gq1b-ganglioside and Acute-Disease

To delineate the clinical features and ocular motor findings in acute vestibular syndrome (AVS) associated with anti-GQ1b antibodies.. We reviewed 90 patients with positive serum anti-GQ1b antibody in association with various neurological syndromes at Seoul National University Bundang Hospital from 2004 to 2018. The diagnoses included typical Miller Fisher syndrome (n = 31), acute ophthalmoplegia without ataxia (n = 27), Guillain-Barre syndrome with ophthalmoplegia (n = 18), AVS (n = 11), and Bickerstaff brainstem encephalitis (n = 3). Of them, the 11 patients with AVS formed the basis of this study. We also conducted a systematic review on AVS reported in association with anti-GQ1b antibody.. Patients with AVS showed various ocular motor findings that included head-shaking nystagmus (n = 6), spontaneous nystagmus (n = 5), gaze-evoked nystagmus (n = 5), central positional nystagmus (n = 3), canal paresis (n = 2), and abnormal head-impulse tests (n = 1) without any internal or external ophthalmoplegia. Compared to those with other subtypes, patients with AVS mostly showed normal deep tendon reflexes (8 of 11 [73%],. Anti-GQ1b antibody may cause acute vestibulopathy by involving either the central or peripheral vestibular structures. AVS may constitute a subtype of anti-GQ1b antibody syndrome.

Topics: Acute Disease; Adolescent; Adult; Aged; Aged, 80 and over; Autoantibodies; Biomarkers; Child; Female; Follow-Up Studies; Gangliosides; Humans; Male; Middle Aged; Vestibular Diseases; Young Adult

Miller Fisher syndrome (MFS) is an acute polyradiculoneuritis regarded as an uncommon clinical variant of Guillain-Barré syndrome (GBS). MFS is characterized by the acute onset of the clinical triad of ophthalmoplegia, cereballar ataxia and areflexia. Atypical forms of MFS presenting as isolated ophthalmoplegia without ataxia have been rarely described, mostly in adults.. We present two cases of acute isolated bilateral ophthalmoplegia in childhood, both occurring shortly after Campylobacter jejuni enteritis. Serum analysis of anti-ganglioside antibodies revealed elevated levels of anti-GQ1b IgG and IgM. We observed in both children complete spontaneous resolution several weeks after onset.. The cases of the two patients confirm the rare but possible occurrence of atypical MFS in young children a few weeks after gastrointestinal infection. Identification of high levels of anti-GQ1b antibodies in the serum may help confirm the diagnosis of MFS even when its clinical presentation is incomplete.

Topics: Acute Disease; Antibodies; Campylobacter Infections; Campylobacter jejuni; Child; Child, Preschool; Gangliosides; Gastroenteritis; Humans; Male; Miller Fisher Syndrome; Ophthalmoplegia

Although acute inflammatory polyneuropathy (AIP) and immune thrombocytopenic purpura (ITP) are both believed to be immune-mediated disorders, only a few cases have been reported in which these two diseases co-existed. We describe a case of a 67-year-old patient who developed quadriparesis, ophthalmoplegia and severe sensory impairment along with thrombocytopenia. Detailed examinations, including the measurement of anti-ganglioside antibodies and anti-glycoprotein-IIb-IIIa-IgG-producing B-cells, revealed that he developed AIP and ITP. By reviewing past similar reports, we noticed that AIP associated with ITP tends to manifest severe sensory impairment and is often preceded by upper respiratory tract infection, but not by gastrointestinal infection.

Topics: Acute Disease; Aged; Autoantibodies; Gangliosides; Glucocorticoids; Guillain-Barre Syndrome; Humans; Immunoglobulins, Intravenous; Male; Pharyngitis; Platelet Count; Prednisone; Purpura, Thrombocytopenic, Idiopathic

