Parsonage-Turner syndrome

Author: Doctor I. Kolev M.D1 Creation Date: December 2002 Update: July 2004

Scientific Editor: Professor Alexis Brice

1Fédération de Neurologie, Hôpital Salpêtrière, Bâtiment Paul Castaigne 47-83 Bd de l'Hôpital, 75013 Paris, France. [email protected]

Abstract Keywords Disease name and synonyms Excluded diseases Diagnosis criteria / definition Differential diagnosis Frequency Clinical description Management and treatment Etiology Diagnostic methods Unresolved questions References

Abstract Parsonage-Turner is a clinically defined syndrome that is easily confused with other neck and upper extremity abnormalities. Affected patients present with a characteristic pattern of sudden and acute across the top of the shoulder, lasting a few hours to a fortnight, followed by flaccid paralysis of some muscles of the shoulder girdle. Features supporting strongly diagnosis of Parsonage-Turner disease include: -discrepancy for muscles wasting and denervation between muscles innervated by the same nerve; -patchwork distribution of muscles denervation for muscles that are innervated by several nerves or nerve trunk arising from the brachial plexus -dissociation between sparing of the sensory nerve action potential and muscles denervation depending from the same mixed nerves. The incidence has been estimated at approximately 1.64 in 100,000, with a peak rate between the third and fifth decades and a slight male predominance. Although different precipitating factors, such as infection, trauma, surgery, immunization, and autoimmune mechanisms, have been suspected and incriminated in the occurrence of Parsonage-Turner syndrome, the etiology remains unknown. Prognosis is generally favorable, with about 75% of complete recovery within 2 years. Treatment is symptomatic and is based on analgesic drugs and physical therapy.

Keywords Neuralgic amyotrophy – Brachial plexus – Pain – Patchwork amyotrophy and – Symptomatic treatment – Spontaneous recovery – Unknown etiology.

Disease name and synonyms • Seratus magnus paralysis (2) Parsonage-Turner disease was first reported • Multiple neuritis of the shoulder girdle (3) under different names, such as: • Acute brachial radiculitis (4-5) • Localised neuritis of the shoulder girdle In 1948, Parsonage and Turner described similar (1) conditions and isolated a distinct clinical

Kolev I. Parsonage-Turner syndrome. Orphanet Encyclopedia. July 2004. http://www.orpha.net/data/patho/GB/uk-Turner.pdf 1

