Toshihiko Ebisu

Neurenteric cysts with meningomyelocele or meningocele

Two rare cases of neuroenteric cysts with meningomyelocele and meningocele were treated. The mechanism of the development of these anomalies is discussed. It is considered that the terminal, dorsal part of the enteric fistula, which is produced between the endoderm and the ectoderm through a partially duplicated notochord in the development of the embryo, remains after obliteration of the fistula and, consequently, that the mucosa of the enteric remnant is inverted and projects through the skin of the back.

Effects of Atrial Natriuretic Peptide on Brain Oedema: The Change of Water, Sodium, and Potassium Contents in the Brain

We examined the effect of atrial natriuretic peptide (ANP) administration on cerebral oedema in rats. Intravenous ANP infusion with total dose of 120 micrograms/kg and 100 micrograms/kg suppressed the elevation of water and Na contents in left middle cerebral artery (MCA) occluded and cold injured brain tissue, indicating that ANP has a suppressive effect on cerebral oedema. Similar ANP infusion at a low dose of 1 microgram/kg/h for 6 h also resulted in observation of the anti-oedematous effect in both models, with no observable occurrence of the known systemic effects of ANP on systolic blood pressure (SBP), heart rate (HR), hematocrit, or serum electrolyte ion (Na+, K+, Cl-) concentrations. The results thus suggest that the anti-oedematous effect of ANP is attributable to water and Na content control by ANP specific to the damaged tissue, possibly through inhibition of sodium transport. Taken together with a recent study in which it was shown that ANP might inhibit sodium transport in cerebral microvessel, our results suggest that ANP suppresses the development of brain oedema by inhibiting sodium transport and the coupled water influx.

Magnetic resonance imaging of brain contusion

In this study we investigated the time course of brain contusions using magnetic resonance imaging and compared the findings with those of a computed tomography scan. The lesions, which were demonstrated as homogeneous density areas on the computed tomography scan were demonstrated as different intensity areas in the magnetic resonance image. The intensity of the images varied according to the time at which the images were obtained. The findings indicated changes in the nature of the contusions including hematoma hemoglobin, perifocal edema extension, and so on. In conclusion, magnetic resonance imaging is important in the follow-up of chronological change as well as in original diagnosis of brain contusions.

The Investigation of Experimental Brain Tumours Using 31P-MRS and 1H-MRI

In vivo 31P-magnetic resonance spectra (MRS) were obtained by the surface coil method from rat glioma, human glioblastoma, and human neuroblastoma inoculated subcutaneously in CD Fisher rats and hamsters, and the effects of chemotherapy, photoradiation therapy, and radiofrequency hyperthermia as well as 60Co-irradiation were evaluated by sequentially observing spectral changes. In the 31P-spectra of tumour tissue, the nucleoside triphosphate (NTP), phosphomonoesters (PME) peaks were high and the phosphocreatine peak was low compared to those of normal brain. When the antitumour agents were given and were effective, NTP peaks decreased, and inorganic phosphate increased remarkably within several hours after the treatment. 1H-magnetic resonance imaging (MRI) were also obtained in some cases. Necrotic regions was detected by the 1H-MRI as image changes which appeared later than those detected by MRS. It proved practical to monitor the effect of therapy by employing either 31P-MRS or 1H-MRI. However, the image changes which demonstrated the effect of the therapy used closely resembled those changes which occurred with the onset of necrosis in tumour tissue during tumour growth. Several problems for future application of these techniques to human brain tumours are also mentioned.

Effects of Atrial Natriuretic Peptide on Ischaemic Brain Oedema Evaluated by the Proton Magnetic Resonance Method

The effect of atrial natriuretic peptide (ANP) on cerebral oedema in rats was examined by magnetic resonance (MR). After occlusion of the left middle cerebral artery (MCA) to induce cerebral ischaemia, rats received continuous infusion of ANP for 24 h at a total dose of 120 micrograms/kg or 150 micrograms/kg. Proton relaxation times (T1 and T2) of excised oedematous tissue were measured in vitro and the area of the oedematous region was determined in vivo by the use of magnetic resonance imaging (MRI). The administration of ANP was found to decrease the lengthening of both T1 and T2 in the oedematous tissues and shown by MRI to decrease the area of the oedematous region, compared with group receiving saline. The topographic observations in vivo suggest that ANP suppress the development of the oedematous region.

