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EMG: neuropathic changes

MedGen UID:
867363
Concept ID:
C4021727
Finding
Synonyms: EMG: neurogenic abnormalities; EMG: neurogenic changes; EMG: neurogenic findings
 
HPO: HP:0003445

Definition

The presence of characteristic findings of denervation on electromyography (fibrillations, positive sharp waves, and giant motor unit potentials). [from HPO]

Term Hierarchy

CClinical test,  RResearch test,  OOMIM,  GGeneReviews,  VClinVar  
  • EMG: neuropathic changes

Conditions with this feature

Metachromatic leukodystrophy
MedGen UID:
6071
Concept ID:
C0023522
Disease or Syndrome
Arylsulfatase A deficiency (also known as metachromatic leukodystrophy or MLD) is characterized by three clinical subtypes: late-infantile MLD, juvenile MLD, and adult MLD. Age of onset within a family is usually similar. The disease course may be from several years in the late-infantile-onset form to decades in the juvenile- and adult-onset forms. Late-infantile MLD. Onset is before age 30 months. Typical presenting findings include weakness, hypotonia, clumsiness, frequent falls, toe walking, and dysarthria. As the disease progresses, language, cognitive, and gross and fine motor skills regress. Later signs include spasticity, pain, seizures, and compromised vision and hearing. In the final stages, children have tonic spasms, decerebrate posturing, and general unawareness of their surroundings. Juvenile MLD. Onset is between age 30 months and 16 years. Initial manifestations include decline in school performance and emergence of behavioral problems, followed by gait disturbances. Progression is similar to but slower than in the late-infantile form. Adult MLD. Onset occurs after age 16 years, sometimes not until the fourth or fifth decade. Initial signs can include problems in school or job performance, personality changes, emotional lability, or psychosis; in others, neurologic symptoms (weakness and loss of coordination progressing to spasticity and incontinence) or seizures initially predominate. Peripheral neuropathy is common. Disease course is variable – with periods of stability interspersed with periods of decline – and may extend over two to three decades. The final stage is similar to earlier-onset forms.
Neuronopathy, distal hereditary motor, type 2A
MedGen UID:
322471
Concept ID:
C1834692
Disease or Syndrome
Distal hereditary motor neuropathy, type II is a progressive disorder that affects nerve cells in the spinal cord. It results in muscle weakness and affects movement, primarily in the legs.\n\nOnset of distal hereditary motor neuropathy, type II ranges from the teenage years through mid-adulthood. The initial symptoms of the disorder are cramps or weakness in the muscles of the big toe and later, the entire foot. Over a period of approximately 5 to 10 years, affected individuals experience a gradual loss of muscle tissue (atrophy) in the lower legs. They begin to have trouble walking and running, and eventually may have complete paralysis of the lower legs. The thigh muscles may also be affected, although generally this occurs later and is less severe.\n\nSome individuals with distal hereditary motor neuropathy, type II have weakening of the muscles in the hands and forearms. This weakening is less pronounced than in the lower limbs and does not usually result in paralysis.
Muscle cramps, familial
MedGen UID:
371885
Concept ID:
C1834708
Disease or Syndrome
Spinal muscular atrophy, type IV
MedGen UID:
325364
Concept ID:
C1838230
Disease or Syndrome
Spinal muscular atrophy (SMA) is characterized by muscle weakness and atrophy resulting from progressive degeneration and irreversible loss of the anterior horn cells in the spinal cord (i.e., lower motor neurons) and the brain stem nuclei. The onset of weakness ranges from before birth to adulthood. The weakness is symmetric, proximal > distal, and progressive. Before the genetic basis of SMA was understood, it was classified into clinical subtypes based on maximum motor function achieved; however, it is now apparent that the phenotype of SMN1-associated SMA spans a continuum without clear delineation of subtypes. With supportive care only, poor weight gain with growth failure, restrictive lung disease, scoliosis, and joint contractures are common complications; however, newly available targeted treatment options are changing the natural history of this disease.
Charcot-Marie-Tooth disease recessive intermediate A
MedGen UID:
334012
Concept ID:
C1842197
Disease or Syndrome
