电刺激诱发瞬目反射对脑桥梗死患者的预后价值

目的 探讨电刺激诱发瞬目反射(blink reflex,BR)对脑桥梗死患者的预后价值.方法 对43例脑桥梗死患者和37例健康对照组进行电刺激诱发BR的检测,采用欧洲脑卒中评分(The European stroke scale,ESS)和日常生活活动(activity of daily life,ADL)量表对每位患者在BR检查当日和4周末分别进行神经功能缺损程度评分.结果 脑桥梗死组病灶侧R1的潜伏期较对照组明显延长,病灶侧R1的潜伏期较健侧也显著延长(P＜0.001).脑桥梗死组BR各波的异常率以R1最高,占81.4%,而R2和R2′的异常率分别为23.3%和25.6%.R1的异常率显著高于R2和R2′(P＜0.001).双侧脑桥梗死(双侧均有病灶,每侧病灶直径均＞3mm),导致BR各波均未引出.一侧脑桥单个梗死灶,梗死灶直径＞3mm,主要引起R1潜伏期延长;一侧脑桥单个梗死灶,梗死灶直径0.5～3mm,BR各波潜伏期均正常.R1波未引出组神经功能缺损程度最重,ESS评分和ADL评分显著低于R1潜伏期延长组和R1潜伏期正常组(P＜0.001);R1潜伏期正常组预后最好,4周末其ESS评分和ADL评分均较1周内显著提高(P＜0.01和0.001);R1潜伏期延长组次之.结论 脑桥梗死患者的BR异常以R1潜伏期延长为特征.脑桥的病灶主要引起R1异常,进一步提示R1的反射中枢位于脑桥.BR的异常类型可大致反映脑桥梗死病灶的范围,BR的R1异常可作为脑桥梗死患者神经功能缺损程度和预后评价的电生理指标之一.     

Pontine supranuclear facial palsy

Two patients presented with a unilateral supranuclear facial palsy. Additional dysarthria was attributed to the pontine origin documented by magnetic resonance imaging on the contralateral side. The pontine disorder also was indicated by an isolated delay of the blink reflex R1 component or of the masseter reflex. We attribute the facial palsy to a lesion of a supranuclear fiber bundle supplying the facial nucleus. The location of the lesions favors these fibers taking a separate course from the main pyramidal tract at the mid- to upper pontine level.     

Topodiagnostic value of blink reflex R1 changes: a digital postprocessing MRI correlation study

The aim of the study was to investigate the relation of the blink reflex R1 arc to known anatomical brainstem structures. Acute vascular brainstem lesions as identified by magnetic resonance imaging (MRI) of patients with isolated R1 pathology were superimposed into a stereotactic anatomical atlas using a new method of digital postprocessing. Isolated acute brainstem lesions were documented by diffusion-weighted MRI in 12 of 24 patients with unilateral R1 pathology. The lesions were located in the ipsilateral mid- to lower pons. In three patients only, the lesion had partial contact with the principal sensory nucleus of the trigeminal nerve (PSN) on at least one level. In two patients, the lesion involved the medial longitudinal fasciculus. Most lesions were located medially and ventrally to the PSN on transverse slices. Our results underline the high localizing value of changes in the R1 component of the blink reflex in patients with ipsilateral pontine functional deficits. Although available physiological evidence suggests that the R1 component of the blink reflex traverses an oligosynaptic pathway, this MRI study does not support the view that synaptic transmission in the PSN subserves R1. The reflex arc probably descends more medially and ventrally on its course to the facial nucleus.     

