原发性脑干出血30例临床分析

目的：探讨原发性脑干出血的病因，临床表现，治疗及预后，方法：收集我科诊治的30例原发性脑干出血病人，经保守治疗后的有关资料。结果：死亡11例，存活19例，结论：高血压动脉硬化是脑干出血的主要病因，临床表现复杂多样，治疗原则与半球相同，早期脱水甚为重要，并直接决定预后，出血量越多，预后越差。     

原发性脑干出血内科保守治疗预后评估的临床研究

目的研究原发性脑干出血内科保守治疗的疗效及预后评估。方法回顾性分析50例经CT或MRI检查诊断脑干出血的临床和影像学资料。结果首次CT检查诊断脑干出血46例，余4例经MRI检查明确诊断。临床内科治疗治愈14例，好转16例，死亡15例。结论脑干出血的预后与多种因素有关，死亡率与出血量密切相关。同时临床表现和并发症是脑干出血死亡的危险因素，应积极预防和治疗。     

去大脑皮层综合征治疗体会

对于去大脑皮层综合征目前临床上尚无有效治疗方法。19 90～ 2 0 0 0年 ,我院收治该病患者 16例 ,经综合治疗效果较好。现报告如下。一般资料 :本组男 14例 ,女 2例 ;年龄 16～ 60岁 ,平均 3 6岁。原发性脑干损伤 9例 ,原发性脑干损伤加颅内血肿、脑疝4例 ,颅内血肿继发脑干损伤 3例。昏迷时间 82～ 3 0 6天。GCS评分 4分 8例 ,5～ 6分 8例。双侧瞳孔散大 4例、缩小 4例、多变 3例 ,一侧瞳孔散大 5例 ,瞳孔对光反应消失 4例 ,眼球同向注视 3例 ,眼球分离 6例。双侧巴氏征阳性 12例。偏瘫 6例。 CT检查硬膜下血肿 7例 ,脑挫裂伤 13例。治疗…     

重症颅脑损伤并发多脏器功能衰竭35例

重症颅脑损伤并发多脏器功能衰竭(MODS)是导致其病死率增加的主要原因之一。2000年5月至2002年8月,我们共收治重症颅脑损伤患者263例,其中35例并发MODS。现报告如下。 临床资料:本组263例均符合重症颅脑损伤的诊断标准,即格拉期哥昏迷测量表评分(GCS)≤8分,发生MODS者35例,男23例、女12例,年龄8～75岁、平均51岁。GCS≤5分10例(23.26％),原发脑干损伤者9例(37.70％);35例患者     

原发脑干损伤并发神经源性肺水肿19例诊疗体会

目的探讨原发性脑干损伤后合并神经源性肺水肿（NPE）的诊疗体会。方法回顾性分析我院神经外科2003~2009年期间收治的19例原发性脑干损伤并发NPE病例临床资料。结果 19例原发性脑干损伤并发NPE病例均于颅脑损伤或开颅术后24 h内发病,出现呼吸窘迫症状、呼吸频率〉40次/min、双肺可闻及广泛湿罗音。胸片示肺纹理紊乱增强11例,斑片状阴影7例。在吸氧情况下血气分析均为PaO2〈8.0 kPa,PaCO2〉8.2kPa。经对因治疗、有效脱水、气管切开、呼吸机辅助呼吸、物理降温结合冬眠药物降温、大剂量糖皮质激素治疗、缓解气道痉挛、有效抗生素应用等措施治疗,本组存活11例,死亡8例。结论治疗原发性脑干损伤合并NPE应兼顾肺部及颅脑损伤等多方面因素,以提高存活率和治愈率。     

重型脑干出血两种治疗方法对比研究

目的探讨重型脑干出血治疗方法与预后的关系。方法通过复习文献结合我院2007年8月—2009年12月收治的重型脑干出血38例患者,将GCS≤9分17例患者及GCS〈5分21例患者随机分为两组,应用侧脑室穿刺外引流术综合治疗20例为观察组,内科保守治疗18例为对照组,进行预后对比。结果观察组有效率70%,对照组有效率33.3%;与对照组比较应用侧脑室穿刺外引流术综合治疗有效率提高,病死率无明显变化。结论重型脑干出血患者预后凶险,但侧脑室穿刺外引流术综合治疗能提高疗效,有助于改善患者预后。     

