Oculomotor palsy


Oculomotor palsy occurs due to damage of the oculomotor nerve. This is the third of twelve paired cranial nerves. It controls most of the eye movements (cranial nerves IV and VI also do some), constriction of the pupil, and holding the eyelid open.

These video clips illustrate the effects of damage to the oculomotor nerve or 3rd cranial nerve.

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Incomplete oculomotor palsy with pupil sparing caused by compression of the oculomotor nerve by a posterior communicating posterior cerebral aneurysm.

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Incomplete oculomotor palsy with pupil sparing caused by compression of the oculomotor nerve by a posterior communicating posterior cerebral aneurysm.

Jpn J Ophthalmol. 2007 Nov-Dec;51(6):470-3

Authors: Takahashi M, Kase M, Suzuki Y, Yokoi M, Kazumata K, Terasaka S

PURPOSE: To report a patient with agenesis of both internal carotid canals who presented with incomplete oculomotor palsy with pupil sparing. METHODS: The incomplete oculomotor palsy was followed clinically, and the precise anatomical relation of the aneurysm to the subarachnoid oculomotor nerve was investigated during clipping surgery for the aneurysm. RESULTS: A 39-year-old woman with agenesis of both internal carotid arteries was admitted because of diplopia and left blepharoptosis. The left superior palpebral and the superior rectus muscles were severely palsied. The paralysis of the medial rectus muscle was milder than that of the former two muscles, and the inferior rectus was the least affected muscle. The papillary reflexes were normal. Examination during clipping surgery showed that the aneurysm was located below the oculomotor nerve in the subarachnoid space about 6.5 mm from its exit from the midbrain. The differences in severity and resolution time of the palsies of the extraocular muscles suggested that the fibers destined for the superior levator and the superior rectus were concentrated on the caudomedial portion of the subarachnoid oculomotor nerve. The fibers innervating the medial rectus muscle were located within the core of the nerve, and the fibers innervating the pupils and the inferior rectus muscle occupied a more rostral part. CONCLUSIONS: The functional distribution of fibers within the subarachnoid oculomotor nerve about 6.5 mm from its exit from the midbrain succeeds to that of the intraparenchymal oculomotor nerve.

PMID:- oculomotor palsy 18158600 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • Evolution of neurological, neuropsychological and sleep-wake disturbances after paramedian thalamic stroke.
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    Evolution of neurological, neuropsychological and sleep-wake disturbances after paramedian thalamic stroke.

    Stroke. 2008 Jan;39(1):62-8

    Authors: Hermann DM, Siccoli M, Brugger P, Wachter K, Mathis J, Achermann P, Bassetti CL

    BACKGROUND AND PURPOSE: The clinical features and natural course of paramedian thalamic stroke is poorly known. The aim of this study was to characterize the evolution of neurological, neuropsychological, and sleep-wake deficits after paramedian thalamic stroke. METHODS: Forty-six consecutive patients, aged 48.4+/-16.6 years, were studied. Fourteen had bilateral, 16 left-sided, and 16 right-sided lesions. Assessment included neurological examinations, estimation of sleep needs, formal neuropsychological tests (n=27), and polysomnographies (n=31). Functional outcome was followed up over 1 year in 31 patients with the modified Rankin Scale and Barthel index. RESULTS: Oculomotor palsy (76% of patients), mild gait ataxia (67%), deficits of attention (63%), fluency and error control (59%), learning and memory (67%), and behavior (67%) were common in the acute stroke phase. Outcome was excellent with right-sided infarcts but mostly incomplete with bilateral and left-sided lesions. This was mainly related to persistent frontal lobe-related and cognitive deficits found in 100% bilateral and 90% left-sided, but only 33% right-sided strokes. Initially, hypersomnia was present in all patients associated with increased stage 1 sleep, reduced stage 2 sleep, and reduced sleep spindles. Sleep needs improved in patients with bilateral and almost disappeared with unilateral lesions after 1 year. Sleep architecture remained abnormal with the exception of sleep spindles that increased. CONCLUSIONS: Whereas neurological deficits and hypersomnia recover to large extent in patients with paramedian thalamic stroke, the frontal lobe-related and cognitive deficits, which are mainly linked with bilateral and left-sided lesions, often persist. As such, stroke outcome is better in right-sided than bilateral or left-sided infarcts.

    PMID:- oculomotor palsy 18048862 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • Aberrant regeneration of the oculomotor nerve: implications for neurosurgeons.
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    Aberrant regeneration of the oculomotor nerve: implications for neurosurgeons.

    Neurosurg Focus. 2007;23(5):E14

    Authors: Weber ED, Newman SA

    Aberrant regeneration of cranial nerve III, otherwise known as oculomotor synkinesis, is an uncommon but well-described phenomenon most frequently resulting from trauma, tumors, and aneurysms. Its appearance usually follows an oculomotor palsy, but it can also occur primarily without any preceding nerve dysfunction. It is vital that neurosurgeons recognize this disorder because it may be the only sign of an underlying cavernous tumor or PCoA aneurysm. The tumor most often implicated is a cavernous or parasellar meningioma, but any tumor that causes compression or disruption along the course of the oculomotor nerve may cause primary or secondary misdirection. The most common clinical signs of oculomotor synkinesis consist of elevation of the upper eyelid on attempted downward gaze or adduction, adduction of the eye on attempted upward or downward gaze, and constriction of the pupil on attempted adduction. The authors present the largest series of patients with oculomotor synkinesis, including those in whom it developed after neurosurgical intervention, to illustrate various presentations. In addition, the various mechanisms that contribute to synkinesis are reviewed. Last, the treatment strategies for both oculomotor palsies and synkinesis are discussed.

    PMID:- oculomotor palsy 18004962 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • Kernohan's notch phenomenon in chronic subdural hematoma: MRI findings.
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    Kernohan's notch phenomenon in chronic subdural hematoma: MRI findings.

    J Clin Neurosci. 2007 Oct;14(10):989-92

    Authors: Moon KS, Lee JK, Joo SP, Kim TS, Jung S, Kim JH, Kim SH, Kang SS

    We report two cases of Kernohan's notch phenomenon secondary to chronic subdural hematoma detected by MRI. In the first case, the patient was drowsy with an oculomotor palsy and a hemiparesis ipsilateral to the chronic subdural hematoma. MRI in the post-operative period showed no abnormal signal or deformity of the crus cerebri. The neurological signs immediately resolved after trephination. In the second case, the patient was admitted with progressive decrease in their level of consciousness and ipsilateral hemiparesis with the chronic subdural hematoma. MRI on admission revealed an abnormal signal in the contralateral crus cerebri against the chronic subdural hematoma. After surgery, the mental state gradually recovered to normal with some degree of residual hemiparesis. In patients with chronic subdural hematoma, a compressive deformity of the crus cerebri, without abnormal signal on MRI, may predict a better neurological recovery in patients with Kernohan's notch phenomenon.

    PMID:- oculomotor palsy 17823049 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • Effect of gabapentin on oculomotor control and parkinsonism in patients with progressive supranuclear palsy.
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    Effect of gabapentin on oculomotor control and parkinsonism in patients with progressive supranuclear palsy.

    Eur J Neurol. 2007 Sep;14(9):1060-2

    Authors: Poujois A, Vidailhet M, Trocello JM, Bourdain F, Gaymard B, Rivaud-Péchoux S

    The efficacy of gabapentin on motor, oculomotor and frontal lobe symptoms was evaluated in patients with progressive supranuclear palsy (PSP) in a pilot study. Fourteen patients were included and seven of them received gabapentin. Clinical evaluation and horizontal eye movement recordings were performed at inclusion and 5-weeks later. Motor score and saccade latency in the visually guided saccade (VGS) task were identical in the two groups. However, the error rate in the antisaccade task was significantly decreased in the gabapentin group. This preliminary study shows that gabapentin improves reflexive saccade inhibition in patients with PSP but does not improve the latency of VGSs.

    PMID:- oculomotor palsy 17718702 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • Third nerve palsies.
    Related Articles

    Third nerve palsies.

    Semin Neurol. 2007 Jul;27(3):257-68

    Authors: Bruce BB, Biousse V, Newman NJ

    The diagnosis and management of third nerve dysfunction vary according to the age of the patient, the characteristics of the third nerve palsy, and the presence of associated symptoms and signs. Third nerve palsies can result from lesions located anywhere from the oculomotor nucleus to the termination of the third nerve in the extraocular muscles within the orbit, and may be the herald manifestation of underlying neurological emergencies such as intracranial aneurysm, pituitary apoplexy, and giant cell arteritis. Recent advances in noninvasive neuroimaging facilitate early diagnosis, but the management of a patient presenting with isolated third nerve palsy remains a challenge.

    PMID:- oculomotor palsy 17577867 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • An interesting case of a pituitary adenoma apoplexy mimicking an acute meningitis. Case report.
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    An interesting case of a pituitary adenoma apoplexy mimicking an acute meningitis. Case report.

    J Neurosurg Sci. 2007 Jun;51(2):65-9; discussion 68-9

    Authors: Chibbaro S, Benvenuti L, Carnesecchi S, Faggionato F, Gagliardi R

    Apoplexy of a pituitary adenoma is a rare and under-diagnosed clinical occurrence. It results from either infarction or haemorrhage into an adenoma of the pituitary gland. Its clinical presentation more often includes rapid development of impaired consciousness, severe headache, visual disturbance and variable association of oculomotor nerve palsy. Meningeal irritation signs are considered very rare and usually not reported as presenting symptoms. A 33-year-old male suffered a pituitary macroadenoma apoplexy, clinically indistinguishable from an infectious meningitis at presentation. Three days after surgery, the patient developed a left ophthalmoplegia due to 3(rd) nerve palsy, which fully resolved within 2 months. A right pterional craniotomy was performed during which complete tumour removal was achieved. In conclusion the authors believe that, despite many reports in the literature, encouraging conservative management in pituitary apoplexy by administering intravenous steroids, surgery should be undertaken in order to avoid eventual visual field defects, relieve pituitary gland compression and prevent a possible recurrent apoplectic episode or tumor re-growth.

    PMID:- oculomotor palsy 17571037 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • Oculomotor control in children who were born very prematurely.
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    Oculomotor control in children who were born very prematurely.

    Invest Ophthalmol Vis Sci. 2007 Jun;48(6):2595-601

    Authors: Newsham D, Knox PC, Cooke RW

    PURPOSE: Preterm infants are at increased risk of a variety of cerebral lesions, involving the white matter, cortex, cerebellum, thalamus, and caudate nucleus, many of which could compromise the control of eye movement. Visual problems and disorders of binocularity and alignment have been reported, but little if any quantitative assessment of oculomotor control has been undertaken. The purpose of this study was to extend the initial pilot study and quantitatively examine the control of saccades, smooth pursuit, and antisaccades in children who were born very prematurely. METHODS: A group of preterm (PT) children aged 8 to 11 years (<32 weeks' gestation), who had normal IQ (>or=85) and were free of major disabilities (cerebral palsy, blindness, or deafness), and full-term (FT) control subjects of similar age were recruited from a geographically defined cohort. Antisaccades were examined in 36 preterm and 33 full-term subjects and smooth pursuit and saccades in 21 preterm and 19 full-term subjects, by using infrared oculography. Saccade and antisaccade targets were presented at an amplitude of 5 degrees according to a standard synchronous paradigm, and pursuit was assessed by using a step-ramp paradigm with a target velocity of 14 deg/s. RESULTS: There were no statistically significant differences between the preterm and the full-term subjects in relation to saccade gain, latency, duration, peak velocity, or the proportion of express saccades. Smooth-pursuit latencies tended to be slightly longer in the preterm subjects (leftward: P = 0.17, rightward: P = 0.02), but there were no significant differences between them and the full-term subjects in pursuit acceleration, open-loop velocity, or peak slow-eye velocity. The main area of deficit in the preterm children occurred in the voluntary control of saccades, with significantly higher antisaccade directional error rates (PT: 73.3% +/- 18.1%, FT: 54.2% +/- 16.9%, mean +/- SD; P < 0.001). The latency of the antisaccade error tended to be shorter in preterm subjects (P = 0.065), with a greater proportion of errors with latency in the express range (P = 0.08). CONCLUSIONS: Despite the increased risk of cerebral lesions, the control of saccades and pursuit was largely normal in the preterm children, suggesting that pathways at the level of the brain stem were principally intact. However, the preterm children had difficulties with the voluntary control of saccades, particularly in the area of inhibition, which may be indicative of a deficit in the region of the dorsolateral prefrontal cortex. This finding is consistent with other reports in preterm children in whom executive function has been found to be compromised, and both these aspects of behavior are likely to share similar areas of cortical control.

    PMID:- oculomotor palsy 17525189 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • Is migraine with cranial nerve palsy an ophthalmoplegic migraine?
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    Is migraine with cranial nerve palsy an ophthalmoplegic migraine?

    J Headache Pain. 2007 Apr;8(2):119-22

    Authors: Giraud P, Valade D, Lanteri-Minet M, Donnet A, Geraud G, Guégan-Massardier E,

    Ophthalmoplegic migraine (OM) is a rare form of primary headache. Because of its rarity, only a few cases, mostly symptomatic, are reported. We analyse nine cases among 52 973 adults who suffer from headaches with an oculomotor palsy firstly considered as OM. The study was retrospective and multicentric in a database set up in France. The aim of our investigation was to describe the clinical and radiological aspects of these cases and to discuss the diagnosis of OM. We demonstrate that the characteristics of the headaches were identical to usual migraine without oculomotor nerve palsy for each case. The study emphasises the difficulty of the OM diagnosis even with the new IHS criteria because of the rarity of having all characteristics. A wide heterogeneity was noted in cranial imagery and blood tests. We suggest adding the code of probable OM in the IHS classification to increase the knowledge and detection of this type of headache. A biological blood test and an MRI are systematically required to help clinicians in their diagnosis and to exclude alternative aetiology of headache with palsy.

    PMID:- oculomotor palsy 17497265 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • Reoperation for giant false aneurysm of the thoracic aorta: how to reenter the chest?
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    Reoperation for giant false aneurysm of the thoracic aorta: how to reenter the chest?

    Ann Thorac Surg. 2007 May;83(5):1610-4

    Authors: Bachet J, Pirotte M, Laborde F, Guilmet D

    BACKGROUND: Giant false or pseudoaneurysm of the aorta is a rare but dreadful complication occurring several months or years after cardiac or aortic surgery. We describe a surgical approach that allowed safe reentry in the chest in five patients, with a mean follow-up of almost seven years. METHODS: From December 1991 to October 1999, five patients aged 34 to 74 years (mean age, 55 +/- 11.6 years), who had previously undergone a total of nine operations in other institutions, required reoperation for giant false aneurysm of the ascending aorta in a mean delay of 22.6 +/- 20.3 months (3 months to 6 years) after the last surgical procedure. In order to avoid major mediastinal wound and patient's exsanguination during resternotomy, the following technique has been used: femoral artery cannulation; right atrial cannulation through the femoral vein; femoro-femoral full-flow cardiopulmonary bypass; rectal temperature lowered to 25 degrees C; direct cannulation and cross-clamping of both carotid arteries through a direct cervical approach, and selective cerebral perfusion with cold blood (10 degrees C to 12 degrees C); circulatory arrest of the main circuit; chest opening; and mediastinal division. RESULTS: Despite the fact that the false aneurysm was entered in all patients, reopening of the chest has been safe in all cases. In four cases, the aortic repair consisted of complete graft replacement (Dacron) of the compromised aortic segment (ascending aorta in two; both ascending aorta and aortic arch in two). In one case, reimplantation of the left coronary ostium and closure of a fistula with the left ventricle was carried out. One patient with ongoing mediastinitis died from intractable septicemia and multiorgan failure. Presently, two patients are in excellent condition; one suffers from light neurologic sequelae (oculomotor nerves palsy) and one patient had a nonrelated stroke one year postoperatively. CONCLUSIONS: The technique of separate carotid cannulation and selective antegrade brain perfusion with cold blood during circulatory arrest at moderate core hypothermia has, in our opinion, many advantages. In addition to allowing harmless opening of the chest in the presence of most dangerous mediastinal false aneurysms, it implies no general deep hypothermia, reduced duration of cardiopulmonary bypass, and circulatory arrest of the lower part of the body, and safe and permanent brain protection throughout chest opening and mediastinal division. It has allowed us to safely reoperate on patients who are generally considered as a major surgical risk.

    PMID:- oculomotor palsy 17462366 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • A rare case of brainstem encephalitis by Listeria monocytogenes with isolated mesencephalic localization. Case report and review.
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    A rare case of brainstem encephalitis by Listeria monocytogenes with isolated mesencephalic localization. Case report and review.

    Diagn Microbiol Infect Dis. 2007 May;58(1):121-3

    Authors: Reynaud L, Graf M, Gentile I, Cerini R, Ciampi R, Noce S, Borrelli F, Viola C, Gentile F, Briganti F, Borgia G

    We describe a case of brainstem infection by Listeria monocytogenes with right oculomotor palsy and lip drop, facial hypoesthesia, left arm paresthesia, positive blood culture, and sterile liquor in a 63-year-old man. Magnetic resonance imaging revealed an isolated mesencephalic lesion. Localization of this kind accounted for 3% of 111 cases reviewed.

