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A detailed review of the adverse reactions of anticonvulsants is given, focusing on the definitions of drug toxicity, sources of information, patterns of durg utilization, pharmacokinetic variables and different mechanisms of action. The information available in the literature provides a wide spectrum of drug toxicity with no attempt at a practical definition of the reported events. This favors uncertainty among practising physicians, who are led to use the individual items with different attitudes. Suggestions are given for the evaluation, prevention and treatment of anticonvulsant drug toxicity.

Six patients with Steinert disease were treated with selenium and vitamin E, for a 24 month period, including a first phase of 12 months, 6 months wash-out interval and a second treatment phase of 6 months. Mean segmental strength values showed significant improvement during the first 12 months of therapy, while marked reductions of serum enzymes CPK, SGOT, SGPT and γ-GT were observed in some patients. The results support the hypothesis that selenium may play a role in the development of muscle damage in Steinert disease.

A 48 year-old man with chronic subdural hematoma presented with a parkinsonian syndrome. Removal of the hematoma was followed by gradual disappearance of the extrapyramidal symptoms, as in other, rare, published cases.

Cytomegalovirus (CMV) encephalitis is particularly evident in immunodepressed patients. Often diagnosis is difficult and time-consuming because of the complex basic clinical picture of these patients. We describe the diagnostic steps taken in a case of cytomegalovirus encephalitis affecting an elderly patient, classified as immunodepressed and deceased on the thirty-fifth day of hospitalisation in the intensive care unit due to acute myocardial infarction. Treatment with ganciclovir, 30 mg/kg per day, begun at the time of diagnosis, appears to have had a positive effect on the neurologic symptoms.

The diagnostic sensitivity of dermatomal somatosensory evoked potentials (DSEPs) was evaluated in a homogeneous group of fifteen patients with low back pain due to isolated lumbosacral radiculopathy. The normative values from L3 to S1 were defined, as were the parameters of abnormality. In seven patients with pseudoradicular or referred leg pain, a negative neurological examination and images indicative of protrusion or paramedian disc hernia, the DSEPs were normal in six cases and slightly altered in one. In eight patients with deafferentiation leg pain, clinical signs of root damage and images indicative of an intraforaminal hernia, the DSEPs showed varying degrees of alteration which could generally be correlated to the severity of the clinical picture. This method can therefore be useful in differentiating pain due to stimulation of the receptors of the osteoarticular structures or the root sheath, in which the DSEPs are normal, from pain due to direct root damage, in which the DSEPs are altered. This functional evaluation of anatomical damage provides further information which may help to achieve a better therapeutic approach.

MRI makes it possible to study the in vivo brain and spinal cord morphology of patients with hereditary ataxia. We performed T1-and T2-weighted studies in eleven patients with Friedreich's disease (FD), five with “late onset” FD and ten with early onset cerebellar ataxia with retained tendon reflexes (EOCA). Cervical cord atrophy was constant in FD and “late onset” FD and often associated with atrophy of the cerebellum and of the brainstem; T2-weighted studies showed posterior column degeneration in the cervical cord. The most frequent finding in EOCA was cerebellar atrophy, pure or associated with cervical cord or brainstem atrophy; the cerebellar atrophy was marked in a few cases and was related to disease duration.

We report the case of a 56-year-old woman who was accidentally poisoned when she ingested choke cherries whose pulp contained cyanide, and describe the acute clinical picture, the neurological sequelae and the neuroradiological findings. After recovery from coma, the patient showed signs of a parkinsonian syndrome, retrobulbar neuritis and sensory-motor neuropathy. MRI showed abnormal signal intensities involving the basal ganglia. Since no memory deficits were observed, we argue that the parkinsonian syndrome was caused by cyanide intoxication rather than by subcortical damage due to hypoxia.

Lisuride was investigated for therapeutic effects in 19 patients with advanced Parkinson disease, no longer satisfactorily responding to routine L-Dopa therapy. The patients were treated with oral Lisuride (0.6–2.5 mg/die) and L-Dopa. The follow-up was at least 6 months. We noted a significant improvement on the Webster Rating Scale at 1st, 3td and 6th months. Disability and on-off phenomen were reduced. Side effects were few. Lisuride is a valuable tool in this type of patient.