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We investigated the presence of soluble intercellular adhesion molecule-1 (sICAM-1) and soluble tumor necrosis factor receptor (sTNF-R) antigens in the CSF of patients with multiple sclerosis (MS) using a double-determinant ELISA. Patients with acute relapsing MS during an exacerbation (p0.001) and those with chronic progressive MS (p0.001) had significantly increased CSF levels of sICAM-1 compared with subjects with other neurologic diseases. CSF levels of sTNF-R were also significantly increased in patients with acute relapsing MS during an exacerbation (p0.001) and chronic progressive MS (p0.001) compared with subjects with other neurologic diseases. CSF levels of sICAM-1 and sTNF-R were positively correlated in patients with acute relapsing MS during an exacerbation (r = 0.81, p0.01) and chronic progressive MS (r = 0.86, p0.001). These results suggest that active immune reactions involving ICAM-1 and TNF-R production are present within the CNS and that both sICAM-1 and sTNF-R are important immunologic markers of the clinical activity of MS.

We investigated the cytotoxic effect of peripheral blood T cells on cerebral endothelium in patients with MS. We examined in vitro the damage to 51Cr-labelled dissociated human brain endothelial cells produced by mitogen-stimulated T cell lines from patients with MS and controls. Endothelial targets were lysed by T-lymphocytes from patients with acute relapsing MS during an exacerbation at every target-effector cell ratio tested compared with controls (P < 0.001). The percentage of endothelial targets lysed was not significantly increased by incubation with T cells from patients with acute relapsing MS in remission and chronic progressive MS, compared with that of normal subjects. Relapsing MS patients during an exacerbation had significantly higher interleukin-1 (IL-1)-alpha concentrations in cultures of targets with effector cells than normal subjects (P < 0.02). Experiments of major histocompatibility complex (MHC)-restricted cytotoxicity in MS demonstrated incomplete blocking of specific lysis by either anti-MHC class I or class II monoclonal antibody (mAb). These results indicate that cytotoxicity of T cells for cerebral endothelial cells may play a role in the initiation of immune response in acute relapsing MS during an exacerbation which appears to cause an increase in blood-brain barrier (BBB) permeability.

We evaluated the presence of soluble intercellular adhesion molecule-1 (sICAM-1) antigen in the sera of patients with multiple sclerosis and human T-lymphotropic virus type I (HTLV-I)-associated myelopathy (HAM) using an enzyme-linked immunosorbent assay. Patients with multiple sclerosis in the active phase had higher sICAM serum levels than did control subjects (p < 0.01). In addition, a significantly increased serum level of sICAM-1 was found in patients with HAM (p < 0.001). Furthermore, we found a positive correlation with HAM sICAM-1 and tumor necrosis factor-alpha levels in the sera of patients with multiple sclerosis in the active phase (r = 0.88, p < 0.01) and in those with HAM (r = 0.86, p < 0.01). These results suggest that serum sICAM-1 may be related to clinical activity in patients with multiple sclerosis and the detection of sICAM-1 could be useful as a marker of inflammatory disease.

Neuropeptide Y is distributed abundantly not only in the brain, but also in the gastrointestinal tract and suppresses intestinal muscle contraction in isolated muscle preparations. The purpose of the present study was to determine whether centrally administered neuropeptide Y modulated gastric emptying and intestinal transit in conscious rats. Graded doses of neuropeptide Y were administered intracisternally 1 min before ingestion of test meals through an oral tube. Four hours after ingestion of 60 Amberlite pellets, the rats were sacrificed and residual pellets in the stomach and the small intestine segments were counted to calculate the solid meal transit rate. The liquid meal transit rate was calculated 1 hr after 0.07% phenol red ingestion by determining the residual phenol red in the stomach and the small intestine segments. Neuropeptide Y elicited potent suppression of gastric emptying and intestinal transit of both solid and liquid meals. Pretreatment with propranolol antagonized, whereas phentolamine did not affect, the suppressive effect of central neuropeptide Y. Although carbachol blocked the effects of neuropeptide Y, neither atropine nor hexamethonium altered the actions of neuropeptide Y. In conclusions, centrally administered neuropeptide Y strongly inhibited gastrointestinal transit by stimulating a beta-adrenergic pathway.

