Blink reflex in patients with an ischaemic lesion of the brain-stem verified by MRI

The electrically elicited blink reflex was investigated in 25 patients with ischaemic lesions of the pons or the medulla oblongata. Only patients with a lesion on MRI appropriate to the clinical syndrome were included. Twenty patients had an infarction of the pons, bilateral in 5. Additional 5 patients had an infarction of the dorsolateral medulla oblongata. Patients with hemispheric lesions were excluded. Four of the 5 patients with Wallenberg's syndrome showed delayed R2 components to stimulation ipsilateral to the lesion. Additional loss of the ipsilateral R1 component was observed in 1 patient. Fifteen of the 20 patients with pontine infarctions had pathological blink reflexes. All 6 patients with a unilateral pons lesion and an abnormality of R1 had this abnormality on the side contralateral to the lesion. In 3 cases with bilateral pontine infarction R1 was abnormal on one side or on either side. Of 11 patients with a normal R1, 6 had isolated abnormalities of R2 without consistent correlation to the side of the lesion. We conclude that abnormalities of the blink reflex are of minor localizing value in pontine infarction. This may be explained by the fact that a pontine infarction affects either the reflex arch itself or descending pathways that have a modulating influence on the reflex arch. Infarctions of the medulla oblongata, however, have characteristic abnormalities that have already been described.     

Blink reflex in hemiplegia.

An electrophysiological study of the blink reflex was undertaken in 20 normal subjects and in 28 patients complaining of central facial palsy caused by unilateral hemispheral damage. In normal subjects, the latency, amplitude and organization of R1 and R2 responses are well known. Habituation of R2 responses occurred between 1 and 2 c/sec stimulation rate. R1 responses habituated at a higher stimulation rate (5 c/sec). In patients with unilateral hemispheral lesion, our results showed that changes in the blink reflex responses were bilateral. On the hemiplegic side the responses showed a decreased amplitude, while they were facilitated on the "normal" side. However, there was no change in latency of the two components of the reflex, on both sides. On the other hand, habituation of the late component occurred on the hemiplegic side for low stimulation rates: (0.5--1 c/sec), while on the "normal" side there was less habituation (3--4 c/sec), as compared with normal subjects. These results agree with those of experimental studies on cortical modulatory influences on brain-stem nuclei. They suggest a tactile origin of the two components of the blink reflex.     

Blink reflex in facial-hypoglossal anastomosis

Summary The blink reflex was investigated in two patients after a facial-hypoglossal anastomosis had been performed. In each case the first component of the blink reflex could be demonstrated with normal latency on the operated side after ipsilateral supraorbital stimulation. These findings give further evidence that the first component of the blink reflex is not monosynaptic in nature. The second component of the blink reflex was distinctly retarded in the first case and was not seen at all in the second case. The second component of the blink reflex is influenced strongly by alteration of the intrabulbar and efferent part of the reflex circuits; it shows some correlation with voluntary motor activity.Stipendiary of the Humboldt Foundation.     

Blink reflex in hemiplegia

Data about the influence of hemispheric lesions on the blink reflex are conflicting. 21 hemiplegic patients and 11 control subjects were investigated. The duration, latency and electric area of electrically evoked blink reflex responses were evaluated by common electromyographic techniques. A depression of the ipsilateral and the consensual late response after stimulation of the paretic side was the most evident finding. However, also a certain increase of the early response and a depression of the late response of the paretic side independent of the side of stimulation emerged. Concerning the parameters taken into account, the evaluation of the latency period seems to be the most significant and reliable. Determination of the electric area provides additional useful data which, however, may easily lead to mistakes.     

Blink reflex in patients with hemifacial spasm. Observations during microvascular decompression operations

The blink reflex cannot normally be elicited during surgical anesthesia using inhalation anesthetics. However, in patients with hemifacial spasm (HFS) the early component of the reflex response (R1) can be elicited on the affected side but not on the unaffected side during such anesthesia. The electromyographic (EMG) response from the mentalis muscle to stimulation of the supraorbital nerve was recorded during microvascular decompression (MVD) of the facial nerve to relieve HFS and compared to the response from the same muscle to stimulation of the zygomatic branch of the facial nerve in four patients. During the operation before the facial nerve was decompressed, contractions in both the orbicularis oculi and the mentalis muscles could be elicited by stimulation of the supraorbital nerve (mean latencies 12.2 +/- 1.9 and 12.9 +/- 2.0 ms, respectively). When the facial nerve had been decompressed the blink reflex could no longer be elicited, and there was no response from the mentalis muscle to stimulation of the zygomatic branch of the facial nerve. Compound action potentials (CAP) recorded from the 7th cranial nerve in response to stimulation of the supraorbital nerve had latencies of 7.5 ms +/- 1.4 ms to the negative peak.     

