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Biomedical subjects

H Ishimitsu

Publications and source records attributed to H Ishimitsu.

At least 19 recordsLinked to original sources
PubMed2001

[Extraaxial primary malignant lymphoma associated with calcified chronic subdural hematoma: a case report].

The authors report the case of a 54-year-old male with extraaxial primary malignant lymphoma associated with calcified chronic subdural hematoma. He slowly developed progressive headache accompanied by a bulge in the left forehead. Skull radiogram showed a large biconvex calcification in the left frontoparietal region, with concave change in the overlying bone. Computed tomograms and magnetic resonance images revealed a left frontoparietal chronic subdural hematoma surrounded by a calcified rim, with marginal enhancement in the frontal portion extending upward to the subcutaneous tissue through the underlying bone. The lesion was suspected to be an infectious calcified hematoma. The patient underwent a craniotomy for the removal of the hematoma. It was observed that the tumor was located mainly in the epidural and subdural space. The extent of the tumor corresponded with the enhanced area of the lesion in the preoperative neuroimages. The histological diagnosis was malignant lymphoma of B cell origin. General examination, which included bone marrow study and Ga scintigraphy, failed to prove systemic lymphoma. Extraaxial primary malignant lymphoma is extremely rare, and this is the first report of a lymphoma associated with calcified chronic subdural hematoma. The authors review the literature and discuss the clinical features and the pathogenesis of the lesion.

Brain Neoplasms↗
PubMed1999

[Congenital arteriovenous malformation of the scalp with a drainage to the transverse sinus: a case report].

Arteriovenous malformation (AVM) of the scalp is uncommon, and a subtype which has connection with the intracranial dural sinus is extremely rare. Only 3 cases have been reported. We present a case of congenital AVM of the scalp which was connected with the intracranial venous sinus. A 27-year-old woman had been noted as having a pulsatile soft mass in the midline of the occipital region since her birth. She visited our hospital because of pain and enlargement of the mass. The patient had had no history of trauma. Physical examination revealed a pulsatile scalp mass in the midline of the occipital region, measuring 3.5 x 3.5 x 1 cm. A loud bruit was ausculated. Tenderness was noted. The skin over the mass was slightly reddish. No focal neurological deficits were noted. Plain skull films demonstrated a round defect in the midline of the occipital bone. Magnetic resonance imaging (MRI) demonstrated a subcutaneous mass with low signal intensity and an infratentorial mass with flow void. 3D CT angiograms demonstrated a subcutaneous vascular mass with a single large vein draining into the right transverse sinus. External carotid angiograms revealed a vascular lesion within the scalp with supply from the branches of the bilateral occipital arteries and the meningeal arteries. The nidus penetrated the skull and connected to a dilated varix, which had a draining vein shunting into the right transverse sinus. After embolization of the right meningeal feeding arteries, surgery was performed. The vascular lesion penetrated the skull and the dura. The infratentorial mass was in the epiarachnoid space and was fed by a small pial artery. The mass was excised completely after interruption of the pial artery and the draining vein. Postoperative course was uneventful. Histologically, the subcutaneous mass and infratentorial vascular mass were shown to be AVM and varix, respectively.

Adult↗
PubMed1998

[Cervical myelopathy caused by bilateral vertebral artery compression].

We report a rare case of myelopathy caused by compression of the upper cervical cord by the bilateral anomalous vertebral arteries. A 49-year-old man had dragged his right foot for 4 years. He also complained of a tingling sensation in his right arm and occipitalgia. Neurological examination disclosed right hemiparesis, hypalgesia in the right half of the body and hypertonicity of the lower extremities. MRIs showed a flow void area which compressed and distorted the spinal cord bilaterally at the level of the atlas. A vertebral angiogram showed that the bilateral vertebral arteries had pierced the dura matter under the posterior arch of the atlas, turned upward and laterally in the vertebral canal, making vascular loops at the level of the atlas. 3D CT angiography showed the loops convex medially in the anterior part of the vertebral canal. With these findings, we diagnosed the patient as suffering compression of the cervical cord by the bilateral anomalous vertebral arteries. Suboccipital craniectomy and C1 laminectomy were performed. When the dura mater was opened, the dorsolateral aspect of the spinal cord was found to be compressed and indented markedly by the vertebral arteries. To decompress the spinal cord, the vertebral arteries were retracted dorsolaterally by means of Gore-tex tape and anchored to the spinous process of the axis. Postoperatively, his neurological symptoms improved. Postoperative MRIs showed that the spinal cord was decompressed and had recovered its contour. A review of the literature revealed that only 3 such cases as this one have been reported. The clinical features of these rare cases are nonspecific myelopathy and concomitant occipitalgia or neck pain. The main cause of this rare entity seemed to be the compression of the vertebral artery through its course when it enters the vertebral canal between the atlas and the axis.

