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

We profiled personality changes that were measured cross-sectionally on the Blessed Dementia Scale in 80 patients with Alzheimer's disease who were examined at a dementia clinic. The most common personality changes were diminished initiative/growing apathy (61.3%), relinquishment of hobbies (55.0%), and increased rigidity (41.3%). The least frequent personality change was sexual misdemeanor (3.8%). Discriminant function analysis showed that the Global Deterioration Scale, the Clinical Rating Scale for Symptoms of Psychosis in Alzheimer's Disease, and the duration of dementia symptoms were the best predictors to classify personality change in an overall score of personality. However, cognitive impairment, as measured by the Blessed Memory-Information-Concentration Test and Mini-Mental State Examination, was not a good predictor of overall personality change. Personality and behavioral changes are common in Alzheimer's disease and may not be attributed entirely to intellectual impairment.
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PMID:Personality changes in Alzheimer's disease. 153 33

Severe closed head-injury results in a multitude of long-lasting cognitive deficits. ERPs can effectively complement the more traditional behavioural measures to provide information that is not available through any other means. It is now fairly clear that a late positive wave, P3, associated with contextual updating is attenuated and prolonged in a variety of conditions in the head-injured. It is also possible that measures of selective attention such as the processing negativity may be abnormal in this group. A more definitive statement will, however, have to wait the results of further investigations. A number of investigators have now indicated that cognitive processing is slowed in the head-injured. Again, ERPs have been instrumental in explaining why it is slowed. Decision-making time as measured by RT is generally longer than P3 latency. Because P3 latency is delayed in the head-injured, the time required for evaluation of the stimulus (recognition and classification) is slowed in the head-injured. The additional delay in RT must, however, be explained by other processes, most probably a response bias that perhaps emphasizes accuracy at a cost of speed. Such a strategy can be manipulated if the patient is provided with cues about their speed of responding. Finally, ERPs have been instrumental in explaining possible reasons for cognitive slowing. A powerful CNV technique may permit the categorization of the head-injured into at least 2 distinctive groups: those that tend to underprocess information (perhaps as a result of apathy or a lack of motivation) and those that tend to overprocess (perhaps as a result of an inefficient and needless processing of irrelevant information resulting in fatigue). The extent to which the different modes of information processing are related to the site of brain injury and possible personality change remains an issue of speculation.
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PMID:Electrophysiological assessment of cognitive disorder in closed head-injured outpatients. 228 30

The symptoms of hypothyroidism are protean and include apathy, somnolence, lethargy, personality change, and intellectual deterioration. Many of these symptoms may be related to hypothyroid-induced sleep disorders. Hypothyroidism is associated with abnormal ventilatory drive, abnormal sleep architecture, and sleep apnea. Central, obstructive, and mixed patterns of sleep apnea are commonly observed in hypothyroidism. A case of severe sleep apnea in a grossly myxedematous patient who improved dramatically following thyroid replacement alone is presented. Myxedema is a reversible cause of sleep apnea, and thyroid function testing should be considered in its diagnostic work-up.
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PMID:Sleep apnea, sleep disorders, and hypothyroidism. 276 18

We report behavioral and cognitive characteristics of 12 patients with caudate nuclei lesions, 11 unilateral and one bilateral. These patients developed an acute behavioral change characterized by apathy, disinhibition, or a major affective disturbance. The pattern of personality change correlated with size and location of lesion within the caudate but not the laterality. Seven patients were further compared with matched controls on a series of neuropsychological tests. Their performance was impaired on tasks requiring planning and sequencing. They had short attention spans and decreased free recall of episodic and semantic items with good recognition memory scores. Similar behavioral and cognitive changes also occur in early Huntington's disease, frontal-lesioned patients, and caudate-lesioned animals, and correspond to disturbances of specific frontal-caudate circuits. These results implicate the caudate nuclei in mediating prefrontal behaviors and possibly in the conceptual integration of memories.
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PMID:Neurobehavioral changes associated with caudate lesions. 279 71

In a longitudinal prospective study of dementia, 158 patients were investigated post mortem. Sixteen patients were classified as frontal lobe dementia (FLD) of non-Alzheimer type and four cases as Pick's disease. Positive heredity for dementia was reported in 50% of these cases compared to 30% in a reference group of patients with Alzheimer's disease (AD). The typical clinical picture in FLD and Pick's disease was that of a slowly progressive dementia, at an early stage dominated by personality change, lack of insight, disinhibition, and later on stereotypy and increased apathy. There was also a progressive dynamic aphasia ending in mutism and amimia. Memory and spatial functions were comparatively spared. Disinhibition, oral/dietary hyperactivity, and echolalia were more consistently found in Pick's disease compared to FLD. The differential diagnosis against AD, cerebrovascular dementia, and other degenerative dementias and against affective disorders and psychotic reactions are discussed.
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PMID:Frontal lobe degeneration of non-Alzheimer type. II. Clinical picture and differential diagnosis. 368 54

