U.S. flag

An official website of the United States government

Format

Send to:

Choose Destination

Upper limb spasticity

MedGen UID:
220882
Concept ID:
C1273957
Finding
Synonym: Spasticity of the upper limbs
SNOMED CT: Upper limb spasticity (394680009)
 
HPO: HP:0006986

Term Hierarchy

CClinical test,  RResearch test,  OOMIM,  GGeneReviews,  VClinVar  
  • CROGVUpper limb spasticity

Conditions with this feature

Troyer syndrome
MedGen UID:
97950
Concept ID:
C0393559
Disease or Syndrome
Troyer syndrome is characterized by progressive spastic paraparesis, dysarthria, pseudobulbar palsy, distal amyotrophy, short stature, and subtle skeletal abnormalities. Most affected children exhibit delays in walking and speech and difficulty in managing oral secretions, followed by increased lower-limb spasticity and slow deterioration in both gait and speech. Mild cerebellar signs are common. The most severely affected individuals have choreoathetosis. Emotional lability / difficulty in controlling emotions and affective disorders, such as inappropriate euphoria and/or crying, are frequently described. Life expectancy is normal.
Hereditary spastic paraplegia 26
MedGen UID:
373138
Concept ID:
C1836632
Disease or Syndrome
SPG26 is an autosomal recessive form of complicated spastic paraplegia characterized by onset in the first 2 decades of life of gait abnormalities due to lower limb spasticity and muscle weakness. Some patients have upper limb involvement. Additional features include intellectual disability, peripheral neuropathy, dysarthria, cerebellar signs, extrapyramidal signs, and cortical atrophy. The disorder is slowly progressive (summary by Boukhris et al., 2013). For a discussion of genetic heterogeneity of autosomal recessive SPG, see SPG5A (270800).
Hereditary spastic paraplegia 5A
MedGen UID:
376521
Concept ID:
C1849115
Disease or Syndrome
Spastic paraplegia-5A (SPG5A) is an autosomal recessive neurologic disorder with a wide phenotypic spectrum. Some patients have pure spastic paraplegia affecting only gait, whereas others may have a complicated phenotype with additional manifestations, including optic atrophy or cerebellar ataxia (summary by Arnoldi et al., 2012). The hereditary spastic paraplegias (SPG) are a group of clinically and genetically diverse disorders characterized by progressive, usually severe, lower extremity spasticity; see reviews of Fink et al. (1996) and Fink (1997). Inheritance is most often autosomal dominant (see 182600), but X-linked (see 303350) and autosomal recessive forms also occur. Genetic Heterogeneity of Autosomal Recessive Spastic Paraplegia Autosomal recessive forms of SPG include SPG7 (607259), caused by mutation in the paraplegin gene (602783) on chromosome 16q24; SPG9B (616586), caused by mutation in the ALDH18A1 gene (138250) on 10q24; SPG11 (604360), caused by mutation in the spatacsin gene (610844) on 15q21; SPG15 (270700), caused by mutation in the ZFYVE26 gene (612012) on 14q24; SPG18 (611225), caused by mutation in the ERLIN2 gene (611605) on 8p11; SPG20 (275900), caused by mutation in the spartin gene (607111) on 13q12; SPG21 (248900), caused by mutation in the maspardin gene (608181) on 15q21; SPG26 (609195), caused by mutation in the B4GALNT1 gene (601873) on 12q13; SPG28 (609340), caused by mutation in the DDHD1 gene (614603) on 14q22; SPG30 (610357), caused by mutation in the KIF1A gene (601255) on 2q37; SPG35 (612319), caused by mutation in the FA2H gene (611026) on 16q23; SPG39 (612020), caused by mutation in the PNPLA6 gene (603197) on 19p13; SPG43 (615043), caused by mutation in the C19ORF12 gene (614297) on 19q12; SPG44 (613206), caused by mutation in the GJC2 gene (608803) on 1q42; SPG45 (613162), caused by mutation in the NT5C2 gene (600417) on 10q24; SPG46 (614409), caused by mutation in the GBA2 gene (609471) on 9p13; SPG48 (613647), caused by mutation in the KIAA0415 gene (613653) on 7p22; SPG50 (612936), caused by mutation in the AP4M1 gene (602296) on 7q22; SPG51 (613744), caused by mutation in the AP4E1 gene (607244) on 15q21; SPG52 (614067), caused by mutation in the AP4S1 gene (607243) on 14q12; SPG53 (614898), caused by mutation in the VPS37A gene (609927) on 8p22; SPG54 (615033), caused by mutation in the DDHD2 gene (615003) on 