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Hand tremor

MedGen UID:
68689
Concept ID:
C0239842
Finding; Sign or Symptom
Synonyms: Hand tremors; Tremors (in hands)
 
HPO: HP:0002378

Definition

An unintentional, oscillating to-and-fro muscle movement affecting the hand. [from HPO]

Term Hierarchy

Conditions with this feature

Wilson disease
MedGen UID:
42426
Concept ID:
C0019202
Disease or Syndrome
Wilson disease is a disorder of copper metabolism that can present with hepatic, neurologic, or psychiatric disturbances, or a combination of these, in individuals ranging from age three years to older than 50 years; symptoms vary among and within families. Liver disease includes recurrent jaundice, simple acute self-limited hepatitis-like illness, autoimmune-type hepatitis, fulminant hepatic failure, or chronic liver disease. Neurologic presentations include movement disorders (tremors, poor coordination, loss of fine-motor control, chorea, choreoathetosis) or rigid dystonia (mask-like facies, rigidity, gait disturbance, pseudobulbar involvement). Psychiatric disturbance includes depression, neurotic behaviors, disorganization of personality, and, occasionally, intellectual deterioration. Kayser-Fleischer rings, frequently present, result from copper deposition in Descemet's membrane of the cornea and reflect a high degree of copper storage in the body.
Congenital sensory neuropathy with selective loss of small myelinated fibers
MedGen UID:
6916
Concept ID:
C0020075
Disease or Syndrome
Hereditary sensory and autonomic neuropathy type V (HSAN5) is a condition that primarily affects the sensory nerve cells (sensory neurons), which transmit information about sensations such as pain, temperature, and touch. These sensations are impaired in people with HSAN5.\n\nThe signs and symptoms of HSAN5 appear early, usually at birth or during infancy. People with HSAN5 lose the ability to feel pain, heat, and cold. Deep pain perception, the feeling of pain from injuries to bones, ligaments, or muscles, is especially affected in people with HSAN5. Because of the inability to feel deep pain, affected individuals suffer repeated severe injuries such as bone fractures and joint injuries that go unnoticed. Repeated trauma can lead to a condition called Charcot joints, in which the bones and tissue surrounding joints are destroyed.
Kugelberg-Welander disease
MedGen UID:
101816
Concept ID:
C0152109
Disease or Syndrome
Spinal muscular atrophy (SMA) is characterized by muscle weakness and atrophy resulting from progressive degeneration and irreversible loss of the anterior horn cells in the spinal cord (i.e., lower motor neurons) and the brain stem nuclei. The onset of weakness ranges from before birth to adulthood. The weakness is symmetric, proximal > distal, and progressive. Before the genetic basis of SMA was understood, it was classified into clinical subtypes based on maximum motor function achieved; however, it is now apparent that the phenotype of SMN1-associated SMA spans a continuum without clear delineation of subtypes. With supportive care only, poor weight gain with growth failure, restrictive lung disease, scoliosis, and joint contractures are common complications; however, newly available targeted treatment options are changing the natural history of this disease.
Spinal muscular atrophy, type II
MedGen UID:
95975
Concept ID:
C0393538
Disease or Syndrome
Spinal muscular atrophy (SMA) is characterized by muscle weakness and atrophy resulting from progressive degeneration and irreversible loss of the anterior horn cells in the spinal cord (i.e., lower motor neurons) and the brain stem nuclei. The onset of weakness ranges from before birth to adulthood. The weakness is symmetric, proximal > distal, and progressive. Before the genetic basis of SMA was understood, it was classified into clinical subtypes based on maximum motor function achieved; however, it is now apparent that the phenotype of SMN1-associated SMA spans a continuum without clear delineation of subtypes. With supportive care only, poor weight gain with growth failure, restrictive lung disease, scoliosis, and joint contractures are common complications; however, newly available targeted treatment options are changing the natural history of this disease.
Charcot-Marie-Tooth disease X-linked dominant 1
MedGen UID:
98290
Concept ID:
C0393808
Disease or Syndrome
