Developmental changes in electrically elicited blink reflex in infancy and childhood

Developmental changes in electrically elicited blink reflex (BR) in 118 normal subjects, aged from 32 weeks of conceptional age to 14 years of age. During the waking state, R1 and bilateral R2 responses were always elicited. The latency of R1 shortened rapidly during the neonatal period, reaching the adult value at 3 months of age. The latency of R2 and contralateral R2 (CR2), which were elicited synchronously after 3 years of age, shortened slowly during childhood and reached the adult value at 6 years of age. The conduction indexes of R1, R2 and CR2, which were calculated as head circumference/latency (m/sec), increased rapidly during the neonatal period and reached the adult values at 6 years of age. The influence of NREM sleep on BR in neonates was different from those in infants and children. While BR of neonates in NREM sleep showed similar to that seen in wakefulness, BR of infants and children after one month of age was suppressed during NREM sleep. BR pattern in NREM sleep in infants and children after 6 months of age was similar to that seen in adults.     

电刺激诱发瞬目反射对脑桥梗死患者的预后价值

目的 探讨电刺激诱发瞬目反射(blink reflex,BR)对脑桥梗死患者的预后价值.方法 对43例脑桥梗死患者和37例健康对照组进行电刺激诱发BR的检测,采用欧洲脑卒中评分(The European stroke scale,ESS)和日常生活活动(activity of daily life,ADL)量表对每位患者在BR检查当日和4周末分别进行神经功能缺损程度评分.结果 脑桥梗死组病灶侧R1的潜伏期较对照组明显延长,病灶侧R1的潜伏期较健侧也显著延长(P＜0.001).脑桥梗死组BR各波的异常率以R1最高,占81.4%,而R2和R2′的异常率分别为23.3%和25.6%.R1的异常率显著高于R2和R2′(P＜0.001).双侧脑桥梗死(双侧均有病灶,每侧病灶直径均＞3mm),导致BR各波均未引出.一侧脑桥单个梗死灶,梗死灶直径＞3mm,主要引起R1潜伏期延长;一侧脑桥单个梗死灶,梗死灶直径0.5～3mm,BR各波潜伏期均正常.R1波未引出组神经功能缺损程度最重,ESS评分和ADL评分显著低于R1潜伏期延长组和R1潜伏期正常组(P＜0.001);R1潜伏期正常组预后最好,4周末其ESS评分和ADL评分均较1周内显著提高(P＜0.01和0.001);R1潜伏期延长组次之.结论 脑桥梗死患者的BR异常以R1潜伏期延长为特征.脑桥的病灶主要引起R1异常,进一步提示R1的反射中枢位于脑桥.BR的异常类型可大致反映脑桥梗死病灶的范围,BR的R1异常可作为脑桥梗死患者神经功能缺损程度和预后评价的电生理指标之一.     

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

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

Relationship between electroencephalographic abnormality and late blink reflex responses in infantile spasms and EIEE]

Electrically elicited blink reflex (BR) were analyzed in seven patients with age dependent epileptic encephalopathies (5 patients with infantile spasms and 2 with EIEE). Four patients with infantile spasms showed prolonged latency of the late BR responses (R2). In 2 patients with EIEE showing suppression burst pattern on EEG, R2 was not detectable. R2 abnormality in BR might reflect the dysfunction of the brainstem reticular formation in age dependent epileptic encephalopathies.     

Maturation of blink reflex in children

The blink reflex was examined in 57 subjects aged from neonate to adult in the alert state. The ipsilateral late response (R2) was elicited in all subjects and considered most suitable to evaluate maturational changes of the blink reflex. In a few subjects older than 3 years and of adults, the ipsilateral early response (R1) was difficult to observe. The contralateral late response (R2') could not be obtained in 32% of neonates and infants. From the observation about developmental change of an interference pattern, a latency shortening of R2 and a latency difference between R2' and R2, the blink reflex in children may be considered as mature at no later than 5 years of age. In addition, the R2 latency tended to increase temporarily through 1 or 2 years from late infancy. The reflex circuit evaluated by the blink reflex in children may partially change its makeup after the early infantile period and is almost fully mature at no later than 5 years.     

