Weakness in both lower limbs for 1 week and blepharoptosis for 3 days in a boy aged 1 year and 7 months. / ç”·æ€§å¹¼å„¿åŒä¸‹è‚¢æ— åŠ›1周伴眼睑下垂3 d.

A boy, aged 1 year and 7 months, was hospitalized due to weakness in both lower limbs and blepharoptosis, which showed progressive aggravation and developed into irregular breathing. Neurological examinations showed lethargy, blepharoptosis, grade 4 muscle strength of both upper limbs, grade 3 muscle strength of both lower limbs, and disappearance of tendon reflex. Laboratory tests revealed albuminocytological dissociation in cerebrospinal fluid, disappearance of H reflex, and positive serum anti-GD1b IgG. The boy was finally diagnosed with Guillain-Barré syndrome (GBS) overlapping with Miller-Fisher syndrome and Bickerstaff brainstem encephalitis. He recovered and was discharged after treatment including immunoglobulin, plasma exchange, and respiratory support. The GBS overlap syndromes in children have strong clinical heterogeneity due to the injury of both peripheral nerve and brainstem, among which anti-GD1b antibody-related GBS overlap syndromes have special clinical manifestations and complex neuroelectrophysiological changes and are thus difficult to diagnose. Nerve conduction velocity tests, especially H reflex test, should be performed for children with weakness in both lower limbs and blepharoptosis.

Transient Isolated Lower Bulbar Palsy With Elevated Serum Anti-GM1 and Anti-GD1b Antibodies During Aripiprazole Treatment.

BACKGROUND: Transient bulbar palsy without involvement of the facial or extraocular muscles is a rare presentation. It is considered a form of cranial polyneuropathy, a variant of Guillain-Barré syndrome that is related to the autoimmune mechanisms induced by preceding infections or vaccinations. However, drug-induced cranial polyneuropathy has not previously been reported. We describe a boy with isolated bulbar palsy and positive serum antiganglioside antibodies during aripiprazole treatment. PATIENT DESCRIPTION: This 12-year-old boy was admitted with a seven-day history of dysarthria, tongue discomfort, and tinnitus. Three weeks before symptom onset, aripiprazole was added to the patient's medications for attention-deficit hyperactivity disorder. On examination, he showed curtaining of the pharyngeal wall, tongue fasciculation and deviation, and a weak gag reflex. Cranial magnetic resonance imaging suggested lower cranial nerve involvement. Serum anti-GM1 IgG and anti-GD1b IgG antibodies were positive. After stopping aripiprazole, his bulbar symptoms improved. However, on readministration of aripiprazole seven weeks later, dysarthria recurred and again resolved after stopping the drug. CONCLUSION: We describe the first patient with anti-GM1 IgG and anti-GD1b IgG antibodies-associated transient cranial polyneuropathy presenting as isolated bulbar palsy. These findings could be an adverse effect of aripiprazole treatment.

A Case of Squamous Cell Lung Cancer Representing as Guillain-Barre Syndrome Associated with Monospecific Anti-GD1b IgG / 대한임상신경생리학회지

We report a case with squamous cell lung cancer with concomitant Guillain-Barre syndrome (GBS) as a paraneoplastic syndrome. A 67-year-old patient who was previously diagnosed as metastatic squamous cell lung cancer developed mild symmetrical weakness, paresthesia and sensory ataxia. Nerve conduction study showed sensorimotor polyneuropathy. Analysis of cerebrospinal fluid showed high tilter for monospecific anti-GD1b IgG antibody without onconeuronal antibodies. After treatment with intravenous immunoglobulin, the patient's symptoms improved.

Acute and chronic ataxic neuropathies with disialosyl antibodies: a continuous clinical spectrum and a common pathophysiological mechanism.

Acute ataxic neuropathies with disialosyl antibodies include Fisher syndrome, ataxic Guillain-Barré syndrome (GBS), and acute sensory ataxic neuropathy. Fisher syndrome and ataxic GBS are more strongly associated with IgG anti-GQ1b and anti-GT1a than with anti-GD1b antibodies, whereas the association is reversed in the case of acute sensory ataxic neuropathy. Chronic ataxic neuropathy with disialosyl antibodies is associated with IgM paraprotein to GD1b and GQ1b, which occasionally reacts with GT1a. The clinical, electrophysiological, and pathological features, along with experimental findings, suggest that acute and chronic ataxic neuropathies with disialosyl antibodies form a continuous clinical and pathophysiological spectrum characterized by a complement-mediated disruption at the nodal region and are better classified in the new category of nodo-paranodopathies.

Antibodies to the Antiganglioside GD1b in a Guillain-Barre Syndrome Patient with Bilateral Cerebellar Lesions

No abstract available.

Acute Sensory Neuropathy Associated with anti-GD1b Ig G Antibody

Acute sensory neuropathy (ASN) is rare and is characterized by acute onset of sensory ataxia, loss of deep tendon reflexes and impaired vibratory and joint position sensations. Similar to Guillain-Barre syndrome (GBS) with prominent sensory ataxia, a few cases of ASN associated with antiganglioside antibodies have been reported. This suggests that a common autoimmue mechanism operates in some cases of ASN and of GBS with sensory ataxia. We report a patient with ASN associated with anti-GD1b IgG antibody.