CHRONIC RECURRENT GUILLAIN-BARRÉ SYNDROME
R E P O R T O F 3 C A S E S
ANTÔNIO RODRIGUES DE MELLO * — MARCOS R. G. DE FREITAS *! ¡ LEILA CHIMELLI ***
S U M M A R Y — T h e c l a s s i c a l G u i l l a i n B a r r e s y n d r o m e i s a n a c u t e o r s u b a c u t e p o l y r a d i c u l o -n e u r o p a t h y w h o s e m a i -n c l i -n i c a l f e a t u r e s a r e p r o g r e s s i v e w e a k -n e s s o f t h e l i m b s , d e c r e a s e o r a b s e n c e o f t e n d o n r e f l e x e s , a n d s e n s o r y c h a n g e s . A l t h o u g h i n m o s t o f t h e c a s e s t h e r e is c o m p l e t e r e c o v e r y i n w e e k s o r m o n t h s , s o m e p a t i e n t s h a v e a s l o w a n d p r o g r e s s i v e r e l a p s i n g c o u r s e a n d p r e s e n t t h i c k e n i n g o f t h e p e r i p h e r a l n e r v e s . I n t h i s p a p e r w e d e s c r i b e t h r e e c a s e s o f t h e c h r o n i c a n d r e l a p s i n g v a r i e t y o f G u i l l a i n - B a r r é s y n d r o m e , t w o o f w h i c h had p r o m i n e n t h y p e r t r o p h i c c h a n g e s i n t h e p e r i p h e r a l n e r v e s w i t h o n i o n b u l b f o r m a t i o n s T h e c l i n i c a l a n d p a t h o l o g i c a l f e a t u r e s o f t h i s d i s e a s e a r e r e v i e w e d . T h e t h r e e p a t i e n t s i m p r o v e d w i t h t h e u s e o f s t e r o i d s .
Síndrome de Guillain-Barré crônica recorrente: registro de 3 casos.
R E S U M O — A s í n d r o m e d e G u i l l a i n - B a r r é c l á s s i c a é p o l i r r a d i c u l o n e u r o p a t i a a g u d a ou s u b - a g u d a , c u j o s p r i n c i p a i s a s p e c t o s c l í n i c o s s ã o : f r a q u e z a p r o g r e s s i v a d o s m e m b r o s , r e d u ç ã o o u a u s ê n c i a d e r e f l e x o s t e n d i n o s o s e a l t e r a ç õ e s s e n s i t i v a s . E m b o r a n a m a i o r i a d o s c a s o s h a j a r e c u p e r a ç ã o c o m p l e t a e m s e m a n a s o u m e s e s , e m a l g u n s p a c i e n t e s o c u r s o é l e n t o , p r o g r e s s i v o o u r e c i d i v a n t e e h á e s p e s s a m e n t o d o s n e r v o s p e r i f é r i c o s . N o p r e s e n t e a r t i g o d e s c r e v e m o s t r ê s c a s o s d a v a r i e d a d e c r ô n i c a e r e c i d i v a n t e d a s í n d r o m e d e G u i l l a i n - B a r r é , d o i s d o s q u a i s t i n h a m a l t e r a ç õ e s h i p e r t r ó f i c a s p r o e m i n e n t e s n o s n e r v o s p e r i f é r i c o s c o m f o r m a ç õ e s e m b u l b o d e c e b o l a . O s a s p e c t o s c l í n i c o s e p a t o l ó g i c o s d e s t a d o e n ç a s ã o r e v i s t o s . Os t r ê s p a c i e n t e s m e l h o r a r a m c o m o u s o d e e s t e r ó i d e s .
The Guillain-Barré ( G B ) syndrome is a polyradiculoneuropathy whose main clinical features are progressive weakness of the limbs, decrease or absence of tendon
reflexes, sensory changes and, less frequently, cranial nerve involvement2
. The cerebrospinal fluid ( C S F ) shows albuminous-cytologic dissociation, and there is
electro-physiological evidence of slow nerve conduction. In the peripheral nervous system the main pathological finding is demyelination 2,20. While in most patients the illness
is acute or sub-acute with complete recovery in weeks or months, some cases have a slow and progressive relapsing course, and present thickening of the peripheral
nerves 2,8,3. In spite of the clinical presentation and the variety of names given by various authors 9.21 to the latter forms, they share with the classical GB syndrome
electrophysiological, humoral and pathological findings.
In the present paper three cases of the chronic and relapsing variety of G B
syndrome are described, which are also unusual for some morphological findings
in the peripheral nerves.
