Psychiatry and Clinical Psychopharmacology

Rapid onset apathy following basal ganglia infarct: a case report

Psychiatry and Clinical Psychopharmacology 2014; 24: Supplement S199-S199
Read: 528 Published: 17 February 2021

Apathy is conventionally defined as an absence or lack of feeling, emotion, interest or concern and often correlated with cognitive deficits, functional impairment and depression. Akinetic mutism is characterized by profound apathy and lack of verbal and motor output despite preserved alertness. We reported here the case of a 36-year-old male with no history of neuropsychiatric disorders and had pure apathy and akinetic mutism after the onset of a left brain vascular lesion located in the head of the caudate nucleus. Mr. B, a 36-year-old married man, was admitted to the psychiatry service with the complaints of severe slowness of movements and speaking. He did not eat, drink and speak spontaneously. The complaints of the patient had started the in two months slowly. He had not history of any psychiatric and neurologic disorder. He had not any history of alcohol and substance use and family history of any psychiatric disorder. According to his psychiatric examination; He was alert and his affect was apathic. He had spoken spontaneously rarely, the tempo and rhythm of his speech was decreased. His associations were normal and goal directed. His mood was euthymic and there was not any finding of depression. His psychomotor activity was severely decreased and had not revealed voluntary movements and goal-directed behavior. MRI findings showed gliotic ischemic lesion of left corona radiata and nucleus caudatus. The neuropsychiatric assessment of the patient revealed decreased problem solving ability, impaired memory and abstract thinking. Scale for the Assessment of Negative Symptoms (SANS) scores was 91. He was prescribed risperidon 4 mg/day per oral. The symptoms of the patient were significantly improved. The SANS scores were 39 and 34, respectively. This case highlights the key role of the lesions of basal ganglia in the development of pure apathy and akinetic mutism. It is proposed that apathy may be explained by the impact of lesions or dysfunctions of the basal ganglia, because these lesions or dysfunctions lead to diminished extraction of the relevant signal within the frontal cortex, thereby inhibiting the capacity of the frontal cortex to select, initiate, maintain and shift programs of action. The case which we illustrated here, also alerts the physician about the neuropsychiatric syndromes, which mimics the negative symptoms of the psychosis and may challenge the differential diagnosis

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