syndrome under the neutral term of "Neuralgic involvement of an immune mechanism in amyotrophy; the shoulder-girdle syndrome" (6). Parsonage-Turner syndrome (6-13-18-19-20-21- Subsequently, further appellations have been 22-48-49). proposed, such as: -Paralytic brachial neuritis (7-8) Neuralgic amyotrophy of the lumbar plexus -Acute shoulder neuritis (9) Similar conditions involving lumbo-sacral plexus -Acute scapula-humeral palsy (10) rather than brachial plexus have been described. -Brachial plexus neuropathy (11) Although the clinical features and evolution are This terminology underlines the persistent lack of very similar, pelvis belt neuralgic amyotrophy is knowledge concerning the pathogenic process excluded from Parsonage-Turner syndrome (23). and the localization of lesions in this syndrome. Nevertheless, the "Parsonage-Turner syndrome" Diagnosis criteria / definition (12) appellation has the advantage of referring to Parsonage-Turner disease is a rare and clinically a well-recognized and a well-identified clinical defined syndrome of unknown etiology, which entity, without addressing the issues of consists of sudden pain followed by muscle- localization or pathogenic process. weakness and wasting of the shoulder girdle and upper arm. Usually "without any constitutional Excluded diseases disturbance, pain starts suddenly across the top Hereditary neuralgic amyotrophy (HNA) or of the shoulder-blade (…) and lasts from a few Hereditary brachial plexus neuropathy hours to a fortnight (…) Then, a flaccid paralysis (HBPN) of some of the muscles of the shoulder girdle Familial occurrences of the Parsonage-Turner and often of the arm develops". Sensory syndrome led to the individualization of impairment is more often limited to "a patch of Hereditary neuralgic amyotrophy (HNA) or numbness over the outer side of the upper arm. Hereditary brachial plexus neuropathy (HBPN). When the paralysis appears, the severe pain Clinical features of HNA are identical to those of usually stops" (6). the sporadic form. Family history, a marked tendency of relapse, cases beginning more Differential diagnosis frequently in childhood, and in some cases, At the disease onset, the pain around the minor dysmorphic features, enable distinguishing shoulder girdle may be a sign leading to the hereditary forms from the sporadic variety misdiagnosis, as acute pain can occur in (13). An autosomal-dominant transmission mode numerous other shoulder affections (13-24), linked to 17q25 locus is admitted in most HNA such as: families (14), but recent data tend towards a • Rotator cuff tears genetic heterogeneity (15). • Adhesive capsulitis • Calcific tendonitis Hereditary neuropathy with liability to • Shoulder arthritis pressure palsies (HNPP) • Local bone affection HNPP is a distinct genetic disorder and recurrent • Cervico-brachial neuralgia brachial plexopathy might be its only expression • Herpes Zoster (16). When muscles are subsequently affected with paralysis and wasting, other conditions involving Diabetic amyotrophy the second motor neurone can be discussed, Proximal diabetic neuropathy, which consists of especially: muscle-weakness and, exceptionally, wasting in • Discogenic nerve root compression the proximal part of the lower limbs, involves the • Tumors of the spinal cord or brachial plexus scapulo-humeral region (17). • Infiltrative tumor of the nerve root or brachial Neuralgic amyotrophy as a complication of plexus such as Pancoast-Tobias syndrome serotherapy • Outlet syndrome such as neuralgia of the This entity, known since 1910, is clinically supra scapular nerve, the long thoracic identical to Parsonage-Turner syndrome, except nerve, or the thoracic outlet syndrome that the delay between pain and paralysis is • Traumatic compressive nerve injuries shorter, and sometimes preceded by generalized • Cervical artery dissection urticaria. This condition is usually considered • Anterior poliomyelitis distinct from Parsonage-Turner syndrome • Amyotrophic lateral sclerosis because of the well-identified precipitating factor. The acute onset of pain followed by its rapid However, numerous authors consider it as the resolution or decrease, as weakness and prototypic form of the Parsonage-Turner paralysis occur, constitute a disease pattern syndrome, and use this argument to support the characteristic of Parsonage Turner syndrome.

Kolev I. Parsonage-Turner syndrome. Orphanet Encyclopedia. July 2004. http://www.orpha.net/data/patho/GB/uk-Turner.pdf 2

