INTRODUCTION

 

Eye cannot close and constantly weeps, mouth dribbles, speech is interfered with and mastication is impaired, delicate shades of continence are lost, Joy, happiness, sorrow, shock, surprise; all the emotions have for their common expression, the same blank stare; all of this refers to a situation called Bell’s palsy.¹

        It can strike almost anyone at any age; however, it disproportionately attacks pregnant women and people who have diabetes, influenza, or a cold. M: F ratio is equal, but it is twice as common in females for the 10-19 year age group and 1.5 times more common in males for the >40 age group; left/right sides are equally involved being bilateral in less than 1%; recurrence rate is about 10% and can be ipsi-/bi-lateral; diabetics have 4.5 times more risk to develop Bell's palsy; family history of Bell's palsy is present in 10% of patients.²

    Bell’s palsy induces a wide range of facial movement dysfunction from mild paresis to total paralysis. The pathophysiology associated with this injury is suspected to be due to edema within the facial nerve, with maximal injury in the labyrinthine segment.  

     A carefully planned electrodiagnostic study is paramount in the evaluation of nerve injuries. They are useful for establishing prognosis for return of facial nerve function and for determining endpoint of degeneration by serial testing.

Conventional EMG testing in the acute phase is primarily a complementary test as it is unable to distinguish a totally neurapraxic injury from a completely degenerated nerve or a regenerating nerve. Early in the disease, EMG will not demonstrate any voluntary motor units, and if voluntary active motor units are present, the nerve is probably intact with incomplete injury. After 10-14 days, fibrillation potentials become evident (degeneration). Then the axons will regenerate through the intact neural tubules allowing complete return of motor function to the muscle fiber innervated by that nerve fiber (reinnervation). Polyphasic potentials are seen during nerve regeneration and may be seen as early as 4-6 weeks after onset of paralysis. EMG may be complementary to NET, MST, and ENoG during the first 3-4 days after injury.⁴

NET, MST and ENoG are most useful in evaluating acute paralysis while the nerve is in the degenerative phase, however, they may show normal results for the first 3-4 days after nerve injury. This is due to the stimulating and recording electrodes being both distal to the lesion.  It takes about 3-4 days for the nerve degeneration to reach the site of stimulation. Also NET, MST, ENoG will only work if the patient has unilateral involvement since the tests are of value in the presence of a "normal" contralateral side for comparison.

Nerve excitability test (NET) and maximal stimulation test (MST) are quantitative  measures of   the electrical excitability of the peripheral nerves. These tests are often used to assess the prognosis of Bell’s palsy. If they are performed within a few days after the onset of Bell’s palsy, they will give valuable information regarding the eventual prognosis of the condition.⁵

Undoubtly, there are some types of injuries that may necessitate the use of unconventional studies to adequately assess the degree of axon loss in each individual nerve branch or fascicle.

Single fiber EMG (SFEMG) is a technique to study the microphysiology of an individual motor unit.  It  can be employed to study the process of denervation and reinnervation. The selectivity of the technique results from the small recording surface (25 um in diameter), which is exposed at a port on the side of the electrode, which is 3 mm from the tip.⁶      

Electrophysiologically, the process of reinnervation can be monitored by SFEMG. Fiber density will increase as early as three weeks. The fiber density will continue to increase and will reach a plateau when reinnervation is completed. Early in reinnervation ,with early contact of the new axon sprout with the previously denervated muscle fibers, jitter is greatly increased and if transmission fails at this site, concomitant blocking, or neurogenic blocking, can occur . The previously denervated muscle fiber has atrophied and with reinnervation ,it now conducts impulses at slower speeds. As it recovers, if its muscle fiber propagation velocity becomes variable , this can add to the increased jitter recorded early in reinnervation. With time and maturation of the new axon sprout and new endplate structures, the blocking stops and the jitter reverts towards normal. In some cases it may take 1 to 1 ½ years for the jitter to revert back to normal, while in some other cases there are individual motor units which never regain normal transmission.⁷

The use of SFEMG provides satisfactory information on  the quality and quantity of axonal regeneration following an injury. Misdirect regeneration and developing synkinesia is a problem that can be prevented with early diagnosis and intense rehabilitative course.

