The usefulness of large decompressive craniectomy in cases of severe contusion with thin subdural hematoma has been reported by Ransohoff et al. The beneficial effects of this procedure, however, still remained obscure from the standpoints that its mechanism and limits within which effectiveness can reasonably be expected were not clear. The present study was designed to obtain an index of the limits for effective decompressive craniectomy mainly in terms of intracranial pressure, cerebral blood flow, electroencephalogram, and far field acoustic response from both animal experiments and clinical investigations.
Experimental results indicated that decompressive craniectomy was useless if the intracranial pressure was more than 60 mmHg and the vasomotor index (the ratio of intracranial pressure and systemic arterial pressure) was more than 0.5 with reduced perfusion pressure, impaired venous return, and if there was an 80-90% decrease in cerebral blood flow. It was also shown that such conditions coincided with the absence of far field acoustic response as an expression of the brainstem function.
In clinical studies of 60 cases of severe brain contusion with thin subdural hematoma following large decompressive craniectomy, intracranial pressure, cerebral blood flow, angiogram, CT scan and far field acoustic responses were retrospectively checked in both the survival and dead groups. It was found that effective results by this procedure was difficult to obtain whenever the II-VII was in far field acoustic response was absent, the vasomotor index was more than 0.5 and when non-filling angiograms were observed.
Thus, indication for large decompressive craniectomy for the treatment of severe brain contusion with thin subdural hematoma is established based on the analysis of these results.

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Translational acceleration impact was applied to elicit cerebral concussion and contusion in subhuman primates (12 Japanese monkeys and 2 baboons) using a HYGE sled and a slider-impactor system.
All animals were concussed more than 15 seconds by force ranging from 240 to 960 G (duration; 17.5-3.5 msec.) in average head accelerations. Five monkeys among 8 with frontal impact died within 27 minutes. This well correlated with thoracic trauma, including rib fracture and small mediastinal hemorrhage. Only one animal (baboon) among 6 with occipital impact died immediately and the cerebro-spinal junction was found traumatically severed. Bradycardia, apnea, systemic hypotension and depression of EEG activity occurred immediately after impact in every animal. No visible intracranial pathology, such as brain contusion, subdural hematoma, or intracerebral hematoma was noticed. Microscopic examination revealed central chromatolysis of nerve cells and degeneration of Purkinje cells. However, these findings did not correlate with the post-impact state of the animals nor with biomechanical data.
Our experiment suggests that translational acceleration impact to the brain does not usually cause gross morphological changes. Secondly, the so-called brain concussion might be the result of the cumulative effect of, 1) transient medullary paralysis, 2) cardio-respiratory depression of cervical cord origin, as well as, 3) cardiocirculatory insufficiency due to thoracic impact (primary shock). If severe, these factors would generate a vicious cycle to lead to a state of circulatory catastrophe which ends in death only.

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Six hundred and eight carotid angiograms of 266 patients with ruptured intracranial aneurysms were analyzed to investigate the sequential changes of the type and severity of vasospasm. Furthermore, the present study was undertaken to analyze the effects of vasospasm upon clinical states, cerebral blood flow and prognosis of the patients.
Vasospasm was simply classified according to its extent into four types; diffuse (narrowing of intraarterial diameter over 2 cm in length including at least one part of C₁, A₂ and M₁), peripheral (narrowing of the diameter over 2 cm in length in the distal parts), multi-local (multiple, localized narrowing) and local (single, localized narrowing). Diffuse type of vasospasm was further divided into two groups by its degree of severity. Namely, vasospasm reducing the caliber of an artery by more than 50% was defined as severe (diffuse severe), while mild vasospasm represented reduction in the caliber of 25 to 50% (diffuse mild). In order to obtain an indicator of objective measure of vasospasm, a ratio between each diameter of the arteries (C₁, A₂, M₁) to the diameter of the canalicular portion of the internal carotid artery was calculated from 32 normal carotid angiograms (A-P projection). Fifty or 75% of the normal ratio were used as measurement controls.
The results were as follows : 1) Vasospasm which occurred within 3 days after the onset was seen in only 3 of 79 cases (3.8%). However, the incidences of vasospasm increased as the time passed and reached its peak at the period between 8th and 15th day, when vasospasm was seen in 83 of 106 cases (78%). The type of narrowing was diffuse in most of these cases. Thereafter, the occurrence of vasospasm gradually decreased and the type of narrowing tended to change from diffuse to local or multi-local types. Only few cases showed vasospasm after 50th day. 2) It was noted that in all of the 8 preoperative patients, on whom carotid angiography was performed more than twice, vasospasm changed from diffuse to local or multi-local types. 3) Most of the patients with diffuse type of vasospasm, especially with diffuse severe type, showed decreased values of mean CBF, and showed focal ischemia in the regions supplied by the involved arteries. In patients with multi-local or local types of vasospasm, there was little difference in mean CBF as compared to the patients without vasospasm, though there frequently existed focal ischemia in patients with multi-local type of vasospasm. 4) Diffuse type of vasospasm tended to have effects on the clinical state and outcome of patients. It was evident that narrowing of the arterial lumen by more than 50% and diffuseness of vasospasm (diffuse-severe type of vasospasm) caused cerebral ischemia.
It was concluded that the present method of classifying the degree of vasospasm was useful in determining the clinical significance of vasospasm.

