Diagnosis Of Miller-Fisher Syndrome Research Articles

Pediatric Miller Fisher syndrome mimicking anti-histaminic drug toxicity

Background: Miller Fisher syndrome (MFS) is a rare condition in childhood, characterized by acute-onset ataxia, ophthalmoplegia, and areflexia. It is mostly preceded by viral and bacterial infections, and the pathogenesis is speculated to be an immune response to cross-reacting antigens. We describe a case of acute ataxia which was initially misdiagnosed as antihistaminic toxicity and later emerged to be MFS. Clinical Description: A 4.5-year-old girl presented with acute-onset ataxia, giddiness, and limb pain, following toxic ingestion of an antihistaminic drug (chlorpheniramine) that had been prescribed for an upper respiratory infection. The absence of waning symptoms, new manifestations, and undetectable drug levels prompted us to consider an alternate diagnosis. Management: Magnetic resonance imaging of the cranium and spine was unremarkable. Hence, a central nervous system infection was considered. Cerebrospinal fluid (CSF) analysis revealed albumin-cytologic dissociation, a negative viral panel, and sterile culture. Serum anti-GQ1b antibody of immunoglobulin G type was positive. A nerve conduction study revealed absent H-reflexes in both gastrocnemius muscles. A diagnosis of MFS was made based on clinical features, CSF albumin-cytologic dissociation, positive anti-GQ 1b antibody, and absent H reflexes. She was treated with intravenous immunoglobulin therapy, following which there was an improvement in 1 week and complete recovery within 3 months. Conclusion: Although a rare entity, we need to consider MFS in the differential diagnosis of ataxia when the neurological signs persist beyond the expected time duration so that investigations can be planned accordingly and timely immunotherapy initiated.

Fleeting diplopia and wobbly feet: Miller-Fisher syndrome-presenting as bilateral abducent nerve palsy

A case report of a healthy young male, presented with binocular diplopia of sudden onset with mild bilateral abduction limitation, progressed rapidly to near total ophthalmoplegia. Rest of the ophthalmic examination, blood pressure, and magnetic resonance imaging of brain were normal. Basic blood work-up was normal except mildly raised serum triglycerides. He gave a history of mild giddiness and ataxia. Neurological evaluation done showed absent deep tendon reflexes and serum anti-GQ1b antibody was raised. A diagnosis of Miller-Fisher syndrome was made and he was given intravenous immunoglobulin. Post-treatment his ocular motility recovered well, with minimal residual diplopia noted for distance. In individuals with abducent nerve palsy, normal imaging, and no systemic risk factors, a careful history asking for subtle neurological symptoms and a complete central nervous system examination is warranted to rule out conditions like Miller-Fisher syndrome which may not be a familiar entity to many ophthalmologists.

Antibodies to Glycolipids in Guillain-Barré Syndrome, Miller Fisher Syndrome and Related Autoimmune Neurological Diseases.

Guillain-Barré syndrome (GBS) and Miller Fisher syndrome (MFS) are acute immune-mediated neuropathies, often preceded by an infection. Anti-glycolipid antibodies are frequently detected in patients' sera in the acute-phase. In particular, IgG anti-GQ1b antibodies are positive in as high as 90% of MFS cases. Anti-glycolipid antibodies are useful for the diagnosis of GBS and MFS. In addition, those antibodies may be directly involved in the pathogenetic mechanisms by binding specifically to the regions where the target glycolipid antigen is densely localized. This was proven by the development of animal models of anti-glycolipid antibody-mediated neuropathies. The presence of antibodies that specifically recognize a new conformational epitope formed by two gangliosides (ganglioside complex) in the acute-phase sera of some GBS patients suggested existence of a carbohydrate-carbohydrate interaction between glycolipids. Further intensive research is needed to clarify this point.

