CC BY-NC-ND 4.0 · Arq Neuropsiquiatr 2018; 76(01): 60-61
DOI: 10.1590/0004-282X20170169
IMAGES IN NEUROLOGY

Delayed hemiparkinsonism after closed head injury

Hemiparkinsonismo tardio após traumatismo craniano fechado
Monalisa da Silveira Dias
1   Hospital de Base do Distrito Federal, Unidade de Neurologia, Centro de Distúrbios do Movimento e Doença de Parkinson, Brasília DF, Brasil;
,
Pedro Renato Brandão
1   Hospital de Base do Distrito Federal, Unidade de Neurologia, Centro de Distúrbios do Movimento e Doença de Parkinson, Brasília DF, Brasil;
2   Congresso Nacional, Câmara dos Deputados, Departamento Médico, Brasília DF, Brasil;
,
Talyta Grippe
1   Hospital de Base do Distrito Federal, Unidade de Neurologia, Centro de Distúrbios do Movimento e Doença de Parkinson, Brasília DF, Brasil;
3   Universidade de Brasília, Faculdade de Medicina, Programa de Pós Graduação, Brasília DF, Brasil;
,
Cassio Jovem
4   Clínica Villa Rica, Brasília DF, Brasil;
5   Hospital de Base do Distrito Federal, Departamento de Radiologia, Brasília DF, Brasil;
,
Marcelo Gomes
6   Núcleos Medicina Nuclear, Brasília DF, Brasil.
,
Flávio Faria Pereira
1   Hospital de Base do Distrito Federal, Unidade de Neurologia, Centro de Distúrbios do Movimento e Doença de Parkinson, Brasília DF, Brasil;
› Author Affiliations

A 40-year-old man complained of insidiously-reduced right arm dexterity, which started three years previously. He had had a severe closed head injury 19 years before. At the examination, he presented with rigidity, akinesia, and dystonia uniquely over the right side. According to Crouzon and Justin-Besancon, the criteria for traumatic secondary parkinsonism are severe trauma, brain concussion, and a temporal relationship between the trauma and symptoms[1]. In this patient, presynaptic dopaminergic imaging corroborated nigrostriatal denervation induced, presumably, by a previous traumatic hemorrhage. As a result, neuroimaging ([Figures 1] and [2]) showed specific features that validated the diagnosis of parkinsonism secondary to a traumatic etiology[2],[3].

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Figure 1 Magnetic resonance imaging, with T2 (A), and susceptibility weighted imaging (B), discloses, in detail, a focal lesion with hemosiderin deposits, over the left cerebral peduncle and substantia nigra.
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Figure 2 Scintigraphic imaging with single photon emission computed tomography shows normal 99mTc-TRODAT uptake in the right striatum, and absence of the radionuclide concentration on the left side.


Publication History

Received: 18 November 2016

Accepted: 05 September 2017

Article published online:
30 August 2023

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