    PMID:- oculomotor palsy 17408902 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • Occurrence of oculomotor dysfunctions in acquired brain injury: a retrospective analysis.
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    Occurrence of oculomotor dysfunctions in acquired brain injury: a retrospective analysis.

    Optometry. 2007 Apr;78(4):155-61

    Authors: Ciuffreda KJ, Kapoor N, Rutner D, Suchoff IB, Han ME, Craig S

    BACKGROUND: The purpose of this retrospective study was to determine the frequency of occurrence of oculomotor dysfunctions in a sample of ambulatory outpatients who have acquired brain injury (ABI), either traumatic brain injury (TBI) or cerebrovascular accident (CVA), with associated vision symptoms. METHODS: Medical records of 220 individuals with either TBI (n = 160) or CVA (n = 60) were reviewed retrospectively. This was determined by a computer-based query spanning the years 2000 through 2003, for the frequency of occurrence of oculomotor dysfunctions including accommodation, version, vergence, strabismus, and cranial nerve (CN) palsy. RESULTS: The majority of individuals with either TBI (90%) or CVA (86.7%) manifested an oculomotor dysfunction. Accommodative and vergence deficits were most common in the TBI subgroup, whereas strabismus and CN palsy were most common in the CVA subgroup. The frequency of occurrence of versional deficits was similar in each diagnostic subgroup. CONCLUSION: These new findings should alert the clinician to the higher frequency of occurrence of oculomotor dysfunctions in these populations and the associated therapeutic, rehabilitative, and quality-of-life implications.

    PMID:- oculomotor palsy 17400136 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • Abnormalities of the oculomotor nerve in congenital fibrosis of the extraocular muscles and congenital oculomotor palsy.
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    Abnormalities of the oculomotor nerve in congenital fibrosis of the extraocular muscles and congenital oculomotor palsy.

    Invest Ophthalmol Vis Sci. 2007 Apr;48(4):1601-6

    Authors: Lim KH, Engle EC, Demer JL

    PURPOSE: High-resolution magnetic resonance imaging (MRI) can now directly demonstrate innervation to extraocular muscles and quantify optic nerve size. A quantitative MRI technique was developed to study the oculomotor nerve (CN3) and applied to congenital fibrosis of extraocular muscles (CFEOM) and congenital oculomotor palsy. METHODS: The subarachnoid portions of the CN3s were imaged with a 1.5-T MRI scanner and conventional head coils, acquiring heavily T(2)-weighted oblique axial planes 1-mm thick and parallel to the optic chiasm. Thirteen normal subjects, 14 with CFEOM, and 3 with congenital CN3 palsy were included. Digital image analysis was used to measure CN3 diameter, which was correlated with motility findings. RESULTS: In CFEOM, CN3 diameter was bilaterally subnormal in eight subjects, unilaterally subnormal in three subjects, and normal in three subjects. Mean +/- SD CN3 diameter in CFEOM was 1.14 +/- 0.61 mm, significantly smaller than the diameter in normal subjects, which measured 2.01 +/- 0.36 mm (P < 0.001). CN3 diameter variably correlated with clinical function. One subject with congenital CN3 palsy showed bilateral CN3 hypoplasia, but CN3 diameter was normal in two other subjects with congenital CN3 palsy. CONCLUSIONS: Unilateral or bilateral hypoplasia of CN3 is quantitatively demonstrable using MRI in many cases of CFEOM and occasionally in congenital CN3 palsy. Variations in CN3 diameter in CFEOM and congenital CN3 palsy suggest mechanistic heterogeneity of these disorders that may be clarified by further imaging and genetic studies.

    PMID:- oculomotor palsy 17389489 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • Surgery for mesencephalic cavernoma: case report.
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    Surgery for mesencephalic cavernoma: case report.

    Surg Neurol. 2007 Apr;67(4):413-7; discussion 417-8

    Authors: Li ST, Zhong J

    BACKGROUND: Intrinsic midbrain tumor has been one of the most challenging therapeutic tasks in neurosurgery because of its prognosis and risks associated with surgical procedures. We encountered a rare case of cavernoma located in the anterior-mesencephalic region presented as parkinsonism tremor. CASE DESCRIPTION: A 42-year-old woman had a resting tremor for 10 years. This tremor involved the left shoulder and the proximal and distal limb, which was exacerbated by any attempted movement and became grossly uncontrollable. She showed a partial right ophthalmoplegia with mydriasis. Her right upper and lower extremities had normal strength, but her left extremities had three-fifth strength. Her sensation was intact. Magnetic resonance imaging demonstrated a popcorn-like rounded lesion in the right ventral midbrain adjacent to the medial cerebral peduncle. To access this anterior-medial portion of the midbrain, we chose a frontotemporal transsylvian route via an orbitozygomatic craniotomy. With a longitudinal pial incision between the frontopontine fibers and the pyramidal tracts in the peduncle, the cavernoma was totally removed en bloc. After the operation, the tremor dramatically disappeared. The muscle strength of her left lower extremity improved to four fifths, whereas the upper extremity was still the same. The preoperative left oculomotor palsy seemed to have no improvement. CONCLUSIONS: Clinically manifested cavernoma due to repeated hemorrhage needs surgical intervention. With an optimal surgical approach, fairly safe entry zones on the anterior face of the rostral brainstem may be accessible, which provides a successful resection of a mesencephalic cavernoma without postoperative complications.

    PMID:- oculomotor palsy 17350419 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • Outcome of oculomotor nerve palsy from posterior communicating artery aneurysms: comparison of clipping and coiling.
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    Outcome of oculomotor nerve palsy from posterior communicating artery aneurysms: comparison of clipping and coiling.

    Neurosurgery. 2007 Mar;60(3):E582; author reply E582

    Authors: Mansour N, Choudhari KA

    PMID:- oculomotor palsy 17327781 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • Anterior and nasal transposition of the inferior oblique muscles in patients with missing superior oblique tendons.
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    Anterior and nasal transposition of the inferior oblique muscles in patients with missing superior oblique tendons.

    J AAPOS. 2007 Feb;11(1):29-33

    Authors: Hussein MA, Stager DR, Beauchamp GR, Stager DR, Felius J

    INTRODUCTION: Patients with missing superior oblique (SO) tendons present with overelevation/underdepression in adduction. Unilateral cases often exhibit abnormal head postures, whereas in bilateral cases, there may be a marked V-pattern with upgaze exotropia. These patients may have craniosynostosis. METHODS: Nine children with unilateral (n = 2) or bilateral (n = 7) absent SO tendons underwent anterior and nasal transposition of the inferior oblique (IO) muscles, some in combination with horizontal rectus recession for horizontal strabismus. They were evaluated 6 to 46 months postoperatively for alignment and oculomotor examination. Cyclodeviations were not evaluated in most children. RESULTS: Postoperatively, all patients improved. Both unilateral cases were orthotropic with no abnormal head posture. In the bilateral cases, vertical deviation in adduction and exotropia in upgaze had largely cleared, although some symptoms remained, most notably vertical deviation in side gaze (3 patients) and V-pattern esotropia in downgaze (2 patients). A patient missing both SO tendons as well as the left superior rectus muscle, who had the anterior and nasal transposition on the right side only, remained with 25(Delta) left hypotropia. CONCLUSIONS: Anterior and nasal transposition of the IO muscle reduces overelevation in adduction and helps eliminate or reduce divergence of the eyes in upgaze, but esodeviation may persist in downgaze. This procedure was most effective in unilateral absence of the SO tendon. It is likely to benefit patients with severe congenital fourth nerve palsy in which standard IO muscle weakening procedures have been ineffective.

    PMID:- oculomotor palsy 17307680 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • Atypical parkinsonism in Guadeloupe: a common risk factor for two closely related phenotypes?
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    Atypical parkinsonism in Guadeloupe: a common risk factor for two closely related phenotypes?

    Brain. 2007 Mar;130(Pt 3):816-27

    Authors: Lannuzel A, Höglinger GU, Verhaeghe S, Gire L, Belson S, Escobar-Khondiker M, Poullain P, Oertel WH, Hirsch EC, Dubois B, Ruberg M

    In Guadeloupe, there is an abnormally high frequency of atypical parkinsonism. Only one-third of the patients that develop parkinsonian symptoms were reported to present the classical features of idiopathic Parkinson disease and one-third a syndrome resembling progressive supranuclear palsy (PSP). The others were unclassifiable, according to established criteria. We carried out a cross-sectional study of 160 parkinsonian patients to: (i) define more precisely the clinical phenotypes of the PSP-like syndrome and the parkinsonism that was considered unclassifiable in comparison with previously known disorders; (ii) define the neuropsychological and brain imaging features of these patients; (iii) evaluate to what extent a candidate aetiological factor, the mitochondrial complex I inhibitor annonacin contained in the fruit and leaves of the tropical plant Annona muricata (soursop) plays a role in the neurological syndrome. Neuropsychological tests and MRI were used to classify the patients into those with Parkinson's disease (31%), Guadeloupean PSP-like syndrome (32%), Guadeloupean parkinsonism-dementia complex (PDC, 31%) and other parkinsonism-related disorders (6%). Patients with a PSP-like syndrome developed levodopa-resistant parkinsonism, associated with early postural instability and supranuclear oculomotor dysfunction. They differed, however, from classical PSP patients by the frequency of tremor (>50%), dysautonomia (50%) and the occurrence of hallucinations (59%). PDC patients had levodopa-resistant parkinsonism associated with frontosubcortical dementia, 52% of these patients had hallucinations, but, importantly, none had oculomotor dysfunction. The pattern of neuropsychological deficits was similar in both subgroups. Cerebral atrophy was seen in the majority of the PSP-like and PDC patients, with enlargement of the third ventricle and marked T2-hypointensity in the basal ganglia, particularly the substantia nigra. Consumption of soursop was significantly greater in both PSP-like and PDC patients than in controls and Parkinson's disease patients. In conclusion, atypical Guadeloupean parkinsonism comprises two forms of parkinsonism and dementia that differ clinically by the presence of oculomotor signs, but have similar cognitive profiles and neuroimaging features, suggesting that they may constitute a single disease entity, and both were similarly exposed to annonaceous neurotoxins, notably annonacin.

    PMID:- oculomotor palsy 17303592 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • Ruptured anterior communicating artery aneurysm causing bilateral oculomotor nerve palsy: a case report.
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    Ruptured anterior communicating artery aneurysm causing bilateral oculomotor nerve palsy: a case report.

    J Korean Med Sci. 2007 Feb;22(1):173-6

    Authors: Kang SD

    A rare case of bilateral third cranial nerve palsy due to a ruptured anterior communicating artery aneurysm is presented. A 68-yr-old woman was semicomatose with bilaterally fixed dilated pupil, abducted eyes, and ptosis. A computed tomography demonstrated extensive hemorrhage spreading around the both Sylvian and interhemisheric fissure without focal mass effect. Intracranial pressure via extraventricular drainage before surgery was 15-50 mmHg. Three months later, brain MRI showed infarction of left posterior cerebral artery territory and lacuna infarction of the pons. Eleven months after aneurysm repair, nerve palsy improved slowly and recovered partially. The patient communicated well with simple words. The author reviewed and discussed the possible mechanism of this rare neuro-ophthalmological manifestation in view of a false localizing sign.

    PMID:- oculomotor palsy 17297277 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • Magnetic resonance imaging segmentation techniques using batch-type learning vector quantization algorithms.
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    Magnetic resonance imaging segmentation techniques using batch-type learning vector quantization algorithms.

    Magn Reson Imaging. 2007 Feb;25(2):265-77

    Authors: Yang MS, Lin KC, Liu HC, Lirng JF

    In this article, we propose batch-type learning vector quantization (LVQ) segmentation techniques for the magnetic resonance (MR) images. Magnetic resonance imaging (MRI) segmentation is an important technique to differentiate abnormal and normal tissues in MR image data. The proposed LVQ segmentation techniques are compared with the generalized Kohonen's competitive learning (GKCL) methods, which were proposed by Lin et al. [Magn Reson Imaging 21 (2003) 863-870]. Three MRI data sets of real cases are used in this article. The first case is from a 2-year-old girl who was diagnosed with retinoblastoma in her left eye. The second case is from a 55-year-old woman who developed complete left side oculomotor palsy immediately after a motor vehicle accident. The third case is from an 84-year-old man who was diagnosed with Alzheimer disease (AD). Our comparisons are based on sensitivity of algorithm parameters, the quality of MRI segmentation with the contrast-to-noise ratio and the accuracy of the region of interest tissue. Overall, the segmentation results from batch-type LVQ algorithms present good accuracy and quality of the segmentation images, and also flexibility of algorithm parameters in all the comparison consequences. The results support that the proposed batch-type LVQ algorithms are better than the previous GKCL algorithms. Specifically, the proposed fuzzy-soft LVQ algorithm works well in segmenting AD MRI data set to accurately measure the hippocampus volume in AD MR images.

    PMID:- oculomotor palsy 17275624 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • Protein S deficiency manifesting simultaneously as central retinal artery occlusion, oculomotor nerve palsy, and systemic arterial occlusive diseases.
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    Protein S deficiency manifesting simultaneously as central retinal artery occlusion, oculomotor nerve palsy, and systemic arterial occlusive diseases.

    Eye. 2007 May;21(5):684-6

    Authors: Loh BK, Lee SY, Goh KY

    PMID:- oculomotor palsy 17259919 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • Outcome of oculomotor nerve palsy from posterior communicating artery aneurysms: comparison of clipping and coiling.
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    Outcome of oculomotor nerve palsy from posterior communicating artery aneurysms: comparison of clipping and coiling.

    Neurosurgery. 2007 Jan;60(1):E208; author reply E208

    Authors: Stiebel-Kalish H, Rappaport HZ

    PMID:- oculomotor palsy 17228235 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • Oculomotor nerve schwannoma located in the oculomotor cistern.
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    Oculomotor nerve schwannoma located in the oculomotor cistern.

    Surg Neurol. 2007 Jan;67(1):83-8; discussion 88

    Authors: Tanriover N, Kemerdere R, Kafadar AM, Muhammedrezai S, Akar Z

    BACKGROUND: OSs are extremely rare tumors, most often located in the interpeduncular cistern or the CS. We report an OS located predominantly within the oculomotor cistern, the arachnoid sac that surrounds the nerve for a short distance in the roof of the CS. We discuss a possible growth pattern for cavernous OSs. CASE DESCRIPTION: We report the case of a 34-year-old woman presenting with a right oculomotor nerve palsy. Magnetic resonance imaging revealed a mass within the borders of the roof of the CS extending forward toward the superior orbital fissure. A right pterional approach was undertaken, and the roof of the CS was opened just above the oculomotor nerve toward the superior orbital fissure. Although the part of the OS inside the oculomotor cistern was excised completely while preserving the anatomical continuity of the nerve, a subtotal removal was performed for the more anterior part of the tumor toward the superior orbital fissure. At 5 months follow-up, her third nerve paresis had improved dramatically. CONCLUSIONS: Resection of cavernous OSs within the oculomotor cistern, where the third nerve is clearly separated from the adjacent neurovascular structures, is feasible with functional preservation of the nerve. The chance of occurrence of the nerve palsy may increase as the resection proceeds more anteriorly toward the superior orbital fissure.

    PMID:- oculomotor palsy 17210311 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • High-resolution magnetic resonance imaging of the extraocular muscles and nerves demonstrates various etiologies of third nerve palsy.
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    High-resolution magnetic resonance imaging of the extraocular muscles and nerves demonstrates various etiologies of third nerve palsy.

    Am J Ophthalmol. 2007 Feb;143(2):280-287

    Authors: Kau HC, Tsai CC, Ortube MC, Demer JL

    PURPOSE: The etiology of third nerve palsy is usually diagnosed by history, motility examination, and presence of lid and pupil involvement, as well as cranial and vascular imaging. We used high-resolution magnetic resonance imaging (hrMRI) of the oculomotor nerve and affected extraocular muscles (EOMs) to investigate oculomotor palsy. DESIGN: Prospective, noncomparative, observational case series in an academic referral setting. METHODS: Twelve patients with nonaneurysmal oculomotor palsy of 0.75 to 252 months' duration were studied. In the orbit and along the intracranial oculomotor nerve, hrMRI at 1- to 2-mm thickness was performed. Coronal plane images of each orbit were obtained in multiple, controlled gaze positions. Structural abnormalities of the oculomotor nerve and associated changes in EOM volume and contractility were evaluated. RESULTS: Cases were categorized as tumor related, congenital, diabetic, traumatic, and idiopathic according to clinical characteristics and hrMRI findings. Reduction of volume and contractility of affected EOMs were noted in six patients; however, there was no marked EOMs atrophy in two cases of diabetic oculomotor palsy, and there were four cases of aberrant regeneration. hrMRI demonstrated the oculomotor nerve at the midbrain and at EOMs in all cases, and in two cases with previous normal neuroimaging elsewhere that demonstrated contrast-enhancing tumors on the oculomotor nerve. One patient with apparently unilateral congenital inferior division oculomotor palsy had no detectable ipsilateral and a hypoplastic contralateral oculomotor nerve exiting the midbrain. CONCLUSIONS: hrMRI provides valuable information in patients with oculomotor palsy, such as structural abnormalities of the orbit and oculomotor nerve, and atrophy and diminished contractility of innervated EOMs. This information could be helpful in diagnosis and management of oculomotor palsy.

