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Recurrent brachial plexus neuropathy and giant cell arteritis
Recurrent brachial plexus neuropathy and giant cell arteritis R.A. Dierckx”, G. Ebinger*, P. Herregodts*, B. Maillet* * *
A. Michotte*, B. Carly* *, E. Schmedding*,
Introduction Summary
The syndrome of Parsonage and Turner’ or neuralgic amyotrophy or sporadic brachial plexus neuropathy is a clinical entity characterized by the acute or subacute onset of pain and weakness, with occasional atrophy of shoulder muscles1,2. Its etiology still remains unclear. An immune-mediated mechanism has been suggested2,3 because of the analogy with the brachial neuropathy of serum sickness, in which immune complex mechanisms operate. Rarely the condition may also be familia14.5,6.Differential diagnosis includes brachial plexus involvement secondary to tumoral, vascular, traumatic, compressive, infectious’, inflammatory’, physical9 or toxiclo causes. We report a patient who presented with this clinical picture and at the same time suffered from giant cell arteritis. Features of particular interest are the simultaneous occurrence a few days after an upper respiratory tract illness and the recurrence of the brachial plexus neuropathy. Case report
A 73-year-old woman sought medical attention in April 1987 because of a left arm palsy. Two months before admittance she suffered for 3
A 73-year-old woman presented with a recurrent form of sporadic brachial plexus neuropathy, the so-called Parsonage and Turner syndrome. This diagnosis is based on clinical and electromyographic findings. Interestingly a biopsy of the temporal artery demonstrated a giant cell arteritis. The clinical picture started 2 weeks after an upper respiratory tract illness. The possible viral etiology of giant cell arteritis is considered. We think an immunological rather than ischemic disturbance may have caused the recurrent brachial plexus neuropathy. This case report suggests that giant cell arteritis be considered in the investigation of the Parsonage and Turner syndrome. Key words: sporadic brachial plexus neuropathy, Parsonage and Turner syndrome, giant cell arteritis.
days of an upper respiratory tract illness. Six weeks before admission she developed fever accompanied by a right arm palsy. This clinical picture was characterized by acute onset and pain. She also complained of a throbbing holocranial headache and fatigue. A routine laboratory examination at that time showed a slightly elevated sedimentation rate of 24 mm/lb.
*Dept. of Neurology, * *Dept. of Surgery and * * *Dept. of Pathology, University Hospital, Vrije Universiteit Brussel, Laarbeeklaan 101, B-1090 Brussels, Belgium. Address for correspondence Antwerpen, Belgium.
and reprint requests: R. Dierckx, Nucleaire Diagnostiek, A. Z. Middelheim,
Lindendreef
1, B-2020
Accepted 13.3.89 Clin Neurol Neurosurg 1990. Vol92-1
71
Fig. 1. Giant cells (g) concentrated on either side of the intimal-medial junction where only small fragments of the internal elastic lamina (arrows) remained (Orcein-stain, 250 X).