8p11; SPG55 (615035), caused by mutation in the MTRFR gene on 12q24; SPG56 (615030), caused by mutation in the CYP2U1 gene (610670) on 4q25; SPG57 (615658), caused by mutation in the TFG gene (602498) on 3q12; SPG61 (615685), caused by mutation in the ARL6IP1 gene (607669) on 1p12; SPG62 (615681), caused by mutation in the ERLIN1 gene on 10q24; SPG63 (615686), caused by mutation in the AMPD2 gene (102771) on 1p13; SPG64 (615683), caused by mutation in the ENTPD1 gene (601752) on 10q24; SPG72 (615625), caused by mutation in the REEP2 gene (609347) on 5q31; SPG74 (616451), caused by mutation in the IBA57 gene (615316) on 1q42; SPG75 (616680), caused by mutation in the MAG gene (159460) on 19q13; SPG76 (616907), caused by mutation in the CAPN1 gene (114220) on 11q13; SPG77 (617046), caused by mutation in the FARS2 gene (611592) on 6p25; SPG78 (617225), caused by mutation in the ATP13A2 gene (610513) on 1p36; SPG79 (615491), caused by mutation in the UCHL1 gene (191342) on 4p13; SPG81 (618768), caused by mutation in the SELENOI gene (607915) on 2p23; SPG82 (618770), caused by mutation in the PCYT2 gene (602679) on 17q25; SPG83 (619027), caused by mutation in the HPDL gene (618994) on 1p34; SPG84 (619621), caused by mutation in the PI4KA gene (600286) on 22q11; SPG85 (619686), caused by mutation in the RNF170 gene (614649) on 8p11; SPG86 (619735), caused by mutation in the ABHD16A gene (142620) on 6p21; SPG87 (619966), caused by mutation in the TMEM63C gene (619953) on 14q24; SPG89 (620379), caused by mutation in the AMFR gene (603243) on 16q13; and SPG90B (620417), caused by mutation in the SPTSSA gene (613540) on 14q13. Additional autosomal recessive forms of SPG have been mapped to chromosomes 3q (SPG14; 605229), 13q14 (SPG24; 607584), 6q (SPG25; 608220), and 10q22 (SPG27; 609041). A disorder that was formerly designated SPG49 has been reclassified as hereditary sensory and autonomic neuropathy-9 with developmental delay (HSAN9; 615031).
Hereditary spastic paraplegia 29
MedGen UID:
346682
Concept ID:
C1857855
Disease or Syndrome
A complex form of hereditary spastic paraplegia characterised by a spastic paraplegia presenting in adolescence, associated with the additional manifestations of sensorial hearing impairment due to auditory neuropathy and persistent vomiting due to a hiatal or paraoesophageal hernia. The phenotype has been mapped to a locus on chromosome 1p31.1-p21.1.
Amyotrophic lateral sclerosis type 2, juvenile
MedGen UID:
349246
Concept ID:
C1859807
Disease or Syndrome
ALS2-related disorder involves retrograde degeneration of the upper motor neurons of the pyramidal tracts and comprises a clinical continuum of the following three phenotypes: Infantile ascending hereditary spastic paraplegia (IAHSP), characterized by onset of spasticity with increased reflexes and sustained clonus of the lower limbs within the first two years of life, progressive weakness and spasticity of the upper limbs by age seven to eight years, and wheelchair dependence in the second decade with progression toward severe spastic tetraparesis and a pseudobulbar syndrome caused by progressive cranial nerve involvement. Juvenile primary lateral sclerosis (JPLS), characterized by upper motor neuron findings of pseudobulbar palsy and spastic quadriplegia without dementia or cerebellar, extrapyramidal, or sensory signs. Juvenile amyotrophic lateral sclerosis (JALS or ALS2), characterized by onset between ages three and 20 years. All affected individuals show a spastic pseudobulbar syndrome (spasticity of speech and swallowing) together with spastic paraplegia. Some individuals are bedridden by age 12 to 50 years.
Hereditary spastic paraplegia 8
MedGen UID:
400359
Concept ID:
C1863704
Disease or Syndrome
Hereditary spastic paraplegia 8 (SPG8) is a slowly progressive pure spastic paraplegia of the lower limbs (i.e., pyramidal signs including hyperreflexia, spasticity, and occasionally clonus without other neurologic findings). Some affected individuals have urinary urgency that usually becomes apparent at the same time as the spasticity. Onset is between ages ten and 59 years. Affected individuals often become wheelchair dependent. While intra- and interfamilial phenotypic variability is high, SPG8 is typically more severe than other types of hereditary spastic paraplegia.