    PMID:- oculomotor palsy 17173848 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • Early-onset ophthalmoplegia in Leigh-like syndrome due to NDUFV1 mutations.
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    Early-onset ophthalmoplegia in Leigh-like syndrome due to NDUFV1 mutations.

    Pediatr Neurol. 2007 Jan;36(1):54-7

    Authors: Laugel V, This-Bernd V, Cormier-Daire V, Speeg-Schatz C, de Saint-Martin A, Fischbach M

    Mitochondrial disorders can be linked to mutations in both mitochondrial and nuclear deoxyribonucleic acid, corresponding to various clinical phenotypes. Mutations in nuclear genes, including NDUFV1, have been associated with severe encephalomyopathies in infants, but genotype-phenotype correlations have remained elusive. This report details the complete clinical, biochemical, and molecular data of a 7-year-old male who presented at the age of 7 months with progressive ophthalmoplegia and later developed cerebellar ataxia, spasticity, and dystonia. Complex I deficiency was demonstrated in muscle, and two pathogenic missense mutations were present in the NDUFV1 gene. Ketogenic diet has seemingly improved the oculomotor palsy but has been unable to correct other neurologic symptoms. Considering other cases from the literature, this report broadens our understanding of genotype-phenotype correlations for NDUFV1 mutations and illustrates a potential and partial efficacy of ketogenic diet in complex I deficient patients.

    PMID:- oculomotor palsy 17162199 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • Joubert syndrome surviving to adulthood associated with a progressive movement disorder.
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    Joubert syndrome surviving to adulthood associated with a progressive movement disorder.

    Mov Disord. 2007 Jan 15;22(2):262-5

    Authors: Gunzler SA, Stoessl AJ, Egan RA, Weleber RG, Wang P, Nutt JG

    A 48-year-old man presented with a progressive gait disorder. He had longstanding ataxia, oculomotor apraxia, motor delay, and cognitive impairment, diagnosed as cerebral palsy. Physical examination revealed ataxia, oculomotor apraxia, extrapyramidal signs, and a wide-based, shuffling gait. Magnetic resonance imaging showed vermian aplasia, consistent with Joubert syndrome. Positron emission tomography scan revealed normal fluorodopa uptake, but elevated raclopride binding, compatible with dopamine deficiency. This case demonstrates that a patient with Joubert syndrome may survive into adulthood and present as a chronic neurologic disorder with subacute extrapyramidal signs.

    PMID:- oculomotor palsy 17149728 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • Guillain-Barré syndrome.
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    Guillain-Barré syndrome.

    Optometry. 2006 Nov;77(11):540-6

    Authors: Gurwood AS, Drake J

    Guillain-Barré syndrome (GBS) is an acute, demyelinating polyneuropathy involving the spinal roots, peripheral nerves, and often the cranial nerves. Although its exact mechanism remains unclear, an autoimmune etiopathology is theorized. It is characterized by rapidly progressing, symmetrical muscular weakness starting in the legs and ascending to the trunk and arms. Additionally, deep tendon reflexes are lost. Approximately half of the patients with GBS have cranial nerve palsies, with unilateral or bilateral facial nerve (CN VII) palsy being the most common. Paralysis of the muscles of the tongue, lips, palate, larynx, and pharynx from lesions involving cranial nerves IX, X, and XI and weakness of the muscles of mastication (CN V) are the next most common cranial nerve abnormalities. Ocular muscle palsy is not common, only occurring in approximately 10% of patients. The Miller Fisher variant of GBS is a distinct syndrome in which the only neurologic deficits are oculomotor palsies, areflexia, and ataxia. We present the rare case of a 45-year-old woman with GBS whose ocular muscles were affected. The oculomotor disturbance and limb weakness occurred within a few days of one another. Basic anatomic considerations are reviewed along with the pathophysiology and clinical features of GBS.

    PMID:- oculomotor palsy 17145565 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • Dystonia in Parkinson's disease.
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    Dystonia in Parkinson's disease.

    J Neurol. 2006 Dec;253 Suppl 7:VII7-13

    Authors: Tolosa E, Compta Y

    Dystonia can occasionally be found in idiopathic Parkinson's disease. It is very uncommon in untreated patients and is more frequently seen as a complication of its treatment. In this review, the various types of dystonia occurring in PD, the differential diagnosis with other parkinsonian syndromes associated with dystonia and treatments available are revised. Dystonia unrelated to treatment can be typical (blepharospasm, torticollis), atypical (parkinsonian writer's cramp, camptocormia, anismus), or occurring in earlyonset Parkinson disease (the so-called kinesigenic foot dystonia, considered a hallmark of early-onset Parkinson's disease). Early and prominent dystonia in untreated patients with parkinsonism should raise the suspicion of other entities other than Parkinson's disease, such as progressive supranuclear palsy, multiple system atrophy or corticobasal degeneration. In patients on chronic dopaminergic treatment, peak-dose dystonia, diphasic dystonia and off-dystonia can be seen. The later constitutes the major dystonic feature of chronic levodopa therapy, and a wide variety of strategies are available to manage this complication. Among them, deep brain stimulation of the subthalamic nucleus has proved to be the most effective one. Dystonic reactions (mainly involving oculomotor cranial nerves and limbs) in operated patients (especially carriers of deep brain stimulation (DBS) devices) are increasingly being reported, constituting a new type of dystonia in patients with Parkinson's disease: dystonia linked to surgical treatment.

    PMID:- oculomotor palsy 17131231 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • Isolated nuclear oculomotor nerve palsy due to a solitary midbrain metastasis: a rare presentation.
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    Isolated nuclear oculomotor nerve palsy due to a solitary midbrain metastasis: a rare presentation.

    Indian J Ophthalmol. 2006 Dec;54(4):286-7

    Authors: Modi M, Singla V, Bhatia R, Reddi R

    PMID:- oculomotor palsy 17090891 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • Hepatocellular carcinoma metastasizing to the skull base involving multiple cranial nerves.
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    Hepatocellular carcinoma metastasizing to the skull base involving multiple cranial nerves.

    World J Gastroenterol. 2006 Nov 7;12(41):6727-9

    Authors: Kim SR, Kanda F, Kobessho H, Sugimoto K, Matsuoka T, Kudo M, Hayashi Y

    We describe a rare case of HCV-related recurrent multiple hepatocellular carcinoma (HCC) metastasizing to the skull base involving multiple cranial nerves in a 50-year-old woman. The patient presented with symptoms of ptosis, fixation of the right eyeball, and left abducens palsy, indicating disturbances of the right oculomotor and trochlear nerves and bilateral abducens nerves. Brain contrast-enhanced computed tomography (CT) revealed an ill-defined mass with abnormal enhancement around the sella turcica. Brain magnetic resonance imaging (MRI) disclosed that the mass involved the clivus, cavernous sinus, and petrous apex. On contrast-enhanced MRI with gadolinium-chelated contrast medium, the mass showed inhomogeneous intermediate enhancement. The diagnosis of metastatic HCC to the skull base was made on the basis of neurological findings and imaging studies including CT and MRI, without histological examinations. Further studies may provide insights into various methods for diagnosing HCC metastasizing to the craniospinal area.

    PMID:- oculomotor palsy 17075993 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • Myasthenic ptosis with synkinetic override in a child with congenital oculomotor nerve palsy.
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    Myasthenic ptosis with synkinetic override in a child with congenital oculomotor nerve palsy.

    J AAPOS. 2006 Oct;10(5):484-5

    Authors: Brodsky MC

    PMID:- oculomotor palsy 17070490 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • Magnetic resonance imaging demonstrates neuropathology in congenital inferior division oculomotor palsy.
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    Magnetic resonance imaging demonstrates neuropathology in congenital inferior division oculomotor palsy.

    J AAPOS. 2006 Oct;10(5):473-5

    Authors: Wu TE, Isenberg SJ, Demer JL

    PMID:- oculomotor palsy 17070486 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • Corticotroph tumor progression after adrenalectomy in Cushing's Disease: A reappraisal of Nelson's Syndrome.
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    Corticotroph tumor progression after adrenalectomy in Cushing's Disease: A reappraisal of Nelson's Syndrome.

    J Clin Endocrinol Metab. 2007 Jan;92(1):172-9

    Authors: Assié G, Bahurel H, Coste J, Silvera S, Kujas M, Dugué MA, Karray F, Dousset B, Bertherat J, Legmann P, Bertagna X

    CONTEXT: Adrenalectomy is a radical treatment for hypercortisolism in Cushing's disease. However, it may lead to Nelson's syndrome, originally defined by the association of a pituitary macroadenoma and high plasma ACTH concentrations, a much feared complication. OBJECTIVE: The objective of the study was to reconsider Nelson's syndrome by investigating corticotroph tumor progression based on pituitary magnetic resonance imaging scan and search for predictive factors. DESIGN: This was a retrospective cohort study. SETTING: The complete medical records of Cushing's disease patients at Cochin Hospital were studied. PATIENTS: Patients included 53 Cushing's disease patients treated by adrenalectomy between 1991 and 2002, without previous pituitary irradiation. MEASUREMENTS: Clinical data, pituitary magnetic resonance imaging data, and plasma ACTH concentrations for all patients and pituitary gland pathology data for 25 patients were recorded. Corticotroph tumor progression-free survival was studied by Kaplan-Meier, and the influence of recorded parameters was studied by Cox regression. INTERVENTION: There was no intervention. RESULTS: Corticotroph tumor progression ultimately occurred in half the patients, generally within 3 yr after adrenalectomy. A shorter duration of Cushing's disease (adjusted hazard ratio: 0.884/yr), and a high plasma ACTH concentration in the year after adrenalectomy [adjusted hazard ratio per 100 pg/ml (22 pmol/liter): 1.069] were predictive of corticotroph tumor progression. In one case, corticotroph tumor progression was complicated by transitory oculomotor nerve palsy. During follow-up, corticotroph tumor progression was associated with the increase of corresponding ACTH concentrations (odds ratio per 100 pg/ml of ACTH variation: 1.055). CONCLUSION: After adrenalectomy in Cushing's disease, one should no longer wait for the occurrence of Nelson's syndrome: modern imaging allows early detection and management of corticotroph tumor progression.

    PMID:- oculomotor palsy 17062771 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • Primary germinoma arising from the midbrain.
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    Primary germinoma arising from the midbrain.

    Acta Neurochir (Wien). 2006 Nov;148(11):1197-200; discussion 1200

    Authors: Koizumi H, Oka H, Utsuki S, Sato S, Tanizaki Y, Shimizu S, Suzuki S, Iizuka T, Sakai F, Fujii K

    A 29-year-old man presented with diplopia, dysarthria, anisocoria, oculomotor nerve paralysis, abducens nerve paralysis, right facial palsy, and spastic hemiparetic gait. Magnetic resonance imaging (MRI) showed a homogenously enhanced mass in the midbrain. MRI-guided stereotactic biopsy was performed, and the histologic diagnosis was pure germinoma. The tumor disappeared after chemotherapy and radiotherapy. Germinoma should be included in the differential diagnosis of midbrain lesions in young adults. MRI-guided stereotactic biopsy provided a helpful diagnostic clue in a patient with a midbrain lesion.

    PMID:- oculomotor palsy 17039305 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • Isolated ocular motor nerve palsy in dural carotid-cavernous sinus fistula.
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    Isolated ocular motor nerve palsy in dural carotid-cavernous sinus fistula.

    Eur J Neurol. 2006 Nov;13(11):1221-5

    Authors: Wu HC, Ro LS, Chen CJ, Chen ST, Lee TH, Chen YC, Chen CM

    The incidence of dural carotid-cavernous sinus fistula (DCCF) presenting as isolated ocular motor nerve palsies without congestive ocular features is unknown. We reviewed the DCCF patients in our hospital during the last 10 years to elucidate the clinical and neuroradiological features of DCCF with isolated ocular motor nerve palsy. Eleven amongst the 33 DCCF patients presented isolated ocular motor nerve palsy. All the 11 patients underwent brain CT/CT angiography (CTA) and/or MRI/MR angiography (MRA), before the digital subtraction angiography (DSA). The compromised nerves were the oculomotor nerve in eight (72.7%), abducens nerve in two (18.2%) and trochlear nerve in one (9.1%). Brain CT and/or CTA were conducted in four patients but all unremarkable. MRI and/or MRA were performed in nine patients and six of them showed compatible findings of DCCF. The diagnoses of DCCFs were confirmed by DSA and all were posterior-draining type. The outcome was good, with a total recovery rate of 54.5% within 12 months. Thirty-three percent (11 of 33) of our DCCF patients presented with isolated ocular motor nerve palsy, which is not uncommon. MRI and MRA are of value in the initial evaluation, but DSA is necessary for the accurate diagnosis and treatment planning.

    PMID:- oculomotor palsy 17038036 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • Isolated oculomotor nerve palsy as the presenting clinical manifestation of a meningeal carcinomatosis: a case report.
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    Isolated oculomotor nerve palsy as the presenting clinical manifestation of a meningeal carcinomatosis: a case report.

    Neurol Sci. 2006 Sep;27(4):288-90

    Authors: Nardone R, Herz M, Egarter-Vigl E, Tezzon F

    We present a previously unreported case of isolated oculomotor nerve palsy as the inaugural clinical sign of meningeal carcinomatosis (MC). Gadolinium-enhanced magnetic resonance images (MRI) were unremarkable. Cerebrospinal fluid (CSF) analysis showed malignant cells consistent with a pulmonary adenocarcinoma; the chest CT revealed a small pulmonary mass in the upper right lobe. This case highlights the importance of considering MC in all patients who develop sudden oculomotor palsy; lumbar punctures should always be performed on patients with normal MRI when other possible causes of oculomotor palsy have been ruled out.

    PMID:- oculomotor palsy 16998736 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • Traumatic oculomotor nerve palsy.
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    Traumatic oculomotor nerve palsy.

    J Clin Neurosci. 2006 Oct;13(8):852-5

    Authors: Kaido T, Tanaka Y, Kanemoto Y, Katsuragi Y, Okura H

    Traumatic isolated oculomotor nerve palsy is not common. Oculomotor nerve palsy without internal ophthalmoplegia (pupil sparing) is extremely rare. We report a case of this condition in a child. An 11-year-old boy was transferred to our hospital after a head injury in a traffic accident. Neuro-ophthalmic examination showed that the left eye had limited adduction, supraduction, and infraduction, incomplete convergence and left ptosis, but no internal ophthalmoplegia. Magnetic resonance imaging indicated mild bending of the ipsilateral oculomotor nerve at the posterior petroclinoid ligament. One month after injury, movement of the patient's eyes was normal on examination, but there was mild diplopia. The suggested mechanism of the oculomotor nerve palsy with pupil sparing in this case is stretching of the oculomotor nerve at the posterior petroclinoid ligament, maintaining an intact pupillomotor nerve.

    PMID:- oculomotor palsy 16978866 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • Abducens-oculomotor synkinesis associated with internuclear ophthalmoplegia and acquired abducens nerve palsy.
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    Abducens-oculomotor synkinesis associated with internuclear ophthalmoplegia and acquired abducens nerve palsy.

    J Pediatr Ophthalmol Strabismus. 2006 Jul-Aug;43(4):246-9

    Authors: Wutthiphan S, Foster SR, Poonyathalang A, Pongpech S

    We report a case of acquired abducens-oculomotor synkinesis, internuclear ophthalmoplegia, and abducens nerve palsy following brainstem hemorrhage. Weakening surgery on the medial rectus muscle did not eliminate the synergistic movement. The mechanism responsible for the abducens-oculomotor synkinesis is discussed.

    PMID:- oculomotor palsy 16915907 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • Intrasellar cavernous hemangioma.
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    Intrasellar cavernous hemangioma.

    J Clin Neurosci. 2006 Jul;13(6):672-5

    Authors: Chuang CC, Jung SM, Yang JT, Chang CN, Pai PC

    Reports of intrasellar cavernous hemangioma are rare. They are usually incidental findings at autopsy, or initially mistaken for pituitary adenoma and treated accordingly. There are no specific symptoms. Cranial nerve palsy has occasionally been reported in patients with cavernous hemangioma, with or without sellar extension. However, intrasellar cavernous hemangioma with extension into the cavernous sinus resulting in oculomotor palsy has not been reported. We present a rare case of intrasellar cavernous hemangioma and discuss the diagnosis and management. Total surgical removal is recommended. However, attempts to resect the parasellar component of the lesion may be associated with high morbidity. Therefore, surgical cranial nerve decompression in the acute stage followed by stereotactic radiosurgery for the residual lesion may be an alternative.

    PMID:- oculomotor palsy 16815022 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • Clinical features of double infection with tick-borne encephalitis and Lyme borreliosis transmitted by tick bite.
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    Clinical features of double infection with tick-borne encephalitis and Lyme borreliosis transmitted by tick bite.

