Restless legs syndrome pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Mohamadmostafa Jahansouz M.D.[2]
Overview
Pathophysiology
Pathogenesis
- Generally most scientists consider restless legs syndrome(RLS) as a central nervous system (CNS)-related disorder, but no specific lesion has been found to be associated with the syndrome.
- It is thought that RLS is the result of central nervous system anatomic lesions.[1]
- Findings in imaging of CNS witch suggest the relation between the anatomic lesions in CNS and RLS include:[1][2][3][4]
- Presence of morphologic changes in the somatosensory cortex, motor cortex and thalamic gray matter in MRI
- Abnormal bilateral cerebellar and thalamic activation during the manifestation of sensory symptoms, with additional red nucleus and reticular formation activity during periodic leg movements (PLMS), in functional MRI study
- Evidences of the role of the limbic and opioid systems in SPECT and PET studies
- Low brain iron concentrations and dysfunction of iron metabolism and intracellular iron
- The "iron-dopamine model" explains that iron deficiency in the brain causes an abnormality in the dopaminergic system leading to manifestation of RLS.
- RLS symptoms seem to depend on abnormal spinal sensorimotor integration at the spinal cord level and abnormal central somatosensory processing
- In animal models, studies suggest that the All dopaminergic system and the D3 receptor participates in RLS symptoms
Genetics
- Genes involved in the pathogenesis of RLS include: RLS 1: 12q and RLS 2: 14q and RLS 3: 9p and RLS 4: 2q and RLS 5: 20p.[1]
- 40% of cases of RLS are familial and are inherited in an autosomal dominant fashion with variable penetrance.
Associated Conditions
Conditions which may be associated with RLS include:[5][6][7]
- Hypertension
- cardiovascular deseases
- Anxiety
- Depression
- Iron deficiency
- Anemia
- Kidney diseases
- Stroke
- Parkinson disease
- Polyneuropathy
- Multiple sclerosis
Microscopic Pathology
- The exact neuroanatomical substrate imbalance which causes restless legs syndrome (RLS) is unknown.[8]
- Chronic ischemic changes were found in some brain tissue samples of patients whit RLS.[8]
References
- ↑ 1.0 1.1 1.2 Miyamoto M, Miyamoto T, Iwanami M, Suzuki K, Hirata K (2009). "[Pathophysiology of restless legs syndrome]". Brain Nerve. 61 (5): 523–32. PMID 19514512.
- ↑ Li X, Allen RP, Earley CJ, Liu H, Cruz TE, Edden RAE; et al. (2016). "Brain iron deficiency in idiopathic restless legs syndrome measured by quantitative magnetic susceptibility at 7 tesla". Sleep Med. 22: 75–82. doi:10.1016/j.sleep.2016.05.001. PMC 4992945. PMID 27544840.
- ↑ Etgen T, Draganski B, Ilg C, Schröder M, Geisler P, Hajak G; et al. (2005). "Bilateral thalamic gray matter changes in patients with restless legs syndrome". Neuroimage. 24 (4): 1242–7. doi:10.1016/j.neuroimage.2004.10.021. PMID 15670702.
- ↑ Guo S, Huang J, Jiang H, Han C, Li J, Xu X; et al. (2017). "Restless Legs Syndrome: From Pathophysiology to Clinical Diagnosis and Management". Front Aging Neurosci. 9: 171. doi:10.3389/fnagi.2017.00171. PMC 5454050. PMID 28626420.
- ↑ Katsi V, Katsimichas T, Kallistratos MS, Tsekoura D, Makris T, Manolis AJ; et al. (2014). "The association of Restless Legs Syndrome with hypertension and cardiovascular disease". Med Sci Monit. 20: 654–9. doi:10.12659/MSM.890252. PMC 3999161. PMID 24747872.
- ↑ Cotter PE, O'Keeffe ST (2006). "Restless leg syndrome: is it a real problem?". Ther Clin Risk Manag. 2 (4): 465–75. PMC 1936366. PMID 18360657.
- ↑ Trenkwalder C, Allen R, Högl B, Paulus W, Winkelmann J (2016). "Restless legs syndrome associated with major diseases: A systematic review and new concept". Neurology. 86 (14): 1336–43. doi:10.1212/WNL.0000000000002542. PMC 4826337. PMID 26944272.
- ↑ 8.0 8.1 Pittock SJ, Parrett T, Adler CH, Parisi JE, Dickson DW, Ahlskog JE (2004). "Neuropathology of primary restless leg syndrome: absence of specific tau- and alpha-synuclein pathology". Mov Disord. 19 (6): 695–9. doi:10.1002/mds.20042. PMID 15197711.