To provide new insights into metabolic changes in the brain of patients with dementia, we performed in vivo localized proton magnetic resonance spectroscopy in nine patients with primary degenerative dementia and in three patients with normal-pressure hydrocephalus. We compared the results with those in 26 healthy volunteers. Measurements of regional cerebral blood flow were performed in seven patients by means of single photon emission computed tomography with amphetamine I 123 as a tracer. The magnetic resonance spectra constantly showed three major peaks corresponding to N-acetylaspartate (NAA), creatine and phosphocreatine (Cr), and choline-containing compounds. There were no age-related changes in the mean area ratio of NAA to Cr in neurologically normal volunteers. The NAA/Cr ratio was significantly reduced in patients with primary degenerative dementia. The reduction of the NAA/Cr ratio was observed even in dementia patients with no significant brain atrophy or reduction in regional cerebral blood flow. No significant reduction of the NAA/Cr ratio was seen in patients with normal-pressure hydrocephalus. The NAA/Cr ratio might reflect the number and/or activity of neuronal cells in the brain. Proton magnetic resonance spectroscopy may well provide a useful tool for early detection of, and further pathophysiological study of, primary degenerative dementia.

The production of interleukin-1 (IL-1) by peripheral blood mononuclear cells (MNC) was assessed in patients with relapsing multiple sclerosis (MS) in both the active and inactive phase, in chronic progressive MS patients, in other neurological diseases, and in healthy subjects. Production was determined by measuring the IL-1 concentration in cultures with MNC supernatants using enzyme-linked immunosorbent assay (ELISA). IL-1 in sera of MS patients and healthy subjects also was investigated. MNC IL-1 alpha production was significantly higher in MS patients (180.2 +/- 177.5 pg/ml) than in healthy subjects (66.2 +/- 66.0 pg/ml) (P less than 0.05). Relapsing MS patients in the active phase had significantly higher MNC IL-1 alpha concentrations (360.1 +/- 130.0 pg/ml) than normal subjects (P less than 0.001), but MNC IL-1 alpha production in patients with relapsing MS in the inactive phase (65.3 +/- 52.8 pg/ml) or chronic progressive MS (80.9 +/- 71.9 pg/ml) was not increased significantly. MNC IL-1 beta production in MS patients was not elevated significantly. IL-1 alpha and -1 beta were not detected in sera of MS patients. The correlation between increased IL-1 alpha production and the clinical course of MS suggests that activated MNC may play a role in the pathogenesis of MS.

We studied the efficacy of preischemic and postischemic systemic treatment with a new calcium antagonist nilvadipine in a permanent focal cerebral ischemia model of spontaneously hypertensive rats. Rats that underwent microsurgical middle cerebral artery occlusion were blindly assigned to a single intraperitoneal injection of nilvadipine (0.32 mg/kg) or the same amount of polyethylene glycol either 15 minutes before, immediately after, 1 hour after, or 3 hours after occlusion of the left middle cerebral artery. Neurologic conditions of rats were closely examined, and rats were killed 24 hours later. Removed brains were sliced coronally, stained with triphenyltetrazolium choloride, and the size of infarct was determined. Although no neurologic improvements were observed in the treated rats, the area of infarcts was significantly reduced in the groups treated before, immediately after, and 1 hour after occlusion of the middle cerebral artery. Treatment started 3 hours after occlusion was ineffective.

Somatosensory evoked potentials (SEPs) were monitored during 55 aneurysm procedures in 49 patients to investigate the relationship between central conduction time (CCT) and neurological status in the immediate postoperative period. Significant CCT prolongation was observed in 15 cases. The postoperative neurological status deteriorated in nine of the 15 cases, compared with three of 40 cases without appreciable CCT changes. This difference was significant at p less than 0.05. The CCT prolongation was ascribable to temporary vascular occlusion in half of the cases. Intraoperative SEP monitoring is useful in predicting neurological morbidities in the immediate postoperative period in patients with cerebral aneurysm.

