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

Schizophrenia is a serious and disabling mental disorder with symptoms such as auditory hallucinations, disordered thinking and delusions, avolition, anhedonia, blunted affect and apathy. In this review article we seek to present the current scientific findings from linkage studies and susceptible genes and the pathophysiology of white matter in schizophrenia. The article has been reviewed in two parts. The first part deals with the linkage studies and susceptible genes in schizophrenia in order to have a clear-cut picture of the involvement of chromosomes and their genes in schizophrenia. The genetic linkage results seem to be replicated in some cases but in others are not. From these results, we cannot draw a fine map to a single locus or gene, leading to the conclusion that schizophrenia is not caused by a single factor/gene. In the second part of the article we present the oligodendrocyte-related genes that are associated with schizophrenia, as we hypothesize a potential role of oligodendrocyte-related genes in the pathology of the disorder.
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PMID:The myelin-pathogenesis puzzle in schizophrenia: a literature review. 1792 96

Deficit schizophrenia is a relatively homogeneous subtype of patients which is considered helpful to explore the pathogenesis of schizophrenia. The aim of the present study was to reexamine the clinical characteristics of deficit (n=30) and nondeficit schizophrenia (n=93) in a Chinese sample and investigate the differences of neurocognitive function among the two subtypes of schizophrenia and the normal controls (n=103). Schizophrenia patients completed the Brief Psychiatric Rating Scale (BPRS), Scale for the Assessment of Negative Symptoms (SANS) and Scale for the Assessment of Positive Symptoms (SAPS). Additionally, all participants completed an abbreviated version of the Wechsler Adult Intelligence Scale (WAIS-RC) and a neuropsychological test battery examining the executive functions, visuospatial abilities and explicit memory related to the frontal, parietal, and temporal lobe functions. The deficit group received higher scores than the nondeficit group on the BPRS anergia factor and SANS affective flattening, alogia, avolition-apathy, anhedonia-asociality subscales, but not on the SAPS. Both two schizophrenia subgroups performed more poorly on the WAIS-RC and neuropsychological tests than the normal controls. Moreover, deficit patients performed worse than nondeficit patients on the prorated IQ, the Trail Making Test, Wisconsin Card Sorting test and Block Design test. The present study replicated symptom profiles in deficit vs. nondeficit schizophrenia in the Chinese sample. Furthermore, this study suggested that deficit schizophrenia is associated with frontal and parietal lobe impairment, and that temporal lobe dysfunction may be a common basis for cognitive impairment in schizophrenia as a whole.
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PMID:Psychopathology and neuropsychological impairments in deficit and nondeficit schizophrenia of Chinese origin. 1824 36

Although still considered a paradigmatic movement disorder, Parkinson's disease (PD) is associated with a broad spectrum of non-motor symptoms. These include disorders of mood and affect with apathy, anhedonia and depression, cognitive dysfunction and hallucinosis, as well as complex behavioural disorders. Sensory dysfunction with hyposmia or pain is almost universal, as are disturbances of sleep-wake cycle regulation. Autonomic dysfunction including orthostatic hypotension, urogenital dysfunction and constipation is also present to some degree in a majority of patients. Whilst overall non-motor symptoms become increasingly prevalent with advancing disease, many of them can also antedate the first occurrence of motor signs - most notably depression, hyposmia or rapid eye movement sleep behaviour disorder (RBD). Although exact clinicopathological correlations for most of these non-motor features are still poorly understood, the occurrence of constipation, RBD or hyposmia prior to the onset of clinically overt motor dysfunction would appear consistent with the ascending hypothesis of PD pathology proposed by Braak and colleagues. Screening these early non-motor features might, therefore, be one approach towards early 'preclinical' diagnosis of PD. This review article provides an overview of the clinical spectrum of non-motor symptoms in PD together with a brief review of treatment options.
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PMID:Non-motor symptoms in Parkinson's disease. 1835 32

