With the cooperation of 60 neurosurgical centers in Japan, a prospective randomized placebo-controlled double-blind trial of a new calcium antagonist AT877 (hexahydro-1-(5-isoquinolinesulfonyl)-1H-1,4-diazepine hydrochloride, or fasudil hydrochloride) was undertaken to determine the drug's effect on delayed cerebral vasospasm in patients with a ruptured cerebral aneurysm. A total of 276 patients, who underwent surgery within 3 days after subarachnoid hemorrhage (SAH) of Hunt and Hess Grades I to IV, were entered into the study. Nine patients were excluded because of protocol violation. The remaining 267 patients received either 30 mg AT877 or a placebo (saline) by intravenous injection over 30 minutes, three times a day for 14 days following surgery. Demographic and clinical data were well matched between the two groups. It was found that AT877 reduced angiographically demonstrable vasospasm by 38% (from 61% in the placebo group to 38% in the AT877 group, p = 0.0023), low-density regions on computerized tomography associated with vasospasm by 58% (from 38% to 16%, p = 0.0013), and symptomatic vasospasm by 30% (from 50% to 35%, p = 0.0247). Furthermore, AT877 reduced the number of patients with a poor clinical outcome associated with vasospasm (moderate disability or worse on the Glasgow Outcome Scale at 1 month after SAH) by 54% (from 26% to 12%, p = 0.0152). There were no serious adverse events reported in the AT877 group. This is the first report of a placebo-controlled double-blind trial that has demonstrated a significant reduction in angiographically revealed vasospasm by intravenous drug therapy.

Saccular aneurysms arising at locations other than at arterial divisions are extremely rare. The authors describe eight such aneurysms that protruded from the dorsal wall of the internal carotid artery (ICA) and were unrelated to any arterial junction. Radical surgery was performed in all eight cases. The aneurysms were saccular with a fragile wide or semifusiform neck. Intraoperative rupture occurred in three cases. From this experience, it is emphasized that these unusual protruding aneurysms of the dorsal ICA should be clipped with the clip blade parallel to the parent artery. In addition to clipping, complete wrapping with fascia or Bemsheet (cellulose fabric) is often advisable to prevent slippage of clips or postoperative rupture of residual aneurysm.

In a series of 32 surgical cases of carotid-ophthalmic artery aneurysm, seven of the lesions were located in the "carotid cave." This special type of aneurysm is usually small and projects medially on the anteroposterior view of the angiogram. At surgery, it is located intradurally at the dural penetration of the internal carotid artery (ICA) on the ventromedial side, appears to be buried in the dural pouch (carotid cave), and is often difficult to find, dissect, and clip. The aneurysm extends into the cavernous sinus space, and the parent ICA penetrates the dural ring obliquely. An ipsilateral pterional approach was used in all 32 cases, and ring clips were used exclusively because the aneurysms were located ventromedially. Clipping was successful in five cases. All patients returned to their preoperative occupation, although vision worsened postoperatively in two cases. The technical steps required for successful obliteration of this aneurysm are summarized as follows: 1) exposure of the cervical ICA; 2) unroofing of the optic canal and removal of the anterior clinoid process; 3) exploration of the ICA around the dural ring and opening of the cavernous sinus; 4) direct retraction of the ICA and optic nerve; and 5) application of multiple ring clips to conform to the natural curvature of the carotid artery; a curved-blade ring clip is especially useful. The relevant topographic anatomy is discussed.

We showed that normovolaemic induced hypertension therapy was effective in reducing ischaemic symptoms attributed to cerebral vasospasm in 41 patients after subarachnoid haemorrhage. By inducing hypertension to 25% to 50% above normal systolic arterial blood pressure, we observed that in 17 of 24 cases (71%) neurological deficits improved. In four cases of haemorrhagic infarction, the blood pressure rose to over 50% of systolic arterial pressure, and a low density area was confirmed on computerized tomography (CT) scan prior to vasospasm. Induced hypertension was therefore not considered when a low density area was revealed on CT scan. Restriction of fluid input is usually a factor in producing hypovolaemia after a neurosurgical operation. Intravascular volume expansion has been reported effective in reversing ischaemic deficits. However, according to Poiseuille's equation, increasing blood volume to a state of hypervolaemia can not enhance flow. The cerebral blood flow (CBF) was raised by increasing perfusion pressure, reducing viscosity, or increasing blood vessel diameter. Intravascular volume expansion elevates not only systemic arterial pressure, but also pulmonary artery wedge pressure over 18 mmHg and cardiac index over 2.2. Since pulmonary oedema and congestive heart failure may develop, one should monitor haemodynamic parameters with the Swan-Ganz catheter as a preventive measure. We emphasize that normovolaemic induced hypertension, maintaining haemodynamics subset 1 of the comparable haemodynamic subsets, is effective in raising perfusion pressure of CBF.

Subdural fluid collections appeared in 15 cases (39%) after removal of 38 intra- and paraventricular tumours in the third or lateral ventricle through 18 frontal and 20 parietal transcortical approaches. Transient fluid collections which disappeared within 2 weeks occurred in 6 cases (16%) and persistent ones in 9 cases (24%). Four of the 9 cases (11%) of collections required surgical treatment because of positive clinical signs and symptoms. Two cases had expansive fluid collections and the other two contained subdural haematomas at surgery. The risk factors likely to contribute to a persistent collection were preoperative ventriculomegaly (frontal horn index greater than 0.38) and a frontal transcortical approach. A symptomatic collection should be considered as a potential complication of the transcortical approach to intraventricular tumours and some methods should be devised to prevent it when intra- or paraventricular tumours with ventriculomegaly are removed.