Brainstem Examination Lecture
"Clinical Evaluation of the Brain-stem and Cerebellum"
The brain-stem is one of the most confusing and complicated areas of neuroanatomy and consequently brainstem examination (focusing on cranial nerve function) is one of the hardest parts of the neurological examination to perform and interpret.
This lecture on brain-stem examination focuses on the key clinical features of brain-stem and cerebellar dysfunction such as diplopia,
involvement.The clinical problem and answer section emphasizes the need for a clear understanding of the functions of the major pathways and the signs resulting in their dysfunction.
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Brainstem examination slideshow transcript
Slide 1: BRAIN STEM, CEREBELLUM and NEURO-OPTHALMOLOGY Submitted to AskTheNeurologist.Com in 2007
Brainstem examination Slide 2: GROSS ANATOMY
Brainstem examination Slide 3: LATERAL VIEW
Slide 4: LOCATION OF CRANIAL NERVE NUCLEI WITHIN BRAINSTEM
Slide 5: CRANIAL NERVE 5 Note that although all fibres enter the brainstem at the level of the pons, those concerned with pain and temperature descend as low as C3
Slide 6: PATHWAYS INVOLVED IN HORIZONTAL GAZE LEFT FRONTAL EYE FIELD
Slide 7: INTERNUCLEAR OPTHALMOPLEGIA ( INO)
Slide 8: THE FACIAL NERVE Therefore a lesion at or distal to the facial nucleus will result in weakness of the upper as well as the lower part of the face:- this is what is know as a “ peripheral facial palsy ”
Slide 9: The Long Tracts Note sites of decussation of major tracts : Spinothalamic Cuneate / Gracile Corticospinal
Brainstem examination Slide 10: LONG TRACT DECUSSATION • Spinothalamic Spinal cord • Gracile / Cuneate Medulla Medulla • Corticospinal Therefore: - Lesions at medulla and below can result in dissociated sensory syndromes - Lesions above the medulla will result in a contralateral upper motor neuron syndrome
Slide 11: The Corticobulbar Tract • Accompanies the corticospinal tract: can assume decussation occurs at level of nucleus Connects with the brain-stem motor nuclei Each tract connects bilaterally with most cranial nerve motor nuclei EXCEPT: Part of VII dealing with lower face is innervated unilaterally Sometimes XII innervated unilaterally
Brainstem examination Slide 12: Bulbar Palsy Pseudobulbar Palsy • Upper motor neuron • Lower motor neuron therefore bilateral damage therefore signs of necessary denervation present • Inappropriate spells of • Tongue wasting and crying / laughing fasciculation • Jaw jerk and gag reflex increased Dysarthria, dysphagia, weight loss, risk of aspiration pneumonia present in both cases
Slide 13: LATERAL MEDULLARY (WALLENBERG’S) SYNDROME LESION SITE IN LATERAL MEDUL SYNDROME ( BLUE)
Slide 14: CLINICAL FEATURES OF LMS I • VERTIGO, NYSTAGMUS • VESTIBULAR NUCLEI IPSILATERAL DESCENDING HORNER’S SYMPATHETIC TRACT SYNDROME IPSILATERAL INFERIOR CEREBELLAR CEREBELLAR SIGNS PEDUNCLE DYSPHONIA AND NUCLEUS AMBIGUUS DYSPHAGIA
Brainstem examination Slide 15: CLINICAL FEATURES OF LMS II LOSS OF IPSILATERAL SPINAL TRACT AND FACIAL PAIN AND NUCLEUS OF TEMPERATURE TRIGEMINAL NERVE SENSATION LOSS OF GRACILE AND IPSILATERAL CUNEATE NUCLEI VIBRATION AND PROPRIOCEPTION IN LIMBS AND TRUNK
Slide 16: CLINICAL FEATURES OF LMS III LOSS OF SPINOTHALAMIC TRACT CONTRALATERAL PAIN AND TEMPERATURE SENSATION IN LIMBS AND TRUNK HICCUPS UNKNOWN NUCLEUS AND LOSS OF TASTE TRACTUS SOLITARIUS
Slide 17: Blood supply of Brainstem and Cerebellum 1) Ant. cerebral 2) Internal carotid 3) Middle cerebral 4) Post. communicating 5) Sup. cerebellar 6) Basilar 7) Ant. Inf. cerebellar 8) Vertebral 9) Ant. Spinal 10) Post. Spinal 11) Post. Inf. Cerebellar 12) Post cerebral 13) Mesencephalic
Slide 18: Somatotopy of cerebellum Midline lesions: • nystagmus •Titubation •Trunk / gait ataxia Hemispheric lesions: • nystagmus posterior • ipsilateral limb signs
Brainstem examination Slide 19: Basic Plan of Cerebellar connections DN= Dentate nucleus T = Thalamus RN = Red nucleus Each cerebellar cortex controls ipsilateral side of body Efferents to cortex leave cerebellum via superior cerebellar peduncle Note: red nucleus is present in midbrain and ultimately controls contralateral half of body
Slide 20: DSCT= dorsal spinocerebellar tract VSCT= ventral spinocerebellar tract VSCT is crossed in the cord but crosses back within cerebellum
Slide 21: Fronto-ponto Cerebellar tract Right Cerebral cortex Note that right side of cortex ultimately controls left cerebellar hemisphere Fronto-ponto-cerebellar fibres enter cerebellum via middle cerebellar peduncle
