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July2007 Vol.44 Issue:      2 Table of Contents
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Neurogenic Thoracic Outlet Associated With Carpal Tunnel Syndrome: Is This A Clinical Example of Double Crush Hypothesis?

Osama M.M.A. Elazouni1, Adham M.M. Ismail1, Ghada S. Nageb2, Said A. Elmonem3

Departments of Neurology1, Rheumatology & Rehabilitation2, Radiology3, Zagazig University


Aim of the work: The aim of this study was to assess the possible contribution of the double crush hypothesis (DCH) for the association of carpal tunnel syndrome (CTS) with neurogenic thoracic outlet syndrome (NTOS)which -if confirmed- can explain some of the not uncommonly persistent CTS cases despite being confirmed and properly treated, particularly that NTOS is potentially treatable. Subjects and Methods: 137 CTS patients {91 (66.4%) females, 46(33.6%) males}, with mean age 39.4, ranging from 23 to 48 years, were included in the study based solely on electrophysiological criteria of CTS (distal motor latency to abductor pollicis brevis > 4 ms, 3 rd digit to wrist orthodromic sensory conduction velocity < 45m/s, or orthodromic median/ulnar latency difference of the 4th digit > 0.4 ms). Patients who proved suffering peripheral neuropathy or entrapment of ulnar nerve were excluded. Twenty apparently healthy individuals, age and sex matched with patients were included as a control group. The patients and control groups were subjected to clinical  neurological evaluation. Electrophysiological work up including motor/sensory conduction study of median and ulnar nerves on both sides, and bilateral medial antebrachial cutaneous nerve (MABCN) antidromic sensory, considering side to side MABCN sensory nerve action potentials (MABCN SNAP) amplitude ratio of >2.0 as abnormal. Electrophysiological criteria used for confirming (NTOS), were low median compound motor action potentials (CMAP), low ulnar SNAP, low or normal ulnar CMAP,  normal or reduced interference pattern of C8 T1-innervated muscles, and MABCN SNAP interside amplitude ratio >2.0(the latter was used as a mandatory inclusion criterion). Patients with atypical upper limb pain have undertaken cervical plain X ray. Control group was subjected to complete neurophysiological studies. Student t test was used to compare means of two groups. Results: Ulnar nerve SNAP amplitudes were found normal. Reduction of median CMAP was reported in 19 patients (13.86%) and it was bilateral in 7 (36.84%). Antidromic MABCN SNAP interside amplitude ratios showed values <2.0 and mean ±SD was 1.273±0.221. Needle examination showed incomplete interference pattern in abductor pollicis brevis muscles in 11 patients (8%). 3 patients (5.26%), 2 males, and 1 female had bilateral bony cervical ribs but non had evidence of NTOS. Conclusions: Neurophysiologically confirmed CTS was not proved to associate NTOS, and the hypothesized relationship between them could not be obtained. This might inspire us to revisit DCH for re-evaluation. Finally, NTOS is still a rare medical condition and scrutinizing suspected cases with thorough clinical assessment, and electrophysiological work up is a must. (Egypt J. Neurol. Psychiat. Neurosurg., 2007, 44(2): 407-419)



             The term ‘thoracic outlet syndrome (TOS)’ was described  by Schenard  in 20051 and referred to a group of disorders affecting the brachial plexus, the subclavian vessels, or both at any point between the base of the neck and the axilla. TOS was further sub classified into vascular, neurogenic, and vascular-neurogenic combined forms2. Neurogenic thoracic outlet syndrome (NTOS) is caused by compression of the lower trunk of the brachial plexus by a fibrous band (true NTOS) and this syndrome is exceedingly rare3. NTOS consists of unilateral wasting of the hand associated with a rudimentary cervical rib or elongated C7 transverse process. During surgery a fibrous band is found over which the lower brachial plexus is stretched and angulated4. 

Kothari et al. in 19984 reawakened interest in the syndrome and described the neurophysiological findings. The authors showed that nerve conduction studies were quite helpful in localizing the lesion to the lower trunk of the brachial plexus affecting predominantly the C8-T1 roots4,5. Currently the accepted electrophysiological criteria for true NTOS are low amplitude median compound motor action potentials (CMAP), low ulnar sensory nerve action potentials (SNAP), relatively low or normal ulnar CMAP, and normal median SNAP(4,5,6), and these abnormalities are usually not seen with other lower trunk brachial plexopathies such as those due to injury, tumour, or radiation6.

