In the first part of the paper supplementary information on Flechsig’s personality and his attitude to work is given which had not been sufficiently appreciated in English biographical notices. This is followed by translated excerpts from “Gehirn and Seele”, published in 1896, in which Flechsig introduced his myelogenetic localization of the cerebral cortex.

The second part is mainly a review of recent advances in neuroanatomical and neurophysiological research within those cortical regions in which Flechsig had been interested. A comparison between recent advances and Flechsig’s work demonstrates that Flechsig had definitive ideas on the solution of some of the outstanding problems but had been unable to resolve these with the techniques available at his time.

Eight patients with a histologically proven angiographically occult arteriovenous malformation of the brain had plain and infused computed tomographic (CT) examinations. In five cases angiography revealed a hypovascular mass and in three cases the angiogram was normal. On CT examination a high density lesion (six cases) and ventricular asymmetry (five cases) were demonstrated. In three patients presenting with intracerebral hemorrhage, the high density appearance and ventricular compression were accounted for by the presence of hematoma. In three of five seizure patients the high density lesion was associated with calcification while ipsilateral (one case) and contralateral (one case) enlargement of the lateral ventricle was seen. In five of the eight cases the vascular nature of the lesion was suggested by vascular enhancement of the infused CT scan. Glioma was a common misdiagnosis.

Multimodality evoked potentials testing including PVEPs, SEPsand BAEPs was done in 112 patients who were known or suspected to have multiple sclerosis. The incidence of abnormal evoked potential findings in each of these systems was considered in patients in the different diagnostic categories of M.S. Results were also evaluated with respect to the presence of abnormal clinical visual, somatosensory, or brainstem signs. The PVEP was found to be the most frequently abnormal even in patients without clinical involvement in the visual system (45% of patients with definite, probable, or possible M.S.), the SEP was less frequently abnormal in the absence of clinical signs (35% in patients with M.S.), and the BA EP showed the lowest frequency of abnormalities in patients without brainstem signs (14% in patients with M.S.). Combining the three types of evoked potentials significantly increased the percentage of M. S. patients having abnormal findings, compared to any of these tests alone, with 97% of “definite” M.S. patients, 86% of “probable” M.S. patients and 63% of “possible” M. S. patients having at least one of these EP tests abnormal.

The eye movements of a patient with a left lateral medullary infarct (Wallenberg’s syndrome) were recorded using the scleral search coil in magnetic field technique. When asked to look at spontaneously appearing targets, saccades to the left were generally accurate hut those to the right reached the target by multiple step refixation saccades. Large amplitude rightward saccades were possible between two continuously visible targets or when making voluntary saccades in the dark.

Vertical saccades, up or down, between spontaneously appearing targets were always associated with a leftward eye movement (lateropulsion). Voluntary vertical saccades between continuously visible targets showed that upward movements had left lateropulsion but downward movements were normal. Vertical voluntary saccades in the dark were oblique, upward saccades showing left lateropulsion and downward saccades showing rightward deviation. The aberrant horizontal components of vertical saccades had amplitude and velocity characteristics for components of normal oblique saccades. Possibly impaired assessment of vertically with incorrect eye position information produced by the infarct accounts for the lateropulsion of saccades in Wallenberg’s syndrome.

The authors report on a patient with a ruptured anterior communicating aneurysm treated surgically on the day following her subarachnoid hemorrhage (SAH). Repeated measurements of cerebral blood flow (rCBF) were carried out using the inhalational Xenon 133 method. Dramatic acute increases in rCBF occurred, coincident with clinical improvement, following mannitol, CSF drainage and dopamine. Later, further elevation to normal levels occurred following ventriculo-peritoneal shunting.

Using a method of a gradual increase of bromocriptine with a concomitant reduction of Sinemet® (levodopa 250 mg + carhidopa 25 mg), 19 patients with advanced Parkinson’s disease have been treated for periods of up to 22 months and 16 of them have shown improvements of varying degrees. Eighteen patients were able to tolerate bromocriptine addition, with early transient adverse effects occurring in seven cases. In contrast to several previously reported studies, it was found necessary to withdraw bromocriptine in only one case.

