Shuhei Miyazaki

Growth of totally thrombosed giant aneurysm within the posterior cranial fossa

SummaryWe report a case in which growth of a totally thrombosed giant aneurysm of the posterior cranial fossa was demonstrated by computed tomography (CT) scans repeated after 4 years. A magnetic resonance (MR) image demonstrated an onion-skin-like, laminated structure within a calcified wall. The laminated structure had developed around an old thrombosis, without any communication to the flowing blood. It showed intensities indicating recent clots, revealing that the giant aneurysm had grown by recurrent intramural hemorrhage rather than by intraluminal accumulation of thrombotic materials. This case illustrates that totally thrombosed giant aneurysms still have the potential of growth.

Characterization and Modification of Brain Activity with Deep Brain Stimulation in Patients in a Persistent Vegetative State: Pain‐Related Late Positive Component of Cerebral Evoked Potential

A series of eight patients in a persistent vegetative state (PVS) were subjected to chronic deep brain stimulation (DBS) for the purpose of promoting recovery from the PVS. The characteristics of the brain activity in these patients were evaluated from the late positive component of the cerebral evoked potential in response to painful stimuli (pain‐related P250). While any neurological scoring system for the comatose state includes evaluations of motor reactions to painful stimuli, the pain‐related P250 is unique in terms of its ability to assess the cortical responsiveness to painful stimuli directly and quantitatively without involving functions of the motor system. It was found that the pain‐related P250 was more or less depressed in patients in a PVS. It was repeatedly demonstrated in four patients, however, that the pain‐related P250 could be transiently increased by preceding stimulation of the mesencephalic reticular formation. Furthermore, a persistent increase in the pain‐related P250 was produced in these four patients following chronic DBS of the mesencephalic reticular formation or nonspecific thalamic nuclei for more than 6 months, and this was correlated with the clinical improvements. These results imply that responsiveness at the cortical level to pain is depressed in the PVS. It also appears that some fraction of the depression may, however, be functionally produced and potentially reversible.

Magnetic resonance imaging of cavernous sinus cavernous hemangiomas.

SummaryRadiological findings of surgically verified cavernous hemangiomas of the cavernous sinus are presented with special reference to the appearance in magnetic resonance imaging. Differences in radiological features of the cavernous sinus cavernous hemangiomas and intracerebral cavernous hemangiomas are discussed.

Electrophysiological evidence favoring intracaudate axon collaterals of GABAergic caudate output neurons in the cat.

Stimulation of the entopeduncular nucleus in the cat was shown to evoke inhibitory responses with a short onset-latency in the caudate nucleus isolated from its afferents. These inhibitory responses are shown to be GABAergic, and some of them are suggested to be monosynaptic in nature.

Post-ischemic potentiation of Schaffer collateral/CA1 pyramidal cell responses of the rat hippocampus in vivo: involvement of N-methyl-d-aspartate receptors

The present study examined the functional changes in the hippocampal CA1 pyramidal cell system in vivo occurring after 12-min forebrain ischemia in the rat. A population excitatory postsynaptic potential and orthodromic population spike of CA1 pyramidal cells to stimulation of the Schaffer collaterals were potentiated at 6-8 h post-ischemia. These changes were not associated with an increase in excitability of the CA1 pyramidal cells as evaluated from the antidromic population spike induced by alveus stimulation, suggesting the presence of an increased synaptic efficacy. The post-ischemic potentiation was prevented by pretreatment with the N-methyl D-aspartate (NMDA) receptor antagonist, MK801, in a dose-dependent manner. These findings suggest that 12-min forebrain ischemia in the rat activates NMDA receptors, which results in an increase in synaptic efficacy to the CA1 pyramidal cells at 6-8 h post-ischemia.

Oedema Fluid Formation Within Contused Brain Tissue as a Cause of Medically Uncontrollable Elevation of Intracranial Pressure: The Role of Surgical Therapy

In patients with focal cerebral contusions, medical therapies have generally been advocated unless haemorrhages significantly contributing to the elevated intracranial pressure (ICP) exist. We report here several lines of clinical evidence which indicate that (1) enormous amount of extracellular oedema fluid is formed within contused brain tissue, (2) the formation of extracellular oedema fluid within contused brain tissue alone can be a cause of medically uncontrollable elevation of ICP and (3) surgical excision of the contused brain tissue provides excellent control of the elevated ICP in such patients. The excision of contused brain tissue appears to be the only therapy currently available to alleviate the formation of extracellular oedema fluid in cerebral contusions. We believe that, if ICP is elevated primarily by extracellular oedema due to cerebral contusions and the elevated ICP is medically uncontrollable, surgical excision of contused brain tissue should be carried out without delay regardless of the size of associated haemorrhages.

