Serotonergic projections from the midbrain periaqueductal gray and nucleus raphe dorsalis to the nucleus parafasccicularis of the thalamus

By a double-labeling method combining the retrograde tracing of horseradish peroxidase and the immunocytochemical technique, serotonin-like immunoreactive neurons in the midbrain periaqueductal gray (PAG) and nucleus raphe dorsalis (DR) of the rat were observed to send projection fibers to the nucleus parafascicularis of the thalamus bilaterally with an ipsilateral dominance. These serotonin-containing projecting neurons were observed mainly at the middle-caudal levels of the ventrolateral subdivision of the PAG and less at the middle-rostral levels of the DR.     

Imaging of shifted stimulated echoes and multiple spin echoes

It is shown that a repetitive pulse sequence consisting of two 90° pulses and gradients in a 1:2 ratio around the second 90° pulse generates interscan shifted stimulated echoes (SSTEs) and intrascan multiple spin echoes (MSEs). Separation of these two types of signals is accomplished using specific gradient crusher schemes. The intensity of the SSTEs is an order of magnitude larger than that of the MSEs and determines the signal contrast if both effects are selected simultaneously. The SSTE sequence generates improved contrast between gray and white matter, even at high field, which is explained in terms of increased inverse T₁-weighting for the interscan echo. The MSE image has low signal to noise and no detectable contrast. The effect of interscan diffusion weighting is also discussed.     

脑梗死后再发缺血性卒中与脑出血患者微血管病变及预后的比较

【目的】探讨脑梗死后再发缺血性卒中与脑出血患者的临床特点、影像学上微血管病变及预后的异同。【方法】连续收集急性复发性卒中的住院病例（初发事件为脑梗死，复发事件包括脑梗死或脑出血），详细记录临床资料。观察脑内微出血及自质病变的严重程度，随访有无严重血管事件及死亡的发生。【结果】175例再发脑梗死患者。19例复发事件为脑出血的患者进入本研究。155例（88．6％）再发脑梗死患者，以及18例（94．7％）脑出血患者存在自质病变。77例（44％）再发脑梗死患者和16例（84．2％）脑出血患者存在脑内微出血。脑出血组自质病变的严重程度及微出血的数目均明显高于再发脑梗死组（P=0．033，0．016），脑出血组的死亡率及再发脑出血的危险性明显增高（P=0．034，0．036）。【结论】严重的脑自质病变及微出血的出现与脑梗死后再发脑出血有关。多发微出血提示出血风险增高。如复发事件为脑出血，则其死亡率及再次复发脑出血的风险均明显增加。     

Binswanger's disease in the absence of chronic arterial hypertension

Summary The cerebral changes are described in a woman of 54 who suffered from Binswanger's encephalopathy: there were no signs or symptoms of chronic arterial hypertension. The disease presented as dementia of about 3 years duration. Computed tomography of the brain 2. 5 years before her death showed bilateral widespread hypodense lesions in the cerebral white matter. She died of an asthmatic attack. Autopsy disclosed extensive bilateral degeneration of the central white matter, lacunes and gliosis. Severe obliterative arteriolosclerosis occurred in the meningeal vessels and those supplying the affected parts of the brain. Light microscopy showed that the most severe lesions occurred in the arterioles. Immunohistochemistry demonstrated profound extravasation of plasma proteins chiefly albumin, indicating dysfunction of the blood-brain barrier. Thus, the lesions characteristic of Binswanger's encephalopathy may develop in the absence of chronic arterial hypertension. Additional pathogenic factors, possibly genetic predisposition to vascular injury may play a role in the development of this condition.Supported by grants from the Swedish Medical Research Council, Project No 12X-03020 and 1987 Års Stiftelse för Strokeforskning     

An Autopsied Case of Interferon Encephalopathy

Abstract: A 78-year-old male with renal carcinoma was treated with a high dose infusion of interferon-alpha (IFN-alpha) for eight months. The patient had evidence of organlc brain syndrome such 88 : dysfunction of memory, slowing of behavior, and development of mental confusion that appeared eight months after the treatment. MRI at the time of mental confusion revealed difise white matter lesions. Neuropathologic findings were compatible to Binswanger's disease and Senile Dementia of Alzheimer Type (SDAT), Preexisting neurologic abnormalities including intracerebral arteriosclerosis and cerebral atrophy may increase susceptibility to unacceptably severe IFN neurotoxicity.     

