Biomedical subjects
Publications and source records attributed to K Okuchi.
The case of a 63-year-old man with acute obstructive hydrocephalus is presented. To the authors' knowledge, this is the first reported case of acute obstructive hydrocephalus associated with nonketotic hyperosmolar diabetic coma. It is believed that the plasma hyperosmolality resulted in osmotic endothelial injury leading to brain-stem edema.
A case of a traumatic vertebral arteriovenous fistula associated with a hangman's fracture is reported. A 45-year-old male fell down about 2 meters and struck his parietooccipital region against the ground. Profuse nasal bleeding developed. He was transferred to a local hospital, where his respiration was ataxic and blood pressure was low. After intubation, he was transferred to our emergency department. Cervical x-p revealed fracture of C1, C2 and subluxation of C2 body. Because of uncontrollable nasal bleeding, the bilateral maxillary arteries were embolized with spongel. At this time, right vertebral angiograms demonstrated a vertebral arteriovenous fistula with an pseudoaneurysm located at C2 level. On the 13th hospital day, direct balloon occlusion of the fistula was attempted; this could not be achieved because the subclavian and vertebral arteries were tortuous and the balloon catheter could not be introduced to the level of the fistula in the vertebral artery. The patient was only observed until follow-up angiogram on the 24th hospital day revealed enlargement of the pseudoaneurysm. We performed trapping of both the proximal and distal ends of the involved vertebral artery; from C5 to C1. Postoperative course was uneventful, hangman's fracture was fixed with a Halo vest. Four months after operation, fistula and pseudoaneurysm were not opacified on angiogram. We believe that transvascular techniques are the treatment of choice for vertebral arteriovenous fistulas. However, as the next best thing, we can use trapping for the patient whose vessels are too tortuous to introduce the balloon catheter to the involved vessel.
Only 27 cases of dural AVM fed by the anterior ethmoid artery have been reported in the literature. Their nidi were usually in the dura mater. In our case, the nidus was located in the brain parenchyma, although its feeder was the dural artery. A 75-year-old man was admitted to our department because of disturbed consciousness. CT scan showed intracerebral hemorrhage in the left frontal region with ventricular perforation, and subarachnoid hemorrhage in the suprasellar cistern. Left carotid angiography revealed an AVM in the anterior cranial fossa, fed by the anterior ethmoidal artery and drained by a cortical vein, which was dilated with some vascular sacs. A left frontal craniotomy was performed. The subcortical hematoma was removed, and then, after retracing the frontal lobe, two feeders penetrating the dura mater were identified and clipped. The nidus of the AVM with aneurysmal vascular dilatation could be seen on the cortical surface. It was coagulated and removed en-bloc. Histologically, the malformation consisted of thickened dilated veins and distorted small arteries. Postoperative angiography revealed no vascular anomaly. The patient was discharged with mild aphasia and mild right hemiparesis.
Traumatic hemorrhage in the ambient cistern is thought to be an indirect indication of brain stem injury. In many cases such brain stem lesions cannot be clearly demonstrated by conventional CT scans. Magnetic resonance imaging (MRI) provides a more sophisticated display of the brain stem with improved contrast resolution of structures not appreciated on CT. We present four patients with traumatic ambient cistern hematoma on CT. They showed consciousness disturbance at the initial neurological examination and a Glasgow Coma Scale (GCS) of 7-10. All patients had hemothorax or clavicular fracture ipsilateral to the ambient cistern hematoma that suggested a severe mechanical force from the same direction. Axial, coronal and sagittal MRI scans were obtained with a super-conductive 1.5 T unit (Picker) within 6 days after trauma. Two standard pulse sequences were used; (1) Spin-echo (TR/TE = 500/20) or Inversion Recovery (TR/TI/TE = 3300/600/30) to obtain T1-weighted information and (2) Spin-echo (TR/TE = 2000/100) to obtain T2-weighted information. In case 1 (3-year-old girl) the hematoma which was thought to be located in the ambient cistern on CT was found to be present in the subpial region in the tegmentum on MRI. On T2 weighted image, a high signal intensity area was seen in the perifocal area. This area was demonstrated as a low density area on CT. This patient has remained in a persistent vegetative state 6 months after trauma. In case 3 (31-year-old man) CT demonstrated no abnormal findings in the brain stem. MRI demonstrated a high intensity area in the right cerebral peduncle and left tegmentum.(ABSTRACT TRUNCATED AT 250 WORDS)
We describe a 44-year-old man found to have a diffusely calcified astrocytoma originating in the left frontoparietal region and extending along the axonal fibres into the opposite cerebral hemisphere and brain stem. Computed tomography and magnetic resonance imaging clearly demonstrated the spread of the tumour. The tumour was partially resected and histologically diagnosed as an astrocytoma. A correct preoperative diagnosis was difficult, because the lesion was very slow-growing and its widespread calcification mimicked congenital or inflammatory calcium deposits.