高血压脑出血的规范化微创外科治疗

目的 探讨高血压脑出血(HICH)的规范化外科治疗。方法 制定HICH人选标准，将患者随机分为小骨窗开颅血肿清除术组(小骨窗组)和颅骨钻孔血肿清除术组(颅骨钻孔组)，观察两组患者的术后GCS评分、临床神经功能缺损评分变化，并进行疗效评价。结果 HICH发病后早期(8～24小时)尤其是12小时内手术者，术后再出血发生率高。GCS6～8分者小骨窗组的病死率及致残率比颅骨钻孔组低，而GCS9～15分者以颅骨钻孔组的病死率及致残率较低。结论 HICH发病后，经内科保守治疗病情稍稳定，血压控制在180／105mmHg内，12～24小时内手术效果好；GCS6～8分者首选小骨窗开颅血肿清除术，GCS9～15分者首选颅骨钻孔血肿清除术。     

原发性脑干损伤90例诊治体会

1992年4月～2001年4月，我院共收治原发性脑干损伤患者90例，现将诊断及治疗情况总结如下。     

原发性脑干出血50例临床及预后分析

目的探讨原发性脑干出血的临床类型及预后。方法对资料完整的50例原发性脑干出血的临床资料进行回顾性分析。结果原发性脑干出血50例患者中，脑桥出血45例，中脑出血5例，无延髓出血。结论脑干出血死亡率高，轻型脑干出血预后较好，部分病人可完全治愈。出血量〉5ml，累及延髓者，预后差。     

重型颅脑损伤继发吸入性肺炎的护理

重型颅脑损伤患者由于不同程度的昏迷、吞咽反射减弱或消失、高颅压所致呕吐,易造成患者胃内容物、分泌物或脑脊液的误吸,影响呼吸道畅而致吸入性肺炎。我院于2002～2004年收治重型颅脑损伤继发吸入性肺炎患者21例。现将护理体会报告如下。1一般资料本组男15例、女6例,年龄10～72岁,平均41岁;致伤原因及损伤部位:车祸16例、重物砸伤3例、坠落伤2例,病人均行头颅CT检查:急性硬膜下血肿8例、急性硬膜外血肿6例、原发性脑干损伤3例、广泛脑挫裂伤4例;脑损伤昏迷时间超过6h,GCS评分<8分(本组GCS评分<5分占有5例),并发呕吐、鼻、口腔有大量血…     

脑干梗死后全身炎症反应综合征及其临床意义

目的观察脑干梗死后全身炎症反应综合征（SIRS）的发生情况，并探讨其病因及高危因素。方法根据116例脑干梗死住院患者的体温、心率、呼吸频率及白细胞计数确定是否存在SIRS，分析与SIRS发生相关的因素。结果116例脑干梗死患者中，SIRS70例，46例无SIRS。脑干梗死后SIRS的发生与脑干梗死的危重程度及基础疾病密切相关。存在SIRS的患者死亡率较无SIRS者明显升高。结论脑干梗死后出现SIRS提示疾病仍在进展，预后较差；除脑干梗死本身的严重程度外，患者并存的躯体疾病也是激发SIRS的重要因素。     

脑外伤与心电图异常关系的分析

目的:分析脑外伤患者脑伤情况与心电图异常率之间的关系.方法:选择同一时间段内住院治疗的161例脑外伤患者,比较、分析不同损伤程度、部位的脑伤患者心电图异常率,以及随着治疗心电图异常的恢复情况.结果:共出现心电图异常83例(51.55%),以各种心律失常、T波及ST段改变、左室高电压等最为常见.Glasgow评分越低、脑...     

Identification of discrete functional subregions of the human periaqueductal gray

