Blink Reflex Excitability Recovery Research Articles

Blink reflex excitability in patients with Hemifacial spasm exhibiting different abnormal discharge patterns: from early isolated discharges to later grouped bursts or tonic spasms.

We studied blink reflex (BR) and BR excitability recovery (BRER) in patients with hemifacial spasm (HFS) exhibiting different abnormal discharge patterns. We hypothesized that patients with groups of clonic or tonic burst activities appear later in the disease course and may have more excitability of the BR circuit at the brainstem compared to patients with isolated twitchings, which occur earlier. We included 124 patients with botulinum toxin-naive HFS (mean age 50.6 ± 13.3years) and 40 healthy subjects. We performed surface polymyography on facial muscles in patients and classified them according to the abnormal discharge pattern: isolated discharges, grouped bursts forming random sequences, tonic spasms, and a combination of these activities. Then, we recorded BR and BRER at 200, 600, and 1000ms interstimulus intervals. We compared disease duration, R1 and R2 latencies, R2 area-under-the-curve (AUC), and BRER% (i) between healthy subjects and patients and (ii) among groups of patients with different abnormal discharge patterns. There were isolated discharges in 28 patients, grouped bursts forming random sequences in 42, and continuous muscle activity with tonic spasms in one. The remaining patients had combinations. Mean R1 and R2 latencies were significantly longer, and mean R2 AUC was significantly higher on the symptomatic side of patients compared to healthy subjects. The mean BRER was enhanced on both sides in patients than in healthy subjects (p < 0.001). However, it was similar among patient groups with different abnormal discharge patterns (p > 0.05). The mean disease duration in patients with isolated discharges was shorter (3.3 ± 2.0years) than those with grouped bursts or tonic spasms (p = 0.002; Kruskal-Wallis test). Our study observed that excitability at the brainstem was similar in HFS patients with different abnormal discharge patterns, suggesting that the difference in discharge patterns in HFS may be due to a reason other than the difference in BR excitability.

In the spotlight: How the brainstem modulates information flow

ObjectiveThe blink reflex (BR) to supraorbital nerve (SON) stimulation is reduced by either a low-intensity prepulse stimulus to digital nerves (prepulse inhibition, PPI) or a conditioning SON stimulus (SON-1) of the same intensity as the test (SON-2) stimulus (paired-pulse paradigm). We studied how PPI affects BR excitability recovery (BRER) to paired SON stimulation. MethodsElectrical prepulses were applied to the index finger 100 ms before SON-1, which was followed by SON-2 at interstimulus intervals (ISI) of 100, 300, or 500 ms. ResultsBRs to SON-1 showed PPI proportional to prepulse intensity, but this did not affect BRER at any ISI. PPI was observed on the BR to SON-2 only when additional prepulses were applied 100 ms before SON-2, regardless of the size of BRs to SON-1. ConclusionsIn BR paired-pulse paradigms, the size of the response to SON-2 is not determined by the size of the response to SON-1. PPI does not leave any trace of inhibitory activity after it is enacted. SignificanceOur data demonstrate that BR response size to SON-2 depends on SON-1 stimulus intensity and not SON-1 response size, an observation that calls for further physiological studies and cautions against unanimous clinical applicability of BRER curves.

Spontaneous, Voluntary, and Reflex Blinking in Clinical Practice.

Blinking is one of the motor acts performed more frequently by healthy human subjects. It involves the reciprocal action of at least two muscles: the orbicularis oculi shows a brief phasic activation while the levator palpebrae shows transient inhibition. In clinical practice, noninvasive recording of the orbicularis oculi activity is sufficient to obtain useful information for electrodiagnostic testing. Blinking can be spontaneous, voluntary, or reflex. Although the analysis of spontaneous blinks can already furnish interesting data, most studies are based on reflex blinking. This article is a review of some of the alterations that can be observed in blinking, focusing in four patterns of abnormality that can be distinguished in the blink reflex: (1) afferent versus efferent, which allows characterization of trigeminal or facial lesions; (2) peripheral versus central, which distinguishes alterations in nerve conduction from those involving synaptic delay; (3) upper versus lower brainstem lesions, which indicates the lesions involving specific circuits for trigeminal and somatosensory blink reflexes; and (4) asymmetric abnormal excitability pattern, which shows a unilateral alteration in the descending control of excitability in brainstem circuits. The blink reflex excitability recovery curve to paired stimuli may provide information about other modulatory inputs to trigemino-facial circuits, such as those proposed for the connection between basal ganglia and trigeminal neurons. Finally, prepulse inhibition of blink reflex reflects the motor surrogate of subcortical gating on sensory volleys, which is still another window by which electrodiagnosis can document motor control mechanisms and their abnormalities in neurologic diseases.