However, electro-physiological and imaging arm, develops (6-7). Usually, studies are useful in distinguishing the above appears suddenly, but sometimes gradually conditions from Parsonage-Turner syndrome (6- increases over two or three days, or even one 11-13-24). week in rare cases. Paralysis is of lower motor neurone type, with flaccidity and rapid wasting of Frequency the affected muscles. Tendon reflexes might be Firstly described in military personnel during the affected, depending on the severity and extent of Second World War, Parsonage-Turner muscular paralysis and wasting. Hypoactive syndrome seems rare. In the general population reflexes are frequently encountered, and of Rochester, Minnesota, the incidence has been fasciculations are occasionally seen (6-7-8-10- estimated at about 1.64 in 100,000 (25). Ages of 11). affected patients range from 3 months to 84 Depending on the supposed anatomical site of years (26), with the highest incidence occurring the lesion, several patterns of weakness are between the third and fifth decades (6-7-11-27- reported: weakness involving muscles that are 28-29-30), and the average age at onset has innervated by either one peripheral nerve, been estimated to 38 years from review of several peripheral nerves, one or several nerve- literature series(31). A male predominance is root, or a combination of nerve-roots and reported in the civilian population, with a male- peripheral nerves. The most frequent pattern of to-female ratio ranging from 1.74:1 to 4:1 (11-25- weakness corresponds to the involvement of 26). several peripheral nerves, among which axillary, suprascapular, long thoracic and Clinical description musculocutaneous nerves are the most Local pain around the shoulder girdle is the commonly affected (6-7-8-10-11). Radial (11-7), prevalent presenting symptom (6-7-8-10-11). It is anterior interosseous (7-10-33-36), and median usually sudden and often severe, insufferable, nerves (37), are also occasionally reported to be sometimes awakening patients during the night. affected. The involvement of the phrenic nerve, It worsens progressively for some hours or even resulting in diaphragm paralysis with dyspnea is two days. Described as a constant severe ache rarely, but classically, reported. This involvement associated with tenderness of the muscles, the is probably underestimated, as it is frequently pain is not affected by coughing. However, it is associated with asymptomatic presentation. accentuated by arm movements and muscular Regarding nerve-root involvement pattern, C5 pressure, but almost unaltered by movements of and C6 are the most commonly affected; C4 and the neck. The pain is commonly distributed C7 are also involved, but more rarely. across the back of the scapula and the tip of the Accordingly, the weakness will affect the deltoid, shoulder. It often radiates down the outer side of which is the muscle the most frequently involved, the arm and up along the neck, and seldom and the supraspinatus, infraspinatus, serratus spreads down as far as the outer side of the anterior, biceps, triceps, and wrist and finger forearm, below the elbow. There is no exact extensors (6-7-8-11-38-39). Muscle involvement correlation between the localisation of the pain is usually unilateral, although bilateral and the distribution of the subsequent muscle involvement is not uncommon, with an paralysis. However, in general, pain radiating asymmetrical pattern of affected muscles. below the elbow is associated with involvement Weakness and pain area do not coincide of the biceps or triceps, and radiation into the perfectly. Muscular atrophy occurs rapidly in neck involves the sternocleidomastoid and different degrees of severity. The resulting trapezius. Similarly, most of the patients with clinical feature is a patchwork of weakness and bilateral paralysis also initially suffer from atrophy in one or several muscles, principally bilateral pain. Usually the severe pain lasts from around the shoulder blade. a few hours to three weeks, and then disappears In the early stages of the affection, many rather suddenly while the muscular wasting and patients report a localised numbness, although weakness occur. A less severe pain may persist there is no residual sensory impairment at the considerably longer. Severe pain may later stages when weakness has already sometimes last days or even weeks after appeared (6-7). Sensory impairment at the later appearance of the weakness. Occasionally, stages is usually mild and the most commonly muscular weakness and pain occur involved area is a small strip over the outer side simultaneously. Although lack of pain is of the upper arm, corresponding to the extremely uncommon in Parsonage-Turner distribution of the circumflex nerve. Nerve-root syndrome, it has been already reported in the distribution of muscle weakness is usually original series of Parsonage and Turner(6). associated with sensory impairment occurring As the pain subsides, flaccid paralysis of some down the outer side of the arm and forearm in muscles of the shoulder girdle, and often of the

Kolev I. Parsonage-Turner syndrome. Orphanet Encyclopedia. July 2004. http://www.orpha.net/data/patho/GB/uk-Turner.pdf 3

