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Show Journal 01 ellllleal Neuro- oplllizalmology 12( 1), 57- 63,1992 The Miller Fisher Syndrome Review of the Literature Peter Berlit, M. D. and Josef Rakicky, M. D. The triad of ataxia, aretlexia and ophthalmoplegia was first described as a variant of the Guillain- Barre syndrome in 1932 by Collier. In 1956, Miller Fisher reported three patients with ataxia, aretlexia, and ophthalmoplegia as a separate entity. Since then, 223 cases of Miller Fisher syndrome have been published. The male/ female ratio is 2: 1 with a mean age of 43.6 years at the onset of the disease. A viral infection preceded the neurological symptoms in 71.8% of cases with an average symptomiree interval of 10 days. First symptoms were diplopia ( 38.60/ c) or ataxia ( 20.60/ c). An aretlexia was present in 81.6% of cases. Cranial nerves other than the oculomotor nerves were involved in 127 cases ( 56.9%): cranial nerves 7 ( 45.7%), 9 and 10 ( 39.9%), and 12 ( 13%) were involved. In 53 cases a tetraparesis occurred. An elevated protein value was present in 134 patients ( 64.4%); cerebrospinal tluid findings were normal in 56 patients. Eighteen patients showed a mild pleocytosis. Besides the cerebellar type of ataxia, initial disturbances of consciousness ( n = 8), supranuclear oculomotor signs ( n = 22), and pathology findings in electroencephalography ( n = 38), computed tomography ( n = 8), and magnetic resonance imaging ( n = 2) were reported as evidence for a central nervous system involvement in the Miller Fisher syndrome. The prognosis of Miller Fisher syndrome was good- recovery occurred after a mean time period of 10.1 weeks. Residual symptoms were present in 74 cases ( 33.2%), and a recidivism of the Miller Fisher syndrome was reported in seven patients. Eight patients died. Of six patients with autopsy findings, four exhibited central nervous system lesions. The Miller Fisher syndrome is apparently a variant of the Guillain- Barre syndrome with irequent central nervous system involvement and a benign outcome in the majority of cases. Key Words: Miller Fisher syndrome- Guillain- Barre syndrome- Aretlexia- Ataxia- Ophthalmoplegia. From the Neurology Department at the Mannheim Clinic of the University of Heidelberg, Mannheim, Germany. Address correspondence and reprint requests to Dr. Peter Berlit, Neurol. Klinik am Klinikum Mannheim der Universitat Heidelberg, Theodor Kutzer Ufer, 0- 6800 Mannheim, Germany. 57 ,~, 1992 Raven Press, Ltd, New York As early as 1 year after the first description of the Guillain- Barre syndrome in 1916 ( 1), variants with involvement of the cranial nerves and the central nervous system were reported ( 2-- 4). The triad of ataxia, areflexia, and ophthalmoplegia was first described as a variant of the Guillain- Barre syndrome in 1932 by Collier ( 5). During the following years, there were several reports about the combination of bilateral ophthalmoplegia and widespread paralysis of the extremities in acute polyneuritis ( 611). In 1956, Miller Fisher reported three patients with ataxia, areflexia, and ophthalmoplegia without prominent signs of peripheral neuropathy as a separate entity ( 12). Since then, patients presenting with ataxia, areflexia, and ophthalmoplegia as their leading symptoms are referred to as having the Miller Fisher syndrome. ( Since one author is responsible for defining this condition, the hyphen between the names should be avoided.) Since 1956, 223 cases of Miller Fisher syndrome have been described in the world literature. The majority of cases are cited under the name of Miller Fisher, some primarily as ataxia, areflexia, and ophthalmoplegia with reference to the Miller Fisher syndrome. In the discussion about the localization of ataxia, areflexia, and ophthalmoplegia, both a pure peripheral nerve affection ( 13-- 16) and a primary central nervous system lesion in the sense of a brainstem- encephalitis ( 17- 21) are suggested. In this report, we try to reevaluate the clinical picture, the course, and the possible pathogenesis and localization of Miller Fisher syndrome by a review of the literature. AGE AND SEX DISTRIBUTION The male/ female ratio of the 223 patients in the literature is approximately 2: 1. The mean age at the onset of the disease is 43.6 years. There are reports of about 32 ( 14.3%) children