    J Neurol Neurosurg Psychiatry. 2006 Dec;77(12):1350-3

    Authors: Logina I, Krumina A, Karelis G, Elsone L, Viksna L, Rozentale B, Donaghy M

    BACKGROUND: In Latvia and other endemic regions, a single tick bite has the potential to transmit both tick-borne encephalitis (TBE) and Lyme borreliosis. OBJECTIVE: To analyse both the clinical features and differential diagnosis of combined tick-borne infection with TBE and Lyme borreliosis, in 51 patients with serological evidence, of whom 69% had tick bites. RESULTS: Biphasic fever suggestive of TBE occurred in 55% of the patients. Meningitis occurred in 92%, with painful radicular symptoms in 39%. Muscle weakness occurred in 41%; in 29% the flaccid paralysis was compatible with TBE. Only two patients presented with the bulbar palsy typical of TBE. Typical Lyme borreliosis facial palsy occurred in three patients. Typical TBE oculomotor disturbances occurred in two. Other features typical of Lyme borreliosis detected in our patients were distal peripheral neuropathy (n = 4), arthralgia (n = 9), local erythema 1-12 days after tick bite (n = 7) and erythema chronicum migrans (n = 1). Echocardiogram abnormalities occurred in 15. CONCLUSIONS: Patients with double infection with TBE and Lyme borreliosis fell into three main clinical groups: febrile illness, 3 (6%); meningitis, 15 (30%); central or peripheral neurological deficit (meningoencephalitis, meningomyelitis, meningoradiculitis and polyradiculoneuritis), 33 (65%). Systemic features pointing to Lyme borreliosis were found in 25 patients (49%); immunoglobulin (Ig)M antibodies to borreliosis were present in 18 of them. The clinical occurrence of both Lyme borreliosis and TBE vary after exposure to tick bite, and the neurological manifestations of each disorder vary widely, with considerable overlap. This observational study provides no evidence that co-infection produces unusual manifestations due to unpredicted interaction between the two diseases. Patients with tick exposure presenting with acute neurological symptoms in areas endemic for both Lyme borreliosis and TBE should be investigated for both conditions. The threshold for simultaneous treatment of both conditions should be low, given the possibility of co-occurrence and the difficulty in ascribing individual neurological manifestations to one condition or the other.

    PMID:- oculomotor palsy 16754695 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • Superior divisional oculomotor nerve palsy caused by midbrain neurocysticercosis.
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    Superior divisional oculomotor nerve palsy caused by midbrain neurocysticercosis.

    Parasitol Int. 2006 Sep;55(3):223-5

    Authors: Chotmongkol V, Sawanyawisuth K, Limpawattana P, Phuphatham A, Chotmongkol R, Intapan PM

    Superior divisional oculomotor nerve palsy caused by intrinsic brainstem disease occurs rarely. We herein report, to our knowledge, the first case of midbrain neurocysticercosis presenting as isolated superior divisional paresis of the oculomotor nerve. A 25-year-old woman presented with acute onset of headache and ptosis-upgaze palsy of the right eye. Results of the CT scan and MRI of the brain were compatible with neurocysticercosis at the left midbrain. She was dramatically responded to albendazole treatment. The diagnosis was confirmed by positive enzyme-linked immunosorbent assay (ELISA) test for cysticercus in her serum.

    PMID:- oculomotor palsy 16737842 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • Cervico-oculo-Acoustic syndrome in a male with consanguineous parents.
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    Cervico-oculo-Acoustic syndrome in a male with consanguineous parents.

    Can J Neurol Sci. 2006 May;33(2):237-9

    Authors: Di Maio L, Marcelli V, Vitale C, Menzione M, De Giorgio A, Briganti F, Perretti A, Marciano E, Filla A, De Michele G

    BACKGROUND: The cervico-oculo-acoustic syndrome comprises Klippel-Feil anomaly, sensorineural deafness and Duane's retraction syndrome. Polygenic, autosomal dominant, and X-linked inheritance have been hypothesized. The disorder has rarely been reported in males. CASE REPORT: A 42-year-old male, born of consanguineous parents, presented with Duane's syndrome, mixed hearing loss, C2-C3 fusion, neck stiffness, and right facial palsy. A variety of cardiac, neurological and urogenital anomalies occurred in his relatives. The electro-oculographic studies showed impaired abduction and adduction of the right eye and impaired abduction of the left eye. Vergence, vertical eye movements and peripheral vestibular responses were normal. Somatosensory evoked potentials showed absence of the N13 peak and brainstem auditory evoked potentials bilateral delay of the I-III interpeak latencies. CONCLUSIONS: Consanguinity of the patient's parents, not previously reported, suggests autosomal recessive inheritance, but autosomal dominant inheritance is indicated by the family history. The pattern of the oculomotor deficit is consistent with bilateral dysplasia of the abducens nuclei with preserved internuclear neurons in the right abducens nucleus. Neurophysiological investigations revealed lower brainstem and cervical cord involvement.

    PMID:- oculomotor palsy 16736738 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • Outcome of oculomotor nerve palsy from posterior communicating artery aneurysms: comparison of clipping and coiling.

    Outcome of oculomotor nerve palsy from posterior communicating artery aneurysms: comparison of clipping and coiling.

    Neurosurgery. 2006 Jun;58(6):1040-6; discussion 1040-6

    Authors: Chen PR, Amin-Hanjani S, Albuquerque FC, McDougall C, Zabramski JM, Spetzler RF

    OBJECTIVE: Recovery of posterior communicating artery aneurysm-induced oculomotor nerve palsy (ONP) after aneurysm coiling has been reported. However, the coil mass may compromise recovery of the nerve. Therefore, we compared the outcome of coiling and clipping for this indication. METHODS: We retrospectively compared the outcomes of ONP in 13 patients, six of whom underwent endovascular coiling and seven of whom underwent surgical clipping. RESULTS: Six of the seven surgical patients with ONP recovered completely, compared with two of the six patients in the endovascular group. Of the patients with more than 1 year of follow-up, all six surgical patients recovered completely, compared with two of four endovascular patients (P = 0.05). In addition, preoperative complete or partial ONP also was associated with degree of resolution by survival analysis (P = 0.03). All patients with partial ONP in the surgical group and two of three patients in the endovascular group recovered without residual deficits, whereas three of the four patients with complete ONP in the clipping group and none in the coiling group recovered completely. Regardless of the treatment method, time to complete resolution of ONP was 6 months in both groups. CONCLUSION: Clipping posterior communicating artery aneurysms was associated with a higher probability of complete recovery from ONP than coiling. Degree of preoperative ONP also affected recovery. If patients can tolerate surgery, it should be considered the treatment of choice.

    PMID:- oculomotor palsy 16723882 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • High-resolution magnetic resonance imaging demonstrates abnormalities of motor nerves and extraocular muscles in patients with neuropathic strabismus.
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    High-resolution magnetic resonance imaging demonstrates abnormalities of motor nerves and extraocular muscles in patients with neuropathic strabismus.

    J AAPOS. 2006 Apr;10(2):135-42

    Authors: Demer JL, Ortube MC, Engle EC, Thacker N

    INTRODUCTION: Although the ocular motility examination has been used traditionally in the diagnosis of strabismus that is a result of cranial nerve (CN) abnormalities, magnetic resonance imaging (MRI) now permits the direct imaging of lesions in CN palsies. METHODS: Prospectively, nerves to extraocular muscles (EOMs) were imaged with T1 weighting in orbits of 83 orthotropic volunteers and 96 strabismic patients in quasicoronal planes using surface coils. Intraorbital resolution was 234-312 microns within 1.5- to 2.0-mm thick planes. CNs were imaged at the brainstem using head coils and T2 weighting, yielding 195 micron resolution in planes 1.0-mm thick in 6 normal volunteers and 22 patients who had oculomotor (CN3), trochlear (CN4), or abducens (CN6) palsies and Duane syndrome. RESULTS: Oculomotor (CN3) and abducens (CN6) but not trochlear (CN4) nerves were demonstrable in the orbit and skull base in all normal subjects. Patients with congenital CN3 palsies had hypoplastic CN3s both in orbit and skull base, with hypoplasia of involved EOMs. Patients with chronic CN6 and CN4 palsies exhibited atrophy of involved EOMs. Patients with Duane syndrome exhibited absence or hypoplasia of CN6 in both orbit and brainstem regions, often with mild hypoplasia and apparent misdirection of CN3 to the lateral rectus muscle. Unlike CN6 palsy, patients with Duane syndrome exhibited no EOM hypoplasia. Patients with congenital fibrosis exhibited severe hypoplasia of CN3, moderate hypoplasia of CN6, and EOM hypoplasia, particularly severe for the superior rectus and levator muscles. CONCLUSION: High-resolution MRI can directly demonstrate pathology of CN3 and CN6 and affected EOM atrophy in strabismus caused by CN palsies. Direct imaging of CNs and EOMs by MRI is feasible and useful in differential diagnosis of complex strabismus.

    PMID:- oculomotor palsy 16678748 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • Endodermal cyst of the oculomotor nerve: case report.
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    Endodermal cyst of the oculomotor nerve: case report.

    Neurosurgery. 2006 May;58(5):E994; discussion E994

    Authors: Okunaga T, Tsutsumi K, Hayashi T, Nagata I

    OBJECTIVE: Endodermal cysts are commonly found in the anterior spinal cord. Reports of intracranial cases are uncommon. We report a case of endodermal cyst located on the left oculomotor nerve. CLINICAL PRESENTATION: A 16-year-old female experienced diplopia followed by headache. Neurological examinations revealed left oculomotor nerve palsy. Magnetic resonance imaging scans showed a well-defined multilocular cystic mass in the proximity of the left oculomotor nerve at its exit from the midbrain. INTERVENTION: This patient underwent biopsy and drainage of the cyst. At surgery, the cyst seemed to be intrinsic to the oculomotor nerve and could not be totally resected. Pathological examination confirmed the diagnosis of endodermal cyst. CONCLUSION: Intracranial endodermal cysts are rare, particularly when associated with the cranial nerves. To our knowledge, this is the second case of endodermal cyst located on the oculomotor nerve. A detailed discussion and review of these case reports are presented.

    PMID:- oculomotor palsy 16639308 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • Visuospatial functions in atypical parkinsonian syndromes.
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    Visuospatial functions in atypical parkinsonian syndromes.

    J Neurol Neurosurg Psychiatry. 2006 Apr;77(4):454-6

    Authors: Bak TH, Caine D, Hearn VC, Hodges JR

    OBJECTIVES: Visuospatial deficits have been occasionally reported but never systematically studied in atypical parkinsonian syndromes. The interpretation of existing studies is complicated by the possible influence of motor and frontal executive deficits. Moreover, no attempt has been made to distinguish visuoperceptual from visuospatial tasks. The aim of the present study was to assess visuoperceptual and visuospatial abilities in three atypical parkinsonian syndromes while minimising the influence of confounding variables. METHODS: Twenty patients with multiple system atrophy (MSA), 43 with progressive supranuclear palsy (PSP), and 25 with corticobasal degeneration (CBD) as well as 30 healthy age matched controls were examined with the Visual Object and Space Perception Battery (VOSP). RESULTS: Visuospatial functions were intact in MSA patients. PSP patients showed mild deficits related to general cognitive decline and the severity of oculomotor symptoms. The CBD group showed the most pronounced deficits, with spatial tasks more impaired than object based tasks. Performance on object based, but not spatial, tasks was related to general cognitive status. The extent of the visuospatial impairment could not be predicted from disease duration or severity. CONCLUSION: Visuospatial functions are not consistently impaired in atypical parkinsonian syndromes. The degree and pattern of impairment varies across the diseases, suggesting that the observed deficits could have a different neural basis in each condition. The distinction between the object based ("ventral stream") and the space oriented ("dorsal stream") processing might be useful in the interpretation of visuospatial deficits in parkinsonian syndromes, especially in CBD.

    PMID:- oculomotor palsy 16543521 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • Oculomotor nerve palsy evaluated by diffusion-tensor tractography.
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    Oculomotor nerve palsy evaluated by diffusion-tensor tractography.

    Neuroradiology. 2006 Jun;48(6):434-7

    Authors: Yamada K, Shiga K, Kizu O, Ito H, Akiyama K, Nakagawa M, Nishimura T

    INTRODUCTION: The aim of the study was to test the feasibility of the tractography technique based on diffusion-tensor imaging (DTI) for the assessment of small infarcts involving the brainstem. METHODS: A patient who presented with an isolated left third cranial nerve palsy underwent magnetic resonance examination. Images were obtained by use of a whole-body, 1.5-T imager. Data were transferred to an off-line workstation for fiber tracking. RESULTS: The conventional diffusion-weighted imaging (DWI) performed using a 5 mm slice thickness could only depict an equivocal hyperintensity lesion located at the left paramedian midbrain. An additional thin-slice DTI was performed immediately after the initial DWI using a 3 mm slice thickness and was able to delineate the lesion more clearly. Image postprocessing of thin-slice DTI data revealed that the lesion location involved the course of the third cranial nerve tract, corresponding with the patient's clinical symptoms. CONCLUSION: The tractography technique can be applied to assess fine neuronal structures of the brainstem, enabling direct clinicoradiological correlation of small infarcts involving this region.

    PMID:- oculomotor palsy 16538477 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • An unusual presentation of a pituitary tumour in the early postpartum period.
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    An unusual presentation of a pituitary tumour in the early postpartum period.

    Anaesth Intensive Care. 2006 Feb;34(1):79-82

    Authors: Paech MJ

    The case of a parturient, who first presented with a partial oculomotor nerve palsy shortly after caesarean delivery while participating in a clinical trial, is presented. The anaesthesia for the caesarean delivery involved a combined spinal-epidural with intrathecal bupivacaine and postoperative epidural pethidine patient-controlled analgesia. The trial was examining the possible effects of magnesium infusions on acute and chronic pain. The partial oculomotor nerve palsy was an unusual presentation and the signs and symptoms were transient. Magnetic resonance imaging confirmed the presence of a presumed pituitary macroadenoma. Possible reasons for the timing of onset and the rapid resolution of symptoms, and the implications and management of pituitary pathology in the peripartum period, are considered. The uncomplicated course of a later caesarean delivery in the same patient, using the same anaesthesia technique, is also noted.

    PMID:- oculomotor palsy 16494155 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • Ophthalmic zoster sine herpete presenting as oculomotor palsy after marrow transplantation for acute myeloid leukemia.
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    Ophthalmic zoster sine herpete presenting as oculomotor palsy after marrow transplantation for acute myeloid leukemia.

    Haematologica. 2005 Dec;90(12 Suppl):EIM04

    Authors: Hon C, Au WY, Cheng VC

    PMID:- oculomotor palsy 16464763 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • Phaeohyphomycosis: an unusual pituitary mass.
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    Phaeohyphomycosis: an unusual pituitary mass.

    Br J Neurosurg. 2005 Oct;19(5):442-5

    Authors: Yeung IY, Whitelaw BC, Hortobágyi T, Bódi I, Petrou MA, Connor SE, Thomas NW

    A 64-year-old Caucasian woman presented with left eye pain and a transient left oculomotor nerve palsy. Subsequent imaging revealed a mass involving the sphenoid sinus and sella with suprasellar extension. A trans-sphenoidal hypophysectomy was performed. Histopathology showed a fungal infection consistent with phaeohyphomycosis. Development of this lesion is probably attributed to allergic rhinitis and insulin-dependent diabetes mellitus. Intravenous amphotericin and itraconazole treatment resulted in full recovery and the patient remains well at 6-month postoperative follow-up.

    PMID:- oculomotor palsy 16455570 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • Oculomotor nerve schwannoma mimicking ophthalmoplegic migraine.
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    Oculomotor nerve schwannoma mimicking ophthalmoplegic migraine.

    Neuropediatrics. 2005 Dec;36(6):395-8

    Authors: Murakami T, Funatsuka M, Komine M, Hirayama Y, Suzuki H, Shishikura K, Aihara Y, Shibata K, Hori T, Kobayashi M, Osawa M

    Ophthalmoplegic migraine (OM) is a rare variant of migraine characterized by recurrent attacks of severe headache followed by oculomotor nerve palsy. The recent revision of the International Headache Classification has reclassified OM from a subtype of migraine, defined as a functional headache, to the neuralgia category. We describe a case of an 11-year-old girl with pathologically confirmed oculomotor nerve schwannoma who had been suffering from symptoms mimicking OM. For five years, she has been under treatment for OM, an initial diagnosis which was corroborated by brain magnetic resonance imaging (MRI). Usually, most OM attacks occur during one period in a lifetime and remit completely. In contrast, however, her attacks became more frequent and were not controlled by medication. After surgery, the frequency of OM attacks was reduced. From this experience, we hypothesize that optic nerve tumor is one condition that can mimic OM, without apparent signs suggestive of intracranial mass. To our knowledge, this is the first report to describe a pathologically confirmed case of oculomotor nerve schwannoma mimicking OM.

    PMID:- oculomotor palsy 16429381 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • Oculomotor nerve palsy in childhood.
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    Oculomotor nerve palsy in childhood.