Alterations of nocturnal sleep in patients with HIV infection

Nocturnal sleep of 14 patients with HIV infection was characterized by longer sleep onset latency, shorter total sleep time, reduced sleep efficiency, more time spent awake and in Stage 1. There was significantly less sleep Stage 2 than in healthy controls. REM latency was slightly reduced and correlated negatively with depressive symptomatology, while percentages of REM and slow wave sleep were normal. Patients without complaints at the time of the investigation exhibited similar sleep abnormalities. The results stress the usefulness of polysomnography as a sensitive methodology for detection and monitoring of CNS affection in HIV positive patients.     

Development of the blink reflex during the 1st 3 years of a child's life

The blink reflex was elicited in 42 awake and quiet children from birth to 3 years of age. The R1 ipsilateral reflex response was always recorded. Its latency decreased significantly during the first 6 months of life whereas the VIIth nerve motor conduction velocity increased markedly; its threshold stimulus was lower in children after 1 year of age. R2 responses, especially contralateral ones, were sometimes absent in infants under 9 months of age; beyond that age, they were constant and bilateral. The ipsilateral R2 latency response diminished during the first 6 months of life, and the R2 reflex threshold became lower in infants above 1 year of age. When elicited after crying, in 22 children, the reflex components were facilitated; R1 response occasionally appeared bilaterally, its amplitude increased and its threshold was lower. During REM sleep, in 12 children, the reflex responses were similar to those recorded during quiet wakefulness. On the contrary, non-REM sleep recorded in 12 children markedly depressed the reflex responses; this inhibition was more pronounced for R2 responses.     

Changes in the VEP in preterm neonates with arousal states, as assessed by EEG monitoring

The effect of sleep state on the visual evoked potentials (VEPs) in neonates was investigated in 7 preterm infants. Polygraphic monitoring including EEG, EOG, ECG, respirogram and submental EMG for the purpose of sleep staging was carried out on all infants simultaneously with VEP testing. Awake-sleep stages were classified into 4 states: awake, transitional or atypical, quiet sleep and active sleep. VEPs were recorded from Oz, referenced to Fz, in response to binocular stimulation with light-emitting diode goggles. Polygraphic and EEG data were analyzed separately. Reproducible VEPs that were appropriate for their ages were seen in all infants in the awake state. The N300 was the most reliable component across sleep states but there was a significant decrease in amplitude with quiet sleep. There were no significant differences among awake, atypical or active sleep states. The other two VEP components followed the same trends as the N300. The P200, present in the older infants, disappeared in both active and quiet sleep states; the P400 was typically variable but reliably present in the awake or atypical states. When a distinction is made between quiet sleep and other arousal states, consistent and significant differences emerge. Our results emphasize the need to test infants in the same arousal states in studies of VEPs in order to make valid comparisons of latency or amplitude changes, particularly with longitudinal or follow-up studies.     

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

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

Features of the blink reflex in individuals at risk for Huntington's disease.

The aim of the study was to correlate the features of the blink reflex (BR) with the genetic abnormalities and the clinical findings in patients with Huntington's disease (HD) and asymptomatic gene carriers. Twenty patients with HD and 20 relatives were studied. Mutation analysis was performed for the CAG expansion within the HD gene using HD 333-HD 447 as oligonucleotide primers. The BR was elicited transcutaneously by electrical stimulation of the right supraorbital nerve. The recovery curve of the R2 and R3 responses after a conditioning stimulus was evaluated. R2 latency and duration and R3 duration were significantly increased in HD patients and in presymptomatic carriers in comparison with controls; reduced R2 recovery was also clear in both HD and gene-carrier relatives. In HD patients, the R2 latency increase correlated significantly with the severity of facial chorea. The R2 abnormalities are probably caused by impaired suprasegmental control by the basal ganglia over brainstem interneurons, which may precede the onset of involuntary movements, probably conditioning the severity of facial chorea during development of the disease.     

Reverse sleep state misperception

A 71-year-old woman with a 3-year history of excessive daytime sleepiness and an increased need for sleep did not feel restored upon awakening and had daytime fatigue despite a full night's sleep. She was evaluated with polysomnography (PSG). She significantly underestimated her sleep latency and awake time after sleep onset. The following morning, she stated that she had slept all night, when in fact she had extremely poor sleep efficiency and prolonged sleep latency. Another PSG and a two-week long actigraphy confirmed her misperception. Therefore, she perceived physiologic wakefulness, by PSG and actiraphy criteria, as subjective sleep, in direct contrast to 'conventional' sleep state misperception, in which patients usually present with a complaint of insomnia but have normal sleep quality and duration by PSG criteria. This patient may have a previously undescribed variation of sleep state misperception that the authors have tentatively named 'reverse' sleep state misperception.     

