Cerebrospinal Fluid Albuminocytological Dissociation Research Articles

Lesion Localization and Prognosis Using Electrodiagnostic Studies in Facial Diplegia: A Rare Variant of Guillain-Barre Syndrome.

BackgroundThe etiology of facial nerve palsy is diverse and includes herpes zoster virus, Guillain-Barre syndrome (GBS), otitis media, Lyme disease, sarcoidosis, human immunodeficiency virus, etc. The lower motor neuron type facial nerve palsy is usually caused by an ipsilateral facial nerve lesion; however, it may be caused by a central lesion of the facial nerve nucleus and tract in the pons. Facial diplegia is an extremely rare condition that occurs in approximately 0.3% to 2.0% of all facial palsies. Electrodiagnostic studies including direct facial nerve conduction, facial electromyography (EMG), and blink reflex studies are useful for the prognosis and lesion localization in facial nerve palsy.MethodologyThis retrospective, observational study was conducted at the Neurophysiology Unit, Hamad General Hospital, Doha, Qatar. This study included 11 patients with bilateral facial weakness who visited for electrodiagnostic studies in the neurophysiology laboratory.ResultsIn total, eight (72.7%) patients had facial diplegia, eight (72.7%) had hypo/areflexia, seven (63.6%) had facial numbness, and five (45.5%) had cerebrospinal fluid albuminocytological dissociation. The most frequent cause of facial diplegia in this study was GBS (81.9%). Direct facial nerve conduction stimulation showed that nine (81.8%) patients had bilateral facial nerve low compound muscle action potential amplitudes. The bilateral blink reflex study showed that eight (88.8%) patients had absent bilateral evoked responses. Finally, the EMG study showed that five (55.5%) patients had active denervation in bilateral sample facial muscles.ConclusionsBilateral facial nerve palsy is an extremely rare condition with a varied etiology. Electrodiagnostic studies are useful in detecting the underlying pathophysiologic processes, prognosis, and central or peripheral lesion localization in patients with facial diplegia.

Porphyric neuropathy.

Acute hepatic porphyrias are inherited metabolic disorders that may present with polyneuropathy, which if not diagnosed early can lead to quadriparesis, respiratory weakness, and death. Porphyric neuropathy is an acute to subacute motor predominant axonal neuropathy with a predilection for the upper extremities and usually preceded by a predominantly parasympathetic autonomic neuropathy. The rapid progression and associated dysautonomia mimic Guillain-Barré syndrome but are distinguished by the absence of cerebrospinal fluid albuminocytologic dissociation, progression beyond 4 wk, and associated abdominal pain. Spot urine test to assess the porphyrin precursors delta-aminolevulinic acid and porphobilinogen can provide a timely diagnosis during an acute attack. Timely treatment with intravenous heme, carbohydrate loading, and avoidance of porphyrinogenic medications can prevent further neurological morbidity and mortality.

Guillain-Barré syndrome: clinical features, treatment choices and outcomes in an Australian cohort.

Guillain-Barré syndrome (GBS) causes acute neuromuscular weakness. Severe cases are life-threatening and many are left disabled. Intravenous immunoglobulin (IVIg) and plasma exchange (PE), along with supportive care, are the mainstays of treatment. Treatment choice is influenced by multiple factors. The clinico-epidemiological features of GBS in Australia have not been reviewed in 30 years and few studies have assessed contemporary treatment choices. To investigate the clinico-epidemiological features, choice of treatment, clinical course and outcomes of GBS patients in an Australian tertiary metropolitan hospital. A retrospective observational study was performed of GBS presentations to a tertiary hospital in Sydney, Australia, over 5 years. Clinico-epidemiological features, treatment choices, clinical course and outcomes were assessed. We reviewed 46 GBS patients (54% male), average age 55 years. Antecedent infection was identified in 61%. Twenty-eight per cent had preceding immunogenic events or conditions. Acute inflammatory demyelinating polyradiculoneuropathy was the most common subtype (78%). Cerebrospinal fluid albumino-cytologic dissociation was present in 43%. Electrodiagnostic testing most frequently demonstrated demyelination (64%). Ninety-eight per cent received immunotherapy, mostly IVIg (93%). Twenty-two per cent received further treatment due to treatment-related fluctuations or lack of improvement. Thirteen per cent required ICU admission and 46% needed rehabilitation. There were no deaths or need for mechanical ventilation. Seventy-one per cent of the follow-up cohort had residual disability at 6 months, but this was generally mild. The clinico-epidemiological features are consistent with previous cohorts. Our experience in a large Australian tertiary centre demonstrates a clear preference for IVIg over PE.

