Here’s a concise comparison of Chronic Inflammatory Demyelinating Polyradiculoneuropathy (CIDP), Amyotrophic Lateral Sclerosis (ALS), Acute Inflammatory Demyelinating Polyradiculoneuropathy (AIDP), and Lambert-Eaton Myasthenic Syndrome (LEMS) based on key clinical and diagnostic features:

FeatureCIDPALSAIDPLEMS
PathophysiologyAutoimmune demyelination of peripheral nervesDegeneration of upper and lower motor neuronsAcute autoimmune demyelination of peripheral nervesAutoimmune attack on presynaptic voltage-gated calcium channels
OnsetChronic, progressive or relapsing (>2 months)Progressive, insidious (months to years)Acute, rapid (days to weeks)Subacute to chronic
SymptomsSymmetric weakness, sensory loss, hyporeflexia/areflexiaMuscle weakness, atrophy, fasciculations, spasticity, hyperreflexiaSymmetric weakness, sensory loss, areflexia, often post-infectionProximal weakness, fatigability, autonomic dysfunction (e.g., dry mouth), hyporeflexia
Motor InvolvementProximal and distal, lower motor neuron (LMN)Upper motor neuron (UMN) + LMNProximal and distal, LMNProximal, improves with repeated activity (facilitation)
Sensory InvolvementCommon (numbness, tingling)Rare (sensory sparing)Common (paresthesia, sensory loss)Rare (sensory sparing)
Autonomic InvolvementRareRareCommon (e.g., dysautonomia, heart rate variability)Common (e.g., dry mouth, constipation)
ReflexesReduced or absentHyperreflexic (UMN) or mixedAbsent or reducedReduced, may improve with exercise
Electrophysiology (EMG/NCS)Demyelinating features (slow conduction, conduction block)Denervation, fasciculations, no sensory involvementDemyelinating features, acute onsetReduced CMAP amplitude, facilitation with high-frequency stimulation
Cerebrospinal Fluid (CSF)Elevated protein, normal cell count (albuminocytologic dissociation)NormalElevated protein, normal cell countNormal
Associated ConditionsNone specific, may have monoclonal gammopathyFrontotemporal dementia (some cases)Post-infectious (e.g., Campylobacter, CMV, EBV)Small cell lung cancer (paraneoplastic, ~50% of cases)
TreatmentImmunotherapy (IVIG, corticosteroids, plasmapheresis)Supportive, riluzole, edaravoneIVIG, plasmapheresis3,4-DAP, immunotherapy, treat underlying malignancy
PrognosisVariable, often responds to treatmentPoor, progressive (median survival 2-5 years)Good with treatment, most recover within monthsVariable, depends on underlying malignancy and treatment response

Key Differentiators:

  • CIDP: Chronic, treatable, demyelinating neuropathy with sensory and motor involvement.
  • ALS: Progressive motor neuron disease with UMN and LMN signs, no sensory loss, poor prognosis.
  • AIDP: Acute form of CIDP (Guillain-BarrĂ© syndrome), often post-infectious, good recovery with treatment.
  • LEMS: Neuromuscular junction disorder, often paraneoplastic, with characteristic facilitation and autonomic symptoms.

For precise diagnosis, clinical evaluation, EMG/NCS, CSF analysis, and sometimes antibody testing (e.g., anti-VGCC for LEMS) are critical.

Disclaimer: owerl is not a doctor; please consult one. Don’t share information that can identify you.

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