Clinicoradiological comparison between vascular parkinsonism and Parkinson's disease.

OBJECTIVE: To compare the clinical and radiological features of vascular parkinsonism (VP) and Parkinson's disease (PD). METHODS: Cross-sectional study where 15 patients with VP (8 (53.3%) men; aged 75.7 ± 10.4 years) and 30 patients with PD (17 (56.7%) men; aged 67.3 ± 7.5 years) underwent motor and cognitive evaluation and brain MRI. RESULTS: Patients with VP were, on average, 8.4 years older (p = 0.004); all had arterial hypertension. They presented with a sudden onset of parkinsonism (80%) and a rapidly progressive clinical course (53.3%). Predominant lower body parkinsonism (p<0.001), postural instability (p=0.003) with freezing of gait (p<0.001) and falls (p<0.001), urinary incontinence (p < 0.001) and pyramidal signs (p<0.001) were more common in patients with VP. Movement Disorders Society's Unified PD Rating Scale (MDS-UPDRS) scores were higher in patients with VP (p=0.005 in 'OFF' state and p<0.001 in 'ON' state). They had greater cognitive impairment and 12 (80%) fulfilled diagnostic criteria for probable vascular dementia. Most patients with VP had brain MRI changes: multiple lacunar infarcts (66.7%) or extensive white matter disease (26.7%). CONCLUSIONS: VP can be clinically distinguished from PD based on sudden onset of parkinsonism at an older age, characterised by lower body predominance, urinary incontinence, pyramidal signs, postural instability with freezing of gait and falls, and dementia.

Signos extrapiramidales en pacientes con multinfartos encefálicos profundos (Parkinsonismo vascular) / Extrapyramidal findings in patiens with deep cerebral multiple infarcts (vascular parkinsonism)

Fueron seleccionados prospectivamente 44 pacientes con multinfartos cerebrales profundos. Estos se dividieron en dos grupos, uno compuesto por los pacientes con signos extrapiramidales (n=29), y el otro sin ellos (grupo control)(n=15). El 65,9 por ciento de los casos seleccionados tuvieron signos extrapiramidales de grado leve a moderado, constituyendo un síndrome hipocinético rígido sin temblor. Todos los pacientes de ambos grupos tuvieron otros defectos neurológicos, su distribución no fue diferente entre los grupos comparados. La localización topográfica de los infartos, la presencia de leukoaraiosis y la dilatación de los ventrículos fue semejante en ambos grupos. El origen de los signos extrapiramidales es explicado por una génesis fisiopatológica funcional, más que estructural, secundaria a una hipoxia persistente relacionada con el daño vascular multifocal (AU)