Pontocerebellar hypoplasia type 6
MedGen UID:
370596
Concept ID:
C1969084
Congenital Abnormality
Pontocerebellar hypoplasia (PCH) is a heterogeneous group of disorders characterized by an abnormally small cerebellum and brainstem and associated with severe developmental delay (Edvardson et al., 2007). For a phenotypic description and a discussion of genetic heterogeneity of PCH, see PCH1 (607596).
Hereditary spastic paraplegia 18
MedGen UID:
442343
Concept ID:
C2749936
Disease or Syndrome
Spastic paraplegia-18B (SPG18B) is a severe autosomal recessive neurologic disorder characterized by onset in early childhood of progressive spastic paraplegia resulting in motor disability. Most affected individuals have severe psychomotor retardation. Some may develop significant joint contractures (summary by Alazami et al., 2011 and Yildirim et al., 2011).
Hereditary spastic paraplegia 44
MedGen UID:
413042
Concept ID:
C2750784
Disease or Syndrome
A very rare, complex form of hereditary spastic paraplegia characterised by a late-onset, slowly progressive spastic paraplegia associated with mild ataxia and dysarthria, upper extremity involvement (i.e. loss of finger dexterity, dysmetria), and mild cognitive impairment, without the presence of nystagmus. A hypomyelinating leucodystrophy and thin corpus callosum is observed in all cases and psychomotor development is normal or near normal. Caused by mutations in the GJC2 gene (1q41-q42) encoding the gap junction gamma-2 protein.
Hereditary spastic paraplegia 46
MedGen UID:
473687
Concept ID:
C2828721
Disease or Syndrome
Autosomal recessive spastic paraplegia-46 (SPG46) is a neurodegenerative disorder characterized by onset in childhood of slowly progressive spastic paraplegia and cerebellar signs. Some patients have cognitive impairment, cataracts, and cerebral, cerebellar, and corpus callosum atrophy on brain imaging (summary by Boukhris et al., 2010 and Martin et al., 2013). For a discussion of genetic heterogeneity of autosomal recessive spastic paraplegia, see SPG5A (270800).
Hereditary spastic paraplegia 37
MedGen UID:
422458
Concept ID:
C2936880
Disease or Syndrome
A pure form of hereditary spastic paraplegia with a childhood to adulthood-onset of slowly progressive spastic gait, extensor plantar responses, brisk tendon reflexes in arms and legs, decreased vibration sense at ankles and urinary dysfunction. Ankle clonus is also reported in some patients.
Megalencephalic leukoencephalopathy with subcortical cysts 2A
MedGen UID:
462705
Concept ID:
C3151355
Disease or Syndrome
The classic phenotype of megalencephalic leukoencephalopathy with subcortical cysts (MLC) is characterized by early-onset macrocephaly, often in combination with mild gross motor developmental delay and seizures; gradual onset of ataxia, spasticity, and sometimes extrapyramidal findings; and usually late onset of mild mental deterioration. Macrocephaly, observed in virtually all individuals, may be present at birth but more frequently develops during the first year of life. The degree of macrocephaly is variable and can be as great as 4 to 6 SD above the mean in some individuals. After the first year of life, head growth rate normalizes and growth follows a line parallel to and usually several centimeters above the 98th centile. Initial mental and motor development is normal in most individuals. Walking is often unstable, followed by ataxia of the trunk and extremities, then minor signs of pyramidal dysfunction and brisk deep-tendon stretch reflexes. Almost all individuals have epilepsy from an early age. The epilepsy is typically well controlled with anti-seizure medication, but status epilepticus occurs relatively frequently. Mental deterioration is late and mild. Disease severity ranges from independent walking for a few years only to independent walking in the fifth decade. Some individuals have died in their teens or twenties; others are alive in their fifties. An improving phenotype has a similar initial presentation with delayed mental or motor development, followed by an improving clinical course: macrocephaly usually persists, but some children become normocephalic; motor function improves or normalizes; hypotonia and clumsiness may persist in some or neurologic examination may become normal. Some have intellectual disability that is stable, with or without autism. Epilepsy and status epilepticus may occur.