Medial antebrachial cutaneous nerve (MABCN) SNAP is of value for early diagnosis of NTOS7. This nerve is derived from the C8-T1 roots and is a branch of the medial cord of the brachial plexus and as the nerve goes distally it lies nearby the basilic vein and subsequently branches to supply the median forearm8. Despite that previous electrophysiological criteria for diagnosing NTOS (low median CMAP, low ulnar SNAP, relatively low or normal ulnar CMAP, and normal median SNAP), were not all reported in all NTOS cases, MABCN sensory response was abnormal in all cases in patients studied in two studies7,9. In 2004, Seror10 has studied the ability to diagnose mild lower brachial plexus lesion only through abnormal MABCN conduction study and defined abnormality by an interside amplitude radio of SNAP equal or greater than 2. The author found that MABCN testing was abnormal in all the patients when all other motor and sensory nerve conductions of median and ulnar nerves were normal.     

Carpal tunnel syndrome (CTS) is a constellation of symptoms associated with localized compression of the median nerve at the wrist. The pathophysiology of CTS is not fully understood but mechanical aspects of injury within the carpal tunnel are most likely. The issues of ischaemia, mechanical trauma, ectopic impulse generation, demyelination, tendonitis, elevated carpal tunnel pressure, mechanical factors, small and large fiber involvement and the variability of symptoms are presented11. In 2002, a consensus conference was organized and identified a combination of symptoms (numbness, tingling, burning and pain in combination with nocturnal symptoms) plus abnormal median nerve function based upon nerve conduction studies as the best ‘gold standard’ for diagnosis of CTS11.   

The double crush hypothesis (DCH) suggests that a peripheral nerve which is compressed proximally is more liable to be compressed distally than a nerve that has not sustained proximal compression12. This hypothesis was supported by studies in the humans13-15 and animal models16-18.

The comparison of NTOS with CTS is interesting in that CTS as NTOS is a chronic entrapment neuropathy that usually displays a clinical pattern of transient complaints and absence of amyotrophy and hypoesthesia for a long time. Improvements in the methods of CTS electro diagnosis have led to diagnosis at an earlier stage. As a proof of this, Seror10 noted that amyotrophy and hypoesthesia were found respectively in 50 and 80%, of patients. Most of the authors would be interested in discovering early cases of NTOS before occurrence of amyotrophy and hypoesthesia, so that this study was designed aiming at answering the question about the likelihood of NTOS to associate CTS as an example of DCH.  NTOS is a potentially treatable co morbidity which may contribute to the not uncommon persistent CTS cases despite being properly diagnosed and treated, so early accurate diagnosis may be of help.




        This study was conducted at Clinical Neurophysiology units of Neurology department and Rheumatology & rehabilitation department, Zagazig university hospitals. A hundred and thirty seven patients (91 (66.4%) females, 46 (33.6%) males) were included in this study. They were  referred for neurophysiological assessment, a diagnosed CTS based on clinical parameters (permanent hypoesthesia or intermittent symptoms of burning, tingling, and paraesthesia in the radial 3 & half digits especially at night or upon awakening,+/- thenar muscle atrophy). Patients were included in the study solely based on electrophysiological proofs of CTS, otherwise they were excluded. Twenty apparently healthy individuals {13 (65%) females and 7 (35%) males}, age and sex matched with patients, were included in the study as a healthy control group. Patients who proved clinically and/or electrophysiologically suffering peripheral neuropathy or entrapment of ulnar nerve at wrist or elbow were excluded. Neuropathy was defined by the presence of two or more abnormalities on electrophysiological testing of the nerves examined with regard to distal latency, conduction velocity, amplitude of action potentials, and F wave latency19.


All patients were subjected to the followings:

(1)    Neurological clinical evaluation: stressing on symptoms/signs of peripheral neuropathy (pain, tingling and numbness, stocking and glove hypoesthesia, bilateral distal symmetric weakness, wasting, hypotonia, hyporeflexia, vasomotor changes etc),  thoracic outlet syndrome (atypical pain, burning sensation, numbness in digits 4-5 and inner side of the forearm, clumsiness, cramps of the upper limbs, weakness of muscles supplied by C8-T1 not limited to single nerve distribution), as well as signs of entrapment neuropathy of median nerve at wrist, and ulnar nerve at wrist or elbow (paresthesia at the sensory distributions of the median and ulnar nerves, pain etc).

