"Narcolepsy drug treatment can greatly impact on the lives of this often under-diagnosed condition characterized by an uncontrollable urge to fall asleep irrespective of the amount of hours sleep the person gets"
People with narcolepsy often get misdiagnosed as being depressed, lazy, or as suffering from "chronic fatigue syndrome" or fibromyalgia.
A physician experienced in diagnosing and treating sleep disorders should be able to separate these possibilities and initiate effective treatment.
The drugs provigil (modafinil) and ritalin (methylphenidate) are often highly effective in treating the symptoms of excessive sleepiness or "hypersomnia" associated with narcolepsy.
Latest research articles below, but you can search for something specific here
Sleep and aging: 2. Management of sleep disorders in older people.
CMAJ. 2007 May 8;176(10):1449-54
Authors: Wolkove N, Elkholy O, Baltzan M, Palayew M
The treatment of sleep-related illness in older patients must be undertaken with an appreciation of the physiologic changes associated with aging. Insomnia is common among older people. When it occurs secondary to another medical condition, treatment of the underlying disorder is imperative. Benzodiazepines, although potentially effective, must be used with care and in conservative doses. Daytime sedation, a common side effect, may limit use of benzodiazepines. Newer non-benzodiazepine drugs appear to be promising. Rapid eye movement (REM) sleep behaviour disorder can be treated with clonazepam, levodopa-carbidopa or newer dopaminergic agents such as pramipexole. Sleep hygiene is important to patients with narcolepsy. Excessive daytime sleepiness can be treated with central stimulants; cataplexy may be improved with an antidepressant. Restless legs syndrome and periodic leg-movement disorder are treated with benzodiazepines or dopaminergic agents such as levodopa-carbidopa and, more recently, newer dopamine agonists. Treatment of obstructive sleep apnea includes weight reduction and proper sleep positioning (on one's side), but may frequently necessitate the use of a continuous positive air-pressure (CPAP) device. When used regularly, CPAP machines are very effective in reducing daytime fatigue and the sequelae of untreated obstructive sleep apnea.
Narcolepsy drug treatment Narcolepsy drug treatment PMID: 17485699 [PubMed - indexed for MEDLINE]
A review of pediatric nonrespiratory sleep disorders.
Chest. 2006 Oct;130(4):1252-62
Authors: Moore M, Allison D, Rosen CL
Sleep problems are extremely common during childhood, from infancy to adolescence. Despite the prevalence of sleep problems, childhood sleep disorders are often underrecognized and undiagnosed, despite being either preventable or treatable. Sleep impacts almost all aspects of a child's functioning, and thus the increased recognition and treatment of sleep disorders will positively affect a child's well-being. Children experience the same broad range of sleep disturbances encountered in adults, including sleep apnea, insomnia, parasomnia, delayed sleep phase, narcolepsy, and restless legs, but their clinical presentation, evaluation, and management may differ. Although snoring and sleep apnea may be the most common indication for an overnight sleep study in a child, one quarter of children presenting to a sleep clinic for evaluation will have a second sleep diagnosis, which is often nonrespiratory in nature. Especially in children, ruling out sleep apnea is rarely the end point of the sleep evaluation. Clinicians involved in sleep medicine must be prepared to recognize, evaluate, and manage plans for sleep disorders across the lifespan of the patient. This article will provide an updated review of nonrespiratory pediatric sleep disorders within a developmental framework.
Narcolepsy drug treatment Narcolepsy drug treatment PMID: 17035465 [PubMed - indexed for MEDLINE]
Hypersomnia related to CNS disorders can be due to a variety of conditions. In this review, we discuss the diagnosis and treatment of narcolepsy with and without cataplexy, idiopathic hypersomnia, recurrent hypersomnia, and related illnesses. Research has provided insight into the underlying etiologies of these disorders, such as the genetic influences on disease development and the fundamental role of hypocretins in narcolepsy. We define the current utility of diagnostic testing, including sleep studies, neuroimaging techniques, and laboratory investigations. New treatment options for hypersomnia are discussed.
Narcolepsy drug treatment Narcolepsy drug treatment PMID: 16963696 [PubMed - indexed for MEDLINE]
General anesthesia and chronic amphetamine use: should the drug be stopped preoperatively?
