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Biomedical subjects

J F Greden

Publications and source records attributed to J F Greden.

At least 37 records · Page 2Linked to original sources

Depression in stroke rehabilitation.

Despite recent advances in understanding the pathophysiology of poststroke depression, major questions remain. They include the relative importance of lesion location and size and the confounding effects of time since stroke, age, prior history of depression, and cerebral atrophy. To evaluate these issues, we systematically assessed depressive features, functional status, and brain structure with computer tomography scans in 91 men undergoing stroke rehabilitation. Forty percent met DSM-III criteria for major depressive disorder. Mood disturbance was more severe for patients with right than with left hemisphere lesions, correlated with functional disability and lesion size, and was associated with previous history of depression. Age, time since stroke, and atrophy did not correlate with mood. Depression is common in delayed stroke recovery, regardless of lesion location. Because there are no demographic or anatomic features that predict the absence of depression, depression screening should be part of the assessment of all patients undergoing stroke rehabilitation.

Activities of Daily Living↗

Dissociation between pituitary and adrenal suppression to dexamethasone in depression.

OBJECTIVE: To determine if corticotroph nonsuppression, as reflected by beta-endorphin nonsuppression, occurs before cortisol nonsuppression (defined as a cortisol level of > 140 nmol/L) when examining multiple time points in a day. SETTING: The General Medical Clinical Research Center and Inpatient Depression Research Unit, Ann Arbor, Mich. DESIGN: Multiple blood samples were obtained through an intravenous catheter around the time points of 8 AM, noon, and 4 PM and assayed for beta-endorphin and cortisol. PATIENTS: Patients meeting Research Diagnostic Criteria for the diagnosis of major depressive disorder, primary and simple. A total of 73 subjects, both inpatients and outpatients, were studied. INTERVENTION: Samples were obtained both at baseline and 1 day after administration of 1 mg of dexamethasone at 11:30 PM. MEASUREMENTS AND RESULTS: Overall 39 patients (53%) demonstrated beta-endorphin nonsuppression after administration of dexamethasone at any of the three time points, while only eight patients (11%) demonstrated cortisol nonsuppression at any of these time points. Cortisol nonsuppression, but not beta-endorphin nonsuppression, was associated with lower concentrations of dexamethasone in plasma. Baseline cortisol and menopausal status were significantly associated with beta-endorphin nonsuppression in women.

Adult↗

Cholinergic hyperactivity and negative symptoms: behavioral effects of physostigmine in normal controls.

Intravenous infusion of physostigmine (a centrally active anticholinesterase agent) in normal subjects leads to a syndrome of psychomotor inhibition; this has been proposed as a model for selected symptoms of depression. In view of its similarity to the negative schizophrenic syndrome, we compared the 'physostigmine syndrome' to the negative symptom profile by evaluating the behavioral effects of intravenous physostigmine infusion in seven normal volunteers. Observer ratings and self description revealed significant withdrawal, apathy, alogia, lethargy, decreased energy, slowed thoughts, diminished affective responsivity, and reduced hedonic capacity. Subjects did not report sadness, ideas of hopelessness, worthlessness, or guilt. These findings support the implication of cholinergic hyperactivity as one mechanism in the pathophysiology of negative schizophrenic symptoms.

Adult↗

Sleep deprivation in depressed adolescents and psychiatric controls.

Up to 70% of depressed adults have an antidepressant response to sleep deprivation. To study the effects of sleep deprivation on depression severity and level of arousal in psychiatrically disturbed adolescents, we deprived 17 patients of sleep for 36 hours. Severity of depression and subjective arousal were assessed at baseline, during sleep deprivation, and after 1 night's recovery sleep. We found that severely depressed adolescents showed a significant decrease in depression severity, whereas depressed patients in remission and psychiatric controls worsened after sleep deprivation. Patients with depression in remission showed a significant decrease in subjective arousal after sleep deprivation. In contrast to findings in depressed adults, the effects of sleep deprivation persisted after 1 night of recovery sleep, and diurnal variation of mood did not predict response to sleep deprivation. These findings are consistent with those reported in the adult literature, and suggest a common psychophysiology between adult and adolescent depression.

Adolescent↗

The DST as a predictor of outcome in depression: a meta-analysis.

OBJECTIVE: The authors undertook a review of the literature on the dexamethasone suppression test (DST) as a predictor of course and outcome in major depression, to illustrate clinical and pathophysiological implications of studying the relation between biological measures and course of illness in psychiatry. METHOD: In computerized searches and cross-references, 144 articles were found that related DST results to prediction of treatment response or outcome. Meta-analysis was performed on pooled data from all of the studies and separately on data from selected studies that had used stricter methodology. RESULTS: 1) Baseline DST status did not predict response to antidepressant treatment or outcome after hospital discharge. 2) Non-suppression of cortisol on the baseline DST predicted poorer response to placebo. 3) Persistent nonsuppression of cortisol on the DST after treatment was associated with high risk of early relapse and poor outcome after discharge. CONCLUSIONS: Baseline DST results may be devoid of prognostic value, but posttreatment nonsuppression of cortisol on the DST is strongly associated with poor outcome. Persistent nonsuppression may reflect a partially treated index episode or identify sicker patients who are unresponsive to treatment. The findings reiterate the importance of studying biological measures in relation to multiple validators of psychiatric illness beyond cross-sectional diagnosis.