An atypical course of a 71-year old man with right arm weakness and ataxia: Expert commentary

Dr Khemani and colleagues have presented a diagnostically challenging case of a sporadic, adult onset ataxia (SAOA) syndrome resembling Multiple System Atrophy cerebellar type (MSA-C), with an atypical presentation of focal amyotrophy, eventually diagnosed as spinocerebellar ataxia type 3 (SCA3) [ [1] Khemani P. Elliott M. Levine T. An Atypical Clinical Course of a 71-Year-Old Man with Right Arm Weakness and Ataxia. Parkinsonism Relat Disord, 2022 Abstract Full Text Full Text PDF Scopus (0) Google Scholar ]. The patient had presented elsewhere three years prior, with a Miller Fisher syndrome (MFS) associated with an elevated antiGQ1b antibody titer. However, as the patient had become wheelchair bound over the subsequent three years, the initial diagnosis of MFS is perhaps questionable. When evaluating ataxic disorders, it is important to establish the disease onset and course accurately. As the patient had a progressive cerebellar syndrome, the possible causes could be categorized broadly as: primary autoimmune (paraneoplastic or non-paraneoplastic); or neurodegenerative (sporadic or genetic). Primary autoimmune cerebellar ataxia encompassing paraneoplastic ataxia syndromes, and immune-mediated ataxias (gluten ataxia and anti-GAD65 ataxia) may present insidiously, with accumulating disability especially if timely and appropriate immunosuppressive therapies are not instituted [ [2] Hadjivassiliou M. Graus F. Honnorat J. Jarius S. Titulaer M. Manto M. Hoggard N. Sarrigiannis P. Mitoma H. Diagnostic criteria for primary autoimmune cerebellar ataxia-guidelines from an international task force on immune-mediated cerebellar ataxias. Cerebellum. 2020; 19: 605-610 Crossref PubMed Scopus (35) Google Scholar ].

Bilateral Sixth nerve palsy in a pediatric patient as first presentation of atypical miller fisher syndrome

AbstractPurposeTo describe a case of bilateral sixth nerve palsy in the setting of an atypical Miller Fisher Syndrome (MFS), extremely rare in the pediatric population and barely documented in the literatureMethodsWe present a case of a 12‐year‐old girl who came to the emergency room for diplopia of 24 hours. She had no history of a previous infectious or febrile process, except for an episode of abdominal pain 8 days earlier. The examination revealed bilateral sixth nerve palsy. Hospital admission was decided. Two days later the clinical picture worsened, appearing swallowing difficulty, decreased strength and muscle tone in all 4 extremities. The tendon reflexes were preserved. Craniospinal MRI and lumbar puncture were normal. The electroneurogram was consistent with early stage of polyradiculoneuritis. Autoimmunity tests showed positive anti‐GT1a antibodies and negative anti‐GQ1b antibodies.ResultsBased on the findings, treatment with immunoglobulin and intravenous corticosteroids was decided. Clinical resolution was progressive and the oculomotor alteration completely remitted at 2 months.ConclusionsMFS is a rare autoimmune disease characterized by the classic triad of ophthalmoplegia, ataxia, and areflexia. It is considered a variant of Guillain‐Barré syndrome. There are few cases or series of cases described in the literature on MFS and its behavior in pediatrics. Therefore, almost all clinical and laboratory findings have been described in adults, but in pediatrics, there is still uncertainty. This can lead to difficulties in the diagnosis of MFS in these patients. MFS should always be suspected in the context of acute diplopia or oculomotor paralysis in pediatrics, especially if it is bilateral; despite that its bilateral character seems to be less than in adults. Fortunately, even in these patients, it maintains its self‐limited behavior, so a full recovery is expected.Mane S, (2020) Miller Fisher in a Child. Journal of Pediatric Neurosciences.

Miller Fisher syndrome following BNT162b2 mRNA coronavirus 2019 vaccination

BackgroundThe coronavirus disease 2019 (COVID-19) pandemic, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), began in late 2019. One of the vaccines approved against COVID-19 is the BNT162b2 mRNA COVID-19 vaccine (Pfizer/BioNTech).Case presentationWe present the case of a 71-year-old man with no history of the SARS-CoV-2 infection or any recent viral or bacterial illnesses who presented with bilateral oculomotor palsy and limb ataxia after BNT162b2 mRNA COVID-19 vaccination. The diagnosis of Miller Fisher syndrome (MFS) was established based on physical examination, brain magnetic resonance imaging (MRI), cerebrospinal fluid analysis (CSF), and positron emission tomography (PET). There was no evidence of other predisposing infectious or autoimmune factors, and the period from COVID-19 vaccination to the appearance of neurological symptoms was similar to that of other vaccines and preceding events, such as infection.ConclusionGuillain–Barré syndrome (GBS) and its variants after COVID-19 vaccination are extremely rare. Note that more research is needed to establish an association between MFS and COVID-19 vaccines. In our opinion, the benefits of COVID-19 vaccination largely outweigh its risks.

