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Resting tremor

MedGen UID:
66697
Concept ID:
C0234379
Sign or Symptom
Synonyms: Rest Tremor; Rest Tremors; Resting Tremor; Resting Tremors; Tremor, Rest; Tremor, Resting
SNOMED CT: Resting tremor (25082004)
 
HPO: HP:0002322

Definition

A resting tremor occurs when muscles are at rest and becomes less noticeable or disappears when the affected muscles are moved. Resting tremors are often slow and coarse. [from HPO]

Term Hierarchy

Conditions with this feature

Early-onset parkinsonism-intellectual disability syndrome
MedGen UID:
208674
Concept ID:
C0796195
Disease or Syndrome
Waisman syndrome is an X-linked neurologic disorder characterized by delayed psychomotor development, impaired intellectual development, and early-onset Parkinson disease (summary by Wilson et al., 2014).
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.
Progressive external ophthalmoplegia with mitochondrial DNA deletions, autosomal dominant 1
MedGen UID:
371919
Concept ID:
C1834846
Disease or Syndrome
POLG-related disorders comprise a continuum of overlapping phenotypes that were clinically defined long before their molecular basis was known. Most affected individuals have some, but not all, of the features of a given phenotype; nonetheless, the following nomenclature can assist the clinician in diagnosis and management. Onset of the POLG-related disorders ranges from infancy to late adulthood. Alpers-Huttenlocher syndrome (AHS), one of the most severe phenotypes, is characterized by childhood-onset progressive and ultimately severe encephalopathy with intractable epilepsy and hepatic failure. Childhood myocerebrohepatopathy spectrum (MCHS) presents between the first few months of life and about age three years with developmental delay or dementia, lactic acidosis, and a myopathy with failure to thrive. Other findings can include liver failure, renal tubular acidosis, pancreatitis, cyclic vomiting, and hearing loss. Myoclonic epilepsy myopathy sensory ataxia (MEMSA) now describes the spectrum of disorders with epilepsy, myopathy, and ataxia without ophthalmoplegia. MEMSA now includes the disorders previously described as spinocerebellar ataxia with epilepsy (SCAE). The ataxia neuropathy spectrum (ANS) includes the phenotypes previously referred to as mitochondrial recessive ataxia syndrome (MIRAS) and sensory ataxia neuropathy dysarthria and ophthalmoplegia (SANDO). About 90% of persons in the ANS have ataxia and neuropathy as core features. Approximately two thirds develop seizures and almost one half develop ophthalmoplegia; clinical myopathy is rare. Autosomal recessive progressive external ophthalmoplegia (arPEO) is characterized by progressive weakness of the extraocular eye muscles resulting in ptosis and ophthalmoparesis (or paresis of the extraocular muscles) without associated systemic involvement; however, caution is advised because many individuals with apparently isolated arPEO at the onset develop other manifestations of POLG-related disorders over years or decades. Of note, in the ANS spectrum the neuropathy commonly precedes the onset of PEO by years to decades. Autosomal dominant progressive external ophthalmoplegia (adPEO) typically includes a generalized myopathy and often variable degrees of sensorineural hearing loss, axonal neuropathy, ataxia, depression, parkinsonism, hypogonadism, and cataracts (in what has been called "chronic progressive external ophthalmoplegia plus," or "CPEO+").
Fragile X-associated tremor/ataxia syndrome
MedGen UID:
333403
Concept ID:
C1839780
Disease or Syndrome
FMR1 disorders include fragile X syndrome (FXS), fragile X-associated tremor/ataxia syndrome (FXTAS), and fragile X-associated primary ovarian insufficiency (FXPOI). Fragile X syndrome occurs in individuals with an FMR1 full mutation or other loss-of-function variant and is nearly always characterized in affected males by developmental delay and intellectual disability along with a variety of behavioral issues. Autism spectrum disorder is present in 50%-70% of individuals with FXS. Affected males may have characteristic craniofacial features (which become more obvious with age) and medical problems including hypotonia, gastroesophageal reflux, strabismus, seizures, sleep disorders, joint laxity, pes planus, scoliosis, and recurrent otitis media. Adults