A total of 44 patients suffering from slow-progressive schizophrenia with affective disorders prevalence were examined. A long latent stage was defined as Bonn's "masked mania", two variants of the development were singled out in the active period of the disease. The first variant was characterized by depressive disorders and "mixed states" type of a clinical picture. The patients were optimistic, demonstrating high self-estimation in spite of depressive complaints, flaccidity, suppression, weakness, apathy and pseudoneurotic disorders. Accelerated development of associations was retained and motor retardation was absent Personality changes were limited by emotional and psychopathic ones. The second variant represented affective paranoia, delusional disorders formed on the basis of chronic hypomania. Its expressivity correlated with the intensity of hypomanic effect. Personality changes included thought disturbances, autization, mild decrease of the energy potential.
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PMID:[Slowly progressive schizophrenia with signs of chronic hypomania during its course]. 682 56

The subcortical dementias are a heterogeneous group of disorders in which the predominant pathological lesions occur in subcortical structures such as basal ganglia, brainstem nuclei, and the cerebellum. When the cerebral cortex is involved, the lesions are most often in the frontal lobes. These pathologic lesions are associated with cognitive changes that include bradyphrenia, personality change (apathy, depression, irritability), memory impairment, and impaired manipulation of acquired knowledge (calculation, abstraction). Aphasia, apraxia, and agnosia are commonly seen in the cortical dementias, but are absent in the subcortical dementias. Progress in research on the anatomy and connectivity of cortical-subcortical structures has led to refinement in our understanding of the cortical dementias. Despite the connectivity between the cortical and subcortical structures, patterns of cognitive impairment in subcortical dementias remain distinct.
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PMID:Subcortical dementia: a neurobehavioral approach. 881

Frontotemporal dementia is a progressive dementing illness characterized clinically by personality change, disinhibition, and apathy. Neuropathologically, neuronal cell loss, astrogliosis, and microvacuolation are present in the superficial frontotemporal cortical layers, with variable involvement of subcortical and limbic structures. The clinical picture and anatomical distribution of the degenerative changes, as well as motor neuron involvement, differentiate four neuropathological groups: 1) frontal lobe type, 2) thalamostriatal type, 3) motor neuron type, and 4) asymmetrical type. The authors review the results of four large postmortem studies with a special emphasis on cliniconeuropathological correlation.
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PMID:Frontotemporal dementia: a clinicopathological review of four postmortem studies. 884 92

We report a patient who underwent a resection of the right lateral frontal lobe after a venous thrombosis of the superior sagittal sinus. The patient showed inertia, obsessive-compulsive behavior and disinhibition two weeks after the operation and hyperlogia and hypergraphia four weeks later, all of which disappeared within six weeks. General intelligence, language and memory were consistently preserved, though the scores of the performance IQ and the visual memory were relatively decreased. A few months after the operation emotional and personality change such as impatience and apathy became evident. We suggest that the right lateral prefrontal area is concerned with personality and behavior and that the widespread resection holds general intelligence, language and memory within normal range but relatively decreases non-verbal cognitive function that requires manual responses.
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PMID:[A neuropsychological study on a patient with the resection of the right lateral frontal lobe]. 943 Sep 99

The group of Frontotemporal dementias (FTD) is composed of non-Alzheimer forms of dementia characterized clinically by behavioural and personality change leading to apathy and mutism. The disorder is associated with a progressive atrophy of the frontal, anterior temporal and anterior parietal lobes of the brain with several types of underlying pathology. One type (frontal lobe degeneration) is characterized by a microvacuolar degeneration of the outer cortical laminae along with a mild and mainly subpial gliosis and a loss of nerve cells, mostly from layers II and III. Another type shows transcortical tissue cavitation and florid gliosis with neuronal degeneration characterized by the presence of tau and ubiquitin positive inclusion bodies and alpha beta-crystallin-positive ballooned neurones: such changes have been termed 'Pick-type histology', and form the basis for the modern definition of 'Pick's disease'. The aetiological relationship between these two histological types is presently unknown. Both histologies can be differently distributed topographically throughout the brain to produce syndromes of progressive language disorder, when affecting bitemporal lobes or the left hemisphere preferentially, or progressive apraxia when parietal and motor regions are involved. Either pathology can be combined with or overlaps with that of classical motor neurone disease to produce motor neurone disease dementia. The underlying cause of FTD is unknown but genetic factors are strongly implicated. About half of cases show a previous family history of a similar disorder. In several families bearing a FTD clinical and pathological phenotype, linkage to chromosome 17 has been established but the pathology of this group appears distinctive and its relation to other forms of FTD awaits further elucidation. It is still possible that the many clinical and pathological variants of FTD may reflect different phenotypic expressions of a particular genetic change(s) at a single locus on this chromosome.
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PMID:Dementia of frontal type and dementias with subcortical gliosis. 954 90


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