Brendan T. Carroll

Eating attitudes in college males

Three hundred and forty male college students participated in a survey study of eating attitudes. Participants completed a survey including demographic data, a weight history, and the Eating Attitudes Test (EAT-26). Twelve subjects or 3.5% of the population had elevated scores of 20 or above on the EAT-26. Elevated scores correlated significantly with body building and with a past history of obesity. Fully 65% of the men reported weighing within 5 percentage points of their ideal weight. The authors suggest that males who are overinvested in their bodies and physical appearances are at higher risk for developing eating disorders.

Elevated CSF protein in male patients with depression

Abstract Elevation of total protein is the most frequent pathologic finding in the cerebrospinal fluid (CSF) examination. It occurs in a variety of situations such as inflammation or tumors of the central nervous system (CNS), degenerative disorders, and subarachnoid hemorrhage, or as a result of traumatic taps. It has also been reported, for unknown reasons, in patients with psychiatric disease. In a study of hormone changes in depression, 9 of 24 (38%) patients (13 male, 11 female) were found to have elevated CSF protein levels (>45 mg/dl), whereas no elevations were found in healthy controls (8 male, 9 female). Eight of the patients with the elevated CSF protein levels were male (62%) and one was female (9%). Depressed patients had significantly higher CSF protein levels (44.7 ± 18.0 mg/dl) than controls (31.5 ± 6.0 mg/dl) (t = 3.32, df = 30.37, p = 0.002). No relationship was found between CSF protein levels and (1) the use of medication (tricyclic antidepressants, lithium carbonate, or monoamine oxidase inhibitors) or (2) post-dexamethasone suppression test cortisol levels. Female controls, however, tended to have lower protein levels than male controls, whereas female patients had significantly lower levels than male patients. Protein electrophoresis was performed on 21 of the 41 subjects (13 patients, 8 controls). Male patients had nonsignificantly higher absolute concentrations of CSF albumin and the globulin fractions when compared to male controls. These differences in CSF protein do not suggest monoclonal CSF protein production, nor are they the result of this elevated peripheral protein. They suggest increased polyclonal production of CSF protein and/or increased blood-brain barrier permeability in male depressed patients, and a tendency to such in female depressed patients.

Pituitary-adrenal axis response to arginine vasopressin in patients with major depression.

Arginine vasopressin (AVP) was administered to 21 patients with major depression and 20 normal control subjects. Thirty-two subjects also underwent an overnight dexamethasone suppression test. The patient group did not differ significantly from the control group in adrenocorticotropic hormone (ACTH) or cortisol response. Dexamethasone suppression status did not affect ACTH or cortisol response. This study supports the hypothesis that unlike the response to corticotropin releasing hormone, the ACTH response to AVP is not attenuated in depression.

Catatonia Due to a General Medical Condition (Organic Catatonia)

While much has been written about catatonia, there are only a few scholarly reviews focused on catatonia due to a general medical condition, also referred to as organic catatonia. There has been a long list of causative conditions that account for the development of organic catatonia which are informative but not clinically helpful. We performed a literature search using the term ‘catatonia’ covering the last ten years. We found 31 titles of catatonia due to drugs and 76 titles of catatonia due to a general medical condition. Of these, 9 were catatonia due to NMDA antibody associated encephalitis. In order to update this body of knowledge, we have revisited the differential diagnosis of catatonia and attempted to delineate catatonia due to a general medical condition from phenomenologically similar but etiologically disparate conditions. We also focused on catatonia due to systemic lupus erythematosis. We also present a case of catatonia due to hydrocephalus to illustrate treatment issues. In spite of the pharmacologic treatment for catatonia, this patient has not improved. We hope that this review and discussion will aid in the identification and treatment of catatonia due to a general medical condition. Medical causes must be addressed to ensure the best outcome.