GDAP1-related hereditary motor and sensory neuropathy (GDAP1-HMSN) is a peripheral neuropathy (also known as a subtype of Charcot-Marie-Tooth disease) that typically affects the lower extremities earlier and more severely than the upper extremities. As the neuropathy progresses, the distal upper extremities also become severely affected. Proximal muscles can also become weak. Age at onset ranges from infancy to early childhood. In most cases, disease progression causes disabilities within the first or second decade of life. At the end of the second decade, most individuals are wheelchair bound. Disease progression varies considerably even within the same family. The neuropathy can be either of the demyelinating type with reduced nerve conduction velocities or the axonal type with normal nerve conduction velocities. Vocal cord paresis is common. Intelligence is normal. Life expectancy is usually normal, but on occasion may be reduced because of secondary complications.
Pontocerebellar hypoplasia type 1A
MedGen UID:
335969
Concept ID:
C1843504
Disease or Syndrome
Pontocerebellar hypoplasia (PCH) refers to a group of severe neurodegenerative disorders affecting growth and function of the brainstem and cerebellum, resulting in little or no development. Different types were classified based on the clinical picture and the spectrum of pathologic changes. PCH type 1 is characterized by central and peripheral motor dysfunction associated with anterior horn cell degeneration resembling infantile spinal muscular atrophy (SMA; see SMA1, 253300); death usually occurs early. Genetic Heterogeneity of Pontocerebellar Hypoplasia Also see PCH1B (614678), caused by mutation in the EXOSC3 gene (606489); PCH1C (616081), caused by mutation in the EXOSC8 gene (606019); PCH1D (618065), caused by mutation in the EXOSC9 gene (606180); PCH1E (619303), caused by mutation in the SLC25A46 gene (610826); PCH1F (619304), caused by mutation in the EXOSC1 gene (606493); PCH2A (277470), caused by mutation in the TSEN54 gene (608755); PCH2B (612389), caused by mutation in the TSEN2 gene (608753); PCH2C (612390), caused by mutation in the TSEN34 gene (608754); PCH2D (613811), caused by mutation in the SEPSECS gene (613009); PCH3 (608027), caused by mutation in the PCLO gene (604918); PCH4 (225753), caused by mutation in the TSEN54 gene; PCH5 (610204), caused by mutation in the TSEN54 gene; PCH6 (611523), caused by mutation in the RARS2 gene (611524); PCH7 (614969), caused by mutation in the TOE1 gene (613931); PCH8 (614961), caused by mutation in the CHMP1A gene (164010); PCH9 (615809), caused by mutation in the AMPD2 gene (102771); PCH10 (615803), caused by mutation in the CLP1 gene (608757); PCH11 (617695), caused by mutation in the TBC1D23 gene (617687); PCH12 (618266), caused by mutation in the COASY gene (609855); PCH13 (618606), caused by mutation in the VPS51 gene (615738); PCH14 (619301), caused by mutation in the PPIL1 gene (601301); PCH15 (619302), caused by mutation in the CDC40 gene (605585); PCH16 (619527), caused by mutation in the MINPP1 gene (605391); and PCH17 (619909), caused by mutation in the PRDM13 gene (616741) on chromosome 6q16.
X-linked distal spinal muscular atrophy type 3
MedGen UID:
335168
Concept ID:
C1845359
Disease or Syndrome
A rare distal hereditary motor neuropathy with characteristics of slowly progressive atrophy and weakness of distal muscles of hands and feet with normal deep tendon reflexes or absent ankle reflexes and minimal or no sensory loss, sometimes mild proximal weakness in the legs and feet and hand deformities in males.
Neuronopathy, distal hereditary motor, autosomal recessive 3
MedGen UID:
337659
Concept ID:
C1846823
Disease or Syndrome
Autosomal recessive distal hereditary motor neuronopathy-3 (HMNR3), also known as distal spinal muscular atrophy (DSMA) and distal hereditary motor neuronopathy (dHMN or HMN), is characterized by distal muscle weakness and wasting without significant sensory involvement. For a discussion of genetic heterogeneity of autosomal recessive HMN, see HMNR1 (604320). Harding (1993) classified autosomal recessive distal hereditary motor neuronopathy as dHMN IV (HMN4) and dHMN III (HMN3). Both have juvenile onset and differ only by less severe involvement in HMN3. However, Viollet et al. (2004) reported an extended Lebanese kindred in which both HMN III and HMN IV occurred, suggesting that the same gene was involved in both phenotypes (see Irobi et al., 2006).
Nemaline myopathy 2
MedGen UID:
342534
Concept ID:
C1850569
Disease or Syndrome
