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Biomedical subjects

M M Hoehn

Publications and source records attributed to M M Hoehn.

At least 19 recordsLinked to original sources
PubMed1992

The natural history of Parkinson's disease in the pre-levodopa and post-levodopa eras.

Since Parkinson's disease was first described by James Parkinson in 1817, the natural history has been confounded by various treatment modalities: the replenishment of deficient dopamine, the addition of the dopamine agonists, and the more recent addition of drugs whose putative action may slow the natural history of the disease. Nevertheless it remains a disease that is slowly and inexorably progressive over several decades. The quality of life during this progression can be improved, and the duration of life before inanition produces life-threatening complications can be extended. New approaches to identifying the disease before the overt symptoms appear and to slowing the progression of the underlying pathophysiology are being explored but to date have not produced significant changes in the prognosis for the individual patient.

Humans↗
PubMed1990

An examination of male-female differences in progression and mortality of Parkinson's disease.

We conducted disability and mortality studies to determine if the male preponderance usually found in Parkinson's disease (PD) was reflected in different courses of the diseases in the 2 sexes. We analyzed longitudinal disability score in 47 men and 23 women with PD followed for 6 years at UCLA. We found no significant differences between the sexes in mean disability scores in any of the 6 years. Mean dopa dosage was significantly higher in men, possibly reflecting their generally larger body mass. Choreoathetosis, dementia, or other side effects did not differ between the 2 groups. We obtained observed to expected mortality ratios in 239 men and 132 women followed for 3,831 person-years from records of 4 medical centers. Using the sex-specific US Life Tables to calculate expected mortality, we found the observed to expected ratio for the men was 1.7457 and for the women 2.4740, a significantly greater excess in female mortality. Analyses of mortality using tables which are not sex-specific will fail to uncover the decreased longevity in women with PD. We conclude that, despite the male preponderance in PD, men and women acquire it at the same age, have the same progression and duration of disease, and die at the same age; whereas, in the general population, women have a longer life expectancy than men. It is not known what factors protect women from incurring PD and what lowers their life expectancy to that of men when they do have the disease.

Disability Evaluation↗
PubMed1989

Effect of age at onset on progression and mortality in Parkinson's disease.

We examined longitudinal disability scores in 54 patients with Parkinson's disease followed for 6 years at UCLA. We sorted data into 3 groups based on age at onset of symptoms: group A, onset under 50 years; group B, 50 to 59 years; group C, 60 years or older. There were no significant differences between groups initially. All 3 groups improved dramatically when levodopa was given, but group A showed significantly less disability in years 4, 5, and 6 than did group C. The groups did not differ with respect to side effects. To determine if age at onset affected mortality, we sorted records from 4 geographically diverse centers into the same 3 groups. Results on 359 patients followed for 3,314 person-years, covering a period of 17 years after onset of symptoms, showed that group A had the most favorable observed-to-expected mortality ratio, 1.82, compared with 2.17 and 2.20 for groups B and C respectively, but the difference was not statistically significant. Results from the disability analyses indicate that patients with onset of Parkinson's disease under 50 years of age may have a more favorable prognosis than those whose symptoms begin in later years.

Aging↗
PubMed1979

Neuropsychological impairment with schizophrenia vs. acute and chronic cerebral lesions.

Performed detailed neuropsychological evaluations with 25 recently hospitalized schizophrenics in whom systematic neurologic workups had failed to reveal CNS disease. Efforts were made to minimize possible effects of drug-induced extrapyramidal symptoms on test performance. Although the schizophrenics showed some neuropsychological impairment relative to 25 normals, their deficits were not as severe as those of patients known to have either acute or chronic brain disorders (N = 25). The diagnostic accuracy achieved by the tests supports their use in short-term treatment facilities when the differential diagnosis includes schizophrenia and brain disorder, especially acute brain disorder. Schizophrenics' neuropsychological impairment was more correlated with degree of EEG abnormality than with degree of psychosis, which suggests a possible organic basis for the deficits that they showed on testing.

Acute Disease↗
PubMed1978

Dopamine excretion and vulnerability to drug-induced Parkinsonism. Schizophrenic patients.

Before and during a standardized course of trifluoperazine therapy, 18 schizophrenic patients underwent repeated examinations for extrapyramidal motor signs, clinical psychopathology, and urinary excretion of free and conjugated forms of dopamine and its metabolites. Patients excreting more free dopamine and metabolites, or showing less complete conjugation, before drug treatment, were much less likely than others to develop parkinsonian akinesia and rigidity during drug treatment. Neither catatonic rigidity nor akinesia before treatment was predictive of a parkinsonian response to trifluoperazine, but pretreatment tremor may have been. The severity of schizophrenic psychopathology was unrelated to dopamine excretion. This study of schizophrenic patients, and our previous research in Parkinson's disease, suggest that urinary dopamine excretion may reflect dopaminergic function of the extrapyramidal motor system in both conditions.