Diagnosis of Guillain-Barré syndrome and validation of the Brighton criteria in Malaysia.

We aimed to evaluate the key diagnostic features of Guillain-Barré syndrome (GBS) in Malaysian patients and validate the Brighton criteria. This was a retrospective study of patients presenting with GBS and Miller Fisher syndrome (MFS) between 2010 and 2019. The sensitivity of the Brighton criteria was evaluated. A total of 128 patients (95 GBS, 33 MFS) were included. In the GBS cohort, 92 (97%) patients presented with symmetrical limb weakness. Reflexes were depressed or absent in 90 (95%) patients. Almost all patients (94, 99%) followed a monophasic disease course, with 5 (5%) patients experiencing treatment-related fluctuations. Cerebrospinal fluid (CSF) albuminocytological dissociation was seen in 62/84 (73%) patients. Nerve conduction study (NCS) revealed neuropathy in 90/94 (96%) patients. In GBS patients with complete dataset (84), 56 (67%) patients reached level 1 of the Brighton criteria, 21 (25%) reached level 2, 3 (4%) reached level 3, and 4 (5%) reached level 4. In MFS, the clinical triad was present in 25 (76%) patients. All patients had a monophasic course. CSF albuminocytological dissociation was present in 10/25 (40%) patients. NCS was normal or showed sensory neuropathy in 25/33 (76%) patients. In MFS patients with complete dataset (25), 5 (20%) patients reached level 1 of the Brighton criteria, 14 (56%) reached level 2, 2 (8%) reached level 3, and 4 (16%) reached level 4. Inclusion of antiganglioside antibodies improved the sensitivity of the Brighton criteria in both cohorts. In the Malaysian cohort, the Brighton criteria showed a moderate to high sensitivity in reaching the highest diagnostic certainty of GBS, but the sensitivity was lower in MFS.

Update: the Miller Fisher variants of Guillain-Barré syndrome.

This article will update and review the Miller Fisher variants (MFV) of Guillain-Barré syndrome (GBS) including the clinical presentation, diagnostic testing, and treatment. Although the diagnosis of GBS and MFV can be made on clinical grounds, cerebrospinal fluid (CSF) analysis, nerve conduction studies, imaging (e.g. ultrasound and MRI), and serologic testing can help to confirm the diagnosis. Some patients may need immunotherapy with either intravenous immunoglobulin (IVIg) or plasma exchange, and recent studies suggest that complement inhibition combined with IVIg could be of benefit, but further studies are needed to prove efficacy. GBS is characterized by an acute, ascending polyneuropathy, ataxia, areflexia, and CSF albuminocytologic dissociation. The MFV of GBS is associated with ophthalmoplegia. Clinicians should have high index of suspicion for MFV of GBS in patients with acute ophthalmoplegia in order to establish the diagnosis, perform appropriate evaluation, and start treatment. SDC VIDEO LINK:.

Pathophysiology of Ataxia in Fisher Syndrome

Fisher syndrome is regarded as a peculiar inflammatory neuropathy associated with ophthalmoplegia, ataxia, and areflexia. The disorder is associated with preceding infection, cerebrospinal fluid albumino-cytological dissociation, and spontaneous recovery, and regarded as a variant of Guillain-Barré syndrome. The discovery of anti-GQ1b IgG antibodies led to dramatic advances in understanding the pathophysiology of Fisher syndrome. The lesions in Fisher syndrome are determined by expression of ganglioside GQ1b in the human nervous system. This review article focuses on the pathophysiology of ataxia in Fisher syndrome. Current evidence suggests that antibody attack on Group Ia neurons in the dorsal root ganglia is mainly responsible for the sensory ataxia. Involvement of the muscle spindles might also contribute to the development of ataxia.

Guillain-Barré syndrome in Bangladesh: validation of Brighton criteria.

