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.     

Neurophysiological evaluation of trigeminal and facial nerves in patients with chronic inflammatory demyelinating polyneuropathy

Cranial neuropathy is clinically uncommon in patients with chronic inflammatory demyelinating polyneuropathy (CIDP), but there is little information on the neurophysiological examination of cranial nerve involvement. To determine the incidence of trigeminal and facial nerve involvement in patients with CIDP, the direct response of the orbicularis oculi muscle to percutaneous electric stimulation of the facial nerve and the blink reflex (induced by stimulation of the supraorbital nerve) were examined in 20 CIDP patients. The latency of the direct response was increased in 12 patients (60%) and an abnormal blink reflex was observed in 17 patients (85%). There was no correlation between electrophysiological findings and the latencies of the direct and R1 responses and disease duration or clinical grade in CIDP patients. Nevertheless, the prevalence of subclinical trigeminal and facial neuropathy is extremely high in patients with CIDP when examined by neurophysiological tests.     

Comparative neurophysiological study for the diagnosis of mild polyneuropathy in patients with diabetes mellitus and glucose intolerance

This article evaluates diagnostic sensitivity of minimal F-wave latency, sural/radial amplitude ratio (SRAR), dorsal sural/radial amplitude ratio (DSRAR), sympathetic skin response (SSR), and R-R interval variability (RRIV) for detecting early polyneuropathy in patients with glucose intolerance and diabetic patients. F-wave latencies were more prolonged in diabetic patients with normal and abnormal nerve conduction studies than control subjects (p < .001). SRAR was lower, SSR latency was more prolonged, and RRIV was lower in diabetic patients with abnormal nerve conduction studies than healty controls (p < .001). SSR latency was more prolonged and RRIV was lower in diabetic patients with normal nerve conduction studies than healty controls (p < .01, p < .05, respectively). DSRAR was lower in diabetic patients with normal and abnormal nerve conduction studies than control subjects (p < .001). DSRAR was also lower in patients with glucose intolerance than control subjects (p < .01). DSRAR was the most sensitive and specific test in either of diabetic patients with normal nerve conduction studies (sensitivity 66%, specificity 90%) and diabetic patients with abnormal nerve conduction studies (sensitivity 100%, specificity 90%). DSRAR is the most reliable method for detection of early nerve pathology. Patients with glucose intolerance might have subclinical neuropathy that can be demonstrated with DSRAR analysis.     

The role of blink reflex R1 latency as an electrophysiological marker in diabetic distal symmetrical polyneuropathy

ObjectiveStudies showed a relatively prolonged blink R1 latency in patients with diabetic distal symmetrical polyneuropathy (DSPN) compared to that without DSPN. We tested the hypothesis that blink R1 latency would provide a diagnostic alternative to nerve conduction studies (NCS) in DSPN and act as a marker of the severity of NCS abnormalities in DSPN.MethodA total of 109 patients with type 2 diabetes underwent blink reflex studies and NCS. We used the composite amplitude scores of nerve conductions (CAS), which consisted of motor (tibial, peroneal and ulnar) and sensory (sural and ulnar) amplitudes for estimating the severity of NCS.ResultsPatients with DSPN had longer blink R1, R2, and contralateral R2 latencies (P < 0.0001, P = 0.001, and P = 0.031, respectively) and higher CAS (P < 0.0001). Area under curve on receiver operating characteristic curve analysis in diagnosing occurrence of DSPN in blink R1 latency was 0.772 (P < 0.0001). Multiple linear regression analysis showed that blink R1 latency was independently associated with CAS.ConclusionBlink R1 latency may be valuable in auxiliary diagnosis and in determining the severity of NCS abnormalities in DSPN.SignificanceBlink R1 latency can be added as a supplemental marker of severity of NCS in DSPN, especially if the patient’s sural amplitudes has a floor effect.     

