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Biomedical subjects

H Toyooka

Publications and source records attributed to H Toyooka.

At least 199 records · Page 11Linked to original sources
PubMed1984

[Significance of hematoma irrigation with trephination therapy (HITT) in the management of acute subdural hematoma].

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)

Adult↗
PubMed1984

[Auditory evoked brain-stem responses (ABRs) in brain dead status].

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)

Adult↗
PubMed1983

[Some practical problems of clinical diagnosis of brain death].

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)

Adolescent↗
PubMed1979

An analgesic action of intranvenously administered lidocaine on dorsal-horn neurons responding to noxious thermal stimulation.

Using extracellular single-unit recording techniques, effects of intravenously administered lidocaine on dorsal-horn nociceptive neurons were studied in cats made decerebrate whose spinal cords had been transected. Thirty-seven neurons in Rexed lamina V responding to high-threshold mechanical and noxious thermal stimuli (radiant heat, using Hardy-Wolff-Goodell dolorimeter) were studied. Lidocaine hydrochloride, 2.5, 5, and 10 mg/kg, iv, produced dose-related suppression of both spontaneous activity and responses of these neurons to noxious thermal stimulation. Spontaneous discharge frequencies at maximum suppression, observed 3--7 min after administration of each of the three doses of lidocaine were 64 +/- 14 (mean +/- 1 SE), 32 +/- 8, and 25 +/- 9 per cent of control values, respectively; responses to noxious thermal stimuli were 83 +/- 5, 52 +/- 8, and 39 +/- 7 per cent of the control values, respectively. Threshold skin temperature to noxious thermal stimulation increased from 44.7 +/- 0.4 C (control) to 46.3 +/- 0.7 C with lidocaine, 5 mg/kg (P less than 0.05), to 47.8 +/- 0.8 C with lidocaine, 10 mg/kg (P less than 0.01). The times necessary for recovery varied in a dose-related fashion. Plasma lidocaine concentrations 5 min after lidocaine, 5 mg/kg, averaged 3.6 +/- 0.7 microgram/ml. These data support the clinical impression that intravenously administered lidocaine produces analgesia at plasma concentrations of 3--10 microgram/ml. It is suggested that lidocaine may block conduction of nociceptive impulses, at least in part, by suppression of spinal-cord nociceptive neurons.

Analgesics↗
PubMed1979

Effects of morphine sulfate on dorsal-horn neuronal responses to graded noxious thermal stimulation in the decerebrate cat.

Effects of morphine sulfate upon activity of the neurons of dorsal-horn lamina V as evoked by graded noxious thermal stimuli applied on the receptive field were studied in spinal cord-transected, decerebrate cats utilizing an extracellular microelectrode recording technique. All single units studied (n = 30) responded to noxious thermal as well as to noxious mechanical stimulation. Their spontaneous discharge frequency was 9.7 +/- 1.5 (mean +/- 1 SE) impulses/sec (IPS), the threshold skin temperature was 44.8 +/- 0.2 C, and a linear correlation existed between skin temperature and discharge frequency at 6.7 +/- 0.6 IPS/degree C. Morphine, 1 and 2 mg/kg, iv, suppressed spontaneous activity by 53 +/- 6 and 84 +/- 6 per cent, respectively; increased threshold skin temperature to 46.5 +/- 0.3 and 47.9 +/- 0.5 C, respectively, and maintained the linear correlation between skin temperature and discharge frequency but depressed the mean slope of the regression line to 4.5 +/- 0.7 and to 2.4 +/- 0.4 IPS/degree C, respectively. Naloxone, 0.02--0.04 mg/kg, iv, reversed all of these changes produced by morphine. The results of the present study are, to the authors' knowledge, the first demonstration of the suppressive effect of morphine on the spinal nociceptive neurons in Rexed lamina V as they respond to graded noxious thermal stimuli. These results may explain the analgesic action of morphine at the spinal level.

Animals↗
PubMed1979

Effects of ketamine on nociceptive cells in the medial medullary reticular formation of the cat.

Anatomic, physiologic and behavioral evidence suggests that the neurons in the nucleus reticularis gigantocellularis of the medial medullary reticular formation may act as a relay station for the transmission of nociceptive information from the spinal cord to higher brain centers. The nucleus reticularis gigantocellularis may also be the site of action of analgesic agents, such as ketamine hydrochloride. Utilizing extracellular microelectrodes in 23 decerebrate cats, the authors measured the effect of ketamine on neurons in the nucleus reticularis gigantocellularis that were excited by electrical stimulation of peripheral nerves. The frequency of spontaneous single-unit firing activity in the nucleus reticularis gigantocellularis was suppressed by 31 +/- 11 (mean +/- 1 SE) and by 62 +/- 7 per cent with ketamine, 1.0 and 2.5 mg/kg, iv, respectively. The frequency of evoked single-unit activity was suppressed by 57 +/- 9 and 79 +/- 5 per cent with ketamine, 1.0 and 2.5 mg/kg, respectively. Ketamine produces significant depression of single-unit activity of the cells in the nucleus reticularis gigantocellularis, suggesting that this may be an important site of its analgesic action.

Animals↗