When conventional treatment for status epilepticus fails, general anaesthesia is recommended. We present our experience with isoflurane, an inhalational anaesthetic, in the management of four patients with status epilepticus which occurred soon after surgery for motor area lesion. The seizures were controlled with relatively small concentrations of isoflurane. Hypotension, the only adverse effect of isoflurane, was managed easily with the use of dopamine in physiological saline. Although status epilepticus occurring soon after surgery is transient, it carries a risk of persistent brain damage if active treatment is not instituted promptly. Isoflurane general anaesthesia may be recommended to control it in the intensive neurosurgical care.
Although it is well known that Wallenberg's syndrome is caused by occlusion of the vertebral artery (VA) or the posterior inferior cerebellar artery (PICA), the etiology of the occlusion is rarely documented. During the course of Wallenberg's syndrome, patients often complain of headache. We thought that these headaches might be caused by dissecting aneurysm (DA) of the vertebral artery, and so we studied the incidence of DA in our cases with Wallenberg's syndrome. Although many variants exist, Wallenberg's syndrome encompasses several neurological symptoms due to a disorder of the nucleus and nerve tracts located in the lateral part of the medulla. We diagnosed our patients as having Wallenberg's syndrome on the basis of symptoms such as loss of pain and temperature sensation in the unilateral face and contralateral body, cerebellar ataxia, and dysphasia. We investigated 22 cases of Wallenberg's syndrome over a five-year period, and excluded patients who developed subarachnoid hemorrhage upon onset of the syndrome. Our cases can be divided into two groups; one with severe stenosis or occlusion of VA (n = 15) and the other with occlusion of PICA (n = 5). The angiograms of the two remaining patients showed no abnormal findings. The mean age of the VA group (42.5 yrs.) was younger than that of the PICA group (64.2 yrs.). The age distribution of the PICA group is similar to that of other occlusive cerebrovascular diseases. Seven cases of the VA group demonstrated aneurysmal dilatation and luminal stenosis, and so they were diagnosed as having dissecting aneurysm of VA.(ABSTRACT TRUNCATED AT 250 WORDS)
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BACKGROUND AND PURPOSE: Very few reports are available on changes in the human hippocampus after cardiac arrest. The objective of this study was to investigate if specific hippocampal volume losses can be demonstrated in the human brain following reperfusion after cardiac arrest. METHODS: We assessed the volumes of the hippocampal formation (HF) and temporal lobe excluding HF (TL) as the contrast using magnetic resonance (MR)-imaging-based volumetry in 11 vegetative patients after cardiac arrest and in 22 healthy controls of similar age, sex and body size distribution. The measured volumes were normalized for differences in the head size among subjects by dividing by the total intracranial volume (TICV). The MR images of the 11 patients were obtained between days 8 and 21 after cardiac arrest. RESULTS: The observed volumes of HFs and TLs of both patient and control groups were as follows: right HF volume (HFV): 2.67 +/- 0.19 (mean +/- SD, cm(3)) in patients versus 3.89 +/- 0.44 in controls; left HFV: 2.72 +/- 0.17 versus 3.74 +/- 0.35; right TL volume (TLV): 73.37 +/- 6.54 versus 80.08 +/- 7.62, and left TLV: 72. 45 +/- 6.77 versus 78.59 +/- 6.68. The normalized indices (HFV/TICV and TLV/TICV) were as follows: right HF: 0.0021 +/- 0.0002 (mean +/- SD) in patients versus 0.0031 +/- 0.0001 in controls, p < 0.0001, left HF: 0.0022 +/- 0.0002 versus 0.0030 +/- 0.0001, p < 0.0001, right TL: 0.058 +/- 0.002 versus 0.064 +/- 0.004, p = 0.0007, and left TL: 0.058 +/- 0.002 versus 0.062 +/- 0.004, p = 0.0014. The HFV-TLV ratios (HFV/TICV divided by TLV/TICV) of both groups were: right HFV-TLV ratio: 0.037 +/- 0.004 in patients versus 0.049 +/- 0. 004 in controls, p < 0.0001, left HFV-TLV ratio: 0.038 +/- 0.004 versus 0.048 +/- 0.004, p < 0.0001. CONCLUSIONS: The patient group had HFs that were 26.8-30.6% smaller than those of the control group, but in the patient group, the TLs slightly decreased in size by only 7.8-8.2% of the volume of those in the control group within 21 days after cardiac arrest. The volume reductions in the bilateral HFs of patients after cardiac arrest were significantly larger than those in the bilateral TLs. We speculate that this specific rapid hippocampal shrinkage reflects its greater vulnerability to global brain ischemia.