with Miller Fisher syn- 58 P. BERLlT AND ]. RAKICKY drome ( 22,23). There were 21 boys ( 9.4%) and 11 girls ( 4.9%). In the reports of adult patients, there were 113 men ( 50.7( 7c.) and 51 women ( 22.9%). In 27 cases, no sex was given ( 12.2%). The age of the oldest patient was 80 years; the youngest child was 14 months old. The sex distribution in the different age groups of all the patients reported is summarized in Fig. 1. As in the Guillain- Barre syndrome, the majority of patients with Miller Fisher syndrome develop their symptoms after some kind of viral infection ( 12- 80); the respiratory tract ( n = 132; 59.2%) is by far the most common site of infection. The various events that precede ataxia, areflexia, and ophthalmoplegia are shown in Table 1. The average time between the preceding event and the Miller Fisher syndrome was 10 days, the longest interval being 5 weeks. In 24 cases ( 12.6%), no preceding illness was mentioned. Only 12 of the reported patients ( 5.4%) had an elevated leukocyte count at the time of admission. INITIAL SYMPTOMS ophthalmoplegia was reported in 72 patients ( 32.3%). In 42 patients ( 18.8%), sufficient data were missing. An accompanying unilateral or bilateral ptosis was present in 105 patients ( 47.1 %). The ophthalmoplegia developed asymmetrically in 108 patients. Supranuclear ocular symptoms in Miller Fisher syndrome were described by several investigators. Signs of internuclear ophthalmopathia ( 50, 59, 63, 72, 75, 76, 81), the one- and- ahalf- syndrome ( 19), the Parinaud syndrome ( 82), and preserved optokinetic nystagmus in complete ophthalmoplegia ( 34, 41, 46, 54, 56, 59, 67, 71, 72) were mentioned. Meienberg described one patient with convergence spasms ( 48). The ataxia was characterized as cerebellar in the majority of cases, with stand and gait ataxia suggesting a lesion of the paleocerebellum. In 201 patients, ataxia was attributed to be cerebellar in origin ( 90.1 %). Only two patients presented with a sensory ataxia ( 0.9%) ( 35,83). In 20 cases ( 9%), data were missing. Areflexia was documented in 182 patients ( 81.6%): in 41 cases no description of the reflex status had been given ( 18.4%). The initial symptoms of Miller Fisher syndrome are given in Table 2. Diplopia and ataxia were responsible for one- third and one- fourth of initial symptoms, respectively. In most patients, the full picture of ataxia, areflexia, and ophthalmoplegia was reached in 5 to 10 days, so, in general, a subacute course of the disease can be presumed. Cardinal Symptoms A complete ophthalmoplegia including the parasympathic fibers to the m. sphincter pupillae was described in 109 patients ( 48.9%). A pure external Other Symptoms Involvement of cranial nerves other than the ocular nerves was cited in 127 patients ( 56.9%). The facial nerve was most frequently affected ( n = 102; 45.7%), followed by the lower cranial nerves: dysphagia as a possible sign of cranial nerves 9 and 10 lesions ( n = 89; 39.9%) and dysarthria as a possible symptom of cranial nerve 12 paresis ( n = 29; 13%). Only in 2 patients was dysarthria described as cerebellar ( 56). Other involved cranial nerves were 1 ( n = 2), 5 ( n = 11), 8 ( n = 2), and 11 ( n = 6). In facial palsy, 50 1:==:=::::;---------------~ FIG. 1. Age and sex distribution in Miller Fisher syndrome ( n = 223). 43 15 - 34 35 - 60 > 60 Age ( years) - 1/ 1 c: CIl 30 +: III Q. 0 20 Z 10 0 < 15 MILLER FISHER SYNDROME 59 TABLE 2. Initial symptoms of Miller Fisher syndrome ( n = 223) TABLE 1. Anteceding events in Miller Fisher syndrome ( n = 223) Other infections 19 ( 8.5) Gastrointestinal infection 11 20, 25, 32, 36, 38,40,42, 59, 60 Childhood infections 4 17,20,50,54 Urogenital infection 1 15 Tonsilitis 1 19 Spondylitis 1 61 Q · fever 1 81 Others 10 ( 4.5) Vaccination 3 43, 47, 56 Delivery 2 26, 52 Alcohol excesse 2 33,71 Cholesteatom surgery 1 17 Digitalis intoxication 1 16 Insect bite 1 22 None 24 ( 10.8) No data available 39 ( 17.4) a preserved Bell phenomenon instead of complete ophthalmoplegia was observed by some investigators ( 12,21,23,26,34,35,67,84). Only in 2 patients was facial palsy of central origin described ( 50,73). A paresis of the extremities was described in 63 patients ( 28.3%). In only 1 case published as Miller Fisher syndrome was there a severe tetra paresis ( 56). Most of these patients