Search

Previous randomized clinical trials have so far failed to establish the efficacy of extracranial-intracranial(EC-IC)bypass in the prevention of secondary ischemic strokes. For patients with a recent transient ischemic attack or ischemic stroke ipsilateral to a stenosis or occlusion of the middle cerebral or carotid artery, EC-IC bypass is not recommended as per the American heart association/American stroke association guidelines(Class III, Level of Evidence A). However, patients with severe hemodynamic impairment(misery perfusion)are at high risk of developing stroke, and EC-IC bypass is recommended as per the Japan stroke guideline 2021, provided that the patients show cerebral blood flow less than 80% from baseline and cerebral vascular reserve less than 10%. Perioperative management is also important in preventing ischemic complications and hyperperfusion. Some adjunctive drugs, including minocycline and edaravone, have been reported to be effective against brain damage from hyperperfusion. Regarding Moyamoya disease, EC-IC bypass has been established as a recommended strategy for ischemic presentation, hemorrhagic presentation, hemodynamic impairment, and choroidal anastomosis. EC-IC bypass is also necessary for specific types of aneurysms, including fusiform and thrombotic, as well as in the dissection of aneurysms that are difficult to clip.

Involuntary movement is a rare clinical manifestation of transient ischemic attack (TIA). However, limb-shaking TIA is well described presentation of carotid occlusive disease. We present the case of a patient who developed limb-shaking TIA associated with high-grade stenosis of middle cerebral artery (M1), which was treated with percutaneous transluminal angioplasty (PTA). The procedure was performed successfully without complication and the symptom disappeared immediately after the procedure. The patient remained free of symptoms at the 38-month follow-up. There was no tendency of restenosis of M1. In this case, PTA was technically feasible and beneficial for limb-shaking TIA with M1 stenosis. Limb-shaking TIA can be a symptom of high-grade stenosis of M1.

Aplastic or twig-like middle cerebral artery (Ap/T-MCA) is a rare anatomical anomaly, which can be associated with intracranial hemorrhage and cerebral ischemia. A 52-year-old woman who presented with sudden headache was admitted to our hospital. Computed tomography (CT) and magnetic resonance imaging showed no abnormality; however, magnetic resonance angiogram revealed an occlusion or severe stenosis in the left middle cerebral artery. Three-dimensional CT angiography demonstrated severe stenosis in the left middle cerebral artery. The patient was discharged without any neurological deficit; however, she subsequently complained of temporary weakness in the right hand. It was possibly due to a transient ischemic attack; therefore, cilostazol 200 mg/day was administered for prevention of cerebral ischemia. Single photon emission computed tomography(with or without administration of acetazolamide)showed neither significant decrease in the cerebral blood flow nor cerebrovascular reactivity; hence, surgical revascularization was not performed. However, two years after the initial admission, she was urgently admitted to our hospital with sudden headache and nausea followed by aphasia and weakness of the right extremities. CT images showed diffuse subarachnoid hemorrhage and intracerebral hemorrhage in the left temporo-parietal lobe. Cerebral angiography revealed that the left middle cerebral artery was Ap/T-MCA without cerebral aneurysms. The patient was treated conservatively, and she eventually recovered without any neurological deficit except mild aphasia. Since Ap/T-MCA is associated with both hemorrhagic and ischemic stroke, antiplatelet therapy should be administered carefully. Moreover, it is necessary to consider extracranial-intracranial bypass to reduce hemodynamic stress on the abnormal vessels.

Symptomatic cervical carotid artery stenosis is one of the common causes of ischemic stroke in octogenarians. The records for 90 consecutive patients with symptomatic cervical carotid artery stenosis treated by carotid endarterectomy(CEA)were analyzed retrospectively. The patients were divided into two groups:21 patients aged 80 years or over and 69 patients aged less than 80 years. CT angiography revealed that ulcer formation was significantly more common and the length of carotid artery stenosis was significantly greater in the octogenarians. Histological examination of the plaque revealed no significant difference between the two groups in terms of ulcer formation, lipid content, and intraplaque hemorrhage. However, all three of these pathological findings were present in a significantly higher number of octogenarians. No significant difference was observed for new ischemic lesions on diffusion-weighted MR imaging, neurological complications, or cardiac and pulmonary complications. However, treatment with an albumin preparation and loop diuretics was significantly more common in octogenarians after CEA. The present study suggests that with careful postoperative management CEA can be safely performed in symptomatic patients aged 80 years or over with almost the same risk as that for patients aged less than 80 years.