Witin 2 weeks the patient recovered of the right arm palsy, but she remained febrile and asthenic. No EMG studies were done till this point. Three weeks before hospitalisation she developed a painful progressive palsy, this time of the left arm. The weakness progressed in the next hours. It was especially marked proximally and accompanied by a moderate amyotrophy of the left shoulder girdle. The past medical history was otherwise unremarkable. There was no family history of neuralgic amyotrophy. On admittance physical examination was normal except for a temperature of 37,6” C. Neurological examination showed a wasting of the left deltoid and supraspinatus muscles. The weakness was most pronounced in the left deltoid, triceps and biceps muscles. Myotatic reflexes were weak in both upper extremities, especially on the left. There was an hypesthesia on the radial surface of the forearm. Further exam72
ination disclosed no abnormalities. Routine laboratory examination now demonstrated a markedly raised sedimentation rate: 121 mmlh; the fibrinogen equaled 702 mg/lOO ml; the hemoglobine was 9.7 g/lOOml, the erythrocyte count was 3.4 10Ymm”. the hematocrite was 30.5%. Serum protein was 7.2 g/100 ml and electrophoresis revealed a low albumin fraction: 3.1 g/100 ml, raised alfal-: 0.4 g/lOOml and alfa2 globulin: 1 g/100 ml and - to a higher extent raised gamma globulin: 2 g/100 ml. The Waaler Rose test was negative, rheumatoid antigen was 98 IU WHO and the C reactive protein was 180 ug/ml. LE test was negative, tissue antibodies were negative. Fundoscopic examination was normal. Lumbar puncture yielded clear cerebrospinal fluid (CSF). Cytological and biochemical examination were normal. The CSF was sterile. The agar gel electrophoresis and isoelectric focusing of CSF proteins showed no abnormalities. Several blood cultures were negative. Viral serological examination showed no significant rise of antibody titers. Serological examination for Borrelia Burgdorferii was equally negative. Electromyographic examination of the left arm showed severe denervation in several muscles innervated by the upper trunc, the lateral and posterior cords. No denervation was found in serratus anterior and paraspinal cervical muscles. No signs of involvement of the medial cord were found on electromyographic investigation, motor nerve conduction studies and F wave studies. Roentgenographic examination of the cervical spine and left shoulder were normal. A CT scan of the lower cervical spine performed without and with administration of contrast was normal. CT scan, NMR and 67-Gallium scintigraphy of the left plexus region demonstrated no pathological changes. A biopsy of the left deltoid muscle revealed signs of neurogenic induced muscular atrophy and a biopsy of the temporal artery demonstrated an active giant cell arteritis (Fig. 1). Based on the clinical history, the electromyographic findings and the biopsy of the temporal artery the tentative diagnosis of a recurrent brachial plexus neuropathy related to a giant cell arteritis was made. Treatment with prednisolone 60 mg/day was instaured. This therapy
prompted a disappearance of the constitutional symptoms the following days. The tenth day the sedimentation rate was 45 mrn/lh and the patient was dismissed. The next 3 months the patient made a complete neurological recovery. Discussion Except for headache the manifestations suggesting an underlying vasculitis in our patient were constitutional symptoms and fever of undetermined origin I1. The routine laboratory examination supported the hypothesis of a giant cell arteritis. Its existence finally was demonstrated by a biopsy of the superficial temporal artery”. It should be stressed that clinically inspection of the temporal arteries revealed no signs of inflammation. Polymyalgica rheumatica may have accompanied the temporal arteritis and may have contributed to the shoulder pains. However, polymyalgia rheumatica cannot stand for all the manifestations confined to the shoulder girdle: the neurological symptomatology reflected a topographical distribution and plexus involvement was further evidenced by the electromyographical findings. Clinically, the first symptoms of giant cell arteritis developed concommitantly with the first episode of brachial plexus neuropathy. Although brachial plexus neuropathy constitutes no classical complication of giant