As conceived by Wilder Penfield the Montreal Neurological Institute (MNI) integrated neurology, neurosurgery, and allied disciplines within a single institution, where research and teaching complemented patient care. The MNI’s success influenced the creation of the National Institute of Neurological Diseases and Blindness (NINDB), as Pearce Bailey, its first Director, sought to replicate the MNI’s clinical and research model. He turned to MNI trainees Maitland Baldwin and Milton Shy to head the NINDB’s Surgical and Medical Neurology Branches, respectively. They in turn recruited other MNI trainees who continued their work at the NINDB bringing clinical neuroscience to the USA.

Wilder Penfield was appointed as Chair of McGill University’s newly created Department of Neurology and Neurosurgery in 1930 and Director of the Montreal Neurological Institute (MNI) in 1933. The departmental structure allowed Penfield to develop his own research priorities, and the MNI’s clinics and laboratories allowed residents to train in neurosurgery and in basic science under one roof. This paper reviews the research performed by neurosurgical residents under Penfield’s direction from 1934 to 1945 and argues that their initiation to laboratory research contributed to the emergence of neuroscience following the Second World War.

This paper reviews the history of neurology and neurosurgery at McGill University from their origins within the Departments of Medicine and of Surgery at the Royal Victoria Hospital in 1894, to the creation of an autonomous Department of Neurology and Neurosurgery in 1928 at the Montreal Neurological Institute. The argument is made that the collaboration of James Stewart and James Bell and of Colin Russel and Edward Archibald in the diagnosis and treatment of neurological patients created an institutional culture that favored the integration of neurology, neurosurgery, and allied disciplines within a departmental structure and the creation of the Montreal Neurological Institute.

Analyses of between-sex differences have provided a powerful starting point for evolutionarily informed work on human sexuality. This early work set the stage for an evolutionary analysis of within-sex differences in human sexuality. A comprehensive theory of human sexual strategies must address both between-sex differences and within-sex differences in evolved psychology and manifest behavior.

Psychosurgery refers to the surgical interruption of the white matter fibres joining the frontal cortex to the remainder of the cortical mantle and to the thalamus, in an attempt to mitigate the manifestations of psychosis. It reached its heyday following World War Two and was abandoned with the introduction of major tranquilisers such as chlorpromazine. Wilder Penfield, unlike most of his contemporaries, had a jaundiced view of psychosurgery. This paper addresses Penfield’s early experience with experimental, penetrating brain trauma and with the surgical resection of frontal, epileptogenic lesions, which explain his antagonism towards psychosurgery.

Acute vasospasm of the transclivally exposed basilar artery of anesthetised cats was produced by the subarachnoid injection of platelet-rich plasma (PRP) treated with enough adenosine diphosphate (ADP) to induce platelet aggregation and secretion. Vasorelaxation was produced by the topical application of the calcium antagonist verapamil. Changes in the internal diameter of the basilar artery were determined by measuring the blood column diameter from photomicrographs taken sequentially, at 5 minute intervals, through the operating microscope. Changes in blood vessel diameter are expressed as a plus or minus percentage of the pretreatment diameter. Arterial blood pressure and blood gas values were kept in the physiological range for the cat.

The subarachnoid injection of PRP-ADP produced severe constriction of the basilar artery (mean constriction at 5 minutes after injection: -40.7% ± 2.8 SEM). Platelet-free plasma, ADP alone and Elliott’s A solution had no spasmogenic effect when injected into the subarachnoid space. The topical application of the calcium channel blocker verapamil (0.1 mg per kg) 30 minutes after the injection of PRP-ADP, with the basilar artery still in spasm (mean constriction: -23% ± 3.5 SEM), produced prompt and dramatic vasodilation (mean dilation at 5 minutes after application: + 52.7% ±18.1 SEM). This spasmolytic effect persisted in a decremental fashion for the 60 minute period of observation, by which time the previously constricted vessel had returned to its normal size. These observations indicate that the platelet fraction of whole blood may be involved in the genesis of acute vasospasm following subarachnoid hemmorhage and that this phenomenon can be readily reversed by calcium antagonism.

