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Falls

MedGen UID:
39084
Concept ID:
C0085639
Finding
Synonym: Fall
SNOMED CT: Falls (161898004); Fall (1912002)
 
HPO: HP:0002527

Definition

A sudden movement downward, usually resulting in injury. [from NCI]

Term Hierarchy

CClinical test,  RResearch test,  OOMIM,  GGeneReviews,  VClinVar  
  • CROGVFalls

Conditions with this feature

Supranuclear palsy, progressive, 2
MedGen UID:
324446
Concept ID:
C1836148
Disease or Syndrome
Congenital myopathy 23
MedGen UID:
324513
Concept ID:
C1836447
Disease or Syndrome
Nemaline myopathy is divided into six types. In order of decreasing severity, the types are: severe congenital, Amish, intermediate congenital, typical congenital, childhood-onset, and adult-onset. The types are distinguished by the age when symptoms first appear and the severity of symptoms; however, there is overlap among the various types. The severe congenital type is the most life-threatening. Most individuals with this type do not survive past early childhood due to respiratory failure. The Amish type solely affects the Old Order Amish population of Pennsylvania and is typically fatal in early childhood. The most common type of nemaline myopathy is the typical congenital type, which is characterized by muscle weakness and feeding problems beginning in infancy. Most of these individuals do not have severe breathing problems and can walk unassisted. People with the childhood-onset type usually develop muscle weakness in adolescence. The adult-onset type is the mildest of all the various types. People with this type usually develop muscle weakness between ages 20 and 50.\n\nNemaline myopathy is a disorder that primarily affects skeletal muscles, which are muscles that the body uses for movement. People with nemaline myopathy have muscle weakness (myopathy) throughout the body, but it is typically most severe in the muscles of the face; neck; trunk; and other muscles close to the center of the body (proximal muscles), such as those of the upper arms and legs. This weakness can worsen over time. Affected individuals may have feeding and swallowing difficulties, foot deformities, abnormal curvature of the spine (scoliosis), and joint deformities (contractures). Most people with nemaline myopathy are able to walk, although some affected children may begin walking later than usual. As the condition progresses, some people may require wheelchair assistance. In severe cases, the muscles used for breathing are affected and life-threatening breathing difficulties can occur.
Myosin storage myopathy
MedGen UID:
374868
Concept ID:
C1842160
Disease or Syndrome
Autosomal dominant myosin storage congenital myopathy-7A (CMYO7A) is a skeletal muscle disorder with wide phenotypic variability. The age at symptom onset can range from early childhood to late adulthood. Affected individuals have proximal muscle weakness affecting the upper and lower limbs and distal muscle weakness of the lower limbs, resulting in gait difficulties and scapular winging (scapuloperoneal myopathy). Additional features may include thin habitus, high-arched palate, foot drop, pes cavus, calf pseudohypertrophy, and decreased reflexes. The severity is also variable: some patients develop respiratory insufficiency, joint contractures, and scoliosis in the first decades, whereas others are clinically unaffected, but show subtle signs of the disorder on examination. Serum creatine kinase may be normal or elevated. The disease is usually slowly progressive and most patients remain ambulatory. Skeletal muscle biopsy can show different abnormalities, including hyaline bodies, type 1 fiber predominance, congenital fiber-type disproportion (CFTD), and nonspecific myopathic changes with myofibrillar disarray. Intrafamilial variability is common (Dye et al., 2006; Pegoraro et al., 2007; review by Tajsharghi and Oldfors, 2013). For a discussion of genetic heterogeneity of congenital myopathy, see CMYO1A (117000).
Syndromic X-linked intellectual disability Hedera type
MedGen UID:
337257
Concept ID:
C1845543
Disease or Syndrome
The Hedera type of X-linked syndromic intellectual developmental disorder (MRXSH) is characterized by global developmental delay apparent from infancy and progressive neurologic decline with abnormal movements, spasticity, and seizures. Brain imaging shows volume loss of cortical white and gray matter, thin corpus callosum, and myelination defects, consistent with a neurodegenerative process. Only males are affected (summary by Hirose et al., 2019).
