Four hundred and ninetytwo ulnar nerves were studied in 237 patients with cubital tunnel syndrome and 233 subjects without clinically apparent ulnar neuropathy. Terminal motor and sensory latencies, motor and sensory conduction velocities, sensory action potential amplitudes and dispersions, and needle electromyography were analysed by a 0 to 10 rating — the EMG score. The patients were clinically graded from 1 (least severe) to 4 (most severe). The median EMG scores of these were 0.9/10 (N=70): 1.6/10 (N=81); 4.7/10 (N=46); and 7.1/10 (N=56), respectively. The median EMG score for the controls was 0.6/10 (N=239) and 14.7% had asymptomatic ulnar entrapments. This incidence reached 30% in controls who were 60years or older. In 25 other controls, the above sulcus sensory action potential was analysed. Its mean dispersion was 4.9 ± 1.0 s-3. This measurement was significantly prolonged in 84.6% of 13 studies in which the EMG score was 0/10. These patients had either sensory symptoms only or an additional mild sensory deficit. Comparison of the EMG score obtained with sequential studies would allow one to objectively evaluate improvement or deterioration of the clinical state, giving a rational means of determining the need for surgery.

Fifteen regional cerebral blood flow studies (rCBF) were conducted on 14 patients with arteriovenous malformations (AVM). Only one patient was studied at the time of a hemorrhage. None of the patients were operated upon. All patients had angiographically demonstrated lesions. All the CT scans performed demonstrated the lesions. rCBF was increased in the involved hemisphere compared to the non-involved hemisphere and the difference was greater when the malformations were superficial. There was a higher incidence of high flow regions in the involved hemisphere of patients with AVMs compared to our normal control group and patients with subarachnoid hemorrhage (SAH) from aneurysms. Flow rales within the involved hemisphere demonstrated abnormal distributions and greater variability than normals. Some peaks previously demonstrated in the intraarterial flow studies are not apparent using the inhalation method. This noninvasive technique has a potential to provide additional useful information on the natural history of this disorder.

A World Health Organization Expert Committee has concluded that symptoms of methylmercury poisoning may appear at blood concentrations of 200-500 ng Hg/ml. Blood levels in this range have been found in several Indian and Inuit communities in Canada. The syndrome of severe methylmercury poisoning (Hunter-Russell syndrome) is well described. However, diagnosis of less severe cases is difficult. This paper reviews the present situation in Canada. The problems of diagnosis currently being encountered are discussed and are illustrated by the case of an individual who had one of the highest blood concentrations (551 ng Hg/ml) ever described in fish-eating populations outside of the outbreaks in Minamata and Niigata in Japan. Although mercury concentrations in brain were estimated to have been in the “symptomatic” range at least once in the two years prior to his death, neurohisiological examination was normal. Detailed examination by two teams of neurologists revealed effects that may be associated with methylmercury poisoning but a definitive diagnosis remained elusive.

Brain edema (BE) research lacks quantitative regional methods. We modified the method of Pappius and McCann (1969), who used radioactive iodinated I125 serum albumin (RISA) as a label for vasogenic BE fluid. To correct for intravascular plasma volume we used Cr51 labelled red blood cells and calculated equivalent extravascular plasma volume (EVPV). The modified RISA method was compared with a standard method for measuring increased tissue water, i.e. the change in wef.dry weights. Anesthetized rabbits were subjected to unilateral cortical freeze injury and sacrificed three hours later. The lesion corresponding to the area of blood brain barrier (BBB) breakdown was delineated by Evan's blue staining. That area and the two adjacent poles were sectioned. The contralateral hemisphere was used as the control. Good agreement was found between the two methods. By the modified RISA method, 4.08% of the wet weight of the injured hemisphere was EVPV while the decrease in dry weight corresponded to 5.56% edema. In the freeze lesion, however, where BBB breakdown occurred extravascular (EV)protein exceeded EV water, while adjacent to the lesion in the area with intact BBB, EV water exceeded EV protein. This suggests that the diffusion rate for water through brain tissue exceeds that of albumin in the early stages of vasogenic BE formation. We conclude that the modified RISA method is a satisfactory measure of regional vasogenic BE in acute animal experiments.

The few existing neuropathological, neurochemical, and neuropharacological studies have shed little light on the pathophysiology of spasmodic torticollis (ST). The relevance of experimental ST in animals and drug-induced ST in man to idiopathic ST is unclear.

Most pharmacotherapeutic endeavors have focused on drugs affecting basal ganglia function. Unfortunately, problems of sample size, clinical heterogeneity of patient population, research design, objective evaluation of response, documentation of key data, and adequacy of duration of follow-up make interpretation of published results difficult. Because of the heterogeneity of ST, investigations aimed at establishing a neurotransmitter profile for each patient by observing the acute response to a test dose of drugs affecting cholinergic, dopaminergic, serotonergic, and gammaaminobutyric acid systems may provide a more rational basis to the selection of treatment.

In reinnervatedskin transferred from the foot to the hand, sensory thresholds approach normal values — an observation not predicted by the theoretical relationship between innervation density and tactile acuity. Therefore, we suggest that innervation density is not the major factor determining tactile acuity. Rather, the hand region of the central somesthelic map may be specialized to provide a calibre of function unavailable to other regions.

The aim of medical management of a patient with a recently ruptured intracranial aneurysm is to preserve residual brain function and prevent systemic complications. Surgery should be performed as soon as the patient is in good neurological condition. Most fatalities result from the destructive effects of the initial hemorrhage, but delayed ischemic neurologic deficit can result from vasospasm and rebleeding. Systemic complications of the brain damaged state result in a smaller proportion of deaths.

Common medical problems are reviewed as well as their medical management. In particular, some special problems related to subarachnoid hemorrhage such as cerebral edema and herniations, rebleeding, and vasospasm are also considered. Major recent advances have been the introduction of antifibrinolytic therapy, the realization of the importance of maintaining blood volume and pressure, as well as general advances in respiratory care.

HLA-A, B, and C typing was carried out on five families with classical Friedreich's Ataxia (F.A.). Segregation patterns in a total of 16 offspring. 10 with the disease and 6 without, indicated no association between F.A. and HLA.

In vitro experiments using the equilibrium dialysis technique were performed to determine the binding of valproic acid to plasma components in the absence and presence of therapeutic concentrations of phenytoin. The free fraction of valproic acid was found to be dependent on the total valproic acid concentration. Phenytoin did not influence valproic acid protein binding.

Because of the high concentrations of ɣ-aminobutyric acid (GABA) in the cerebellar cortex and nuclei, an attempt was made to enhance GABAergic transmission in patients with cerebellar disease. Maximum tolerated doses of sodium valproate, a drug which inhibits the degradation of GABA, failed to influence cerebellar deficits in a double blind crossover study on six patients.