Jendrassik maneuver effect on spinal and brainstem reflexes.

The effect of Jendrassik Maneuver (JM) has been extensively studied on monosynaptic reflexes in numerous muscles below the level at which the maneuver was performed. Here we hypothesize that the effect of JM could be observed also on other reflexes, indicating a widespread influence of performing a motor act such as the JM. We examined polysynaptic reflexes caudal (i.e., the withdrawal reflex of the lower extremities) and rostral (i.e., the blink reflex to supraorbital nerve stimulation) to the level of JM contraction. We have assessed soleus tendon (T) reflex; withdrawal reflex in tibialis anterior and soleus muscle; blink reflex (BR), blink reflex excitability recovery curve (BR-ER) and prepulse inhibition of the blink reflex. Our results showed that (1) T-reflex amplitude increased during JM and decreased just after and 15min after JM; (2) no change in the withdrawal reflex; (3) R2 area of BR reduced significantly just after or 15min after JM; (4) Prepulse inhibition in BR reduced significantly during JM; (5) no change in BR-ER. Our results indicate that JM leads to generalized effects on neural excitability at both caudal and rostral levels. Furthermore, JM has a selective effect on excitability of reflex circuitries.

Adult-Onset Gilles de la Tourette Syndrome: Psychogenic or Organic? The Challenge of Abnormal Neurophysiological Findings

Gilles de la Tourette syndrome (GTS) is characterized by multiple motor and vocal tics. Adult-onset cases are rare and may be due to “reactivation” of childhood tics, or secondary to psychiatric or genetic diseases, or due to central nervous system lesions of different etiologies. Late-onset psychogenic motor/vocal tics resembling GTS have been described. Neurophysiology may serve to differentiate organic from functional GTS. Altered blink reflex pre-pulse inhibition (BR-PPI), blink reflex excitability recovery (BR-ERC), and short-interval intracortical inhibition (SICI) have been described in GTS. We report a 48-years-old male, who developed numerous motor/vocal tics 2 months after sustaining non-commotional craniofacial trauma in a car accident. Both his father and brother had died earlier in car crashes. He presented with blepharospasm-like forced lid closure, forceful lip pursing, noisy suction movements, and deep moaning sounds, occurring in variable combinations, without warning symptoms or internal “urge.” Tics showed low distractibility and these increased with attention. Standard magnetic resonance imaging, electroencephalography, and evoked potentials were unremarkable. Neuropsychology diagnosed moderately impaired intellect, attention, and executive functions. Psychiatric assessment revealed somatization disorder and generalized anxiety. BR-PPI was unremarkable, while BR-ERC was enhanced, even showing facilitation at short intervals. SICI was markedly reduced at 1 and 3 ms and intracortical facilitation (ICF) was enhanced at 10 ms. The patient fulfilled Fahn and Williams' diagnostic criteria for a psychogenic movement disorder. Neurophysiology, however, documented hyperexcitability of motor cortex and brainstem. We suggest that—similar to what has been reported in psychogenic dystonia—a pre-existing predisposition may have led to the functional hyperkinetic disorder in response to severe psychic stress.

Brainstem reflex excitability after high-frequency repetitive transcranial magnetic stimulation in healthy and spinal cord injury subjects

