BRAINSTEM REFLEXES: ELECTRODIAGNOSTIC TECHNIQUES ...

INVITED REVIEW ABSTRACT: An overview is provided on the physiological aspects of the 

brainstem reflexes as they can be examined by use of clinically applicable 

neurophysiological tests. Brainstem reflex studies provide important information 

about the afferent and efferent pathways and are excellent physiological 

tools for the assessment of cranial nerve nuclei and the functional 

integrity of suprasegmental structures. In this review, the blink reflex after 

trigeminal and nontrigeminal inputs, corneal reflex, levator palpebrae inhibitory 

reflex, jaw jerk, masseter inhibitory reflex, and corneomandibular reflex 

are discussed. Following description of the recording technique, physiology, 

central pathways, and normative data of these reflexes, including an account 

of the recording of recovery curves, the application of these reflexes is 

reviewed in patients with various neurological abnormalities, including trigeminal 

pain and neuralgia, facial neuropathy, and brainstem and hemispherical 

lesions. Finally, simultaneous electromyographic recording from 

the orbicularis oculi and the levator palpebrae muscles is discussed briefly in 

different eyelid movement disorders. 

© 2002 Wiley Periodicals, Inc. Muscle Nerve 26: 14–30, 2002 

BRAINSTEM REFLEXES: ELECTRODIAGNOSTIC 

TECHNIQUES, PHYSIOLOGY, NORMATIVE DATA, 

AND CLINICAL APPLICATIONS 

M. ARAMIDEH, MD, PhD, 1,2 and B.W. ONGERBOER DE VISSER, MD, PhD 1 

1 Department of Neurology and Clinical Neurophysiology Unit, Academic Medical Center, Meibergdreef 9, 1105 AZ, 

Amsterdam, The Netherlands 

2 Department of Neurology/Clinical Neurophysiology, Medical Center Alkmaar, P.O. Box 501, 1800 AM, 

Alkmaar, The Netherlands 

Accepted 1 February, 2002 

The recording of brainstem reflexes provides valuable 

information on the functional integrity of the 

brainstem and allows the afferent and efferent pathways 

of these reflexes to be assessed. Many structural 

abnormalities, such as tumors or infarcts at the level 

of the brainstem, may cause abolition of these reflexes. 

Recording of different brainstem reflexes is 

helpful to exclude structural lesions or, conversely, 

to localize more accurately lesions within the brainstem. 

In the latter case, tailored magnetic resonance 

imaging (MRI) of this region may be sufficient. Recording 

of the brainstem reflexes also plays an important 

role in the selection of patients for additional 

MRI and in assessing objectively functional 

abnormalities of the cranial nerves by elucidating 

Abbreviations: LP, levator palpebrae superioris muscle; MIR, masseter 

inhibitory reflex; OO, orbicularis oculi muscle; R1, early response of blink 

reflex; R2, late response of blink reflex; SP1, first silent period; SP2, second 

silent period 

Key words: blink reflex; brainstem reflexes; corneal reflex; cranial nerves; 

masseter reflex 

Correspondence to: M. Aramideh; e-mail: m.Aramideh@mca.nl 

© 2002 Wiley Periodicals, Inc. 

Published online 1 May 2002 in Wiley InterScience (www. 

interscience.wiley.com). DOI 10.1002/mus.10120 

subtle changes in one or more variables of the reflex 

features, such as amplitude or latency of the responses. 

67 Studies of different reflex responses also 

provide information about the physiology and 

pathophysiology of segmental and suprasegmental 

control mechanisms on the brainstem reflexes and 

help to differentiate between the segmental and suprasegmental 

origin of abnormalities. 

This article provides an overview on the recording 

techniques, physiology, and normative data of 

different brainstem reflexes. Clinical applications 

are discussed briefly in patients with trigeminal and 

facial neuropathies, brainstem or hemispheric lesions, 

and extrapyramidal or eyelid movement disorders. 

ORBICULARIS OCULI REFLEXES 

Blink Reflex. The British physician Overend 85 first 

elicited the blink reflex by tapping one side of the 

forehead. Kugelberg 62 analyzed the blink reflex electromyographically 

by electrically stimulating the supraorbital 

nerve. Reflex responses from the inferior 

portion of both orbicularis oculi muscles may be recorded 

simultaneously by surface or needle elec- 

14 Brainstem Reflexes MUSCLE & NERVE July 2002

trodes. Stimuli should be delivered at intervals of 7 s 

or longer, while the subject is kept alert. 14 The afferent 

limb of the reflex is mediated by the ophthalmic 

division of the trigeminal nerve. 25,62 The facial 

nerve subserves the efferent limb. 

The electrical stimulation of the supraorbital 

nerve elicits two responses (Fig. 1); the first or early 

response, R1, is a brief unilateral response that occurs 

with a latency of about 10 ms in the orbicularis 

oculi muscle ipsilateral to the side of stimulation. 

The second or late response, R2, has a latency of 

about 30 ms. The R1 response is regarded as delayed 

if its latency exceeds 13.0 ms and R2 is regarded as 

delayed if its latency exceeds 41 ms. 59,80 A latency 

difference between the two sides exceeding 1.5 ms 

for R1 and 5.0 ms 59 or 8.0 ms 80 for R2 is also considered 

abnormal. 

Stimulation of the infraorbital nerve always 

evokes an R2 response but not necessarily an R1. 

When R1 is not present, it is difficult to evaluate R2, 

because of its wide range in latency. An absent R2, 

however, is certainly abnormal. 

The R1 response is conducted through the pons 

and is relayed via an oligosynaptic arc, probably consisting 

of one or two interneurons, located in the 

vicinity of the main sensory nucleus of the trigeminal 

nerve 56,74,90 (Fig. 1). For the R2 responses, it has 

been established that afferent impulses are conducted 

through the descending spinal tract of the 

trigeminal nerve in the pons and medulla oblongata 

before they reach the caudal spinal trigeminal 

nucleus. 58,82 From there, impulses are relayed by a 

medullary pathway that ascends bilaterally to reach 

the facial nuclei in the pons. These trigeminofacial 

connections are thought to pass through the lateral 

tegmental field, which lies medial to the spinal trigeminal 

nucleus. 50,82 The observations of Aramideh 

et al. 6 established that the uncrossed, ascending trigeminofacial 

pathway originates at the level of the 

lower medulla oblongata and that the contralateral 

R2 response is established by way of an ascending 

trigeminofacial connection that crosses the midline 

at the level of the lower third of the medulla oblongata. 

The blink reflex is influenced by many suprasegmental 

structures, including the motor cortex, the 

postcentral area of the cortex, and the basal ganglia. 

38 

Blink Reflexes Evoked by Nontrigeminal Inputs. Somatosensory 

Blink Reflex. An electrical stimulus to 

peripheral nerves, specifically the median nerve at 

the wrist, may induce responses in the orbicularis 

oculi muscles. 71,94 The circuits involved in these re- 

FIGURE 1. (A) Normal early (R1) and bilateral late (R2) responses 

of the blink reflex. Responses are shown from the right 

(r) and left (l) OO muscles after stimulation of the right (r*) and (l*) 

supraorbital nerves. (B) Diagram showing the presumed location 

of the bulbar interneurons subserving the two components of the 

blink reflex. (VII, facial nucleus; VII N, facial nerve; VI, abducens 

nucleus; Vp, principal trigeminal nucleus; Vm, trigeminal motor 

nucleus; V N, trigeminal nerve; MED RET, medial reticular field; 

LAT RET, lateral reticular field). 

sponses are not fully understood. However, the somatosensory-induced 

blink reflex may be part of a 

generalized activation of the startle circuit 53 or the 

expression of a release phenomenon. 72 Electrical 

Brainstem Reflexes MUSCLE & NERVE July 2002 15

stimulation of the median nerve may also induce 

responses in lower facial muscles, as an electrophysiological 

equivalent of the palmomental reflex. 31 

Acoustic Blink Reflex. Sound induces a response 

in the orbicularis oculi muscle, which may be isolated 

and limited to this muscle or involve neck and 

extremity muscles as in the generalized auditory 

startle reaction. When the response is limited to the 

orbicularis oculi, it is known as the auditory blink 

reflex. Some authors consider the acoustic blink reflex 

the least expression of the generalized startle 

response. 99 However, different physiological features 

with regard to habituation and latency of the 

acoustic blink reflex and the startle reaction have 

been described. 18 Specific circuits have been proposed 

for the acoustic blink reflex 51 and the startle 

reaction. 30 In practical terms, however, if two different 

responses are indeed generated by sound stimulation 

in the orbicularis oculi muscles, they cannot 

be easily differentiated in single individuals in routine 

practice. The latency of the orbicularis oculi 

response to sound is usually between 40 and 60 ms. 

Photic Blink Reflex. Yates and Brown 100 studied 

the orbicularis oculi reflex responses evoked by light 

stimuli using a photic stimulator. In a control group, 

the authors obtained optimal responses of shortest 

latency (50.0 ms ± 4.5 ms) with the stimulator held at 

a distance of 200 mm in front of the eyes. Afferent 

optic fibers probably enter the brainstem in the pretectum 

and impulses are then conveyed to the facial 

nuclei in the pons. 92 It seems that the cerebral cortex 

is not involved in the generation of the photic 

blink reflex, as experimental ablation of occipital 

cortex does not influence the response. 97 Further 

research is required to trace the central circuit mediating 

this reflex. 

