title: Echogenicity of substantia nigra determined by transcranial ultrasound correlates with severity of parkinsonian symptoms induced by neuroleptic therapy.
abstract: BACKGROUND
  Increased echogenicity of the substantia nigra (SN) detected by transcranial sonography is a characteristic ultrasound feature of Parkinson's disease. This ultrasound feature can also be detected in a subgroup of healthy adults. In recent studies, healthy subjects with this ultrasound feature showed a reduced [(18)F]-Dopa uptake on positron emission tomography (PET), indicating a subclinical alteration of the nigrostriatal system. This study was designed to evaluate whether the severity of neuroleptic side effects is related to the echo-feature of the SN.
  
  
  METHODS
  In the retrospective part of the study, 93 psychiatric patients with either definite and severe parkinsonism after neuroleptic treatment (n = 52) or with no or minimal parkinsonian symptoms (n = 41) were included and underwent transcranial sonography to measure the extension of hyperechogenic areas at the SN. In addition, in the prospective part 11 patients with an acute psychotic episode requiring first-ever neuroleptic treatment underwent ultrasound examination. Subsequently, neuroleptic-induced parkinsonian signs were assessed prospectively.
  
  
  RESULTS
  In the retrospective part of the study, patients with severe neuroleptic-induced parkinsonism had more extended echogenic signals at the SN than those with low echogenic SN (U-test; p <.01). The prospective part of the study showed that the severity of parkinsonian symptoms correlated with the echogenicity of the substantia nigra (Spearman's rank: p <.01).
  
  
  CONCLUSIONS
  Increased echogenicity of the substantia nigra is associated with impaired function of the nigrostriatal system that can be disclosed by neuroleptic drugs.
authors.affiliation: Department of Neurology, Bayerische Julius-Maximilians-Universität, Würzburg, Germany.
authors.forename: D
authors.initials: D
authors.lastname: Berg
authors.forename: B
authors.initials: B
authors.lastname: Jabs
authors.forename: U
authors.initials: U
authors.lastname: Merschdorf
authors.forename: H
authors.initials: H
authors.lastname: Beckmann
authors.forename: G
authors.initials: G
authors.lastname: Becker
mesh_terms: D000208:Acute Disease; D000328:Adult; D000978:Antiparkinson Agents / Q000493:pharmacokinetics; D014150:Antipsychotic Agents / Q000009:adverse effects*; D003342:Corpus Striatum / Q000000981:diagnostic imaging / Q000378:metabolism; D005260:Female; D006801:Humans; D007980:Levodopa / Q000493:pharmacokinetics; D008297:Male; D008875:Middle Aged; D020734:Parkinsonian Disorders / Q000139:chemically induced* / Q000175:diagnosis*; D011446:Prospective Studies; D011618:Psychotic Disorders / Q000188:drug therapy / Q000523:psychology; D012189:Retrospective Studies; D013378:Substantia Nigra / Q000000981:diagnostic imaging* / Q000378:metabolism; D014055:Tomography, Emission-Computed; D014463:Ultrasonography
chemical_list: D000978:Antiparkinson Agents; D014150:Antipsychotic Agents; D007980:Levodopa