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Abstract Neuropsychiatric events in SLE have been documented to have a wide range of prevalence, which vary from 14% up to more than 80% in adults. This variation mirrors the shortage in definitions of individual presentations and the absence of standardization for investigation. Different patterns of SLE related neuropathies have been documented in 10–20% of lupus patients. Their clinical presentation relies upon the diameter of the affected nerve, the type of demyelinating or axonal lesions and their acute or chronic occurrence.(21) Routine nerve conduction studies just mirror the activity of the fast conducting myelinated A nerve fibers, which are physiologically irrelevant to pain. The overwhelming neuropathic symptoms are related to abnormalities of other smaller nerve fibers. Thus, Skin sympathetic response (SSR) and quantitative sensory testing (QST); which can evaluate small nerve fiber function; (22) ought to be in this manner applied to patients with lupus related PN. Matrix metalloproteinases (MMPs) are group of zinc-containing endoproteinases that can degrade a variety of extracellular matrix components, the up-regulation of MMP-9 within the vessel walls maybe responsible for the vascular damage seen in SLE and the resulting chronic combined axonal degeneration and demyelinating type of neuropathy frequently found in SLE,(18) thus further studies are needed to evaluate and test the hypothesis that serum MMP-9 levels are associated with PN in patients with SLE. In the literature researches on the peripheral nervous system in lupus patients are mostly represented by case reports or case series with few number of patients.(23) Moreover, the peripheral neuropathy (PN) has not been well described in SLE in terms of onset, severity, clinical associations, and electrophysiological findings. Therefore, more studies are necessary to characterize PN in SLE with respect to the patient’s clinical lupus manifestations, serologic markers, and electrophysiological findings. |