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Aphasia

MedGen UID:
8159
Concept ID:
C0003537
Mental or Behavioral Dysfunction
Synonyms: Alogia; Alogias; Anepia; Anepias; Deafness, Word; Logagnosia; Logagnosias; Logamnesia; Logamnesias; Logasthenia; Logasthenias; Word Deafness
SNOMED CT: Aphasia (87486003); Loss of power of expression or comprehension (87486003); Aphasic disturbance (87486003)
 
HPO: HP:0002381
Monarch Initiative: MONDO:0000598

Definition

An acquired language impairment of some or all of the abilities to produce or comprehend speech and to read or write. [from HPO]

Conditions with this feature

Landau-Kleffner syndrome
MedGen UID:
79465
Concept ID:
C0282512
Disease or Syndrome
GRIN2A-related speech disorders and epilepsy are characterized by speech disorders in all affected individuals and a range of epilepsy syndromes present in about 90%. Severe speech disorders observed can include dysarthria and speech dyspraxia, and both receptive and expressive language delay/regression; more mildly affected individuals may display subtly impaired intelligibility of conversational speech. Epilepsy features include seizure onset usually between ages three and six years, focal epilepsy with language and/or global developmental regression, and electroencephalogram (EEG) showing continuous spike-and-wave discharges in sleep or very active centrotemporal discharges. Seizure types include seizures associated with aura of perioral paresthesia, focal or focal motor seizures (often evolving to generalized tonic-clonic), and atypical absence seizures. Epilepsy syndromes can include: Landau-Kleffner syndrome (LKS), epileptic encephalopathy with continuous spike-and-wave during sleep (ECSWS), childhood epilepsy with centrotemporal spikes (CECTS), atypical childhood epilepsy with centrotemporal spikes (ACECTS), autosomal dominant rolandic epilepsy with speech dyspraxia (ADRESD), and infantile-onset epileptic encephalopathy.
Flynn-Aird syndrome
MedGen UID:
91009
Concept ID:
C0343108
Disease or Syndrome
A rare genetic disease characterized by childhood onset of bilateral progressive sensorineural hearing loss, ocular anomalies (myopia, cataract, retinitis pigmentosa), central and peripheral nervous system features (dementia, epilepsy, ataxia, peripheral neuropathy), ectodermal features (skin atrophy, alopecia, dental caries), and skeletal anomalies (bone cysts, joint stiffness, scoliosis, kyphosis). Laboratory examination may reveal elevated cerebrospinal fluid protein.
Inherited Creutzfeldt-Jakob disease
MedGen UID:
155837
Concept ID:
C0751254
Disease or Syndrome
Genetic prion disease generally manifests with cognitive difficulties, ataxia, and myoclonus (abrupt jerking movements of muscle groups and/or entire limbs). The order of appearance and/or predominance of these features and other associated neurologic and psychiatric findings vary. The three major phenotypes of genetic prion disease are genetic Creutzfeldt-Jakob disease (gCJD), fatal familial insomnia (FFI), and Gerstmann-Sträussler-Scheinker (GSS) syndrome. Although these phenotypes display overlapping clinical and pathologic features, recognition of these phenotypes can be useful when providing affected individuals and their families with information about the expected clinical course. The age at onset typically ranges from 50 to 60 years. The disease course ranges from a few months in gCJD and FFI to a few (up to 4, and in rare cases up to 10) years in GSS syndrome.
MASA syndrome
MedGen UID:
162894
Concept ID:
C0795953
Disease or Syndrome
L1 syndrome involves a phenotypic spectrum ranging from severe to mild and includes three clinical phenotypes: X-linked hydrocephalus with stenosis of the aqueduct of Sylvius (HSAS). MASA (mental retardation [intellectual disability], aphasia [delayed speech], spastic paraplegia [shuffling gait], adducted thumbs) syndrome including X-linked complicated hereditary spastic paraplegia type 1. X-linked complicated corpus callosum agenesis. Males with HSAS are born with severe hydrocephalus, adducted thumbs, and spasticity; intellectual disability is severe. In less severely affected males, hydrocephalus may be subclinically present and documented only because of developmental delay; intellectual disability ranges from mild (IQ: 50-70) to moderate (IQ: 30-50). It is important to note that all phenotypes can be observed in affected individuals within the same family.
