The Clinical Properties of Deep Small Basal Ganglia Infarctions: Lacune or Small Striatocapsular Infarction?.
- Author:
San JUNG
1
;
Seok Beom KWON
;
Sung Hee HWANG
Author Information
1. Department of Neurology, Hallym University College of Medicine, Seoul, Korea. neurojs@hallym.ac.kr
- Publication Type:Original Article
- Keywords:
Basal Ganglia;
Lacune;
Striatocapsular infarction
- MeSH:
Angiography;
Aphasia;
Basal Ganglia*;
Cerebral Infarction;
Diffusion Magnetic Resonance Imaging;
Humans;
Infarction*;
Magnetic Resonance Imaging;
Perfusion;
Reflex, Babinski;
Reflex, Stretch;
Risk Factors;
Stroke;
Stroke, Lacunar;
Visual Fields
- From:Journal of the Korean Neurological Association
2004;22(4):295-301
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: Small subcortical infarctions of basal ganglia can be divided into either lacunes or striatocapsular infarctions by size of lesion. However, there are some controversies concerning the size criteria of lacune and striatocapsular infarction. To better understand differences among these patients, we elucidated clinical and other properties of deep small basal ganglia infarctions (DSBIs), which could not be clearly classified as either lacunes or striatocapsular infarction by their sizes only. METHODS: We analyzed 27 patients with acute ischemic lesion of basal ganglia with which the size varying from 1.5 cm to 3 cm in their maximal diameters. We assessed clinical features, laboratory data, stroke risk factors, and radiologic findings such as MRI and MR angiography. RESULTS: These patients could be largely divided into two distinct groups, either with or without associated cortical symptoms and signs. The most common clinical feature was motor weakness that was found in all but one patient. Sensory disturbances, altered deep tendon reflexes, and positive Babinski signs were also commonly found. Ten of the 27 patients showed cortical manifestations such as eyeball deviation, visual field defect, aphasia and neglect. Eight of the 10 patients with cortical manifestations showed MCA or ICA stenotic lesions. CONCLUSIONS: We found that many patients with 1.5 cm to 3 cm sized DSBIs could have the features of either lacune or striatocapsular infarction. Careful evaluation of clinical and radiologic findings should be performed in patients with clinically appearing lacunar syndrome in order to differentiate lacunar infarction of small vessel disease from striatocapsular infarction of other various pathophysiologies. Echocardiogram, cerebral angiogram and perfusion and diffusion MRI could be recommended for further evaluation and to better understand the pathogenesis in these patients.