Anesth Analg. 2006 Jul;103(1):203-6, table of contents
Authors: Fischer SP, Schmiesing CA, Guta CG, Brock-Utne JG
Prescription amphetamines are being used more often for several medical conditions. Anesthesia concerns focus on the cardiovascular stability of patients who may be catecholamine-depleted and thus have a blunted response to intraoperative hypotension. Previously we reported one case of a patient receiving chronic amphetamine therapy who had a stable intraoperative course. We now report eight additional patients taking chronic prescription amphetamines who underwent a safe general anesthesia and outcome. Predominantly prescribed for narcolepsy and attention deficit hyperactivity disorder, amphetamine drugs had been given to these 8 patients for 2 to 10 yr. Ages ranged from 22 to 77 yr and genders were equally divided. All required general anesthesia for their surgical procedures and 6 of the 8 patients were tracheally intubated. Anesthesia operating room times ranged from 30 min to 4.25 h. The authors conclude that amphetamine use need not be stopped before surgery and anesthesia.
Narcolepsy drug treatment Narcolepsy drug treatment PMID: 16790654 [PubMed - indexed for MEDLINE]
Clinical analysis of anti-Ma2-associated encephalitis.
Brain. 2004 Aug;127(Pt 8):1831-44
Authors: Dalmau J, Graus F, Villarejo A, Posner JB, Blumenthal D, Thiessen B, Saiz A, Meneses P, Rosenfeld MR
Increasing experience indicates that anti-Ma2-associated encephalitis differs from classical paraneoplastic limbic or brainstem encephalitis, and therefore may be unrecognized. To facilitate its diagnosis we report a comprehensive clinical analysis of 38 patients with anti-Ma2 encephalitis. Thirty-four (89%) patients presented with isolated or combined limbic, diencephalic or brainstem dysfunction, and four with other syndromes. Considering the clinical and MRI follow-up, 95% of the patients developed limbic, diencephalic or brainstem encephalopathy. Only 26% had classical limbic encephalitis. Excessive daytime sleepiness affected 32% of the patients, sometimes with narcolepsy-cataplexy and low CSF hypocretin. Additional hormonal or MRI abnormalities indicated diencephalic-hypothalamic involvement in 34% of the patients. Eye movement abnormalities were prominent in 92% of the patients with brainstem dysfunction, but those with additional limbic or diencephalic deficits were most affected; 60% of these patients had vertical gaze paresis that sometimes evolved to total external ophthalmoplegia. Three patients developed atypical parkinsonism, and two a severe hypokinetic syndrome with a tendency to eye closure and dramatic reduction of verbal output. Neurological symptoms preceded the tumour diagnosis in 62% of the patients. Brain MRI abnormalities were present in 74% of all patients and 89% of those with limbic or diencephalic dysfunction. Among the 34 patients with cancer, 53% had testicular germ-cell tumours. Two patients without evidence of cancer had testicular microcalcification and one cryptorchidism, risk factors for testicular germ-cell tumours. After neurological syndrome development, 17 of 33 patients received oncological treatment (nine also immunotherapy), 10 immunotherapy alone, and six no treatment. Overall, 33% of the patients had neurological improvement, three with complete recovery; 21% had long-term stabilization, and 46% deteriorated. Features significantly associated with improvement or stabilization included, male gender, age <45 years, testicular tumour with complete response to treatment, absence of anti-Ma1 antibodies and limited CNS involvement. Immunosuppression was not found to be associated with improvement but was clearly effective in some patients. Fifteen patients (10 women, five men) had additional antibodies to Ma1. These patients were more likely to have tumours other than testicular cancer and to develop ataxia, and had a worse prognosis than patients with only anti-Ma2 antibodies (two women, 21 men); 67% of deceased patients had anti-Ma1 antibodies. Anti-Ma2 encephalitis (with or without anti-Ma1 antibodies) should be suspected in patients with limbic, diencephalic or brainstem dysfunction, MRI abnormalities in these regions, and inflammatory changes in the CSF. In young male patients, the primary tumour is usually in the testis, in other patients the leading neoplasm is lung cancer.