Nemaline myopathy-2 (NEM2) is an autosomal recessive skeletal muscle disorder with a wide range of severity. The most common clinical presentation is early-onset (in infancy or childhood) muscle weakness predominantly affecting proximal limb muscles. Muscle biopsy shows accumulation of Z-disc and thin filament proteins into aggregates named 'nemaline bodies' or 'nemaline rods,' usually accompanied by disorganization of the muscle Z discs. The clinical and histologic spectrum of entities caused by variants in the NEB gene is a continuum, ranging in severity. The distribution of weakness can vary from generalized muscle weakness, more pronounced in proximal limb muscles, to distal-only involvement, although neck flexor weakness appears to be rather consistent. Histologic patterns range from a severe usually nondystrophic disturbance of the myofibrillar pattern to an almost normal pattern, with or without nemaline bodies, sometimes combined with cores (summary by Lehtokari et al., 2014). Genetic Heterogeneity of Nemaline Myopathy See also NEM1 (255310), caused by mutation in the tropomyosin-3 gene (TPM3; 191030) on chromosome 1q22; NEM3 (161800), caused by mutation in the alpha-actin-1 gene (ACTA1; 102610) on chromosome 1q42; NEM4 (609285), caused by mutation in the beta-tropomyosin gene (TPM2; 190990) on chromosome 9p13; NEM5A (605355), also known as Amish nemaline myopathy, NEM5B (620386), and NEM5C (620389), all caused by mutation in the troponin T1 gene (TNNT1; 191041) on chromosome 19q13; NEM6 (609273), caused by mutation in the KBTBD13 gene (613727) on chromosome 15q22; NEM7 (610687), caused by mutation in the cofilin-2 gene (CFL2; 601443) on chromosome 14q13; NEM8 (615348), caused by mutation in the KLHL40 gene (615340), on chromosome 3p22; NEM9 (615731), caused by mutation in the KLHL41 gene (607701) on chromosome 2q31; NEM10 (616165), caused by mutation in the LMOD3 gene (616112) on chromosome 3p14; and NEM11 (617336), caused by mutation in the MYPN gene (608517) on chromosome 10q21. Several of the genes encode components of skeletal muscle sarcomeric thin filaments (Sanoudou and Beggs, 2001). Mutations in the NEB gene are the most common cause of nemaline myopathy (Lehtokari et al., 2006).
Adult-onset proximal spinal muscular atrophy, autosomal dominant
MedGen UID:
340120
Concept ID:
C1854058
Disease or Syndrome
Spinal muscular atrophy is characterized by degeneration of the anterior horn cells in the spinal cord, leading to symmetric muscle weakness and wasting. See also autosomal recessive adult-onset proximal spinal muscular atrophy (SMA4; 271150), caused by defect in the SMN1 gene (600354), and autosomal dominant childhood-onset proximal SMA (158600).
Autosomal recessive distal spinal muscular atrophy 1
MedGen UID:
388083
Concept ID:
C1858517
Disease or Syndrome
Autosomal recessive distal hereditary motor neuronopathy-1 (HMNR1) is characterized by distal and proximal muscle weakness and diaphragmatic palsy that leads to respiratory distress. Without intervention, most infants with the severe form of the disease die before 2 years of age. Affected individuals present in infancy with inspiratory stridor, weak cry, recurrent bronchopneumonia, and swallowing difficulties. The disorder is caused by distal and progressive motor neuronopathy resulting in muscle weakness (summary by Perego et al., 2020). Genetic Heterogeneity of Autosomal Recessive Distal Hereditary Motor Neuronopathy See also HMNR2 (605726), caused by mutation in the SIGMAR1 gene (601978); HMNR3 (607088) (encompassing Harding HMN types III and IV), which maps to chromosome 11q13; HMNR4 (611067), caused by mutation in the PLEKHG5 gene (611101); HMNR5 (614881), caused by mutation in the DNAJB2 gene (604139); HMNR6 (620011), caused by mutation in the REEP1 gene (609139); HMNR7 (619216), caused by mutation in the VWA1 gene (611901); HMNR8 (618912), caused by mutation in the SORD gene (182500); HMNR9 (620402), caused by mutation in the COQ7 gene (601683); HMNR10 (620542), caused by mutation in the VRK1 gene (602168); and HMNR11 (620854), caused by mutation in the RTN2 gene (603183).
Monomelic amyotrophy
MedGen UID:
356265
Concept ID:
C1865384
Disease or Syndrome
Monomelic amyotrophy, also known as Hirayama disease, is characterized by insidious onset of weakness and wasting of the muscles of the hand and forearm. It is usually unilateral, but can be bilateral. It occurs most commonly as a sporadic condition, is most common in young men, and follows a relatively benign course after a few years of progression (Nalini et al., 2004; Misra et al., 2005).
Neuronopathy, distal hereditary motor, autosomal recessive 4
MedGen UID:
369682
Concept ID:
C1970211
Disease or Syndrome