    Can J Ophthalmol. 2005 Oct;40(5):645-53

    Authors: Ng YS, Lyons CJ

    BACKGROUND: The management of children with oculomotor nerve palsy is complicated by their variable presentation, amblyopia, potential loss of binocularity, and associated neurological disease. Our purpose was to evaluate the causes, neurological associations, treatment, and sensorimotor outcomes of a group of children who developed oculomotor nerve palsy. METHODS: We identified 18 children aged 14 years or younger, of whom 13 (72%) were less than 8 years old, through a retrospective record review of all children with oculomotor nerve palsy seen between January 1995 and January 2001 by one of the authors (C.J.L.). RESULTS: Congenital-onset oculomotor nerve palsy was the most frequent presentation, followed by traumatic, neoplastic, vascular, and migrainous or para-infectious etiologies. Pupil sparing was seen in 1 patient with neoplastic etiology. Primary aberrant regeneration was the presenting sign in a child with neurofibromatosis type 2. Amblyopia developed in 7 (39%) children and was successfully treated in 5 of the 7 (71%). Stereopsis was maintained in 6 (33%) children of whom 2 were within the amblyogenic age group. Six (33%) patients underwent strabismus surgery, and 3 of them (50%) achieved orthotropia and maintained stereopsis. INTERPRETATION: Children with oculomotor nerve palsy require neuroimaging. Their pupillary signs, unlike those of adults, are not helpful in differentiating compressive etiologies from other causes. Good visual acuity was obtained in children within the amblyogenic age group with appropriate occlusion therapy. Stereopsis was uncommon in children who developed third nerve palsy during the amblyogenic period; preservation of stereopsis was dependent either on rapid and complete recovery, or on the child's adoption of a compensatory head position.

    PMID:- oculomotor palsy 16391633 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • Pseudotumor cerebri with transient oculomotor palsy.
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    Pseudotumor cerebri with transient oculomotor palsy.

    Indian J Pediatr. 2005 Dec;72(12):1047-8

    Authors: Chansoria M, Agrawal A, Ganghoriya P, Raghu Raman B

    Pseudotumor cerebri is a clinical syndrome characterized by raised intracranial pressure with normal ventricular size, anatomy and position. Headache, vomiting and diplopia are the most common symptoms. Signs include those of raised intracranial pressure including papilledema and absence of focal neurological signs. A secondary cause is identifiable in 50% of children; the most common predisposing conditions are otitis media, viral infection and medications. Management is mainly directed towards identifying and treating the cause and measures to reduce the raised intracranial pressure. Though it is mostly a self limited condition, optic atrophy and blindness can occur. Oculomotor nerve palsy is very rarely associated with pseudotumor cerebri. We report a unique case of pseudotumor cerebri who had left Oculomotor palsy with sparing of the pupillary fibres, which resolved following treatment with oral acetazolamide.

    PMID:- oculomotor palsy 16388155 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • Concomitant ectatic posterior communicating artery and tentorial meningioma as a source of oculomotor palsy: case report.
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    Concomitant ectatic posterior communicating artery and tentorial meningioma as a source of oculomotor palsy: case report.

    Neurosurgery. 2005 Dec;57(6):E1316; discussion E1316

    Authors: Babbitz JD, Harsh GR

    OBJECTIVE AND IMPORTANCE: Although non-aneurysmal vascular compression of the oculomotor nerve is rare, it should be considered in the evaluation of unilateral oculomotor palsy. CLINICAL PRESENTATION: A 36-year-old non-diabetic man presented with two months of intermittent retro-orbital headache and third nerve paresis caused by compression of the oculomotor nerve between an ectatic, atherosclerotic posterior communicating artery (PComA) and a small tentorial meningioma. At operation, the subarachnoid portion of the nerve, prevented from migrating posteriorly and laterally by the meningioma, was grooved by the apex of the artery's loop. INTERVENTION: Microvascular decompression (MVD) of the artery loop from the nerve and resection of the meningioma were performed. Postoperatively, the patient's retro-orbital headache and oculomotor paresis, with the exception of mild anisocoria, resolved. Tumor infiltrating the posterior tentorium and lateral cavernous sinus was treated by Cyberknife radiosurgery five months later. One year after surgery, the patient had improvement in his headaches, full extra-ocular movements, and minimal residual anisocoria. CONCLUSION: Only one other report describes MVD of the third nerve from PComA compression. A review is presented of MVD carried out for similar cases of non-aneurysmal vascular compression of the oculomotor nerve. By analogy from cases in which an aneurysm is the compressing vascular structure, prompt surgical treatment is advocated. Complete evaluation of an isolated third nerve palsy should include MRI sequences designed to detect vascular compression of cranial nerves.

    PMID:- oculomotor palsy 16331147 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • Posttraumatic pneumocephalus-induced bilateral oculomotor nerve palsy.
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    Posttraumatic pneumocephalus-induced bilateral oculomotor nerve palsy.

    Clin Neurol Neurosurg. 2005 Dec;108(1):84-6

    Authors: Aygun D, Doganay Z, Baydin A, Akyol M, Senel A, Nural MS, Otal Y, Guven H

    Bilateral third nerve palsy often points to the involvement of its nucleus. Third nerve palsy as a result of posttraumatic nuclear involvement is an extremely rare condition. A 23-year-old man presented with a depressed skull fracture after acute head trauma and had Glasgow Coma Scale Score of 9. The diameters of the pupils were 6.5 and 7.5 mm and they were not reactive to light stimulation. There was bilateral ptosis. Computed tomography (CT) relieved bilateral perimesensephalic pneumocephalus. We suggested that bilateral oculomotor nerve paresis might develop in association with posttraumatic bilateral perimesensephalic pneumocephalus, which affected the nucleus of the third nerve.

    PMID:- oculomotor palsy 16311155 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • Bilateral third nerve palsy and temporal arteritis.
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    Bilateral third nerve palsy and temporal arteritis.

    Arch Neurol. 2005 Nov;62(11):1766-8

    Authors: Lazaridis C, Torabi A, Cannon S

    BACKGROUND: Bilateral oculomotor palsy is a rare manifestation of temporal arteritis, and to our knowledge only 1 case has been described in the literature. OBJECTIVE: To investigate a possible case of temporal arteritis in a patient with bilateral third nerve palsy. DESIGN: Case report and review. SETTING: University hospital. PATIENT: A 65-year-old man had subacute pupil-sparing bilateral third nerve palsy. RESULTS: Temporal artery biopsy findings and response to corticosteroids are consistent with temporal arteritis. CONCLUSION: Temporal arteritis is a rare cause of ophthalmoplegia in elderly persons and may be unrecognized.

    PMID:- oculomotor palsy 16286553 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • Bilateral chronic subdural hematoma cases showing rapid and progressive aggravation.
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    Bilateral chronic subdural hematoma cases showing rapid and progressive aggravation.

    Surg Neurol. 2005 Nov;64(5):444-9; discussion 449

    Authors: Kurokawa Y, Ishizaki E, Inaba K

    BACKGROUND: We have analyzed the records of our own hospitalized cases of bilateral chronic subdural hematoma (cSDH) to reveal the prognosis. METHODS: Ninety-eight cases of cSDH were operated at our hospital over a 6-year period, in which 14 cases were classified as being bilateral. Among these 14 cases, 6 cases showed a rapid and aggressive clinical course. Therefore, complicated risk factors, the initial data on coagulofibrinolytic examination, magnetic resonance imaging appearance, and prognosis were analyzed. RESULTS: Of the 6 cases, 5 showed a rapid aggravation as they awaited surgery. The period of the aggravation since the initial diagnosis harboring cSDH was 19 to 54 hours. One case was at first neurologically free from any disturbance but 17 hours later experienced a generalized seizure. All 6 cases experienced consciousness disturbance. In addition, 3 of them manifested oculomotor palsy. Two cases showed an abnormality of coagulofibrinolytic activity. No significant risk factors were revealed. In 4 cases, T(2)-weighted images (T2WIs) revealed the hematoma of a mixed high and low intensity, indicating that the hematoma consisted of both liquid and solid parts of a freshly formed blood clot. In 2 cases, the hematoma showed a low intensity in T(1)-weighted image (T1WI), indicating a recent bleeding of a significant amount. CONCLUSION: The bilateral cases of cSDH should be treated as early as possible with simultaneous decompression of bilateral hematoma pressure, even if the patient shows minimal neurologic deficits. Mixed high and low intensity in T2WI or low intensity in T1WI is the most predictable factor to show rapid aggravation.

    PMID:- oculomotor palsy 16253697 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • Primary central nervous system lymphoma of the brain stem responding favorably to radiosurgery: a case report and literature review.
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    Primary central nervous system lymphoma of the brain stem responding favorably to radiosurgery: a case report and literature review.

    Surg Neurol. 2005 Nov;64(5):400-5; discussion 405

    Authors: Campbell PG, Jawahar A, Fowler MR, Delaune A, Nanda A

    OBJECTIVE: To explore various therapeutic alternatives and evaluate the clinical results of patients with primary central nervous system lymphoma (PCNSL). We report a case of PCNSL with involvement of the brain stem managed with radiosurgery using the Leksell gamma knife as the treatment modality. CASE DESCRIPTION: A 55-year-old white woman presented with complaints of weakness on the left side of her body and double vision associated with a frontal headache. Nervous system examination revealed right-sided oculomotor palsy and left-sided motor paresis, grade 2/5, in both upper and lower limbs. Her Karnofsky performance score was 50. A contrast-enhanced magnetic resonance imaging scan of the brain revealed an irregular space-occupying lesion in the pons that enhanced uniformly with gadolinium. A frame-based stereotactic biopsy was performed revealing a B-cell malignant lymphoma. Subsequently, stereotactic radiosurgery using the Leksell gamma knife was performed. A dose of 11 Gy was delivered to the tumor margin. A follow-up magnetic resonance imaging scan after 2 months revealed a 50% reduction in the size of the enhancing lesion. CONCLUSION: Our own results and limited evidence from the literature suggest stereotactic radiosurgery as a potentially safe and effective treatment option in patients with PCNSL.

    PMID:- oculomotor palsy 16253683 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • Clinical and pathologic evidence of corticobasal degeneration and progressive supranuclear palsy in familial tauopathy.
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    Clinical and pathologic evidence of corticobasal degeneration and progressive supranuclear palsy in familial tauopathy.

    Arch Neurol. 2005 Sep;62(9):1453-7

    Authors: Tuite PJ, Clark HB, Bergeron C, Bower M, St George-Hyslop P, Mateva V, Anderson J, Knopman DS

    BACKGROUND: Corticobasal degeneration (CBD) and progressive supranuclear palsy (PSP) are neurodegenerative tauopathies. Sporadic and familial cases of PSP and CBD have been noted, but both have not been reported in a single family. OBJECTIVE: To describe the clinical, oculomotor, balance, functional imaging, histopathologic, and genetic studies in a family with CBD and PSP. DESIGN: A report of the clinical and pathological features in a familial tauopathy. SETTING: University of Minnesota.Patients We evaluated 2 siblings and clinically assessed 20 additional family members. MAIN OUTCOME MEASURES: Demonstration of salient features in deceased and living family members. RESULTS: Histopathologically confirmed CBD in one sibling and PSP in another deceased sibling were demonstrated; both had clinical features of corticobasal syndrome. In addition, 3 siblings had probable PSP by clinical criteria. Genetic studies of 4 affected family members demonstrated the H1/H1 haplotype but did not reveal pathogenic tau mutations. The family history revealed consanguinity. CONCLUSIONS: This is the first report, to our knowledge, of CBD and PSP in 2 individuals in a single family who presented with corticobasal syndrome and had other affected siblings with clinical PSP. Despite clinical and pathologic heterogeneity, a unifying genetic etiology appears likely in this familial tauopathy.

    PMID:- oculomotor palsy 16157754 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • Intrinsic hematoma of the oculomotor nerve: case report and review of the literature.
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    Intrinsic hematoma of the oculomotor nerve: case report and review of the literature.

    Neurosurgery. 2005 Aug;57(2):E370; discussion E370

    Authors: Ratilal BO, Galo SM, Luiz CA

    OBJECTIVE AND IMPORTANCE: Intrinsic oculomotor nerve hematoma is an exceptional cause of third nerve palsy. This case report illustrates the clinical, radiological, and intraoperative relevance of this rare pathological finding. CLINICAL PRESENTATION: A 25-year-old woman with a 12-year history of gross total resection of cerebellar medulloblastoma and posterior whole-brain radiotherapy presented with complete left oculomotor palsy. Magnetic resonance imaging revealed a left-sided, perimesencephalic cistern, small, round lesion with a fluid level. Digital subtraction angiography demonstrated no evidence of vascular abnormalities. INTERVENTION: A pterional craniotomy was performed, and the left oculomotor nerve was exposed. A blackish intrinsic lesion was detected in its cisternal segment near the uncus. The lesion was incised, and liquid compatible with a subacute noncoagulated hematoma was drained. Three months after surgery, the patient had partial recovery from diplopia and extraocular muscle function. CONCLUSION: We reviewed the literature and found four cases of oculomotor nerve intrinsic hematoma. These cases were all associated with hematological diseases, trauma, or solid tumors, and, as a group, these patients had poor outcomes. In the present report, the possibility of radiotherapy-induced vasculopathy as a predisposing factor is discussed. Surgical removal of an intrinsic nerve hematoma is probably helpful in the functional recovery of these patients.

    PMID:- oculomotor palsy 16094140 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • Isolated oculomotor nerve palsy from minor head trauma.
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    Isolated oculomotor nerve palsy from minor head trauma.

    Br J Sports Med. 2005 Aug;39(8):e34

    Authors: Chen CC, Pai YM, Wang RF, Wang TL, Chong CF

    Isolated third cranial nerve palsies in head trauma patients can be the result of direct or indirect damage to the oculomotor nerve. They are usually associated with severe head trauma. We reported a case of isolated oculomotor nerve palsy associated with minor head injury. No initial loss of consciousness was recalled. Computed tomography (CT), magnetic resonance imaging (MRI), and magnetic resonance angiography (MRA) of the brain were normal. Previous reports in the literature were reviewed and the possible mechanism of injury was discussed. Head injuries are commonly seen in sports settings. Our case illustrated that even minor head trauma can cause isolated oculomotor nerve palsy in the absence of abnormal brain imaging findings.

    PMID:- oculomotor palsy 16046322 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • Unilateral oculomotor nerve palsy induced by combination therapy of interferon-alpha2b and ribavirin.
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    Unilateral oculomotor nerve palsy induced by combination therapy of interferon-alpha2b and ribavirin.

    Intern Med. 2005 Jun;44(6):682-3

    Authors: Nakamura A, Tojo K, Takasu K, Kaneko K, Komastu H, Ikeda S

    PMID:- oculomotor palsy 16020909 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • Isolated oculomotor nerve palsy in Churg-Strauss syndrome.
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    Isolated oculomotor nerve palsy in Churg-Strauss syndrome.

    Intern Med. 2005 Jun;44(6):638-40

    Authors: Tsuda H, Ishikawa H, Majima T, Sawada U, Mizutani T

    A 30-year-old man with bronchial asthma complained of horizontal diplopia. Partial oculomotor nerve palsy with restrictions of elevation and adduction, and mydriasis was observed in the left eye. Cranial magnetic resonance imaging demonstrated an infarct lesion in the territory of the left superior median mesencephalic branch of the posterior cerebral artery. Based on bronchial asthma, hypereosinophilia, mononeuropathy multiplex, pulmonary eosinophilia and positive perinuclear antineutrophil cytoplasmic antibody in the serum, the patient was diagnosed as having Churg-Strauss syndrome. This is the first case of oculomotor nerve palsy due to midbrain infarction associated with Churg-Strauss syndrome.

    PMID:- oculomotor palsy 16020896 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • Delayed oculomotor nerve palsy after bilateral cervical zoster in an immunocompetent patient.
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    Delayed oculomotor nerve palsy after bilateral cervical zoster in an immunocompetent patient.

    Neurology. 2005 Jul 12;65(1):170

    Authors: Karmon Y, Gadoth N

    PMID:- oculomotor palsy 16009918 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • Isolated oculomotor palsy following minor head trauma.
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    Isolated oculomotor palsy following minor head trauma.

    Neurology. 2005 Jul 12;65(1):169

    Authors: Levy RL, Geist CE, Miller NR

    PMID:- oculomotor palsy 16009916 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • MRA or CTA, that's the question.
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    MRA or CTA, that's the question.

    Surv Ophthalmol. 2005 Jul-Aug;50(4):406-10

    Authors: Vaphiades MS, Horton JA

    A 26-year-old woman developed a painful left pupil-involving oculomotor palsy. Magnetic resonance imaging of the brain and orbits with and without fat suppression and gadolinium and magnetic resonance angiography of the head were normal. A computed tomographic angiogram showed a left 7-mm posterior communicating artery aneurysm. The different neuroimaging modalities used to diagnose intracranial aneurysms are discussed.

    PMID:- oculomotor palsy 15967194 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • Incarceration of the inferior oblique muscle branch of the oculomotor nerve in two cases of orbital floor trapdoor fracture.
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    Incarceration of the inferior oblique muscle branch of the oculomotor nerve in two cases of orbital floor trapdoor fracture.