The midbrain periaqueductal gray (PAG) region is organized into distinct subregions that coordinate survival-related responses during threat and stress [Bandler R, Keay KA, Floyd N, Price J (2000) Brain Res 53 (1):95–104]. To examine PAG function in humans, researchers have relied primarily on functional MRI (fMRI), but technological and methodological limitations have prevented researchers from localizing responses to different PAG subregions. We used high-field strength (7-T) fMRI techniques to image the PAG at high resolution (0.75 mm isotropic), which was critical for dissociating the PAG from the greater signal variability in the aqueduct. Activation while participants were exposed to emotionally aversive images segregated into subregions of the PAG along both dorsal/ventral and rostral/caudal axes. In the rostral PAG, activity was localized to lateral and dorsomedial subregions. In caudal PAG, activity was localized to the ventrolateral region. This shifting pattern of activity from dorsal to ventral PAG along the rostrocaudal axis mirrors structural and functional neurobiological observations in nonhuman animals. Activity in lateral and ventrolateral subregions also grouped with distinct emotional experiences (e.g., anger and sadness) in a factor analysis, suggesting that each subregion participates in distinct functional circuitry. This study establishes the use of high-field strength fMRI as a promising technique for revealing the functional architecture of the PAG. The techniques developed here also may be extended to investigate the functional roles of other brainstem nuclei.The periaqueductal gray (PAG) is a small tube-shaped region of the midbrain involved in survival-related responses and homeostatic regulation important for affective responses and stress (1–3). Subregions of the PAG underlie distinct, coordinated behavioral responses to threat. For example, stimulation in the lateral/dorsolateral portion produces active-coping responses (e.g., “fight” or “flight”) that involve increasing heart rate and arterial pressure, redistribution of the blood to the limbs, and a fast-acting, nonopioid-mediated analgesia. Stimulation in the ventrolateral portion produces passive-coping responses (i.e., disengagement, freezing) that involve reduced heart rate, decreased reactivity to the environment, and a longer-term, opioid-mediated analgesic response. These responses occur even when inputs to PAG from the cortex are severed (1, 4).The considerable animal literature on the critical role of the PAG in coordinating emotional responses has led to a surge of interest in studying the PAG in humans. The PAG plays a central role in neurobiologically inspired theories of human emotion (5), the neural circuitry underlying depression and anxiety (3, 6), autonomic regulation (7), and pain (8–11). To examine PAG function in humans, researchers have relied primarily on functional MRI (fMRI). To date, dozens of human neuroimaging studies have observed increased activation in the vicinity of the PAG during administration of painful and aversive stimuli (8, 12–16) and across a variety of emotional states (17).Unfortunately however, standard fMRI is fundamentally limited in its resolution, making it uncertain which fMRI results lie in the PAG and which lie in other nearby nuclei. The overarching issue is size and shape. The PAG is small and is shaped like a hollow cylinder with an external diameter of ∼6 mm, a height of ∼10 mm, and an internal diameter of ∼2–3 mm. The cerebral aqueduct, which runs through the middle, can prevent detecting activations within the PAG [type II errors (18)] and also can create artificial activations that appear to be in the PAG but are not [type I errors (19)], making the PAG particularly challenging to image among the subcortical nuclei. Standard smoothing and normalization procedures, even with high-resolution scanning, incorporate signal from the aqueduct (Fig. 1). This signal can be overpowering. The variability of signal in the aqueduct can be an order of magnitude greater than that of the surrounding PAG. (Figs. S1 and S2).Open in a separate windowFig. 1.The PAG imaged at high resolution. The transaxial slice on the left shows the PAG from a functional scan at ultra-high field strength (7-T) and high resolution (0.75 mm isotropic). Scanning the PAG at lower resolutions prevents clear separation of the PAG from the aqueduct and surrounds. (A) The mean functional image for a single run at the 0.75-mm isotropic resolution used in this study shows the PAG crisply as indicated by the red arrow. (B) Downsampling the image to a resolution of 1.5 mm isotropic begins to blur the boundary between the PAG and its surrounds because of partial-volume effects. (C) Further downsampling the image to a resolution of 3 mm isotropic eliminates the ability to distinguish PAG from the aqueduct with any degree of confidence. (D–F) Smoothing with a standard 4-mm kernel further increases the partial-volume effects that blend signal from PAG with the aqueduct and surrounds, as shown for 0.75 mm isotropic (D), 1.5 mm isotropic (E), and 3 mm isotropic (F) resolutions. Most neuroimaging studies use a 3-mm isotropic resolution with a 4-mm or higher smoothing kernel. We addressed these issues by separating PAG voxels from the aqueduct before additional image processing (i.e., using the image shown in A) so that only voxels within the PAG are incorporated into later stages of analysis. The top of the transaxial image corresponds to the anterior portion of the head; the bottom corresponds to the posterior portion of the head.Standard neuroimaging techniques also are fundamentally limited in capturing the remarkable functional organization that is internal to the PAG. In addition to being differentiated into columns (1, 4), the PAG also is organized rostrocaudally. In caudal PAG, neurons that contain endogenous opioids and neuropeptides involved in nonopioid analgesia are concentrated in the ventrolateral columns, whereas in rostral PAG this concentration is greater in the lateral and dorsomedial columns (20, 21). Mirroring this distribution, administration of anxiogenic drugs produces greater neural activity in caudal, ventrolateral PAG and rostral, dorsolateral PAG [as measured from c-Fos expression (22)]. Connections from the central nucleus of the amygdala terminate more extensively in lateral and dorsal rostral PAG and ventrolateral caudal PAG (23). The ability to resolve which of these circuits is involved in a given behavior is crucial for understanding the implications of PAG activity in a given situation and for mapping homologies across species.Resolving activity to subregions of the PAG requires greater precision than provided by any study to date. Indeed, the overwhelming majority of previous studies have used 1.5- or 3-T MRI systems that typically cannot exceed an isotropic resolution of 1.5–2 mm without incurring significant losses in the signal-to-noise ratio (SNR) and significant increases in image distortion. This resolution already introduces substantial partial-volume effects (Fig. 1) that merge signal from the PAG with the exceedingly variable signal in the aqueduct (Fig. S2). Standard intersubject normalization and smoothing procedures that generally increase SNR but diminish localization accuracy further aggravate these issues. Ultimately, standard fMRI techniques—even those using high-resolution scanning—are incapable of capturing the functional organization of the PAG in humans.To overcome these obstacles, we used ultra-high field (7-T) fMRI combined with 32-channel parallel imaging (24), which can boost sensitivity by as much as an order of magnitude compared with low-field strength magnets (1.5–3 T) and volume coils (25). Higher-field strength magnets also provide greater sensitivity to the susceptibility effects that underlie the blood-oxygenation level–dependent (BOLD) signal measured in fMRI (26) and greater sensitivity to microvasculature (27, 28). At a nominal voxel resolution of 0.75 mm isotropic (Fig. 1A), we isolated the PAG directly from the functional scans and separated activity in the PAG from activity in the aqueduct (Fig. S1).We examined activity in the PAG while participants viewed aversive images (29), which included images of burn victims, gory injuries, and other content related to threat, harm, and loss, or while they viewed neutral images. Although prior studies have demonstrated activity in the vicinity of the PAG during the viewing of aversive images (15), we first tested whether the PAG definitively showed greater activity during to these images when signal was separated from the aqueduct and surrounding brainstem nuclei. Next, we used two approaches to test whether activity was localized to subregions of the PAG. In one approach, we segmented the PAG along dorsal/ventral and rostral/caudal divisions and examined whether activity was localized within specific segments. In a second but related approach, we performed analyses on a voxel-by-voxel basis to test whether high-field strength imaging can map the functional architecture of PAG at the voxel level. Given that discrete voxels identified in this approach necessarily would reside within just a few millimeters of each other, we performed a factor analysis to discover whether they carried similar or unique information during emotional responses.     