GJB1 disorders are typically characterized by peripheral motor and sensory neuropathy with or without fixed CNS abnormalities and/or acute, self-limited episodes of transient neurologic dysfunction (especially weakness and dysarthria). Peripheral neuropathy typically manifests in affected males between ages five and 25 years. Although both men and women are affected, manifestations tend to be less severe in women, some of whom may remain asymptomatic. Less commonly, initial manifestations in some affected individuals are stroke-like episodes (acute fulminant episodes of reversible CNS dysfunction).
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+").
Familial pseudohyperkalemia
MedGen UID:
324588
Concept ID:
C1836705
Disease or Syndrome
'Familial pseudohyperkalemia' (PSHK) is a term that was coined to describe conditions in which a patient presents with pseudohyperkalemia as a result of a temperature-based abnormality in the transport of potassium (K) and sodium (Na) across the red cell membrane, in association with essentially normal hematology. PSHK can be considered to be the clinically benign, nonhemolytic cousin of hereditary stomatocytic leaky-cell, congenital hemolytic anemias (see 194380) (summary by Gore et al., 2002). For a discussion of clinical and genetic heterogeneity of the hereditary stomatocytoses, see 194380.
Spinal muscular atrophy, type IV
MedGen UID:
325364
Concept ID:
C1838230
Disease or Syndrome
Spinal muscular atrophy (SMA) is characterized by muscle weakness and atrophy resulting from progressive degeneration and irreversible loss of the anterior horn cells in the spinal cord (i.e., lower motor neurons) and the brain stem nuclei. The onset of weakness ranges from before birth to adulthood. The weakness is symmetric, proximal > distal, and progressive. Before the genetic basis of SMA was understood, it was classified into clinical subtypes based on maximum motor function achieved; however, it is now apparent that the phenotype of SMN1-associated SMA spans a continuum without clear delineation of subtypes. With supportive care only, poor weight gain with growth failure, restrictive lung disease, scoliosis, and joint contractures are common complications; however, newly available targeted treatment options are changing the natural history of this disease.
Rolandic epilepsy-paroxysmal exercise-induced dystonia-writer cramp syndrome
MedGen UID:
334104
Concept ID:
C1842531
Disease or Syndrome
Rolandic epilepsy with paroxysmal exercise-induced dystonia and writer's cramp (EPRPDC) is an autosomal recessive neurologic disorder characterized by onset of focal seizures in infancy and exercise-induced dystonia in childhood. Features usually include involuntary movements, including facial movements, and difficulties with fine motor skills of the hand. Seizures often respond to medication and remit with age; the dystonia tends to persist (summary by Luthy et al., 2019).
Pontocerebellar hypoplasia type 1A
MedGen UID:
335969
Concept ID:
C1843504
Disease or Syndrome
Pontocerebellar hypoplasia (PCH) refers to a group of severe neurodegenerative disorders affecting growth and function of the brainstem and cerebellum, resulting in little or no development. Different types were classified based on the clinical picture and the spectrum of pathologic changes. PCH type 1 is characterized by central and peripheral motor dysfunction associated with anterior horn cell degeneration resembling infantile spinal muscular atrophy (SMA; see SMA1, 253300); death usually occurs early. Genetic Heterogeneity of Pontocerebellar Hypoplasia Also see PCH1B (614678), caused by mutation in the EXOSC3 gene (606489); PCH1C (616081), caused by mutation in the EXOSC8 gene (606019); PCH1D (618065), caused by mutation in the EXOSC9 gene (606180); PCH1E (619303), caused by mutation in the SLC25A46 gene (610826); PCH1F (619304), caused by mutation in the EXOSC1 gene (606493); PCH2A (277470), caused by mutation in the TSEN54 gene (608755); PCH2B (612389), caused by mutation in the TSEN2 gene (608753); PCH2C (612390), caused by mutation in the TSEN34 gene (608754); PCH2D (613811), caused by mutation in the SEPSECS gene (613009); PCH3 (608027), caused by mutation in the PCLO gene (604918); PCH4 (225753), caused by mutation in the TSEN54 gene; PCH5 (610204), caused by mutation in the TSEN54 gene; PCH6 (611523), caused by mutation in the RARS2 gene (611524); PCH7 (614969), caused by mutation in the TOE1 gene (613931); PCH8 (614961), caused by mutation in the CHMP1A gene (164010); PCH9 (615809), caused by mutation in the AMPD2 gene (102771); PCH10 (615803), caused by mutation in the CLP1 gene (608757); PCH11 (617695), caused by mutation in the TBC1D23 gene (617687); PCH12 (618266), caused by mutation in the COASY gene (609855); PCH13 (618606), caused by mutation in the VPS51 gene (615738); PCH14 (619301), caused by mutation in the PPIL1 gene (601301); PCH15 (619302), caused by mutation in the CDC40 gene (605585); PCH16 (619527), caused by mutation in the MINPP1 gene (605391); and PCH17 (619909), caused by mutation in the PRDM13 gene (616741) on chromosome 6q16.