Blink reflex abnormalities in chronic alcoholics

PURPOSE: The aim of the present study was to evaluate the efficacy of blink reflex as a method for obtaining early diagnosis of cranial nerve involvement in alcoholic patients. MATERIALS AND METHODS: The study was conducted on 30 male alcoholics with a mean age of 43 years. They had histories of alcohol abuse for at least 6 years (mean: 25). At the time of recording, they had undergone detoxification treatment for a mean of 27 days. RESULTS: R1 (early response), R2Y (second ipsilateral response), and R2C (second contralateral response) latencies in alcoholics were prolonged relative to controls and the differences were statistically significant (p < 0.02, p < 0.001, p < 0.001, respectively). According to the defined criteria, 40% of the patients had abnormal responses, and the most common abnormality was the unilateral prolongation of R1 (13%). CONCLUSION: Finding abnormal blink reflex responses in alcoholic patients has suggested that blink reflex testing is a useful method for the evaluation of subclinical cranial nerve involvement in alcoholic patients. Blink reflex testing may be useful in detecting early changes and in the follow-up of alcoholic disorder.     

Blink reflex in young children with medullary kink in Chiari malformation.

We studied the blink reflex (especially the late components ipsi- and contralateral to stimulation site, R2 and R2') in 17 patients under 6 years of age; 12 with Chiari malformation, 1 with Dandy-Walker syndrome and 4 with brainstem tumor. We investigated the correlation between the R2 or R2' and neuro-image findings. Out of various features of the brainstem lesion revealed by MRI or CT examinations, the medullary kink characteristic in Chiari malformation was most responsible for abnormality of R2 and R2'. In addition, the fact that the disturbance of R2 and R2' in patients with Chiari malformation was more apparent in younger children than older ones confirms the intrinsic vulnerability of the blink reflex in the younger age groups as noted in normal children.     

Blink reflex in patients with Wallenberg’s syndrome

Knowledge of the neural circuits involved in Wallenberg’s syndrome (WS) is incomplete. Study of the blink reflex (BR) in patients with WS can help in reaching a better understanding of the physiopathology underlying clinical symptoms and may help in the prediction of clinical outcome. We evaluated the BR in response to supraorbital nerve electrical stimuli in 20 patients with WS. All patients were studied within the 1st week after onset of symptoms, and 10 of them were also studied repeatedly during a follow-up period of 3–12 months. At the first examination the long latency bilateral responses (R2 and R2c) to stimulation of the supraorbital nerve of the affected side were absent in 11, delayed in 4, and normal in 5 patients. At follow-up, there was a normalization of the BR in all patients who had absent or delayed responses at the first examination except for one patient whose responses remained absent at the 9th month. Late responses elicited on the side of the lesion by stimulation of the non-affected supraorbital nerve were normal in all but one patient. This patient died from cardiorespiratory arrest within the 1st month of the illness. One patient with normal BR responses also died in the acute phase. The BR is abnormal in most patients with acute WS and tends to normalize in a mean period of 7 months. BR pattern is not a predictor of early fatal complications in patients with this syndrome. Received: 18 March 1996 Received in revised form: 18 June 1996 Accepted: 26 June 1996     

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 reflexes and the silent period in tetanus

Abnormalities of the silent period (SP) and blink reflexes occur in diseases that interfere with inhibitory pathways, such as tetanus and stiff-person syndrome (SPS). The SP is abnormal in tetanus but not in SPS. Studies of the blink reflex in tetanus are limited. In this report, a patient with generalized tetanus is described. The masseteric-and mixed-nerve SP was absent or truncated. In contrast to SPS, blink reflex studies revealed no bilateral R1 component, and a discrete R3 was only present ipsilateral to right supraorbital stimulation. This reflects the distinct inhibitory pathways underlying these disorders.     

