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CIDP is an immune-mediated neuropathy characterized by a relapsing or progressive course1 12 The diagnostic approach requires detailed clinical examination, combined with supportive laboratory and electrodiagnostic abnormalities and occasionally a nerve biopsy (Fig 12 1) Various research criteria for CIDP have been developed but none have been universally accepted (Tables 12 2 and 12 3)1,9,13 15 CIDP may account for 10 33% of initially undiagnosed peripheral neuropathies in large tertiary referral centers1,4,16 By de nition, symptoms and signs of the neuropathy must be progressive for at least 2 months, which distinguishes CIDP from Guillain Barre syndrome (GBS) or the most common form of GBS, namely acute acquired in ammatory demyelinating neuropathy (AIDP)1,13 Differentiating AIDP from CIDP can be dif cult early on, as it is not always possible to determine in the rst few weeks how many patients will continue to progress over 2 months and how many will reach a plateau Further, some patients have a subacute onset over 4 8 weeks, a variant some have called
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SECTION II
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TABLE 12 1 COMPARISON OF THE CHRONIC ACQUIRED IMMUNE-MEDIATED DEMYELINATING POLYNEUROPATHIES
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CIDP Clinical Features Weakness Symmetric proximal and distal weakness
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DADS
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MADSAM Asymmetric, distal > proximal, arms > legs Yes; asymmetric Asymmetrically reduced or absent Demyelinating features including CB Abnormal Usually elevated Rarely present Rarely present Demyelinating/ remyelinating features are common
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MMN Asymmetric, distal > proximal, arms > legs No Asymmetrically reduced or absent Demyelinating features including CB Normal Usually normal Rarely present Frequently present Demyelinating/ remyelinating features are scant, if present
Sensory loss Re exes Electrophysiology CMAPs
None or only mild symmetric distal weakness Yes; symmetric Yes; distal and symmetric Symmetrically reduced Symmetrically or absent reduced or absent Demyelinating features Demyelinating including CB features excluding CB Abnormal Abnormal Usually elevated Occasionally present, usually IgG or IgA Rarely present Demyelinating/ remyelinating features are common Usually elevated IgM usually present (most anti-MAG) Rarely present Demyelinating/ remyelinating features are common, with IgM deposition evident in paranodal regions Poor Poor Poor Poor
SNAPs Laboratory Findings CSF protein Monoclonal protein GM1 antibodies Sensory nerve biopsies
Treatment Response Prednisone Plasma exchange IVIG Cyclophosphamide
Yes Yes Yes Yes
Yes Not adequately studied Yes Not adequately studied
No No Yes Yes
CIDP, chronic in ammatory demyelinating polyneuropathy; DADS, distal acquired demyelinating symmetrical; MADSAM, multifocal acquired demyelinating sensory and motor; MMN, multifocal motor neuropathy; CMAPs, compound motor action potentials; SNAPs, sensory nerve action potentials; CB, conduction block; CSF, cerebrospinal uid; MAG, myelin-associated glycoprotein; IVIG, intravenous immunoglobulin With permission from Saperstein DS, Katz JS, Amato AA, Barohn RJ The spectrum of the acquired chronic demyelinating polyneuropathies Muscle Nerve 2001;24:311 324, Table 4, p 213
patients, particularly large- ber modalities (vibration and touch)1,3,21,22,28 Some patients exhibit sensory ataxia and gait imbalance Most patients with CIDP are are exic or at least hypore exic Symptomatic autonomic neuropathy (eg, orthostatic hypotension, incontinence, and impotence) can occur but is uncommon21,30,31 Rare patients may have only sensory symptoms and signs, a so-called chronic sensory demyelinating neuropathy 32 34 However, in most such cases, nerve conduction studies (NCS) reveal slowing of the motor nerves as well It is not unusual for CIDP to present with sensory symptoms and then later develop motor abnormalities35 In our experience, patients with a demyelinating neuropathy who have sensory signs out of proportion to muscle weakness often
have an IgM monoclonal gammopathy with or without antibodies directed against myelin-associated glycoprotein (MAG) Whenever a pure sensory neuropathy is present, consideration should be given to other diseases as well, such as Sj gren syndrome or a paraneoo plastic neuronopathy, which are associated with sensory ganglionitis36 However, there are indeed rare cases of demyelination that appears to be focused on the sensory roots (chronic demyelinating sensory polyradiculopathy), which likely falls into end of the spectrum of CIDP37 This is distinguished from sensory ganglionopathies and anti-MAG neuropathies by the clinical absence or reduction of muscle stretch re exes but normal routine sensory SNAPs On the other hand, H-re exes and somatosensory-evoked potentials are
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CHRONIC INFLAMMATORY DEMYELINATING POLYNEUROPATHY
Progressive or relapsing proximal paresis, distal paresis, or both, with or without hypoesthesia and reduced or no tendon reflexes
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