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In order to evaluate glucose metabolism in brain death, 18F-FDG-PET scans were performed in three patients with clinically highly suspected brain death. One case was caused by head trauma and other two cases were by subarachnoid hemorrhage. All of them were in deep coma without spontaneous breathing, whose intracranial pressure was remarkably elevated up to the level of mean arterial pressure. Nineteen frames of dynamic scan were started soon after intravenous injection of 18F-FDG for one minute per frame, followed by 10 minutes of static scan which started 40 minutes after the injection. Both in dynamic and static scan, no significant intracranial accumulation of 18F-FDG was seen in all of three cases. This finding can be interpreted as the evidence that there is no significant glucose utilization from blood in the brain. This is the first report of clinical application of 18F-FDG-PET to brain death. Our results support the clinical diagnosis of brain death and 18F-FDG-PET can be of value for the assessment of glucose metabolism in patients with suspected brain death.

A 62-year-old woman was admitted complaining of clumsiness in both hands. On neurological examination, bilateral hand muscles were weak, both legs were spastic and hyperreflexic, all the extremities were hypoesthetic. Urological examination revealed detruser sphincter dyssynergia. Spinal CT scan demonstrated an iso density mass lesion in the cervical spinal cord, and it was markedly enhanced. On MRI, it was also markedly enhanced by Gd-DTPA. The operative finding was that an oval shaped tumor was buried in the spinal cord and was totally removed. Its histological diagnosis was neurofibroma. Intramedullary neurofibroma is rare and only 18 cases have been reported. In this case the tumor seemed to have arisen at the root entry zone and to have grown sub-pially.

Two patients with atrophy and weakness of intrinsic had muscles innervated by the deep branch of the ulnar nerve except abductor digiti quinti muscle and without any sensory symptoms were reported. They were house-wives aged thirty and fourty-four, respectively, without any specific history of trauma or occupation. Neurological and neurophysiological examination pointed out that the lesion situated in the deep branch of the ulnar nerve. Both of them were operated on. At operation, no abnormal structure were found in the canal of Guyon, though, the deep branch of the ulnar nerve was enlarged at the pisio-hamate hiatus where the branch to the abductor digiti quinti has taken off. In one of the cases, microsurgical removal of the epineurium of the deep branch revealed that each funiculus has lost its course into irregularly enlarged mass, which thought to be neoplastic change. In this case the deep branch was replaced by cable grafts about two centimeters in length by using the sural nerve. Histological findings of this case were as follows: there was no neoplastic or inflammatory change, there was no normal axon pa surviving and that very little regenerated axon and marked interneural fibrosis were observed, which indicates that the nerve lesion was caused by chronic compression. In the other case, the attachment of the membranous tendon of the flexor digiti quinti brevis and opponence digiti quinti muscle to the hook of the hamate was removed. No marked improvement was obtained in both of the cases, because they were too late to be operated on (ten and three years has passed since they noticed muscular atrophy, respectively).

A case of myelopathy caused by hypertrophy of the posterior longitudinal ligament at the cervical spine is reported. A 71-year-old man was hospitalized with myelopathy with progressed during the last two months. Plain X-ray of the cervical spine revealed only mild spondylotic change. Myelography demonstrated completely blocked contrast medium at C4 to C5 vertebral height due to epidural mass. This epidural mass was localized ventral to the spinal cord from C3 to C5. CT scan revealed slightly high density area behind the vertebral body. On surgery, no evidence of disc fragment but only hypertrophied posterior longitudinal ligament which was removed was found to be a cause of cord compression. Excellent recovery of neurological symptoms after operation was obtained. On histological study, remarkable hypertrophy, edema, hyalinoid degeneration and a little calcification of the ligament was found, which did not show any evidence of new bone formation. HPLL was characterized by thickened and broad epidural mass in the ventral side of cervical cord with Hounsfield number of 90-156 on CT scan, which is not very easy to differentiate from metastatic epidural tumor. The cause of HPLL is not well elucidated, though, this may be a new category of compression myelopathy.

