IMPACT OF DIFFERENT INJURY SITES IN S-D RATS’ OCULOMOTOR NERVES

目的：研究不同部位损伤对Sprague-Dawley(以下简称S-D)大鼠动眼神经功能修复的影响及可能机制。方法：经幕下和眶上裂切断和修复动眼神经，术后通过前庭眼反射评估眼外肌在垂直、水平方向的恢复程度，经右侧上直肌注射HRP逆行追踪中脑动眼神经核团内神经元分布，动眼神经组织学、解剖学研究。结果：经眶上裂干预动眼神经的实验组大鼠新生神经纤维对眼外肌支配的特异性较高，其眼外肌功能恢复程度明显优于经幕下干预动眼神经的实验组大鼠。结论：动眼神经损伤部位距离眼外肌越近，最终的神经功能恢复水平就越好，其机理可能与再生神经纤维通过损伤部位时的迷行程度有关。     

成年S-D大鼠动眼神经核的显微解剖学研究

目的研究成年S-D大鼠动眼神经核的显微解剖学特征。方法成年S-D大鼠30只,经右眼球结膜入路行单眼外肌肌鞘内注射辣根过氧化物酶(HRP),逆行标记中脑动眼神经运动神经元,48小时后取中脑组织切片还原显色(TMB法),并在光镜和电镜下观察。结果动眼神经核的运动神经元直径平均为(19.20±1.15)μm,单侧核内的运动神经元总数为(1467±57.55)个,其中支配内直肌(424±41.39)个,支配上直肌(338±19.90)个,支配下直肌(238±20.01)个,支配下斜肌(276±16.72)个,支配提上睑肌(191±8.51)个。各组神经元有相对固定的解剖位置,其中下斜肌神经元位于核的背侧中间部,下直肌神经元位于核的背内侧,内直肌神经元位于核的腹内侧,上直肌神经元位于核的腹外侧,提上睑肌神经元位于核的外侧中部。结论动眼神经核内的运动神经元按功能不同集中分布(形成各个亚核),各亚核之间存在不同程度重叠,单一眼外肌均有来自双侧的运动神经元支配。     

动眼神经功能修复实验研究

目的研究成年SD大鼠动眼神经损伤后功能修复的机制。方法成年SD大鼠45只,随机分为4组:第一组:正常对照组(10只),动眼神经不损伤,其余35只大鼠均在海绵窦内切断右侧动眼神经主干,第二组为损伤对照组(5只)不予缝合,第三组和第四组立即用11-0无创缝线行端端对位缝合,定期观察动眼神经功能并进行神经组织学和解剖学研究。结果动眼神经包含粗细两种纤维,直径呈双峰分布。动眼神经核内运动神经元按功能不同集中分布(形成亚核)。动眼神经损伤后,核内的神经元数量减少(仅为损伤前的1/3)、亚核分布特征消失,再生轴突的数量明显增加,超过损伤前的水平,但以细纤维为主,双峰分布特征消失。瞳孔括约肌的功能恢复速度与最终的恢复水平明显优于眼外肌。结论动眼神经损伤后神经元的数量减少和非特异性增生及其再生轴突在效应器上的迷行分布影响了动眼神经的功能恢复。     

损毁丘脑底核阻止6-OHDA对大鼠多巴胺能神经元的损伤作用

目的 观察不同时期毁损丘脑底核对大鼠中脑黑质多巴胺神经元6－羟基多巴胺（6－OHDA）损伤的保护作用。方法 将60只Wistar大鼠随机分为6组,每组10只。对照组采用6－OHDA立体定向注入大鼠右侧前脑内侧束（MFB）和中脑被盖腹侧区（VTA）,制成偏侧帕金森病（PD）模型。实验组分为第Ⅰ、Ⅱ、Ⅲ、Ⅳ和Ⅴ组,分别于6－OHDA注射前7d、注射后1h、2h、3d、7d 5个不同时间点,局部注射海藻氨酸（KA）破坏STN。4周后处死大鼠,采用免疫组化染色方法,定量测量各组大鼠黑质致密区（SNc）区TH免疫阳性反应神经元数目。实验数据采用方差分析和t检验统计学处理。结果 第Ⅰ、Ⅱ、Ⅲ、Ⅳ、Ⅴ实验组以及对照组的注射侧TH神经元存活数目分别为71．46±6．84、57．07±5．54、51．09±4．85、12．68±2．67、4．15±1．60和3．40±1．54个每张切片,为对侧的96．7％、72．9％、69．8％、17．2％、5．6％及4．4％。各实验组注射侧TH神经元均比对照组同侧数目多（P ＜ 0．05）,但Ⅴ组无显著性差异（P ＞0．05）。各实验组之间比较,均有明显差异,其中以Ⅰ组TH神经元存活的数量最多（P ＜0．01）。结论 早期毁损丘脑底核（STN）可减轻6－OHDA对黑质致密部多巴胺（DA）能神经元的损伤和细胞数量的缺失;晚期毁损对其无明显     