Assessing blink reflex circuits by three different afferent routes in Parkinson’s disease

ObjectiveDegeneration of nuclei of the brainstem, especially parts of the vagal nuclei complex and the reticular formation, in Parkinson’s disease (PD) may in part be responsible for nonmotor signs like obstipation, cardiac dysfunction and rapid eye movement sleep behavior disorder (RBD). The aim of the study was to establish a new blink reflex (BR) variant involving the vagal nuclei complex and the reticular formation and to investigate BR comprehensively using 3 different afferent routes in PD.MethodsIn this cross-sectional observational study in 30 PD patients and 30 age and sex matched healthy controls, BR was elicited by stimulation of the auricular branch of the vagus nerve (ABVN) and compared to conventional BR variants evoked by the trigeminal and median nerve.ResultsBRs could be elicited reliably by stimulation of ABVN in both groups. In none of the three BR variants, latencies or amplitudes differed between PD patients and controls. In PD, BR parameters were not related to cognition or presence of RBD.ConclusionThe present study did not provide evidence for malfunctioning of neural circuits subserving BRs elicited by three different afferents in PD.SignificanceBrainstem circuits mediating these BR variants may be spared from neurodegeneration in PD.     

Multimodality evoked potentials in severe athetoid cerebral palsy: correlation with clinical features and all-night polygraphical data.

We examined the correlation between the clinical and electrophysiological features, short latency somatosensory evoked potentials (SSEPs), auditory brainstem responses (ABRs), electrically elicited blink reflexes (BRs) and all-night polysomnographical examination (PSG) data in eight patients with severe athetoid cerebral palsy (ACP). Absence ABRs were observed in cases who had suffered from severe neonatal hyperbilirubinemia (posticteric ACP), and in most of them gaze abnormalities and a significant reduction in rapid eye movements during REM sleep, as observed on PSG, coexisted. Prolongation of the interpeak latency, N13-N20, of SSEPs existed concurrently with disturbed late components of BRs in two cases of posticteric ACP. The phasic contractions of the submental muscle during sleep were impaired in most of the patients. Multimodality evoked potentials together with PSGs seem to be useful for assessing brainstem dysfunctions in ACP and might also be of use for elucidating the pathogenesis of the episodic sudden death in ACP.     

Auditory evoked potentials during sleep in normal children from ten days to three years of age.

Auditory evoked potentials (AEPs) to clicks of moderate intensity were studied in 130 normal sleeping children from 10 days to 3 years of age. Latencies of the principal response components were found to decrease with log age, i.e., change was most rapid during the first year of life. From 15 days of age to 3 years, mean latencies decreased as follows: P2 from 230 to 150, N2 from 535 to 320 and P3 from 785 to 625 msec. Variance was quite high, especially at younger ages. The fact that decreases in the latencies of the various components proceeded at different rates suggest that the components reflect quasi-independent neural substrates. The components of shortest latency displayed the weakest relationship to age. Findings with respect to latency for the subset of data obtained during stage 2 sleep were similar to those for the total population which contained responses recorded during several sleep stages. The amplitude of AEP components increased with age with the exception of N1P2 which decreased. Observations with regard to amplitude held both for the overall data recorded during several sleep stages and stage 2 data for components N0P1, N1P2 and N2P3. The amplitude trends for P1N1 and P2N2 were, however, not significant for the stage 2 subset. The maturation of the morphology of the AEP was characterized by a relative increase in the prominence of long latency components. The most striking change was the development of P3. High amplitude, V shaped P3 waves were also associated with stage 3-4 sleep. The changes which were delineated by this study for infancy and early childhood appear to be continuations of developmental trends reported for premature infants and neonates. AEPs are a reliable elicited measure which correlate well with maturation. They, therefore, can be a useful tool both in the study of central nervous system development and in the diagnosis of sensory and neurologic abnormalities.     

