PubMed Health⌕ Search

Biomedical subjects

T Shigeno

Publications and source records attributed to T Shigeno.

At least 55 records · Page 3Linked to original sources
PubMed1989

[Surgical treatment of spasmodic torticollis: effectiveness of microvascular decompression].

We report two patients of spasmodic torticollis who underwent different types of surgery according to their pathogenetic mechanisms. The first case was a 42-year-old man who had two years history of right-sided antecollis. EMG of the sternocleidal muscle on the affected side showed pathological findings. Characteristic findings on the vertebral angiography were a low position of the branching of tortuous PICA. At operation, we confirmed sandwich-like compression of left accessory nerve between the PICA and vertebral artery. Decompression of the nerve from these arteries led to a remarkable relief of the symptom. The second case was a 70-year-old man whose neck had been forced to bend backward; retrocollis over two years. EMG study was negative. The vertebral angiography showed no abnormality, either. Because there was no evidence of vascular compression on both accessory nerves at surgery, we chose bilateral C1-3 anterior root section which was effective in consequence. We found so far sixteen cases of spasmodic torticollis in the literature including ours who were benefited by microvascular decompression (MVD). All of them presented antecollis or horizontal type. The characteristic operative finding was the compression of the accessory nerve located at between the dural perforation of the vertebral artery and dural attachment of C1 dentate ligament. We can therefore propose a mechanism that the compression at the junction of the central and peripheral myelin causes such a neuroexcitatory symptom as in cases of facial spasm and trigeminal neuralgia.(ABSTRACT TRUNCATED AT 250 WORDS)

Accessory Nerve↗
PubMed1989

[The effectiveness of FID-CT (functional image of dynamic CT) for the evaluation of early cerebral ischemia].

A computer program was newly developed to display the ischemic area from the serial dynamic CT scan, namely the functional image of the dynamic CT (FID-CT). The principles of FID-CT are as follows; Seven rapid-sequence dynamic CT scans were taken following a peripheral bolus intravenous injection of 40 ml of iopamidol. As the data from each scan can be separated into three consecutive segments, we obtained 21 images during 44 seconds. Time density curves of each pixel were calculated employing Gamma variate fitting method. Eight functional parameters obtained from this curve were displayed with gray-scale pixel by pixel. These eight images were functional images obtained from dynamic CT. Only three or four minutes were required to complete all the calculations. Twenty-two patients were examined with both FID-CT and 123I-SPECT. In each case, the lesion detected by FID-CT was remarkably consistent with that shown by SPECT. Two representative cases were presented. The authors believe that FID-CT is a very useful diagnostic method in the acute stage of cerebral ischemia because the method can be quickly and easily performed and it discloses the ischemic area with fair certainty.

Aged↗
PubMed1987

A novel concept on the pathogenetic mechanism underlying ischaemic brain oedema: relevance of free radicals and eicosanoids.

A survey on literature reports and our own experimental studies on the pathogenetic mechanisms underlying ischaemic brain oedema is given and a new concept proposed. In regional incomplete ischaemia the lipoxygenase activity is enhanced, presumably caused by an increase of free radicals and hydroperoxides, leading to an enhancement of endothelial Na+, K+-AtPase and increased sodium and water transport from blood to brain. The aggravation of brain oedema and post-ischaemic hypoperfusion following recirculation appears to be mainly due to an activation of the cyclo-oxygenase pathway with release of oxidants from PGG2, which causes non-specific but detrimental damage to the endothelial and parenchymal cells. This new concept may open future perspectives in treatment which are briefly discussed.

Animals↗
PubMed1987

Quantitative assessment of early brain damage in a rat model of focal cerebral ischaemia.

A method for the volumetric assessment of early cerebral infarction, together with its statistical and biological validation, is described. In halothane anaesthetised rats the stem of the right middle cerebral artery was occluded and 3 hours later (with full monitoring of respiratory and cardiovascular status) the animals were killed by perfusion fixation. In normotensive normocapnic animals the volume of infarction was 52 +/- 4 mm3 in the cerebral cortex and 21 +/- 1 mm3 in the corpus striatum. The reproducibility of the volumetric assessment was found to be excellent (coefficient of correlation 0.995 on 18 replicate measurements). The minimum number of stereotactic levels which must be assessed to yield accurate volumetric measurements of infarction is 8. The method is sensitive at detecting alterations in the amount of infarction. For example, it can readily detect the increase in amount of structural damage in cerebral cortex following a transient episode of hypotension. This approach allows an objective assessment of drug therapy and management strategies in the treatment of cerebral infarction.

