Brilish
lownal
of Dernuilnhnij
( 1 9 4 2 ) 1 2 f i . (•>^ l -
Blisters, ulceration and autonomic neuropathy in carpal tunnel syndrome N.H.COX. D.M.LARGE.* VV.D.PATERSON AND F.A.IVI-f ls of Dermntohiin and 'Medicine. Ciimberltind Infirmarii. Carlisle CA2 THY, U.K. of Drrmalolocju. Drulmrii Hospititt, Durham, U.K.
Accepted lor publication I S IJecetnbcr 1991
Summary
We describe three patients with trophic ulceration and blistering of the lingertips associated with carpal tunnel syndrome. One of the patients also had non-insulin-dependent diabetes mellitus. Autonomic neuropathy distal to the carpal tunnel was probably present in all subjects at the time of presentation; in the patient with recent symptoms the skin was warm, and sweating was virtually absent, whilst the other two patients described cold skin, consistent with prolonged autonomic neuropathy.
Prominent dermatological signs are rare in carpal tunnel syndrome (CTS) and almost all the reported cases have been in European literature.' ' Reported skin iibnormalities include ulceration. blistering, hypohidrosis and other features of autonomic neuropathy, vasospasm or Raynaud's phenomenon, and irritant contact dermatitis. Dermatologists may therefore be involved in diagnosis or management of such cases.
Case reports Case 1
A 62-year-old woman with well-controlled, non-insulin-dependent diabetes mellitus and hypertension, both of 8 years' duration, had a 6-month history of paraesthesiae. sensory loss and functional deficit in the thumb, index and middle fingers ot the right hand. Blisters and subsequent ulcers of both palmar and dorsal aspects of the tips of the affected digits were a prominent early feature. She had long-standing osteoarthritis of the neck, shoulders and hands but no history of Raynaud's phenomenon or connective tissue disease. Apart from marked Heberden's nodes, the clinical abnormalities in the hands were confined to the Hrst three digits and radial aspect of the right hand. The digits were dusky, swollen, dry, markedly warmer than other digits of either hand, and several healing ulcers were present (Fig. 1). Sensation (light touch, pinprick and temperature) was grossly impaired, and there was marked thenar wasting with loss of power of the median nerve-innervated muscles, especially abductor pollicis Correspondence: Dr N.H,Cnx,
Figure I. I lands of Case 1, Swelling of index and middle lini^er tips on the right hand with a healed ulcer of the middle finger, and marked thenar wasting.
brevis. Tinel's test was positive, and starch-iodine testing to identify sweat-duct orifices demonstrated virtually complete anhidrosis in the affected sensory distribution. There were patchy areas of mild loss of light touch and vibration sensation in the feet, and absent knee and ankle reflexes, suggesting chronic peripheral neuropathy. However, the only clinical evidence of neunjpathy in the arms was that in the median nerve distribution of the right hand. Previous radiology of the neck and shoulder had demonstrated changes of osteoarthritis only, and no osteolysis was observed in X-rays of the hands. ESR was 611
612
N.A.COX ('( al.
4 mm/h. and results of thyroid biochemistry were within the normal range. Nerve conduction studies, steroid injection, and surgical treatment were refused by the patient. Case 2
A 75-year-old man had bilateral carpal tunnel syndrome, previously treated by steroid injection on the right 12 years ago and by surgical decompression on the left 4 years ago. The surgical treatment was performed 6 months after development of symptoms, and produced complete resolution, but the steroid injections in the right hand had been of no benefit. He was referred because of development of blisters and subsequent ulcers on the tips of the right index and middle fingers. There was a history of possible injury preceding the first blister but he denied that subsequent blistering was associated with trauma. He had osteoarthritis and had previously had hip replacement surgery. Examination revealed marked decrease in touch and pinprick sensation in the median nerve sensory distribution, more prominent in the right hand, and an ulcer on the right index finger from which a bacteriology culture produced scanty Staphylococcus aureus and a profuse growth of F.schcricbia coU. The affected area was colder than unaffected skin, but no other abnormality of autonomic function was noted in the records and there was no comment regarding thenar wasting. Surgical deeompression was considered but a previous orthopaedic opinion was not optimistic for recovery and further intervention was declined.
