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July2007 Vol.44 Issue:      2 Table of Contents
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An Electro-Physiologic Study of Trigeminal Brainstem Circuits in Migraine

Nihal El-Shazly1, Fouad Abd Allah2, Hanan Hosni1, Gihan Ramzy2, Mona T. El-Ghoniemy3

Departments of Clinical Neurophysiology1, Neurology2, Neurosurgery3, Cairo University



ABSTRACT

Objective: The study aimed at investigating functional changes in the trigeminal and optic nerves brainstem connections in migraine patients. Methods: Trigeminal somatosensory evoked potentials (TSER's), electric blink reflex (EBR) and light stimulus evoked blink reflex (LBR) were carried out interictally on 18 patients suffering from migraine without aura and 12 healthy controls. TSER’s latencies (N1, P1, N2, and P2), EBR latencies (R1, ipsilateral and contralateral R2) as well as LBR latencies (direct and indirect responses) and their amplitudes were recorded and compared to healthy controls. Results: The ipsilateral and the contralateral R2 components of the EBR (R2i, R2c) showed a highly significant delay as compared to the control group (p<0.000). N1, P1 and N2 latencies in patients were significantly longer than the control group bilaterally. P1 latencies showed the most significant prolongation of latency (p<0.0000). The latencies of the LBR direct and indirect responses were significantly prolonged in the patient group (p<0.000) and had a double fold amplitude compared to those of the control group. Conclusion: Migraine patients show a disruption in the central circuits not only at the level of the brainstem but possibly within the higher cerebral regions as well.

(Egypt J. Neurol. Psychiat. Neurosurg., 2007, 44(2): 693-703)

 

 




INTRODUCTION

 

Migraine is a common, chronic incapacitating neurovascular disorder. It affects an estimate of 12% of the population1,2. The pathophysiology of migraine is incompletely understood, however understanding the nature of that disorder is important to provide the basis for treatment policy. Different theories were proposed to explain the pathophysiology of migraine, one proposes a generator in the brainstem, the second deals with the cortical spreading depression theory, the third proposes a genetic mutation of the calcium channels and the fourth is based on the pathophysiological role of serotonin. Activation of the trigemino-vascular system and its central brainstem projections may explain the prolonged headache and the associated symptoms of migraine.1, 3, 4

This study aims at determining the possible involvement of the brainstem trigeminal and optic nerve connections in patients suffering from migraine using different neurophysiologic techniques.

Studying of the central trigeminal brainstem circuits is easy and feasible by a variety of neurophysiologic methods one of them is the electric blink reflex (EBR). Higher central trigeminal connections can be neurophysiologically tested through the trigeminal somatosensory evoked responses (TSER). Optic nerve brainstem connections can be studied using LBR.

Blink reflex can be elicited by flashes of light, corneal touch, electrical stimulation of the 5th nerve and muscle stretch5. The early and late blink discharges evoked by stimulation of the supra-orbital nerve (EBR) are abnormal in lesions that involve the Vth or the VIIth cranial nerves, brain stem or cerebral hemispheres6. The response consists of an early ipsilateral R1 component that is mediated by a simple reflex arc running to the pons through the sensory root of the trigeminal nerve. The later R2 component appears bilaterally and represents a polysynaptic reflex arc that involves the spinal tract and nucleus7. Methods to evoke the blink reflex other than electric stimulation of the Vth nerve branches are attractive because they test peripheral and central neural connections specifically related to the type of stimulus, light or auditory. 8, the auditory evoked blink reflex to single clicks is commonly absent in healthy individuals and thus has a limited diagnostic value. The LBR, on the contrary, is present in all healthy subjects and is reliable in testing the integrity of the prethalamic visual connections8. Limited information is known about the exact pathway of the reflex, and central brainstem connections of the optic nerve to the VIIth nerve complex, however there is evidence that afferent optic fibers probably enter the brainstem in the pretectum and impulses are then conveyed to the facial nuclei in the pons. It seems that the cerebral cortex is not involved in the generation of the LBR as experimental ablation of occipital cortex does not influence the response LBR is not blocked or delayed by hemispherectomy8, but the reflex is lost in rostral brainstem lesions8,9. Combined light and electric evoked blink responses examination allow different brainstem levels to be examined.

