U.S. flag

An official website of the United States government

Format

Send to:

Choose Destination

Apraxia

MedGen UID:
8166
Concept ID:
C0003635
Mental or Behavioral Dysfunction
Synonyms: Dyspraxia; Verbal apraxia
SNOMED CT: Apraxia (68345001); Dyspraxia (6950007)
 
HPO: HP:0002186
Monarch Initiative: MONDO:0000665

Definition

A defect in the understanding of complex motor commands and in the execution of certain learned movements, i.e., deficits in the cognitive components of learned movements. [from HPO]

Conditions with this feature

Gerstmann-Straussler-Scheinker syndrome
MedGen UID:
4886
Concept ID:
C0017495
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.
Wieacker-Wolff syndrome
MedGen UID:
163227
Concept ID:
C0796200
Disease or Syndrome
Wieacker-Wolff syndrome (WRWF) is a severe X-linked recessive neurodevelopmental disorder affecting the central and peripheral nervous systems. It is characterized by onset of muscle weakness in utero (fetal akinesia), which results in arthrogryposis multiplex congenita (AMC) apparent at birth. Affected boys are born with severe contractures, show delayed motor development, facial and bulbar weakness, characteristic dysmorphic facial features, and skeletal abnormalities, such as hip dislocation, scoliosis, and foot deformities. Additional features include global developmental delay with poor or absent speech and impaired intellectual development, feeding difficulties and poor growth, hypotonia, hypogenitalism, and spasticity. Carrier females may be unaffected or have mild features of the disorder (summary by Hirata et al., 2013 and Frints et al., 2019).
X-linked intellectual disability-psychosis-macroorchidism syndrome
MedGen UID:
163232
Concept ID:
C0796222
Disease or Syndrome
The spectrum of MECP2-related phenotypes in females ranges from classic Rett syndrome to variant Rett syndrome with a broader clinical phenotype (either milder or more severe than classic Rett syndrome) to mild learning disabilities; the spectrum in males ranges from severe neonatal encephalopathy to pyramidal signs, parkinsonism, and macroorchidism (PPM-X) syndrome to severe syndromic/nonsyndromic intellectual disability. Females: Classic Rett syndrome, a progressive neurodevelopmental disorder primarily affecting girls, is characterized by apparently normal psychomotor development during the first six to 18 months of life, followed by a short period of developmental stagnation, then rapid regression in language and motor skills, followed by long-term stability. During the phase of rapid regression, repetitive, stereotypic hand movements replace purposeful hand use. Additional findings include fits of screaming and inconsolable crying, autistic features, panic-like attacks, bruxism, episodic apnea and/or hyperpnea, gait ataxia and apraxia, tremors, seizures, and acquired microcephaly. Males: Severe neonatal-onset encephalopathy, the most common phenotype in affected males, is characterized by a relentless clinical course that follows a metabolic-degenerative type of pattern, abnormal tone, involuntary movements, severe seizures, and breathing abnormalities. Death often occurs before age two years.
Alzheimer disease 3
MedGen UID:
334304
Concept ID:
C1843013
Disease or Syndrome
Alzheimer's disease can be classified as early-onset or late-onset. The signs and symptoms of the early-onset form appear between a person's thirties and mid-sixties, while the late-onset form appears during or after a person's mid-sixties. The early-onset form of Alzheimer's disease is much less common than the late-onset form, accounting for less than 10 percent of all cases of Alzheimer's disease.\n\nIndividuals with Alzheimer's disease usually survive 8 to 10 years after the appearance of symptoms, but the course of the disease can range from 1 to 25 years. Survival is usually shorter in individuals diagnosed after age 80 than in those diagnosed at a younger age. In Alzheimer's disease, death usually results from pneumonia, malnutrition, or general body wasting (inanition).\n\nAs the disorder progresses, some people with Alzheimer's disease experience personality and behavioral changes and have trouble interacting in a socially appropriate manner. Other common symptoms include agitation, restlessness, withdrawal, and loss of language skills. People with Alzheimer's disease usually require total care during the advanced stages of the disease.