(2)    Electrophysiological studies: These studies were carried out using System PLUS Micromed Via Giotto 4, 1-31021 Mogliano Veneto (TU)- Italy as follows: Motor conduction studies of median, and ulnar nerves on both sides: The median nerve was stimulated by surface electrodes at wrist (palmer midwrist 6.5 cm proximal to active recording electrode on abductor pollicus brevis muscle), and elbow (in the antecubital fossa). The ulnar nerve was stimulated at wrist 7 cm proximal to active recording electrode on abductor digiti minimi, as well as below and above the elbow. Recording was done by monopolar surface electrodes over abductor pollicis brevis for median, and abductor digiti minimi muscle for ulnar nerve.  Distal motor latencies in msec were estimated from stimulus artefact to the beginning of CMAP. CMAP amplitudes were measured peak to peak and motor conduction velocities in different segments were calculated. Inter side as well as segmental comparisons regarding conduction velocities were calculated as well. Median and ulnar F-wave latencies were recorded after 10 supra maximal stimulations at wrist and the shortest latencies were obtained20,21.


Sensory conduction studies of both median and ulnar nerves on both sides: Orthodromic sensory studies of median and ulnar nerves were done by ring electrode stimulation of the digit 3 for median and digit 4 for median and ulnar nerves, and recording by surface electrodes at wrist on median and ulnar nerves20,21.

MABCN: MABCN was studied bilaterally with antidromic technique. The antidromic study of the anterior branch of the MABCN was performed with bipolar stimulation 1 to 3 cm above and before the medial epicondyle and bipolar recording 8 to 12 cm distally on the anterior medial aspect of the forearm. Averaging was applied and the amplitudes in µV were measured from peak to peak. The mandatory inclusion criterion was the interside amplitude ratio greater than 2.0 for  a unilateral abnormal MABCN. The studies were done bilaterally with the same settings22. 

                Electromyography: was performed with concentric needle examination of the abductor pollicis brevis, abductor digiti minimi, and first dorsal interosseous muscles. The followings were looked for (1) activities at rest (fibrillation potentials), (2)individual motor unit potentials morphology, and (3) interference patterns.

Electrophysiological criteria used in this study for diagnosing CTS were distal motor latency to abductor pollicis brevis greater than 4 ms, digit 3 to wrist orthodromic sensory conduction velocity lower than 45 m/s, or orthodromic median/ulnar latency difference of the 4th digit greater than 0.4 ms23. In cases of bilateral CTS, nerve conduction results from more profoundly affected limbs were processed.

The current study evaluated electrophysiologically the lower brachial plexus lesion, (neurogenic pattern of C8-T1 affection), based on Kothari et al. criteria which are low amplitude of median nerve CMAP, low amplitude of ulnar nerve SNAP, low or normal amplitude of ulnar CMAP as well as normal or slightly reduced interfernce pattern of some C8-T1 innervated muscles4, but MABCN interside amplitude ratio grater than 2.0 by antidromic technique was mandatory for the diagnosis according to Seror10 postulation. Stimulus duration applied was 0.2 ms, intensity from 5-15 mA), lower/upper filter sittings: 20-2000 Hz, time base 20 ms, gain for division 2 µV, and averaging for 50 sweeps.    


(3)    Plain X ray of cervical spine: That was carried out looking for cervical ribs or elongated C7 processes  for 57 patients (31 females, 26 males) having pain numbness and/or tingling, and heaviness vague and generalized over the upper limb,+/- symptom provocation by repetitive or stressful activity of the involved limb,+/- positive Tinel sign.

Healthy controls were subjected to neurological examination exactly the same as patients as well as complete electrophysiological study and their values were used as our norm. 

Finally, results were collected and data base processing was done using statistical package of social sciences (SPSS) version 8(24). Student ״ t״ test was used and the results were considered significant if P-value ‹0.05, while P-value >0.05 indicates non significant and P<0.001 highly significant values.




Total patients included in this study were 137 pts, 91 females (66.4%) and 46 males (33.6%). Age of these patients was ranging from 23 to 48 years and the mean value ± SD was 39.43±7.46 years. Control group included 7 (35%) males and 13 (65%) females, their age was ranging from 19 to 53 years with mean age ±SD (38.60±11.74) which showed a non significant relationship on comparing with that of patients (p=0.713).


Electrophysiological studies:

In electrodiagnosis of CTS, most of the patients subjected to the study showed bilateral entrapment of median nerve at wrist followed in frequency by right unilateral lesion as shown in table (1).

Sensory nerve action potentials of the ulnar nerve studies were done bilaterally for all patients and the mean values ± SD were (14.088±4.832 µV). Bilateral CMAP amplitude measurement of the median nerves in all patients showed reduction of CMAP amplitudes in 19 (13.86%) patients, 7 (36.84%) patients of them were bilateral. The mean CMAP amplitudes for the normal group was 12.137±6.081 mV compared to 2.989±0.580 mV for the abnormal group with statistically highly significant relationship (p<0.001).