TSERs can be obtained by electrical stimulation of the trigeminal nerve10,11,12. Lip stimulation was found to be the best standardized method of stimulation to obtain consistent reliable and reproducible TSER's with high degree of bilateral representation. The general picture shows a number of waves between 2 ms and 115 ms 13 The  short latency waves (within 3 ms) are of peripheral origin, that may be  in the Gasserian ganglion, or the trigeminal nerve.14 These early potentials are followed by at least two longer latency waves (N1 of 12-15 ms and P1 of 19-22 ms) that may originate in deep brainstem structures, Furthermore, potential waves with a very long latency (> 100 ms) follow when the response is produced by painful stimulation. The origins of the long and very long latency waves is still a matter of debate and are believed to originate more proximal than the brain stem15,16. The most consistent response consists of four very constant deflexions (N1, P1, N2, P2 and N3) forming a W-shaped complex of mean duration 31.27 ms.  All the components with the exception of N3 are always bilaterally detectable.15-23

 

PATIENTS AND METHODS

 

The study was carried on 30 subjects (18 patients and 12 age and sex matched controls). The patient group consisted of 18 migraine patients among those coming to the Neurology out-patient clinic, in Kasr El-Eini Hospital.

According to the Headache Classification Committee of the International Headache Society24 all the patients were classified as migraine without aura.

The control group: consisted of 12 age and sex matched controls recruited from the hospital staff and the relatives of the patients.

Excluded from the study were types of headache other than migraine, patients with neurological deficits other than headache, patients with renal, hepatic or blood disorders, patients with ENT or ophthalmologic diseases causing headache or drug intake causing headache. All patients had no prophylactic treatment (only simple analgesics). All patients were subjected to meticulous history taking and neurological examination and headache questionnaire according to Headache Classification Committee of the International Headache Society24.

 

I)             Neurophysiologic studies:

Blink reflex and trigeminal somatosensory evoked potentials were carried out in the same session.

 

Studies were all interictal.

1)      LBR: (Technique modified after Yates & Brown, 1981)8

The LBR was carried out on a 2 channel Nihon Kohden Neduropack 2 machine. The patient was seated on a comfortable chair and asked to look downward at an angle of 15o-20o to eliminate any background EMG activity in the Orbicularis Oculi muscle. The room was darkened and the patient was given 5 minutes to adapt to darkness. The active electrode (Ag/AgCl disc electrode 1 cm in diameter) was placed on the Orbicularis Oculi muscle in the inferior lateral quadrant bilaterally, reference was placed at the inner side of the nose and the ground electrode was placed on the forehead. Stimuli were delivered by a photic stimulator of total energy output 1.2 joules. The flash placed 20 cm from the eyes. Stimuli were delivered at random intervals at least 3 seconds apart to avoid habituation. The sweep speed was adjusted at 200ms high cut 100 HZ, low cut 0.5 Hz. Each eye was tested separately while the other eye was covered by an eye patch.

 

2)            EBR:

The EBR was carried on a Schwartzer Myos 4 machine. The active electrode was placed on the belly of the orbicularis oculi muscle below the outer canthus bilaterally. The reference electrode was placed on the side of the nose and the ground electrode was placed on the forehead. The impedance was kept below 5 KOhm. The sweep speed was adjusted at 60 ms, the band pass was 1-2500Hz. Square wave electrical pulses were randomly delivered to the supraorbital nerves at an inter-stimulus interval of at least 30 seconds (to avoid habituation), pulse duration was 0.2 ms. The intensity of the stimulus was gradually increased till the threshold provoking a response was defined this was followed by a gradual reduction of the intensity till the response vanishes. This procedure was repeated twice to define the minimum intensity that provokes a blink response. The intensity of stimulation was then adjusted at the value that provokes maximum response amplitude.  Two trials were carried out to ensure reliability and reproducibility.

