Although the occurrence of so-called late cerebral vasospasm after subarachnoid hemorrhage (SAH) due to ruptured cerebral aneurysm is well-known, its etiology still remains obscure. The authors previously reported that C1q (q-subfraction of the first complement component) binding substance, formed in blood-stained cerebrospinal fluid, might trigger the activation of the complement system in the subarachnoid space and develop cerebral vasospasm. This time, the authors investigated constricted cerebral arterial walls after SAH by immunofluorescent technique to see what immunological changes they were subject to, following the activation of the complement system and in the course of the possible production of chemical mediators (anaphylatoxin, etc.). One hundred and thirty-eight major intracranial arterial specimens obtained from patients with and without central nervous system disorders at autopsy were examined for deposits of immunoglobulin G (IgG), immunoglobulin A (IgA), immunoglobulin M (IgM), the third complement component (C3) or fibrinogen in the arterial walls. In cases of SAH with definite or probable vasospasm, deposits of both IgG and C3 in the arterial media were observed in 74% of the arterial specimens examined. However, these deposits could not be found at all in the patients who died within 48 hours after aneurysmal rupture. The frequency of the deposits of both IgG and C3 was 42% in hypertensive intracerebral hematoma, 44% in cerebral infarction, 42% in brain tumor, 75% in meningoencephalitis. Deposits of IgA, IgM or fibrinogen were also observed in the media, but with much less frequency than those of IgG or C3 in all cases. The significance of deposits of IgG and C3 in the media found in cases with late vasospasm after SAH is unclear at present, but it is thought that they represent an antibody to degenerated arterial smooth muscles due to constriction and complement bound to the antibody. In other words, it is highly likely that those deposits indicate arteritis or an inflammatory process in the arterial wall.

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Tissue polypeptide antigen (TPA), a tumor associated antigen and first described in 1957 by Björklund et al., is a surface antigen and has an approximate molecular weight between 20, 000 and 45, 000. TPA is a single-chain polypeptide having 4 subfractions, and is released from propagating cells. TPA in serum, cerebrospinal fluid (CSF) or intratumoral cystic fluid of patients with brain tumor was assayed by the radioimmunoassay technique and found quite useful as a brain tumor marker. TPA level in serum was significantly elevated in patients with glioblastoma, metastatic brain tumor, malignant lymphoma and pituitary adenoma. TPA was elevated in malignant tumors, probably because more TPA was produced in propagating tumor cells. However, elevated TPA levels were also found in non-malignant diseases, for example, hepatitis and infection. Therefore, elevation of the TPA level should be considered indicative of a brain tumor when other diseases can be excluded. TPA in serum was found useful for differentiating glioblastoma and metastatic brain tumor. If TPA level in serum exceeded 150 U./l, it was more likely a metastatic brain tumor. TPA level in cystic fluid was elevated in metastatic brain tumor, craniopharyngioma and pineal teratocarcinoma, and it was suggested that TPA was increased in tumors of epithelial origin. TPA in the CSF was not noticeable in normal CSF, but was markedly elevated in meningeal carcinomatosis. TPA in CSF was positive in 13 (81%) out of 16 patients of brain tumors with proven leptomeningeal dissemination, and leptomeningeal dissemination was verified in 13 (68%) out of 19 patients with positive TPA in CSF. TPA in CSF is considered quite useful in clinical observation of brain tumors.

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The authors investigated the distribution and range of ependymal cell defects and dynamics of these defects in a group of patients with non-communicating hydrocephalus and in the controls without central nervous system lesions. Ependymal defects in the control group were found at specific sites in the lateral ventricles, namely, roof and medial wall of the anterior horn, lateral wall of the posterior horn, and ventral wall of the inferior horn and these defects occupied a wider range in the hydrocephalic group. The thickness of the ventricular wall in the hydrocephalic group was greater than that in the controls, due to subependymal glial proliferation, and this increase was especially marked in the area of ependymal defects. From the findings at the junctional areas of the ventricular wall with and without the ependymal cells, it was suggested that proliferation of the subependymal glial fibers was a major factor in the spread of the defects. In cases with edema in the periventricular white matter of the hydrocephalic group, the distribution of edema did not match the area of ependymal cell defects and was more localized than the defects.