Multiple congenital anomalies-hypotonia-seizures syndrome 2
MedGen UID:
477139
Concept ID:
C3275508
Disease or Syndrome
Multiple congenital anomalies-hypotonia-seizures syndrome-2 (MCAHS2) is an X-linked recessive neurodevelopmental disorder characterized by dysmorphic features, neonatal hypotonia, early-onset myoclonic seizures, and variable congenital anomalies involving the central nervous, cardiac, and urinary systems. Some affected individuals die in infancy (summary by Johnston et al., 2012). The phenotype shows clinical variability with regard to severity and extraneurologic features. However, most patients present in infancy with early-onset epileptic encephalopathy associated with developmental arrest and subsequent severe neurologic disability; these features are consistent with a form of developmental and epileptic encephalopathy (DEE) (summary by Belet et al., 2014, Kato et al., 2014). The disorder is caused by a defect in glycosylphosphatidylinositol (GPI) biosynthesis. For a discussion of genetic heterogeneity of MCAHS, see MCAHS1 (614080). For a discussion of nomenclature and genetic heterogeneity of DEE, see 308350. For a discussion of genetic heterogeneity of GPI biosynthesis defects, see GPIBD1 (610293).
Hereditary spastic paraplegia 54
MedGen UID:
761341
Concept ID:
C3539495
Disease or Syndrome
Spastic paraplegia-54 (SPG54) is a complicated form of spastic paraplegia, a neurodegenerative disorder affecting fibers of the corticospinal tract. Affected individuals have delayed psychomotor development, intellectual disability, and early-onset spasticity of the lower limbs. Brain MRI shows a thin corpus callosum and periventricular white matter lesions. Brain magnetic resonance spectroscopy shows an abnormal lipid peak (summary by Schuurs-Hoeijmakers et al., 2012). For a general phenotypic description and a discussion of genetic heterogeneity of autosomal recessive spastic paraplegia, see 270800.
Early-onset progressive diffuse brain atrophy-microcephaly-muscle weakness-optic atrophy syndrome
MedGen UID:
934638
Concept ID:
C4310671
Disease or Syndrome
PEBAT is an autosomal recessive neurodevelopmental disorder characterized by severely delayed psychomotor development apparent soon after birth or in infancy, profound intellectual disability, poor or absent speech, and seizures. Most patients are never able to walk due to hypotonia or spasticity. Brain imaging shows cerebral and cerebellar atrophy, thin corpus callosum, and secondary hypomyelination. The disorder shows progressive features, including microcephaly, consistent with a neurodegenerative process (summary by Miyake et al., 2016; Flex et al., 2016).
Spastic paraplegia 80, autosomal dominant
MedGen UID:
1682111
Concept ID:
C5193084
Disease or Syndrome
Spastic paraplegia-80 (SPG80) is an autosomal dominant juvenile-onset neurologic disorder characterized by onset of progressive spasticity and hyperreflexia affecting mainly the lower limbs and resulting in difficulty walking or loss of independent ambulation, sometimes as early as the second decade. Some patients may have cerebellar signs and mild cognitive impairment, but most have a pure form of the disorder (summary by Farazi Fard et al., 2019). For a general phenotypic description and a discussion of genetic heterogeneity of autosomal dominant spastic paraplegia, see SPG3A (182600).
Developmental and epileptic encephalopathy, 76
MedGen UID:
1673011
Concept ID:
C5193113
Disease or Syndrome
Developmental and epileptic encephalopathy-76 (DEE76) is an autosomal recessive neurodevelopmental disorder characterized by early-onset, usually refractory, seizures, severely delayed global development, hypotonia, peripheral spasticity, and abnormalities on brain imaging, mainly cerebral atrophy and delayed myelination. Some patients may have additional features, such as scoliosis or microcephaly. The disorder may result in death in childhood (summary by Bell et al., 2019). For a general phenotypic description and a discussion of genetic heterogeneity of DEE, see 308350.
Spastic paraplegia 81, autosomal recessive
MedGen UID:
