To determine the current recovery rates and causes for morbidity and mortality in patients suffering aneurysmal subarachnoid hemorrhage (SAH).

We reviewed a recent consecutive series of 95 patients with ruptured intracranial aneurysms who presented to our hospital between 1994 and 1995. When administered, active treatment consisted of early surgery for aneurysm clipping and aggressive prevention and treatment of SAH-related complications.

Eighty-eight (93%) of the patients were admitted within 24 hours of rupture. One-quarter of the patients in this series did not undergo aneurysm clipping due to poor neurological condition on presentation. Of the 75 patients initially considered for active treatment, 83% underwent surgery within 48 hours of rupture, all received nimodipine, 16% received tissue plasminogen activator to lyse subarachnoid or intraventricular clots, 40% underwent hypertensive treatment, and 7% underwent transluminal balloon angioplasty for vasospasm. At one year followup, 29% of patients had died, 7% had severe disabilities, 13% had moderate disabilities, 51% had made a good recovery, and 64% of all surviving patients had returned to their previous work status. Primary and contributing causes of death and disability, affecting 47 patients at one year, were: direct effects of the initial hemorrhage (79% of affected patients), surgical complications (13%), vasospasm (11%), rebleeding (11%) and medical complications (13%).

Almost two-thirds of patients suffering aneurysm rupture make a satisfactory recovery with modern treatment. While vasospasm has become a less common cause of poor outcome following SAH, surgical complications remain an important problem.

In previous studies we reported an increased prevalence of Parkinson's disease in several kibbutzim of Southern Israel (cluster kibbutzim). Subsequent studies revealed a significant prevalence of subjects presenting extrapyramidal signs (preparkinsonism) in the same kibbutzim. On follow-up worsening of these signs was observed in some of the older subjects, some of them actually being diagnosed as suffering from I-Dopa responsive Parkinson's disease. The current study was designed to evaluate possible etiologic factors for the development of preparkinsonism.

317 subjects over the age of 40, living in five kibbutzim were examined and interviewed. 95 subjects presenting extrapyramidal signs were compared with 95 control subjects. They were matched for age, sex and length of residence in the kibbutz. Odds ratios were computed to identify exposure variables for logistic regression analyses. Detectors for carbamates and organic phosphates were applied at different sites of these kibbutzim.

The severity and frequency of the extrapyramidal signs were higher in the older age groups, more in the “cluster”, than in other kibbutzim. A very strong association was found between field crop work exposure, particularly cotton, and preparkinsonism (p = 0.0007) and a slightly weaker association for landscape work. The detectors picked up abundant pesticide traces (carbamates and organic phosphates) in the residential areas fairly distant from sites of aerial spray.

We assume a chronic passive exposure of the residents in these kibbutzim to pesticides, in addition to any occupational exposures.

Constructional impairment following left vs. right hemisphere damage has been extensively studied using drawing tasks. A confounding factor in these studies is that right-handed patients with left hemisphere damage (LHD) are often forced by weakness to use their non-dominant (left) hand or hemiparetic dominant hand. Qualitative differences in the drawing characteristics of left and right hand drawings by normal subjects have not previously been characterized. The present study was undertaken to determine the qualitative differences between left and right hand drawings of normal subjects.

Thirty right-handed, elderly subjects without a history of neurological disease were asked to draw, from memory, seven objects using the right and left hand. Half of the subjects were randomly assigned to draw with the left hand first, and half the right hand first. Right and left hand drawings were compared using a standardized scoring system utilized in several previous studies of drawing in focal and diffuse neurological disease. Each drawing was scored on eighteen criteria. Right and left hand drawing scores were then compared using the t-test for paired samples or the Wilcoxon matched-pairs test

Drawings made using the left hand were found to be significantly simpler, more tremulous and of poorer overall quality than drawings made by the same subjects using the right hand.

The deficits found in left versus right hand drawings of normals are similar to those found in patients with LHD, suggesting that much of the drawing impairment seen following LHD is due to an elementary motor disturbance related to use of the non-dominant hand.