Acute ophthalmoparesis without ataxia was designated as 'atypical Miller Fisher syndrome' as it presents with progressive, relatively symmetrical ophthalmoplegia, but without ataxia nor limb weakness, in the presence of anti-GQ1b antibody. Idiopathic intracranial hypertension is characterized by signs of raised intracranial pressure occurring in the absence of cerebral pathology, with normal composition of cerebrospinal fluid and a raised opening pressure of more than 20 cmH. A 28-year-old gentleman with body mass index of 34.3 was referred to us for management of double vision of 2 weeks duration. His symptom started after a brief episode of upper respiratory tract infection. His best corrected visual acuity was 6/6 OU. He had bilateral sixth nerve palsy worse on the left eye and bilateral hypometric saccade. His deep tendon reflexes were found to be hyporeflexic in all four limbs. No sensory or motor power deficit was detected, and his gait was normal. Plantar reflexes were downwards bilaterally and cerebellar examination was normal. Both optic discs developed hyperaemia and swelling. Magnetic resonance imaging of brain was normal and lumbar puncture revealed an opening pressure of 50 cmH. Acute ophthalmoparesis without ataxia can present with co-occurrence of raised intracranial pressure. It is important to have a full fundoscopic assessment to look for papilloedema in patients presenting with Miller Fisher syndrome or acute ophthalmoparesis without ataxia.

Topics: Abducens Nerve Diseases; Acetazolamide; Acute Disease; Administration, Oral; Adult; Ataxia; Autoantibodies; Diplopia; Diuretics; Gangliosides; Humans; Immunoglobulin G; Magnetic Resonance Imaging; Male; Ophthalmoplegia; Ophthalmoscopy; Pseudotumor Cerebri

A 61-year-old man developed double vision subsequent to diarrheal illness. Mixed horizontal-vertical gaze palsy in both eyes, diminution of tendon reflexes, and gaze nystagmus were noted. His horizontal gaze palsy was accompanied by gaze nystagmus in the abducent direction, indicative of the disturbance in central nervous system. Neither limb weakness nor ataxia was noted. Serum anti-GQ1b antibody was detected. Brain magnetic resonance imaging (MRI) findings were normal. The patient was diagnosed as having acute ophthalmoparesis. The ophthalmoparesis and nystagmus gradually disappeared in 3 months. The accompanying nystagmus suggests that central nervous system disturbance may also be present with acute ophthalmoparesis.

Topics: Acute Disease; Biomarkers; Gangliosides; Humans; Immunoglobulin G; Male; Middle Aged; Miller Fisher Syndrome; Nystagmus, Pathologic; Ophthalmoplegia

Ophthalmoplegia without ataxia, areflexia or both has been designated as atypical Miller Fisher syndrome (MFS) or acute ophthalmoplegia (AO). This entity, first reported by Chiba et al. is associated with anti-GQ1b IgG antibodies.We report a patient with isolated acute ophthalmoplegia with high titer of anti-GQ1b IgG antibody activity in the acute phase in whom treatment with intravenous immunoglobulin (IVIg) led to the clinical recovery and the decrease in antibody titer.

Topics: Acute Disease; Adult; Blepharoptosis; Diplopia; Enzyme-Linked Immunosorbent Assay; Female; Gangliosides; Humans; Immunoglobulin G; Immunoglobulins, Intravenous; Miller Fisher Syndrome; Neural Conduction; Neurologic Examination

Antiganglioside antibodies are found in various neurological disorders that constitute a continuum from peripheral neuropathy to encephalitis. However, nystagmus has rarely been described in patients with ataxia associated with antiganglioside antibodies.. From January 2008 to July 2009, we identified 3 patients with acute ataxia and nystagmus in 2 University Hospitals of Korea, who were found to have anti-GD1b, anti-GM1, or anti-GQ1b antibodies.. In addition to acute ataxia, all 3 patients showed various combinations of nystagmus, which included central positional nystagmus (n = 3), vertical nystagmus (n = 1), and periodic alternating nystagmus (n = 1). The spontaneous and positional nystagmus were mostly detectable only with the elimination of fixation and magnification of the eyes using video goggles. Two patients also exhibited gaze-evoked nystagmus that was noticeable without the aid of video goggles. Patients had serum IgG antibodies to GD1b, GM1, or GQ1b. Cerebrospinal fluid examination, nerve conduction studies, and brain MRI were normal. In all patients, the symptoms and signs resolved over 3-12 months.. Various forms of nystagmus with acute ataxia may be a sole or predominant manifestation of disorders related to antiganglioside antibodies. The nystagmus indicates a central pathology involving the cerebellum or brainstem in this antibody-associated disorder. Antiganglioside antibodies should be measured in patients with nystagmus and acute ataxia of undetermined etiology.