may have mitral valve prolapse or aortic root dilatation. The physical and behavioral features seen in males with FXS have been reported in females heterozygous for the FMR1 full mutation, but with lower frequency and milder involvement. FXTAS occurs in individuals who have an FMR1 premutation and is characterized by late-onset, progressive cerebellar ataxia and intention tremor followed by cognitive impairment. Psychiatric disorders are common. Age of onset is typically between 60 and 65 years and is more common among males who are hemizygous for the premutation (40%) than among females who are heterozygous for the premutation (16%-20%). FXPOI, defined as hypergonadotropic hypogonadism before age 40 years, has been observed in 20% of women who carry a premutation allele compared to 1% in the general population.
Autosomal dominant Parkinson disease 8
MedGen UID:
339628
Concept ID:
C1846862
Disease or Syndrome
LRRK2 Parkinson disease (PD) is characterized by features consistent with idiopathic PD: initial motor features of slowly progressive asymmetric tremor at rest and/or bradykinesia, cogwheel muscle rigidity, postural instability, and gait abnormalities that may include festination and freezing. Certain nonmotor symptoms in LRRK2-PD, especially REM sleep behavior disorder and cognitive decline, may occur at similar or slightly reduced frequency compared to typical idiopathic* PD. Onset is generally after age 50, although early-onset (in the 20s) and late-onset (in the 90s) disease has been described. * Idiopathic PD refers to the presence of signs and symptoms of PD for which the etiology is currently unknown and in which there is no known family history of PD.
Dystonia 5
MedGen UID:
342121
Concept ID:
C1851920
Disease or Syndrome
GTP cyclohydrolase 1-deficient dopa-responsive dystonia (GTPCH1-deficient DRD) is characterized by childhood-onset dystonia and a dramatic and sustained response to low doses of oral administration of levodopa. This disorder typically presents with gait disturbance caused by foot dystonia, later development of parkinsonism, and diurnal fluctuation of symptoms (aggravation of symptoms toward the evening and alleviation of symptoms in the morning after sleep). Initial symptoms are often gait difficulties attributable to flexion-inversion (equinovarus posture) of the foot. Occasionally, initial symptoms are arm dystonia, postural tremor of the hand, or slowness of movements. Brisk deep-tendon reflexes in the legs, ankle clonus, and/or the striatal toe (dystonic extension of the big toe) are present in many affected individuals. In general, gradual progression to generalized dystonia is observed. Intellectual, cerebellar, sensory, and autonomic disturbances generally do not occur.
Autosomal recessive early-onset Parkinson disease 7
MedGen UID:
344049
Concept ID:
C1853445
Disease or Syndrome
Parkinson's disease is a progressive disorder of the nervous system. The disorder affects several regions of the brain, especially an area called the substantia nigra that controls balance and movement.\n\nOften the first symptom of Parkinson's disease is trembling or shaking (tremor) of a limb, especially when the body is at rest. Typically, the tremor begins on one side of the body, usually in one hand. Tremors can also affect the arms, legs, feet, and face. Other characteristic symptoms of Parkinson's disease include rigidity or stiffness of the limbs and torso, slow movement (bradykinesia) or an inability to move (akinesia), and impaired balance and coordination (postural instability). These symptoms worsen slowly over time.\n\nGenerally, Parkinson's disease that begins after age 50 is called late-onset disease. The condition is described as early-onset disease if signs and symptoms begin before age 50. Early-onset cases that begin before age 20 are sometimes referred to as juvenile-onset Parkinson's disease.\n\nParkinson's disease can also affect emotions and thinking ability (cognition). Some affected individuals develop psychiatric conditions such as depression and visual hallucinations. People with Parkinson's disease also have an increased risk of developing dementia, which is a decline in intellectual functions including judgment and memory.
Autosomal recessive early-onset Parkinson disease 6
MedGen UID:
342982
Concept ID:
C1853833
Disease or Syndrome