Anti-Ganglioside Antibody Negative Miller Fisher Syndrome with Atypical Features: A Case Report

Miller Fisher Syndrome (MFS), a variant of Guillain Barre Syndrome (GBS), is an immune-mediated neuropathy presenting with the classical clinical triad of ophthalmoplegia, ataxia, and areflexia. Although the clinical triad is the cardinal diagnostic clue, it can also present with a variety of other atypical neurological symptoms and signs beyond the classical triad. IgG anti-GQ1b antibodies are a powerful serological marker for the diagnosis of MFS, however, they can be absent in 10-15% cases of MFS. Here, we are describing a case of a 55-year old lady with an anti-ganglioside negative case of MFS with ptosis and bulbar palsy, who improved with IVIg.

Miller Fisher syndrome in a patient with pulmonary tuberculosis

Miller Fisher syndrome (MFS) is characterized by the acute ophthalmoparesis, ataxia and areflexia. We describe the case of 70-year-old man with cardinal symptom of MFS and active pulmonary tuberculosis (Tb). A thorough evaluation led to the diagnosis of MFS and treatment with intravenous immunoglobulin (IVIg) was started. The complete resolution of ophthalmoparesis and ataxia was observed from the fourth day of IVIg treatment. This is the first report to describe a case of MFS that developed in patient pulmonary tuberculosis. Key Words: Miller Fisher syndrome · Tuberculosis · Guillain-Barré syndrome.

Miller Fisher syndrome with bilateral vocal cord paralysis: a case report

BackgroundMiller Fisher syndrome is a variant of acute inflammatory demyelinating polyneuropathy classically characterized by ataxia, ophthalmoplegia, and areflexia. Miller Fisher syndrome can present with uncommon symptoms such as bulbar, facial, and somatic muscle palsies and micturition disturbance.Case presentationWe describe the case of a 76-year-old white man with new-onset ataxia, stridor, areflexia, and upper and lower extremity weakness who required intubation at presentation. An initial work-up including imaging studies and serum tests was inconclusive. Eventually, neurophysiological testing and cerebrospinal fluid analysis suggested a diagnosis of Miller Fisher syndrome. Our patient responded to treatment with intravenous immunoglobulin and supportive therapy.ConclusionThe occurrence of acute or subacute descending paralysis with involvement of bulbar muscles and respiratory failure can often divert clinicians to a diagnosis of neuromuscular junction disorders (such as botulism or myasthenia gravis), vascular causes like stroke, or electrolyte and metabolic abnormalities. Early identification of Miller Fisher syndrome with appropriate testing is essential to prompt treatment and prevention of further, potentially fatal, deterioration.

Miller Fisher syndrome presenting with bilaterally impaired adduction in horizontal gaze and dissociated nystagmus of the abducting eyes

AbstractThe patient is a 58‐year‐old woman presenting a 5‐day history of diplopia that started 2 weeks after an upper respiratory tract infection. Neurological examination revealed bilaterally impaired adduction in horizontal gaze with dissociated nystagmus of the abducting eyes, which resembled dissociated nystagmus observed in internuclear ophthalmoplegia (INO). She also exhibited slightly impaired abduction and impaired supraduction in both eyes, right‐sided ptosis, and slight truncal ataxia. There were no abnormal findings on contrast‐enhanced MRI of the brain. The diagnosis of Miller Fisher syndrome was confirmed by positive serum anti‐GQ1b and GT1a antibodies. The patient fully recovered without specific treatment. Impaired adduction in horizontal gaze with dissociated nystagmus of the abducting eye is generally presumed to be indicative of INO, a lesion in the medial longitudinal fasciculus. We presumed that an imbalance between severely restricted adduction and preserved abduction of the opposite eye led to the unique ocular motility disturbances observed in our patient.

One-sided triangle: A case of double vision

A 51-year-old woman presented with acute diplopia and was found to have ptosis and complete bilateral external and internal ophthalmoplegia. She had normal reflexes and gait. Serological testing showed elevated levels of GQ1b ganglioside autoantibodies, making the diagnosis of Miller Fisher syndrome. This case illustrates an atypical presentation of the Miller Fisher variant of Guillain-Barre syndrome, which should be considered in all patients presenting with bilateral ophthalmoplegia.

