B vitamin deficiency is a leading cause of neurological impairment and disability throughout the world. Multiple B vitamin deficiencies often coexist, and thus an understanding of the complex relationships between the different biochemical pathways regulated in the brain by these vitamins may facilitate prompter diagnosis and improved treatment. Particular populations at risk for multiple B vitamin deficiencies include the elderly, people with alcoholism, patients with heart failure, patients with recent obesity surgery, and vegetarians/vegans. Recently, new clinical settings that predispose individuals to B vitamin deficiency have been highlighted. Moreover, other data indicate a possible pathogenetic role of subclinical chronic B vitamin deficiency in neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, and amyotrophic lateral sclerosis. In light of these findings, this review examines the clinical manifestations of B vitamin deficiency and the effect of B vitamin deficiency on the adult nervous system. The interrelationships of multiple B vitamin deficiencies are emphasized, along with the clinical phenotypes related to B vitamin deficiencies. Recent advances in the clinical determinants and diagnostic clues of B vitamin deficiency, as well as the suggested therapies for B vitamin disorders, are described.

There was a low chance (<10%) of being offered surgery if there were bilateral lesions on MRI and extratemporal lobe epilepsy. Patients should be given advice on the risk/benefit ratio and of realistic outcomes of epilepsy surgery; this may help reduce the number of patients who refuse surgery after comprehensive workup.

SUMMARYThis study aimed to determine clinical features of adult patients with gelastic seizures recorded on video -electroencephalography (EEG) over a 5-year period. We screened video-EEG telemetry reports for the occurrence of the term "gelastic" seizures, and assessed the semiology, EEG features, and duration of those seizures. Gelastic seizures were identified in 19 (0.8%) of 2,446 admissions. The presumed epileptogenic zone was in the hypothalamus in one third of the cases, temporal lobe epilepsy was diagnosed in another third, and the remainder of the cases presenting with gelastic seizures were classified as frontal, parietal lobe epilepsy or remained undetermined or were multifocal. Gelastic seizures were embedded in a semiology, with part of the seizure showing features of automotor seizures. A small proportion of patients underwent epilepsy surgery. Outcome of epilepsy surgery was related to the underlying pathology; two patients with hippocampal sclerosis had good outcomes following temporal lobe resection and one of four patients with hypothalamic hamartomas undergoing gamma knife surgery had a good outcome. KEY WORDS: Gelastic seizures, Hypothalamic hamartoma, Temporal lobe epilepsy, Epilepsy surgery.Gelastic seizures are the hallmark of seizures arising from the hypothalamus, with hypothalamic hamartoma being the most frequent underlying pathology.1 Such seizure types are rare and are more likely to be diagnosed in childhood. Gelastic seizures in the setting of hypothalamic hamartomas are associated with childhood onset, intractable seizures, precocious puberty and, commonly, cognitive impairment. 1Functional imaging studies and intracranial electroencephalography (EEG) recordings have shown that seizures originate in the hamartomas. 2,3Recent reports have indicated that there is secondary independent epileptogenesis, 4 which is facilitated by the plethora of connections between the hypothalamus and other brain areas, particularly the temporal lobe. The hypothalamus is unlikely to be the symptomatogenic zone of gelastic seizures, as laughter and mirth involves a complex brain network involving the cingulate and basal temporal cortex. 5 This contention is supported by the fact that gelastic seizures are seen not only with hypothalamic hamartomas, but also with seizures arising from the temporal and frontal lobes.6-8 Most of these cases, with gelastic seizures arising from brain structures other than the hypothalamus, have been reported in adults. Case series of gelastic seizures in an adult cohort are lacking, and it remains to be determined whether hypothalamic hamartomas are the leading underlying pathology, and whether adults with gelastic seizures and hypothalamic hamartomas have secondary epileptogenic zones. Such information would be important, since it would prompt (1) more careful evaluation in adults with gelastic seizures and hypothalamic hamartomas and (2) would lead to a better understanding of brain areas involved in gelastic seizures. BRIEF COMMUNICATIONWe aimed to quantify the occurre...