Corneal Reflex. Technique of Recording. During recording 

of the corneal reflex responses, the subject 

lies supine on a bed or sits in a reclining chair. Responses 

are recorded simultaneously from the two 

eyes, with surface electrodes positioned as for recording 

of the blink reflex responses. The optimal 

time to stimulate the cornea is between spontaneous 

blinks. The cornea can be stimulated mechanically 

or electrically. With mechanical stimulation, orbicularis 

oculi responses are evoked by successive manual 

application of a small metal sphere, 2 mm in diameter, 

to the cornea. 83 The examiner holds the upper 

eyelid open with one finger. When the sphere 

touches the cornea, contact is made between the 

subject and an electronic trigger circuit, which delivers 

a pulse. When the corneal reflex is studied by 

electrical stimulation, the cornea is touched lightly 

with a thin saline-soaked cotton thread connected to 

the cathode of a constant-current stimulator. The 

anode is placed on the earlobe or forearm. 1 Square 

pulses, 1 ms in duration, of 0.1 to 3 mA are delivered 

manually, and the oscilloscope is triggered by the 

stimulus. Electrical shocks excite the A-delta nerve 

fibers directly. To measure the reflex threshold and 

for studying the recovery curve with the doubleshock 

technique (vide infra), it is necessary to use 

electrical stimulation, which provides a controlled 

and reproducible stimulus. 

Physiology and Normative Data. The corneal reflex 

is typically nociceptive and serves to protect the 

eye. The cornea is innervated by unmyelinated (C) 

and small myelinated (A-delta) fibers. 66 After penetrating 

the cornea, the myelinated axons lose myelin 

and both types of axons terminate in the stroma 

and epithelium as free nerve endings. The mechanical 

or electrical stimulation of the cornea gives rise 

to a bilateral contraction of the orbicularis oculi, 

leading to closure of the eyelids. 

Three pairs of latency times should be assessed 

from stimulus artifact to onset of the electromyographic 

(EMG) response (Fig. 2). In contrast to the 

blink reflex, the corneal reflex does not evoke an 

early R1 response. When the cornea is touched mechanically, 

the latency time of the direct (ipsilateral) 

response should not exceed the consensual (contralateral) 

response latency by more than 8 ms. The 

latencies of the direct responses, evoked by stimulation 

of both corneas separately, should never differ 

by more than 10 ms. This also applies to the consensual 

response latencies. 83 With an electrical stimulus, 

the difference between the direct and consensual 

responses never exceeds 5 ms, and the difference 

between direct responses should never exceed 8 ms. 

The reflex threshold in normal subjects rarely exceeds 

0.5 mA. 1 Mechanical and electrical stimuli 

elicit reflex responses with similar latency times. Absolute 

latency values range from 36 ms to 64 ms with 

mechanical stimulation and from 35 ms to 50 ms 

with electrical stimulation. This wide range of latencies 

narrows if control subjects are divided into 

groups that take age into account. 

Central Pathway. The reflex afferents are A- 

delta fibers 25 passing through the long ciliary nerves 

and the ophthalmic division of the trigeminal sensory 

root to reach the pons. 32,74 The central circuit is 

grossly similar to that of the R2 responses of the 

blink reflex (Fig. 2). The corneal reflex differs from 

R2, however, because it is a purely nociceptive reflex. 

The corneal reflex is relayed through different and 

fewer interneurons than R2, 84 and it is far more resistant 

to suprasegmental influences. 27 


muscle is innervated by the third cranial nerve. The 

inhibitory reflex of the LP can be examined together 

with the OO excitatory reflex. 8 

Technique of Recording. The EMG recordings 

from the LP and the OO muscles can be obtained 

with the subject supine. To record from the LP, a 

bipolar needle electrode is inserted through the skin 

in the middle portion of the upper eyelid and directed 

toward the LP, while the subject looks downward 

and keeps the eyelids gently closed. The subject 

is then asked to open the eyes. This maneuver results 

in EMG activity from the LP, which can be verified 

on the monitor and by the sound signal. To record 

from the OO, a bipolar needle electrode is inserted 

into the upper or lower eyelids. The position of the 

needles is adjusted depending on the response obtained 

when the subject blinks or closes the eyes 

gently (Fig. 3). Supraorbital nerve stimulation, similar 

to that used for eliciting the blink reflex, can be 

used in the absence of spontaneous blinking, while 

the subject keeps the eyes open voluntarily. 

FIGURE 2. Normal corneal reflex. (A) Responses from the right 

(r) and left (l) OO muscles after mechanical stimulation of the 

right (r*) and (l*) cornea. (B) Presumed central pathways subserving 

the corneal reflex. (For key abbreviations, see legend to 

Fig. 1.) 

Afferent impulses descend along the spinal trigeminal 

tract, reach below the obex at the level of 

the trigeminal subnucleus caudalis, and ascend 

along a multisynaptic chain of interneurons in the 

lateral tegmental field before impinging on the facial 

motoneurons. 

LEVATOR PALPEBRAE INHIBITORY REFLEX 

The levator palpebrae superioris (LP) muscle and 

the orbicularis oculi (OO) muscle act antagonistically 

during various movements of the eyelid. The LP 

Physiology and Normative Data. Stimulation of the 

supraorbital nerve evokes two silent periods in the 

LP muscle 8 (Fig. 4). The first or early silent period is 

designated SP1, and the second or late period is SP2. 

In contrast to the R1 response of the OO muscle, the 

SP1 occurs bilaterally, regardless of the stimulation 

site. The latency of SP1 varies from 9 to 13 ms and is 

slightly shorter than the latency of the corresponding 

R1 response after ipsilateral stimulation. The SP1 

has a duration of 12 to 15 ms. Previous experimental 

work, including tracing studies, has shown that a 

small percentage of the LP motoneurons have axon 

collaterals to both LP muscles. 96 Whether these motoneurons 

are involved in the generation of SP1 is 

unclear. The latency of SP2 varies from 27 to 35 ms 

and is again slightly shorter than that of the corresponding 

R2 responses. The SP2 has a duration of 32 

to 50 ms. 

There is a slight variability in the features of the 

LP inhibitory reflex, depending on the prestimulus 

contraction level of the LP muscle and the stimulus 

intensity; when the prestimulus contraction of the 

levator is weak, SP1 and SP2 may form a single, large 

inhibitory period. At lower stimulus intensities, SP1 

may not be evoked. The SP2 latency decreases and 

its duration increases following supramaximal stimulation 

of the supraorbital nerve. 

The antagonistic behavior between OO and LP 

muscles can therefore be observed not only during 

closure and opening of the eyelids, or during spontaneous 

or voluntary blinks, but also during the 


FIGURE 3. Electromyograms from the LP and OO muscles, 

showing the reciprocal inhibition between the two muscles in a 

healthy subject. (A) When the subject is asked to close the eyes, 

LP activity ceases abruptly, followed by contraction of OO. (B) 

Note the occurrence of dense bursts of action potentials with high 

amplitude preceding the return of LP activity on the order “open 

eyes,” following the inhibition of OO. (C) Total inhibition of the LP 

muscle activity and a brief contraction of the OO during two spontaneous 

blinking (Aramideh et al. 5 ). 

evoked blink reflex. Preliminary data indicate that 

inhibition of the LP muscle is probably relayed 

through central pathways other than those involved 

in R1 and R2 responses of the OO muscle. The data 

obtained from the examination of the recovery curve 

of LP inhibition responses are also in agreement 

with this assumption (vide infra). 

JAW REFLEXES 

Jaw Jerk. The jaw jerk induced by a tap on the 

chin was first described by De Watteville. 34 It is also 

called the jaw reflex, mandibular reflex, or masseter 

reflex. Without EMG recording, the clinical value of 

the mandibular reflex is generally confined to the 

distinction between normal and brisk reactions, because 

in healthy subjects, the movement of the mandible 

is often undetectable. Furthermore, on clinical 

examination alone, unilateral interruption of the reflex 

arc cannot be detected. 

Technique of Recording. To elicit the jaw jerk, the 

examiner puts one finger on the subject’s chin and 

taps it with a reflex hammer provided with a microswitch 

that triggers the sweep of the oscilloscope. 

45,80,81 Electromyographic responses are recorded 

simultaneously from the two sides by surface 

electrodes. The active electrode is placed on the 

masseter muscle belly, in the lower third of the distance 

between the zygoma and the lower edge of the 

mandible, and the reference electrode is placed below 

the mandibular angle. Reflex responses can also 

be recorded by a small-diameter concentric-needle 

electrode inserted into each masseter. In this case, a 

ground electrode is taped onto the forehead, neck, 

or upper arm. To ensure a constant latency, taps 

should be delivered at intervals of 5sormore. 

Physiology and Normative Data. The reflex afferents 

are Ia fibers from muscle spindles of the jawclosing 

muscles. The reflex latency, which provides 

the most useful parameter, should be evaluated in 

several trials or measured on the averaged signal. 