Guillain-Barré syndrome has a diverse clinical phenotype related to geographical origin. To date, the majority of large-scale studies on Guillain-Barré syndrome (GBS) have been conducted in developed countries. We aimed to evaluate the key diagnostic features and assess the suitability of the Brighton criteria in 344 adult GBS patients from Bangladesh. All patients fulfilled the National Institute of Neurological Diseases and Stroke (NINDS) diagnostic criteria. Standardized data on demographic characteristics and clinical features, cerebrospinal fluid (CSF) analysis, and nerve conduction study (NCS) results were elaborated to measure the sensitivity of Brighton criteria. Most patients (88%) were admitted to hospital after the nadir weakness. Symmetrical weakness and reduced reflexes were found in 98% of patients. CSF albuminocytologic dissociation was detected in 238/269 (89%) cases and abnormal nerve physiology in 258/259 (>99%) cases. Only 27 (8%) patients received either intravenous immunoglobulin (IVIg) or plasmapheresis. In total, 200 (58%) patients met level 1 of the Brighton criteria; 97 (28%) patients met level 2; 42 (12%) patients met level 3; and 5 (2%) patients met level 4. This analysis showed that despite the heterogeneity of GBS in Bangladesh, the Brighton criteria showed a high sensitivity in the diagnosis of GBS.

Paraparetic Guillain‐Barré syndrome: Nondemyelinating reversible conduction failure restricted to the lower limbs

Paraparetic Guillain-Barré syndrome (GBS) is a rare subtype of GBS characterized by leg weakness and areflexia in the absence of neurological involvement of the arms, cranial nerves, or respiratory muscles. Onset is characterized by lower back, buttock, or leg pain, followed by development of symmetric flaccid limb weakness in the absence of sensory disturbance. We describe an elderly woman who developed postinfectious symmetric flaccid leg weakness in the absence of sensory disturbance. Serial nerve conduction studies were carried out over 5 months. Antecedent infection, a monophasic disease course, and the presence of cerebrospinal fluid albuminocytological dissociation suggested a diagnosis of paraparetic GBS. Serial nerve conduction studies demonstrated nondemyelinating reversible conduction failure, which was restricted to the legs. Axonal neuropathy was supported by the presence of anti-GM1 IgG antibodies. These findings suggest that patients with paraparetic GBS have axonal neuropathy, which is restricted to the lower limbs. Muscle Nerve 55: 281-285, 2017.

Polyneuritis cranialis: oculopharyngeal subtype of Guillain-Barré syndrome.

Guillain-Barré syndrome (GBS) constitutes a spectrum of related post-infectious neuropathies, which are characterized by their anatomical patterns of weakness and neurological involvement. Historically, the term polyneuritis cranialis has been used to describe some patients with GBS presenting with multiple cranial neuropathies in the absence of limb weakness. We examine previous reports of polyneuritis cranialis to determine disease characteristics and define new diagnostic criteria. Disease characteristics were determined from 15 historical case reports of patients presenting with isolated 'polyneuritis cranialis', 'cranial polyneuropathy', 'multiple cranial neuropathy' and 'multiple cranial neuropathies' due to GBS. Median age was 40 years. 80% displayed antecedent infectious symptoms. In all cases, disease course was monophasic with clinical improvement within weeks or months. Initial symptoms were ocular (73%) or bulbar (33%). Mean number of cranial nerves involved was 6 (range, 3-10). 93% displayed ocular signs, 73% facial weakness or numbness and 87% bulbar signs. In 3 patients (20%), there was significant asymmetry. Cerebrospinal fluid albuminocytological dissociation was present in 67% of cases. Serum anti-ganglioside antibodies were tested for in 8 of 15 patients and anti-GQ1b antibodies were found in 3 patients, whilst anti-GT1a antibodies were found in 1 patient. Polycranial neuritis (the oculopharyngeal subtype of GBS) can be defined in patients with disease characteristics of GBS who display ocular and pharyngeal weakness in the absence of limb weakness or ataxia. In half of cases tested for, anti-ganglioside antibodies were present and most frequently against GQ1b.