Crossed linguo-buccal reflex in post-stroke patients

A pathological crossed orofacial reflex, called crossed linguo-buccal reflex in the present study, was observed in approximately 1/3 of post-stroke patients with central facial palsy. Stroking with pressure two or three times with a split wooden tongue-blade to the tongue or palate contralateral to the central facial palsy elicited a reflex movement consisting of retraction of the angle of mouth and medio-posterior withdrawal of the buccal mucosa on the paretic side. Seventy-seven patients with central hemifacial palsy caused by a unilateral cerebral lesion were examined clinically, electromyographically and by computed tomography (CT) and magnetic resonance imaging (MRI). In addition, three men with bilateral cerebral lesions and bilateral crossed linguo-buccal reflexes were electromyographically examined. Twenty-two patients with unilateral cerebral lesions had this reflex. It was found that this reflex was most frequently observed in patients with a capsulo-caudate lesion involving the head of the caudate nucleus, the anterior limb and genu of the internal capsule. The electromyogram of the reflex showed increased activity in the orbicularis oris, depressor anguli oris, risorius, zygomaticus major and buccinator muscles on the paretic side with a long latency (254-856 ms), and a prolonged after-discharge after the stimulation. Reciprocal inhibition was observed in patients with bilateral positive reflexes. These findings suggest that liberation of the polysynaptic brainstem reflex in the medulla oblongata and pons from the indirect corticobulbar inhibition may underlie the occurrence of the crossed linguo-buccal reflex in post-stroke patients.     

Diffusion-weighted magnetic resonance imaging (MRI) in acute brain stem infarction]

Diffusion-weighted magnetic resonance imaging (DWI) provides one of the earliest demonstrations of ischemic lesions. However, some lesions may be missed in the acute stage due to technical limitation of DWI. We therefore conducted the study to clarify the sensitivity of DWI to acute brain stem infarctions. Twenty-eight patients with the final diagnosis of brain stem infarction(midbrain 2, pons 9, medulla oblongata 17) who had been examined by DWI within 24 hours of onset were retrospectively analyzed for how sensitively the initial DWI demonstrated the final ischemic lesion. Only obvious(distinguishable with DWI alone without referring clinical symptoms and other informations) hyperintensity on DWI was regarded to show an ischemic lesion. Sixteen(57.1%) out of 28 patients had brain stem infarctions demonstrated by initial DWI. In the remaining 12 cases, no obvious ischemic lesion was evident on initial DWI. Subsequent MRI studies obtained 127 hours, on average after the onset showed infarction in the medulla oblongata in 11 cases and in the pons in one case. Negative findings of DWI in the acute stage does not exclude possibility of the brain stem infarction, in particulary medulla oblongata infarction.     

The orbicularis oculi response after hemispheral damage.

The corneal and blink reflexes were evaluated in 20 normal subjects and in 30 patients with motor deficits secondary to unilateral hemispheral lesions of vascular origin. In the normal population there were no differences between subjects below and subjects above 50 years of age. In the patients the reflex evoked by electrical stimulation of the cornea of the clinically affected side was depressed in 24 out of 30 cases. The depression mainly affected the afferent branch of the circuit, which triggers both homolateral and contralateral orbicularis oculi discharge (afferent abnormality). In three cases the depression was exerted concomitantly on the efferent branch (afferent and efferent abnormality) and only in one case was it limited to the efferent branch (efferent abnormality). The late R2 component of the blink reflex was depressed in 15 out of 30 patients. The early R1 component was slightly facilitated on the affected side. The changes of the corneal reflex and of the R2 component of blink reflex were similar, but the blink reflex had a greater safety factor. The patients with an abnormal corneal reflex had more extensive damage than had the patients with normal corneal response, as shown by computer tomography, but the site of the lesion was comparable in the two groups. Conduction through the brain stem circuits mediating the orbicularis oculi response is normally under pyramidal facilitatory influences while facial motoneurons are subjected to pyramidal inhibition. After pyramidal damage the transmission of impulses in the brain stem was slowed down, ultimately to a degree that abolished the reflex. Removal of pyramidal inhibition on facial motoneurons is probably the basis of the slight facilitation of the R1 component of the blink reflex.     

Blink reflex in patients with hemispheric cerebrovascular accident (CVA). Blink reflex in CVA