81,101 

The mean latency in healthy subjects is 6.8 ms 

(SD, 0.8 ms), with a range of 5 to 10 ms 28 (Fig. 5). 

Comparison of the latency of the jaw jerk responses, 

recorded simultaneously on the two sides, is of great 

value. A difference of more than 0.8 ms or a consistent 

unilateral absence of the reflex is abnormal. 

This reflex is strongly influenced by dental occlusion 

and can be asymmetrical or even absent in patients 

with temporomandibular disorders. 24 Changing the 

position of the mandible or the level of preinnervation 

may markedly reduce or worsen the asymmetry 

in patients with dental problems but not in patients 

with a lesion along the reflex arc. A bilaterally absent 

reflex in elderly subjects has no definite clinical significance, 

because this may occur in healthy subjects. 

Central Pathway. Whether the afferent fibers 

travel in the trigeminal motor root 69,87 or the trigeminal 

sensory root 41,46,73 is still controversial (Fig. 5). 

Unique among the primary sensory neurons, these 

afferents have their cell body in the central nervous 

system, in the trigeminal mesencephalic nucleus, 

rather than in the ganglion. Collaterals from the trigeminal 

mesencephalic nucleus descend to the midpons 

to activate monosynaptically jaw-closing motoneurons 

of the ipsilateral side only. 

Masseter Inhibitory Reflex. The masseter inhibitory 

reflex (MIR), also called the cutaneous silent 


FIGURE 4. (A) Superimposition of three traces of the right LP muscle (upper traces) and the right OO muscle (lower traces) after 

stimulation of the ipsilateral right supraorbital nerve (R*). The ipsilateral stimulation causes an ipsilateral early (SP1) and late (SP2) period 

in the LP and an ipsilateral R1 and R2 in the OO. (B) The superimposition of three traces is as in (A), after stimulation of the contralateral 

left supraorbital nerve (L*). In contrast to R1 response, regardless of the stimulation site, SP1 could still be evoked (Aramideh et al. 8 ). 

period or exteroceptive suppression reflex was first 

described by Hoffman and Tonnies 49 as the inhibitory 

component of the tongue–jaw reflex seen after 

electrical stimulation of the tongue. The EMG silent 

period (SP) refers to a transitory relative or absolute 

decrease in EMG activity evoked in the midst of an 

otherwise sustained contraction. 90 

Technique of Recording. The MIR is recorded bilaterally 

with the electrodes placed as described for 

the jaw jerk. Subjects are seated upright and are instructed 

to clench the teeth as hard as possible for a 

period of 2–3 s, with the aid of auditory feedback. 

The reflex can be measured properly only if the patient 

is able to clench the teeth and produce a full 

interference pattern in the EMG. It may be necessary 

to use a concentric-needle electrode, instead of surface 

electrodes, particularly when the signal is contaminated 

by facial muscle activity. 

Single electrical shocks, 0.2 ms in duration, are 

delivered to the mentalis or infraorbital nerves, 

through surface electrodes placed over the homonymous 

foramina. A stimulus intensity of about 2–3 

times the reflex threshold (usually 20–50 mA) yields 

the best results. It is always necessary to examine 

several trials, usually 8 to 16, allowing 10–30 s of rest 

between contractions. Some authors measure the latency 

at the last EMG peak, some at the last crossing 

of the isoelectric line, and others at the beginning of 

the electric silence. Each of these methods is clinically 

satisfactory if the same criterion is maintained 

and intraindividual differences between right and 

left stimulations are examined. 

Physiology and Normative Data. Mechanical or 

electrical stimulation, applied anywhere within the 

mouth or on the facial skin of the maxillary and 

mandibular trigeminal divisions, evokes a reflex inhibition 

in the jaw-closing muscles. These reflexes 

probably play a role in the reflex control of mastication 

by preventing intraoral damage that could occur 

with uncontrolled contraction of jaw-closing 

muscles and in jaw movements during speech. 

The MIR consists of two electrical silent periods 

interrupting the voluntary EMG activity in the ipsilateral 

and contralateral masseter muscles 43,79,81,90 

(Fig. 6). The early silent period, SP1, has a latency of 

10–15 ms. The late silent period, SP2, has a latency 

of 40–50 ms. A latency difference between the ipsilateral 

and contralateral responses exceeding 2 ms 

for SP1 or 6 ms for SP2 is abnormal. 

In a few subjects, little or no EMG activity occurs 

between the two SPs, for example, SP1 and SP2 

merge in a single long-lasting SP, even when the 

strength of contraction is maximal. In this case, the 

latency to the resumption of EMG activity is taken as 

a measure of SP2. The interside latency difference 


FIGURE 5. (A) Normal jaw-jerk responses from the right (R) and 

left (L) masseter muscles. The lower traces are made by averaging, 

and arrows mark the latency times. (B) Presumed central 

pathways subserving the jaw-jerk responses. (Ophth, ophthalmic 

trigeminal root; Max, maxillary trigeminal root; Mand, mandibular 

trigeminal root; Mot Root N V, trigeminal motor root; NIII, oculomotor 

nerve; N VI= abducens nerve; Ncl Mes N V, mesencephalic 

nucleus of the trigeminal nerve; Ncl Mot N V, motor nucleus of 

the trigeminal nerve; Ncl Princ N V, principal sensory nucleus of 

the trigeminal nerve; Ncl Tract Spin N V, nucleus of the trigeminal 

spinal tract.) 

FIGURE 6. (A) Normal early (SP1) and late (SP2) phase of the 

MIR. The responses are shown from the right (upper trace) and 

left (lower trace) masseter muscles after stimulation of the right 

(R*) mental nerve. (B) Presumed location of the bulbar interneurons 

subserving the SP1 and SP2 of the MIR. (For key abbreviations, 

see legend to Fig. 5). 

when recording from one muscle should not exceed 

8 ms. 

If full-wave rectification is available, 8–16 trials 

should be averaged. The latency and duration of SPs 

can be measured from the intersection of the rectified 

and averaged signal and a line indicating 80% of 

the background EMG level. In 100 normal subjects 

aged 15–80 years, the mean latency of SP1 was 11.8 

ms (SD, 0.8) and of SP2 was 45 ms (SD, 5.2). The 

duration of SP1 was 20 ms (SD, 4) and the duration 

of SP2 was 40 ms (SD, 15). 28 

Probably because electrical stimuli yield a mixed 

nociceptive and nonnociceptive input, whether the 

SP1, SP2, or both components are nociceptive reflexes 

remains controversial. 37,70 Both inhibitory responses 

can nevertheless be elicited with innocuous 

mechanical stimuli, and indirect evidence supports 

the view that the afferents belong to the intermediately 

myelinated A beta group. 22,89 

Central Pathway. After stimulation of the mental 

or infraorbital nerve, impulses reach the pons 

through the sensory mandibular or maxillary root of 

the trigeminal nerve, respectively 81 (Fig. 6). The SP1 


esponse is probably mediated by one inhibitory interneuron, 

located close to the ipsilateral trigeminal 

motor nucleus. The inhibitory interneuron projects 

onto jaw-closing motoneurons bilaterally. The whole 

circuit lies in the midpons. 79 The afferents for SP2 

descend in the spinal trigeminal tract and connect 

with a polysynaptic chain of excitatory interneurons, 

probably located in the lateral reticular formation, 

at the level of the pontomedullary junction. The 

last interneuron of the chain is inhibitory and 

gives rise to ipsilateral and contralateral collaterals 

that ascend medial to the right and left spinal trigeminal 

complexes to reach the trigeminal motoneurons. 

79 

Corneomandibular Reflex. The trigemino– 

trigeminal corneomandibular reflex is elicited clinically 

by touching the cornea with a dry wisp of cotton 

wool. 47,48 The reflex response is a slight protrusion 

and contralateral deviation of the mandible due to 

contraction of the inferior head of the lateral pterygoid 

muscle. The corneomandibular reflex must not 

be confused with the trigeminofacial corneomental 

reflex. 10,98 This latter response, seen as a subtle 

movement of the skin over the chin caused by contraction 

of the mental muscle, occurs in many 

healthy subjects. Electromyographic investigation 

has demonstrated that the corneomandibular reflex 

is absent in healthy subjects and can be recorded in 

patients with corticobulbar tract lesions. 77 

Technique of Recording. For EMG recording, the 

cornea is touched with a 2-mm–diameter metal 

sphere, connected to an electronic trigger circuit, 

identical to the arrangement used for corneal reflex 

response recordings. 77 The lateral inferior pterygoid 

muscle can be studied best with a unipolar wire electrode. 

This is composed of a fine Teflon-coated wire, 

0.1 mm in diameter, threaded into the tip of a 4-cm 

disposable needle. The needle is positioned in the 

mandibular notch, just in front of the condylar head 

and about 1 cm below the zygomatic arch, and is 

then placed approximately perpendicular to the sagittal 

plane and advanced to a depth of about 4 cm. 

