Intracerebral temperature monitoring in severely head injured patients

Summary In a series of 6 severely head injured patients, intraventricular as well as rectal, bladder and jugular vein temperature is recorded. The relationship between these temperatures in different conditions is evaluated. Intracerebral temperature is 0.5±0.2 °C (mean ± SD) higher than bladder temperature except in conditions such as brain death. It is concluded that rectal temperature is not representative and therefore not a good alternative to the measurement of brain temperature. More data on human intracerebral temperature are mandatory as well as prospective studies correlating intracerebral temperature with final outcome in head injury.     

A comparision of brain biopsy and CSF-PCR in the diagnosis of CNS lesions in AIDS patients

Twenty patients with AIDS who had intracranial lesions underwent both brain biopsy and cerebro-spinal fluid (CSF) examination to compare histological diagnosis with the polymerase chain reaction (CSF-PCR) for the identification of infectious agents. CSF-PCR was performed for herpes simplex virus, varicella zoster virus, cytomegalovirus (CMV), JC virus (JCV), Epstein-Barr virus (EBV), Toxoplasma gondii and Mycobacterium tuberculosis. A definitive diagnosis was obtained by brain biopsy in 14 patients (2 with astrocytoma, 12 with brain infection). CSF-PCR was positive for EBV DNA in 3 of 3 cases of primary cerebral lymphoma, positive for JCV DNA in 6 of 7 biopsy-proven (and one autopsy-proven) cases of progressive multifocal leukoencephalopathy (PML). CSF-PCR was positive for CMV DNA in one biopsy-proven and one autopsy-proven case of CMV encephalitis (the former also had PML) and positive for M. tuberculosis DNA in one case of tuberculous encephalitis. None of the five toxoplasmic encephalitis cases (one definite, four presumptive) were T. gondii DNA positive. There was close correlation between histology and CSF-PCR for CMV encephalitis, PML and PCL. Antitoxoplasma therapy affected the sensitivity of both histological and CSF-PCR methods. Received: 8 November 1995 Received in revised form: 9 July 1996 Accepted: 19 July 1996     

Immunohistochemical mapping of nitric oxide synthase in the rat hypothalamus and colocalization with neuropeptides

The localization and distribution of nitric oxide synthase in the hypothalamus have been studied with an immunohistochemical technique using antibodies to neuronal rat nitric oxide synthase. Subsequent double-labeling experiments examined the colocalization patterns of nitric oxide synthase and several peptides. Our results demonstrate a widespread occurrence of nitric oxide synthase-immunoreactive nerve cell bodies and processes throughout the hypothalamus, especially in various parts of the preoptic region, in the supraoptic and paraventricular nuclei, the lateral hypothalamic area, the ventromedial and dorsomedial nuclei, the arcuate nucleus and various parts of the mammillary region. Double labeling experiments showed that nitric oxide synthase-like immunoreactivity coexists with substance P-like immunoreactivity in the medial preoptic area, with oxytocin-, cholecystokinin- and galanin message-associated peptide-like immunoreactivity in the supraoptic nucleus, with enkephalin-, oxytocin- and corticotropin releasing factor-like immunoreactivity in the paraventricular nucleus and with enkephalin-like immunoreactivity in the arcuate nucleus. Furthermore, in the ventromedial nucleus, nitric oxide synthase-like immunoreactivity coexisted with enkephalin-, substance P-, and somatostatin-like immunoreactivity, and in the dorsomedial nucleus with enkephalin-, galanin message-associated peptide- and substance P-like immunoreactivity. In the mammillary region nitric oxide synthase-like immunoreactivity coexisted with enkephalin-, cholecystokinin-, and substance P-like immunoreactivity. Among these neuropeptides, enkephalin and substance P were most frequently found in nitric oxide synthase-immunoreactive neurons. We conclude that nitric oxide synthase-immunoreactive neurons contain neuropeptides in various parts of the hypothalamus, and that nitric oxide in the hypothalamus may be involved in a variety of neuroendocrine and autonomic functions.     

