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Polyneuropathy

 Multi Focal Motor Neuropathy

Small fiber neuropathy

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Paraproteinemias and/or plasma cell dyscrasias

CIDP is seen with monoclonal gammopathies (eg MGUS), most frequently gammopathy of immunoglobulin M (IgM)
Evidence suggests that CIDP with IgM MGUS has specific clinical and electrophysiologic characteristics
Usually predominance of distal weakness with sensory symptoms greater than motor
Multiple sclerosis
Reports describe CNS white matter changes in patients with CIDP
Whether a true association exists between CIDP and multiple sclerosis remains unclear
 
Systemic lupus erythematosus
Chronic active hepatitis (B or C)
CIDP associated with hepatitis should be differentiated from cryoglobulinemic vasculitis
The latter causes either symmetric distal sensorimotor polyneuropathy or mononeuropathy multiplex but on pathologic examination shows wallerian degeneration and not the segmental demyelination seen in CIDP
 
Inflammatory bowel disease
CIDP has been described in association with Crohn disease and other inflammatory bowel conditions, although no direct correlation between the two afflictions is known
The mechanism of development of CIDP is presumed to be an autoimmune abnormality that is also causing the primary problem in inflammatory bowel disease, although the details are not known
Diabetes mellitus
Increasing evidence supports the suggestion that some patients with diabetes who have severe neuropathy or unusually progressive neuropathy may have CIDP superimposed on their diabetic disorder
Diabetes may predispose patients to CIDP
Pregnancy
Known to worsen CIDP
Worsening usually occurs in the third trimester or in the postpartum period

 

CIDP: Monitoring and Prognosis
Sometimes difficult to assess the activity of a chronic neuropathy
Nerve biopsy can be used to detect active nerve lesions and inflammatory infiltrates
Axonal loss has more long-term prognostic impact than active demyelination or inflammatory infiltrates in demyelinating disorders of the peripheral and central nervous systems

 

CIDP: Diagnosis
The diagnosis of CIDP is typically based on the clinical presentation, absence of other causes of the neuropathic syndrome, and results of electrodiagnostic studies
Presence of increased cerebrospinal fluid (CSF) protein and demyelinating changes on nerve biopsy are supportive of the diagnosis, but these are not always present
Because of the clinical heterogeneity and the lack of a diagnostic test, various diagnostic criteria have been proposed
In one series of patients all of whom had proximal and distal weakness and in whom 95% of patients had improvement with treatment, only 30% had the classic triad of slow nerve conduction velocity, elevated CSF protein and demyelination on nerve biopsy
 
American Association of Neurology: Criteria
Developed criteria for the identification of patients with CIDP for research studies
Pathologic criteria
Electrophysiologic criteria: Require 3 demyelinating range abnormalities (either slow conduction velocity, prolonged distal motor latencies or F wave latencies or conduction block) in 2 nerves
Criteria are not sensitive and may miss more than 50 % of patients with CIDP
Specificity approaches 100%
Majority of patients seen in clinical practice fail to meet all of the criteria

 

Laboratory Studies: CSF
Protein level is increased significantly in 80% of patients
Usually between 50 and 200 mg/dL, but can be higher
10% of patients also have mild lymphocytic pleocytosis (<50 cells) and increased gamma globulin (usually associated with HIV infection)
CBC, sedimentation rate, antinuclear antibody, biochemistry profile, and serum and urine immunoelectrophoresis are necessary to exclude important associated systemic disorders
 

 
              Shifa