A case of amelanotic malignant melanoma of the esophagus in a 76-year-old woman is reported. A whitish polypoid tumor, measuring 3 x 2 x 2.7 cm, surrounded by black pigmented mucosa, was detected in the middle intrathoracic esophagus. The tumor showed a lobulated surface lined by squamous cell layer, and had epithelioid and polyhedral cells forming alveolar clusters. Melanin pigments or stainability for the dihydroxyphenylalanine (DOPA) reaction were only observed in a few tumor cells. Junctional changes and mucosal melanosis, however, were found freely in the mucosa around the tumor. Many tumor cells showed a strongly positive immunohistochemical reaction for neuron specific enolase (NSE) and S100 protein. The patient died of widespread metastases six months after surgery. Further, a review of 106 reported cases of primary esophageal malignant melanoma, including 29 autopsies, was made; the melanomas were found to include 10 of amelanotic type, eight of which had been misdiagnosed at biopsy. Junctional changes could be found in the mucosa over or around the tumor, in four cases, and mucosal melanosis in one. Lymph node metastasis was the most frequently observed development at autopsy regardless of whether the tumor was amelanotic or melanotic. For correct diagnoses of melanomas of the amelanotic type, peripheral mucosal findings, such as junctional changes or melanosis, should be helpful; and, in order to obtain a good prognosis, a careful resection of the regional lymph nodes could prove valuable.

Magnetic resonance studies of 27 consecutive preoperative and 33 postoperative patients with cerebral aneurysm and subarachnoid hemorrhage were reviewed. Magnetic resonance imaging using a 0.5- or 0.22-Tesla unit was at least as accurate as computed tomography scan for detection of acute subarachnoid hemorrhage. Magnetic resonance imaging was superior to computed tomography scan for demonstrating blood in the ventricles or posterior fossa subarachnoid space, transependymal migration of the cerebrospinal fluid, and several kinds of iatrogenic intracranial pathologies in postoperative patients. Ischemic lesions, particularly fresh lesions caused by delayed cerebral vasospasm, were much better shown on magnetic resonance imaging than on computed tomography scan. Nonferromagnetic Sugita clips caused significant artifacts, but the area of artifacts was consistently smaller, and a reasonable evaluation of structures relatively closer to the clip was possible with magnetic resonance imaging rather than computed tomography scan.

Magnetic resonance imaging of 31 meningiomas in 29 patients was retrospectively reviewed and compared with pathologic specimens in 25 tumors to investigate how magnetic resonance imaging could delineate a tumor-brain interface. The thick, collagenous connective tissue, which was seen around four tumors, was shown as a low signal intensity rim on both a T1-weighted image and a T2-weighted image. A rim of low signal intensity on a T1-weighted image and high signal intensity on a T2-weighted image most likely represented cerebrospinal fluid space: this finding was seen around eight tumors. No distinct rim could be identified in five tumors. Of these five, two tumors grew invasively into the brain. Although mixed features predominated in meningiomas, magnetic resonance imaging could well delineate a tumor-brain relationship in most of the cases.

Diagnosis of hydrocephalus after aneurysmal subarachnoid hemorrhage has been facilitated by CT, but the true incidence and pathogenesis of the condition remain to be clarified. Extent of ventricular dilatation does not necessarily correlate with clinical symptoms and the indication of shunting operation is by no means definite.

Effects of a novel calcium 2+ antagonist, KB-2796, on neurologic outcome and size of infarction were studied in the rat model of focal cerebral ischemia. Neurologic deficits were examined from 1 to 24 hours after occlusion of the middle cerebral artery and size of infarction was measured at 24 hours postocclusion. When KB-2796 (10 mg/kg, IP) was given immediately after, or 1 hour after, middle cerebral artery occlusion, marked improvement in neurologic score was seen 1 to 3 hours postocclusion. When given immediately after middle cerebral artery occlusion, size of infarction was also markedly smaller when compared with the control rat. The present study suggests that the calcium 2+ antagonist KB-2796 has brain-protective effects against ischemia even with its administration after induction of ischemia.

