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Sleep and headache have both generated curiosity within the human mind for centuries. The relationship between headache and sleep disorders is very complex. While Lieving in 1873 first observed that headaches were linked to sleep, Dexter and Weitzman in 1970 described the relationship between headache and sleep stages. Though our understanding of sleep and headache relationship has improved over the years with expanding knowledge in both fields and assessment tools such as polysomnography, it is still poorly understood. Headache and sleep have an interdependent relationship. Headache may be intrinsically related to sleep (migraine with and without aura, cluster headache, hypnic headache, and paroxysmal hemicrania), may cause sleep disturbance (chronic migraine, chronic tension-type headache, and medication overuse headache) or a manifestation of a sleep disorder like obstructive sleep apnea. Headache and sleep disorder may be a common manifestation of systemic dysfunction-like anemia and hypoxemia. Headaches may occur during sleep, after sleep, and in relation to different sleep stages. Lack of sleep and excessive sleep are both considered triggers for migraine. Insomnia is more common among chronic headache patients. Experimental data suggest that there is a common anatomic and physiologic substrate. There is overwhelming evidence that cluster headache and hypnic headaches are chronobiological disorders with strong association with sleep and involvement of hypothalamus. Cluster headache shows a circadian and circannual rhythmicity while hypnic headache shows an alarm clock pattern. There is also a preferential occurrence of cluster headache, hypnic headache, and paroxysmal hemicrania during REM sleep. Silencing of anti-nociceptive network of periaqueductal grey (PAG), locus ceruleus and dorsal raphe nucleus doing REM sleep may explain the preferential pattern. Sleep related headaches can be classified into (1) headaches with high association with obstructive sleep apnea, which includes cluster headache, hypnic headache, and headache related to obstructive sleep apnea; and (2) headaches with high prevalence of insomnia, medication overuse, and psychiatric comorbidity including chronic migraine and chronic tension-type headache. The initial step in the management of sleep related headache is proper diagnosis with exclusion of secondary headaches. Screening for sleep disorders with the use of proper tests including polysomnography and referral to sleep clinic, when appropriate is very helpful. Control of individual episode in less than 2 hours should be the initial goal using measures to abort and prevent a relapse. Cluster headache responds very well to injectable Imitrex and oxygen. Verapamil, steroids and lithium are used for preventive treatment of cluster headache. Intractable cluster headache patients have responded to hypothalamic deep brain stimulation. Hypnic headache patients respond to nightly caffeine, indomethacin, and lithium. Paroxysmal hemicrania responds very well to indomethacin. Early morning hea...

SUMMARYLately, few case reports have brought forth limited cases of levetiracetam (LEV)-induced thrombocytopenia. To estimate the burden of LEV-induced thrombocytopenia, we reviewed medical records of 758 patients aged 18 years or older who received LEV during their stay at the University Hospital from June 2005 to December 2008. In patients identified with thrombocytopenia, records were reviewed to establish a cause of thrombocytopenia and possible causal role of LEV. Of 758 patients, 29 patients were identified with thrombocytopenia while on LEV therapy. For 23 patients, an alternative cause for thrombocytopenia was established; 4 patients had preexisting thrombocytopenia without any appreciable change in platelet count after addition of LEV. One patient had limited data for identifying the cause of thrombocytopenia. A single patient had clear temporal co-relation and association of thrombocytopenia with LEV therapy. LEV-induced thrombocytopenia is a rare but reversible complication of LEV therapy. The mechanism remains unknown.

SUMMARYExperimental studies suggest that 5-hydroxytryptamine (5-HT) receptors play a role in epileptogenesis and seizure propagation. Ondansetron, a 5-HT 3 receptor antagonist, has been reported to have proconvulsant and anticonvulsant effects in animals. We describe three patients who developed seizures after receiving ondansetron. There were two females and one male. Ages ranged from 38-56 years. None had a previous or family history of seizures. Four milligrams (mg) of ondansetron was given intravenously for severe nausea and vomiting in association with migraine, gastritis, and diabetic ketoacidosis. A generalized tonicclonic seizure occurred in each patient-12, 15, and 22 min after injection. Brain magnetic resonance imaging (MRI) and electroencephalography (EEG) were normal in all patients. Although no antiepileptic drugs were given, none had seizure recurrence subsequently. The temporal relationship between ondansetron administration and seizures, lack of EEG or MRI abnormalities, and absence of seizure recurrence suggest that the seizures were causally related to ondansetron in our patients.