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.     

Electrophysiological study on hemifacial spasm--usefulness in the etiological diagnosis and pathophysiological mechanism

Electrophysiological studies were performed in 30 patients with idiopathic hemifacial spasm (idiopathic HFS), who underwent microvascular decompression with abolishment of spasm, and 10 patients with symptomatic hemifacial spasm (symptomatic HFS) secondary to Bell's palsy. (1) The maximum firing rate of abnormal discharges recorded from the orbicularis oris muscle during spasm in patients with idiopathic and with symptomatic HFS, and that of discharges recorded on the intact side during voluntary contraction in idiopathic HFS patients measured 181 +/- 71 Hz, 68.4 +/- 36.9 Hz, 56.3 +/- 21.8 Hz, respectively. Thus, the maximum firing rate of the discharges during spasm in idiopathic HFS patients was exceedingly higher than that in symptomatic HFS patients. (2) Electroneurography, performed to evaluate quantitatively degeneration of the facial nerve, revealed that the ENoG value (90.2 +/- 16.5%) in idiopathic HFS patients were higher than that (57.6 +/- 26.8%) in symptomatic HFS patients. (3) In blink reflex examined, synkinetic potentials (S1, S2), synchronous to the potentials consisting of the early (R 1) and late component (R 2) in the orbicularis oculi muscle, were recorded from the orbicularis oris muscle on the affected side in all patients with idiopathic and with symptomatic HFS. In sequential recording of blink reflex potentials (R 1, R 2) and synkinetic potentials (S 1, S 2), the recording pattern of synkinetic potentials was divided into variable and constant type. In the variable type, synkinetic potentials appeared unsteadily and the difference in latency between R 1 and S 1 was varied. In the constant type, synkinetic potentials appeared steadily and the difference in latency between the two was not varied.(ABSTRACT TRUNCATED AT 250 WORDS)     

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.     

Excitability of facial nucleus and related brain-stem reflexes in hemifacial spasm, post-facial palsy synkinesis and facial myokymia.

OBJECTIVE: To compare the electrophysiological excitability characteristics of the facial nucleus and related structures in hemifacial spasm (HFS), post-facial palsy synkinesis (PFPS) and facial myokymia (FM). METHODS: Facial F-waves, blink reflex recoveries and magnetically elicited silent periods (SP) were prospectively studied in 17 HFS, 17 PFPS, 8 FM cases and in 13 controls. Earlier unpublished observations on abnormal impulse transmission in 36 HFS and 29 PFPS cases were also included. RESULTS: Enhanced F-waves were recorded on the symptomatic side in PFPS and HFS cases with a tendency to be more pronounced in PFPS. HFS and PFPS groups both showed an earlier blink reflex recovery, more prominent in PFPS patients, when stimulated and/or recorded on the symptomatic side. Unelicitable SPs were encountered after 24/39 stimulations in 5 patients with PFPS and rarely in HFS cases. Duration of elicitable SPs did not change remarkably. FM group had similar characteristics as normal controls in the 3 electrophysiological tests. Latencies of the lateral and synkinetic spread responses were significantly prolonged in the earlier PFPS group as compared to HFS. In two-point stimulation, both groups showed a greater latency shift in late responses, again more pronounced in PFPS. CONCLUSIONS: PFPS and HFS cases had similar enhanced excitability patterns at the facial nucleus and related brain-stem structures, more marked on the symptomatic side and more obvious in the PFPS group. Findings elicited in the FM group were thought to be caused by asynchronous hyperactivity of facial motoneurons. SIGNIFICANCE: In this comparative electrophysiological study, similar excitability patterns were found in HFS and PFPS groups, albeit with different intensities.     

Reorganization of sensory input at brainstem in hemifacial spasm and postparalytic facial syndrome

We hypothesized the filtering of sensory input from face and hand at brainstem may reorganize in hemifacial spasm (HFS) and postparalytic facial syndrome (PFS). Thus, we examined the prepulse inhibition of blink reflex (BR-PPI) in HFS and PFS. We included 12 healthy subjects, 13 patients with HFS, and 11 patients with PFS. Baseline BR, BR recovery at interstimulus interval (ISI) of 300 ms and BR-PPI at ISI of 100 ms were performed on the right sides of healthy subjects and on both sides of patients. Within-subject analysis showed baseline BR and BR-PPI were similar between asymptomatic and symptomatic sides of patients with HFS whereas BR recovery was higher on the symptomatic side. In the PFS group, latency of R2 during baseline BR recording was longer (p = 0.022) and R2 amplitude (p = 0.046) was reduced on the symptomatic side compared to asymptomatic side. Reduction of R2 area in BR-PPI recordings was also the lowest in HFS compared to other two groups (p = 0.000); however, it was also lower in patients with PFS compared to healthy subjects (p = 0.018). BR-PPI was decreased on both sides of patients. The mean R2 recovery was higher on both sides of patients with HFS and PFS (p = 0.007). Filtering of facial sensory input is decreased probably to monitor and to correct the sequence of facial movements in these disorders.     

