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

We examined six patients with an abrupt change in behavior after infarction involving the inferior genu of the internal capsule. The acute syndrome featured fluctuating alertness, inattention, memory loss, apathy, abulia, and psychomotor retardation, suggesting frontal lobe dysfunction. Contralateral hemiparesis and dysarthria were generally mild, except when the infarct extended into the posterior limb. Neuropsychological testing in five patients with left-sided infarcts revealed severe verbal memory loss. Additional cognitive deficits consistent with dementia occurred in four patients. A right-sided infarct caused transient impairment in visuospatial memory. Functional brain imaging in three patients showed a focal reduction in hemispheric perfusion most prominent in the ipsilateral inferior and medial frontal cortex. We infer that the capsular genu infarct interrupted the inferior and anterior thalamic peduncles, resulting in functional deactivation of the ipsilateral frontal cortex. These observations suggest that one mechanism for cognitive deterioration from a lacunar infarct is thalamocortical disconnection of white-matter tracts, in some instances leading to "strategic-infarct dementia."
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PMID:Confusion and memory loss from capsular genu infarction: a thalamocortical disconnection syndrome? 841 58

This paper discusses the definition of apathy, reviews its differential diagnosis, and proposes a classification for the conditions that may produce it. Apathy is defined as diminished motivation not attributable to diminished level of consciousness, cognitive impairment, or emotional distress. In its differential diagnosis, abulia, akinesia and akinetic mutism, depression, dementia, delirium, despair, and demoralization must be ruled out. Classification of apathy is organized in terms of its adaptive and functional consequences, its relationship to personality or to sociocultural or environmental events, and its association with psychiatric, neurological, and medical disorders. An approach to assessment and treatment is proposed.
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PMID:Differential diagnosis and classification of apathy. 240 72

Six patients with small cell lung cancer developed a slowly progressive neurologic syndrome characterized by apathy, abulia, memory loss, gait ataxia, and corticospinal tract signs 26 to 50 months (mean, 35.2 months) after prophylactic cranial irradiation and systemic chemotherapy. In each case this was accompanied by CT and/or MRI evidence of changes in the periventricular white matter. These patients are long-term survivors (41 to 69 months) and do not have CNS metastases.
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PMID:Delayed leukoencephalopathy in survivors with small cell lung cancer. 303 38

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

On the basis of a psychopathological analysis of art work of schizophrenics (over 300 pictures painted by 35 patients) two main tendencies were elucidated. The first one was a tendency, marked to one or another degree, towards geometrization of the forms followed by their deformation and decomposition into the constituent elements. This tendency was mostly seen in the patients with appreciable abnormalities in the thinking sphere (diffuse and inconsistent judgements). The second tendency was manifested by striving for compositions resembling with pictures of children and cheap popular prints. In the group of the patients with this tendency there prevailed subjects with a noticeable shift in the emotional-volitional sphere towards apathy and abulia. It is inferred that the data obtained are specific enough and may be used as additional-diagnostic criteria for delimitation of the defect conditions.
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PMID:[Various features of the artistic creativity of schizophrenic patients in a handicapped state]. 710 89

The authors analyze the personality of cranial-traumatized patients in the years that follow the accident or neuro-surgery. They point out the negative aspect of the behaviors noted: abulia, apathy, selfdenial, passiveness, and especially the failure to recognize the very special syndrome, that is no pure psychosis, nor actual neurosis, not even dementia that is well-known by the neuro-surgeons, badly-known by the experts and forgotten in the tables. The evolution of this syndrome of long duration, it lasts from two to five years, according to circumstances, and for some symptoms or occasionally chronic patients.
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PMID:[Privative syndrome of brain-injured patients (aboulia, asthenia, apathy, ataraxia)]. 722 81

The mechanisms of dementia resulting from small deep infarctions are incompletely understood. The thesis underlying the concept of "multi-infarct dementia" is that multiple lesions have a synergistic effect on mental functions, resulting in dementia irrespective of specific location or volume. In this report, we summarize our experience with six patients reported previously along with additional patients examined subsequently, whose clinical features and brain imaging findings allow an alternative formulation for dementia resulting from lacunar stroke. The six initial patients presented with an abrupt change in behavior after acute infarction involving the inferior genu of the internal capsule documented by computed tomography (CT) and magnetic resonance imaging (MRI). The acute syndrome featured fluctuating alertness, inattention, memory loss, apathy, abulia, and psychomotor retardation suggesting frontal lobe dysfunction. Contralateral hemiparesis and dysarthria were generally mild, except when the infarct extended into the posterior limb. Neuropsychological testing in five patients with left-sided infarcts revealed severe verbal memory loss. Additional cognitive deficits consistent with dementia were evident in four patients. A right-sided infarct caused transient impairment in visuospatial memory. Functional brain imaging in three patients using 133xenon regional cerebral blood flow (rCBF) and single photon emission computed tomography (SPECT) showed focal reduction in hemispheric perfusion most prominent in the ipsilateral inferior and medial frontal cortex. Perfusion was also defective in the medial and laterial temporal cortex. Important pathways of the limbic system traverse the inferior capsule in the region of the genu. Corticothalamic and thalamocortical fibers form the thalamic peduncles which detach from the internal capsule and enter the thalamus at its rostral and caudal poles and along its dorsal surface. The anterior thalamic peduncle, conveys reciprocal connections between the dorsomedial nucleus and the cingulate gyrus, as well as the prefrontal and orbitofrontal cortex. The inferior thalamic peduncle carries fibers which connect the thalamus with orbitofrontal, insular, and temporal cortex, as well as the amygdala via the ansa peduncularis to the ventral amygdalofugal pathway. Thus, damage to one or both white-matter tracts may occur with infarctions in the region of the inferior genu, causing striking frontal behavioral effects and memory loss in our patients associated with functional deactivation of the ipsilateral frontal and temporal cortex.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Strategic infarcts in vascular dementia. A clinical and brain imaging experience. 776 29