1711668
Concept ID:
C5394033
Disease or Syndrome
Spastic paraplegia-81 (SPG81) is an autosomal recessive neurologic disorder with onset in infancy. Affected individuals have delayed motor development, progressive spasticity, and other neurologic impairment, including impaired intellectual development and speech delay. Some patients may have additional features, including bifid uvula, microcephaly, seizures, and variable ocular anomalies. One severely affected patient was reported to have cortical visual loss, sensorineural deafness, and achievement of almost no developmental milestones. Brain imaging shows white matter abnormalities, hypomyelination with progressive white matter loss, and sometimes cerebral atrophy. These significant additional abnormalities enable classification of this disorder as a complicated form of SPG (summary by Ahmed et al., 2017 and Horibata et al., 2018). For a discussion of genetic heterogeneity of autosomal recessive spastic paraplegia, see SPG5A (270800).
Kohlschutter-Tonz syndrome-like
MedGen UID:
1781649
Concept ID:
C5543202
Disease or Syndrome
Den Hoed-de Boer-Voisin syndrome (DHDBV) is characterized by global developmental delay with moderately to severely impaired intellectual development, poor or absent speech, and delayed motor skills. Although the severity of the disorder varies, many patients are nonverbal and have hypotonia with inability to sit or walk. Early-onset epilepsy is common and may be refractory to treatment, leading to epileptic encephalopathy and further interruption of developmental progress. Most patients have feeding difficulties with poor overall growth and dysmorphic facial features, as well as significant dental anomalies resembling amelogenesis imperfecta. The phenotype is reminiscent of Kohlschutter-Tonz syndrome (KTZS; 226750). More variable features of DHDBV include visual defects, behavioral abnormalities, and nonspecific involvement of other organ systems (summary by den Hoed et al., 2021).
Spastic paraplegia 85, autosomal recessive
MedGen UID:
1794263
Concept ID:
C5562053
Disease or Syndrome
Autosomal recessive spastic paraplegia-85 (SPG85) is a neurologic disorder characterized by the onset of motor symptoms in the first few years of life. Affected individuals have spasticity and hyperreflexia of the lower limbs resulting in gait abnormalities. Older patients may have upper limb involvement and demonstrate axonal polyneuropathy. Additional features include optic atrophy, dysarthria, dysphagia, ataxia, and urinary incontinence. Brain imaging may show cerebellar atrophy (summary by Wagner et al., 2019). For a discussion of genetic heterogeneity of autosomal recessive spastic paraplegia, see SPG5A (270800).
Spastic paraplegia 87, autosomal recessive
MedGen UID:
1813069
Concept ID:
C5774182
Disease or Syndrome
Autosomal recessive spastic paraplegia-87 (SPG87) is a neurologic disorder characterized by the onset of lower limb spasticity in infancy or early childhood. Affected individuals have mildly delayed walking, spastic gait, and hyperreflexia; the upper limbs and bulbar regions are not affected. Some patients may also have mild intellectual disability or speech problems. Thus, SPG87 can manifest as either a pure or a complex disorder (Tabara et al., 2022). For a discussion of genetic heterogeneity of autosomal recessive SPG, see SPG5A (270800).
Megalencephalic leukoencephalopathy with subcortical cysts 3
MedGen UID:
1841261
Concept ID:
C5830625
Disease or Syndrome
Megalencephalic leukoencephalopathy with subcortical cysts-3 (MLC3) is a neurodegenerative disorder characterized by increased head circumference in infancy followed by progressive motor and cognitive decline in early childhood. Affected individuals either do not achieve walking or lose independent ambulation in the first or second decades. Cognitive impairment is variable and accompanied by poor speech and dysarthria. Most patients have early-onset seizures, which may be mild or refractory. Brain imaging shows unremitting megalencephalic leukoencephalopathy with subcortical cysts and swelling of the cerebral white matter (Passchier et al., 2023). For a discussion of genetic heterogeneity of megalencephalic leukoencephalopathy with subcortical cysts, see MLC1 (604004).

