Little attention has been paid to an early Canadian experiment in neuronal regeneration and what may have been the world's first attempt to replace a damaged spinal cord with a transplant. In 1905, a paper entitled “Regeneration of the Axones of Spinal Neurones in Man” was published in the Montreal Medical Journal. It had been read at the Panamerican Congress in Panama. The author was David Alexander Shirres, a Scot who had trained in Aberdeen in neurology and neuropathology. He came to Canada in 1902 to assume the position of neurologist at the Montreal General Hospital, with the responsibility of establishing clinics and teaching undergraduates about the mysteries of the nervous system. To my knowledge, he was the first man in Canada to be appointed as a neurologist. (There were others, notably James Stewart, who devoted most of their time and writing to diseases of the nervous system but considered themselves to be internists. Stewart, for example, left the MGH to become the first chief of medicine at the Royal Victoria Hospital in Montreal.)

ALS symptom spread results from local spread of the neuronal degeneration because contiguous areas are more quickly involved than non-contiguous areas. Local spread to contiguous areas of motor neuron dysfunction is faster at the brainstem, cervical and lumbar regions than spread to non-continguous areas. The time for caudal-rostral symptomatic spread of ALS to involve a distant region is a function of the distance of that region from the site of onset. The time for spread to the bulbar region is shorter following arm onset than leg onset. Spread to non-contiguous areas is faster within the spinal cord than from the spinal cord to the bulbar region. These kinetics are consistent with axonal transport of the etiological agent in a manner similar to spread of poliovirus in poliomyelitis patients. Spread from the bulbar region to the spinal cord, on the other hand, occurs faster than symptom spread from the limb region to the bulbar region in limb onset patients. This rapid limb involvement following bulbar onset is more dramatic in males compared with females. Females with leg onset, on the other hand, show more rapid involvement of the opposite leg, either arm or bulbar structures than males. Gender effects may determine the course of ALS depending on the original site of onset.

Selective amygdalohippocampectomy (AHE) offers a real chance of cure only in patients with welldefined, precisely localized “epileptogenic area”, i.e. seizure focus. Therefore, a priori only a small proportion of all patients with epilepsy can meet the criteria for selective surgical interventions. From the evidence in patients meeting the criteria for AHE, we conclude that this technique is to be preferred to the “standard” anterior temporal lobectomy and represents a more selective but still effective surgical treatment of epilepsy.

The relative failure of symptomatic therapeutic trials for Alzheimer's disease using non-selective cholinergic agonists brings about the need for longitudinal studies with parallel designs aimed at disease stabilization, using trophic substances or amyloid suppressors.

We have briefly reviewed the experimental and clinical evidence for the importance of the amygdala and hippocampal formation in temporal lobe epilepsy. More specifically, we have analyzed our own experience in patients with temporal lobe epilepsy investigated with intracerebral stereotaxic electrodes and operated by various modalities of resection. Our results, in agreement with previous experimental and clinical work, provide further evidence for an overwhelming predominance of limbic participation in temporal lobe epilepsy. As a result, more and more selective procedures are being carried out involving the mesial structures. However, this shift has been slow and progressive because of the proven value of cortico-amygdalo-hippocampectomy which provides excellent results on seizure tendency with low morbidity.

In this review we summarize a number of technical and methodological approaches that have been used in our laboratory to study human brain slices maintained in vitro. The findings obtained in the course of these studies appear to be relevant in establishing he mechanisms that underlie physiological phenomena of the human brain such as synaptic plasticity or responses to neuroactive drugs. Moreover, these data are important for understanding certain fundamental mechanisms of epilepsy. In this respect, however, we aution that the mechanisms that apply to different forms of clinical epilepsy might be ifficult to find given the variability present in the pathogenesis of human epilepsy.