Forty patients with cranial bone defects after craniectomy underwent extensive cerebrospinal fluid (CSF) hydrodynamic investigations by means of a CSF infusion test before and after cranioplasty. The results of these investigations were related to the clinical signs of the patients before and after cranioplasty and to the size and location of the skull bone defect. Twenty-two patients were considered to have "the syndrome of the trephined" (ST). The remaining patients were either free of symptoms or had symptoms not related to ST. CSF hydrodynamic variables that were changed before and normalized after cranioplasty include the following: Resting pressure, sagittal sinus pressure, buffer volume, elastance at resting pressure and pulse variations at resting pressure. The changes were statistically significant mainly in ST patients who were also relieved of their symptoms after cranioplasty.

No abstract

A case is reported of a giant aneursym of the intracavernous portion of the left internal carotid artery that was treated initially with a left common carotid artery ligation. Six months later the aneurysm was partially removed. During this time the development and evolution of thrombus formation, a serpentine channel, and a hypervascular capsule was easily followed with recreated computerized tomography and angiography of the aneurysm.

Radiographically verified spontaneous disappearance of medium-sized arterial cerebral aneurysms is seldom reported, and only three times in connection with antifibrinolytic therapy (EACA). In our clinic repeat angiograms have shown non-filling of the aneurysms in three patients during treatment with tranexamic acid (AMCA) two, three, and four weeks respectively after primary bleeds. Initially, all three patients had severe radiological vasospasm associated with neurological deterioration. Follow-up angiograms have demonstrated partial reappearance of the aneurysm after one month in one patient and complete disappearance of the aneurysms in the other two patients after 9 and 22 months respectively. In two cases occlusion of cerebral arteries occurred. With regard to the higher risk of severe vasospasm and occlusion of cerebral arteries in our opinion it should not be a therapeutic goal to try to achieve a thrombosis of a ruptured aneurysm with antifibrinolytic drugs. The reason for spontaneous aneurysm thrombosis during treatment with AMCA may be a local inhibition of plasminogen activators in and around the aneurysm wall. It may also be related to the sympathomimetic property of the drug, with vasospasm and a subsequent flow-reduction inside the aneurysm or a possible interaction with other drugs and substances.

A randomized controlled clinical trial was carried out to study the effect of tranexamic acid (AMCA, Cyklokapron; AB Kabi, Stockholm, Sweden) in the prevention of early rebleeding after the rupture of an intracranial aneurysm. The incidence of vasospasm, hydrocephalus, cerebral ischemic and thromboembolic complications, morbidity, and mortality was also evaluated. The series comprises 59 patients, 30 treated with tranexamic acid and 29 controls. The treatment was stopped if there was rebleeding, operation, or discharge from the hospital. There were 6 recurrent hemorrhages in 6 patients in the tranexamic acid-treated group and 11 recurrences in 7 patients in the control group. Recurrent hemorrhages occurred later in tranexamic acid-treated patients than in controls. Five patients in each group died from rebleeding. Five additional treated patients and 2 controls died from cerebral ischemic dysfunction. The results suggest that tranexamic acid may protect patients with ruptured aneurysms from rebleeding for 1 or 2 weeks, but that it also may produce cerebral ischemic complications.