Antidromic MABCN SNAP interside amplitude ratio was done and none of the patient had ratio more than 2 and the mean ±SD values were 1.273±0.221 as shown in table (1).

Needle examination showed incomplete interference pattern in abductor pollics brevis muscles in 11 (8%) cases, 8 (72.7%) females and 3 (27.3%) males and was bilateral in 7 (63.6%) cases 6 (85.7%) females and 1 (14.3%) male.

Fifty seven patients (41.6%), presented with atypical pain in the upper limbs {31 (54.4%) females, 26 (45.6%) males} were subjected to plain cervical x ray and 3 (5.26%) of them (2 males and 1 female) had bilateral bony cervical ribs as shown in figure 3. The electrophysiological testing for them was as shown in table (2).

Electrophysiological values of the control group as shown in tables (3), (4) and (5) were used in the study as a reference values for diagnosing abnormal cases that were excluded (peripheral neuropathy, entrapment of ulnar nerve at wrist or elbow).

Table 1. Neurophysiological parameter results used for detection of CTS and NTOS.





No & %



No & %



No & %


Bilateral cases

No &%

Unilateral cases

No &%




Orth.Median     SCV/ m/s








29 pts



35.58±9.2 m/s


62 pts



28 pts



18 pts



Latencies/ msec





21 pts



56 pts


21 pts


14 pts


Median DML/ msec

94 pts




23 pts



39 pts


19 pts


13 pts



MABCN ratio









interside amplitude ratio



*Digit 3 to wrist orthodromic sensory conduction velocity lower than 45 m/s

(orth = orthodromic, SCV= sensory conduction velocity).

+Orthodromic median/ulnar latency difference of the 4th digit greater than 0.4 ms

# Median distal motor latency (DML) to abductor pollicis brevis greater than 4 ms.

++Medial antebrachial cutaneous nerve (MABCN) interside amplitude ratio >2.0



Fig. (1): Orthodromic median/ulnar latency difference of the 4th digit in ms.




Fig. (2): MABCN recorded on right and left sides by antidromic technique,

interside SNAP amplitude ratio was calculated.

Table 2. Results of Neurophysiological parameters of the three patients presented with cervical ribs in cervical plain X-ray examination.



Median CMAP


Ulnar SNAP



Needle Examination





1st  patient, Male






Incomplete interference pattern of right Abductor pollics brevis

2nd patient, Male






Within normal.

3rd patient, Female






Within normal.

*Abnormal values




Fig. (3): Plain cervical x ray showing bilateral bony cervical ribs.


Table 3. Mean values of distal latencies (DL), conduction velocities (CV), and CMAP amplitudes in motor nerves in upper and lower limbs of control group.


NC variables


Nerves studied

Distal latencies

Motor conduction velocities

CMAP amplitudes




Median nerve

3.0±0.3 msec

60.3±4.7 m/sec

16.0±6.0 mV

Ulnar nerve

2.4±0.3 msec

64.1±6.2 m/sec

14.0±4.0 mV

Radial nerve

2.2±0.4 msec

63.8±5.1 m/sec

15.0±5.3 mV

Common Peroneal

3.9±0.4 msec

53.7±3.6 m/sec

12.0±3.5 mV

Posterior Tibial

3.7±0.5 msec

49.3±3.2 m/sec

19.6±7.1 mV

Values beyond ‘two standard deviations’ from normal were considered abnormal.



Table 4. F response in control group.


Nerve (distal site)

Mean (msec)

Range (msec)

Ulnar (hypothenar)

Median (thenar)

Posterior tibial (AHB)

Common peroneal (EDB)









Values beyond ‘two standard deviations’ from normal were considered abnormal.

AHB:Abductor hallucis brevis

EDB: Extensor digitorum brevis


Table 5. Mean values of distal latencies (DL), conduction velocities (CV), and SNAP amplitudes in sensory nerves in upper and lower limbs of control group.


NC variables


Nerves studied

Distal latencies

Sensory conduction velocities

SNAP amplitudes




Median nerve

2.8±0.1 msec

61.0±4.9 m/sec

35.0±12.0 µV

Ulnar nerve

2.5±0.1 msec

60.0±5.2 m/sec

15.0±4.2 µV

Radial nerve

2.6±0.2 msec

59.0±4.1 m/sec

28.0±4.0 µV

Sural nerve

3.1±0.3 msec

48.2±3.5 m/sec

16.3±5.9 µV

Values beyond ‘two standard deviations’ from normal were considered abnormal.