BackgroundThe excitability of brainstem interneuronal circuits is partly under control from descending inputs. Since high frequency repetitive transcranial magnetic stimulation (rTMS) modulates cortical output, we hypothesized that it will also modulate brainstem functions. Such modulation may be different in healthy subjects than in subjects with spinal cord injury (SCI), submitted to an altered integration of body afferent inputs. MethodsIn this randomized, double-blind, sham-controlled trial, we recruited 22 subjects with SCI assigned to either real (n = 11) or sham (n = 11) rTMS and nine healthy subjects, who served as control group, receiving both real (at 20 Hz, with double cone coil over vertex) and sham rTMS separated by at least one week. We recorded the blink reflex (BR) to supraorbital nerve (SON) electrical stimulation and its modification by another conditioning SON, to study the BR excitability recovery (BRER), or a prepulse electrical stimulus to the right index finger, to study the BR inhibition by prepulse (BRIP). Subjects were examined immediately before and after either sham or real rTMS. ResultsReal but not sham rTMS significantly reduced the area of the BR R2 response in both SCI and healthy subjects. There were no changes in BRER and BRIP. ConclusionrTMS over the vertex modulates brainstem reflexes with no significant differences between SCI and healthy subjects.

Role of mesial temporal lobe structures in sensory processing in humans: a prepulse modulation study in temporal lobe epilepsy.

Prepulse modulation (PPM) is an electrophysiological method which enables to assess sensory processing in vivo. Reflex responses may be facilitated or inhibited (prepulse inhibition, PPI) after a weak stimulus. Theoretically, in animal studies, the generator of PPI involves pedunculopontine nucleus which is modulated by various structures, including amygdala. We aimed to investigate whether or not there was a role of limbic structures in the generation of PPM in humans. For this purpose, we studied PPM of the blink reflex (BR) in 10 patients with mesial temporal lobe epilepsy (MTLE group) and in nine patients who had previously undergone amygdala resection for medically resistant MTLE (surgery group). A control group including 19 healthy volunteers was formed. Blink reflex, BR-PPM and BR excitability recovery were recorded in all participants. Two components of BR, first early ipsilateral component (R1) and second late bilateral components (R2 and R2c) were identified. All BR parameters after single stimulation were normal in all groups. Compared to healthy subjects, R2-PPI was more pronounced in the surgery group whereas there was a R2-PPI deficit in the MTLE group. R2-PPI deficit in the MTLE group was more prominent on the lesion side. Ipsilesional R1 facilitation was more evident at ISI of 100ms in both MTLE and surgery groups compared to healthy subjects. BR excitability recovery was not different between groups. MTLE in humans leads to a PPI deficit. Interestingly, removal of amygdala in humans with MTLE probably provides more efficient functioning of PPI network. Amygdala and hippocampus play roles in the human R2-PPI circuit. Modulation of R1 facilitation is unilateral whereas the modulation of R2-PPI is bilateral, though asymmetric.

Blink reflex and prepulse inhibition in fibromyalgia

Patients with fibromyalgia syndrome (FMS) show increased sensory processing of nociceptive and non-nociceptive stimuli. They perceive somatosensory stimuli differently and show altered cortical sensory representation maps following peripheral stimulation. Altered sensory gating may play a causal role. Blink 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. Unconditioned blink reflex characteristics (R1 latency and amplitude, R2 and R2c latency and area-under-the-curve) did not differ significantly between patients and controls. However, 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, but patients showed significantly less R2 area suppression than controls (patients: to 80.0 ± 28.9%, controls: to 47.8 ± 21.7%). The general pattern of corresponding changes in R2c was similar. Blink 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. Reduced blink reflex prepulse inhibition concurs with altered sensory gating in patients with FMS.

Transcranial Direct Current Stimulation (tDCS) Enhances the Excitability of Trigemino-Facial Reflex Circuits.

Transcranial direct current stimulation (tDCS) causes a tiny burning sensation through activation of local cutaneous trigeminal afferents. Trigeminal sensory inputs from tDCS may generate excitability changes in the trigemino-facial reflex circuits. Sixteen healthy volunteers were submitted to 20 minutes tDCS sessions with two types of electrode-montage conditions: 1. Real vs Sham 'bi-hemispheric' tDCS (cathode/anode: C4/C3), for blinded assessment of effects, and 2. 'uni-hemispheric' tDCS (cathode/anode: Fp3/C3), for assessment of laterality of the effects. Supraorbital nerve stimuli were used to obtain blink reflexes before, during (10 minutes from onset) and after (30 minutes from onset) the tDCS session. Outcome measures were R2 habituation (R2H) to repeated stimuli, the blink reflex excitability recovery (BRER) to paired stimuli and the blink reflex inhibition by a prepulse (BRIP). Real but not sham bi-hemispheric tDCS caused a significant decrease of R2H and leftward shift of BRER curve (p < 0.05 for all measures). The effects of uni-hemispheric tDCS on BRER and BRIP were larger on ipsilateral than on contralateral blink reflexes (p < 0.05). Excitability changes were still present 10 minutes after the end of stimulation in a lesser extent. This study shows that 20 minute tDCS enhances the excitability of trigemino-facial reflex circuits. The finding of larger ipsilateral than contralateral effects suggests that sensitization through cutaneous trigeminal afferents adds on other possible mechanisms such as activation of cortico-nuclear or cortico-reticular connections.

