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Lacunar Infarction Caused by Chronic Subdural Hematoma
Shoko Merrit Yamada1, Yusuke Tomita1, Yoshinori Takaya1
1Department of Neurosurgery, Teikyo University Mizonokuchi Hospital.
Insights
Chronic subdural hematoma (CSDH) patients with rapid motor decline may have lacunar infarctions. Imaging can identify these, suggesting specific treatment approaches for better recovery.
Area of Science:
- Neurology
- Radiology
- Neurosurgery
Background:
- Chronic subdural hematoma (CSDH) typically resolves with surgery, but some patients experience poor motor recovery.
- Investigating cerebral infarctions is crucial in CSDH patients with persistent hemiparesis post-surgery.
Observation:
- Among 284 CSDH patients with motor weakness, 82 underwent pre-operative MRI and MRA due to rapid hemiparesis progression.
- Small lacunar infarctions were found on the hematoma side in 5 elderly patients (all >80 years) with hypertension and/or diabetes.
- MRA revealed a characteristic shift of the middle cerebral artery (M1) in all 5 patients with lacunar infarction, compared to only 5.2% without infarction.
Findings:
- CSDH-associated lacunar infarctions may result from arterial distortion rather than typical risk factors like lipohyalinosis.
- These infarctions were small, associated with mild hemiparesis, and had a good prognosis with physical rehabilitation.
- Pre-operative MR imaging is recommended for CSDH patients presenting with sudden or rapidly worsening motor weakness.
Implications:
- Understanding the cause of lacunar infarction in CSDH can refine treatment strategies, potentially avoiding unnecessary anti-platelet therapy.
- Early detection via MRI/MRA can guide management and improve patient outcomes in complex CSDH cases.
- This study highlights the importance of neuroimaging in diagnosing specific causes of neurological deficits in CSDH patients.
Abstract:
In chronic subdural hematoma (CSDH) patients, motor functions usually recover quickly after burr-hole surgery; however, in a rare case, the hemiparesis showed poor improvement after surgery. In that case, investigation of cerebral infarctions is important. Among the 284 CSDH patients with motor weakness, magnetic resonance image (MRI) and MR angiography (MRA) were acquired in 82 patients before surgery when the hemiparesis progressed rapidly. Small lacunar infarction was identified on the hematoma side in five cases; all were older than 80 years with hypertension, and diabetes mellitus had been diagnosed in two. In all the five patients (100%), MRA demonstrated a downward or upward shift of the M1 portion of the middle cerebral artery on the hematoma side, where the perforating arteries originate. Conversely, only 4 CSDH patients (5.2%) without lacunar infarction demonstrated M1 downward shift. The risk factors of lacunar infarction were high in the five detected cases; however, distortion, twisting, or elongation of the lenticulostriate arteries might be a cause of the lacunar infarctions, rather than the formation of lipohyalinosis or microatheroma in the arteries. Therefore, anti-platelet treatment might not be necessary for CSDH-inducing lacunar infarction. The lacunar infarctions caused by CSDH were small, the patients' hemiparesis was mild, a prognosis of all the patients was good, and they recovered well from the motor weakness after physical rehabilitation. MR examinations before surgery are recommended for CSDH patients especially when a patient complains of sudden onset or rapid deterioration of motor weakness.
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