Migraine, familial hemiplegic, 1
MedGen UID:
331388
Concept ID:
C1832884
Disease or Syndrome
Familial hemiplegic migraine (FHM) falls within the category of migraine with aura. In migraine with aura (including FHM) the neurologic symptoms of aura are unequivocally localizable to the cerebral cortex or brain stem and include visual disturbance (most common), sensory loss (e.g., numbness or paresthesias of the face or an extremity), and dysphasia (difficulty with speech). FHM must include motor involvement, such as hemiparesis (weakness of an extremity). Hemiparesis occurs with at least one other symptom during FHM aura. Neurologic deficits with FHM attacks can be prolonged for hours to days and may outlast the associated migrainous headache. FHM is often earlier in onset than typical migraine, frequently beginning in the first or second decade; the frequency of attacks tends to decrease with age. Approximately 40%-50% of families with CACNA1A-FHM have cerebellar signs ranging from nystagmus to progressive, usually late-onset mild ataxia.
CARASIL syndrome
MedGen UID:
325051
Concept ID:
C1838577
Disease or Syndrome
HTRA1 disorder is a phenotypic spectrum in which some individuals have few to no symptoms and others manifest with the more severe CARASIL (cerebral autosomal recessive arteriopathy with subcortical infarcts and leukoencephalopathy) phenotype. Those who have a heterozygous HTRA1 pathogenic variant may have mild neurologic findings (sometimes identified only on neuroimaging) or mild-to-moderate neurologic signs and symptoms of CARASIL. In this chapter, the term "classic CARASIL" refers to the more severe phenotype associated with biallelic pathogenic variants, and "HTRA1 cerebral small vessel disease" (HTRA1-CSVD) refers to the milder phenotype associated with a heterozygous HTRA1 pathogenic variant. Classic CARASIL is characterized by early-onset changes in the deep white matter of the brain observed on MRI, and associated neurologic findings. The most frequent initial symptom is gait disturbance from spasticity beginning between ages 20 and 40 years. Forty-four percent of affected individuals have stroke-like episodes before age 40 years. Mood changes (apathy and irritability), pseudobulbar palsy, and cognitive dysfunction begin between ages 20 and 50 years. The disease progresses slowly following the onset of neurologic symptoms. Scalp alopecia and acute mid- to lower-back pain (lumbago) before age 30 years are characteristic. The most frequent initial symptom in individuals with HTRA1-CSVD is slowly progressive gait disturbance after age 40 years, which may be followed by the development of mood changes and cognitive dysfunction. A majority of affected individuals have a stroke-like episode after age 40 years. Spondylosis and alopecia are seen in a minority of individuals with HTRA1-CSVD.
Familial developmental dysphasia
MedGen UID:
374015
Concept ID:
C1838630
Disease or Syndrome
A severe form of developmental verbal apraxia with characteristics of a deficit in spontaneous speech, writing, grammatical judgment and repetition, defective articulation, moderate to severe degree of dyspraxia, a reduced use of consonant clusters and comprehension delay. Hearing and intelligence are normal. Inheritance is autosomal dominant with full penetrance.
Syndromic X-linked intellectual disability 12
MedGen UID:
333405
Concept ID:
C1839792
Mental or Behavioral Dysfunction
X-linked intellectual disability, Wilson type is characterised by severe intellectual deficit with mutism, epilepsy, growth retardation and recurrent infections. It has been described in three males from three generations of one family. The causative gene has been localised to the 11p region of the X chromosome.
GRN-related frontotemporal lobar degeneration with Tdp43 inclusions
MedGen UID:
375285
Concept ID:
C1843792
Disease or Syndrome