Nocturnal polysomnography in obsessive–compulsive disorder

To determine if sleep abnormalities occur in obsessive–compulsive disorder (OCD), 2 nights of sleep electroencephalographic (EEG) recordings were obtained from 13 medication-free outpatients with OCD and 13 age- and sex-matched normal volunteers. Patients were awake more on night 2 than on night 1, whereas control subjects had less time awake on night 1; no other differences between groups were found on sleep latency, sleep time, minutes of movement, sleep efficiency, rapid eye movement (REM) latency or amount of stage 1, 2, 3, or 4 or REM sleep. Within the patient group, total scores on the Yale–Brown Obsessive–Compulsive Scale were negatively correlated with total sleep time (r=−0.51, P=0.07), sleep efficiency (r=−0.51, P=0.07), and duration of stage 1+2 sleep (r=−0.49, P=0.09) but not with REM time (r=−0.05, P=0.87) or latency (r=−0.26, P=0.39). Previous sleep studies in OCD have had divergent results, especially regarding REM latency; our results suggest that many OCD patients have essentially normal sleep EEG findings.     

Maturation of the blink reflex in infants

The blink reflex was elicited in 50 children from birth to 3 years of age. In the awake state, the R1 response was always obtained; R2 responses, especially contralateral ones, were more difficult to elicit under 9 months of age. R1 latency and VIIth motor nerve conduction variations were a good witness of the peripheral nervous system maturation. The influence of the different states of waking and sleeping on these reflex responses was studied. These results and some of the mechanisms that underlie these changes are discussed.     

Delayed blink reflex in dementia with Lewy bodies

Blink reflexes (BR) to electric stimuli of the supraorbital nerve were recorded in 26 patients with dementia with Lewy bodies (DLB), 26 patients with multiple system atrophy, 26 patients with Parkinson's disease, with or without REM sleep behaviour disorder (RBD), and in 20 patients with Alzheimer's disease and 20 with progressive supranuclear palsy without RBD, and compared with recordings in 30 healthy controls. BR were significantly delayed (p<0.001) only in DLB patients in comparison with controls and with the other groups of patients; 14 (53.8%) patients had BR latency above 2 SD of the control mean, ranging from 36.1 to 46.3 ms. BR latency was not related to the presence of RBD, while a Spearman correlation rho of 0.68 was found for scores assessing the presence of cognitive fluctuations. R2 delay was prominently (71.5%) bilateral.     

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.     

Familial congenital facial diplegia: electrophysiologic and genetic studies

A 13-year-old boy with autosomal-dominant congenital facial diplegia was evaluated by electrophysiologic and genetic investigations. Thirteen members of his family were affected over 4 generations. The electrophysiologic studies revealed blink reflex abnormalities. Both R1 and R2 responses were prolonged on the left side after ipsilateral stimulation, while R2 was also delayed by contralateral stimulation. Ipsilateral R1 and R2 were of normal latencies when the right side was stimulated. A third ipsilateral response at 63 msec of latency could be obtained when stimulating the left side. These findings suggest functional damage to the brainstem. Further support for this interpretation was provided by the prolonged time between waves I and V, bilaterally, documented by study of brainstem auditory evoked potentials.     

Sleep, subcortical stimulation and kindling in the cat.

A longitudinal study of the effects of sleep on amygdaloid kindling showed that kindling disrupted normal sleep patterns by reducing REM sleep and increasing awake time. Few interictal spike discharges were observed during the awake stage, while a marked increase in discharge was observed during the light and deep sleep stages. No discharges were observed during REM sleep. During the immediate post-stimulation period the nonstimulated amygdala showed a much higher rate of spike discharge. On the other hand, there was an increase in spike discharge in the stimulated amygdala during natural sleep without preceding amygdaloid stimulation. Amygdaloid stimulation at the generalized seizure threshold during each sleep stage resulted in a generalized convulsion. The influence of subcortical electrical stimulation on kindled amygdaloid convulsions was investigated in a second experiment. Stimulation of the centre median and the caudate nucleus was without effect on kindled convulsions, while stimulation of the mesencephalic reticular formation at high frequency (300 Hz) reduced the latency of onset of kindled generalized convulsions. Stimulation of the nucleus ventralis lateralis of the thalamus at low frequency (10 Hz) prolonged the convulsion latency, and at high current levels blocked the induced convulsion. Stimulation in the central gray matter at low frequency (10 Hz) also blocked kindled amygdaloid convulsions.