A case of Herpes zoster of the mandibular nerve in an 80 year old man is reported. Herpes zoster infection affecting only the mandibular branch of the trigeminal nerve is rare, ft is proposed that the distribution of lesions is a consequence of a unique latent site of the virus within neurons of the gasserian ganglion innervating the mandibular division of the trigeminal nerve.

A rare abnormality of the vertebral artery is described in a 63-yearold male. The right vertebral artery consisted of several minute endothelial lined channels which failed to perfuse at autopsy. The anterior spinal artery showed areas of muscular media dysplasia. These anomalies were associated with large posterior communicating arteries. The terminal event was precipitated by thrombotic occlusion of the left vertebral artery. The embryological aspect of these anomalies are discussed.

Subdural empyema is a serious intracranial infection. C. T. scanning is the most accurate examination method in this disease. Increasing reliance on C. T. scanning makes it important to realize that even an enhanced scan may produce a false negative result, as outlined in this case.

A case is reported of traumatic chronic extradural hematoma in a child who had previously undergone a craniotomy for a different lesion. Perforations made in the bone flap served as vents for extrusion of the hematoma fluid into the subgaleal space, thus decompressing the intracranial space. This resulted in a benign clinical course.

Balint's syndrome is usually attributed to bilateral parieto-occipital lesions. In several reported cases involvement of the frontal lobes was also documented and could be responsible for the “spasmodic fixation” often recorded in these patients. We report a case of Balint's syndrome in a patient with bilateral frontal and parieto-occipital metastases demonstrated by CTscan and confirmed by postmortem examination.

Anxiety seems to be an inherent and perhaps necessary component of civilization. However, the biological basis of anxiety has always been as obscure as the definition of anxiety itself. The importance of anxiety to our mental wellbeing was noted by Freud (1933) who considered it a “nodalpoint”. As in the case of schizophrenia, there have been as many hypotheses to explain anxiety as there have been investigators with different techniques for studying it. The benzodiazepines, introduced clinically in I960, are now the most widely-used anxiolytic drugs. From the time of their introduction, it was felt that an explanation of the mode of action of benzodiazepines might shed considerable light on the basis of anxiety. The discovery, in 1977, of a specific benzodiazepine receptor, uniquely localized in the CNS, was the major turning point in this search (Squires and Braestrup, 1977; Mohler and Okada, 1977).

A case of hereditary sensory neuropathy is described resembling Dyck's Type I hereditary sensory neuropathy. Sensory testing revealed marked pain impairment in feet and hands shading at mid calf to normal at mid thigh and shading above the wrist to normal at the elbow. Other sensory modalities including temperature were intact except painful heat and painful cold and they produced very little if any discomfort. Stimuli at 0° C or 45° to 70° C elicited a temperature response but not pain. Sural nerve biopsy findings (including elecironmicroscopy) were consistent with a diagnosis of Type I hereditary sensory neuropathy, but also showed evidence of abortive axonal regeneration and profound Schwann cell vacuolation.

Experimental evidence is cited in support of the proposal that benzodiazepines exert their anxiolytic effects by inhibiting the uptake of adenosine by central neurons and glia.

Six years after apparent complete recovery from intestinal Whipple's disease, a 56 year old man developed insidious progressive somnolence and gait ataxia. Studies showed hydrocephalus with obstruction of the aqueduct and CSF leukocytosis and elevated protein. Arachnoid biopsy during craniotomy revealed chronic inflammatory infiltration with PAS-positive macrophages. The patient died 5 years later despite two courses of antibiotic therapy. This is the first report of histologically confirmed cerebral Whippie's disease during life.

Whipple's disease is a systemic infectious disorder. Cerebral involvement even in neurologically asymptomatic patients should be sought with periodic CSF cytologic studies and a search for hydrocephalus. The possibility of cerebral Whipple's disease should be considered in the presence of unexplained hydrocephalus and/or chronic inflammatory changes in the spinal fluid, especially in those with past or active intestinal disease.

The authors present a simple system for disability scoring and functional staging of an ataxic patient, based on modifications of a previous scheme advocated by De Falco and collaborators (1979). This system was tested under field conditions in 47 ataxic subjects and found to be useful and functional.

Nuclei of the extrapyramidal system contain among the highest levels of GABA and its synthesizing enzyme glutamic acid decarboxylase (GA D) in the central nervous system. In recent years the anatomical organization of GABAergic neurons in the extrapyramidal system has been the subject of considerable experimental enquiry. In this note, current knowledge concerning the origin and projections of GABAergic neurons in certain extrapyramidal nuclei is briefly reviewed.

The validity of a synaptosomal model to monitor drug-induced changes in the y-aminobutyric acid (GABA) content of nerve endings is reviewed. Examples of data obtained using the model are presented and the possibility of using the model for research on antipsychotic drugs is discussed.

We have studied a large family of which seven members suffer from a progressive disease with onset in the first decade. The first symptoms were gait ataxia and clumsiness in all cases, followed by progressive development of severe distal amyotrophy reminiscent of Charcot-Marie-Tooth disease. In four patients a postural tremor which was relieved by pharmacological agents was also evident in the limbs or head.

Cerebellar atrophy was confirmed on CT scan. Motor nerve conduction velocities were in the low normal range, while sensory nerve conduction was markedly decreased. All patients had impaired proprioception and vibration sense. The laboratory investigation revealed a normal CSF protein level and elevated serum bilirubin.

The patients reported in this study apparently suffer from an original recessive form of spinal and olivocerebellar degeneration associated with a neuronal form of Charcot-Marie-Tooth disease.