The spectrum of GRN frontotemporal dementia (GRN-FTD) includes the behavioral variant (bvFTD), primary progressive aphasia (PPA; further subcategorized as progressive nonfluent aphasia [PNFA] and semantic dementia [SD]), and movement disorders with extrapyramidal features such as parkinsonism and corticobasal syndrome (CBS). A broad range of clinical features both within and between families is observed. The age of onset ranges from 35 to 87 years. Behavioral disturbances are the most common early feature, followed by progressive aphasia. Impairment in executive function manifests as loss of judgment and insight. In early stages, PPA often manifests as deficits in naming, word finding, or word comprehension. In late stages, affected individuals often become mute and lose their ability to communicate. Early findings of parkinsonism include rigidity, bradykinesia or akinesia (slowing or absence of movements), limb dystonia, apraxia (loss of ability to carry out learned purposeful movements), and disequilibrium. Late motor findings may include myoclonus, dysarthria, and dysphagia. Most affected individuals eventually lose the ability to walk. Disease duration is three to 12 years.
L-2-hydroxyglutaric aciduria
MedGen UID:
341029
Concept ID:
C1855995
Disease or Syndrome
2-hydroxyglutaric aciduria is a condition that causes progressive damage to the brain. The major types of this disorder are called D-2-hydroxyglutaric aciduria (D-2-HGA), L-2-hydroxyglutaric aciduria (L-2-HGA), and combined D,L-2-hydroxyglutaric aciduria (D,L-2-HGA).\n\nThe main features of D-2-HGA are delayed development, seizures, weak muscle tone (hypotonia), and abnormalities in the largest part of the brain (the cerebrum), which controls many important functions such as muscle movement, speech, vision, thinking, emotion, and memory. Researchers have described two subtypes of D-2-HGA, type I and type II. The two subtypes are distinguished by their genetic cause and pattern of inheritance, although they also have some differences in signs and symptoms. Type II tends to begin earlier and often causes more severe health problems than type I. Type II may also be associated with a weakened and enlarged heart (cardiomyopathy), a feature that is typically not found with type I.\n\nL-2-HGA particularly affects a region of the brain called the cerebellum, which is involved in coordinating movements. As a result, many affected individuals have problems with balance and muscle coordination (ataxia). Additional features of L-2-HGA can include delayed development, seizures, speech difficulties, and an unusually large head (macrocephaly). Typically, signs and symptoms of this disorder begin during infancy or early childhood. The disorder worsens over time, usually leading to severe disability by early adulthood.\n\nCombined D,L-2-HGA causes severe brain abnormalities that become apparent in early infancy. Affected infants have severe seizures, weak muscle tone (hypotonia), and breathing and feeding problems. They usually survive only into infancy or early childhood.
Migraine, familial hemiplegic, 2
MedGen UID:
355962
Concept ID:
C1865322
Disease or Syndrome
Familial hemiplegic migraine (FHM) falls within the category of migraine with aura. In migraine with aura (including FHM) the neurologic symptoms of aura are unequivocally localizable to the cerebral cortex or brain stem and include visual disturbance (most common), sensory loss (e.g., numbness or paresthesias of the face or an extremity), and dysphasia (difficulty with speech). FHM must include motor involvement, such as hemiparesis (weakness of an extremity). Hemiparesis occurs with at least one other symptom during FHM aura. Neurologic deficits with FHM attacks can be prolonged for hours to days and may outlast the associated migrainous headache. FHM is often earlier in onset than typical migraine, frequently beginning in the first or second decade; the frequency of attacks tends to decrease with age. Approximately 40%-50% of families with CACNA1A-FHM have cerebellar signs ranging from nystagmus to progressive, usually late-onset mild ataxia.
Hemolytic uremic syndrome, atypical, susceptibility to, 1
MedGen UID:
412743
Concept ID:
C2749604
Finding