    Jpn J Ophthalmol. 2005 May-Jun;49(3):246-52

    Authors: Kakizaki H, Zako M, Iwaki M, Mito H, Katori N

    BACKGROUND: Incarceration of the inferior oblique muscle (IO) branch of the oculomotor nerve may occur in cases of orbital floor trapdoor fracture. CASES: Two orbital floor trapdoor fracture cases, with lesions located just outside of the inferior rectus muscle but without its incarceration, were examined pre- and postoperatively for visual acuity, intraocular details, the nine diagnostic ocular positions of gaze, binocular single vision field with the Hess chart, and by computed tomography (CT). One case was also examined by magnetic resonance imaging (MRI; T1-weighted images). A forced duction test was conducted intraoperatively. OBSERVATIONS: Each case presented good visual acuity and neither globe showed any injury. Motility disturbance of the IO was shown in each case by binocular single vision field testing and the Hess chart. The possibility of the incarceration of the IO branch of the oculomotor nerve, which runs from the incarcerated lesion to the superior belly of the IO, in an orbital floor trapdoor fracture was shown on CT and MRI. Intraoperative forced duction testing revealed a restriction due to the incarceration of the connective tissue septa. CONCLUSIONS: As inferred from the CT and MRI analyses conducted in this study, IO palsy may be one of the causes of ocular motility disturbance of the IO in an orbital floor trapdoor fracture, in addition to the ocular motility disturbance due to the connective tissue septa.

    PMID:- oculomotor palsy 15944833 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • Apraxia in movement disorders.
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    Apraxia in movement disorders.

    Brain. 2005 Jul;128(Pt 7):1480-97

    Authors: Zadikoff C, Lang AE

    The definition of apraxia specifies that the disturbance of performed skilled movements cannot be explained by the more elemental motor disorders typical of patients with movement disorders. Generally this does not present a significant diagnostic problem when dealing with 'higher-level' praxic disturbances (e.g. ideational apraxia), but it can be a major confound in establishing the presence of limb-kinetic apraxia. Most motor disturbances characteristic of extrapyramidal disorders, particularly bradykinesia and dystonia, will compromise the ability to establish the presence of loss of dexterity and deftness that constitutes this subtype. The term 'apraxia' has also been applied to other motor disturbances, such as 'gait apraxia' and 'apraxia of eyelid opening', that perhaps are misnomers, demonstrating the lack of a coherent nomenclature in this field. Apraxia is a hallmark of corticobasal degeneration (CBD) and historically this has received the most attention among the movement disorders. Corticobasal degeneration is characterized by various forms of apraxia affecting limb function, particularly ideomotor apraxia and limb-kinetic apraxia, although buccofacial and oculomotor apraxia can be present as well. The syndrome of parkinsonism and prominent apraxia, designated the 'corticobasal syndrome' (CBS), may be caused by a variety of other central nervous system pathologies including progressive supranuclear palsy (PSP), Alzheimer's disease, dementia with Lewy bodies and frontotemporal dementias. Distinct from the CBS, PSP and Parkinson's disease can demonstrate varying degrees of apraxia on selected tests, especially in those patients with more severe cognitive dysfunction. Diseases that cause the combination of apraxia and a primary movement disorder most often involve a variety of cerebral cortical sites as well as basal ganglia structures. Clinical-pathological correlates and functional imaging studies are compromised by both this diffuse involvement and the confusion experienced in the clinical evaluation of apraxia in the face of the additional elemental movement disorders. Finally, although apraxia results in clear disability in patients with the CBS, it is not clear how milder ideomotor apraxia found on specific testing contributes to patients' overall day-to-day motor disability.

    PMID:- oculomotor palsy 15930045 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • Weber's syndrome and sixth nerve palsy secondary to decompression illness: a case report.
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    Weber's syndrome and sixth nerve palsy secondary to decompression illness: a case report.

    Undersea Hyperb Med. 2005 Mar-Apr;32(2):95-101

    Authors: Padilla W, Newton HB, Barbosa S

    We describe the first case of Weber's Syndrome to present as a manifestation of decompression illness in a recreational scuba diver. Weber's Syndrome is characterized by the presence of an oculomotor nerve palsy and contralateral hemiparesis. The patient was a 55 year-old male with a past medical history of a pulmonary cyst, in whom symptoms developed after a multilevel drift dive to a depth of 89 feet for 53 minutes, exceeding no-decompression limits. Symptom onset was within 30 minutes of surfacing and included the Weber's Syndrome, a sixth nerve palsy, dizziness, nausea, sensory loss, and ataxia. The patient received four U.S. Navy Treatment Tables with complete resolution of all neurological signs and symptoms. The mechanism of injury remains unclear, but may involve aspects of both air gas embolism and decompression sickness. Individuals with pre-existing pulmonary cysts may be at increased risk for dive-related complications.

    PMID:- oculomotor palsy 15926301 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • Involvement of the cranial nerves and their nuclei in spinocerebellar ataxia type 2 (SCA2).
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    Involvement of the cranial nerves and their nuclei in spinocerebellar ataxia type 2 (SCA2).

    Acta Neuropathol. 2005 Jun;109(6):617-31

    Authors: Gierga K, Bürk K, Bauer M, Orozco Diaz G, Auburger G, Schultz C, Vuksic M, Schöls L, de Vos RA, Braak H, Deller T, Rüb U

    Although the cranial nerves, their nuclei and related fiber tracts are crucial for a variety of oculomotor, somatomotor, somatosensory, auditory, vestibular-related, autonomic and ingestion-related functions, knowledge regarding the extent of their involvement in spinocerebellar ataxia type 2 (SCA2) patients is incomplete. Accordingly, we performed a pathoanatomical analysis of these structures in six clinically diagnosed SCA2 patients. Unconventionally thick serial sections through the brainstem stained for lipofuscin pigment (aldehyde-fuchsin) and Nissl material (Darrow red) showed that all oculomotor, somatomotor, somatosensory, auditory, vestibular and autonomic cranial nerve nuclei may undergo neurodegeneration during SCA2. Similarly, examination of myelin-stained thick serial sections revealed that nearly all cranial nerves and associated fiber tracts may sustain atrophy and myelin loss in SCA2 patients. In view of the known functional role of the affected cranial nerves, their nuclei and associated fiber tracts, the present findings provide appropriate pathoanatomical explanations for some of the disease-related and unexplained symptoms seen in SCA2 patients: double vision, gaze palsy, slowing of saccades, ptosis, ingestion-related malfunctions, impairments of the optokinetic nystagmus and the vestibulo-ocular reaction, facial and tongue fasciculation-like movements, impaired centripetal transmission of temperature-related information from the face, dystonic posture of the neck, as well as abnormalities of the brainstem auditory evoked potentials.

    PMID:- oculomotor palsy 15906049 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • Embolic stroke with a patent foramen ovale and Behcet's disease.
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    Embolic stroke with a patent foramen ovale and Behcet's disease.

    Intern Med. 2005 Apr;44(4):326-7

    Authors: Ishida C, Furui E, Sakashita Y, Yamada M

    We report a case of a 53-year-old man with Behcet's disease (BD) and paradoxical stroke. This patient suddenly developed sensory aphasia, right oculomotor palsy, nystagmus, and left ataxic hemiparesis. MR images showed fresh embolic infarcts in the midbrain and the left parietotemporal lobe. He presented with uveitis, oral aphthous ulcers and genital ulcers. An electrocardiogram revealed no abnormalities, and a transesophageal echocardiogram disclosed a patent foramen ovale. Since venous involvement is common in BD, we suspected the presence of smaller thrombi probable in this patient. We conclude that embolic stroke is a notable complication of BD with right-to-left shunting.

    PMID:- oculomotor palsy 15897645 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • Y-configured dual intracranial stent-assisted coil embolization for the treatment of wide-necked basilar tip aneurysms.
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    Y-configured dual intracranial stent-assisted coil embolization for the treatment of wide-necked basilar tip aneurysms.

    Neurosurgery. 2005 May;56(5):1035-40; discussion 1035-40

    Authors: Thorell WE, Chow MM, Woo HH, Masaryk TJ, Rasmussen PA

    OBJECTIVE: Despite advances in both the surgical and endovascular treatment of intracranial aneurysms, wide-necked basilar tip aneurysms (i.e., basilar tip aneurysms in which both posterior cerebral arteries emanate from the base of a wide-necked aneurysm) represent a subset of aneurysms that continues to pose technical challenges in treatment. We sought to demonstrate the safety and short-term durability of a novel dual stent-assisted coil embolization technique. METHODS: Two Neuroform stents (Boston Scientific/Target, Fremont, CA) were deployed in the posterior cerebral arteries and the basilar artery, one passing through the interstices of the other in a Y-configuration, thereby recreating an aneurysm neck and enabling safe coil delivery while preserving the parent vessels. RESULTS: Seven patients with unruptured, asymptomatic, wide-necked basilar tip aneurysms involving both posterior cerebral arteries and ranging in size from 7 to 20 mm underwent treatment with this stent-assisted coiling technique. Two stents were successfully deployed in six of the patients and one stent was successfully deployed in the seventh. One patient developed a transient internuclear ophthalmoplegia, and another experienced transient partial right oculomotor nerve palsy. All aneurysms had complete or near-complete embolization with the initial procedure. Follow-up angiography performed 6 months (six patients) and 1 year (one patient) after treatment demonstrated coil compaction and slight recanalization in one patient and recanalization requiring retreatment in another. All patients were neurologically intact at least 6 months after the initial procedure, as well as subsequent procedures, without clinical signs of subarachnoid hemorrhage. CONCLUSION: These initial technical and clinical results are highly encouraging, and this technique may significantly improve the endovascular treatment of intracranial aneurysms.

    PMID:- oculomotor palsy 15854251 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • Pure midbrain infarction: clinical, radiologic, and pathophysiologic findings.
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    Pure midbrain infarction: clinical, radiologic, and pathophysiologic findings.

    Neurology. 2005 Apr 12;64(7):1227-32

    Authors: Kim JS, Kim J

    OBJECTIVE: To describe the clinical features, MRI findings, and the pathogenesis of the pure midbrain infarction. METHODS: Forty patients with infarcts limited to the midbrain were studied. MRI and angiography (mostly MR angiography) were performed in all patients. RESULTS: Clinical manifestations included gait ataxia in 27 (68%) patients, dysarthria in 22 (55%), limb ataxia in 20 (50%), sensory symptoms in 17 (43%), third nerve palsy in 14 (35%), definitive limb weakness (< or =IV/V) in nine (23%), and internuclear ophthalmoplegia in five (13%). According to MRI findings, the lesions were categorized into four groups. The anteromedial group (n = 18) was characterized by oculomotor disturbances (89%), ataxia (89%, bilateral in 17%), and sensory changes (39%) usually restricted to the perioral and hand areas. Lesions restricted to the subcortical area (n = 10) were usually related to small vessel disease (SVD) (78%), whereas those involving the medial surface (n = 8) were caused by large vessel disease (LVD) (78%). The anterolateral group (n = 11) was characterized by ataxia (70%) and definitive hemiparesis (30%) usually caused by LVD (82%). The combined group (n = 6) had frequent oculomotor disturbances (83%), definitive hemiparesis (67%), and ataxia (50%) and was usually associated with LVD (67%). The lateral group (n = 2) was characterized by prominent sensory symptoms. The prognosis was generally good except for one patient with a bilateral lesion. CONCLUSION: Clinical-radiologic correlation study yields four distinct subgroups: anteromedial, anterolateral, combined, and lateral. Large vessel disease and small vessel disease are usual pathogenic mechanisms, whereas cardiogenic embolism is rare.

    PMID:- oculomotor palsy 15824351 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • Intraoperative motor mapping of the cerebral peduncle during resection of a midbrain cavernous malformation: technical case report.
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    Intraoperative motor mapping of the cerebral peduncle during resection of a midbrain cavernous malformation: technical case report.

    Neurosurgery. 2005 Apr;56(2 Suppl):E439; discussion E439

    Authors: Quiñones-Hinojosa A, Lyon R, Du R, Lawton MT

    OBJECTIVE AND IMPORTANCE: Brainstem cavernous malformations that seem to come to a pial or ependymal surface on preoperative magnetic resonance imaging studies may, in fact, be covered by an intact layer of neural tissue. For cavernous malformations in the cerebral peduncle, intraoperative stimulation mapping with a miniaturized probe can determine whether this overlying tissue harbors fibers in the corticospinal tract. In addition, intermittent monitoring with transcranial motor evoked potentials (TcMEPs) helps to protect this vital pathway during resection of the lesion. CLINICAL PRESENTATION: A 20-year-old woman collapsed after a cavernous malformation in the left cerebral peduncle hemorrhaged into the pons, midbrain, and thalamus. She presented with right hemiparesis and left oculomotor palsy. INTERVENTION: The cavernous malformation was completely resected through a left orbitozygomatic craniotomy and transsylvian approach. Stimulation mapping of the cerebral peduncle with a Kartush probe (Medtronic Xomed, Inc., Jacksonville, FL) identified the corticospinal tract lateral to the lesion, and a layer of tissue over the lesion harbored no motor fibers. TcMEP monitoring helped to guide the resection, with increased voltage thresholds and altered waveform morphologies indicating transient impaired motor conduction. All TcMEP changes returned to baseline by the end of the procedure, and the patient's hemiparesis improved after surgery. CONCLUSION: Stimulation mapping of the corticospinal tract and intermittent TcMEPs is a safe and simple surgical adjunct. Expanded monitoring of the motor pathway during the resection of cerebral peduncle cavernous malformations may improve the safety of these operations.

    PMID:- oculomotor palsy 15794843 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • Surgical clipping of complex basilar apex aneurysms: a strategy for successful outcome using the pretemporal transzygomatic transcavernous approach.
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    Surgical clipping of complex basilar apex aneurysms: a strategy for successful outcome using the pretemporal transzygomatic transcavernous approach.

    Neurosurgery. 2005 Apr;56(2 Suppl):261-73; discussion 261-73

    Authors: Krisht AF, Kadri PA

    OBJECTIVE: Complex basilar apex aneurysms (large size, wide and complex neck, tortuous parent vessels) continue to pose a challenge in treatment. Endovascular treatment has a high risk of recanalization, and surgical treatment is limited by the space and time necessary to achieve safe clipping. To overcome these obstacles, a modification of previously reported approaches was developed. The pretemporal transzygomatic transcavernous approach and a clipping strategy were used in the treatment of 21 high-complexity basilar apex aneurysms. METHODS: By use of the pretemporal route, the zygomatic notch was widened, the anterior clinoid was removed, the cavernous sinus was partially exposed, and the oculomotor nerve was mobilized. The depth of the field was widened by further cavernous exposure and the removal of the posterior clinoid. Temporary clips were applied to the basilar trunk perforator-free zone to preserve visualization of the aneurysm neck and perforators and to maintain collateral flow to the brainstem. RESULTS: Twenty-one high-complexity basilar apex aneurysms, 11 of which caused subarachnoid hemorrhage, were treated. Twenty (95%) were successfully clipped (Glasgow Outcome Scale scores, 4 or 5 in 90.5% at discharge; Rankin Disability Score, 1 in 90.5% at 1-yr follow-up). Complications were transient oculomotor palsy in all patients, small thalamic infarct in one patient, and cerebrospinal fluid leak in another. There was no surgical mortality. Delayed follow-up angiography in 19 of the 21 patients showed no residual aneurysm. CONCLUSION: We report the largest series of a unique, challenging group of complex basilar apex aneurysms treated with the pretemporal transzygomatic transcavernous approach, which provided improved safety of clipping by 1) increased visualization of the basilar apex and perforator arteries, 2) improved maneuverability of clip application, 3) a safer perforator-free location, and 4) preservation of brainstem collateral flow.

    PMID:- oculomotor palsy 15794823 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • Incomplete oculomotor nerve palsy caused by an unruptured internal carotid-anterior choroidal artery aneurysm--case report--.
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    Incomplete oculomotor nerve palsy caused by an unruptured internal carotid-anterior choroidal artery aneurysm--case report--.

    Neurol Med Chir (Tokyo). 2005 Mar;45(3):143-7

    Authors: Kurokawa Y, Ishizaki E, Inaba K

    A 59-year-old woman visited our institute with the chief complaint of dizziness which persisted whenever she tried to focus on objects. She had not experienced apparent double vision and had no history of intracranial bleeding. Neurological examination revealed no abnormality except for exotropia at the mid-position and at upper gaze. Cerebral angiography revealed that the intracranial portion of the left internal carotid artery ran more horizontally and also identified an unruptured left internal carotid-anterior choroidal artery (IC-AChA) aneurysm of 3.0 mm diameter. The aneurysm at the origin of the AChA was confirmed during surgery. The proximal lateral wall of the aneurysm was in contact with the oculomotor nerve. This contact was released after complete obliteration of the aneurysm. The exotropia resolved 3 months later. Oculomotor nerve palsy usually indicates the presence of internal carotid-posterior communicating artery (IC-PcomA) aneurysm. Since sacrifice of the AChA will result in severe neurological deficits, accurate neuroimaging information is needed prior to the operation. Conventional angiography and/or three-dimensional computed tomography angiography should be performed to ascertain whether the aneurysm is an IC-PcomA or IC-AChA aneurysm, even if some neurosurgeons insist that conventional angiography is not always needed before surgery for an unruptured aneurysm.

    PMID:- oculomotor palsy 15782005 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • Upper cranial nerve palsy resulting from spontaneous carotid dissection.
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    Upper cranial nerve palsy resulting from spontaneous carotid dissection.