白蛋白减轻大鼠液压颅脑损伤伤后脑水肿和神经功能障碍的剂量效应

目的 探讨白蛋白在治疗大鼠液压颅脑损伤后神经功能恢复和脑组织含水量的剂量效应。方法 将96只SD大鼠随机分为4组,液压打击致伤。伤后30min经尾静脉注射2g/kg(n=24,Ⅰ组)、1.2g/kg(n=24,Ⅱ组)、0.8g/kg(n=24,Ⅲ组)、0.4g/kg(n=24,Ⅳ组)20％人血白蛋白。每组取12只伤前、伤后当日、伤后连续7d进行行走、平衡和记忆实验,记录神经功能恢复情况。另每组12只伤后48h取双侧大脑半球测湿重、干重,计算脑组织含水量。结果 实验Ⅰ组动物的行走实验、平衡实验、记忆均优于其他组(P<0.01)。实验Ⅰ组的脑组织含水量为78.09±0.42％,Ⅱ组为79.01～0.66％,Ⅲ组为78.89±0.45％,Ⅳ组为79.03±0.35％,Ⅰ组脑水肿程度明显低于其它组(P<0.01)。结论 伤后早期使用大剂量白蛋白对大鼠液压颅脑损伤有明显促进神经功能恢复和减轻脑水肿的作用。     

损毁丘脑底核阻止6—OHDA对大鼠多巴胺能神经元的损？…

目的观察不同时期毁损丘脑底核对大鼠中脑黑质多巴胺神经元６－羟基多巴胺（６－ＯＨＤＡ）损伤的保护作用。方法将６０只Ｗｉｓｔａｒ大鼠随机分为６组,每组１０只。对照组采用６－０ＨＤＡ立体定向注入大鼠右侧前脑内侧束（ＭＦＢ）和中脑被盖腹侧区（ＶＴＡ）,制成偏侧帕金森病（ＰＤ）模型。实验组分为第Ⅰ、Ⅱ、Ⅲ、Ⅳ和Ⅴ组,分别于６－ＯＨＤＡ注射前７ｄ、注射后１ｈ、２ｈ、３ｄ、７ｄ５个不同时间点,局部注射海藻氨酸（     

人脐带间充质干细胞移植对大鼠脊髓损伤神经功能恢复的评价

目的 观察人脐带间充质干细胞（human umbilical cordmesenchymal stem cell，hUCMSC）移植对大鼠脊髓损伤神经功能恢复的影响。方法 SD大鼠70只，随机分为3组：脊髓半切＋hUCMSC组（n=30）、脊髓半切＋PBS组（n=30）和假手术组（n=10）。脊髓半切＋hUCMSC组和PBS组又分为头侧注射、尾侧注射和头尾两侧注射三个亚组。移植后1、7、14、21、28d观察大鼠神经功能恢复情况，应用免疫组化检测移植到脊髓的hUCMSC胶质纤维酸性蛋白（GFAP）和神经元特异性烯醇化酶（NSE）表达情况。结果 大鼠脊髓半切损害后，hUCMSC组动物较PBS组有明显的神经功能恢复。植入后28d在宿主脊髓中存活的hUCMSC细胞MABl281（mouse antiuman nuclei monoclonal antibody）染色阳性，免疫组化双标染色显示MABl28l阳性细胞亦分别有NSE或GFAP表达并向损伤部位迁移，hUCMSC来源的GFAP阳性细胞可见明显的树突生长。结论 hUCMSC移植到宿主损伤脊髓后可以存活、向损伤部位迁移，并向神经元样和星形胶质细胞分化，且可促进大鼠脊髓损伤后神经功能恢复。hUCMSC作为一种来源广泛的干细胞用于治疗脊髓损伤可能具有重要的价值。     

