The neonatal cat model of kaolin-induced hydrocephalus is associated with progressive and severe ventriculomegaly. In this experiment we studied the evolution of the histopathological changes in hydrocephalic (n = 23) cats from 5–168 days after the induction of hydrocephalus along with age-matched controls (n = 10). In the periventricular white matter, extracellular edema and axonal damage were present within days of the onset of hydrocephalus. This was followed by reactive gliosis, white matter atrophy, and in some animals gross cavitation of the white matter. Even in the chronic, apparently compensated state there was ongoing glial cell death. Six cats were shunted an average of 23.6 ± 6.5 days after the induction of hydrocephalus because they were no longer able to feed independently. In spite of clinical improvement the white matter changes persisted. Overt cortical changes were minimal except where areas of white matter destruction encroached upon the deep layers. The white matter changes are very similar to those seen in periventricular leukomalacia and suggest that ischemia plays a role in neonatal brain injury caused by hydrocephalus.

The PC 10, a monoclonal antibody against proliferating cell nuclear antigen (PCNA), is known to show immunoreactivity in routinely processed paraffin embedded tissue. This antibody was applied to 72 astrocytic tumours from surgical biopsy material obtained in a ten year period. The PCNA labelling index (LI) obtained by image analysis was compared with patient’s survival, age at diagnosis, and Karnofsky score as well as the histological grade of tumour. The survival analysis shows that patients with tumour PCNA LI of more than 6% have significantly poorer prognosis than those with 6% and below. In addition, there is also good correlation between PCNA LI with age, Karnofsky and tumour grade. This study suggests that although the PCNA expression of astrocytoma could be a useful predictor of patient’s outcome, it is not an independent prognostic factor but has derived its statistical association with survival secondarily through its relationship with tumour grade, age and Karnofsky score.

We report three patients with striatonigral degeneration highlighting the correlation between magnetic resonance imaging (MRI) and the pathological changes. The “slit-like void signal” observed in the putamen is typical of striatonigral degeneration and can be used to assist diagnosis during life. Our histochemical studies support the concept that increased iron deposition in the putamen is responsible for this MRI picture.

In our centre, 111 patients have been treated with linear accelerator stereotactic radiosurgery. Angiographic, CT and MRI images are generated and the target coordinates calculated in 3 dimensions. For CT scanning, cross sections of perpendicular and oblique fiducial markers are seen. For follow-up CT scans done without the frame, a virtual frame is generated by means of a computer program that places fiducial markers on each CT scan cut, as if the patient had been wearing the OBT frame and the scan produced with the gantry parallel to the base of the frame. The position of the oblique marker may be calculated by knowing the thickness and position of each CT cut. Various natural fiducial markers (bony landmarks) are identified by coordinates in the scan with the patient wearing the real frame and in the scan with the virtual frame applied. A transformation matrix is utilized to establish the equivalence between the original CT scan with the real frame applied and subsequent scans without the real frame but with the virtual frame applied. In effect, the virtual frame is re-applied in exactly the same position as the real frame. Lesion measurements may then be duplicated and growth or regression accurately established. The uncertainty in this system of re-application resides in possible patient movement, CT scan slice thickness and inter-observer error in the identification of natural fiducial markers.

We studied the electrophysiological changes occurring in six patients with tethered cord syndrome. Evidence of spinal malformations was provided by magnetic resonance imaging. The functional assessment of the spinal cord was performed by analysing both spinal and cortical somatosensory evoked potentials. The evoked electrospinogram was recorded from the thoracic and lumbosacral spinous processes. The N22 lumbosacral potential was selectively affected, being rostrocaudally displaced and reduced in amplitude or even absent in patients with neurological signs indicating a segmental lower cord lesion. Inter-peak somatosensory evoked potentials latency was normal in all cases, suggesting that ascending axonal potentials in the dorsal column fibres may be synchronized. Segmental potentials of the lumbosacral response, originating from the post-synaptic activity of dorsal horn interneurons, are selectively affected in this syndrome resulting from the rostrocaudal displacement of the spinal cord due to tethering. Our findings in the clinical field are consistent with previous experimental evidence indicating a different sensitivity of the gray vs. white matter to progressive stretching.