Blink reflex abnormalities in children with Tourette syndrome

Tourette syndrome (TS) is a common disorder which typically occurs during childhood or early adolescence. There is no definitive diagnostic test for TS. The objective of this study was to demonstrate whether neurophysiological abnormalities of the blink reflex can be observed in children with TS. We enrolled 15 children with TS, diagnosed according to DSM IV Diagnostic Criteria, and 15 controls. The blink reflex was elicited by stimulating the supraorbital nerve in order to measure the early response (R1), homolateral and contralateral R2 (late) responses, amplitude of R1 and duration of R2. The mean duration of R2 was significantly longer in TS patients than in the controls ( P  < 0.001, Student's t -test). An abnormal pattern of the blink reflex can be, even in childhood, an early neurophysiologic marker of TS, which is not related to the duration of TS or to the age of onset.     

Blink reflex recovery in facial weakness: an electrophysiologic study of adaptive changes

OBJECTIVE: To study the electrophysiologic effects of unilateral facial weakness on the excitability of the neuronal circuitry underlying blink reflex, and to localize the site of changes in blink reflex excitability that occur after facial weakness. BACKGROUND: Eyelid kinematic studies suggest that adaptive modification of the blink reflex occurs after facial weakness. Such adaptations generally optimize eye closure. A report of blepharospasm following Bell's palsy suggests that dysfunctional adaptive changes can also occur. METHODS: Blink reflex recovery was evaluated with paired stimulation of the supraorbital nerve at different interstimulus intervals. Comparisons were made between normal control subjects and patients with Bell's palsy who either recovered facial strength or who had persistent weakness. RESULTS: Blink reflex recovery was enhanced in patients with residual weakness but not in patients who recovered facial strength. Facial muscles on weak and unaffected sides showed enhancement. In patients with residual weakness, earlier blink reflex recovery occurred when stimulating the supraorbital nerve on the weak side. Sensory thresholds were symmetric. CONCLUSION: Enhancement of blink reflex recovery is dependent on ongoing facial weakness. Faster recovery when stimulating the supraorbital nerve on the paretic side suggests that sensitization may be lateralized, and suggests a role for abnormal afferent input in maintaining sensitization. Interneurons in the blink reflex pathway are the best candidates for the locus of this plasticity.     

Blink reflex in stroke: follow-up and correlation with function and CT parameters

Blink reflex (BR) was examined serially in patients 1, 2 and 3 months after unilateral hemispheric cerebrovascular accident and compared with functional state and CT findings of lesion extent and location. BR R2 components were depressed and correlated with lesion size. Initial walking ability was correlated with latency and amplitude of both direct and consensual R2 elicited by stimulation of the paretic side. No correlation was found between BR and arm function or the final ambulatory ability. A model suggesting a close association between BR projection-facilitating fibers and those mediating facial movements is presented.     

Blink reflex excitability cycle in hemifacial spasm

We studied electrically elicited blink reflex responses in patients with hemifacial spasm (HFS) by applying single isolated, as well as paired (conditioning and test), stimuli at both sides of the face. Responses after single stimuli were of larger size on the side of the spasm compared with the uninvolved side and controls. With paired stimuli, the inhibitory effect of the conditioning stimuli upon the test stimuli late response (R2), which was always observed in normals, was significantly less pronounced at short interstimuli intervals. This resulted in an enhanced recovery curve of R2, which was observed on the side of the spasm and the contralateral, clinically normal side. Patients with longer disease duration showed more striking abnormalities of the recovery curve. We suggest that there is enhanced excitability of facial motoneurons and of those brainstem interneurons that mediate the blink reflex pathway in patients with HFS.     

Blink reflex in Parkinson's disease with levodopa-induced dyskinesia

We have studied the electrically evoked blink reflex (R1 and R2 components) in 40 parkinsonian patients with levodopa-induced dyskinesia (15 with facial dyskinesia, 13 with limb-truncal dyskinesia and 12 with mixed dyskinesia). R2 latencies (both ipsilateral and contralateral) were significantly prolonged in dyskinetic patients. These findings are indicative of decreased excitability of brainstem interneurones in the dyskinetic parkinsonians. We found no correlation between the neurophysiological pattern of blink reflex and the localization of dyskinesia.     