Brainstem examination Slide 22: Symptoms and signs of cerebellar disease (VANISH’D) •
• Ataxia - usually falls towards lesion • Nystagmus – increased with gaze towards lesion • Intention Tremor • Scanning speech • Hypotonia • Dysdiadochokinesia + Dysmetria
Brainstem examination Slide 23: Approach to differential diagnosis of cerebellar dysfunction Acute Chronic Focal CVA Neoplastic asymmetric - ischaemia Demyelination - haemorrhage ( usually) Demyelination Diffuse Drug intoxication: Drugs: - alcohol - phenytoin • ethanol/ BZD/ Barbs Symmetric Hereditary – SCA, FA, WD • anticonvulsants Paraneoplastic Wernicke encephalopathy ( usually) Creutzfeldt-Jacob disease Hypothyroidism
Brainstem examination Slide 24: Approach to localisation within brainstem Left Right Midbrain Pons Medulla A combination of long-tract and brainstem signs may allow accurate location of a brainstem lesion
Slide 25: Case 1* • Right facial paralysis affecting upper and lower face + diplopia + left hemiparesis ( arm and leg) • What is the likely cause of the diplopia and where is the lesion?
Brainstem examination Slide 26: Answer 1 • Diplopia likely to be due to a right VIth nerve lesion – the VIIth nerve passes around the nucleus of VI just below the 4th ventricle in the pons • Right pons
Slide 27: Case2 • A 72 year old man with a right hemiplegia. On examination in addition to the hemiplegia with pyramidal signs his tongue deviates to the left and is atrophic and fasciculating on the left side
Slide 28: Answer 2 • Left medulla Combination of XII LMN lesion on left, and right UMN hemiplegia places lesion in the left medulla above the decussation of the pyramidal tract
Slide 29: brainstem examination Case 3* • A 26 year old woman with horizontal diplopia on looking to left and right. On examination impaired adduction of both eyes on attempted lateral gaze with relative preservation of convergence. In addition dysmetria and intention tremor of right hand.
Slide 30: Answer 3 The patient has features of - a lesion of the medial longitudinal fasciculus bilaterally - a lesion of the right cerebellum ( or its connections) - A bilateral MLF lesion is almost pathognomonic of MS and the addition of cerebellar signs strengthens the diagnosis
Slide 31: brainstem examination Case 4 * • A 24 year old woman with vertical diplopia maximal on looking up and horizontal diplopia maximal on looking right, difficulty swallowing, ptosis more pronounced on left, facial weakness more pronounced on right. Sensation in tact.
Slide 32: Answer 4 • No single brainstem lesion can account for all these features. • Myaesthenia gravis may present in this way with a combination of pure motor signs attributable to NMJ dysfunction of muscles innervated by various brainstem nuclei.
Slide 33: brainstem examination Case 5* • A 65 year old lady with a right sided ptosis, right pupil dilatation, diplopia, left sided cerebellar and pyramidal signs
Slide 34: Answer 5 • Right Midbrain • Eye signs are due to right III palsy. • Contralateral cerebellar signs due to damage to right Red Nucleus • Contralateral pyramidal signs due to damage to corticospinal tract
Slide 35: brainstem examination Case 6* • A 84 year old lady with sudden onset of a left hemiparesis and deviation of both eyes to the left side
Slide 36: Answer 6 • Right pons • The combination of gaze deviation and hemiparesis usually occurs with large hemispheric CVA’s; in such a case the eyes deviate to the side of the lesion ( due to destruction of the frontal gaze centre) • In case 8 the eyes deviate away from the lesion (left) due to the destruction of the right pontine paramedian reticular formation (PPRF)
Slide 37: What is Nystagmus? • Rhythmic oscillation of the eyes • Fast phase ( saccade) • Slow phase ( smooth-pursuit – like)
Slide 38: Describing nystagmus 1. Position of gaze in which occurs or is most prominent 2. Direction ( of FAST phase) 3. Precipitating / exacerbating factors 4. Fatiguing / persistent 5. Associated symptoms - Vertigo - Oscillopsia – feeling that vision is jerky
Slide 39: Brainstem examination Example: - Vestibular neuronitis left side • Most prominent on gaze towards right • Horizontal right – sided nystagmus with a rotatory component • Exacerbated by quick head movements • Associated with severe vertigo + / - vomiting • Persistent / may fatigue Illustrates following rule: Nystagmus is always most prominent on gaze towards the direction of the fast phase
Slide 40: Nystagmus may be……… 1.Physiological Central 3.Pathological Peripheral this is THE most important distinction to be made in assessing nystagmus!