Hemolytic-uremic syndrome (HUS) is characterized by hemolytic anemia, thrombocytopenia, and renal failure caused by platelet thrombi in the microcirculation of the kidney and other organs. The onset of atypical HUS (aHUS) ranges from the neonatal period to adulthood. Genetic aHUS accounts for an estimated 60% of all aHUS. Individuals with genetic aHUS frequently experience relapse even after complete recovery following the presenting episode; 60% of genetic aHUS progresses to end-stage renal disease (ESRD).
Potocki-Lupski syndrome
MedGen UID:
444010
Concept ID:
C2931246
Disease or Syndrome
Potocki-Lupski syndrome (PTLS) is characterized by cognitive, behavioral, and medical manifestations. Cognitively, most individuals present with developmental delay, later meeting criteria for moderate intellectual disability. Behaviorally, issues with attention, hyperactivity, withdrawal, and anxiety may be seen. Some individuals meet criteria for autism spectrum disorder. Medically, hypotonia, oropharyngeal dysphagia leading to failure to thrive, congenital heart disease, hypoglycemia associated with growth hormone deficiency, and mildly dysmorphic facial features are observed. Medical manifestations typically lead to identification of PTLS in infancy; however, those with only behavioral and cognitive manifestations may be identified in later childhood.
Vasculitis due to ADA2 deficiency
MedGen UID:
854497
Concept ID:
C3887654
Disease or Syndrome
Adenosine deaminase 2 deficiency (DADA2) is a complex systemic autoinflammatory disorder in which vasculopathy/vasculitis, dysregulated immune function, and/or hematologic abnormalities may predominate. Inflammatory features include intermittent fevers, rash (often livedo racemosa/reticularis), and musculoskeletal involvement (myalgia/arthralgia, arthritis, myositis). Vasculitis, which usually begins before age ten years, may manifest as early-onset ischemic (lacunar) and/or hemorrhagic strokes, or as cutaneous or systemic polyarteritis nodosa. Hypertension and hepatosplenomegaly are often found. More severe involvement may lead to progressive central neurologic deficits (dysarthria, ataxia, cranial nerve palsies, cognitive impairment) or to ischemic injury to the kidney, intestine, and/or digits. Dysregulation of immune function can lead to immunodeficiency or autoimmunity of varying severity; lymphadenopathy may be present and some affected individuals have had lymphoproliferative disease. Hematologic disorders may begin early in life or in late adulthood, and can include lymphopenia, neutropenia, pure red cell aplasia, thrombocytopenia, or pancytopenia. Of note, both interfamilial and intrafamilial phenotypic variability (e.g., in age of onset, frequency and severity of manifestations) can be observed; also, individuals with biallelic ADA2 pathogenic variants may remain asymptomatic until adulthood or may never develop clinical manifestations of DADA2.
Intellectual disability, autosomal dominant 29
MedGen UID:
863578
Concept ID:
C4015141
Mental or Behavioral Dysfunction
SETBP1 haploinsufficiency disorder (SETBP1-HD) is characterized by hypotonia and mild motor developmental delay; intellectual abilities ranging from normal to severe disability; speech and language disorder; behavioral problems (most commonly attention/concentration deficits and hyperactivity, impulsivity), and refractive errors and strabismus. Typically children with SETBP1-HD whose intellect is in the normal or borderline range (IQ 80-90) were diagnosed following genetic testing for behavioral problems and/or severe speech and language disorders (respectively: the inability to produce sounds in words correctly, and deficits in the understanding and/or expression of words and sentences). To date, 47 individuals with SETBP1-HD have been reported.
Inclusion body myopathy with Paget disease of bone and frontotemporal dementia type 1
MedGen UID:
1641069
Concept ID:
C4551951
Disease or Syndrome