    J Neurol. 2005 Apr;252(4):453-6

    Authors: Wessels T, Röttger C, Kaps M, Traupe H, Stolz E

    INTRODUCTION : Upper cranial nerve palsy has a variety of causes such as cerebral and nerve ischemia, diabetes, infectious and non-infectious meningitis, subarachnoid hemorrhage and intracranial aneurysm. CASE 1 : A 45-year-old man suffered from holocephalic headaches and a right-sided neck pain for two weeks. He presented to our emergency department because of a sudden ptosis of the right eye. On admission neurological examination revealed a right sided Horner's syndrome and hypesthesia of the right side of the face. Magnetic resonance angiography identified a circumscribed dissection of the right extracranial internal carotid artery originating from the carotid bifurcation. Conventional angiography 2 weeks later showed a nearly recanalized artery. CASE 2 : A 55-year-old previously healthy man without cardiovascular risk factors developed right sided neck pain when loading a seeder with several sacks of crop. A few hours later he noticed a left-sided weakness. On admission a severe left sided hemiparesis and a mild neglect were present. Duplex sonography revealed a right-sided distal internal carotid artery (ICA) occlusion. The next morning the patient complained of double vision; he had a right-sided pupil-sparing oculomotor palsy. The diagnosis of ICA dissection was confirmed by conventional angiography, at that time showing a partially recanalized ICA without involvement of the cavernous region by the dissection. CONCLUSION : ICA dissection must be included in the differential diagnosis of upper cranial nerve palsy and should be assessed by duplex ultrasound and magnetic resonance imaging. A possible explanation is nerve ischemia due to a transient or permanent interruption of the blood supply by compression of the vasa nervorum originating from the intracranial carotid artery.

    PMID:- oculomotor palsy 15739041 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • Subacute subdural haematoma presenting with oculomotor nerve palsy, reduced vision, and hallucinations.
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    Subacute subdural haematoma presenting with oculomotor nerve palsy, reduced vision, and hallucinations.

    Eye. 2006 Jan;20(1):125-6

    Authors: Mulholland C, Knox FA

    PMID:- oculomotor palsy 15688047 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • Vertical-torsional oscillations and dissociated bilateral horizontal gaze palsy in a patient with a pontine cavernous angioma.
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    Vertical-torsional oscillations and dissociated bilateral horizontal gaze palsy in a patient with a pontine cavernous angioma.

    J Neurol Neurosurg Psychiatry. 2005 Feb;76(2):283-5

    Authors: Washio N, Suzuki Y, Yamaki T, Kase M, Ohtsuka K

    We report the case of a 16 year old girl with vertical-torsional oscillations. She had a 4 year history of bilateral horizontal gaze palsy caused by a cavernous angioma in the medial part of the dorsal pons. She presented with vertical oscillopsia that had worsened during the past 3 months. Unilateral three dimensional eye movements and bilateral horizontal eye movements were recorded using a magnetic search coil method and direct current electro-oculography, respectively. She had vertical-torsional oscillations (average frequency: 3.0 Hz) leaving vertical saccades and pursuits intact. The average amplitudes of the vertical and torsional components were 2.0 degrees and 0.6 degrees , respectively. Her horizontal rapid eye movements were severely impaired; however, her horizontal pursuits and slow phases of vestibulo-ocular reflex were only partially impaired (gain<0.3, oculomotor range<+/-9 degrees ). Convergence and divergence were intact. Lesions involving the medial part of the dorsal pons and bilateral paramedian pontine reticular formation can induce vertical and torsional oscillations without disruption of vertical rapid eye movements.

    PMID:- oculomotor palsy 15654054 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • Botulinum neurotoxin serotype A: a clinical update on non-cosmetic uses.
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    Botulinum neurotoxin serotype A: a clinical update on non-cosmetic uses.

    Am J Health Syst Pharm. 2004 Nov 15;61(22 Suppl 6):S11-23

    Authors: Charles PD

    PURPOSE: Clinical experience with botulinum toxin type A for non-cosmetic uses that are approved by the Food and Drug Administration (FDA) and various other non-cosmetic uses that are not approved by FDA, including some applications that are widely known and others that currently are emerging, is discussed. SUMMARY: FDA-approved indications for botulinum toxin type A (Botox) include the temporary treatment of cervical dystonia (a neuromuscular disorder involving the head and neck), the oculomotor disorders strabismus (improperly aligned eyes) and blepharospasm (involuntary contraction of the eye muscles), and severe primary axillary hyperhidrosis (excessive sweating). Other uses of botulinum toxin type A that are widely known but not approved by FDA include spastic disorders associated with injury or disease of the central nervous system including trauma, stroke, multiple sclerosis, or cerebral palsy and focal dystonias affecting the limbs, face, jaw, or vocal cords. Treatment and prevention of chronic headache and chronic musculoskeletal pain are emerging uses for botulinum toxin type A. CONCLUSION: Many of the conditions for which botulinum toxin type A has been explored are common and difficult to treat. Temporary improvement in symptoms is associated with botulinum toxin type A injection, and repeat treatment often is required. The drug is well tolerated and has a wide margin of safety.

    PMID:- oculomotor palsy 15598005 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • The neuropsychiatry of Parkinson's disease and related disorders.
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    The neuropsychiatry of Parkinson's disease and related disorders.

    Psychiatr Clin North Am. 2004 Dec;27(4):801-25

    Authors: Lauterbach EC

    Parkinson's disease is associated with classical Parkinsonian features that respond to dopaminergic therapy. Neuropsychiatric sequelae include dementia, major depression, dysthymia, anxiety disorders, sleep disorders, and sexual disorders. Panic attacks are particularly common. With treatment, visual hallucinations, paranoid delusions, mania, or delirium may evolve. Psychosis is a key factor in nursing home placement, and depression is the most significant predictor of quality of life. Clozapine may be the safest treatment for psychotic features, but more research is needed to establish the efficacy of antidepressant treatments. Dementia with Lewy bodies, the second most common dementia in the elderly, may present in association with systematized delusions, depression, or RBD. Early evidence suggests the utility of rivastigmine, donepezil, low-dose olanzapine, and quetiapine in treating DLB. Parkinson-plus syndromes generally lack a good response to dopaminergic treatment and evidence additional features, including dysautonomia, cerebellar and pontine features, eye signs, and other movement disorders. MSA is associated with dysautonomia and RBD. SND (MSA-P) is associated with frontal cognitive impairments, but dementia, psychosis, and mood disorders have not been strikingly apparent unless additional pathological findings are present. In SDS (MSA-A), impotence is almost ubiquitous; urinary incontinence is frequent; depression is occasional, and sleep apnea should be treated to avoid sudden death during sleep. OPCA neuropsychiatric correlates await further definition. Progressive supranuclear palsy neuropsychiatric features include apathy, subcortical dementia, pathological emotionality, mild depression and anxiety, and lack of appreciable response to donepezil. CBD usually is recognized by early frontal dementia with ideomotor apraxia, often in the right upper extremity, attended later by poorly responsive unilateral Parkinsonism, with additional signs including cortical reflex myoclonus, limb dystonia, alien limb, oculomotor apraxia when asked to look horizontally, depression, personality changes, and, occasionally, Kluver-Bucy syndrome. The neuropsychiatry of FTDP-17 involves apraxia, executive impairment, personality changes, hyperorality, and occasional psychosis. Future research in these Parkinsonian disorders should target the characterization of neuropsychiatric sequelae and their treatment.

    PMID:- oculomotor palsy 15550293 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • Recurrent oculomotor nerve palsy: a rare presentation of neurocysticercosis.
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    Recurrent oculomotor nerve palsy: a rare presentation of neurocysticercosis.

    Neurol India. 2004 Sep;52(3):402

    Authors: Mokta JK, Mahajan S, Machhan P, Mokta KK, Patial RK, Prashar BS

    PMID:- oculomotor palsy 15472451 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • Giant cell arteritis, oculomotor nerve palsy, and acute hearing loss.
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    Giant cell arteritis, oculomotor nerve palsy, and acute hearing loss.

    Scand J Rheumatol. 2004;33(4):279-80

    Authors: Loffredo L, Parrotto S, Violi F

    PMID:- oculomotor palsy 15370728 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • Distribution of tuft-shaped astrocytes in the cerebral cortex in progressive supranuclear palsy.
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    Distribution of tuft-shaped astrocytes in the cerebral cortex in progressive supranuclear palsy.

    Acta Neuropathol. 2004 Nov;108(5):399-405

    Authors: Iwasaki Y, Yoshida M, Hattori M, Goto A, Aiba I, Hashizume Y, Sobue G

    The deposition of abnormal levels of tau protein is a major neuropathological feature of progressive supranuclear palsy (PSP), and the presence of tuft-shaped astrocytes is a neuropathological hallmark of PSP. We examined the topographic distribution of tuft-shaped astrocytes in the cerebral hemisphere by Gallyas-Braak silver staining in three Japanese autopsy cases of typical PSP. The distribution of tuft-shaped astrocytes was relatively uniform between cases. Tuft-shaped astrocytes were identified predominantly in posterior frontal areas such as the precentral gyrus and premotor and supplementary motor areas (Brodmann areas 4, 6 and 8). Tuft-shaped astrocytes were most dense in areas of cortical convexity, and they were more abundant in the crests of the cerebral gyri than in the valleys of the cerebral sulci. The temporal, parietal and occipital cortices, including the hippocampal formation and cingulate gyrus, were relatively free of tuft-shaped astrocytes. We confirmed involvement of the cerebral cortex in the pathology of PSP, and showed the widespread presence of tuft-shaped astrocytes, particularly in the precentral gyrus and premotor and supplementary motor areas, to be an essential neuropathological feature of PSP. The extra-pyramidal and pyramidal signs, supranuclear oculomotor abnormalities and other cortical signs associated with PSP may be related to the high density of tuft-shaped astrocytes in the precentral gyrus and premotor and supplementary motor areas. Dementia, apraxia, aphasia and frontal lobe signs may also result, at least in part, from this cortical involvement.

    PMID:- oculomotor palsy 15365723 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • Unusual neuro-ophthalmic presentation of anterior communicating artery aneurysm with third nerve paresis.
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    Unusual neuro-ophthalmic presentation of anterior communicating artery aneurysm with third nerve paresis.

    J Clin Neurosci. 2004 Sep;11(7):776-8

    Authors: Satyarthee GD, Mahapatra AK

    Paresis of the oculomotor nerve associated with subarachnoid haemorrhage is considered a hallmark of aneurysms located at the junction of the internal carotid artery and posterior communicating artery. Third nerve palsy can also be caused by those aneurysms located in the intracavernous part of the internal carotid artery, basilar artery, posterior cerebral artery and superior cerebellar artery. However, oculomotor nerve paresis caused by an anterior communicating artery aneurysm is a very uncommon occurrence. We report a case of an elderly female with sudden severe headache who developed an acute third nerve paresis. Angiography revealed an anterior communicating artery aneurysm. Management and the pertinent literature are reviewed along with the mechanism of third nerve compression.

    PMID:- oculomotor palsy 15337148 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • Prolonged visual disturbance secondary to isolated sphenoid sinus disease.
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    Prolonged visual disturbance secondary to isolated sphenoid sinus disease.

    Laryngoscope. 2004 Jun;114(6):986-90

    Authors: Lee LA, Huang CC, Lee TJ

    OBJECTIVES/HYPOTHESIS: The objective was to evaluate the efficacy of endoscopic sinus surgery in patients with isolated sphenoid sinus disease with visual disturbances of more than 72 hours' duration. STUDY DESIGN: Retrospective review. METHODS: A sequential series of patients with isolated sphenoid sinus disease with visual disturbances who underwent endoscopic surgery performed by the same surgeon between 1995 and 2002 were reviewed. Patients with malignant tumors were excluded from the study. Patients were evaluated preoperatively and postoperatively to record the effects of this approach on visual acuity and diplopia. RESULTS: The study population included six women and seven men with a mean age of 56.2 years (age range, 31-75 y). Eight eyes had vision loss attributable to compressive optic neuropathy (27%) and optic neuritis (27%); seven eyes with diplopia had abducens palsy (40%) and oculomotor nerve palsy (7%). Sphenoid sinus lesions included sinusitis (38%), mucocele (31%), and aspergillosis (31%). The mean interval between the onset of visual disturbances and surgery was 6.6 months (range, 3 d-3.5 y). Visual disturbances improved in 60% of the patients (P <.01). There was better improvement in diplopia than in vision loss (P <.01). The results of endoscopic sinus surgery for patients with abducens palsy and aspergillosis were excellent (83% and 80%, respectively). Optic neuritis and visual disturbances lasting for more than 6 months were regarded as poor prognostic factors. CONCLUSION: The study supports the treatment of visual disturbances resulting from isolated sphenoid sinus disease by endoscopic sinus surgery. A timely operation may prevent permanent sequelae.

    PMID:- oculomotor palsy 15179200 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • Selective and sequential therapy of oculomotor and palpebral sequelae resulting from biopsy of dorsal midbrain sarcoidosis.
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    Selective and sequential therapy of oculomotor and palpebral sequelae resulting from biopsy of dorsal midbrain sarcoidosis.

    Klin Monatsbl Augenheilkd. 2004 May;221(5):404-7

    Authors: Klainguti G, Spahn B, Borruat FX

    BACKGROUND: Biopsy of a dorsal mesencephalon lesion often leads to neuro-ophthalmological complications, namely dorsal mesencephalic syndrome, skew deviation, IV (th) palsy, or Horner's syndrome. HISTORY AND SIGNS: A 26-year-old man underwent a biopsy of the quadrigeminal plate for a lesion which revealed to be neurosarcoidosis. Post-operative complications included a left homonymous hemianopia, a left III (rd) nucleus palsy, a bilateral IV (th) palsy and a bilateral internuclear ophthalmoplegia. Palpebral fissures were narrowed to 2 mm on both sides. In primary gaze there was 24 degrees of exotropia, 17 degrees of right hypertropia and 30 degrees of exyclorotation. THERAPY AND OUTCOME: After 24 months of stable evolution, three oculomotor surgical procedures were performed including: surgery on both horizontal muscles of the left eye; shortening of both superior oblique muscles; resection of the right lateral rectus muscle, and posterior fixation of an inferior rectus muscle. Bilateral brow suspension on the frontal muscle of both superior eyelids was then performed. Evolution was favorable with a binocular single field of vision measuring 17 degrees horizontally and 20 degrees vertically centered on the primary gaze. Palpebral fissures measured 7 to 8 mm in primary gaze. CONCLUSIONS: The neuro-ophthalmological sequelae which followed the biopsy of a neurosarcoidosis lesion of the quadrigeminal plate were so severe that this patient was completely handicapped. A four-step surgery correcting the horizontal, torsional, vertical components, then the bilateral ptosis allowed the patient to recover both a satisfying function and esthetical aspect.

    PMID:- oculomotor palsy 15162292 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • Midbrain ischemia presenting as vertical gaze palsy: value of diffusion-weighted magnetic resonance imaging.
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    Midbrain ischemia presenting as vertical gaze palsy: value of diffusion-weighted magnetic resonance imaging.

    Cerebrovasc Dis. 2004;18(1):3-7

    Authors: Seifert T, Enzinger C, Ropele S, Storch MK, Fazekas F

    BACKGROUND: Conventional magnetic resonance imaging may fail to identify very small but clinically relevant acute subcortical brain infarcts. Diffusion-weighted magnetic resonance imaging (DWI) is very sensitive and specific for acute cerebral ischemia and should contribute to the early detection of such lesions. METHODS: We analyzed 6 patients who presented with acute vertical gaze palsy and in whom DWI was performed within 1-6 days from symptom onset. RESULTS: DWI accurately identified ischemia in an area supplied by the posterior thalamosubthalamic paramedian artery in all patients. T(2)-weighted and FLAIR imaging failed to identify the clinically relevant lesion in 2 and 3 patients, respectively. CONCLUSION: DWI improves the clinicoanatomical correlation in patients presenting with supranuclear oculomotor disturbances.

    PMID:- oculomotor palsy 15159614 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • Neurosyphilis presenting with gummatous oculomotor nerve palsy.
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    Neurosyphilis presenting with gummatous oculomotor nerve palsy.

    J Neurol Neurosurg Psychiatry. 2004 May;75(5):789

    Authors: Seeley WW, Venna N

    PMID:- oculomotor palsy 15090587 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • Severe preeclampsia presenting as third nerve palsy.
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    Severe preeclampsia presenting as third nerve palsy.

    Am J Perinatol. 2004 Apr;21(3):153-5

    Authors: Bonebrake RG, Fleming AD, Carignan EM, Hoover DK

    Preeclampsia is a common complication of pregnancy and often manifests in severe cases with neurological symptoms. We present the first documented case of preeclampsia associated with third nerve palsy. A 19-year-old primigravida presented at 31 2/7 weeks' gestation with preeclampsia. In addition to classic preeclampsia symptoms, the patient had atypical visual disturbances. Exhaustive neurological and ophthalmological examinations revealed a third nerve palsy with no etiology other than preeclampsia. Deteriorating renal function necessitated preterm delivery. She ultimately underwent a cesarean section. Two months postpartum, the patient has shown complete spontaneous resolution of third nerve palsy. In this case of severe preeclampsia manifested by third nerve palsy, we hypothesize that the mechanism is attributed to vasospasm of the vessels supplying the oculomotor nerve.

    PMID:- oculomotor palsy 15085498 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • Tumors metastatic to the pituitary gland: case report and literature review.
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    Tumors metastatic to the pituitary gland: case report and literature review.