Miller Fisher Syndrome and Neuroborreliosis: A Clinical Conundrum

SESSION TITLE: Nervous System Disorders in the ICU 2 SESSION TYPE: Affiliate Case Report Poster PRESENTED ON: Tuesday, October 31, 2017 at 01:30 PM - 02:30 PM INTRODUCTION: Miller Fisher Syndrome (MFS) is a variant of Guillain-Barre Syndrome (GBS) accounting for 5% of GBS cases. It is characterized by ophthalmoplegia, areflexia, and ataxia. Neuroborreliosis (NB) is a common complication of Lyme disease (LD), which can mimic, or even trigger GBS. We identified a rare case of MFS in a patient with acute Lyme serologies. Given the potential similarities in clinical presentation, it can be challenging to differentiate NB from MFS. CASE PRESENTATION: A 26-year-old woman presented to the Emergency Department after awakening with ptosis, ataxia, diplopia, and dysarthria. She denied any sick contacts, travel, or tick bites. Vital signs on presentation were normal. Neurological examination was significant for bilateral ptosis and ophthalmoplegia with decreased extraocular movements in all directions, normal strength, intact sensation, decreased deep tendon reflexes in all extremities, dysmetria on bilateral finger-to-nose testing, and normal plantar reflexes. Neuroimaging, which included CT head, MRI brain, MRA head and neck, and MRV brain, were unremarkable. Laboratory studies were significant for the presence of CSF Ganglioside GQ1B Ab titers at 1:3200; CSF albuminocytologic dissociation (WBC 5u/L, protein 63mg/dL); negative CSF anti-B.burgdorferi antibodies; and positive serum anti-B.burgdorferi IgM with positive 23 and 41 kDa bands on western blot. This data suggested MFS as the diagnosis. The patient was admitted to the ICU for close respiratory monitoring with serial vital capacity (VC) and negative inspiratory force (NIF) measurements. She was concurrently treated with 5 days of IVIG and ceftriaxone. Neurological improvements were observed on day 4 of her treatment. DISCUSSION: The constellation of signs and symptoms that characterize MFS are nonspecific, and can be seen in LD manifesting with cranial neuropathies. The presence of positive Lyme serologies in the setting of the classic MFS presentation can result in a diagnostic dilemma, but MFS should be ruled out as it can progress to respiratory failure. B. burgdorferi infection is rarely associated with GBS. Its potential to be an inciting factor is based on the hypothesis that it can mount autoimmune responses. Diagnosis of MFS requires CSF analysis, and is supported by the presence of albumincytologic dissociation, and Anti-GQ1b antibodies (90% sensitivity and specificity). Treatment is based on standard therapy for GBS (plasma exchange vs. IVIG). There are no specific guidelines available catered to the MFS variant. CONCLUSIONS: Our case demonstrates that although rare, B. burgdorferi infection may be a potential inciting factor for the development of GBS and MFS. In the setting of positive Lyme serologies and cranial neuropathies that include ophthalmoplegia, both LD and GBS should also be considered in the diagnosis. Reference #1: Lo YL. Clinical and immunological spectrum of the Miller Fisher syndrome. Muscle Nerve 2007; 36:615. DISCLOSURE: The following authors have nothing to disclose: Di Pan, Sung Lee, Nader Ishak Gabra, Joseph Mathew No Product/Research Disclosure Information

A Case of Miller Fisher Syndrome and Literature Review

Miller Fisher syndrome (MFS) was first recognized by James Collier in 1932 as a clinical triad of ataxia, areflexia, and ophthalmoplegia. Later, it was described in 1956 by Charles Miller Fisher as a possible variant of Guillain-Barré syndrome (GBS). Here, we write a case of a patient with atypical presentation of this clinical triad as the patient presented with double vision initially due to unilateral ocular involvement that progressed to bilateral ophthalmoplegia. He developed weakness of the lower extremities and areflexia subsequently. A diagnosis of MFS was made due to the clinical presentation and the presence of albuminocytologic dissociation in the cerebrospinal fluid (CSF) along with normal results of brain imaging and blood workup. The patient received intravenous immune globulin (IVIG), and his symptoms improved. The initial diagnosis of MFS is based on the clinical presentation and is confirmed by cerebral spinal fluid analysis and clinical neurophysiology studies. This case which emphasizes the knowledge of a rare syndrome can help narrow down the differentials to act promptly and appropriately manage such patients.

