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Query: UMLS:C0085632 (apathy)
 4,089 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The neurological analysis of complex behavioral states associated with serious brain disease not infrequently is a difficult task. In many such cases, the signs of minor degrees of akinetic mutism were found when deliberately looked for. Recognition of this feature greatly facilitated interpretation. The ancient term abulia is suggested for the specific neurological syndrome comprising slowness, decreased responsiveness, apathy, etc. Akinetic mutism is its extreme form. A lesser degree of abulia is here termed abulia minor. The attributes of abulia minor are described, and the neurological conditions with which it had been found associated are listed. Preliminary conclusions as to the anatomical localization of the syndrome are presented. The literature on akinetic mutism is reviewed, and a few special observations are commented on--paradoxical activity, the telephone effect, and reflex attention. The application of the newer knowledge of cerebral neurotransmitters to akinetic mutism is illustrated. At the beginning of the study the focus was on abulia, but it was natural that sooner or later the contrasting state of behavioral hyperactivity or agitation would have to come under equal scrutiny. A list of conditions in which psychomotor agitation was a feature has been compiled from personal files. The localization of the disease process in hyperactive states is compared with that in abulia. A few special observations on hyperactive states are presented, along with a note on a unique syndrome termed anideation. There has gradually emerged a concept of a continuum of behavioral activity extending from abulia at one end through eukinesia to hyperactivity at the other end. Involvement of specific fundamental integrative circuits is postulated. This morning we have been enthralled by Computers in Neurosurgery, Neurobiology in Neurosurgery, and Humanism in Neurosurgery. What could be more natural for a neurologist than to talk about Neurology in Neurosurgery. And how best to pay homage to the great lady of Medicine than by offering a modest example of her handiwork. Thus, I am led to discuss a neurological theme which has recently occupied my attention. To anticipate a little, I shall be talking about two somewhat opposite states: on the one hand there is abulia--slowness, apathy, and lack of spontaneity--and on the other hand, agitation and hyperactivity. By way of explanation, this study originated during the bedside examination of patients with brain damage and serious impairment of analysis appeared not only formidable but even impossible.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Honored guest presentation: abulia minor vs. agitated behavior. 614 34

Akinetic mutism is a wakeful state of severe apathy and paucity of volitional movement. Evidence indicates a possible dopaminergic hypofunction within the anterior cingulate cortex. The authors present three cases of acute onset akinetic mutism successfully treated with intramuscular olanzapine.
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PMID:Treatment of akinetic mutism with intramuscular olanzapine: a case series. 1830 90

Akinetic mutism is characterized by profound apathy and a lack of verbal and motor output for action, despite preserved alertness. The condition usually follows bilateral damage to the medial frontal subcortical circuits. We report a 59-year-old right-handed woman who was admitted to the neurology ward with sudden-onset akinetic mutism. Her medical history included an ischemic stroke 3 years earlier, with residual anomia and mild agraphia but no motor dysfunction. On this admission, a cranial computed tomography scan disclosed an acute left superior cerebellar infarction embracing the vermis, and a prior left inferior parietal infarct. Electroencephalogram showed bilateral frontal delta-wave activity. Four weeks later, we performed a technetium-99m hexamethylpropyleneamine oxime single-photon emission computed tomography (Tc-HMPAO SPECT) scan to study the patient's frontal lobe function. The SPECT scan revealed the causative bifrontal hypoperfusion, more prominent on the right, while the structurally evident cerebellar infarction was predictably masked by subacute hyperperfusion phenomenon. Contralateral frontal diaschisis is an established sequela of cerebellar infarction. Because this patient also had lesions in the left parietal region, her left prefrontal area was critically deprived of its major reciprocally connected cortical counterparts (right prefrontal and left parietal), and also became dysfunctional. Her resulting bilateral frontal dysfunction is a common cause of akinetic mutism.
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PMID:Akinetic mutism without a structural prefrontal lesion. 2381 68

Akinetic mutism (AM) is a rare neurological disorder characterized by the presence of an intact level of consciousness and sensorimotor capacity, but with a simultaneous decrease in goal-directed behavior and emotions. Patients are in a wakeful state of profound apathy, seemingly indifferent to pain, thirst, or hunger. It represents the far end within the spectrum of disorders of diminished motivation. In recent years, more has become known about the functional roles of neurocircuits and neurotransmitters associated with human motivational behavior. More specific, there is an increasing body of behavioral evidence that links specific damage of functional frontal-subcortical organization to the occurrence of distinct neurological deficits. In this review, we combine evidence from lesion studies and neurophysiological evidence in animals, imaging studies in humans, and clinical investigations in patients with AM to form an integrative theory of its pathophysiology. Moreover, the specific pharmacological interventions that have been used to treat AM and their rationales are reviewed, providing a comprehensive overview for use in clinical practice.
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PMID:On the pathophysiology and treatment of akinetic mutism. 3204 73