Shigeru Tani

Induction of Cerebral Thrombosis With Phenytoin in Rats

BACKGROUND AND PURPOSE This study was conducted to explore whether intra-arterial infusion of phenytoin causes cerebral ischemia and to examine the mechanism of cerebral ischemia induced by phenytoin. METHODS Ten rats were infused with phenytoin (150 microL, 3.75 mg) retrogradely from the left external carotid artery, followed by perfusion of carbon black transcardially. The removed brain was photographed from above, and the nonperfused area was compared with control rats (n = 10) with the use of an image analyzer. Eight animals with or without phenytoin treatment were perfusion-fixed for transmission electron microscopic analyses of cerebral vasculature. To determine the effect of tissue plasminogen activator (TPA) on phenytoin-infused rat cerebrum, 20 rats were treated with or without TPA (120,000 IU) 5 minutes after the phenytoin infusion (n = 10 each). RESULTS All rats suffered from respiratory distress 25 to 40 minutes after the injection and received carbon black transcardially. The nonperfused area was seen in the territory of the left internal carotid artery. Thrombi were observed from arterioles to capillaries. Under electron microscopy, endothelial cells were partially exfoliated, and the vascular lumen was obstructed by thrombi predominantly consisting of platelets. Eight rats with TPA survived more than 60 minutes, whereas only 2 rats survived without the treatment (P < .005). Nonperfused areas were 7 +/- 5% and 50 +/- 11% of cerebral surface area in rats with and without TPA treatment, respectively (P < .001). CONCLUSIONS Intra-arterial infusion of phenytoin results in a nonperfused area in rat cerebrum primarily due to thrombosis of arterioles and capillaries.

[Radiation-Induced Malignant Peripheral Nerve Sheath Tumor of the High Cervical Spine].

UNLABELLED CASE A 30-year-old woman presented with posterior cervical pain and left-sided omalgia. The patient had a history of non-Hodgkins lymphoma for which she had received prophylactic whole-brain irradiation(including at the upper cervical level)17 years previously. A magnetic resonance imaging(MRI)scan obtained 1 month previously showed an intradural extramedullary mass lesion at the left C1/2 level. We initially considered the tumor to be a benign schwannoma, but the patient subsequently developed left hemiparesis and was consequently admitted 2 days after her first visit. A second MRI scan showed that the tumor had progressed markedly. Hence, the patient underwent emergency surgical excision of the tumor. However, the tumor could only be partially removed because it had strongly adhered to the ventral aspect of the spinal cord. The tumor was pathologically diagnosed as a malignant peripheral nerve sheath tumor(MPNST). The residual tumor was subjected to local irradiation and surgery, but the treatment was unsuccessful, and the patient died on the 91st day of her illness. Conclusion:We report a case of radiation-induced high cervical MPNST arising from a benign schwannoma. All 9 previously reported cases of radiation-induced spinal MPNST were reviewed. Intraspinal MPNST of the high cervical region are extremely rare and are associated with a very poor prognosis. The 5-year survival rate of such tumors is markedly worse than that of other types of MPNST, and no standard treatment has been established for this condition.

Phenytoin‐induced cerebral thrombosis in rats: cerebral ultrastructure, water content and ischaemic volume in the acute phase

A new rat model for multifocal cerebral thrombosis has recently been reported (Tani et al., 1994; 1995). Ultrastructural changes in the cerebral neocortex in the acute phase were investigated in order to characterize the early pathological events in this model. A bolus injection of alkaline phenytoin solution (pH 10.8) into one internal carotid artery in the rat caused severe endothelial injury accompanied by thrombosis in the cerebral vasculature within 5 minutes, and severe oedema of the ipsilateral hemisphere within an hour. Cerebral water content was measured by the simple dry–wet method, and cerebral surface area and the surface area and volume of the ischaemic zone were measured using computer‐aided image analysis. Good correlations were demonstrated between cerebral water content and cerebral surface area, and between the surface area and volume of the ischaemic zone. We report here that quantitative evaluation of acute cerebral damage induced by phenytoin solution is possible with high reliability using simple image analysis.

Microvascular decompression for hypoglossal nerve palsy secondary to vertebral artery compression: A case report and review of the literature.

Background: Neurovascular-compression syndrome (NCS) is described as a prominent pathological contact between cranial nerves and vessels. Trigeminal neuralgia, hemifacial spasm, and glossopharyngeal neuralgia are typical clinical entities associated with NCS. On the other hand, the hyoglossal nerve is rarely affected by NCS. Case Description: We present a case of hypoglossal nerve palsy (HNP) secondary to vertebral artery (VA) compression. A 47-year-old man presented to our hospital with a 1-month history of dysarthria and dysphagia. Neurological examination revealed left HNP, with an intact swallowing reflex and no oropharyngeal or palatal weakness. Magnetic resonance imaging (constructive interference in steady state) revealed left hypoglossal nerve compression by the V4 segment of the left atherosclerotic VA. He underwent microvascular decompression (MVD) surgery. Intraoperatively, the VA was compressing the hypoglossal nerve. The left VA was moved and attached to the dura matter using a polytetrafluoroethylene (Teflon®) sheet and fibrin glue. Postoperatively, the patient exhibited gradual recovery of HNP in 3 months without dysfunction of lower cranial nerves. Conclusion: In patients with isolated HNP, vascular compression should be considered as a cause of these symptoms, and subsequent MVD can lead to resolution.