Charlevoix-Saguenay spastic ataxia
MedGen UID:
338620
Concept ID:
C1849140
Disease or Syndrome
Autosomal recessive spastic ataxia of Charlevoix-Saguenay (ARSACS) is clinically characterized by a progressive cerebellar ataxia, peripheral neuropathy, and spasticity. Disease onset of classic ARSACS is often in early childhood, leading to delayed walking because of gait unsteadiness in very young toddlers, while an increasing number of individuals with disease onset in teenage or early-adult years are now being described. Typically the ataxia is followed by lower-limb spasticity and later by peripheral neuropathy – although pronounced peripheral neuropathy has been observed as a first sign of ARSACS. Oculomotor disturbances, dysarthria, and upper-limb ataxia develop with slower progression than the other findings. Brain imaging demonstrates atrophy of the superior vermis and the cerebellar hemisphere with additional findings on MRI, such as linear hypointensities in the pons and hyperintense rims around the thalami. Many affected individuals (though not all) have yellow streaks of hypermyelinated fibers radiating from the edges of the optic disc noted on ophthalmologic exam, and thickened retinal fibers can be demonstrated by optical coherence tomography. Mild intellectual disability, hearing loss, and urinary urgency and incontinence have been reported in some individuals.
Leber congenital amaurosis 14
MedGen UID:
442375
Concept ID:
C2750063
Disease or Syndrome
Autosomal recessive childhood-onset severe retinal dystrophy is a heterogeneous group of disorders affecting rod and cone photoreceptors simultaneously. The most severe cases are termed Leber congenital amaurosis, whereas the less aggressive forms are usually considered juvenile retinitis pigmentosa (Gu et al., 1997). For a general phenotypic description and a discussion of genetic heterogeneity of Leber congenital amaurosis, see LCA1 (204000); for retinitis pigmentosa, see 268000.
Oxoglutaricaciduria
MedGen UID:
414553
Concept ID:
C2752074
Disease or Syndrome
Oxoglutarate dehydrogenase deficiency (OGDHD) is an autosomal recessive disorder associated with features of infantile- and pediatric-onset basal ganglia-associated movement disorders, hypotonia, developmental delays, ataxia, and seizures (summary by Yap et al., 2021).
Mitochondrial DNA deletion syndrome with progressive myopathy
MedGen UID:
767513
Concept ID:
C3554599
Disease or Syndrome
Autosomal dominant progressive external ophthalmoplegia-6 (PEOA6) is characterized by muscle weakness, mainly affecting the lower limbs, external ophthalmoplegia, exercise intolerance, and mitochondrial DNA (mtDNA) deletions on muscle biopsy. Symptoms may appear in childhood or adulthood and show slow progression (summary by Ronchi et al., 2013). For a general phenotypic description and a discussion of genetic heterogeneity of autosomal dominant progressive external ophthalmoplegia, see PEOA1 (157640).
Myopathy, tubular aggregate, 2
MedGen UID:
862994
Concept ID:
C4014557
Disease or Syndrome
Any tubular aggregate myopathy in which the cause of the disease is a mutation in the ORAI1 gene.
Autosomal recessive early-onset Parkinson disease 23
MedGen UID:
896607
Concept ID:
C4225186
Disease or Syndrome
Parkinson disease-23 (PARK23) is a progressive neurodegenerative disorder characterized by young-adult onset of parkinsonism associated with progressive cognitive impairment leading to dementia and dysautonomia. Some individuals have additional motor abnormalities. Affected individuals become severely disabled within a few decades (summary by Lesage et al., 2016).
Congenital myasthenic syndrome 11
MedGen UID:
902189
Concept ID:
C4225367
Disease or Syndrome
Congenital myasthenic syndrome associated with AChR deficiency is a disorder of the postsynaptic neuromuscular junction (NMJ) clinically characterized by early-onset muscle weakness with variable severity. Electrophysiologic studies show low amplitude of the miniature endplate potential (MEPP) and current (MEPC) resulting from deficiency of AChR at the endplate. Treatment with cholinesterase inhibitors or amifampridine may be helpful (summary by Engel et al., 2015). For a discussion of genetic heterogeneity of CMS, see CMS1A (601462).
Supranuclear palsy, progressive, 1
MedGen UID:
1640811
Concept ID:
C4551863
Disease or Syndrome