presented with a mild accompanying tetra paresis ( n = 54). A hemiparesis was present in 6 patients ( 73,79,85). In one of his original patients, Miller Fisher described a monoparesis of the right arm ( 12), Sensory symptoms were present in 99 patients ( 44.4%). In the majority ( n = 52), there were paresthesias and dysesthesia of all four extremities. Both legs of 39 patients were affected. Involvement of the arm and leg on one side of the body or of one arm only were each described in 4 circumstances. A pallhypesthesia was observed in 42 patients ( 18.8%), but it was never severe enough to explain the ataxia of the patients. Only a few investigators report on quantitative electrophysiological findings; some methods were mentioned only in single cases, which makes the findings difficult to interpret. Generalized slowing of electroencephalography activity was documented in 36 of 66 available case reports ( 54.5%). Localized slowing was mentioned in only 2 circumstances ( 12,17). There was no case with epileptiform discharges. Electromyography findings were given for 99 patients. Signs of demyelination were present in 38 of these patients ( 38.4%): in 11 patients a primarily axonal lesion was suggested ( 11.1 %). Combined findings were obtained in 18 patients ( 18.2%). In 32 patients, the electromyography findings were normal ( 32.3%). Pathological acoustic evoked potentials findings have been reported twice ( 17,88); the blink reflex was pathological in one case report ( 61). CEREBROSPINAL FLUID FINDINGS In most of the reports, cerebrospinal fluid findings are mentioned ( n = 208; 93.3%) but usually without a statement about the time of lumbar puncture. An elevated protein value was present in 134 patients ( 64.4%), 2.8 gil ( 87 patients) and 5.2 gil ( 67 patients) being the highest protein measurements. The rise in protein usually developed over 1- 3 weeks. Eighteen patients showed an initial pleocytosis ( 8.1%). The highest cell count was 1,350/ 3 cells ( 17). Cerebrospinal fluid findings were normal in 56 cases ( 26.9%). NEUROPHYSIOLOGICAL FINDINGS Other reported symptoms include headache ( n = 34), disturbance of consciousness ( n = 24), fever ( n = 13), vomitus ( n = 8), and irritability ( n = 3). In 9 patients, plantar responses were reported as being extensor ( 17,18,33,62,70); 5 patients developed bladder problems during the course of their disease ( 20, case 8; 40; 69; 79, cases 2 and 4). Epileptic fits were reported by Bickerstaff ( 20) and Al Din ( 17). Myoclonias, tremor, and other extrapyramidal symptoms were reported by Bickerstaff ( 20) and Ropper ( 86). A respiratory insufficiency developed during the course of the disease in 11 patients. No. cases (%) n (%) References 132 ( 59.2) 12,14,15,17, 18,21, 24- 37, 39, 41, 44- 53, 55- 59, 62- 70, 72- 79 Anteceding event Symptom Respiratory infection Diplopia Ataxia Headache Dysphagia Facial palsy Paresthesias of arms or legs Ptosis No data available 86 ( 38.6) 46 ( 20.6) 7 ( 3.1) 7 ( 31) 5 ( 2.2) 4 ( 1.8) 2 ( 0.9) 66 ( 29.7) NEURORADIOLOGICAL FINDINGS Computed tomography examinations were performed for 66 patients. Pathological findings were infratentorial hypodensities in eight patients ( 12.1%) ( 17,46,75), The majority ( n = 58; 87.9%) of JClm Neuro- ophtlullmol, Vol. ] 2, No. ], ] 992 60 P BERLIT AND f. RAKICKY investigations yielded normal results. Brainstem and mesencephalic lesions were reported in two ( 75,79) of five reports on the basis of magnetic resonance imaging. COURSE OF THE DISEASE The prognosis of Miller Fisher syndrome was generally good, with recovery after a mean of 10.1 weeks. The shortest interval to remission was 14 days; the longest, 18 months. Frequent residual symptoms were hyporeflexia or areflexia ( n = 36; 16.1 %). The other 2 cardinal symptoms of ataxia and ophthalmoplegia persisted in 11 patients ( 4.9%). Both ataxia and diplopia were usually mild and did not interfere with the activities of daily life. Other persisting symptoms ( n = 16; 7.2%) were psychic changes ( n = 4), facial weakness ( n = 4), and extrapyramidal symptoms such as tremor ( n = 3). Most patients showed a complete remission without any residual symptoms ( n = 119; 53.4%). There are no data about the course of the disease for 30 patients ( 13.5' 7c.). Recidivism has been reported for seven patients ( 15,19,23,25,38,64,69,88), the