The effect of hypoxia on traumatic head injury in rats: alterations in neurologic function, brain edema, and cerebral blood flow.

We evaluated the effects of early posttraumatic hypoxia on neurologic function, magnetic resonance images (MRI), brain tissue specific gravities, and cerebral blood flow (CBF) in head-injured rats. By itself, an hypoxic insult (PaO2 40 mm Hg for 30 min) had little effect on any measure of cerebral function. After temporal fluid-percussion impact injury, however, hypoxia significantly increased morbidity. Of rats subjected to impact (4.9 +/- 0.3 atm) plus hypoxia, 71% had motor weakness contralateral to the impact side 24 h after injury, while only 29% of rats subjected to impact alone had demonstrable weakness (p less than 0.05). Lesions observed on MR images 24 h after injury were restricted to the impact site in rats with impact injury alone, but extensive areas with longer T1 relaxation times were observed throughout the ipsilateral cortex in rats with impact injury and hypoxic insult. Brain tissue specific gravity measurements indicated that much more widespread and severe edema developed in rats with impact injury and hypoxia. [14C]Iodoantipyrine autoradiography performed 24 h after injury showed that there was extensive hypoperfusion of the entire ipsilateral cortex in rats with impact injury and hypoxia. These results show that large areas of impact-injured brain are extremely vulnerable to secondary insults that can irreparably damage neural tissue, and provide experimental evidence for the observed adverse effects of hypoxia on outcome after human head injury.

Effect of hypoxia on traumatic brain injury in rats: Part 1. Changes in neurological function, electroencephalograms, and histopathology.

The effect of hypoxia on neurological function, compressed spectral array electroencephalography, and histopathology in head-injured rats was evaluated. By itself, an hypoxic insult (PaO2, 40 mm Hg for 30 minutes) caused no neurological deficit. Twenty per cent of rats injured by a 5-atmosphere temporal fluid percussion impact were hemiparetic contralateral to the side of impact, whereas 80% had no deficit 24 hours after injury. Seventy per cent of rats with both fluid impact injury and hypoxic insult, however, either had a definite hemiparesis, showed no spontaneous movement, or died (P less than 0.02). Impact alone produced an initial depression in electroencephalogram power that was prolonged in rats with hypoxic insult; the most dramatic effect was found in the injured hemisphere, with shorter and less profound effects in the contralateral hemisphere. Perfusion staining of injured cerebral tissue in vivo with 2,3,5-triphenyltetrazolium chloride showed an area of extensive ischemia around the impact site in rats with hypoxic insult. This ischemic area was not present in rats with either impact injury or hypoxia alone. We conclude that posttraumatic hypoxia clearly increases the severity of impact injury in this rat model. These findings suggest that hypoxia, which is common in head-injured patients, very likely worsens the effect of impact injury and may account for much of the diffuse neurological dysfunction in patients with severe craniocerebral trauma.

Effect of hypoxia on traumatic brain injury in rats: Part 2. Changes in high energy phosphate metabolism.

The effect of different degrees of hypoxia on phosphate metabolism in the brains of impact-injured rats was studied using in vivo phosphorus-31 magnetic resonance (P-31 MR) spectroscopy. Sequential changes in P-31 MR spectra within 60 minutes of insult were compared among rats with hypoxia alone, impact injury alone, or a combined impact-hypoxic insult. Hypoxia alone (PaO2 of 40 mm Hg for 30 minutes) caused no remarkable changes in phosphorus spectra except a decrease in intracellular pH. In impact-injured rats, the concentration of inorganic phosphate (Pi) increased, but signals for phosphocreatine (PCr) and beta-adenosine triphosphate (beta-ATP) did not change, and the ratio of PCr/Pi changed only slightly to 7% below control value. When rats with a fluid percussion impact injury of 5 atm were subjected to hypoxic conditions of a PaO2 of 40 mm Hg for 15 minutes, the PCr/Pi ratio decreased by 14%, a value significantly below that of the impact alone group (P less than 0.05). After longer periods of hypoxia (PaO2 of 40 mm Hg for 30 minutes) in impact-injured rats, there were marked increases of Pi and significant decreases in signals for PCr and beta-ATP, which caused a marked decrease in the PCr/Pi ratio to 39% below control values (P less than 0.001). Milder hypoxia (PaO2 of 50 mm Hg for 30 minutes) plus impact injury caused smaller changes in high energy metabolite concentrations, and the PCr/Pi ratio decreased to 15% below control values.(ABSTRACT TRUNCATED AT 250 WORDS)

The effects of hypovolemic hypotension on high-energy phosphate metabolism of traumatized brain in rats.

