Polyneuropathy

2011 ◽  
Author(s):  
Michael Donaghy
Keyword(s):  
Conduction Block ◽  
Distal Limb ◽  
Nerve Roots ◽  
Demyelinating Neuropathies ◽  
Temperature Sensations ◽  
Acquired Demyelinating Neuropathies ◽  
Cardinal Sign ◽  
Distal Limb Muscle ◽  
Tendon Reflexes ◽  
Nerve Root Involvement

Typically polyneuropathy will cause the combination of distal limb muscle weakness, loss of tendon reflexes, and reduced distal limb sensation. There is variable involvement of the autonomic innervation, damage to which causes a dry, vasodilated foot or hand. Loss of tendon reflexes is a cardinal sign of polyneuropathy, often restricted to the ankle jerks in axonal degeneration, but involving more proximal reflexes in acquired demyelinating neuropathies which may involve more proximal segments or the nerve roots. Clinical features suggestive of demyelinating or conduction block polyneuropathy include: a relative lack of muscle wasting in relation to the degree of weakness because no denervation has occurred; weakness of proximal muscles as well as distal, because of nerve root involvement; and disproportionate loss of joint position and vibration sensations compared to relative preservation of pain and temperature sensations which are carried by unmyelinated fibres.

scholarly journals Surgical placement of rectus sheath catheters in a cadaveric cystectomy model

2018 ◽  
Vol 100 (2) ◽  
pp. 120-124 ◽  
Author(s):  
ECP Chedgy ◽  
G Lowe ◽  
R Tang ◽  
C Krebs ◽  
A Sawka ◽  
...  
Keyword(s):  
Abdominal Surgery ◽  
Surface Area ◽  
Nerve Root ◽  
Rectus Sheath ◽  
Rectus Muscle ◽  
Midline Incision ◽  
Nerve Roots ◽  
The Mean ◽  
Peritoneal Spread ◽  
Nerve Root Involvement

Introduction Surgically inserted rectus sheath catheters (RSCs) are used increasingly for analgesia after cystectomy and other abdominal surgery. Currently, there is little information on the optimal positioning of RSCs to allow maximal spread of local anaesthetic. This study sought to assess the spread of dye injected via RSCs and to highlight the extent of its coverage in a fresh unembalmed cadaveric cystectomy model in order to confirm the nerve endings that are likely to be anaesthetised with RSCs. Methods Four cadavers underwent lower midline incision with limited bladder mobilisation. A RSC was inserted into the eight hemiabdomens. The RSCs were positioned either anterior (n=5) or posterior to the rectus muscle (n=3). Dye was injected down the RSCs to evaluate spread. The eight hemiabdomens were dissected anatomically to determine the surface area of dye spread and nerve root involvement. Results The mean surface area of dye spread with anteriorly placed RSCs was 30.6cm2 anterior and 25.9cm2 posterior to the rectus muscle. The mean surface area of dye spread with posteriorly placed RSCs was 11.3cm2 anterior and 37.3cm2 posterior to the rectus muscle. The mean number of nerve roots stained with anteriorly and posteriorly placed RSCs was 3.8 and 2.7 respectively. Subcutaneous spread of dye was seen with one anterior RSC insertion. Peritoneal spread was seen with one anteriorly positioned RSC. Conclusions This study has demonstrated efficient nerve root infiltration with anteriorly and posteriorly positioned RSCs. It appears that dye spreads between the fibres of the rectus muscle rather than out laterally to the nerve roots when spreading from its initial compartment.

scholarly journals Sphingomyelin as a myelin biomarker in CSF of acquired demyelinating neuropathies

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Giovanna Capodivento ◽  
Davide Visigalli ◽  
Martina Garnero ◽  
Roberto Fancellu ◽  
Michela Demetra Ferrara ◽  
...  
Keyword(s):  
Demyelinating Neuropathies ◽  
Acquired Demyelinating Neuropathies

scholarly journals Nodopathies of the peripheral nerve: an emerging concept

2015 ◽  
Vol 86 (11) ◽  
pp. 1186-1195 ◽  
Author(s):  
Antonino Uncini ◽  
Satoshi Kuwabara
Keyword(s):  
Peripheral Nerve ◽  
Axonal Degeneration ◽  
Conduction Block ◽  
Good Prognosis ◽  
Apparent Paradox ◽  
Nodal Region ◽  
Demyelinating Neuropathies ◽  
Temporal Dispersion ◽  
Peripheral Nerve Diseases ◽  
Nerve Conduction Block