Gentle removal of the needle leaves the wire electrode 

in place. Its free end is connected to a preamplifier 

lead through a tightly coiled steel spring. An 

inactive surface electrode is located over the posterior 

zygoma. Pterygoid electrode placement can be 

checked by recording EMG activity during downward 

and contralateral mandible movement. A pair 

of surface electrodes placed ipsilaterally over the 

lateral half of the chin will allow simultaneous examination 

of reflex discharges in the mentalis 

muscle. 

Latency and Central Pathway of Responses. After 

mechanical stimulation of the cornea, the average 

latency of the EMG response (Fig. 7) in the lateral 

inferior pterygoid muscle is 73.3 ms (SD, 7.4), and 

the interside difference is 5 ms (range 0–12 ms). 77 

The long latency suggests multiple intramedullary 

synaptic connections. Afferent impulses for the corneomandibular 

reflex and afferent impulses for the 

corneal reflex pass along similar fibers, whereas ascending 

trigemino–trigeminal interneuronal connections 

probably run in the bulbar lateral reticular 

formation. Efferent impulses to the lateral inferior 

pterygoid muscle are mediated through the trigeminal 

motor root. 

FIGURE 7. Example of the corneomandibular reflex responses. 

Upper two traces show responses from the right (r) and left (l) 

inferior head of the lateral pterygoid muscle obtained by stimulation 

of the right (r*) cornea. The lower two traces show the 

responses evoked by stimulation of the left (l*) cornea. 


INTEGRATIVE FUNCTIONS OF THE BRAINSTEM 

Recovery Curves to Paired Stimuli. Because of passive 

mechanisms (e.g., afterhyperpolarization potential) 

or the intervention of negative feedback circuits, 

the excitability of a reflex circuit is depressed 

after the passage of an earlier impulse. With the 

double-shock technique, it is possible to draw the 

recovery curve (or excitability cycle) of a given reflex 

and thus obtain a measure of the excitability of the 

reflex circuit. 55 

Stimulus intensity and position of the stimulating 

and recording electrodes are the same as used in 

standard reflex studies. Electrical stimuli of equal 

intensity are delivered in pairs, at varying interstimulus 

intervals. The first shock is called the “conditioning” 

stimulus, and the second shock is the “test” 

shock. The size (amplitude, duration, or area) of 

the conditioning and test responses are measured, 

and that of the test response is expressed as a percentage 

of the conditioning response. The recovery 

curve is drawn by plotting the size of the test response, 

as a percentage of the conditioning response, 

on the y-axis and the time-interval on the 

x-axis 55 (Fig. 8). 

Recovery of Orbicularis Oculi Reflexes. A complete 

excitability cycle of the orbicularis oculi reflex can be 

examined with 10-ms time intervals between 10 ms 

and 100 ms, and 100-ms intervals between 100 ms 

and 1500 ms. However, it is not clinically necessary to 

check all these intervals. 

The test R1 summates with the conditioning R1 

or R2 at short (up to 60–70 ms) interstimulus intervals. 

The apparent facilitation may reach 250% at 

30–40-ms intervals. With longer intervals, R1 is affected 

little by the conditioning shock. It may be 

slightly reduced (80% at the 100-ms interval) and 

slowly recovers to 90–100% of the conditioning response 

at intervals of 200–500 ms. 55 

Test R2 is usually completely abolished at interstimulus 

intervals shorter than 200 ms; it then slowly 

recovers, reaching about 40–50% at the 500-ms 

interval and 70–90% at the 1500-ms interval 3,35 

(Fig. 8). 

The recovery of the corneal reflex parallels but is 

more rapid than that of R2. The test corneal reflex 

already measures about 30% at the 200-ms interval, 

whereas R2 of the blink reflex is still abolished, and 

reaches 90–100% at the 1500-ms interval. 20,55 

As the same motoneurons are shared by the various 

orbicularis oculi reflexes, the difference in recovery 

times (progressively longer for R1, corneal 

reflex, and R2) is commonly attributed to differences 

in the interneuronal net. The R2 of the blink 

FIGURE 8. Recovery curve of the R2 response of the blink reflex. 

Rectified and averaged (n = 6) EMG responses are presented at 

intervals from 220 ms to 10 s between conditioning and test 

stimuli, in a control subject (A) and in a patient with blepharospasm 

(B). (C) Complete recovery curves for both subjects. The 

patient (B) shows significantly less suppression at intervals 

smallerthan1s(S1,conditioning stimulus; S2, test stimulus). 

reflex response is most susceptible to changes in excitability, 

and the R2 recovery curve has provided 

valuable information in research and clinical settings. 

It may also be valuable to measure the recovery 

index. 3,35 


Recovery of Levator Palpebrae Inhibitory Reflex. 

With the recording needle positioned as for 

recording of the levator palpebrae EMG activity and 

the inhibition reflex (see earlier), the recovery of the 

inhibition periods of the levator palpebrae muscle 

can be examined with the recovery curve of the orbicularis 

oculi responses 8 (Fig. 9). The durations of 

the two silent periods are measured, and that of the 

test response is expressed as a percentage of the conditioning 

response. The recovery curve is drawn by 

plotting the size of the test response, as a percentage 

of the conditioning response, on the y-axis and the 

time-interval on the x-axis. 

At interstimulus intervals higher than 500 ms, the 

percentage of inhibition recovery of the second silent 

period (SP2) is similar to that of the excitability 

recovery of the R2 response (Fig. 9). At lower intervals, 

the recovery curve of SP2 is shifted upward, i.e., 

SP2 recovers faster than the corresponding R2 response. 

For example, at 200 ms where the R2 response 

is completely abolished, the SP2 could still be 

recruited at a level of about 20–30%. These findings 

are in accord with our earlier hypothesis that responses 

are probably relayed on different central 

pathways. 

Recovery of Masseter Inhibitory Reflex. The recovery 

cycle of the MIR is studied by delivering paired 

stimuli at interstimulus intervals of 100 ms, 150 ms, 

250 ms, and 500 ms, with the same low-rate stimulation 

and alternation of “clench” and “rest” phases 

described for the assessment of the reflex values. 

The recovery curve is drawn by plotting the timeintervals 

on the x-axis and the size (area or duration) 

of the test response as a percentage of the size of the 

conditioning on the y-axis (Fig. 10). 

The recovery of SP1 in normal subjects varies 

from about 85% at 100-ms intervals to approximately 

96% at 500 ms. The recovery of SP2 varies from 24% 

at 100 ms to 79% at 500 ms. The function of correlation 

between time interval (milliseconds) and size 

of the test response (percent) is linear for SP1 (y = 

0.02 ×+ 85) and logarithmic in base 10 for SP2 (y = 

75 log ×− 120). 29 

Recovery can also be evaluated by simply measuring 

the duration of SP1 and SP2 in nonrectified recordings, 

and for clinical use, it may be sufficient to 

measure the recovery of SP2 at the 250-ms interval. 

24,28 

CLINICAL APPLICATIONS 

Trigeminal Neuropathy. For diagnosing extra-axial 

trigeminal nerve lesions, the short-latency responses, 

such as R1 of the orbicularis oculi muscle, SP1 of the 

MIR, and the jaw jerk, are far more sensitive than are 

FIGURE 9. (A) Recovery curve of SP2 of the LP (L. Palpebrae) 

and (B) recovery curve of the R2 response of the OO (O. Oculi). 

(C) Recovery curves of both muscles together. At higher stimulus 

intervals, e.g., 1 s and 0.5 s, the percentage of inhibition recovery 

of the SP2 was similar to that of the excitability recovery of the R2 

response. At lower stimulus intervals, the recovery curve of inhibition 

responses were shifted upward, i.e., SP2 recovered faster 

than did corresponding R2 response; at 200 ms, where R2 response 

did not show any recovery, the SP2 could still be recorded 

for about 20–30 %. The SP1 is not examined systematically 

(Aramideh et al. 8 ). 

the long-latency responses, such as R2 of the blink 

reflex and SP2 of the MIR. One reason is that they 

are supplied by fewer reflex afferents. In addition, 


they exhibit less variability and have a smaller normal 

range than do polysynaptic responses. 9,57,78 

The blink reflex may be abnormal, with lesions of 

the supraorbital nerve branch or more proximal lesions 

affecting the ophthalmic division of the trigeminal 

nerve. An abnormal corneal reflex can reflect 

damage to the long ciliary nerves or the ophthalmic 

division where ciliary nerves join the ophthalmic 

root. Blink and corneal reflexes are not necessarily 

both affected, because they are mediated by different 

sets of afferents and different central circuits. 

11,75 Furthermore, the corneal reflex is more 

sensitive, because it is mediated by fewer afferents 

than is the blink reflex. In lesions of the infraorbital 

nerve or, more proximally, of the maxillary root, the 

blink reflex and the MIR may be abnormal after infraorbital 

nerve stimulation. Damage to the mental 

nerve or the trigeminal mandibular root may cause 

MIR abnormalities. 

To localize the site of lesion, it is helpful to study 

trigeminal reflexes evoked from all three divisions. 

Abnormalities in all divisions of the trigeminal nerve 

indicate a trigeminal root lesion in the middle or 

posterior cranial fossa. 

