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C H Kellner

Publications and source records attributed to C H Kellner.

At least 19 recordsLinked to original sources
PubMed1991

Brain MRI in obsessive-compulsive disorder.

Magnetic resonance imaging (MRI) brain scans were performed on 12 patients with obsessive-compulsive disorder and 12 healthy controls. Measurements of the area of the head of the caudate nucleus, cingulate gyrus thickness, intracaudate/frontal horn ratio, and area of the corpus callosum did not differ between the two groups. These limited data do not support the presence of a consistent gross brain structural abnormality in obsessive-compulsive disorder. Further studies using other anatomic measurements and other brain structural imaging techniques are warranted.

Adult↗
PubMed1991

TV and ECT.

Explore the source record for details and available documents.

Depressive Disorder↗
PubMed1989

Abnormalities of the septum pellucidum in schizophrenia.

The authors present two cases of schizophrenia in young males who have malformations of the septum pellucidum, a thin sheet of cells and fibers located in the midline of the brain that separates the lateral ventricles. These cases are discussed in the context of newly proposed neurodevelopmental models of schizophrenia.

Adult↗
PubMed1988

Ventricular-brain ratio and life course of illness in patients with affective disorder.

The relationship between ventricular-brain ratio (VBR) on computed tomography of the brain and life course of illness was assessed in 59 hospitalized patients with recurrent affective disorder. In contrast to the implications of some, but not all, prior studies. VBR was not positively related to episode frequency, severity, pattern, or chronicity. In fact, when analyzed by sex, in both males and females, VBR was inversely related to several measures of illness chronicity.

Adult↗
PubMed1987

Intravenous procaine as a probe of limbic system activity in psychiatric patients and normal controls.

Evidence from animal and human studies suggests that procaine hydrochloride may selectively activate limbic system structures and suppress neocortical structures. We administered a series of intravenous bolus doses of procaine hydrochloride to 31 subjects (7 with affective disorders, 17 with borderline personality disorder, and 7 healthy normal volunteers). Dose-related cognitive and sensory distortions and illusions were observed; affective experiences ranged widely from euphoric to dysphoric. Topographic electroencephalogram (EEG) analysis indicated selective increases in fast activity (26-45 Hz) over the temporal lobes; the degree of increase in this activity correlated with degree of dysphoria experienced. Procaine was associated with increases in secretion of cortisol, adrenocorticotrophic hormone (ACTH), and prolactin, but not with growth hormone. These preliminary data are consistent with the possibility that procaine might serve as a clinically useful probe of psychosensory, affective, electrophysiological, and endocrine effects referable to the limbic system.

Adrenocorticotropic Hormone↗
PubMed1987

Neuroendocrine effects of limbic activation by electrical, spontaneous, and pharmacological modes: relevance to the pathophysiology of affective dysregulation in psychiatric disorders.

1. Literature is reviewed that implicates various limbic structures (particularly amygdala and hippocampus) in the modulation of stress-associated neuroendocrine systems. 2. Procaine and related local anesthetics may show a selective proclivity for activating limbic structures. 3. Procaine stimulates ACTH-cortisol and prolactin, but not growth hormone secretion. This pattern is most comparable to that elicited by stimuli which act bilaterally on temporal lobe and limbic areas. 4. Procaine may be a useful agent for helping to elucidate the anatomic and physiologic basis for mood, endocrine, and cognitive dysregulation associated with stress and affective disorders. 5. The endocrine concomitants of limbic activation may have relevance to the course and symptom complex of affective disorders and related psychiatric conditions.

Adrenocorticotropic Hormone↗
PubMed1986

Responses to corticotropin-releasing hormone in the hypercortisolism of depression and Cushing's disease. Pathophysiologic and diagnostic implications.

Primary depression can be associated with substantial hypercortisolism, thus prompting some researchers to suggest that depression shares pathophysiologic features with Cushing's disease. Clinically, depression can be difficult or impossible to distinguish from mild or early Cushing's disease that is associated with depressive features. The purpose of this study was to evaluate whether the pituitary-adrenal responses to ovine corticotropin-releasing hormone could help to clarify the mechanism of hypercortisolism in depression and in Cushing's disease and to assist in the differential diagnosis of these disorders. As compared with controls (n = 34), depressed patients (n = 30) had basal hypercortisolism (P less than 0.001) that was associated with attenuated plasma ACTH responses to ovine corticotropin-releasing hormone (P less than 0.001). This indicates that in patients with depression, the corticotroph cell in the pituitary responds appropriately to the negative feedback of high cortisol levels. In contrast, patients with Cushing's disease (n = 29) had plasma ACTH hyperresponsiveness to ovine corticotropin-releasing hormone (P less than 0.001), despite basal hypercortisolism (P less than 0.001), which indicates a gross impairment of the mechanism by which cortisol exerts negative feedback on the pituitary. Less than 25 percent of the patients with depression or Cushing's disease had peak ACTH responses that overlapped. We conclude that the pathophysiologic features of hypercortisolism in depression and Cushing's disease are distinct in each of the disorders and that the ovine corticotropin-releasing hormone stimulation test can be helpful in their differential diagnosis.

Adrenocorticotropic Hormone↗