急性创伤昏迷大鼠中脑calpain Ⅱ、Nach6的表达

目的通过随机分组研究急性创伤昏迷大鼠中脑钙蛋白酶Ⅱ（CalpainⅡ）及电压门控钠通道亚型（Nach6）的早期表达变化。方法雄性sD大鼠12只，随机分为两组：假手术对照组（n=6）；急性创伤昏迷组（n=6）。建立急性创伤昏迷大鼠模型，1h后通过实时定量PCR法检测中脑钙蛋白酶Ⅱ及电压门控钠通道亚型（Nach6）变化。结果逆转录酶-多聚酶链反应（RT-PCR）法结果显示钙蛋白酶Ⅱ在创伤昏迷组的中脑表达相对含量增加（P〈0．01），电压门控钠通道亚型（Nach6）在创伤昏迷组的中脑组织表达相对含量增加（P〈0．05）。结论急性创伤昏迷早期钙蛋白酶Ⅱ激活、钠离子内流导致中脑神经细胞及胶质细胞损伤可能为急性创伤昏迷早期分子生物学机制之一。     

FOREL H野神经元与垂直动眼运动神经元的兴奋性联系

本实验采用电生理学方法，研究了猫中·间脑结合部Ｆｏｒｅｌ＇ｓｆｉｅｌｄＨ（ＦＦＨ）神经元与垂直动眼运动神经元的兴奋性联系形式。在下直肌动眼运动神经元（ＩＲＯＭＮ）池中给予电刺激可使ＦＦＨ神经元产生逆行兴奋。在４５个被同侧ＩＲＯＭＮ池刺激逆行激活的ＦＦＨ神经元中，８个亦可被对侧的ＩＲＯＭＮ池刺激逆行激活。另一方面，电刺激一侧ＦＦＨ内侧部，在双侧各垂直ＯＭＮ池中均诱发了兴奋性单突触电场电位；在同侧诱发的电场电位的振幅明显大于对侧，并旦同侧ＦＦＨ今诱发此电场电位的有效区域明显大于对侧。上述结果表明，中·间脑ＦＦＨ神经元与垂直动眼运动神经元的兴奋性联系为双侧性，但同侧联系较为优势。     

侧脑室微量注射左旋多巴治疗大鼠帕金森病

目的观察经侧脑室注射左旋多巴对帕金森病（PD）大鼠的影响。方法应用“羟基多巴胺立体定向脑内注射制备偏侧损毁的PD大鼠模型，并用阿扑吗啡（APO）皮下注射诱发大鼠向健侧旋转。将24只PD大鼠随机分为4组（n=6），经侧脑室注入生理盐水组为对照组，余3组分别经侧脑室注射浓度为0．1μg／μl、1μg／μl和5μg／μl的左旋多巴1μl，4μl／d，连续1周；观察在注射后不同时间大鼠旋转行为以及中脑黑质多巴胺能神经元数量的变化。结果经侧脑室注射1μg/μl和5μg/μl的左旋多巴后。与对照组相比，PD大鼠向健侧的旋转圈数明显减少（P〈0．01），左旋多巴效果在2h左右达到高峰，且中脑黑质多巴胺能神经元的数量也明显增多（P〈0．01）。结论经侧脑室注射适当剂量的左旋多巴可有效地改善PD大鼠的旋转行为，并增加中脑黑质多巴胺能神经元数量。     

Regenerating nerve fiber innervation of extraocular muscles and motor functional changes following oculomotor nerve injuries at different sites

In the present study, the oculomotor nerves were sectioned at the proximal (subtentorial) and distal (superior orbital fissure) ends and repaired. After 24 weeks, vestibulo-ocular reflex evaluation confirmed that the regenerating nerve fibers following oculomotor nerve injury in the superior orbital fissure had a high level of specificity for innervating extraocular muscles. The level of functional recovery of extraocular muscles in rats in the superior orbital fissure injury group was remarkably superior o...     