Animals↗
PubMed1985

Pure cortical ischemia versus striatal ischemia. Circulatory, metabolic, and neuropathologic consequences.

Selective ischemic damage was produced either involving only the cortex or together with the striatum by occlusion of the middle cerebral artery proximal or distal to the lenticulostriate artery in the rat. The consequences in local cerebral blood flow, local cerebral glucose utilization, and neuropathology were investigated in the acute stage of ischemia. Caudate damage produced by proximal occlusion resulted in such secondary alterations as enhanced blood flow and metabolism in areas remote from the main lesion, such as in the globus pallidus and substantia nigra ipsilateral to occlusion. After distal occlusion, however, there were two patterns distinctly different from each other in the appearance of the autoradiograms. One was ipsilateral and the other was contralateral enhancement of blood flow and metabolism involving the striato-pallido-nigral axis without any striatal damage. We therefore suggest that these secondary alterations in circulation and metabolism contribute to a varied neurological dysfunction after focal cerebral ischemia. Furthermore, our currently introduced model of selective ischemic lesioning is important in studying the roles of cortical and striatal influences in ischemic pathophysiology.

Animals↗
PubMed1985

Blow-out fracture of the orbit in 4 children.

4 cases of blow-out fractures of the orbit in children are presented. Four 6- to 12-year-old boys were successfully operated on via an orbital and transsinus approach. As material for restoration of the broken orbital floor, Silastic was used in 3 patients.

Child↗
PubMed1985

Recirculation model following MCA occlusion in rats. Cerebral blood flow, cerebrovascular permeability, and brain edema.

A new model for establishing a successful and consistent arterial recirculation has been devised following middle cerebral artery (MCA) occlusion in the rat. A snare ligature was introduced at the stem of the MCA just distal to the lenticulostriate branches, and occlusion and recirculation were performed by pulling and releasing the thread. This method had an advantage over the use of a small clip which caused damage to the artery without good recirculation. Study of local cerebral blood flow using carbon-14 (14C)-iodoantipyrine, of cerebrovascular permeability using 14C-aminoisobutyric acid, and of brain-water content using the microgravimetric technique was performed upon recirculation following various periods of occlusion and compared with the results in permanent ischemia. A reactive hyperemia was noted within the previously ischemic area immediately upon recirculation following either a 30-minute or a 2-hour ischemic period. One or 2 hours later, delayed hypoperfusion developed in this region, but the circulation over the periphery of the ischemic area recovered well. Cerebrovascular permeability was not, however, altered during the time courses studied. Topographic changes in tissue specific gravity were compared between permanent and transient ischemia in the corresponding time-courses. Although there was a greater decrease in tissue specific gravity following recirculation when the ischemic period was maintained longer, edema formation was resolved by recirculation. Further study is required to determine thresholds of ischemic brain damage and edema formation at recirculation following focal cerebral ischemia.

Aminoisobutyric Acids↗
PubMed1985

[The pathomechanism underlying ischemic brain edema: the role of Na+, K+-ATPase of the brain microvessels].