[Trigeminal neuralgia caused by cerebellopontine angle lipoma:a case report and review of the literature].

A 59-year-old man presented with right trigeminal neuralgia of the second branch, which had been treated with carbamazepine. The pain could not be controlled adequately because of side effects. CT and MRI revealed a 2-cm lesion in the right cerebellopontine angle. Retrosigmoid lateral suboccipital craniectomy was performed, and a soft yellowish mass was found to be associated with the 5th, 7th, and 8th cranial nerves, anterior inferior cerebellar artery, and small vessels. The lipoma was partially resected from around the root entry zone(REZ)of the 5th nerve and small vessels were coagulated around the REZ. After surgery, there was no trigeminal neuralgia, but facial numbness and cerebellar signs were noted. Postoperative MRI showed decompression of the trigeminal nerve and venous infarction in the middle cerebellar peduncle. Reviewing similar cases, we found 19 lipoma patients presenting with trigeminal neuralgia. Symptoms of involvement of other cranial nerves were also present in 11 patients, and 14 were younger than 30 years old. Of 17 surgical cases, total resection was not attempted apart from one case. Although pain relief was achieved in all surgical cases, complications developed in 11. Surgery should be performed only in patients with disabling and uncontrolled symptoms.

Intraoperative and Postoperative Bleeding in Microvascular Decompression for Trigeminal Neuralgia

OBJECTIVE The surgical approach for the trigeminal nerve involves veins connected to the superior petrosal and tentorial sinus, and we should pay special attention to these veins. We investigated intraoperative and postoperative bleeding using our database. METHODS A prospectively accumulated database of 247 microvascular decompression surgeries for trigeminal neuralgia over the past 10 years was analyzed. Intraoperative and postoperative bleeding was confirmed with surgical records, videos, and computed tomography. Of 235 patients, 161 were female; 85 patients were >70 years old at the time of surgery; 96 surgeries involved the left side. RESULTS Intraoperative venous bleeding was encountered in 29 surgeries (12%): from the superior petrosal vein/sinus in 18 and the hemispheric bridging vein/tentorial sinus in 11. Massive bleeding occurred from the superior petrosal sinus owing to tear of the entrance of the superior petrosal vein in 4 surgeries and from the tentorial sinus in 3; bleeding was controlled by Surgicel with fibrin glue. Postoperative bleeding occurred in 11 surgeries (4%): intracerebellar hematoma in 2, subarachnoid hemorrhage in 3, subdural hemorrhage in 3, supratentorial subdural hemorrhage in 2, and supratentorial epidural hematoma in 1. These lesions were associated with intraoperative bleeding in 1 case, a trans-horizontal fissure approach in 1 case, coagulation of the petrosal vein in 2 cases, and unknown reasons in 7 cases. Cure without medication was achieved in 218 surgeries at an average follow-up of 4.2 years. CONCLUSIONS Microvascular decompression for trigeminal neuralgia involves potential risks of intraoperative and postoperative bleeding.

Nonspastic hemifacial spasm confirmed by abnormal muscle responses

Background: Hemifacial spasm is usually diagnosed by inspection which mainly identifies involuntary movements of orbicularis oculi. Assessing abnormal muscle responses (AMR) is another diagnostic method. Case Description: We report a case of left hemifacial spasm without detectable involuntary facial movements. The patient was a 48-year-old man with a long history of subjective left facial twitching. On magnetic resonance imaging (MRI), the left VIIth cranial nerve was compressed by the left anterior inferior cerebellar artery (AICA), which was in turn compressed by the left vertebral artery. We initially treated him with botulinum toxin. We were able to record AMR, and hemifacial spasm occurred after AMR stimulation, although no spasm was detectable by inspection. Subsequently, we performed microvascular decompression with transposition of the AICA that compressed the VIIth cranial nerve. His hemifacial spasm resolved by 5 weeks after surgery and was not induced by AMR stimulation. Conclusion: Hemifacial spasm can sometimes be diagnosed by detecting AMR rather than by visual inspection. We propose that such hemifacial spasm should be termed nonspastic hemifacial spasm.

Clinical features of bilateral trigeminal neuralgia

Among 238 patients with bilateral trigeminal neuralgia(TN)who visited our hospital between April 2007 and June 2014, 5(2%)were surgically treated by microvascular decompression(MVD). The initial symptom was on the right side in four and on both sides in one patient. Intervals between the initial and second onset on the other side(left)were two months, and four, six, and eight years. None of the patients showed involvement of the first branch of the trigeminal nerve. The patients with bilateral TN were younger than the 154 patients with unilateral TN who were treated surgically by MVD in this period(45 vs. 65 years), and the bilateral TN patients predominantly were women(4/5 vs. 99/154). In the surgical field, the trigeminal nerve and root entry zone were compressed more by veins in the bi lateral TN patients than in the unilateral TN(4/5 vs. 60/154, respectively)patients. We could not identify any differences in MRI CISS before versus after the onset of left trigeminal neuralgia, suggesting that compression is not the sole cause of the symptom.

Multifocal cerebral infarction induced by phenytoin in rats

Recently we developed a new rat model for multifocal cerebral thrombosis and reported the macroscopic and histopathologic findings together with therapeutic effects of a recombinant tissue plasminogen activator in the acute phase (1, 2). However, most of the animals died or became moribund within 1 hour after the administration of the causative agent, phenytoin, in the original method. We have now investigated whether a smaller dosage of phenytoin can induce a chronic and multifocal cerebral infarction with a lower mortality rate.