A blink reflex consists of an early unilateral component, R1, and a late bilateral component, R2. During an acute phase of hemispheric cerebrovascular accident, R1 and R2 were abnormal in 30 and 50 of 66 patients, respectively. Paired stimuli usually corrected R1 but not R2, which was profoundly suppressed. The discrepancy between polysynaptic R2 and oligosynaptic R1 indicates a greater disfacilitation at the level of interneurons than at the motoneuron, which serves as the final common path. Abnormality of R2 occurred bilaterally with stimulation on the affected side of face and contralaterally after stimulation on the normal side in 31 patients. This finding suggests a diffuse loss of internuncial excitability, contralateral to the hemispheric lesion. Changes of R2 implicated the brainstem pathways forming the afferent and efferent arc of the reflex in 7 and 8 patients, respectively. The remaining 4 comatose patients had no R2 irrespective of stimulus sites. Clinical localization of the hemispheric lesion showed no consistent correlation with the type of blink reflex abnormalities. The CT scans revealed widely scattered changes in 29 patients with abnormal blink reflex but with a tendency to overlap in the inferior Rolandic area. This contrasted with conspicuous sparing of the inferior post-central region in 10 patients with normal blink reflex. These findings suggest the presence of crossed facilitation to this reflex from wide areas of the cortex but most prominently from the sensory representation of the face.     

Electrophysiological brainstem investigations in obstructive sleep apnoea syndrome

Phasic inspiratory genioglossus activity prevents pharyngeal airway collapse in healthy subjects during sleep and is diminished or absent in obstructive sleep apnoea syndrome (OSAS), thus leading to pharyngeal obstruction. Case reports of OSAS after pontomedullary lesions indicate that impaired inspiratory genioglossal activity may result from brainstem lesions. We therefore investigated brainstem functions in 18 awake patients with OSAS using brainstem auditory evoked potentials, blink reflex, masseter reflex, masseter inhibitory reflex (in 11 of 18 patients), magnetic evoked potentials of the tongue and electrooculography with vestibular testing. Fifteen of 18 patients showed no electrophysiological abnormalities. One patient had a left pontine and two patients a bilateral pontomesencephalic lesion, although a causal connection with OSAS was not conclusively confirmed. Our results do not support the assumption of a relevant structural brainstem lesion in OSAS patients with normal neurological findings.     

Pontine lesions mimicking acute peripheral vestibulopathy

OBJECTIVES: Clinical signs of acute peripheral vestibulopathy (APV) were repeatedly reported with pontine lesions. The clinical relevance of such a mechanism is not known, as most studies were biased by patients with additional clinical signs ofbrainstem dysfunction. METHODS: Masseter reflex (MassR), blink reflex (BlinkR), brainstem auditory evoked potentials (BAEPs), and DC electro-oculography (EOG) were tested in 232 consecutive patients with clinical signs of unilateral APV. RESULTS: Forty five of the 232 patients (19.4%) had at least one electrophysiological abnormality suggesting pontine dysfunction mainly due to possible vertebrobasilar ischaemia (22 patients) and multiple sclerosis (eight patients). MassR abnormalities were seen in 24 patients, and EOG abnormalities of saccades and following eye movements occurred in 22 patients. Three patients had BlinkR-R1 abnormalities, and one had delayed BAEP waves IV and V. Clinical improvement was almost always (32 of 34 re-examined patients) associated with improvement or normalisation of at least one electrophysiological abnormality. Brain MRI was done in 25 of the 44 patients and confirmed pontine lesions in six (two infarcts, three inflammations, one tumour). CONCLUSIONS: Pontine dysfunction was suggested in 45 of 232 consecutive patients with clinical signs of APV on the basis of abnormal electrophysiological findings, and was mainly attributed to brainstem ischaemia and multiple sclerosis. The frequency of pontine lesions mimicking APV is underestimated if based on MRI established lesions only.     

Feeding function, blink reflex and MRI in the severely handicapped

Blink reflexes were studied in 41 patients with severe handicaps, and were correlated with feeding problems and other lower brainstem symptoms such as drooling, an absent gag reflex and stridor. Ventrodorsal diameters of the pons and medulla oblongata on sagittal MRI were also studied in 29 of the cases. The patients were divided into three groups: tube feeding (25 cases), oral feeding (13 cases) and mixed feeding (3 cases). In the tube feeding group, all but three cases showed a prolonged or absent R1 component, and all cases showed prolonged or absent R2 and R2' components. These abnormalities were significantly more frequent in the tube than in the oral feeding group. The patients with drooling, stridor or an absent gag reflex more frequently showed prolonged or absent components than the patients without these symptoms. The brainstem size on MRI was not different between the tube and oral feeding group. These results suggest that the blink reflex, particularly its late components, is a useful indicator for evaluating feeding function and other lower brainstem functions.     

