Postictal noserubbing (PIN) has been identified as a good, albeit imperfect, lateralizing and localizing sign in human partial epilepsy, possibly related to ictal autonomic activation.

PIN was studied prospectively in a group of consecutive patients admitted for video-EEG monitoring, with the laterality of noserubbing correlated with electrographic sites of seizure onset, intra- and interhemispheric spread, and sites of seizure termination.

PIN was significantly more frequent in temporal than extratemporal epilepsy (p<0.001; 23/41 (56%) patients and 41/197 (21%) seizures in temporal lobe epilepsy compared with 4/34 (12%) patients and 12/167 (7%) seizures in extratemporal epilepsy). The hand used to rub the nose was ipsilateral to the side of seizure onset in 83% of both temporal and extratemporal seizures. Seizures with contralateral PIN correlated with spread to the contralateral temporal lobe on scalp EEG (p<0.04). All extratemporal seizures with PIN showed spread to temporal lobe structures. One patient investigated with intracranial electrodes showed PIN only when ictal activity spread to involve the amygdala: seizures confined to the hippocampus were not associated with PIN. PIN was not observed in 63 nonepileptic events in 17 patients. Unexpectedly, one patient with primary generalized epilepsy showed typical PIN after 1/3 recorded absence seizures.

This study confirms PIN as a good indicator of ipsilateral temporal lobe seizure onset. Instances of false lateralization and localization appear to reflect seizure spread to contralateral or ipsilateral temporal lobe structures, respectively. Involvement of the amygdala appears to be of prime importance for induction of PIN.

We investigated the in vitro effects of low- and high-dose methylprednisolone (MP) on the cytokine-induced expression of HLA-DR, ICAM-1 and VCAM-1 on human brain microvessel endothelial cells (HBMECs).

Brain endothelium was obtained from microvessels included in the apparently normal white matter of surgical specimens of nine patients. Cells were stained with monoclonal antibodies anti-HLA-DR, anti-ICAM-1 and anti-VCAM-1 and analysed by flow cytometry as fluorescence histograms. The mean fluorescence intensity (MFI) of HBMECs treated with different stimuli was calculated.

3-IFN-induced HLA-DR was down-regulated in a dose-dependent manner by MP. High-dose MP reduced the TNF-3-induced ICAM-1 and VCAM-1 expression.

The down-regulation of adhesion molecules on cerebral endothelial cells could decrease mononuclear cell transmigration through the blood brain barrier and consequently the perivascular infiltrates. The results add support to the rationale for high-dose MP treatment in multiple sclerosis relapses.

We examined the lateralizing value of postictal language and motor deficits and studied their underlying mechanisms.

The total sample consisted of 35 patients (26 temporals, 8 frontals, 1 parietal) with a good postsurgical outcome (Engel's class I and II). Postictal examination was blindly reviewed on videotapes. In 15 cases (29 seizures), postictal language manifestations were analyzed in relation with the diffusion of the epileptic discharge recorded by intracerebral EEG. Language dominance was determined by the intracarotid amobarbital test.

Postictal aphasia was observed only when (1) seizure originated in the dominant hemisphere and (2) ictal activity spread to language areas (Wernicke and/or Broca areas). When the epileptic focus was in the nondominant hemisphere, no postictal aphasia was observed even if there was secondary generalization of ictal activity affecting the language areas of the dominant hemisphere. Postictal motor deficits also had a strong lateralizing value even when seizures were secondarily generalized.

Postictal aphasia in temporal epilepsies and postictal motor deficits in temporal and extra temporal epilepsies provided excellent lateralizing information. Postictal deficits appear to be the result of inhibitory mechanisms induced by previous ictal activity of the structures related to these functions.

To compare the clinical characteristics, natural history, and therapeutic outcome of patients with cervical dystonia (CD) with head tremor (HT+) and without head tremor (HT-).

We prospectively evaluated 114 consecutive patients of CD over a 9-month period with a detailed questionnaire. Chi-square and t-tests were employed for statistical analysis.

Seventy-eight (68.4%) patients had head tremor and 27 of them (34.6%) had tremor as one of the first symptoms. Age at onset of symptoms were similar in HT+ and HT- groups; however there was a higher prevalence in women in the former group (66.7% vs. 41.7%; p=0.01). HT+ patients had more frequent positive family history of essential-like hand/head tremor (21.8% vs. 5.5%; p<0.05), associated neck pain (92.3% vs. 77.8%; p<0.05), and essential-like hand tremor (40% vs. 8.3%; p<0.001). They also appeared to have more frequent history of preceding head/neck trauma (14.1% vs. 8.3%), frequent head rotation (88.5% vs. 69.4%) and antecollis (12.8% vs. 5.5%) but less often head tilt (37.2% vs. 47.2%) and gestes antagonistes (60.2% vs. 75%) than the HT- patients; however these differences were not statistically significant. The frequency of prior psychiatric illnesses, the incidence of dystonias in other parts of the body, frequency of retrocollis and shoulder elevation, and spontaneous remission were similar in the two groups.