Inclusion body myopathy associated with Paget disease of bone (PDB) and/or frontotemporal dementia (IBMPFD) is characterized by adult-onset proximal and distal muscle weakness (clinically resembling a limb-girdle muscular dystrophy syndrome), early-onset PDB, and premature frontotemporal dementia (FTD). Muscle weakness progresses to involve other limb and respiratory muscles. PDB involves focal areas of increased bone turnover that typically lead to spine and/or hip pain and localized enlargement and deformity of the long bones; pathologic fractures occur on occasion. Early stages of FTD are characterized by dysnomia, dyscalculia, comprehension deficits, and paraphasic errors, with minimal impairment of episodic memory; later stages are characterized by inability to speak, auditory comprehension deficits for even one-step commands, alexia, and agraphia. Mean age at diagnosis for muscle disease and PDB is 42 years; for FTD, 56 years. Dilated cardiomyopathy, amyotrophic lateral sclerosis, and Parkinson disease are now known to be part of the spectrum of findings associated with IBMPFD.
Mitochondrial complex 1 deficiency, nuclear type 12
MedGen UID:
1648278
Concept ID:
C4746984
Disease or Syndrome
Polycystic lipomembranous osteodysplasia with sclerosing leukoencephalopathy 2
MedGen UID:
1648374
Concept ID:
C4748657
Disease or Syndrome
Polycystic lipomembranous osteodysplasia with sclerosing leukoencephalopathy-2 (PLOSL2), or Nasu-Hakola disease, is a recessively inherited presenile frontal dementia with leukoencephalopathy and basal ganglia calcification. In most cases the disorder first manifests in early adulthood as pain and swelling in ankles and feet, followed by bone fractures. Neurologic symptoms manifest in the fourth decade of life as a frontal lobe syndrome with loss of judgment, euphoria, and disinhibition. Progressive decline in other cognitive domains begins to develop at about the same time. The disorder culminates in a profound dementia and death by age 50 years (summary by Klunemann et al., 2005). For a discussion of genetic heterogeneity of polycystic lipomembranous osteodysplasia with sclerosing leukoencephalopathy, see 221770.
Frontotemporal dementia and/or amyotrophic lateral sclerosis 8
MedGen UID:
1728824
Concept ID:
C5436881
Disease or Syndrome
Frontotemporal dementia and/or amyotrophic lateral sclerosis-8 (FTDALS8) is an autosomal dominant neurodegenerative disorder characterized by adult-onset dementia manifest as memory impairment, executive dysfunction, and behavioral or personality changes. Some patients may develop ALS or parkinsonism. Neuropathologic studies show frontotemporal lobar degeneration (FTLD) with tau (MAPT; 157140)- and TDP43 (605078)-immunoreactive inclusions (summary by Dobson-Stone et al., 2020). For a discussion of genetic heterogeneity of FTDALS, see FTDALS1 (105550).
Amyotrophic lateral sclerosis 26 with or without frontotemporal dementia
MedGen UID:
1771903
Concept ID:
C5436882
Disease or Syndrome
Amyotrophic lateral sclerosis-26 with or without frontotemporal dementia (ALS26) is an autosomal dominant neurodegenerative disorder characterized by adult onset of upper and low motor neuron disease causing bulbar dysfunction and limb weakness (ALS). Patients may also develop frontotemporal dementia (FTD) manifest as primary progressive aphasia, memory impairment, executive dysfunction, and behavioral or personality changes. Although patients may present with 1 or the other diseases, all eventually develop ALS. Neuropathologic studies of the brain and spinal cord show TDP43 (605078)-immunoreactive cytoplasmic inclusions that correlate with clinical features and Lewy body-like cytoplasmic inclusions in lower motor neurons (summary by Mackenzie et al., 2017). For a discussion of genetic heterogeneity of amyotrophic lateral sclerosis, see ALS1 (105400).
Developmental and epileptic encephalopathy 103
MedGen UID:
1809962
Concept ID:
C5677002
Disease or Syndrome
Developmental and epileptic encephalopathy-103 (DEE103) is characterized by onset of various types of seizures in the first year of life, most of which are refractory to treatment. Affected individuals show global developmental delay with impaired intellectual development ranging from mild to severe. Additional features may include hypotonia, ataxia, and behavioral abnormalities, including autism and hyperactivity (Schwarz et al., 2022). For a general phenotypic description and a discussion of genetic heterogeneity of DEE, see 308350.