Blink reflex with stimulation of the mental nerve. Methodology, reference values, and some clinical vignettes

Introduction - In order to develop an objective electrophysiological method for detecting and grading lesions in the inferior alveolar nerve (IAN) and its terminal branch, the mental nerve (MN), the normal physiology of the blink reflex (BR) with stimulation of the distribution of the MN was evaluated and reference values for the MN BR test obtained. Material and methods - The BR responses to electrical stimulation of the distribution of the MN on each side were recorded in all 44 healthy adults. The onset latencies and peak-to-peak amplitudes were measured and analysed. The effects of the stimulation site, the size of the stimulating electrode, and facilitation by eye closure and mathemathical task on the MN BR responses were tested. Results - A small paediatric stimulating electrode was found to be efficient for dermatomal stimulation of the MN distribution. The MN BR responses consisted of an ipsilateral late component (R2i) on the side of the stimulation and a contralateral component (R2c) with similar latency. The latencies were longer and the stimulation thresholds needed to evoke a reflex response were higher with stimulation of the MN, when compared with the BRs with supraorbital nerve stimulation. Eye closure resulted in facilitation of the MN BR in the form of latency shortening, while mathematical task did not have any significant effect on the responses. In addition, the test was found useful in the diagnosis of iatrogenic IAN lesions after extraction of third molars in two patients, and after an orthognathic operation in one patient. Conclusion - Contrary to some previous reports, constant MN BR responses can be elicited in healthy adults, which enables further clinical application of this test.     

The corneal reflex and the R2 component of the blink reflex

A reflex contraction of the human orbicularis oculi muscles can be evoked by stimulation of either the supraorbital region ("blink reflex") or the cornea ("corneal reflex"). We found that the latency of the corneal reflex was longer, and the duration was longer than the R2 component of the blink reflex. The absolute refractory period of the R2 component of the blink reflex was longer after supraorbital than after corneal conditioning stimulation. When the R2 component of the blink reflex was habituated by repetitive stimuli, stimulation of the cornea still evoked a reflex, but supraorbital stimulation produced only a depressed R2 response. These findings suggest that the two reflexes do not have identical neural connections.     

Blink reflex recovery curves in blepharospasm,torticollis spasmodica,and hemifacial spasm

R1 and R2 blink reflex responses to single and paired stimuli were investigated in 23 control subjects: 21 patients with blepharospasm (BSP), 20 patients with torticollis spasmodica (TS), and 23 with hemifacial spasm (HFS). For paired stimuli, we compared measurements of area and peak responses at two and three times R2 threshold. R1 and R2 indices were calculated as the average of the recovery values at 0.5-, 0.3-, and 0.21-s interstimulus intervals to test individual patients. Peak amplitude measurements at three times R2 threshold were optimal. The R2 index was abnormal in 67% of BSP patients, 37% of TS patients, and 50% of HFS patients on the affected side and 20% on the unaffected side. A normal R2 index in one third of patients with BSP may indicate that different pathophysiological mechanisms are involved in this type of focal dystonia. © 1996 John Wiley & Sons, Inc.     

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.     

Blink reflex in primary lateral sclerosis

OBJECTIVE: To investigate the underlying pathophysiology of primary lateral sclerosis (PLS) regarding possible changes in blink reflex (BR) circuit. METHODS: BR was studied in 10 patients in whom diagnosis of PLS was established by comparing them to two control groups: ten patients with amyotrophic lateral sclerosis (ALS) and 30 healthy volunteers. All patients were followed up annually for a 5 year period. A typical evoked potential study of the BR was employed. RESULTS: Significantly lower values of R(2) and R(2)' amplitude were found both in the PLS and ALS groups compared with the healthy control group. All these differences were highly significant (p<0.001). R(1) amplitude and latency, as well as R(2) and R(2)' latencies, were normal in all patients. Annually recorded follow up data revealed no significant changes in BR values for PLS patients. In contrast, for ALS patients, BR progressively disappeared following clinical impairment. CONCLUSIONS: The study suggests that BR is abnormal in PLS. It also adds some clues regarding PLS pathophysiology and can be helpful as a marker of ALS progression.