Case 3
A 51-year-old woman with morbid obesity and gross varicose leg ulceration was noted to have painless ulceration of the tips of the right index and middle fingers. She gave a history of loss of fine touch sensation of 9 years duration in thumb and index fingers of both hands, and the affected digits felt cold. Several fingertip blisters had developed, at least some of which were caused by thermal burns, and had led to persistent ulceration. Examination revealed decreased sensation, thenar wasting, and reduced power in median nerveinnervated muscles as described for Case 1. and a diagnosis of bilateral carpal tunnel syndrome was made. Nerve-conduction studies, performed at the Regional Neurology Unit, showed slowing of sensory conduction velocities (finger to wrist) and increased distal motor latency for both median nerves, more marked on the
right, consistent with carpal tunnel syndrome. No specific endocrinologicai cause for her obesity was demonstrated, and obesity was believed to be the cause of the carpal tunnel compression. Bilateral surgical treatment was followed by rapid healing of the ulcers. Case records of the presenting features were not available, but review of clinical photographs revealed the affected fingers to be swollen and slightly dusky; these features were consistent with a chronic autonomic neuropathy although specific testing was not performed at the time. At review 11 years later, she described residual mild sensory loss and loss of power of opposition, but no worsening of symptoms and no recurrence of ulceration. She had warm fingers, and no apparent deficit of sweating as demonstrated by the starch-iodine test.
Discussion There are few reports of blistering of the digits in CTS.'' Trauma to the digits, vasomotor or autonomic factors, and secondary infection may all be involved." Although only one of our patients admitted thermal damage or trauma preceding blisters and ulceration. ali had such severity of sensory loss that either physical or thermal trauma could have occurred without any immediate symptoms. All three patients described blisters before the ulceration: infection was only demonstrated in one {Case 2) at the time of presentation, but ulcers in the first patient had healed following use of antiseptic preparations and bacteriology samples had not been taken. None of the patients was able to attend at the time of development of a fresh blister, so the possibility that the blisters were due to infection of minor areas of trauma cannot be excluded. However, primarily infective causes of fingertip bullae. such as blistering distal dactylitis, do not cause subsequent trophic ulceration. Diabetic bullosis was a possible diagnosis in Case 1 but there is no reason why this should have been localized to the area of sensory loss, and this disorder does not cause trophic ulcers. It is probable that the neuropathy was the most important factor in all our patients. Autonomic dysfunction in CTS is probably underestimated as it is less obvious from symptoms or routine neurological examination than the motor and sensory features of the syndrome. It is, however, a frequent component of the syndrome^ because the autonomic fibres carried by the median nerve traverse the carpal tunnel before the nerve divides. Decreased or absent sweating.** '* swelling of the hand.'* and increased temperature due to vasomotor abnormalities'"'* are all
SKIN SIGNS IN CARPAL TUNNEL SYNDROME
features of the autonomic neuropathy and were all present in our first case. Marked swelling of the affected digits was a feature in Case 3. Other features of autonomic neuropathy which have been reported in CTS include 'contact dermatitis' of thefingertips.**which was presumed to be irritant in type and related to lack of sweating, and also the more serious complication of osteolysis which can occur'''' in digits where there is long-term ulceration. The constellation of features in patients with prominent autonomic damage in CTS is therefore similar to some features of reflex sympathetic dystrophy (Sudek's atrophy).'" and CTS has been associated with this disorder. The cold skin in our Cases 2 and 5. who both had long-standing C1'S, would also be compatible with the dystrophic or atrophic stages of refiex sympathetic dystrophy, but no investigation of sweating was performed at the time of presentation. Although diabetes is associated with neuropathy of various types, including a symmetrical peripheral neuropathy (of which CTS can be the first indication), autonomic neuropathy, and mononeuritis multiplex, the features in our first case were more suggestive of true CTS. She had abnormalities of motor and sensory function, as well as vasomotor and sweating abnormalities, in a distribution suggesting CTS rather than a mixed peripheral neuropathy. However, a peripheral nerve dysfunction can be due to a combination of factors acting simultaneously, and it is likely that CTS and polyneuropathy co-exist in some diabetic patients." '^ As surgical treatment can produce freedom from symptoms." it is important to consider CTS in diabetic patients with neuropathy affecting the hands. It is also likely that the combined autonomic and sensory dysfunction is important in the pathogenesis of fingertip ulceration, as a recent study demonstrated that autonomic dysfunction was a better predictor of diabetic foot ulceration than peripheral sensory nerve function;" there is no reason why this finding should be specific to either diabetes or to foot ulceration. and it could apply to hand ulceration in our non-diabetic patients also. Aggravation of Raynaud's syndrome by development of CTS'"" and vasospasm related to CTS''' have been reported, and also connective tissue disorders associated with CTS."' but careful objective studies have not demonstrated the frequency of Raynaud's phenomenon to be any greater in patients with CTS than that expected in the general population.'' 'I'wo of our patients had swollen dusky cold fingers but not the variability of colour which is diagnostic of Raynaud's phenomenon. Treatment of patients with blisters and trophic ulcers in CTS. apart from local therapy, is by surgical decompression of the carpal tunnel. Although complete resolu-
613
tion of all symptoms is perhaps unlikely, this treatment may abolish blistering and ulceration (and therefore the secondary problems of infection and osteolysis). Two of four patients with trophic ulcers reported by Besson et a!.' (including one with blisters) clearly improved after surgery, and a further patient with blisters and osteolysis developed blisters less frequently. Unfortunately, two of our patients with blisters declined, or were advised against, surgical intervention, but there was complete and prolonged healing of ulceration in the other patient despite some residual sensory deficit.