A rare genetic neuromuscular disease characterized by proximal muscle weakness with an early involvement of foot and hand muscles following normal motor development in early childhood, a rapidly progressive disease course leading to generalized areflexic tetraplegia with contractures, severe scoliosis, hyperlordosis, and progressive respiratory insufficiency leading to assisted ventilation. Cranial nerve functions are normal and tongue wasting and fasciculations are absent. Milder phenotype with a moderate generalized weakness and slower disease progress was reported. There is evidence the disease is caused by homozygous mutation in the gene encoding pleckstrin homology domain-containing protein, family G member 5 (PLEKHG5) on chromosome 1p36.
Neuronopathy, distal hereditary motor, type 2B
MedGen UID:
382017
Concept ID:
C2608087
Disease or Syndrome
Some individuals with distal hereditary motor neuropathy, type II have weakening of the muscles in the hands and forearms. This weakening is less pronounced than in the lower limbs and does not usually result in paralysis.\n\nOnset of distal hereditary motor neuropathy, type II ranges from the teenage years through mid-adulthood. The initial symptoms of the disorder are cramps or weakness in the muscles of the big toe and later, the entire foot. Over a period of approximately 5 to 10 years, affected individuals experience a gradual loss of muscle tissue (atrophy) in the lower legs. They begin to have trouble walking and running, and eventually may have complete paralysis of the lower legs. The thigh muscles may also be affected, although generally this occurs later and is less severe.\n\nDistal hereditary motor neuropathy, type II is a progressive disorder that affects nerve cells in the spinal cord. It results in muscle weakness and affects movement, primarily in the legs.
Neuronopathy, distal hereditary motor, type 2C
MedGen UID:
461969
Concept ID:
C3150619
Disease or Syndrome
Any neuronopathy, distal hereditary motor in which the cause of the disease is a mutation in the HSPB3 gene.
Spinocerebellar ataxia type 36
MedGen UID:
483339
Concept ID:
C3472711
Disease or Syndrome
Spinocerebellar ataxia-36 (SCA36) is a slowly progressive neurodegenerative disorder characterized by adult-onset gait ataxia, eye movement abnormalities, tongue fasciculations, and variable upper motor neuron signs. Some affected individuals may develop hearing loss (summary by Garcia-Murias et al., 2012). For a general discussion of autosomal dominant spinocerebellar ataxia, see SCA1 (164400).
Actin accumulation myopathy
MedGen UID:
777997
Concept ID:
C3711389
Disease or Syndrome
Congenital myopathy-2A (CMYP2A) is an autosomal dominant disorder of the skeletal muscle characterized by infantile- or childhood-onset myopathy with delayed motor milestones and nonprogressive muscle weakness. Of the patients with congenital myopathy caused by mutation in the ACTA1 gene, about 90% carry heterozygous mutations that are usually de novo and cause the severe infantile phenotype (CMYP2C; 620278). Some patients with de novo mutations have a more typical and milder disease course with delayed motor development and proximal muscle weakness, but are able to achieve independent ambulation. Less frequently, autosomal dominant transmission of the disorder within a family may occur when the ACTA1 mutation produces a phenotype compatible with adult life. Of note, intrafamilial variability has also been reported: a severely affected proband may be identified and then mildly affected or even asymptomatic relatives are found to carry the same mutation. The severity of the disease most likely depends on the detrimental effect of the mutation, although there are probably additional modifying factors (Ryan et al., 2001; Laing et al., 2009; Sanoudou and Beggs, 2001; Agrawal et al., 2004; Nowak et al., 2013; Sewry et al., 2019; Laitila and Wallgren-Pettersson, 2021). The most common histologic finding on muscle biopsy in patients with ACTA1 mutations is the presence of 'nemaline rods,' which represent abnormal thread- or rod-like structures ('nema' is Greek for 'thread'). However, skeletal muscle biopsy from patients with mutations in the ACTA1 gene can show a range of pathologic phenotypes. These include classic rods, intranuclear rods, clumped filaments, cores, or fiber-type disproportion, all of which are nonspecific pathologic findings and not pathognomonic of a specific congenital myopathy. Most patients have clinically severe disease, regardless of the histopathologic phenotype (Nowak et al., 2007; Sewry et al., 2019). ACTA1 mutations are the second most common cause of congenital myopathies classified histologically as 'nemaline myopathy' after mutations in the NEB gene (161650). ACTA1 mutations are overrepresented in the severe phenotype with early death (Laing et al., 2009). For a discussion of genetic heterogeneity of congenital myopathy, see CMYP1A (117000). For a discussion of genetic heterogeneity of nemaline myopathy, see NEM2 (256030).
