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Biomedical subjects

J F Neil

Publications and source records attributed to J F Neil.

At least 37 records · Page 2Linked to original sources
PubMed1980

MHPG excretion in depression.

3-Methoxy-4-hydroxyphenylethyleneglycol (MHPG) was measured in 24-hour urine collections obtained from 44 drug-free patients hospitalized for a major depressive disorder, MHPG was significantly lower in a group of three biopolar 1 patients than in a group of unipolar patients. The excretion of MHPG did not significantly differ among patients classified as psychoatic, agitated, or retarded subtypes of depression as compared to patients not assigned to these subtypes.

Adult↗
PubMed1980

MHPG excretion and EEG sleep in primary depression.

Measures of daily urinary 3-methoxy-4-hydroxyphenylglycol (MHPG) excretion and electroencephalographic (EEG) sleep data were examined in 30 patients hospitalized for depression. This sample (mean age = 35 years) comprised 17 females and 13 males, all of whom were drug-free for 2 weeks and met Research Diagnostic Criteria for primary depressive disorder. Data analyses were conducted on the entire group, as well as the male, female, unipolar, and recurrent subgroups. No significant relationships were observed between total MHPG excretion and rapid eye movement (REM) or non-REM sleep variables. In particular, the absence of an interrelatedness of MHPG and REM sleep fails to confirm earlier findings in a smaller patient sample. These results, therefore, raise new questions about the proposed role of central noradrenergic activity in the mediation of REM sleep in depression.

Adult↗
PubMed1980

RBC and plasma choline levels in control and depressed individuals: a critical evaluation.

Red blood cell (RBC) and plasma choline (Ch) were measured in 78 depressed, drug-free patients and in 23 normal, drug-free control subjects. RBC Ch levels displayed a huge variability among the patients, in contrast to those measured in normal controls. Plasma Ch levels, on the other hand, were more consistent within each group, and were correlated with age among the two populations studied. RBC Ch levels would appear to be independent of plasma Ch levels, and to be highly individualized and reproducible within each subject. A segment of the depressed population exhibited significantly higher RBC Ch levels than those seen in the normal control population. A clinical correlation of RBC and plasma Ch levels within the depressed population indicated that the patients with RBC Ch levels exceeding 35 nmole/ml might represent a diagnostically distinct subpopulation with specific clinical characteristics. Results presented here, although preliminary, suggest a role for RBC Ch as a biological marker in certain categories of depressive illness.

Adolescent↗
PubMed1980

Urinary MHPG and clinical response to amitriptyline in depressed patients.

The authors treated 18 rigorously diagnosed depressed patients with amitriptyline after baseline urine samples were collected for the measurement of 3-methoxy-4-hydroxphenylglycol (MHPG). Neither age nor severity of depression before treatment correlated with MHPG excretion. There was also no significant correlation between baseline MHPG excretion and clinical response at the end of at least 25 days' treatment with amitriptyline. The authors discuss the relevance of amitriptyline and nortriptyline plasma levels to MHPG and the noradrenergic/serotonergic theories of depression.

Adolescent↗
PubMed1980

Age, dementia, dyskinesias, and lithium response.

Nineteenth-century neuropsychiatrists felt that the aged bipolar patient usually developed chronic mania, which eventually turned into dementia. The authors' elderly patients seemed to experience few such denouements, so they evaluated the course and treatment response of 81 bipolar patients over the age of 55. Fifty-six responded well to lithium. Advanced age had no effect on course or outcome. However, with increased clinical evidence of neurological illness there was an increased incidence of chronic mania, a poorer response to lithium, and more frequent and severe neurotoxicity. Extrapyramidal syndromes were particularly devastating.

Age Factors↗
PubMed1980

EEG sleep alterations in olivopontocerebellar degeneration.

All-night polygraphic recordings of the electroencephalogram, horizontal electrooculogram, and submental electromyogram were performed in two patients with familial olivopontocerebellar degeneration. Sleep was characterized by subnormal measurements of both rapid eye movement (REM) and delta (slow-wave) sleep. Phasic eye movements were reduced out of proportion to tonic components of REM sleep. These findings lend further support to theories linking the pontine nuclei to the primary regulation of sleep in both experimental animals and humans.

Adolescent↗
PubMed1979

Familial psychosis and diverse neurologic abnormalities in adult-onset Gaucher's disease.