The spectrum of clinical manifestations of MAPT-related frontotemporal dementia (MAPT-FTD) has expanded from its original description of frontotemporal dementia and parkinsonian manifestations to include changes in behavior, motor function, memory, and/or language. A recent retrospective study suggested that the majority of affected individuals have either behavioral changes consistent with a diagnosis of behavioral variant FTD (bvFTD) or, less commonly, a parkinsonian syndrome (i.e., progressive supranuclear palsy, corticobasal syndrome, or Parkinson disease). Fewer than 5% of people with MAPT-FTD have primary progressive aphasia or Alzheimer disease. Clinical presentation may differ between and within families with the same MAPT variant. MAPT-FTD is a progressive disorder that commonly ends with a relatively global dementia in which some affected individuals become mute. Progression of motor impairment in affected individuals results in some becoming chairbound and others bedbound. Mean disease duration is 9.3 (SD: 6.4) years but is individually variable and can be more than 30 years in some instances.
Charcot-Marie-Tooth disease, dominant intermediate G
MedGen UID:
1642893
Concept ID:
C4693509
Disease or Syndrome
CMTDIG is an autosomal dominant neurologic disorder with a highly variable phenotype. Most affected individuals have onset in the first or second decades of slowly progressive distal motor weakness and atrophy, resulting in gait instability and distal upper limb impairment, as well as distal sensory impairment. More severely affected individuals may have pes cavus and claw hands and become wheelchair-bound, whereas other affected individuals have later onset with a milder disease course. Electrophysiologic studies tend to show median motor nerve conduction velocities (NCV) in the 'intermediate' range, between 25 and 45 m/s (summary by Berciano et al., 2017). In a review of intermediate CMT, Berciano et al. (2017) noted that advanced axonal degeneration may induce secondary demyelinating changes resulting in decreased NCV and attenuated compound muscle action potential (CMAP) in median nerve conduction studies. They thus suggested that testing the upper arm, axilla to elbow, may provide more accurate assessment of NCV and CMAP and reveal an intermediate phenotype (review by Berciano et al., 2017). For a discussion of genetic heterogeneity of CMTDI, see 606482.
Intellectual disability, autosomal dominant 58
MedGen UID:
1648488
Concept ID:
C4748195
Disease or Syndrome
Mitochondrial complex 1 deficiency, nuclear type 2
MedGen UID:
1648466
Concept ID:
C4748737
Disease or Syndrome
Progressive myoclonic epilepsy type 8
MedGen UID:
1680582
Concept ID:
C5190825
Disease or Syndrome
Progressive myoclonic epilepsy-8 (EPM8) is a rare autosomal recessive form of progressive myoclonic epilepsy with phenotypic variability including ataxia and other movement disorders in addition to myoclonus (summary by Godeiro et al., 2018). For a discussion of genetic heterogeneity of progressive myoclonic epilepsy, see EPM1A (254800).
Mitochondrial DNA depletion syndrome 18
MedGen UID:
1713890
Concept ID:
C5394140
Disease or Syndrome
Mitochondrial DNA depletion syndrome-18 (MTDPS18) is an autosomal recessive neuromuscular disorder characterized by early-onset progressive weakness and atrophy of the distal limb muscles, resulting in loss of ambulation as well as atrophy of the intrinsic hand muscles with clawed hands. Affected individuals may also develop scoliosis and have hypo- or hyperreflexia and decreased pulmonary vital capacity. Examination of skeletal muscle shows neurogenic atrophy and combined mitochondrial oxidative phosphorylation deficiency associated with mtDNA depletion. The clinical phenotype is reminiscent of spinal muscular atrophy (see SMA, 253300) and the metabolic profile is reminiscent of 2-aminoadipic 2-oxoadipic aciduria (AMOXAD; 204750), which is caused by mutation in the DHTKD1 gene (614984) (summary by Boczonadi et al., 2018). For a discussion of genetic heterogeneity of autosomal recessive mtDNA depletion syndromes, see MTDPS1 (603041).
Muscular dystrophy, limb-girdle, autosomal recessive 26
MedGen UID:
1718449
Concept ID:
C5394268
Disease or Syndrome
Autosomal recessive limb-girdle muscular dystrophy-26 (LGMDR26) is a muscle disorder characterized by adult-onset weakness that primarily affects the proximal muscles of the lower limbs. The disorder is slowly progressive, with later involvement of the upper limbs and fatty replacement of muscle tissue apparent on MRI. Some patients may have calf hypertrophy. Serum creatine kinase is significantly elevated, and skeletal muscle biopsy shows typical dystrophic features with normal ultrastructural findings. There is no cardiac or respiratory involvement (summary by Vissing et al., 2019). For a discussion of genetic heterogeneity of autosomal recessive limb-girdle muscular dystrophy, see LGMDR1 (253600).