Charcot-Marie-Tooth disease axonal type 2CC
MedGen UID:
934757
Concept ID:
C4310790
Disease or Syndrome
Axonal Charcot-Marie-Tooth disease type 2CC is an autosomal dominant peripheral neuropathy that predominantly affects the lower limbs, resulting in muscle weakness and atrophy and gait impairment. Other features include distal sensory impairment and less severe involvement of the upper limbs. The age at onset and severity are variable (summary by Rebelo et al., 2016). For a phenotypic description and a discussion of genetic heterogeneity of axonal CMT type 2, see CMT2A (118210).
MYH7-related skeletal myopathy
MedGen UID:
1647391
Concept ID:
C4552004
Disease or Syndrome
Laing distal myopathy is characterized by early-onset weakness (usually before age 5 years) that initially involves the dorsiflexors of the ankles and great toes and then the finger extensors, especially those of the third and fourth fingers. Weakness of the neck flexors is seen in most affected individuals and mild facial weakness is often present. After distal weakness has been present for more than ten years, mild proximal weakness may be observed. Life expectancy is normal.
Myofibrillar myopathy 4
MedGen UID:
1648314
Concept ID:
C4721886
Disease or Syndrome
Myofibrillar myopathy-4 (MFM4) is an autosomal dominant disorder characterized by adult-onset distal muscle weakness primarily affecting the lower limbs at onset. Affected individuals usually present with gait difficulties in their forties, followed by slow progression with eventual involvement of the hands and proximal muscles of the lower limbs. Rare patients may develop cardiomyopathy. Skeletal muscle biopsy shows myopathic changes with myofibrillar changes (Selcen and Engel, 2005; Griggs et al., 2007). For a phenotypic description and a discussion of genetic heterogeneity of myofibrillar myopathy, see MFM1 (601419).
Charcot-Marie-Tooth Disease, axonal, type 2GG
MedGen UID:
1794143
Concept ID:
C5561933
Disease or Syndrome
Charcot-Marie-Tooth disease type 2GG (CMT2GG) is an autosomal dominant axonal peripheral neuropathy characterized by slowly progressive distal muscle weakness and atrophy primarily affecting the lower limbs and causing difficulty walking. The onset is usually in adulthood, although rare patients may have mild symptoms from childhood. Some individuals may also have involvement of the hands. Although most patients have hypo- or areflexia at the ankles, distal sensory impairment is not always present, indicating a spectrum of disease encompassing both distal hereditary neuropathy and axonal CMT. Electrophysiologic studies are consistent with a axonal process (summary by Mendoza-Ferreira et al., 2020). For a discussion of genetic heterogeneity of axonal CMT, see CMT2A1 (118210).
Autosomal dominant childhood-onset proximal spinal muscular atrophy without contractures
MedGen UID:
1830501
Concept ID:
C5780022
Disease or Syndrome
Spinal muscular atrophy (SMA) is a hereditary neuromuscular disorder characterized by degeneration of spinal cord motor neurons resulting in muscle weakness. SMALED shows autosomal dominant inheritance with muscle weakness predominantly affecting the proximal lower extremities (Harms et al., 2010). The most common form of SMA (see, e.g., SMA1, 253300) shows autosomal recessive inheritance and is due to mutation in the SMN1 gene (600354) on chromosome 5q. Genetic Heterogeneity of Lower Extremity-Predominant Spinal Muscular Atrophy See also SMALED2A (615290) and SMALED2B (618291), both of which are caused by mutation in the BICD2 gene (609797) on chromosome 9q22. SMALED2A and SMALED2B differ in age at onset and severity, with SMALED2B being more severe.
Werdnig-Hoffmann disease
MedGen UID:
1845578
Concept ID:
C5848259
Disease or Syndrome
Spinal muscular atrophy (SMA) is characterized by muscle weakness and atrophy resulting from progressive degeneration and irreversible loss of the anterior horn cells in the spinal cord (i.e., lower motor neurons) and the brain stem nuclei. The onset of weakness ranges from before birth to adulthood. The weakness is symmetric, proximal > distal, and progressive. Before the genetic basis of SMA was understood, it was classified into clinical subtypes based on maximum motor function achieved; however, it is now apparent that the phenotype of SMN1-associated SMA spans a continuum without clear delineation of subtypes. With supportive care only, poor weight gain with growth failure, restrictive lung disease, scoliosis, and joint contractures are common complications; however, newly available targeted treatment options are changing the natural history of this disease.