PINK1 type of young-onset Parkinson disease is characterized by early onset (mean age 33 years) of tremor, bradykinesia, and rigidity that are often indistinguishable from other causes of Parkinson disease. Lower-limb dystonia may be a presenting sign. Postural instability, hyperreflexia, abnormal behavior, and psychiatric manifestations have been described. The disease is usually slowly progressive. Individuals have a marked and sustained response to oral administration of levodopa (L-dopa), frequently associated with L-dopa-induced fluctuations and dyskinesias.
Autosomal dominant Parkinson disease 1
MedGen UID:
357008
Concept ID:
C1868595
Disease or Syndrome
Parkinson disease is the second most common neurogenic disorder after Alzheimer disease (AD; 104300), affecting approximately 1% of the population over age 50. Clinical manifestations include resting tremor, muscular rigidity, bradykinesia, and postural instability. Additional features are characteristic postural abnormalities, dysautonomia, dystonic cramps, and dementia (Polymeropoulos et al., 1996). For a general phenotypic description and a discussion of genetic heterogeneity of Parkinson disease, see 168600.
Autosomal recessive juvenile Parkinson disease 2
MedGen UID:
401500
Concept ID:
C1868675
Disease or Syndrome
Parkin type of early-onset Parkinson disease (PARK-Parkin) is characterized by the cardinal signs of Parkinson disease (PD): bradykinesia, resting tremor, and rigidity. The median age at onset is 31 years (range: 3-81 years). The disease is slowly progressive: disease duration of more than 50 years has been reported. Clinical findings vary; hyperreflexia is common. Lower-limb dystonia may be a presenting sign and cognitive decline appears to be no more frequent than in the general population. Dyskinesia as a result of treatment with levodopa frequently occurs.
Autosomal recessive Parkinson disease 14
MedGen UID:
414488
Concept ID:
C2751842
Disease or Syndrome
Parkinson's disease can also affect emotions and thinking ability (cognition). Some affected individuals develop psychiatric conditions such as depression and visual hallucinations. People with Parkinson's disease also have an increased risk of developing dementia, which is a decline in intellectual functions including judgment and memory.\n\nGenerally, Parkinson's disease that begins after age 50 is called late-onset disease. The condition is described as early-onset disease if signs and symptoms begin before age 50. Early-onset cases that begin before age 20 are sometimes referred to as juvenile-onset Parkinson's disease.\n\nOften the first symptom of Parkinson's disease is trembling or shaking (tremor) of a limb, especially when the body is at rest. Typically, the tremor begins on one side of the body, usually in one hand. Tremors can also affect the arms, legs, feet, and face. Other characteristic symptoms of Parkinson's disease include rigidity or stiffness of the limbs and torso, slow movement (bradykinesia) or an inability to move (akinesia), and impaired balance and coordination (postural instability). These symptoms worsen slowly over time.\n\nParkinson's disease is a progressive disorder of the nervous system. The disorder affects several regions of the brain, especially an area called the substantia nigra that controls balance and movement.
Parkinson disease, late-onset
MedGen UID:
463618
Concept ID:
C3160718
Disease or Syndrome
Parkinson's disease can also affect emotions and thinking ability (cognition). Some affected individuals develop psychiatric conditions such as depression and visual hallucinations. People with Parkinson's disease also have an increased risk of developing dementia, which is a decline in intellectual functions including judgment and memory.\n\nGenerally, Parkinson's disease that begins after age 50 is called late-onset disease. The condition is described as early-onset disease if signs and symptoms begin before age 50. Early-onset cases that begin before age 20 are sometimes referred to as juvenile-onset Parkinson's disease.\n\nOften the first symptom of Parkinson's disease is trembling or shaking (tremor) of a limb, especially when the body is at rest. Typically, the tremor begins on one side of the body, usually in one hand. Tremors can also affect the arms, legs, feet, and face. Other characteristic symptoms of Parkinson's disease include rigidity or stiffness of the limbs and torso, slow movement (bradykinesia) or an inability to move (akinesia), and impaired balance and coordination (postural instability). These symptoms worsen slowly over time.\n\nParkinson's disease is a progressive disorder of the nervous system. The disorder affects several regions of the brain, especially an area called the substantia nigra that controls balance and movement.