Professional guidelines

PubMed

Lefaucheur JP, Aleman A, Baeken C, Benninger DH, Brunelin J, Di Lazzaro V, Filipović SR, Grefkes C, Hasan A, Hummel FC, Jääskeläinen SK, Langguth B, Leocani L, Londero A, Nardone R, Nguyen JP, Nyffeler T, Oliveira-Maia AJ, Oliviero A, Padberg F, Palm U, Paulus W, Poulet E, Quartarone A, Rachid F, Rektorová I, Rossi S, Sahlsten H, Schecklmann M, Szekely D, Ziemann U
Clin Neurophysiol 2020 Feb;131(2):474-528. Epub 2020 Jan 1 doi: 10.1016/j.clinph.2019.11.002. PMID: 31901449
Volkmer A, Rogalski E, Henry M, Taylor-Rubin C, Ruggero L, Khayum R, Kindell J, Gorno-Tempini ML, Warren JD, Rohrer JD
Pract Neurol 2020 Apr;20(2):154-161. Epub 2019 Jul 29 doi: 10.1136/practneurol-2018-001921. PMID: 31358572Free PMC Article
Berthier ML
Drugs Aging 2005;22(2):163-82. doi: 10.2165/00002512-200522020-00006. PMID: 15733022

Recent clinical studies

Etiology

Zhang H, Hinzen W
PLoS One 2022;17(12):e0278676. Epub 2022 Dec 6 doi: 10.1371/journal.pone.0278676. PMID: 36473005Free PMC Article
Walker GM, Fridriksson J, Hillis AE, den Ouden DB, Bonilha L, Hickok G
Am J Speech Lang Pathol 2022 Nov 16;31(6):2722-2740. Epub 2022 Nov 4 doi: 10.1044/2022_AJSLP-22-00071. PMID: 36332139Free PMC Article
Cherney LR, Carpenter J
Handb Clin Neurol 2022;185:197-220. doi: 10.1016/B978-0-12-823384-9.00010-4. PMID: 35078599
Puppala GK, Gorthi SP, Chandran V, Gundabolu G
Neurol India 2021 Sep-Oct;69(5):1144-1152. doi: 10.4103/0028-3886.329593. PMID: 34747778
Marshall CR, Hardy CJD, Volkmer A, Russell LL, Bond RL, Fletcher PD, Clark CN, Mummery CJ, Schott JM, Rossor MN, Fox NC, Crutch SJ, Rohrer JD, Warren JD
J Neurol 2018 Jun;265(6):1474-1490. Epub 2018 Feb 1 doi: 10.1007/s00415-018-8762-6. PMID: 29392464Free PMC Article

Diagnosis

Puppala GK, Gorthi SP, Chandran V, Gundabolu G
Neurol India 2021 Sep-Oct;69(5):1144-1152. doi: 10.4103/0028-3886.329593. PMID: 34747778
Sheppard SM, Sebastian R
Expert Rev Neurother 2021 Feb;21(2):221-234. Epub 2020 Dec 10 doi: 10.1080/14737175.2020.1855976. PMID: 33231117Free PMC Article
Gonzalez R, Rojas M, Rosselli M, Ardila A
Arch Clin Neuropsychol 2021 May 21;36(4):455-464. doi: 10.1093/arclin/acaa072. PMID: 32978628
Dietz A, Wallace SE, Weissling K
Am J Speech Lang Pathol 2020 May 8;29(2):909-913. Epub 2020 Feb 27 doi: 10.1044/2019_AJSLP-19-00041. PMID: 32109137Free PMC Article
Marshall CR, Hardy CJD, Volkmer A, Russell LL, Bond RL, Fletcher PD, Clark CN, Mummery CJ, Schott JM, Rossor MN, Fox NC, Crutch SJ, Rohrer JD, Warren JD
J Neurol 2018 Jun;265(6):1474-1490. Epub 2018 Feb 1 doi: 10.1007/s00415-018-8762-6. PMID: 29392464Free PMC Article

Therapy

Sheppard SM, Sebastian R
Expert Rev Neurother 2021 Feb;21(2):221-234. Epub 2020 Dec 10 doi: 10.1080/14737175.2020.1855976. PMID: 33231117Free PMC Article
Coleman ER, Moudgal R, Lang K, Hyacinth HI, Awosika OO, Kissela BM, Feng W
Curr Atheroscler Rep 2017 Nov 7;19(12):59. doi: 10.1007/s11883-017-0686-6. PMID: 29116473Free PMC Article
Brady MC, Kelly H, Godwin J, Enderby P, Campbell P
Cochrane Database Syst Rev 2016 Jun 1;2016(6):CD000425. doi: 10.1002/14651858.CD000425.pub4. PMID: 27245310Free PMC Article
Langhorne P, Bernhardt J, Kwakkel G
Lancet 2011 May 14;377(9778):1693-702. doi: 10.1016/S0140-6736(11)60325-5. PMID: 21571152
Berthier ML
Drugs Aging 2005;22(2):163-82. doi: 10.2165/00002512-200522020-00006. PMID: 15733022

