Biomedical subjects

T Tsubokawa

Publications and source records attributed to T Tsubokawa.

At least 73 records · Page 4Linked to original sources

PubMed1993

Dynamic changes in cytochrome oxidase activity in the rat somatosensory cortex following thalamocortical deafferentation.

The changes in cytochrome oxidase (CYO) activity in the primary somatosensory cortex (SI) induced by unilateral lesions restricted to the posterior ventrobasal region of the thalamus were investigated by histochemical techniques and photometric semi-quantitation in the rat. The CYO activity decreased rapidly and dramatically in layer IV of the lesioned side, reaching its lowest level within 2 weeks, and remained depressed at 8 weeks post-lesion. Segmentations normally seen in layer IV corresponding to barrels remained absent. While less marked decreases were also noted in other layers, obvious recovery was subsequently observed, attaining levels comparable to those on the intact size at 6 or 8 weeks post-lesion. The persistent decrease in layer IV appears to reflect a reduced thalamocortical activation of the dendritic profiles and neuronal perikarya. The recovery in other layers may represent an increase in the resting level of the initially depressed neuronal activity near to the original levels. The persistent reduction of function in the inhibitory surround, which is normally activated by thalamocortical input, may contribute to the increase in CYO activity.

Afferent Pathways↗

PubMed1993

Pituitary adenoma combined with Rathke's cleft cyst--case report.

A rare pituitary adenoma associated with Rathke's cleft cyst was discovered incidentally in a 44-year-old male admitted after head trauma. Neurological and physiological examination found no abnormalities, except for panhypopituitarism. Computed tomography and magnetic resonance imaging demonstrated a solid mass in the sellar cavity with suprasellar extension, associated with a cystic mass extending into the third ventricle. The tumor was removed subtotally by the transcranial approach. Light microscopy demonstrated that the cyst wall was composed of ciliated columnar cells, cuboidal cells, and goblet cells, and the solid part indicated chromophobe pituitary adenoma. Immunohistochemistry demonstrated that a few adenoma cells were positive for prolactin and the cyst wall cells were positive for cytokeratin and negative for S-100 protein.

Adenoma↗

PubMed1993

Chronic motor cortex stimulation in patients with thalamic pain.

Analysis of the authors' experience over the last 10 years has indicated that excellent pain control has rarely been obtained by thalamic relay nucleus stimulation in patients with thalamic pain. In the present study, 11 patients with thalamic pain were treated by chronic stimulation of the precentral gyrus. In eight patients (73%), the stimulation system was internalized since excellent pain control was achieved during a 1-week test period of precentral gyrus stimulation. In contrast, no clear effect was noted or the original pain was even exacerbated by postcentral gyrus stimulation. The effect of precentral stimulation was unchanged in five patients (45%) for follow-up periods of more than 2 years. In the remaining three patients, the effect decreased gradually over several months. This outcome was significantly better than that obtained in an earlier series tested by the authors with thalamic relay nucleus stimulation (p < 0.05). The pain inhibition usually occurred at intensities below the threshold for production of muscle contraction (pulse duration 0.1 to 0.5 msec, intensity 3 to 8 V). When good pain inhibition was achieved, the patients reported a slight tingling or mild vibration sensation during stimulation projected in the same area of distribution as their pain. The authors discuss the possibility that, in deafferentation pain, sensory neurons below the level of deafferentation cannot exert their normal inhibitory influences toward deafferented nociceptive neurons because of the development of aberrant connections. Thus, while stimulation of the first- to third-order sensory neurons at the level of the thalamic relay nucleus or below cannot bring about good pain inhibition in patients with thalamic pain, activation of hypothetical fourth-order sensory neurons through precentral stimulation may be able to inhibit deafferented nociceptive neurons within the cortex. None of the patients developed either observable or electroencephalographic seizure activity.

Afferent Pathways↗

PubMed1993

Histological and ultrastructural findings of benign intracranial cysts.

Since benign intracranial cysts have similar clinical and neuroradiological imaging appearances, it is difficult to distinguish between these cysts. Thus an electron microscopic study plays an important role in definite diagnosis of these non-tumorous benign cystic lesions, and also in determination of their origins. Arachnoid cysts occurring in 5 patients, epithelial cysts occurring in 2 patients, 2 cases of Rathke's cleft cysts, and one case of pineal cyst, were electron- and light-microscopically observed, and their characteristic features and differences were described. The structure of the arachnoid cyst wall was similar to that of normal arachnoid membrane. The inner surface of the arachnoid membrane. The inner surface of the arachnoid cyst wall was formed of one or several layers of arachnoid cells with slender processes, which contained large extracellular spaces, but not microvilli. As for epithelial cysts, microvilli and surface-coating material were present on the surface of epithelial cysts, and a well-developed basement membrane was continuously observed under the epithelial cells. Rathke's cleft cysts, which may basically be classified as epithelial cysts, are lined by columnar or cuboidal ciliated epithelium. The wall of the pineal cyst is composed of normal pineal tissue, and there are three layers, which have a lining of glial cells in the inner layer, a few sheets of pineal cells in the middle layer, and a fibrous capsule in the outer layer.

