Intracranial calcification in Raine syndrome.

We report the fourth case of a patient recognised with Raine syndrome, a distinct lethal sclerosing bone dysplasia, and we describe the association with intracranial calcification demonstrable by ultrasound and CT.

Diagnostic dilemma and therapeutic non-compliance in a case of intracranial tuberculoma.

A case of extensive intracranial tuberculoma is presented. The patient had been treated for 5 years with a standard antituberculosis regimen but she had been grossly non-compliant. This had led to emergence of multi-resistant Mycobacterium tuberculosis producing progressive disease and extensive cranial nerve damage and proptosis. The unusual CT and angiographic appearances cast doubt on the original diagnosis and a brain biopsy was necessary. Mycobacterium tuberculosis resistant to isoniazid, rifampicin, ethambutol, ethionamide, pyrazinamide, clofazimine and PAS was cultured from the brain biopsy specimen and from an associated groin abscess. A novel regimen of isoniazid, cycloserine, amikacin and ciprofloxacin produced clinical improvement of symptoms and radiological resolution.

Computed tomographic features of primary brain lymphoma.

Head computed tomographic (CT) examinations of 14 patients with primary brain lymphoma were reviewed to assess the CT features of the presenting and subsequent lesions. Presenting lesions were single in 62% and multiple in 38%. Lesions tended to be iso- or hyperdense and homogeneously enhancing. They were commonly located in the deep hemispheric regions, corpus callosum, and posterior fossa. Despite these characteristic patterns, the diagnosis of lymphoma was initially considered in just three patients. Follow-up CT showed good initial response to radiotherapy in 10 patients although mortality was high and posttherapy changes were frequent. Consideration of primary brain lymphoma by radiologists is important, as needle biopsy and radiotherapy may be preferred to a surgical resection.

Major cerebral arterial and venous disease in osteopetrosis.

Two patients with osteopetrosis were studied in whom severe stenosis of one or both internal carotid arteries was demonstrated. One patient had autosomal dominant osteopetrosis and the other patient had the autosomal recessive form of the disease. In one patient, probable occlusion of one internal jugular vein and retrograde thrombosis of the contributing dural venous sinuses was present. Venous drainage of parts of the brain occurred through dilated emissary and scalp veins. It appears that major extracranial vessels may be impinged upon by dysplastic bone in osteopetrosis, although this is the first report of such an occurrence. A posterior fossa aneurysm was present in one case, and may have been related to abnormal intracranial hemodynamics.

Radiographic-pathologic correlation in cerebral amyloid angiopathy. A review of 12 patients.

Twelve patients with pathologically proven cerebral amyloid angiopathy (CAA), causing intracerebral hemorrhage, were reviewed to determine the clinical and radiographic features. All 12 patients were 62 years of age or older and presented with acute neurological syndromes. The computed tomographic scan (CT) in each showed a relatively large intracerebral lobar hemorrhage located in a cortical and subcortical area. The finding of a lobar intracerebral hematoma in an elderly patient should suggest CAA as a cause.

Intracranial metrizamide mimicking white matter disease.

We report two patients in whom brain penetrance of grey matter by metrizamide, introduced for myelography thirty hours earlier, mimics the periventricular lucency of white matter disease on cranial computed tomography.

Doppler flow maps of the carotid artery compared with the findings on angiography.

One noninvasive method of evaluating the condition of the carotid arteries is by the Echoflow Doppler device, which produces colour-coded images of the flow pattern in the arteries. Normal velocities are represented in red, accelerated flow in yellow and turbulences in blue. The authors present the results of Echoflow studies in 317 patients who also underwent cerebral angiography. Of 660 normal carotid vessels, 21 showed appreciable abnormalities on Echoflow study (false positive 3.2%). Of 87 vessels with stenosis of 50% or more, the Echoflow study showed normal flow in 26 (false negative 29.9%). The Echoflow study indicated no abnormalities in 3 of 22 patients with severe stenosis (more than 80%) (false negative 13.6%). Of nine patients with carotid occlusion, the Echoflow study gave normal findings in one (false negative 11.1%). Sensitivity was 70.1%, specificity was 96.9%, with a positive predictive accuracy of 93.9%. Sources of error include misidentification of arteries, signal attenuation (acoustic shadow), hemodynamic changes and timing of the Echoflow study relative to angiography. Combined studies with B-mode ultrasonography and spectral analysis of the Doppler signal should reduce error. These studies should not be used to replace angiography, but to help select for angiography patients for whom the study might be contraindicated because of advanced age or cardiac disease.

Amnesia after femorocerebral angiography.

The charts and radiographs of 12 of 1,520 patients who developed amnesia after transfemoral cerebral angiography performed with local anesthesia and minimal sedation were retrospectively reviewed. In three younger patients, exacerbation of organic or idiopathic temporal lobe epilepsy was thought to be the cause of the amnesia, while the amnesia of the nine patients over 40 years old had the characteristics of transient global amnesia. Eight of the patients had had similar episodes before angiography, and three others had other evidence of vertebrobasilar disease. Emboli from atheromatous debris or catheter clot due either to catheter manipulation problems, an inexperienced operator, or the use of a large catheter were considered likely causes in 11 cases, while in three patients contrast emboli or toxicity may have been the etiologic factor.

Cerebral edema associated with meningiomas.

The cerebral edema, as judged by computed tomographic scan, associated with supratentorial meningiomas was assessed in 55 cases. No relationship to the occurrence or the degree of edema could be established with respect to meningioma location, histological type, tumor vascularity, cellularity, number of mitotic figures, necrosis, calcification, or cortical invasion. The larger the meningioma, the more likely the presence of and the severity of cerebral edema. The edema is a significant factor in the occurrence of clinical signs and symptoms. A biopsy of cerebral cortex and white matter underlying a transitional meningioma in a patient with associated cerebral edema demonstrated perivascular astrocytic end-feet swelling in the cortex and considerable extracellular fluid in the white matter. The ultrastructural appearance is similar to that seen with primary and metastatic brain tumors and with experimental vasogenic cerebral edema.