\n\nMemory loss is the most common sign of Alzheimer's disease. Forgetfulness may be subtle at first, but the loss of memory worsens over time until it interferes with most aspects of daily living. Even in familiar settings, a person with Alzheimer's disease may get lost or become confused. Routine tasks such as preparing meals, doing laundry, and performing other household chores can be challenging. Additionally, it may become difficult to recognize people and name objects. Affected people increasingly require help with dressing, eating, and personal care.\n\nAlzheimer's disease is a degenerative disease of the brain that causes dementia, which is a gradual loss of memory, judgment, and ability to function. This disorder usually appears in people older than age 65, but less common forms of the disease appear earlier in adulthood.
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.
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).
Spinocerebellar ataxia type 17
MedGen UID:
337637
Concept ID:
C1846707
Disease or Syndrome
Spinocerebellar ataxia type 17 (SCA17) is characterized by ataxia, dementia, and involuntary movements, including chorea and dystonia. Psychiatric symptoms, pyramidal signs, and rigidity are common. The age of onset ranges from three to 55 years. Individuals with full-penetrance alleles develop neurologic and/or psychiatric symptoms by age 50 years. Ataxia and psychiatric abnormalities are frequently the initial findings, followed by involuntary movement, parkinsonism, dementia, and pyramidal signs. Brain MRI shows variable atrophy of the cerebrum, brain stem, and cerebellum. The clinical features correlate with the length of the polyglutamine expansion but are not absolutely predictive of the clinical course.
Alzheimer disease 4
MedGen UID:
376072
Concept ID:
C1847200
Disease or Syndrome
Alzheimer's disease is a degenerative disease of the brain that causes dementia, which is a gradual loss of memory, judgment, and ability to function. This disorder usually appears in people older than age 65, but less common forms of the disease appear earlier in adulthood.\n\nMemory loss is the most common sign of Alzheimer's disease. Forgetfulness may be subtle at first, but the loss of memory worsens over time until it interferes with most aspects of daily living. Even in familiar settings, a person with Alzheimer's disease may get lost or become confused. Routine tasks such as preparing meals, doing laundry, and performing other household chores can be challenging. Additionally, it may become difficult to recognize people and name objects. Affected people increasingly require help with dressing, eating, and personal care.\n\nAs the disorder progresses, some people with Alzheimer's disease experience personality and behavioral changes and have trouble interacting in a socially appropriate manner. Other common symptoms include agitation, restlessness, withdrawal, and loss of language skills. People with Alzheimer's disease usually require total care during the advanced stages of the disease.\n\nIndividuals with Alzheimer's disease usually survive 8 to 10 years after the appearance of symptoms, but the course of the disease can range from 1 to 25 years. Survival is usually shorter in individuals diagnosed after age 80 than in those diagnosed at a younger age. In Alzheimer's disease, death usually results from pneumonia, malnutrition, or general body wasting (inanition).\n\nAlzheimer's disease can be classified as early-onset or late-onset. The signs and symptoms of the early-onset form appear between a person's thirties and mid-sixties, while the late-onset form appears during or after a person's mid-sixties. The early-onset form of Alzheimer's disease is much less common than the late-onset form, accounting for less than 10 percent of all cases of Alzheimer's disease.
Mast syndrome
MedGen UID:
343325
Concept ID:
C1855346
Disease or Syndrome
