Shoji Naruse

Discrimination of brain abscess from necrotic or cystic tumors by diffusion-weighted echo planar imaging.

Diagnostic difficulties in discriminating brain abscess from necrotic or cystic tumors using conventional CT and MRI have been reported. In this article, we examine the diagnostic ability of diffusion-weighted imaging to discriminate brain abscess from necrotic or cystic tumors. In previous reports, necrotic or cystic tumors show low signal intensity in diffusion-weighted imaging, indicating a high apparent diffusion coefficient (ADC). In contrast, in our study, high signal intensity was observed in the abscess fluid, associated with low ADC.

Initial MRI findings of non-traumatic osteonecrosis of the femoral head in renal allograft recipients

Fifty-one renal allograft recipients (15-62 years old, mean: 37 years) were monitored for 2.5-6.5 years (average: 4.3 years) after surgery by using magnetic resonance imaging (MRI) to find (i) initial signs of osteonecrosis of the femoral head (ONF), (ii) the presence of bone marrow edema as an initial sign of ONF, (iii) any changes of MRI patterns, and (iv) the relationship between these MRI findings and prognosis. MRI was performed preoperatively (baseline), and whenever possible during the 6-9th week, 12-16th week, 12th month, and yearly thereafter. T1- and T2-weighted images were obtained by using a spin echo technique. Abnormalities were first detected on MRI of 23 femoral heads in 13 patients between 6 weeks and 12 months. All lesions first showed a low intensity band on T1-weighted images and a high intensity band on T2-weighted images. No symptoms or diffuse patterns, such as bone marrow edema, preceded the appearance of the band pattern. After the 12th month, no new abnormal findings on MRI were detected. The lesions were classified into Type A, B, or C, according to the location. 12 of the 16 Type C femoral head lesions, which extend beyond the medial two thirds of the weight-bearing portion of the acetabulum, became symptomatic 7-14 months after transplantation and then progressed to collapse. Bone marrow edema appeared with radiological collapse and symptoms. With the exception of five lesions in three patients who failed to be MR imaged until 12 months postoperatively, all lesions were first detected on MRI within 16 weeks after transplantation. We therefore postulate that the ischemic event that causes ONF will have occurred within 12 weeks after transplantation, considering the time lag of reparative reaction to the dead bone.

Dynamic activity-induced manganese-dependent contrast magnetic resonance imaging (DAIM MRI)

Activity‐induced manganese‐dependent contrast (AIM) MRI is a hemodynamic‐independent functional MRI method that used manganese ion as an MR‐detectable contrast agent. In AIM, MnCl2 is infused intra‐arterially after the blood‐brain barrier (BBB) is opened with a hyperosmolar agent. Upon functional stimulation of the brain, Mn2+ accumulates in the active region(s) by entering active cells through voltage‐gated Ca2+ channels, causing local signal increases in T1‐weighted images. The contrast of AIM MRI depends strongly on the depth of anesthesia, and the low levels used in somatosensory stimulation studies can lead to significant nonspecific accumulation of manganese ion throughout the brain. The purpose of this study was to produce an AIM functional map of somatosensory stimulation, which separates the stimulation‐specific signal increase from the nonspecific activation due to light anesthesia. A dynamic AIM (DAIM) paradigm was developed, which used sequential MR scans during MnCl2 infusion, prior to and following functional stimulation of the brain. Stimulation‐specific functional maps were produced using time‐course analysis. The new method was tested during glutamate administration and electric stimulation of the rat forepaw. It was shown that DAIM maps are better confined to the specific region of brain activated by somatosensory stimulation as compared to AIM MRI. Magn Reson Med 48:927–933, 2002.

In vivo measurement of energy metabolism and the concomitant monitoring of electroencephalogram in experimental cerebral ischemia

The energy metabolites in rat brain in vivo were measured by using topical magnetic resonance (TMR) during the whole course of ischemia, in combination with the concomitant monitoring of electroencephalogram (EEG). Immediate loss of high energy phosphorus compounds, phosphocreatine (PCr) and ATP, resulted in the flattening of EEG after the induction of ischemia. PCr and ATP returned to almost normal level 30 min after recirculation of the ischemic brain, but EEG showed no recovery and the abnormality lasted for 12 h. The measurement of in vivo 31P-NMR is essential for the decision of the convalescence of cellular function in the brain.