References 1 PlisttT R, Zur Klinik der Haut- und Nageiveranderungen beim Carpal-Tunndsyndrom, Hatitarzt 1954; 5; 540-2, 2 Lagrot F. Micheou P. Costagliola M. Mansat C, A propos d'une rormt' ulcerantc du syndrome du canal carpicn, iFre) Mem Arad Chir \9(->(y.92: 1(19-71, i BoLivier M, I-ejcunc H, Rouillat M, Marionncl), Les formes ulccromultilantes du syndrome du caniil Ciirpien, iFrcl (Hng, Atistr,! Rev RInim Mai Osteoartic 1979:46: K-.9-7h, 4 Difonzo EM, Moretti S, Baldini MA cl al. Quadro tutanco distrotico iilcerativo in forso di sindronie del canale carpale, (Ita) (Hng. Abstr.l G Hal Dermatol Venereol 1986: 121: 9 J - 5 , 5 Neau |P. Cil R. Boissonnot L ef d/, llkerations cutanees et osteolyse dans II' syndrome du canal carpien, IFrel lEng, Abstr,) Rev Neitrol 1987; 14J: J(li-5. f> I'avcsi c;, Medici D, lirunibilla S *•( til. Carpal tunnel syndrome presenting with prominent skin syrnplums, ttal j \eiirol Sri 1988: 9: 173-4, 7 Besson i. Courturier F, De Ciamcomini P et al. Atleinte du nerf median associee a des lesions cutanees et des troubles trophiques desdoigts. (Fre) Press Med 1989: 18: 1207, H Spinner R|. Bachman |W. Amadio PC. The many faces of carpal tunnel syndrome, MaifO Clinic Pnneedinqs ] 9S9; 64: S29- 36, 9 I'ast A, Parikh S. Ducommun K|, Dermatitis-sympathetic dysfunction in carpal tunnel syndrome, A case report, Clin Drthop ] 989; 247; 124-f-., 10 Shelton RM, I^wi.s CW, Reflex sympathetic dystrophy: a review. / Am Acad liermatot 1990; 22: 51 3-20, 1 1 Walter-Sack I. Zollner N, Maskiertes Karpaltunnelsyndrom bei diabetischer Polyneuropatliie (Ger,) (Fng, Abstr,) Dlsih Med Woihensihr 1980; 105: 19-21, 1 2 ()/aki I, Baba M, Matsunaga M, Takebe K, Deleterious effect of the carpal tunnel syndrome on nerve conduction in diabetic polyneuropathy, Ekrlromnotfr Clin Neuroplnisiol 19SS; 28: 301-6, 1 i McFadden IP. Corrall K|M, O'Brien IAD, Autonomic and sensory nerve function in diabetic foot ulceration, Clin Exp Lhrnuitol 1991; 16: 19 3-6, 14 Waller IXI. Dathan IR. Raynaud's syndrome and carpal tunnel syndrome. Postgrad Med I 1985: 61: 161-2, 1 5 Linscheid RL. Peterson LFA. Juergens |I.. Carpal-tunnel syndrome associated wilh vasospasm, / Hone joint Stiri} 1967: 49: 1141-6, 16 Winkelmann RK, Connolly SM, Doyle JA, Carpal tunnel syndrome in cutaneous connective tissue disease: generalized morphoea. lichen sclerosus, fasciitis. discoid lupus erythematosus, and iupus panniculitis, / Am Aaul DernuUal 1982; 7: 94-9, 17 Loebe M. Heidrich H, The carpal tunnel syndrome—a disease underlying Raynaud's phenomenon? Angiology 1988: 59: 8 9 1 901.
lownal
of Dernuilnhnij
( 1 9 4 2 ) 1 2 f i . (•>^ l -
Blisters, ulceration and autonomic neuropathy in carpal tunnel syndrome N.H.COX. D.M.LARGE.* VV.D.PATERSON AND F.A.IVI-f ls of Dermntohiin and 'Medicine. Ciimberltind Infirmarii. Carlisle CA2 THY, U.K. of Drrmalolocju. Drulmrii Hospititt, Durham, U.K.