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.

Blink reflex prepulse inhibition and excitability recovery: Influence of age and sex

ObjectiveAge and sex affect various reflexes in healthy humans. Their respective influence on prepulse inhibition (PPI) of the trigeminofacial blink reflex (BR) and BR excitability recovery has not as yet been investigated in detail. MethodsWe studied the trigeminofacial BR bilaterally in 62 healthy volunteers (31 males, age 41.0±13.2years, mean±SD, 31 females, 39.2±11.7years) following right supraorbital nerve stimulation. Single sweeps were recorded either alone (n=8) or conditioned by a prepulse applied 100ms earlier to the dominant index finger though ring electrodes (n=8). Latency and amplitude of the ipsilateral R1 component, as well as latency and area-under-the-curve of the ipsilateral R2 and contralateral R2c components were measured in single traces and then averaged per subject. BR excitability recovery was established bilaterally following right supraorbital nerve stimulation with paired pulses. Six responses were averaged on-line per interstimulus interval (ISI 160, 300, and 500ms). ResultsUnconditioned BR did not differ significantly between males and females, but R2 and R2c latencies increased with age. Prepulse stimulation caused significant facilitation of R1 (latency and amplitude), and inhibition of R2 and R2c (latency and area), irrespective of age. PPI of R2 and R2c area was significantly more pronounced in men. BR excitability recovery was significantly influenced by age, but not by sex. Multiple regression showed inverse correlation of age with conditioned R2 and R2c area at ISI 300ms and 500ms (P<0.01 each), indicating reduced excitability recovery. No parameter showed significant interaction of age×sex. ConclusionThese data indicate less pronounced PPI of the trigeminofacial BR in females, concurring with previous reports of sex differences in protective reflexes, but also suggesting less rigorous filtering of information flow to the brain in females. Reduced BR excitability to paired-pulse stimulation may counteract age-related disinhibition of brainstem interneuronal circuitry. SignificanceThe present findings allow new insight into human brainstem physiology.

Narcolepsy–cataplexy: deficient prepulse inhibition of blink reflex suggests pedunculopontine involvement

Hypocretin (orexin) deficiency plays a major role in the pathophysiology of narcolepsy-cataplexy. In animal models, hypocretinergic projections to the pedunculopontine nucleus are directly involved in muscle tone regulation mediating muscle atonia - a hallmark of cataplexy. We hypothesized that pedunculopontine nucleus function, tested with prepulse inhibition of the blink reflex, is altered in human narcolepsy-cataplexy. Twenty patients with narcolepsy-cataplexy and 20 healthy controls underwent a neurophysiological study of pedunculopontine nucleus function. Blink reflex, prepulse inhibition of the blink reflex and blink reflex excitability recovery were measured. Blink reflex characteristics (R1 latency and amplitude, and R2 and R2c latency and area under the curve) did not differ between patients and controls (P > 0.05). Prepulse stimulation significantly increased R2 and R2c latencies and reduced R2 and R2c areas in patients and controls. However, the R2 and R2c area suppression was significantly less in patients than in controls (to 69.8 ± 14.4 and 74.9 ± 12.6%, respectively, versus 34.5 ± 28.6 and 43.3 ± 29.5%, respectively; each P < 0.001). Blink reflex excitability recovery, as measured by paired-pulse stimulation, which is not mediated via the pedunculopontine nucleus, did not differ between patients and controls (P > 0.05). Our data showed that prepulse inhibition is reduced in narcolepsy-cataplexy, whereas unconditioned blink reflex and its excitability recovery are normal. Because the pedunculopontine nucleus is important for prepulse inhibition, these results suggest its functional involvement in narcolepsy-cataplexy.