Parkinson disease 17
MedGen UID:
481763
Concept ID:
C3280133
Disease or Syndrome
VPS35-related Parkinson disease (VPS35-PD) is defined as Parkinson disease caused by heterozygous VPS35 pathogenic variants. Currently, the only known VPS35 variant with confirmed pathogenicity is c.1858G>A (p.Asp620Asn). Except for a younger age of onset, VPS35-PD is clinically indistinguishable from Parkinson disease of unknown cause (so-called sporadic Parkinson disease). Variability among 50 individuals reported with molecularly confirmed VPS35-PD includes age of onset (mean: 51.0±8.7 years; range: 34-68 years), Parkinson subtype (tremor, akinetic rigid, mixed), first motor symptom, course of the disease (unilateral onset and slow disease progression are typical; dyskinesia and motor fluctuations may occur), and presence/absence of neuropsychiatric manifestations (including depression, schizophrenia, learning difficulties, mild cognitive impairment, and dementia).
Parkinson disease 18, autosomal dominant, susceptibility to
MedGen UID:
481901
Concept ID:
C3280271
Finding
Parkinson disease-18 is an autosomal dominant, adult-onset form of the disorder. It is phenotypically similar to idiopathic Parkinson disease (summary by Chartier-Harlin et al., 2011). For a general phenotypic description and a discussion of genetic heterogeneity of Parkinson disease (PD), see 168600.
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).
X-linked parkinsonism-spasticity syndrome
MedGen UID:
813052
Concept ID:
C3806722
Disease or Syndrome
A rare genetic neurological disorder with characteristics of parkinsonian features (including resting or action tremor, cogwheel rigidity, hypomimia and bradykinesia) associated with variably penetrant spasticity, hyperactive deep tendon reflexes and Babinski sign. There is evidence this disease is caused by hemizygous mutation in the ATP6AP2 gene on chromosome Xp11.
Parkinson disease 11, autosomal dominant, susceptibility to
MedGen UID:
896658
Concept ID:
C4083045
Finding
Parkinson's disease is a progressive disorder of the nervous system. The disorder affects several regions of the brain, especially an area called the substantia nigra that controls balance and movement.\n\nOften the first symptom of Parkinson's disease is trembling or shaking (tremor) of a limb, especially when the body is at rest. Typically, the tremor begins on one side of the body, usually in one hand. Tremors can also affect the arms, legs, feet, and face. Other characteristic symptoms of Parkinson's disease include rigidity or stiffness of the limbs and torso, slow movement (bradykinesia) or an inability to move (akinesia), and impaired balance and coordination (postural instability). These symptoms worsen slowly over time.\n\nGenerally, Parkinson's disease that begins after age 50 is called late-onset disease. The condition is described as early-onset disease if signs and symptoms begin before age 50. Early-onset cases that begin before age 20 are sometimes referred to as juvenile-onset Parkinson's disease.\n\nParkinson's disease can also affect emotions and thinking ability (cognition). Some affected individuals develop psychiatric conditions such as depression and visual hallucinations. People with Parkinson's disease also have an increased risk of developing dementia, which is a decline in intellectual functions including judgment and memory.
Autosomal recessive early-onset Parkinson disease 23
MedGen UID:
896607
Concept ID:
C4225186
Disease or Syndrome
Parkinson disease-23 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).
Parkinson disease 22, autosomal dominant
MedGen UID:
907886
Concept ID:
C4225238
Disease or Syndrome
Any Parkinson disease in which the cause of the disease is a mutation in the CHCHD2 gene.
Parkinsonism with polyneuropathy
MedGen UID:
1783451
Concept ID:
C5543299
Disease or Syndrome