Results of this study showed that none of the neurophysiologically proved CTS patients included, had reduction of Ulnar nerve SNAP amplitude. This can be explained in two ways: firstly, patients who showed electrophysiological evidence of ulnar nerve entrapment at wrist or elbow (segmental, and or inter side comparative significant slowing) were excluded from this study, secondly, none of patients showed evidence of lower brachial plexus lesion that could have contributed to a low ulnar nerve SNAP5. 

Motor study of the median nerve showed that CMAP amplitude was significantly reduced in 19 (13.86%) patients, and that the reduction was bilateral in 7 (36.84%). This finding could be a sequel of severe prolonged entrapment of median nerve at wrist complicated by secondary  axonal lesion. This explanation might be supported by the fact that nearly 37% of those 19 patients were having bilateral CTS, which usually builds up sequentially, thus taking some time long enough for axonal pathology to ensue. Another possible explanation is coexistence of  a lower brachial plexus lesion. As a matter of fact, median nerve CMAP represents mainly a motor function of T1, which is also represented sensorily by MABCN SNAP5,25,26. So if there is a lesion  compromising T1, one can expect affection of median CMAP, and of MABCN SNAP as well, which was not the case in our study. In conclusion, it can be reported that the reduction of median CMAP was mostly a consequence of entrapment of median nerve at wrist rather than of a lower brachial plexus lesion.          

Neurophysiological study of MABC nerve in all CTS patients showed within normal SCV, and inter side amplitude ratio. The mean values ± SD of inter side amplitude ratio was 1.273±0.221, which is less than the ratio of 2.0 required for the diagnosis of predominantly T1, and to a lesser extent, C8 involvement in lesion of lower trunk, as well as medial cord of the brachial plexus. In fact, MABCN predominantly carries sensory fibres from the T1 root, which is the first to suffer from angulation on cervical rib, or fibrous bands connecting the first thoracic rib to the scalene tubercle or other spine structures27. Kothari and colleagues4, in their study on patients with electrophysiologically proven NTOS have supported the findings of Nishida et al.7 and recommended that the MABCN sensory study be performed when other standard electro-physiological tests have failed to confirm or satisfactorily localize a lower trunk brachial plexopathy. Subsequently, we can conclude that neurophysiologically evidenced NTOS could not be detected in our CTS patients and we might state that NTOS is still rare in CTS patients, at least less than 1 per 137 patients that meets with Seror22  findings.

As far as concordance of prominent C7 transverse processes or cervical ribs with NTOS is concerned, bilateral bony cervical ribs were reported in three patients. These patients showed within normal MABCN SNAP inter side amplitude ratio, ulnar SNAP amplitudes, and median CMAP amplitudes except one male patient who showed bilateral reduction of median nerve CMAP, and incomplete interference pattern of abductor pollicis brevis and considered as severe CTS with secondary axonal lesion of the median nerve. This observation could tell us that not all  cases of cervical ribs are associated with NTOS, while NTOS cases are frequently (12-100%) associated with cervical rib as compared with the 0.2 or 0.5% expected in the general population5,28,29.

The above mentioned findings may conclude that NTOS is rare , and its association with CTS may be a mere coincidence, or both have a common aetiology. This calls for re-evaluation of the DCH., particularly as an aetiological factor for the clinical association of CTS and NTOS

Although the DCH has some experimental and considerable clinical support, present understanding of the anatomy and physiology of peripheral nerves is largely inconsistent with the most common clinical example of this hypothesis which is CTS superimposed on a cervical radiculopathies (CR).CR leading to disruption in axoplasmic flow proximal to the dorsal root ganglion would not be expected to cause distal dysfunction or demyelination of that same axon30. Wilbourn and Gilliatt30 suggested that the most common clinical example of the DCH is an increased predisposition to CTS in patients with CR, and reported it as physiologically unsound, where a radicular lesion should have no effect on frequency of CTS and CR should have no effect on distal sensory conduction studies, no effect on distal myelin, and minimal effect on distal motor axon function of the median nerve.

Based on the fact that median sensory component is of C6/C7 origin, and its motor component is primarily of C8 origin, Richardson et al.31 hypothesized that C6 and/or C7 cases would demonstrate an increased frequency of median sensory mononeuropathy, and C8 cases would demonstrate an increased frequency of median motor mononeuropathy. They also hypothesized that median sensory and motor response parameters among the same groups would be altered in ways consistent with a proximal influence on distal nerve conduction studies. Although median mononeuropathy was unexpectedly common (22.1%) among cases of CR (which may explain the clinical acceptance of the double crush hypothesis), none of their hypothesis on pattern of median neuropathy determined according to the affected cervical root was supported. This study found no evidence to support a neurophysiological explanation for the double crush hypothesis.