We devised a semiconductor film strain transducer (SFT) for continuous measurements of epidural or subdural intracranial pressure and blood pressure. The metal diaphragm of this transducer facing the dura mater was made of high quality stainless steel (sus 27, 30μ in thickness). A strip of SFT element is bonded on the counter surface of the diaphragm at its center, and the rim of the diaphragm is fixed at the edge of the stainless steel cylindrical housing base. The inner space is sealed except for an 1 mm diameter polyethylene tube which is used to balance the inner space pressure against the outer. For the detection of SFT resistance change a bridge method was employed. The transducer was calibrated by a comparison method, giving both positive and negative air pressure. We also developed a new telemetric system consisting of transducer bridge circuits with IC amplifier and transmitter circuits. The miniature transmitter measures only 5×1×3 cm in size, but it was still too large to be implanted. The transmitter and its receiving system utilize the pulse transmitting circuits (3 and 80 MHz), and its radius of action is approximately 10 meters. The SFT was used for continuous recording of epidural pressure (EDP) in 41 neurosu rgical patients for a period ranging from one to nine days (3.5 days on an average). No untoward complications such as infection or hemorrhage at the site of implantation were experienced. Induction of general anesthesia caused an acute rise in the EDP in almost all cases. Intraoperative recording of the EDP was performed in the supine, sitting and prone positions. The sitting position proved to be very useful in reducing the EDP for posterior fossa craniectomy. Irrespective of the positioning of the patients, the EDP was restored to a lower and adequate level as soon as an extreme flexion or rotation of the neck was corrected. In one case the development of a postoperative intracerebral hematoma was detected by monitoring the EDP. Telemetric monitoring of the EDP was performed in two patients during their daily life in the neurosurgical ward, such as eating, drinking, sitting, standing or going to stool. The EDP and systemic blood pressure were recorded simultaneously in one of them. When those patients went to stool, the EDP increased sharply at the beginning of straining and the diastolic pressure also increased at the same time, but the systolic pressure decreased. At the end of straining both the systolic and diastolic pressure increased. Of particular interest was the fact that the magnitude of the EDP rise during straining at stool differed significantly by the posture of the patients, such as lying on a bed-pan, seating on a toilet or squatting over a Japanese style toilet.

The so called “spontaneous” carotid-cavernous fistulae are mostly dural shunts between the meningeal branches of internal or external carotid arteries and dural veins in the vicinity of cavernous sinus. The spontaneous external carotid-cavernous fistula could be treated by ligation or embolization of branches of external carotid artery. On the other hand, the direct closure of internal carotid-cavernous fistula is quite a challenge to neurosurgeons. Here is a report of a technique for direct closing of a spontaneous internal carotid-cavernous fistula which does not impair internal carotid blood flow. Exposure of cavernous sinus wall is achieved by means of a frontotemporal craniotomy. Operative angiography is performed in order to establish the topographical relationship of internal carotid artery, Parkinson's triangle of the cavernous sinus and fistula. Fine copper on copper compound wire is threaded transdurally into the lumen of the sinus. A direct current (0.2 mA to 2 mA) is applied to the copper wire for 1 to 2 minutes. The closure of fistula is verified by operative angiograms. Our experiences of the three cases suggest that electrothrombosis is an ideal treatment of spontaneous internal carotid-cavernous fistula.

Tentorial herniation is caused by a pressure gradient between supra and infratentorial compartments and the herniated brain is burdened with a force, which is called shear strain at the edge of the tentorium. The purpose of the present study is to clarify the relationships between increased intracranial pressure, the pressure gradient and the tentorial shear strain. Twenty-three monkeys were used and intracranial pressure was raised by inflation of an epidural balloon placed in the right temporal region. The supratentorial pressure was found to be always higher than the infratentorial pressure and the pressure gradient became greater as intracranial pressure increased. The shear strain at the tentorial edge began to develop as soon as the balloon was expanded, and showed a slow and steady increase even when the intracranial pressure was only slightly increased and the pressure gradient did not have any effect. The degree of the tentorial edge descent observed by X-ray was, however, variable depending upon the animals used. The tentorial edge ceased to descend at the moment the tentorial shear strain was 80-140 mm Hg. At this point and thereafter, the characteristics of both herniated brain and tentorial edge changed from elastic to plastic, and the damage caused by the strained tentorial edge is thought to be tremendously extensive. Our dynamical study of transtentorial herniation shows clearly that the magnitude of shear strain was greater as a local forced pressure than supra and infratentorial pressure.