Prognosis

Lin HL, Tsai CF, Liu SP, Muo CH, Chen PC
J Stroke Cerebrovasc Dis 2022 Dec;31(12):106838. Epub 2022 Oct 22 doi: 10.1016/j.jstrokecerebrovasdis.2022.106838. PMID: 36283235
Grönberg A, Henriksson I, Stenman M, Lindgren AG
Neuroepidemiology 2022;56(3):174-182. Epub 2022 Mar 23 doi: 10.1159/000524206. PMID: 35320798
De Cock E, Batens K, Hemelsoet D, Boon P, Oostra K, De Herdt V
Eur J Neurol 2020 Oct;27(10):2014-2021. Epub 2020 Jun 30 doi: 10.1111/ene.14385. PMID: 32515514
Flowers HL, Skoretz SA, Silver FL, Rochon E, Fang J, Flamand-Roze C, Martino R
Arch Phys Med Rehabil 2016 Dec;97(12):2188-2201.e8. Epub 2016 Apr 8 doi: 10.1016/j.apmr.2016.03.006. PMID: 27063364
Code C, Petheram B
Int J Speech Lang Pathol 2011 Feb;13(1):3-10. doi: 10.3109/17549507.2010.520090. PMID: 21329405

Clinical prediction guides

Walker GM, Fridriksson J, Hillis AE, den Ouden DB, Bonilha L, Hickok G
Am J Speech Lang Pathol 2022 Nov 16;31(6):2722-2740. Epub 2022 Nov 4 doi: 10.1044/2022_AJSLP-22-00071. PMID: 36332139Free PMC Article
Rangus I, Fritsch M, Endres M, Udke B, Nolte CH
J Neurol 2022 Jan;269(1):368-376. Epub 2021 Jun 8 doi: 10.1007/s00415-021-10640-4. PMID: 34100990Free PMC Article
Gonzalez R, Rojas M, Rosselli M, Ardila A
Arch Clin Neuropsychol 2021 May 21;36(4):455-464. doi: 10.1093/arclin/acaa072. PMID: 32978628
Brown J, Thiessen A
Am J Speech Lang Pathol 2018 Mar 1;27(1S):504-515. doi: 10.1044/2017_AJSLP-16-0190. PMID: 29497760
Lazar RM, Boehme AK
Curr Neurol Neurosci Rep 2017 Sep 19;17(11):83. doi: 10.1007/s11910-017-0797-z. PMID: 28929424

Recent systematic reviews

Li B, Deng S, Sang B, Zhu W, Zhuo B, Zhang M, Qin C, Lyu Y, Du Y, Meng Z
Neural Plast 2022;2022:5635596. Epub 2022 Apr 21 doi: 10.1155/2022/5635596. PMID: 35494482Free PMC Article
Liu Q, Li W, Yin Y, Zhao Z, Yang Y, Zhao Y, Tan Y, Yu J
Neurol Sci 2022 Feb;43(2):863-872. Epub 2021 Nov 24 doi: 10.1007/s10072-021-05743-9. PMID: 34816318
Payne LE, Gagnon DJ, Riker RR, Seder DB, Glisic EK, Morris JG, Fraser GL
Crit Care 2017 Nov 14;21(1):276. doi: 10.1186/s13054-017-1856-1. PMID: 29137682Free PMC Article
Brady MC, Kelly H, Godwin J, Enderby P, Campbell P
Cochrane Database Syst Rev 2016 Jun 1;2016(6):CD000425. doi: 10.1002/14651858.CD000425.pub4. PMID: 27245310Free PMC Article
Simmons-Mackie N, Raymer A, Armstrong E, Holland A, Cherney LR
Arch Phys Med Rehabil 2010 Dec;91(12):1814-37. doi: 10.1016/j.apmr.2010.08.026. PMID: 21112422

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