It is unclear why CR and CTS seem to coincide  frequently.  May be  both disorders have  common  predisposing factors such as upper extremity overuse, or osteoarthritis leading to both cervical foraminal and carpal canal stenosis32,33. Previous work has identified an increased incidence of CTS in patients with cervical arthritis13, and small carpal canal size34. Upper extremity weakness and pain in patients with CR may cause changes in biomechanics and usage patterns leading to increased upper extremity oedema with resultant increased carpal canal pressures33.

Many studies supporting the DCH have often defined CR by clinical or radiological evidence and this may raise the possibility of misdiagnosis34,35.

Finally we can summarize that neurophysiologically assessed CTS was not proved to be  associated with NTOS that was defined neurophysiologically as ‘low median nerve CMAP amplitude, low ulnar nerve SNAP amplitude, and side to side MABCN SNAP amplitude ratio greater than 2, and the hypothesized relationship between them could not be obtained, and this might call for re-evaluation of the DCH. Also not all cases of cervical rib would be accompanied by NTOS. And we can conclude that NTOS is a rare medical condition, and patients presenting with pain in upper limbs even with x-ray evidenced cervical ribs do not have to be diagnosed as cases of NTOS, unless after thorough clinical examination and specific/ sensitive electrophysiological work up.  




1.      Schenardi C. Whiplash injury. TOS and double crush syndrome. Forensic medical aspects. Acta Neurochir Suppl. 2005;92:25-7.

2.      Gomez E, Bastida R, Oleaga L, et al.. [Diagnosis of thoracic outlet syndrome by angio-MRI] Radiologia. 2006 Sep-Oct; 48(5): 295-300. Spanish.

3.      Hug U, Jung FJ, Guggenheim M, et al.   ["True neurologic thoracic outlet syndrome" -- anatomical features and electrophysiological long-term follow-up of lateral thenar atrophy] Handchir Mikrochir Plast Chir. 2006 Feb; 38(1):42-5.

4.      Kothari MJ, Macintosh K, Heistand M, et al. Medial antebrachial cutaneous sensory studies in the evaluation of neurogenic thoracic outlet syndrome. Muscle Nerve 1998;21:647-649.

5.      HurteventJF. [Neurophysiological explorations of thoracic outlet syndrome] Rev Med Interne. 1999 Sep; 20 Suppl 5:494S-496S.

6.      Hachulla E, Gillard J, Duquesnoy B. [Clinical aspects of thoracic outlet syndrome] Rev Med Interne. 1999 Sep;20 Suppl 5:464S-467S.

7.      Nishida T, Price SJ, Minieka MM. Medial antebrachial cutaneous nerve conduction in true neurogenic thoracic outlet syndrome. Electromyogr Clin Neurophysiol 1993; 33: 285-288.

8.      Race CM, Saldana MJ. Anatomic course of the medial cutaneous nerves of the arm. J Hand Surg 1991;16A:48-52.

9.      Lazaro-Blazquez D, Soto O. Combined median and medial antebrachial cutaneous neuropathies: an upper-arm neurovascular syndrome. Electromyogr Clin Neurophysiol. 2004 Apr-May; 44(3): 187-91.

10.    Seror P. Medial antebrachial cutaneous nerve conduction study, a new tool to demonstrate mild lower brachial plexus lesions. A report of 16 cases. Clinical Neurophysiology 2004; 115:2316-2322.

11.    Werner RA, Andary M. Carpal tunnel syndrome: pathophysiology and clinical neurophysiology. Clinical Neurophysiology 2002; 113: 1373-1381.

12.    Narakas AO. The role of thoracic outlet syndrome in the double crush syndrome. Ann Chir Main Memb Super. 1990;9(5):331-40. Review.

13.    Niwa H, Yanagi T, Hakusui S, Ando T, et al. [Double crush syndrome in patients with cervical spondylosis or ossification of posterior longitudinal ligament--a clinicophysiological study] Rinsho Shinkeigaku. 1994 Sep; 34(9): 870-6.

14.    Kwon HK, Hwang M, Yoon DW. Frequency and severity of carpal tunnel syndrome according to level of cervical radiculopathy: double crush syndrome? Clin Neurophysiol. 2006 Jun; 117(6): 1256-9.

15.    Simpson RL, Fern SA. Multiple compression neuropathies and the double crush syndrome. Orthop Clin North Am 1996; 27: 381-388.

16.    Dahlin LB, Lundborg G. The neurone and its response to peripheral nerve compression. J Hand Surg  1990; 15: 5-10.

17.    Olmarker K, Rydevik B. Single versus double level nerve root compression: an experimental study on the porcine cauda equina with analyses of nerve impulse conduction properties. Clin Orthop 1992; 279: 35-39.