Retinal dystrophy with leukodystrophy
MedGen UID:
1715138
Concept ID:
C5394315
Disease or Syndrome
Retinal dystrophy and leukodystrophy (RDLKD) is a peroxisomal enzyme deficiency caused by impaired very long chain fatty acid (VLCFA) metabolism. Patients exhibit ataxia and spastic paraparesis as well as developmental delay, and may show facial dysmorphism (Ferdinandusse et al., 2017).
Intellectual developmental disorder with paroxysmal dyskinesia or seizures
MedGen UID:
1727046
Concept ID:
C5436894
Disease or Syndrome
Intellectual developmental disorder with paroxysmal dyskinesia or seizures (IDDPADS) is an autosomal recessive complex neurologic disorder characterized by global developmental delay with impaired intellectual development and language delay. In addition, most patients develop a paroxysmal hyperkinetic movement disorder in the first months or years of life manifest as sudden falls or backward propulsion, eye or head deviation, and dystonic limb posturing followed by chorea and dyskinetic movements. The episodes are pharmacoresistant to anticonvulsant medication. EEG may show interictal abnormalities, but are usually not consistent with epilepsy. However, some patients may also develop epileptic seizures or only have seizures without a movement disorder (summary by Doummar et al., 2020).
Mitochondrial complex 2 deficiency, nuclear type 4
MedGen UID:
1782861
Concept ID:
C5543176
Disease or Syndrome
Mitochondrial complex II deficiency nuclear type 4 (MC2DN4) is a severe autosomal recessive disorder characterized by early-onset progressive neurodegeneration with leukoencephalopathy. Acute episodes of neurodegeneration are often triggered by catabolic stress such as infection or fasting.
Developmental delay, impaired speech, and behavioral abnormalities
MedGen UID:
1794167
Concept ID:
C5561957
Disease or Syndrome
Developmental delay, impaired speech, and behavioral abnormalities (DDISBA) is characterized by global developmental delay apparent from early childhood. Intellectual disability can range from mild to severe. Additional variable features may include dysmorphic facial features, seizures, hypotonia, motor abnormalities such as Tourette syndrome or dystonia, and hearing loss (summary by Cousin et al., 2021).
Neurodevelopmental disorder with hypotonia and dysmorphic facies
MedGen UID:
1794184
Concept ID:
C5561974
Disease or Syndrome
Neurodevelopmental disorder with hypotonia and dysmorphic facies (NEDHYDF) is characterized by global developmental delay and hypotonia apparent from birth. Affected individuals have variably impaired intellectual development, often with speech delay and delayed walking. Seizures are generally not observed, although some patients may have single seizures or late-onset epilepsy. Most patients have prominent dysmorphic facial features. Additional features may include congenital cardiac defects (without arrhythmia), nonspecific renal anomalies, joint contractures or joint hyperextensibility, dry skin, and cryptorchidism. There is significant phenotypic variability in both the neurologic and extraneurologic manifestations (summary by Tan et al., 2022).
Autosomal recessive spastic paraplegia type 78
MedGen UID:
1799316
Concept ID:
C5567893
Disease or Syndrome
Autosomal recessive spastic paraplegia-78 is an adult-onset neurodegenerative disorder characterized predominantly by spasticity and muscle weakness of the lower limbs, resulting in gait difficulties and loss of ambulation in some patients. Affected individuals also have cerebellar signs, such as dysarthria, oculomotor disturbances, and limb and gait ataxia; brain imaging shows cerebellar atrophy. Some patients may have mild cognitive impairment or frank dementia. The phenotype is highly variable (summary by Estrada-Cuzcano et al., 2017). Biallelic mutation in the ATP13A2 gene also causes Kufor-Rakeb syndrome (KRS; 606693), a neurodegenerative disorder with overlapping features. Patients with KRS have earlier onset and prominent parkinsonism. Loss of ATP13A2 function results in a multidimensional spectrum of neurologic features reflecting various regions of the brain and nervous system, including cortical, pyramidal, extrapyramidal, brainstem, cerebellar, and peripheral (summary by Estrada-Cuzcano et al., 2017).