Parkinsonism with polyneuropathy (PKNPY) is an autosomal dominant disorder characterized by asymmetrical tremor-dependent parkinsonism. The age of onset ranges from the late forties to mid-sixties, and patients have a good response to levodopa (summary by Lin et al., 2020).
Dyskinesia with orofacial involvement, autosomal dominant
MedGen UID:
1790407
Concept ID:
C5551343
Disease or Syndrome
ADCY5 dyskinesia is a hyperkinetic movement disorder (more prominent in the face and arms than the legs) characterized by infantile to late-adolescent onset of chorea, athetosis, dystonia, myoclonus, or a combination of these. To date, affected individuals have had overlapping (but not identical) manifestations with wide-ranging severity. The facial movements are typically periorbital and perioral. The dyskinesia is prone to episodic or paroxysmal exacerbation lasting minutes to hours, and may occur during sleep. Precipitating factors in some persons have included emotional stress, intercurrent illness, sneezing, or caffeine; in others, no precipitating factors have been identified. In some children, severe infantile axial hypotonia results in gross motor delays accompanied by chorea, sometimes with language delays. The overall tendency is for the abnormal movements to stabilize in early middle age, at which point they may improve in some individuals; less commonly, the abnormal movements are slowly progressive, increasing in severity and frequency.
Parkinson disease 24, autosomal dominant, susceptibility to
MedGen UID:
1794179
Concept ID:
C5561969
Finding
Parkinson disease-24 (PARK24) is an autosomal dominant disorder characterized by classic Parkinson disease features, including adult onset, asymmetric limb involvement initially, and slowly progressive motor dysfunction. PARK24 shows incomplete penetrance, consistent with the presence of the PSAP mutation being a susceptibility factor for development of the disease (Oji et al., 2020). For a phenotypic description and a discussion of genetic heterogeneity of Parkinson disease, see 168600.
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).
Hereditary spastic paraplegia 9A
MedGen UID:
1800401
Concept ID:
C5568978
Disease or Syndrome
Autosomal dominant spastic paraplegia-9A is a neurologic disorder characterized by onset of slowly progressive spasticity mainly affecting the lower limbs. The age at onset usually ranges from adolescence to adulthood, and patients have gait difficulties, motor neuropathy, and dysarthria. Additional variable features include cerebellar signs, cataract, pes cavus, and urinary urgency (summary by Coutelier et al., 2015). For a general phenotypic description and a discussion of genetic heterogeneity of autosomal dominant spastic paraplegia, see SPG3A (182600).
Neurodevelopmental disorder with or without variable movement or behavioral abnormalities
MedGen UID:
1802087
Concept ID:
C5676908
Disease or Syndrome
Neurodevelopmental disorder with or without variable movement or behavioral abnormalities (NEDMAB) is an autosomal dominant disorder characterized by mildly to severely impaired intellectual development and, in some patients, movement abnormalities consisting of tremors, cerebellar ataxia, or extrapyramidal symptoms. Movement abnormalities have onset in childhood or adolescence. Other variable features include autism spectrum disorder or autistic features and epilepsy.
Intellectual developmental disorder with language impairment and early-onset DOPA-responsive dystonia-parkinsonism
MedGen UID:
1805453
Concept ID:
C5677001
Disease or Syndrome
Intellectual developmental disorder with language impairment and early-onset dopa-responsive dystonia-parkinsonism (IDLDP) is a neurodevelopmental disorder characterized by global developmental delay affecting motor, cognitive, and speech domains apparent in early childhood or infancy. Some patients may have normal early development in infancy before symptom onset. There is phenotypic heterogeneity and the severity is highly variable; less severely affected individuals have only mild deficits and are able to attend special schools. About half of patients develop various types of seizures that may be refractory or responsive to treatment. Most patients also show movement abnormalities, often hypotonia early in the disease course with later development of dopa-responsive dystonia or parkinsonism (Ramos et al., 2019, Wirth et al., 2020; Singh et al., 2020).

