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Biomedical subjects

B M Allan

Publications and source records attributed to B M Allan.

5 recordsLinked to original sources
PubMed1999

MR imaging of brachial plexopathy in breast cancer patients without palpable recurrence.

OBJECTIVE: To investigate the role of MR imaging in detecting brachial plexus (BP) abnormalities in breast cancer patients with plexopathy but without palpable masses. DESIGN: MR imaging of the BP was performed on 26 breast cancer patients with brachial plexopathy without palpable regional masses, using 0.5 T and 1.5 T imaging systems. Findings were correlated with the clinical diagnoses. PATIENTS: Twenty-six patients with brachial plexopathy and history of breast cancer were enrolled in the study. All patients presented with plexopathy symptoms. Fourteen patients were positive and 12 patients were indeterminate for BP metastasis according to clinical criteria. RESULTS AND CONCLUSION: MR imaging demonstrated masses involving the BP representing metastases in two patients. Nine patients had other regional abnormalities with a normal brachial plexus. It is concluded that MR imaging is useful in the assessment and direction of therapy of brachial plexopathy in breast cancer patients by detecting both metastases to the BP as well as other abnormalities, unrelated to the BP, which may explain the patient's symptoms.

Adult↗
PubMed1982

A double-blind clinical trial of isoniazid in Huntington disease.

Isoniazid (INH) was given to nine patients with Huntington disease (HD) in a double-blind, placebo-controlled crossover trial. In an earlier open trial, three of six patients had improved, and one of them remained improved after 7 years on INH. Only one patient benefited in the present trial. All patients excreted small amounts of hydrazine in their urine while taking INH, and it is this INH metabolic that elevates GABA content in brain. GABA concentrations were markedly increased in CSF during INH therapy. Lack of clinical improvement in most HD patients despite elevation of brain GABA content suggests that in the minority who are benefited, INH may be acting by some mechanism other than increase of GABAergic neuronal function.

Adult↗
PubMed1980

Failure of aminooxyacetic acid therapy in Huntington disease.

Seven patients with Huntington disease were treated with aminooxyacetic acid (AOAA), an inhibitor of gamma-aminobutyric acid aminotransferase (GABA-T), in an effort to alleviate symptoms by increasing brain GABA content. AOAA was given orally in a placebo-controlled crossover trial in which patients, relatives, and three of the evaluating physicians remained blind. Toxic symptoms occurred in all seven patients when AOAA dosage was increased beyond 2 mg per kilogram per day, and included drowsiness, ataxia, seizures, and psychotic behavior. In five patients who took AOAA for 4 months, no clinical improvement was observed. Biochemical monitoring showed that less inhibition of hepatic GABA-T enzyme activity was achieved than in patients treated with large doses of isoniazid. Results of this trial neither support nor exclude the possible therapeutic usefulness of increasing brain GABA content in Huntington disease.

Acetates↗