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This paper reports the treatment of cerebral vasospasm by topical application of lidocaine in 3 patients with ruptured aneurysm. Each case had shown vasospasm of the smooth narrowing type on preoperative angiogram performed on the 9th day after the subarachnoid hemorrhage attack. Direct aneurysmal operation was carried out on the 9th day in I case and on the 10th day in 2 cases. After clipping of the aneurysm, subarachnoid clot was removed and cottonoids soaked in 1-4% of lidocaine was applied over the spastic arteries. After 10-15 minutes, the vessels showed marked dilatation in each instance. Postoperative angiograms also showed relief of the spasm of the arteries which had been in contact with lidocaine during the operation.
Pharmacological basis of spasmolytic action of lidocaine and its indication for clinical use are discussed.

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Ischemic changes in small vessels, especially in capillaries, were investigated by electron microscope. Samples were taken from the ischemic foci in the thalamus of 18 dogs which were subjected to various cerebrovascular occlusions from 15 minutes to 24 hours by our method of producing thalamic infarction in dogs.
After 30 minute occlusion, swelling of perivascular astrocytic processes was seen. After 1 hour occlusion, swelling of pericytes was seen. After 2 hours occlusion, swelling of endothelial cells was seen. Blebs were found in the lumen of capillaries after 3 hours. Dehiscence of tight junctions was rarely observed after 6 hours occlusion, but after 12 hours occlusion it was frequently found in capillaries and venuoles which had succumbed to necrosis. Diapedesis from necrotic capillaries and venuoles was found in the 12 hour occlusion group. After 24 hours occlusion, numerous neutrophiles appeared within the blood vessels and some of them infiltrated into softened areas.

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From December 1974 to October 1977, 11 transsphenoidal microsurgical operations were performed on 11 patients with functioning pituitary microadenomas. Of these patients, 6 had symptoms of hypersecretion of human growth hormone (acromegaly with or without diabetes mellitus), and the remaining 5 showed symptoms due to hypersecretion of prolactin (galactorrhea with or without amenorrhea).
Preoperatively, elevated serum HGH concentration was observed in the acromegalic patients (12-86 ng/ml), and they were responsive to intravenous TRH. Elevated serum prolactin (PRL) concentration was also observed in 3. The secretional function of other anterior pituitary hormones was normal or slightly decreased.
Elevated serum PRL concentration was noticed in all of the patients with galactorrhea (200-1050 ng/ml), and they were variably responsive to intravenous TRH. The other anterior pituitary hormones were normal or slightly decreased.
Neuroradiological examination revealed that each adenoma was an enclosed tumor without suprasellar extension. The sella turcica was of almost normal size, but discrete bulging of the sellar wall was seen. Anteroposterior tomograms showed unilaterally depressed sellar floor, and lateral projection revealed double contour of the sellar wall.
Selective gross total removal was attempted through the transsphenoidal procedure. The adenomas were found within the pituitary gland just adjacent to the discrete bulging of the sellar floor. The size of the tumor varied from 5 to 10 mm in diameter. A small cyst was found within the adenoma tissue in 2 patients with galactorrhea, who, as others, had not undergone prior therapy.
Diabetes inspidus was a postoperative hazard in 4 cases. Neither operative deaths nor complications were recorded. Postoperatively, a marked decrease of serum HGH concentration below 5 ng/ml and relief of clinical symptoms was obtained in 4 acromegalic patients. In one of the other 2 patients, because of insufficient reduction of serum HGH concentration, postoperative irradiation was given, but no responsiveness was noted. In the patients with galactorrhea, the elevated serum PRL concentration was significantly reduced immediately after the operation, and there was no further lactation.
During follow-up period ranging from 1 to 34 months, regular menstration was observed in 6 out of 9 female patients, biphasic basal body temperature in 2, and pregnancy in 1 patient.
In the patients who underwent removal of the microprolactinoma, there was a tendency of gradual increase of serum PRL concentration, and galactorrhea recurred in 1 patient. Ethanol fixation of the tumor bed should have been undertaken during surgery.