With the drugs currently available, bromocriptine has a role in the management of patients with advanced Parkinson’s disease. The method described here may allow a greater number of patients to be given a trial with this drug.

One hundred multiple sclerosis (MS) patients and hospital controls were compared for coexisting illnesses, and other illnesses among their family members. The patients and controls were compared for allergy, migraine, and cancer among themselves and for a family history of these illnesses. The findings were negative. However a relationship was found between multiple sclerosis and diabetes mellitus. More MS patients than controls were either diabetic or reported a blood relative with diabetes. MS patients who reported another blood relative with MS were also more likely to report a family history of diabetes mellitus than MS patients who had no other relative with multiple sclerosis.

This case was presented as an interesting example of a global arteriovenous malformation (AVM) involving muscle, bone, extradural and intradural spaces of the cervical region.

A twenty-eight year old male in October, 1976, fell at work sustaining a blow to his lower back. The following day he complained of cervical pain. Physical examination was negative and he had a full range of movement of his cervical spine.

Plain films and tomograms of the cervical spine showed a lytic honeycomblesion of C2 and C3, and a 4 mm. subluxation of C3 on C4 (Fig. 1). The bone scan showed increased flow and decreased static activity in the upper cervical region. The radiological diagnosis was vertebral hemangioma; tumor, infection and histiocytosis were unlikely but important differential considerations.

A case of Fisher’s variant of Guillain Barré Syndrome is presented. Treatment with exchange transfusion coincided with clinical improvement. This is the first case of Fisher’s variant treated in this manner.

A patient presenting with palatal myoclonus was diagnosed as suffering from possible multiple sclerosis. A reduction of cerebrospinal 5-hydroxy-indole-acetic acid suggested a decreased central serotonergic turnover. A therapeutic trial with clonazepam, a serotonergic agonist, improved the myoclonus symptomatically. The possible involvement of serotonergic inhibitory systems in the expression of palatal myoclonus is discussed.

In a sibship of four, Friedreich’s ataxia and minimal lesion nephrotic syndrome occurred in two siblings, a third sibling had Friedreich’s ataxia, but no evidence of nephrotic syndrome; the fourth sibling had neither condition. The chance of Friedreich’s ataxia and minimal lesion nephrotic syndrome occurring in two siblings is small, and suggested a common immunological abnormality. High dose prednisone and antimetabolites given for the nephrotic syndrome did not appear to affect the course of Friedreich’s ataxia.

The two siblings with Friedreich’s ataxia and nephrotic syndrome developed epilepsy at age 15 years. All three children with Friedreich’s ataxia had abnormal electroencephalograms (EEGs). These epileptiform EEG abnormalities were probably inherited from the mother, who had spike wave epilepsy. The neurologic deficits of Friedreich’s ataxia, in turn, may have allowed the EEG trait to be expressed as a seizure disorder. The progressive ataxia and epileptic, sometimes myoclonic, seizures in these patients and the dentate nucleus changes in the autopsied patient were consistent with the diagnosis of dyssynergia cerebellaris myoclonica. This suggested that the latter disorder may represent a coincidence of two genetic entities: Friedreich’s ataxia and spike wave epilepsy.

Experiments were conducted to evaluate the effect of two intertrial intervals of 1-Hz brain stimulation on kindling behavior 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 between determinations. On each day experimental rats were stimulated with 1-Hz current on the first and third trials for 120 seconds duration and with 60-Hz current for 30 seconds on the second trial (1-60-1 group). A second group was stimulated with 60-Hz current on each trial (60-60-60 group). A third group received no stimulation on Trials 1 and 3 and 60-Hz current on Trial 2 (X-60-X group). In Experiment I, the intertrial interval was 3 hours; a 24 hour interval was used in Experiment 2. The results were similar in both experiments. For the 1-60-1 group, there was a steady increase in the intensity required to elicit a convulsion with 60-Hz current from ETI to ETI. However, the 24 hour interval produced a lesser effect than did the 3 hour interval (or the 1 hour interval used in previous experiments). Rats in the other groups maintained relatively stable values from ETI to ETI, with a slight decline occurring. Suppression of convulsive behaviour on daily trials was present with the 1-60-1 groups, and nonexistent with the other groups.