The effect of age on blink reflex excitability recovery

Background: The effect of age on blink reflex excitability recovery has not as yet been investigated.

Abnormalities of prepulse inhibition do not depend on blink reflex excitability: a study in Parkinson's disease and Huntington's disease

Objective Prepulse inhibition of the blink reflex is a robust phenomenon with an interesting physiology and a large potential for clinical applicability. In the study presented here we investigated whether the blink reflex inhibition by a prepulse (BRIP) is influenced by the blink reflex excitability recovery (BRER). Methods The study was undertaken in 20 patients with Parkinson's disease (PD), 20 patients with Huntington's disease (HD) and 20 healthy volunteers. BRER was determined by measuring the size of the response to a test supraorbital nerve stimulus as a percentage of the response to a conditioning stimulus at inter-stimuli intervals of 100–1000 ms. BRIP was determined as the percentage reduction induced in the response to a supraorbital nerve stimulus by either a low intensity auditory click or a weak third finger somatosensory stimulus, applied with a leading interval of 50–110 ms. Results There was a negative correlation between the percentage BRER and the percentage BRIP (Pearson's correlation coefficient of −0.37). BRER was enhanced in 14 PD patients (70%) and 6 HD patients (30%), while it was depressed in 10 HD patients (50%). BRIP was significantly reduced in 15 PD patients (75%) and 16 HD patients (80%). No significant correlation was found between abnormally enhanced BRER and abnormally reduced BRIP in all patients as a group ( χ 2=2.4; P=0.11). A weak correlation was found in PD patients ( P=0.019), and no correlation was observed in HD patients ( P=0.8). Conclusions Our results indicate that an abnormally reduced BRIP was not always accompanied by an abnormally enhanced BRER in patients with HD. The two tests likely assess specific and distinct brainstem functions, and provide different types of information. While BRIP may be the result of a widespread integrative processing of sensory stimuli, BRER likely reflects the excitability of a chain of brainstem inter-neurons. Significance BRER and BRIP provide independent information on the state of functionally separate circuits that converge on trigemino-facial brainstem inter-neurons.

Blink Reflex Excitability Recovery Curves in Patients with Dysfunctions after Facial Nerve Palsy

The blink reflex excitability recovery curves were studied in 12 patients with postparalytic facial dysfunctions (PPFD) and 12 healthy control subjects. The inhibitory effects of the conditioning stimuli on the ipsilateral R2 and contralateral R2 responses observed in control subjects were significantly less in patients with PPFD. The enhanced recovery of the R2 responses was similar on the affected side and unaffected side in the patients. These results indicate that patients with PPFD have an increased excitability of central interneurons which mediate the R2 pathway. It is suggested that not only changes in the peripheral facial nerve but also changes in the central nervous system may contribute to the onset of PPFD.

The `geste antagonistique' induces transient modulation of the blink reflex in human patients with blepharospasm

The mechanism of action of the `geste antagonistique', or sensory trick, used by patients with dystonic blepharospasm (BSP) to transiently diminish their symptoms is presently unknown. In this paper we examined the effects induced by a sensory trick consisting of finger contact with the face on the electrically induced blink reflex and the blink reflex excitability recovery curve to paired stimuli. The results were compared with those obtained in a group of six healthy volunteers who mimicked the manoeuvre used by the patients as a sensory trick. In all subjects, the area of R2 was significantly reduced, and the amplitude of R1 was significantly enhanced, during a mean of 10 min after the onset of finger-face contact in comparison to rest. However, there were no changes in the blink reflex excitability recovery curve. The contact-induced effect on the magnitude of the R2 component of the blink reflex is probably caused by sensory gating on trigeminal afferents. Such a reduction in the gain of trigemino-facial reflexes may partly underly the transient benefit experienced by patients with BSP with the use of sensory tricks.

Distinctive abnormalities of facial reflexes in patients with progressive supranuclear palsy.

