A review of the convulsive seizures of 153 alcoholics is followed by a proposed classification with the aim of defining more precisely the pattern of so-called alcoholic epilepsy and distinguishing it from the other alcohol-related seizures (due to sudden changes in alcohol intake: convulsive inebriation or alcohol withdrawal seizures) and seizures in which alcohol is only one of the pathogenetic factors. Particular attention is devoted to an analysis and comparison of alcohol withdrawal seizures and alcoholic epilepsy, which are a source of nosological confusion. The results of oral glucose tolerance tests suggest an etiopathogenesis for alcoholic epilepsy based on the carbohydrate metabolism.

Classic statistical method (mean, standard deviation, variance) were used to analyze peripheral nerve conduction tests and visual evoked potentials in 13 chronic alcoholics and in 11 chronic alcoholics who had abstained for at least one year, in order to assess the repercussions of alcohol on the PNS and on the visual pathways and their reversibility. The sensory fibers were more affected than the motor fibers, and while the damage to the motor fibers was transient the damage to the sensory fibers was permanent and also significantly different, at least in the early stages, in the two lower limbs. Our results showed constant involvement, without clinical symptoms, of the visual potential, especially of the earliest component N70 and of the amplitude of the response. This would suggest greater involvement of the peripheral visual nervous structures, that is retino-geniculo-cortical, than of the more properly cortical structures, though these are also affected. For the visual damage too withdrawal of alcohol seems to determine a regression, though only partial, of the neurophysiological changes. The simultaneous involvement of VEP and peripheral nerve function is at variance with the assertion that optic nerve damage is a very rare event in alcoholism.

An immunocompetent adult developed cytomegalovirus (CMV) meningoencephalitis with paroxysmal neurologic symptoms of a self-limited nature and with a favourable outcome. Consistent with known cases in the clinical literature, two clinical forms of CMV meningoencephalitis will be identified: a monophasic form and a paroxysmal form. The clinical, diagnostic and therapeutic aspects of the two types will be analysed, and a pathogenetic hypothesis for the paroxysmal type will be proposed.

The aim of the study was to assess the occurrence and the clinical features of primary headaches in a sample of players of the Italian Soccer League first division. The design of the study allowed a retrospective and prospective diagnosis of primary headaches according to the International Classification of Headache Disorders-II edition (ICHD-II), using anonymous questionnaires, which had to be filled out at regular times during the playing season. A total of 83 athletes playing in four different clubs were involved; four of them changed football team during the season and so did not complete the study. During the championship three soccer players reported headache (3.6%) with features fulfilling ICHD-II criteria for episodic tension-type headache. Important and prolonged physical effort was reported as aggravating factor in one case, but no attacks occurred during competitive matches. The same athletes had reported a personal history of episodic tension-type headache. In conclusion, the occurrence of primary headaches among professional soccer players of Italian first division championship appear to be strikingly lower, as compared to that found in the general population. A possible explanation could be given by the selection operated by a career which is not compatible with unpredictable, disabling attacks.

A 30-year-old man without previous attacks of migraine, despite a family history of migraine, presented with moderate headache and temporary focal neurological signs and symptoms. The patient had had, two weeks previously, a prodromic flu-like illness. Cerebrospinal fluid (CSF) analysis showed lymphocytic pleocytosis and increased total protein. Extensive microbiological determinations were negative. Routine hematological, immunological, blood and urine tests were normal. Electroencephalography showed a focal slowing in the right temporal area. Brain SPECT, performed during a symptom-free period, revealed decreased tracer uptake in the left temporal and insula cortices,topographicallyconsistent with abnormalities on brainstem auditory evoked potentials. Computed tomography and magnetic resonance imaging of the brain were normal. A cardiovascular examination provided normal results. The patient completely recovered within 2 days. This condition is suggestive of "headache with neurologic deficits and CSF lymphocytosis" (HaNDL syndrome). I hypothesize that this syndrome could be produced by the direct action of a virus.