Regional cerebral blood flow measurements and neuropsychological testing were conducted before and after venesection on 6 patients with polycythemia secondary to chronic obstructive pulmonary disease. Venesection resulted in lowered viscosity and hematocrit, and an accompanying improvement in cerebral perfusion and mental function. Blood flow was significantly increased in the left cerebral hemisphere following phlebotomy, and there was significant improvement in sensory I mental function. Cerebral function would appear to be related to blood flow alterations influenced by the viscosity of the blood.

A computer program was developed to analyse the relative amount of EMG activity in an agonist-antagonist pair of muscles while subjects performed voluntary flexion-extension movements at the wrist to track a visual target. The data were presented to the subjects in the form of a vector display, the angle and length of which was determined from calculation of EMG power in the two muscles.

This new approach to EMG biofeedback was evaluated in two hemiplegic patients and three patients with cerebellar incoordination. Over a training period of several weeks, all the subjects were able to modify the pattern of EMG activity in the muscles to reduce the amount of inappropriate coactivation of flexors and extensors and to produce more sustained and regular activation of individual muscle groups.

A female child, TK, was born January 12, 1965, and was initially admitted to the Hospital for Sick Children, Toronto, on January 13, 1972, at age seven years with a sevenday history of runny nose, earache, headache, and fever. On the day before admission, she had a grand mal seizure and lumbar puncture revealed purulent cerebrospinal fluid (C.S.F.) which grew pneumococci. She was treated with antibiotics, her meningitis resolved, and she was discharged home nine days after admission.

We present the first case of central pontine myelinolysis (CPM) confirmed by high resolution computerized tomography (CT) in which auditory brainstem responses (A BR) revealed impaired conduction beyond the mid pons. The combined use of CT and A BR in the diagnosis of central pontine myelinolysis is discussed.

Twenty-two patients were carefully defined as having progressive dementia without other known cause and not complicated by clinical or laboratory evidence of multiinfarct dementia. Their degree of dementia measured by the ESD correlated highly with EEG disturbance (r=-0.79). The LPRS correlated 0.73 with ventricular enlargement. Although the EEG and CT scan only correlated significantly with each other in advanced cases, a combined index of EEG and CT Scan change, (Physical Meaasures Index) achieved a correlation of 0.93 with a combined index of psychological change (Psychological Measures Index). The results indicate the possibility of using physical and psychological measures to monitor quantitative change in Alzheimer's Disease, the EEG contributing more initially and the CT scan more in the most advanced cases.

An ABA within-subject study design was used to assess the effect of dietary phenylalanine restriction on the visual attention span of three mentally retarded males (9, 15, and 21 years old)with phenylketonuria. Visual attention span was measured by recording the amount of time the subjects visually fixated pictures projected on a screen according to a standardized test protocol. After 4-6 weeks of baseline testing (A-phase), each subject was placed on a phenylalaninerestricted diet, designed to maintain plasma phenylalanine levels at 0.3 - 0.9 mM, for 8-14 weeks (B-phase). A return to baseline phenylalanine intake (A-phase) was achieved by surreptitiously adding sufficient L-phenylalanine to the therapeutic diets to increase plasma concentrations of the amino acid to pretreatment levels. Diet treatment (B-phase) was associated with highly significant improvementsin visual attention span in two subjects (multivariate analysis of variance, P <<0.001); the third subject, the most retarded, showed no effect. No objectivelydemonstrable change in behavior was documented in any subject. However, the results support the view that phenylalanine toxicity extends beyond early childhood and that some component of the toxicity is reversible, even in severely retarded patients with phenylketonuria.

A 28 year old female presented with clinical and electrical evidence indicative of L5 motor radiculopathy. Subsequently she was found to have symptoms and signs of multiple sclerosis. When clinical assessment and investigation fail to disclose a cause then demyelinating disease should he considered in the differential diagnosis of motor radiculopath.

Necropsy findings consistent with spongiform encephalopathy of the Creutzfeldt-Jakob type are described in the brain of a 48-year-old woman whose prolonged course and clinical features had suggested Alzheimer's presenile dementia. Six other members of her family in two generations have also died of progressive presenile dementing illnesses of Alzheimer type, lasting 5-10 years.

Autopsies showed a post-viral temporal lobe encephalopathy in one and spongiform (C-J) lesions in another. Neuropathological studies in this family add weight to the idea that Alzheimer's disease and Creutzfeldt-Jakob disease represent different manifestations of a genetic predisposition to “slow virus” encephalopathies.

A case of intraventricular hemorrhage secondary to a ruptured aneurysm of the posterior inferior cerebellar artery in a child is presented. Treatment is discussed and the literature is reviewed.

The case history to be presented spans most of the lifetime of a young lady who is now twenty-two years old, and it reflects the stages of development of our knowledge of several important neurosurgical concepts.

Charles River CD male rats were randomly divided into 3 groups of five each and placed on folate deficient, folate excess, and control diets respectively. Glutamate decarboxylase GA D y-aminohutyrate aminotransferase (GABA-T), choline acetyltransferase (ChAc), and acetylcholinesterase (AChE) were assayed in the rat brains after 6 weeks of dietary treatment. Neither folate deficiency nor folate supplementation influenced the enzymes associated with GABA and acetylcholine metabolism.