Mast syndrome (MASTS) is an autosomal recessive complicated form of hereditary spastic paraplegia in which progressive spastic paraparesis is associated in more advanced cases with cognitive decline, dementia, and other neurologic abnormalities. Symptom onset usually occurs in adulthood, and the disorder is progressive with variable severity. Brain imaging shows thinning of the corpus callosum. The disorder occurs with high frequency in the Old Order Amish (summary by Simpson et al., 2003). For a discussion of genetic heterogeneity of autosomal recessive spastic paraplegia, see SPG5A (270800).
Retinal vasculopathy with cerebral leukoencephalopathy and systemic manifestations
MedGen UID:
348124
Concept ID:
C1860518
Disease or Syndrome
Retinal vasculopathy with cerebral leukoencephalopathy and systemic manifestations (RVCL-S) is a small-vessel disease that affects highly vascularized tissues including the retina, brain, liver, and kidneys. Age of onset is often between 35 and 50 years. The most common presenting finding is decreased visual acuity and/or visual field defects. Neurologic manifestations may include hemiparesis, facial weakness, aphasia, and hemianopsia. Migraines and seizures are less frequently described. Renal manifestations may include mild-to-moderate increase in serum creatinine and mild proteinuria; progression to end-stage renal disease (ESRD) is uncommon. Hepatic manifestations frequently include mildly elevated levels of alkaline phosphatase and gamma-glutamyltransferase (GGT). Less common findings include psychiatric disorders, hypertension, mild-to-moderate anemia, and Raynaud phenomenon.
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.
Rett syndrome, congenital variant
MedGen UID:
462055
Concept ID:
C3150705
Disease or Syndrome
The congenital variant of Rett syndrome is a severe neurodevelopmental disorder with features of classic Rett syndrome (RTT; 312750), but earlier onset in the first months of life. Classic Rett syndrome shows later onset and is caused by mutation in the MECP2 gene (300005).
Mitochondrial complex III deficiency nuclear type 2
MedGen UID:
767519
Concept ID:
C3554605
Disease or Syndrome
Mitochondrial complex III deficiency nuclear type 2 is an autosomal recessive severe neurodegenerative disorder that usually presents in childhood, but may show later onset, even in adulthood. Affected individuals have motor disability, with ataxia, apraxia, dystonia, and dysarthria, associated with necrotic lesions throughout the brain. Most patients also have cognitive impairment and axonal neuropathy and become severely disabled later in life (summary by Ghezzi et al., 2011). The disorder may present clinically as spinocerebellar ataxia or Leigh syndrome, or with psychiatric disturbances (Morino et al., 2014; Atwal, 2014; Nogueira et al., 2013). For a discussion of genetic heterogeneity of mitochondrial complex III deficiency, see MC3DN1 (124000).
Leukoencephalopathy, progressive, with ovarian failure
MedGen UID:
863025
Concept ID:
C4014588
Disease or Syndrome
Progressive leukoencephalopathy with ovarian failure is an autosomal recessive neurodegenerative disorder characterized by loss of motor and cognitive skills, usually with onset in young adulthood. Some patients may have a history of delayed motor development or learning difficulties in early childhood. Neurologic decline is severe, usually resulting in gait difficulties, ataxia, spasticity, and cognitive decline and dementia. Most patients lose speech and become wheelchair-bound or bedridden. Brain MRI shows progressive white matter signal abnormalities in the deep white matter. Affected females develop premature ovarian failure (summary by Dallabona et al., 2014).
Short stature, microcephaly, and endocrine dysfunction
MedGen UID:
895448
Concept ID:
C4225288
Disease or Syndrome
In patients with SSMED, short stature and microcephaly are apparent at birth, and there is progressive postnatal growth failure. Endocrine dysfunction, including hypergonadotropic hypogonadism, multinodular goiter, and diabetes mellitus, is present in affected adults. Progressive ataxia has been reported in some patients, with onset ranging from the second to fifth decade of life. In addition, a few patients have developed tumors, suggesting that there may be a predisposition to tumorigenesis. In contrast to syndromes involving defects in other components of the nonhomologous end-joining (NHEJ) complex (see, e.g., 606593), no clinically overt immunodeficiency has been observed in SSMED, although laboratory analysis has revealed lymphopenia or borderline leukopenia in some patients (Murray et al., 2015; Bee et al., 2015; de Bruin et al., 2015; Guo et al., 2015).