Adult↗
PubMed1978

A32390A, a new biologically active metabolite. I. Discovery and fermentation studies.

A32390A is an isonitrile-containing derivative of diacyl D-mannitol. The compound is produced in fermentation as the major component of a metabolic complex known as A32390. A32390A inhibits dopamine-beta-hydroxylase reduces heart and adrenal norepinephrine levels, lowers blood pressure in hypertensive rats, and possesses antibiotic activity vs. Gram-positive bacteria and fungi, including Candida albicans. A32390 is produced in submerged culture by a mold, a species of Pyrenochaeta, NRRL-5786. Glucose and sucrose are among the best carbon sources for the biosynthesis of A32390. Mannitol, although a substituent of the A32390A molecule, supports little or no biosynthesis of the compound when employed as the major carbon source for the fermentation. The addition of crotonic acid derivatives. ethanol, or L-histidine to the fermentation medium enhances the level of A32390 produced.

Alcohols↗
PubMed1978

Hypothalamic atrophy.

A patient, who has been followed for thirteen years, developed the first symptoms of progressive hypothalamic atrophy at the age of 39. The diagnosis was confirmed by pneumoencephalography five years after onset. Hypothalamic dysfunction was manifested clinically by loss of libido, impotence, obesity, polydypsia, somnolence, and rage attacks. Assessment of endocrinologic function demonstrated low serum levels of testosterone, FSH, and LH, a diabetic glucose tolerance curve, decreased basal and hypoglycemic stimulated levels of HGH, and progressively increasing levels of serum prolactin. Repeated pneumoencephalography revealed an initial, and then progressive, enlargement of the third ventricle which was later associated with generalized, but proportionately less severe, atrophy of the cerebellum and cerebral hemispheres. Analysis of the physiologic and endocrinologic mechanisms underlying these abnormalities suggests diffuse hypothalamic damage, especially in the ventromedial area. The decreased somnolence and increased libido and potency which accompanied therapy with levodopa suggest damage to dopaminergic and noradrenergic pathways. Slowly progressive hypothalamic atrophy, confirmed by pneumoencephalography, but without specific etiology, has not been reported previously. This article describes such a patient followed over thirteen years, and the efficacy of therapy with levodopa in ameliorating certain aspects of his disease.

Adult↗
PubMed1977

Effects of levodopa on the renin-aldosterone system.

Plasma renin activity and plasma aldosterone, supine and erect, and urinary aldosterone levels were measured in 18 patients on normal sodium diets and 11 patients on low sodium diets, all of whom also were on long-term levodopa therapy. Of the 230 hormone measurements, 185 were normal, 11 were high, and 34 were low. Most of the low levels were in 3 patients who had recently received fludrocortisone for orthostatic hypotension, and the renin-aldosterone systems might have been suppressed by it. In another phase of this study, 4 subjects were maintained on a constant diet for 6 wk, while the effect of gradually increasing dosages of levodopa on mineral balance and renin-aldosterone was determined. In 3 of the 4 patients there was a mild natriuretic effect of levodopa (previously demonstrated for acute levodopa therapy). There were no significant consistent changes in renin or aldosterone levels while levodopa was being administered. These studies indicate that levodopa does not usually suppress the elements of the renin-aldosterone system and that such a mechanism is unlikely to be the cause of orthostatic hypotension during the course of levodopa therapy. Since levodopa may induce natriuresis, in this situation unchanged lvels of renin and aldosterone may, however, represent an inappropriately low set of this hormonal system.

Aldosterone↗
PubMed1977

The Parkinsonian syndrome and its dopamine correlates.

The urinary excretion of free dopamine in 37 untreated parkinsonian patients correlated negatively with the severity of rigidity and akinesia (p less than 0.025) and with total neurologic deficit (p less than 0.05). In a parallel study of psychiatric patients, those with the lowest levels of urinary free dopamine before treatment were the most vulnerable to, and developed the most severe, secondary parkinsonian rigidity (p less than 0.005), akinesia (p less than 0.05), and total deficit (p less than 0.01) when they were subsequently treated for two weeks with trifluoperazine. In neither study was there a significant correlation between free urinary dopamine and tremor. These studies directly associate the level of free dopamine in the urine with the severity of the parkinsonian syndrome. Therefore, although many peripheral sources contribute to urinary free dopamine, a small decrease in the level may actually reflect the severity of the disturbance of central dopamine metabolism and the known deficiency of dopamine in the neurons of the parkinsonian brain.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1977

Spinal myoclonus.