Multiple cranial neuropathy variant of guillain–barré syndrome: A case series

Prompt identification of the rare cranial variant of Guillain-Barré syndrome (GBS) is crucial, but the clinical characteristics remain poorly defined. We conducted a retrospective review of 12 GBS patients hospitalized from 1995 to 2009 with multiple cranial nerve (CN) impairment at disease onset. Eight patients had impairment of CN IX and X; 3 of CN VII; and 1 of CN VII, IX, and X. All patients had areflexia or hyporeflexia, 6 had Lasegue sign, and 5 required tracheostomy and mechanical ventilation. All patients had cerebrospinal fluid (CSF) albuminocytologic dissociation within 2-3 weeks after onset. Electrophysiological studies showed motor conduction velocity and F-wave abnormalities in 10 of 12 and 10 of 11 patients, respectively. Treatment with intravenous immunoglobulin was effective. Bilateral CN IX, X, and/or VII impairment with areflexia or hyporeflexia, early abnormal F-wave response, nerve conduction abnormalities, and CSF albuminocytologic dissociation support a diagnosis of this GBS cranial variant.

Ataxic Guillain–Barré syndrome and acute sensory ataxic neuropathy form a continuous spectrum

BackgroundAtaxic Guillain–Barré syndrome is characterised by profound ataxia with negative Romberg sign and no ophthalmoplegia. Its nosological relationship to acute sensory ataxic neuropathy has yet to be discussed.MethodsMedical records were...

Neurologic Manifestations of Pandemic (H1N1) 2009 Virus Infection

To the Editor: In April 2009, the outbreak of influenza A pandemic (H1N1) 2009 virus was reported. Subsequently, the disease spread throughout the world, and the pandemic alert level was raised to level 6 in June by the World Health Organization. Pandemic (H1N1) 2009 virus infection spread to Thailand and is now found throughout Thailand. Similar to the effects of other viruses, pandemic (H1N1) 2009 virus may cause neurologic complications. Associated neurologic symptoms were first reported from Dallas, Texas, USA: 4 children experienced unexplained seizures or had an alteration of consciousness level that was associated with this virus (1). We report an adult patient with pandemic (H1N1) 2009 infection who had neurologic complications. A 34-year-old man, previously healthy, was admitted to Chaiyaphum Hospital in Chaiyaphum, Thailand, on August 24, 2009, with influenza-like symptoms. Two days after admission, progressive quadriparesis with bilateral, symmetric paresthesia (glove-and-stocking pattern), and areflexia developed. His motor weakness (grades III/V) began in both legs and then involved both arms and hands. Other neurologic examinations showed limitation of extraocular movement in all directions, normal pupil size and light reflex, and facial diplegia. A lumbar puncture was performed, and cerebrospinal fluid (CSF) contained neither leukocytes nor erythrocytes, with a protein level of 19.5 mg/dL. On day 3 after the patient’s admission, acute respiratory failure developed. A nasopharyngeal aspirate specimen was positive for pandemic (H1N1) 2009 virus by PCR. The patient received oseltamivir, zanamivir, and ventilator support. His chest radiograph showed diffuse alveolar infiltration. On day 10, his motor weakness worsened to grade 0, and his consciousness level was diminished to a drowsy state. A computed tomography scan of the brain showed diffuse white matter lesions (Figure). Repeated lumbar punctures continued to show CSF findings within the reference range. An electrophysiologic study, electromyogram, and nerve conduction study showed polyneuropathy, axonopathy type. Guillain-Barre syndrome was suspected, and intravenous immunoglobulin was given for 5 days. Tests for GQ1b and GM1 antibodies were carried out at Oxford University; results were negative. Figure Computed tomography images of the brain of an adult patient with pandemic (H1N1) 2009 virus infection and neurologic signs. A noncontrast study showed hypodense lesions in both occipital lobes (A) and in both upper parietal lobes (B). Other laboratory tests showed mild transaminitis and negative results for syphilis testing and for serologic tests for HIV, hepatitis B virus, hepatitis C virus, Japanese encephalitis virus, herpes simplex virus, and Mycoplasma pneumoniae. A CSF antigen test was negative, and CSF culture was negative for bacteria. Meropenem was given to treat ventilator-associated pneumonia, which was caused by β-lactam–resistant Klebsiella pneumoniae. After a month of treatment, the patient regained consciousness, his motor strength improved considerably, and he was able to be gradually removed from the ventilator. After 3 months, he was discharged with self-assisted status. Our report shows neurologic manifestations associated with pandemic (H1N1) 2009 virus infection in an adult. The manifestation of progressive quadriplegia with diffuse sensory loss is compatible with a polyneuropathy. The neurologic signs developed 2 days after the respiratory tract signs. Although a diagnosis of Guillain-Barre syndrome was considered initially, according to the National Institute of Neurologic Disorders and Stroke criteria (2), some clinical features did not support this diagnosis. These included the lack of CSF albuminocytologic dissociation, the fact that the clinical signs occurred during the outbreak of pandemic (H1N1) 2009 virus infection rather than after it, and the fact that antibodies were not found in gangliosides. CSF albuminocytologic dissociation and serum ganglioside antibodies may be found in 85%–90% of Guillain-Barre syndrome patients (2). Alternatively, the patient might have had central nervous system complication from pandemic (H1N1) 2009 virus infection. Acute disseminated encephalomyelitis is a condition that might occur within 30 days after an infectious process (3). It can lead to quadriplegia and diffuse white matter lesions. The clinical feature that makes acute disseminated encephalomyelitis less likely in this patient was the CSF findings in the reference range. In summary, however, we believe that pandemic (H1N1) 2009 virus infection can cause neurologic complications affecting both the peripheral and central nervous systems in adult patients.