A case of superior sagittal sinus thrombosis followed by a subdural hematoma is reported. A 33-year-old woman, who presented with serious neurological deficits, made a remarkable recovery with mild residual. She had a thin subdural fluid collection, which eventually developed into a subdural hematoma. After evacuation of the hematoma, she had no neurological deficits. Treatment of cerebral venous and dural sinus thrombosis is discussed.

A case of a 6-year-old boy with a large meningioma is reported. The patient had an enlarged head, the Foster Kennedy syndrome, and roentgenological evidence of increased intracranial pressure. A computed tomography scan and magnetic resonance image showed a huge tumor in the right parietooccipital region. The tumor was totally resected with the involved right transverse sinus in staged operations. Histology was transitional meningioma. The incidence of intracranial meningiomas is low in childhood. The literature is reviewed, and some peculiarities of childhood meningiomas are discussed.

Rapid-sequence computed tomographic scanning with time-density analysis for selected regions of interest seems to be a useful, noninvasive test to confirm a total arrest of cerebral circulation in the diagnosis of brain death.

✓ Cerebral autoregulation and vasomotor responsiveness to carbon dioxide (CO2) were measured quantitatively by the use of the autoregulation index and chemical index, respectively, in normal baboons before and after intravertebral and intracarotid infusion of the anticholinesterase agent, neostigmine methylsulfate (Prostigmin). Continuous measurements were made of cerebral blood flow (measured as bilateral internal jugular venous outflow), arterial and cerebral venous pO2 and pCO2, cerebral arteriovenous oxygen differences, and endotracheal CO2. The effect of intravertebral infusion of neostigmine (12.5 µg/kg body weight) was compared to intracarotid infusion of neostigmine (25 µg/kg body weight) for assessment of any specific action of the drug on a hypothetical cholinergic vasomotor center, presumed to be located in the territory of the vertebrobasilar supply. No significant or persistent changes in cerebral blood flow (CBF) and cerebral metabolic rate for oxygen (CMRO2) followed either intravertebral or intracarotid infusion of neostigmine. Cerebral vascular resistance (CVR) and cerebral perfusion pressure (CPP), however, decreased significantly after intravertebral infusion. Cerebral autoregulatory vasoconstriction during increases of CPP was significantly reduced following both intravertebral and intracarotid infusion. Cerebral autoregulatory vasodilatation was not altered as CPP was lowered. Cerebral vasodilatory reactivity to CO2 inhalation was significantly enhanced following intravertebral neostigmine but not following intracarotid neostigmine. Cerebral vasoconstrictive response to hyperventilation was not influenced by neostigmine. These results support the view that central cholinergic cerebrovascular influences exist, and are vasodilatory in nature.

一般に後交通動脈瘤といえば, ほとんどが「いわゆる」内頸動脈-後交通動脈分岐部動脈瘤を指しており, 後交通動脈自体から発生した「真の」動脈瘤は稀である.我々は最近, くも膜下出血によって発症した「真の」後交通動脈瘤の1症例を経験したので, 文献的考察を加えて報告する.症例は40歳の女性で, 激しい頭痛と嘔吐を主訴として某病院に搬入され, CTでくも膜下出血と診断された.当科での発作の翌日に行った右内頸動脈撮影で後交通動脈自体から発生している嚢状動脈瘤を認め, 同日, 右前頭側頭開頭によりネッククリッピングを行った.動脈瘤は脳血管撮影で認められた如く, 内頸動脈-後交通動脈分岐部より約3mm遠位で後交通動脈本幹に頸部を持っており, その発生部位に穿通枝は認められなかった.ネッククリッピングは容易であり, 術後も障害を残さずに発症から29日目に退院となった.