Topics: Acute Disease; Adolescent; Adult; Ataxia; Autoantibodies; Autoantigens; Autoimmune Diseases; Cerebrospinal Fluid; Dizziness; Enzyme-Linked Immunosorbent Assay; Female; G(M1) Ganglioside; Gangliosides; Humans; Immunoglobulin G; Male; Nystagmus, Pathologic; Postural Balance; Sensation Disorders; Vertigo

Topics: Acute Disease; Adult; Autoantibodies; Autonomic Nervous System Diseases; Blepharoptosis; Bradycardia; Cranial Nerve Diseases; Cranial Nerves; Diplopia; Disease Progression; Early Diagnosis; Gangliosides; Humans; Immunoglobulins, Intravenous; Male; Miller Fisher Syndrome; Oculomotor Nerve Diseases; Ophthalmoplegia; Respiratory Tract Infections; Treatment Outcome; Vagus Nerve Diseases; Virus Diseases

Anti-GQ1b IgG antibody syndrome comprises a wide range of diseases presenting with ophthalmoplegia and ataxia. Anti-GQ1b antibodies have been strongly associated in the literature with Miller Fisher Syndrome, with acute ophthalmoplegia associated with Guillain-Barré syndrome, and with isolated ophthalmoplegia. Acute ophthalmoplegia presents as various combinations of external and internal ophthalmoplegia. Reported here is a novel case of isolated ptosis as a manifestation of ophthalmoplegia. The present finding of bilateral ptosis and areflexia with anti-GQ1b IgG antibody positivity helps confirm the existence of the syndrome. Further research is needed on diagnosis and treatment.

Topics: Acute Disease; Ataxia; Autoantibodies; Autoimmune Diseases of the Nervous System; Blepharoptosis; Child, Preschool; Gangliosides; Humans; Immunoglobulin G; Immunoglobulins, Intravenous; Immunologic Factors; Male; Ophthalmoplegia; Reflex; Syndrome; Treatment Outcome

Anti-GQ1b antibody has been found in Miller Fisher syndrome (MFS), Guillain-Barré syndrome (GBS) with ophthalmoplegia, Bickerstaff brainstem encephalitis (BBE), and acute ophthalmoplegia without ataxia (AO). The aim of this study was to determine the clinical features of AO associated with anti-GQ1b antibody.. We retrospectively collected 34 patients with anti-GQ1b antibody syndrome. Of these patients, 31 patients had ophthalmoplegia. The patients with ophthalmoplegia were classified into MFS (n = 13), AO (n = 11), GBS with ophthalmoplegia (n = 6), and BBE (n = 1). We analyzed clinical features and patterns of external and internal ophthalmoplegia of AO, and neuro-ophthalmologic findings were compared with those of other anti-GQ1b syndromes with ophthalmoplegia.. AO was observed in 11 (32.4%) of the 34 patients with anti-GQ1b antibody. External ophthalmoparesis was present in all the patients and included mixed horizontal-vertical (n = 7), pure horizontal (n = 3), and pure vertical gaze palsy (n = 1). Binocular involvement was common, but unilateral ophthalmoparesis was also observed in 27.3%. Other findings included ptosis (n = 5, 45.5%) and internal ophthalmoplegia (n = 6, 54.5%). Other anti-GQ1b antibody syndromes had prominent neurologic signs including ataxia, weakness, and facial palsy in addition to ophthalmoplegia. The patterns of neuro-ophthalmologic findings did not differ between AO and other anti-GQ1b antibody syndromes with ophthalmoplegia.. Acute ophthalmoplegia (AO) commonly occurs in anti-GQ1b antibody syndrome and manifests as various combinations of external and internal ophthalmoplegia. Internal ophthalmoplegia is fairly common and unilateral involvement may occur in AO.