The cerebral pathology in a case of tricyclic antidepressant overdose by amitriptyline is described. A review of the literature of similar cases is summarized. The relation of the cerebral lesions to the development of a hypertensive episode possibly induced by amitriptyline is discussed.

Constriction of a peripheral nerve may precipitate a primary problem or prevent recovery from a pre-existing one. Any surgical technique to minimize subsequent constrictive scar formation would be advantageous. In this study, using rat femoral nerves, various modes of protection were evaluated. Wrapping the nerve with free fat seemed to offer the best prophylaxis.

Experiments were conducted to evaluate the effect of various durations of 1-Hz brain stimulation on kindling behaviour induced by 60-Hz sine wave stimulation. In two experiments the effective threshold intensity (ETI) to elicit a convulsion was determined on four separate occasions with 5 days of daily trials interspersed between determinations. On each day experimental rats were stimulated with I-Hz current on the first and third trials for 5, 15, 30, 60, 120, 180, or 600 seconds duration and with 60-Hz current for 30 seconds on the second trial. A steady increase in the intensity required to elicit a convulsion with 60-Hz current from ETI2 to ETI4 resulted for all rats with durations of 15 seconds or greater. Rats stimulated only with 60-Hz sine waves, and those in the 5 second group, maintained relatively stable values from ETI1 to ETI4 with a slight decline occurring. Suppression of convulsive behavior on daily trials was modest in the 15 second group, pronounced with the 30 second group, and drastic with the other groups. The 600 second group had the greatest suppressive effect operating. The suppression effect did not appear to be due to tissue damage inasmuch as most of the experimental rats (except the 600 seconds one) convulsed again at previous low ETI levels following a 15 or 16 day rest at the end of the experiment. This result suggests that the suppression effect is a relatively transient event.

An ultrastructural study of the sympathetic ganglia, dorsal sympathetic chain, and Auerbach's plexus is described in the streptozotocin diabetic rat. The observations cover the first six weeks following induction of diabetes. Degenerative changes began to appear in the axonal plasma membranes and axoplasm of unmyelinated fibers at 24 hours and were widespread by two weeks. Axonal sprouting and regenerating axons began to appear and increase in number through the 6th week. Chromatolysis in ganglion cells in sympathetic ganglia became apparent by two weeks as did degenerative changes in axons of Auerbach's plexus. This somewhat later appearance of changes in ganglion cells and Auerbach's plexus suggested the primary changes occurred in the postganglionic fibers. The cycle of change from degeneration to regeneration in the areas examined suggests either a possible toxic effect of strepiozotocin or a combination of metabolic disturbances as a cause of this neuropathy.

An experiment was tonducted to evaluate the effect of various frequencies of brain stimulation on kindling behavior induced by 60-Hz sine wave stimulation. The effective threshold intensity (ETI) to elicit a convulsion was determined on four separate occasions with 5 days of daily trials between determinations. On each day experimental rats were stimulated with current of a specific frequency on the first and third trials for 60 seconds duration and with 60-Hz current for 30 seconds on the second trial (one hour intertrial interval). There were five experimental groups, one each for I, 5, 10, 30, and 60-Hz stimulation. A sixth group received no stimulation on trials I and 3 and 60-Hz current on trial 2. Suppression of convulsive behavior induced by the 60-Hz stimulation trial was present for all ETI determinations with I-Hz and5- Hz stimulation; the mean ETI increased on each successive determination. Suppression was prominent also for the 10-Hz group until the ETI4 determination. Suppression was moderate for the 30-Hz and 60-Hz groups. Overall, it appeared that the interference effect gradually increased with remoteness from the 60-Hz point.

A patient exhibited confusion, dysphasia, and striking asterixis 18 hours after metrizamide myelography. The symptoms lasted for a day and a half. While metrizamide is a useful contrast medium, side effects are not unusual and can, on occasion, be quite severe.

Injury to peripheral nerves complicating deep intramuscular injections of antibiotic and other agents is well recognized and can result in significant permanent neurological deficit. The purpose of this paper is to review the subject of nerve injection injuries, and report on a series of recent experimental studies carried out in this laboratory designed to improve our understanding of the pathophysiology of this condition and help provide a rational basis for its treatment. A wide variety of chemotherapeutic, prophylactic, and local anaesthetic agents in common use were injected into the sciatic nerve of the adult Wistar rat. Both intrafascicular and extrafascicular injections were examined. Results revealed that the site of injection was the most crucial factor in determining the degree of nerve fiber injury. Following intrafascicular injection, the degree of injury varied significantly, depending upon the specific agent injected. The most severe injuries were associated with wide-spread axonal and myelin degeneration. Pathological alterations in the nerve were evident as early as 30 minutes following injection injury. Regeneration was a constant finding in nerve damage by injection of the various agents. The mechanism of injury appeared to be a direct toxic effect of the injected compound on neural tissue, with an associated break down of the bloodnerve barrier.

The prevalence of Horner's syndrome in the MS patient population is 2 - 3%. Using pharmacologic testing in three patients the lesions were localized to the central or intermediate sympathetic neurons. It is likely that demyelination of the central sympathetic neuron accounts for this probable manifestation of MS.