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Published on: July 21, 2013
Acute caudate vascular lesions
E Kumral1, D Evyapan, K Balkir
1Division of Cerebrovascular and Neuropsychology Unit, Department of Neurology, Faculty of Medicine, Ege University, Izmir, Turkey. ekumral@med.ege.edu.tr
Insights
This study analyzed caudate nucleus strokes, finding small-artery disease and cardiac embolism as common causes. Behavioral and neurological deficits often resulted from damage to specific caudate subnuclei and nearby structures.
Area of Science:
- Neurology
- Neuroscience
- Vascular Neurology
Background:
- Caudate nucleus lesions, including infarcts and hemorrhages, present unique clinical challenges.
- Understanding the demographic, risk factor, and clinical profiles of caudate stroke is crucial for diagnosis and management.
Purpose of the Study:
- To evaluate demographic features, risk factors, clinical profiles, and behavioral abnormalities in patients with caudate nucleus lesions.
- To differentiate between caudate infarct and hemorrhage presentations and outcomes.
Main Methods:
- Retrospective analysis of patients with acute caudate stroke confirmed by CT or MRI over a 5-year period.
- Database review including risk factors, clinical features, stroke type, mechanism, and vascular territories.
Main Results:
- Thirty-one patients (mean age 62.3 years) experienced acute caudate stroke (25 infarcts, 6 hemorrhages).
- Key risk factors for infarct included hypertension, hypercholesterolemia, and diabetes mellitus. Small-artery disease (59%) and cardiac embolism (20%) were primary causes.
- Common neurological deficits included abulia, psychic akinesia, frontal system abnormalities, speech deficits, and neglect syndromes.
Conclusions:
- Caudate nucleus vascular lesions, particularly with neighboring structure involvement, constitute a distinct stroke syndrome.
- Small-artery disease and cardiac embolism are significant etiologies. Clinical presentation of caudate hemorrhage can mimic subarachnoid hemorrhage.
- Behavioral abnormalities are linked to specific caudate subnuclei damage and anterior limb of internal capsule lesions.
Background And Purpose:
We sought to evaluate demographic features, risk factors, clinical profiles, and behavioral abnormalities in patients with caudate lesion, either with infarct or with hemorrhage involving the caudate nucleus.
Methods:
We studied all patients with acute caudate stroke confirmed by CT or MRI who were admitted to our stroke unit over a 5-year period. A database containing risk factors, clinical features, type and mechanism of stroke, and caudate vascular territories was analyzed.
Results:
Thirty-one patients had acute caudate stroke (24 men and 7 women; mean age, 62.3 years). Caudate infarct was present in 25 patients and caudate hemorrhage in 6. The main risk factors for caudate infarct were hypertension (64%), hypercholesterolemia (32%), diabetes mellitus (28%), and previous myocardial infarct (20%). Hypertension was present in 4 patients (67%) with caudate hemorrhage, and arteriovenous malformation was present in 1 patient (17%). Small-artery disease was diagnosed in 14 patients (59%), cardiac embolism in 5 patients (20%), and large-artery disease in 2 patients (8%), and 2 patients (8%) had mixed etiology. The most frequent neurological abnormalities were abulia and psychic akinesia (48%), frontal system abnormalities (26%), speech deficits in patients with left-sided lesions (23%), and neglect syndromes in those with right-sided lesions (10%). Fifteen patients with caudate infarct (60%) and 3 patients with hemorrhage (50%) were able to return to normal daily life. Patients with infarct in the territory of the lateral lenticulostriate arteries extending to neighboring structures showed more frequent motor and neuropsychological deficits than those with infarct in the territory of the anterior lenticulostriate arteries.
Conclusions:
The clinical presentation of patients with caudate hemorrhage mimicked subarachnoid hemorrhage with or without motor and neuropsychological signs. Caudate vascular lesions with concomitant neighboring structure involvement represent a specific stroke syndrome, usually caused by small-artery disease and in one fifth of the patients caused by cardiac embolism. The behavioral abnormalities were mostly due to medial, lateral, and ventral caudate subnuclei damage and coexisting lesion of the anterior limb of the internal capsule.
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