PubMed Health⌕ Search

Biomedical subjects

Max Fink

Publications and source records attributed to Max Fink.

At least 19 recordsLinked to original sources
PubMed2003

Catatonia in psychiatric classification: a home of its own.

OBJECTIVE: The authors assess the present position of catatonia in diagnostic classification systems and consider the merits of designating catatonia as a separate diagnostic category with defined criteria. METHOD: Following the logical steps to establish diagnostic validity when the etiology of a syndrome is unknown, the authors review the literature on the features that delineate catatonia as a syndrome, the prevalence and response to treatment of catatonia, and the conditions that are associated with catatonia. RESULTS: Catatonia is a well-defined syndrome that can be reliably ascertained. Although more than 40 motor signs of catatonia are known, the presence of two prominent features for 24 hours or longer is sufficient to identify the syndrome. Catatonia is found in about 10% of acutely ill psychiatric inpatients and is more commonly observed in persons with mood disorder than in those with schizophrenia. It is found in many conditions and presents mainly as retarded-stuporous or excited-delirious forms. Catatonia responds to specific treatments, including sedative anticonvulsants (barbiturates and benzodiazepines) and ECT. CONCLUSIONS: Catatonia can be distinguished from other behavioral syndromes by a recognizable cluster of clinical features. Catatonia is sufficiently common to warrant classification as an independent syndrome. It can be reliably identified, has a typical course when appropriately treated, responds to specific treatments, and is worsened by other treatments. It is associated with many pathophysiologic processes and most often with mood disorder. These findings, which are consistent with established methods of defining distinct diagnostic groupings, support consideration of catatonia as an individual category in psychiatric diagnostic systems.

Adolescent↗
PubMed2002

Electrotherapeutics.

Explore the source record for details and available documents.

Electroconvulsive Therapy↗
PubMed2002

Catatonia and ECT: Meduna's biological antagonism hypothesis reconsidered.

Catatonia is a motor syndrome with abnormalities in neuroendocrine regulation. Both the motor syndrome and the neuroendocrine abnormalities respond rapidly to electroconvulsive therapy (ECT). This rapid efficacy supports a neuroendocrine hypothesis of the mode of action of ECT and encourages neuroendocrine studies of catatonia.

Amobarbital↗
PubMed1993

Blood Pressure, Memory, and Electroconvulsive Therapy.

Blood pressure changes recorded during electroconvulsive therapy (ECT) in 23 psychiatric in-patients with major depressive disorders correlated with and predicted the degree of anterograde memory changes measured 48-72 h after ECT. The Randt memory test was the principal measure of memory change. A subgroup of older patients with cardiovascular illness received trimethaphan, a ganglionic blocker that impedes a hypertensive surge during the treatment. They did not differ in memory function from a younger subgroup that did not receive trimethaphan. Control of the hypertensive response in the older age group counterbalanced the additional memory dysfunction that was anticipated as a result of advanced age and cardiovascular pathology.

Journal Article↗
PubMed1993

Caffeine Pretreatment Enhances Clinical Efficacy and Reduces Cognitive Effects of Electroconvulsive Therapy.

In an open clinical trial, depressed patients received age-dosed, brief-pulse electroconvulsive therapy (ECT) either with or without 500 mg i.v. caffeine sodium benzoate before each treatment. Caffeine-pretreated patients required fewer ECT treatments, and after three to four treatments, their Hamilton Depression Scale (HDS) scores were significantly lower. At the end of the ECT course, both groups reached the same reduction in HDS scores. Of five memory tests, one showed better performance at the end of the ECT course for the caffeine-pretreated compared with the non-caffeine-pretreated patients. The results argue that caffeine-modified ECT differs from unmodified ECT in speed of response and the effects on cognitive tests.

Journal Article↗
PubMed1993

Reversible Dementia and Affective Disorder: The Rip Van Winkle Syndrome.

The diagnostic separation of the reversible dementia of an affective disorder from the dementia secondary to structural brain pathology remains a clinical challenge. A 58-year-old woman had been diagnosed as having Alzheimer's dementia for 9 years before antidepressant treatment with electroconvulsive therapy (ECT) resolved the dementia syndrome. The patient has functioned well for 8 years on maintenance treatment with lithium, with ECT given every 7-8 weeks. By the summer of 1993, she had undergone 132 ECT. Until specific and reliable pre-morbid tests for the diagnosis of irreversible dementias of the Alzheimer's and multiinfarct types are developed, antidepressant treatment trials are encouraged in elderly patients with a dementia syndrome. Extensive maintenance ECT schedules are safe.

Journal Article↗
PubMed1993

Post-ECT Delirium.

A confusional state accompanied by restlessness is a frequent occurrence at the end of an induced seizure in electroconvulsive therapy (ECT). Delirium, which usually lasts <1 h, occurs in up to 12% of patients. It is most frequent during the initial treatments of a series. The occurrence of delirium in one treatment is not a harbinger of its reappearance in later treatments. Usually gentle reassurance is sufficient to help the patient, but some instances warrant the administration of diazepam, midazolam, a barbiturate, or droperidol.

Journal Article↗