Glycosylphosphatidylinositol biosynthesis defect 15
MedGen UID:
1615160
Concept ID:
C4540520
Disease or Syndrome
GPIBD15 is an autosomal recessive disorder characterized by delayed psychomotor development, variable intellectual disability, hypotonia, early-onset seizures in most patients, and cerebellar atrophy, resulting in cerebellar signs including gait ataxia and dysarthria. The disorder is caused by a defect in glycosylphosphatidylinositol (GPI) biosynthesis (summary by Nguyen et al., 2017). For a discussion of genetic heterogeneity of GPI biosynthesis defects, see GPIBD1 (610293).
Polycystic lipomembranous osteodysplasia with sclerosing leukoencephalopathy 1
MedGen UID:
1648386
Concept ID:
C4721893
Disease or Syndrome
Polycystic lipomembranous osteodysplasia with sclerosing leukoencephalopathy (PLOSL) is characterized by fractures (resulting from radiologically demonstrable polycystic osseous lesions), frontal lobe syndrome, and progressive presenile dementia beginning in the fourth decade. The clinical course of PLOSL can be divided into four stages: 1. The latent stage is characterized by normal early development. 2. The osseous stage (3rd decade of life) is characterized by pain and tenderness, mostly in ankles and feet, usually following strain or injury. Fractures are typically diagnosed several years later, most commonly in the bones of the extremities. 3. In the early neurologic stage (4th decade of life), a change of personality begins to develop insidiously. Affected individuals show a frontal lobe syndrome (loss of judgment, euphoria, loss of social inhibitions, disturbance of concentration, and lack of insight, libido, and motor persistence) leading to serious social problems. 4. The late neurologic stage is characterized by progressive dementia and loss of mobility. Death usually occurs before age 50 years.
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.
Autosomal recessive spinocerebellar ataxia 20
MedGen UID:
1684324
Concept ID:
C5190595
Disease or Syndrome
Autosomal recessive spinocerebellar ataxia-20 is a neurodevelopmental disorder characterized by severely delayed psychomotor development with poor or absent speech, wide-based or absent gait, coarse facies, and cerebellar atrophy (summary by Thomas et al., 2014).
Hao-Fountain syndrome
MedGen UID:
1719035
Concept ID:
C5393908
Disease or Syndrome
Hao-Fountain syndrome (HAFOUS) is a neurodevelopmental disorder characterized by global developmental delay, variably impaired intellectual development with significant speech delay, behavioral abnormalities, such as autism, and mild dysmorphic facies. Additional features are variable, but may include hypotonia, feeding problems, delayed walking with unsteady gait, hypogonadism in males, and ocular anomalies, such as strabismus. Some patients develop seizures and some have mild white matter abnormalities on brain imaging (summary by Fountain et al., 2019).
Leukoencephalopathy, diffuse hereditary, with spheroids 1
MedGen UID:
1794139
Concept ID:
C5561929
Disease or Syndrome
CSF1R-related adult-onset leukoencephalopathy with axonal spheroids and pigmented glia (ALSP) is characterized by executive dysfunction, memory decline, personality changes, motor impairments, and seizures. A frontal lobe syndrome (e.g., loss of judgment, lack of social inhibitors, lack of insight, and motor persistence) usually appears early in the disease course. The mean age of onset is usually in the fourth decade. Affected individuals eventually become bedridden with spasticity and rigidity. The disease course ranges from two to 30 or more years (mean: 8 years).
Neurodevelopmental disorder, nonprogressive, with spasticity and transient opisthotonus
MedGen UID:
1794250
Concept ID:
C5562040
Disease or Syndrome