Head tremor is common in CD and is more commonly associated with hand tremor and family history of tremor or other movement disorders. This supports a possible genetic association between CD and essential tremor (ET). Linkage studies are required to evaluate the genetic association between CD and ET.

Traditionally, odontoid fractures have been treated with different bracing techniques resulting in variable degrees of successful healing. Surgical intervention is becoming more widely practiced as a primary intervention. The purpose of this report was to survey our recent experience in southern Alberta to determine potential outcome differences in management strategies.

We retrospectively reviewed the charts of 520 patients diagnosed with cervical spine fractures over a six-year period from January 1990, through December 1996. Patients were identified through the medical records database of the two Level 1 trauma facilities, on the basis of ICD-9 diagnostic coding.

Ninety-three fractures of the odontoid process were identified, of which 85 were acute and eight were chronic. There were 57 Type II (67%) and 27 Type III (32%) acute odontoid fractures. Of these, 64 were managed conservatively (bracing), whereas 20 were treated surgically. Thirteen patients underwent anterior screw fixation, seven patients had posterior cervical fusion. Eleven patients died in the acute phase, two as a result of their high cervical cord injury and nine from unrelated medical causes. Fifty-six of the remaining 82 patients (68%) were located with a minimum of three months follow-up (range three months to eight years). Satisfactory results were obtained in 76% of all acute patients treated by bracing, but only 50% in those over the age of 65. In the surgically managed group, all patients (100%) went on to develop stable fusions.

Our results indicate that while conservative management of odontoid fractures with external bracing results in fracture healing in most cases, surgical fusion may provide superior rates of bony union with acceptable morbidity. This difference in outcome lends itself to formal investigation through a prospective randomized trial.

The incidence of head/neck trauma preceding cervical dystonia (CD) has been reported to be 5-21%. There are few reports comparing the clinical characteristics of patients with and without a history of injury. Our aim was to compare the clinical characteristics of idiopathic CD (CD-I) to those with onset precipitated by trauma (CD-T). Methods: We evaluated 114 consecutive patients with CD over a 9-month period. All patients were interviewed using a detailed questionnaire and had a neurological examination. Their clinical charts were also reviewed.

We evaluated 114 consecutive patients with CD over a 9-month period. All patients were interviewed using a detailed questionnaire and had a neurological examination. Their clinical charts were also reviewed.

Fourteen patients (12%) had mild head/neck injury within a year preceding the onset of CD. Between the two groups (CD-I and CD-T), the gender distribution (F:M of 3:2), family history of movement disorders (32% vs. 29%), the prevalence of gestes antagonistes (65% vs. 64%), and response to botulinum toxin were similar. There were non-specific trends, including an earlier age of onset (mean ages 43.3 vs. 37.6), higher prevalence of neck pain (86% vs. 100%), head tremor (67% vs. 79%), and dystonia in other body parts (23% vs. 36%) in CD-T.

CD-I and CD-T are clinically similar. Trauma may be a triggering factor in CD but this was only supported by non-significant trends in its earlier age of onset.

To assess the feasibility and the toxicity of adjuvant high dose tamoxifen (TAM) and postoperative brain irradiation for patients with newly-diagnosed glioblastoma multiforme (GBM).

Twelve patients with histopathologically confirmed GBM entered the study. There were nine males and three females, with median age of 48.8 years (range 30-75 years). Karnofsky performance status (KPS) was 60-70% for four patients and 80-100% for eight patients. Based on the Radiation Therapy Oncology Group recursive partition analysis, there were three class III patients, six class IV, one class V, and two class VI. Eleven patients underwent partial surgical tumor resection and one patient had a near complete resection. Two weeks post surgery, the patients were started on high dose TAM (120mg/m2 P.O. BID for three months). Two weeks from date of starting TAM, external beam radiotherapy (RT) was given at a dose of 59.4 Gy/33 qd fractions/6.5 weeks. Patients were assessed weekly for toxicity during treatment. Imaging studies were done at the end of two weeks of TAM, then monthly.

