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Biomedical subjects

U McMonagle

Publications and source records attributed to U McMonagle.

4 recordsLinked to original sources
PubMed1996

[Secondary cerebral vasculitis in suppurative meningitis. Clinical aspects and findings in color-coded transcranial duplex ultrasound].

Transcranial Doppler ultrasonography carried out in cases of bacterial meningitis has often shown a reversible increase in blood flow velocity in basal cerebral arteries, that is interpreted as caused by segmental vasospasm brought on by vasculitis. We report for the first time on findings of transcranial colour-coded duplex ultrasonography performed on a patient with pneumococcal meningitis who suffered a subcortical infarction in the territory of the right middle cerebral artery. Doppler ultrasonography revealed an increase in blood flow velocity of the right middle basal cerebral artery, while the B-scan revealed thickening of the main trunk on the right. These findings suggest an inflammatory thickening of the blood vessel wall with secondary narrowing of the lumen as a result of secondary vasculitis.

Adult↗
PubMed1996

Paroxysmal convergence spasm in multiple sclerosis.

Paroxysmal phenomena are rare but relatively typical clinical symptoms of multiple sclerosis (MS) caused by abnormal excitation in demyelinated plaques. We report the case of a 25-year-old woman with ocular convergence spasms as a new type of paroxysmal phenomenon in MS. MRI revealed the associated brainstem lesion in the region of the medial longitudinal fasciculus. Bromocriptine treatment was successful in resolving the paroxysms.

Adult↗
PubMed1994

Wernicke's encephalopathy--causes to consider.

Wernicke's encephalopathy (WE) is a thiamine deficiency disorder and is characterized clinically by the triad of ocular abnormalities, ataxia and disturbances of consciousness. We report on 3 patients with WE, of whom 2 had insufficient thiamine substitution. In the first patient symptoms disappeared during thiamine substitution. In the second patient acute WE was the terminating event in the sequence of parenteral nutrition, lactic acidosis and cardio-pulmonary decompensation. Possibly due to hereditary deficits WE developed in the third patient despite sufficient thiamine substitution. Attention to thiamine deficiency should be paid in all patients with history of alcoholism, malnutrition, malabsorption, tumors, inflammation, other severe diseases and in parenteral hyperalimentation. In order to prevent WE thiamine should be substituted with at least 100 mg/day i.v. or i.m.

Adult↗