Whole-Body [18F]FDG PET in the Management of Metastatic Brain Tumours

Summary Background To determine its roles in the diagnosis and the systemic evaluation of metastatic brain tumours, whole-body positron emission tomography (PET) using [¹⁸F]FDG was performed in 20 consecutive patients. Methods  All patients were thought to be suffering or needing to be differentiated from metastatic brain tumours. Nine patients had multiple brain lesions; six were older and showed a rim-enhancing lesion with surrounding oedema; seven had homogeneously enhancing periventricular lesion(s) on computed tomography (CT) and/or magnetic resonance (MR) imaging, thought to be central nervous system lymphomas. Two patients had skull mass(es) and two patients had a solid mass suspected to be, respectively, a haemorrhagic metastasis and a metastatic malignant melanoma. All of them received whole-body [¹⁸F]FDG PET and conventional systemic work-up for metastasis in order to compare the results of the two methods. Results  Metastatic brain tumours were diagnosed on whole-body [¹⁸F]FDG PET in eleven patients who had extracranial and intracranial hypermetabolic lesions. In nine of these, a conventional work-up also detected primary lesions which on whole-body [¹⁸F]FDG PET were seen to be hypermetabolic foci. Systemic lymph node metastases were detected by whole-body [¹⁸F]FDG PET only in two patients and histological diagnosis was possible by biopsy of lymph nodes rather than of brain lesions. In the remaining nine patients who had only intracranial hypermetabolic foci, histological diagnosis was made by craniotomy or stereotactic biopsy. It was confirmed that seven of nine patients were suffering from a primary brain tumour and two from metastatic carcinoma. None of the nine showed evidence of systemic cancer on conventional work-up. Histological diagnoses of the primary brain tumours were four cases of primary central nervous system lymphoma and one each of multifocal glioblastoma, Ewing's sarcoma, and cavernous angioma.  Patients felt no discomfort during the whole-body [¹⁸F]FDG PET procedure and there were no complications. The false negative rate in [¹⁸F]FDG PET and in conventional work-up was 15.4% and 30.7% respectively. There were no false positives on either [¹⁸F]FDG PET or conventional work-up. Conclusion  It is suggested that whole-body [¹⁸F]FDG PET is a safe, reliable, and convenient method for the diagnosis and systemic evaluation of patients thought to be suffering or needing to be differentiated from a metastatic brain tumour.     

脑内转移瘤误诊原因分析

提高脑内转移瘤影诊断的准确性。材料与方法：脑转移瘤与脑内其他病变术前相互误诊的４２例作回顾性影像分析。结果：脑内转移瘤误诊的主要原因是由于影像的不典型表现，病变部位的影响，特殊因素的影响，如临床病病史的误导，少见肿瘤，少见表现。     

Invited. Brain edema development after MRI-guided focused ultrasound treatment

The aim of this study was to investigate a potential technique for image-guided minimally invasive neurosurgical interventions. Focused ultrasound (FUS) delivers thermal energy without an invasive probe, penetrating the dura mater, entering through the cerebrospinal fluid (CSF) space, or harming intervening brain tissue. We applied continuous on-line monitoring by MRI to demonstrate the effect of the thermal intervention on the brain tissue. For this, seven rabbits had a part of their skull removed to create access for the FUS beam into the brain through an acoustic window of 11 mm in diameter. Dura was left intact and skin was sutured. One week later, the rabbits were sonicated for 3 seconds with 21 W acoustic power, and the FUS focus was visualized with a temperature-sensitive T1-weighted MRI pulse sequence. The tissue reaction was documented over 7 days with T2-weighted images of the brain. The initial area of the central low signal intensity in the axial plane was .4 ± .3 mm², and for the bright hyperintensity surrounding the lesion, it was 2.3 ± .6 mm² (n = 7). In the coronal plane, the corresponding values were .4 ± .1 mm² and 3.4 ± .9 mm² (n = 5). The developing brain edema culminated 48 hours later and thereafter diminished during the next 5 days. Histology revealed a central necrosis in the white matter surrounded by edematous tissue with inflammatory cells. In summary, the image-guided thermal ablation technique described here produced a relatively small lesion in the white matter at the targeted location. This was accomplished without opening the dura or the need for a stereotactical device. MRI allowed on-line monitoring of the lesion setting and the deposition of thermal energy and demonstrated the tissue damage after the thermal injury.     

抑郁症的基础与认知激活脑SPECT显像

目的通过抑郁症患者基础和认知激活局部脑血流（ｒＣＢＦ）灌注显像的半定量分析，评估抑郁症患者的脑血流灌注异常。方法选择２７例未经抗抑郁治疗、ＩＣＤ１０分类为中度抑郁发作伴躯体症状的患者，１５例年龄匹配的健康人作正常对照。２７例患者中２１例、１５例健康人中１３例行双日法基础与认知激活脑ｒＣＢＦ显像；另６例患者及２例健康人仅行基础脑ＳＰＥＣＴ显像。认知激活采用Ｗｉｓｃｏｎｓｉｎ卡片分类试验。半定量分析在横断面图像７～１１帧上进行，将各ＲＯＩ的平均计数与同侧小脑的最高计数相除，得到各ＲＯＩ的ｒＣＢＦ比值。结果抑郁症左额叶和左颞叶的基础ｒＣＢＦ值均为０７２０，明显低于对照组（０７６４和０７５０，Ｐ＜００５）；左额、左颞、左顶叶的认知激活ｒＣＢＦ值分别为０７１９、０６９０及０７０１，明显低于对照组（０７８２、０７５２和０７６６，Ｐ＜００１和Ｐ＜００５）。结论①抑郁症患者存在左额叶、左颞叶的局部血流低灌注。②额叶、颞叶皮层低灌注可能是引起抑郁症认知障碍、心境低落的原因。③Ｗｉｓｃｏｎｓｉｎ卡片分类试验认知激活脑ＳＰＥＣＴ显像有助于提高抑郁症的诊断准确性     