Median follow-up was 40 weeks (range 22-84 weeks). In one patient, TAM was associated with significant vomiting, necessitating the TAM dose to be decreased at three weeks and then stopped at two months. One other patient had bilateral deep venous thrombosis after 51/2 weeks on TAM, although the relationship to TAM was not firmly established. There were no radiological responses after two weeks of TAM or at the end of RT. The median time to progression was 17.7 weeks (range 5.1- 43.8 weeks). Median survival time was 33.4 weeks (range 10-79.7). Actuarial survival at 48 and 74 weeks was 40% and 15%, respectively.

Our study shows that adjuvant high dose TAM is feasible and relatively well-tolerated. Furthermore, the combined use of high dose TAM and RT postoperatively was not associated with any significant increase in radiation-induced neurological toxicity. However, high dose TAM does not appear to improve treatment results.

The purpose of this study was to obtain information from Canadian neurosurgeons regarding their opinions on, and utilization of, intracranial pressure (ICP) monitoring for severe traumatic brain injury (TBI).

A brief survey was sent to practicing Canadian neurosurgeons questioning them about their utilization of, and confidence in, intracranial pressure monitoring in the management of patients with severe TBI.

One hundred and ninety-six surveys were mailed. There were 103 responses for a response rate of 52.6%. The vast majority of responding neurosurgeons (98.1%) utilized ICP monitoring in the management of patients with severe TBI, with most (63.4%) using it in more than 75% of their patients, 14.9% using it in 50-75% of patients, 14.9% in 25-50% of patients, and 6.9% using it in less than 25% of patients. The level of confidence that routine monitoring improves outcome from severe TBI ranged from 23.3% having a low level of confidence, 56.3% having an intermediate level of confidence, to 20.4% having a high level of confidence. Most respondents (78.6%) felt that some form of prospective trial evaluating the role of ICP monitoring in improving outcome from severe TBI was warranted; 17.4% felt such a trial was not warranted and 3.9% were uncertain.

While ICP monitoring has gained almost universal acceptance among responding Canadian neurosurgeons, their level of confidence that routine monitoring improves outcome from severe TBI was quite variable, with only 20.4% of respondents having a high level of confidence. Over 75% of respondents felt that some form of prospective trial evaluating the utility of ICP monitoring is warranted. This information is being used in consideration of a prospective trial addressing this issue.

“Blister-like” aneurysms of the supraclinoid internal carotid artery have recently been recognized as having unique pathological and clinical features. Little is known regarding their optimal treatment modality.

We report a case of a “blister-like” aneurysm of the internal carotid artery treated with Guglielmi detachable coil (GDC) embolization. Case Report: A 55-year-old man presented with a Hunt & Hess grade II subarachnoid hemorrhage. Computed tomography revealed diffuse subarachnoid blood. Cerebral angiography demonstrated a broad-based bulge on the medial wall of the right distal internal carotid artery. The patient was taken to the operating room and underwent a right pterional craniotomy and wrapping of this unclippable aneurysm. On postoperative day 11, he developed signs of vasospasm, and repeat angiography showed remarkable growth of the aneurysm. The aneurysm was believed to be amenable to endovascular therapy and was treated by GDC embolization. The patient recovered well and remained neurologically intact on follow-up examinations. Repeat cerebral angiography was performed three and nine months following his initial presentation and revealed a significant aneurysm neck remnant. This neck remnant was treated by repeat GDC embolization 13 months following his subarachnoid hemorrhage.

“Blister-like” aneurysms of the internal carotid artery are important to recognize and are difficult to manage using traditional surgical approaches. Early repeated cerebral angiography is indicated and, where appropriate, endovascular therapy should be considered in the management of these patients.

The aim of the study was to test the validity of the controversial subdivision of essential tremor (ET) patients into electrophysiological subgroups.

We evaluated a hundred patients with ET using surface electromyographic (EMG) recordings of antagonist forearm muscles and distinguished three groups: the first group showed synchronous activity of antagonistic muscles, the second showed alternating activity of antagonist muscles; and the third group consisted of patients whose EMG recordings were not compatible with the other two groups. We compared patients with synchronous and alternating activity in terms of sex, age at onset, duration of illness, family history of tremor, symmetry and frequency of tremor, and the scores of a disability scale.

The only significant difference between the patients with synchronous and alternating activity was that the patients with synchronous activity were more disabled.

This result adds to the evidence for distinct electrophysiological subgroups of ET with distinct clinical properties.

The objective of this study was to evaluate the pattern of cognitive disturbances in Nigerian Africans with newly diagnosed epilepsy, prior to onset of drug therapy.