Professional guidelines

PubMed

Minelli C, Luvizutto GJ, Cacho RO, Neves LO, Magalhães SCSA, Pedatella MTA, Mendonça LIZ, Ortiz KZ, Lange MC, Ribeiro PW, Souza LAPS, Milani C, Cruz DMCD, Costa RDMD, Conforto AB, Carvalho FMM, Ciarlini BS, Frota NAF, Almeida KJ, Schochat E, Oliveira TP, Miranda C, Piemonte MEP, Lopes LCG, Lopes CG, Tosin MHS, Oliveira BC, Oliveira BGRB, Castro SS, Andrade JBC, Silva GS, Pontes-Neto OM, Carvalho JJF, Martins SCO, Bazan R
Arq Neuropsiquiatr 2022 Jul;80(7):741-758. Epub 2022 Sep 29 doi: 10.1055/s-0042-1757692. PMID: 36254447Free PMC Article
Black L, Gaebler-Spira D
Hand Clin 2018 Nov;34(4):455-464. Epub 2018 Aug 18 doi: 10.1016/j.hcl.2018.06.003. PMID: 30286960
Simpson DM, Hallett M, Ashman EJ, Comella CL, Green MW, Gronseth GS, Armstrong MJ, Gloss D, Potrebic S, Jankovic J, Karp BP, Naumann M, So YT, Yablon SA
Neurology 2016 May 10;86(19):1818-26. Epub 2016 Apr 18 doi: 10.1212/WNL.0000000000002560. PMID: 27164716Free PMC Article

Recent clinical studies

Etiology

Senarath ID, Thalwathte RD, Pathirage M, Kularatne SAM
PLoS One 2023;18(5):e0283321. Epub 2023 May 26 doi: 10.1371/journal.pone.0283321. PMID: 37235581Free PMC Article
Delgado MR, Tilton A, Carranza-Del Río J, Dursun N, Bonikowski M, Aydin R, Maciag-Tymecka I, Oleszek J, Dabrowski E, Grandoulier AS, Picaut P; Dysport in PUL study group
Dev Med Child Neurol 2021 May;63(5):592-600. Epub 2020 Nov 18 doi: 10.1111/dmcn.14733. PMID: 33206382Free PMC Article
Mahmood A, Veluswamy SK, Hombali A, Mullick A, N M, Solomon JM
Arch Phys Med Rehabil 2019 Apr;100(4):751-768. Epub 2018 Nov 16 doi: 10.1016/j.apmr.2018.10.016. PMID: 30452892
Guo J, Qian S, Wang Y, Xu A
Int J Rehabil Res 2019 Mar;42(1):31-35. doi: 10.1097/MRR.0000000000000316. PMID: 30211721Free PMC Article
Dong Y, Wu T, Hu X, Wang T
Eur J Phys Rehabil Med 2017 Apr;53(2):256-267. Epub 2016 Nov 11 doi: 10.23736/S1973-9087.16.04329-X. PMID: 27834471