Prognostic significance of the electrically elicited blink reflex in neonates

The electrically elicited blink reflex was examined in ten normal neonates, 11 postasphyxial neonates, and 3 congenital hydrocephalus cases. The blink reflex was elicited in all cases. In normal neonates, the latencies and amplitudes were 10.9 +/- 0.7 msec and 159 +/- 62 microV at R1, 34.3 +/- 1.4 msec and 123 +/- 30 microV at R2, and 40.7 +/- 2.3 msec and 84 +/- 25 microV at R'2 respectively. Ischemic-hypoxic brain damage during the neonatal period mainly influenced the late components of the blink reflex. The blink reflex of the postasphyxial neonates showed significantly prolonged latencies of R2 and R'2. The amplitudes were increased in cases with a fair prognosis and decreased in cases with a poor prognosis. A case of congenital hydrocephalus with mental retardation also showed the prolonged latencies of R2 and R'2 in neonatal period. The blink reflex in neonates appears to be useful in predicting the outcome in cases of neonatal asphyxia and congenital hydrocephalus.     

Effects of Monotherapy and Polytherapy on the Blink Reflex in Epileptic Patients

We performed the blink reflex (BR) in 20 normal volunteers, 13 epileptic patients receiving antiepileptic drug (AED) monotherapy, and 13 epileptic patients receiving AED polytherapy. Comparison of R1, ipsilateral and contralateral R2 and VIIth nerve latencies in the three groups showed no statistically significant differences in R1 and VIIth nerve latencies among the three groups. There were statistically significant differences between the polytherapy group and the monotherapy and control groups in comparisons of ipsilateral and contralateral R2. There were no significant differences between the monotherapy group and the control group for ipsilateral and contralateral R2. We hypothesized that AED polytherapy might interfere with synaptic transmission in the polysynaptic pathway of the blink reflex, prolonging the latency of R2. These results provide further evidence of the pathophysiologic effects associated with polytherapy in epileptic patients.     

Mandibular nerve involvement in diabetic polyneuropathy and chronic inflammatory demyelinating polyneuropathy

Sensory complaints in the area of the mandible and mouth often escape notice or remain undiagnosed. Using electromyographic recording of the trigeminal reflexes and motor responses, we sought trigeminal dysfunction in 50 patients with peripheral neuropathy, and tried to gain pathophysiological information on the mechanisms provoking trigeminal damage. Trigeminal reflex recordings (early and late blink reflex after supraorbital stimulation, early and late masseter inhibitory reflex after mental stimulation, and jaw jerk) disclosed abnormalities caused by sensory trigeminal neuropathy in 8 out of 15 patients with chronic inflammatory demyelinating polyneuropathy (CIDP), 13 out of 23 patients with severe diabetic polyneuropathy, and in none of 12 patients with mild diabetic polyneuropathy. Six patients had abnormal motor responses in facial or masseter muscles. The response affected most frequently was the masseter early inhibitory reflex (also called first silent period, SP1) after mental nerve stimulation, its latency being strongly delayed. We found these long delays not only in patients with CIDP, but also in diabetic patients with severe polyneuropathy. We conclude that peripheral polyneuropathies often cause subclinical damage to the trigeminal nerve, especially to its mandibular branch. We believe that the nerve fibers running along the alveolar–mandibular pathway are more exposed to damage because of their cramped anatomical route in the mandibular canal and below the internal pterygoid muscle and fascia. © 1998 John Wiley & Sons, Inc. Muscle Nerve 21: 1673–1679, 1998     

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.     

Abnormal vasoreaction to arousal stimuli--an early sign of diabetic sympathetic neuropathy demonstrated by laser Doppler flowmetry.

Early diagnosis of diabetic autonomic neuropathy contributes to the prevention of serious complications and improves the prognosis of patients with diabetes. Common tests of peripheral autonomic function are the quantitative sudomotor axon reflex test or the sympathetic skin response (SSR). Quantitative sudomotor axon reflex test is quantifiable but technically demanding. Sympathetic skin response cannot be quantified easily. To study whether measurement of skin vasomotion is suited to assess early sympathetic peripheral neuropathy, we monitored skin blood flow at the index finger pulp using laser Doppler flowmetry before and after electrical stimulation. We assured that the stimulus was sufficient to elicit an efferent sympathetic response by monitoring palmar SSR ipsilateral to the flow measurement. In 21 diabetic patients with at least stage one polyneuropathy and 21 age-matched controls, SSR was recorded from one palm and sole following electrical stimulation at the contralateral wrist. Sympathetic skin response was present at the palms in all patients and controls and absent at the sole of two patients only. Eight patients (38.9%) had abnormal SSR, with absent plantar responses in two patients, prolonged plantar latencies in six patients, and prolonged volar SSR latencies in two patients. Skin blood flow responses were more often abnormal (46.1%) than SSR (P < 0.05), responses were delayed in two patients and absent in another 8 patients. Skin blood flow retest reliability was high with a repeatability coefficient of 10.64% in controls and 12.34 % in patients. Skin blood flow monitoring after sympathetic stimulation provides a reproducible parameter of sympathetic vasomotor control and complements the diagnostic value of SSR testing.     