Blink reflex R2 changes and localisation of lesions in the lower brainstem (Wallenberg's syndrome): an electrophysiological and MRI study

OBJECTIVES: Pathways of late blink reflexes are detected by high resolution MRI. Electronically matched stroke lesions superimposed to an anatomical atlas show the suspected course. METHODS: Fifteen patients with infarction of the lower brainstem, MRI lesions and electrically elicited blink reflexes were examined. The involved structures in patients with R2 and R2c blink reflex changes were identified by biplane high resolution MRI with individual slices matched to an anatomical atlas at 10 different levels using digital postprocessing methods. RESULTS: The blink reflexes were normal in five of 15 patients (33%) and showed loss or delay of R2 and R2c to stimulation ipsilaterally to lesion (R2-i and R2c-i) in eight (53%). Loss or delay of R2-i/R2c-i was seen in lesions covering the entire trigeminal spinal tract and nucleus (TSTN) at at least one level. These infarctions were located more dorsally within the medulla. Patients with normal blink reflexes showed lesions sparing or involving the TSTN only partially. They more often had incomplete Wallenberg's syndromes and MRI lesions were located more ventrally. CONCLUSIONS: Using digital postprocessing MRI methods it was possible to identify central pathways of late blink reflex in patients with Wallenberg's syndrome. This method is suggested as a new approach to identify incompletely understood functional structures of the brainstem.     

Midbrain vs. pontine medial longitudinal fasciculus lesions: the utilization of masseter and blink reflexes

Masseter (MR) and blink reflexes (BL) were investigated in 51 patients with internuclear ophthalmoplegia (INO) due to multiple sclerosis (28) and lacunar infarction (23). The MR was abnormal in 20 of 23 cases with bilateral INO and in 21 of 28 with unilateral INO. The R1 component of the BL (BL-R1) was abnormal in 7 of 23 patients with bilateral INO and 10 of 28 with unilateral INO. Combined MR and BL-R1 changes occurred in 8 of 28 cases with unilateral INO and 7 of 23 with bilateral INO. The findings provide evidence for a rostral/caudal localization of lesions within the medial longitudinal fasciculus causing INO on the basis of MR and BL-R1 abnormalities. An abnormality limited to MR suggests a midbrain location in 58.8% of patients while abnormal BL-R1 with or without an associated MR change suggests a rostral pontine location in 35.3%.     

Wallenberg's lateral medullary syndrome with loss of pain and temperature sensation on the contralateral face: clinical,MRI and electrophysiological studies

Thirteen patients with Wallenberg's lateral medullary syndrome (WLMS) were studied. Clinical and magnetic resonance imaging (MRI) evidence demonstrated infarction in the dorsolateral medulla which produced loss of pain and temperature sensation on one side of the face ipsilateral to the lesion in seven patients. However, in another six patients, the infarction in a similar location produced the same sensory loss on the contralateral face. This is the first report of an analysis comparing these two conditions in WLMS patients, confirmed by MRI. The finding of normal blink reflex and somatosensory evoked potentials (stimulation on median nerve) in the two groups of patients may indicate that the impulses travel along the central pathways of touch, vibration and joint position sensation instead of the pathways for pain and temperature, because the patients had normal sensation of touch, vibration and joint position but impairment of pain and temperature sensation. In addition, it is suggested that the pathways of late blink reflex (R2) pass through the medial lemniscus in the ventromedial medulla instead of the spinal trigeminal tract in the dorsolateral medulla. Further, the observation of the much longer lantencies (about 29 ms) of the normal R2 raises the possibility that the impulses may travel along the longer pathways through the opposite medial lemniscus and up to the thalamus or cortex where they project to bilateral motoneurons of the orbicularis oculi muscles. Although the alternative of R2 travelling only by the shorter pathways through the brain stem is not excluded, this is not supported by current data.     