cell arteritis12~13~14, their simultaneous independent appearance, might be considered more than hazardous. Moreover while the giant cell arteritis persisted, a second episode of brachial plexus neuropathy was seen, which was not attributable to any other cause: no clinical, X-ray or laboratory evidence for infection, malignancy or other systemic disease was found. In this regard, particular attention was paid to Bannwarth’s syndrome or Lyme disease, a newly recognized spirochetal infection caused by Borrelia Burgdorferii15. The spectrum of its neurological manifestations includes brachial plexus neuropathy15. This possible cause was excluded by serological and CSF examination’6. The recurrent, familial form of neuralgic amyotrophy was excluded based on the negative family history, the absence of associated con-
genital defects and the late age of onset4*5.6. Giant cell arteritis is known to affect almost any vessels, especially large and middle sized arteries12,14,17. However, the vasculitic process may also affect smaller arteries of the skeletal musclesls, kidney” and peripheral nerves *O,Hence both larger feeding arteries as well as the vasae nervorum could have been affected in our patient. The neurological complications are mostly due to subsequent infarctions12,13x14. The complete spontaneous recovery of the first episode of brachial plexus neuropathy in two weeks time pleads against this hypothesis. On the contrary, we think an immunological disturbance affecting the brachial plexus to be a more plausible explanation. A focal character of neurological manifestations exists also in other disorders with autoimmunological processes such as e.g. systemic lupus erythematodes*‘. A demyelinating process would appear to be more compatible with the rapid recovery of the right arm function. Unfortunately, EMG evidence for this clinical observation is lacking. Although we are at a loss to explain the precise pathophysiological mechanisms, we think the association of brachial plexus neuropathy and giant cell arteritis in our patient to be more than coincidental. In chronological order the whole symptomatology developed eleven days after the occurrence of an infectious upper respiratory tract disorder, probably of viral nature. A non-specific febrile illness, preceding the onset of the disorder, has been reported in the syndrome of Parsonage and Turner’***. A genetic predisposition has been suggested in the development of giant cell arteritis”, in which case an infectious agent may have constituted the triggering factor for its appearance. The syndrome of Parsonage and Turner usually carries a good prognosis2.23.24.In temporal arteritis and polymyalgia rheumatica however treatment with corticosteroids is mandatory25. Even then, caution is warranted as complications may occur despite treatment26,27. Although there exists a benign course in the Parsonage and Turner syndrome, it is tempting to attribute its recurrency in this case to the vasculitic process. This 73
would support a potential beneficial effect of the corticotherapy on the brachial plexus neuropathy. In a review of 84 cases with the syndrome of Parsonage and Turner recurrence was found in only 4 patients 23. In the population of Rochester on 11 patients with neuralgic amyotrophy from 1970 to 1981 only one developed an affection of the opposite arm 5 years later3. This case suggests that giant cell arteritis be considered in the investigation of sporadic brachial plexus neuropathy. This possible cause may often go unrecognized because of different factors: - the heterogenous clinical picture of giant cell arteritis*‘,*’ - its consideration only over the age of 503”and _ the problems in interpreting biopsies due to the segmental character of the vasculitis”‘. Literature PARSONAGE MJ, TURNER JWA. Neuralgic amyotrophy. The shoulder girdle syndrome. Lancet 1948; i:973-8. MUMENTHALER M, NARAKAS A, GILLIATT w. Brachial plexus disorders. In Dyck PJ, Thomas PK, Lamber EH, Bunge R (eds). Peripheral Neuropathy, 2. Philadelphia. Saunders, 1984: 1389-94. BEGHI E,KURLARD ET,MULDERDW,NIC~LOSIA. Brachial plexus neuropathy in the population of Rochester. Minnesota. Ann neurol 1985: 320-3. SERRATRlCE G, POUGET J, PELLISSIER JF. Des fOUTleS familiales du syndrome de Parsonage et Turner aux h&rbdopathies tomaculaires du plexus brachial. Revue du Rhumatisme 1985; 11:625-9. AVIAKSINENEM,LIVANAINENM,KARLIP~~U~. Iiereditary recurrent brachial plexus neuropathy with dysmorphic features. Acta Neurol Stand 1985; 71:309-16. ARTS WFM,BUSCHHFM,VANDENBRAND HJ etal.Hereditary neuralgic amyotrophy. Clinical, genetic, electrophysiological and histopathoIogical studies. J Neurol Sci 1983; 62:261-79. GEIGERI.R,MAN~ALLEL,PENNA~,TUCKERSH. Familial neuralgic amyotrophy. Report of three families with review of the literature. Brain 1984; 97:87-102. RAI I, LEITERSDORF G, KLEINMAN Y. Acute bilateral plexus neuritis associated with hypersensitivity vasculitis. A case report and a review of the literature. Klin Wochenschr 1985; 63~543-5. RAWLINGS
