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 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.     

Electrophysiologic analysis of aberrant regeneration after facial nerve paralysis.

The blink reflex, ordinarily elicited only in the orbicularis oculi and not in other facial muscles, can be used to detect synkinetic movements objectively. In 26 of 29 patients tested at least 4 months after facial nerve degeneration, an aberrant blink reflex was recorded in the orbicularis oris on the affected side. Of the remaining three, one had injury to only a peripheral branch of the facial nerve and experienced a return of function with no evidence of synkinesis; in the other two, the affected side of the face was totally paralyzed in the absence of facial nerve regeneration. Synkinetic movements ultimately will occur in nearly all cases following facial nerve degeneration provided that the facial nerve regenerates from a proximal site.     

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.     

The influence of age in peripheral facial palsy on brainstem reflex excitability

BACKGROUND: Neuronal plasticity is expected to be different at different ages and adaptive changes developing after peripheral facial palsy (PFP) may provide a clue in this respect. AIMS: To investigate the difference in the reorganization developing after facial nerve damage between patients who developed PFP at childhood-youth and middle-old age. PATIENTS AND METHODS: Twenty-two patients were divided into two groups according to the age-at-onset of PFP; young (PFP 1), and elderly (PFP 2). Two age-matched control groups (C 1 and C 2) comprised of 32 healthy subjects were included in the study. The latency, R(2) area, and recovery of the R(2) area of the blink reflex were investigated. STATISTICAL ANALYSIS: ANOVA and Bonferroni tests were used. RESULTS: The R(2) areas were significantly greater on the intact side of the PFP 1 group as compared to that in the control group ( P =0.012). The recovery of R2 component was significantly enhanced on the symptomatic (P = 0.027), and intact (P = 0.041) sides in PFP 1 as compared to that in the C 2 group at the stimulus interval of 600 ms. Significant enhanced recovery was noted at 200 ms stimulus interval on the symptomatic side of the two PFP groups (PFP 1, P = 0.05 and PFP 2, P = 0.025) and on the intact side of the PFP 1 group (P =0.035) as compared to that in the control groups. CONCLUSION: Young age-at-onset of PFP is associated with more prominent excitability changes developing at the neuronal and interneuronal level.     

Partial restoration of blink reflex function after spinal accessory-facial nerve anastomosis.

Functional motor control requires perfect matching of the central connections of motoneurons with their peripheral inputs. It is not known, however, to what extent these central circuits are influenced by target muscles, either during development or after a lesion. Surgical interventions aimed at restoring function after peripheral nerve lesions provide an opportunity for studying this interaction in the mature human nervous system. A patient was studied in whom the spinal accessory nerve was anastomosed into a lesioned facial nerve, allowing voluntary contractions of the previously paralysed muscles. This procedure, in addition to replacing the facial neurons at peripheral synapses, allowed a new short latency trigeminospinal accessory reflex of the R1 blink reflex type to be demonstrated, implying that trigeminal neurons had sprouted towards spinal accessory motoneurons over a distance of at least 1 cm. These results show an unexpected influence of the periphery in remodelling central connectivity in humans. The motoneuronal excitability for this R1 reflex response was therefore studied to compare the convergent properties of facial motoneurons (normal side) with those of the spinal accessory motoneurons (operated side) using a classic double shock technique with variable interstimulus intervals (conditioning test stimulus). On the normal side, conditioning stimuli (to the ipsilateral or contralateral infraliminar supraorbital nerve) produced a clearcut facilitation of the R1 blink reflex when the interstimulus interval was 30-80 ms. By contrast, a similar procedure had no effect on the R1 blink reflex mediated via the trigeminal-spinal accessory reflex arc. These data indicate that despite the heterotopic sprouting of some axons from neurons in the XIth nucleus, motoneurons involved in the newly formed reflex arc remain totally inexcitable by other trigeminal afferents and seem unable to ensure a physiological functioning of the normal blink reflex. Thus the functional relevance of the recovered R1 blink response remains unclear.     

Contralateral early blink reflex in patients with facial nerve palsy: indication for synaptic reorganization in the facial nucleus during regeneration.

Fifty patients with Bell's palsy and 30 patients with etiologically different symptomatic peripheral facial nerve palsy were studied by means of electrically evoked blink reflexes 1-23 days after onset of paresis. Their results were compared with a normal control group of 30 healthy subjects. In a significant number of patients (64% in Bell's palsy and 53% in symptomatic facial nerve palsy) a contralateral early blink reflex response (R1) could be elicited upon stimulation of the normal side as compared to 13% in the control group. It is suggested that this result may be explained by synaptic reorganization of the facial nucleus leading to functional unmasking of pre-existing crossed trigemino-facial reflex pathways during regeneration. This view is in line with previous experimental data in animals on the time course of structural changes in the facial nucleus after lesioning of the ipsilateral facial nerve.     