The focal involuntary muscular contractions of spinal myoclonus have been associated with neoplastic, infectious, traumatic, and degenerative lesions of the spinal cord. Four patients are described here. In two, the myoclonus is associated with severe cervical spondylitis. One patient had herpes zoster. In the fourth, a segment of thoracic spinal cord is narrow and probably atrophic. Both tetrabenazine and clonazepam were therapeutically effective.

Clonazepam↗
PubMed1976

A trial of antilymphocyte globulin in the treatment of chronic progressive multiple sclerosis.

Twenty-three patients with chronic progressive multiple sclerosis (MS), resistant to steroid therapy, were treated with antilymphocyte globulin (ALG) and prednisone (30 mg by mouth daily). Twelve patients completed a full course of therapy (2 ml ALG i.m. daily for 2 weeks and 2 ml i.m. on alternate days for 2 weeks) and 6 others completed at least 2 weeks of daily injections. Six patients experienced an overall improvement of at least 15% using a comprehensive neurological scoring system. Three other patients had limited, but functionally useful improvement in specific neurologic functions. Six months after the completion of therapy, no patient had deteriorated to a level of function below that noted prior to treatment. Adverse reactions, which often necessitated stopping treatment, included fever, local inflammatory reactions, local rash, general malaise, mild anaphylactoid reactions, and enlargement and tenderness of regional lymph nodes. Because of the short duration of immunosuppression and the toxic side effects of ALG, we do not feel that ALG treatment yet deserves to be intorduced as a standard treatment in clinical practice. However, the improvement or arrest of progression seen in these patients who were deteriorating progressively despite steroid therapy would seem to justify a continued search for a safer method of suppressing immunity in MS patients.

Adult↗
PubMed1976

Age distribution of patients with Parkinsonism.

The modal age at onset of the parkinsonian syndrome during the past thrity years is less than a decade higher than it was in the late 19th and early 20th centuries, suggesting that the same disease entity is affecting parkinsonian patients now as then. The evidence points to the existence of two distinct clinical entities: 1) parkinsonism secondary to encephalitis lethargica, which had its greatest influence on the epidemiology of parkinsonism between 1920 and 1945; and 2) classic parkinsonism, which has undergone little change in the past hundred years.

Adult↗
PubMed1976

Dopamine correlates of neurological and psychological status in untreated Parkinsonism.

Thirty-seven untreated Parkinsonism patients showed significant positive correlations among decreased excretion of free dopamine, MMPI scores indicative of schizophrenic-like looseness of thinking, and the severity of all Parkinsonism signs except tremor. The data could indicate that abnormalities of dopamine metabolism may underlie both the motor and mental abnormalities of Parkinsonism.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1976

Low urinary dopamine and prediction of phenothiazine-induced Parkinsonism: a preliminary report.

Psychiatric patients who excreted larger amounts of urinary free dopamine before treatment were significantly more likely than patients excreting smaller amounts to develop parkinsonian side effects during moderate-dose trifluoperazine therapy. If this finding is replicated, urinary free dopamine determinations could prove valuable in indicating which patients should receive those antipsychotic drugs least likely to produce extrapyramidal side effects.

Adult↗
PubMed1976

A30641, a new epidithiodiketopiperazine with antifungal activity.

A new antibiotic, designated A30641, having in vitro activity against Gram-positive bacteria and fungi has been isolated from a strain of Aspergillus tamarii. Chemical and physical characterization indicate that it is a member of the class of antibiotics containing the epidithiodiketopiperazine moiety.

Animals↗
PubMed1975

Levodopa-induced postural hypotension. Treatment with fludrocortisone.

Six parkinsonian patients with symptomatic postural hypotension secondary to levodopa therapy were treated with 0.05 to 0.2 mg of fludrocortisone acetate daily for six to ten months. Severe orthostatic light-headedness and frequent syncope had previously been alleviated only be reducing the dosage of levodopa to levels producing less than optimal antiparkinsonian benefits. In all six patients, symptoms were alleviated satisfactorily, and supine and upright blood pressures returned to normal levels during treatment with fludrocortisone acetate. There were no adverse reactions. Fludrocortisone acetate is an effective and safe drug for the treatment of severe and otherwise intractable postural hypotension secondary to therapy with levodopa.

Aged↗
PubMed1975

Acute overdose with levodopa. Clinical and biochemical consequences.

A 61-year-old parkinsonian patient ingested up to 100 gm of levodopa during a period of 12 hours. Signs of parkinsonism were completely alleviated. Adverse effects included initial hypertension followed rapidly by hypotension of a few hours' duration, prolonged symptomatic postural hypotension, sinus tachycardia, mental confusion, insomnia, and anorexia. The effects of the overdose gradually subsided over 1 week. Analyses of serum and urine for dopa and its metabolites confirmed the overdose, which biochemically resulted in apparent saturation of two enzymatic pathways that inactivate dopamine: conjugation with sulfuric acid and O-methylation.

Acute Disease↗