Recent clinical studies

Etiology

Elkhateeb N, Selim R, Soliman NA, Atia FM, Abouelwoun II, Elmonem MA, Helmy R
Pediatr Nephrol 2022 Jul;37(7):1555-1566. Epub 2021 Nov 18 doi: 10.1007/s00467-021-05343-x. PMID: 34791528
Aras YG, Aydemir Y, Güngen BD, Güngen AC
Int J Chron Obstruct Pulmon Dis 2018;13:1857-1862. Epub 2018 Jun 7 doi: 10.2147/COPD.S159738. PMID: 29922052Free PMC Article
Cronin NJ, Peltonen J, Ishikawa M, Komi PV, Avela J, Sinkjaer T, Voigt M
Clin Biomech (Bristol, Avon) 2010 Jun;25(5):476-82. Epub 2010 Mar 2 doi: 10.1016/j.clinbiomech.2010.01.018. PMID: 20193974
Cho SC, Katzberg HD, Rama A, Kim BJ, Roh H, Park J, Katz J, So YT
Muscle Nerve 2010 Mar;41(3):324-8. doi: 10.1002/mus.21511. PMID: 19882633
Curatolo M, Arendt-Nielsen L, Petersen-Felix S
Phys Med Rehabil Clin N Am 2006 May;17(2):287-302. doi: 10.1016/j.pmr.2005.12.010. PMID: 16616268

Diagnosis

Abdel-Mannan O, Eyre M, Löbel U, Bamford A, Eltze C, Hameed B, Hemingway C, Hacohen Y
JAMA Neurol 2020 Nov 1;77(11):1440-1445. doi: 10.1001/jamaneurol.2020.2687. PMID: 32609336Free PMC Article
Bromberg MB
Muscle Nerve 2020 Feb;61(2):131-142. Epub 2019 Oct 23 doi: 10.1002/mus.26718. PMID: 31579956
Leonardis L, Podnar S
Neurophysiol Clin 2017 Dec;47(5-6):405-412. Epub 2017 Aug 24 doi: 10.1016/j.neucli.2017.07.003. PMID: 28844760
Davis CG
J Forensic Leg Med 2013 Feb;20(2):74-85. Epub 2012 Jul 4 doi: 10.1016/j.jflm.2012.05.004. PMID: 23357391
Rapin I
Adv Neurol 1986;43:65-85. PMID: 3080854