Accepted lor publication I S IJecetnbcr 1991
Summary
We describe three patients with trophic ulceration and blistering of the lingertips associated with carpal tunnel syndrome. One of the patients also had non-insulin-dependent diabetes mellitus. Autonomic neuropathy distal to the carpal tunnel was probably present in all subjects at the time of presentation; in the patient with recent symptoms the skin was warm, and sweating was virtually absent, whilst the other two patients described cold skin, consistent with prolonged autonomic neuropathy.
Prominent dermatological signs are rare in carpal tunnel syndrome (CTS) and almost all the reported cases have been in European literature.' ' Reported skin iibnormalities include ulceration. blistering, hypohidrosis and other features of autonomic neuropathy, vasospasm or Raynaud's phenomenon, and irritant contact dermatitis. Dermatologists may therefore be involved in diagnosis or management of such cases.
Case reports Case 1
A 62-year-old woman with well-controlled, non-insulin-dependent diabetes mellitus and hypertension, both of 8 years' duration, had a 6-month history of paraesthesiae. sensory loss and functional deficit in the thumb, index and middle fingers ot the right hand. Blisters and subsequent ulcers of both palmar and dorsal aspects of the tips of the affected digits were a prominent early feature. She had long-standing osteoarthritis of the neck, shoulders and hands but no history of Raynaud's phenomenon or connective tissue disease. Apart from marked Heberden's nodes, the clinical abnormalities in the hands were confined to the Hrst three digits and radial aspect of the right hand. The digits were dusky, swollen, dry, markedly warmer than other digits of either hand, and several healing ulcers were present (Fig. 1). Sensation (light touch, pinprick and temperature) was grossly impaired, and there was marked thenar wasting with loss of power of the median nerve-innervated muscles, especially abductor pollicis Correspondence: Dr N.H,Cnx,
Figure I. I lands of Case 1, Swelling of index and middle lini^er tips on the right hand with a healed ulcer of the middle finger, and marked thenar wasting.
brevis. Tinel's test was positive, and starch-iodine testing to identify sweat-duct orifices demonstrated virtually complete anhidrosis in the affected sensory distribution. There were patchy areas of mild loss of light touch and vibration sensation in the feet, and absent knee and ankle reflexes, suggesting chronic peripheral neuropathy. However, the only clinical evidence of neunjpathy in the arms was that in the median nerve distribution of the right hand. Previous radiology of the neck and shoulder had demonstrated changes of osteoarthritis only, and no osteolysis was observed in X-rays of the hands. ESR was 611
612
N.A.COX ('( al.
4 mm/h. and results of thyroid biochemistry were within the normal range. Nerve conduction studies, steroid injection, and surgical treatment were refused by the patient. Case 2
A 75-year-old man had bilateral carpal tunnel syndrome, previously treated by steroid injection on the right 12 years ago and by surgical decompression on the left 4 years ago. The surgical treatment was performed 6 months after development of symptoms, and produced complete resolution, but the steroid injections in the right hand had been of no benefit. He was referred because of development of blisters and subsequent ulcers on the tips of the right index and middle fingers. There was a history of possible injury preceding the first blister but he denied that subsequent blistering was associated with trauma. He had osteoarthritis and had previously had hip replacement surgery. Examination revealed marked decrease in touch and pinprick sensation in the median nerve sensory distribution, more prominent in the right hand, and an ulcer on the right index finger from which a bacteriology culture produced scanty Staphylococcus aureus and a profuse growth of F.schcricbia coU. The affected area was colder than unaffected skin, but no other abnormality of autonomic function was noted in the records and there was no comment regarding thenar wasting. Surgical deeompression was considered but a previous orthopaedic opinion was not optimistic for recovery and further intervention was declined.