Professional guidelines

PubMed

Wieling W, Kaufmann H, Claydon VE, van Wijnen VK, Harms MPM, Juraschek SP, Thijs RD
Lancet Neurol 2022 Aug;21(8):735-746. doi: 10.1016/S1474-4422(22)00169-7. PMID: 35841911Free PMC Article
Montero-Odasso MM, Kamkar N, Pieruccini-Faria F, Osman A, Sarquis-Adamson Y, Close J, Hogan DB, Hunter SW, Kenny RA, Lipsitz LA, Lord SR, Madden KM, Petrovic M, Ryg J, Speechley M, Sultana M, Tan MP, van der Velde N, Verghese J, Masud T; Task Force on Global Guidelines for Falls in Older Adults
JAMA Netw Open 2021 Dec 1;4(12):e2138911. doi: 10.1001/jamanetworkopen.2021.38911. PMID: 34910151Free PMC Article
Izquierdo M, Merchant RA, Morley JE, Anker SD, Aprahamian I, Arai H, Aubertin-Leheudre M, Bernabei R, Cadore EL, Cesari M, Chen LK, de Souto Barreto P, Duque G, Ferrucci L, Fielding RA, García-Hermoso A, Gutiérrez-Robledo LM, Harridge SDR, Kirk B, Kritchevsky S, Landi F, Lazarus N, Martin FC, Marzetti E, Pahor M, Ramírez-Vélez R, Rodriguez-Mañas L, Rolland Y, Ruiz JG, Theou O, Villareal DT, Waters DL, Won Won C, Woo J, Vellas B, Fiatarone Singh M
J Nutr Health Aging 2021;25(7):824-853. doi: 10.1007/s12603-021-1665-8. PMID: 34409961

Recent clinical studies

Etiology

Xu Q, Ou X, Li J
Front Public Health 2022;10:902599. Epub 2022 Oct 17 doi: 10.3389/fpubh.2022.902599. PMID: 36324472Free PMC Article
Ang GC, Low SL, How CH
Singapore Med J 2020 Mar;61(3):116-121. doi: 10.11622/smedj.2020029. PMID: 32488276Free PMC Article
Cuevas-Trisan R
Phys Med Rehabil Clin N Am 2017 Nov;28(4):727-737. doi: 10.1016/j.pmr.2017.06.006. PMID: 29031339
Sherrington C, Tiedemann A
J Physiother 2015 Apr;61(2):54-60. Epub 2015 Mar 18 doi: 10.1016/j.jphys.2015.02.011. PMID: 25797882
Fuller GF
Am Fam Physician 2000 Apr 1;61(7):2159-68, 2173-4. PMID: 10779256