A family is described in which adult-onset Gaucher's disease developed, followed years later by atypical psychotic disorders with neurologic and electroencephalographic abnormalities. A biochemical investigation of primary and secondary enzyme alterations in the index case was performed in an attempt to identify a pattern that might be specific to this clinical profile. The literature pertaining to CNS involvement in adult patients with Gaucher's disease is also reviewed. An etiologic link may exist between the inherited metabolic disorder and associated neuropsychiatric impairment. The biochemical basis of this hypothesized association remains unclear, however, and further enzymatic and pathologic investigations are warranted.

Acid Phosphatase↗
PubMed1979

EEG sleep in primary depression. A longitudinal placebo study.

Characteristic EEG sleep changes in depression are highlighted by a sleep continuity disturbance, delta sleep reduction, and a shortened REM latency. Since these findings have been derived primarily from only a few baseline recordings, questions regarding their persistence and/or variability have not been previously addressed. As part of an extensive set of investigations of EEG sleep in depression, we examined nightly the sleep of 12 hospitalized, non-delusional, primary depressives who were involved in a program of active psychosocial treatment intervention and received only placebo during a 5-week study period. EEG sleep findings revealed a relative lack of change across time, particularly in those parameters reported to be associated with a primary or 'biologic' depressive episode. While some degree of clinical improvement was noted, the group failed to achieve a state of remission or even partial remission as determined by the Hamilton Rating Scale. It appears that the major sleep alterations associated with such disorders persist for up to at least 5 weeks in the absence of pharmacologic or other somatic intervention.

Adult↗
PubMed1979

EEG sleep and affective psychoses: I. Schizoaffective disorders.

The sleep electroencephalogram (EEG) was studied in 41 depressed inpatients. EEG sleep records were compared for two diagnostic subgroups; patients with psychotic depression (n = 29) or with schizoaffective disorders (n = 12). As was true in the previous pilot study, no major EEG sleep variables distinguished the patients with psychotic depression from those with schizoaffective disorders. These data are consistent with the theory that all psychotic depressive states may have certain common psychobiologic features such as shortened rapid eye movement (REM) sleep latency.

Depressive Disorder↗
PubMed1979

Patterns of utilization of a neuropsychiatric assessment unit.

During a one-year period an inpatient psychiatric ward specializing in the evaluation of neuropsychiatric disorders admitted 306 patients for neurodiagnostic services and 119 general psychiatric patients for brief treatment. About half the neurodiagnostic patients were referred by sources not affiliated with the unit, and about a quarter came from outside the immediate area, indicating that a variety of community agencies relied on the unit as a referral facility. In nearly 60 per cent of the cases evaluated, suspected medical or neurologic abnormality was confirmed and the probable etiology determined, while in only a small percentage was a previously unsuspected abnormality detected; this combination of outcomes suggests that most referrals were appropriate and that the unit's main function was to clarify etiologic relationship and design treatment plans.

Diagnostic Services↗
PubMed1978

Platelet monoamine oxidase in affective disorders.

Platelet monoamine oxidase (MAO) activity was determined with tryptamine as substrate for 61 drug-free patients who had a primary major depressive disorder and for 32 normal controls. Although there were no significant differences between the mean platelet MAO activity of 19 bipolar patients (4.94 nmoles/hr/mg of protein), 42 unipolar patients (4.97 nmoles), and the controls (4.78 nmoles), an analysis of variance indicated that the variance of the bipolar group was significantly greater than that of the other groups. This suggests that there may be subgroups of bipolar patients that differ in their platelet MAO activity but that appear to be distinct from the bipolar I vs bipolar II classification.

Adult↗
PubMed1977

Adjustment of lithium dose during lithium-chlorothiazide therapy.

There has been a long-held belief that lithium salts cannot be used in the presence of thiazide diuretics. Recently, however, thiazides have been demonstrated to be not only safe, but actually indicated in two situations in which lithium salts are used. The first is in the treatment of lithium-induced nephrogenic diabetes insipidus and the second is in severe manic depressive illness in which high doses of lithium do not produce therapeutic serum or intraeythrocytic lithium concentrations. This new information now makes it possible for some manic depressive patients with serious medical illnesses (such as hypertension or congestive heart failure), in whom thiazide diuretics are routinely used, to be treated cautiously with lithium carbonate. This paper analyzes data from 13 patients taking lithium carbonate and varying doses of chlorothiazide in order to indicate the approximate magnitude of downward adjustment of daily lithium dose which the clinician must make to safely give 500, 750, and 1,000 mg/day of chlorothiazide.

Chlorothiazide↗