the C5-C6 cases, and extending to the neck side suggested to maintain full range of motion. when C4 root is involved. In fact, areas of Active rehabilitation is undertaken only when sensory impairment correspond to the some recovery of the affected muscle(s) is distribution of the nerve or nerve-root already obtained. Furthermore, all the upper supposedly affected, which is itself based on body muscles should undergo rehabilitative distribution of weakness. However, in several exercises, and not only those presenting clinical cases, the degrees of sensory impairment and weakness (42). It is also recommended that weakness corresponding to the distribution of strength recovery reaches a plateau before the same nerve do not correlate (6-7-8-10-11- patient returns to sports (44). 25-26-28-31). However, the recovery delay does not seem to From the observation of few cases in which be improved by these physical therapies (11). sensory impairment was absent and the pattern Surgical stabilization of the scapula to the of muscles affected by weakness did not thorax, or tendon transfers have been performed correspond to any peripheral nerve or nerve root with benefit in patients who did not achieve distribution, Parsonage and Turner (6) recovery (43). suggested that the lesion could probably also affect the spinal cord (anterior horn cells). Etiology The exact cause of brachial neuritis remains Management and treatment unknown. Numerous authors have proposed Prognosis is generally good, since recovery of various precipitating events or factors. These strength and sensation usually begins factors, suggested to contribute to the spontaneously, as early as 1 month after development of brachial neuritis, are found in symptoms onset, with about 75% of complete approximately 30 to 85% of the cases (1-6-7-8- recovery within 2 years (11). However, the 11-26-28-35), 3 to 14 days preceding the onset period of time for complete recovery is very of pain. The most frequently reported factors are variable, ranging from 6 months to 5 years (7- infection, viral diseases, trauma, heavy exercise, 24). It seems that the delay in recovering surgery, immunization, and autoimmune strength depends on the severity and duration of mechanisms (vaccinations, serotherapy, foreign pain, weakness, or both (6-8-11-39). serum injection, subcutaneous injections of Furthermore, patients with involvement of allergens, immunogenic substances, pregnancy) proximal and upper trunk lesions have the most (6-7-8-10-11-13-27-28-30-32-33-34-45). rapid recovery(11). Although not very common, Although commonly admitted, the contributing relapse might nevertheless occur within a few role of these factors has not been proved and months to several years after full recovery (6-7- remains hypothetical. 8-11-38-40-41). In general, complete restoration The particular case of post-serotherapy to normal strength and function usually occurs neuralgic amyotrophy (18-19-20-21-22) must be within five years. underlined. This well-known condition is an However, prognosis is influenced by the duration occasional complication of serum injection. of the resulting incapacity, some patients having Although incompletely elucidated, the experienced impairment persisting sometimes physiopathology of this process lies in the thirty years after the onset (31). The occurrence occurrence of perineural oedema, similar to the of diaphragmatic forms must be taken into mechanism involved in urticaria in serum account in the diagnostic approach of dyspnea. sickness (6). Several authors consider that No specific treatment has yet been proved neuralgic amyotrophy following foreign serum efficient in Parsonage-Turner syndrome. In the injection should not be distinguished from the early stages, pain may require treatment. Parsonage-Turner syndrome (48-49). Common analgesic drugs are usually sufficient. In a way similar to post-serotherapy neuralgic However, in many cases, high pain intensity amyotrophy, and on the basis that numerous requires morphine administration. immune events are recognized as precipitating Corticosteroids administration does not provide factors for Parsonage-Turner disease, an allergic any significant benefit, with the exception of a or hypersensitivity reaction mechanism is few patients who experienced some pain relief commonly suggested in the etiology of the (11). Rest is recommended (42), and disorder (6-9-28-45). Rare cases reported in immobilization of the affected upper extremity anatomo-pathological studies are suggestive of may be helpful in relieving the pain and in an inflammatory-immune pathogenesis (50). preventing stretching of the affected muscles Furthermore, some authors underline that the (10-43). particular evolution of Parsonage-Turner As pain subsides, physical therapy is disease, i.e. sudden pain onset and recommended. Passive range of motion spontaneous recovery, is similar to the exercises of the shoulder and elbow (38-43) are

Kolev I. Parsonage-Turner syndrome. Orphanet Encyclopedia. July 2004. http://www.orpha.net/data/patho/GB/uk-Turner.pdf 4