Slide 41: IS IT NORMAL?? Physiological Pathological Never asymmetrical Usually asymmetrical Horizontal only Horizontal, vertical or rotational Fatigues Usually persistent Present only at extremes May be present at any of horizontal gaze position of gaze
Slide 42: Central vs Peripheral ( guidelines) Peripheral ( vestibular ) Central Unidirectional Uni or Bidirectional Horizontal usually with Horizontal, vertical or rotational component rotatory Vertigo severe Vertigo mild May be associated with May be associated with tinnitus or hearing loss other cranial nerve, cerebellar or long-tract signs
Slide 43: Diplopia “ The subjective feeling of seeing double” May be: 4. Monocular ( present even when one eye open) 5. Binocular ( present only when 2 eyes open) Monocular diplopia is either due to a local (ocular) process, “non- organic” in origin or very rarely from visual cortical dysfunction Therefore almost all neurological causes of diplopia are “ binocular ”
Slide 44: Binocular diplopia…questions 1. Horizontal vs Vertical ? 2. Worse on looking in which direction? 3. Worse on focussing near or far ? RULES 2) Diplopia is maximal on gaze in the direction of action of the weak muscle. 3) The false image is projected towards the direction of action of the weak muscle
Slide 45: Anatomical sites which may cause diplopia 1. Internuclear ( INO ) 2. Nucleus 3. Fascicle 4. Cranial nerve 5. Neuromuscular junction (NMJ)*** 6. Muscle 7. Local distortion of orbit *** ANY type of diplopia or gaze disturbance may be due to a problem at the NMJ….usually Myaesthenia Gravis …and often with ptosis
Slide 46: Example of a patient with Myaesthenia Gravis The examiner is lifting the patient’s eyelids for 2 reasons: - Good examination technique! - In this case the patient has bilateral ptosis
Slide 47: Which of the following patients cannot have MG? • Right eye totally paralysed, left eye moves freely but with ptosis • Inability of both eyes to move to left with no diplopia • Bilateral inability to look up with bilateral ptosis • Left eye deviated down and laterally with ptosis on left and left pupil larger than right Myaesthenia Gravis NEVER causes pupil asymmetry ( anisocoria) …..which brings us onto the next subject…..
Slide 48: Anisocoria “ Inequality between the 2 pupils” Pupils may be : - equal ( to within 1mm) - unequal due to surgery / trauma usually irregular) - unequal due to a neurological condition
Slide 49: The 2 neurological causes of anisocoria 1. One pupil too big 2. One pupil too small Parasympathetic---------------------------------------Sympathetic Constricts (Ach) Dilates (Nad) Travels in III Symp fibres
Slide 50: Anisocoria rules 1. Darkness exaggerates failure of dilation 2. Bright light exaggerates failure of constriction 3. If unilateral ptosis is present assume that the eye with the ptosis is sick!
Slide 51: Patient with a left IIIrd nerve palsy: - Left sided ptosis - Left pupil > Right - Medial rectus weakness seen on attempted gaze to right
Slide 52: Right – sided Horner’s Syndrome
Slide 53: Horner’s syndrome • Due to interruption of sympathetic input to eye - Ptosis - Miosis ( constriction ) - Anhidrosis ( lack of sweating on side of face) Lesion sites - hypothalamus, brainstem, cervical cord - cervical sympathetic chain and ganglion - fibres running next to carotid artery
Slide 54: Sphincter pupillae muscle Pathways involved in the pupillary light reflex
Slide 55: Left RAPD ( relative afferent pupillary defect) AKA Marcus-Gunn pupil For example a patient with multiple sclerosis who is suffering from acute left sided optic neuritis Step 1 small reaction of BOTH pupils to light on L Step 2 Normal (large) Step 3 reaction of BOTH pupils to Dilatation of BOTH light on R pupils with light on L when compared to Step 2
Slide 56: A lesion here would cause RAPD A lesion beyond the chiasm would NOT cause RAPD
Slide 57: Case 7* • Right facial paralysis with sparing of the forehead, right hemiparesis affecting arm>leg, diplopia maximal on looking right, left ptosis, left pupil larger than right, tongue deviation to right side
Slide 58: Answer 7 • Left midbrain • The UMN facial weakness places lesion above pons; remember that supra-nuclear innervation of each XIIth nerve nucleus is often unilateral therefore tongue deviation may occur • The IIIrd nerve palsy places lesion in midbrain
Slide 59: Question 8* • A 23 year old obese woman with acne with a 3 month history of headaches vomiting and transient visual symptoms. Over last 3 days horizontal diplopia maximal on looking left and into distance; except for the diplopia and one other abnormality the neurological examination is normal.
Slide 60: Answer 8 • The “other abnormality” is papilloedema • This woman is exhibiting classical features of raised intracranial pressure (likely in this case to be due to pseudotumour cerebri). A VIth nerve palsy may occur as a false localising sign in any case of raised intracranial pressure.
Slide 61: THE END For presentation requests and downloads please visit AskTheNeurologist.Com