Decompressive craniectomy in the management of acute traumatic subdural hematoma (acute SDH) has been advocated as a treatment for the cerebral edema or swelling associated with it. The bony decompression with dural grafting seems successful in some patients, but surely enhances cerebral swelling and exacerbates edema in others. Whether the external or internal decompression could be justified is therefore a subject of controversy for the surgical treatment of choice. The authors, herein, proposed the new method with small craniectomy, 3 cm in diameter and irrigation with Nelaton's catheter for acute SDH with cerebral edema or swelling, that is the hematoma irrigation with trephination therapy (HITT) and performed it in 27 adult cases, 19 to 84 years of age (20 males and 7 females), who were transported within 24 hours after trauma and hospitalized in Department of Emergency Medicine, University of Tokyo Hospital during the period from January, 1982 to January, 1984, whose Glasgow coma scale points were 3 to 8 on admission, 16 cases (59%) of whom showed unilateral or bilateral absence of light reflex. The patients were all placed under the intensive care, using artificial ventilation (27 cases, 100%), hemodynamic management with Swan-Ganz catheter insertion (10 cases, 37%), continuous intracranial pressure monitoring (27 cases, 100%) and barbiturate therapy (13 cases, 48%). Ten cases (37%) recovered, 3 (11%) fell in vegetative state, 2 of whom died of medical complications afterwards and 14 (52%) could not avoid progressive deterioration to result in brain death.(ABSTRACT TRUNCATED AT 250 WORDS)

Auditory evoked brain-stem responses (ABRs) were recorded in 19 out of 52 brain dead cases in Department of Emergency Medicine, University of Tokyo Hospital from May, 1981 to January, 1984. The causes of brain death were severe head injury (9 cases), cerebro-vascular disease (7 cases), anoxia (2 cases), hydrocephalus (1 case). Eleven cases of them fulfilled the clinical criteria which included absence of cortical and brain-stem functions excluding severe hypothermia and depressant drug intoxication. The remainders who were subjected to barbiturate therapy were diagnosed as brain death for non-filling phenomenon in cerebral angiography. Results were as follows; Fourteen cases (74%) had no identifiable ABR waves. One case (5%) had only 1st wave. Three cases (16%) had 1st and 2nd waves. One case (5%) had 1st, 2nd, and 3rd waves. In spite of definition of clinical brain death, 5 cases had at least 1st wave, and therefore these datum suggested that ABR might have less clinical utility in diagnosis of brain death. Each case did not necessarily demonstrate the total extinction of ABRs, as was shown in (2) to (4) mentioned above. The clinical status which met the criteria of brain death might therefore possibly imply any conditions in which brain death was impending gradually to result in the total brain death of cerebrum through medulla oblongata. Under these circumstances, how barbiturate might produce ABRs abnormality remained unsolved, though it has been said not to produce ABRs abnormality. Among 8 cases under barbiturate therapy, there were 5 cases with no identifiable waves and 3 cases with 1st and 2 nd waves.(ABSTRACT TRUNCATED AT 250 WORDS)

The authors experienced thirty brain deaths including eighteen head injuries and seven cerebrovascular accidents during the period from Nov. 1980 to Dec. 1982 and encountered with some practical problems on clinical diagnosis of brain death. In sixteen patients subjected to barbiturate (pentobarbital) therapy, the attempt to meet the criteria of brain death made it necessary to confirm the total cerebrocirculatory arrest as well as to measure the serum concentration of pentobarbital and assure its level low enough. But as a result of the angiograms performed in twenty-four cases the cerebral angiography sometimes failed to give sufficient evidence to confirm it not merely because of the angiographical intracranial delayed opacification but also because of the dissociation of filling between supra- and infratentorial spaces or between right and left hemispheres. And besides the contrast enhancement of cerebral vessels was verified in computed tomograms of two cases among ten cases who had already met the criteria and demonstrated angiographical nonfilling phenomenon. The angiographical narrowing of C 1-2, A 1, M 1 portions or basilar artery observed on serial angiograms preceding the angiographical nonfilling phenomenon was regarded as direct vascular compression by cerebral swelling or vasospasm and considered to suggest that brain death might be impending. At present the continuous monitoring of intracranial pressure performed in twenty-six cases proved to be a convincing guide to suspicion of brain death or impending brain death according to decrease in cerebral perfusion pressure and appearance of so-called plateau waves recorded in four cases.(ABSTRACT TRUNCATED AT 250 WORDS)