Benign osteoblastoma of the temporal bone of an infant

Benign osteoblastoma is a rare neoplasm of bone tissue most commonly involving the vertebral column and long bones. Occurrence in the calvarium is extremely rare, and no cases in infants have previously been described. We report a case of benign osteoblastoma occurring in the temporal squama of an infant. The clinical features of this type of tumor occurring in the calvarium are briefly discussed.

Temporal pattern of survival and dendritic growth of fetal hippocampal cells transplanted into ischemic lesions of the adult rat hippocampus

Cell suspensions obtained from the fetal hippocampus were transplanted into the adult rat hippocampus at 1 or 4 weeks after transient forebrain ischemia. Only when the ischemia induced death of most of the CA1 pyramidal cells of the host hippocampus and transplantation was performed at 1 week after the ischemia, did a large number of transplanted cells survive and the most extensive dendritic growth was demonstrated by microtubule-associated protein 2 immunohistochemistry. The dendrites of the cells located in the ventral part were oriented ventrally, lining up similarly to the parallel arrangements of apical dendrites of normal CA1 pyramidal cells. These findings suggest that certain forms of trophic factors, which appear to occur in association with the presence of free terminals of afferent fibers during the earlier period after ischemic insult, are involved in the survival of and dendritic growth from transplanted hippocampal cells.

Supranormal levels of serotonin and its metabolite after raphe cell transplantation in serotonin-denervated rat hippocampus ☆

Transplantation of fetal raphe cells (14 days of gestation) into the adult rat hippocampus, 2 weeks following serotonin (5-HT)-denervation with intracisternal injection of 5,7-dihydroxytryptamine, can restore 5-HT and 5-hydroxyindoleacetic acid (5-HIAA) levels in the hippocampus to far beyond normal values. Transplantation into the unilateral hippocampus produces asymmetrical turning behavior after administration of the 5-HT releasor, p-chloroamphetamine (IP), comparable to the behavior reported for rats with 5-HT denervation of the unilateral hippocampus. The effect is blocked by prior depletion of 5-HT with p-chlorophenylalanine (IP). The asymmetry in 5-HT levels are correlated with the behavioral change. These data indicate that a large amount of 5-HT is released from nerve terminals of transplanted raphe cells, and suggest that the supranormal levels of 5-HT and 5-HIAA after raphe cell transplantation are neurochemical correlates of 5-HT hyper-innervation of the hippocampus which has been reported previously.

N-methyl-D-aspartate receptor-mediated, prolonged afterdischarges of CA1 pyramidal cells following transient cerebral ischemia in the rat hippocampus in vivo.

We previously reported the post-ischemic potentiation (PIP) of synaptic efficacy in hippocampal Schaffer collateral/CA1 responses of the rat beginning at 6-8 h following 12 min transient cerebral ischemia in vivo. The present study demonstrated that repetitive stimulation with a relatively low frequency (5 Hz, 6 s), which produced short-lasting afterdischarges (ADs; duration, 4.49 +/- 4.26 s; n = 7) in sham-controls, resulted in prolonged ADs (duration, 26.33 +/- 12.63 s; n = 6; P < 0.001) at the same period after ischemia. The PIP was not affected by 2-amino-5-phosphonovalerate (APV) administered via microdialysis at 7 h post-ischemia. The prolonged ADs in response to repetitive stimulation were, however, reversed to short-lasting ADs (duration, 7.13 +/- 1.44 s; n = 4; P < 0.02) by the same procedure, leaving the response to single stimulation unaffected. These findings suggest that, during the reperfusion period, Ca2+ influx into the CA1 pyramidal cells can be greatly increased through N-methyl-D-aspartate (NMDA) receptor-coupled ion channels if appropriately timed multiple synaptic inputs bombard these cells. Such Ca2+ influx may contribute to delayed death of CA1 pyramidal cells after transient cerebral ischemia if synaptic activity is maintained at relatively high levels during the reperfusion period.