脑胶质瘤干细胞的体外培养与生物学特性观察

目的体外培养人脑胶质瘤干细胞并观察其生物学特性。方法应用无血清培养技术,从手术中获取的人脑胶质瘤组织培养得到肿瘤干细胞,诱导其分化后与原肿瘤组织细胞进行比较。应用细胞免疫荧光技术鉴定肿瘤干细胞表面标志物。结果分别在间变性星形细胞瘤和胶质母细胞瘤中培养得到悬浮生长的肿瘤干细胞球,其能在体外自我更新、增殖,形成新的克隆性细胞球,保持连续稳定的传代,能表达神经干细胞表面标志物CD 133。在含血清培养基中能够分化为与原肿瘤组织相似的贴壁生长的细胞。结论人脑胶质瘤中存在一定量的肿瘤干细胞,能够自我更新增殖、诱导分化、表达干细胞标志物CD 133。为探讨脑胶质瘤的发病机制奠定了基础。     

非典型脑干梗死190例临床特征分析

脑干梗死是指椎基底动脉及其分支血管狭窄或闭塞引起中脑、桥脑或延髓缺血、坏死、软化,出现相应的神经系统症状,临床上较为常见,占脑梗死的20%～30%。经典脑干梗死常有眩晕、复视、构音     

骨髓间充质干细胞对大脑中动脉缺血再灌注大鼠治疗作用的研究

目的探讨骨髓间充质干细胞(MSC)对大脑中动脉缺血再灌注大鼠的治疗作用。方法雄性SD大鼠30只,以线栓法制成缺血再灌注模型,成功大鼠23只,随机分为3组,早期MSC治疗组(8只)、晚期MSC治疗组(8只)和对照组(7只)。术后每3天对各组大鼠进行神经功能评估,28天后处死大鼠,荧光倒置显微镜下观察MSC进入大鼠体内后神经元特异性烯醇化酶的表达。结果早期MSC治疗组大鼠神经功能恢复较对照组明显提前,MSC治疗14天后与对照组比较无显著差异。MSC治疗28天后梗死灶边缘可见少量神经元特异性烯醇化酶和5-溴脱氧尿嘧啶双染细胞。晚期MSC治疗组大鼠神经功能恢复与对照组比较无显著差异。结论大鼠大脑中动脉缺血再灌注后早期静脉注射MSC治疗可明显加速神经功能的恢复。     

