A 1995 National Institute of Neurological Disorders (NINDS) study found benefit for intravenous tissue plasminogen activator (tPA) in acute ischemic stroke (AIS). The symptomatic intracranial hemorrhage (SICH) rate in the NINDS study was 6.4%, which may be deterring some physicians from using this medication.

Starting December 1, 1998, patients with AIS in London, Ontario were treated according to NINDS criteria with one major exception; those with approximately greater than one-third involvement of the idealized middle cerebral artery (MCA) territory on neuroimaging were excluded from treatment. The method used to estimate involvement of one-third MCA territory involvement bears the acronym ICE and had a median kappa value of 0.80 among five physicians. Outcomes were compared to the NINDS study.

Between December 1, 1998 and February 1, 2000, 30 patients were treated. Compared to the NINDS study, more London patients were treated after 90 minutes (p<0.00001) and tended to be older. No SICH was observed. Compared to the treated arm of the NINDS trial, fewer London patients were dead or severely disabled at three months (p=0.04). Compared to the placebo arm of the trial, more patients made a partial recovery at 24 hours (p=0.02), more had normal outcomes (p=0.03) and fewer were dead or severely disabled at three months (p=0.004).

The results of the NINDS study were closely replicated and, in some instances, improved upon in this small series of Canadian patients, despite older age and later treatment. These findings suggest that imaging exclusion criteria may optimize the benefits of tPA.

Since 1991 the author has routinely performed awake craniotomy for intra-axial brain tumors with low complication rate and low resource utilization. In late 1996 a pilot study was initiated to assess the feasibility of performing craniotomy for tumor resection as an outpatient procedure.

A rigorous protocol was developed and adhered to, based around the patient's arrival at hospital at 6:00 a.m, undergoing image-guided awake craniotomy with cortical mapping, and being discharged by 6:00 p.m.

During the 48 month period from December 1996 to December 2000, 245 awake craniotomies were performed and of those, 46 patients were entered into the outpatient craniotomy protocol. Pathology in the 46 intent-to-treat group was: 21 metastasis, 19 glioma, and six miscellaneous. Four patients required conversion to inpatients and one patient was readmitted later the same evening due to headache. Thus 41/46 patients successfully completed the protocol (89%). There were five complications in the 46 intent-to-treat group (10.9%).

Outpatient craniotomy for brain tumor is a feasible option which appears safe and effective for selected patients. Besides being resource-friendly, the procedure may be psychologically less traumatic to patients than standard craniotomy for brain tumor. Proper prospective studies including satisfaction surveys would help resolve these issues and will be the next step.

The optimal surgical treatment of atlanto-axial instability remains controversial despite the variety of modifications and supplemental techniques currently available.

We describe a modification of the Brooks posterior wiring technique supplemented with transarticular screws for C1-C2 instability.

This method has been implemented in 30 patients in our institution with no radiological failures.

The modification provides several technical advantages and potentially stronger fixation compared to methods currently in use.

As part of an investigation of a suspected "outbreak" of Bell's palsy in the Greater Toronto Area, a population-based sample of patients with Bell's palsy was investigated electrophysiologically to help understand the spectrum of abnormalities that can be seen in this setting.

Two hundred and twenty-four patients were surveyed, of whom 91 underwent formal neurological assessment. Of the latter, 44 were studied electrophysiologically using standard techniques. Thirty-two of the 44 patients fulfilled clinical criteria for Bell's palsy.

A wide range of electrophysiological changes was observed. Blink responses were the most useful test showing diagnostic sensitivity of 81% and specificity of 94% compared to the contralateral control side. Needle electromyography was additionally helpful in only one patient of six with normal conduction studies.

There is a wide spectrum of electrophysiological abnormalities in Bell's palsy. Blink reflex latencies may be under-utilized in the assessment of the facial nerve in Bell's palsy. Facial EMG is not generally useful in routine assessment.

The aims of the present study were: i) to measure levels of the dopamine metabolite homovanillic acid (HVA), the serotonin metabolite 5-hydroxindoleacetic acid (5HIAA) and precursor tryptophan, as well as the noradrenaline metabolite 3-methoxy-4-hydroxyphenylethylene glycol (MHPG) and thiamine in the cerebrospinal fluid (CSF) of patients with Friedreich's ataxia (FA), olivopontocerebellar atrophy (OPCA), and the autosomal recessive spastic ataxia of Charlevoix-Saguenay (ARSAC), as compared with sex- and age-matched control subjects.

