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Increasing evidence suggests that manganese deposition is responsible for the T1-weighted magnetic resonance imaging (MRI) signal hyperintensity consistently observed in pallidum of cirrhotic patients. However, the relationship between blood manganese and the etiology or severity of liver disease, as well as the neurological symptomatology in these patients, has not been well established. In the present study, blood manganese concentrations were measured by atomic absorption spectrometry together with MRI and neurological evaluation in 57 cirrhotic patients with various etiologies and severity of liver disease. Blood manganese concentrations were elevated in 67% of cirrhotic patients and were significantly higher in patients with previous portacaval anastomoses or transjugular intrahepatic portosystemic shunt (TIPS). Pallidal signal hyperintensity was observed in 88% of patients, and significant correlations were demonstrated between blood manganese and pallidal index (PI) (a measure of pallidal signal hyperintensity), as well as Child-Pugh score. Assessment of extrapyramidal symptoms using the Columbia rating scale revealed a significant incidence of tremor, rigidity, or akinesia in up to 89% of cirrhotic patients. However, there was no significant correlation between blood manganese and extrapyramidal symptoms, although severity of akinesia was significantly greater in Child-Pugh C patients. Extrapyramidal symptoms could result from a toxic effect of manganese on basal ganglia dopaminergic function. These findings further support a role for manganese in the etiology of pallidal MRI signal hyperintensity in patients with chronic liver disease.

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BACKGROUND: Embolization via a persistent trigeminal artery, one of the embryonic vascular connections that may persist between the carotid and basilar arteries, is an unusual occurrence. CASE DESCRIPTION: We describe a 76-year-old man with bilateral occipital infarctions presumably related to an ulcerated left carotid stenosis. Clinically, a left inferior homonymous quadrantanopia was present. CONCLUSIONS: Anomalous connections between the carotid and the usual posterior circulation territory should be considered in evaluating patients with vertebrobasilar stroke. When they are identified, patients with symptoms attributable to the pontine vertebrobasilar territory supplied by the anomaly may be considered for carotid endarterectomy in the presence of concomitant severe carotid stenosis detected angiographically. Proper identification and treatment of such cases would be expected to prevent recurrence of disabling strokes in the vertebrobasilar circulation. These anomalies will likely be overlooked by ultrasound techniques and depend on good intracranial arteriographic images.

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Over the last decade, transcranial Doppler examination of the cerebral vessels has been made possible by the development of a high-intensity, low-frequency (2 MHz) pulse probe. The middle, the anterior and the posterior cerebral arteries, the cavernous portion of the carotid artery and the basilar artery can thus be easily studied transtemporally or transorbitally or from below the foramen magnum. The transcranial Doppler examination is already used clinically to study arteriosclerosis and in the diagnosis and follow-up of vasospasm and arteriovenous malformations. This review describes the examination procedure and summarizes and illustrates its major indications.

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Six patients with an aortoiliac vascular disease and a peripheral neurological deficit are presented. Clinical and electromyographic findings revealed lumbosacral plexus, sciatic and femoral nerve lesions. A correlation is made between the level of the vascular lesion (aortic, aortoiliac or distally) and the type of peripheral nerve deficit observed. In a patient complaining of pain, weakness, or numbness in a leg, the differential diagnosis should include aortoiliac vascular disease. The peripheral neurological symptoms may be the initial manifestation of the vascular disease or may appear in the early post-operative period.

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The circulating 25-hydroxyvitamin D [25(OH)D] and 1,25-dihydroxyvitamin D [1,25-(OH)2D] concentrations were studied in a patient receiving increasing doses of phenytoin. The plasma 1,25(OH)2D concentrations were independent of the dose of phenytoin administered, as well as of the drug plasma concentrations. The plasma 25(OH)D concentrations were, on the other hand, increased by low phenytoin concentration but rapidly declined when the dose of phenytoin was increased and/or as the length of time of exposure to the drug increased. A linear relationship (R = 0.9651, P less than 0.05) was found between the plasma 25(OH)D concentrations and the dose/plasma phenytoin concentration ratio, suggesting that chronic phenytoin administration may have a dose-related effect on the circulating 25(OH)D concentrations.

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Hypermetabolism of phenytoin is not frequently recognized as a cause of treatment failure. We report the case of a 37-year-old male in whom detailed pharmacokinetic investigation revealed that hypermetabolism, rather than lack of compliance or poor absorption, was responsible for low plasma levels of phenytoin. An increase of his daily dose of phenytoin to 800 mg resulted in adequate plasma levels and good seizure control. Additional studies with two model drugs metabolized by the liver--aminopyrine and antipyrine--showed that he was also a fast metabolizer for these substrates, suggesting a nonspecific induction of hepatic drug metabolizing enzymes. Low plasma phenytoin levels should not be systematically ascribed to lack of compliance, and increased phenytoin metabolism should be considered as an occasional cause of treatment failure.

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