An unsulfated form of human cholecystokinin (hCCK-33) was synthesized by successive azide condensations of seven peptide fragments, followed by deprotection with 1 M trimethylsilyl trifluoromethanesulfonate/trifluoroacetic acid. The phenolic group of Tyr (position 27) was selectively sulfated with pyridine-SO3 complex, after reversible masking of other functional groups with hard base (F-)-labile protecting groups, i.e., the amino functions with 9-fluorenyl-methyloxycarbonyl group and the hydroxyl functions of 4 Ser residues with tert-butyldiphenylsilyl groups. In terms of pancreatic protein output and capillary blood flow in dogs, the relative potency of synthetic hCCK-33 with respect to that of synthetic CCK-8 (taken as 1 on a molar basis) was 0.9. In terms of gastric acid and pepsin output in rat in vivo assays, synthetic hCCK-33 was about 2- to 3-fold more potent than CCK-8 on a molar basis.

A 36-residue peptide amide corresponding to the entire amino acid sequence of chicken antral peptide was synthesized by assembling seven peptide fragments via the azide, followed by thioanisole-mediated deprotection with trimethylsilyl bromide and trimethylsilyl trifluoromethanesulfonate in trifluoroacetic acid.The synthetic peptide stimulated gastric secretion, but not pancreatic secretion.

A 59-year-old female had episodes of vertigo for 13 years, right tinnitus for 6 years, and right hearing difficulty for 2 years. She had no facial nerve dysfunction or other neurological deficits. Postcontrast computed tomography (CT) did not show abnormalities, but a wide, high-window CT scan revealed erosion of the petrous pyramid on the right side. Magnetic resonance imaging clearly delineated the entirety of a small tumor transecting the petrous bone. At operation a neurinoma was found to originate from the facial nerve proximal to the geniculate ganglion; it was totally removed. This case is unique in that she had a long history of signs and symptoms of acoustic nerve disturbance, but no facial nerve dysfunction whatsoever.

Cerebral blood flow (CBF) was measured in four elderly hydrocephalic patients with dementia with the use of the 133-Xe inhalation method. The patients had no signs and symptoms of increased intracranial pressure. They all had a triad of normal pressure hydrocephalus (NPH) except one patient, who lacked incontinence. Dementia, evaluated with the dementia rating scale by Hasegawa, decreased markedly after shunting procedures in two patients and after removal of posterior fossa tumors in the other two patients. The average hemispheric CBF was subnormal in three patients, and within normal range in the fourth patient before operation. It did not increase when dementia disappeared within 7 to 21 days postoperatively. The mean CBF was 41.4 ml/100 g/min before operation, and 40.8 ml/100 g/min after operation when dementia disappeared. The cerebral circulation time (CCT) was measured by the dynamic computed tomography (CT) in three of them. The mean CCT was prolonged before operation, 13.0 sec, and returned to normal range, 7.5 sec, when dementia abated after operation. This reduction and normalization of CCT reflect an improvement in the microcirculation within the brain. The results of this study demonstrate that disappearance of dementia following surgical intervention in hydrocephalic patients, possibly including those with NPH, is not always accompanied or preceded by an increase in CBF as measured by the conventional method. However, the postoperative disappearance of dementia is accompanied by an improvement in microcirculation which can be measured by the dynamic CT.

A 74-year-old female developed a subdural hematoma in association with a large hemorrhagic infarct. The hemorrhagic infarct was treated conservatively by steroid and a dehydrating agent. The subdural hematoma enlarged over a 10-day period and it was evacuated through a burr hole. The patient survived with residual neurological deficits. Although subdural hematomas associated with cerebrovascular lesions are not uncommon, ones with intracerebral hemorrhage or hemorrhagic infarct are rare.