Acute Cerebral Hemorrhage Changes the Nocturnal Surge of Plasma Melatonin in Humans

The diurnal rhythm of plasma melatonin was studied in 46 Chinese patients with acute cerebral hemorrhage. The state of consciousness of each patient was assessed clinically. The individual sites of lesion were determined by computerized tomography scanning. One to five days after stroke, blood samples were collected by venipuncture at 1000 and 1400 h in the daytime and 0200 and 0400 h at night. Plasma melatonin was extracted by dichloromethane and determined by radioimmunoassay. It was found that patients with lesions in the brain stem or in the third and lateral ventricles had melatonin levels significantly different from the other subjects in that these values were lower and lacking a nocturnal rise. These results are consistent with the presumptive retina-pineal pathway proposed in humans. Dramatic blunting or obliteration of the nocturnal melatonin surge in the blood was also observed in some patients with lesions in the frontal lobe, fronto-parietal lobe, parieto-temporal lobe, and basal ganglia. These brain regions are not involved in the retina-pineal pathway described in rodents or humans. Thus, our results suggest that brain regions other than the presumptive retina-pineal neural pathway may play an important role in the generation and/or regulation of the diurnal production and/or secretion of pineal melatonin in humans. However, a global functional disturbance caused by cerebral hemorrhage cannot be ruled out in some cases. It should be noted that many of the lesions leading to a change in the nocturnal rise of plasma melatonin were unilateral lesions. The significance of this finding is presently unknown. In addition, patients without a nocturnal rise of plasma melatonin were mostly comatose. They had lesions in the basal ganglion, fronto-parietal lobe, brain stem, and lateral and third ventricles. The latter findings suggest that in the brain, certain regions responsible for the state of consciousness of the individual may also be important to the dirunal rhythm of pineal melatonin secretion.     

Intractable vomiting due to a brainstem lesion in the absence of neurological signs or raised intracranial pressure

^a St Mark's Hospital, Northwick Park, Watford Road, Middlesex HA1 3UJ, UK, ^b Stobhill General Hospital, Glasgow     

PYY Regulates Pancreatic Exocrine Secretion Through Multiple Receptors in the Awake Rat

Peptide YY (PYY) is one of several regulatory peptides reported to modulate pancreatic secretion. PYY circulates in two forms, PYY_1–36 and PYY_3–36, and binds to multiple receptor subtypes. We sought to determine if PYY_1–36 or PYY_3–36 regulates neurally mediated pancreatic secretion through the Y1, Y2, and/or Y5 receptor subtypes. Experiments were conducted in awake, surgically recovered rats. In order to determine the effects of the PYYs on basal pancreatic secretion, either PYY_1–36, [Pro³⁴] PYY_1–36 (a Y1/Y5 agonist), or PYY_3–36 (a Y2/Y5 agonist) were infused for 40 min at doses of 0, 12.5, 25, or 50 pmol/kg/hr while measuring pancreatic juice volume and protein. PYY_1–36 increased pancreatic protein secretion at 25 and 50 pmol/kg/hr (P < 0.05) in a dose-dependent manner (P < 0.001, R ² = 0.990). The Y2/Y5 receptor agonist PYY_3–36 significantly inhibited pancreatic juice volume and protein at 12.5 and 25 pmol/kg/hr, but stimulated protein secretion at higher doses (P < 0.001, R ² = 0.995). The Y1/Y5 agonist, [Pro³⁴] PYY_1–36, had no significant effect on basal pancreatic exocrine secretion. Therefore, PYY_1–36, PYY_3–36 and [Pro³⁴] PYY_1–36 produced different, dose-dependent changes on basal pancreatic exocrine secretion. Inhibition of pancreatic secretion by circulating PYY_1–36 and PYY_3–36 are primarily mediated by the Y2 receptor. Since [Pro³⁴] PYY_1–36 did not change pancreatic secretion, it can be concluded that circulating PYY_1–36 or PYY_3–36 does not modulate pancreatic secretion through the Y1 or Y5 receptors. Since the stimulatory effects of PYY_1–36 on pancreatic secretion could not be explained by the actions of PYY_3–36 or [Pro³⁴] PYY_1–36 on Y1 or Y2 receptors, and since PYY_1–36 fails to bind to Y3 or Y4 receptors, we also conclude that PYY_1–36 may stimulate pancreatic secretion in a dose-dependent mechanism through a PYY receptor subtype different from Y1, Y2, Y3, Y4 or Y5.