        The aim of our study is to demarcate the extracranial etiology of facial nerve paralysis, to delineate the value of serial single fiber electromyography in estimating degree of degeneration of fibers in Bell’s palsy and to monitor the course of regeneration and also give hints about clinical and technical diagnostic and prognostic scenarios that outline decision-making and patient treatment protocols in such a disease.

 

PATIENTS AND METHODS

 

        Eighteen patients afflicted by acute isolated  cases of Bell’s palsy participated in this research. Onset of illness with Bell’s palsy never exceeded their first two weeks. There were 12 males (66.6%) and 6 females(33.3%)with a mean age of 33.11±17.39 years .

 

Methods:

All patients had the following assessments and tests:

1-     Careful history taking and meticulous neurological examination with thorough cranial nerve evaluation. This narrows the scope of the differential diagnosis.

2-     Further clinical grading of the degree of Bell’s palsy was achieved via the “House-Brackmann Classification of Facial Function”: Such grading was accomplished in two sessions; one with the first experience with the patient, and the second session  one month from the onset of illness.  Table (1) views the classification used in the present research.

3-     Electrophysiological study:

Equipment: A reporter  ESAOTE BIOMEDICA instrument was used.

The study was performed in two sessions within the 1^st 2 weeks and one month from the onset of illness.  In each setting the following tests were done:

a-   Conventional EMG was carried using concentric needle electrodes:

      The frontalis and orbicularis oris muscles were tested  at rest ,during mild & maximum contraction.

b-   NET: was performed only on the first visit.

Methods:

Both facial nerves were stimulated and when minimal twitching of the distal facial muscles as the orbicularis oculi or orbicularis oris occurs, the intensity (strength) of the stimulus should be recorded in milliamperes.

 

I.    A difference of 4 mA or more in the nerve excitability test between the symptomatic and asymptomatic sides, indicates partial nerve degeneration.

II.   Absence of any response  beyond 20 mA indicates complete nerve degeneration.

 c-     NCV: was performed on the affected and unaffected side. 

The facial nerve was stimulated in front of the ear tragus with bipolar electrodes. Responses to maximal electrical stimulation were recorded by concentric needle electrodes in the frontalis and orbicularis oris muscles. The  peak-to-peak amplitude of the evoked compound action potential was compared to the amplitude of the normal side.  A reduction of the amplitude of the CMAP to 5 % or less of normal(95% reduction) is indicative of poor prognosis in Bell’s palsy.

 

Data analysis:

The evoked responses were analyzed for:

I-      The amplitude of the compound muscle action potential.

Mean amplitude ± SD

II-     The latency of the compound muscle action potential:

Mean latency ± SD

III-   The percentage of degeneration

IV-   The duration of the compound muscle action potential.

 

d-            SFEMG

SFEMG studies were performed in the frontalis muscle. The single fiber needle was inserted into the weakened slightly contracting muscle with the subject comfortably seated. A clear, high-pitched sound of a single-fiber discharge indicates a suitable site for further study. Careful rotation ,advancement or retraction of the needle maximizes the potential on the oscilloscope. The needle is then further advanced until another single fiber action potential is recorded; at least 20 peak pairs were recorded.

 

Recommended criteria:

a-     Peak to peak amplitude > 200 uV.

b-     Rise time from positive to negative peak <300 us.

 

A constant waveform of the successive tracings confirms a  suitable single fiber discharge for the following automatic analysis:

1-     FD (fiber density): the number of simultaneously firing single muscle fibers is counted for at least 5ms interval after the triggering spike.

2-     MISI (mean inter spike interval): was calculated by dividing the total duration by the number of intervals(number of spikes minus –1).

3-     MCD (mean consecutive difference or jitter): it is expressed as the mean value of consecutive differences; it represents the degree of variability in the interpotential interval (IPI).

4-     MSD (mean sorted interval difference):it is a parameter similar to the MCD where the differences are calculated on potentials of non consecutive traces.

N.B.: we use MSD if the MCD/MSD  exceeds 1.25.

5-     Range :it represents the range of variability of the ISI.

6-     Blocking: it represents the percent value of blocks.

7-     R-RV: it represents the percent value of the R-R variability.

8-     Firing rate: is the firing rate of a single fiber discharge.

9-     MIDI (mean interdischarge interval): It represents the mean value of differences in conduction time from the common branching point to each fiber within the same motor unit.