G, ARRIAGADA
R, FONTAINE F ef al. Plexite
brachiale post-radiothtrapique: experience de I’Institut Gustave-Roussy. Bull Cancer (Paris) 1983; 70:77-83. SHEROKMAN B,FILLING-KATZ HR,TELLD. Brachialplex-
74
us neuropathy following high-dose cytarabine in acute monoblastic leukemia. Cancer Treatment Reports 1985: 69:1005-6. CALAMIA KT, HUNDER GG. Giant cell arteritis (temporal arteritis) presenting as fever of undetermined origin. Arthr Rheumat 1981; 24:1414-S. FAIICHALD P, RYGVOLD O.@)YCTESE B. Temporal arteritis and polymyalg~a rheumatica. Clinical and biopsy findings. Ann Int Med 1972; 77:X45-52. J0NASSON F.~‘IJLLENJ~,tLIoN KA. Temporal arteritis: a 14-year epidemiological, clinical and prognostic study. Scot Med J 1979; 24:111-7. GEKBERN,V~-RNON-ROBERTS B. Polymyalgiarheumatic. Klinisch-histologische Studie an 4hFllIen. Z Rheumatol 1977; 361275-84. PACHNER AR, STEERE AC'.The triad of neurologic manifestations of Lyme disease: meningitis, neuritis and radiculoneuritis. Neurology 1985; 35:47-53. HENKIKSSON A, LINK N, <'RU% M, 5TIERNSTEDT G. IIIllIlU-
noglobulin abnormalities in cerebrospinal fluid and blood over the course of ~ymphocytic meningoradicul~tis (Bann~arth~s syndrome). Ann Neurol 1986: 20:337-45. I‘:'ITl.INGER RE, IIUNDER
G
LE. POiyIXl@giZI
rheumatica and giant cell arteritis. Ann Rev Med 1978: 29:15-22. TORVIK A, BERNTZEN AE. Necrotizing vasculitis without visceral involvement. Acta Med Stand 1968; 184:69-77. IAI.LGREN L
A. Michotte*, B. Carly* *, E. Schmedding*,
Introduction Summary
The syndrome of Parsonage and Turner’ or neuralgic amyotrophy or sporadic brachial plexus neuropathy is a clinical entity characterized by the acute or subacute onset of pain and weakness, with occasional atrophy of shoulder muscles1,2. Its etiology still remains unclear. An immune-mediated mechanism has been suggested2,3 because of the analogy with the brachial neuropathy of serum sickness, in which immune complex mechanisms operate. Rarely the condition may also be familia14.5,6.Differential diagnosis includes brachial plexus involvement secondary to tumoral, vascular, traumatic, compressive, infectious’, inflammatory’, physical9 or toxiclo causes. We report a patient who presented with this clinical picture and at the same time suffered from giant cell arteritis. Features of particular interest are the simultaneous occurrence a few days after an upper respiratory tract illness and the recurrence of the brachial plexus neuropathy. Case report
A 73-year-old woman sought medical attention in April 1987 because of a left arm palsy. Two months before admittance she suffered for 3
A 73-year-old woman presented with a recurrent form of sporadic brachial plexus neuropathy, the so-called Parsonage and Turner syndrome. This diagnosis is based on clinical and electromyographic findings. Interestingly a biopsy of the temporal artery demonstrated a giant cell arteritis. The clinical picture started 2 weeks after an upper respiratory tract illness. The possible viral etiology of giant cell arteritis is considered. We think an immunological rather than ischemic disturbance may have caused the recurrent brachial plexus neuropathy. This case report suggests that giant cell arteritis be considered in the investigation of the Parsonage and Turner syndrome. Key words: sporadic brachial plexus neuropathy, Parsonage and Turner syndrome, giant cell arteritis.
days of an upper respiratory tract illness. Six weeks before admission she developed fever accompanied by a right arm palsy. This clinical picture was characterized by acute onset and pain. She also complained of a throbbing holocranial headache and fatigue. A routine laboratory examination at that time showed a slightly elevated sedimentation rate of 24 mm/lb.