We report an 82-year-old man with crescendo brainstem TIA and left upper-limb ischemia due to the left proximal subclavian artery stenosis. Angiography revealed that the left proximal subclavian artery was stenotic. The right vertebral artery was considered to be aplastic or occlusive. Neurosonography, especially the echo-Doppler study of the left vertebral artery, showed that the subclavian artery steal phenomenon did not occur. This study has enabled us to opt for axillo-axillary bypass. We preferred to avoid percutaneous transluminal angioplasty in order to avoid the risk of embolization. The patient received the axillo-axillary bypass operation. He has been free of TIAs and the left upper-limb ischemia since the surgery. We have evaluated his blood circulation fully, by comparing his state before and after the axillo-axillary bypass grafting.

Since October 1967 we have performed 76 microsurgical STA--cortical MCA bypass operations. Recently we have had two cases, who died from intracerebellar hematoma following bypass operation. Intracerebellar hematoma is reported primarily due to hypertension (50-80%), and to comprise 10% of all spontaneous intracranial hematomas. Diagnosis of this lesion is frequently missed but can be made by the typical clinical picture (respiratory irregularity, pinpoint pupils, absence of oculovestibular responses, loss of consciousness), and the CT-Scan. If the correct diagnosis is made and operation promptly performed, many patients with subacute or acute intracerebellar hematoma can be saved. The 2 cases presented here had a history of hypertension and anticoagulation (including Colfarit), but had sustained the bypass operation well and showed no neurological deficit immediately after the operation. They had received Rheomacrodex intra- and postoperatively. Quite soon postoperatively, however, the systolic blood pressure rose to 210 mmHg and the patients complained of severe headache. They were treated symptomatically with analgesics and antihypertensive drugs. A short time later they became comatose and died. In order to prevent this complication after bypass surgery, postoperative management of hypertension is mandatory. The combination of antithrombic agents, Colfarit and Rheomacrodox, might have played a role in inducing the hemorrhages. Furthermore strong analgesics should be withheld to prevent their masking neurological deterioration. Intracerebellar hematoma must always be considered in hypertensive or anticoagulated patients, especially because it can be cured with prompt diagnosis and operative treatment.

A rare case with the episodes of vertebrobasilar TIAs which were caused by carotid ulcerative lesion and by persistence of proatlantal intersegmental artery is reported. This 69-year-old man was admitted on 14th Feb. 1985 with complaints of three attacks of vertigo, diplopia, nausea, vomiting and dysequilibrium lasting about 1 hour. His past history and family history were unremarkable. On admission, physical and neurological examinations revealed nothing particular, except bilateral carotid bruits. On the right side, innocent low pitched bruit was detected, however on the left side, carotid bruit was high pitched and was regarded as pathological. Blood pressure was 180/80 mmHg. Pulse rate was 66/min and cardiac arrhythmia was not detected by EKG. He also had no history of cardiac arrhythmia as mentioned above. CT scans and MRI showed only mild brain atrophy and no brain stem nor cerebellar lesions. Left carotid angiogram revealed ulcerative lesion of the common carotid bifurcation which was compatible with high pitched bruit. And at the level of the C2 vertebra, persistent proatlantal intersegmental artery originated from the left internal carotid artery which, after running upward, joined to the horizontal portion of the left vertebral artery above the atlas. Internal carotid and the vertebrobasilar vasculature beyond the proatlantal intersegmental artery were normal except slight irregularity of carotid siphon. Right carotid and vertebral angiograms revealed no abnormality and basilar artery was opacified clearly again via right vertebral artery.(ABSTRACT TRUNCATED AT 250 WORDS)

Delayed neurologic deterioration from vasospasm remains the greatest cause of morbidity and mortality following subarachnoid hemorrhage. The authors performed superficial temporal artery-middle cerebral artery bypass in three patients with symptomatic vasospasm and studied its effects on cerebral hemodynamics. All three patients responded neurologically to the bypass procedure within 24 hours. The average cerebral blood flow in the region supplied by the spastic middle cerebral artery increased from 40 ml/100 g/min to 49 ml/100 g/min after bypass. Angiography disclosed dilatation of donor vessels during the peak of spasm, followed by their decrease in caliber coincident with alleviation of vasospasm. The authors conclude that superficial temporal artery-middle cerebral artery anastomosis for the management of symptomatic vasospasm can increase blood flow in the ischemic region supplied by the spastic artery. This management strategy may lower the incidence of death and disability from vasospasm after subarachnoid hemorrhage.

