Cranial nerve, spinal root and plexus hypertrophy in chronic inflammatory demyelinating polyneuropathy

Shah, Sachit; Chandrashekar, HS; Manji, Hadi; Davagnanam, Indran

doi:10.1136/practneurol-2011-000040

Cited by 11 publications

(14 citation statements)

References 3 publications

(4 reference statements)

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“…MR scanning of the brachial and lumbrosacral plexuses with gadolinium should be requested looking for evidence of nerve root or plexus hypertrophy or enhancement (figure 4). 41 Useful sequences are STIR and T1 weighted images, with and without gadolinium, but data continue to emerge on the specificity and sensitivity of MRI findings 42. In cases where there has been no significant deterioration over time either clinically or electrophysiologically, it is reasonable to consider sequencing of the GJB1 gene, or an alternative genetic diagnosis.…”

Section: Second-line Investigationsmentioning

confidence: 99%

CIDP: mimics and chameleons

2014

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Section: Second-line Investigationsmentioning

confidence: 99%

CIDP: mimics and chameleons

2014

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“…3 Additionally, hypertrophy of cranial nerves in CIDP patients has occasionally been described in case reports or case series; however, its precise frequency has not been determined. [4][5][6][7][8] Blink reflex testing, which measures the reflex time from stimulation of the afferent trigeminal supra-orbital nerve to generation of a compound muscle action potential (CMAP) of the orbicularis oculi muscle by the efferent facial motor branch, 9 is used to assess trigeminal and facial nerve function. Although blink reflex abnormalities in CIDP patients have been reported, [10][11][12] their frequencies vary, which reflect CIDP's etiological heterogeneity.…”

Section: Introductionmentioning

confidence: 99%

Optic, trigeminal, and facial neuropathy related to anti‐neurofascin 155 antibody

Ogata

Inamizu

et al. 2020

Ann Clin Transl Neurol

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Objective: To characterize the frequency and patterns of optic, trigeminal, and facial nerve involvement by neuroimaging and electrophysiology in IgG4 antineurofascin 155 antibody-positive (NF155 +) chronic inflammatory demyelinating polyneuropathy (CIDP). Methods: Thirteen IgG4 NF155 + CIDP patients with mean onset age of 34 years (11 men) were subjected to neurological examination, blink reflex, and visual-evoked potential (VEP) testing, and axial and/ or coronal T2-weighted head magnetic resonance imaging (MRI). Results: Among 13 patients, facial sensory impairment, facial weakness, and apparent visual impairment were observed in three (23.1%), two (15.4%), and two (15.4%) patients, respectively. All 12 patients tested had blink reflex abnormalities: absent and/or delayed R1 in 11 (91.7%), and absent and/or delayed R2 in 10 (83.3%). R1 latencies had strong positive correlations with serum anti-NF155 antibody levels (r = 0.9, P ≤ 0.0001 on both sides) and distal and F wave latencies of the median and ulnar nerves. Absent and/or prolonged VEPs were observed in 10/13 (76.9%) patients and 17/26 (65.4%) eyes. On MRI, hypertrophy, and high signal intensity of trigeminal nerves were detected in 9/ 13 (69.2%) and 10/13 (76.9%) patients, respectively, whereas optic nerves were normal in all patients. The intra-orbital trigeminal nerve width on coronal sections showed a significant positive correlation with disease duration. Interpretation: Subclinical demyelination frequently occurs in the optic, trigeminal, and facial nerves in IgG4 NF155 + CIDP, suggesting that both central and peripheral myelin structures of the cranial nerves are involved in this condition, whereas nerve hypertrophy only develops in myelinated peripheral nerve fibers.

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“…Additional studies have looked at the role of lumbosacral root and sciatic nerve imaging to assess disease severity and progression, as well as to support a diagnosis of a postinfectious radiculoneuropathy found in patients with AIDP and chronic inflammatory demyelinating radicluoneuropathy [91][92][93][94][95] . Though a limited resource, neuroimaging is becoming more available in many parts of Africa and may become a more viable resource for the future.…”

Section: Neuroimagingmentioning

confidence: 99%

Diagnosis and Management of Pediatric Peripheral Neuropathies In Resource-Poor Settings

Wilmshurst

2013

Future Neurol.

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The diagnosis of a peripheral neuropathy in a child who resides in the majority of resource-poor settings is based on the history taken and the clinical examination. The majority of children, unless they demonstrate additional clinical markers, will lack a more definitive diagnosis beyond the label ‘peripheral neuropathy’. The treatable, typically acquired conditions, which are prevalent in these settings, are the priority to identify. This would include neuroinfections, neuroinflammation, toxins and vitamin deficiencies. The management of children with peripheral neuropathies in resource-poor settings must be approached in a different manner to that of more ‘resource-equipped’ settings. Secondary or tertiary centers are scarce, often significant distances away from the patient, and this leads to long delays before access is possible. Most children present to primary healthcare settings and are seen by practitioners with little training in the features suggestive of a peripheral neuropathy. As such, basic aids to assist the healthcare worker in the early recognition and interventions of a child with a peripheral neuropathy are important. In addition, there must be recognition of the child with a rapidly progressive neuropathy where a life-threatening condition is present, and urgent referral to a tertiary setting made wherever possible.

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Cranial nerve, spinal root and plexus hypertrophy in chronic inflammatory demyelinating polyneuropathy

Cited by 11 publications

References 3 publications

CIDP: mimics and chameleons

CIDP: mimics and chameleons

Optic, trigeminal, and facial neuropathy related to anti‐neurofascin 155 antibody

Diagnosis and Management of Pediatric Peripheral Neuropathies In Resource-Poor Settings

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