Ian Lam Leong,Tsz Huen Ng,Kunal Sen,Ella Burchill,Harry Costello,James B Badenoch,Jan Coebergh,Robert A McCutcheon,Akshay Nair,Michael Browning,Quentin J M Huys,Glyn Lewis,Andrew Lees,Anthony S David,Jonathan P Rogers
{"title":"纹状体多巴胺传递减少作为精神运动迟缓的跨诊断底物。","authors":"Ian Lam Leong,Tsz Huen Ng,Kunal Sen,Ella Burchill,Harry Costello,James B Badenoch,Jan Coebergh,Robert A McCutcheon,Akshay Nair,Michael Browning,Quentin J M Huys,Glyn Lewis,Andrew Lees,Anthony S David,Jonathan P Rogers","doi":"10.1093/brain/awaf335","DOIUrl":null,"url":null,"abstract":"Psychomotor retardation, defined as generalised slowing of movement and speech, is a feature of several neurological and psychiatric disorders. In this review, we discuss the hypothesis that reduced striatal dopaminergic transmission is a transdiagnostic substrate for psychomotor retardation underlying the motor features of conditions such as Parkinson's disease, drug-induced parkinsonism, neuroleptic malignant syndrome, catatonia and depression. We examine the evidence across clinical, epidemiological, neuroimaging, laboratory and therapeutic studies. Parkinsonian disorders share slowed movement and a reduction in verbal output with catatonia and depression. Bradyphrenia, slowed cognitive processing, also occurs in Parkinson's disease and depression. In addition, there are close epidemiological relationships between depression and Parkinson's disease, and between catatonia and neuroleptic malignant syndrome. Neuroimaging studies also generally support the association of psychomotor retardation with reduced dopaminergic transmission, particularly in the dorsal striatum. Cerebrospinal fluid measurement of homovanillic acid (a dopamine catabolite) yields inconsistent results and is very nonspecific. Parkinson's disease and catatonia generally respond well to dopaminergic medication. In contrast, dopamine antagonists can induce both parkinsonism and catatonia. Our review is limited by the variability in measurement of psychomotor retardation and difficulty distinguishing between cognitive and motor slowing. It is also likely that other neurotransmitters, such as GABA and serotonin, play an important role in psychomotor speed. It is possible that dopaminergic deficits in psychiatric disorders represent functional disruptions, in contrast to the structural damage to the substantia nigra in Parkinson's disease. We propose further research be conducted into the effects of levodopa and dopamine agonists in depression with psychomotor retardation. Alternative neuroimaging methods such as PET sequences with shorter imaging protocols and neuromelanin-MRI should also be explored.","PeriodicalId":9063,"journal":{"name":"Brain","volume":"29 1","pages":""},"PeriodicalIF":11.7000,"publicationDate":"2025-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Reduced striatal dopamine transmission as a transdiagnostic substrate of psychomotor retardation.\",\"authors\":\"Ian Lam Leong,Tsz Huen Ng,Kunal Sen,Ella Burchill,Harry Costello,James B Badenoch,Jan Coebergh,Robert A McCutcheon,Akshay Nair,Michael Browning,Quentin J M Huys,Glyn Lewis,Andrew Lees,Anthony S David,Jonathan P Rogers\",\"doi\":\"10.1093/brain/awaf335\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Psychomotor retardation, defined as generalised slowing of movement and speech, is a feature of several neurological and psychiatric disorders. In this review, we discuss the hypothesis that reduced striatal dopaminergic transmission is a transdiagnostic substrate for psychomotor retardation underlying the motor features of conditions such as Parkinson's disease, drug-induced parkinsonism, neuroleptic malignant syndrome, catatonia and depression. We examine the evidence across clinical, epidemiological, neuroimaging, laboratory and therapeutic studies. Parkinsonian disorders share slowed movement and a reduction in verbal output with catatonia and depression. Bradyphrenia, slowed cognitive processing, also occurs in Parkinson's disease and depression. In addition, there are close epidemiological relationships between depression and Parkinson's disease, and between catatonia and neuroleptic malignant syndrome. Neuroimaging studies also generally support the association of psychomotor retardation with reduced dopaminergic transmission, particularly in the dorsal striatum. Cerebrospinal fluid measurement of homovanillic acid (a dopamine catabolite) yields inconsistent results and is very nonspecific. Parkinson's disease and catatonia generally respond well to dopaminergic medication. In contrast, dopamine antagonists can induce both parkinsonism and catatonia. Our review is limited by the variability in measurement of psychomotor retardation and difficulty distinguishing between cognitive and motor slowing. It is also likely that other neurotransmitters, such as GABA and serotonin, play an important role in psychomotor speed. It is possible that dopaminergic deficits in psychiatric disorders represent functional disruptions, in contrast to the structural damage to the substantia nigra in Parkinson's disease. We propose further research be conducted into the effects of levodopa and dopamine agonists in depression with psychomotor retardation. 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Reduced striatal dopamine transmission as a transdiagnostic substrate of psychomotor retardation.
Psychomotor retardation, defined as generalised slowing of movement and speech, is a feature of several neurological and psychiatric disorders. In this review, we discuss the hypothesis that reduced striatal dopaminergic transmission is a transdiagnostic substrate for psychomotor retardation underlying the motor features of conditions such as Parkinson's disease, drug-induced parkinsonism, neuroleptic malignant syndrome, catatonia and depression. We examine the evidence across clinical, epidemiological, neuroimaging, laboratory and therapeutic studies. Parkinsonian disorders share slowed movement and a reduction in verbal output with catatonia and depression. Bradyphrenia, slowed cognitive processing, also occurs in Parkinson's disease and depression. In addition, there are close epidemiological relationships between depression and Parkinson's disease, and between catatonia and neuroleptic malignant syndrome. Neuroimaging studies also generally support the association of psychomotor retardation with reduced dopaminergic transmission, particularly in the dorsal striatum. Cerebrospinal fluid measurement of homovanillic acid (a dopamine catabolite) yields inconsistent results and is very nonspecific. Parkinson's disease and catatonia generally respond well to dopaminergic medication. In contrast, dopamine antagonists can induce both parkinsonism and catatonia. Our review is limited by the variability in measurement of psychomotor retardation and difficulty distinguishing between cognitive and motor slowing. It is also likely that other neurotransmitters, such as GABA and serotonin, play an important role in psychomotor speed. It is possible that dopaminergic deficits in psychiatric disorders represent functional disruptions, in contrast to the structural damage to the substantia nigra in Parkinson's disease. We propose further research be conducted into the effects of levodopa and dopamine agonists in depression with psychomotor retardation. Alternative neuroimaging methods such as PET sequences with shorter imaging protocols and neuromelanin-MRI should also be explored.
期刊介绍:
Brain, a journal focused on clinical neurology and translational neuroscience, has been publishing landmark papers since 1878. The journal aims to expand its scope by including studies that shed light on disease mechanisms and conducting innovative clinical trials for brain disorders. With a wide range of topics covered, the Editorial Board represents the international readership and diverse coverage of the journal. Accepted articles are promptly posted online, typically within a few weeks of acceptance. As of 2022, Brain holds an impressive impact factor of 14.5, according to the Journal Citation Reports.