disease- free interval being 1 ( 69) to 29 years ( 64). The course of the relapse was as benign as the first episode in all cases. Eight patients died during the course of the disease ( 13,14,16,17,20,28,38,57,89). Secondary infections ( pneumonia, sepsis) were the cause of death in four patients. One patient died because of a pulmonary embolism ( 17). Autopsy findings were reported for six patients. Inflammatory lesions in the brainstem were described by AI- Din ( 17), Bickerstaff ( 20), and Bignami and Servi ( 28). Dehaene et al. ( 13) found demyelination of the cranial nerves with chromatolysis of the mesencephalon. Similar findings with involvement of anterior horn cells were reported by Gronnet and Lubon ( 14). In the case report by Phillips et al. ( 16), segmental demyelination of the ocular nerves was the only pathological finding at autopsy. In the last three reports mentioned, there were no changes in the brainstem. None of the autopsy reports showed inflammatory lesions in the cerebellum. Some loss of Purkinje cells was described by Bignami and Servi ( 28). Data about treatment in Miller Fisher syndrome are sparse. A corticosteroid therapy was established for 32 patients ( 14.3%). These cases did not differ from the others in terms of duration and degree of remission. Plasmapheresis was performed in seven patients: some authors ( 27,46,65) saw some positive effect in patients who became respiratory insufficient. In the large majority of reports no specific treatment was given, or data are missing ( n = 188; 84.4%). THE LOCALIZAnON AND NATURE OF MILLER FISHER SYNDROME Miller Fisher himself ( 12) was uncertain about the localization of the ataxia, areflexia, and ophthalmoplegia triad. Though the loss of tendon reflexes and the cerebrospinal fluid findings did make the syndrome similar to the Guillain- Barre syndrome, the striking symmetry of ophthalmoplegia with conjugate palsies during recovery and the cerebellar type of ataxia suggested, in his opinion, an involvement of the central nervous system. Weighting the different findings against each other, he concluded, " The clinical signs in question are reluctantly interpreted as manifestations of an unusual and unique disturbance of peripheral neurons." This interpretation was challenged in 1957 by Bickerstaff ( 20), who reported histological features suggestive of brainstem encephalitis in one of eight patients with symmetrical ophthalmoplegia and ataxia. Since then, the triad of ataxia, areflexia, and ophthalmoplegia is referred to either as Miller Fisher syndrome or as Bickerstaff encephalitis. Even in the most recent literature, the nature of this clinical entity with benign prognosis remains unclear ( 79,81). In general, there are three major interpretations of the nature of the Miller Fisher syndrome: ( a) The Miller Fisher syndrome is a variant of the Guillain- Barre syndrome- an idiopathic inflammation of peripheral neurons. The central nervous system- findings reported are either secondary or patients have been wrongly classified as having Miller Fisher syndrome ( 13,15,16,34-- 36,41,44,61, 63,65,69,82,83,87,88,90). ( b) The Miller Fisher syndrome is a brainstem encephalitis without involvement of peripheral nerves. The areflexia is due to a lesion of the mesencephalon and the upper pontine reticular formation ( 17,20,28,29,53,59,60,74,75,81,84,85). ( c) The Miller Fisher syndrome is caused by a brainstem affection, which is accompanied by a polyneuritis ( 14,19,22,23,25,27,33,36,39, 40,50,55,62,67,70,81,91,93). In Table 3, we have tried to summarize both the arguments in favor of a central nervous system lesion and those suggestive of a primary peripheral disease. In fact, some of the characteristics of the Miller Fisher syndrome resemble those of Guil- MILLER FISHER SYNDROME TABLE 3. Evidence of central and peripheral origin of Miller Fisher syndrome 61 Clinical: Neurophysiological: Neuroradiology: CSF: Neuropathological: Central origin Symmetry of ophthalmoplegia Internuclear ophthalmoplegia or preserved convergence One and a half syndrome Convergence spasmus Parinaud syndrome Preserved optokinetic nystagmus Cerebellar ataxia Facial palsy of central origin Preserved Bell phenomenon Hemiparesis or hemihypesthesia Disturbances of consciousness Epileptic fits Extrapyramidal signs Blink reflexes Acoustic