To clarify the effect of hypovolemic hypotension on high-energy phosphate metabolism in head injury, sequential changes in in vivo phosphorus-31 magnetic resonance (31P MR) spectra were compared in 35 rats after impact injury with and without hypotension. Fourteen rats were subjected to hypotension alone (mean arterial blood pressure (MABP) of either 40 or 30 mm Hg for 60 minutes), seven to fluid-percussion impact injury (4 to 5 atm) alone, and 14 to impact injury and hypotension (MABP of 40 to 30 mm Hg). Impact injury alone caused a transient decrease in the phosphocreatine (PCr) level and an increase in the inorganic phosphate (Pi) value. While hypotension alone produced only small changes on 31P MR spectra, impact injury plus hypotension caused pronounced changes. Impact injury and an MABP of 40 mm Hg caused a 50% decrease in PCr concentration and an approximately twofold increase in Pi level, which were significantly greater than values in rats with impact injury alone. Impact injury and an MABP of 30 mm Hg also caused a significant decrease in adenosine triphosphate value, which was not observed in rats with impact injury alone or with an MABP of 30 mm Hg alone. Decreases in intracellular pH were greater in rats with impact injury and hypotension. After traumatic injury, the brain is extremely vulnerable to hypovolemic hypotension, as reflected in the loss of high-energy phosphates in brain.

Cervical myelopathy caused by the anomalous vertebral artery. A case report.

STUDY DESIGN: A case of cervical myelopathy caused by an anomalous vertebral artery is reported. OBJECTIVES: To report a case of high cervical myelopathy resulting from spinal cord compression by an anomalous vertebral artery. Authors believe that this is the first reported case in which the nutrient artery to the abnormal artery originated from the posterior inferior cerebellar artery. SUMMARY OF BACKGROUND DATA: Although fenestration of the vertebral artery is net an unusual anomaly to the best of the authors knowledge, three cases of high cervical myelopathy resulting from the anomaly were reported. There is no reported case in which an abnormal artery originated from the posterior inferior cerebellar artery. METHODS: The clinical features of the case are reported and discussed with a review of the previously documented cases. RESULTS: The cord compression war relieved surgically, and the patient's symptoms improved postoperatively. CONCLUSIONS: A fenestrated vertebral artery should be included in the differential diagnosis of the upper cervical or the craniovertebral junctional lesions of unknown origin. Magnetic resonance imaging is useful for the diagnosis. In the present case, there was an anomalous branch entered as a nutrient artery from the posterior inferior cerebellar artery. Careful management for similar abnormal arteries includes surgery.

The PCr/Pi ratio in in vivo injured rat brain.

A new ratio, R+ = PCr/(mP + Pi), is proposed to analyses brain metabolism after injury. The Pcr/Pi and PCr/(mP + Pi) ratios of a series of injured rat brains show similar trends in the case of well-defined Pi and mP peaks, while they diverge in the case of mutual overlap.

Brain death in moderately injured rat brains by in vivo P-31 NMR spectroscopy.

In the course of a systematic in vivo P-31 NMR study of moderately insulted rat brains, some brains died after such injury. Changes in high-energy phosphate metabolism of these brains after injury were rationalised by the aid of a model based on the depletion of an insoluble Pi pool followed by depletion of PCr and ATP pools.

Fluctuating visual field defects in Rathke's cleft cysts: MRI analysis.

This is the first report that the authors are aware of concerning fluctuating visual field defects in patients with Rathke's cleft cysts. Among 11 patients with histologically proven Rathke's cleft cyst, three patients presented with a visual field defect which spontaneously resolved. The symptom became overt again in the subsequent 1 to 14 month follow-up period and a surgical procedure was then chosen. Magnetic resonance imaging (MRI) observation clearly revealed change in the cyst size without signal intensity change in two cases. In the remaining case, multiple spotty high intensities on T1-weighted images were found corresponding to fluctuations in the clinical course. In the last case, enlargement of the cyst was considered to be due to repeated haemorrhage. In the other two cases, minor haemorrhage, undetectable on MRI, may have played a role in the increased cyst size. Another possible mechanism is an imbalance between secretion from, and absorption into, the cyst wall. The size change and neurological fluctuations were previously unknown aspects of the natural history of this lesion. Surgical indications for such patients with transient symptoms followed by cyst size reduction have been controversial, since pituitary cystic lesions may enlarge again or disappear. Our observations suggest that this change in cyst size may be more frequently noted in cases with iso- or high intensity cysts on T1-weighted images, indicating the need for closer observation of patients with this MRI finding.

[Single burr hole irrigation without drainage in chronic subdural hematoma].

