Autoimmune diseases

CIDP with Diseases
by: M.C |JUlY 4, 2020


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.
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

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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