Related Experiment Video

Updated: Jul 20, 2026

Nerve Ultrasound Protocol to Detect Dysimmune Neuropathies
08:56

Nerve Ultrasound Protocol to Detect Dysimmune Neuropathies

Published on: October 7, 2021

Clinical heterogeneity in mild chronic inflammatory demyelinating polyneuropathy

Y A Rajabally1, S Jacob, R J Abbott

  • 1Neuromuscular Clinic, Department of Neurology, University Hospitals of Leicester, Leicester General Hospital, Leicester, UK. yusuf.rajabally@uhl-tr.nhs.uk

European Journal of Neurology
|August 26, 2006
PubMed

Insights

Mild chronic inflammatory demyelinating polyneuropathy (CIDP) presents variably, causing diagnostic challenges. Early electrophysiological confirmation and potential treatment with intravenous immunoglobulins are crucial for managing this condition.

Area of Science:

  • Neurology
  • Clinical Electrophysiology

Background:

  • Chronic inflammatory demyelinating polyneuropathy (CIDP) is an autoimmune disorder affecting peripheral nerves.
  • Mild variants of CIDP can present with subtle or atypical symptoms, complicating diagnosis.

Observation:

  • Three patients presented with an unusually mild and variable clinical course of CIDP.
  • Diagnostic uncertainty was present in all cases due to the non-specific presentation.
  • Cerebrospinal fluid protein levels were elevated in only one patient.

Findings:

  • Extensive electrophysiological studies confirmed CIDP in all three patients.
  • Histological examination supported the diagnosis in one patient.
  • Two patients treated with intravenous immunoglobulins showed significant clinical improvement.

Implications:

  • Recognizing mild CIDP is essential for timely diagnosis and intervention.
  • Early treatment may prevent progression to more severe neurological deficits.
  • Immunomodulatory therapies, such as intravenous immunoglobulins, can be effective in managing mild CIDP.

More Related Videos

Comprehensive Autopsy Program for Individuals with Multiple Sclerosis09:41

Comprehensive Autopsy Program for Individuals with Multiple Sclerosis

Published on: July 19, 2019

Rat Model of Widespread Cerebral Cortical Demyelination Induced by an Intracerebral Injection of Pro-Inflammatory Cytokines09:46

Rat Model of Widespread Cerebral Cortical Demyelination Induced by an Intracerebral Injection of Pro-Inflammatory Cytokines

Published on: September 21, 2021

Related Concept Videos

Multiple Sclerosis l: Introduction01:19

Multiple Sclerosis l: Introduction

Multiple sclerosis is a chronic autoimmune disease of the central nervous system (CNS) that affects the brain, spinal cord, and optic nerves. It is an inflammatory demyelinating disorder and a leading cause of neurological disability in young adults.EpidemiologyMS commonly begins between 20 and 40 years of age and is twice as common in women. Its exact cause remains unclear, but genetic susceptibility contributes, with higher risk in first-degree relatives and identical twins. A greater...
Local Anesthetics: Differential Sensitivity of Nerve Fibers01:24

Local Anesthetics: Differential Sensitivity of Nerve Fibers

Local anesthetics (LAs) block the sodium channels of nerve trunks, sensory nerve endings, and neuromuscular junctions. Although LAs can block all kinds of nerves, the sensitivity of nerve fibers differs according to nerve types and structures. LAs are known to block myelinated fibers faster than unmyelinated ones. Also, they block pain or sensory neurons at low concentrations without affecting the motor neurons involved in muscle contractions. This helps relieve labor pain without affecting the...
Peripheral Arterial Disease II: Clinical Manifestations and Diagnostic Evaluation01:21

Peripheral Arterial Disease II: Clinical Manifestations and Diagnostic Evaluation

Clinical manifestationsPeripheral Arterial Disease (PAD) manifests through a range of symptoms, from the characteristic intermittent claudication to atypical presentations and severe complications in advanced stages. Intermittent claudication, a hallmark symptom of PAD, presents as exercise-induced muscle pain that typically resolves within minutes of rest. This pain is reproducible and stems from inadequate blood flow, leading to the accumulation of lactic acid produced during anaerobic...
Myasthenia Gravis ll: Pathophysiology01:22

Myasthenia Gravis ll: Pathophysiology

The disease process of myasthenia gravis begins at the neuromuscular junction, where antibodies attack key proteins needed for muscle activation. This immune reaction weakens signal transmission, leading to the characteristic muscle fatigue and weakness that define the condition.Immune-Mediated DamageIn most individuals, antibodies target acetylcholine receptors (AChRs) on the postsynaptic membrane of muscle cells. By blocking acetylcholine binding, these antibodies prevent the nerve signal...
Diabetic Neuropathy01:22

Diabetic Neuropathy

DefinitionDiabetic neuropathy is nerve damage caused by long-standing diabetes mellitus. It results directly from prolonged high blood sugar levels.PathophysiologyThe pathophysiology of diabetic neuropathy involves both metabolic and vascular disturbances triggered by chronic hyperglycemia.Metabolic injury: Elevated glucose levels activate the polyol pathway within nerve cells, leading to the accumulation of sorbitol and fructose. This increases oxidative stress, disrupts normal nerve...
Parkinson Disease ll: Pathophysiology01:24

Parkinson Disease ll: Pathophysiology

Parkinson disease (PD) is a progressive neurodegenerative disorder primarily affecting movement, with additional non-motor features. Its pathophysiology involves complex interactions among genetic susceptibility, environmental exposures, and cellular dysfunction, including dopaminergic neuron loss, protein aggregation, and mitochondrial impairment.Selective NeurodegenerationA key feature is the degeneration of dopaminergic neurons in the substantia nigra pars compacta, leading to reduced...