Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085632 (apathy)
 4,089 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Episodes of depression and acute psychosis in two patients receiving propranolol hydrochloride are described, and the literature on propranolol-induced depression and psychosis is reviewed. A 42-year-old woman developed severe depression, marked apathy, social withdrawal, and anorexia after taking propranolol hydrochloride (80 mg/day) for three months to control her hypertension. Five days after the dose was reduced to 40 mg/day, there was a major improvement in her depressive symptoms, with a complete resolution in eight days. Upon rechallenge with 80 mg/day of propranolol, she again experienced depressive symptoms. Atenolol 50 mg/day was substituted for the propranolol therapy, and she exhibited a complete remission of her depression. The second patient was a 63-year-old man who had been taking propranolol hydrochloride 160 mg/day for three months without incident. Because of an increased frequency of anginal attacks, the dosage was increased to 240 mg/day. Within two days, he demonstrated such agitation, excitement, and combativeness that he had to be controlled with a 25-mg dose of methotrimeprazine. When the propranolol dose was reduced to 160 mg/day, his psychotic symptoms rapidly cleared. However, when the dose was subsequently increased to 200 mg/day, he again showed increased agitation. After substituting atenolol 100 mg/day for propranolol, the patient's mental status returned to normal. Both of these patients experienced symptoms that were temporarily associated with propranolol. Both patients were subsequently controlled without symptoms with atenolol therapy. Propranolol is a highly lipophilic beta blocker that achieves high concentrations in the brain. When continued beta-blocking therapy is necessary or beta blockade is indicated, a weakly lipophilic agent such as atenolol is indicated.
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PMID:Propranolol-induced depression and psychosis. 398 22

Traumatic brain injury (TBI) can lead to changes in eating behavior patterns. This report describes the case of a patient with alcohol dependence presenting with behavioral changes and eating disorder following frontal lobe trauma. A 42-year-old male, premorbidly well-adjusted presented with alcohol use in dependent pattern for years. He sustained a subdural hematoma in the frontal lobe following a road traffic accident 10 years back. Post-TBI, the patient, started having low frustration tolerance, aggressive outbursts, disinhibition, difficulty in persisting with tasks, apathy, amotivation, and craving for food with inability to control intake on the sight of food. On testing, a deficit in frontal lobe functions was seen. Magnetic resonance imaging scan showed large areas of gliosis and encephalomalacia involving both frontal lobes with parenchymal loss. Eating disorders have been reported after TBI. This case report underscores a major role of frontal-subcortical circuits in regulation of eating habits.
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PMID:Secondary Eating Disorder: A Reality? Case Report of Post Brain Injury Sequelae. 2851 63

A 42-year-old woman presented with a 6-month history of diffuse headache of moderate intensity and gradual onset of generalized weakness, imbalance, apathy, memory decline, hypophonia, dysphagia, constipation and urinary incontinence. Clinical examination revealed several elements of a frontal lobe dysfunction including apathy with motor impersistence, presence of primitive reflexes, generalized hyperreflexia with bilateral Hoffman sign and ankle clonus. The biological workup was unremarkable and a brain computed tomography scan identified a giant olfactory groove meningioma. A prompt neurosurgical intervention helped to reverse the symptoms. This case illustrates the benefits of actively looking for treatable conditions in young patients presenting with acute or subacute dementia and emphasizes the pivotal role of early brain imaging.
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PMID:A 42-year-old woman with subacute reversible dementia: A cautionary tale. 2987 18