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Biomedical subjects

F O Walker

Publications and source records attributed to F O Walker.

51 records · Page 3Linked to original sources
PubMed1989

An open label trial of dextromethorphan in Huntington's disease.

Because of its interactions at N-methyl-D-aspartate and haloperidol specific sigma receptors, dextromethorphan may have symptomatic or protective effects in Huntington's Disease (HD). Escalating doses of dextromethorphan in 11 HD patients produced side effects of dysarthria, rash, and incoordination. At maximum doses, performance declined on a variety of measures of HD, including functional rating scales and quantitative exam scores, consistent with dose-related side effects. Windows of symptomatic benefit were not found. Serum levels of dextromethorphan and its metabolites, including the active compound dextrorphan, showed atypical relationships to dose and side effects, suggesting complex pharmacokinetics. Although not beneficial symptomatically, further trials of dextromethorphan as protective therapy in HD may be warranted.

Adult↗
PubMed1989

Gadolinium-enhanced MRI: a superior technique for the diagnosis of intraspinal metastases.

Intraspinal medullary metastases are difficult to demonstrate radiographically. We describe the value of gadolinium-DTPA-enhanced magnetic resonance imaging in the diagnosis of intraspinal medullary metastases. This safe, sensitive procedure should be a requisite study in myelogram-negative patients with symptomatology indicative of a cord lesion.

Contrast Media↗
PubMed1989

Dysphagia in Huntington's disease.

Although not the most obvious symptom of Huntington's disease (HD), difficulty swallowing, or dysphagia, is a common symptom and may be associated with fatal complications. Management of dysphagia requires an understanding of the process of normal food ingestion and how this process is impaired in HD. This article describes HD and how it interferes with food intake. An effective nursing approach to the management of dysphagia is presented.

Adult↗
PubMed1988

Tabes dorsalis: electrodiagnostic features.

Electrodiagnostic data have not been previously reported in tabes dorsalis. A patient with tabes dorsalis is described whose nerve conduction studies and median nerve somatosensory evoked responses (SEPs) were normal. H-reflexes were absent. SEPs of the tibial nerve suggested posterior column dysfunction. These electrodiagnostic findings correlate precisely with the known pathology of tabes dorsalis.

Afferent Pathways↗
PubMed1988

Evidence for a role of haloperidol-sensitive sigma-'opiate' receptors in the motor effects of antipsychotic drugs.

Haloperidol exhibits a high affinity for a subclass of sigma- "opiate" binding sites which have a unique anatomic distribution and a unique drug selectivity pattern. These binding sites differ from phencyclidine-sensitive sigma-receptors and are found in many brain areas involved in the control of movement. 1,3-Di-o-tolylguanidine (DTG), a highly selective ligand for the haloperidol-sensitive sigma-receptor, produced marked dystonia in rats after microinjection into the red nucleus, a motor area rich in this receptor. Haloperidol and another sigma-ligand [(+)-SKF 10,047] produced similar effects. On the other hand, clozapine, an antipsychotic drug which fails to bind to sigma-receptors and fails to induce movement disorders in humans, failed to induce these dystonic reactions in rats. Phencyclidine was also without effect, as were injections of the active compounds in sites distant to the red nucleus. Microinjections of DTG in the substantia nigra produced vigorous contralateral circling behavior at extremely low doses. These findings suggest that sigma-binding sites represent biologically functional receptors that are active in the neural control of movement. Since haloperidol (and many other antipsychotic drugs) exhibit an affinity for sigma-receptors which is at least equal to its affinity for dopamine receptors, these data raise the further possibility that sigma-receptors are involved in the motor side effects of antipsychotic drugs.

Animals↗
PubMed1987

Chorea-amyotrophy with chronic hemolytic anemia: a variant of chorea-amyotrophy with acanthocytosis.

We studied two siblings with chorea and amyotrophy of adult onset and spherocytic hemolytic anemia. Autopsy revealed an atrophic striatum with iron deposition and spheroid bodies. Degeneration of the substantia nigra and spinal cord anterior horns was seen without iron deposition. The disorder seems to be a variant of the chorea-amyotrophy-acanthocytosis syndrome, and the pathology may account for evidence of parkinsonism and amyotrophy in that syndrome. Acanthocytosis may not be the only hematologic abnormality in this disorder.

Acanthocytes↗
PubMed1984

Benzodiazepine and GABA receptors in early Huntington's disease.

We compared autoradiographic measurements of GABA and benzodiazepine receptors in the brains of two early cases of Huntington's disease (HD), five controls, and four advanced cases of HD. These receptors increase in lateral globus pallidus and decrease in putamen early in the disease, before there is any extensive cell loss and atrophy. The cause of these receptor changes is unknown, but could imply dysfunction rather than death of striatal neurons.

Benzodiazepines↗
PubMedDate not supplied

Failure of meperidine to anesthetize human median nerve. A blinded comparison with lidocaine and saline.

BACKGROUND AND OBJECTIVES: Although meperidine safely produces clinical spinal anesthesia, the responsible mechanism is unknown. This study was undertaken to test the possibility that this drug acts as a local anesthetic by investigating its ability to inhibit conduction in a human peripheral nerve. METHODS: In a blinded fashion, the abilities of 5-mL injections of meperidine (0.5% and 1.5%), lidocaine (0.25%), and saline to produce median nerve block were tested in eight volunteer subjects, and these four solutions were compared with standard local anesthetic solutions that had been tested in previous studies. The extent of local anesthesia was measured objectively by electrodiagnostic tests, namely, compound motor action potentials (CMAPs) and sensory nerve action potentials (SNAPs), as well as by qualitative tests of sensation. RESULTS: Lidocaine (0.25%) prolonged median SNAP latency from 3.1 ms to 3.3 ms (P < .015) and prolonged mean CMAP latency from 4.1 ms to 4.7 ms (P < .002). The SNAP amplitude trended downward after lidocaine (0.25%), but the decrease did not reach statistical significance (35 microV to 25 microV, P < .19). Neither meperidine solution (0.5% or 1.5%) nor saline inhibited SNAP or CMAP amplitudes or prolonged SNAP or CMAP latencies. Also, in contrast to previous findings with more potent local anesthetic solutions (eg, lidocaine 1%, mepivacaine 1%, and bupivacaine 0.33%), none of the four solutions tested in this study altered subjective sensations of hot, cold, or pinprick. Meperidine 1.5% produced systemic side effects, including vertigo, nausea, and flushing, in all subjects. CONCLUSIONS: Meperidine produced no signs of local anesthesia, even when given at a dose (75 mg) and concentration (1.5%) that consistently produced systemic side effects. Thus, the coequivalent ability of meperidine and lidocaine to produce spinal anesthesia contrasts with their discordant ability to produce local anesthesia. This disparity suggests that meperidine may produce spinal anesthesia through mechanisms other than inhibition of sodium channel function.

Action Potentials↗
PubMedDate not supplied

Somesthetic and electrophysiologic effects of topical 0.025% capsaicin in man.

As a topical agent, capsaicin reportedly blocks pain without otherwise impairing sensation. Ten subjects underwent blinded, multiple-dose application of topical 0.025% capsaicin or control emollient to skin test sites in order to evaluate capsaicin effectiveness and toxicity. Clinical changes in somesthetic perception of pinprick, heat and cold developed, but neurogenic flare responses were unchanged. Clinical and electrophysiologic measures of large fiber and autonomic function were unaffected by capsaicin. This study indicates that 0.025% capsaicin is a safe topical agent with demonstrable clinical effects on small fiber function but not on large fiber or autonomic function.

Administration, Cutaneous↗