A Guillain-Barré syndrome variant with prominent facial diplegia

To determine the clinical features of a Guillain-Barré syndrome variant with prominent facial diplegia, we retrospectively reviewed approximately 8,600 cases referred to our neuroimmunological laboratory for serological tests during the past seven years. Patients' histories, neurological signs, and laboratory and electrophysiological data were clarified based on their clinical records. Sera obtained during the acute phase were tested for prior infectious serology and anti-ganglioside antibodies. In 22 patients, clinical signs such as acute progressive bifacial weakness, paresthesias in the distal dominant limbs, and hypo- or areflexia, were compatible with a Guillain-Barré syndrome variant, facial diplegia and paresthesias. Other cranial nerve involvements, limb weakness, and ataxia were absent or minimal. Clinical courses were monophasic, the nadir being reached within four weeks. Eighteen patients (86%) had had infectious symptoms within the four weeks preceding the onset of neurological illness. In the infection serology tests, anti-cytomegalovirus IgM antibodies were the most frequent (35%). All the patients had cerebrospinal fluid albuminocytologic dissociation. In nerve conduction studies, 14 (64%) showed demyelination in their limbs. Anti-GM2 IgM antibodies were detected in four patients who had anti-cytomegalovirus IgM antibodies. Patients with conditions similar to facial diplegia and paresthesias, but lacking either distal paresthesias or hyporeflexia, were regarded as having marginal facial diplegia and paresthesias, because they also frequently had features of Guillain-Barré syndrome, such as an antecedent infection or cerebrospinal fluid albuminocytologic dissociation. Our findings are further evidence of a facial variant of Guillain-Barré syndrome and provide important information essential for its diagnosis.

Electrodiagnostic and Clinical Aspects of Guillain-Barré Syndrome: An Analysis of 142 Cases

The incidence of Guillain-Barré syndrome (GBS) and its subtypes varies throughout the world. We present a retrospective analysis of 142 GBS cases, treated at our center, aimed at classifying GBS electrophysiologically, to study the sequential electrophysiological changes in cases with acute inflammatory demyelinating polyradiculoneuropathy (AIDP), and to look for any clinical and cerebrospinal fluid parameters that can also help in distinguishing the subtypes. One hundred twenty-one (85.2%) cases had AIDP, 15 (10.6%) had acute motor axonal neuropathy, and 6 (4.2%) were unclassifiable. Motor conduction blocks and temporal dispersion could be observed from days 3 and 5 onward, respectively. Progression of motor conduction slowing in AIDP was most impressive in the median nerves. Varying affection of deep tendon reflexes, cranial nerves, and cerebrospinal fluid albuminocytological dissociation can also help make a distinction between AIDP and acute motor axonal neuropathy. Sural sparing, a marker of demyelinating neuropathy, is more commonly seen in later than in early stages of AIDP.