Humans↗
PubMed1994

Pediatric cerebellar infarction caused by atlantoaxial subluxation--case report.

An 11-year-old girl developed cerebellar infarction presenting as a posterior fossa mass lesion after stretching and flexing her neck. Cerebral angiography demonstrated irregular narrowing of the right vertebral artery at the C2 level and x-rays of the upper cervical spine showed atlantoaxial subluxation with os odontoideum. She underwent surgical decompression with removal of infarcted tissue. The cerebellar infarction probably resulted from occlusion of the vertebral artery, followed by brain swelling due to recanalization.

Atlanto-Axial Joint↗
PubMed1994

[Anterior decompression of the thoracic spine through the posterior approach: its usefulness, indications, technique, and the preservation of postoperative spinal stability].

Three patients with thoracic myelopathy were operated on using a modified surgical approach, anterior decompression of the thoracic cord through the posterior approach. The usefulness of and indication for this approach were discussed. Operative technique is as follows. In the prone position, laminae are removed widely enough to include the medial half of the facets and pedicles. This creates cavities lateral to the dural sac as deep as the diameter of the spinal canal. Through these cavities the anterior wall of the spinal canal and the posterior portion of the intervertebral disc are drilled out to make a space into which lesions are pulled away from the dural sac. The lesions can be removed under direct vision with minimum retraction to the dural sac. Our technique preserves the integrity of the spinous processes and supra/inter spinal ligaments, which do not restrict access to the cord and have the potential to be one of the supports of the spine. Postoperative course was uneventful in all of the patients. This approach has several advantages. It can be applied to any levels of the thoracic spine and can be used for decompression all around the thoracic cord. The procedure is minimumly invasive. The indications for this operation are considered to be 1) lesions at the level of T3, 2) anterior lesions associated with OYL at the same or adjacent level, 3) multilevel lesions which need staged operations, 4) laterally protruded discs and 5) lesions in elderly or high risk patients.

Cordotomy↗
PubMed1991

Peduncular hallucinosis associated with ruptured basilar-superior cerebellar artery aneurysm--case report.

A 65-year-old female developed peduncular hallucinosis 3 days after rupture of a basilar-superior cerebellar artery aneurysm. There were no neurological deficits except slight anisocoria when she first complained of hallucinations. Vasospasm of the perforating arteries to the upper brainstem, rather than direct brainstem damage caused by the bleeding, was probably the cause. Peduncular hallucinosis is possibly the only localizing sign of ruptured upper posterior circulation aneurysm.

Aged↗
PubMed1990

[Diffuse hemispheric low density on CT scan following acute interhemispheric subdural hematoma in an infant. Case report].

A 17-month-old boy was admitted to our hospital in a semicomatose state after a minor head injury. Computed tomography (CT) scans revealed a posterior interhemispheric and a thin convexity subdural hematoma. Two and a half hours later, repeated CT scans disclosed a development of the right hemispheric diffuse low density and an enlargement of the interhemispheric subdural hematoma. Decompressive craniectomy and removal of the hematoma was performed immediately. On the second postoperative day, the diffuse low density areas developed in the contralateral frontal and temporal lobes. On the 14th postoperative day, the gyri which had been low in density were markedly enhanced with contrast enhancement. On the 16th postoperative day, CT scans showed a diffuse hemispheric gyral high density with bleeding in the right parieto-occipital lobe. A right occipital lobectomy and removal of the hematoma was performed. Histological examination suggested cerebral infarction probably due to venous congestion. It is also suggested that the diffuse hemispheric gyral high density observed on the 16th postoperative day was the hemorrhagic cerebral infarction.

Acute Disease↗
PubMed1989

[Effect of external decompression on the development of delayed ischemic neurological deficits after subarachnoid hemorrhage].

The protective effect of a large decompressive craniectomy against delayed ischemic neurological deficits (DIND) was evaluated in patients operated on after subarachnoid hemorrhage due to a ruptured aneurysm. In 54 cases, a large decompressive craniectomy was performed (Group D), and 41 patients underwent conventional craniotomy (Group ND). Transient DIND appeared in three (17%) of the 18 Group D patients of Hunt and Kosnik grade I or II, but permanent deficits were not observed in this group. In Group ND, permanent DIND developed in seven (21%) of the 33 grade I or II patients, despite their having received the same medical care. This difference was statistically significant. However, there were no differences in outcome among patients of grades III, IV, and V. These results suggest that, at least in patients of grade I or II, a large decompressive craniectomy, performed early, will prevent DIND after subarachnoid hemorrhage. The procedure may prevent the increase in intracranial pressure and decrease in perfusion pressure brought on by vasospasm and the development of brain edema.

Adult↗
PubMed1989

[Atypical computed tomographic features of meningioma: a case report].