Peripheral and central oculomotor organization in the goldfish, Carassius auratus

Peripheral and central oculomotor organization was studied in the goldfish. The sizes of the extraocular muscles were quantified by counting the fibers contained in a given muscle and by area measurements of the cross-sectional surfaces. All the muscles were of approximately similar size. Kinematics were determined by electrical stimulation of a given muscle. The macroscopic appearance and kinematics of the muscles had the characteristics of other lateral-eyed animals (e.g., rabbit). Locations of extraocular motor neurons were found by retrograde transport of horseradish peroxidase (HRP) following injections into individual extraocular muscles. The eye muscles were innervated by four ipsilateral (lateral rectus, medial rectus, inferior oblique, inferior rectus) and two contralateral (superior rectus, superior oblique) motor neuron pools. The oculomotor nucleus was found in the midbrain, at the level of the caudal zone of the inferior lobe of the hypothalamus. Inferior rectus motor neurons were located rostrally in the oculomotor nucleus, whereas medial rectus, superior rectus, and inferior oblique motor neurons were intermingled in its more caudal portions. All labelled cells were located dorsally and medially to the medial longitudinal fasciculus (MLF) in close proximity to either the floor of the ventricle or the midline region. Occasionally, motor neurons were interspersed within the fiber bundles of the MLF or the exiting fibers of the oculomotor nerve. The trochlear nucleus, containing superior oblique motor neurons, was found in the immediate lateral and caudal neighborhood of the oculomotor nucleus, where its rostral border overlapped with the caudal border of the latter. The abducens nucleus, containing lateral rectus motor neurons, was located in the posterior brainstem in the neighborhood of the vestibular nuclear complex. This nucleus was divided into a rostral and a caudal portion. The axons of ipsilaterally projecting motor neurons headed toward their respective nerve roots via the shortest possible route, as did the axons of superior rectus motor neurons, which crossed the midline without detour to enter the contralateral oculomotor nerve. In contrast, trochlear motor neuron axons arched around the dorsal aspect of the ventricle through the cerebellar commissure to reach the contralateral trochlear nerve. The morphology of individual motor neurons was visualized by intrasomatic injection of HRP. Cell somata had oblong shapes, and their large dendrites were oriented laterally and ventrally. The axons did not collateralize within the midbrain region or the oculomotor nerve as far as they could be traced.(ABSTRACT TRUNCATED AT 400 WORDS)     

Crossed innervation of the superior rectus.

We studied two patients which showed a paralysis of the oculomotor nerve on one side and isolated paralysis of the superior rectus on the other side. On the side of oculomotor nerve paralysis, midbrain infarct extending from the paramedian tegmentum to crus cerebri was demonstrated in one case who showed no recovery, and a small lacuna in midbrain tegmentum in another one who showed complete recovery. On the side of isolated paralysis of the superior rectus, no lesion was demonstrated by CT and MRI, and no clinical signs of the involvement of fiber tracts or nuclei were evident in both cases. A unilateral lesion of oculomotor nerve nucleus caused a paralysis of the contralateral superior rectus.     

A case of partial fascicular oculomotor paresis caused by midbrain infarction]

We report a 74-year-old man with an ischemic lesion in the ventral midbrain. He presented with contralateral ptosis and marked upward gaze paresis of the right eye. Neurological examination revealed partial oculomotor nerve palsy caused by impairment of the right levator palpebrae, superior rectus and inferior oblique muscles. This finding is highly suggestive of a possible lesion in the midbrain affecting the oculomotor fascicular fibers. Magnetic resonance images showed an ischemic lesion in the paramedian area of the right midbrain tegmentum. The coronal view of T 2-weighted imaging clearly demonstrated to be the site of lesions below the red nucleus. It seemed to be coincidental with the impaired site of involving the caudal part of oculomotor fascicular fibers emerging from the nucleus. This report is considered to be a typical case of partial fascicular oculomotor paresis based on impairment of the caudal part of oculomotor fascicles for the levator palpebrae, superior rectus, and inferior oblique muscles. This is a valuable case to be documented in which neurological site of lesions are consistent with those found in radiological study.     