Bell's palsy-induced blepharospasm relieved by passive eyelid closure and responsive to apomorphine.

OBJECTIVE: We describe the case of a woman with Bell's Palsy-induced blepharospasm (BPIB) of the right eye that appeared simultaneously with a complete left facial nerve palsy. The involuntary spasm was relieved by passive lowering of the upper eyelid on the paretic side. METHODS: The recovery curve of the blink reflex was evaluated on the non-paretic side in baseline conditions, after subcutaneous apomorphine and placebo administration and 8 months later, at recovery from the palsy. RESULTS: We found increased recovery of the test-R2 responses at short interstimulus intervals at baseline, which was normalised by apomorphine but not by placebo. At recovery the blink reflex R2 recovery curve returned to normal. CONCLUSIONS: This report demonstrates for the first time a response of BPIB to a dopamine agonist. SIGNIFICANCE: Our findings are in agreement with an animal model of blepharospasm that suggests a combined role of weakness of the orbicularis oculi muscle and a dysfunction of the dopaminergic system in the pathogenesis of this disorder.     

Electrophysiological study of ephaptic axono-axonal responses in hemifacial spasm

One of the classic features of hemifacial spasm (HFS) is spread of the blink reflex responses to muscles other than the orbicularis oculi. The pathophysiological mechanisms underlying the generation of such abnormal responses include lateral spread of activity between neighboring fibers of the facial nerve and hyperexcitability of facial motoneurons. In this report we present evidence for another mechanism that can contribute to the generation of responses in lower facial muscles resembling the R1 response of the blink reflex. In 13 HFS patients, we studied the responses induced in orbicularis oris by electrical stimuli applied at various sites between the supraorbital and zygomatic areas. We identified responses with two different components: an early and very stable component, with an onset latency ranging from 10.5 to 14.8 ms, and a more irregular longer-latency component. Displacement of the stimulation site away from the supraorbital nerve and towards the extracranial origin of the facial nerve caused a progressive shortening of response latency. These features indicate that, in our patients, the shortest latency component of the orbicularis oris response was likely generated by antidromic conduction in facial nerve motor axons followed by axono-axonal activation of the fibers innervating the lower facial muscles. Our results suggest that motor axono-axonal responses are generated by stimulation of facial nerve terminals in HFS.     

The effect of paired stimuli on blink reflex latencies in normal subjects

Introduction: In this study we assessed the effect of paired stimuli on the latencies and amplitudes of the blink reflex. Methods: Blink reflexes were performed with single and paired (5‐ms interstimulus interval) stimuli in 47 patients. The changes in latencies between paired and single stimuli were calculated. Results: Paired stimulation produced two types of R1 waveform morphologies: single‐ and double‐peaked waveforms. Increases in R1 and contralateral R2 latencies with paired stimulation were significantly higher in those with single‐peaked R1 responses compared to those with double‐peaked R1 responses. Conclusions: Interpreting the blink reflex latencies using paired stimulation requires visualization of the R1 waveform morphology. A double‐peaked R1 response requires no change in normal latency values, but the latency of a single‐peaked R1 should be interpreted from the second shock artifact. The effect on the R2 latency is variable. Muscle Nerve, 2011     

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.     

Fear conditioned potentiation of the acoustic blink reflex in patients with cerebellar lesions

OBJECTIVE: To investigate whether the human cerebellum takes part in fear conditioned potentiation of the acoustic blink reflex. METHODS: A group of 10 cerebellar patients (eight patients with lesions involving the medial cerebellum, two patients with circumscribed lesions of the cerebellar hemispheres) was compared with a group of 16 age and sex matched healthy control subjects. The fear conditioned potentiation paradigm consisted of three phases. During the first, habituation phase subjects received 20 successive acoustic blink stimuli. In the subsequent fear conditioning phase, subjects passed through 20 paired presentations of the unconditioned fear stimulus (US; an electric shock) and the conditioned stimulus (CS; a light). Thereafter, subjects underwent the potentiation phase, which consisted of a pseudorandom order of 12 trials of the acoustic blink stimulus alone, 12 acoustic blink stimuli paired with the conditioned stimulus, and six conditioned stimuli paired with the unconditioned stimulus. The EMG of the acoustic blink reflex was recorded at the orbicularis oculi muscles. The potentiation effect was determined as the difference in normalised peak amplitude of the blink reflex evoked by pairs of CS and acoustic blink stimuli and evoked by the acoustic stimulus alone. RESULTS: In the habituation phase, short term habituation of the acoustic blink reflex was preserved in all cerebellar patients. However, in the potentiation phase, the potentiation effect of the blink reflex was significantly reduced in patients with medial cerebellar lesions compared with the controls (mean (SD) potentiation effect (%), patients: -6.4 (15.3), controls: 21.6 (35.6)), but was within normal limits in the two patients with lateral lesions. CONCLUSIONS: The present findings suggest that the human medial cerebellum is involved in associative learning of non-specific aversive reactions-that is, the fear conditioned potentiation of the acoustic 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.     