T r a b a l h o d a s D i s c i p l i n a s d e N e u r o l o g i a e d e N e u r o p a t o l o g i a , F a c u l d a d e d e M e d i c i n a , U n i v e r s i d a d e F e d e r a l F l u m i n e n s e : * P r o f e s s o r E m é r i t o d a U N I R I O ; P r o f e s s o r A d j u n t o d e N e u r o l o g i a ; *** P r o f e s s o r A d j u n t o d e N e u r o p a t o l o g i a .
C A S E R E P O R T S
C a s e 1 — L W M , a 1 2 - y e a r - o l d g i r l , p r e s e n t e d in J u n e 1958 w e a k n e s s a n d p a r a e s t h e s i a of all 4 l i m b s s t a r t i n g in t h e l o w e r l i m b s w h i c h p r o g r e s s e d r a p i d l y . S h e d e n i e s a n y t o x i c o r a l c o h o l i c i n g e s t i o n a n d t h e r e is n o s i m i l a r c a s e in t h e f a m i l y . N e u r o l o g i c a l e x a m i n a t i o n s h o w e d t e t r a p a r e s i s , r e d u c e d t e n d o n r e f l e x e s , a n d s l i g h t d i s t a l s u p e r f i c i a l h y p o e s t h e s i a in a r m s a n d l e g s ; c r a n i a l n e r v e s w e r e n o r m a l . C S F e x a m i n a t i o n s h o w e d 14 c e l l s / m m a , p r o t e i n s 138 m g / d l . R o u t i n e b l o o d t e s t s w e r e n o r m a l . S h e r e c o v e r e d c o m p l e t e l y a f t e r 30 d a y s . In 1972 at t h e a g e o f 26 s h e h a d a r e c u r r e n c e . T h e r e w a s g e n e r a l i z e d d e e p a r e f l e x i a , s u p e r f i c i a l h y p o e s t h e s i a in t h e l a t e r a l a s p e c t o f t h e f e e t . T h e c u b i t a l n e r v e s w e r e t h i c k e n e d a n d t h e b r a c h i a l p l e x u s w a s p a l p a b l e a n d v i s i b l e o n b o t h s i d e s . E l e c t r o m y o g r a p h i c f i n d i n g s s u g g e s t e d a p e r i p h e r a l n e r v e d i s o r d e r . S h e i m p r o v e d a g a i n b u t in 1974 s h e h a d a n e w r e c u r r e n c e w h i c h i m p r o v e d w i t h d e x a m e t h a s o n e . T h r e e m o n t h s later, a f t e r t h e s t e r o i d h a d b e e n d i s c o n t i n u e d t h e r e w a s a n e w r e c u r r e n c e w i t h u n i l a t e r a l p e r i p h e r a l f a c i a l p a l s y . T h e r e w e r e t h r e e o t h e r r e c u r r e n c e s i n J u n e a n d D e c e m b e r 1975 a n d in D e c e m b e r 1981, f o l l o w i n g r e d u c t i o n o f t h e s t e r o i d d o s e . T h e C S F e x a m i n a t i o n i n 1981 s h o w e d 1.7 c e l l s / m m ^ , 216 m g / d l p r o t e i n , a n d 1 6 % o f g a m m a g l o b u l i n . A t t h i s o c c a s i o n t h e b i o p s y o f a s u p r a c l a v i c u l a r m a s s s h o w e d an e n l a r g e d n e r v e , w h i c h w a s e x a m i n e d h i s t o l o g i c a l l y . T h e s p e c i m e n c o n s i s t e d o f a t h i c k n e r v e w h i c h w a s p r o c e s s e d f o r p a r a f f i n e m b e d d i n g . L o n g i t u d i n a l s e c t i o n s s t a i n e d w i t h h a e m a t o x i l i n a n d e o s i n ( H E ) s h o w e d e x t r e m e l y l a r g e n e r v e f i b r e s s u r r o u n d e d b y n u m e r o u s S c h w a n n c e l l n u c l e i . O n t r a n s v e r s e s e c t i o n s it s h o w e d c o n c e n t r i c p r o l i f e r a t i o n o f S c h w a n n c e l l s w i t h t h e a p p e a r a n c e o f o n i o n b u l b s ( F i g . l a ) . L y m p h o c y t e s , m a i n l y a r o u n d b l o o d v e s s e l s w e r e a l s o s e e n ( F i g . l b ) . T h e a p p e a r a n c e s w e r e t h o s e o f a h y p e r t r o p h i c c h r o n i c i n f l a m m a t o r y n e u r o p a t h y . T h e p a t i e n t d i e d s o o n a f t e r last r e c u r r e n c e w i t h c a r d i o r e s p i r a -t o r y f a i l u r e . P o s -t m o r -t e m e x a m i n a -t i o n w a s n o -t p e r f o r m e d .
