The analgesic effects of transcutaneous electrical nerve stimulation (TENS) and vibratory stimulation (VS), used both separately and simultaneously, were compared in 24 patients suffering from chronic pain. We tested the hypothesis that these combined procedures might improve the pain reducing effects obtained with a single type of stimulation, since they make it possible to recruit a larger number of large diameter afferents and/or to increase the discharge frequencies. Four 35-minute treatment sessions (VS, TENS, VS+TENS, Sham stimulation) were run with each patient. The vibrations (100 Hz) and TENS (100 Hz) were applied to the surface of the painful region. The sham stimulation treatment consisted of positioning the TENS electrodes without actually delivering any current. The short form of the McGill pain questionnaire was used to assess the subjects' pain levels. The assessments took place immediately after any treatment (Oh.), and again 4 hours and 24 hours later. The results showed that dual stimulation not only alleviated pain in more cases than either VS or TENS alone, but also had stronger and more long-lasting analgesic effects. On the other hand, all three types of stimulation used produced stronger analgesic effects than those obtained with the sham stimulation.

The authors present clinical experience with 28 cases of ruptured anterior cerebral artery (ACA) aneurysms managed personally during a 36 month period, and 10 unruptured ACA aneurysms. The cases included five giant aneurysms and four distal ACA aneurysms. Management strategy was uniform and included early operative intervention (except in the setting of deteriorating neurologic deficit, not attributable to hydrocephalus or hematoma), and vasospasm prophylaxis including calcium channel blockers and hypervolemic hemodilution and arterial hypertension. Modern diagnostic adjuncts including transcranial doppler were used as they became available. Good outcome (outcome grade 1 or 2) was observed at 6 months in 71% (20/28) of ruptured cases and in 90% (9/10) of unruptured cases; fair outcome (outcome grade 3) was observed in 14% (4/28) of ruptured cases and in 10% of unruptured cases; bad outcome (outcome grade 4 or 5) was observed in 14% (4/28) of ruptured cases. There were no instances of rebleeding after admission to the hospital. There was a single mortality in a patient moribund on admission. Delayed ischemic deterioration (DID) was documented in 46% (13 of 28) of the ruptured cases, and was a major source of morbidity in 7 of the 9 instances of fair or poor outcome in the series. Management outcome, including the occurrence of subtle neuropsychological difficulties commonly described in cases with ACA aneurysms, is discussed with relation to the incidence of DID, the clinical course of DID, and the possible impact of various therapeutic strategies.

Thiamine status was evaluated using the erythrocyte transketolase activation assay in 20 alcoholic patients admitted on a voluntary basis to a Detoxification Unit. Electromyographic evaluation revealed significant reductions of motor and sensory conduction velocities in the alcoholic group. 38% of alcoholic patients had at least one abnormal peripheral nerve conduction parameter. Findings were consistent with an axonal type of neuropathy. 30% of alcoholic patients showed significant erythrocyte transketolase activation deficits indicative of severe thiamine deficiency. In the case of peroneal nerve, reduced conduction velocities were negatively correlated with abnormal transketolase parameters. These findings are consistent with a contributory (but not exclusive) role of thiamine deficiency in the pathogenesis of alcoholic peripheral neuropathy. Deficiencies of other vitamins as well as direct neurotoxic effects of alcohol could also be involved in this phenomenon.

The value of CT as a routine screening procedure in the investigation of cognitive impairment is being increasingly challenged. To address this issue, we reviewed the records of 175 patients with intellectual deficits admitted to a Behavioural Neurology Unit over a two-year period. In the vast majority of cases, ie. 82%, the CT served essentially to confirm the clinical impression and added no new diagnostic information that impacted the management of the presenting problem. In 15% of cases the CT scan was helpful for diagnosis, especially in the differentiation between Alzheimer's disease and multi-infarct dementia.

The anticonvulsant effects of amitriptyline, imipramine, nortriptyline and desipramine were tested against focal and generalized seizures, triggered from either the amygdala or the cortex in fully kindled rats. Tests were administered on a 72- or a 24-hour schedule. Significant seizure suppression was achieved with only one drug, amitriptyline, and it occurred only at toxic or near-toxic doses. The differential, low-dose suppression of amygdala-kindled seizures, reported in earlier studies, was not seen in the present experiments. It may occur only in the short-interval test paradigms used by previous experimenters.

Mitral valve prolapse has been associated with an increased risk of transient or lasting ischemic events. Recurrence is uncommon after initiation of antiplatelet or anticoagulant therapy. In this communication we report two patients, both female, who had mitral valve prolapse as the major risk factor for cerebrovascular disease and who developed cerebral infarction despite anticoagulation. The cerebral infarctions were bilateral and extensive in one patient and led to the patient's death. In the second case, three infarctions resulted in moderate disability.