Blink reflex alterations in recently diagnosed diabetic patients

Objective. The aim of the present study was to determine the frequency of blink reflex alterations and to examine the influence of hyperglycemia in inducing the alterations in recently diagnosed Type 2 diabetes mellitus patients.Methods. A cross-sectional study was carried out on patients having asymptomatic diabetes with a period of evolution under 10 years. In all 47 patients (26 women and 21 men), serum glycemia levels were determined and the latency onset of the blink reflex components were measured.Results. The average patient age was 44.5±11.0 (mean ± SD) years with a diabetes evolution period of 4.3±2.9 (mean ± SD) years. After a fasting serum glucose test, the diabetic patients were catalogued as normoglycemic (⩽126 mg/dl) or as hyperglycemic (>26 mg/dl) and subjected to a blink reflex test. The results obtained from the diabetic patients were compared with those from a non-diabetic control group. 14.8–31.9% of the diabetic patients showed alterations in blink reflex component latencies. The differences compared with the control group were significant (p<0.05).Conclusions. Diabetes, as is well-known, can affect the central and peripheral nervous system and there does not appear to be a link between glycemic levels and blink reflex components. However, blink reflex alterations were present even in diabetic patients with a relatively short period of disease evolution.     

Adductor T reflex abnormalities in patients with decreased patellar reflexes

The adductor reflex (AR) is a tendon reflex that has various features that differ from other tendon reflexes. This reflex was tested in different disorders presenting with diminished patellar reflexes such as diabetic lumbosacral radiculoplexus neuropathy (DLRPN), L2–L4 radiculopathy, and distal symmetric diabetic neuropathy (diabetic PNP). The AR and crossed‐AR (elicited by tapping the contralateral patellar tendon) were recorded using concentric needle electrodes. Additionally, the patellar T reflex (vm‐TR) and vastus medialis H reflex (vm‐HR) were recorded using surface electrodes. AR was recorded in only one out of eight patients with DLRPN, but it was recorded in 21 out of 22 patients with L2–L4 radiculopathy (95.5%). Of these reflexes, only AR showed prolonged latency in the L2–L4 radiculopathy group. The latencies of AR, vm‐TR, and vm‐HR were prolonged in patients with diabetic PNP. We conclude that AR can be useful in the differential diagnosis of some lower motor neuron disorders that present with patellar reflex disturbance. Muscle Nerve 40: 264–270, 2009     

Femoral nerve involvement in diabetics

Background and purpose:  In this study, the conduction of the femoral nerve has been evaluated in diabetic patients without clinical signs of femoral nerve involvement and in a group of healthy subjects.
Methods:  Forty-eight patients have been included in the study. Patients have been examined in terms of neuropathy and their neuropathy scores have been calculated. In addition to the nerve conduction studies have been performed. The findings of the diabetic patients have been compared with those of the 26 healthy volunteers.
Results:  There has been a statistically significant difference between diabetics and the healthy volunteers in the control group in terms of both femoral nerve motor latency and amplitude. The femoral latencies of patients have significantly been related to the total neuropathy score. A significant difference between diabetic patients without polyneuropathy and the controls was observed with respect to their femoral latencies.
Conclusion:  In our study, femoral nerve conduction abnormalities have been determined in diabetics who clinically did not have femoral nerve involvement. It has been observed that these abnormalities become more evident as the polyneuropathy of the patients becomes more serious. Our study has shown that femoral nerve conductions may increase the sensitivity of the diagnosis of polyneuropathy.     