 

3)            TSER:

TSER’s were carried on a 2 channel Nihon Kohden Neuropack 2 machine. The active electrode was placed contralateral to the side of stimulation on the C5 and C6 positions (mid way between C3 and T3, C4 and T4 respectively according to the 10-20 international system). The reference electrode was placed on the Fpz position and the earlobe served as a ground .The impedance was kept below 5 KOhm the band pass was 1-3000 Hz, the sweep was adjusted at 100 ms. The stimulating electrode was fixed on the lips 1 cm from the angle of the mouth, the cathode was placed on the upper lip and the anode on the lower lip, 0.2 ms square wave electrical impulses were delivered to the lips at a frequency of 2 Hz, the intensity of stimulation was gradually increased to define the sensory threshold then the stimulus intensity was adjusted at 3 folds the sensory threshold. Two hundred stimuli were averaged and recorded. Two trials were carried out for each to ensure reproducibility and reliability.

 

Wave identification:

(i)     LBR: The latency was measured to the earliest EMG response

(ii)   EBR: R1 component: a biphasic or triphasic response on the same side of the stimulation, appearing around 10 ms,

R2 component: A polyphasic bilateral response appearing both ipsilateral to stimulation (R2i) as well as contralaterally R2c

(iii)  TSER: A W shaped response consisting of an early negative deflexion, N1 (N8)  appearing around 8 ms, followed by a positive deflexion, P1 (P14 ) around 14 ms, then a negative deflexion, N2 (N23) around 23 ms and finally another positive deflexion, P2 (P 37) around 37 ms.

 

II)        Statistical Methods:

Data were entered on an IBM compatible computer and were analyzed using the mean, standard deviation. To test the significance of differences between the two means, the student t-test was applied.

 

RESULTS

 

I.             Clinical data:

The study was carried on 18 patients suffering from migraine without aura, 13 females (72.2%) and 5 males (27.8%) of mean age 30.1±8.5 years as well as 12 age and sex matched controls, 8 females (66.7%) and 4  males (33.3%)  of mean age 31.0±11.6 years .

All the patients had migraine without aura. The duration of illness from the onset of the disease to the time of examination range between 6-40 months, mean duration was 20.0±12.5 months.

The headache was throbbing in character in 8 patients (44.4%), bursting in 4 patients (22.2%) and dull aching in 6 patients (33.3%). The Frequency of the attacks ranged between 1-9 attacks per month, mean frequency 4.4±2.64 attacks/ month. The duration of the attacks ranged between 5- 24 hours, mean duration 10.7±5.08 hours. Sixteen patients (88.9%) had other symptoms associated with headache and 2 (11.1%) did not have any associated symptoms. Among the 16 patients, 8 (50%) had headache associated with nausea, 2(12.5%) had vomiting, 12 (75%) had blurred vision and photophobia, 7 (43.7%) had vague manifestations and 1 (6.25%) had palpitation.

 

II.            Neurophysiologic data:

1.                   LBR :

LBR was elicited bilaterally in all patients as well as the control group (100%). The response recorded ipsilateral to the stimulation site was termed the direct response while that elicited on the opposite side was termed indirect response.

The mean latency of the recorded responses was significantly longer in the patients as compared to the control group on both the symptomatizing and non-symptomatizing sides (Table 1). The mean amplitude of the evoked response as well showed an almost double fold increase in the patients as compared to the control group (Table 2).

The maximum and minimum latencies and amplitudes of the direct and indirect responses are shown in tables (3) and (4).

Neither the latency nor the amplitude of the LBR showed a significant difference in  either the direct or the indirect responses on the symptomatizing compared to the opposite side (p>0.05). In patients who had bilateral attacks (6 patients) the side of the most frequent attacks was compared to the opposite side, and as well showed a non-significant difference in all the response parameters (p>0.05).

The duration of migraine and the frequency of the attacks showed a non-significant correlation (p> 0.05) to the latencies and amplitudes of direct and indirect responses of the LBR.

 

2.             EBR: 

Mean±SD of EBR threshold was 6.0±0.17 Uv and 11.9±2.7 Uv in patients and control respectively on the symptomatizing side and 5.8±2.6 Uv, 10.6±1.3 Uv in cases and control groups on the opposite side (Fig. 1).

A highly significant low (p<0.000) threshold of the EBR was found in the patient group as compared to the control group on both sides (threshold of EBR in migraine was almost half of that in the control group).

In migraineurs the threshold for EBR was low bilaterally regardless of the side of migraine attacks (p>0.05).

The latency of both the R2i and R2c components was significantly longer in the patient group as compared to the controls on both the symptomatizing and non - symptomatizing sides; however the R1 showed a non-significant difference (Tables  5 and 6).