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In order to elucidate the mechanism of the normal pressure hydrocephalus (NPH), results of continuous intracranial pressure monitoring were analyzed.
The subjects were 37 patients, consisting of 23 with NPH symptoms and 14 without, in whom continuous intracranial pressure monitoring was performed. In patients with cerebral aneurysm the monitoring was performed through the ventricular drainage within one week after operation. In 6 of these patients, the monitoring was repeated after the recurrence of NPH symptoms. Shunt operations were carried out in 16 patients. The pre and post-operative sizes of the ventricle were compared with each other by computerized tomography (CT) scan. The results indicated that 19 patients manifested pressure waves, and 8 were without NPH symptoms. No difference was found between the results of two monitorings in any of the 6 aneurysmal patients. The shunt was effective in all 6 patients with pressure waves, and in 4 out of 10 patients without pressure waves. Reduction of the ventricular size was observed in 6 patients by CT scan, 5 of whom had shown pressure waves. CT scan disclosed frontal damage in most of the NPH patients. Thus, the pressure wave frequently appeared even in patients without NPH symptoms. Though the efficacy rate of shunt operation wa: higher in patients with a pressure wave, some effects were observed even in the patients without z pressure wave.
The pressure wave might not indicate an abnormal circulation or absorption of cerebrospina: fluid but the functional capacity of the brain itself. Occurrence of NPH appears to be dependent tc some extent on factors such as the severity and site of the brain damage and the preexisting functional capacity of the brain itself as well as the circulation of cerebrospinal fluid.

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A new flexible detachable balloon apparatus has been developed. It consists of three parts; a silicone balloon, a teflon introducing catheter, and stainless steel coaxial catheter. A coaxial catheter with a stainless steel tubular spring is used to afford a higher degree of flexibility for better navigation in the various angulations of the intracranial vasculature. A miter valve is used as a self-sealing system at the base of the balloon.
Twelve patients with carotid-cavernous fistulas (CCF) (traumatic: 10 cases, spontaneous: 2 cases) were treated using two types of detachable balloon systems, namely, Debrun's latex balloon and the authors' newly developed silicone balloon. Good results were obtained in 11 cases, although four patients required occlusion of the carotid artery. The carotid blood flow was preserved in 8 (67%) out of 12 cases. In cases of total steal shown by carotid angiography, the treatment was more difficult and more than one balloon was sometimes necessary to occlude the fistula. The neurological complications were a case of oculomotor palsy and one of visual impairment, both cases recovering within one week. Postoperative angiography revealed carotid stenosis in one case and a venous pouch in two cases.
The detachable balloon techniques should be the standard form of treatment for high flow CCF, particularly if traumatic in origin, when adequate experience has been obtained by the radiologicalneurosurgical team.

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Since 1981, nine patients with carotid-cavernous fistula were treated by an intravascular occlusion technique. In these cases detachable balloon catheters were chosen for the treatment, using techniques almost identical to those described by Debrun. The balloon was introduced by the transcarotid route, inflated with metrizamide at a concentration of 240 mgI/ml, and detached without hardening materials. During the procedure, a Doppler ultrasonic flow detector was utilized for constant monitoring of the orbital bruit.
Internal carotid artery patency was preserved in 6 cases. In these cases, abducens nerve palsy disappeared within a week, whereas oculomotor nerve palsy persisted for two to three weeks. In two of the three remaining cases, internal carotid artery was permanently occluded with detachable balloons. Before the permanent occlusion, the intravascular occlusion test was performed by interrupting the carotid flow while monitoring the patient's neurologic signs. No ischemic sequelae were encountered. In the third case, no occlusion of either the fistula or internal carotid artery was accomplished. Thus, 8 of the 9 patients were considered to be successfully treated. Two patients, in whom carotid-cavernous fistula was selectively occluded, experienced a transient hemiparesis. In the eight successfully treated patients no recurrent symptoms were observed during the follow-up period, ranging between 7 and 26 months.
In conclusion, the detachable balloon catheterization technique proved very valuable in treating traumatic carotid-cavernous fistula by the intraarterial route.