As many as 20% of individuals with the clinical diagnosis of Parkinson's disease (PD) do not have the characteristic neuropathologic features of PD at post mortem. The striatonigral degeneration (SND) subtype of multiple system atrophy is one of the categories of pathology which may be incorrectly diagnosed as PD on the basis of clinical presentation. SND may be associated with increased iron deposition in the putamen which can be detected with magnetic resonance imaging.

We have estimated regional brain iron content in a patient with probable SND, using a novel imaging method developed in our laboratory, and have compared the results in this patient to those which we have previously reported in patients with PD and in age-matched controls.

We observed that putamenal iron content was increased in our SND patient, beyond the 95% confidence limit for inclusion in the PD group, even when considering clinical severity. In contrast, pallidal and thalamic iron were within the PD range.

The demonstration of increased putamenal iron content may be a useful adjunctive investigative procedure in patients with suspected SND.

Results from the Canadian Collaborative Project on Genetic Susceptibility to Multiple Sclerosis (MS)-Phase 1 (CCPGSMS-Phase 1) together with other family data published since 1982 have led to the following conclusions about the etiology of MS: (i) genetic and non-genetic (environmental) factors are involved in the etiology of MS on a population basis; (ii) the familial aggregation of MS is genetic; (iii) maternal factors do not influence the risk for siblings to develop MS; and (iv) MS appears to be oligogenic. The present paper describes the rationale and methodology for the CCPGSMS-Phase 2.

The CCPGSMS-Phase 2 is a nation-wide collaborative effort involving all the 15 Canadian MS clinics. A series of structured questionnaires is administered to MS index cases, spouse controls and mothers of index cases and spouse controls (if available) by trained interviewers. Blood samples are taken for molecular genetic studies. This national effort is coordinated by the MS Clinics in Vancouver and London.

The CCPGSMS-Phase 2 is in progress so specific results are not available. The study is designed to (i) increase the database for genetic epidemiological/molecular genetic research and (ii) gather population-based data to further our understanding of the non-genetic factors in the etiology of MS.

It is anticipated that the results from this study will impact on the eventual prevention, cure and treatment of MS.

Tropical Spastic Paraparesis/HTLV-I Associated Myelopathy (HAM/TSP) is a chronic, progressive myelopathy endemic to the Caribbean. In HAM/TSP, peripheral motor pathways have been assessed using electromyography and nerve conduction studies; central motor pathways have been assessed to a limited extent using electrocortical stimulation. We used magnetic cortical stimulation (a painless alternative to electrocortical stimulation) and F-wave analysis to study conduction in the central and peripheral motor pathways in 18 HTLV-I seropositive, Jamaican TSP patients (ages 29- 70 years; duration of symptoms 3-20 years) and 22 normal controls.

Magnetic cortical stimulation was effected using a 9 cm diameter undamped MES10 coil. F-waves and M-responses were elicited by electrical stimulation of the ulnar nerve at the wrist, and deep peroneal stimulation at the knee. Stimulation and recording of response latencies in abductor digitii minimi (ADM) and tibialis anterior (TA) were carried out using a Cadwell Excel system.

With cortical stimulation, response latencies (TMCTs) to ADM and TA were prolonged in the patients relative to controls. F-wave and M-response latencies were unaffected, suggesting no peripheral pathology. Latency (CMCT) between cortex and lumbar cord was significantly prolonged; that between cortex and C7/T1, also, but less markedly (P < 0.0005). Amplitudes of cortically evoked responses were significantly reduced only in the lower limbs (TA). CMCT increased as the disease progressed from mild to moderate, thereafter remaining largely unchanged.

Meta-analysis of interlaboratory control data revealed no significant differences in TMCTs between our controls and others studied using similar techniques. The observations are consistent with pathology affecting mainly the thoracolumbar cord in HAM/TSP.

The relationship of ictal and post-ictal cephalic pain to migraine remains debatable. We hereby report 2 patients whose post-ictal migraine-like symptoms ameliorated in response to oral sumatriptan.

