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CIDP presenting as recurrent severe back pain without weakness or sensory loss
Dirk Bäumer1, David James Grant2, Ravi Knight3
1Wessex Neurological Centre, University Hospital Southampton, Southampton, UK.
Insights
This study describes a rare case of relapsing polyradiculoneuropathy, a variant of chronic inflammatory demyelinating polyradiculoneuropathy. The patient experienced recurrent severe back pain and high cerebrospinal fluid protein, with symptoms resolving after treatment.
Area of Science:
- Neurology
- Immunology
Background:
- Guillain-Barré syndrome is an autoimmune disorder affecting the peripheral nervous system.
- Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) is a progressive or relapsing disorder characterized by demyelination of peripheral nerves.
Observation:
- A 71-year-old woman presented with severe back pain, limb weakness, and cranial nerve dysfunction, initially diagnosed as Guillain-Barré syndrome.
- She experienced three subsequent episodes of severe back pain with elevated cerebrospinal fluid (CSF) protein, but without neurological deficits.
- Specialized tests revealed proximal demyelination and inflammation of the lumbosacral plexus.
Findings:
- The patient's recurrent symptoms, despite normal routine nerve conduction studies, suggest a relapsing proximal polyradiculoneuropathy.
- This presentation is proposed to be part of the spectrum of chronic inflammatory demyelinating polyradiculoneuropathy (CIDP).
Implications:
- This case expands the understanding of CIDP spectrum disorders.
- It highlights the importance of considering atypical presentations of inflammatory polyradiculoneuropathies, especially in recurrent cases with high CSF protein.
Abstract:
A 71-year-old woman presented with severe back pain, limb weakness and cranial nerve dysfunction associated with high cerebrospinal fluid (CSF) protein; we diagnosed Guillain-Barré syndrome and her symptoms completely resolved after intravenous immunoglobulin. Over the next 4 years, she had three further episodes of excruciating back pain accompanied by raised CSF protein, but without weakness, sensory loss, or abnormalities in routine nerve conduction studies. Sensory evoked potentials suggested proximal demyelination and lumbosacral plexus imaging suggested inflammation. We argue that this is a relapsing proximal polyradiculoneuropathy on the spectrum of chronic inflammatory demyelinating polyradiculoneuropathy.
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