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.
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.
A 26-year-old male was injured in a motorcycle accident and arrived unconscious at a local general hospital. Lack of improvement despite intensive care prompted his referral to the neurosurgical department, approximately 10 hours after the accident. On neurological examination his Glasgow Coma Scale score was 8, and mild right hemiparesis and right radial nerve palsy were noted. There was no skull fracture. Computed tomography disclosed intraventricular hemorrhage and small hemorrhagic foci in the prepontine area and the border between the gray and white matter. No hemorrhage was demonstrated in the corpus callosum. Magnetic resonance imaging (MRI) was performed 3 weeks after admission with a 0.5-tesla resistive Vista magnetic resonance scanner. The inversion recovery technique was used, with a repetition time (TR) of 2100 msec, an inversion time of 500 msec, and an echo time (TE) of 40 msec, for T1-weighted images. The spinecho technique was used, with a TR of 2000 msec and a TE of 80 msec, for T2-weighted images. In the body and splenium of the corpus callosum, T1-weighted images showed a spotty area of low signal intensity with an irregular margin; this area was of high signal intensity on T2-weighted images. On repeat MRI performed 4 months after injury, T1-weighted images showed, in the same region, granular low signal intensity, while T2-weighted images showed high signal intensity. The MRI findings in the subacute and chronic stages of diffuse axonal injury are discussed.