Case 3
A 51-year-old woman with morbid obesity and gross varicose leg ulceration was noted to have painless ulceration of the tips of the right index and middle fingers. She gave a history of loss of fine touch sensation of 9 years duration in thumb and index fingers of both hands, and the affected digits felt cold. Several fingertip blisters had developed, at least some of which were caused by thermal burns, and had led to persistent ulceration. Examination revealed decreased sensation, thenar wasting, and reduced power in median nerveinnervated muscles as described for Case 1. and a diagnosis of bilateral carpal tunnel syndrome was made. Nerve-conduction studies, performed at the Regional Neurology Unit, showed slowing of sensory conduction velocities (finger to wrist) and increased distal motor latency for both median nerves, more marked on the
right, consistent with carpal tunnel syndrome. No specific endocrinologicai cause for her obesity was demonstrated, and obesity was believed to be the cause of the carpal tunnel compression. Bilateral surgical treatment was followed by rapid healing of the ulcers. Case records of the presenting features were not available, but review of clinical photographs revealed the affected fingers to be swollen and slightly dusky; these features were consistent with a chronic autonomic neuropathy although specific testing was not performed at the time. At review 11 years later, she described residual mild sensory loss and loss of power of opposition, but no worsening of symptoms and no recurrence of ulceration. She had warm fingers, and no apparent deficit of sweating as demonstrated by the starch-iodine test.
Discussion There are few reports of blistering of the digits in CTS.'' Trauma to the digits, vasomotor or autonomic factors, and secondary infection may all be involved." Although only one of our patients admitted thermal damage or trauma preceding blisters and ulceration. ali had such severity of sensory loss that either physical or thermal trauma could have occurred without any immediate symptoms. All three patients described blisters before the ulceration: infection was only demonstrated in one {Case 2) at the time of presentation, but ulcers in the first patient had healed following use of antiseptic preparations and bacteriology samples had not been taken. None of the patients was able to attend at the time of development of a fresh blister, so the possibility that the blisters were due to infection of minor areas of trauma cannot be excluded. However, primarily infective causes of fingertip bullae. such as blistering distal dactylitis, do not cause subsequent trophic ulceration. Diabetic bullosis was a possible diagnosis in Case 1 but there is no reason why this should have been localized to the area of sensory loss, and this disorder does not cause trophic ulcers. It is probable that the neuropathy was the most important factor in all our patients. Autonomic dysfunction in CTS is probably underestimated as it is less obvious from symptoms or routine neurological examination than the motor and sensory features of the syndrome. It is, however, a frequent component of the syndrome^ because the autonomic fibres carried by the median nerve traverse the carpal tunnel before the nerve divides. Decreased or absent sweating.** '* swelling of the hand.'* and increased temperature due to vasomotor abnormalities'"'* are all
SKIN SIGNS IN CARPAL TUNNEL SYNDROME
features of the autonomic neuropathy and were all present in our first case. Marked swelling of the affected digits was a feature in Case 3. Other features of autonomic neuropathy which have been reported in CTS include 'contact dermatitis' of thefingertips.**which was presumed to be irritant in type and related to lack of sweating, and also the more serious complication of osteolysis which can occur'''' in digits where there is long-term ulceration. The constellation of features in patients with prominent autonomic damage in CTS is therefore similar to some features of reflex sympathetic dystrophy (Sudek's atrophy).'" and CTS has been associated with this disorder. The cold skin in our Cases 2 and 5. who both had long-standing C1'S, would also be compatible with the dystrophic or atrophic stages of refiex sympathetic dystrophy, but no investigation of sweating was performed at the time of presentation. Although diabetes is associated with neuropathy of various types, including a symmetrical peripheral neuropathy (of which CTS can be the first indication), autonomic neuropathy, and mononeuritis multiplex, the features in our first case were more suggestive of true CTS. She had abnormalities of motor and sensory function, as well as vasomotor and sweating abnormalities, in a distribution suggesting CTS rather than a mixed peripheral neuropathy. However, a peripheral nerve dysfunction can be due to a combination of factors acting simultaneously, and it is likely that CTS and polyneuropathy co-exist in some diabetic patients." '^ As surgical treatment can produce freedom from symptoms." it is important to consider CTS in diabetic patients with neuropathy affecting the hands. It is also likely that the combined autonomic and sensory dysfunction is important in the pathogenesis of fingertip ulceration, as a recent study demonstrated that autonomic dysfunction was a better predictor of diabetic foot ulceration than peripheral sensory nerve function;" there is no reason why this finding should be specific to either diabetes or to foot ulceration. and it could apply to hand ulceration in our non-diabetic patients also. Aggravation of Raynaud's syndrome by development of CTS'"" and vasospasm related to CTS''' have been reported, and also connective tissue disorders associated with CTS."' but careful objective studies have not demonstrated the frequency of Raynaud's phenomenon to be any greater in patients with CTS than that expected in the general population.'' 'I'wo of our patients had swollen dusky cold fingers but not the variability of colour which is diagnostic of Raynaud's phenomenon. Treatment of patients with blisters and trophic ulcers in CTS. apart from local therapy, is by surgical decompression of the carpal tunnel. Although complete resolu-
613
tion of all symptoms is perhaps unlikely, this treatment may abolish blistering and ulceration (and therefore the secondary problems of infection and osteolysis). Two of four patients with trophic ulcers reported by Besson et a!.' (including one with blisters) clearly improved after surgery, and a further patient with blisters and osteolysis developed blisters less frequently. Unfortunately, two of our patients with blisters declined, or were advised against, surgical intervention, but there was complete and prolonged healing of ulceration in the other patient despite some residual sensory deficit.