Professional guidelines

PubMed

Cattaneo C, Jost WH
J Integr Neurosci 2023 Sep 8;22(5):132. doi: 10.31083/j.jin2205132. PMID: 37735139
Shahien M, Elaraby A, Gamal M, Abdelazim E, Abdelazeem B, Ghaith HS, Negida A
Neurol Sci 2023 Feb;44(2):461-470. Epub 2022 Oct 7 doi: 10.1007/s10072-022-06420-1. PMID: 36205810
Rabiei Z, Solati K, Amini-Khoei H
Pharm Biol 2019 Dec;57(1):355-362. doi: 10.1080/13880209.2019.1618344. PMID: 31141426Free PMC Article

Recent clinical studies

Etiology

Li LY, Liu SF, Zhuang JL, Li MM, Huang ZP, Chen YH, Chen XR, Chen CN, Lin S, Ye LC
Rev Neurosci 2023 Oct 26;34(7):719-735. Epub 2022 Dec 2 doi: 10.1515/revneuro-2022-0093. PMID: 36450297
Sarica A, Quattrone A, Crasà M, Nisticò R, Vaccaro MG, Bianco MG, Gramigna V, De Maria M, Vescio B, Rocca F, Quattrone A
J Neurol 2022 Nov;269(11):6029-6035. Epub 2022 Jul 19 doi: 10.1007/s00415-022-11291-9. PMID: 35852601
Zach H, Dirkx MF, Roth D, Pasman JW, Bloem BR, Helmich RC
Neurology 2020 Sep 15;95(11):e1461-e1470. Epub 2020 Jul 10 doi: 10.1212/WNL.0000000000010316. PMID: 32651292
Cacabelos R
Int J Mol Sci 2017 Mar 4;18(3) doi: 10.3390/ijms18030551. PMID: 28273839Free PMC Article
Earhart GM, Falvo MJ
Compr Physiol 2013 Apr;3(2):833-48. doi: 10.1002/cphy.c100047. PMID: 23720332

Diagnosis

Liu Z, Cheung HH
Int J Mol Sci 2020 Oct 29;21(21) doi: 10.3390/ijms21218060. PMID: 33137927Free PMC Article
Louis ED
Continuum (Minneap Minn) 2019 Aug;25(4):959-975. doi: 10.1212/CON.0000000000000748. PMID: 31356289
Reich SG, Savitt JM
Med Clin North Am 2019 Mar;103(2):337-350. Epub 2018 Dec 3 doi: 10.1016/j.mcna.2018.10.014. PMID: 30704685
Zhang PL, Chen Y, Zhang CH, Wang YX, Fernandez-Funez P
J Med Genet 2018 Feb;55(2):73-80. Epub 2017 Nov 18 doi: 10.1136/jmedgenet-2017-105047. PMID: 29151060
Lew M
Pharmacotherapy 2007 Dec;27(12 Pt 2):155S-160S. doi: 10.1592/phco.27.12part2.155S. PMID: 18041935