Reorganization of sensorimotor gating after peripheral facial palsy starts at brainstem*

Background and objective We aimed to analyze the alterations in sensorimotor gating at brainstem after peripheral facial palsy (PFP). To examine sensorimotor gating, we used prepulse modulation (PPM) of blink reflex (BR). We also recorded BR recovery to identify excitability changes in the facial nucleus.

Patients and method We included 33 patients and 39 recordings. Control group was composed of 16 healthy subjects. Simultaneous bilateral baseline BR, BR recovery at ISI of 300-ms and BR-PPM at ISI of 100-ms recordings were performed after stimulation of trigeminal nerve on right sides of healthy subjects and on both sides of patients. Severity of PFP and time lapse from the onset was noted.

Results Mean R1 amplitude was increased, whereas mean R2 and R2c magnitude were reduced in all groups after prepulse stimulation. However, multivariate ANOVA showed significance at group level (patients and healthy subjects), at prepulse level (no prepulse and 100-ms prepulse) and group and prepulse level. Suppression of R2 or R2c was lower on both sides of patients compared to healthy subjects and the deficit first started on the symptomatic side.

Conclusion Suppression of R2 and R2c after prepulse stimulation is reduced in PFP suggesting decreased filtering of facial sensory input at brainstem level. Trigeminal sensitization at brainstem develops early after PFP.     

Bell's palsy-induced blepharospasm

We report two patients with blepharospasm that appeared during the recovery phase of Bell's palsy. It is well known that hemifacial spasm occasionally appears after Bell's palsy; however, blepharospasm associated with Bell's palsy has been rarely reported so far. Blepharospasm appeared within a month after the onset of Bell's palsy, suggesting that a certain causal relationship may be present between Bell's palsy and blepharospasm. We speculate that corneal irritation caused by lagophthalmos contributes to the induction of blepharospasm. Another speculation is that abnormal afferent input from the paralyzed side contributes to the abnormal sensitization of the blink reflex, thereby facilitating the induction of abnormal facial motor outputs such as blepharospasm. Received: 17 May 2001, Accepted: 27 August 2001     

Interaction between the blink reflex and the abnormal muscle response in patients with hemifacial spasm: results of intraoperative recordings

Patients with hemifacial spasm (HFS) have an abnormal muscle response (AMR) that can be elicited by stimulating one branch of the facial nerve and recording electromyographically from muscles innervated by other branches of the facial nerve. In addition, the R1 component of the blink reflex can be elicited from the affected side in patients with HFS who are undergoing microvascular decompression (MVD) operations under inhalation anesthesia. A synkinetic component of the blink reflex response that corresponds to the R1 component can be recorded from the mentalis muscle. In the present study we show that the blink reflex elicited by electrical stimulation of the supraorbital nerve can suppress the AMR elicited by electrical stimulation of the temporal branch of the facial nerve in patients with HFS when the interval between stimulation of the supraorbital nerve and stimulation of the temporal branch of the facial nerve (interstimulus interval, ISI) is such that the blink reflex response would appear later than the AMR if they had been elicited independently. Within a short range of ISIs the two responses suppress each other partially or totally. We find evidence that the suppression of the AMR is the result of an interaction in the facial motonucleus. We believe that the results of the present study support the hypothesis that the facial motonucleus is hyperactive in patients with HFS, and we suggest that the AMR is a result of backfiring from the facial motonucleus and that it may thus be an exaggerated F-response.     

Abnormal muscle responses in hemifacial spasm: F waves or trigeminal reflexes?

OBJECTIVE: In patients with hemifacial spasm (HFS), abnormal muscle responses (AMR) are frequently present. The objective of this study was to investigate whether the afferent input of AMR is mediated by antidromic facial nerve stimulation or orthodromic trigeminal nerve stimulation. METHODS: AMR in the orbicularis oris muscle were recorded in 28 patients with HFS. When AMR were present, they were recorded after subthreshold stimulation of the facial nerve and weak stimulation delivered to the skin. RESULTS: AMR were recordable in 24 (86%) of the patients, and usually consisted of the early constant component (mean onset latency, 10.0 ms) and late variable component (35.3 ms), similar to R1 and R2 of the blink reflex. The early or late components of AMR, or both, were frequently elicited after subthreshold stimulation of the facial nerve (43%) and skin stimulation (88%). CONCLUSIONS: AMR are likely to be mediated by trigeminal afferent inputs, rather than antidromic activation of the facial nerve, and are a type of trigeminal reflex.     

Myokymic discharges and enhanced facial nerve reflex responses after recovery from idiopathic facial palsy.

A functional disorder of facial muscle activity commonly occurs in patients after recovery from Bell's palsy with axonal degeneration. The postparalytic facial dysfunction is probably related to the aberrant growing of regenerating axons, although other theories such as ephaptic transmission, spontaneous generation of impulses, and enhancement of motoneuron excitability should also be considered. In this work, we have carried out a comparative electrophysiological study of both sides of the face in 23 patients who had recovered from a unilateral Bell's palsy with axonal degeneration. At rest, spontaneous firing of motor units was observed in muscles of the previously paralyzed side. Direct motor responses to facial nerve stimulation were smaller in the muscles of the previously paralyzed side, but reflex responses obtained in the same muscles by stimulation of either the facial or trigeminal nerve were larger when compared with those of the contralateral side. These data indicate that patients with "postparalytic facial dysfunction" may have an increased background muscle activity, as well as an enhanced recruitment of facial motoneurons to reflex activation in the side of the previous paralysis. These findings are compatible with an enhanced level of motoneuron excitability in the facial nucleus.     