Adult↗

PubMed1993

[A case of penetrating head injury caused by nail-gun].

A rare case of penetrating head injury caused by a nail-gun was described. A 24-year-old male was admitted to our hospital due to head injury. He had handled a nail-gun at a construction site. On admission the patient was fully conscious with no neurological defects. A small wound was observed at the left front-temporal region. Skull films showed a large nail embedded in the skull cavity. A computed tomographic (CT) scan, changing level of window, demonstrated intracerebral hematoma, fragment of skull bone and nail. Cerebral angiography (CAG) showed extravasation at the left frontal region. Emergency operation was performed and his recovery was uneventful. Twenty-two craniocerebral injuries caused by nail-guns have been reported in world medical literature but this was the first report in Japan. The characteristics of craniocerebral nail-gun injuries were less damage and better prognosis compared with gunshot injuries. However intracranial infection and vascular injury were possible lethal complications. In this case, preoperative examination, such as CT scan and CAG was valuable and the early operation for the sake of safety was very effective.

Adult↗

PubMed1993

[Central neurocytoma--report of a case].

The authors present a case of central neurocytoma in a 23-year-old male with increased intracranial pressure syndrome. Computed tomographic (CT) scans and magnetic resonance images showed a large tumor mass with no evidence of calcification in the right lateral ventricle extending towards the third ventricle. A right transcortical-transventricular approach was performed and the tumor was totally removed. The postoperative course was uneventful and no further treatment was administered. CT shows no evidence of tumor recurrence after the six months from his surgery. Light microscopic findings suggested a diagnosis of oligodendroglioma. However, ultrastructural examinations demonstrated many dense-core or clear vesicles, microtubules and synaptic like structures within the abundant cytoplasmic processes of the tumor cells which suggested neuronal differentiation. Immunohistochemical examinations showed the tumor cells to be positive for neuron-specific enolase, sporadically positive for synaptophysin, and negative for glial fibrillary acidic protein. The final histological diagnosis was central neurocytoma. Central neurocytoma was first described by Hassoun et al, in 1982. Since then, 96 cases have been reported in the literatures. Their clinicopathological features, neuroradiological findings and prognosis are discussed.

Adult↗

PubMed1992

Excitatory amino acid antagonist administered via microdialysis attenuates lactate accumulation during cerebral ischemia and subsequent hippocampal damage.

Our previous studies have shown that kynurenic acid (KYN), a broad-spectrum antagonist of excitatory amino acids (EAAs), administered in situ through a dialysis probe can delay the massive ionic fluxes in the rat hippocampus during cerebral ischemia. The present experiments demonstrated that the same procedure attenuates the increase in extracellular concentration of lactate ([lactate]e) during ischemia as measured by microdialysis. This finding suggests that the lactate accumulation is partially caused by a sudden increase in energy demand due to the rapid ionic fluxes through EAA-coupled ion channels. This inference is consistent with the hypothesis that the earlier ionic event during ischemia is a cause of energy depletion, rather than the result merely of energy failure. The present experiments also revealed that KYN administered by the same procedure attenuates death of hippocampal CA1 pyramidal cells after 5-min transient ischemia in gerbils. Since lactate accumulation is likely to be an important factor affecting cell viability, the protective effect of KYN may be attributable, in part, to inhibition of lactate accumulation.

Amino Acids↗

PubMed1992

Early cellular swelling during cerebral ischemia in vivo is mediated by excitatory amino acids released from nerve terminals.

This study demonstrates ischemic cellular swelling in vivo detected as changes in the concentration of 14C-sucrose pre-perfused into the extracellular space (ECS) as an ECS marker. Microdialysis was utilized as a means of perfusion and measurement of the extracellular concentration of 14C-sucrose ([14C-sucrose]e). Concomitant with an abrupt increase in [K+]e at 1-3 min following the ischemia induction, [14C-sucrose]e was also rapidly elevated. Since sucrose is not taken up by either cells or capillaries, the absolute amount of 14C-sucrose in the ECS must be unchanged. The increase therefore appears to represent a relative decrease in water volume in the ECS resulting from a movement of water into the cells, i.e. cellular swelling. Ca(2+)-free perfusate containing Co2+, which has been shown to block excitatory amino acid release during cerebral ischemia, significantly delayed the increase in [14C-sucrose]e and [K+]e. Kynurenic acid, a broad-spectrum antagonist of excitatory amino acids, administered in situ through the dialysis probe also significantly delayed the increase in [14C-sucrose]e and [K+]e. These findings indicate that the early cellular swelling occurring during cerebral ischemia is a result of massive ionic fluxes mediated by excitatory amino acids which are released by a Ca(2+)-dependent exocytotic process from the nerve terminals.