Miller Fisher syndrome associated with polymyoclonus

AbstractWe described a 35‐year‐old man who presented with diplopia, dysarthria, loss of deep tendon reflexes, and rapidly progressive unsteadiness in standing and walking. Two days after admission, frequent, irregular, and shock‐like movements appeared in the hands and abdomen. On laboratory examination, serum immunoglobulin G antibodies against GQ1b, GT1a and GD1b were all positive. Electrophysiologically, recording of the involuntary movements with surface electromyography showed irregular sharp discharges especially during weak muscle contraction. The clinical diagnosis of Miller Fisher syndrome associated with polymyoclonus was made, and all neurological symptoms including myoclonus improved after intravenous injection of immunoglobulin. The distribution of myoclonus and electrophysiological data suggested that the myoclonus, though different from propriospinal or spinal segmental myoclonus in the distribution and propagation, might still be of spinal cord origin.

PP08.12 – 2493: Atypical Miller Fisher syndrome presenting as acute isolated bilateral ophthalmoplegia: Report of two nex patients with serological specificity

Objective Miller Fisher syndrome (MFS) is an acute polyradiculoneuritis regarded as an uncommon clinical variant of Guillain-Barre syndrome (GBS) asociated with antiGQ 1b positvie serology. MFS is characterized by the acute onset of a clinical triad of ophthalmoplegia, cereballar ataxia and areflexia. Atypical forms of MFS presenting as ophthalmoplegia without ataxia, have been scarcely described. Methods A detailed clinical and serological description of 2 young childhood cases of acute isolated bilateral ophthalmoplegia. Results Case 1 6-year-old boy presented with acute onset of diplopia, ten days after he experienced diarrhea and fever. Neurologic examination showed bilateral isolated sixth nerve palsy, more prominent on the left. Investigations including brain imaging, lumbar puncture and fundoscopic exam were normal. C. jejuni serology showed elevated IgG and IgA. Analysis of anti-ganglioside antibodies by ELISA in serum obtained immediately after admission revealed high levels of anti-GQ1b, anti-GT1a and anti-GD3 IgG and IgM. Case 2 4-year-old boy admitted with limited abduction of both eyes, as well as adduction paresis of the right eye. Two weeks before, the boy suffered from a febrile episode with diarrhea. All investigations carried out on admission were normal. ELISA for anti-ganglioside antibodies was performed on the serum obtained 2 weeks after onset and revealed elevated titers of anti-GQ1b and anti-GT1a IgG and IgM. Serology was positive to C. jejuni. We observed a complete spontaneous resolution 8 weeks after onset in both children. Conclusion The two patients we decribed confirm the rare but possible occurrence of atypical MFS in young children a few weeks following gastrointestinal infection. Identification of high titers of anti-GQ1b IgG associated with positive serology for C. jejuni enabled the diagnosis of atypical MFS. This paper highlights the relevance of measuring serum anti-GQ1b IgG level in the diagnostic work-up of acute isolated ophthalmoplegia of unknown aetiology in a child.

Miller-Fisher Syndrome: Is the ataxia central or peripheral?

A 50-year-old man presented with a brief history of slurred speech, unsteadiness, double vision and paraesthesia. He had been unwell for 12 days with campylobacter gastroenteritis. On examination, there was ophthalmoplegia, nystagmus, areflexia and lower limb and gait ataxia. Serological testing was positive for GQ1b antibody in keeping with the diagnosis of Miller Fisher Syndrome (MFS). He was treated with two courses of intravenous immunoglobulins and made a good recovery, only displaying mild gait ataxia when reviewed in clinic 2.5 months later.There has long been a debate as to whether the ataxia in MFS originates in the cerebellum or it is more peripheral. In this case, magnetic resonance spectroscopy (MRS) revealed a reduced NAA/Cr ratio in the cerebellar vermis and right cerebral hemisphere, suggestive of cerebellar dysfunction. The NAA/Cr normalised 2.5 months later reflecting the clinical recovery. The findings on MRS suggest that the cerebellum is involved in MFS.

Clinical Features of Miller-Fisher Syndrome in Pregnancy.