*Dept. of Neurology, * *Dept. of Surgery and * * *Dept. of Pathology, University Hospital, Vrije Universiteit Brussel, Laarbeeklaan 101, B-1090 Brussels, Belgium. Address for correspondence Antwerpen, Belgium.
and reprint requests: R. Dierckx, Nucleaire Diagnostiek, A. Z. Middelheim,
Lindendreef
1, B-2020
Accepted 13.3.89 Clin Neurol Neurosurg 1990. Vol92-1
71
Fig. 1. Giant cells (g) concentrated on either side of the intimal-medial junction where only small fragments of the internal elastic lamina (arrows) remained (Orcein-stain, 250 X).
Witin 2 weeks the patient recovered of the right arm palsy, but she remained febrile and asthenic. No EMG studies were done till this point. Three weeks before hospitalisation she developed a painful progressive palsy, this time of the left arm. The weakness progressed in the next hours. It was especially marked proximally and accompanied by a moderate amyotrophy of the left shoulder girdle. The past medical history was otherwise unremarkable. There was no family history of neuralgic amyotrophy. On admittance physical examination was normal except for a temperature of 37,6” C. Neurological examination showed a wasting of the left deltoid and supraspinatus muscles. The weakness was most pronounced in the left deltoid, triceps and biceps muscles. Myotatic reflexes were weak in both upper extremities, especially on the left. There was an hypesthesia on the radial surface of the forearm. Further exam72
ination disclosed no abnormalities. Routine laboratory examination now demonstrated a markedly raised sedimentation rate: 121 mmlh; the fibrinogen equaled 702 mg/lOO ml; the hemoglobine was 9.7 g/lOOml, the erythrocyte count was 3.4 10Ymm”. the hematocrite was 30.5%. Serum protein was 7.2 g/100 ml and electrophoresis revealed a low albumin fraction: 3.1 g/100 ml, raised alfal-: 0.4 g/lOOml and alfa2 globulin: 1 g/100 ml and - to a higher extent raised gamma globulin: 2 g/100 ml. The Waaler Rose test was negative, rheumatoid antigen was 98 IU WHO and the C reactive protein was 180 ug/ml. LE test was negative, tissue antibodies were negative. Fundoscopic examination was normal. Lumbar puncture yielded clear cerebrospinal fluid (CSF). Cytological and biochemical examination were normal. The CSF was sterile. The agar gel electrophoresis and isoelectric focusing of CSF proteins showed no abnormalities. Several blood cultures were negative. Viral serological examination showed no significant rise of antibody titers. Serological examination for Borrelia Burgdorferii was equally negative. Electromyographic examination of the left arm showed severe denervation in several muscles innervated by the upper trunc, the lateral and posterior cords. No denervation was found in serratus anterior and paraspinal cervical muscles. No signs of involvement of the medial cord were found on electromyographic investigation, motor nerve conduction studies and F wave studies. Roentgenographic examination of the cervical spine and left shoulder were normal. A CT scan of the lower cervical spine performed without and with administration of contrast was normal. CT scan, NMR and 67-Gallium scintigraphy of the left plexus region demonstrated no pathological changes. A biopsy of the left deltoid muscle revealed signs of neurogenic induced muscular atrophy and a biopsy of the temporal artery demonstrated an active giant cell arteritis (Fig. 1). Based on the clinical history, the electromyographic findings and the biopsy of the temporal artery the tentative diagnosis of a recurrent brachial plexus neuropathy related to a giant cell arteritis was made. Treatment with prednisolone 60 mg/day was instaured. This therapy