Apathy is a common condition in Parkinson's disease (PD) and is generally defined as a lack of motivation. It is associated with more severe cognitive dysfunction and a decrease in activities of daily living (ADL) performance. Anhedonia, the inability to experience pleasure, can be a symptom of both depressive and apathetic syndromes. The Movement Disorder Society (MDS) commissioned a task force to assess the clinimetric properties of apathy and anhedonia scales in PD patients. A systematic literature review was conducted to identify scales that have either been validated or used in PD patients. Apathy scales identified for review include the Apathy Evaluation Scale (AES), the Apathy Scale (AS), the Apathy Inventory (AI), and the Lille Apathy Rating Scale (LARS). In addition, item 4 (motivation/initiative) of the Unified Parkinson's Disease Rating Scale (UPDRS) and item 7 (apathy) of the Neuropsychiatric Inventory (NPI) were included. Anhedonia scales identified for review were the Snaith-Hamilton Pleasure Scale (SHAPS) and the Chapman scales for physical and social anhedonia. Only the AS is classified as "recommended" to assess apathy in PD. Although item 4 of the UPDRS also meets the criteria to be classified as recommended, it should be considered for screening only because of the obvious limitations of a single item construct. For the assessment of anhedonia, only the SHAPS meets the criteria of "Suggested." Information on the validity of apathy and anhedonia scales is limited because of the lack of consensus on diagnostic criteria for these conditions.
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PMID:Apathy and anhedonia rating scales in Parkinson's disease: critique and recommendations. 2010 64

To explore the relationship between depression and cognitive impairment in non-demented PD patients, we evaluated neurological and neuropsychological asset in 65 patients with a diagnosis of major depressive disorder (dPD) according to DSM-IV criteria and 60 patients without depression (nPD). Compared with nPD patients, dPD patients had significantly higher scores on behavioral rating scales and performed worse on the Frontal Assessment Battery (FAB), Semantic Fluency Task, Copying Task (CT), and Stroop Test. Three dPD subgroups were identified based on the first two DSM-IV criteria: patients fulfilling criterion 1 (depressed mood; group 1); patients fulfilling criterion 2 (apathy/anhedonia; group 2); patients fulfilling criteria 1 and 2 (group 3). Patients of group 2 scored significantly lower than patients of group 1 on the CT, FAB and phonological fluency task. Patients of groups 2 and 3 scored significantly lower than nPD patients on visuoconstructional and frontal tasks. Similar results were obtained in dPD patients stratified in four subgroups based on cut-off scores of the Apathy Evaluation Scale and the Snaith Hamilton Pleasure Scale. In summary, PD patients with concomitant apathy and anhedonia may show more severe cognitive impairments. Since such patients are diagnosed to be affected by depression according to clinical DSM-IV criteria, we suggest that DSM-IV criteria may not distinguish an affective from a cognitive disorder in PD.
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PMID:Relationship between depression and cognitive dysfunctions in Parkinson's disease without dementia. 1937 Mar 1

The course of negative and positive symptoms was studied in neuroleptic-treated patients over a 3-year period, in consideration also of the initial phase of illness (post-acute or chronic). This study was carried out in a broadly defined schizophrenic sample, in order not to give preference to one diagnostic subgroup over another. Forty-six patients were evaluated every year for 3 years, 23 in the post-acute group and 23 in the chronic group. Aggravations of the Clinical Global Impression (CGI) and of the SANS total score were observed, regardless of the group (chronic or post-acute). This global aggravation confirmed Kraepelin's concept of dementia praecox; moreover, this aggravation was not due to an increase in the number of patients relapsing, or to an aggravation of akinesia. Three types of negative and positive symptom courses were observed: i) the mean sub-scores of positive symptoms, such as hallucinations, delusions, positive formal thought disorders, and of negative symptoms such as flattening affect, avolition/apathy and attentional impairment, did not vary significantly over time in either group; ii) the mean sub-scores of bizarre behavior and alogia fluctuated over time (p < 0.05) and only poverty of speech was perfectly stable among the items constituting alogia; iii) the mean subscores of anhedonia/asociality worsened significantly over time irrespective of the groups (p < 0.05), and among the items constituting anhedonia, recreational interest-activities and intimacy-closeness abilities worsened (p < 0.05 and p < 0.01, respectively). This aggravation was neither due to an increase in neuroleptic doses nor to the duration and chronicity of illness. However, negative symptoms, except anhedonia, can be reversible in some patients. The very strong stability of anhedonia, whatever the group, emphasize the importance of taking anhedonia into account in future diagnostic classifications.
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PMID:Stability of positive and negative symptoms in schizophrenic patients: a 3-year follow-up study. 1969 45

Deficits in odor identification have been most frequently described in schizophrenia (SZ). A relationship between dysfunction in odor identification and negative symptoms of SZ has also been reported. Furthermore, deficit SZ (a subtype of the illness with primary, enduring negative symptoms) has been found to be associated with a particularly poor performance on odor identification tests indicating that deficits in smell identification could be differentially expressed in some subtypes of SZ. We describe correlations of performance on smell identification with positive and negative symptoms of SZ. Patients with SZ (n=15) and normal controls (n=19) were tested by the University of Pennsylvania Smell Identification Test (UPSIT). Psychopathology was assessed with the Scales for the Assessment of Positive and Negative Symptoms (SAPS and SANS). SZ patients performed more poorly on the UPSIT test than did normal controls. Consistent with previous findings, we observed a correlation of SANS with UPSIT performance. In particular, specific subdomains of SANS, such as blunted affect, apathy and anhedonia, were associated with odor identification deficits. Furthermore, UPSIT score predicts these subdomains of negative symptoms. No correlation was observed between positive symptom and odor identification deficits. Our study further reinforces a relation between olfactory identification deficit and negative symptoms in SZ and suggests that smell identification could be a candidate endophenotype relevant to negative symptoms of SZ.
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PMID:Negative symptoms of schizophrenia correlate with impairment on the University of Pennsylvania smell identification test. 1981 72

