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Updated: Mar 14, 2026

Establishing a Mouse Model of a Pure Small Fiber Neuropathy with the Ultrapotent Agonist of Transient Receptor Potential Vanilloid Type 1
Published on: February 13, 2018
SLE Neuropathy-Anything New?
1Associate Professor of Medicine and I/C Rheumatology, Hinduhridaysamrat Balasaheb Thakeray Medical College and R.N. Cooper Hospital; Visiting Consultant Rheumatologist, Sevenhills Hospital, Mumbai, Maharashtra.
Abstract:
SLE (systemic lupus erythematosus) is a multisystem autoimmune disorder of unknown aetiology which can present with myriad clinical presentation. The neurological manifestations of SLE consist of central nervous system (CNS) and peripheral nervous system manifestations (PNS). The CNS manifestations are aseptic meningitis, cerebrovascular accidents (stroke), demyelinating disorders, headache, involuntary movements like chorea, myelopathy, acute confusional states, cognitive dysfunction, mood disorder, seizures, psychosis and cranial nerve palsies.1 The PNS manifestations are Guillain Barre syndrome (GBS), autonomic disorder, mononeuropathy, polyneuropathy and plexopathy.1 Neuropathy in SLE can be clinically classified as mononeuritis multiplex and symmetrical and asymmetrical polyneuropathy. Symmetrical polyneuropathy being the most commonly seen clinical entity amongst the neuropathies in SLE. The neuropathy can be slowly progressive or acute in onset. Electrophysiologically, neuropathy is classified as axonal neuropathy, small fibre neuropathy, demyelinating neuropathy, mixed axonal-demyelinating sensorimotor polyneuropathy and plexopathy. Axonal neuropathy is further divided into sensory, sensorimotor and mononeuritis multiplex. Demyelinating neuropathy can be of two types: acute inflammatory demyelinating polyneuropathy (AIDP) and sensory demyelinating polyneuropathy. Anecdotal case reports also suggest that CIDP can occur as part of SLE neuropathy.2.
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