Diagnosis

Fitoussi F, Lallemant-Dudek P
Orthop Traumatol Surg Res 2024 Feb;110(1S):103763. Epub 2023 Nov 20 doi: 10.1016/j.otsr.2023.103763. PMID: 37992866
Crowe CS, Pino PA, Rhee PC; Upper Extremity Spasticity Working Group
J Hand Surg Eur Vol 2023 Nov;48(10):986-997. Epub 2023 Sep 17 doi: 10.1177/17531934231192843. PMID: 37717178
Wang C, Peng L, Hou ZG, Zhang P
IEEE Trans Neural Syst Rehabil Eng 2021;29:2242-2251. Epub 2021 Nov 3 doi: 10.1109/TNSRE.2021.3121780. PMID: 34673492
Shiner CT, Vratsistas-Curto A, Bramah V, Faux SG, Watanabe Y
Disabil Rehabil 2020 Jul;42(15):2170-2177. Epub 2019 Mar 31 doi: 10.1080/09638288.2018.1555620. PMID: 30929536
Flinn SR, Craven K
Top Stroke Rehabil 2014 Jul-Aug;21(4):296-302. doi: 10.1310/tsr2104-296. PMID: 25150661

Therapy

Senarath ID, Thalwathte RD, Pathirage M, Kularatne SAM
PLoS One 2023;18(5):e0283321. Epub 2023 May 26 doi: 10.1371/journal.pone.0283321. PMID: 37235581Free PMC Article
Delgado MR, Tilton A, Carranza-Del Río J, Dursun N, Bonikowski M, Aydin R, Maciag-Tymecka I, Oleszek J, Dabrowski E, Grandoulier AS, Picaut P; Dysport in PUL study group
Dev Med Child Neurol 2021 May;63(5):592-600. Epub 2020 Nov 18 doi: 10.1111/dmcn.14733. PMID: 33206382Free PMC Article
Salazar AP, Pinto C, Ruschel Mossi JV, Figueiro B, Lukrafka JL, Pagnussat AS
Ann Phys Rehabil Med 2019 Jul;62(4):274-282. Epub 2018 Dec 22 doi: 10.1016/j.rehab.2018.11.004. PMID: 30582986
Guo J, Qian S, Wang Y, Xu A
Int J Rehabil Res 2019 Mar;42(1):31-35. doi: 10.1097/MRR.0000000000000316. PMID: 30211721Free PMC Article
Dong Y, Wu T, Hu X, Wang T
Eur J Phys Rehabil Med 2017 Apr;53(2):256-267. Epub 2016 Nov 11 doi: 10.23736/S1973-9087.16.04329-X. PMID: 27834471

Prognosis

Tedesco Triccas L, Kennedy N, Smith T, Pomeroy V
Physiotherapy 2019 Jun;105(2):163-173. Epub 2019 Jan 11 doi: 10.1016/j.physio.2019.01.004. PMID: 30745061
Posteraro F, Crea S, Mazzoleni S, Berteanu M, Ciobanu I, Vitiello N, Cempini M, Gervasio S, Mrachacz-Kersting N
Eur J Phys Rehabil Med 2018 Aug;54(4):536-544. Epub 2017 Sep 4 doi: 10.23736/S1973-9087.17.04815-8. PMID: 28870058
Noland ME, Lalonde DH, Yee GJ, Rohrich RJ
Plast Reconstr Surg 2016 Sep;138(3):519e-530e. doi: 10.1097/PRS.0000000000002480. PMID: 27556628
Cheung DK, Climans SA, Black SE, Gao F, Szilagyi GM, Mochizuki G
Neurorehabil Neural Repair 2016 Jan;30(1):63-70. Epub 2015 May 20 doi: 10.1177/1545968315585357. PMID: 25995383
Sheean G, Lannin NA, Turner-Stokes L, Rawicki B, Snow BJ; Cerebral Palsy Institute
Eur J Neurol 2010 Aug;17 Suppl 2:74-93. doi: 10.1111/j.1468-1331.2010.03129.x. PMID: 20633180