Seventh nerve palsies may be the only clinical sign of small pontine infarctions in diabetic and hypertensive patients

Backgroud: Small brainstem infarctions are increasingly recognized as a cause of isolated ocular motor and vestibular nerve palsies in diabetic and/or hypertensive patients. This raises the question whether there are also isolated 7^th nerve palsies due to pontine infarctions in patients with such risk factors for the development of cerebrovascular diseases. Methods: Over an 11-year-period, we retrospectively identified 10 diabetic and/or hypertensive patients with isolated 7^th nerve palsies and electrophysiological abnormalities indicating pontine dysfunction. All patients had examinations of masseter and blink reflexes, brainstem auditory evoked potentials, direct current electro-oculography including bithermal caloric testing, and T1- and T2-weighted MRI (slice thickness: 4–7 mm). Results: Electrophysiological abnormalities on the side of the 7^th nerve palsy included delayed masseter reflex latencies (4 patients), slowed abduction saccades (4 patients), vestibular paresis (2 patients), and abnormal following eye movements (2 patients). Electrophysiological abnormalities were always improved or normalized at re-examination, which was always associated with clinical improvement. MRI revealed an ipsilateral pontine infarction in 2 patients. Another 2 had bilateral hyperintense intrapontine lesions, and one an ipsilateral cerebellar infarction. Conclusions: Simultaneous improvement or recovery of abnormal clinical and electrophysiological findings strongly indicated that both were caused by the same actual pontine lesions. A 7^th nerve palsy may be the only clinical sign of a pontine infarction in diabetic and/or hypertensive patients. Such mechanism may be underestimated if based on MRI only. Received: 24 January 2002, Received in revised form: 22 May 2002, Accepted: 4 June 2002 Correspondence to Frank Th?mke, MD     

The correlation between vertebral artery asymmetry and pontine infarction--an MR angiography study]

The purpose of this study is to evaluate the correlation between variation of the vertebral artery (VA) and the incidence of pontine infarction. A total of 206 patients were examined using magnetic resonance imaging (MRI) and 3-dimension time-of-flight MR angiography (MRA) of the brain. Of these, 54 patients had pontine infarctions (23 symptomatic and 31 asymptomatic), and the majority of them were located in the pontine base. The sites of dominant lesion in the pons were right in 18 cases, left in 8 cases, and bilateral in 28 cases. The number of patients with VA asymmetry (the ratio of internal diameters 1:2 or more) were 89 (43.2%). Of these, 67 patients had small diametric VA of right side, and 22 of left side. Among the 117 patients with normal VA pattern, 19 (16.2%) had infarction, while among the 89 patients with VA asymmetry, 35 (39.3%) had infarction. The patients with small diametric VA of right side significantly had infarctions in the same side of the pons. The results of this study suggest that VA asymmetry is considered to be one of the risk factors of pontine infarction and that MRA can be useful in the examination of the cerebral artery as a valuable and non-invasive screening method.     

脑卒中对瞬目反射的影响

目的 :探讨脑干以上节段的病变对瞬目反射 ( BR)的影响。方法 :共 3 0例脑卒中患者作了 BR检测。于眶上切迹处以方波脉冲电流刺激眶上神经。双侧下眼轮匝肌分别记录 ,刺激同侧所记录的两个波为 R1 、R2 ,刺激的对侧所记录到的一个波为 R'2 。结果 :( 1 ) BR2例正常、2 8例异常。 ( 2 )在这 2 8例 56侧中 BR各成分的异常率分别为 R1 :4 8.2 % ( 2 7/56)、R2 :69.6% ( 3 9/56)、R'2 :57.1 % ( 3 3 /56)。 ( 3 )两个或以上的 BR成分缺如者 9例 ,其中 5例有神志的改变、2例有失语、2例神志清楚。结论 :大脑半球病变对 BR总的影响是抑制性的。 BR的异常与病人的神志状况及有否失语密切相关 ,而与病变部位、是否有中枢性面瘫、偏瘫、面部感觉障碍以及检测的时间间隔均关系不大。     

Significance of the blink reflex in the Wallenberg syndrome

The blink reflex was studied in 38 cases with lateral medullary lesions (Wallenberg syndrome). Twenty-one blink reflexes were abnormal. The most common abnormality is an afferent delay in the late reflex on the side of the lesion with a normal early reflex. This abnormality is not pathognomonic of the Wallenberg syndrome. The physiopathogeny is discussed.     