The surgical treatment of chronic subdural hematoma has evolved from membranectomy through craniotomy to burr hole irrigation. The latter approach is based on utilization of the natural absorptive process that is thought to be part of the life cycle of the hematoma. To test this theory, the authors treated fifty-nine patients with chronic subdural hematoma according to the following protocol. Local anesthesia was induced with a modified neuroleptanalgesic procedure. A single burr hole was drilled, usually in the posterior frontal region, and irrigation was carried out until the washing was clear. Subdural drainage was not employed. Patients were permitted to walk about on the following day. The outcome was better than that achieved with conventional treatment. Such complications as tension pneumocephalus and intracranial hematoma were not observed, and only one patient (1.7%) had a recurrence. The results of this study indicate that single burr hole irrigation without drainage is a very simple and effective treatment for chronic subdural hematoma. The absence of subdural drainage may be an important feature, since drainage may contribute to the development of certain postoperative complications. Also, the simplified procedure allows patients early mobility, which may be of particular benefit to the elderly.

[Neurinoma with intrasellar extension: a case report].

A 64-year-old female visited Kawatetsu Chiba Hospital complaining of left retro-orbital pain. A month before, she had experienced ptosis and diplopia, that had been releaved two days later by corticosteroid. On admission, she had no neurological deficits except for minimal anisocoria, with the left pupil larger than the right. There was no cutaneous manifestation of von Recklinghausen's disease. Skull X-ray films showed depression of the floor of the sella turcica on the left side. CT scans demonstrated a parasellar enhancing mass with intrasellar extension. Left carotid angiogram showed intracavernous portion of the internal carotid artery displaced laterally, inferiorly, and anteriorly. With a tentative diagnosis of laterally extending pituitary adenoma, a transsphenoidal operation was carried out, which disclosed a solid tumor locating beside the medially-displaced pituitary gland. The histological diagnosis was typical neurinoma. Parasellar neurinoma is not so common. It is usually difficult to determine the origin of the parasellar neurinoma. Trigeminal neurinoma arising from the Gasserian ganglion is generally recognized to be the most frequent. However, the absence of the trigeminal nerve involvement, unusual CT findings, and angiographical changes in the present case were all different from those of the typical trigeminal neurinoma. We believe that the tumor of this case originated from the oculomotor nerve. Fifteen cases of neurinoma of the oculomotor, trochlear, and abducens nerve have been reported to date. Their clinical features were reviewed.

[Hemorrhagic type of moyamoya disease].

Clinical picture of Moya Moya Disease was analyzed in 18 cases. In 16 cases whose CT scan were available at the time of the first bleeding, hematoma at the basal ganglia was noted in 43.8%, primary ventricular hemorrhage in 37.5%, thalamic hemorrhage with ventricular rupture in 12.5% and subcortical hemorrhage in 6.3%. The frequencies shown above were well correlated to previous reports. In MRI performed 1 year or more after primary ventricular hemorrhage, the primary bleeding site was demonstrated at the lateral wall of the lateral ventricle, in proton weighted and T2 weighted images. MRI can detect the site of old bleeding points and its chronological change if the study is repeated. In a follow-up period of 5.4 years, 27.8% of the cases had rebleeding one or more times. As a result, good outcome was noted in 72.2% after the 1st bleeding, and in 55.6% after re-bleedings. Death occurred in 5.6% of patients after the 1st bleeding and in 22.2% after further rebleeding. Rebleeding worsened the outcome. Therefore, prevention of rebleeding is important. From a therapeutic viewpoint, although a direct relation between rebleeding and untreated hypertension could not be established, blood pressure control is critical at both the acute and the chronic stages. Reconstructive vascular surgery is a recommendable method for properly selected patients.

[A case of systemic lupus erythematosus associated with spontaneous bilateral epidural hematomas].

The authors reported a case of systemic lupus erythematosus (SLE) associated with bilateral epidural hematomas which had developed without any recent trauma. A 34-year-old male suddenly suffered from a severe headache and vomited several times. He had no neurological deficits on admission, but CT scans of the head revealed abnormal high density areas over the parieto-occipital regions beneath the calvarium bilaterally. At the operation, fresh epidural clots were removed. There were neither evidence of trauma nor abnormal structures which might have led to the development of the clots. He was discharged a month later, being free from any signs and symptoms. One year later, arthralgia progressed and cutaneous ulceration appeared on his feet. On the second admission, butterfly rash on the face, alopecia, polyarthritis and arthralgia, photosensitivity, systemic purpura and proteinuria were noted. With detailed immunological examinations and renal biopsy, he was diagnosed as SLE. SLE is often associated with neurologic and psychic disorders and there are some cases of intracranial hemorrhage among them. However, the association with epidural hematoma has not been reported to date. We think the degeneration of the dural vessels caused by underlying SLE resulted in the development of these epidural hematomas. We also reviewed the literature about spontaneous epidural hematoma and about bilateral epidural hematomas.