CSF amine related compound levels and thiamine results were compared in 40 FA, 44 OPCAand nine ARSAC patients with those of 94 sex- and age-matched subjects. Neuroimaging (CT scans and single photon emission computed tomographies i.e. SPECT) were carried out in all patients and controls. Genetic studies were conducted on OPCApatients. CSF amine related compounds were measured by high performance liquid chromatography, whereas CSF thiamine levels were measured by a microbiological method.

FA patients had significantly lower CSF HVA, 5HIAA and thiamine values than control patients and a trend for lower MHPG levels. In OPCA patients, CSF HVA, MHPG and thiamine values were markedly lower whereas CSF 5HIAA values showed only a trend towards lower levels; in ARSAC patients only thiamine and HVA CSF values were lower than those in control subjects.

After presenting the relationships between neurochemical findings on one side, the degree of ataxia, the degree of cerebellar atrophy and the SPECT findings on the other, the authors concluded that replacement and neuroprotective clinical trials in these patients would have to include two or three drugs because the neurotransmitter deficiencies are multiple.

Multiple sclerosis (MS) is a disease characterised by perivascular infiltrates and demyelination of the white matter in the central nervous system. Although the precise cause of MS remains unknown, some investigations have been carried out on antioxidant mechanisms in these patients.

In this study, malondialdehyde (MDA), as a lipid peroxidation marker, and ceruloplasmin (Cp) and transferrin (Trf), as antioxidant proteins, levels were determined in cerebrospinal fluid (CSF) and serum of 30 MS patients before and after corticosteroid therapy and in 20 control subjects. Transferrin and Cp levels were measured by the nephelometric method and MDAwas measured spectrophotometrically.

Mean MDAserum and MDACSF levels were found to be highest in the pretreatment group and lowest in the control group. Although there was no significant difference in terms of serum Trf level, serum Cp was found higher in pre- and posttreatment groups than in the control groups. Ceruloplasmin and Trf levels of CSF were not detectable using the nephelometric method. A significant correlation was found between MDACSF and MDAserum in the pretreatment group (r=0.58).

These data revealed that lipid peroxidation was increased in serum and particulary in CSF of MS patients and was reduced with corticosteroid therapy.

In recent years, an increased prevalence of Parkinson's disease (PD) in southern Israel was observed. The aim of this study was to determine which exposures are associated with PD in the urban population of this region.

Ninety-three PD patients living in towns were compared to 93 age and sex matched controls. A previously validated questionnaire, including demographic data, education, data on exposures, previous diseases, family history and habits, was administered.

In multivariate logistic regression analysis, it was found that history of work in construction sites was the strongest predictor of PD risk, followed by exposure to pesticides. In contrast, there was a negative association with smoking and history of mechanical factory employment. When the same statistical analysis was limited to association of PD with smoking, pesticides and construction work, the latter was found to be the strongest risk factor.

The risk factors for PD in this population are work on a construction site and exposure to pesticides.

Traumatic retroperitoneal hematoma in the iliacus muscle is an unusual but potentially serious cause of femoral compression neuropathy.

We describe the clinical, imaging, and management features of a case of traumatic iliacus retroperitoneal hematoma with delayed manifestation of femoral neuropathy.

The anatomical substrate for hematoma formation with subacute compression of the femoral nerve is emphasized. A subacute compartment syndrome with progressive edema, swelling and ischemia of iliacus compartment is suggested as the underlying cause. Early fasciotomy with or without hematoma evacuation should be considered in order to provide rapid decompression and to minimize the chance of permanent nerve injury.

Meige syndrome is a movement disorder that includes blepharospasm and oromandibular dystonias. Its etiology may be idiopathic (primary) or it may arise secondary to focal brain injury. Acute respiratory distress as a feature of such dystonias occurs infrequently. A review of the literature on Meige syndrome and the relationship between dystonias and respiratory compromise is presented.