Electrodiagnostic features of hereditary neuropathy with liability to pressure palsies

OBJECTIVE: Because diagnosis of hereditary neuropathy with liability to pressure palsies (HNPP) frequently is missed or delayed, we looked for electrodiagnostic features that raise suspicion of the disorder by making comparisons with two more common diseases that mimic it electrophysiologically: chronic inflammatory demyelinating polyneuropathy (CIDP) and diabetic polyneuropathy. METHODS: A retrospective review of the neuromuscular laboratory database was performed. RESULTS: Nine HNPP subjects, 22 with CIDP and 49 with diabetic polyneuropathy. Of all the HNPP nerves studied, abnormally slow sensory nerve conduction velocity (SNCV) was found in 93%, prolonged distal motor latencies (DML) in 78%, slow motor nerve conduction velocity in 31%, and prolonged F-wave latencies in 90%. Mean SNCV for HNPP was 85.6%+/-10.6% of the lower limit of normal and significantly slower than for CIDP (114.3%+/-20.1%; p<0.0001) or diabetes (108.1%+/-14.8%; p<0.0001). Excluding the carpal tunnel site from the analysis did not alter this observation: Mean DML were more prolonged in HNPP, even without median nerve data in the analysis (118.5%+/-31.0% of the upper limit of normal), than in CIDP (103.2%+/-31.6%; p<0.05) or diabetes (86.3%+/-18.3%; p<0.0001). Mean HNPP motor nerve conduction velocity was within normal limits. CONCLUSIONS: According to findings, hereditary neuropathy with liability to pressure palsies (HNPP) has a distinctive background polyneuropathy independent of superimposed entrapment neuropathy. It is characterized by diffuse sensory nerve conduction velocity (SNCV) slowing and prolongation of distal motor latencies with relatively infrequent and minor reduction of motor nerve conduction velocities. This indicates disproportionate distal conduction slowing in the disorder.     

Blink reflex abnormalities in Tourette syndrome.

OBJECTIVE: Tourette syndrome (TS) is a not uncommon disorder which represents the most complex manifestation of the spectrum of tic disorders, with onset during childhood or early adolescence. There are no definitive tests for diagnosis of TS. The objective of this study has been to demonstrate whether neurophysiological abnormalities of the blink reflex can be observed in patients affected with TS and correlate with the severity of TS. METHODS: We enrolled 17 patients with Tourette syndrome, diagnosed according to DSM IV Diagnostic Criteria, and 10 healthy volunteers. Tic severity was assessed using a self rating scale (Tourette Syndrome Symptom List, TSSL) and examiner ratings (Yale Global Tic Severity Scale (YGTSS), and Tourette-Syndrome Global Scale (TSGS)). 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. RESULTS: We observed a mean duration of R2 significantly longer in the patient group than in the control group (P<0.01, Student t test), without any statistically significant differences of R1 and R2 latencies and of R1 amplitude between the patient group and the control group. Correlations between changes in clinical rating scores and R2 duration were tested by simple linear regression analysis, which has not demonstrated a significant correlation between TSSL scores, clinical rating scores (measured by TSGS and YGTSS) and duration of R2. CONCLUSIONS: A pattern as to excitability of the blink reflex can be a frequent abnormality in TS patients, not correlated with its severity.     

Blink reflex measurement of effects of trichloroethylene exposure on the trigeminal nerve.

Trichloroethylene (TCE) exposure is known to have specific toxic effects on cranial nerves, the trigeminal nerve (V) in particular. The electrophysiological measurement of the blink reflex (BR) can quantify latency changes in the Vth and VIIth cranial nerve reflex arc. Prior study looked at the blink reflex measurement in a community group exposed to TCE in their drinking water. This study evaluated the use of the electrophysiologic blink reflex as an indicator of neurotoxic effects of TCE in occupationally exposed workers. The BR was tested in individual cases with documented histories of exposure to known chemical neurotoxins including TCE (n = 18). When compared with the nonexposed laboratory control values (n = 30), the subjects with a significant history of TCE exposure demonstrated the most prolonged latencies (greater than or equal to 3.0 SD above the nonexposed group mean) in the R1 component of the blink reflex measurement. The electrophysiological study of the blink reflex has application in assessing TCE exposure and in documenting the neurotoxic effects of that exposure on trigeminal nerve functions in humans.     