Clinical prediction guides

Danchenko N, Johnston KM, Whalen J
J Med Econ 2022 Jan-Dec;25(1):919-929. doi: 10.1080/13696998.2022.2092354. PMID: 35730362
Dabrowski E, Chambers HG, Gaebler-Spira D, Banach M, Kaňovský P, Dersch H, Althaus M, Geister TL, Heinen F
Pediatr Neurol 2021 Oct;123:10-20. Epub 2021 May 21 doi: 10.1016/j.pediatrneurol.2021.05.014. PMID: 34339951
Delgado MR, Tilton A, Carranza-Del Río J, Dursun N, Bonikowski M, Aydin R, Maciag-Tymecka I, Oleszek J, Dabrowski E, Grandoulier AS, Picaut P; Dysport in PUL study group
Dev Med Child Neurol 2021 May;63(5):592-600. Epub 2020 Nov 18 doi: 10.1111/dmcn.14733. PMID: 33206382Free PMC Article
Guo J, Qian S, Wang Y, Xu A
Int J Rehabil Res 2019 Mar;42(1):31-35. doi: 10.1097/MRR.0000000000000316. PMID: 30211721Free PMC Article
Dong Y, Wu T, Hu X, Wang T
Eur J Phys Rehabil Med 2017 Apr;53(2):256-267. Epub 2016 Nov 11 doi: 10.23736/S1973-9087.16.04329-X. PMID: 27834471

Recent systematic reviews

Jarratt Barnham I, Alahmadi S, Spillane B, Pick A, Lamyman M
Hand Surg Rehabil 2022 Sep;41(4):426-434. Epub 2022 Apr 28 doi: 10.1016/j.hansur.2022.04.006. PMID: 35490985
Tedesco Triccas L, Kennedy N, Smith T, Pomeroy V
Physiotherapy 2019 Jun;105(2):163-173. Epub 2019 Jan 11 doi: 10.1016/j.physio.2019.01.004. PMID: 30745061
Salazar AP, Pinto C, Ruschel Mossi JV, Figueiro B, Lukrafka JL, Pagnussat AS
Ann Phys Rehabil Med 2019 Jul;62(4):274-282. Epub 2018 Dec 22 doi: 10.1016/j.rehab.2018.11.004. PMID: 30582986
Mahmood A, Veluswamy SK, Hombali A, Mullick A, N M, Solomon JM
Arch Phys Med Rehabil 2019 Apr;100(4):751-768. Epub 2018 Nov 16 doi: 10.1016/j.apmr.2018.10.016. PMID: 30452892
Dong Y, Wu T, Hu X, Wang T
Eur J Phys Rehabil Med 2017 Apr;53(2):256-267. Epub 2016 Nov 11 doi: 10.23736/S1973-9087.16.04329-X. PMID: 27834471

Supplemental Content

Table of contents

    Clinical resources

    Practice guidelines

    • PubMed
      See practice and clinical guidelines in PubMed. The search results may include broader topics and may not capture all published guidelines. See the FAQ for details.
    • Bookshelf
      See practice and clinical guidelines in NCBI Bookshelf. The search results may include broader topics and may not capture all published guidelines. See the FAQ for details.

    Consumer resources

    Recent activity

    Your browsing activity is empty.

    Activity recording is turned off.

    Turn recording back on

    See more...