Amino Acids↗

PubMed1992

Intraparenchymal blood-fluid levels in traumatic intracerebral haematomas.

Blood-fluid levels within the cerebral parenchyma are observed more frequently on CT and MRI in traumatic intracerebral haematomas than in those of other aetiologies. The intraparenchymal blood-fluid interface can be formed without a fluid cavity. It is suggested that the blood-fluid levels represent layering of red blood cells within areas of contusion necrosis as well as extensive contusion oedema. The more extensive the damage to brain tissue, the more often blood-fluid levels formed. A poorer outcome can be therefore predicted when an intraparenchymal blood-fluid interface is seen.

Arteriovenous Malformations↗

PubMed1992

Growth of a giant aneurysm following complete thrombosis by detachable balloon occlusion.

A giant basilar artery aneurysm demonstrating growth and causing neurological deterioration even after complete detachable balloon occlusion is reported. Autopsy revealed total thrombosis of the aneurysm and a hemiconcentric, onion skin-like, laminated structure. Numerous vascular channels and multiple fresh intramural hemorrhages were noted within the outer margin of the aneurysmal wall. Repeated intramural hemorrhages appeared to have been responsible for the aneurysmal laminated structure and contributed to progressive aneurysmal growth. This case demonstrates that the growth of some giant aneurysms is not dependent upon the continuity with the parent artery, and progressive enlargement cannot always be prevented by balloon occlusion.

Basilar Artery↗

PubMed1992

Primary Ewing's sarcoma of the temporal bone.

Primary cranial Ewing's sarcoma is exceptionally rare. Only ten cases of such a tumor had been reported heretofore in the literature. We describe a case of primary Ewing's sarcoma occurring in the temporal bone. The tumor was surgically excised, and the patient underwent radiation and chemotherapy. Neither recurrence nor distant metastasis was noted at 12 months after surgery. Although the prognosis of Ewing's sarcoma in general is often poor because of early metastasis to the lungs and/or to other bones, a review of the literature suggested that the same tumor occurring in the cranium can often be successfully managed by intensive therapy with radical excision and radiochemotherapy. This inference was supported by the case reported here.

Adult↗

PubMed1992

Appearance of collagen fibers in the cerebral vascular wall following subarachnoid hemorrhage.

Ultrastructural examinations of the cerebral vascular wall following subarachnoid hemorrhage (SAH) demonstrated that collagen fibrils developed in the muscle layer near the adventitia in the early stage of SAH and increased in number and volume with time. These findings suggest that accelerating factors of collagen synthesis in the muscle layer may be released from the adventitial side, and collagen synthesis is induced by extravascular factors. The changes of collagen volume with time suggest collagen to be an important phenomenon of persistent vasospasm after SAH. Histoimmunological studies showed that increased collagen fibers in the tunica media were mainly type III collagen, implying that cerebral vasospasm may be related to chemical inflammation.

Animals↗

PubMed1992

[A study of factors regulating ciliary activity using cultured human paranasal sinus mucosa].

Whether temperature, pH, osmotic pressure, Ca2+, Mg2+, and ATP have promotive effects on ciliary activity was investigated by a photo-electric method using cultured human ethmoid sinus mucosa. The results obtained were as follows: 1. Ciliary activity was reversible between 11 and 43 degrees C. It was activated with rising temperature, and inactivated at 40 degrees C. A temperature between 36 and 40 degrees C was optimal for activation of ciliary activity. 2. In the case of brief immersion (30 min.) in solutions between pH 4.5 and 8.5 ciliary activity was reversible, and with prolonged immersion (72 h) between pH 6.5 and 7.5 it was also reversible. with brief immersion within 30 min, pH 8.5 was an activating factor. 3. Ciliary activity was reversible in solutions between 143 and 1,140mOsm/Kg for 30 min. However, the ciliary reaction was different even at the same osmotic pressure according to the substance, NaCl or glucose, used to adjust it. Inhibited beating was reversible after prolonged immersion (72 h) in an osmotic pressure between 285 and 423mOsm/Kg adjusted by NaCl, and between 285 and 570mOsm/Kg adjusted by glucose. Any osmotic pressure of 428mOsm/Kg adjusted by NaCl activated ciliary activity. 4. Neither Ca2+ nor Mg2+, between 10(-2) and 10(-6) Mol, increased ciliary activity. 5. Between 10(-3) and 10(-5) Mol of Na-ATP, given exogenously, slightly activated ciliary movement, while Mg-ATP of 10(-3) Mol also activated it but only slightly. It is important to bear in mind the above results in administering local aerosol therapy for nasal and paranasal sinus diseases.