Respiratory insufficiency following acutely elevated intracranial pressure (ICP) may occur as a result of pulmonary edema which is supposed to be caused by increased sympathetic discharge from the central nervous system. Supporting experimental studies have been reported concerning this immediate respiratory consequence, while delayed respiratory consequences with an elevated ICP remain poorly characterized clinically. We studied delayed effects of an increased ICP on respiratory functions (pulmonary shunt ratio (Qs/Qt), respiratory index (A-aDO2/PaO2), oxygenation index (PaO2/FIO2) ), extravascular lung water (EVLW), and hemodynamics [cardiac index (CI), mean arterial pressure (MAP), mean pulmonary arterial pressure (MPAP), pulmonary capillary wedge pressure (PCWP), systemic vascular resistance (SVR), pulmonary vascular resistance (PVR)] in 15 cases with head injury, 4 with cerebrovascular diseases, and one with hypoxic brain damage. Ten cases had either aspiration, long bone fractures (the syndrome of fat embolism), or pneumonia, and the 10 cases without these pulmonary insults were defined as the cases without pulmonary complications and studied further. Pulmonary functions deteriorated as the ICP rose in the total cases, but in the cases without pulmonary complications, the correlations between the pulmonary functions and the ICP were not significant. None of the hemodynamic parameters correlated with the ICP in both the total cases and the cases without pulmonary complications.(ABSTRACT TRUNCATED AT 250 WORDS)

In the present study, the authors analysed the serial angiographical findings progressing to brain death and their relation to the intracranial pressure (ICP) and the cerebral perfusion pressure (CPP). Seventy two patients, from four to eighty four years old (fourty six males and twenty six females) admitted in the Department of Emergency Medicine, University of Tokyo Hospital during the period from January, 1981 to April, 1986, were studied. Their underlying diseases were supratentorial primary brain lesions except two cases with asphyxias which progressed to brain death. ICP was continuously measured and CPP was calculated as the pressure gradient between the mean arterial blood pressure (MAP) and ICP. The direct carotid angiography was performed to follow the cerebral circulation. Fourty five patients were subjected to barbiturate (pentobarbital sodium) therapy. The degree of the intracranial filling staged as "Non-filling", "Siphon-filling", "Partial-filling", "Delayed-filling", "All-filling" correlated significantly with ICP and CPP. These relationships, however, disappeared once ICP exceeded MAP. When "Non-filling" angiogram was obtained, clinical signs had already showed brain death. On the other hand, minimal flow ("Siphon-filling", "Partial-filling", "Delayed-filling") were still demonstrated in six brain death cases while ICP was approaching its "peak" value. This study showed that clinical diagnosis of brain death preceded the Non-filling phenomenon, suggesting that, for the demonstration of the cerebral circulatory arrest, the angiograms should be performed after the clinical diagnosis of brain death was established and CPP became zero. The evaluation of the extremely slow and minimal filling is still a matter of discussion.(ABSTRACT TRUNCATED AT 250 WORDS)

The effect of high frequency jet ventilation (HFJV) on intracranial pressure (ICP) in the series of seven patients with severe head injury was studied. These patients received mechanical ventilation for respiratory failure accompanied with neural damage or circulatory shock and for ICP control by decreasing PaCO2. ICP was measured continuously by subarachnoid catheter method connected to Gould P-50 strain-gage transducer and controlled by hyperventilation and/or osmotic diuretics during acute phase. Arterial pressure, central venous pressure and intratracheal pressure were measured continuously in the same way. Arterial blood gases were analysed by BG-I of Technicon Co. Ltd. At the weaning from respirator, two methods were applied. One was conventional IMV (with PEEP) and/or CPAP by using IMV mode of Servo 900 respirator or T-piece together with PEEP valve and another was new-fashioned HFJV. Mean intratracheal pressure (mPit) was fixed at 0 mmHg (control value), 5, 10 and 15mmHg in both methods by adjusting PEEP valve or driving pressure of HFJV. The result is that in the same patients ICP was significantly lower during HFJV than IMV/CPAP when mPit was 5 and 10mmHg. Only three cases having been studied at 15mmHg of mPit because circulatory condition would not permit it, significant difference of ICP between HFJV and IMV/CPAP was not detected. PaCO2, being suspected to be the cause of lower ICP of HFJV group, was studied too. But blood gas analysis showed no significant difference neither PaCO2 nor PaO2. The fluctuation of CVP reflecting the change of intrathracic pressure was smaller in HFJV group than in IMV/CPAP group.(ABSTRACT TRUNCATED AT 250 WORDS)