Topics: Acute Disease; Adolescent; Aged; Autoantibodies; Female; Gangliosides; Humans; Male; Middle Aged; Ophthalmoplegia; Retrospective Studies; Syndrome

Miller Fisher syndrome (MFS) is a rare and usually monophasic polyradiculoneuropathy characterised by ophthalmoplegia, decreased or absent tendon reflexes, and ataxia. The objective of this study was to report a case of recurrent MFS with a clinical presentation virtually indistinguishable from botulism. The patient was a young man with two episodes of increasing external ophthalmoplegia, ptosis, and ataxia with a long asymptomatic interval in between. The second episode occurred after consumption of rotten fish and was accompanied by gastrointestinal symptoms and an anticholinergic syndrome. Very rarely, MFS can present with a recurrent course. The importance of this case of recurrent MFS lies not only in its long asymptomatic period and identical clinical presentation, but also in its instructiveness regarding the differential diagnosis of MFS, particularly life-threatening botulism.

Topics: Acute Disease; Adult; Autoantibodies; Botulism; Diagnosis, Differential; Diplopia; Gangliosides; Humans; Male; Miller Fisher Syndrome; Recurrence

A patient with acute oropharyngeal palsy associated with internal ophthalmoplegia was reported. A 13-year-old boy had fever and diarrhea for two days. Ten days after resolution of these symptoms, he noticed difficulty in speaking (day 1). Neurological findings on day 4 included bilateral mydriasis, right abducens nerve palsy, nasal voice with absent pharyngeal reflex. Although superficial sensation was preserved, vibratory sensation was reduced in distal limbs. Tendon reflexes were generally absent. Neither ataxia nor dysautonomia was seen. Serum anti-glycolipid antibody assay on day 4 disclosed elevated IgG antibodies to GQ1b and GT1a. His cerebrospinal fluid on day 21 contained 6 mononuclear cells/microl with 137 mg/dl of total protein. Nerve conduction study on day 5 showed minimal sensory nerve involvement. Quantitative sudomotor axon reflex test was normal in the lower extremities. Low dose pilocarpine eyedrops dilated his pupils. Although mild cerebellar-like ataxia appeared on day 5, intravenous immunoglobulin (0.4 g/kg/day for four days) rapidly improved his neurological abnormalities. IgG anti-GQ1b antibody might contribute not only oropharyngeal weakness but also internal ophthalmoplegia in this patient.

Topics: Acute Disease; Adolescent; Autoantibodies; Gangliosides; Humans; Immunoglobulin G; Male; Miller Fisher Syndrome; Ophthalmoplegia; Oropharynx; Paralysis

To prospectively study anti-GQ1b antibody positive cases of acute ophthalmoparesis (AO) clinically and electrophysiologically.. Nine consecutive cases presenting with predominantly acute ophthalmoplegia were assessed clinically and had stimulated single fibre electromyography (SFEMG) of the orbicularis oculi at presentation. All had magnetic resonance imaging brain scans and anti-GQ1b antibody titres determined.. Four cases had elevated anti-GQ1b antibody titres and abnormal SFEMG studies, which improved in tandem with clinical recovery over three months. Five other anti-GQ1b antibody negative cases were diagnosed as diabetic related cranial neuropathy, idiopathic cranial neuropathy, ocular myasthenia gravis, and Tolosa-Hunt syndrome. All five cases showed complete recovery over a three month period.. This study demonstrated electrophysiologically the dynamic improvement of neuromuscular transmission of anti-GQ1b antibody positive cases of AO, in tandem with clinical recovery. SFEMG is of value in differentiating weakness due to neuromuscular transmission defect from neuropathy in these clinical situations.

Topics: Acute Disease; Autoantibodies; Autoimmune Diseases; Electromyography; Electrophysiology; Gangliosides; Humans; Male; Middle Aged; Ophthalmoplegia; Prospective Studies

Topics: Abducens Nerve Diseases; Acute Disease; Child; Female; Gangliosides; Humans; Immunoglobulin G; Ophthalmoplegia; Recovery of Function