18.    Suzuki Y, Shirai Y. Motor nerve conduction analysis of double crush syndrome in a rabbit model. J Orthop Sci. 2003; 8(1): 69-74.

19.    Shin JB, Seong YJ, Lee HJ, et al. The usefulness of minimal F-wave latency and sural/radial amplitude ratio in diabetic polyneuropathy. Yonsei Med J. 2000 Jun; 41(3): 393-7. 

20.    Sethi RK, Thompson LL. The Electromyographer’s Handbook, Little Brown and Company Boston/Toronto, 2nd edition, 1989; pp.131-166.

21.    Delisa JA, Lee HJ, Baran EM, et al. Manual of Nerve Conduction and Clinical Neurophysiology. Raven Press, New York, 3rd edition, 1994; pp. 42-183.

22.    Seror P. The medial antebrachial cutaneous nerve: antidromic and orthodromic conduction studies. Muscle Nerve 2002; 26: 421-423.

23.    Seror P. Sensitivity of the various tests for the diagnosis of the carpal tunnel syndrome. J Hand Surg 1994; 19B: 725-8.

24.    Dean AG, Dean G, Colmbeir D. EP1-INFO, Data Processing, Statistics and Epidemiology, Soft Ware Computer, package on microcomputer CDC, Atlanta, USA, 2000.

25.    Abe M, Ichinohe K, Nishida J. Diagnosis, treatment, and complications of thoracic outlet syndrome. J Orthop Sci. 1999; 4(1): 66-9. Review.

26.    Wilbourn AJ: Brachial plexus disorders, in Dyck PJ, Thomas PK (eds): Peripheral Neuropathy, 3rd ed. Philadelphia, Saunders, 1993, pp. 911-950.

27.    Levin KH, Wilbourn AJ, Maggiano HJ. Cervical rib and median sternotomy related brachial plexopathies: a reassessment. Neurology 1998; 1407: 1407-13.

28.    Le Forestier N, Maisonobe T, Moulonguet A, et al. True neurogenic outlet syndrome: electrophysiological diagnosis in six cases. Muscle Nerve 1998; 21: 1129-34.

29.    Gillard J, Duquesnoy B. [Thoracic outlet syndromes: the viewpoint of the rheumatologist] Rev Med Interne. 1999 Sep; 20 Suppl 5: 481S-486S.

30.    Wilbourn AJ, Gilliatt RW. Double-crush syndrome: a critical analysis. Neurology 1997; 49: 21-29.

31.    Richardson JK, Forman GM, Riley B. An electrophysiological exploration of the double crush hypothesis. Muscle Nerve 1999;22:71-77.

32.    Braddom R. Management of common cervical pain syndromes. In: DeLisa JA, editor. Rehabilitation medicine-principles and practice, 2nd ed. Philadelphia: J.B. Lipincottt; 1993. pp.1036-1046.

33.    Flak M, Durmala J, Czernicki K, Dobosiewicz K. Double crush syndrome evaluation in the median nerve in clinical, radiological and electrophysiological examination.  Stud Health Technol Inform. 2006; 123: 435-41.

34.    Choi SJ, Ahn DS.  Correlation of clinical history and electrodiagnostic abnormalities with outcome after surgery for carpal tunnel syndrome.  Plast Reconstr Surg. 1998 Dec; 102(7): 2374-80.

35.    Nakase H, Lida J, Matsuda R, et al. [Clinical study of cervical myeloradiculopathy with carpal tunnel syndrome, double crush syndrome]  2005 Oct; 57(10): 883-7.



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ان الهدف من هذا البحث هو تقييم او اختبار افتراضية التحطيم المزدوجه ومثال لذلك هو دراسة معدل حدوث متلازمة مخرج القفص الصدرى العصبية مع متلازمة النفق الرسغى.


طرق البحث :

اشتملت هذه الدراسة على 137 مريضآ من مرضى متلازمة النفق الرسغى وكانوا 91 (66.4%) من المرضى الاناث و 46 (33.6%) من المرضى الزكور وقد تراوحت اعمار المرضى مابين 23 الى 48 عامآ وقد تم تشخيص  متلازمة النفق الرسغى معتمدا اساسآ على المعايير الكهروفسيولوجيه وهى تضمنت الاتى: ضعف قوة الجهد الكهربى الحركى  للعصب.

  • فترة الخفاء الحركى القصوى لعضلة الابهام المبعده القصيرة اكثر من 4 ملى/ثانية.
  • سرعة التوصيل الحسى المعتدل من الاصبع الثالث الى الرسغ اقل من 45 متر/ثانية.
  • الفرق بين الخفاء الحسى المعتدل للعصب الاوسط و الزندى للاصبع الرابع اكثر من 0.4 ملى/ثانيه.