Pathophysiological Investigation of Experimental Cerebral Ischaemia Using in vivo 31P-NMR Spectroscopy and 1H-MRI

The cerebral energy metabolism and brain oedema were investigated in three experimental cerebral ischaemia models using 31P-NMR spectroscopy (MRS) and 1H-NMR imaging (MRI) in the same subject animal. These measurements were performed also in experimental brain oedema models and the findings were compared with each other. 31P-MRS showed an ischaemic pattern in all of the cerebral ischaemia models, that is, ATP and PCr peaks decreased, and the Pi peak increased and shifted to a higher resonant frequency. However, 31P-MRS did not show any remarkable change in the brain oedema models. On the other hand, 1H-MRI clearly demonstrated brain oedema in the brain oedema model. In the cerebral ischaemia models, 1H-MRI findings differed depending upon the type of model, namely the most marked brain oedema was detected in the unilateral middle cerebral arterial occlusion model and no marked change was detected in the temporary four vessel occlusion model. It was thought that this difference depended on the severity of the ischaemic insult. Accordingly, the fundamental pathophysiological problem of cerebral ischaemia was the energy metabolism disturbance with the brain oedema being associated with this disturbance but occurring secondarily. However, in the brain oedema model the main pathological change was the increase in tissue water.

Diagnostic Imaging of Brain Function and Metabolism by Magnetic Resonance Methods

Brain metabolism and function were examined by using multimodality magnetic resonance methods. In magnetic resonance spectroscopy (MRS) and chemical shift imaging (CSI), various intrinsic metabolites in the brain were detected and their distribution was visualized. Energy metabolism and phospholipid metabolism can be examined by using the 31P nucleus. Increased phosphomonoesters in brain tumors and infant brain indicate the changes of phospholipid metabolism. Decreased phosphocreatine and increased lactate in acute cerebral infarction indicate the impairment of aerobic metabolism. Amino acids, choline, creatine, and lactate can be detected by using the nucleus. Decrease of N-acetyl aspartate (NAA) in brain tumors, degenerative diseases, and cerebral infarction indicated the loss of neurons. Increased lactate was observed in hypoxic cell fractions such as malignant tumors and infarction. In diffusion weighted imaging (DWI), anisotropy of water diffusion was detected in the white matter. The apparent diffusion coefficient (ADC) was different among three types of brain edema, between benign astrocytoma and cerebral infarction, and between arachnoid and epidermoid cysts. In functional magnetic resonance imaging (fMRI) using the gradient echo method on conventional MRI scanners, a rapid increase of signal intensity was observed in the primary cortical area corresponding to each activation task such as finger movements, photic stimulation, and hearing of words. The fMRI was also obtained during complex tasks such as imagination of hand grasping. The multimodality MR methods using various analytical techniques, such as MRS, CSI, DWI, and fMRI, are unique and useful methods to examine brain metabolism and function noninvasively; consequently, these are promising methods for examining the pathophysiology of various cerebral disorders.

Neuroimaging of Cerebral Metabolism in Severe Diffuse Brain Injury in Chronic Stage: Part 2. MR Spectroscopy and Spectroscopic Imaging

We have developed the 31P- and 1H-magnetic resonance spectroscopic imaging (MRSI) and applied them to severe diffuse brain injury(SDBI) in the chronic stage. The three patients are all young male and had the so called diffuse axonal injury (DAI) by the traffic accident. The DAI was judged by neurological symptoms, computed tomography (CT) and magnetic resonance imaging (MRI). 31P- and 1H-MRSI were performed 2 to 16 months after injury. The decrease of phosphocreatine (PCr) was observed by 31P-MRSI and the decrease of NAA by 1H-MRSI in the wide area of the brain. The decrease of NAA reflects the neuronal damage and consequently indicates the functional deterioration. Therefore, it is suggested that the amount of NAA could be the indicator of neuronal function and 1H-MRSI is useful for the examination of the neurological condition in SDBI.

Cerebral Hemodynamics and Metabolism in Severe Diffuse Brain Injury in Chronic Stage: Positron Emission Tomography

The authors measured the cerebral hemodynamics and metabolism in patients with severe diffuse brain injury (SDBI) in the chronic stage using positron emission tomography (PET). In this study, regional cerebral blood flow (rCBF), oxygen extraction fraction (rOEF), cerebral blood volume (rCBV), cerebral metabolic rate for oxygen (rCMRO2), cerebral metabolic rate for glucose (rCMRGlu), and cerebral metabolic rate were measured in three patients with SDBI in the chronic stage. The patients were all male, and aged 17, 19 and 25 years. The Glasgow Coma Scale score on admission was 3,4 and 3, respectively. In all patients, the cause of injury had been a traffic accident, computed tomography and magnetic resonance imaging revealed findings of so-called diffuse axonal injury (DAI), and the clinical course was also typical of that of DAI. The PET studies were performed 2 to 16 months after injury. The clinical condition of the patients at that time was vegetative state in two and severely disabled in one. PET revealed misery perfusion and low metabolism in two and matched low perfusion and low metabolism in one. It is interesting that any slight difference in clinical state was correlated with a slight difference in PET findings in every patients. The authors stress the usefulness of PET study in the investigation of SDBI in the chronic stage and in the assessment of its prognosis.