It is unclear how the brain enables a subject to discriminate between two or more sensory stimuli and to respond appropriately to them. This process must include the ability to detect and identify the stimuli, and to select and initiate an appropriate motor response. With the advent of improved computer technology, this behavior can now be studied in the laboratory, not only by monitoring the input to (stimulus) and output from the brain (response), but also by measuring the associated electrical activity of the brain in order to gain an understanding of how this task is accomplished. In this paper we discuss our work in this area and its relevance to understanding the neural organization of the decision to make a movement in response to a sensory stimulus.

One of the most lethal properties of high grade gliomas is their ability to invade the surrounding normal brain tissue, as infiltrated cells often escape surgical resection and inevitably lead to tumour recurrence. The consequent poor prognosis and survival rate underscore the need to further understand and target the cellular mechanisms that underly tumour invasiveness. Proteases which degrade the surrounding stromal cells and extracellular matrix proteins have been demonstrated to be critical effectors of invasion for tumours of both central and peripheral origin. Within the nervous system, the role of metalloproteinases as well as other classes of proteases in mediating the invasive phenotype of high grade gliomas has been an intense area of research. We present in this article a review of this literature and address the possibility that these proteases and the biochemical pathways that regulate their expression, such as protein kinase C, may represent potential targets in the therapy of high grade gliomas.

Familial cerebral aneurysms are currently the subject of burgeoning interest. We review the pertinent, recent reports on this topic in the light of our study of 17 families with familial cerebral aneurysms. The prevalence of familial cerebral aneurysms ranges from 5-28%. The sex distribution displays a female bias. Mothers are more often affected than fathers and daughters more than sons. There is no site predilection for familial cerebral aneurysms but they tend to occur at the same (or mirror) site within families. The age at rupture of familial cerebral aneurysms is younger, especially in females, than for sporadic aneurysms. They tend to rupture within the same decade in families, and within five years of each other in identical twins. The size of ruptured familial cerebral aneurysms appears to be smaller, especially in women, than sporadic aneurysms. The pattern of inheritance is unknown. A poor outcome of rupture is more frequent in familial cerebral aneurysms cases than in sporadic ones. Angiographic screening of family members at risk, especially first degree relatives, appears justified.

Anterior temporal resection may effectively relieve therapy-resistant seizures in children and give social, psychological and economic benefits. Epidemiological and prognostic data demonstrate that this is an under-utilised procedure: although an estimated 677 Ontario children per year would be candidates for anterior temporal resection, only 18 were performed in a 12 month period.

The study of cellular adhesion molecules offers crucial understanding of cellular interactions. Their name implies an underestimation of their function, as intercellular glue. In fact, they play vital roles in tissue development and intra- and intercellular signaling. In neurology, cellular adhesion molecules are already providing welcome new insight into neurodevelopmental anomalies, autoimmune demyelination, and invasive tumours. Cellular adhesion molecule manipulation has led to several therapeutic options which are the subject of ongoing clinical investigation.

The neurotrophins comprise a family of secreted proteins that elicit profound responses in cells of the developing and mature vertebrate nervous system including the regulation of neuronal survival and differentiation. The molecular mechanisms by which the neurotrophins exert their effects have been the subject of intense investigation. The neurotrophins elicit responses in neurons via members of the Trk family of receptors and the p75 neurotrophin receptor. Once activated, neurotrophin receptors trigger a large number of biochemical events that propagate the neurotrophin signal from the plasma membrane to the interior of the cell. An important target of the neurotrophin-induced signaling pathways is the nucleus, where neurotrophin-induced signals are coupled to alterations in gene expression. These neurotrophin-induced changes in gene expression are critical for many of. the phenotypic effects of neurotrophins including the regulation of neuronal survival and differentiation.

Initiation of oral contraceptive (OC) therapy in migraine may worsen pre-existing migraine or change the pattern of the individual migraine attacks. Many women experience no change in their migraine and a few show improvement. Evidence is accumulating that migraine increases ischemic stroke risk and that this risk is higher in migraine with aura than in migraine without aura. OCs also increase stroke risk, and the increased stroke risk attributable to each of migraine and OC therapy may be additive. The risk of ischemic stroke in young women is very low and likely remains acceptably low in young women with migraine without aura and in those with a simple migraine aura when OCs are prescribed. However, the presence of a complex or prolonged migraine aura, or of additional stroke risk factors such as increased age, smoking, and hypertension likely increases the ischemic stroke risk further in patients with migraine when OCs are prescribed. Whether OCs can be prescribed safely for the patient with migraine depends upon many factors including patient age, type of migraine, and the presence or absence of other stroke risk factors.

The ipsilateral primary motor cortex (M1) plays a role in voluntary movement. In our studies, we used repetitive transcranial magnetic stimulation (rTMS) to study the effects of transient disruption of the ipsilateral M1 on the performance of finger sequences in right-handed normal subjects. Stimulation of the M1 ipsilateral to the movement induced timing errors in both simple and complex sequences performed with either hand, but with complex sequences, the effects were more pronounced with the left-sided stimulation. Recent studies in both animals and humans have confirmed the traditional view that ipsilateral projections from M1 to the upper limb are mainly directed to truncal and proximal muscles, with little evidence for direct connections to distal muscles. The ipsilateral motor pathway appears to be an important mechanism for functional recovery after focal brain injury during infancy, but its role in functional recovery for older children and adults has not yet been clearly demonstrated. There is increasing evidence from studies using different methodologies such as rTMS, functional imaging and movement-related cortical potentials, that M1 is involved in ipsilateral hand movements, with greater involvement in more complex tasks and the left hemisphere playing a greater role than the right.