Diagnosis of intracranial meningiomas with computed tomography (CT) is usually easy. However, some authors have reported cases preoperatively misdiagnosed because of atypical computed tomographic features. We report a case of non-cystic meningioma presenting a ring enhanced mass lesion, with CT scan. A 48-year-old male was admitted to our hospital on January 5, 1987, because of progressive monoparesis of his left lower limb. This had continued for 1 1/2 years. Neurological examination revealed monoparesis, hypesthesia and decreased deep sensation of the left lower limb. X-ray films of the skull appeared normal. A CT scan demonstrated a ring-like high density mass attached to the falx in the right frontoparietal area with perifocal low density. The ring-like high density was irregularly increased with contrast enhancement. Right carotid angiograms showed a doughnut like tumor stain without meningeal blood supply. Brain scintigrams revealed a dense round hot lesion in the frontoparietal area at 5 minutes, and the hot lesion was still visualized after 90 minutes. We diagnosed a cystic parasagittal meningioma. A right frontoparietal craniotomy was performed, and total removal of the parasagittal tumor was made. The center of the tumor was very soft but it could not be said that it was not cystic. Histologically the tumor was a meningotheliomatous meningioma. The center of the tumor, which was very soft, was necrotic with arteriolar hyalinization. The meningioma cells survived around the patent vessels. These intact meningioma cells were scattered like islands in extensive necrosis. This is so called "oasis phenomenon" indicating that the necrosis of the tumor was caused by intratumoral ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Carotid Arteries↗
PubMed1986

[Opsoclonus-polymyoclonia syndrome suppressed with reserpine].

A 38-year-old man was admitted to Iwakuni National Hospital on July 6, 1978, with the complaints of difficulty seeing and walking. Two weeks before admission, he first experienced dizziness and it slowly progressed to uncontrollable tremor-like movements of the whole body. On admission, he was alert, oriented and afebrile. He had not experienced nausea, vomiting nor headache. He showed irregular horizontal oscillations of the eyes. Electronystagmographic study showed that this jerky eye movement appeared especially with changes of fixation of the eyes. It was also recorded during conjugate eye movement, and while he closed his eyes. He was ataxic, unable to walk, but no other abnormalities in cerebellar functions were observed. Spinal tap was performed and yielded watery clear cerebrospinal fluid containing 9/mm3 mononuclear cells. Clonazepam was given, 1.5 mg per day, for three days followed by doses of 3 mg per day. Improvement in walking was observed one week after starting the medication, when reserpine was started at a dose of 1 mg per day and increased to a dose of 1.5 mg per day in three days. One week after starting reserpine, opsoclonus improved markedly and he became able to read again. He was discharged home on September 3, 1978. Six months after admission, reserpine was decreased to 0.5 mg per day. Difficulty in reading developed within a month. Reserpine was given 1.0 mg per day and the doses was continuously given for next three months. One year after admission, he is back to his former occupation without medication. He complains of slight difficulty in reading for more than an hour, and in watching TV.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1980

[Effect of various kinds of glucocorticoids on experimental brain edema (author's transl)].

Although the effectiveness of glucocorticoids for the treatment of cerebral edema has been widely accepted in neurosurgical practice, but its mechanism is still obscure. Also the dose equivalent of various kinds of glucocorticoid preparation is still uncertain. Only the dose equivalent determined by the test examining an antiinflammatory effect on a growth of glanulation, has been applied for the treatment of brain edema. The authors attempted to establish the dose equivalent of each kinds of glucocorticoid for the treatment of cerebral edema. Cold induced cerebral edema was produced by touching a metal probe at the temperature of -90 degrees C for 3 minutes on the right parietal cortex of rat brain. Hydrocortisone (16 mg/kg), prednisolone (3.2 mg/kg), methylprednisolone (3.2 mg/kg), dexamethasone (0.8 mg/kg) and betamethasone (0.8 mg/kg) were administered at the time of 3 hours prior or after the cold injury. The animals were sacrificed 24 hours after injury and the grade of brain edema was determined by the changes of water content in the brain tissue. For this purpose, the authors developed a new method of measuring water content in the brain tissue using tritiated water and a liquid scintillation counter. In the group of animals which were treated with prednisolone, dexamethasone or betamethasone, the water content was significantly decreased compared to the value of non-treated animals. But in the animals treated with hydrocortisone or methylprednisolone, no significant changes of the water content was observed. But in the animals treated with double doses of hydrocortisone (32 mg/kg) or methylprednisolone (6.4 mg/kg), cerebral edema was improved significantly. From these results the authors concluded that the dose equivalent of each kinds of glucocorticoid for the treatment of the brain edema was as follows: hydrocortisone: prednisolone: methylprednisolone: dexamethasone: betamethasone = 40 : 4 : 8 : 1 : 1.

Animals↗