Recent years have seen major progress in our understanding of the clinical pathophysiology of autoimmune neuropathies particularly with the identification and analysis of antibodies to gangliosides and related glycolipids in the serum of patients. Anti-glycolipid antibodies react with epitopes on the carbohydrate region of glycolipid molecules and can be routinely measured by standard immunoassays. In multifocal motor neuropathy, IgM anti-GM1 antibodies that cross react with GD1b and asialo-GM1 are detectable in around 50p. 100 of cases. This condition may clinically resemble certain forms of lower motor neurone disease. IgM anti-GD1b antibodies are found in IgM paraproteinaemic neuropathy characterised by profound sensory ataxia. In the anti-myelin associated glycoprotein (anti-MAG) IgM paraproteinaemic neuropathy, antibodies also react with the acidic glycolipids, sulphated glucuronyl paragloboside and its higher lactosaminyl homologue (SGPG and SGPLG). Thus a variety of chronic syndromes can be defined by their anti-glycolipid antibody profile. In Guillain-Barré syndrome, anti GM1, GM1b, GD1a and GalNAc-GD1a antibodies are found in patients with acute motor axonal neuropathy (AMAN) and anti-GQ1b IgG antibodies are a very sensitive and specific marker for the Miller Fisher syndrome. Many other anti-glycolipid antibodies are being increasingly identified in other neuropathy subtypes. The article will summarise existing clinical and serological information in this field.

Topics: Acute Disease; Antibodies; Autoimmune Diseases of the Nervous System; beta-Galactosidase; Chronic Disease; Gangliosides; Globosides; Humans

To examine the clinical features of acute ophthalmoparesis (AO) (without ataxia) associated with anti-GQ1b immunoglobulin G (IgG) antibody.. Retrospective observational case series.. Twenty-one subjects with AO (without ataxia) who had anti-GQ1b IgG.. Clinical features of 21 subjects with AO were analyzed.. 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.. 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.

Topics: Abducens Nerve Diseases; Acute Disease; Adolescent; Adult; Aged; Autoantibodies; Autoimmune Diseases; Campylobacter Infections; Campylobacter jejuni; Child; Diplopia; Female; Gangliosides; Gastrointestinal Diseases; Humans; Immunoglobulin G; Male; Middle Aged; Miller Fisher Syndrome; Ophthalmoplegia; Paresthesia; Retrospective Studies

Miller-Fisher syndrome (MFS) is characterized by variable ophthalmoplegia, ataxia, and tendon areflexia. It seems to be a variant of Guillain-Barré syndrome (GBS), but unlike in GBS, there is a primitive involvement of the ocular motor nerves, and in some cases there is brainstem or cerebellum direct damage. The unusual case of MFS in the current study started with a bilateral areflexical mydriasis and a slight failure of accommodative-convergence. Ocular-movement abnormalities developed progressively with a palsy of the upward gaze and a bilateral internuclear ophthalmoplegia to a complete ophthalmoplegia. In the serum of this patient, high titers of an IgG anti-GQ1b ganglioside and IgG anti-cerebellum. anti-Purkinje cells in particular, were found. The former autoantibody has been connected to cases of MFS, of GBS with associated ophthalmoplegia, and with other acute ocular nerve palsies. The anti-cerebellum autoantibody could explain central nervous system involvement in MFS. The role of these findings and clinical implications in MFS and in other neuro-ophthalmologic diseases are discussed.

Topics: Accommodation, Ocular; Acute Disease; Autoantibodies; Cerebellum; Child; Convergence, Ocular; Dexamethasone; Gangliosides; Humans; Immunoglobulin G; Immunoglobulins, Intravenous; Male; Miller Fisher Syndrome; Mydriasis; Ophthalmoplegia; Plasmapheresis; Purkinje Cells

IgG anti-GQ1b antibody was present in a patient with acute ataxia and areflexia without ophthalmoplegia or elementary sensory loss. Sensory nerve conduction studies and somatosensory evoked potentials were normal, but postural body sway analysis showed dysfunction of the proprioceptive afferent system. The clinical presentation and laboratory results for this patient resemble those of Miller Fisher syndrome, except for the lack of ophthalmoplegia. This case may represent part of an IgG anti-GQ1b syndrome.