inflammatory dysimmune process of the delayed imaging of the thorax, even if there is no clinical over-sensitiveness type (30). evidence for a diaphragmatic weakness. Several studies provide additional evidence for an allergic or autoimmune mechanism. Sierra et Unresolved questions al (51) showed that blood lymphocytes in Although some arguments are in favor of a patients with neuralgic amyotrophy are possible immune mechanism, the specifically sensititized to brachial plexus nerves. etiopathogenesis of Parsonage-Turner disease In addition, Vriesendorp et al (52) determined remains unknown. Furthermore, the rare cases that complement-fixing antibodies to peripheral of conduction block reported suggest a possible nerve myelin and terminal complement activation focal demyelination (47-53), which may occur products are increased in serum of patients in during the early stage of the affection, when the acute phase of neuralgic amyotrophy. electromyographical studies are rarely performed. Moreover, the precise location of the Diagnostic methods lesion on the nerve root, either among the The Parsonage-Turner disease is a clinical brachial plexus, or in the nerve trunk is also syndrome and there is no existing diagnostic uncertain. Particularly, the cases with distal study providing a specific result that allows muscles involvement may result from a partial diagnosis confirmation. The results of most of plexus trunk lesion or a distal terminal nerve laboratory studies are normal, and their aim is to lesion (31). Thus, the diversity of appellations eliminate conditions in differential diagnosis. for Parsonage-Turner diseases reflects entirely There is no evidence for an inflammatory or these uncertainties as to the localization and the infectious process. Cerebrospinal fluid is usually pathogenic process. normal or might show a slight increase in the More recently, many cases of clinical variations total protein (8-11-28). Imaging studies such as of Parsonage-Turner disease have been brachial plexus and cervical MRI are helpful in reported (37-54). These variants forms include eliminating any local pathological process, which focal and distal forms, sensory isolated forms, is associated with a differential diagnosis and some involve cranial nerves (31). Therefore, condition. High intensity signals on T2-weighted it seems that the nosographic framework of images in shoulder muscles before development neuralgic amyotrophy is widening, and that the of have been described, but are condition should be considered as a multifocal not specific (46). neuropathy involving mostly, but not only, nerves Electromyographical studies are more useful as of the upper extremity. they give the precise pattern of muscles involvement, and subsequently the hypothetical References localisation of the nerve lesion(s). They can also 1. Spillane JD. Localised neuritis of the shoulder be helpful in detecting sub-clinical involvement of girdle. Lancet 1943; 245:532-535. unsuspected muscles, or in ruling out a 2. Richardson JS. Serratus magnus palsy. traumatic or compressive nerve or trunk lesion. Lancet 1942; 242:618-619. In neuralgic amyotrophy, electromyographical 3. Burnard ED, Fox FG. Multiple neuritis of the findings usually reveal acute denervation shoulder girdle. N Z med J 1942; 41:243-247. resulting from an axonal neuropathy. However, 4. Dixon GJ, Dick TBS. Acute brachial radiculitis some rare studies reported evidence of proximal : Course and prognosis. Lancet 1945; 249:707- conduction block, suggesting focal proximal 708. demyelination (47). 5. Turner JWA. Acute brachial radiculitis. Br Med The following features are highly suggestive of J 1944; 2:592-594 Parsonage-Turner disease diagnosis: 6. Parsonage MJ, Turner JWA. Neuralgic -discrepancy for muscles wasting and amyotrophy: The shoulder-girdle syndrome. denervation between muscles innervated by the Lancet 1948; 1:973-978. same nerve; 7. Turner JWA, Parsonage MJ. Neuralgic -patchwork distribution of muscles denervation amyotrophy (paralytic brachial neuritis) with for muscles that are innervated by several special reference to prognosis. Lancet 1957; nerves or nerve trunk arising from the brachial 2:209-212. plexus; 8. Magee KR, DeJong RN. Paralytic brachial -dissociation between sparing of the sensory neuritis. Discussion of clinical features with nerve action potential and muscles denervation review of 23 cases. JAMA 1960; 174:1258-1262. depending from the same mixed nerves. 9. Höök O. Acute shoulder neuritis. A syndrome Similarly, diaphragmatic denervation supports characterised by pain, paralysis and muscular also diagnosis of Parsonage-Turner disease atrophy. Acta psychiat (Kbh ) 1950; 25:209-223. (31). Diaphragmatic involvement may also be revealed by radiography or ultrasonography

Kolev I. Parsonage-Turner syndrome. Orphanet Encyclopedia. July 2004. http://www.orpha.net/data/patho/GB/uk-Turner.pdf 5