prompted a disappearance of the constitutional symptoms the following days. The tenth day the sedimentation rate was 45 mrn/lh and the patient was dismissed. The next 3 months the patient made a complete neurological recovery. Discussion Except for headache the manifestations suggesting an underlying vasculitis in our patient were constitutional symptoms and fever of undetermined origin I1. The routine laboratory examination supported the hypothesis of a giant cell arteritis. Its existence finally was demonstrated by a biopsy of the superficial temporal artery”. It should be stressed that clinically inspection of the temporal arteries revealed no signs of inflammation. Polymyalgica rheumatica may have accompanied the temporal arteritis and may have contributed to the shoulder pains. However, polymyalgia rheumatica cannot stand for all the manifestations confined to the shoulder girdle: the neurological symptomatology reflected a topographical distribution and plexus involvement was further evidenced by the electromyographical findings. Clinically, the first symptoms of giant cell arteritis developed concommitantly with the first episode of brachial plexus neuropathy. Although brachial plexus neuropathy constitutes no classical complication of giant cell arteritis12~13~14, their simultaneous independent appearance, might be considered more than hazardous. Moreover while the giant cell arteritis persisted, a second episode of brachial plexus neuropathy was seen, which was not attributable to any other cause: no clinical, X-ray or laboratory evidence for infection, malignancy or other systemic disease was found. In this regard, particular attention was paid to Bannwarth’s syndrome or Lyme disease, a newly recognized spirochetal infection caused by Borrelia Burgdorferii15. The spectrum of its neurological manifestations includes brachial plexus neuropathy15. This possible cause was excluded by serological and CSF examination’6. The recurrent, familial form of neuralgic amyotrophy was excluded based on the negative family history, the absence of associated con-
genital defects and the late age of onset4*5.6. Giant cell arteritis is known to affect almost any vessels, especially large and middle sized arteries12,14,17. However, the vasculitic process may also affect smaller arteries of the skeletal musclesls, kidney” and peripheral nerves *O,Hence both larger feeding arteries as well as the vasae nervorum could have been affected in our patient. The neurological complications are mostly due to subsequent infarctions12,13x14. The complete spontaneous recovery of the first episode of brachial plexus neuropathy in two weeks time pleads against this hypothesis. On the contrary, we think an immunological disturbance affecting the brachial plexus to be a more plausible explanation. A focal character of neurological manifestations exists also in other disorders with autoimmunological processes such as e.g. systemic lupus erythematodes*‘. A demyelinating process would appear to be more compatible with the rapid recovery of the right arm function. Unfortunately, EMG evidence for this clinical observation is lacking. Although we are at a loss to explain the precise pathophysiological mechanisms, we think the association of brachial plexus neuropathy and giant cell arteritis in our patient to be more than coincidental. In chronological order the whole symptomatology developed eleven days after the occurrence of an infectious upper respiratory tract disorder, probably of viral nature. A non-specific febrile illness, preceding the onset of the disorder, has been reported in the syndrome of Parsonage and Turner’***. A genetic predisposition has been suggested in the development of giant cell arteritis”, in which case an infectious agent may have constituted the triggering factor for its appearance. The syndrome of Parsonage and Turner usually carries a good prognosis2.23.24.In temporal arteritis and polymyalgia rheumatica however treatment with corticosteroids is mandatory25. Even then, caution is warranted as complications may occur despite treatment26,27. Although there exists a benign course in the Parsonage and Turner syndrome, it is tempting to attribute its recurrency in this case to the vasculitic process. This 73