References 1 PlisttT R, Zur Klinik der Haut- und Nageiveranderungen beim Carpal-Tunndsyndrom, Hatitarzt 1954; 5; 540-2, 2 Lagrot F. Micheou P. Costagliola M. Mansat C, A propos d'une rormt' ulcerantc du syndrome du canal carpicn, iFre) Mem Arad Chir \9(->(y.92: 1(19-71, i BoLivier M, I-ejcunc H, Rouillat M, Marionncl), Les formes ulccromultilantes du syndrome du caniil Ciirpien, iFrcl (Hng, Atistr,! Rev RInim Mai Osteoartic 1979:46: K-.9-7h, 4 Difonzo EM, Moretti S, Baldini MA cl al. Quadro tutanco distrotico iilcerativo in forso di sindronie del canale carpale, (Ita) (Hng. Abstr.l G Hal Dermatol Venereol 1986: 121: 9 J - 5 , 5 Neau |P. Cil R. Boissonnot L ef d/, llkerations cutanees et osteolyse dans II' syndrome du canal carpien, IFrel lEng, Abstr,) Rev Neitrol 1987; 14J: J(li-5. f> I'avcsi c;, Medici D, lirunibilla S *•( til. Carpal tunnel syndrome presenting with prominent skin syrnplums, ttal j \eiirol Sri 1988: 9: 173-4, 7 Besson i. Courturier F, De Ciamcomini P et al. Atleinte du nerf median associee a des lesions cutanees et des troubles trophiques desdoigts. (Fre) Press Med 1989: 18: 1207, H Spinner R|. Bachman |W. Amadio PC. The many faces of carpal tunnel syndrome, MaifO Clinic Pnneedinqs ] 9S9; 64: S29- 36, 9 I'ast A, Parikh S. Ducommun K|, Dermatitis-sympathetic dysfunction in carpal tunnel syndrome, A case report, Clin Drthop ] 989; 247; 124-f-., 10 Shelton RM, I^wi.s CW, Reflex sympathetic dystrophy: a review. / Am Acad liermatot 1990; 22: 51 3-20, 1 1 Walter-Sack I. Zollner N, Maskiertes Karpaltunnelsyndrom bei diabetischer Polyneuropatliie (Ger,) (Fng, Abstr,) Dlsih Med Woihensihr 1980; 105: 19-21, 1 2 ()/aki I, Baba M, Matsunaga M, Takebe K, Deleterious effect of the carpal tunnel syndrome on nerve conduction in diabetic polyneuropathy, Ekrlromnotfr Clin Neuroplnisiol 19SS; 28: 301-6, 1 i McFadden IP. Corrall K|M, O'Brien IAD, Autonomic and sensory nerve function in diabetic foot ulceration, Clin Exp Lhrnuitol 1991; 16: 19 3-6, 14 Waller IXI. Dathan IR. Raynaud's syndrome and carpal tunnel syndrome. Postgrad Med I 1985: 61: 161-2, 1 5 Linscheid RL. Peterson LFA. Juergens |I.. Carpal-tunnel syndrome associated wilh vasospasm, / Hone joint Stiri} 1967: 49: 1141-6, 16 Winkelmann RK, Connolly SM, Doyle JA, Carpal tunnel syndrome in cutaneous connective tissue disease: generalized morphoea. lichen sclerosus, fasciitis. discoid lupus erythematosus, and iupus panniculitis, / Am Aaul DernuUal 1982; 7: 94-9, 17 Loebe M. Heidrich H, The carpal tunnel syndrome—a disease underlying Raynaud's phenomenon? Angiology 1988: 59: 8 9 1 901.