10. Gathier JC, Bruyn GW. La paralysie huméro- Rochester, Minnesota, 1970-1981. Ann Neurol scapulaire aiguë. Psychiat Neurol Neurochir 1985; 18:320-323. (Amst ) 1960; 63:307-332. 26. Devathasan G, Tong HI. Neuralgic 11. Tsairis P, Dyck PJ, Mulder DW. Natural amyotrophy: criteria for diagnosis and a clinical history of brachial plexus neuropathy. Report on with electromyographic study of 21 cases. Aust 99 patients. Arch Neurol 1972; 27:109-117. N Z J Med 1980; 10:188-191. 12. Ducros JJ. Le syndrome de Parsonage et 27. Serratrice G, Baudoin D, Pouget J, Blin O, Turner. Thèse (Bordeaux) 1958. Guieu R. Formes typiques et atypiques de 13. Pourel J. Syndrome de Parsonage et Turner. névralgie amyotrophiante de l'épaule : 86 cas. Encycl Med Chir (Elsevier Paris) 1982; Appareil Rev Neurol (Paris) 1992; 148:47-50. locomoteur:14347-A-10. 28. Weikers NJ, Mattson RH. Acute paralytic 14. Wehnert M, Timmerman V, Spoelders P, brachial neuritis. A clinical and electrodiagnostic Meuleman J, Nelis E, Van Broeckhoven C. study. 1969; 19:1153-1158. Further evidence supporting linkage of 29. Flaggman PD, Kelly JJ, Jr. Brachial plexus hereditary neuralgic amyotrophy to chromosome neuropathy. An electrophysiologic evaluation. 17q. Neurology 1997; 48:1719-1721. Arch Neurol 1980; 37:160-164. 15. Kuhlenbaumer G, Meuleman J, De Jonghe 30. Vighetto A, Grand C, Confavreux C, Aimard P, Falck B, Young P, Hunermund G et al. G. Le syndrome de Parsonage et Turner et ses Hereditary Neuralgic Amyotrophy (HNA) is frontières. 29. cas. Rev Neurol (Paris) 1988; genetically heterogeneous. J Neurol 2001; 144:494-498. 248:861-865. 31. Kolev I. Le syndrome de Parsonage et 16. Orstavik K, Skard HM, Young P, Stogbauer Turner et ses formes atypiques ; un cadre F. Brachial plexus involvement as the only nosologique revisité. Thèse (Paris) 2001. expression of hereditary neuropathy with liability 32. Juillet P, Savelli A, Rigal J, Bouvier S. Le to pressure palsies. Muscle Nerve syndrome de Parsonage et Turner. Rev Neurol 2001;24:1093-6. (Paris) 1964; 2:135-147. 17. Ogawa K, Sasaki H, Kishi Y, Yamasaki H, 33. Subramony SH. AAEE case report #14: Okamoto K, Yamamoto N et al. A suspected neuralgic amyotrophy (acute brachial case of proximal diabetic neuropathy neuropathy). Muscle Nerve 1988; 11:39-44. predominantly presenting with scapulohumeral 34. Gathier JC, Bruyn GW. Handbook of clinical muscle weakness and deep aching pain. Neurology. North Holland Publishing, Diabetes Res Clin Pract 2001; 54:57-64. Amsterdam 1970;77-86. 18. Lhermitte J. Paralysies amyotrophiques 35. Martin WA, Kraft GH. Shoulder girdle disociées du plexus brachial à type supérieur neuritis: a clinical and electrophysiological consécutive à la sérothérapie. Rev Neurol evaluation. Mil Med 1974; 139:21-25. (Paris) 1919; 26:894-900. 36. Wong L, Dellon AL: Brachial neuritis 19. Brodin P, Lhermitte J. Paralysie presenting as anterior interosseous nerve amyotrophique spontanée des racines compression-Implications for diagnosis and supérieures du plexus brachial ; leur treatment: A case report. J Hand Surg 1997; ressemblance avec les paralysies post- 22A:536-539. sérothérapiques. Rev Neurol (Paris) 1932; 37. England JD, Sumner AJ: Neuralgic 41:86-91. amyotrophy: An increasingly diverse entity. 20. Bataille JGJ. Contribution à l'étude des Muscle Nerve 1987; 10:60-68. paralysies postsérothérapiques antidiphtériques. 38. Aymond JK, Goldner JL, Hardaker WT: Thèse (Paris) 1934. Neuralgic amyotrophy. Orthop Rev 1989; 21. Dyke SC. Peripheral nerve lesions after 18:1275-1279. antitetanic serum. Lancet 1918; 1:570. 39. Dillin L, Hoaglund FT, Scheck M: Brachial 22. Smith HP, Smith HP Jr. Phrenic paralysis neuritis. J Bone Joint Surg 1985; 67A:878-880. due to serum neuritis. Amer J Med 1955; 40. Favero K, Hawkins R, Jones M: Neuralgic 19:808-813. amyotrophy. J Bone Joint Surg 1987; 69A:195- 23. Marra TR. The clinical and electrodiagnostic 198. features of idiopathic lumbo-sacral and brachial 41. Ferrini L, Della-Torre P, Perticoni G. plexus neuropathy: a review of 20 cases. Cantisani TA: Neuralgic amyotrophy of the Electromyogr Clin Neurophysiol 1987; 27:305- shoulder girdle: The Parsonage-Turner 315. syndrome. Ital J Orthop Traumatol 1986; 12:223- 24. McCarty EC, Tsairis P, Warren RF. Brachial 231. neuritis. Clin Orthop 1999;368:37-43. 42. Hershman EB: Brachial plexus injuries. Clin 25. Beghi E, Kurland LT, Mulder DW, Nicolosi A. Sports Med 1990; 9:311-329. Brachial plexus neuropathy in the population of