Hereditary motor and sensory neuropathy, Okinawa type
MedGen UID:
346886
Concept ID:
C1858338
Disease or Syndrome
Okinawa-type hereditary motor and sensory neuropathy (HMSNO) is an autosomal dominant neurodegenerative disorder characterized by young adult onset of proximal or distal muscle weakness and atrophy, muscle cramps, and fasciculations, with later onset of distal sensory impairment. The disorder is slowly progressive and clinically resembles amyotrophic lateral sclerosis (ALS; see 105400) (summary by Ishiura et al., 2012).
Tremor, hereditary essential, 1
MedGen UID:
349909
Concept ID:
C1860861
Disease or Syndrome
Essential tremor may be the most common human movement disorder. The main feature of essential tremor is postural tremor of the arms, but the head, legs, trunk, voice, jaw, and facial muscles also may be involved. Aggravated by emotions, hunger, fatigue, and temperature extremes, the condition may cause a functional disability or even incapacitation. Autosomal dominant inheritance can be demonstrated in most families (summary by Higgins et al., 1997). Deng et al. (2007) provided a detailed review of the genetics of essential tremor. Genetic Heterogeneity of Essential Tremor Other forms of hereditary essential tremor include ETM2 (602134), mapped to chromosome 2p25-p22; ETM3 (611456), mapped to chromosome 6p23; ETM4 (614782), caused by mutation in the FUS gene (137070) on chromosome 16p11; ETM5 (616736), caused by mutation in the TENM4 gene (610084) on chromosome 11q14; and ETM6 (618866), caused by mutation in the NOTCH2NLC gene (618025) on chromosome 1q21.
Torsion dystonia 7
MedGen UID:
355560
Concept ID:
C1865818
Disease or Syndrome
Idiopathic torsion dystonia (ITD) is a clinically and genetically heterogeneous group of movement disorders characterized by sustained dystonic muscle contractions causing involuntary twisting movements and/or postures, where causes such as cerebral lesions (especially of the basal ganglia), drugs, or other neurologic disorders have not been found. Adult-onset torsion dystonia usually remains focal and is localized in the upper part of the body (summary by Leube et al., 1996).
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\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 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.
Hereditary spastic paraplegia 46
MedGen UID:
473687
Concept ID:
C2828721
Disease or Syndrome
Autosomal recessive spastic paraplegia-46 (SPG46) is a neurodegenerative disorder characterized by onset in childhood of slowly progressive spastic paraplegia and cerebellar signs. Some patients have cognitive impairment, cataracts, and cerebral, cerebellar, and corpus callosum atrophy on brain imaging (summary by Boukhris et al., 2010 and Martin et al., 2013). For a discussion of genetic heterogeneity of autosomal recessive spastic paraplegia, see SPG5A (270800).
Cerebellar dysfunction with variable cognitive and behavioral abnormalities
MedGen UID:
766575
Concept ID:
C3553661
Disease or Syndrome
Cerebellar dysfunction with variable cognitive and behavioral abnormalities (CECBA) is an autosomal dominant neurologic disorder with significant phenotypic heterogeneity, even within families. The disorder is most often diagnosed through genetic analysis with retrospective clinical phenotyping. Symptom onset is usually in early childhood, although later onset, even in adulthood, has been reported. Most affected individuals show global developmental delay from early childhood, particularly of motor and language skills. Many have mild intellectual disability; behavioral and psychiatric abnormalities such as autism and obsessive-compulsive disorder are also often observed. The movement disorder is prominent and may include cerebellar signs such as ataxia, tremor, dysmetria, poor coordination, and dysarthria. Other abnormal movements including spasticity, myoclonus, and dystonia have been reported, thus widening the phenotypic spectrum. Brain imaging is usually normal, but may show cerebellar atrophy or nonspecific white matter lesions. Variable dysmorphic facial features may also be present (summary by Thevenon et al., 2012; Jacobs et al., 2021; Wijnen et al., 2020).
Charcot-Marie-Tooth disease X-linked dominant 6
MedGen UID:
