I. Diagnosis: 1. Onset after middle age with a history of long-term hypertension; 2. Clinical presentation is consistent with one of the cavernous syndromes (pure motor light hemiparesis, pure sensory stroke, ataxic light hemiparesis, dysarthria-hand clumsiness syndrome, sensorimotor stroke, cavernous state); 3. CT or MRI imaging can confirm the presence of a lesion consistent with neurological deficits; 4. 4, EEG, lumbar puncture or DSA have no positive findings; 5, the prognosis is good and most patients can recover within a short period of time. Differential diagnosis: In addition to infarction, the etiology of cavernous syndrome includes small cerebral hemorrhage, infection, cysticercosis, smoker’s disease, brain abscess, extracranial carotid artery occlusion, cerebral bridge hemorrhage, demyelinating disease and metastases, etc. Therefore, attention should be paid to differentiate non-infarct cavernous lesions in clinical diagnosis. Treatment: There is no effective treatment method, mainly to prevent disease recurrence: 1. Effective control of hypertension and various types of cerebral atherosclerosis is the key to prevent this disease; 2. Application of aspirin, ticlopidine, etc. to inhibit platelet aggregation and reduce recurrence; 3. Appropriate application of vasodilator drugs such as pulse bolus to increase the blood supply of brain tissue and promote neurological recovery in the acute stage; 4. Calcium antagonists such as nimodipine and flunarizine can reduce vasospasm, improve cerebral blood circulation and reduce the recurrence rate of lacunar infarction; 5. Prognosis: The disease has a good prognosis, with a low mortality and disability rate, but is prone to recurrence.