Head injury patients often complicate facial and/or multiple injuries other than cranio-cerebral insults and perplex the emergency staffs. The authors used Brighton epistaxis balloon for such patients with massive nasal bleeding and reported the utility of the balloon not only in such state of emergency but also for a few days to control the hemorrhage mostly caused by craniobasal fractures or rupture of the adjacent vessels. One hundred and twenty-nine patients were transported and hospitalized in Department of Emergency Medicine, University of Tokyo Hospital, Tokyo, Japan during the period from October, 1981 to January, 1983. Nasal bleeding was noted in 29 cases of them and the balloon was used in 10 cases, who were from 19 to 76 years of age, all males and suffered from basal fractures or craniofacial injuries. Six cases of them were also accompanied with fractures in the extremities or pelvis, hemopneumothorax and/or intra-abdominal bleeding and could not but put on "Military anti-shock trousers" for the management of hypovolemic shock, hence the nasal bleeding should be managed immediately in the emergency room. In these situations the balloon was inserted into both nasal cavities in all the patients, to control successfully the nasal hemorrhages one of which contaminated cerebrospinal fluid and three of which were sure to be pulsatile due to arterial injury. The Brighton epistaxis balloon is to be removed within twelve or twenty-four hours, but in the authors' cases the mean duration for the hemostasis was 58.9 hours for 6 survivors and 49.6 hours for all 10 cases.(ABSTRACT TRUNCATED AT 250 WORDS)

The continuous intracranial pressure monitoring has been widely applied in intensive or critical care, but there are various kinds of methods for its monitoring at present. One hundred and forty-one cases mostly with severe head injury were subject to the intracranial pressure recordings in the critical care ward in Department of Emergency Medicine, University of Tokyo Hospital, from October, 1980 through May, 1983, and in Neurosurgical Unit, Showa General Hospital, in April and May, 1984. The authors made several methodological trials for the monitorings in them and compared with one another from the aspect of clinical practice. The subarachnoid catheter was inserted into the subarachnoid or sometimes into the subdural spaces by way of the burr hole in 112 cases and proved not to demonstrate in some cases the intracranial pressure waves clearly due to so called damping phenomenon but to indicate the reliable values, or trustworthy mean pressures in all the cases except for impending brain dead patients with swollen hemispheres and least cerebrospinal fluid remained in intracranial subarachnoid spaces. The ventricular fluid pressure was monitored in nine cases and was most dependable as well as the subarachnoid pressure. The ventricular cannulation and its maintenance were, however, difficult when the ventricles were compressed or deviated, which were often experienced in acute severe head injury and also in impending brain death just because of the same above mentioned reasons. These demerits were attempted to be conqured with epidural pressure monitorings such as the fiberoptic sensor (Ladd) in 17 cases, the intracranial catheter tip pressure transducer (Gaeltec) in nine cases and the sensor of bioimplantable polymer (Plastimed) in three cases.(ABSTRACT TRUNCATED AT 250 WORDS)

In this study, thermal-dye double-indicator dilution method using Lung water computer (Edwards Laboratories) was used to detect the changes of extravascular lung water (EVLW) in 14 patients, including 8 head injuries, one multiple injury, and 5 burns. The coefficient of variation of multiple readings at the same time was 5.04 +/- 3.64% (M +/- SD, n = 180), so reproducibility was excellent. EVLW showed no correlation with cardiac index, Qs/Qt ratio, PAO2/PaO2 ratio, and PaO2/FiO2 ratio, but did show significant correlation with pulmonary capillary wedge pressure (PCWP) (r = 0.50, n = 54, p less than 0.01). In non-septic period of burn patients, EVLW showed good correlation with COP-PCWP gradient (r = -0.75, n = 54, p less than 0.01), better correlation than with PCWP only. In septic period, it had no correlation with the gradient, probably due to the enhanced pulmonary capillary permeability. Although it is very difficult to determine the threshold of EVLW to diagnose pulmonary edema, the elevation of EVLW appeared earlier than the changes of X-ray films. In estimate of EVLW, we must always take into consideration changes in effective vascular bed and pulmonary capillary permeability. The measurement of EVLW was also of much help in the differential diagnosis of pulmonary edema and other lung diseases.