 

Statistical analysis:

       Data were included in a database and analyzed  by means of statistical software package namely SPSS Windows V.8. All variables were expressed as means and standard deviations (SD). Two-Independent-Samples test was performed  to compare the diabetic and non-diabetic groups on each variable and Wilcoxon Rank W test  to compare the distributions of two variables for a single group. Pearson’s correlation was also  performed to measure how  each pair of variables are related;  correlation coefficients  range in value from -1(negative correlation) and +1 (positive correlation).

 

RESULTS

 

This study  was carried out in 18 patients with acute Bell’s palsy (12 males and 6 females); their ages ranged from 9 to 65  years with a mean age of  33.11±17.39; 5 (27.8%)  of cases were diabetic. We classified our sample based on the presence of diabetes into group I and group II (Table 8).

 

I-             Clinical data (Tables 1, 2):

According to House Brackmann grading, 7 patients (38.9%) had grade III, 8 (44.4%) had grade IV, and 3 (16.7%)  patients had grade V. 11 (61.1%) of cases had left facial palsy, 5 (27.8%) have right paresis and only 2 cases (11.1%) had bilateral affection.

 

II-           Electrophysiological data:

Table (3) is a summary table describing the sensitivity of each test in detecting signs of denervation and early signs of reinnervation within the first two weeks.

 a-            On EMG  testing:

*       Signs of denervation were present in only 1 case (5.5%).

*       Broad polyphasic MUPs were detected in 4 cases (22.2%).

 b-           On single fiber EMG:

*       FD was normal (<2) in 13 cases (72.2%).

*       Mean jitter was abnormal (>45 us) in 13 cases (72.2%).

*       Mean sorted interval difference was abnormal (>45 us) in 13 cases (72.2%).

*       Percentage of blocking was abnormal (>40%) in 16 cases (88.8%).

 c-            On nerve excitability test (NET):

*       A side-to-side difference > 4 mA was found in 7 cases(38.8%).

 d-    On NCV, percentage of degeneration >90% was demonstrated in 17 cases (94.4%).

 

Table (4) correlates the age, duration of illness and degree of paralysis with the electrophysiological parameters:

*      A highly statistically significant positive correlation was found between the degree of clinical paralysis and reduction in the interference pattern (P<002).

*      A statistically significant positive correlation was also found between the degree of clinical paralysis and the percentage of degeneration (P<0.01) ,the jitter (MCD ) (P<0.05) , MSD (P<0.04), FD (P<0.04) and the percentage of blocking (P<0.03).

               

Table 5 (I & II) compares the electrophysiological  parameters (Conventional EMG and NCV on the two sessions: Group A (represents the first visit) and group B (represents the second one):

*      The percentage of polyphasic MUPs  was significantly increased (P<0.05) ,while the reduction in the interference pattern was significantly decreased (P<0.03).

*      The latency of the compound motor action potentials(CMAP) was unaffected while its amplitude and duration were significantly increased (P<0.02 & 0.04). The percentage of degeneration  also significantly improved (P<0.03) .

 

Table (6) compares the parameters of single fiber EMG studies on the two sessions: Group A (represents the first visit) and group B(represents the second one):

*      The percentage of blocking  highly significantly decreased (P<0.003), while the FD was extremely significantly Increased (P< 0.001).

*      The R-R variability was significantly reduced (P<0.02).

 

Table (7) correlates  the electrophysiological  parameters of regeneration In conventional EMG and conduction studies (% of polyphasic MUPs, %of degeneration, NET and SFEMG parameters (FD, mean jitter and percent blocking):

*      A highly statistically significant positive correlation was found between the percentage of polyphasic MUPs and the fiber density (P<004).

*      A statistically significant positive correlation was found between the percentage of polyphasic MUPs and the mean jitter  (P<03).

 

Table (8) compares the clinical data in Group I (diabetic) and group II (non-diabetic).

 

Table 9 (I & II) compares the electrophysiological  parameters (Conventional EMG and NCV in Group I  (diabetic) and group II (non-diabetic):

*      There were no statistically significant difference between Group I & II.

 

Table (10) compares the parameters of single fiber EMG studies  in Group I and group II:

*      There were also no statistically significant difference between Group I & II.

 

 

Table 1. House-Brackmann Classification of facial function.