Diagnosis

Heng H, Jazayeri D, Shaw L, Kiegaldie D, Hill AM, Morris ME
BMC Geriatr 2020 Apr 15;20(1):140. doi: 10.1186/s12877-020-01515-w. PMID: 32293298Free PMC Article
Khalifa M
Stud Health Technol Inform 2019 Jul 4;262:340-343. doi: 10.3233/SHTI190088. PMID: 31349337
Ronthal M
Med Clin North Am 2019 Mar;103(2):203-213. Epub 2018 Dec 20 doi: 10.1016/j.mcna.2018.10.010. PMID: 30704677
Atkinson N, van Rijn RR, Starling SP
Pediatr Emerg Care 2018 Dec;34(12):837-841. doi: 10.1097/PEC.0000000000001186. PMID: 28590993
Candel Romero C, Forner Cordero Á, Sánchez Santos JC, Pereiró Berenguer I
Med Clin (Barc) 2017 Nov 22;149(10):436-438. Epub 2017 Jul 29 doi: 10.1016/j.medcli.2017.04.014. PMID: 28625513

Therapy

Weatherald J, Boucly A, Peters A, Montani D, Prasad K, Psotka MA, Zannad F, Gomberg-Maitland M, McLaughlin V, Simonneau G, Humbert M; Evolving Landscape of Pulmonary Arterial Hypertension and Redesigning Pulmonary Arterial Hypertension Clinical Trials Task Force of the 18th Global CardioVascular Clinical Trialists Forum
Lancet 2022 Nov 26;400(10366):1884-1898. doi: 10.1016/S0140-6736(22)01601-4. PMID: 36436527
Mammenga E, Hansen KA
S D Med 2021 Nov;74(11):506-512. PMID: 35008136
Veronese N, Maggi S, Schofield P, Stubbs B
Maturitas 2017 Aug;102:1-5. Epub 2017 May 4 doi: 10.1016/j.maturitas.2017.05.004. PMID: 28610676
Sherrington C, Michaleff ZA, Fairhall N, Paul SS, Tiedemann A, Whitney J, Cumming RG, Herbert RD, Close JCT, Lord SR
Br J Sports Med 2017 Dec;51(24):1750-1758. Epub 2016 Oct 4 doi: 10.1136/bjsports-2016-096547. PMID: 27707740
Lawrence JM, Reckless JP
Int J Clin Pract 2000 Nov;54(9):614-8. PMID: 11220991

Prognosis

Santos-Lozada AR
JAMA 2023 May 9;329(18):1605-1607. doi: 10.1001/jama.2023.3054. PMID: 37159042Free PMC Article
Tharwani ZH, Bilal W, Khan HA, Kumar P, Butt MS, Hamdana AH, Essar MY, Nashwan AJ, Habib Z, Marzo RR
Inquiry 2023 Jan-Dec;60:469580231167024. doi: 10.1177/00469580231167024. PMID: 37085986Free PMC Article
Naser M, Schilling P, Szalai H, Visintainer P, Pack Q
J Cardiopulm Rehabil Prev 2023 Jan 1;43(1):75-77. Epub 2022 Nov 12 doi: 10.1097/HCR.0000000000000747. PMID: 36374173Free PMC Article
Harris WS, Tintle NL, Imamura F, Qian F, Korat AVA, Marklund M, Djoussé L, Bassett JK, Carmichael PH, Chen YY, Hirakawa Y, Küpers LK, Laguzzi F, Lankinen M, Murphy RA, Samieri C, Senn MK, Shi P, Virtanen JK, Brouwer IA, Chien KL, Eiriksdottir G, Forouhi NG, Geleijnse JM, Giles GG, Gudnason V, Helmer C, Hodge A, Jackson R, Khaw KT, Laakso M, Lai H, Laurin D, Leander K, Lindsay J, Micha R, Mursu J, Ninomiya T, Post W, Psaty BM, Risérus U, Robinson JG, Shadyab AH, Snetselaar L, Sala-Vila A, Sun Y, Steffen LM, Tsai MY, Wareham NJ, Wood AC, Wu JHY, Hu F, Sun Q, Siscovick DS, Lemaitre RN, Mozaffarian D; Fatty Acids and Outcomes Research Consortium (FORCE)
Nat Commun 2021 Apr 22;12(1):2329. doi: 10.1038/s41467-021-22370-2. PMID: 33888689Free PMC Article
Giannoulis D, Calori GM, Giannoudis PV
Eur J Orthop Surg Traumatol 2016 May;26(4):365-70. Epub 2016 Mar 4 doi: 10.1007/s00590-016-1744-4. PMID: 26943870Free PMC Article