Spontaneous and voluntary eyelid motility is often abnormal in patients with progressive supranuclear palsy. In contrast, their eyelid reflex responses are relatively preserved, and only those generated by an acoustic startle have been found absent or severely reduced. We hypothesized that, because of their relevant brainstem pathology, patients with progressive supranuclear palsy might have other brainstem reflex abnormalities which, on detection, could help with their neurophysiological characterization. In this study, we examined facial reflex responses in 14 patients with progressive supranuclear palsy, 12 patients with multisystem atrophy, 10 patients with Parkinson's disease, six patients with corticobasal ganglionic degeneration, 11 patients with various non-parkinsonian neurological illnesses and 10 normal subjects. EMG activity was simultaneously recorded from the orbicularis oculi and mentalis muscles following electrical stimulation of the median nerve at the wrist. Mentalis responses were obtained in two normal subjects and in all patients except one with Parkinson's disease, one with progressive supranuclear palsy and one with corticobasal ganglionic degeneration; there were no differences between groups of subjects regarding latency or peak amplitude. Orbicularis oculi responses were always present in control subjects and patients who exhibited mentalis responses, with the significant exception of patients with progressive supranuclear palsy, in whom only the response of mentalis was obtained. Blink-reflex responses to supraorbital nerve electrical stimuli were present at a normal latency and amplitude in all patients. An abnormally enhanced blink-reflex excitability recovery curve to paired stimuli was found in a similar percentage of patients with progressive supranuclear palsy, multisystem atrophy and Parkinson's disease, but in only two patients with corticobasal ganglionic degeneration. Patients with progressive supranuclear palsy have a functional involvement of circuits mediating orbicularis oculi responses to median nerve electrical stimuli, that is a distinctive feature with respect to other parkinsonian syndromes.

Neurophysiological investigations in patients with head tremor.

We studied 30 patients whose primary complaint was head tremor in an attempt to characterize neurophysiological aspects of their abnormal movement. Based on family medical history and physical examination, 23 patients had definite or probable essential tremor (essential head tremor, EHT). The remaining seven had mild dystonic signs accompanying their head tremor (head tremor plus dystonic signs, HT + DS). We recorded head movement and the electromyographic (EMG) activity of the sternomastoid and splenius capitis muscles, determined the spontaneous blinking rate, and measured the excitability recovery curve of the blink reflex and of the masseteric inhibitory reflex. All patients had tremor bursts at a frequency ranging between 3 and 9 Hz in at least one of the muscles examined. The predominant pattern seen when patients were sitting relaxed and facing forward was that of synchronized EMG bursts in both splenius capitis muscles. Maintenance of extreme head postures demonstrated two types of additional abnormalities: type 1 (enhancement of tremor), which was observed in 11 patients (47.8%) with EHT and in two (28.5%) with HT + DS; and type 2 (activation of neck muscles not required for maintenance of the posture), which was observed in two patients (8.7%) with EHT and in five (71.5%) with HT + DS (chi 2 = 26.4; p < 0.001). Mean blinking rate per minute was 24.9 +/- 14.6 in patients with EHT and 42.3 +/- 10.5 in patients with HT + DS (paired t test, p = 0.001). The blink reflex and masseteric inhibitory reflex excitability recovery curves showed an abnormal interneuronal excitability enhancement in seven (30.4%) of the 23 patients with EHT and in two (28.5%) of the seven with HT + DS (chi 2 = 3.1; p > 0.05). Abnormal patterns of EMG activity of the neck muscles correlated well with the presence of mild dystonic signs. However, the analysis of brainstem interneuronal excitability did not enable recognition of those patients with head tremor who could potentially develop cervical dystonia. The enhancement of brainstem interneuronal excitability found in approximately 30% of patients with head tremor could be related to plastic changes triggered by increased activity of the cranial muscles.

Blink reflex excitability recovery curves in patients with spasmodic dysphonia.

We studied 12 patients with spasmodic dysphonia (SD) and 12 healthy control subjects. The patients, who had no symptomatic involvement of the eyes, were evaluated for increased excitability of blink reflexes, which is characteristic of blepharospasm and generalized dystonia. We measured symptom severity from sound spectrograms of five sentences, including sentence production time, number of pitch phonatory breaks, and percentage of aperiodic phonation. We evoked blink reflexes by electrical and mechanical stimulation, and assessed excitability by obtaining excitability recovery curves and responses to trains of stimuli. Patients and controls differed from each other in test R2 amplitude attenuation across all intervals from 150 to 1,000 msec to electrical and mechanical stimulation. Our results indicate that patients with SD have increased excitability of blink reflexes, which suggests that the dystonia involves not only the larynx but also other anatomical structures.