The authors report eight cases of aneurysm of the anterior cerebral artery proximal to the anterior communicating artery (A 1 segment). In six of these cases, the aneurysms arose from the proximal anterior cerebral artery at the origin of either a cortical branch (one case), the accessory middle cerebral artery (one case), or a perforating branch (four cases). In another case the aneurysm arose at the proximal end of the fenestration, whereas in the one remaining case no branch was present at the site of the aneurysmal neck.

Two cases of accessory middle cerebral arteries associated with cerebral aneurysms are reported, and the literature concerning this rare association is reviewed.

A 63-year-old female with a large meningioma of the middle cranial fossa was admitted. The tumor was fed mainly by the hypertrophied middle meningeal artery. Immediately following a seemingly successful embolization of that artery with gelfoam powder, consciousness of the patient rapidly declined and anisocoria and decerebrate posturing developed. An intratumoral massive hemorrhage ruptured into and extended widely in the subdural space was confirmed by computed tomography scan. The hematoma was evacuated and the tumor was radically removed by emergency craniotomy, and the patient recovered. Therapeutic embolization for meningiomas and other highly vascular intracranial tumors has been established as a useful and relatively safe adjunctive preoperative measure, and an intratumoral massive hemorrhage in the period immediately following this procedure has seldom been reported in the literature. However, the present case shows that it is apparently a potential complication of this procedure. The possible mechanisms of an intratumoral hemorrhage following therapeutic embolization of the feeding arteries are briefly discussed.

A case of traumatic aneurysm of the middle cerebral artery in a patient who suffered a closed head injury with a linear skull fracture is reported. Repeat angiography 7 days after injury disclosed the aneurysm associated with severe vasospasm and intracerebral hematoma. The parent artery appeared to be normal and neither vasospasm nor displacement of the cerebral vessels was present on the previous angiogram obtained 3 days earlier. The aneurysm in this case probably was caused by injury of the arterial wall by the firm sphenoid ridge.

✓ Adenosine 3′,5′-cyclic monophosphate (cyclic AMP) (0.5 mg/kg) was infused into the carotid artery of baboons anesthesized with sodium pentobarbital, causing a biphasic increase in cerebral blood flow (CBF) and reduction in cerebrovascular resistance (CVR) associated in each phase with stimulation of cerebral metabolism evidenced by increased cerebral oxygen consumption (CMRO2) and cerebral glucose consumption (CMRGI). Intracarotid dibutyryl cyclic AMP (0.5 mg/kg) caused a monophasic increase in CBF and reduction of CVR but failed to alter cerebral metabolism. This may be due to its rapid removal from the circulation with ineffective passage across the blood-brain barrier since intracisternal infusion of dibutyryl cyclic AMP caused sustained increase in CBF, CMRO2 and CMRGl and reduction in CVR. Intracarotid AMP (0.4 mg/kg) and adenosine (0.3 mg/kg) caused an immediate and more marked increase in CBF and decrease in CVR unassociated with cerebral metabolic change making it unlikely that the observed effects of cyclic AMP can be attributed to its breakdown products. Cyclic AMP or its dibutyryl derivative may alter cerebral metabolism secondary to neuronal activation but increase in glucose/oxygen utilization ratio after intracarotid cyclic AMP and intracisternal dibutyryl cyclic AMP also suggests an influence on enzymatic regulation of glucose metabolism.

✓ Effects of cholinergic inhibition by atropine on cerebral circulation were studied in 15 baboons anesthetized with sodium pentobarbital. Intravertebral infusion of atropine, 0.1 mg/kg, did not cause any changes in cerebral blood flow (CBF), superior sagittal sinus wedge pressure (SSWP), epidural pressure (EDP), cerebral perfusion pressure, or cerebral vascular resistance under normal conditions. Cerebrovascular responsiveness to carbon dioxide (CO2) inhalation was not influenced by atropine. The presence of cholinergic nerve fibers has been proved in the cerebral blood vessels and the existence of cholinergic mechanism suggested in the brain stem, but it is not likely that the cholinergic nerves have tonic control of cerebral blood vessels in the resting state or affect cerebrovascular responsiveness to CO2. The changes in EDP and those in SSWP showed a very good correlation to each other. There was also a good correlation between the changes in CBF and those in EDP or SSWP.