A case of overlapping Bickerstaff’s brainstem encephalitis and Guillain-Barré syndrome

There is no report on Bickerstaff's brainstem encephalitis (BBE) patients in China. We here report the first case of BBE in China. Clinical features, results of electromyography, electroencephalography (EEG), magnetic resonance imaging (MRI) and cerebrospinal fluid (CSF) examination were studied to clarify the characteristics of this syndrome. A 44-year-old man presented himself at our inpatient department with somnolence and dizziness as his initial symptoms. He developed multiple cranial nerves paralysis especially internal and external ophthalmoplegia, ataxia and tetraparesis within 1 week. His condition rapidly deteriorated, and he experienced coma. Electromyography showed indications of peripheral nerve dysfunction, electroencephalography revealed loss of basic rhythm, MRI demonstrated high-intensity abnormalities on T(2)-weighted images of medulla oblongata, and CSF albuminocytological dissociation was defined abnormally as high protein. Ten months later, he almost completely recovered. BBE, fisher syndrome (FS) and Guillain-Barré syndrome (GBS) are similar clinically; BBE and FS were proposed to be the variant of GBS.

Usefulness of anti-GQ1b IgG antibody testing in Fisher syndrome compared with cerebrospinal fluid examination

Fisher syndrome (FS), a variant of Guillain–Barré syndrome (GBS), is a rare disorder, and there are few reported studies of a large number of patients with FS. Cerebrospinal fluid (CSF) albuminocytological dissociation was found in 59% of 123 FS patients during the first 3 weeks of illness, while serum anti-GQ1b IgG antibody was positive in 85%. Whereas the incidence of CSF albuminocytological dissociation increased from the first to second weeks in FS, anti-GQ1b IgG antibody peaked in the first week, but there was no CSF albuminocytological dissociation. Statistically, anti-GQ1b antibody testing was superior to a CSF examination in supporting a diagnosis of FS during the first 3 weeks of illness, especially in the first week.

Complicaciones neurológicas de la infección por el virus del dengue

Dengue is the most common of the arbovirosis that humans can suffer from. The frequency with which the central nervous system (CNS) is affected by this viral infection remains unknown, although isolated cases with neurological complications have been reported in Asia and South America. In Rio de Janeiro, Brazil, dengue virus infection has become an important public health concern. The authors describe two cases of immune-mediated CNS involvement following classic infection by the dengue virus: one involving post-infectious disseminated acute encephalitis and the other consisting of Guillain-Barré syndrome. In both cases dengue was diagnosed using the ELISA technique, and other viral aetiologies in the cerebrospinal fluid (CSF) were excluded. A 10-year-old female, following a bout of classic dengue, presented symptoms of a diminished level of consciousness, spastic tetraparesis, cerebellar syndrome and frontal symptoms. A resonance brain scan showed areas of hypersignal in T2 sequences in the cerebral peduncle, lentiform nuclei and internal capsule on both sides of the brain, which suggested post-infectious encephalitis. The second patient, a 14-year-old male, presented an areflexive flaccid ascending tetraparesis that suggested acute polyradiculoneuritis, following a bout of classic dengue. CSF albuminocytologic dissociation was also observed. This patient's electroneuromyogram recording showed a polyradiculoneuropathy of a primarily demyelinating nature with an associated axonal component. The immunological mechanisms involved in the pathophysiology of this type of neurological complications after suffering from dengue may be part of the physiological response to the viral infection.

Acute ophthalmoparesis (without ataxia) associated with anti-GQ1b IgG antibody: Clinical features

Objective To examine the clinical features of acute ophthalmoparesis (AO) (without ataxia) associated with anti-GQ1b immunoglobulin G (IgG) antibody. Design Retrospective observational case series. Participants Twenty-one subjects with AO (without ataxia) who had anti-GQ1b IgG. Methods Clinical features of 21 subjects with AO were analyzed. Results Seventeen had symptoms of antecedent infection. Gaze limitation was bilateral in 16 subjects and unilateral in five, indicative that laterality does not always negate AO. Nine subjects showed abducens paresis, and two limitation of abduction and adduction. Eight, who initially had bilateral abducens palsy, subsequently had impairment of adduction and vertical movement. These showed that bilateral abducens palsy followed by oculomotor nerve involvement is characteristic of AO. Muscle stretch reflexes were normal in nine subjects, hypoactive in eight, absent in three, and brisk in one. Distal paresthesias were present in seven subjects. Acellular cerebrospinal fluid (CSF) associated with raised protein concentration was detected in three. Conclusions Antecedent infectious symptoms, characteristic limitation of ocular movement, areflexia, distal paresthesias, and CSF albuminocytologic dissociation are useful markers for diagnosing AO as well as anti-GQ1b IgG. AO can be considered a mild form of Miller Fisher syndrome or a regional variant of Guillain-Barré syndrome.