As a general rule, peripheral lesions are more 

likely to affect both blink reflex components to a 

similar degree (Fig. 11, type B) or more clearly affect 

R1 than R2. It is extremely rare to see absence or 

delay of R2 without accompanying abnormalities of 

R1 in peripheral lesions. By contrast, intra-axial lesions 

often affect R1 and R2 separately. Very discrete 

lesions limited to the upper pons may cause a delay 

or loss of the R1 component without accompanying 

R2 response abnormalities 56 (Fig. 11, type A). The 

most common finding with intra-axial involvement 

of the trigeminal sensory system, such as in multiple 

sclerosis or in olivopontocerebellar atrophy, is of an 

abnormal R2 response with normal R1 response. 

FIGURE 10. Recovery curves of the MIR. (A) Eight rectified and 

averaged signals, recorded in a healthy subject after stimulation 

of the mental nerve. The first (conditioning) shock is indicated by 

the dashed line. The second (test) shock is indicated by the arrows. 

After a second shock with an interstimulus interval of 100 

ms, the test SP2 is almost abolished (A1) and partly recovers with 

an interval of 250 ms (A2). (B) The same as in (A) but in a patient 

with Parkinson’s disease. The test SP2 is only slightly suppressed 

at the interstimulus interval of 100 ms (B1) and completely 

recovers at the interval of 250 ms (B2). (C) Recovery 

curve of the SP2 component of the MIR. Note: x-axis, interstimulus 

interval (ms); y-axis, area of the test response expressed as 

percentage of the conditioning response. The two curves are ± 

standard errors of the estimate in 20 healthy subjects. The two 

squares indicate the recovery value for the 100-ms and 250-ms 

intervals in (B). Note that the recovery of SP2 is enhanced in the 

patient with Parkinson’s disease. 

Trigeminal Pain and Neuralgia. In patients with 

pain in the trigeminal territory, neurophysiological 

testing of trigeminal function offers the clinician 

useful information. Abnormalities are often disclosed 

in divisions that appear clinically unaffected. 

An objective demonstration of dysfunction is provided 

in all patients with pain secondary to a documented 

disease, such as symptomatic trigeminal 

neuralgia, postherpetic neuralgia, vascular malformations, 

benign tumors of the cerebellopontine 

angle, and multiple sclerosis, even in those patients 

who have no clinical signs or complaints other than 

pain. 26,60,78 

Reflex responses are more affected in patients 

with constant pain than in those with paroxysmal 


FIGURE 11. (A) Schematic representation of various lesions within the brainstem (A-E) and corresponding blink reflex response 

abnormalities in the right (R) and left (L) OO muscles after stimulation (*) of the supraorbital nerves (B). Blink reflex responses are either 

delayed (left column) or absent (right column). See text for comments on different types of reflex abnormalities. (VII, facial nucleus; VI, 

abducens nucleus; Vpr, principal trigeminal nucleus; Vmot, trigeminal motor nucleus; Lat. tegm. field, lateral tegmental field; Med. tegm. 

field, medial tegmental field) (Aramideh et al. 6 ). 

pain. This agrees with the common notion that a 

dysfunction of few fibers provokes paroxysmal pain, 

whereas severe damage does not. Indeed, neuralgic 

pain is often relieved by surgical deafferentation, 

whereas constant pain is often worsened. In symptomatic 

trigeminal pains, the trigeminal reflexes 

have a very high sensitivity, probably because they 

allow examination of all three divisions. The most 

sensitive reflexes are the R1 of the blink reflex and 

the SP1 of the MIR. 26 Mild reflex abnormalities occur 

occasionally, 60,81 but in most patients with idiopathic 

trigeminal neuralgia (“tic douloureux”), all 

reflexes are normal. In patients with idiopathic trigeminal 

neuralgia, the presynaptic waves of the scalp 

evoked potential after percutaneous infraorbital 

stimulation are more sensitive than are reflex responses 

64 and in about half of the patients disclose 

abnormalities of the waves originating near the root 

entry into the pons. 63 The finding of any abnormality 

should nonetheless promote further investigation. 

The most commonly reported causes of symptomatic 

neuralgia are benign tumors of the 

cerebellopontine angle and vascular anomalies in 

the posterior fossa impinging on the proximal portion 

of the trigeminal root, and multiple sclerosis 

with a plaque in the root entry zone. 88 As in neuralgia 

secondary to well-documented lesions, the most 

likely site of conduction impairment in idiopathic 

trigeminal neuralgia is the region of the root entry 

into the pons. 26,63 

Facial Neuropathy. Recording the blink reflex, 

whose reflex arc includes the entire facial nerve, may 

provide information right from the onset of the 

palsy, although it has no prognostic value. The R1 

and R2 components are abnormal ipsilaterally to the 

affected side, regardless of the side of stimulation 

(Fig. 11, type C). Although most patients have a complete 

absence of responses, some have a delayed response 

or a response of reduced amplitude. The latter 

findings, or the reappearance of previously 

absent responses, indicate a conduction defect without 

substantial axonal loss, from which the patient 

will recover either completely or almost completely. 

It is common to observe an increased blink rate 

in patients with facial palsy. Pastor et al. 86 reported 

enhanced blink reflex excitability recovery curves in 

two patients examined within the first month after 

onset of a Bell’s palsy. This finding was later confirmed 

by Syed et al., 91 suggesting that plastic 


changes may take place in the central nervous system 

in an attempt to compensate for the eyelid weakness. 

In patients without distal degeneration, the latency 

of R1 is usually delayed by a few milliseconds (2 ms 

in the series reported by Kimura et al. 59 ), and returns 

to normal in 2 to 4 months. 

In patients with substantial degeneration, R1 is 

absent and the direct motor response markedly reduced 

in amplitude for several months or longer. 

Eekhof et al. 36 recorded ephaptic transmission in 

50% of their patients who developed facial synkinesis 

after Bell’s palsy and suggested that there may be 

some alteration in excitability of the facial nucleus. 

Cranial Nerve Involvement in Polyneuropathies. 

Generalized polyneuropathies may induce 

bilateral abnormalities of the trigeminal reflexes. 65 

Kimura 54 has studied the blink reflex in a large series 

of patients with polyneuropathy. In patients with Sjögren’s 

neuronopathy, Valls-Solé et al. 95 found severely 

affected blink reflex and MIR, whereas the jaw 

jerk was spared. The masseter silent period after 

chin taps (tap-SP) tends to be delayed in patients 

with demyelinating neuropathies and normal in patients 

with axonopathies of various origin. Patients 

with chronic inflammatory demyelinating polyneuropathy 

or severe diabetic polyneuropathy often 

have subclinical trigeminal dysfunction. 21 This is 

best disclosed by demonstrating a delay of the first 

silent period SP1 of the MIR after mental nerve 

stimulation. 

Oculomotor, trigeminal, or facial nerve involvement 

may be a mononeuropathic expression of a 

systemic disorder. The trigeminal and facial nerves 

may be involved in patients with Guillain–Barré syndrome. 

Brainstem Lesions. Lesions affecting the mesencephalon, 

pons, or medulla cause different abnormalities, 

which may be revealed by neurophysiological 

examination of brainstem reflexes and functions. 

Changes in jaw jerk, blink reflex, light-evoked blink, 

and corneal reflex have been reported in multiple 

sclerosis. 78 Kimura 56 analyzed the blink reflex obtained 

from 260 patients with suspected multiple 

sclerosis. The R1 response of the blink reflex was 

delayed on one or both sides in 96 of 145 patients 

with a definite diagnosis (66%), 32 of 57 with probable 

multiple sclerosis (56%), and 17 of 58 with possible 

disease (29%). When the reflex was analyzed 

according to clinical localization of the lesion in the 

260 patients, R1 was abnormal in 49 of 63 patients 

with pontine signs (78%) and 59 of 104 with other 

brainstem signs (57%). Kimura 56 also found a delayed 

or absent R1 in 40% of patients in the absence 

of clinical signs of brainstem damage. Alteration of 

R2 was less specific. A combination of trigeminal reflex 

abnormalities, in particular an abnormal jaw 

jerk accompanied by a disorder of one of the other 

reflexes, reflects damage to different levels of the 

trigeminal system and may therefore make an important 

contribution to the diagnosis of multiple sclerosis. 

The finding of an abnormal jaw jerk with normal 

masseteric EMG may reflect a midbrain lesion involving 

structures adjacent to the aqueduct. 73,81 Abnormal 

jaw jerks have been found ipsilateral to midbrain 

lesions. 45,52 These observations have now been verified 

neuroanatomically in midbrain lesions involving 

the mesencephalic tract and nucleus of the trigeminal 

nerve and sparing the trigeminal motor nucleus 

and fibers in the pons. 73 

Lesions affecting the lower pons or the dorsolateral 

medulla oblongata, or both, cause several types 

of blink reflex abnormality, as shown in Figure 11. 

The figure may serve as a guide to relate a specific 

abnormality to the location of the causal lesion in 

the central reflex arc. In general, all the abnormal 

R2 features occurring in the blink reflex also occur 

in corneal reflex responses. 

Wallenberg’s syndrome is commonly associated 

with an abnormality of the corneal reflex and R2 of 

the blink reflex, whereas R1 is spared. 58,74,75,82 In 

most patients, an afferent type of reflex abnormality 

is present (Fig. 11, type B2). 