Nonprogressive neurodevelopmental disorder with spasticity and transient opisthotonus (NEDSTO) is an autosomal recessive complex neurologic disorder characterized by delay of gross motor milestones, particularly walking, associated with axial hypotonia and peripheral spasticity apparent from infancy or early childhood. Affected individuals often show transient opisthotonic posturing in infancy, and later show abnormal involuntary movements, including chorea, dystonia, and dyspraxia. Some patients have impaired intellectual development, although the severity is highly variable; most have speech delay and articulation difficulties and a happy overall demeanor. Brain imaging shows myelination defects in some patients. The disorder is nonprogressive, and many patients may catch up developmentally in the second or third decades (summary by Wagner et al., 2020).
Developmental delay, language impairment, and ocular abnormalities
MedGen UID:
1824035
Concept ID:
C5774262
Disease or Syndrome
Developmental delay, language impairment, and ocular abnormalities (DEVLO) is characterized by delayed acquisition of skills particularly affecting speech and language development, although many patients show mild motor delay. Most affected individuals also have a small head circumference (down to -3 SD) and may have mild dysmorphic features. Variable ocular anomalies include strabismus, cataracts, and cortical visual impairment. Older patients require special schooling and often demonstrate behavioral abnormalities (Laboy Cintron et al., 2022).
Spinocerebellar ataxia 50
MedGen UID:
1824045
Concept ID:
C5774272
Disease or Syndrome
Spinocerebellar ataxia-50 (SCA50) is an autosomal dominant neurologic disorder characterized by cerebellar ataxia, oculomotor apraxia and other eye movement abnormalities, and cerebellar atrophy on brain imaging. Most patients develop symptoms as adults, although childhood onset has rarely been reported. Additional more variable features may include tremor, dysarthria, dysphagia, and cognitive impairment with executive dysfunction (Coutelier et al., 2022; Schoggl et al., 2022).
Frontotemporal dementia and/or amyotrophic lateral sclerosis 1
MedGen UID:
1830423
Concept ID:
C5779877
Disease or Syndrome
C9orf72 frontotemporal dementia and/or amyotrophic lateral sclerosis (C9orf72-FTD/ALS) is characterized most often by frontotemporal dementia (FTD) and upper and lower motor neuron disease (MND); however, atypical presentations also occur. Age at onset is usually between 50 and 64 years (range: 20-91 years) irrespective of the presenting manifestations, which may be pure FTD, pure amyotrophic lateral sclerosis (ALS), or a combination of the two phenotypes. The clinical presentation is highly heterogeneous and may differ between and within families, causing an unpredictable pattern and age of onset of clinical manifestations. The presence of MND correlates with an earlier age of onset and a worse overall prognosis.
Neurodevelopmental disorder with seizures, spasticity, and complete or partial agenesis of the corpus callosum
MedGen UID:
1840932
Concept ID:
C5830296
Disease or Syndrome
Neurodevelopmental disorder with seizures, spasticity, and partial or complete agenesis of the corpus callosum (NEDSSCC) is an autosomal recessive disorder characterized by axial hypotonia and global developmental delay apparent from the first days or months of life. Affected individuals often have feeding difficulties and develop early-onset seizures that tend to be well-controlled. Other features include peripheral spasticity with hyperreflexia, variable dysmorphic features, impaired intellectual development, behavioral abnormalities, and hypoplasia or absence of the corpus callosum on brain imaging (Faqeih et al., 2023).
Intellectual developmental disorder, autosomal dominant 73
MedGen UID:
1841272
Concept ID:
C5830636
Mental or Behavioral Dysfunction
Autosomal dominant intellectual developmental disorder-73 (MRD73) is a highly variable neurodevelopmental disorder characterized by impaired intellectual development that ranges from mild to severe, speech delay, behavioral abnormalities, and nonspecific dysmorphic facial features (Janssen et al., 2022).
Myoclonic epilepsy of Lafora 1
MedGen UID:
1844054
Concept ID:
C5848203
Disease or Syndrome
Any Lafora disease in which the cause of the disease is a variation in the EPM2A gene.