高血压大鼠中脑导水管周围灰质内nNOS样阳性神经元的变化

目的：观察高血压大鼠中脑导水管周围灰质(PAG)内神经元型一氧化氮合酶(nNOS)样阳性神经元数量的变化。方法：用双肾双夹法建立高血压大鼠模型，ABC法显示PAG内nNOS样阳性神经元并进行定量分析。结果：nNOS样阳性神经元分布于PAG的背外侧区。PAG内nNOS样阳性神经元的数量、光密度在对照组各时期无明显变化；在高血压大鼠7d时的数量略减少，光密度略下降；而在30d、70d则数量、光密度逐渐减少，与对照组比较差异显著。结论：中脑PAG内nNOS样阳性神经元及阳性产物的减少可能与其对心血管功能活动、感觉信息传导的影响以及高血压的形成和发展有关。     

Mapping corpus callosum deficits in autism: an index of aberrant cortical connectivity.

BACKGROUND: Volumetric studies have reported reductions in the size of the corpus callosum (CC) in autism, but the callosal regions contributing to this deficit have differed among studies. In this study, a computational method was used to detect and map the spatial pattern of CC abnormalities in male patients with autism. METHODS: Twenty-four boys with autism (aged 10.0 +/- 3.3 years) and 26 control boys (aged 11.0 +/- 2.5 years) underwent a magnetic resonance imaging (MRI) scan at 3 Tesla. Total and regional areas of the CC were determined using traditional morphometric methods. Three-dimensional (3D) surface models of the CC were also created from the MRI scans. Statistical maps were created to visualize morphologic variability of the CC and to localize regions of callosal thinning in autism. RESULTS: Traditional morphometric methods detected a significant reduction in the total callosal area and in the anterior third of the CC in patients with autism; however, 3D maps revealed significant reductions in both the splenium and genu of the CC in patients. CONCLUSIONS: Statistical maps of the CC revealed callosal deficits in autism with greater precision than traditional morphometric methods. These abnormalities suggest aberrant connections between cortical regions, which is consistent with the hypothesis of abnormal cortical connectivity in autism.     

Blood-brain barrier dysfunction in Binswanger’s disease; an immunohistochemical study

Binswanger’s disease is pathologically characterized by a combination of diffuse cerebrovascular white matter lesions and lacunar infarcts in the basal ganglia and white matter. Although a blood-brain barrier (BBB) dysfunction has been implicated in the pathogenesis of these white matter (WM) lesions, few authors have addressed this problem. In the present study, we describe BBB dysfunction and its regional differences in the brains of Binswanger’s disease patients. Twelve brains from Binswanger’s disease patients (group III) were examined and compared with those from five patients with non-neurological disease (group I) and five cortical infarct patients without significant WM lesions (group II). Immunohistochemistry was performed for glial fibrillary acidic protein and vimentin as astroglial cell markers, and for immunoglobulins, complements and fibrinogen as extravasated serum protein markers. The grading scores for IgG extravasation were significantly higher in group III as compared to group I, in both the periventricular WM and the subcortical WM (P < 0.01). In group III, the scores in the periventricular WM and subcortical WM were significantly higher than in the subcortical U fibers and cerebral cortex (P < 0.01 for the periventricular WM; P < 0.001 for the subcortical WM), respectively. Clasmatodendritic astroglia, which had swollen cell bodies and large cytoplasmic vacuoles with disintegrated processes, incorporated the serum components IgG, IgM, C3d, C1q and fibrinogen, both in the periventricular WM and subcortical WM in 5 out of 12 (42%) Binswanger’s disease brains. These results indicate that WM lesions in Binswanger’s disease are accompanied by BBB dysfunction, although it remains uncertain whether BBB dysfunction is secondary to either chronic cerebral ischemia or arterial hypertension. Received: 25 April 1997 / Revised, accepted: 21 July 1997     

Magnetization Transfer and T2 Relaxation Components in Tissue

T₂ relaxation makes an important contribution to tissue contrast in magnetic resonance (MR) imaging. Many tissues are known to exhibit multicomponent T₂ relaxation that suggests some compartmental segregation of mobile protons on a T₂ timescale. Magnetization transfer (MT) is another relaxation mechanism that can be used to produce tissue contrast in MR imaging. The MT process depends strongly on water-macromolecular interactions. To investigate the relationship between multicomponent T₂ relaxation and the MT process, multiecho T₂ measurements have been combined with MT measurements for freshly excised samples of cardiac muscle, striated muscle, and white matter. For muscle, short T₂ components show greater MT than long T₂ components, consistent with the belief that they represent distinct water environments. For white matter, quantitative MT measurements were identical for the two major T₂ components, apparently because of exchange between the T₂ compartments on a timescale characteristic of the MT experiment. Implications for accurate modeling of MT in tissue and the use of MT for MR image contrast are discussed.