Isolated crossed superior rectus palsy in a midbrain infarction]

A 61-year-old man suddenly heard tinnitus and diplopia at night during watchinng television. A few days later he visited at our hospital. Neurologically he exibited marked isolated right superior rectus palsy which was also indicated by the Hess test. No other neurological abnormalities were found such as other ocular muscle paresis, cranial nerve palsies, hemiparesis, sensory impairement or cerebellar ataxia. MRI showed a left medial thalamic infarction extending to a rostral part of the midbrain anterolateral to the cerebral aqueduct at the superior colliculi level. Unilateral superior rectus palsy can rarely be caused by a contralateral midbrain infarction, because fibers from the subnucleus subserving the superior rectus decussate within the oculomoter nerve complex. In this case the crossing fibers toward the contralateral superior rectus may have been selectively involved by a tinny lesion in the area of the oculomotor nucleus. The patient had a slightly narrowed right palpebral fissure. It is indicated that crossing fibers toward the contralateral levator muscle of the eyelid may be also involved. The patient's diplopia completely resolved two months later after the onset.     

Isolated superior rectus palsy due to contralateral midbrain infarction

BACKGROUND: Isolated superior rectus palsy due to a contralateral midbrain lesion has not been reported. CASE DESCRIPTION: A 71-year-old woman suddenly developed diplopia. Examination showed that she had isolated superior rectus paresis. Magnetic resonance imaging showed a tiny infarct at the area of the oculomotor nucleus on the contralateral side. CONCLUSION: Isolated superior rectus palsy may be caused by a contralateral midbrain lesion that selectively involves crossing superior rectus nerve fibers.     

Location of motoneurons in the oculomotor nucleus and the course of their axons in the oculomotor nerve

Subdivisions of the oculomotor nucleus, and the course of axons in the brainstem and more peripherally in the oculomotor nerve of the cat, were studied by directly applying horseradish peroxidase solution to the transected nerve-branch stump in the orbit. The medial rectus subdivision consisted of two subgroups, and intermingling between subdivisions was found. About 20% of the motoneurons controlling the medial rectus muscle were scattered in the medial longitudinal fasciculus or a more ventrolateral area. A few motoneurons controlling the inferior rectus or inferior oblique muscle were also located in the medial longitudinal fasciculus. Axons to the superior branch that supplied the superior rectus and levator muscle coursed in the dorsolateral half of the oculomotor nerve. In contrast, those to the medial rectus, inferior rectus, and inferior oblique muscles were scattered diffusely in the oculomotor nerve.     

Bilateral ptosis and upper gaze palsy with pupil sparing caused by midbrain hemorrhage]

The arrangement within the midbrain oculomotor nerve complex and crossed innervation of the superior rectus muscle are not elucidated in humans. A 65-year-old woman visited our hospital complaining of difficulty opening her eyes. Neurological examination revealed bilateral ptosis and impaired supraduction. The pupils prompty constricted to light. Results of CT and MRI demonstrated that there was a hematoma located in the dorsal midbrain tegmentum that spared the rostral mid-brain. It was presumed that the nerves of the superior rectus and levator palpebrae lie in the midbrain tegmentum more dorsally and medially than the others. Furthermore, crossed innervation of the superior rectus muscle can explain that lesions located in the dorsal midbrain tegmentum cause more often impaired supraduction.     

Midbrain infarction presenting isolated inferior rectus nuclear palsy]

We presented a patient of isolated inferior rectus muscle palsy from midbrain lacunar infarction involving the oculomotor nucleus. The patient noticed sudden onset diplopia gazing to the right side, especially to the right-lower direction. He did not have any other symptom, and neurological examination revealed no other findings. Brain MRI documented the focal hyperintense lesion on T2-weighted images in the right-median midbrain ventral to the aqueduct at the level of the superior colliculus. This lesion involved the right oculomotor nucleus, especially the dorso-lateral subnucleus extend to the inferior rectus muscle. The oculomotor nuclear complex consists of one unpaired subnucleus and four paired subnuclei. Among them, the inferior rectus subnucleus lies dorso-laterally. So nucleus lesion may cause isolated weakness of one of muscles innervated by the oculomotor nerve. Among them the isolated inferior rectus muscle palsy can occur relatively.