p a r t i a l r e m i s s i o n o f t h e w e a k n e s s , a n d b e t w e e n t h e r e l a p s e s s h e e x p e r i e n c e d o n l y l i t t l e d i f f i c u l t y in w a l k i n g . T h e r e i s n o h i s t o r y o f t o x i c o r a l c o h o l i c i n g e s t i o n a n d n o d i a b e t e s . N o s i m i l a r c a s e s o c c u r r e d in t h e f a m i l y . N e u r o l o g i c a l e x a m i n a t i o n — C o a r s e p o s t u r a l t r e m o r in h a n d s , a t a x i c t y p e o f g a i t w i t h s u p p o r t . T e t r a p a r e s i s p r e d o m i n a n t l y d i s t a l a n d m o r e m a r k e d in l o w e r l i m b s , g e n e r a l i z e d h y p o t o n i a , p r o p r i o c e p t i v e a t a x i a o f all l i m b s , s u p e r f i c i a l a n d d e e p h y p o e s t e s i a i n l o w e r l i m b s . C r a n i a l n e r v e s n o r m a l . P e r i p h e r a l n e r v e s p a l p a b l e b u t n o t t h i c k e n e d . C S F e x a m i n a t i o n — I n J a n u a r y 1983: 0 c e l l s / m m 3 , p r o t e i n s 1 5 0 m g / d l ; in M a y 1986: 26 c e l l s / m m - 3 ( 6 0 % p o l y m o r p h s a n d 4 0 % m o n o n u c l e a r ) , p r o t e i n s 3 2 5 m g / d l . R o u t i n e b l o o d a n d u r i n e t e s t s w e r e n o r m a l . E l e c t r o n e u r o m y o g r a p h y s h o w e d s e v e r e i n v o l -v e m e n t o f d i s t a l n e u r o c o n d u c t i o n . S u r a l n e r -v e b i o p s y — A s e g m e n t o f n e r -v e , 2 c m i n l e n g h t w a s f i x e d p a r t l y in 1 0 % f o r m a l i n f o r p a r a f f i n e m b e d d i n g a n d p a r t l y in 3 % g l u t a r a l d e h y d e in 0.05 M N a c a c o d y l a t e b u f f e r f o r A r a l d i t e e m b e d d i n g a n d f o r t e a s i n g . P a r a f f i n s e c t i o n s s t a i n e d w i t h H E s h o w e d a p p a r e n t l y n o r m a l n e r v e f i b r e s w i t h s o m e i n c r e a s e in n u m b e r o f S c h w a n n c e l l s . N o i n f l a m m a t o r y c e l l s w e r e s e e n . O n e m i c r o n t h i c k A r a l d i t e s e c t i o n s s t a i n e d w i t h t o l u i d i n e b l u e s h o w e d s o m e c l u s t e r s o f s m a l l m y e l i n a t e d a x o n s i n s i d e s i n g l e S c h w a n n c e l l s i n d i c a t i n g r e g e n e r a t i o n . S o m e c o n c e n t r i c p r o l i f e r a t i o n o f S c h w a n n c e l l c y t o p l a s m s u r r o u n d i n g m y e l i n a t e d f i b r e s w i t h t h i n m y e l i n s h e a t h w e r e a l s o s e e n ( F i g . 2 ) . T h i s w a s
c o n f i r m e d in t h i n s e c t i o n s w h e r e s o m e S c h w a n n c e l l s d e v o i d o f a x o n s ( F i g . 3 a ) a n d n a k e d a x o n s ( F i g . 3 b ) c o u l d b e o b s e r v e d . O n l y f e w u n m y e l i n a t e d f i b r e s w e r e p r e s e n t . S i n g l e t e a s e d f i b r e s s h o w e d s e g m e n t a l d e m y e l i n a t i o n a n d a g r e a t v a r i a t i o n o f i n t e r n o d a l l e n g h t . T h e f e a t u r e s w e r e s u g g e s t i v e o f a c h r o n i c d e m y e l i n a t i n g n e u r o p a t h y w i t h s i g n s o f r e m y e l i n a -t i o n , a x o n a l r e g e n e r a -t i o n a n d b e g i n n i n g o f o n i o n b u l b f o r m a -t i o n . W i -t h p r e d n i s o n e , e v e n a f t e r r e d u c t i o n o f t h e d o s e , s i g n i f i c a n t i m p r o v e m e n t w a s o b t a i n e d a n d s h e w a s a b l e t o w a l k w i t h o u t s u p p o r t .