would support a potential beneficial effect of the corticotherapy on the brachial plexus neuropathy. In a review of 84 cases with the syndrome of Parsonage and Turner recurrence was found in only 4 patients 23. In the population of Rochester on 11 patients with neuralgic amyotrophy from 1970 to 1981 only one developed an affection of the opposite arm 5 years later3. This case suggests that giant cell arteritis be considered in the investigation of sporadic brachial plexus neuropathy. This possible cause may often go unrecognized because of different factors: - the heterogenous clinical picture of giant cell arteritis*‘,*’ - its consideration only over the age of 503”and _ the problems in interpreting biopsies due to the segmental character of the vasculitis”‘. Literature PARSONAGE MJ, TURNER JWA. Neuralgic amyotrophy. The shoulder girdle syndrome. Lancet 1948; i:973-8. MUMENTHALER M, NARAKAS A, GILLIATT w. Brachial plexus disorders. In Dyck PJ, Thomas PK, Lamber EH, Bunge R (eds). Peripheral Neuropathy, 2. Philadelphia. Saunders, 1984: 1389-94. BEGHI E,KURLARD ET,MULDERDW,NIC~LOSIA. Brachial plexus neuropathy in the population of Rochester. Minnesota. Ann neurol 1985: 320-3. SERRATRlCE G, POUGET J, PELLISSIER JF. Des fOUTleS familiales du syndrome de Parsonage et Turner aux h&rbdopathies tomaculaires du plexus brachial. Revue du Rhumatisme 1985; 11:625-9. AVIAKSINENEM,LIVANAINENM,KARLIP~~U~. Iiereditary recurrent brachial plexus neuropathy with dysmorphic features. Acta Neurol Stand 1985; 71:309-16. ARTS WFM,BUSCHHFM,VANDENBRAND HJ etal.Hereditary neuralgic amyotrophy. Clinical, genetic, electrophysiological and histopathoIogical studies. J Neurol Sci 1983; 62:261-79. GEIGERI.R,MAN~ALLEL,PENNA~,TUCKERSH. Familial neuralgic amyotrophy. Report of three families with review of the literature. Brain 1984; 97:87-102. RAI I, LEITERSDORF G, KLEINMAN Y. Acute bilateral plexus neuritis associated with hypersensitivity vasculitis. A case report and a review of the literature. Klin Wochenschr 1985; 63~543-5. RAWLINGS
G, ARRIAGADA
R, FONTAINE F ef al. Plexite
brachiale post-radiothtrapique: experience de I’Institut Gustave-Roussy. Bull Cancer (Paris) 1983; 70:77-83. SHEROKMAN B,FILLING-KATZ HR,TELLD. Brachialplex-
74
us neuropathy following high-dose cytarabine in acute monoblastic leukemia. Cancer Treatment Reports 1985: 69:1005-6. CALAMIA KT, HUNDER GG. Giant cell arteritis (temporal arteritis) presenting as fever of undetermined origin. Arthr Rheumat 1981; 24:1414-S. FAIICHALD P, RYGVOLD O.@)YCTESE B. Temporal arteritis and polymyalg~a rheumatica. Clinical and biopsy findings. Ann Int Med 1972; 77:X45-52. J0NASSON F.~‘IJLLENJ~,tLIoN KA. Temporal arteritis: a 14-year epidemiological, clinical and prognostic study. Scot Med J 1979; 24:111-7. GEKBERN,V~-RNON-ROBERTS B. Polymyalgiarheumatic. Klinisch-histologische Studie an 4hFllIen. Z Rheumatol 1977; 361275-84. PACHNER AR, STEERE AC'.The triad of neurologic manifestations of Lyme disease: meningitis, neuritis and radiculoneuritis. Neurology 1985; 35:47-53. HENKIKSSON A, LINK N, <'RU% M, 5TIERNSTEDT G. IIIllIlU-
noglobulin abnormalities in cerebrospinal fluid and blood over the course of ~ymphocytic meningoradicul~tis (Bann~arth~s syndrome). Ann Neurol 1986: 20:337-45. I‘:'ITl.INGER RE, IIUNDER
G
LE. POiyIXl@giZI
rheumatica and giant cell arteritis. Ann Rev Med 1978: 29:15-22. TORVIK A, BERNTZEN AE. Necrotizing vasculitis without visceral involvement. Acta Med Stand 1968; 184:69-77. IAI.LGREN L