In predicting MRI results in patients with symptoms 

and signs related to classic trigeminal nerve 

dysfunction, Majoie et al. 67 showed that reflex studies 

yielded a sensitivity of 100%, a specificity of 81%, 

a positive predictive value of 57%, and a negative 

predictive value of 100%. However, the authors emphasized 

that further investigations in larger group 

of patients with different signs and symptoms related 

to trigeminal dysfunction are required. 

Hemispheric Lesions. Ischemic or hemorrhagic lesions 

or tumors in the cerebral hemispheres may 

alter some components of the corneal reflex and 

MIR responses. 23,61,75,76 Studying patients in the 

early phase after a stroke, Fisher et al. 42 reported 

delayed R1 responses, which subsequently returned 

to normal. During chronic states, however, changes 

in R2 may persist for several weeks or even longer. In 

hemispheric disorders, corneal and late blink reflex 

responses may be absent or diminished bilaterally 

when the affected side of the face is stimulated (similar 

to type B2 in Fig. 11). Stimulation of the normal 

side often reveals an additional absence or diminu- 


tion of the consensual response (similar to type D in 

Fig. 11). Because the polysynaptic R2 is more profoundly 

inhibited than is the oligosynaptic R1, interruption 

of corticobulbar pathways to the reflex system 

is more likely to result in diminished facilitation 

of interneurons. The descending facilitatory influence 

on the bulbar pathway itself probably originates 

in wide areas of the cortex, but the most common 

site of origin is the lower postcentral area, which 

corresponds to the sensory representation of the 

face. 61,76 By contrast, in chronic pyramidal tract lesions, 

the R1 response may be slightly facilitated on 

the paretic side. This facilitation is explained by removal 

of corticobulbar inhibitory influences on facial 

motoneurons as they impinge on spinal motoneurons. 

Extrapyramidal Disorders. In extrapyramidal disorders, 

facial reflexes with short latencies (jaw jerk, R1 

of the blink reflex, and SP1 of the MIR) are unaltered. 

This observation indicates that the afferent 

and efferent fibers of the reflex arc and the brainstem 

monosynaptic or oligosynaptic circuits are not 

directly affected by these diseases. In contrast, reflexes 

with longer latencies and polysynaptic pathways, 

which are subject to strong suprasegmental influence, 

are often altered due to a change in the 

excitability of the interneuronal pool. 

Patients with Parkinson’s disease often show an 

enhanced excitability of brainstem interneurons that 

leads to a rapid recovery of the blink reflex responses. 

55 Similar abnormalities have been described 

in the excitability recovery curve of the 

MIR 29 (Fig. 10). 

In Huntington’s disease, R2 shows an increased 

latency and enhanced habituation. 2,16,39,69 In contrast, 

the MIR, including recovery curves of SP1 and 

SP2, is normal. 16,29 

Eyelid Movement Disorders. Eyelid kinematics are 

best investigated using electromagnetic recordings. 

17,19,40 Furthermore, synchronous EMG recording 

from the levator palpebrae and the orbicularis 

oculi muscles provides valuable information on possible 

disturbances of the reciprocal activity between 

these two muscles in various eyelid movement abnormalities. 

5 

Blepharospasm. Blepharospasm is a focal dystonia 

of the eyelids 68 characterized by tremulous, phasic, 

or clonic discharges in the orbicularis oculi. The 

antagonistic activity between the orbicularis oculi 

and the levator palpebrae muscles is disturbed in 

some patients, and a minority of patients also have 

involuntary levator palpebrae inhibition (vide infra). 

Although in some patients with blepharospasm, the 

R2 response is prolonged, 12 the reflex data are usually 

normal. 33,35 Patients with blepharospasm have 

abnormal enhancement of brainstem interneuronal 

excitability, as shown by recovery curves of the R2 

response (Fig. 8), similar to that found in patients 

with parkinsonism. 3,12,29,93 However, the pathophysiology 

underlying such abnormality may be different 

in the two disorders. In a group of 33 patients with 

involuntary eyelid closure, Aramideh et al. 3 showed 

that recovery of R2 was enhanced in all patients with 

pure blepharospasm. The exact pathophysiology of 

dystonia is unknown (see Berardelli et al. 13 for a 

review). 

Apraxia of Eyelid Opening. Patients with apraxia 

of eyelid opening, also known as involuntary levator 

palpebrae inhibition, have difficulty in initiating the 

act of lid opening on command. 15,44 Many patients 

also exhibit an inability to keep the eyelids open for 

FIGURE 12. An EMG recording in a patient with involuntary levator 

palpebrae inhibition (apraxia of eyelid opening) and blepharospasm. 

(A) The patient shows involuntary inhibition periods 

(IIPs) of the LP muscle, causing drooping of the eyelids and 

periods of suppression of LP activity resulting in inability to open 

the eyelids voluntarily on the command “open eyes.” (B) Dense 

burst of phasic discharges during spasms of the OO muscle are 

accompanied by inhibition of LP activity (Aramideh et al. 8 ). 


a long period of time (Fig. 12). Apraxia of eyelid 

opening may accompany blepharospasm. Synchronous 

needle EMG recording from the levator palpebrae 

and the orbicularis oculi muscles reveals involuntary 

inhibition of the levator palpebrae muscle 

activity causing inability to keep the eyelids open or 

to reopen them after involuntary closure of the lids. 5 

The blink-reflex–excitability recovery curve is normal 

in these patients. 3 

Orbicularis Oculi Motor Persistence. Involuntary 

levator palpebrae inhibition should be differentiated 

from “motor persistence of the orbicularis oculi” 

muscle. 4,7 Following voluntary closure of the eyelids 

on command (Fig. 13), the patients with the latter 

abnormality are also unable to open the lids on command. 

However, needle EMG recording shows that 

these patients are unable to suppress the activity of 

the orbicularis oculi muscle. 7 

FIGURE 13. Orbicularis oculi motor persistence. The EMG recording 

shows that after voluntary closure of the eyelid and upon 

the command to “open eyes,” patient is unable to suppress the 

contraction of the OO. After about 1 s, the density of the bursts of 

action potentials in the orbicularis gradually begins to diminish 

and is accompanied by an increase in intensity and frequency of 

the discharges in the LP. The eyelid opens when the orbicularis 

muscle activity is almost completely inhibited (at open arrow) 

(Aramideh et al. 7 ). 

REFERENCES 

1. Accornero N, Berardelli A, Bini G, Cruccu G, Manfredi M. 

Corneal reflex elicited by electrical stimulation of the human 

cornea. Neurology 1980;30:782–785. 

2. Agostino R, Berardelli A, Cruccu G, Pauletti G, Stocchi F, 

Manfredi M. Correlation between facial involuntary movements 

and abnormalities of blink and corneal reflexes in 

Huntington’s chorea. J Neurol Neurosurg Psychiatry 1988; 

3:281–289. 

3. Aramideh M, Eekhof JLA, Bour LJ, Koelman JHTM, Speelman 

JD, Ongerboer de Visser BW. Electromyography and 

blink reflex recovery in involuntary eyelid closure: a comparative 

study. J Neurol Neurosurg Psychiatry 1995;58: 

692–698. 

4. Aramideh M, Koelman JHTM, Speelman JD, Ongerboer de 

Visser BW. Eyelid movement disorders and electromyography. 

Lancet 2001;357:805–806. 

5. Aramideh M, Ongerboer de Visser BW, Devriese PP, Bour 

LJ, Speelman JD. Electromyographic features of levator palpebrae 

superioris and orbicularis oculi muscles in blepharospasm. 

Brain 1994;117:27–38. 

6. Aramideh M, Ongerboer de Visser BW, Koelman JHTM, Majoie 

CB, Holstege G. The late blink reflex abnormality due to 

lesions of the lateral tegmental field. Brain 1997;120: 

1685–1692. 

7. Aramideh M, Ongerboer de Visser BW, Koelman JHTM, 

Speelman JD. Motor persistence of orbicularis oculi muscle 

in eyelid opening disorders. Neurology 1995;45:897–902. 

8. Aramideh M, Valls-Solé J, Cruccu G, Ongerboer de Visser 

BW. Cranial nerves and brain stem reflexes: electrodiagnostic 

techniques, physiology and normative data. In: Brown 

WF, Bolton CF, Aminoff MJ, editors. Neuromuscular function 

and disease. Philadephia: WB Saunders; 2002. p 

433–454. 

9. Auger RG, McManis PG. Trigeminal sensory neuropathy associated 

with decreased oral sensation and impairment of 

the masseter inhibitory reflex. Neurology 1990;40:759–763. 

10. Benedek L, Von Angyal L. Ueber die Palmomentalen und 

corneomentalen Reflexe. Z Neurol Psychiat 1941;172: 

632–638. 

11. Berardelli A, Cruccu G, Manfredi M, Rothwell JC, Day BL, 

Marsden CD. The corneal reflex and R2 component of the 

blink reflex. Neurology 1985;35:797–801. 

12. Berardelli A, Rothwell JC, Day BL, Marsden CD. Pathophysiology 

of blepharospasm and oromandibular dystonia. Brain 

1985;108:593–609. 

