The pathogenesis of symptomatic vasospasm following subarachnoid hemorrhage is still unclear. To clarify this, we analyzed changes of blood coagulation activities between 65 poor risk aneurysmal patients treated by a combination with ticlopidine, albumin and nicardipine (so called TAN therapy) and in 52 untreated patients with symptomatic vasospasm. The hypercoagulable state was scored according to the Disseminated Intravascular Coagulation (DIC) scoring system. Our clinical studies showed that severe SAH following aneurysmal rupture caused the hypercoagulable state. There were good correlations between the degree of hypercoagulation and the severity of the symptomatic vasospasm. TAN therapy reduced the DIC scores by antiplatelet agent and prevented the occurrence of the symptomatic vasospasm in severe SAH. These facts support the beneficial effects of TAN therapy in prevention of symptomatic vasospasm in severe SAH.
The dolichoectatic basilar artery was found in 23 cases during a 10-year period. The 19 males and 4 females ranged in age from 30 to 69 years (mean: 55 years). Hypertension was noted in 17 patients. In seventeen (74%) of the present cases this anomaly could be visualized with CT scan. Seven patients (30%) presented with pontine infarction, which was identified on CT scan in all cases. Vertebro-basilar insufficiency was found in four patients. One patient had transient ischemic attacks. There were facial spasms in four patients and impairment of the lower cranial nerves in one. One patient exhibited cerebellar hemorrhage. In two patients this anomaly was found incidentally. Associated intracranial aneurysms were identified in seven patients, including fusiform aneurysms in 4 and saccular aneurysms in 3. Three patients had an accompanying hydrocephalus. The dolichoectatic basilar artery is associated with various consequences especially in relation to the pathogenesis of brainstem infarction. When this anomaly is diagnosed by CT findings, even if it is clinically asymptomatic, it may be better to treat these patients with medical therapy used to prevent ischemic stroke.
Operative mortality and morbidity for intracerebral aneurysms has recently reduced with microsurgical technique, so more functional prognosis such as visual disturbance due to fundal hemorrhages has been studied. Here vitreous hemorrhage secondary to ruptured cerebral aneurysms (Terson syndrome) was attentioned. Three patients had more over 2 hours of unconsciousness and one patient experienced repeated episodes of subarachnoid hemorrhage within a week. This suggested rapid increased intracranial pressure resulted in vitreous hemorrhage through the venous congestion, which had been reported by Castrén (1963). All patients became blind because of severe vitreous hemorrhage. First case was followed over 7 years with only conservative therapy, but failed to improve. Another 3 cases regained visual acuity soon after operation. We emphasized vitreous hemorrhage as an important functional prognostic factor after ruptured intracerebral aneurysms and effective results of vitrectomy was showed.
In the pathogenesis of symptomatic vasospasm after subarachnoid hemorrhage (SAH), hyperactivity of the platelet, hypercoagulable state and impairment of cerebral microcirculation are considered to play important roles. The authors assess the incidence and clinical course fo symptomatic vasospasm in 88 aneurysmal patients with a uniform management protocol of antiplatelet, Ca blocking agent, and hypervolemic therapy. All patients received an antiplatelet agent (Ticlopidine) and a Ca blocking agent (Nicardipine) after surgery was performed within 48 hours following SAH. The flow velocity of the middle cerebral artery (MCA. FV) was measured after surgery by transcranial Doppler sonography (TCD), and when MCA. FV exceeded 120 cm/sec within seven days after SAH, hypervolemic therapy was started with albumin and Hetastarch. Nine patients (10%) developed characteristic signs and symptoms of symptomatic vasospasm in spite of these managements, but major neurological deficits from vasospasm occurred only in three patients (3%). In the total series, 70 patients (80%) had a good outcome and only five patients (5.7%) died of cardiac, pulmonary complication or sepsis. There were no fatal complications attributable to the antiplatelet agent, Ca? blocking agent or hypervolemic therapy.This management strategy may lower the incidence of death and disability from vasospasm after SAH.
The hydrocephalic oedema in normal-pressure hydrocephalus (NPH) was evaluated by measurement of the relaxation time of protons of the water molecules of brain tissue. Patients with NPH were divided into two groups: shunt responders and shunt non-responders. In the group of shunt responders both T1 and T2 of periventricular white matter were significantly prolonged compared to those of controls, and shortened after shunting. Both T1 and T2 of white matter were significantly longer than of gray matter, while a reversed relationship was seen in normal controls. However, in the group of shunt non-responders, T1 of white matter was significantly prolonged, while T2 of the same area not. There was no change in either T1 or T2 of this region after shunting. Both T1 and T2 were almost the same in white and gray matter in shunt non-responders. It is suggested that periventricular abnormalities seen in various diseases may be distinguished on the basis of the relaxation behavior of protons of tissue water.
Cavernous sinus thrombosis (CST) is classified into aseptic and septic types on the basis of its pathognosis. Aspetic CST includes the primary and secondary types, in which the former is an unknown etiology. We have recently experienced a rare case of aseptic primary CST which showed initially the intraorbital congestive symptoms. This 64 years male admitted to our clinic with the complaints of non-pulsatile exophthalmosis and conjunctival congestion of left eye. On admission, he showed mild external ophthalmoplegia and clinical evidence of intraorbital congestion (choked disc, retinal vein thrombosis, retinal hemorrhage) on the left side. The blood examination, including the thyroid studies, revealed no abnormal findings except for mild anemia and increased ESR. In carotid angiography, there was occlusion of Sylvian vein and cavernous sinus in the affected side. Orbital venography and retrograde jugular venography demonstrated the occlusion of superior ophthalmic vein, cavernous sinus and inferior petreous sinus in left side. CT scan revealed parasellar enhanced area in the normal pattern. Enhanced orbital CT scan revealed the hypertrophy of left external occular muscles and optic nerve with a tomogram of the dilatated superior ophthalmic vein. Aseptic primary CST was diagnosed on the basis of clinical course, cavernous sinography and CT findings.