A 60-year-old woman suffered a cerebral anoxic event secondary to manual strangulation. She developed progressive blepharospasm combined with oromandibular and cervical dystonias. Neuroimaging demonstrated bilateral damage localized to the globus pallidus. Years later, she presented to the emergency department in intermittent respiratory distress associated with facial and cervical muscle spasms.

Increasing frequency and severity of the disorder was noted over years. The acute onset of respiratory involvement required intubation and eventual tracheotomy. A partial therapeutic benefit of tetrabenazine was demonstrated.

Meige syndrome is a movement disorder that includes blepharospasm and oromandibular dystonias. Its etiology may be idiopathic (primary) or it may arise secondary to focal brain injury. Acute respiratory distress as a feature of such dystonias occurs infrequently. A review of the literature on Meige syndrome and the relationship between dystonias and respiratory compromise is presented.

A 60-year-old woman suffered a cerebral anoxic event secondary to manual strangulation. She developed progressive blepharospasm combined with oromandibular and cervical dystonias. Neuroimaging demonstrated bilateral damage localized to the globus pallidus. Years later, she presented to the emergency department in intermittent respiratory distress associated with facial and cervical muscle spasms.

Increasing frequency and severity of the disorder was noted over years. The acute onset of respiratory involvement required intubation and eventual tracheotomy. A partial therapeutic benefit of tetrabenazine was demonstrated.

Meige syndrome is a movement disorder that includes blepharospasm and oromandibular dystonias. Its etiology may be idiopathic (primary) or it may arise secondary to focal brain injury. Acute respiratory distress as a feature of such dystonias occurs infrequently. A review of the literature on Meige syndrome and the relationship between dystonias and respiratory compromise is presented.

A 60-year-old woman suffered a cerebral anoxic event secondary to manual strangulation. She developed progressive blepharospasm combined with oromandibular and cervical dystonias. Neuroimaging demonstrated bilateral damage localized to the globus pallidus. Years later, she presented to the emergency department in intermittent respiratory distress associated with facial and cervical muscle spasms.

Increasing frequency and severity of the disorder was noted over years. The acute onset of respiratory involvement required intubation and eventual tracheotomy. A partial therapeutic benefit of tetrabenazine was demonstrated.

This case highlights two interesting aspects of Meige's syndrome: (1) Focal bilateral basal ganglia lesions appear to be responsible for this patient's movement disorder which is consistent with relative overactivity of the direct pathway from striatum to globus pallidus internal and substantia nigra pars reticularis; (2) Respiratory involvement in a primarily craniofacial dystonia to the point of acute airway compromise.

Carcinomatous transformation of pituitary adenomas is uncommon, and is generally accompanied by nuclear accumulation of p53 protein. Pituitary carcinoma lacking accumulation of p53 protein is very rare, only two such cases being previously reported.

A patient presented with visual disturbance and cranial nerve palsies and was found to have a suprasellar mass. He underwent both transphenoidal and transfrontal excision of a nonfunctioning pituitary adenoma which recurred several times. The third recurrence was accompanied by multiple dural-based metastases. Despite aggressive surgical management, he continued to develop additional intracranial lesions and died two years after the discovery of metastatic disease. Specimens from 1984, 1995, 1997 and 1998 were available for histological and immunocytochemical analysis. Antibodies recognizing the pituitary hormones (ACTH, PRL, GH, FSH, LH and TSH), as well as cytokeratin, epithelial membrane antigen (EMA), glial fibrillary acidic protein (GFAP) and chromogranin A were applied to investigate the lineage of the neoplasm. Antisera specific for Ki-67 (MIB-1) and p53 protein were also applied to further delineate the biology of the tumour.

Although cytokeratin and chromogranin A were detected in neoplastic cells, no expression of pituitary hormones was demonstrable, indicative of a nonfunctioning, null-cell pituitary adenoma. Nuclear pleomorphism and mitotic activity increased with subsequent resections. Abnormal accumulation of p53 protein was not observed, neither in early resections nor in the metastatic deposits.

Failure to demonstrate p53 protein accumulation does not ensure a favourable outcome for pituitary adenoma. Accordingly, pituitary carcinoma may occur in the absence of p53 accumulation. The factors which underlie aggressive behaviour of pituitary neoplasms are uncertain but are under investigation.