Catatonia in Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition [Editorial]

As international scholars of catatonia, we are concerned that the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-V) proposes to delete the codes 295.2 (schizophrenia, catatonic type) and 293.89 (catatonia secondary to a medical condition) and to substitute a noncoded “catatonia specifier” as the principal identifier. We believe that these changes will badly serve clinical practice and research. We advocate a unique and broadly defined code for catatonia in DSM-V. n nCatatonia is common among hospitalized psychiatric patients, including adults, adolescents, and occasionally children. In the 10 principal prospective studies from sites around the world, catatonia syndrome was identified in a mean (SEM) percentage of 9.8% (1.4%) of adult admissions (Table 1). These patients have multiple signs of catatonia (commonly >5); 68% (6%) are mute, and 62% (3%) are negativistic or withdrawn. Some are unable to eat, requiring parenteral nutrition and/or medication. n n n nTABLE 1 n nProspective Studies of the Incidence of Catatonia n n n nOnce catatonia is recognized, first-line treatment with benzodiazepines usually brings prompt relief, although high doses may be needed. If catatonia persists, electroconvulsive therapy is often rapidly beneficial. Every prospective study confirms that catatonia syndrome exists, occasionally becomes malignant, and requires prompt treatment. n nUnder the proposed new guidelines for DSM-V, patients with catatonia syndrome will lack an informative diagnosis. Mutism, negativism, and withdrawal prevent assessment for mood, cognitive, and psychotic symptoms and impede proper delineation of episodes of prior illness. Without findings for a specific diagnosis, it is rational to use a provisional diagnosis of the catatonia syndrome to allow tests and treatments to proceed. Lacking recognition and treatment, catatonia may persist or worsen with adverse or life-threatening results. On the other hand, when patients with catatonia are identified and treated, they become verbal and interactive, allowing interviews and more definitive diagnoses, regardless of the primary pathological findings. n nWhen patients cannot provide information, clinicians may conflate or misdiagnose catatonia with schizophrenia (as in the DSM-IV schema), impute a psychotic process, foster the unproven use of neuroleptics, and risk adverse effects, such as conversion to malignant catatonia or the neuroleptic malignant syndrome. Similarly, assignment of catatonia to “psychosis not otherwise specified” (298.9, DSM-IV and DSM-V) would be erroneous because these patients often either lack hallucinations and delusions or cannot be assessed for them. n nThe proposed elimination of DSM-IV “catatonia due to a general medical condition” (293.89) renders the coding for catatonia arising from general medical conditions problematic. At clinical presentation, the medical/toxic factors are rarely known, as time is often needed to identify these etiologies. n nWe also note that noncoded specifiers are not useful for research on nosology, treatment, and outcome. n nTo address all these issues, we urge inclusion in DSM-V of a specific diagnostic code for catatonia. One simple option is to retain the 293.89 code but revise its formulation to broadly encompass the catatonia syndrome without imputing a link to either primary psychiatric or general medical conditions. A unique and broadly defined code would foster recognition of the catatonia syndrome and permit research on nosology, treatment, and outcome. These goals are not met with the DSM-V plan for noncoded modifiers.

AbstractElevated csf protein in male patients with depression

Elevation of total protein is the most frequent pathologic finding in the cerebrospinal fluid (CSF) examination. It occurs in a variety of situations, such as inflammation or tumors of the central nervous system (CNS), degenerative disorders, and subarachnoid hemorrhage, or as a result of traumatic taps. It has also been reported, for unknown reasons, in patients with psychiatric disease. In a study of hormone changes in depression, 9 of 24 (38%) patients (13 male, 11 female) were found to have elevated CSF protein levels (greater than 45 mg/dl), whereas no elevations were found in healthy controls (8 male, 9 female). Eight of the patients with the elevated CSF protein levels were male (62%) and one was female (9%). Depressed patients had significantly higher CSF protein levels (44.7 +/- 18.0 mg/dl) than controls (31.5 +/- 6.0 mg/dl) (t = 3.32, df = 30.37, p = 0.002). No relationship was found between CSF protein levels and (1) the use of medication (tricyclic antidepressants, lithium carbonate, or monoamine oxidase inhibitors) or (2) post-dexamethasone suppression test cortisol levels. Female controls, however, tended to have lower protein levels than male controls, whereas female patients had significantly lower levels than male patients. Protein electrophoresis was performed on 21 of the 41 subjects (13 patients, 8 controls). Male patients had nonsignificantly higher absolute concentrations of CSF albumin and the globulin fractions when compared to male controls. These differences in CSF protein do not suggest monoclonal CSF protein production, nor are they the result of this elevated peripheral protein.(ABSTRACT TRUNCATED AT 250 WORDS)