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Biomedical subjects

S Fahn

Publications and source records attributed to S Fahn.

At least 343 records · Page 19Linked to original sources
PubMed1981

L-DOPA (L-3,4-dihydroxyphenylalanine) uptake by human red blood cells.

The uptake of L-DOPA (L-3,4-dihydroxyphenylalanine) was studied in normal human red blood cells in vitro using L-[3-14C]DOPA. Uptake was slow, tending towards a distribution ratio close to unity with a half-time to equilibrium of one hour. Uptake was not Na+-dependent. Concentration dependence studies showed both saturable and non-saturable components of uptake, and inhibition studies using L-leucine and L-tryptophan suggest that the L and T systems of red cell amino acid uptake are involved. A powerful inhibitor of both systems, 3,4-dihydroxy-2-methylpropriophenone (U-0521), is described. It is concluded that uptake is by carrier-mediated facilitated diffusion via the L and T systems for which L-DOPA has low affinity.

Biological Transport↗
PubMed1981

Neuroleptic malignant syndrome caused by dopamine-depleting drugs in a patient with Huntington disease.

Prior reports of neuroleptic malignant syndrome (NMS) concerned patients with psychiatric disorders, usually schizophrenia, who were taking dopamine receptor blocking agents. We report the syndrome in a patient with Huntington disease who was treated with dopamine-depleting agents. He had a negative evaluation for malignant hyperthermia (MH), and we suggest that NMS differs from MH. The occurrence of NMS caused by dopamine-depleting agents suggests that anticholinergic properties of phenotiazines are not the only cause. Central dopaminergic systems probably participate in thermoregulation, and dopamine depletion probably plays a pathogenetic role in this syndrome.

Adolescent↗
PubMed1980

Unilateral Parkinson's disease and contralateral tardive dyskinesia: a unique case with successful therapy that may explain the pathophysiology of these two disorders.

A unique case reported of a patient with right-sided Parkinson's disease and left-sided tardive dyskinesia. This situation occurred because the patient's parkinsonian tremor was treated with antipsychotic drugs. After several months she developed tardive dyskinesia on the left side of the body. Successful treatment was achieved nine years later, using dopamine-depleting drugs (combination reserpine and alpha-methylparatyrosine) to suppress the tardive dyskinesia and trihexyphenidyl to reduce the parkinsonism. Control of the symptoms was complicated with parkinsonism symptoms later increased on the right and developed on the left, due to the dopamine-depleting drugs. A small amount of carbidopa/levodopa restored the proper balance of symptoms, effectively reducing the parkinsonism while not aggravating the tardive dyskinesia. This unique case provides insight into the pathogeneis of Parkinson's disease, the pathogenesis of tardive dyskinesia, their successful therapeutic approaches, and possibly the effect of drugs in blocking the progression of Parkinson's disease.

Aged↗
PubMed1980

Delayed-onset dystonia in patients with "static" encephalopathy.

Eight cases of persistent dystonia appearing one to 14 years after non-progressive cerebral insults are described. Five were due to perinatal anoxia, one to trauma, and two to cerebral infarction. This phenomemon of delayed-onset dystonia has not been described previously, although review of earlier literature reveals several probable examples. Delayed-onset dystonia due to perinatal anoxia is an important diagnostic alternative to dystonia musculorum deformans for dystonia occurring in childhood.

Brain Injuries↗
PubMed1980

Physiologic and pathologic tremors. Diagnosis, mechanism, and management.

Tremor, the commonest of the involuntary movement disorders, is characterized by rhythmical oscillatory movement that occurs at rest or during activity; all tremors cease during sleep. Physiologic tremor is present in normal persons and is asymptomatic. Tremor is considered pathologic when it impairs a patient's function. Clinically, the pathologic tremors may be classified as accentuated physiologic, parkinsonian, essential, and cerebellar. We review here the basic mechanisms and clinical features of various tremors and emphasize recent advances in pathophysiology and management.

Alcoholic Beverages↗
PubMed1979

The role of bromocriptine in the treatment of parkinsonism.

Fifty-three patients with parkinsonism, either with intractable symptoms despite optimum-dosage levodopa therapy or with adverse effects from levodopa limiting its usefulness, were treated with bromocriptine, with gradually increasing doses until benefit or adverse effect was encountered. All were initially maintained on optimal levodopa therapy. Improvement was seen in 26 patients, of whom 19 (36 percent of the total 53 patients) had sustained improvement. Effective doses of bromocriptine ranged from 5 to 90 mg per day. Improvement occurred in all categories of clinical problems, including patients who lost some benefit from chronic levodopa therapy as well as those with adverse effects from levodopa. A high incidence (70 percent) of adverse effects of bromocriptine limited the usefulness of this drug. Since one cannot predict which patients might benefit from bromocriptine, this drug is worth a trial in patients not doing well on levodopa therapy if other means to improve their condition are not successful.

Aged↗
PubMed1979

Analysis of the clinical problems in parkinsonism and the complications of long-term levodopa therapy.

We evaluated the current status of 131 patients with idiopathic parkinsonism who were receiving levodopa therapy. The residual parkinsonian symptoms and signs were tabulated, as were the adverse effects from medication. Response to therapy was correlated with duration of the disease and with duration of treatment. Patients with on-off or wearing-off effects were likely to have been treated for 4 years or longer. Patients treated with levodopa for 4 to 8 years were significantly more impaired with parkinsonism than patients treated for 0 to 3 years, even when patients were matched for total duration of disease. These data suggest that the deterioration of responsiveness after several years of levodopa therapy may be due to the therapy itself. Our findings support the concept that utilization of levodopa therapy should be delayed until a patient becomes significantly impaired in occupational or social situations.

Adolescent↗