Severe amotivation, apathy, and abulia, significantly retard rehabilitation following traumatic brain injury. Preliminary, uncontrolled research has suggested possible benefit with amantadine for this behavioural syndrome. This N of 1, double-blind, placebo-controlled study employed amantadine 100 mg three times daily in one such patient. Therapists and nurses completed inventories scoring efforts towards initiation of therapeutic activities during each session, progress in therapy, and participation in therapy. Four treatment periods (two active medication, two placebo), of 2 weeks duration, were completed. Across four therapists, and for both treatment pairs, the average effect score increased from 0.86 on placebo to 1.74 on amantadine (possible range 0-6, 3 = 'average'). There were no side-effects. The study suggests possible benefit with amantadine for patients with amotivational syndrome after traumatic brain injury; a randomized clinical trial appears warranted and required.
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PMID:N of 1 study: amantadine for the amotivational syndrome in a patient with traumatic brain injury. 787 96

The behavioural and movement disorders reported in 240 patients described in the literature with lesions affecting the caudate nucleus, putamen and the globus pallidus (lentiform nucleus) have been analysed. Reports were classified into two groups: small or isolated lesions involving the said nuclei alone; and large lesions with additional involvement of the adjacent internal capsule and/or periventricular white matter. Amongst the 240 cases, dystonia was the most frequent movement disorder recorded (36%); chorea (8%) and parkinsonism (6%) or dystonia-parkinsonism (3%) were uncommon. The commonest behavioural disturbance was the syndrome of abulia (apathy with loss of initiative and of spontaneous thought and emotional responses) (13%); disinhibition was rare (4%). Confusion usually was associated with intracerebral haemorrhage and depression was a relatively non-specific finding. Aphasia was extremely rare with lesions confined to these basal ganglia structures. Lesions of the caudate nucleus rarely caused motor disorders but were more likely to cause behavioural problems. Chorea has been described in only 6% of those with caudate lesions, and dystonia in only 9%. The most significant behavioural disturbance described in 28% of those with caudate lesions was the syndrome of abulia, sometimes alternating with disinhibition (11%). Lesions of the lentiform nuclei rarely caused abulia (10%) and did not produce disinhibition, but they commonly caused dystonia (49%), particularly when the putamen was involved (63%). Bilateral lesions of the lentiform nuclei, either of the globus pallidus or of the putamen, caused parkinsonism (19%) or dystonia-parkinsonism (6%) infrequently. The prominence of the behavioural disturbance of abulia with caudate lesions emphasizes the more complex cognitive role of this basal ganglia structure. The frequent occurrence of dystonia and less commonly of parkinsonism with lentiform lesions emphasize the motor roles of putamen and globus pallidus.
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PMID:The behavioural and motor consequences of focal lesions of the basal ganglia in man. 792 71

The present paper reports on five patients who developed apathy as a peculiar side effect of antidepressants. Their behavioral and psychopathological changes were primarily due to the near-absence of emotional experience, a key characteristic that distinguishes apathy from avolition and abulia. The emergence of apathy in the course of an antidepressant treatment should raise the suspicion of an adverse effect of the drug and lead to its prompt withdrawal. A sample of the relevant clinical evidence favoring the distinction of apathy confined to a single sensory domain ("unimodal apathy") from apathy confined to more than one sensory realm ("multimodal apathy") is reviewed. From a pathophysiological standpoint, it would appear that neural nets centered in the amygdala-temporo polar cortex are critical for the integration of sensory perceptions and mental imagery with appropriate emotional tone and quality as well as with their accompanying somatic markers, as they receive afferents from the major projection systems of the prosencephalon and lie in nodes strategic to modify the ongoing activity of multiple parallel brain systems. The fact that one common symptom can be produced by such a heterogeneous family of substances points to a shared neurochemical mechanism of action. At present, discrete cerebral serotoninergic circuits would appear to be suitable candidates for such a role. Cases as these may be critical for the understanding of the cerebral organization of emotions in man, lending support to the notion that distinct neurochemical systems mediate discrete psychopathological symptoms.
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PMID:[Multimodal iatrogenic apathy]. 898 78


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