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Biomedical subjects

J H Pincus

Publications and source records attributed to J H Pincus.

At least 19 recordsLinked to original sources
PubMed1992

Protein redistribution diet remains effective in patients with fluctuating parkinsonism.

Forty-three carbidopa-levodopa (Sinemet)-treated parkinsonian patients with protein-sensitive motor fluctuations were started on the protein redistribution diet within the past 48 months. Thirty patients (70%) are still using the diet successfully after more than 12 months (mean duration, 33.6 months; range, 12 to 48 months). The diet was discontinued in the other 13 cases. In 10 of these 13 patients, the protein redistribution diet was discontinued for a variety of reasons, despite continued sensitivity to dietary protein; in only three patients (7%), those with the most severe and complicated disease, was the protein redistribution diet stopped because of its limited therapeutic benefit. The protein redistribution diet is a simple adjunct to the treatment of Parkinson's disease that can significantly prolong the efficacy of levodopa therapy in many fluctuating "end-stage" patients.

Adult↗
PubMed1991

Standard and controlled-release levodopa/carbidopa in patients with fluctuating Parkinson's disease on a protein redistribution diet. A preliminary report.

Ten patients with Parkinson's disease (PD) with motor fluctuations that responded to a protein redistribution diet were studied. All 10 patients were receiving standard Sinemet (levodopa/carbidopa). Five randomly selected patients were changed from standard Sinemet to a controlled-release form of Sinemet. The other five patients continued to receive standard Sinemet. To maintain the same degree of control of PD in the five patients switched to the controlled-release form of Sinemet, the daily levodopa intake increased. While receiving optimal therapy (standard Sinemet or controlled-release Sinemet) and a protein redistribution diet, all 10 patients then underwent hourly videotaping and blood sampling (for plasma levodopa levels) during 2 consecutive days. Videotapes were blindly reviewed for PD disability, dyskinesia, and the time required to walk a measured distance. Comparing the two groups, standard Sinemet with controlled-release Sinemet, respectively, mean levodopa requirements were 505 and 1895 mg, plasma levodopa levels were 6.1 and 17.6 mumol/L, and abnormal involuntary movement scale scores were 14 and 26. Their mean PD disability scores did not differ statistically or clinically. Also no statistically significant differences were noted in either their mean walking times or their mean daily dose frequencies.

Antiparkinson Agents↗
PubMed1989

Cryptococcal meningitis. False-negative antigen test results and cultures in nonimmunosuppressed patients.

All cases of cryptococcal meningitis at Yale-New Haven (Conn) Hospital seen during a 4 1/2-year period were reviewed to calculate the rate of false-negative antigen test results and cultures preceding diagnosis. Of 13 patients, 9 were immunosuppressed and were diagnosed following the initial lumbar puncture, with both antigen test results and cultures positive in all cases. Among 4 nonimmunosuppressed patients, the rate of false-negative antigen test results was 77%, and of cultures, 89%. The diagnosis was consequently delayed in 3, 2 of whom died despite treatment. Cryptococcal meningitis may be underdiagnosed and undertreated to a significant degree in nonimmunosuppressed patients.

Acquired Immunodeficiency Syndrome↗
PubMed1988

Neuropsychiatric, psychoeducational, and family characteristics of 14 juveniles condemned to death in the United States.

Of the 37 juveniles currently condemned to death in the United States, all of the 14 incarcerated in four states received comprehensive psychiatric, neurological, neuropsychological, and educational evaluations. Nine had major neurological impairment, seven suffered psychotic disorders antedating incarceration, seven evidenced significant organic dysfunction on neuropsychological testing, and only two had full-scale IQ scores above 90. Twelve had been brutally physically abused, and five had been sodomized by relatives. For a variety of reasons the subjects' vulnerabilities were not recognized at the time of trial or sentencing, when they could have been used for purposes of mitigation.

Adolescent↗
PubMed1988

Protein redistribution diet restores motor function in patients with dopa-resistant "off" periods.

Sixteen parkinsonians with acquired drug-resistant "off" periods without dyskinesia were placed on a diet in which virtually all protein was concentrated in the evening meal. Restoration of sensitivity to levodopa resulted in 88%. Ten patients (62%) have continued to comply with the diet for 7 months (mean). Two patients were studied in detail. Immobility correlated with elevated plasma levels of large neutral amino acids (LNAA), normality with low LNAA.

Amino Acids↗
PubMed1987

Influence of dietary protein on motor fluctuations in Parkinson's disease.