Pulsatile compression of the rostral ventrolateral medulla in hypertension

The rostral ventrolateral medulla (RVLM) has been known to be a major regulating center of sympathetic and cardiovascular activities. An association between essential hypertension and neurovascular compression of the RVLM has been reported in clinical observations, including magnetic resonance imaging (MRI) studies. To reconfirm this relationship, we performed MRI using a high-resolution 512 x 512 matrix in patients with essential and secondary hypertension and in normotensive subjects. The duration of hypertension and the degree of organ damage by hypertension were not significantly different between the two hypertension groups. Neurovascular compression of the RVLM was observed in 74% of the essential hypertension group, and the incidence of compression was significantly higher than in the secondary hypertension group (11%) or in the normotensive group (13%) (P < .01). These results from the clinical studies suggest that neurovascular compression of the RVLM is, at least in part, causally related to essential hypertension. Although blood pressure elevation by pulsatile compression of the RVLM in an experimental baboon model has already been reported, its underlying mechanism is not well known. Accordingly, we performed experiments to investigate whether pulsatile compression of the RVLM would increase arterial pressure and to elucidate the mechanism of the pressor response in rats. Sympathetic nerve activity, arterial pressure, heart rate, and plasma levels of epinephrine and norepinephrine were increased by pulsatile compression of the RVLM. The pressor response was abolished by intravenous treatment with hexamethonium or RVLM injection of kainic acid. In summary, the results from the MRI studies suggest that neurovascular compression of the RVLM is, at least in part, causally related to essential hypertension. This was supported by the results from experimental studies using rats indicating that pulsatile compression of the RVLM increases arterial pressure by enhancing sympathetic outflow.

Significance of proton relaxation time measurement in brain edema, cerebral infarction and brain tumors

We examined the proton relaxation times in vitro in various neurological diseases using experimental and clinical materials, and consequently obtained significant results for making a fundamental analysis of magnetic resonance imaging (MRI) as followings. 1) In the brain edema and cerebral infarction, T1 prolonged and T2 separated into two components, one fast and one slow. Prolongation of T1 referred to the volume of increased water in tissue. The slow component of T2 reflects both the volume and the content of increased edema fluid in tissue. 2) In the edematous brain tissue with the damaged Blood-Brain-Barrier (BBB), the slow component of T2 became shorter after the injection of Mn-EDTA. Paramagnetic ion could be used as an indicator to demonstrate the destruction of BBB in the brain. 3) After the i.v. injection of glycerol, the slow component of T2 became shorter in the edematous brain with the concomitant decrease of water content. The effects of therapeutic drug could be evaluated by the measurement of proton relaxation times. 4) Almost all tumor tissue showed a longer T1 and T2 values than the normal rat brain, and many of them showed two components in T2. It was difficult to determine the histology of tumor tissue by the relaxation time alone because of an overlap of T1 and T2 values occurred among various types of brain tumors. 5) In vivo T1 values of various brain tumor were calculated from the data of MRIs by zero-crossing method, and they were compared with the in vitro T1 values which were measured immediately after the surgical operation. Though the absolute value did not coincide with each other due to differences in magnetic field strength, the tendency of the changes was the same among all kinds of tumors. It is concluded that the fundamental analysis of proton relaxation times is essentially important not only for the study of pathophysiology in many diseases but also for the interpretation of clinical MRI.

