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JournalISSN: 0895-0172

Journal of Neuropsychiatry and Clinical Neurosciences 

American Psychiatric Association Publishing
About: Journal of Neuropsychiatry and Clinical Neurosciences is an academic journal published by American Psychiatric Association Publishing. The journal publishes majorly in the area(s): Dementia & Depression (differential diagnoses). It has an ISSN identifier of 0895-0172. Over the lifetime, 3317 publications have been published receiving 116275 citations. The journal is also known as: Supplement to the Journal of neuropsychiatry and clinical neurosciences & JNCN.


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Journal ArticleDOI
TL;DR: A working model of depression implicating failure of the coordinated interactions of a distributed network of limbic-cortical pathways is proposed to facilitate continued integration of clinical imaging findings with complementary neuroanatomical, neurochemical, and electrophysiological studies in the investigation of the pathogenesis of affective disorders.
Abstract: A working model of depression implicating failure of the coordinated interactions of a distributed network of limbic-cortical pathways is proposed. Resting state patterns of regional glucose metabolism in idiopathic depressed patients, changes in metabolism with antidepressant treatment, and blood flow changes with induced sadness in healthy subjects were used to test and refine this hypothesis. Dorsal neocortical decreases and ventral paralimbic increases characterize both healthy sadness and depressive illness; concurrent inhibition of overactive paralimbic regions and normalization of hypofunctioning dorsal cortical sites characterize disease remission. Normal functioning of the rostral anterior cingulate, with its direct connections to these dorsal and ventral areas, is postulated to be additionally required for the observed reciprocal compensatory changes, since pretreatment metabolism in this region uniquely predicts antidepressant treatment response. This model is offered as an adaptable framework to facilitate continued integration of clinical imaging findings with complementary neuroanatomical, neurochemical, and electrophysiological studies in the investigation of the pathogenesis of affective disorders.

1,505 citations

Journal ArticleDOI
TL;DR: A brief questionnaire form of the NPI (NPI-Q), intended for use in routine clinical practice, is developed and cross-validated in 60 Alzheimer's patients, providing a brief, reliable, informant-based assessment of neuropsychiatric symptoms and associated caregiver distress.
Abstract: The Neuropsychiatric Inventory (NPI) is a validated clinical instrument for evaluating psychopathology in dementia. The authors developed a brief questionnaire form of the NPI (NPI-Q), intended for use in routine clinical practice, and cross-validated it with the NPI in 60 Alzheimer's patients. Test-retest reliability of the NPI-Q was acceptable. The prevalence of analogous symptoms reported on the NPI and NPI-Q differed on average by 5%; moderate or severe symptom ratings differed by less than 2%. The NPI-Q provides a brief, reliable, informant-based assessment of neuropsychiatric symptoms and associated caregiver distress that may be suitable for use in general clinical practice.

1,414 citations

Journal ArticleDOI
TL;DR: The cerebellar cognitive affective syndrome (CCAS) includes impairments in executive, visual-spatial, and linguistic abilities, with affective disturbance ranging from emotional blunting and depression, to disinhibition and psychotic features.
Abstract: Many diseases involve the cerebellum and produce ataxia, which is characterized by incoordination of balance, gait, extremity and eye movements, and dysarthria. Cerebellar lesions do not always manifest with ataxic motor syndromes, however. The cerebellar cognitive affective syndrome (CCAS) includes impairments in executive, visual-spatial, and linguistic abilities, with affective disturbance ranging from emotional blunting and depression, to disinhibition and psychotic features. The cognitive and psychiatric components of the CCAS, together with the ataxic motor disability of cerebellar disorders, are conceptualized within the dysmetria of thought hypothesis. This concept holds that a universal cerebellar transform facilitates automatic modulation of behavior around a homeostatic baseline, and the behavior being modulated is determined by the specificity of anatomic subcircuits, or loops, within the cerebrocerebellar system. Damage to the cerebellar component of the distributed neural circuit subserving sensorimotor, cognitive, and emotional processing disrupts the universal cerebellar transform, leading to the universal cerebellar impairment affecting the lesioned domain. The universal cerebellar impairment manifests as ataxia when the sensorimotor cerebellum is involved and as the CCAS when pathology is in the lateral hemisphere of the posterior cerebellum (involved in cognitive processing) or in the vermis (limbic cerebellum). Cognitive and emotional disorders may accompany cerebellar diseases or be their principal clinical presentation, and this has significance for the diagnosis and management of patients with cerebellar dysfunction.

1,161 citations

Journal ArticleDOI
TL;DR: Research in animals and of cognitive function in normal, brain-injured, and schizophrenic subjects support the theory that a defect in working memory--the ability to guide behavior by representations--may be the fundamental impairment leading to schizophrenic thought disorder.
Abstract: Recent advances in anatomical, behavioral, and physiological techniques have produced new information about the nature of prefrontal function, its cellular basis, and its anatomical underpinnings in nonhuman primates. These findings are changing our views of prefrontal function and providing insight into possible bases for human mental disorder. A major advance is the recognition that various prefrontal areas are engaged in holding information "on line" and updating past and current information on a moment-to-moment basis. Studies of animals and of cognitive function in normal, brain-injured, and schizophrenic subjects support the theory that a defect in working memory--the ability to guide behavior by representations--may be the fundamental impairment leading to schizophrenic thought disorder.

1,050 citations

Performance
Metrics
No. of papers from the Journal in previous years
YearPapers
202330
202265
202118
202056
201960
201839