Transient upbeat nystagmus due to unilateral focal pontine infarction

Upbeat nystagmus is known to be caused by an imbalance of the vertical vestibulo-ocular reflex (VOR), favoring downward VOR activity, due to bilateral lesions of the medulla, ventral tegmentum, anterior cerebellar vermis, adjacent brachium conjunctivum and the midbrain. We report on two patients who had transient upbeat nystagmus due to unilateral pontine infarction that may have disrupted bilateral upward VOR pathways running in the ventral tegmental tracts.     

脑干梗塞急性期弥散MRI的探讨

目的:弥散加权MRI(DW1)因能够在早期、快速、敏感地反映出脑部缺血性病变而成为脑梗塞患者急性期诊断不可缺少的重要的检查方法,但是对于某些部位的某些小的病灶在急性期DW1有时亦不能查出。本研究以脑干梗塞的患者为对象,对急性期DW1的敏感度进一步探讨。方法:以发病24小时以内施行DWI检查的28例患者作为对象;DWI是在1.5Tesl的MR装置下,采用断层回波成像的,与此同时,还进行了T2加权MRI及水抑制成像FLAIR(fluidattenuated inversion recovery)的检查,最终梗塞灶根据平均127小时后的以上所述的MRI检查中的所见及临床症状来综合判断的,只把明确的高信号区域判断为病灶。结果:最终梗塞灶为中脑2例,桥脑9例,延髓17例。通过第一次DWI,检查出病灶的16例(敏感度57.1％),没有明确检查出病灶的12例,其中在这12例患者中有11例是在以后的MRI检查中发现为延髓病变,有1例确认为桥脑病变。从发病开始到施行DWI检查为止,时间越短,病变越不容易查出。结论:应该注意在急性期的DWI中即使没有明确的病灶,也不能否认脑干梗塞,特别是延髓梗塞。     

后循环梗死患者的眼动及前庭功能评价

目的   评价眼动及前庭功能检查对后循环梗死（posterior circulation Infarction,PCI）患者的诊断价值。 方法  纳入22例PCI患者,收集其临床基线资料,包括性别、年龄、首发症状、高血压、糖尿病、吸烟、饮酒史及入院体征等相关指标。患者均行眼动检查：包括凝视试验（gaze test,GT）、扫视试验（saccade test,ST）、平滑跟踪试验（smooth pursuit test,SPT）、视动眼震检查（optokinetic nystagmus test,OPK）;前庭功能检查：包括自发眼震（spontaneous nystagmus,SN）、摇头试验（head shaking test,HST）、固视抑制检查,上述检查均应用眼震视图仪（videonystagmograph,VNG）进行记录。 结果  共纳入22例PCI患者,首发症状：15例（68.2%）为头晕/眩晕,7例（31.8%）为肢体无力麻木。眼动检查提示：异常19例（86.4%）,其中GT异常4例（18.2%）,ST异常11例（50.0%）,SPT异常15例（68.2%）,OPK异常12例（54.5%）。前庭功能检查提示：22例完成SN检查,其中SN阳性8例（36.4%）,包括小脑梗死4例,脑桥梗死3例,左侧延髓背外侧、双侧小脑半球及蚓部梗死1例;17例完成HST检查,其中HST阳性6例（35.3%）,包括小脑梗死2例,脑桥梗死2例,小脑及脑桥梗死1例,右侧小脑及延髓上段梗死1例;19例完成固视抑制检查,其中固视抑制失败8例（42.1%）,包括双侧小脑梗死1例,脑桥梗死4例,左侧延髓梗死1例,右侧小脑及延髓上段梗死1例,左侧延髓背外侧、双侧小脑半球及蚓部梗死1例。以头晕/眩晕为首发症状的患者与以肢体无力、麻木为首发症状的患者相比,眼动及固视抑制检查阳性率高（P分别为0.023和0.045）。 结论  小脑、延髓梗死的患者常以头晕/眩晕起病;眼动检查有助于筛查PCI患者;小脑梗死患者的病灶侧别常与自发、摇头眼震的水平成分一致;脑桥梗死患者HST后可诱发下跳眼震;脑桥、延髓梗死患者常固视抑制失败。