Miller-Fisher syndrome (MFS) is recognized as a variant of Guillain-Barré syndrome (GBS). MFS is a rare disorder that is characterized by the acute onset of ophthalmoplegia, ataxia, and areflexia/hyporeflexia. MFS has a higher incidence in Asia, where the incidence is estimated to be 18%–26% of GBS compared with 3%–5% in the West. The differential diagnosis of MFS includes Wernicke's encephalopathy (WE) which is characterized by a clinical triad (nystagmus and ophthalmoplegia, mental status changes, and ataxia), myasthenia gravis, and brainstem stroke. The association between MFS and pregnancy has not been reported previously. Here, we describe the clinical features of a pregnant woman in early pregnancy with MFS. This case highlights the fact that it is necessary to establish an accurate diagnosis based on the details from the patient's history on appropriate complementary testing in a pregnant patient with MFS.

A CASE OF RECURRENT MILLER FISHER SYNDROME

Introduction Miller Fisher Syndrome (MFS) is classically a post-infectious localized variant of Guillan-Barre Syndrome (GBS), composing a triad of ophthalmoplegia, ataxia and areflexia(1) although variants have been described. In light of this we outline an unusual case of recurrent MFS which challenges the recognised aetiology and/or points to an underlying predisposition. Case A 56-year-old woman presented with subacute progressive ascending weakness, dysasthesia and dysarthria. On examination, there was complex ophthalmoplegia, bilateral lower motor neuron weakness in all limbs with dorsal column sensory loss to the hip and shoulder bilaterally. A clinical diagnosis of MFS was made and supported by nerve conduction studies and a strongly positive anti-gq1b antibody. Following treatment with intravenous immunoglobulin she made a full neurological recovery. However, she also reported two clinically similar episodes in 1980 and 1995 with full recovery, after which she was diagnosed with suspected relapsing remitting Multiple Sclerosis despite normal investigations. Conclusion The risk of recurrence of GBS is reported between 1–6% (2) but recurrent MFS is extremely rare, with only 21 cases in the literature. In this case, the typical clinical presentation of MFS coupled with previous episodes may suggest an underlying predisposition, or even a pathogenic role for anti-gq1b antibody.

An 85-year-old woman with Miller Fisher syndrome

Miller Fisher's syndrome (MFS) commonly presents in the fourth and fifth decades and are rare in people over 70 years. An 85-year-old female with no significant medical history presented with upper extremity anesthesia, ptosis, and unsteady gait. The patient had a history of hypertension and diabetes mellitus. Physical examination showed bilateral total external ophthalmoplegia, areflexia, and cerebellar ataxia. Radiological and laboratory studies were unremarkable. Lumbar puncture showed albuminocytological dissociation. The combined history, physical examination, and lumbar puncture results established a presumptive diagnosis of MFS. Intravenous immunoglobulin was given for 5 days. The patient gradually improved 10 days after the onset of symptoms. Ophthalmoplegia had fully recovered after 6 months. To the best of our knowledge, this case represented the oldest patient with MFS.

Neuropathie optique unilatérale et syndrome de Miller Fisher

Miller Fisher syndrome is an autoimmune neuropathy characterized by the clinical triad of ataxia, areflexia and external ophthalmoplegia. Ophthalmologic involvement in this syndrome is most often represented by motility disorders. The diagnosis is confirmed by the presence of anti-GQ1b antibodies. We report the case of a 65-year-old patient referred by his treating physician to the emergency department for ataxia, dizziness and decreased visual acuity in the left eye. In addition, the patient presented with clinical signs of subacute appendicitis for 2 weeks. After treatment with intravenous immunoglobulin, the patient complained of further decreased visual acuity and oculomotor disorders. On ophthalmological follow-up, he quickly recovered his initial visual acuity and more gradually his ocular motility. Unilateral optical neuropathy does not preclude the diagnosis of Miller Fisher syndrome. On the contrary, in the case of any rapidly progressive ophthalmologic involvement associated with peripheral neurological signs of ataxia, the diagnosis of Miller Fisher syndrome must be considered. Miller Fisher is a rare syndrome for which the diagnosis must be made quickly, so that the patient may benefit from urgent intravenous immunoglobulin therapy. In most cases, ophthalmologic recovery precedes peripheral neurologic recovery by 6 months to 1 year.