Therapy

Elkhateeb N, Selim R, Soliman NA, Atia FM, Abouelwoun II, Elmonem MA, Helmy R
Pediatr Nephrol 2022 Jul;37(7):1555-1566. Epub 2021 Nov 18 doi: 10.1007/s00467-021-05343-x. PMID: 34791528
Dag E, Gokce B, Kocak M
Skinmed 2013 Jul-Aug;11(4):251-2. PMID: 24053013
Schwingenschuh P, Katschnig P, Seiler S, Saifee TA, Aguirregomozcorta M, Cordivari C, Schmidt R, Rothwell JC, Bhatia KP, Edwards MJ
Mov Disord 2011 Dec;26(14):2509-15. Epub 2011 Sep 28 doi: 10.1002/mds.23922. PMID: 21956485Free PMC Article
Cronin NJ, Peltonen J, Ishikawa M, Komi PV, Avela J, Sinkjaer T, Voigt M
Clin Biomech (Bristol, Avon) 2010 Jun;25(5):476-82. Epub 2010 Mar 2 doi: 10.1016/j.clinbiomech.2010.01.018. PMID: 20193974
Velasco F, Carrillo-Ruiz JD, Castro G, Argüelles C, Velasco AL, Kassian A, Guevara U
Pain 2009 Dec 15;147(1-3):91-8. Epub 2009 Sep 29 doi: 10.1016/j.pain.2009.08.024. PMID: 19793621

Prognosis

Biurrun Manresa JA, Sörensen J, Andersen OK, Arendt-Nielsen L, Gerdle B
Clin J Pain 2015 Dec;31(12):1046-53. doi: 10.1097/AJP.0000000000000209. PMID: 25789414
Podnar S, Gregory WT
Neurourol Urodyn 2010 Nov;29(8):1387-92. doi: 10.1002/nau.20893. PMID: 20976812Free PMC Article
Velasco F, Carrillo-Ruiz JD, Castro G, Argüelles C, Velasco AL, Kassian A, Guevara U
Pain 2009 Dec 15;147(1-3):91-8. Epub 2009 Sep 29 doi: 10.1016/j.pain.2009.08.024. PMID: 19793621
Curatolo M, Arendt-Nielsen L, Petersen-Felix S
Phys Med Rehabil Clin N Am 2006 May;17(2):287-302. doi: 10.1016/j.pmr.2005.12.010. PMID: 16616268
Rapin I
Adv Neurol 1986;43:65-85. PMID: 3080854

Clinical prediction guides

Sas D, Gaudel F, Verdier D, Kolta A
Exp Physiol 2024 Jan;109(1):100-111. Epub 2023 Dec 16 doi: 10.1113/EP090769. PMID: 38103003Free PMC Article
Núñez-Cortés R, Horment-Lara G, Tapia-Malebran C, Castro M, Barros S, Vera N, Pérez-Alenda S, Pablo Santelices J, Rivera-Lillo G, Cruz-Montecinos C
J Electromyogr Kinesiol 2023 Aug;71:102793. Epub 2023 May 30 doi: 10.1016/j.jelekin.2023.102793. PMID: 37285714
Ayhan FF, Aykut M, Genç H, Mansız Kaplan B, Soran A
Lymphat Res Biol 2019 Feb;17(1):78-86. Epub 2018 Oct 24 doi: 10.1089/lrb.2018.0011. PMID: 30358471
Dag E, Gokce B, Kocak M
Skinmed 2013 Jul-Aug;11(4):251-2. PMID: 24053013
Ismail M, Gabr K, Shalaby R
J Pediatr Surg 2010 Mar;45(3):533-9. doi: 10.1016/j.jpedsurg.2009.09.013. PMID: 20223316

Recent systematic reviews

Nepal G, Shrestha GS, Rehrig JH, Gajurel BP, Ojha R, Agrawal A, Panthi S, Khatri B, Adhikari I
J Nepal Health Res Counc 2021 Apr 23;19(1):10-18. doi: 10.33314/jnhrc.v19i1.3410. PMID: 33934126

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