13. Berardelli A, Rothwell JC, Hallett M, Thompson PD, Manfredi 

M, Marsden CD. Pathophysiology of primary dystonia. 

Brain 1998;121:1195–1212. 

14. Boelhouwer AJW, Brunia CHM. Blink reflexes and the state 

of arousal. J Neurol Neurosurg Psychiatry 1977;40:58–63. 

15. Boghen D. Apraxia of lid opening: a review. Neurology 1997; 

48:1491–1503. 

16. Bollen E, Arts R, Roos R, van der Velde EA, Buruma OJ. 

Brainstem reflexes and brainstem auditory evoked responses 


in Huntington’s chorea. J Neurol Neurosurg Psychiatry 

1986;49:313–315. 

17. Bour LJ, Aramideh M, Ongerboer de Visser BW. Neurophysiological 

aspects of eye and eyelid movements during 

blinking in man. J Neurophysiol 2000;83:166–176. 

18. Brown P, Rothwell JC, Thompson PD, Britton TC, Day BL, 

Marsden CD. New observations on the normal auditory 

startle reflex in man. Brain 1991;11:1891–1902. 

19. Collewijn H, Van Der Steen J, Steinman RM. Human eye 

movements associated with blinks and prolonged eyelid closure. 

J Neurophysiol 1985;54:11–27. 

20. Cruccu G, Agostino R, Berardelli A, Manfredi M. Excitability 

of the corneal reflex in man. Neurosci Lett 1986;63:320–324. 

21. Cruccu G, Agostino R, Inghilleri M, Innocenti P, Romaniello 

A, Manfredi M. Mandibular nerve involvement in diabetic 

polyneuropathy and chronic inflammatory demyelinating 

polyneuropathy. Muscle Nerve 1998;21:1673–1679. 

22. Cruccu G, Agostino R, Inghilleri M, Manfredi M, Ongerboer 

de Visser BW. The masseter inhibitory reflex is evoked by 

innocuous stimuli and mediated by A beta afferent fibers. 

Exp Brain Res 1989;77:447–450. 

23. Cruccu G, Fornarelli M, Manfredi M. Impairment of masticatory 

function in hemiplegia. Neurology 1988;38:301–306. 

24. Cruccu G, Frisardi G, Pauletti G, Romaniello A, Manfredi M. 

Excitability of the central masticatory pathways in patients 

with painful temporomandibular disorders. Pain 1997;73: 

447–454. 

25. Cruccu G, Inghilleri M, Fraioli B, Guidetti B, Manfredi M. 

Neurophysiological assessment of trigeminal function after 

surgery for trigeminal neuralgia. Neurology 1987;37: 

631–638. 

26. Cruccu G, Leandri M, Feliciani M, Manfredi M. Idiopathic 

and symptomatic trigeminal pain. J Neurol Neurosurg Psychiatry 

1990;53: 1034–1042. 

27. Cruccu G, Leandri MG, Ferracuti S, Manfredi M. Corneal 

reflex responses to mechanical and electrical stimuli in 

coma and narcotic analgesia in humans. Neurosci Lett 1997; 

222:33–36. 

28. Cruccu G, Ongerboer de Visser BW. The jaw reflexes. In: 

Deuschl G, Eisen A, editors. Recommendations for the practice 

of clinical neurophysiology: guidlines of the International 

Federation of Clinical Neurophysiology. Amsterdam: 

Elsevier Science; 1999. p 243–247. 

29. Cruccu G, Pauletti G, Agostino R, Berardelli A, Manfredi M. 

Masseter inhibitory reflex in movement disorders. Huntington’s 

chorea, Parkinson’s disease, dystonia, and unilateral 

masticatory spasm. Electroenceph Clin Neurophysiol 1991; 

81:24–30. 

30. Davis M, Gendelman DS, Tischler MD, Gendelman PM. A 

primary acoustic startle circuit: lesion and stimulation studies. 

J Neurosci 1982;2:791–805. 

31. Dehen H, Bathien N, Cambier J. The palmomental reflex. 

An electrophysiological study. Eur Neurol 1975;13:395–404. 

32. Dengler R, Rechl F, Struppler A. Recruitment of single units 

in human blink reflex. Neurosci Lett 1982;34:301–305. 

33. Deuschl G, Goddemeier C. Spontaneous and reflex activity 

of facial muscles in dystonia, Parkinson’s disease and in normal 

subjects. J Neurol Neurosurg Psychiatry 1998;64: 

320–324. 

34. De Watteville A. Note on the jaw-jerk, or masseteric tendon 

reaction, in health and disease. Brain 1886;8:518–519. 

35. Eekhof JLA, Aramideh M, Bour LJ, Hilgevoord AAJ, Speelman 

JD, Ongerboer de Visser BW. Blink reflex recovery 

curves in blepharospasm, torticollis spasmodica and hemifacial 

spasm. Muscle Nerve 1996;19:10–15. 

36. Eekhof JLA, Aramideh M, Speelman JD, Devriese PP, Ongerboer 

de Visser BW. Blink reflexes and lateral spreading in 

patients with synkinesia after Bell’s palsy and in hemifacial 

spasm. Eur J Neurol 2000;43:141–146. 

37. Ellrich J, Hopf HC, Treede RD. Nociceptive masseter inhibitory 

reflexes evoked by laser radiant heat and electrical 

stimuli. Brain Res 1997;764:214–220. 

38. Esteban A. A neurophysiological approach to brainstem reflexes. 

Blink reflex. Neurophysiol Clin 1999;29:7–38. 

39. Esteban A, Gimenez-Roldan S. Blink reflex in Huntington’s 

chorea and Parkinson’s disease. Acta Neurol Scand 1975;52: 

145–157. 

40. Evinger C, Shaw MD, Peck CK, Manning KA, Baker R. Blinking 

and associated eye movements in humans, guinea pigs 

and rabbits. J Neurophysiol 1984;52:323–339. 

41. Ferguson IT. Electrical study of jaw and orbicularis oculi 

reflexes after trigeminal nerve surgery. J Neurol Neurosurg 

Psychiatry 1978;41:819–823. 

42. Fisher MA, Shahani B, Young RR. Assessing segmental excitability 

after acute rostral lesions: II. The blink reflex. Neurology 

1979;29:45–50. 

43. Godeaux E, Desmedt JE. Exteroceptive suppression and motor 

control of the masseter and temporalis muscles in normal 

man. Brain Res 1975;85:447–458. 

44. Goldstein JE, Cogan DG. Apraxia of lid opening. Arch Ophthalmol 

1965;73:155–159. 

45. Goodwill CJ, O’Tuama L. Electromyographic recording of 

the jaw reflex in multiple sclerosis. J Neurol Neurosurg Psychiatry 

1969;32:6–10. 

46. Goor C, Ongerboer de Visser BW. Jaw and blink reflexes in 

trigeminal nerve lesions. Neurology 1976;26:95–97. 

47. Guberman A. Clinical significance of the corneomandibular 

reflex. Arch Neurol 1982,39:1368–1372. 

48. Guiot G. Valeur localisaterice et pronostique du reflexe corneo-pterygoidien. 

Le phenomene de la diduction lente du 

maxillaire. Sem Hopital Paris 1946;22:1368–1396. 

49. Hoffman P, Tonnies JF. Nachweis des vollig konstanten 

verkommens des Zungen-Kiefer-Reflexes bei Menschen. 

Pflugers Archiv 1948;250:103–108. 

50. Holstege G, Tan J, van Ham JJ, Graveland GA. Anatomical 

observations on the afferent projections to the retractor bulb 

motoneuronal cell group and other pathways possibly related 

to the blink reflex in the cat. Brain Res 1986;374: 

321–334. 

51. Hori A, Yasuhara A, Naito H, Yasuhara M. Blink reflex elicited 

by auditory stimulation in the rabbit. J Neurol Sci 1986; 

76:49–59. 

52. Hufschmidt HJ, Spuler H. Mono- and polysynaptic reflexes 

of the trigeminal muscles in human sclerosis. J Neurol Neurosurg 

Psychiatry 1962;25:332–335. 

53. Karpukhina MV, Gokin AP, Limanskii YP. Activation of pontine 

and bulbar reticulo-spinal neurons in the cat by somatosensory 

stimuli of different modalities. Neurophysiology 

1986;18:329–336. 

54. Kimura J. Conduction abnormalities of the facial and trigeminal 

nerves in polyneuropathy. Muscle Nerve 1982;5: 

149–144. 

55. Kimura J. Disorder of interneurons in parkinsonism. The 

orbicularis oculi reflex to paired stimuli. Brain 1973;96: 

87–96. 

56. Kimura J. Electrical elicited blink reflex in diagnosis of multiple 

sclerosis. Review of 260 patients over a seven-year period. 

Brain 1975;98:413–426. 

57. Kimura J, Daube J, Burke D, Hallett M, Cruccu G, Ongerboer 

de Visser BW, Yanagisawa N, Shimamura M, Rothwell J. 

Human reflexes and late responses. Report of an IFCN committee. 

Electroencephalogr Clin Neurophysiol 1994;90: 

393–403. 

