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Fulltext Opsoclonus

Amin OS, Shwani SS

BMJ Case Rep, 2017 Feb 15;2017.
PMID: 28202488 DOI: 10.1136/bcr-2017-219433
Matched MeSH terms: Gait Ataxia/complications*
Co-occurrence of acute ophthalmoplegia (without ataxia) and idiopathic intracranial hypertension

Yeak J, Zahari M, Singh S, Mohamad NF

Eur J Ophthalmol, 2019 Jul;29(4):NP1-NP4.
PMID: 30280587 DOI: 10.1177/1120672118803532

BACKGROUND: 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 cmH2O during lumbar puncture. We aim to report a rare case of acute ophthalmoplegia with co-occurrence of raised intracranial pressure.
CASE DESCRIPTION: 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 cmH2O. Anti-GQ1b IgG and anti-GT1a IgG antibody were tested positive.
CONCLUSION: 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.

Matched MeSH terms: Ataxia/complications
Polymyoclonus, laryngospasm, and cerebellar ataxia associated with adenocarcinoma and multiple neural cation channel autoantibodies

Lim SY, Mason WP, Young NP, Chen R, Bower JH, McKeon A, et al.

Arch. Neurol., 2009 Oct;66(10):1285-7.
PMID: 19822786 DOI: 10.1001/archneurol.2009.203

OBJECTIVE:
To describe and provide audiovisual documentation of a syndrome of polymyoclonus, laryngospasm, and cerebellar ataxia associated with adenocarcinoma and multiple neural cation channel autoantibodies.

DESIGN:
Case report with video.

SETTING:
University hospitals. Patient A 69-year-old woman presented with subacute onset of whole-body tremulousness and laryngospasm attributed to gastroesophageal reflux.

RESULTS:
Further evaluation revealed polymyoclonus, cerebellar ataxia, and laryngospasm suspicious of an underlying malignant neoplasm. Surface electromyography of multiple limb muscles confirmed the presence of polymyoclonus. The patient was seropositive for P/Q-type voltage-gated calcium channel antibody; subsequently, whole-body fluorine 18 fluorodeoxyglucose positron emission tomography and cervical lymph node biopsy revealed widespread metastatic adenocarcinoma. Follow-up serologic evaluation revealed calcium channel antibodies (P/Q type and N type) and potassium channel antibody.

CONCLUSIONS:
We highlight the importance of recognizing polymyoclonus. To our knowledge, this is also the first description of a syndrome of polymyoclonus, laryngospasm, and ataxia associated with adenocarcinoma and these cation channel antibodies.

Matched MeSH terms: Cerebellar Ataxia/complications*

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