An early MRI change following reversible hypoxic brain injury. A case report.

We describe a patient who suffered reversible hypoxic brain injury. The initial MRI taken 3.5 hours after asphyxiation showed an abnormal lesion on DWI, but he recovered completely from coma. The presence of cytotoxic edema in the acute stage may not necessarily indicate a poor prognosis.

[Effects of microtubule inhibitors on the amelogenesis in rat incisor enamel at the maturation stage: changes of staining patterns of GBHA on the enamel surface].

We investigated the effect of microtubule inhibitors on the amelogenesis in rat incisor enamel at the maturation stage by the glyoxal bis (2-hydroxyanil) (GBHA) staining method. Several red stripes stained with GBHA appeared on the maturation enamel surface of control rats. Colchicine injection (1.3 mg/kg, s.c.) disarranged the GBHA staining stripes and increased the staining area. The ratio of the GBHA staining area to the maturation enamel surface was about 25% in the control, but this value increased about 60% at 8 and 24 hr after the colchicine injection. Lumicolchicine, which does not have the ability to disrupt microtubules, did not cause any significant changes in the enamel surface. The incorporation of 45Ca to the maturation enamel was also reduced by colchicine. Since the hypocalcemic action of microtubule inhibitors may be related to the change of the enamel surface, other drugs, sodium salicylate and sodium fluoride, that have a hypocalcemic action were tested. The staining pattern was not altered by these drugs. Therefore, the hypocalcemic action was independent of the changes of the GBHA staining pattern. These results indicated that the disruption of microtubules in the ameloblasts inhibited calcium movement in the maturation enamel, resulting in the disarrangement of the GBHA staining pattern.

Perceptions of schizophrenic patients and their therapists: application of the semantic differential technique to evaluate the treatment relationship.

This study is an attempt to evaluate the treatment relationship with schizophrenic patients by examining the patients' and their therapists' perceptions of themselves and each other, which are hypothesized to reflect features of the relationship. One hundred fifty-eight schizophrenic patients and 11 psychiatrists who maintained a supportive relationship with the patients as a therapist estimated their perceptions using the semantic differential (SD) technique with 17 adjective pairs. Eight composite scales with sufficient internal consistency were constructed from the estimations. The interrelationship among the perceptual elements, which was represented by correlation analysis of the composite scale scores, seemed consistent with our clinical experience. A factor-analytic study of the scales yielded 3 orthogonal factors that could be assumed to characterize the treatment relationship. The patient-therapist cooperation factor indicated the degree of trust between the two participants, supposedly the affective or relational aspect of the therapeutic alliance. The therapist passivity factor reflects the therapist's passive role-taking and the clinical stability of the patient. The patient strength factor was related to the condition-related and characterological strength of the patient. It is demonstrated that the estimations performed by patients and therapists are valid and useful for evaluation of the treatment relationship in the current status.

The natural course of atraumatic shoulder instability.

Over the years, we have observed a shifting among loose shoulder, voluntary dislocation, habitual dislocation, and sustained subluxation, leading us to the conclusion that they are all varieties of the same condition: atraumatic shoulder instability. For this study, we followed the natural course of atraumatic shoulder instability in 341 patients (573 shoulders) for 3 years or more. There were 467 cases of loose shoulder, 49 cases of voluntary dislocation, 56 cases of habitual dislocation, and 1 case of sustained subluxation. The average follow-up period was 4 years and 6 months. Spontaneous recovery occurred in 50 cases. The average age of patients at the onset of atraumatic shoulder instability who exhibited a change in instability was 14.6 years. The average age of patients at the onset of atraumatic shoulder instability who exhibited no change in shoulder instability was 19.4 years. There was a significant difference of P < .01 in the age of onset between these two groups. The incidence of spontaneous recovery in the group that discontinued overhead sports was 8.7 times greater than in the group that continued to play overhead sports. The incidence of spontaneous recovery in the group that discontinued non-overhead sports was only 1.4 times greater than in the group that continued to play non-overhead sports. However, no instance of spontaneous recovery was observed among patients who changed from playing non-overhead sports to playing overhead sports. The spontaneous recovery of atraumatic shoulder instability encountered in this study shows that it is best to place priority on observing the course of atraumatic shoulder instability for several years and to avoid performing unnecessary surgery.