On a nearly zero protein diet, 11 patients with Parkinson's disease with the "on-off" effect demonstrated great sensitivity to levodopa (L-dopa)-carbidopa and reduced fluctuations. Eight patients required a 41% reduction in total L-dopa dosage and discontinuation of all adjuvant therapy to reduce the preponderance of chorea. On a high-protein diet, all patients were immobilized by bradykinesia for most of the day. A low-protein dietary regimen during the daytime offers an important technique for the control of fluctuations in patients with Parkinson's disease who are receiving L-dopa-carbidopa.

Aged↗
PubMed1987

Plasma levels of amino acids correlate with motor fluctuations in parkinsonism.

Seven patients with Parkinson's disease who experienced severe motor fluctuations in response to levodopa were studied in detail with relation to the effect of dietary protein on their motor function. The levodopa dose for each patient was not changed during the period of study, and no other antiparkinsonian drugs were used. Regular and high-protein diets resulted in a marked elevation in the plasma concentrations of large neutral amino acids (LNAAs) that are known to compete with levodopa for transport across the blood-brain barrier. Despite elevated plasma levodopa levels, all patients with elevated LNAA levels experienced parkinsonian symptoms. When the amino acid level dropped while plasma levodopa levels were elevated, patients experienced relief of these symptoms. On a low-protein diet, LNAA levels remained low and all patients were consistently dyskinetic throughout the day, even though the mean plasma levodopa levels were somewhat lower than when the patients consumed a high-protein diet. A redistribution diet that is virtually protein free until supper and then unrestricted until bedtime is tolerated by patients because this simple manipulation permits near-normal daytime motor function.

Amino Acids↗
PubMed1986

Phenytoin reduces early acetylcholine release after depolarization.

Phenytoin 10 microM inhibits the K-evoked release of acetylcholine (ACh) from synaptosomes, a process which is biphasic. Phenytoin acts only on the early phase of release. Replacement of external Na with Li does not modify phenytoin's effect. Phenytoin augments the spontaneous release of ACh from resting synaptosomes but this effect is eliminated in Li media. It is likely that phenytoin reduces K-evoked Ca uptake and the Na/Ca exchange by separate mechanisms.

Acetylcholine↗
PubMed1986

Phenytoin: mechanisms of its anticonvulsant action.

Phenytoin is a major anticonvulsant drug that is very effective in controlling a wide variety of seizure disorders while impairing neurological function little, if at all. Early work suggested the hypothesis that the drug's effects were due to a selective block of high-frequency neuronal activity. This theory is reevaluated in the light of accumulated observations on the effects of phenytoin in many neuronal and synaptic preparations. Most of these observations can be explained by a use- and frequency-dependent suppression of the sodium action potential by phenytoin, with a consequent filtering out of sustained high-frequency neuronal discharges and synaptic activity. The molecular mechanism for this is a voltage-dependent blockade of membrane sodium channels responsible for the action potential. Through this action, phenytoin obstructs the positive feedback that underlies the development of maximal seizure activity, while normal brain activity, proceeding at lower neuronal firing rates, is spared its depressant action. Other mechanisms of action that may contribute to the drug's efficacy and selectivity are also discussed.

Action Potentials↗
PubMed1986

Phenytoin, tetrodotoxin, and acetylcholine release.

To determine if phenytoin reduces depolarization-linked acetylcholine release from synaptosomes solely by interacting with Na+, the effect of phenytoin (100 to 200 microM) and/or tetrodotoxin (1 microM) on ACh release was assayed in synaptosomes depolarized with either KCl 56 mM or veratridine 10 microM. Phenytoin reduced release in both depolarizing solutions. In KCl the effect of phenytoin was greater at 200 microM than 100 microM but with veratridine, phenytoin 200 microM was not more effective than 100 microM. Tetrodotoxin failed to affect release induced by KCl but the effect of tetrodotoxin and phenytoin on veratridine-stimulated release was much greater than that with phenytoin alone 100 microM. In conclusion, the inhibition of acetylcholine release by phenytoin must be independent of any effect of the drug on Na conductance.

Acetylcholine↗
PubMed1986

Psychiatric, neurological, and psychoeducational characteristics of 15 death row inmates in the United States.

The authors present the results of clinical evaluations of 15 death row inmates, chosen for examination because of the imminence of their executions and not for evidence of neuropsychopathology. All had histories of severe head injury, five had major neurological impairment, and seven others had other, less serious neurological problems (e.g., blackouts, soft signs). Psychoeducational testing provided further evidence of CNS dysfunction. Six subjects had schizophreniform psychoses antedating incarceration and two others were manic-depressive. The authors conclude that many condemned individuals probably suffer unrecognized severe psychiatric, neurological, and cognitive disorders relevant to considerations of mitigation.

Adult↗