 

 

 

Table 2. Grading of our patients according to House-Brackmann classification:

 

Table 3. Electrophysiological tests carried  for our patients.

  

	No. of patients	%
EMG: - At rest - Mild contraction  (presence of polyphasics)	1 4	5.5% 22.2%
NET	7	38.8%
NCV:  (percentage of degeneration :> 90%)	17	94.4%
Single fiber EMG: -FD (<2) -Mean jitter(>45us) -MSD (>45us) -Blocking (>40%)	13 13 16 16	72.2% 72.2% 88.8% 88.8%

 

Table 4. Correlates the age, duration of illness and degree of paralysis with the electrophysiological parameters.

 

*P<0.05 (significant), ** P<0.01 (highly significant), r-value: Pearson correlation coefficient.

 

 

Table  5 I and II. Compares the electrophysiological  parameters (Conventional EMG and NCV on the two sessions: Group A (represents the first visit) and group B (represents the second one).

 

Table  5 I:

* P< 0.05 ( significant)

 

Table 5 II:

* P< 0.05 ( significant)

 

Table 6. Compares the parameters of single fiber EMG studies on the two sessions: Group A (represents the first visit) and group B (represents the second one).

 

*** P< 0.001 (extremely significant)

** P< 0.01 (highly significant)

*   P< 0.05 ( significant)

 

Table 7. Correlates  the electrophysiological  parameters of regeneration In conventional EMG and conduction studies (% of polyphasic MUPs, % of degeneration, NET and SFEMG parameters (FD, mean jitter and percent blocking).

 

Variable	Single fiber EMG parameters
	FD		Mean  jitter		% blocking
	r	P	r	P	r	P
A- EMG studies:     -%of polyphasic MUPs	-.25	0.3	-.01	0.9	.06	0.8
B- NCV    - NET    - %of degeneration	-.04	0.8	.14	0.6	-.21	0.3
	.66	0.004**	.53	0.03*	.46	0.08

 

*P<0.05 (significant), ** P<0.01 (highly significant), r-value: Pearson correlation coefficient.

 

Table 8. Compares the clinical data in Group I (diabetic) and group II (non-diabetic).

 

* P<0.05 (significant)

 

Table  9 I and II. Compares the electrophysiological  parameters (Conventional EMG and NCV in Group I  (diabetic) and group II (non-diabetic).

Table  9 (I):

 

* P< 0.05 ( significant)

 

Table  9 (II):

 

* P<0.05 ( significant

Table 10. Compares the parameters of single fiber EMG studies  in Group I and group II.

 

* P< 0.05 ( significant)

 

 

DISCUSSION

 

There have been no extensive studies in patients of the time course and dynamics of denervation and reinnervation following nerve trauma, particularly in the early stages.

Our study was designed to follow the course of reinnervation aiming at better management of patients afflicted by Bell’s palsy.

Eighteen patients with acute facial palsy were studied , 7 cases had grade III, 8  cases had grade IV and 3 cases had grade V; according to House-Brackmann grading of facial palsy, ⁸

The process of degeneration and reinnervation of facial nerve fibers was monitored over one month from the onset of illness; five out of the 18 cases are diabetic under insulin therapy. Diabetics have 4.5 times more risk to develop Bell's palsy. Left/right side’s affection was unequally involved in our sample as 11 cases had left sided affection, 5 cases had right one and the remaining 2 cases had bilateral affection. 

Conventional EMG during the first two weeks gave  little informative data, signs of denervation were detected in only 1 case, presence of polyphasic MUPs was found in only 4 (22.2 %)cases, noting the onset of reinnervation, the remaining cases showed broad MUPs. Although, this could have a definite value in identifying an incomplete lesion despite  the clinical absence of facial function, needle EMG is not a reliable indicator of prognosis. The presence of some motor units in cases with paralysis that appears with visual inspection to be complete, is of particular prognostic value when a facial palsy follows surgery ;the survival of some units indicates the nerve is in continuity.

By one month, the percentage of polyphasicity was increased ,as it was detected in 11(61.1 %) cases. Polyphasic MUPs suggest desynchronized discharge or drop-off of individual fibers.

There was also a statistically significant improvement in the degree of reduction of the interference pattern (P<0.03) indicating maturation of new axon sprouts and that the muscle fibers now discharge more synchronously.