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Because of the hazard of further intracranial hemorrhage, heparin was not used in cases of disseminated intravascular coagulation (DIC) following head injury. A low dose (6, 000-10, 000 U./day) of heparin, however, could be safely administered without any risk of bleeding and was effective in the early treatment of the authors' series.
Seven patients with DIC that occurred after severe head injury were studied. Of these, three had acute subdural hematomas, three had combined intracranial hematomas and one presented with cerebral contusion. All seven patients received either evacuation of intracranial hematoma or resection of contused brain. DIC was diagnosed within the first 48 hours of injury in five patients and 4 days after injury in two. At the diagnosis the platelet counts were decreased (4.2-9.4×10⁴/mm³) and FDP value was increased in all the patients. Hypofibrinogenemia was shown in four patients. Gastrointestinal bleeding was found in four patients, delayed intracerebral hematomas in two, and intracranial rebleeding in two. A low dose of heparin (6, 000-8, 000 U./day) was administered to six patients following the DIC diagnosis. The treatment was successful without any side effects, such as a bleeding tendency, in four patients. In two of these four patients, gastrointestinal bleeding improved and the delayed or recurrent intracranial hematoma did not increase in three. Two patients died. One died from massive gastrointestinal bleeding. In this patient the coagulation studies were first performed 4 days after injury and the treatment in this instance started too late to improve the DIC.
The present study suggests that the administration of a low dose heparin may be an effective therapy for patients with DIC following head injury.

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Hemodynamics of 7 diabetes insipidus (DI) patients secondary to severe head injuries were examined. In DI, without administration of Pitressin® (vasopressin), systemic vascular resistance (SVR) and pulmonary vascular resistance (PVR) were markedly decreased while central venous pressure (CVP) and pulmonary capillary wedge pressure (PCWP) were rather low. In DI with administration of Pitressin®, mean arterial pressure (MAP), SVR, and PVR were significantly increased. Cardiac index (CI) was decreased, but not significantly. Changes of CVP and PCWP were not significant. It seems that the elevation of MAP is caused by the increase of SVR and that Pitressin® acts mainly on the resistance vessel, and not on the capacitance vessel.
Until recently, it was believed that physiological function of antidiuretic hormone (ADH) is diuresis and that the pressor effect of ADH plays no evident role under physiological conditions. But recent reports from several different laboratories indicate that ADH participates in the normal daily regulation of arterial pressure. The results of this study seems to support this hypothesis.
In DI patients, SVR is markedly decreased and the hemodynamics are rather hypervolemic. In this state, Pitressin® causes decrease of urine volume and increase of body fluid. In the administration of this drug, the possibility of edema of the brain, lung and other organs must be taken into consideration. Pitressin® also causes vasoconstriction of coronary vessels and increase of oxygen demand of myocardial muscle by increase of afterload due to elevated SVR and possibly myocardial ischemia.

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Among 199 cases with cerebral infarction 23 cases ( 11.6%) developed hemorrhagic infarction on repeated computerized tomography (CT) scans. The hemorrhagic pattern was classified into 3 groups according to the CT findings; massive type (12 cases), partial type (6 cases), and scattered type (6 cases). Massive type hemorrhagic infarction was accompanied by cerebral swelling and mass effect and was observed, as a rule, within 4 days from clinical onset of the infarction, although there were a couple of exceptional cases, who developed hemorrhage over 2 weeks after the onset. Scattered type hemorrhagic infarction did not show mass effect and was always found after more than 8 days from the onset and no clinical evidence of symptomatic deterioration was encountered. Partial type hemorrhagic infarction appeared from within 4 days to 3 weeks after the onset. Mass effect was exceptional and symptomatic change was infrequent. Overall mortality of the non-hemorrhagic infarction was 15.3%, whereas it was 13% with hemorrhagic infarction, and the mass effect was the principal cause of mortality. Cardiac diseases were found to be the main risk factor in developing hemorrhagic infarction, while hypertension and diabetes mellitus did not appear to be significantly related to hemorrhagic changes of the cerebral infarction. Aspirin and other anticoagulant medication showed no significance either in this study.
It is suggested that the causes of hemorrhage are different in massive type and partial or scattered type hemorrhagic cerebral infarctions.