Demyelination is assumed to be the cause of the majority of cases of isolated optic neuritis. Because of the importance of establishing the presence of optic nerve dysfunction in patients suspected of having multiple sclerosis several new indices of optic nerve conduction have been reported including the visual evoked potential, the edge-light pupil cycle time, and the Pulfrich test. These measures purport to detect optic nerve dysfunction but with varying degrees of success. This study of 93 patients with clearly documented previous optic neuritis was conducted to determine the statistical relationship between these three measures and other clinical diagnostic indices for detection of previous optic nerve disease and the utility of the diagnostic predictors taken individually, and in combination. The other indices used were the presence of detectable optic atrophy, color vision defect and the presence of a relative afferent pupillary defect. The variables were submitted to linear stepwise multiple regression analysis which indicated that the presence of optic atrophy, defective color vision and prolonged pupil cycle time when used in combination provided the most useful diagnostic prediction of previous optic neuritis in this group of patients. The addition of visual evoked potentials, the Pulfrich test or presence of a relative afferent pupillary defect did not significantly increase predictive reliability.

Swollen, degenerate and fragmented neurons of the septal nuclei and the nucleus ansae peduncularis are commonly found in chronic neurological diseases such as Alzheimer’s or Huntington’s disease, and are rarely found in neurologically normal control patients without mental symptoms. These pathological lipid and pigment laden neurons appear to be a common feature of schizophrenia and have been consistently found in a series of unselected young (mean age 38) schizophrenics.

The case history and CT scan of a patient with delayed encephalopathy following carbon monoxide intoxication are described. The patient recovered.

The CT scan revealed symmetrical areas of decreased density at the level of the globus pallidus. This case differs in several ways from other cases of carbon monoxide intoxication in which abnormalities of the CT scan were found.

Crossed adductor reflexes were recorded electromyographically in ten patients with bilateral lesions of the upper motor neuron. Three of these had a femoral neuropathy. Following blows directed to either the tendon of the adductor muscle or to the medial epicondyle of the femur, large amplitude responses of short latency were recorded from the ipsilateral adductor muscle while small amplitude responses of short latency and large amplitude responses of long latency were recorded from the contralateral adductor. The responses of short latency which were recorded from the ipsilateral and contralateral adductor muscles ranged from 18 to 27 ms. The contralateral responses of long latency ranged from 60 to 67 ms. On tapping the patella or patellar tendon, large amplitude responses of short latency were recorded from the contralateral adductor muscles while the ipsilateral adductor responses were absent. These responses resulted from stretch of the ipsilateral and contralateral adductor muscles. The contralateral responses were mediated across the midline by an extraspinal mechanical pathway.

John W. Magladery was born in New Liskeard, Ontario on October 11, 1911. He graduated from Upper Canada College in 1929 and the University of Toronto Medical School in 1935. As a Rhodes scholar, he received the degree of D. Phil, in Neurophysiology from Oxford University in 1937. During World War II, he was a major in the Royal Canadian Army Medical Corps. Post-graduate studies were undertaken at the University of Toronto and the National Hospital, Queen Square.

A case of spinal subdural hematoma occurring in association with anticoagulant therapy is reported. Seven similar cases from the literature are reviewed with emphasis on the clinical features, investigation, and the results of treatment. The prognosis for recovery is good, only if the condition is diagnosed and the clot evacuated before severe spinal cord compression and subsequent ischemic necrosis has occurred.

Five patients were studied to determine whether kinetic interaction occurs between valproic acid and primidone. During concurrent administration of primidone and valproic acid no significant interaction was observed. Primidone and derived phenobarbital levels did not change significantly. No adjustment of primidone dose was required when valproic acid was used as adjunctive therapy.