Unmasking of the trigemino-accessory reflex in accessory facial anastomosis

OBJECTIVE: To evaluate the possible blink reflex responses in facial muscles reinnervated by the accessory nerve. METHOD: Eleven patients with a complete facial palsy were submitted to a surgical repair by an accessory facial nerve anastomosis (AFA). In this pathological group, blink reflex was studied by means of percutaneous electrical stimulation of the supraorbital nerve and recording from the orbicularis oculi muscle. A control group comprised seven normal people and seven patients with a complete Bell's facial palsy; in this group, responses on the sternocleidomastoideus (SCM) muscles were studied after supraorbital nerve stimulation. RESULTS: All the patients with AFA showed a consistent degree of facial reinnervation. Ten out of the 11 patients with AFA showed reflex responses; in six, responses were configured by a double component pattern, resembling the R1 and R2 components of the blink reflex; three patients had an R1-like response and one patient showed a unique R2 component. Mean values of latencies were 15.2 (SD 4.6) ms for the R1 and 85.3 (SD 9.6) ms for the R2. In the control group, eight out of 14 people had evidence of reflex responses in the SCM muscles; these were almost exclusively configured by a bilateral late component (mean latency 63.5 (SD15.9) ms) and only one of the subjects showed an early response at 11 ms. CONCLUSION: The trigemino-accessory reflex response in the pathological group was more complex and of a significantly higher incidence than in the control group. These differences could be tentatively explained by a mechanism of synaptic plasticity induced by the impairment of the efferent portion of the reflex. This could unmask the central linking between the trigeminal and the accessory limbs of the reflex. The findings described could be a demonstration of neurobionomic function in the repairing process of the nervous system.     

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 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.     

The blink reflex in "chronic migraine".

OBJECTIVES: Activation of the trigeminovascular system and sensitisation of brainstem trigeminal nuclei are thought to play an important role in migraine. The aim of this study was to investigate the blink reflex and its habituation in patients with "chronic migraine". METHODS: We studied 35 patients suffering from "chronic migraine" (IHS classification criteria) outside and during a spontaneous attack, and 35 control subjects. An EMG device with a specific habituation test program was used to elicit and record blink reflex responses and to randomly repeat stimulations at different time intervals so as to induce habituation. RESULTS: The R(1) and R(2) latencies, amplitudes and areas of the basal blink reflex were similar in patients studied both outside and during an attack as well as in control subjects, whereas the blink reflex habituation responses were markedly reduced in patients studied outside an attack. The percent changes in the R(2) areas from the baseline values, obtained when stimuli were delivered at time intervals of 10, 5, 4, 3, 2 and 1s, were statistically different (p<0.01-p<0.001) from those of the same patients studied during a migraine attack and of those of control subjects. There was a significant correlation between decreased habituation of the blink reflex and a higher frequency of attacks. The stimulus intensities of the blink reflex (multiples of the detection threshold intensities) were significantly lower (p<0.001) on the side affected, or more severely affected, by headache in patients studied during a migraine attack. CONCLUSIONS: The decreased habituation of the blink reflex outside an attack reflects abnormal excitability in "chronic migraine", which normalizes during the attacks. The inverse correlation between the frequency of attacks and habituation responses confirms the abnormal excitability induced by the high frequency of attacks. Central sensitisation mechanisms (allodynia) may explain the lower detection thresholds observed on the side affected by headache in patients during the attacks. SIGNIFICANCE: The blink reflex and its habituation may help shed light on the subtle neurophysiological changes that occur in migraine patients between and during attacks.     

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.     

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.     

Related timing for peripheral and central plasticity in hypoglossal-facial nerve anastomosis

The aim of this work was to determine the role of peripheral facial muscle reinnervation in the central reorganization of the blink reflex (BR) after hypoglossal-facial anastomosis (HFA). An electrophysiological study was performed on seven patients who underwent HFA after facial nerve transection during surgery for acoustic neuroma. HFA was performed within 15 days after surgery in five patients (group 1) and later for the two others (group 2). We studied the motor responses (MR) and the BR evoked on the affected side, before and over 3 years after the HFA. The MR appeared by the third month for the first group, and by the sixth and twelfth for the second group. After 36 months, the amplitude of MR was significantly higher than its control value, showing hyperinnervation of the facial muscles. Study of the BR evoked only an R1-type blink response that was observed 4 and 6 months after the MR for groups 1 and 2, respectively. This central reorganization appeared closely correlated with muscle reinnervation and its related timing. The occurrence of peripheral nerve-muscle contacts seems to be a necessary condition for reorganization of the trigemino-hypoglossal-facial reflex.     

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.