Five hundred and fifty-three patients were referred to a Canadian dementia clinic for standardized evaluation. The majority (83.5%) had a dementia with Alzheimer’s disease (AD) accounting for 89% of dementias. Patients with probable AD who were followed for five years had variable rates of progression, increased mortality (37.1%, 2.5 times the expected rate) and a high rate of institutionalization (79%). Simple demographic (age) and social factors (marital status) were strong predictors for institutionalization. It was extremely difficult at presentation to predict the rate of progression. The prevalence of AD in autopsied cases was 62.5%. Clinic patients were younger, had milder dementias, and were more likely to have AD than patients identified in the course of a contemporaneous population-based dementia prevalence study.

Twenty-six of 95 adults treated for tuberculous spondylitis, between 1982 and 1993, underwent surgery. Twenty-one exhibited neurological deficits: radicular deficits: 4, and progressive spinal cord syndromes: 17 (incomplete: 13, complete, of acute onset: 4). Vertebral body compression fracture was the most prominent finding. Indications for surgery were neurologic: 11, mechanical: I, etiologic: 1, and mixed: 13. Twelve patients had vertebrectomies, 3 laminotomies and 11 laminectomies. The average follow-up was 23 months. The neurological recovery was complete in 16 cases, partial in 4 cases and unchanged in one case. Bony consolidation occurred after 3–5 months. The medicosurgical treatment produced a very high cure rate, so rapidly, that it became the treatment of choice in our setting. Moreover, that allows to specify the diagnosis. Anterior decompression and fusion is recommended in the cervical and lumbar spine. In the thoracic segment, significant kyphosis is infrequent, so that surgical correction is rarely necessary. Laminotomy may occasionally be indicated for posterior decompression for abscess. Laminectomy is now preferred for uncommon cases of thoracolumbar posterior compression by tuberculous arachnoiditis or associated posterior vertebral tuberculosis. Indications for open biopsy are discussed.

False aneurysm of the intracranial arteries occurs infrequently as a complication of head injury and rarely as a consequence of other pathology. A case of false aneurysm of the supraclinoid internal carotid artery following minor intraoperative injury during clipping of a basilar-superior cerebellar aneurysm by the pterional approach is described. False aneurysm is a potential cause of recurrent intracranial hemorrhage after successful aneurysm clipping. Arterial bleeding which appears to come from the region of a branch origin should be viewed with concern even if it subsides spontaneously.

A 64-year-old man presented with a three day history of progressive Broca’s aphasia, followed within 3 weeks by exclusively right-sided myoclonus, rigidity, and dystonia. Within 4 weeks he was globally aphasie. He died within 7 weeks of onset. In the final week, rigidity and myoclonus became bilateral. CT and MRI were normal. SPECT showed diminished perfusion of the left hemisphere. EEG showed periodic discharges on the left. At autopsy, there were marked cortical spongiform change, neuronal loss, and gliosis throughout the left hemisphere and in the right occipital cortex. Elsewhere in the right hemisphere, spongiform change was non-existent to minimal. There was moderate spongiform change in the molecular layer of the cerebellar cortex, much more marked on the left. Clinical and pathological unilateral cerebral predominance extended to the ipsilateral cerebellum. Creutzfeldt-Jakob disease is an important consideration in patients with rapidly progressive unilateral cerebral signs associated with a movement disorder.

A woman had a left superior cerebellar artery infarct associated with reduced hexamethyl-propileneamine oxime uptake on SPECT scan of the basal ganglia and frontoparietal areas of the opposite hemisphere performed poorly in some neuropsychological tests indicating right hemisphere dysfunction. There was a lengthening of reaction and movement times with the hand ipsilateral to the lesion. These deficits were temporary. A unilateral cerebellar lesion can produce neuropsychological deficits, possibly because of hypoperfusion in contralateral frontoparietal regions, but spontaneous neuropsychological remissions may occur.

Interest in vascular causes for cognitive impairment is increasing, in recognition that such causes are common, and possibly preventable. This has led to attempts to better define vascular dementia and its natural history. Several sets of criteria for the diagnosis of vascular dementia have been proposed. We provide a brief overview of the background to the initiation of a Canadian consensus conference, established by the Consortium of Canadian Centres for Clinical Cognitive Research (C5R) and report the conclusions reached at that conference. To date, no one set of criteria is demonstrably superior to another; we have therefore not endorsed any of the competing sets, nor have we recommended our own. Instead we suggest that empiric studies are required to establish valid criteria. A diagnostic checklist, which combines existing criteria and additional data, is attached for clinicians wishing to participate in such studies.