evoked potentials EEG- slowing CT lesions MRI lesions Pleocytosis; no rise of protein Inflammatory lesions in mesencephalon and brainstem Normal findings in examination of sural nerve biopsy Peripheral origin Areflexia Tetraparesis Distal sensory symptoms ( arms and legs) Facial palsy of peripheral origin Pall hypesthesia Electroneurography & electromyography Normal CT Normal MRI Albuminocytological dissociation Anterior horn and bulbar chromatolysis, CN lesions Normal findings in brainstem and mesencephalon EEG, electroencephalogram; CT, computed tomography; MRI, magnetic resonance imaging, CN, cranial nerve. lain- Barre syndrome. Both diseases frequently folIowan infection, show the elevated protein value in cerebrospinal fluid, and present with pathological electroneurographic findings. However, the prognosis of the Miller Fisher syndrome is much better than that of Guillain- Barre syndrome. Irregularities in electroencephalography and computed tomography are much more common in the Miller Fisher syndrome; nor does this syndrome ever show the involvement of the autonomic system, which is typical of the Guillain- Barre syndrome. The evidence for involvement of brainstem structures in the Miller Fisher syndrome is quite convincing. From a clinical point of view and besides the symmetry of ophthalmoplegia, the findings of internuclear ophthalmoplegia, one and a half syndrome, Parinaud syndrome, and preserved optokinetic nystagmus and Bell phenomenon in facial palsy clearly indicate a supranuclear lesion. Some neuroradiological and autopsy findings support this assumption. On the other hand, several " classical" cases showed no brainstem lesions on autopsy, and no one ever documented the cerebellar inflammation thought to be responsible for the ataxia. The affected peripheral neurons with accompanying chromatolysis of bulbar and anterior horn cells as in the Guillain- Barre syndrome were shown on autopsy several times ( 13,16). On the basis of the 223 case reports analyzed, it seems improbable that the Miller Fisher syndrome is either a pure brainstem or a pure peripheral neuron disease. The different findings listed above seem to support the case for encephalomyeloneuritis. In the meantime, we have learned that in Guillain- Barre syndrome, involvement of central nervous system structures is possible. Still, the interpretation of Miller Fisher ( 12), which puts ataxia, areflexia, and ophthalmoplegia close to the Guillain- Barre syndrome, seems to be plausible. Why should Miller Fisher syndrome not be a variant of the Guillain- Barre syndrome that more frequently involves the central nervous system? The benign course of this clinical entity especially speaks against the assumption of a primary inflammation of the brainstem. Some findings reported seem to be rather unusual for the Miller Fisher syndrome. They include extensor plantar response, disturbance of consciousness, cerebrospinal fluid pleocytosis, epileptic fits, severe tetraparesis of the Landry type, and respiratory insufficiency. In light of these findings, to attribute the patient's disease to Miller Fisher syndrome is a matter of debate. CONCLUSIONS The Miller Fisher syndrome is an idiopathic disease presenting symptoms of ataxia, areflexia, and ophthalmoplegia. It occurs most frequently in the J Oill Neuro- ophthalmol, Vol. 12, No. 1. 1992 62 P BERLIT AND J RAKICKY fifth decade of life and affects men twice as often as women. It has a subacute development after some viral infection of the respiratory tract and shows complete remission after an average 10 weeks in the majority of cases. The diagnosis of Miller Fisher syndrome should be restricted to patients with ataxia, areflexia, and ophthalmoplegia and no other severe neurologic signs. Cerebrospinal fluid studies should be normal or demonstrate some degree of elevated protein value. The main differential diagnoses are Wernicke encephalopathy, vascular brainstem disease, sinusthrombosis, multiple sclerosis, specific inflammations like diphtheria and botulism, and intracranial neoplasms ( 12,17, 20,43,50,55,62- 64,93- 97). Besides cerebrospinal fluid analysis, magnetic resonance imaging seems to be a mandatory test to confirm diagnosis. However, if the classical triad is present, no other investigations are necessary. 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