بالنسبة للمرضى الذين ثبتت إصابتهم بالتهاب الأعصاب الطرفية أو احتباس (اختناق) فى العصب الزندى فى الرسغ او الكوع فقد تم استبعادهم من الدراسة.

ايضآ قد تضمنت هذه الدراسة  عشرين شخصا من الأصحاء ومتجانسين من ناحية السن و الجنس مع المرضى كمجموعة ضابطه.

تم إخضاع المرضى والمجموعة الضابطة الى:

(1)  فحص اكلينيكى للجهاز العصبى مع التركيز على اعراض وعلامات مرض التهاب االاعصاب واختناق العصب الزندى وذلك ليتم استبعادهم و ايضآ متلازمة مخرج القفص الصدرى ومتلازمة النفق الرسغى.

(2)      الدراسات الكهروفسيولوجية للمرضى وكانت كالاتى:

*   دراسات مزدوجه لسرعة التوصيل الحسى/الحركى للعصب الاوسط و الزندى.

*     دراسة مزدوجة للتوصيل الحسى الغير معتدل للعصب المتوسط الجلدى قبل العضدى مع حساب نسبة (معدل) الجهد الحسي بين الطرفين وينبغي أن تكون أكثر من 2.0 وذلك لتشخيص إصابة العصب المتوسط الجلدى قبل العضدى على احد الأطراف.

*   دراسة رسم العضلات  المغذاة من الجذر العصبى العنقى الثامن والظهرى الأول.

بالنسبه الى المعاييرالكهروفسيولوجية التى استخدمت فى هذه الدراسة لتشخيص متلازمة مخرج القفص الصدرى العصبية كانت كالاتى:

·         ضعف قوة الجهد الكهربى الحركى  للعصب الأوسط.

·         ضعف قوة الجهد الكهربى الحسى  للعصب الذندى.

·         ضعف او اعتدال قوة الجهد الكهربى الحركى  للعصب الذندى.

·         ضعف النموذج التداخلى للعضلات المغذاه من الجذر العصبى العنقى الثامن والظهرى الاول.

*   تم عمل أشعة اكس عادية على الفقرات العنقية للمرضى بأعراض الم الطرف العلوي  الغير تقليدي.

أما بالنسبة للمجموعة الضابطة فقد تم دراستها كهروفسيولوجياً دراسة كاملة واخيراً قد تم تجميع البيانات ومقارنة  المتوسطات إحصائيا كما فى النتائج.


نتائج الدراسة :

أظهرت الدراسة النتائج التالية:

(1)   قوة الجهد الكهربى الحسى للعصب الزندى كانت فى خلال النسبة الطبيعية وكان متوسطها مع مقدار الانحراف 14.08±4.8.

(2)  تبين وجود ضعف فى الجهد الحركى للعصب الأوسط فى 19 مريضآ (13.86%) وكان هذا النقص مزدوجا فى 7 (36.84%) من المرضى ومتوسط ذلك ± مقدار الانحراف 12.13±6.08 بالمقارنة مع 2.98±0.58 والفرق بينهم ذو دلالة إحصائية عالية.

(3)  معدل الجهد الحسى للعصب المتوسط الجلدى قبل العضدى للطرفين العلويين فى جميع المرضى كان اقل من 2.0 ومتوسط القيم بالإضافة الى مقدار الانحراف 1.273±0.221

(4)  رسم العضلات اظهر نموذج تداخلى غير كامل لعضلة الإبهام المبعده القصيرة فى 11 مريضا (8 %) وكان ذلك مزدوج في 7 مرضى (63.6 %).

(5)  أظهرت النتائج وجود ضلوع عظمية عنقية فى 3 مرضى ولكن لم يظهر فيهم علامات او موشرات متزامنة مع متلازمة مخرج القفص الصدرى العصبية. 


ملخص البحث :

اظهر البحث بالمؤشرات الكهروفسيولوجية عدم وجود ارتباط بين متلازمة مخرج القفص الصدرى العصبيه ومتلازمة النفق الرسغى وقد تؤدى هذه النتيجة الى إعادة تمحيص ودراسة لافتراضية التحطم المزدوجة واخيراً يمكن القول بان متلازمة مخرج القفص الصدرى العصبيه هى حالة طبية نادرة ولا يجب التسرع بتشخيص وبالتالى علاج هذه المتزامنة الا بعد إجراء فحص اكلينيكى دقيق للجهاز العصبي مصحوب بدراسات كهروفسيولوجية كاملة.

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