Narcolepsy drug treatment Narcolepsy drug treatment PMID: 15215214 [PubMed - indexed for MEDLINE]
Narcolepsy caused by acute disseminated encephalomyelitis.
Arch Neurol. 2004 May;61(5):758-60
Authors: Gledhill RF, Bartel PR, Yoshida Y, Nishino S, Scammell TE
BACKGROUND: Narcolepsy with cataplexy is caused by a selective loss of hypocretin-producing neurons, but narcolepsy can also result from hypothalamic and rostral brainstem lesions. PATIENT: We describe a 38-year-old woman with severe daytime sleepiness, internuclear ophthalmoplegia, and bilateral delayed visual evoked potentials. Her multiple sleep latency test results demonstrated short sleep latencies and 4 sleep-onset rapid eye movement sleep periods, and her cerebrospinal fluid contained a low concentration of hypocretin. Magnetic resonance imaging showed T2 and fluid-attenuated inversion recovery hyperintensity along the walls of the third ventricle and aqueduct, which are consistent with acute disseminated encephalomyelitis. RESULTS: After treatment with steroids, this patient's subjective sleepiness, hypersomnia, and hypocretin deficiency partially improved. CONCLUSIONS: Autoimmune diseases such as acute disseminated encephalomyelitis can produce narcolepsy. Most likely, this narcolepsy is a consequence of demyelination and dysfunction of hypocretin pathways, but direct injury to the hypocretin neurons may also occur.
Narcolepsy drug treatment Narcolepsy drug treatment PMID: 15148155 [PubMed - indexed for MEDLINE]
Modafinil improves recovery after general anesthesia.
Anesth Analg. 2004 Apr;98(4):976-81, table of contents
Authors: Larijani GE, Goldberg ME, Hojat M, Khaleghi B, Dunn JB, Marr AT
Recovery from general anesthesia often involves residual sedation, drowsiness, fatigue, and lack of energy that may last hours to days. Modafinil is a wakefulness-promoting drug approved for patients with excessive daytime sleepiness associated with narcolepsy. We evaluated the effect of single doses of modafinil (200 mg) and placebo in patients recovering from general anesthesia. Thirty-four subjects participated in this prospective, randomized, double-blind study approved by our IRB. Preoperatively, patients were asked to rate various symptoms they had experienced over the previous 24-h using a verbal analog scale (VAS) of 0 to 10 as well as discrete scale when indicated. Postoperatively, once the patient was able to tolerate oral intake and met our institutional discharge criteria, the study drug (modafinil 200 mg or placebo) was administered with a sip of water. Patients were contacted 24 (1) hours after dosing to evaluate postdischarge symptoms. Patients in the placebo group reported significantly more postoperative fatigue (4.8 [3.3] versus 1.4 [1.8]), exhaustion (4.3 [3.3] versus 2.4 [3.1]), or degree of feeling worn out (4.7 [3.6] versus 2.9 [2.4]). Significantly more patients reported moderate to severe fatigue in the placebo group (65% versus 12%). Two major themes of "alertness" and "energy" were expressed by 71% of the patients receiving modafinil versus 18% of those receiving placebo. Patients recovering from general anesthesia can significantly benefit from modafinil. IMPLICATIONS: Modafinil significantly reduces fatigue and improves feelings of alertness and energy in postoperative patients. Patients recovering from general anesthesia can significantly benefit from modafinil administration.