In the present study, the anti-edema effect of AVS [1,2-bis (nicotineamide)-propane] was evaluated using the cat MCA occlusion model with or without recirculation. In the prolonged ischemia (PI) group, cortical edema as assessed by the changes in specific gravity, developed in those cortical areas where the mean 1-CBF was less than 25-30 ml/100 g/min during MCA occlusion (4 hours). In the recirculation group (2 hours' ischemia followed by 2 hours' recirculation: RC group), the ischemic threshold for edema development was almost the same as in the PI group. In both groups, the drop in cortical specific gravity was significantly suppressed by AVS. Regarding the time-course of 1-CBF, there was no difference between the PI-AVS-treated and PI-saline-treated groups. In the RC group, however, the postischemic hypoperfusion was significantly ameliorated by AVS. Based on the present and previous data showing the antiedema effect of AVS, the mechanism of action of AVS was discussed in relation to the pathomechanism underlying ischemic brain edema. Our new concept of ischemic brain edema is briefly stated below. Related in vitro studies have shown the followings: (i) the influx of sodium not of proteins is the principal cause of ischemic brain edema: (ii) the eicosanoid synthetic capacity of the brain microvessel (MV) is increased simultaneous to edema development (iii) an elevation in the level of hydroperoxides enhances the activities of Na+, K+-ATPase as well as the arachidonate cascade of MV. These data suggest that free fatty acids and free radicals liberated following cerebral ischemia stimulate the activity of the MV-Na+, K+-ATPase, which results in increased sodium influx across the BBB. AVS was shown to scavenge hydroxyl radicals and to inhibit the stimulatory effects of a lipid hydroperoxide (15-HPAA) on the activities of Na+, K+-ATPase and the arachidonate cascade of the MV. These actions of AVS may be linked to its antiedema effect.

Animals↗
PubMed1985

Pneumatosis cystoides intestinalis and trichloroethylene exposure.

A case-control study was carried out to assess the association between pneumatosis cystoides intestinalis (PCI) and working conditions, including occupational exposure to organic solvents. Thirteen patients with primary PCI were individually matched with controls by sex, age, and admission year. It was found that there was a close association between the development of primary PCI and occupational exposure to trichloroethylene (TCE). Twelve of 13 patients with PCI (92.3%) were found to have been exposed occupationally to TCE, and the healing and recurrence of PCI in these patients substantially paralleled the profile of their occupational exposure to TCE. Two pairs of patients with PCI had been working in the same factories, where they had degreased camera lenses with TCE. These results suggest that chronic exposure to TCE could be one of the etiological factors in PCI.

Adult↗
PubMed1983

Clinical signs and evoked response alterations associated with chronic experimental cord compression.

Cortical and spinal evoked potentials were used to monitor the effect of experimental chronic cord compression in cats. An implantable compression screw made it possible to maintain the animals unrestrained. The mean compression period was 10 weeks (maximum 16.5 weeks). Compression was increased by stepwise tightening of the screw at intervals of 4 to 7 days under ketamine anesthesia. Evoked potentials were monitored before and after each compression step with repeated recordings, and were analyzed in terms of alterations in amplitude, latency, and waveform. Amplitude response curves were plotted where the amount of compression at each recording was expressed as a percentage of total compression. Changes in spinal evoked potentials occurred rather early (mean 36% of total compression), while obvious cortical evoked potential changes appeared rather late (mean 91% of total compression). Neurological alterations appeared later than alterations in spinal evoked response but prior to alterations in cortical evoked response. Thus, alterations in cortical somatosensory evoked potentials in the presence of chronic spinal compression indicate a severe degree of compression and do not seem to be of diagnostic value in the early detection of chronic spinal cord compression. It is suggested that the monitoring of spinal rather than cortical evoked responses would be more useful in locating and detecting chronic compression spinal cord damage.

Animals↗
PubMed1983

Experimental investigation on the spinal cord evoked injury potential.

Averaged somatosensory evoked potentials from the epidural space in response to sciatic nerve stimulation were recorded in bipolar and common reference mode in cats following various types of injury. An investigation was conducted on the development and properties of the spinal evoked response recorded from the center of the injury site, designated here as the "spinal cord evoked injury potential." Typically it is a two-peak monophasic positive potential, approximately 40 msec in duration, with a slight negative afterwave. With increasing distance from the site of injury, its amplitude rapidly decreases, whereas latency remains constant. The common reference recording technique resulted in an earlier and better demonstration of the evoked injury potential, especially when it was transitory or incomplete. When impairment of conduction developed gradually, the evoked injury potential developed gradually too. In serial recordings along the spinal cord axis, the transition from a normal triphasic to a monophasic evoked injury potential allowed a precise localization of the lesion. These data suggest that the diagnostic value of intraoperative spinal cord monitoring may be increased by adopting a technique that incorporates several epidural recordings with a common reference recording technique. The spinal cord evoked injury potential seems to be a more sensitive indicator of spinal cord injury than the cortical evoked potential. The findings are discussed in the light of the presently developing spinal cord monitoring techniques.

Animals↗