813032
Concept ID:
C3806702
Disease or Syndrome
A rare genetic principally axonal peripheral sensorimotor neuropathy with an X-linked dominant inheritance pattern and the childhood-onset of slowly progressive, moderate to severe, distal muscle weakness and atrophy of the lower extremities, as well as distal, pan modal sensory abnormalities, bilateral foot deformities (pes cavus, clawed toes), absent ankle reflexes and gait abnormalities (steppage gait). Females are usually asymptomatic or only present mild manifestations (mild postural hand tremor, mild wasting of hand intrinsic muscles).
Basal ganglia calcification, idiopathic, 5
MedGen UID:
815975
Concept ID:
C3809645
Disease or Syndrome
Primary familial brain calcification (PFBC) is a neurodegenerative disorder with characteristic calcium deposits in the basal ganglia and other brain areas visualized on neuroimaging. Most affected individuals are in good health during childhood and young adulthood and typically present in the fourth to fifth decade with a gradually progressive movement disorder and neuropsychiatric symptoms. The movement disorder first manifests as clumsiness, fatigability, unsteady gait, slow or slurred speech, dysphagia, involuntary movements, or muscle cramping. Neuropsychiatric symptoms, often the first or most prominent manifestations, range from mild difficulty with concentration and memory to changes in personality and/or behavior, to psychosis and dementia. Seizures of various types occur frequently, some individuals experience chronic headache and vertigo; urinary urgency or incontinence may be present.
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).
Neurodevelopmental disorder with microcephaly, epilepsy, and brain atrophy
MedGen UID:
1637443
Concept ID:
C4693390
Disease or Syndrome
NEDMEBA is an autosomal recessive neurodegenerative disorder characterized by global developmental delay, severe intellectual disability with poor or absent speech and autistic stereotypic behaviors, microcephaly, early-onset generalized seizures, and hypotonia (summary by Marin-Valencia et al., 2018).
Charcot-Marie-Tooth disease, demyelinating, type 1G
MedGen UID:
1648290
Concept ID:
C4748940
Disease or Syndrome
Charcot-Marie-Tooth disease type 1G is an autosomal dominant progressive peripheral sensorimotor neuropathy characterized by distal muscle weakness and atrophy with onset in the first or second decade. Affected individuals have difficulty walking, distal sensory impairment with decreased or absent reflexes, and often have foot deformities. Median motor nerve conduction velocities (NCV) are decreased (less than 38 m/s) and sural nerve biopsy shows myelin defects and onion bulb formation (summary by Hong et al., 2016 and Motley et al., 2016). For a phenotypic description and a discussion of genetic heterogeneity of autosomal dominant Charcot-Marie-Tooth disease type 1, see CMT1B (118200).
Neuropathy, hereditary sensory and autonomic, type 1A
MedGen UID:
1716450
Concept ID:
C5235211
Disease or Syndrome
SPTLC1-related hereditary sensory neuropathy (HSN) is an axonal form of hereditary motor and sensory neuropathy distinguished by prominent early sensory loss and later positive sensory phenomena including dysesthesia and characteristic "lightning" or "shooting" pains. Loss of sensation can lead to painless injuries, which, if unrecognized, result in slow wound healing and subsequent osteomyelitis requiring distal amputations. Motor involvement is present in all advanced cases and can be severe. After age 20 years, the distal wasting and weakness may involve proximal muscles, possibly leading to wheelchair dependency by the seventh or eighth decade. Sensorineural hearing loss is variable.
Arthrogryposis multiplex congenita 5
MedGen UID:
1731112
Concept ID:
C5436453
Disease or Syndrome
Arthrogryposis multiplex congenita-5 (AMC5) is an autosomal recessive disorder characterized by severe joint contractures apparent at birth. Affected individuals usually have hypertonia and abnormal movements suggestive of dystonia, as well as feeding and/or breathing difficulties. More variable features may include poor overall growth, strabismus, dysmorphic facies, and global developmental delay with impaired speech (summary by Kariminejad et al., 2017).
Dystonia 34, myoclonic
MedGen UID:
1805016
Concept ID:
C5676907
Disease or Syndrome
Myoclonic dystonia-34 (DYT34) is an autosomal dominant neurologic disorder characterized by childhood-onset dystonia primarily involving the hands and neck, with a fast tremor with superimposed myoclonus (Balint et al., 2020).