Professional guidelines

PubMed

Spahiu L, Behluli E, Grajçevci-Uka V, Liehr T, Temaj G
J Mother Child 2022 Mar 1;26(1):118-123. Epub 2023 Feb 22 doi: 10.34763/jmotherandchild.20222601.d-22-00034. PMID: 36803942Free PMC Article
Strand EA
Am J Speech Lang Pathol 2020 Feb 7;29(1):30-48. Epub 2019 Dec 17 doi: 10.1044/2019_AJSLP-19-0005. PMID: 31846588
Levin J, Kurz A, Arzberger T, Giese A, Höglinger GU
Dtsch Arztebl Int 2016 Feb 5;113(5):61-9. doi: 10.3238/arztebl.2016.0061. PMID: 26900156Free PMC Article

Recent clinical studies

Etiology

Walther S, Mittal VA, Stegmayer K, Bohlhalter S
Cortex 2020 Dec;133:65-75. Epub 2020 Oct 3 doi: 10.1016/j.cortex.2020.09.017. PMID: 33099076Free PMC Article
Galeoto G, Polidori AM, Spallone M, Mollica R, Berardi A, Vanacore N, Celletti C, Carlizza A, Camerota F
Clin Ter 2020 Sep-Oct;171(5):e454-e465. doi: 10.7417/CT.2020.2257. PMID: 32901792
Sinha S, Kataria A, Kolla BP, Thusius N, Loukianova LL
Mayo Clin Proc 2019 Jun;94(6):1065-1072. doi: 10.1016/j.mayocp.2019.02.018. PMID: 31171116
Catsman-Berrevoets C, Patay Z
Handb Clin Neurol 2018;155:273-288. doi: 10.1016/B978-0-444-64189-2.00018-4. PMID: 29891065
Murray E, McCabe P, Ballard KJ
Am J Speech Lang Pathol 2014 Aug;23(3):486-504. doi: 10.1044/2014_AJSLP-13-0035. PMID: 24686844

Diagnosis

Utianski RL, Josephs KA
Curr Neurol Neurosci Rep 2023 Jul;23(7):353-359. Epub 2023 Jun 3 doi: 10.1007/s11910-023-01275-1. PMID: 37269450Free PMC Article
Heilman KM
Continuum (Minneap Minn) 2021 Dec 1;27(6):1602-1623. doi: 10.1212/CON.0000000000001014. PMID: 34881728
Catrini M, Lier-DeVitto MF
Codas 2019;31(5):e20180121. Epub 2019 Oct 31 doi: 10.1590/2317-1782/20192018121. PMID: 31691745
Botha H, Josephs KA
Continuum (Minneap Minn) 2019 Feb;25(1):101-127. doi: 10.1212/CON.0000000000000699. PMID: 30707189Free PMC Article
Etcharry-Bouyx F, Le Gall D, Jarry C, Osiurak F
Rev Neurol (Paris) 2017 Jul-Aug;173(7-8):430-439. Epub 2017 Aug 26 doi: 10.1016/j.neurol.2017.07.005. PMID: 28844701

Therapy

Gibson E, Koh CL, Eames S, Bennett S, Scott AM, Hoffmann TC
Cochrane Database Syst Rev 2022 Mar 29;3(3):CD006430. doi: 10.1002/14651858.CD006430.pub3. PMID: 35349186Free PMC Article
Miller KJ, Suárez-Iglesias D, Seijo-Martínez M, Ayán C
Rev Neurol 2020 Mar 1;70(5):161-170. doi: 10.33588/rn.7005.2019417. PMID: 32100276
Sinha S, Kataria A, Kolla BP, Thusius N, Loukianova LL
Mayo Clin Proc 2019 Jun;94(6):1065-1072. doi: 10.1016/j.mayocp.2019.02.018. PMID: 31171116
Catsman-Berrevoets C, Patay Z
Handb Clin Neurol 2018;155:273-288. doi: 10.1016/B978-0-444-64189-2.00018-4. PMID: 29891065
Morgan AT, Murray E, Liégeois FJ
Cochrane Database Syst Rev 2018 May 30;5(5):CD006278. doi: 10.1002/14651858.CD006278.pub3. PMID: 29845607Free PMC Article