Peripheral nerve diseases are traditionally classified as demyelinating or axonal. It has been recently proposed that microstructural changes restricted to the nodal/paranodal region may be the key to understanding the pathophysiology of antiganglioside antibody mediated neuropathies. We reviewed neuropathies with different aetiologies (dysimmune, inflammatory, ischaemic, nutritional, toxic) in which evidence from nerve conductions, excitability studies, pathology and animal models, indicate the involvement of the nodal region in the pathogenesis. For these neuropathies, the classification in demyelinating and axonal is inadequate or even misleading, we therefore propose a new category of nodopathy that has the following features: (1) it is characterised by a pathophysiological continuum from transitory nerve conduction block to axonal degeneration; (2) the conduction block may be due to paranodal myelin detachment, node lengthening, dysfunction or disruption of Na+channels, altered homeostasis of water and ions, or abnormal polarisation of the axolemma; (3) the conduction block may be promptly reversible without development of excessive temporal dispersion; (4) axonal degeneration, depending on the specific disorder and its severity, eventually follows the conduction block. The term nodopathy focuses to the site of primary nerve injury, avoids confusion with segmental demyelinating neuropathies and circumvents the apparent paradox that something axonal may be reversible and have a good prognosis.

51-year old man with tingling, burning and progressive limb weakness

2018 ◽  
Vol 18 (5) ◽  
pp. 382-388 ◽  
Author(s):  
Anu Gupta ◽  
Pappula Santhosh Kumar ◽  
Vinod Puri ◽  
Ravindra Kumar Saran ◽  
Poonam Narang ◽  
...  
Keyword(s):  
Peripheral Neuropathy ◽  
Axonal Degeneration ◽  
Correct Diagnosis ◽  
Common Reason ◽  
Demyelinating Neuropathy ◽  
Limb Weakness ◽  
Immune Mediated ◽  
Demyelinating Neuropathies ◽  
Acquired Demyelinating Neuropathies

Peripheral neuropathy is a common reason for referral to neurology. Chronic acquired demyelinating neuropathies are an important and varied group with overlapping presentations, and may have an immune-mediated cause. Their correct diagnosis is important as they respond to different treatments; timely intervention can prevent irreversible axonal degeneration. We present a case that highlights the approach to an adult presenting with a chronic demyelinating neuropathy.

scholarly journals Contactin-1 autoimmunity

2020 ◽  
Vol 7 (4) ◽  
pp. e771
Author(s):  
Divyanshu Dubey ◽  
Josephe A. Honorat ◽  
Shahar Shelly ◽  
Christopher J. Klein ◽  
Lars Komorowski ◽  
...  
Keyword(s):  
Neuropathic Pain ◽  
Conduction Block ◽  
Nerve Biopsy ◽  
Second Line ◽  
Demyelinating Neuropathies ◽  
Characteristic Features ◽  
Clinical Stabilization ◽  
Protein Assays ◽  
Electrophysiologic Studies

ObjectiveTo determine serologic characteristics, frequency, phenotype, paraneoplastic associations, and electrodiagnostic and histopathologic features accompanying contactin-1 autoimmunity.MethodsArchived sera known to produce synaptic tissue-based immunofluorescence patterns were reevaluated, and contactin-1 specificity was confirmed by recombinant protein assays. Screening of 233 chronic/relapsing demyelinating neuropathies for additional cases was performed.ResultsWe identified 10 contactin-1 IgG seropositive cases. Frequency of contactin-1 immunoglobulin (Ig) G among tested Mayo Clinic chronic/relapsing demyelinating neuropathies was 2%. Sensory predominant presentations (n = 9, 90%), neuropathic pain (n = 6, 60%), and subacute progression (n = 5, 50%) were commonly encountered among contactin-1 neuropathies. Two patients had chronic immune sensory polyradiculopathy-like phenotype at presentation. Electrodiagnostic studies were consistent with demyelination (slowed conduction velocities and/or prolonged distal latencies) without conduction block. Markedly elevated CSF protein (median 222 mg/dL, range 69–960 mg/dL), thickening/gadolinium enhancement of nerve roots (4/5), and subperineural edema on nerve biopsy (4/4) were other characteristic features. Three cases were diagnosed with paraneoplastic demyelinating neuropathies (thymoma, n = 1; breast cancer, n = 1; plasmacytoma, n = 1). Four of the 9 patients treated with IV immunoglobulin demonstrated initial clinical improvement, but the favorable response was sustained in only 1 case (median follow-up, 60 months). Sustained clinical stabilization or improvement was observed among 3 of the 6 cases in whom second-line therapies (rituximab, cyclophosphamide, and azathioprine) were used.ConclusionContactin-1 IgG has a distinct sensory predominant presentation commonly associated with neuropathic pain, with demyelinating changes on electrophysiologic studies. A paraneoplastic cause should be considered. Testing of contactin-1 IgG among cases with similar presentations may guide immunotherapy selection, especially second-line immunotherapy consideration.

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