Professional guidelines

PubMed

Mittal SO, Lenka A, Jankovic J
Parkinsonism Relat Disord 2019 Jun;63:31-41. Epub 2019 Jan 26 doi: 10.1016/j.parkreldis.2019.01.023. PMID: 30709779
Niemann N, Jankovic J
Toxins (Basel) 2018 Jul 19;10(7) doi: 10.3390/toxins10070299. PMID: 30029483Free PMC Article
Dauer WT, Burke RE, Greene P, Fahn S
Brain 1998 Apr;121 ( Pt 4):547-60. doi: 10.1093/brain/121.4.547. PMID: 9577384

Recent clinical studies

Etiology

Serin HM, Arslan EA
Acta Clin Croat 2019 Jun;58(2):295-302. doi: 10.20471/acc.2019.58.02.13. PMID: 31819326Free PMC Article
Bond AE, Shah BB, Huss DS, Dallapiazza RF, Warren A, Harrison MB, Sperling SA, Wang XQ, Gwinn R, Witt J, Ro S, Elias WJ
JAMA Neurol 2017 Dec 1;74(12):1412-1418. doi: 10.1001/jamaneurol.2017.3098. PMID: 29084313Free PMC Article
Chen W, Hopfner F, Szymczak S, Granert O, Müller SH, Kuhlenbäumer G, Deuschl G
Parkinsonism Relat Disord 2017 Jul;40:58-63. Epub 2017 Apr 20 doi: 10.1016/j.parkreldis.2017.04.012. PMID: 28442304
Elias WJ, Lipsman N, Ondo WG, Ghanouni P, Kim YG, Lee W, Schwartz M, Hynynen K, Lozano AM, Shah BB, Huss D, Dallapiazza RF, Gwinn R, Witt J, Ro S, Eisenberg HM, Fishman PS, Gandhi D, Halpern CH, Chuang R, Butts Pauly K, Tierney TS, Hayes MT, Cosgrove GR, Yamaguchi T, Abe K, Taira T, Chang JW
N Engl J Med 2016 Aug 25;375(8):730-9. doi: 10.1056/NEJMoa1600159. PMID: 27557301
Pétursson H
Addiction 1994 Nov;89(11):1455-9. doi: 10.1111/j.1360-0443.1994.tb03743.x. PMID: 7841856

Diagnosis

Bungay J, Emokpae O, Relton SD, Alty J, Williams S, Fang H, Wong DC
Annu Int Conf IEEE Eng Med Biol Soc 2023 Jul;2023:1-4. doi: 10.1109/EMBC40787.2023.10340420. PMID: 38083026
Güngen BD, Aras YG, Gül SS, Acar T, Acar BA, Can NU
Eur Rev Med Pharmacol Sci 2022 Apr;26(8):2721-2726. doi: 10.26355/eurrev_202204_28602. PMID: 35503617
Serin HM, Arslan EA
Acta Clin Croat 2019 Jun;58(2):295-302. doi: 10.20471/acc.2019.58.02.13. PMID: 31819326Free PMC Article
Chen W, Hopfner F, Szymczak S, Granert O, Müller SH, Kuhlenbäumer G, Deuschl G
Parkinsonism Relat Disord 2017 Jul;40:58-63. Epub 2017 Apr 20 doi: 10.1016/j.parkreldis.2017.04.012. PMID: 28442304
Pandey S, Sarma N
Parkinsonism Relat Disord 2016 Aug;29:3-9. Epub 2016 Apr 1 doi: 10.1016/j.parkreldis.2016.03.024. PMID: 27062584

Therapy

Serin HM, Arslan EA
Acta Clin Croat 2019 Jun;58(2):295-302. doi: 10.20471/acc.2019.58.02.13. PMID: 31819326Free PMC Article
Bond AE, Shah BB, Huss DS, Dallapiazza RF, Warren A, Harrison MB, Sperling SA, Wang XQ, Gwinn R, Witt J, Ro S, Elias WJ
JAMA Neurol 2017 Dec 1;74(12):1412-1418. doi: 10.1001/jamaneurol.2017.3098. PMID: 29084313Free PMC Article
Elias WJ, Lipsman N, Ondo WG, Ghanouni P, Kim YG, Lee W, Schwartz M, Hynynen K, Lozano AM, Shah BB, Huss D, Dallapiazza RF, Gwinn R, Witt J, Ro S, Eisenberg HM, Fishman PS, Gandhi D, Halpern CH, Chuang R, Butts Pauly K, Tierney TS, Hayes MT, Cosgrove GR, Yamaguchi T, Abe K, Taira T, Chang JW
N Engl J Med 2016 Aug 25;375(8):730-9. doi: 10.1056/NEJMoa1600159. PMID: 27557301
Pandey S, Sarma N
Parkinsonism Relat Disord 2016 Aug;29:3-9. Epub 2016 Apr 1 doi: 10.1016/j.parkreldis.2016.03.024. PMID: 27062584
Pétursson H
Addiction 1994 Nov;89(11):1455-9. doi: 10.1111/j.1360-0443.1994.tb03743.x. PMID: 7841856