Prognosis

Mermelstein S, Barbosa P, Kaski D
Pract Neurol 2024 Jan 23;24(1):11-21. doi: 10.1136/pn-2023-003917. PMID: 38135498
Baumard J, Lesourd M, Guézouli L, Osiurak F
Cogn Neuropsychol 2021 Oct-Dec;38(7-8):490-514. Epub 2022 May 13 doi: 10.1080/02643294.2022.2071152. PMID: 35549825
Botha H, Josephs KA
Continuum (Minneap Minn) 2019 Feb;25(1):101-127. doi: 10.1212/CON.0000000000000699. PMID: 30707189Free PMC Article
Grijalvo-Perez AM, Litvan I
Semin Neurol 2014 Apr;34(2):160-73. Epub 2014 Jun 25 doi: 10.1055/s-0034-1381734. PMID: 24963675
Finney GR
Int Rev Neurobiol 2009;84:263-81. doi: 10.1016/S0074-7742(09)00414-0. PMID: 19501723

Clinical prediction guides

Baumard J, Lesourd M, Guézouli L, Osiurak F
Cogn Neuropsychol 2021 Oct-Dec;38(7-8):490-514. Epub 2022 May 13 doi: 10.1080/02643294.2022.2071152. PMID: 35549825
Baumard J, Le Gall D
Cortex 2021 Aug;141:66-80. Epub 2021 Apr 23 doi: 10.1016/j.cortex.2021.04.001. PMID: 34033988
Walther S, Mittal VA, Stegmayer K, Bohlhalter S
Cortex 2020 Dec;133:65-75. Epub 2020 Oct 3 doi: 10.1016/j.cortex.2020.09.017. PMID: 33099076Free PMC Article
Coslett HB
Continuum (Minneap Minn) 2018 Jun;24(3, BEHAVIORAL NEUROLOGY AND PSYCHIATRY):768-782. doi: 10.1212/CON.0000000000000606. PMID: 29851877
Buxbaum LJ, Randerath J
Handb Clin Neurol 2018;151:349-363. doi: 10.1016/B978-0-444-63622-5.00017-6. PMID: 29519468Free PMC Article

Recent systematic reviews

Gibson E, Koh CL, Eames S, Bennett S, Scott AM, Hoffmann TC
Cochrane Database Syst Rev 2022 Mar 29;3(3):CD006430. doi: 10.1002/14651858.CD006430.pub3. PMID: 35349186Free PMC Article
Miller KJ, Suárez-Iglesias D, Seijo-Martínez M, Ayán C
Rev Neurol 2020 Mar 1;70(5):161-170. doi: 10.33588/rn.7005.2019417. PMID: 32100276
Morgan AT, Murray E, Liégeois FJ
Cochrane Database Syst Rev 2018 May 30;5(5):CD006278. doi: 10.1002/14651858.CD006278.pub3. PMID: 29845607Free PMC Article
Murray E, McCabe P, Ballard KJ
Am J Speech Lang Pathol 2014 Aug;23(3):486-504. doi: 10.1044/2014_AJSLP-13-0035. PMID: 24686844
Ruano L, Melo C, Silva MC, Coutinho P
Neuroepidemiology 2014;42(3):174-83. Epub 2014 Mar 5 doi: 10.1159/000358801. PMID: 24603320

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.

    Recent activity

    Your browsing activity is empty.

    Activity recording is turned off.

    Turn recording back on

    See more...