IgG3 Caspr autoantibodies were found during the acute GBS-like phase, while IgG4 Caspr autoantibodies were present during the chronic phase of disease. Diagnosis and symptoms
Diagnosis is typically made on the basis of presenting symptoms in tandem with electrodiagnostic testing or a nerve biopsy. Doctors may use a lumbar puncture to verify the presence of increased cerebrospinal fluid protein. Differential diagnosis
CIBP variants are among several types of immune-mediated neuropathies recognised. These include:

Chronic inflammatory demyelinating polyneuropathy (CIDP) with subtypes:
Classical CIDP
CIDP with diabetes
CIDP/monoclonal gammopathy of undetermined significance
Sensory CIDP
Multifocal motor neuropathy
Multifocal acquired demyelinating sensory and motor neuropathy (Lewis-Sumner syndrome)
Multifocal acquired sensory and motor neuropathy
Distal acquired demyelinating sensory neuropathy
Guillain–Barré syndrome with subtypes:
Acute inflammatory demyelinating polyradiculoneuropathy
Acute motor axonal neuropathy
Acute motor and sensory axonal neuropathy
Acute pandysautonomia
Miller Fisher syndrome
IgM monoclonal gammopathies with subtypes:
Waldenströms macroglobulinemia
Mixed cryoglobulinemia, gait ataxia, late-onset polyneuropathy syndrome
Myelin-associated glycoprotein-associated gammopathy, polyneuropathy, organomegaly, endocrinopathy, M-protein and skin changes syndrome (POEMS)Other possible diagnoses are

Bickerstaff brainstem encephalitis
Fisher syndrome
Guillain–Barré syndromeFor this reason a diagnosis of chronic inflammatory demyelinating polyneuropathy needs further investigations. The diagnosis is usually provisionally made through a clinical neurological examination. Symptoms
Symptoms such as diminished or absent deep-tendon reflexes and sensory ataxia are common. Other symptoms include proximal and distal muscle weakness in the limbs.Patients usually present with a history of weakness, numbness, tingling, pain and difficulty in walking. They may additionally present with fainting spells while standing up or burning pain in extremities. Some patients may have sudden onset of back pain or neck pain radiating down the extremities, usually diagnosed as radicular pain.
Sural nerve biopsy; biopsy is considered for those patients in whom the diagnosis is not completely clear, when other causes of neuropathy (e.g., hereditary, vasculitic) cannot be excluded, or when profound axonal involvement is observed on EMG. Ultrasound of the peripheral nerves may show swelling of the affected nerves. Magnetic resonance imaging can also be used in the diagnostic workup.In some cases electrophysiological studies fail to show any evidence of demyelination. Though conventional electrophysiological diagnostic criteria are not met, the patient may still respond to immunomodulatory treatments. In such cases, presence of clinical characteristics suggestive of CIDP are critical, justifying full investigations, including sural nerve biopsy. Treatment
First-line treatment for CIDP is currently intravenous immunoglobulin and other treatments include corticosteroids (e.g., prednisone), and plasmapheresis (plasma exchange) which may be prescribed alone or in combination with an immunosuppressant drug. Recent controlled studies show subcutaneous immunoglobulin appears to be as effective for CIDP treatment as intravenous immunoglobulin in most patients, and with fewer systemic side effects.Intravenous immunoglobulin and plasmapheresis have proven benefit in randomized, double-blind, placebo-controlled trials. Despite less definitive published evidence of efficacy, corticosteroids are considered standard therapies because of their long history of use and cost effectiveness. Intravenous immunoglobulin is probably the first-line CIDP treatment, but is extremely expensive.