The reduced interference patterns due to loss of some of the motor fibers were found to be highly significantly correlated with the degree of paralysis. The recruitment interval is actually a sensitive index of weakness.

Nerve excitability test (NET) measures early evidence of nerve degeneration as the earliest evidence   of   degeneration of the nerves after injury is the failure of the nerve to respond to electrical stimulation below the site of injury. This test was performed as soon as possible after the third day after the onset. Our cases were studied within the first two weeks, 3 out of the 18 cases before the 3^rd day, and the test was impaired in only 7 cases (38.8%). Some authors claimed that in some patients (11%), nerve excitability was unimpaired initially, and usually happened after the tenth day, giving erroneous good prognosis, so we must repeat the NET after the tenth day and this may be due , in few patients to degeneration of the facial nerve continuing within the first week.

Most studies found that the CMAP amplitude comparison is the most useful test for formulating a prognosis.

In our study,  a reduction of the amplitude of the CMAP to 10 % or less of normal(90% reduction) was found in 17 out of 18 studied cases indicating  poor prognosis and this in agreement with most studies.

Eitersen² found that in the acute stage of Bell’s palsy, with  a reduction to 10% or less of the contralateral muscle, recovery took six months to a year and the final result was poor.

Moreover, some authors claimed that surgical procedures performed when axonal degeneration has reached 95-100% within 1-14 days after onset, significantly improve the recovery of facial movements.⁹

On monitoring the amplitude of CMAP over one month, we noticed  that it significantly increased with substantial improvement in the percentage of degeneration. This could be of prognostic value, indicating the progression of reinnervation.

It also showed a significant negative correlation with the degree of paralysis. The amplitude of CMAP is proportional to the number of intact motor axons. The degree of axonal loss has direct implications for assessing the degree of damage and estimating the prognosis and the time required for recovery.

The latency of the CMAP was found to be of no prognostic value.

The duration is another factor that could indicate the dynamics of reinnervation. It was significantly increased over the first month. Increased duration is a good index of the motor unit territory. It probably results from usual variability in length, conduction time of regenerating axon terminals and membrane excitability rather than the enlarged territory.

     The use of SFEMG gives information about changes in the topography of the motor unit and in the function of transmission in terminal nerve, motor end plate and muscle fiber. All of this assists in drawing better management of patients afflicted by such illness, that even may require surgical interference in some cases with more than 90% degeneration of the facial nerve fibers. In such cases, time factor plays a major role in terminating a devastating problem.¹⁰

      The parameters of fiber density, mean jitter, and percent blocking must each be followed and related to the type of injury to determine the stage of reinnervation.

      During the first two weeks of illness, mean jitter was found to be increased in 13 cases ,it was significantly positively correlated with the degree of paralysis, however ,it showed a significant reduction after the first month. These findings indicate ongoing reinnervation, and the increased jitter is probably because of the functional immaturity of the newly formed motor-end-plates, both pre-and post-synaptically.

     The time to the peak of abnormality of jitter values will be dependent upon many factors including the number and rate of regrowth of returning axons. The peak may be reached before the second month but may require 6 months which is about the time it takes for the motor endplate to become histologically and histochemically normal.¹¹

         The marked abnormality of jitter during reinnervation suggests that newly formed immature end-plates were not capable of sustaining normal neuromuscular junction (NMJ). The fall in FD and jitter after maximum function has returned suggests that the original axons had resumed function and re-established innervation to the muscle, after which point collateral sprouting at least partially disappeared resulting in remodeling of the motor units.

Janice & Donald⁷ reported that the maximum increase in mean jitter following facial palsy occurred at 37 days, persisted until 67 days, then returned toward normal.

     Muscle fiber propagation slows substantially upon firing because successive action potentials occur in the relative refractory period of the muscle. This delay may differentially affect the activation of two muscle fibers, depending on the lengths of their respective axon terminals. In general, a long IPI and rapid firing rates tend to increase jitter because these factors induce physiologic slowing that influences two muscle fibers differently.¹²

   As a rule, the firing rate affects jitter if the IPI exceeds 4 ms, a computer can sort the IPI on the basis of the interdischarge  interval (IDI) to calculate the corrected MCD, termed mean sorted interval difference (MSD). If firing rate has not affected jitter, MCD/MSD=1. If the ratio exceeds 1.25,one must use MSD instead of MCD, because the firing rate has influenced jitter.¹³

    As in our sample, the MCD/MSD exceeded 1.25, so we used MSD to determine the jitter values. They showed a significant increase in 16 out of the 18 studied cases, eventually, by 30 days they had again reduced to about 50 % of the value.