C O M M E N T S
Currently, the diagnosis of chronic recurrent GB syndrome is based on the following criteria 5 , 2 i: sensory-motor polyneuropathy with slow evolution; progressive
or recurrent course; severe reduction of nerve conduction velocity; increased protein level in the C S F ; absence of any systemic disease or exposure to toxic substances; and finding of segmental demyelination of peripheral nerves. Although Prineas and McLeod 21 and Dalakas and Engel 5 described the illness at all ages from 3 to 60 years, the patients reported by Dyck et al.9 were in their 5th and 6th decade of life. On the other hand there is agreement on the absence of sex predominance. The possibility that a genetic predisposition plays a role in the disease is supported by the findings of Aaams et al.i who observed that their 14 patients belonged to the HLA types A l , B8, D W E and D R W 3 , and those of Stewart et al.23 wh o found a high
incidence of the type HLA D R W 3 .
The main clinical feature is a mixed polyneuropathy, sometimes with predomi-nance of weakness in proximal muscles. This pattern was seen in our case 2, while in the remaining two cases the distal muscles were the most severely involved. Cranial nerve involvement is not as common as in the acute form 5>9,21) and was seen only in
our case 1 who presented unilateral 7th nerve palsy. Postural tremor of the upper limbs has been described in some patients by Prineas and M c L e o d2 1
and Dalakas and E n g e l5
; in our case 2 there was hyperkinesia which disappeared after treatment with steroids. The tremor is attributed to involvement of proprioceptive pathways 5,21. Bilateral extensor plantar reflex, present in our patient 3, had been previously observed by Prineas and M c L e o d2 1
in one of their cases.
According to Dyck and A r n a s o n8
the evolution of the syndrome can follow 3 courses: steadily progressive or relapsing; the progressive course may stabilize and the patient may eventually recover; a relapsing course in which the attacks may be separated by periods of normality. The recurrence can be spontaneous or may follow the reduction or the withdrawal of the steroid therapy 15-17. Regarding the number of recurrences, the patient described by Nattras in 1921 18 presented only two episodes, while that described by Austin 3 in 1958 had 2 0 such episodes over a period of 5 years. The patient reported by Pollard and Selby 19 had two recurrences, both of which followed an injection of tetanus toxoid. Our patients 1 and 2 suffered multiple episodes
(7 in 23 years and 5 in 17 years, respectively), which followed the withdrawal of steroids. On the other hand, the progressive course shown in our three patients was also present in the cases described by Bonduelle and Gruner 4
, Torvik and Lundar 24, and by Freitas and Nascimento i2
.
In addition to the presence of inflammatory cells, oedema and segmental demy-elination and remydemy-elination, other features described in chronic G B syndrome include thickening of peripheral nerves and, at histological and ultrastructural level, hyper-trophic neuropathy 8. The latter abnormality was present in two of our three cases. Hypertrophic neuropathy, first described by Nattras is, is however present in a mino-rity of cases 9«2
i. The return of nerves to normal size in the cases described by Austin 3 was probably due to improvement of the oedema which was present, in addition to changes of hypertrophic neuropathy. These onion bulbs have been inter-preted by many authors as the result of repeated episodes of demyelination 2
5 . Axonal
degeneration has also been reported in cases of chronic and acute GB syndrome 9,ii. Feasby et a l . H described 5 patients with a variant of acute GB polyneuropathy who had severe axonal degeneration in distal nerves without inflammation or demyelination. Although we did not find fibres undergoing axonal degeneration we could observe indirect signs of this change such as Schwann cells devoid of axons and small clusters of myelinated axons indicating regeneration. The differential diagnosis of hypertrophic forms with slow evolution have to be made with hereditary diseases like Dejerine--Sottas and Charcot-Marie-Tooth diseases 7. However, in these two forms there is a family history, dysmorphic changes and they do not improve with the use of steroids.
The use of steroids made the course of chronic GB syndrome more favou-rable 3,5,6,9,10,16,17,21. Remission can be spontaneous or with the use of this drug. Prineas and M c L e o d2
which used the drug. Our three patients had steroids. All improved and two of them became steroid dependent. It has recently been suggested plasmapheresis as an effective method in the treatment of this disease H . 2 2 . However, some more studies are necessary with more patients to evaluate the real efficiency of this therapeutic scheme.
Acknowledgements — W e s h o u l d l i k e t o t h a n k M i s s R i t a C. C u n h a a n d M i s s S u e l y M .
C u n h a f o r t h e t e c h n i c a l a s s i s t a n c e , a n d M i s s R o s e l y C. C u n h a a n d M r . R i c a r d o B a r r e t o f o r the p h o t o g r a p h i c w o r k .
R E F E R E N C E S
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