Antidepressive Agents↗

Antidepressant maintenance medications: when to discontinue and how to stop.

Most depressive disorders, once developed, have a lifetime course. For the majority of patients, the risk for future episodes increases as the number of past episodes increases. The length of the well interval between episodes becomes progressively shorter with each new episode. Those who are older at onset often have higher probabilities of relapse during future years if not maintained on treatment. As the number of episodes grows larger and the patient becomes older, severity often intensifies, treatment responsivity to conventional antidepressants may diminish or even disappear, and the destructive consequences of the disorder progressively worsen. This destructive lifetime pattern can be prevented in many if not most patients since antidepressant and other maintenance medications are being shown to be efficacious in preventing most future episodes of depression, maintaining euthymia, and preserving quality of life. On the basis of these and other still-developing findings (and with the recognition that maintenance strategies have been inadequately tested in depressed children and adolescents), reasonable clinical wisdom might suggest that lifetime pharmacologic maintenance may be indicated for patients 50 years or older at first episode, 40 years or older with two or more prior episodes, or for those with three or more prior episodes. "Maintenance" dosages need to be comparable to established "treatment" dosages until it is proven that lower doses are efficacious; such data now are lacking. When medication is selected for long-term treatment, strong considerations should be given to the agent's side effect profile, since compliance is essential for success.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Electroencephalographic sleep abnormalities in schizophrenia. Relationship to positive/negative symptoms and prior neuroleptic treatment.

Polysomnographic abnormalities in schizophrenia are not well characterized and their associations with schizophrenic symptomatology have not been adequately assessed. To address these issues, we recorded electroencephalographic sleep in 20 drug-naive schizophrenics, 20 drug-free but previously medicated schizophrenics, and 15 normal controls. Drug-naive and previously medicated patients had significantly greater impairment of sleep continuity and shorter rapid eye movement latency when compared with controls. In the previously medicated group, findings were significantly influenced by duration of drug-free status. Rapid eye movement latency was inversely correlated with the severity of negative symptoms (r = -.52) but was unrelated to depressive symptoms. Slow-wave sleep did not differ between schizophrenic patients and normal controls and was unrelated to any clinical parameter. Mechanisms underlying the observed associations between rapid eye movement sleep abnormalities and negative symptoms in the acute phase of schizophrenic illness need to be explored.

Adult↗

Measurement of depression and negative symptoms in schizophrenia.

The validity of the Hamilton Depression Scale (HAM-D) as a measure of depressive symptomatology in schizophrenic patients is questionable since it was not developed for this purpose, nor has it been validated in a schizophrenic population. Accordingly, 80 schizophrenic inpatients were administered the HAM-D, the 18-item Brief Psychiatric Rating Scale (BPRS), and the Scale for the Assessment of Negative Symptoms (SANS) at drug-free baseline and after 4 weeks of neuroleptic treatment. The findings revealed that the HAM-D total score was nonspecific, while individual HAM-D subfactors provided a better index of various symptom complexes. The HAM-D contained a depressive factor that correlated strongly with the BPRS depression factor and a negative symptom factor that correlated strongly with the SANS and the BPRS negative symptom factor. These findings suggest the need to utilize specific assessment techniques rather than global measures when assessing depression in schizophrenia.

Adolescent↗

Clinical predictors of 1-year outcome in schizophrenia.

To assess clinical predictors of 1-year outcome in schizophrenia, 63 patients were studied prospectively. Persistent negative and total symptoms after 4 weeks of neuroleptic treatment accounted for 62% of the variance of 1-year outcome, whereas baseline measures showed no relationship to outcome. Thus, 1-year outcome in schizophrenia can be reasonably predicted on the basis of symptoms persisting after 4 weeks of treatment.

Adult↗

Effect of anticholinergics on positive and negative symptoms in schizophrenia.

Anticholinergic drugs have been assumed to have no effects on schizophrenic symptomatology. Some studies suggest, however, that anticholinergic agents may antagonize the beneficial effect of neuroleptics on positive symptoms and partially ameliorate negative symptoms. Virtually all studies have been conducted in patients receiving concomitant neuroleptic treatment, raising the possibility that neuroleptics may obscure or modify any "true" anticholinergic effect on schizophrenic symptoms. To evaluate the hypothesis that anticholinergics may increase positive and decrease negative schizophrenic symptoms, we assessed the effect of biperiden on symptoms in the medication-free state. We studied the effect of biperiden 8 mg/day for 2 days on positive and negative symptoms in 40 otherwise drug-free schizophrenic inpatients. Biperiden produced a significant increase in positive symptoms (t = 6.7, p < .001) and reduction in negative symptoms (t = -3.4, p < .01). These data indicate that cholinergic modulation significantly affects positive and negative schizophrenic symptoms and suggest the need for systematic trials of cholinergic and anticholinergic agents in the treatment of positive and negative symptoms of schizophrenia, respectively.

Adult↗