COMPARATIVE NEUROPHYSIOLOGICAL STUDY FOR THE DIAGNOSIS OF MILD POLYNEUROPATHY IN PATIENTS WITH DIABETES MELLITUS AND GLUCOSE INTOLERANCE

This article evaluates diagnostic sensitivity of minimal F-wave latency, sural/radial amplitude ratio (SRAR), dorsal sural/radial amplitude ratio (DSRAR), sympathetic skin response (SSR), and R-R interval variability (RRIV) for detecting early polyneuropathy in patients with glucose intolerance and diabetic patients. F-wave latencies were more prolonged in diabetic patients with normal and abnormal nerve conduction studies than control subjects (p < .001). SRAR was lower, SSR latency was more prolonged, and RRIV was lower in diabetic patients with abnormal nerve conduction studies than healty controls (p < .001). SSR latency was more prolonged and RRIV was lower in diabetic patients with normal nerve conduction studies than healty controls (p < .01, p < .05, respectively). DSRAR was lower in diabetic patients with normal and abnormal nerve conduction studies than control subjects (p < .001). DSRAR was also lower in patients with glucose intolerance than control subjects (p < .01). DSRAR was the most sensitive and specific test in either of diabetic patients with normal nerve conduction studies (sensitivity 66%, specificity 90%) and diabetic patients with abnormal nerve conduction studies (sensitivity 100%, specificity 90%). DSRAR is the most reliable method for detection of early nerve pathology. Patients with glucose intolerance might have subclinical neuropathy that can be demonstrated with DSRAR analysis.     

Tendon-reflex testing in chronic demyelinating polyneuropathy

We studied the tendon reflex (T-reflex) in 26 patients with acquired chronic demyelinating polyneuropathy (CDN), including 22 with chronic inflammatory demyelinating polyneuropathy (ClDP). In 7 patients reflexes were brisk or normal on clinical testing. The height adjusted T-reflex was abnormal in 25 (96%) cases, including 6 of 7 patients with brisk or normal reflexes on clinical testing. Mean latency (P < 0.01) and duration (P < 0.05) of the ankle and patellar tendon reflexes were significantly prolonged in the ClDP patients when compared to the controls. Mean latency in the ClDP patients was 152% of normal means. In 7 CIDP patients, the T-reflex latencies were prolonged beyond 150% of normal means. Thus, the T-reflex test is abnormal in a majority of patients with CDN, even in the presence of well-preserved clinical reflexes, and the T-reflex latency is a useful indicator of the presence of a demyelinating peripheral neuropathy in some patients. © 1994 John Wiley & Sons, Inc.     

Blink reflex role in algorithmic genetic testing of inherited polyneuropathies

Introduction: In severely affected inherited polyneuropathy patients, primary demyelination can be difficult to determine by routine extremity limb nerve conduction studies (NCS). Blink reflexes may help classify severe polyneuropathies as either axonal or demyelinating. However, blink reflex studies have not been studied systematically in any genetically confirmed cohort. Methods: Patients with a genetic diagnosis who had undergone blink reflex testing and extremity NCS were identified retrospectively. Blink reflex R1 latency, extremity NCS, and severity were compared. Results: We identified 26 demyelinating and 23 axonal, genetically confirmed cases, including 20 with PMP22 duplications. In 12 (25%), the ulnar CMAP amplitude was ≤0.5 mV making electrophysiological classification difficult. However, the R1‐latency cutoff of >13 ms (demyelinating) robustly classified all patients regardless of severity. Conclusions: We show that blink reflex studies are reliable for identification of inherited demyelinating polyneuropathy regardless of severity and can facilitate algorithmic decisions in genetic testing. Muscle Nerve 55 : 316–322, 2017     

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     

Assessment of pupillary light reflex latency and darkness adapted pupil size in control subjects and in diabetic patients with and without cardiovascular autonomic neuropathy.

Increased pupillary light reflex latencies were found more often than a reduced darkness pupil size in diabetic patients with and without abnormal cardiovascular reflexes. This finding suggests that parasympathetic pupillary dysfunction precedes sympathetic pupillary denervation in diabetic autonomic neuropathy.