Invited. Fukuyama congenital muscular dystrophy: A neuroradiologic review

We reviewed neuroradiologic findings of Fukuyama congenital muscular dystrophy (FCMD) and correlated them with the known neuropathology. All patients showed thick and bumpy cortices with shallow sulci corresponding to polymicrogyria, and approximately half of the patients showed pachygyric cortex with smooth surface corresponding to type II lissencephaly. The two types of cortical dysplasias presented characteristic distributions: the former demonstrated frontal lobe involvement in all and parietotemporal lobe involvement in some, whereas the latter involved the temporo-occipital lobes. Most patients showed prolonged T1 and T2 signal in the white matter, which was indistinct in neonates and infrequently seen in adolescents. Cerebellar polymicrogyria depicted as disorganized cerebellar foliation accompanying cysts were found more than 90% of the patients. In conclusion, brain MRI demonstrates findings consistent with the known neuropathology of FCMD. The detection of the two types of cerebral cortical dysplasia with characteristic distribution and cerebellar abnormalities is helpful in the differential and early diagnosis.     

Changes of circadian blood pressure patterns and cardiovascular parameters indicate lateralization of sympathetic activation following hemispheric brain infarction

The effects of left- and right-sided hemispheric brain infarction on variability in circadian blood pressure and cardiovascular measures were investigated in 35 patients to test for asymmetry of the sympathetic consequences of stroke. No significant differences regarding age, size of infarction or extent and frequency of damage to the insular cortex could be detected between the two groups. Patients with right-sided infarction showed a significantly reduced circadian blood pressure variability [diastolic: -1% (95% CI -4 to 1) vs -6% (-9 to -2);P < 0.05] and a higher frequency of nocturnal blood pressure increase (47% vs 35%;P < 0.05) as compared with patients with left-sided infarction. Right-sided infarction was also associated with higher serum noradrenaline concentrations [546 pg/ml (95% CI 415–677) vs 405 pg/ml (266–544);P < 0.05], and ECG more frequently showed QT prolongation (53% vs 35%;P < 0.05) and cardiac arrhythmias (67% vs 20%;P < 0.005). However, irrespective of the hemisphere damaged, patients with insular infarction showed the most pronounced changes of these parameters. In addition, two patients with right-sided strokes (13%) involving the insula, but none with a left-sided infarction, developed myocardial infarction. These findings suggest lateralization of sympathetic activation with right-sided dominance for sympathetic effects following hemispheric stroke.Supported by the Friedrich-Schiedel-Stiftung     

Formation of pyridinium species of haloperidol in human liver and brain

Recent interest in the neurotoxicity of haloperidol is based on its oxidation in rodents to the pyridinium derivative, HPP⁺, a structural analog of the neurotoxin, 1-methyl-4-phenylpyridinium (MPP⁺). Recently, we reported that HPP⁺ and a newly identified reduced pyridinium, RHPP⁺, were present in blood and urine of haloperidol-treated schizophrenics and that the concentrations of RHPP⁺ exceeded those of HPP⁺. In this study, we examined pathways for formation of RHPP⁺ in subcellular fractions of human liver (n=5) and brain (basal ganglia;n=5). The major pathway was reduction of HPP⁺ (20 µM) to RHPP⁺ in cytosol (0.17–0.39 and 0.03–0.07 µM RHPP⁺/g cytosolic protein per h in liver and brain, respectively). The reactions were inhibited significantly by menadione and in brain also by daunorubicin. The inhibition profile, cytosolic location and strict NADPH dependence suggest that the enzymes involved are ketone reductases. A second pathway was oxidation of reduced haloperidol (50 µM), a major metabolite of haloperidol in blood and brain, to RHPP⁺. In liver microsomes, 0.17–0.63 µmol RHPP⁺ was formed /g microsomal protein per h. A potent inhibitor of the pathway was ketoconazole (IC₅₀, 0.8 µM), which suggests that P-450 3A isozymes could be involved. In brain mitochondria but not microsomes, reduced haloperidol (120 µM) was oxidised to RHPP⁺ at a small but significant rate (0.005–0.020 µmol RHPP⁺/g mitochondrial protein per h) which was not attenuated by SKF 525A, quinidine, ketoconazole, or monoamine oxidase inhibitors. Further studies are warranted to establish the biological importance of these metabolites in vivo.