Therapy

Frei K, Truong DD
J Neurol Sci 2022 Apr 15;435:120194. Epub 2022 Feb 19 doi: 10.1016/j.jns.2022.120194. PMID: 35279634
Deuel LM, Seeberger LC
Neurotherapeutics 2020 Oct;17(4):1434-1455. doi: 10.1007/s13311-020-00900-y. PMID: 32785848Free PMC Article
Louis ED
Continuum (Minneap Minn) 2019 Aug;25(4):959-975. doi: 10.1212/CON.0000000000000748. PMID: 31356289
Reich SG, Savitt JM
Med Clin North Am 2019 Mar;103(2):337-350. Epub 2018 Dec 3 doi: 10.1016/j.mcna.2018.10.014. PMID: 30704685
Cacabelos R
Int J Mol Sci 2017 Mar 4;18(3) doi: 10.3390/ijms18030551. PMID: 28273839Free PMC Article

Prognosis

Liu Z, Cheung HH
Int J Mol Sci 2020 Oct 29;21(21) doi: 10.3390/ijms21218060. PMID: 33137927Free PMC Article
Zach H, Dirkx MF, Roth D, Pasman JW, Bloem BR, Helmich RC
Neurology 2020 Sep 15;95(11):e1461-e1470. Epub 2020 Jul 10 doi: 10.1212/WNL.0000000000010316. PMID: 32651292
Zhang PL, Chen Y, Zhang CH, Wang YX, Fernandez-Funez P
J Med Genet 2018 Feb;55(2):73-80. Epub 2017 Nov 18 doi: 10.1136/jmedgenet-2017-105047. PMID: 29151060
Reichmann H
Neurosci Bull 2017 Oct;33(5):526-534. Epub 2017 Aug 3 doi: 10.1007/s12264-017-0159-5. PMID: 28776303Free PMC Article
Boettcher LB, Bonney PA, Smitherman AD, Sughrue ME
Neurosurg Focus 2015 Jul;39(1):E8. doi: 10.3171/2015.4.FOCUS1563. PMID: 26126407

Clinical prediction guides

Zhang W, Ye Y, Song J, Sang T, Xia T, Xie L, Qiu X, Zeng Q, Luo X
J Integr Neurosci 2023 Oct 30;22(6):157. doi: 10.31083/j.jin2206157. PMID: 38176929
Shahien M, Elaraby A, Gamal M, Abdelazim E, Abdelazeem B, Ghaith HS, Negida A
Neurol Sci 2023 Feb;44(2):461-470. Epub 2022 Oct 7 doi: 10.1007/s10072-022-06420-1. PMID: 36205810
Liu Z, Cheung HH
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Reichmann H
Neurosci Bull 2017 Oct;33(5):526-534. Epub 2017 Aug 3 doi: 10.1007/s12264-017-0159-5. PMID: 28776303Free PMC Article
Hess CW, Hallett M
Semin Neurol 2017 Apr;37(2):109-117. Epub 2017 May 16 doi: 10.1055/s-0037-1601869. PMID: 28511251Free PMC Article

Recent systematic reviews

Nijakowski K, Owecki W, Jankowski J, Surdacka A
Cells 2024 Feb 14;13(4) doi: 10.3390/cells13040340. PMID: 38391952Free PMC Article
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Neurol Sci 2023 Feb;44(2):461-470. Epub 2022 Oct 7 doi: 10.1007/s10072-022-06420-1. PMID: 36205810
Nila IS, Sumsuzzman DM, Khan ZA, Jung JH, Kazema AS, Kim SJ, Hong Y
Ageing Res Rev 2022 Dec;82:101764. Epub 2022 Oct 20 doi: 10.1016/j.arr.2022.101764. PMID: 36273807
Wang KL, Wong JK, Eisinger RS, Carbunaru S, Smith C, Hu W, Shukla AW, Hess CW, Okun MS, Ramirez-Zamora A
Neuromodulation 2022 Aug;25(6):796-803. Epub 2022 Feb 15 doi: 10.1111/ner.13220. PMID: 32578304
Wilke C, Pomper JK, Biskup S, Puskás C, Berg D, Synofzik M
J Neurol 2016 Mar;263(3):558-74. Epub 2016 Jan 25 doi: 10.1007/s00415-016-8021-7. PMID: 26810719

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