Clinical prediction guides

Jewell VD, Capistran K, Flecky K, Qi Y, Fellman S
Occup Ther Health Care 2020 Oct;34(4):307-319. Epub 2020 Sep 9 doi: 10.1080/07380577.2020.1815928. PMID: 32907452
Hshieh TT, Yue J, Oh E, Puelle M, Dowal S, Travison T, Inouye SK
JAMA Intern Med 2015 Apr;175(4):512-20. doi: 10.1001/jamainternmed.2014.7779. PMID: 25643002Free PMC Article
Barry E, Galvin R, Keogh C, Horgan F, Fahey T
BMC Geriatr 2014 Feb 1;14:14. doi: 10.1186/1471-2318-14-14. PMID: 24484314Free PMC Article
Hester AL, Davis DM
J Neurosci Nurs 2013 Oct;45(5):298-305. doi: 10.1097/JNN.0b013e31829d8b44. PMID: 24025469
Morley JE, Malmstrom TK, Miller DK
J Nutr Health Aging 2012 Jul;16(7):601-8. doi: 10.1007/s12603-012-0084-2. PMID: 22836700Free PMC Article

Recent systematic reviews

Xu Q, Ou X, Li J
Front Public Health 2022;10:902599. Epub 2022 Oct 17 doi: 10.3389/fpubh.2022.902599. PMID: 36324472Free PMC Article
Morris ME, Webster K, Jones C, Hill AM, Haines T, McPhail S, Kiegaldie D, Slade S, Jazayeri D, Heng H, Shorr R, Carey L, Barker A, Cameron I
Age Ageing 2022 May 1;51(5) doi: 10.1093/ageing/afac077. PMID: 35524748Free PMC Article
Schoberer D, Breimaier HE, Zuschnegg J, Findling T, Schaffer S, Archan T
Worldviews Evid Based Nurs 2022 Apr;19(2):86-93. Epub 2022 Mar 9 doi: 10.1111/wvn.12571. PMID: 35262271Free PMC Article
Dautzenberg L, Beglinger S, Tsokani S, Zevgiti S, Raijmann RCMA, Rodondi N, Scholten RJPM, Rutjes AWS, Di Nisio M, Emmelot-Vonk M, Tricco AC, Straus SE, Thomas S, Bretagne L, Knol W, Mavridis D, Koek HL
J Am Geriatr Soc 2021 Oct;69(10):2973-2984. Epub 2021 Jul 28 doi: 10.1111/jgs.17375. PMID: 34318929Free PMC Article
Sherrington C, Michaleff ZA, Fairhall N, Paul SS, Tiedemann A, Whitney J, Cumming RG, Herbert RD, Close JCT, Lord SR
Br J Sports Med 2017 Dec;51(24):1750-1758. Epub 2016 Oct 4 doi: 10.1136/bjsports-2016-096547. PMID: 27707740

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