Kolev I. Parsonage-Turner syndrome. Orphanet Encyclopedia. July 2004. http://www.orpha.net/data/patho/GB/uk-Turner.pdf 6

43. DePalma AF: Shoulder-Arm-Hand Pain of 50. Suarez GA, Giannini C, Bosch EP, Barohn Mesodermal, Neurogenic, and Vascular Origin. RJ, Wodak J, Ebeling P et al. Immune brachial In DePalma AF (ed). Surgery of the Shoulder. plexus neuropathy: suggestive evidence for an Ed 3. Philadelphia, JB Lippincott 597-598, 1983. inflammatory-immune pathogenesis. Neurology 44. Hershman EB, Wilbourn AJ, Bergfeld JA: 1996; 46:559-561. Acute brachial neuropathy in athletes. Am J 51. Sierra A, Prat J, Bas J, Romeu A, Montero J, Sports Med 1989; 19:655-659. Matos JA et al. Blood lymphocytes are 45. Klawans HL, Topel JL: Neurologic Aspects of sensitized to branchial plexus nerves in patients the Shoulder. In Post M (Ed). The Shoulder: with neuralgic amyotrophy. Acta Neurol Scand Surgical and Nonsurgical Management. Ed 2. 1991; 83:183-186. Philadelphia, Lea & Febiger 174-175, 1988. 52. Vriesendorp FJ, Dmytrenko GS, Dietrich T, 46. Helms CA, Martinez S, Speer KP: Acute Koski CL. Anti-peripheral nerve myelin brachial neuritis (Parsonage-Turner syndrome): antibodies and terminal activation products of MR imaging appearance-Report of three cases. complement in serum of patients with acute Radiology 1998; 207:255-259. brachial plexus neuropathy. Arch Neurol 1993; 47. Lo YL, Mills KR. Motor root conduction in 50:1301-1303. neuralgic amyotrophy: evidence of proximal 53. Watson BV, Nicolle MW, Brown conduction block. J Neurol Neurosurg Psychiatry JD.Conduction block in neuralgic 1999; 66:586-590. amyotrophy.Muscle Nerve 2001; 24:559-63. 48. Bouche P, Vallat JM. Neuropathies 54. England JD. The variations of neuralgic Périphériques. Polyneuropathies et amyotrophy. Muscle Nerve 1999; 22:435-436. mononeuropathies multiples. Paris: Doin éditeurs, 1992. 49. Gathier JC, Bruyn GW. Handbook of clinical Neurology. North Holland Publishing, Amsterdam 1970; 8:95-111.

Kolev I. Parsonage-Turner syndrome. Orphanet Encyclopedia. July 2004. http://www.orpha.net/data/patho/GB/uk-Turner.pdf 7