Adenosine Triphosphate↗

PubMed1991

Inhibition of rapid potassium flux during cerebral ischemia in vivo with an excitatory amino acid antagonist.

Previous studies have demonstrated that microdialysis is capable of detecting an abrupt and massive increase in extracellular K+ concentration ([K+]e) and a concomitant increase in extracellular concentration of excitatory amino acids (EAAs) during cerebral ischemia in the rat hippocampus in vivo. Following in situ administration of kynurenic acid (KYN), a broad-spectrum antagonist of EAAs, through the dialysis probe (5-10 mM), a delay in reaching the maximum level of increased [K+]e was observed in a dose-dependent manner. The initial component of the rapid increase in [K+]e appears to be mediated by EAAs released from nerve terminals.

Amino Acids↗

PubMed1991

Calcium-dependent component of massive increase in extracellular potassium during cerebral ischemia as demonstrated by microdialysis in vivo.

This study characterizes the physiological features and limitations of K(+)-free dialysis to detect changes in extracellular concentration of K+ ([K+]e) in the rat hippocampus in vivo. It also demonstrates the effects of Ca(2+)-free perfusate containing Co2+ or Mg2+, which blocks Ca2+ entry into the presynaptic nerve terminal, on the abrupt increase in [K+]e detected by this technique during cerebral ischemia. K(+)-free dialysis for 40 min caused no significant changes in the baseline [K+]e. In contrast, Ca(2+)-free dialysis for 40 min significantly reduced the extracellular Ca2+ concentration. Under this condition, together with addition of Co2+ or Mg2+ to the perfusate, the increase in [K+]e was delayed, and a delay in reaching the maximum level was observed in a dose-dependent manner. These results are consistent with the hypothesis that the initial increase in [K+]e during cerebral ischemia is related to the Ca(2+)-dependent exocytotic release of neurotransmitters from depolarized nerve terminals.

Animals↗

PubMed1991

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.

Animals↗

PubMed1991

Calcium-dependent glutamate release concomitant with massive potassium flux during cerebral ischemia in vivo.

The changes in extracellular glutamate ([Glu]e) and potassium ([K+]e) in the rat hippocampus during cerebral ischemia were determined simultaneously by microdialysis in vivo. Biphasic increases in [Glu]e, i.e. an earlier rapid increase concomitant with an abrupt increase in [K+]e followed by a later slow increase, were observed. Dialysis with Ca(2+)-free perfusate containing Co2+ blocked the earlier rapid increase completely but the later slow increase only partially. These findings suggest that Ca(2+)-dependent exocytotic release from the presynaptic nerve terminals is involved predominantly in the earlier rapid increase in [Glu]d. The later slow increase in [Glu]d may be due in part to a breakdown of membrane function resulting from several causes, including a loss of the electrogenic component of the glutamate gradients across the plasma membrane, and a loss of function of the glutamate uptake system.

Animals↗

PubMed1991

Chronic motor cortex stimulation for the treatment of central pain.

Twelve patients with deafferentation pain secondary to central nervous system lesions were subjected to chronic motor cortex stimulation. The motor cortex was mapped as carefully as possible and the electrode was placed in the region where muscle twitch of painful area can be observed with the lowest threshold. 5 of the 12 patients reported complete absence of previous pain with intermittent stimulation at 1 year following the initiation of this therapy. Improvements in hemiparesis was also observed in most of these patients. The pain of these patients was typically barbiturate-sensitive and morphine-resistant. Another 3 patients had some degree of residual pain but considerable reduction of pain was still obtained by stimulation. Thus, 8 of the 12 patients (67%) had continued effect of this therapy after 1 year. In 3 patients, revisions of the electrode placement were needed because stimulation became incapable of inducing muscle twitch even with higher stimulation intensity. The effect of stimulation on pain and capability of producing muscle twitch disappeared simultaneously in these cases and the effect reappeared after the revisions, indicating that appropriate stimulation of the motor cortex is definitely necessary for obtaining satisfactory pain control in these patients. None of the patients subjected to this therapy developed neither observable nor electroencephalographic seizure activity.

Adult↗