A patient in whom vasospasm of not only intracranial but also extracranial arteries was demonstrated after the rupture of an intracranial aneurysm was reported. A 55-year-old male was admitted with a ruptured left IC-PC aneurysm. Intracranial direct operation and continuous ventricular drainage were performed 33 hours after the rupture. Six days after the surgery, right hemiparesis and consciousness disturbances developed. Angiography revealed severe vasospasm of intra-and extracranial arteries, especially branches of the external carotid artery. The symptoms improved markedly following the superior cervical ganglionectomy and perivascular sympathectomy of cervical internal carotid artery on the left side. Vasospasm of the external carotid system, which has not been reported, was further investigated angiographically in 23 patients who had vasospasm of the intracranial arteries after aneurysm rupture. In about 50% of these patients was found vasospasm of the external carotid system too. These changes were not found in control cases without vasospasm of the intracranial arteries. Pathogenesis of the vasospasm of the external carotid system was discussed with particular emphasis on the relationship with the sympathetic nerves.

Diltiazem or papaverine hydrochloride as vasodilators were polymerized with silicon polymer (MDX-4-4210: Dow Co.). The silicon pellets containing the drugs were placed in cisternal drainage tubes made of silicon, and used for the continuous cisternal drainage after the operations of ruptured cerebral aneurysms. This system was tentatively termed 'pellet-cisternal-drain; PCD'. The rate of diffusion of the drug from the pellets was examined in 30 patients who underwent surgery for ruptured cerebral aneurysms in the acute phase on the 0-4th postical days. 73.3% of patients had severe subarachnoid hemorrhage as group 3-4 in Fisher's classification in CT scan. The concentration of either drug in the cerebrospinal fluid on the 2nd to 3rd postoperative days reached the level of the maximum concentration obtained after bolus injection, and the level on the 5th to 10th postoperative days was similar to that observed several hours after bolus injection. The data showed that the sustained release pellet can act as a vasodilator, and its effects on cerebral vessels after an episode of subarachnoid hemorrhage continue for 2 to 3 weeks. All patients except one showed excellent results and returned to normal life.

Long-term outcome and recurrence rate were discussed in 96 patients of TIA out of 792 of cerebral ischemic disease who were admitted to our hospital during the past 11 years. They all had had attacks in the territory of internal carotid artery. Ninety-three patients could be interviewed finally. They included 63 males and 30 females and the age ranged from 36 to 88 years with an average of 60.5 years. The follow-up period ranged from 4 months to 8 years and 10 months with an average of 3 years and 1 month. Cerebral angiography was performed in 88 patients of them and revealed 16 patients of internal carotid artery stenosis, 12 patients of middle cerebral artery stenosis, 19 patients of severe cerebral arteriosclerosis and 41 patients of normal findings. CT scan was performed in 88 patients and showed abnormal findings in 12 patients. Eleven patients of them had lacunar infarction. Twenty-four patients of arterial stenosis (14 patients of internal carotid artery stenosis and 10 patients of middle cerebral artery stenosis) had surgical treatment of STA-MCA anastomosis (the superficial temporal artery-the middle cerebral artery) and carotid endarterectomy because they were considered to be cause of TIA. The other 69 patients were treated conservatively mainly with antiplatelet therapy. Four of 24 surgical treated patients developed another attack of cerebral ischemia thereafter, 2 patients had TIA of the contra-lateral hemisphere, one had cerebral infarction in the territory of posterior cerebral artery and the rest had lacunar infarction in the contra-lateral basal ganglia.(ABSTRACT TRUNCATED AT 250 WORDS)