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Sturge-Weber syndrome is characterized by a facial cutaneous nevus (port-wine stain) and a leptomeningeal angioma, often found ipsilateral to the facial lesion. Epileptic seizures, mental retardation, and focal neurological deficits are the primary neurologic abnormalities of Sturge-Weber syndrome. In a series of 52 adults with Sturge-Weber syndrome, 65% had neurologic deficits including stroke, hemiparesis, spasticity, and/or weakness. Neuroimaging, electroencephalography, and functional testing with Positron emission tomography (PET) and Single-photon emission computed tomography (SPECT) may also help to define the extent of the intracranial lesion for possible epilepsy surgery. Although gyral calcification is a classic feature of Sturge-Weber syndrome, this "tram track" appearance is not always present. Bilateral calcification is common. Calcification often becomes more apparent as the patient becomes older but is sometimes already present at birth. Daily aspirin has been tried in an effort to prevent recurrent vascular thrombosis that may cause neurologic deterioration.
There are four types of cerebral vascular malformations: arteriovenous malformations (AVMs), cavernous malformations (CMs), capillary telangiectasies, and venous malformations. This chapter presents a review of the pertinent literature on CMs regarding epidemiology, genetics, pathology, clinical findings, and therapeutic management with special emphasis placed upon the natural bleeding risk of these malformations. The most sensitive imaging study to detect CMs is magnetic resonance imaging (MRI). Predictive factors for intracranial hemorrhage in patients harboring CMs is a critical issue because the optimal therapeutic management of such lesions is tailored according to the bleeding risk. The main goal of radiosurgical treatment should be a significant reduction in bleeding risk, especially after a latency period of 2 years. By genetic linkage analyses, three cerebral CM loci have been assigned to chromosome 7p, 7q, and 3q. They account for all familial forms of CM, thus constituting a formidable Mendelian model of stroke.
Acute isolated optic neuritis is often the first manifestation of multiple sclerosis (MS), and its management remains controversial. Over the past decade, with the advent of new disease-modifying agents, management of isolated optic neuritis has become more complicated.
To evaluate the current practice patterns of Canadian ophthalmologists and neurologists in the management of acute optic neuritis, and to evaluate the impact of recently published randomized clinical trials.
All practicing ophthalmologists and neurologists in Canada were mailed a survey evaluating the management of isolated acute optic neuritis and familiarity with recent clinical trials. Surveys for 1158 were mailed, and completed surveys were collected anonymously through a datafax system. Second and third mailings were sent to non-respondents 6 and 12 weeks later.
The final response rate was 34.5%. Although many acute optic neuritis patients initially present to ophthalmologists, neurologists are the physicians primarily managing these patients. Ordering magnetic resonance imaging, and treating with high dose intravenous steroids has become the standard of care. However, 15% of physicians (14% of ophthalmologists and 16% of neurologists) continue to prescribe low dose oral steroids, and steroids are being given for reasons other than to shorten the duration of visual symptoms by 73% of ophthalmologists and 50% of neurologists. More neurologists than ophthalmologists are familiar with recent clinical trials involving disease-modifying agents.
Although the management of acute optic neuritis has been evaluated in large clinical trials that were published in major international journals, some ophthalmologists and neurologists are not following evidence-based recommendations.
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