58. Kimura J, Lyon LW. Orbicularis oculi reflex in Wallenberg 

syndrome: alteration of the late reflex by lesion of the spinal 

tract and nucleus of the trigeminal nerve. J Neurol Neurosurg 

Psychiatry 1972;35:228–233. 

59. Kimura J, Powers JM, Van Allen MW. Reflex response of 

orbicularis oculi muscles to supraorbital nerve stimulation. 

Study in normal subjects and in peripheral facial paresis. 

Arch Neurol 1969;21:193–199. 


60. Kimura J, Rodnitzky RL, Van Allen MW. Electrodiagnostic 

study of trigeminal nerve. Orbicularis oculi reflex and masseter 

reflex in trigeminal neuralgia, paratrigeminal syndrome, 

and other lesions of the trigeminal nerve. Neurology 

1970;20:574–583. 

61. Kimura J, Wilkinson T, Damasio H, Adams HR Jr, Shivapour 

E, Yamada T. Blink reflex in patients with hemispheric cerebrovascular 

accident (CVA). J Neurol Sci 1985;67:15–28. 

62. Kugelberg E. Facial reflexes. Brain 1952;75:385–396. 

63. Leandri M, Favale E. Diagnostic relevance of trigeminal 

evoked potentials following infraorbital nerve stimulation. J 

Neurosurg 1991;75:244–250. 

64. Leandri, M, Parodi CL, Favale E. Early trigeminal evoked 

potentials in tumors of the base of the skull and trigeminal 

neuralgia. Electroencephalogr Clin Neurophysiol 1988;71: 

114–124 

65. Lecky BRF, Hughes RAC, Murray NMF. Trigeminal sensory 

neuropathy. A study of 22 cases. Brain 1987;110:1463–1485. 

66. Lele PP, Wedell G. Sensory nerves of the cornea and cutaneous 

sensibility. Exp Neurol 1959;1:334–359. 

67. Majoie CBLM, Aramideh M, Hulsmans FJH, Castelijns JA, 

van Beek EJR, Ongerboer de Visser BW. Correlation between 

electromyographic reflex and MR imaging examinations 

of the trigeminal nerve. Am J Neuroradiol 1999;20: 

1119–1125. 

68. Marsden CD. Blepharospasm-oromandibular dystonia syndrome 

(Brueghel’s syndrome): a variant of adult-onset torsion 

dystonia J Neurol Neurosurg Psychiatry 1976;39: 

1204–1209. 

69. McIntyre AK, Robinson RG. Pathway for the jaw jerk in man. 

Brain 1959;75:385–396. 

70. Miles TS, Turker KS. Decomposition of the human electromyogramme 

in an inhibitory reflex. Exp Brain Res 1987;65: 

337–342. 

71. Miwa H, Imamura N, Kogahara K, Ohori T, Mizuno Y. Somatosensrory 

evoked blink response: findings in patients 

with Miller Fisher syndrome and in normal subjects. J Neurol 

Neurosurg Psychiatry 1995;58:95–99. 

72. Miwa H, Nohara C, Hotta M, Shimo Y, Amemiya K. Somatosensory-evoked 

blink reflex response: investigation of the 

pathophysiological mechanism. Brain 1998;121:281–291. 

73. Ongerboer de Visser BW. Afferent limb of the human jaw 

reflex: electrophysiologic and anatomic study. Neurology 

1982;32:536–546. 

74. Ongerboer de Visser BW. Anatomical and functional organization 

of reflexes involving the trigeminal system in man: 

jaw reflex, blink reflex, corneal reflex and exteroceptive suppression. 

Adv Neurol 1983;39:729–738. 

75. Ongerboer de Visser BW. Comparative study of corneal and 

blink reflex latencies in patients with segmental or with central 

lesions. Adv Neurol 1983;39:757–772. 

76. Ongerboer de Visser BW. Corneal reflex latency in lesions of 

the lower postcentral region. Neurology 1981;31:701–707. 

77. Ongerboer de Visser BW. The recorded corneo-mandibular 

reflex. Electroencephalogr Clin Neurophysiol 1986;63: 

25–31. 

78. Ongerboer de Visser BW, Cruccu G. Neurophysiologic examination 

of the trigeminal, facial, hypoglossal, and spinal 

accessory nerves in cranial neuropathies and brainstem disorders. 

In: Brown WF, Bolton CF, editors. Clinical electromyography. 

Boston: Butterworths; 1993. p 61–92. 

79. Ongerboer de Visser BW, Cruccu G, Manfredi M, Koelman 

JHTM. Effects of brainstem lesions on the masseter inhibitory 

reflex. Functional mechanisms of reflex pathways. Brain 

1990;113:781–792. 

80. Ongerboer de Visser BW, Goor C. Electromyographic and 

reflex study in idiopathic and symptomatic trigeminal neuralgias: 

latency of the jaw and blink reflexes. J Neurol Neurosurg 

Psychiatry 1974;37:1225–1230. 

81. Ongerboer de Visser BW, Goor C. Jaw reflexes and masseteric 

electromyograms in mesencephalic and pontine lesions. 

An electrophysiologic study. J Neurol Neurosurg Psychiatry 

1976;39:90–92. 

82. Ongerboer de Visser BW, Kuypers HGJM. Late blink reflex 

changes in lateral medullary lesions. An electrophysiological 

and neuroanatomical study of Wallenberg’s syndrome. Brain 

1978;101:285–94. 

83. Ongerboer de Visser BW, Mechelse K, Megens PHA. Corneal 

reflex latency in trigeminal nerve lesions. Neurology 

1977;27:1164–1167. 

84. Ongerboer de Visser BW, Moffie D. Effects of brainstem and 

thalamic lesions on the corneal reflex. An electrophysiological 

and anatomical study. Brain 1979;102:595–608. 

85. Overend W. Preliminary note on a new cranial reflex. Lancet 

1896;1:619. 

86. Pastor P, Muñoz E, Valldeoriola F. Enhanced blink rate and 

involuntary contralateral eye closure in patients with Bell’s 

palsy. Muscle Nerve 1998;21:1596. 

87. Pennisi E, Cruccu G, Manfredi M, Palladini G. Histometiric 

study of myelinated fibers in the human trigeminal nerve. J 

Neurol Sci 1991;105:22–28. 

88. Selby G. Diseases of the fifth cranial nerve. In: Dyck PJ, 

Thomas PK, Lambert EH, Bunge E, editors. Peripheral neuropathy. 

Philadelphia: WB Saunders; 1984. p 1224–1265. 

89. Shahani BT. The human blink reflex. J Neurol Neurosurg 

Psychiatry 1970;33:792–800. 

90. Shahani BT, Young RR. Human orbicularis oculi reflexes. 

Neurology 1972;22:149–154. 

91. Syed NA, Delgado A, Sandbrink F, Schulman AE, Hallett M, 

Floeter MK. Blink reflex recovery in facial weakness. An electrophysiological 

study of adaptive changes. Neurology 1999; 

52:834–838. 

92. Tavy DL, van Woerkom TCAM, Bots GTAM, Endtz LJ. Persistence 

of the blink reflex to sudden illumination in a comatose 

patient. Arch Neurol 1984;42:323–324. 

93. Tolosa E, Montserrat L, Bayes A. Blink reflex studies in focal 

dystonias. Enhanced excitability of brainstem interneurones 

in cranial dystonia and spasmodic torticollis. Mov Disord 

1988;3:61–69. 

94. Valls-Solé J, Cammarota A, Alvarez R, Hallett M. Orbicularis 

oculi responses to stimulation of nerve afferents from upper 

and lower limbs in normal humans. Neurosci Lett 1994;650: 

313–316. 

95. Valls-SoléJ, Graus F, Font J, Pou A, Tolosa ES. Normal proprioceptive 

trigeminal afferents in patients with Sjogren’s 

syndrome and sensory neuropathy. Ann Neurol 1990;28: 

786–790. 

96. VanderWerf F, Aramideh M, Ongerboer de Visser BW, Baljet 

B, Speelman JD, Otto JA. A retrograde double fluorescent 

tracing study of the levator palpebrae superioris muscle in 

the cynomolgous monkey. Exp Brain Res 1997;113:174–179. 

97. Weiskrantz L, Wanington EK, Sanders MD, Marshall J. Visual 

capacity in the hemianoptic field following a restricted occipital 

ablation. Brain 1974;97:700–728. 

98. Wieser ST, Muller-Fahlbusch H. Ueber nociceptive reflexe 

des gesichtes. Dtsch Z Nervenheilk 1962;183:530–543. 

99. Wilkins DE, Hallett M, Wess MM. Audiogenic startle reflex of 

man and its relationship to startle syndromes: a review. Brain 

1986;109:561–573. 

100. Yates SK, Brown WF. Light-stimulus–evoked blink reflex: 

methods, normal values, reaction to other blink reflexes, 

and observation in multiple sclerosis. Neurology 1981;32: 

272–281. 

101. Yates SK, Brown WF. The human jaw-jerk: electrophysiologic 

methods to measure the latency, normal values, and changes 

in multiple sclerosis. Neurology 1981;31:632–634.

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