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Mucocele generally exists in the nasal and orbital cavities of extracranial space. Some of them, however, extend intracranially resulting in compression of the brain and cranial nerves.
The authors encountered a very rare case of ethomoid sinus pyocele extending not only intracranially but also into the intradural space. The patient was a 34-old-year male who had a sinusitis 24 years ago. In addition, he suffered severe head injury with fracture of the frontal base of the skull when 15 years old. He was admitted to our hospital on February 7, 1978, with chief complaints of severe headache and vomiting. Neurological examinations on admission revealed left hyposmia and meningeal irritation but no occular signs. Plain and tomogram X-ray films of the skull showed cloudy shadow in the left ethmoid sinus and destruction of the roof of the same sinus. The left common carotid angiogram demonstrated no remarkable changes. CT-scan (axial and coronal sections) showed enhanced dumbbell like mass lesion, due to expansion of the ethmoid sinus mucocele into the intradural space through bone defect at the left frontal base. Removal of the intracranial portion was performed by bifrontal craniotomy on February 22, 1978, and defects of the dura mater and bone of the frontal base were confirmed. The postoperative course was uneventful and he became free from headache and vomiting. The patient is now waiting for otological radical residual extracranial lesion operation.
It is assumed that the ethmoid sinus mucocele extended into the intradural space which was less resistant than the extradural space because of defects of the dura mater and bone of the left frontal base affected by basis fracture. We could not find reports of any other case like this in Japan.

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A case of infantile bilateral chronic subdural hematoma following acute traumatic epidural hematoma is reported.
This male infant had head trauma when 3 months old without initial lost of consciousness. He vomited at night and his lips, face and body turned pale the next morning. Neurological examinations on May 10, 1978, the next day after the trauma, revealed tense, bulging anterior fontanel, conjugate deviation to the left and slight right hemiparesis. Laboratory test data showed marked anemia. CT scans showed midline deviation to the right, a round high density area just beneath the calvarium in the left parietal region with a small low density area within it, and also a slightly high density area over the bifrontal region. Operation disclosed about 170 g of epidural hematoma caused by linear fracture of the posterior branch of middle meningeal artery. Postoperative CT scans showed subdural fluid collection in the bilateral fronto-temporal regions without shift of midline structures. He was discharged with slight right upper monoparesis 15 days after surgery.
In mid-July, he once suffered fever, vomited and showed pallor of face in the morning. Neurological examination on August 10, 1978 revealed slight right upper monoparesis and slightly enlarged head circumferance. CT scans showed high density over the bilateral fronto-temporal regions, especially on the left side with shift of midline structures. Subdural hematomas on the left and right side of 70 ml and 30 ml, respectively, were evacuated through burr holes. Histological findings of the outer membrane of hematomas showed sinusoidal channel layer in the outer layer and moderately fibrous tissue proliferation with old hemorrhages in the inner layer.
The process leading to the development of chronic subdural hematoma in this case is considered as follows: 1) neo-membrane with marked proliferation of capillaries and fibrous tissue began to form during a certain period after head trauma in response to subdural fluid which consisted of a mixture of blood and cerebrospinal fluid; 2) this process was enhanced by the sudden decrease of intracranial pressure after removal of the epidural hematoma; and 3) repeated hemorrhages into the cavity from this neo-membrane may have resulted in causing chronic subdural hematoma.

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