Narcolepsy drug treatment Narcolepsy drug treatment PMID: 15041583 [PubMed - indexed for MEDLINE]
OBJECTIVE: Sleep is a complex neurologic process that is generated by and primarily benefits the brain. Sleep can be disrupted by a wide range of brain injuries, many of which may occur in children with neoplasms of the central nervous system (CNS). The specific sleep problems that have been associated with brain injuries include sleepiness, apnea, insomnia, and loss of circadian rhythmicity. The objective of this study was to characterize the sleep problems seen in children with neoplasms of the CNS through a comprehensive clinical and objective sleep evaluation. METHODS: A retrospective case series review was conducted of all children with neoplasms of the CNS referred to the sleep clinic for a clinical evaluation between 1994 and 2002. The sleep evaluation of the 14 children in this report included a sleep history, a sleep log, and a polysomnogram. In the 12 children with complaints of daytime sleepiness and/or fatigue, a multiple sleep latency test was performed the day after the polysomnogram. Three children also had a 2-week actigraphic study. RESULTS: The most common sleep complaint in this group of children was excessive daytime sleepiness (EDS), present in 9 of the 14 children. In these children, the sleepiness was manifest by 1 or more of the following symptoms: 1) an increase in total sleep time per 24 hours; 2) the resumption of daytime naps that had been previously discontinued at a younger age; 3) an inability to awaken in the morning to begin the days activities; or 4) the inability to remain awake during activities of daily living, such as school. Of the 9 children with daytime sleepiness, 8 had brain tumors requiring neurosurgical procedures at the time of their diagnosis, 6 of whom required ventricular shunting. The children with the most severe sleepiness had evidence of hypothalamic/pituitary injury with deficiencies in both anterior and posterior pituitary hormones. Five of the children with EDS had polysomnographic evidence of symptomatic narcolepsy with rapid eye movement sleep present on 2 or more of the daytime naps. The symptoms of EDS were effectively controlled with modest doses of daytime stimulant medication and/or scheduled naps. Central apnea leading to respiratory insufficiency and requiring mechanical ventilation to correct was present in 2 children with tumors involving the medulla. Although snoring with possible obstructive sleep apnea was the reason for referral to the sleep clinic in 5 children, none of the children in this series had polysomnographic evidence of significant obstructive sleep apnea. The other sleep problems seen in these children were hypoxia in 2 children, fatigue in 3 children, and seizures during sleep in 1 child. The interval between tumor diagnosis and sleep evaluation varied from 0 months to 9 years (mean: 42 months). The treatment of the sleep problems of this group of children took many forms, including stimulants, scheduled naps, mechanical ventilation, supplemental oxygen, and anticonvulsants. CONCLUSIONS: Brain injuries, which invariably are present in children with neoplasms of the CNS, may result in a variety of diagnosable and treatable sleep disorders. The sleep symptoms did not appear to be directly related to the specific therapy the child received, nor the presence of residual tumor. Rather, the primary determinant of the sleep symptoms was the area of the brain that was damaged, regardless of how the damage occurred. Children who sustained damage to the hypothalamic/pituitary region developed EDS regardless of whether the damage was the result of the tumor, surgery, hydrocephalus, or radiation to the whole brain or localized to the suprasellar area. The only children who developed respiratory insufficiency had an injury to the medulla. This observation is consistent with the view that sleep is a specific, albeit complex, neurologic process that is controlled by specific brain regions. EDS and respiratory insufficiency were the most commonly diagnosed severe sleep disorders in these children. The sleep problems of children with brain tumors may develop before, but more often soon after, their tumor diagnosis and treatment. However, the sleep symptoms may not be appreciated by medical providers until years after their onset, which may delay the beginning of effective interventions.
Narcolepsy drug treatment Narcolepsy drug treatment PMID: 12837905 [PubMed - indexed for MEDLINE]
IMPLICATIONS: Amphetamines are powerful, sympathomimetic amines that, when used chronically, can profoundly effect a patient's cardiovascular stability during anesthesia and surgery. Amphetamines are the third most widely abused class of drugs in the United States. They also have legitimate medical use for attention deficit disorder with hyperactivity, exogenous obesity, and narcolepsy. We report a case of a patient with a 40-yr history of chronic amphetamine use having undergone two general anesthesias without complication.
Narcolepsy drug treatment Narcolepsy drug treatment PMID: 10960415 [PubMed - indexed for MEDLINE]
Complex visual hallucinations. Clinical and neurobiological insights.