     Firing rate seems to have also a significant value . The effects of firing rate on jitter may be an indicator of the type of underlying pathology.

     In postsynaptic defect, the rapid firing rate increases jitter even with an IPI of less than 4 ms, on the other hand, in presynaptic disorders ,jitter increases at slow firing rates and decreases at fast rates.

We found a concomitent increase in the firing rate and mean jitter at the onset of illness within the first 15 days, with subsequent reduction thereafter. This indicates the presence of a postsynaptic defect .

The changes in MIPI result from fluctuation in muscle fiber propagation velocity, in most recordings showing an interval of less than 1 ms (from 0.3-0.7 ms); this value increases in early reinnervation.¹³

       The mean interpotential interval (MIPI) was noted to be significantly increased (>1ms),then it showed a tendency toward a significant reduction over the first month of paralysis. Early with reinnervation, the newly formed axon sprouts with  previously denervated muscle fibers, conduct impulses at slower speeds. As they recover, if their muscle fiber propagation velocity becomes variable, this can add to the increased MIPI  recorded early in reinnervation that reverts back to normal with  maturation of the new axon sprouts and new endplate structures.¹⁴

FD was found to be normal within the first two weeks and significantly increased thereafter. This in agreement with the previous serial single-fiber EMG studies carried by Stalberg¹⁰ in the frontalis muscle who  reported  increased jitter with normal fiber density 15 days after facial nerve trauma.

Fiber density is defined as the mean number of associated single fiber potentials that fire almost synchronously with the initially identified potential. It provides a measure of muscle fiber clustering, rather than the total number of muscle fibers within a motor unit. By definition, the lowest possible value is 1.0. An increase in fiber density usually indicates the presence of collateral sprouting. It rivals histochemical fiber grouping in identifying rearrangements within the motor unit. ⁶

Increase in jitter without concurrent increase in FD 15 days after partial injury demonstrates that transmission in the peripheral portion of the motor nerve or the NMJ was abnormal during the period of denervation before reinnervation began. The increase in FD at 21 days indicates that functional contact has been made between collateral sprouts and muscle.

Jitter is defined as the degree of variability in the IPI. Sometimes after increases in the IPI, the second potential fails to appear. This phenomenon is referred to as blocking; blocking in more than one fiber or jitter values exceeding 55 us constitutes an abnormality in any muscle. Jitter values, typically beyond 80-100us, precede the transmission block.¹³

In our study, the percent blocking was increased at the onset of illness, in 13 out of the 18 studied cases and showed a significant reduction after one month. This is a sign of functional improvement and can serve as a guide when estimating the age of reinnervation potentials in different neuropathies. Our results are  in agreement with Stalberg¹⁰  who  recorded increased jitter and blocking at one month. 

Early in reinnervation, blocking is frequently seen at the branching site of the new axon sprout from its parent axon. If transmission fails at this site, concomitent blocking or neurogenic blocking can occur if the new axon sprout has branched to contact more than one muscle fiber. With time and maturation of the new axon sprout and new enplate structures, the blocking stops and the jitter reverts towards normal.¹⁵

FD and blocking were also  found to be significantly positively correlated with the degree of paralysis.

On evaluating the effects of diabetes in  patients with Bell’s palsy ,we found only a significant difference regarding the age and degree of paralysis, however, it showed no statistically added abnormalities on the electrophysiological parameters. One possible explanation, supported by histochemical findings, is that, in diabetic neuropathy, the degenerative process is mainly restricted to the myelin sheath but in the mixed motor and sensory neuropathies both the myelin and the axons are destroyed (Wallerian degeneration), this axonal degeneration causes denervation followed by collateral reinnervation of the muscle fibers.¹⁶

From this study, it appears that  the percentage of degeneration ,percent blocking and mean jitter seem to be the most sensitive indicators of the process of denervation and reinnervation as their abnormalities were recorded as early as 15 days after onset of paralysis. Fiber density (FD) will be elevated as early as four weeks after onset. These abnormalities can be used to note the onset of reinnervation and to allow  better management of patients with Bell’s palsy .

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