There was no significant difference in the latencies of the EBR in relation to the side of migraine (p>0.05).

The duration of migraine and the frequency of the attacks showed a non-significant correlation (p>0.05) to the latency of any of the components of the EBR either ipsilateral or contralateral to migraine side.

 

3.             TSER:

The mean sensory threshold in patient group was 3.3±0.6 Uv ipsilateral to migraine and 2.9±4.0 contralaterally. Mean threshold in the controls was 3.5±0.8 Uv and 3.2±2.4 Uv (Fig. 2).

The mean sensory threshold in the TSER showed a non- significant difference in the patient group compared to the control group (p>0.05) and also there was a non significant correlation with the side of migraine (p>0.05).

Regarding the mean TSER latencies (Tables 7, 8 and Fig. 3), the P1 and the N1 components showed a significant delay in the patient group bilaterally compared to the controls (p<0.000, 0.01 respectively). The N2 component latency showed a significant delay on the symptomatizing side however on the non-symptomatizing side there was an obvious delay in latency however it did no reach the level of statistical significance. (p<0.05, p=0.07 respectively). The P2 component showed a non significant difference in the patient group compared to the controls on both symptomatizing and non-symptomatizing sides.

In the patient group there was a non-significant difference in latencies on the symptomatizing side compared to the opposite side (p>0.05).

The duration of migraine and the frequency of the attacks showed a non-significant correlation (p>0.05) to the latency of any of the components of the EBR on either side.

Table 1. Mean±SD of LBR latencies in milliseconds in cases and control groups.

 

Symptomatizing side

Non -  symptomatizing side

Direct

Indirect

Direct

Indirect

Patients

Controls

Patient

Control

Patients

Controls

Patient

Control

Mean

53.3

50.1

53.5

50.4

52.8

49.8

53.0

50.6

SD

2.2

1.6

1.8

1.56

1.9

1.5

1.8

1.12

p value

<0.000

<0.000

<0.000

<0.000

p<0.000 highly significant, p<0.05 significant, p>0.05 non-significant

 

Table 2. Mean±SD of LBR amplitudes in microvolts in cases and control groups.

 

 

 

Symptomatizing side

Non-symptomatizing side

Direct

Indirect

Direct

Indirect

Patients

Controls

Patient

Control

Patients

Controls

Patient

Control

Mean

5.0

2.5

5.1

2.3

5.2

2.8

4.9

2.9

SD

1.13

0.6

1.13

0.4

1.14

0.3

1.03

0.5

p value

<0.000

<0.000

<0.000

<0.000

p<0.000 highly significant, p<0.05 significant, p>0.05 non-significant

 

Table 3. The Maximum and minimum LBR latencies in milliseconds in cases and controls.

 

 

 

Symptomatizing side

Non-symptomatizing side

Direct

Indirect

Direct

Indirect

Patients

Controls

Patient

Control

Patients

Controls

Patient

Control

Max.

56.3

52.4

56.0

53.2

55.4

52.1

56.0

52.3

Min.

49.8

47.8

50.0

47.7

50.4

47.2

50.0

48.0

 

Table 4. The Maximum and minimum LBR amplitudes in microvolts in cases and controls.

 

Symptomatizing side

Non-symptomatizing side

Direct

Indirect

Direct

Indirect

Patients

Controls

Patient

Control

Patients

Controls

Patient

Control

Max

7.3

3.6

7.0

3.3

7.3

3.4

7.3

3.6

Min

3.1

1.7

2.9

1.9

3.7

2.2

3.6

1.8

 

Fig. (2):Threshold of VBR in cases and controls.

Table 5. Mean±SD of EBR latencies in milliseconds in patients and controls on the symptomatizing side.

 

 

R1

R2i

R2c

Patient

Control

Patient

Control

Patient

Control

Mean

10.3

10.5

34.8

30.7

34.4

32.9

SD

0.5

0.5

2.3

3.8

2.8

2.2

p value

>0.05

< 0.000

< 0.002

p<0.000 highly significant, p<0.05 significant, p>0.05 non-significant

 

Table 6. Mean EBR latencies in milliseconds in patients and controls on the non-symptomatizing side.