Background: Asymptomatic cerebral aneurysms are diagnosed more frequently since the advent of computed tomography and magnetic resonance imaging. Their management is currently empirical. We have used decision analysis to place it on a more analytical basis. Methods: Decision analysis was used to determine the benefit in years of survival free of sequelae resulting from elective surgery of unruptured aneurysms over natural history. We took 2% as the annual rate of rupture (r), 73% as the risk of death or disability with rupture (M), and 6.5% for the average risk of elective surgery (S). Benefit was calculated from the equation L{[1-(1-r)L]M/2-S} [1] for life expectancy (L) corresponding to each quinquennial age group from age 15 to 100 years. Sensitivity analysis was performed to take into account increasing risk of elective surgery based on the size, and accessibility of the aneurysm, and variable risks of rupture and outcome. Results: A gain of at least one year of survival free of neurological sequelae is achieved by surgery compared to natural history for patients whose life expectancy is 19.5 years, corresponding to age 63.5 years for males and 68 years for females. The life expectancy at which a benefit accrues is longer (the patient is younger) for larger, less accessible aneurysms, for lower rates of rupture, and for lesser risks of death or disability from rupture. Conclusions: Elective surgery of unruptured asymptomatic aneurysms achieves an increased survival over the natural history of at least one year free of neurological sequelae in patients whose life expectancy is 19.5 years or more, using our baseline assumptions. Using equation [1], the corresponding life expectancy producing this benefit can be calculated to account for the increased surgical risk of large, poorly accessible aneurysms and for factors affecting natural history.

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.

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.

It is proposed that the basic mechanism of vasospasm which sometimes follows subarachnoid hemorrhage is dependent on increased free intracellular calcium ion produced by spasmogens from closely applied extravasated blood. Relaxation of this spasm occurs when the intracellular cyclic AMP levels are raised, resulting in sequestration of calcium ion by the vascular smooth muscle cell sarcoplasmic reticulum.

We report the occurrence of cerebral aneurysms and subarachnoid hemorrhage (SAH) in a family with Graves' disease (GD). Nine affected individuals across three generations have GD alone; three in the same generation have SAH without GD; and three others in the same sibship have both conditions. The familial association of GD and SAH has not been previously described. The occurrence of these disorders in individuals of the same family and their coexistence in the same individuals suggests a possible genetic determination for some cerebral aneurysms and mayimply a genetic locus related to that of Graves' disease.

We report experience with 11 patients misdiagnosed for years, on the basis of computed tomography (CT) and angiography, as harbouring brainstem tumours in whom magnetic resonance imaging (MRI) demonstrated cavernous angiomas. Seven had undergone external irradiation, 2 had a ventriculo-peritoneal shunt, 2 developed aseptic femur necrosis following corticosteroid treatment, 1 had undergone a biopsy with a pathological diagnosis of glioma. CT had depicted ill-defined, hyperdense, faintly enhancing lesions. Angiography was normal, or showed an avascular mass or subtle venous pooling. MRI delineated discrete lesions, typical of cavernous angiomas, with a mixed hyperintense, reticulated, central core surrounded by a hypointense rim. Six patients subsequently underwent stereotactic radiosurgery without changes in clinical status or lesion. Although hemorrhagic neoplasms may mimic the clinical course and MRI appearance of cavernous angiomas, MRI is useful in the diagnosis of brainstem cavernous angiomas and should be performed in patients with suspected brainstem tumours.

The pathogenic basis of the association between adult polycystic kidney disease (APKD) and cerebral aneurysms is unknown. We have compared cerebral aneurysms in 79 patients with APKD gleaned from the literature to the sporadic aneurysm cases reported by the Cooperative Study to determine if there are significant biological differences between these two groups. Sixty-eight patients had a single aneurysm and 11 (14%) had multiple aneurysms. In APKD patients with subarachnoid hemorrhage from a single aneurysm there was a significant over-representation of males (72%, p < 0.01); and the APKD group had more aneurysms of the middle cerebral artery (37%, p < 0.05). The peak decennial incidence and mean age of rupture of APKD-associated aneurysms was younger (mean age 39.7 years, p < 0.01) and over 77% of APKD-associated aneurysms had ruptured by age 50 versus 42% for sporadic aneurysms (p < 0.001). Cerebral aneurysms co-existed with APKD in the absence of hypertension in 25% of 45 cases where the presence or absence of hypertension was recorded. These biological differences and the occurrence of aneurysms in normotensive APKD patients suggests an etiology which may be independent of hypertension and that APKD-associated aneurysms may be genetically determined. It is hypothesized that cases of inherited, familial cerebral aneurysms could be linked to a genetic defect resembling that which occurs on chromosome 16 in APKD.