Blink reflex in 57 parkinsonian patients with correlation between the clinical and electrophysiological parameters

An electrophysiological study of the blink reflex was undertaken in 25 control subjects and in 57 patients with Parkinson's disease. An increase in the ipsilateral and contralateral late response was the most evident finding. The excitability cycle of recovery of the R2 component of the blink reflex after a prior conditioning shock was enhanced in the patients. A statistically significant correlation was established between the increase in the late response and the severity of akinesia and rigidity.     

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.     

Alterations in excitatory and inhibitory brainstem interneuronal circuits in fibromyalgia: Evidence of brainstem dysfunction

ObjectivePatients with fibromyalgia syndrome (FMS) perceive stimuli differently and show altered cortical sensory representation maps following peripheral stimulation. Altered sensory gating may play a causal role.MethodsBlink reflex, blink reflex excitability recovery, and prepulse inhibition of the blink reflex – representing brainstem excitability – were assessed in 10 female patients with FMS and 26 female healthy controls.ResultsUnconditioned blink reflex characteristics (R1 latency and amplitude, R2 and R2c latency and area-under-the-curve) did not differ significantly between patients and controls. Blink reflex excitability recovery was enhanced in patients versus controls at all intervals tested. Prepulses significantly suppressed R2 area and increased R2 latency in patients and controls. However, R2 area suppression was significantly less in patients than in controls (patients: to 80.0 ± 28.9%, controls: to 47.8 ± 21.7%). The general pattern of corresponding changes in R2c was similar.ConclusionsBlink reflex is normal, whereas blink reflex excitability recovery is enhanced and blink reflex prepulse inhibition is reduced in patients with FMS, suggesting functional changes at the brainstem level in FMS.SignificanceReduced blink reflex prepulse inhibition concurs with altered sensory gating in patients with FMS.     

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.     

The blink reflex in patients with idiopathic torsion dystonia

The blink reflex and its recovery cycle were examined in 57 patients with idiopathic dystonia affecting different parts of the body. The group comprised 9 patients with generalized and 15 with segmental forms, 19 with torticollis, and 14 with focal arm dystonia. None had blepharospasm. The duration and amplitude of the R2 component of the blink reflex showed only minor changes. However, its recovery cycle to paired supraorbital nerve stimuli was abnormal in all groups of patients, except those with focal arm dystonia. These findings may be interpreted as showing abnormal control of the interneuronal networks mediating the blink reflex in patients with dystonia affecting sites other than the facial muscles. The fact that the principal changes were seen in patients with torticollis, and generalized or segmental dystonia, suggests that the extent of dystonia (rather than the severity) and, therefore, the close proximity to the cranial muscles was important in determining the extent of the abnormal interneuron function.     

Sensorimotor integration in patients with parkinsonian type multisystem atrophy

Sensorimotor integration is an essential feature of the central nervous system that contributes to the accurate performance of motor tasks. Some patients with multiple system atrophy with parkinsonian features (MSAp) exhibit clinical signs compatible with an abnormal central nervous system excitability to somatosen– sory inputs, such as action myoclonus or enhanced cutaneo–muscular reflexes. To investigate further the site where such dysfunction in sensorimotor integration takes place, we examined the inhibitory effects of a cutaneous afferent volley at two different levels of the motor system in 10 MSAp patients and in 10 agematched healthy volunteers. Electrical digital nerve stimuli were given as the conditioning stimulus for the motor evoked potentials (MEP) elicited by transcranial magnetic stimulation in hand muscles, and for the blink reflex responses obtained in the orbicularis oculi muscles by supraorbital nerve stimulation. Intervals for the conditioning were 20 to 50ms for the MEP and 90 to 110ms for the blink reflex. The MEP was significantly inhibited in test trials in healthy volunteers, reaching a mean of 32% of the baseline values at the ISI of 35 ms. Significant inhibition occurred also in the blink reflex, in which the R2 response was a mean of 12% of baseline values at the ISI of 100 ms. The inhibitory effects were abnormally reduced in 8 patients on the MEP, and in 7 patients on the blink reflex. There were significant group differences between patients and control subjects in the size of the conditioned MEP and blink reflex. These results suggest that sensorimotor integration is abnormal in patients with MSAp in at least two central nervous system sites: the sensorimotor cortex, and the brainstem reticular formation.     