The present study employs a new framework to categorise the heterogeneous findings on the relationship between impaired reward processing and negative and affective symptoms of schizophrenia. Based on previous behavioural and neuroimaging studies we postulate that "wanting" (i.e. anticipation) of a reward is specifically related to apathy, whereas "liking" (i.e. hedonic impact) is related to anhedonia and depression--symptoms commonly observed in schizophrenia. Fifteen patients with schizophrenia or schizoaffective disorder treated with atypical antipsychotic drugs and fifteen healthy controls performed a probabilistic monetary incentive delay task while undergoing functional magnetic resonance imaging. At the group level we found no significant differences between patients and controls in neural activation during anticipation or receipt of a reward. However, in patients with schizophrenia specific relationships between ventral-striatal activation and symptoms were observed. Ventral-striatal activation during reward anticipation was negatively correlated with apathy, while activation during receipt of reward was negatively correlated with severity of depressive symptoms. These results suggest that the link between negative symptoms and reward anticipation might specifically relate to apathy, i.e. a lack of motivation and drive. Impaired hedonic reward processing might contribute to the development of depressive symptoms in patients with schizophrenia, but it is not directly associated with self-rated anhedonia. These results indicate the necessity of more specifically differentiating negative and affective symptoms in schizophrenia in order to understand the role of the reward system in their pathogenesis.
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PMID:Neural correlates of reward processing in schizophrenia--relationship to apathy and depression. 2000 75

Assessment of molecular defects that underlie cognitive deficits observed in mendelian disorders provides a unique opportunity to identify key regulators of human cognition. Congenital Myotonic Dystrophy 1 (cDM1), a multi-system disorder is characterized by both cognitive deficits and a spectrum of behavioral abnormalities, which include visuo-spatial memory deficits, anxiety and apathy. Decreased levels of DMPK (Dystrophia Myotonica-protein kinase), SIX5, a transcription factor or MBNL1 (Muscleblind-like 1), an RNA splice regulator have been demonstrated to contribute to distinct features of cDM1. Mouse strains in which either Dmpk, Six5 or Mbnl1 are inactivated were therefore studied to determine the relative contribution of each gene to these cognitive functions. The open field and elevated plus maze tasks were used to examine anxiety, sucrose consumption was used to assess motivation, whereas the water maze and context fear conditioning were used to examine spatial learning and memory. Cognitive and behavioral abnormalities were observed only in Mbnl1 deficient mice, which demonstrate behavior consistent with motivational deficits in the Morris water maze, a complex visuo-spatial task and in the sucrose consumption test for anhedonia. All three models of cDM1 exhibit normal spatial learning and memory. These data identify MBNL1 as a potential regulator of emotional state with decreased MBNL1 levels underlying the motivational deficits observed in cDM1.
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PMID:Muscleblind1, but not Dmpk or Six5, contributes to a complex phenotype of muscular and motivational deficits in mouse models of myotonic dystrophy. 2036 Aug 42

The authors assessed the relationship of negative symptoms to demographic, other clinical, and neuropsychological variables to investigate and, to an extent, validate the assessment of individual negative symptoms in older schizophrenic patients. Sixty-four subjects meeting DSM-III-R criteria for schizophrenia, including 39 with onset before age 45 (early-onset schizophrenia, or EOS) and 25 diagnosed with late-onset schizophrenia (LOS) were recruited, along with 35 normal comparison (NC) subjects. All the subjects were assessed, using Scales for the Assessment of Negative Symptoms, other psychiatric rating scales, and a comprehensive neuropsychological evaluation. The prevalence of alogia and anhedonia/asociality was comparable in EOS and LOS groups. The prevalence of affective blunting and avolition/apathy was greater in EOS than in LOS. The authors propose a three-factor model of negative symptoms in older, ambulatory, neuroleptic-treated schizophrenic patients. Limitations of the study, as well as possible implications of findings are discussed.
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PMID:Negative symptoms in late-life schizophrenia. 2162 3


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