CIDPUSA.org Autoimmune diseases
Investigation in peripheral Neuropathy
Investigation
of peripheral neuropathy
Urine--Bence-Jones protein
Biochemistry--Oral glucose tolerance test
Cerebrospinal fluid--Cells, protein, immunoglobulin
oligoclonal bands
Immunology--Anti-HIV antibodies, antineuronal antibodies
(Hu, Yo), antigliadin antibodies, serum angiotensin
converting enzyme, antiganglioside antibodies,
antimyelin associated glycoprotein antibodies
Tests for Sjogren's syndrome--Salivary flow rate,
Schirmer's test, Rose Bengal test, labial gland biopsy
Search for carcinoma, lymphoma, or solitary
myeloma --Skeletal survey, pelvic ultrasonography,
abdominal and chest computed tomography, mammography, or
positron emission tomography
Molecular genetic tests--Peripheral nerve myelin protein
22 gene duplication (the commonest cause of
Charcot-Marie-Tooth disease type 1) or deletion
(hereditary neuropathy with liability to pressure
palsies), connexin 32 mutation (X linked
Charcot-Marie-Tooth disease), PO gene mutation (another
cause of Charcot-Marie-Tooth disease type 1), etc
Chronic axonal neuropathy occurs in patients with many
multisystem hereditary disorders. The diagnosis of these
conditions is usually suggested by the other
neurological and systemic features. Isolated cases of
hereditary neuropathy such as the axonal form of
Charcot-Marie-Tooth disease (type 2) can, however, be
difficult to diagnose. In this disease the symptoms
usually begin in childhood and are associated with pes
cavus and claw toes but may not come to attention until
middle or old age. The family history may not be evident
without examination of the apparently unaffected
relatives. The condition is clinically and genetically
heterogeneous, and several gene loci are involved.
Molecular genetic tests are available for only a tiny
proportion of patients.
Treatment
Any underlying medical cause of peripheral neuropathy,
such as diabetes mellitus or vitamin B-12 deficiency,
should be treated. Chronic inflammatory demyelinating
polyradiculoneuropathy is important to recognise because
it i, plasma exchange, and some
Management
Preventive and palliative treatments include foot care,
weight reduction, and sensible shoes, boots, or
ankle-foot orthoses. Patients with severe leg weakness
may need sticks, crutches, or a walking frame.
Physiotherapists are best placed to prescribe these
aids, which may need to be adapted to take account of
weakness of the hands. Simple wrist splints can help
weak wrist extension. More complex splints for weak
fingers and hands are usually cumbersome and rarely
used. Disabled patients require help from a
multidisciplinary team including an occupational
therapist, who can advise on special utensils and home
adaptations. Some drugs help. Sildenafil may correct
erectile impotence. In the United Kingdom, the NHS will
pay if the neuropathy is due to diabetes mellitus.
Patients with neuropathy may experience pain, which can
be severe and out of proportion to any sensory or motor
deficit. Painful neuropathy is difficult to treat. The
most useful drugs are anticonvulsants, especially
gabapentin and carbamazepine, and tricyclic
antidepressants, especially amitriptyline. The opioid-like
analgesic tramadol has also been shown to be useful in
randomised controlled trials.
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neuropathy
Links:
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B-12 deficiency
- Small Fiber neuropathy
- neurological effects of CIDP
- Nerve Fiber types
- CIDP-EMG
- Multi Focal Motor neuropathy
- M.M.F.
- Lewis Summer
- Tips for CIDP
- Axonal EMG
- CIDP-EMG
- Plasmapheresis
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- CIDP-GBS-Handbook
- CIDP-family issue
- CIDP-Cyclosporin
- Polyneuropathy
- CIDP-GBS children
- Peripheral Neuropathy
- ALS & CIDP
- Types of neuropathy
- alcoholic poly neuropathy
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