A total of 60 consecutive patients (mean age 31.6 ± 17.4, range 14 - 55 years) presenting with a clinical diagnosis of epilepsy were recruited for the study. Sixty healthy volunteers without a history of epilepsy and who were age-, sex- and level of education matched with the epileptic patients, were recruited as controls. The administration of cognitive tests was done with the FePsy computerized neuropsychological test battery. The tests administered were the visual and auditory reaction times, the continuous performance test and the recognition memory tests to assess mental speed, attention and memory respectively. The means of the cognitive performances of the epileptic patients and controls were statistically compared.

Epileptic patients performed worse than the controls across the spectrum of cognitive tasks assessed (P = 0.00001; P < 0.025), with the exception of the β parameter (response bias) of the vigilance test (P = 0.488; P> 0.025).

The cognitive impairments of short-term memory, psychomotor speed and sustained attention observed in this study are similar to those reported in the literature for patients with epilepsy. The results of this study will be useful in the counseling of patients on their educational, social and vocational needs.

Familial autoimmune myasthenia gravis (MG) is rare, although a genetic role for the development of autoimmune MG is suggested by concordance in monozygotic twins and the increased frequency of other autoimmune diseases in family members of myasthenics.

A patient with a family history of MG was evaluated in hospital. Relatives were interviewed and medical records examined for details regarding the diagnosis of MG in three other family members.

The index case first experienced symptoms of MG at age 75 years. She developed generalized MG and required corticosteroids and immunosuppressive therapy to control her disease. Her father developed predominantly bulbar symptoms of MG at age 75 years. He died of complications experienced following a gastrostomy placed for continued difficulty swallowing. His brother developed similar symptoms of MG in his early 60s and died shortly after thymectomy. A 46-year-old nephew of the index case is also beginning to exhibit signs of generalized MG. Acetylcholine receptor antibodies were strongly positive in the index case and her nephew. (The assay was not available for her father and uncle).

Four individuals in three successive generations had diagnoses of autoimmune MG. Study of familial cases such as these may clarify the contribution of genetic factors to the development of this disease.

The occurrence of a unilateral sensory loss in the second trigeminal distribution and the inability to tear following an ipsilateral temporal lobectomy has not been noted despite a number of reports of cranial nerve compromise under similar situations.

A 48-year-old woman experienced complex partial seizures over three years attributable to the presence of cavernous malformations of the right temporal lobe.

An anterior temporal extrahippocampal resection was performed. The surgery was marked by the need for electrocoagulation of the dural base of the temporal lobe where numerous bleeding points were encountered. Postoperatively, the patient experienced an ipsilateral maxillary division sensory loss, absence of tearing, and diminished nasal congestion for an eight-month period until resolution.

Injury of the fibers of the maxillary division of the trigeminal nerve and the adjacent greater superficial petrosal nerve appears to be the cause. No prior account of such an occurrence has been published.

Increases in hydroxyl radical production have been used as evidence of oxidative stress in cerebral ischemia/ reperfusion. Ischemia can also induce increased dopamine release from the striatum that may contribute to hydroxyl radical formation. We have compared hydroxyl radical production in the cortex and striatum as an index of oxidative stress in a rat model of focal cerebral ischemia with cortical infarction.

Using a three vessel occlusion model of focal cerebral ischemia combined with bilateral microdialysis, hydroxylation of 4-hydroxybenzoate (4HB) was continuously monitored in both hemispheres in either the lateral striatum or frontoparietal cortex. The ischemia protocol consisted of one hour equilibration, 30 min of three vessel occlusion, then release of the contralateral common carotid artery (CCA) for 2.5 h.

Induction of ischemia resulted in a 30-fold increase in dopamine release in the lateral striatum. Compared to the nonischemic striatum, the ratio of the hydroxylation product 3,4-dihydroxybenzoate (34DHB) to 4HB (trapping agent) in the ipsilateral striatum increased significantly 30 min after ischemia induction. In contrast, during the 30 min of three vessel occlusion there was no increase in the ratio in the cortex. Following the release of the contralateral CCA, the ratio from the ischemic cortex increased significantly compared to sham-operated animals. However, under all circumstances, the 34DHB/4HB ratio was greater in the striatum than in the cortex.

The increase in the 34DHB/4HB ratio in the lateral striatum coincides with the increased dopamine release suggesting a role for dopamine oxidation in the increased production of hydroxyl radicals. The significant increase in the ratio from the ischemic cortex compared to that from the sham-operated animals is consistent with increased oxidative stress induced by ischemia. However, the lower 34DHB/4HB ratio in the cortex whichdoes not receive dopaminergic innervation compared to the striatum suggests a different mechanism for hydroxyl radical production. Such an alternate mechanism may represent a more toxic oxidative insult that contributes to infarction.