Short-latency somatosensory evoked potential (SEP) was serially monitored in head-injured patients and its clinical significance was evaluated in relation to auditory brain stem response (ABR), prognosis and other parameters such as intracranial pressure (ICP). SEP, ABR, and ICP were monitored serially and automatically in 16 patients with acute head injury. Glasgow Coma Scale (GCS) score was equal to or less than 8 in 14 cases. High dose barbiturate therapy was performed in 7 cases and intracranial hematoma was removed operatively in 14 cases. SEP was recorded from C3'or C4'-Fz leads on the lesion side following stimulation of the contralateral median nerve, and the difference between the two potentials (N20, N13) defined as central conduction time (CCT) was followed at a basic time interval of 10-20 min. The patients were divided into 3 groups according to N20 finding and the prognosis of each group was analyzed. The final outcome (assessed 6 months after injury) was graded according to Glasgow Outcome Scale as follows: good (good recovery, moderate disability), poor (severe disability, persistent vegetative state), death (death). Three patients with no CCT change showed good recovery (table, 11). Out of 7 patients with no N20 on admission, 5 died due to severely increased ICP and the prognosis for the other 2 cases was poor. The last group consisted of 6 patients in whom CCT varied during hospitalization. In 3 out of these 6 cases N20 finally disappeared due to increased ICP and they died in the acute stage.(ABSTRACT TRUNCATED AT 250 WORDS)

A case of 64-year-old Japanese woman with cervical radiculomyelopathy caused by the deposition of both calcium pyrophosphate dihydrate (CPPD) and hydroxyapatite crystals in the cervical ligamentum flavum is reported. The patient developed paresthesia in her both hands and gait disturbance in the previous six months. Neurological examination revealed generalized hyperreflexia and hypesthesia in the C7 region. Neuroradiologically, two nodular opacifications were shown in the C3-4 and C5-6 level. CT scan revealed linear and symmetrical calcifications in the C3-4 and nodular calcifications in the C5-6 level. En bloc laminectomy was performed and the patient was discharged from the hospital with improvements of neurological symptoms. Specimens of the spinal laminae and ligamenta flava were studied by light microscopy, scanning electron microscopy (SEM), energy dispersive X-ray microanalysis (X-MA) on SEM, and an X-ray diffraction study was carried out on the crystals. The results showed A. CPPD crystal depositions throughout the ligamenta flava together with a minimal thickening of the ligaments. The deposition was seen in the midzone of the ligaments forming a plate-like distribution and forming lines in the cut surface, the latter coincided well with the CT finding at the C3-4 level. B. The nodule (7 X 6 X 6 mm in size) at the C5-6 level was composed of two crystals, CPPD and hydroxyapatite, the latter being encased by the former. The thickness of the CPPD layer was quite thin varying from 10 to 100 mu. Myelographically, the spinal cord was most severely compressed by the C5-6 nodule. C. Because of the absence of family histories and predisposing factors, the case was considered one of primary or idiopathic CPPD crystal deposition disease. The origin of the deposition of mixed crystals was discussed and it appeared likely that the central part of CPPD crystal deposition had transformed to hydroxyapatite at the C5-6 level. In the literature a considerable number of cases have been reported under the title, "Calcification of the Ligamentum Flavum", and some of them have been shown to have hydroxyapatite deposition. Considering the great similarities in clinical, radiological and histological findings between the so-called "calcification of the lig. fl." and CPPD crystal deposition disease, the present case was the first to clearly indicate that these two conditions belong to a single category, i.e. CPPD crystal deposition disease.(ABSTRACT TRUNCATED AT 400 WORDS)