Cerebrovascular accidents due to Moyamoya disease, a disorder characterized by arterial stenosis at the base of the brain accompanied by typical net-like collateral vessels, occurred in two young Japanese women with Graves' disease when they were in thyrotoxicosis. In one patient, a second attack of cerebral infarction occurred with the recurrence of thyrotoxicosis. Association of Moyamoya disease and Graves' thyrotoxicosis is rare and the pathegenetic relationship is discussed.

220 patients with isolated and idiopathic spasmodic torticollis were followed and treated over a 14 year period. Each patient was given a short questionnaire leading to the present retrospective data analysis. In most areas, including female preponderance and frequency of postural tremor, the findings confirmed previous studies and highlighted particular points: importance of psychopathological antecedents and association with stressful life-events. The discussion deals with some of the conflicting debates surrounding this unusual disorder. What is the role of psychopathological factors? What is the therapeutic prognosis? The best therapeutic results were obtained by combining anticholinergic drugs, local injections and rehabilitation.

Three fundamental types of cephalic axial skeletal-neural dysrapic disorders are analyzed, including: cranioschisis aperta with encephaloschisis (anencephaly and/or exencephaly), cranioschisis occulta with occipital encephalocele, and the Chiari malformation (occipital bone hypoplasia) with compression, deformation and displacement of hindbrain, cerebellum, and medulla. Both clinical and experimental (vitamin A induced) examples of these malformations are used. The study establishes that these are not simple neurological (neural tube defects) disorders as it has been generally assumed, but complex developmental malformations affecting primarily the formation of the axial basicranium (causing skeletal defects) and the elevation of the neural folds and neurocranium (causing neural defects), and, secondarily, the topography of the facial skeleton or viscerocranium (causing oropharyngeal defects). The pathology of these skeletal, neural, and oropharyngeal defects is analyzed, their embryonic origin explored, and their developmental interrelationships discussed. The study proposes that an early paraxial mesodermal insufficiency may be the original anomaly common to all the different malformations that constitutes this heterogeneous group of dysraphic disorders. At any time during the segmental formation of the embryonic skeletal-neural axis, a simple reduction in the number of paraxial mesodermal cells produced by the Hensen node/primitive streak complex, could impair the formation of the axial skeleton as well as the elevation of the neural folds thus interfering with their closure. The final type of malformation is determined by variations of the degree, time of occurrence, and duration of the paraxial mesodermal insufficiency.

Synapse formation is a complex, incompletely understood process that has received only limited investigation in man despite the importance of synaptic dysfunction in common disorders such as epilepsy and mental retardation. This review explores synaptic differentiation, focussing on the morphologic maturation of synapses. Since differentiation depends on many antecedent developmental events, synaptogenesis can be affected by several factors: errors in neuronal proliferation, migration, and differentiation. The challenge to the neurobiologist is to detect and evaluate the minor alterations in neuronal differentiation that could account for the structural basis of the clinical manifestations. Trisomy 21 is an example of a condition in which the cytoarchitecture of the cerebral cortex is not obviously altered, yet mental retardation is consistently present; research neurobiologic techniques are making possible documentation of its structural basis. Epilepsy is another example in which examination of surgically removed cerebral cortex reveals subtle cortical dysplasias helpful in understanding the basis for the abnormal electrical discharge. Further exploration of synaptogenesis, particularly the influence of gene products and epigenetic factors on synapse maturation, will increase our understanding of the pathogenesis of conditions in which “morphology” seems normal but function is abnormal.

Cerebral dysgenesis encompasses varied disorders of brain development. Based on the understanding of these conditions provided by histopathologists, embryologists, radiologists and developmental pediatricians, surgeons are able to appropriately assist in the care of these patients. The surgeon can offer assessment of the ventriculomegaly that commonly accompanies cerebral dysgenesis in addition to providing methods to control hydrocephalus, to reconstruct cranial and facial malformations and to remove dysfunctional tissue. For most patients, surgical intervention is only one of the many factors that determine developmental prognosis. Based on the foundation built by other specialists, this review discusses cerebral dysgenesis from the perspective of historical and current surgical interventions.

This review identifies the fundamental anatomical and physiological processes that provide the substrates of maturation in the developing nervous system. Cerebral malformations may be viewed from the perspective of aberrations in one or more of these processes. The maturational processes are generally sequential but with considerable temporal precision and overlap: 1) neuronogenesis and gliogenesis, including neural induction by the notochord and primary segmentation of the nervous system; 2) programmed cell death of excess neuroblasts and glioblasts; 3) neuroblast migration; 4) formation and growth of neurites; 5) development of membrane polarity and excitability; 6) synaptogenesis; 7) biosynthesis of neurotransmitters and other secretory products; and 8) myelination of axons. The anatomical and synaptic organization of the fetal brain differs greatly from the mature state. An excess of axonal collaterals, dendritic branches, spines and synapses are formed and later selectively deleted. Transitory neurons, specialized glial cells, synaptic circuits and transient neurotransmitter systems serve as functional elements for a limited time. The clinical expression of these transitory features of the fetal brain are incompletely understood, particularly in the context of embryonic cerebral plasticity.