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• OBJECTIVE. —A retrospective study was performed to delineate the clinical characteristics of symptomatic unruptured aneurysms. DESIGN. —Patient histories, operative reports, and angiograms in 111 patients with 132 unruptured aneurysms were reviewed. SETTING. —Tertiary care university hospital. PATIENTS. —One hundred eleven patients with 132 unruptured intracranial aneurysms were studied. There were 85 women and 26 men, with a mean age of 51.2 years (age range, 11 to 77 years). Many patients were referred by community neurologists and neurosurgeons for further evaluation and neurosurgical management. RESULTS. —Fifty-four symptomatic patients were identified. Group 1 (n=19; mean aneurysm diameter, 2.1 cm) had acute symptoms: ischemia (n=7), headache (n=7), seizure (n=3), and cranial neuropathy (n=2). Group 2 (n=35; mean aneurysm diameter, 2.2 cm) had chronic symptoms attributed to mass effect: headache (n=18), visual loss (n=10), pyramidal tract dysfunction (n=4), and facial pain (n=3). Group 3 (n=57; mean aneurysm diameter, 1.1 cm) had asymptomatic aneurysms. CONCLUSIONS. —Acute severe headache, comparable to subarachnoid hemorrhage headache, but without nuchal rigidity, was associated with the following mechanisms: aneurysm thrombosis, localized meningeal inflammation, and unexplained. Unruptured aneurysms may be misdiagnosed as optic neuritis or migraine, or serve as a nidus for cerebral thromboembolic events. Internal carotid artery and posterior circulation aneurysms were more likely to cause focal symptoms from mass effect than were anterior cerebral artery and middle cerebral artery aneurysms. Weeks to years may elapse before their diagnosis. The absence of subarachnoid blood does not exclude an aneurysm as a cause for acute or chronic neurologic symptoms.

We studied two patients who were given high-dose intravenous steroid therapy and were intubated for status asthmaticus. Both became quadriplegic and wasted within 2 weeks. EMG had myopathic abnormalities. Muscle biopsy revealed severe atrophy of most muscle fibers, with disorganization of myofibrils and selective loss of thick (myosin) filaments. Immunohistologic stains for myosin isoforms confirmed the decrease or absence of this protein. Both patients clinically improved over several months.

We report the simultaneous occurrence of biopsy-proven temporal arteritis in husband and wife. Serologic and viral studies were negative, including viral culture of the wife's temporal artery. The concurrent incidence of giant cell arteritis in a married couple would suggest a common exogenous exposure.

Spinal dural arteriovenous fistulas (SDAVFs) are the most common type of spinal vascular malformation. The arteriovenous shunts, located entirely outside the spinal cord, cause a clinical picture of chronic progressive myelopathy believed to arise from the effects of increased venous pressure and impaired venous drainage on the spinal cord. Despite their well-described clinical and angiographic features, no reports have documented the spinal cord pathology in a case of angiographically or pathologically proven SDAVF. We report such a patient in whom a spinal cord biopsy supported increased venous pressure as a mechanism of neurologic dysfunction.

To describe the clinical features of cardiac injury associated with neurogenic pulmonary edema (NPE) in patients with acute subarachnoid hemorrhage (SAH).

Previous studies have demonstrated that cerebral blood flow (CBF) can be assessed noninvasively by MRI using magnetic labeling of arterial water as a diffusible flow tracer. The purpose of this study was to assess the quality of CBF images obtained from patients with cerebrovascular disease using this method, and to begin to evaluate the potential clinical role for this technique. We recruited 14 patients who presented with stroke, TIA, or severe carotid stenosis and were likely to have altered CBF based on clinical assessment. In many of these patients, CBF imaging disclosed both focal and hemispheric hypoperfusion, either in vascular territories or in watershed regions. In 11 patients with significant proximal arterial stenosis, hemispheric CBF abnormalities localized to the side of most significant stenosis for the anterior circulation distribution. In several patients watershed hypoperfusion was even more pronounced. Our results suggest that good-quality MR CBF images can be obtained reliably from patients with cerebrovascular disease. CBF imaging can be combined with standard structural imaging within a single MRI examination, and provides clinically meaningful information. The capability of measuring CBF easily provides a potentially useful tool for clinical assessment and further investigation of stroke pathophysiology.

We report three patients (two children and one adult) with Guillain-Barré syndrome and magnetic resonance imaging evidence of gadolinium enhancement of the cauda equina and lumbar nerve roots. All three patients exhibited symmetric ascending paralysis and areflexia, and two (one child, one adult) suffered urinary incontinence and retention. Similar enhancement has been observed in patients with chronic inflammatory demyelinating polyneuropathy and suggests proximal nerve inflammation. Magnetic resonance imaging in Guillain-Barré syndrome and chronic imflammatory demyelinating polyneuropathy may have diagnostic utility.

A 57-year-old awake man developed central neurogenic hyperventilation associated with a pontine mass. Serum pH reached as high as 7.72 with serum carbon dioxide of 6 torr. Examination of CSF during overbreathing showed that CSF pH was markedly alkaline. Pathologic study showed a well-differentiated pontine astrocytoma. The combination of alkaline CSF and an infiltrating pontine lesion supports a structural, rather than chemical, mechanism for central hyperventilation.