Two patients, a 27-year-old woman and 41-year-old man were referred for assessment of migraine of 10 years and 4 years duration, respectively. The man described a recent episode of “vacant stare” and the woman has sensitivity to bright colours and light. Neurological examination, visual field testing, CAT scan, MRI scan, and prolonged EEG recordings were accomplished for each patient.

The man had a spontaneous seizure with ictal discharge arising from the right occipital lobe. Bilateral occipital spikes, associated with palinopsia was triggered in the woman by photic stimulation. Both patients developed post-ictal headaches with symptoms similar to their migraines. The symptoms subsided following treatment with oral sumatriptan.

Migraine-like symptoms occurring following occipital lobe seizures may share similar pathophysiological substrates with idiopathic migraine. Serotonergic mechanisms may be implicated.

Intravenous methylprednisolone (IVMP) is the treatment of choice for multiple sclerosis (MS) patients undergoing acute exacerbation of disease symptoms and yet its cost has not been accurately determined. Determination of this cost in different settings is also pertinent to consideration of cost-saving alternatives to in-patient treatment.

Cost analysis from the point of view of the health care system of IVMP treatment of MS patients receiving treatment in association with a selected Toronto teaching hospital in fiscal year 1994/95 was carried out. Costs of any concurrent treatments were excluded.

Total cost for 92 patients, based on a 4 dose regime, was estimated to be $78,527. The the cost per patient was $1,1181.84 for in-patients (IP), $714.64 for out-patients of the MS Clinic (OP) and $774.21 for patients whose treatment was initiated in the Clinic, but completed in the home (HC). Sensitivity analyses indicated: 1) IP treatment was in all cases more expensive than that of OP or HC; 2) the cost savings of OP vs. HC was sensitive to assumptions made regarding Clinic overhead, Clinic nursing costs and Home Care Program overhead.

Alternatives to in-patient care must be considered carefully. In this study, both out-patient and in-home treatment were cost-saving alternatives to in-patient treatment, but large differences in the cost of hospital out-patient vs. in-home care could not be demonstrated.

Dissection of the internal carotid and vertebral arteries is a well recognized cause of stroke, especially in the middle-aged. The exact etiology of this condition is controversial. According to one theory there is an underlying vasculopathy originating from disturbed development of the neural crest. The neural crest gives rise to several tissues, including the tunica media of large cervical arteries and the outflow tract of the heart. We attempted to test the theory that developmental abnormality at the level of the neural crest may play a role in dissection of the large cervical arteries.

We designed a retrospective case control study. By means of transthoracic echocardiography we measured the aortic root diameter in a group of patients with radiographically determined dissection of at least one large artery in the neck. The results were compared to a control group.

In comparison to age matched controls, male patients were found to have a significantly larger aortic root. Although a similar trend was apparent in females, the difference between the patient and control group of females was not statistically significant.

Patients with cervical artery dissections may have other abnormalities in organs arising from the neural crest. A larger prospective clinical study and further research are needed to establish a firm link between dissection of the cervical arteries and abnormalities in other organs.

Adenosine is a powerful natural vasodilator that participates in the control of cerebral and meningeal blood flow. In this context, it could be involved in the pathophysiology of migraine, since it was previously reported that intravenous adenosine can precipitate crises in migraine patients.

We have investigated circulating adenosine levels in 12 patients suffering from migraine without aura, during crises and in crisis-free periods, and have compared the levels noted to those of a population of 10 controls. To determine if there are interactions between adenosine and serotonin, we examined the effect of adenosine and antagonists on the uptake and the release of (14C) serotonin by platelets.

We have reached a dual conclusion: 1) during migraine headaches there is an increase (mean 68%) in circulating adenosine levels and this increase may participate in cephalalgia; 2) activation of A2 receptors by adenosine causes a dose-dependent inhibition of calcium-dependent serotonin uptake by platelets. This inhibition of uptake could participate in the rapid elimination of serotonin in migraine sufferers. As a result of this, the use of adenosine antagonists could be an effective complementary treatment for migraine.