Pure sensory Guillain-Barre syndrome.

Miralles, Francesc; Montero, José Segundo Niño; Rizzoli, René; Matos, J.A.

doi:10.1136/jnnp.55.5.411-a

Cited by 27 publications

(27 citation statements)

References 11 publications

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“…In others, evidence of demyelination was confined to the terminal latencies, as observed in previously reported cases. [9][10][11] This is understandable, given the nature of the clinical presentation of sensory GBS. The difficulty in demonstrating demyelination in sensory nerve conduction is due to the technical limitation of sensory NCS performed with surface electrodes.…”

Section: (M In 2; All In 6)mentioning

confidence: 99%

“…9 The patient developed sensory ataxia with areflexia and proprioception loss over 2 to 3 days following a viral illness, high CSF protein, absent sensory SNAP but demyelinating value of terminal latency, and a 39% decrease in the CMAP on proximal stimulation of the median nerve. The patient had a complete recovery in 1 month.…”

mentioning

confidence: 98%

“…This case clearly meets the strict diagnostic criteria of the sensory variant of GBS as outlined above. 9 In 1996, two cases of acute sensory neuropathy with prolonged terminal latency in the demyelinating range and good recovery in a few months were reported. CSF protein was not examined in these cases.…”

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confidence: 99%

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Sensory Guillain–Barré syndrome

LaGanke²,

Claussen³

2001

Neurology

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Article abstract-Objective: To report eight cases of sensory Guillain-Barré syndrome (GBS). Background: The concept of sensory equivalent to ascending paralysis of GBS was raised in 1958, and the diagnostic criteria for a sensory loss and areflexia variant of GBS were proposed in 1981. However, clinical cases meeting these criteria have been relatively scarce. Methods: During a 13-year period between 1986 and 1999, the authors collected eight cases of an acute sensory demyelinating neuropathy that met most of the proposed diagnostic criteria of a sensory variant of GBS. Results: In all patients, sensory neuropathy was sudden at onset and peaked to maximal deficit within 4 weeks. In five (63%) cases, there was an antecedent viral illness. All patients had objective sensory loss and diminished or absent reflexes. None showed any muscle weakness. In all four patients in whom the spinal fluid was examined during the first 4 weeks, there was albuminocytologic dissociation. All of the patients had electrophysiologic evidence of demyelination in at least two nerves. Demyelination was demonstrated in motor nerve conduction in seven patients and in sensory nerve conduction in one, indicating that motor nerve conduction studies were the key for the diagnosis of demyelinating neuropathy. All patients had sensory nerve conduction abnormalities in at least one nerve. Three patients responded to immunotherapies. All had a favorable outcome, with a monophasic course of disease and no sign of relapse. Conclusion: The current study confirms the existence of sensory GBS.

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Section: (M In 2; All In 6)mentioning

confidence: 99%

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confidence: 98%

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Sensory Guillain–Barré syndrome

LaGanke²,

Claussen³

2001

Neurology

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“…The sensory variant of Guillain–Barré syndrome , which solely involves the large sensory fibres, is rare but can also present as acute sensory ataxia 8. The clinical findings include sensory ataxia, impaired joint position and vibration sense and areflexia, but usually normal strength.…”

Section: Role Of Neurophysiologymentioning

confidence: 99%

“…The clinical findings include sensory ataxia, impaired joint position and vibration sense and areflexia, but usually normal strength. Serum antibodies to GD1b and GQ1b gangliosides may be positive 8. Nerve conduction in both conditions may show demyelinating polyradiculoneuropathy, although in Miller Fisher syndrome they are often either normal or show small SNAPs 7 8.…”

Section: Role Of Neurophysiologymentioning

confidence: 99%

Clinical assessment of the sensory ataxias; diagnostic algorithm with illustrative cases

et al. 2014

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Ataxia is a common neurological syndrome resulting from cerebellar, vestibular or sensory disorders. The recognition and characterisation of sensory ataxia remains a challenge. Cerebellar ataxia is the more common and easier to identify; sensory ataxia is often mistaken for cerebellar ataxia, leading to diagnostic errors and delays. A coherent aetiological work-up is only possible if clinicians initially recognise sensory ataxia. We discuss ways to separate sensory from cerebellar ataxia, the causes of sensory ataxia and the clinico-neurophysiological syndromes causing the sensory ataxia syndromes. We summarise a logical tiered approach as a diagnostic algorithm.

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Acquired demyelinating polyneuropathy presenting as a pure clinical sensory syndrome

Simmons

Tivakaran

1996

Muscle Nerve

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Pure sensory Guillain-Barre syndrome.

Cited by 27 publications

References 11 publications

Sensory Guillain–Barré syndrome

Sensory Guillain–Barré syndrome

Clinical assessment of the sensory ataxias; diagnostic algorithm with illustrative cases

Acquired demyelinating polyneuropathy presenting as a pure clinical sensory syndrome

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