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Occipital artery posterior inferior cerebellar artery anastomosis seems to be less effective for ischemia of the rostral brain stem. The authors performed superficial temporal artery superior cerebellar artery (STA-SCA) anastomosis for the rostral brain stem ischemia with excellent results.
The patient, a 52-year-old female, was admitted because of vertigo and fainting attacks induced by turning the head to the left. She had been on antiplatelet therapy with the stellate ganglion block without improvement. Cerebral angiography revealed severe stenosis of the right vertebral artery in the proximal portion, complete obstruction of the left vertebral artery at its origin, no significant collateral circulation to the upper basilar artery through posterior communicating artery, and stenosis of bilateral internal carotid arteries in the cervical and siphonic portions. Regional cerebral blood flow study by ¹³³Xe showed decreased blood flow in the bilateral occipital lobes. The STA-SCA anastomosis was performed through the subtemporal approach with spinal drainage and intravenous mannitol administration. Postoperatively, the vertigo and fainting attacks disappeared. However, transient sensory aphasia was noted along with a intracerebral hematoma of the temporal lobe. Postoperative cerebral angiography demonstrated excellent visualization of the bilateral superior cerebellar arteries and the ¹³³Xe study showed improvement of the occipital blood flow.

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A 43-year-old woman presented with ataxia and right-sided cranial nerve palsies. Ten years prior to admission, she was operated for a right cerebellopontine (CP) angle epidermoid. Computed tomography (CT) scan, using GE 9800, showed a large high-density mass without enhancement effect in the right CP angle. The density ranged between 60 and 66 Hounsfield units. Surgery revealed a recurrent epidermoid cyst containing a viscid, dark-green fluid without any cholesterol crystal or clots. Chemical analyses of the cyst content disclosed protein and lipid concentrations 25.6 g/dl and 1, 275 mg/dl, respectively. Ion chromatography revealed only a trace of metal ions. Thin layer chromatography of the lipids showed high phospholipids and low triglyceride, indicating that the high density in this case was not caused by an intratumoral hemorrhage but by desquamation of the squamous epithelium with accumulation of sloughed debris.
Two cases of high-density epidermoids subjected to protein analysis were found in the literature. From these data including the authors' it was shown that CT density correlated well with the protein concentration.

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Two patients with abdominal pseudocysts as a complication of peritoneal shunt were reported and a review of the literature relating to this complication was presented.
Each patient had a ventriculo-peritoneal shunt 3 years previously for normal pressure hydrocephalus. Vomiting and abdominal distention were noted. There was no symptoms or signs of increased intracranial pressure. One patient, Case 1, had a left epidural abscess and one previous shunt revision. The other, Case 2, had no history of prior abdominal surgery or shunt infection and the shunt was converted to a ventriculoarterial diversion. Abdominal pseudocysts are not a common complicaton of peritoneal shunt procedures. In this clinic only 2 (0.9%) of 228 peritoneal shunts, which was performed for the treatment of normal pressure hydrocephalus in the past 5 years, developed this complication.
Forty-one cases of abdominal pseudocysts have been reported in the literature. All except one case had abdominal symptoms and/or symptoms of increased intracranial pressure on admission. The clinical signs developed as late as 5 years after catheter insertion, but frequently within 6 months. Associated shunt infection and previous intra-abdominal surgery appeared to be the most constant and related causes in the formation of the pseudocyst. Cerebrospinal fluid shunt into another cavity was considered to be the most reliable treatment of this complication.

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