Brain. 1998 Oct;121 ( Pt 10):1819-40
Authors: Manford M, Andermann F
Complex visual hallucinations may affect some normal individuals on going to sleep and are also seen in pathological states, often in association with a sleep disturbance. The content of these hallucinations is striking and relatively stereotyped, often involving animals and human figures in bright colours and dramatic settings. Conditions causing these hallucinations include narcolepsy-cataplexy syndrome, peduncular hallucinosis, treated idiopathic Parkinson's disease, Lewy body dementia without treatment, migraine coma, Charles Bonnet syndrome (visual hallucinations of the blind), schizophrenia, hallucinogen-induced states and epilepsy. We describe cases of hallucinosis due to several of these causes and expand on previous hypotheses to suggest three mechanisms underlying complex visual hallucinations. (i) Epileptic hallucinations are probably due to a direct irritative process acting on cortical centres integrating complex visual information. (ii) Visual pathway lesions cause defective visual input and may result in hallucinations from defective visual processing or an abnormal cortical release phenomenon. (iii) Brainstem lesions appear to affect ascending cholinergic and serotonergic pathways, and may also be implicated in Parkinson's disease. These brainstem abnormalities are often associated with disturbances of sleep. We discuss how these lesions, outside the primary visual system, may cause defective modulation of thalamocortical relationships leading to a release phenomenon. We suggest that perturbation of a distributed matrix may explain the production of similar, complex mental phenomena by relatively blunt insults at disparate sites.
Narcolepsy drug treatment Narcolepsy drug treatment PMID: 9798740 [PubMed - indexed for MEDLINE]
Role of central alpha-1 adrenoceptors in canine narcolepsy.
J Clin Invest. 1988 Sep;82(3):885-94
Authors: Mignot E, Guilleminault C, Bowersox S, Rappaport A, Dement WC
The role of central alpha-1 adrenergic receptors in cataplexy was investigated in genetically narcoleptic Doberman pinschers. Treatment of narcoleptic dogs with 25-600 micrograms/kg prazosin, a selective alpha-1 adrenergic receptor blocker, exacerbated cataplexy, whereas treatment with the alpha-1 agonist, methoxamine, ameliorated it. Subsequent studies showed that the beneficial effects of classical treatments of human narcolepsy (amphetamines and tricyclic antidepressants) are antagonized by prazosin, suggesting that these drugs are active through an indirect alpha-1 stimulation (via an increase of norepinephrine in the synaptic cleft). Other studies confirmed that the observed effects were not due to peripheral alpha-1 cardiovascular involvement. Atropine, a central anticholinergic agent, but not methylatropine, a peripheral one, completely suppressed the prazosin effect, which suggests that adrenergic and cholinergic systems act sequentially and not independently to generate cataplexy. Little is known about the physiological role of central alpha-1 adrenoceptors. This series of experiments implicates these receptors in narcolepsy-cataplexy.
Narcolepsy drug treatment Narcolepsy drug treatment PMID: 2843574 [PubMed - indexed for MEDLINE]
Neurosarcoidosis associated with hypersomnolence treated with corticosteroids and brain irradiation.
Chest. 1988 Jul;94(1):205-6
Authors: Rubinstein I, Gray TA, Moldofsky H, Hoffstein V
Narcoleptic features developed in a young man with CNS sarcoidosis. This was associated with a structural lesion in the hypothalamus as demonstrated on CT scans of the head. The diagnosis of narcolepsy was established by compatible clinical history and the Multiple Sleep Latency Test. Treatment with high-dose corticosteroids was ineffective, but when the low-dose, whole-brain irradiation was added, complete resolution of the narcoleptic features ensued.
Narcolepsy drug treatment Narcolepsy drug treatment PMID: 3383638 [PubMed - indexed for MEDLINE]
Amphetamine, mazindol, and fencamfamin in narcolepsy.
Br Med J (Clin Res Ed). 1985 Apr 20;290(6476):1167-70
Authors: Shindler J, Schachter M, Brincat S, Parkes JD
Twenty patients with the narcoleptic syndrome were treated separately with dexamphetamine sulphate tablets 10 and 30 mg, Dexedrine Spansules 10 mg, mazindol 4 mg, and fencamfamin hydrochloride 60 mg daily. Each drug was given for four weeks and the effects compared. In these dosages the reported frequency of attacks of narcolepsy was roughly halved with each treatment, dexamphetamine 30 mg daily being only slightly more potent than 10 mg. The subjective effects of Dexedrine tablets and Spansules could not be distinguished by most patients. Effects on mood, alertness, and sympathomimetic side effects were largely inseparable with all these drugs, but a decrease in appetite was not reported by patients with narcolepsy.
Narcolepsy drug treatment Narcolepsy drug treatment PMID: 2859077 [PubMed - indexed for MEDLINE]