    J Clin Endocrinol Metab. 2004 Feb;89(2):574-80

    Authors: Komninos J, Vlassopoulou V, Protopapa D, Korfias S, Kontogeorgos G, Sakas DE, Thalassinos NC

    Tumors metastatic to the pituitary gland are an unusual complication of systemic cancer typically seen in elderly patients with diffuse malignant disease. Breast and lung are the commonest sites of the primary tumor, whereas diabetes insipidus is the most frequent symptom at presentation. Their rarity and usually indolent course, as well as the lack of specific clinical and radiological features, impede their differentiation from other more common sellar area lesions, particularly when history of malignancy is absent. Management of these patients may also be very difficult because the prognosis depends on the course of the primary neoplasm. A 68-yr-old man, with no history of malignancy, presented with recent onset of hypopituitarism, mild diabetes insipidus, headaches, left oculomotor nerve palsy, and progressive bilateral deterioration of visual acuity and visual fields. Magnetic resonance imaging revealed a large sellar mass compressing the optic chiasm and invading the left cavernous sinus, whereas a prolactin elevation at 438.6 ng/ml (19.73 nmol/liter) was noted. Decompression of the sellar region was attempted, and pathology disclosed a metastatic hepatocellular carcinoma. On postoperative investigation, primary liver tumor was identified and confirmed by biopsy. The patient improved transiently but died 3 months after diagnosis because of deterioration of the liver disease. The relevant literature is reviewed in light of this unusual case, illustrating the problems in the diagnosis and management of patients with metastasis to the pituitary.

    PMID:- oculomotor palsy 14764764 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • Gliomatosis cerebri in a young patient showing various cranial nerve manifestations: a case report.
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    Gliomatosis cerebri in a young patient showing various cranial nerve manifestations: a case report.

    Brain Tumor Pathol. 2003;20(2):93-6

    Authors: Izumiyama H, Abe T, Tanioka D, Fukuda A, Kunii N

    A case of gliomatosis cerebri in a 27-year-old man showing various cranial nerve manifestations is described. He was diagnosed as having cranial mononeuritis multiplex (bilateral oculomotor nerve paralysis, left facial nerve paralysis, bulbar palsy manifestations, and hypoglossal nerve paralysis) and was hospitalized in the neurology department on August 1, 2000. Although he continued to visit the neurology department after discharge, his manifestations showed no improvement. He was sent to our department for brain biopsy in August 2001. A biopsy performed at the Sylvian fissure from the frontal lobe/temporal lobe cortex showed high intensity on T2-weighted and Flair magnetic resonance imaging (MRI). The pathological findings were diffuse low-grade astrocytoma infiltrating between the pia mater and the cerebral cortex. We believed that the astrocytoma spreading on the subpia mater was responsible for the various cranial nerve manifestations, and we started whole-brain irradiation (46 Gy) + interferon (IFN)-beta D.I.V. from September 2001. The pathological findings of the brain biopsy showed diffuse astrocytoma. The clinical presentation was dramatically improved after radiotherapy. It seemed that this tumor had spread along the subpia mater and subependyma. When he was discharged in early December, he walked by himself. The characteristic features of this case are that no lesion in the cerebellum or brain stem was found on MRI, even though the main manifestations were cerebello-brain stem manifestations, and biopsy of the cerebral cortex revealed astrocytoma. It should be noted that the clinical manifestations of astrocytoma in some cases are dissociated from the imaging observations.

    PMID:- oculomotor palsy 14756448 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • A model of neuronopathic Gaucher disease.
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    A model of neuronopathic Gaucher disease.

    J Inherit Metab Dis. 2003;26(7):629-39

    Authors: Campbell PE, Harris CM, Harris CM, Sirimanna T, Vellodi A

    Gaucher disease (GD) is a lysosomal disorder involving the accumulation of glucocerebroside in the liver, spleen, bones and brain. Some patients exhibit only systemic disease (type I), but others have additional neurological signs which may lead to rapid neurodegeneration in infancy (type II) or take a more intermediate course (type III). Types II and III are collectively known as neuronopathic Gaucher disease (NGD). Systemic disease can now be treated by enzyme replacement therapy (ERT), but its efficacy in NGD is limited. Two infants who presented with bulbar palsy and failure to thrive were enzymatically diagnosed at 8 months with NGD. They were started on high-dose ERT (120 IU/kg every 2 weeks). Both underwent serial oculomotor assessment and an audiological battery, including visual reinforcement audiometry, otoacoustic emissions, and the auditory brain stem response (ABR). Biochemical markers showed an incomplete systemic response to ERT, but neurological deterioration was relentless, leading to death at 16 and 25 months. Oculomotor testing revealed a complete absence of saccadic eye movements and progressive bilateral sixth nerve palsy in one. Audiological assessment revealed progressive deterioration of ABRs, but with normal peripheral hearing and otoacoustic emissions. Both infants showed neurological deterioration in spite of high-dose ERT. The audiological findings suggested a loss of inner hair cell pathway function with preserved outer hair function, similar to what is seen in auditory neuropathy. The unusual pattern of audiological and oculomotor abnormalities is consistent with an excitotoxic mechanism predisposing nerve cells to glucocerebroside toxicity. Such excitotoxic damage may be amenable to direct therapeutic intervention.

    PMID:- oculomotor palsy 14707511 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • Progression of preexisting trigeminalgia to Tolose-Hunt-like syndrome. The importance of neuroimaging for early differential diagnosis.
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    Progression of preexisting trigeminalgia to Tolose-Hunt-like syndrome. The importance of neuroimaging for early differential diagnosis.

    Neurol Sci. 2003 Nov;24(4):281-5

    Authors: Chmielewska B, Leszek Kamiński M

    Recurrent unbearable, paroxysmal, unilateral facial pain in the distribution of one or more branches of the trigeminal nerve often provoked by sensory stimuli is typical for idiopathic trigeminal neuralgia. The less frequent localization in the area of ophthalmic branch (5%) is particularly controversial and should be distinguished from pathological lesions in the brainstem and middle and posterior cranial fossa and from diseases of the orbit and eye. This case study presents a 79-year-old woman with typical clinical features of 1st division trigeminalgia without any neurological loss and with normal results of laryngological, ophthalmological, and stomatological examinations as well as neuroimaging CT, and MR /MRA evaluation. Only the evoked potential blink and masseter reflexes demonstrated the pathological values in the early phase of illness. After 1 year of pharmacological treatment no improvement was achieved and the pain became neuropathic and paresis of 3rd, 4th and 6th nerves developed, as observed in Tolose-Hunt syndrome. MRI of the orbit revealed a pathological mass in its apex with a connection to the superior orbital fissure. However, treatment with steroids was completely ineffective. Surgical resection of the tumor (leiomyosarcoma) only partially reversed oculomotor palsy and diminished aching. In differential diagnosis of idiopathic and symptomatic trigeminalgia, early MR and MRA imaging is the most essential and sometimes may be the best single test to evaluate lesions even in distant areas of the nervous system branches.

    PMID:- oculomotor palsy 14658050 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • A patient with reversible pupil-sparing Weber's syndrome.
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    A patient with reversible pupil-sparing Weber's syndrome.

    Neurol India. 2003 Sep;51(3):388-9

    Authors: Umasankar U, Huwez FU

    This is a case report of a lady who presented with pupil-sparing Weber's syndrome. She had left oculomotor nerve palsy with normal pupil and right hemiparesis. The patient subsequently made a good recovery. An ischemic lesion of the lower mid-brain was demonstrated on the MRI scan of the brain, which corresponds to the motor nucleus of the oculomotor nerve. The article also describes the neuroanatomy of the oculomotor nerve and how its partial lesions lead to sparing of the pupil. In addition, this case report documents that a pupil-sparing Weber's syndrome could be reversible.

    PMID:- oculomotor palsy 14652448 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • Isolated superior rectus palsy due to contralateral midbrain infarction.
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    Isolated superior rectus palsy due to contralateral midbrain infarction.

    Arch Neurol. 2003 Nov;60(11):1633-5

    Authors: Kwon JH, Kwon SU, Ahn HS, Sung KB, Kim JS

    BACKGROUND: Isolated superior rectus palsy due to a contralateral midbrain lesion has not been reported. CASE DESCRIPTION: A 71-year-old woman suddenly developed diplopia. Examination showed that she had isolated superior rectus paresis. Magnetic resonance imaging showed a tiny infarct at the area of the oculomotor nucleus on the contralateral side. CONCLUSION: Isolated superior rectus palsy may be caused by a contralateral midbrain lesion that selectively involves crossing superior rectus nerve fibers.

    PMID:- oculomotor palsy 14623739 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • Unilateral oculomotor nerve paresis associated with anterior communicating artery aneurysm rupture--two case reports.
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    Unilateral oculomotor nerve paresis associated with anterior communicating artery aneurysm rupture--two case reports.

    Neurol Med Chir (Tokyo). 2003 Oct;43(10):484-7

    Authors: Aiba T, Fukuda M

    Two cases of complete unilateral oculomotor nerve palsy occurred after subarachnoid hemorrhage (SAH) due to a ruptured anterior communicating artery aneurysm. A 61-year-old female suffered left oculomotor nerve paresis after mild SAH. This paresis was probably related to pre-existing oculomotor nerve stretching caused by abnormal positioning of the posterior cerebral and superior cerebellar arteries in the premesencephalic cistern. A 70-year-old female suffered right oculomotor nerve paresis after severe SAH. Elevated intracranial pressure might have caused this paresis, but the reason for the unilateral occurrence was undetermined. Both patients were treated by clipping of the aneurysm, and the signs of oculomotor nerve paresis gradually resolved. A pattern of pupil-sparing paresis was observed during the early recovery stage in both patients.

    PMID:- oculomotor palsy 14620199 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • Generalized Kohonen's competitive learning algorithms for ophthalmological MR image segmentation.
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    Generalized Kohonen's competitive learning algorithms for ophthalmological MR image segmentation.

    Magn Reson Imaging. 2003 Oct;21(8):863-70

    Authors: Lin KC, Yang MS, Liu HC, Lirng JF, Wang PN

    Kohonen's self-organizing map is a two-layer feedforward competitive learning network. It has been used as a competitive learning clustering algorithm. In this paper, we generalize Kohonen's competitive learning (KCL) algorithm with fuzzy and fuzzy-soft types called fuzzy KCL (FKCL) and fuzzy-soft KCL (FSKCL). These generalized KCL algorithms fuse the competitive learning with soft competition and fuzzy c-means (FCM) membership functions. We then apply these generalized KCLs to MRI and MRA ophthalmological segmentations. These KCL-based MRI segmentation techniques are useful in reducing medical image noise effects using a learning mechanism. They may be particularly helpful in clinical diagnosis. Two real cases with MR image data recommended by an ophthalmologist are examined. First case is a patient with Retinoblastoma in her left eye, an inborn malignant neoplasm of the retina frequently metastasis beyond the lacrimal cribrosa. The second case is a patient with complete left side oculomotor palsy immediately after a motor vehicle accident. Her brain MRI with MRA, skull routine, orbital CT, and cerebral angiography did not reveal brainstem lesions, skull fractures, or vascular anomalies. These generalized KCL algorithms were used in segmenting the ophthalmological MRIs. KCL, FKCL and FSKCL comparisons are made. Overall, the FSKCL algorithm is recommended for use in MR image segmentation as an aid to small lesion diagnosis.

    PMID:- oculomotor palsy 14599536 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • Isolated oculomotor nerve palsy in spontaneous internal carotid artery dissection: case report.
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    Isolated oculomotor nerve palsy in spontaneous internal carotid artery dissection: case report.

    Arq Neuropsiquiatr. 2003 Sep;61(3A):668-70

    Authors: Campos CR, Massaro AR, Scaff M

    Partial oculosympathetic palsy followed by ischemic manifestations in brain or retina are the main symptoms of extracranial internal carotid artery (ICA) dissection. Unusually, cranial nerves may be affected. Isolated oculomotor nerve palsy is found only rarely. CASE: We present a 50-year-old nondiabetic man who experienced acute onset of right occipital headache which spread to the right retro-orbital region. Five days later he noticed diplopia and right blurred vision sensation. Neurologic examination disclosed only impaired adduction and upward gaze of right eye, slight ipsilateral pupillary dilatation, without ptosis. Brain MRI was normal. Angiography showed right internal carotid artery dissection with forward occlusion to the base of the skull. Intravenous heparin followed by warfarin was prescribed. The headache and the oculomotor nerve deficit gradually resolved in the next three weeks. DISCUSSION: Isolated oculomotor nerve palsy is underrecognized as a clinical presentation of extracranial ICA dissection. If the angiographic evaluation is incomplete without careful study of extracranial arteries, misdiagnosis may lead to failure to initiate early treatment to prevent thromboembolic complications. For this reason we draw attention to the need for careful evaluation of cervical arteries in patients with oculomotor nerve palsy. Mechanical compression or stretching of the third nerve are possible mechanisms, but the direct impairment of the blood supply to the third nerve seems to be the most plausible explanation.

    PMID:- oculomotor palsy 14513178 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • Orbital roof fractures: management of ophthalmic complications.
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    Orbital roof fractures: management of ophthalmic complications.

    Ophthal Plast Reconstr Surg. 2003 Sep;19(5):359-63

    Authors: Fulcher TP, Sullivan TJ

    PURPOSE: To review the clinical features and management of patients with orbital roof fractures. METHODS: Non-comparative, retrospective case review of 21 patients presenting with orbital roof fractures. RESULTS: The orbital roof fractures in our series resulted from motor vehicle accidents, blunt trauma, head injuries, and penetrating orbital injuries. Associated orbital and ocular injuries included other ipsilateral orbital fractures (16 cases), traumatic optic neuropathy (3 cases), ptosis (2 cases), perforating eye injuries (2 cases), intraorbital foreign bodies (2 cases), and oculomotor nerve palsy (1 case). Six patients required surgical intervention for ophthalmic sequelae, which included motility problems (4 cases), lagophthalmos (1 case), and a retained intraorbital foreign body with a cerebrospinal fluid leak (one case). The outcome of surgery was favorable in all cases, with complete resolution of symptoms in five of six patients. CONCLUSIONS: Orbital and ocular injuries are common in association with orbital roof fractures. A multidisciplinary approach to management is required because facial and cerebral injuries are also common. Most patients can be managed conservatively. The specific ophthalmic indications for surgical intervention are limited, but the outcome in these cases is gratifying.

    PMID:- oculomotor palsy 14506420 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

  • Idiopathic, intrinsic haematoma of the third cranial nerve.
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    Idiopathic, intrinsic haematoma of the third cranial nerve.

    Acta Neurochir (Wien). 2003 Sep;145(9):811-3; discussion 813

    Authors: Lodrini S, Giombini S, Maccagnano E

    We describe an exceptional case of an intrinsic, spontaneous haematoma of the oculomotor nerve and review the literature. We conclude that, even in an elderly patient, an isolated cranial nerve palsy should be extensively investigated and, when necessary, surgically treated, since a good functional recovery is possible.

    PMID:- oculomotor palsy 14505112 [PubMed - indexed for MEDLINE ( oculomotor palsy )]

    Anatomy of the oculomotor nerve

    The oculomotor nerve arises from the anterior aspect of mesencephalon (midbrain). There are two nuclei for the oculomotor nerve:

    * The oculomotor nucleus originates at the level of the superior colliculus. The muscles it controls are the ciliary muscle (affecting accommodation), and all extraocular muscles except for the superior oblique muscle and the lateral rectus muscle.

    * The Edinger-Westphal nucleus supplies parasympathetic fibres to the eye via the ciliary ganglion, and thus controls pupil constriction.

    Exit from brain

    On emerging from the brain, the nerve is invested with a sheath of pia mater, and enclosed in a prolongation from the arachnoid.

    It passes between the superior cerebellar (below) and posterior cerebral arteries (above), and then pierces the dura mater in front of and lateral to the posterior clinoid process, passing between the free and attached borders of the tentorium cerebelli.

    It runs along the lateral wall of the cavernous sinus, above the other orbital nerves, receiving in its course one or two filaments from the cavernous plexus of the sympathetic, and a communicating branch from the ophthalmic division of the trigeminal.

    Superior and inferior branches

    It then divides into two branches, which enter the orbit through the superior orbital fissure, between the two heads of the lateral rectus.

    Here the nerve is placed below the trochlear nerve and the frontal and lacrimal branches of the ophthalmic nerve, while the nasociliary nerve is placed between its two rami:

    * superior branch of oculomotor nerve * inferior branch of oculomotor nerve

    Testing the oculomotor nerve

    Cranial nerves III, IV and VI are usually tested together. The examiner typically instructs the patient to hold his head still and follow only with the eyes a finger or penlight that circumscribes a large "H" in front of the patient. By observing the eye movements and eyelids, the examiner is able to obtain more information about the extraocular muscles, the levator palpebrae superioris muscle, and cranial nerves III, IV, and VI.

    Since the oculomotor nerve controls most of the eye muscles, it may be easier to detect damage to it. Damage to this nerve, termed oculomotor palsy is also known by the down n' out symptoms, because of the position of the affected eye.

    Pupillary reflex

    The oculomotor nerve also controls the constriction of the pupils. This can be tested in two main ways. By moving a finger towards a person's face to induce accommodation, as well as them going cross-eyed, their pupils should constrict.

    Shining a light into their eyes should also make their pupils constrict. Both pupils should constrict at the same time, independent of what eye the light is actually shone on.

    (adapted in part from wikipedia)

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