Neurovascular Compression of the Rostral Ventrolateral Medulla Related to Essential Hypertension

The rostral ventrolateral medulla (RVLM) is thought to serve as a final common pathway for the integration of central cardiovascular information and to be important for the mediation of central pressor responses. An association between essential hypertension and neurovascular compression of the RVLM has been reported. To confirm this relationship and to quantitatively measure the distances between the RVLM and the neighboring arteries, we performed magnetic resonance imaging using a high-resolution 512x512 matrix and magnetic resonance angiography in 49 subjects (21 patients with essential hypertension, 10 patients with secondary hypertension, and 18 normotensive subjects). One patient with essential hypertension was excluded from the evaluations because of inadequate assessment due to poor images. Neurovascular compression of the RVLM was observed in 15 of 20 (75%) patients with essential hypertension. In contrast, neurovascular compression was observed in only 1 of 10 (10%) patients with secondary hypertension and only 2 of 18 (11%) normotensive subjects. The rate of observed neurovascular compression in the essential hypertension group was significantly higher than that in the secondary hypertension group and the normotensive group (P<.01 for both). The distances between the RVLM and the nearest arteries in the essential hypertension group were significantly shorter than those in the other groups (P<.05 for all). On the other hand, the distances between the surface of the medulla oblongata and the nearest arteries did not differ among these three groups. These results suggest that neurovascular compression of the RVLM, but not of the other regions of the medulla oblongata, is particularly related to essential hypertension.

Decreases in Blood Pressure and Sympathetic Nerve Activity by Microvascular Decompression of the Rostral Ventrolateral Medulla in Essential Hypertension

BACKGROUND Neurovascular compression of the rostral ventrolateral medulla, a major center regulating sympathetic nerve activity, may be causally related to essential hypertension. Microvascular decompression of the rostral ventrolateral medulla decreases elevated blood pressure. CASE DESCRIPTION A 47-year-old male essential hypertension patient with hemifacial nerve spasms exhibited neurovascular compression of the rostral ventrolateral medulla and facial nerve. Microvascular decompression of the rostral ventrolateral medulla successfully reduced blood pressure and plasma and urine norepinephrine levels, low-frequency to high-frequency ratio obtained by power spectral analysis, and muscle sympathetic nerve activity. CONCLUSIONS This case suggests not only that reduction in blood pressure by microvascular decompression of the rostral ventrolateral medulla may be mediated by a decrease in sympathetic nerve activity but also that neurovascular compression of this area may be a cause of blood pressure elevation via increased sympathetic nerve activity.

Detection of the anoxic depolarization of focal ischemia using manganese‐enhanced MRI

Mismatch between diffusion‐ and perfusion‐weighted MRI was used to indicate a treatable area following focal ischemia, called the penumbra. Activity‐induced manganese contrast MRI has been reported as a new visualization method for neural activation using manganese ions as a depolarization‐dependent contrast agent. It is well known that energy failure induced by cerebral ischemia produces anoxic depolarization. The purpose of this study was to detect manganese accumulation caused by permanent middle cerebral artery occlusion (MCAO) of rat brain and to compare regional differences between manganese accumulation and decreased apparent diffusion coefficient (ADC). The ratios of signal intensity of manganese‐enhanced MRI in the ipsilateral cortex to that in the contralateral cortex were 171.0 ± 17.5% in MCAO group and 108.4 ± 13.2% in the sham group. In addition, the enhanced region was much smaller than the area which was detected as having a reduced ADC. Magn Reson Med 50:7–12, 2003.

Metabolic and pathological effects of temporal lobe epilepsy in rat brain detected by proton spectroscopy and imaging.

The goal of these experiments was to test the hypothesis that in an animal model of temporal lobe epilepsy (TLE), magnetic resonance spectroscopic measurement of N-acetylaspartate (NAA) and other metabolites, together with magnetic resonance imaging, provides a sensitive in vivo method to localize and monitor the progression of neuronal cell death and gliosis. Seizures were induced in rats by unilateral hippocampal injection of kainate. Magnetic resonance measurements were made from 1 to 84 days using proton spectroscopic imaging (1H-MRSI), T2-weighted imaging (T2WI) and diffusion-weighted imaging (DWI). The results were compared with findings on histological sections. Decreased NAA and creatine levels and increased apparent diffusion coefficient of water were found in the ipsilateral hippocampus after 14 days where neuronal loss and gliosis were observed. In the contralateral hippocampus a significant increase of choline level was observed. These results suggest that 1H-MRSI is a useful in vivo method for localizing neuronal loss and may also indicate additional pathological and metabolic alterations. In addition, DWI may be a useful method for in vivo detection of tissue alterations due to TLE.