Topics: Acute Disease; Adult; Antibodies, Antiphospholipid; Ataxia; Diagnosis, Differential; Evoked Potentials, Somatosensory; Gangliosides; Humans; Immunoglobulin G; Male; Miller Fisher Syndrome; Neural Conduction

Topics: Acute Disease; Aged; Demyelinating Diseases; Female; Gangliosides; Humans; Immunoglobulin G; Nerve Growth Factors; Ophthalmoplegia; Peroneal Nerve; Polyradiculoneuropathy; Tibial Nerve

Topics: Abducens Nerve; Acute Disease; Antibody Specificity; Autoantibodies; Child; Female; Gangliosides; Humans; Immunoglobulin G; Ophthalmoplegia; Pharyngitis; Streptococcal Infections; Streptococcus pyogenes

There have been several case reports of acute ophthalmoparesis without ataxia subsequent to infection or immunization. The nosological position and therapy for acute ophthalmoparesis have yet to be established. Sera from patients are reported to have IgG anti-GQ1b antibody, which is frequently found in sera from patients with Fisher's syndrome. To establish the etiology of acute ophthalmoparesis, I tested sera from 8 patients with acute ophthalmoparesis for anti-GQ1b antibody. High IgG anti-GQ1b antibody titers were present in sera from patients in the acute phase of the illness. I describe the successful treatment with plasmapheresis and intravenous immunoglobulin. Some cases of acute ophthalmoparesis following infection or immunization may be categorized as an auto-immune disease related to Fisher's syndrome.

Topics: Acute Disease; Adult; Antibodies, Anti-Idiotypic; Brain Stem; Encephalitis; Female; Gangliosides; Humans; Immunoglobulin G; Immunoglobulins, Intravenous; Middle Aged; Nerve Growth Factors; Ophthalmoplegia; Plasmapheresis

A 43-year-old male with 2 episodes of sensory impairments in four extremities and liver dysfunction, developed an acute exacerbation of both sensory impairments and liver dysfunction after administration of interferon-alpha. On admission, neurological examination revealed a mild distal weakness of four extremities, moderate impairment of superficial sensation in hands and severe impairment of deep sensation and areflexia in all extremities. Routine laboratory tests were normal except for a mild liver dysfunction. His serum was positive for antinuclear antibody, but negative for anti-DNA antibody and LE-test. Since he was seropositive for hepatitis B (HB) c antibody but seronegative for HBs antigen and antibody, HBe antigen and antibody, he was considered to be a seroconverted carrier of HB virus. Liver biopsy revealed chronic active hepatitis with marked lymphocytic infiltration. CSF examinations were within normal limits. Sensory conduction studies of median and sural nerves showed no response, but motor conduction studies of median and peroneal nerves were within normal limits. Light and electron microscopic examination of biopsied sural nerve disclosed a moderate decrease in large myelinated fibers, but not in either small myelinated or unmyelinated fibers. Thin-layer chromatography with immunostaining showed the presence of anti-GQ1b antibody in his serum. The anti-GQ1b antibody did not react with GT1a. Oral administration of prednisolone alleviated liver dysfunction, muscle weakness and superficial sensory impairment of four extremities, but not in deep sensation.

Topics: Acute Disease; Adult; Autoantibodies; Autoimmune Diseases; Gangliosides; Hepatitis; Humans; Male; Polyneuropathies; Recurrence; Sensation Disorders

We report a patient with a relapsing form of the acute sensory neuropathy syndrome associated with IgM-kappa type monoclonal gammopathy of undetermined significance. He rapidly developed marked sensory ataxia without weakness following an upper respiratory tract infection at age 44. The symptoms reached their maximum in a few days, followed by subsequent gradual improvement over a few weeks. However, unsteady gait remained as a chronic deficit. Stepwise progression of his symptoms occurred over 15 years with 10 similar relapses. Sensory nerve conduction studies showed the absence of action potentials, and sural nerve biopsy revealed the marked loss of large myelinated fibers. The patient's serum had an extremely high titer of an IgM monoclonal antibody directed against gangliosides GD2, GD1b, GT1b, and GQ1b.

Topics: Acute Disease; Adult; Carbohydrate Sequence; Gangliosides; Humans; Immunoglobulin M; Male; Molecular Sequence Data; Nervous System Diseases; Recurrence; Sensation