 

 

R1

R2i

R2c

Patient

Control

Patient

Control

Patient

Control

Mean

10.7

10.9

35.1

32.5

34.8

31.4

SD

2.8

1.3

2.4

3.0

2.6

1.4

p value

>0.05

<0.05

<0.000

p<0.000 highly significant, p<0.05 significant, p>0.05 non-significant

 

Fig. (2): Mean TSER threshold in cases and controls.

 

Table 7. Mean±SD of the TSER latencies in milliseconds on the symptomatizing side.

 

N1

P1

N2

P2

Patient

Control

Patient

Control

Patient

Control

Patient

Control

Mean

8.3

6

19.3

14.3

24.9

22.1

40.2

42.6

SD

1.5

2.3

2

3.1

3.6

2.8

4

2.8

p value

< 0.01

<0.000

<0.05

>0.05

p<0.000 highly significant, p<0.05 significant, p>0.05 non-significant

 

Table 8. Mean±SD of the TSER latencies in milliseconds on non-symptomatizing side.

 

 

N1

P1

N2

P2

Patient

Control

Patient

Control

Patient

Control

Patient

Control

Mean

8.7

7.4

18.9

15

25.5

23.4

37.5

36.8

SD

1.3

1.9

1.1

2.7

4.2

3.9

4.5

3.1

p value

<0.05

<0.000

= 0.07

>0.05

p<0.000 highly significant, p<0.05 significant, p>0.05 non-significant

 

Fig. (3): Mean latencies of TSER in cases and controls.


DISCUSSION

 

Considerable clinical evidence suggest that primary headache syndromes such as cluster headache and migraine conditions  are primarily central in origin and are regulated by the brain . Functional imaging using PET has shed light on the common genesis of both syndromes documenting activation in the midbrain, pons and in the hypothalamic grey mater. These areas are involved in the pain process in a permissive or triggering manner rather than simply as a response to first division nociceptive pain impulses.25 The shared anatomical and physiological substrate for both clinical syndromes is the neural innervations of the cranial circulation. Current theories propose that the primary dysfunction in migraine occurs within the CNS and genetic abnormalities may be responsible for altering the response threshold to migraine specific trigger factors in the brain of migraineur compared to a normal individual. It is generally thought that the local vasodilatation of the intracranial extra- cerebral blood vessels and a consequent stimulation of surrounding trigeminal sensory nervous pain pathways provide a key mechanism underling the generation of headache pain associated with migraine. The activated trigeminal nerves convey nociceptive information to the brainstem nuclei that in turn relay the pain signals to higher centers where headache pain is perceived thus it has been hypothesized that these central neurons may become sensitized as a migraine attack progresses.26-29

Trigeminal somatosensory evoked potentials and blink reflex provide important information about the functional integrity of the trigeminal sensory pathways.28 Van Villet et al.29, studied the TSER and EBR in cluster headache and reported that, the latencies of the TSER’s N1, P1, N2  on the symptomatic side in patients were significantly longer than those of the healthy controls however, the EBR showed non-significant latency differences between the patients and the healthy controls.

As for migraine, most of the studies focused on studying the central connections of the trigeminal nerve in the brainstem by EBR elicited by stimulation of the supra-orbital nerve, Lack of habituation of the EBR is the principal and most reproducible abnormality30-34.

Our study aimed at investigating the central brainstem trigeminal and optic nerve connections at different levels using different forms of the BR (LBR & EBR) as well as more central cortical connections using TSER’s.

Despite that Fahmi et al.35, found that there is a significant delay in the R1 component of the EBR in migraine (10.25±1.0 in controls versus 10.66±2.36 in cases P=0.01) yet our study did not confirm such relation. We agree with previous studies that the latency of the R1 component of the EBR did not differ significantly in the patients and healthy controls bilaterally36,37 (p>0.05). Regarding the R2 component some reported non-significant difference of onset latencies after standard stimulation36, other studies reported shorter latencies in migraine patients35 (mean R2i latency 34.05±3.8 ms in controls versus 32.68±5.5 ms in patients p=0.06, mean R2c latency 34.31±4.28 ms in the controls versus 33.79±5.63 ms in patients) however it was not mentioned whether these latencies were recorded ictally or interictally and whether symptomatizing and non symptomatizing sides were tested separately or not.  In our study significantly longer ipsilateral and contralateral R2 latencies were recorded on both the symptomatizing and non-symptomatizing sides in the patient group compared to the healthy controls. Bank et al.38, reported comparative findings (R2 latency 30-32 ms in the control group and ≥ 35 ms in the patient group, p<0.001). In agreement with Sandrini et al.36, a significant difference was also noted regarding the EBR threshold that was almost half the threshold in the healthy controls on both symptomatizing and non-symptomatizing sides. 