Further evidence for a central reorganisation of synaptic connectivity in patients with hypoglossal-facial anastomosis in man

In normal subjects, electrical stimulation of trigeminal mucosal afferents (lingual nerve - V3) can elicit a short latency (12.5+/-0. 3 ms; mean+/-S.D.) reflex response in the ipsilateral genioglossus muscle (Maisonobe et al., Reflexes elicited from cutaneous and mucosal trigeminal afferents in normal human subjects. Brain Res. 1998;810:220-228). In the present study on patients with hypoglossal-facial (XII-VII) nerve anastomoses, we were able to record similar R1-type blink reflex responses in the orbicularis oculi muscles, following stimulation of either supraorbital nerve (V1) or lingual nerve (V3) afferents. However, these responses were not present in normal control subjects. Voluntary swallowing movements produced clear-cut facilitations of the R1 blink reflex response elicited by stimulation of V1 afferents. In a conditioning-test procedure with a variable inter-stimulus interval, the R1 blink reflex response elicited by supraorbital nerve stimulation was facilitated by an ipsilateral mucosal conditioning stimulus in the V3 region. This facilitatory effect was maximal when the two stimuli (conditioning and test) were applied simultaneously. This effect was not observed on the R1 component of the blink reflex in the normal control subjects. These data strongly suggest that in patients with XII-VII anastomoses, but not in normal subjects, both cutaneous (V1) and mucosal (V3) trigeminal afferents project onto the same interneurones in the trigeminal principal sensory nucleus. This clearly supports the idea that peripheral manipulation of the VIIth and the XIIth nerves induces a plastic change within this nucleus.     

The Effects of Botulinum Toxin a on Ephaptic Transmission in Idiopathic Hemifacial Spasm

Objective: Lateral spreading and synkinetic responses of blink reflex are a sign of ephaptic transmission in idiopathic hemifacial spasm (HFS). The aim of this study was to evaluate the effect of botulinum toxin A (Btx A) on ephaptic transmission in idiopathic HFS. Methods: Thirty-three patients with idiopathic HFS were investigated. Btx A was injected only into the affected orbicularis oculi (OC) muscle. Electrophysiological studies were performed before and three weeks after the Btx A injection. Results: After Btx A, the latencies of motor response and blink reflexes elicited from the OC muscle were significantly increased. The lateral spreading was not obtained in the OC muscle, while the orbicularis oris muscle response was not changed. There were no significant differences in the synkinetic responses of blink reflex. During needle EMG examination, positive sharp waves and fibrilation potentials were observed due to chemodenervation only in the OC muscle. Conclusion: Btx A affects only the neuromuscular junctions of the injected muscle and has no effect upon ephaptic transmission.     

Metaplasticity of the human trigeminal blink reflex

Although synaptic plasticity in the human cerebral cortex is governed by metaplasticity, whether a similar mechanism operates at brainstem level is unknown. In this study in healthy humans we examined the effects and interactions induced by pairing supraorbital nerve high-frequency electrical stimulation (HFS) protocols on the R2 component of the trigeminal blink reflex [Mao, J.B. & Evinger, C (2001) J Neurosci., 21:RC151(1-4)]. Changes in the R2 component were tested by pairing three different priming stimulation protocols inducing long-term potentiation (LTP)-like or long-term depression (LTD)-like effects (LTP-HFS and LTD-HFS), or no change (CONTROL-HFS) with a subsequent test LTP-HFS. Additionally, to examine changes in the R2 component induced by nonspecific factors, two CONTROL-HFS sessions were paired. Priming LTP-, LTD- or CONTROL-HFS potentiated, inhibited or left unchanged the area of the R2 component. Regardless of the type of priming LTP-, LTD- or CONTROL-HFS, the test LTP-HFS induced negligible differences in the R2 component. When two CONTROL-HFS sessions were paired, the test CONTROL-HFS increased the latency and markedly reduced the duration and area of the R2 component. The analysis of the normalized data across the first three experimental sessions, corrected for the inhibitory effects found in the fourth experiment, showed that the test LTP-HFS potentiated the R2 component area of the trigeminal blink reflex only when preceded by a priming LTD-HFS. We propose that homosynaptic metaplasticity might operate in the brainstem circuitry of the blink reflex.