In the study a W shaped response was recorded in TSERS in patient and control groups, with an initial negative deflection (N1, P1, N2, and P2). The patient group showed a significant delay in the earlier middle latency components of the response (N1, P1, N2 components respectively). These waves are believed to originate in the deep brainstem structures15, 16. The delay was most marked in the P1 component (p < 0.0001) and least in N2. Comparable results were found by Van Villet et al.29, in cluster headache but mainly in the later components where the latencies of the TSER’s. N1, P1, N2  were markedly prolonged on the symptomatic side (mean±SD was N1 = 14.8± 2.3 ms, P1 = 20.4±2.5 ms and N2 = 27.2±3.0  ms in the patients, N1 = 13.4±3.6 ms, P1 = 18.1±2.4 and N2=25.0± 2.6 ms in controls, p<0.03) however in cluster headache, the N2 mainly showed the most marked delay. A common functional and neurophysiologic disruption in both syndromes may explain these common findings.

LBR is one of the methods to evoke reflex contraction of the Orbicularis Oculi muscle through stimulation of the optic nerve. It has the privilege of being present in all healthy subjects and can be used to test the central trigeminal pathways in the brainstem. Abnormalities of the EBR are commonly reported in headache, multiple sclerosis etc.  However the LBR has rarely been mentioned. In this study the LBR was recorded in 100% of patients and control groups, the response appeared in the form of a compound muscle action potential of average latency 50.2±1.6 and amplitude of 2.2±2.6 Uv. It has a direct component ipsilateral to the stimulus side and a contralateral indirect component. Such results are comparable with previous studies.8,39 In migraineurs, the latency of both the direct and indirect components of the  LBR was found to be  significantly longer. The delay was bilateral and symmetric on both sides regardless of the migraine side. These findings could be considered as a part of the functional disruption of the brainstem reflexes in migraineurs. The double fold increase in the response amplitude in the patient group remains to be explained.

Studies investigating other forms of trigeminal brainstem reflexes like the trigemino-cervico-spinal reflexes in migraineurs also reported bilaterally absent reflex in 17 out of 20 patients40. These findings together with our findings further emphasize the role of the brainstem as a as a key step in the pathogenesis of migraine not only as a causative factor but also the persistent interictal abnormalities may be considered a consequence of repeated attacks. The bilateral location of the abnormalities with no specific predilection to the migraine side suggests a centrally located dysfunction.

 

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الملخـص العربى

 

دراسة كهروفسيولوجية لدوائر العصب الخامس فى جذع المخ فى حالات الشقيقة

 

يهدف البحث الى ملاحظة التغيرات التى تحدث فى دوائر الكهربية للعصب الخامس و العصب البصرى فى  جذع المخ  عند مرضى الشقيقة باستخدام الجهد المستثار الحسى والمنعكس الرمشى المثار كهربيا لاستثارة العصب الخامس والمنعكس الرمشى المثار ضوئيا لاستثارة العصب البصرى اجرى البحث على ۱۸ مريض يعنون من الشقيقة و ۱۲ فرد من الأصحاء وقد أظهر البحث انه  مقارنة بالأصحاء يوجد هناك  تأخر فى زمن الكمون للموجات N1, P1, N2  للجهد المستثار الحسى للعصب الخامس و R2 component للمنعكس الرمشى المستثار كهربيا كما اظهر البحث تأخر فى زمن الكمون فى رد الفعل المباشر والغير مباشر للمنعكس الرمشى المستثار ضوئيا عند هؤلاء المرضى ولا يوجد علاقة مباشرة بين مدة المرض أو عدد مرات النوبات وبين التغيرات التى تظهر فى أى من الجهد المستثار أو المنعكس الرمشى.



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