Prognosis

Peters J, Maamary J, Kyle K, Olsen N, Jones L, Bolitho S, Barnett Y, Jonker B, Tisch S
Mov Disord 2024 Jan;39(1):173-182. Epub 2023 Nov 14 doi: 10.1002/mds.29658. PMID: 37964429
Gazulla J, Bellosta-Diago E, Izquierdo-Alvarez S, Berciano J
Eur J Neurol 2023 Aug;30(8):2539-2543. Epub 2023 May 19 doi: 10.1111/ene.15840. PMID: 37154409
Cosgrove GR, Lipsman N, Lozano AM, Chang JW, Halpern C, Ghanouni P, Eisenberg H, Fishman P, Taira T, Schwartz ML, McDannold N, Hayes M, Ro S, Shah B, Gwinn R, Santini VE, Hynynen K, Elias WJ
J Neurosurg 2023 Apr 1;138(4):1028-1033. Epub 2022 Aug 5 doi: 10.3171/2022.6.JNS212483. PMID: 35932269Free PMC Article
Shahtalebi S, Atashzar SF, Samotus O, Patel RV, Jog MS, Mohammadi A
Sci Rep 2020 Feb 10;10(1):2195. doi: 10.1038/s41598-020-58912-9. PMID: 32042111Free PMC Article
Krishna V, Sammartino F, Cosgrove R, Ghanouni P, Schwartz M, Gwinn R, Eisenberg H, Fishman P, Chang JW, Taira T, Kaplitt M, Rezai A, Rumià J, Gedroyc W, Igase K, Kishima H, Yamada K, Ohnishi H, Halpern C
Neurosurgery 2020 Aug 1;87(2):229-237. doi: 10.1093/neuros/nyz417. PMID: 31690945

Clinical prediction guides

Bungay J, Emokpae O, Relton SD, Alty J, Williams S, Fang H, Wong DC
Annu Int Conf IEEE Eng Med Biol Soc 2023 Jul;2023:1-4. doi: 10.1109/EMBC40787.2023.10340420. PMID: 38083026
Farashi S, Sarihi A, Ramezani M, Shahidi S, Mazdeh M
BMC Neurol 2023 Nov 24;23(1):420. doi: 10.1186/s12883-023-03468-0. PMID: 38001410Free PMC Article
Li Y, Wolf MD, Kulkarni AD, Bell J, Chang JS, Nimunkar A, Radwin RG
Hum Factors 2021 Nov;63(7):1169-1181. Epub 2020 Apr 14 doi: 10.1177/0018720820916629. PMID: 32286884Free PMC Article
Bond AE, Shah BB, Huss DS, Dallapiazza RF, Warren A, Harrison MB, Sperling SA, Wang XQ, Gwinn R, Witt J, Ro S, Elias WJ
JAMA Neurol 2017 Dec 1;74(12):1412-1418. doi: 10.1001/jamaneurol.2017.3098. PMID: 29084313Free PMC Article
Elias WJ, Lipsman N, Ondo WG, Ghanouni P, Kim YG, Lee W, Schwartz M, Hynynen K, Lozano AM, Shah BB, Huss D, Dallapiazza RF, Gwinn R, Witt J, Ro S, Eisenberg HM, Fishman PS, Gandhi D, Halpern CH, Chuang R, Butts Pauly K, Tierney TS, Hayes MT, Cosgrove GR, Yamaguchi T, Abe K, Taira T, Chang JW
N Engl J Med 2016 Aug 25;375(8):730-9. doi: 10.1056/NEJMoa1600159. PMID: 27557301

Recent systematic reviews

Łajczak PM, Nawrat Z
J Robot Surg 2024 May 31;18(1):235. doi: 10.1007/s11701-024-01991-x. PMID: 38819533Free PMC Article
Eslamian F, Dolatkhah N, Fallah L, Jahanjoo F, Toopchizadeh V, Talebi M
Tremor Other Hyperkinet Mov (N Y) 2023;13:27. Epub 2023 Aug 24 doi: 10.5334/tohm.773. PMID: 37637849Free PMC Article
Tian Z, Li Y, Xie Y, Yang Y, Xu J
Int Urol Nephrol 2022 Oct;54(10):2555-2566. Epub 2022 Mar 11 doi: 10.1007/s11255-022-03169-6. PMID: 35277831
Castillo-Segura P, Fernández-Panadero C, Alario-Hoyos C, Muñoz-Merino PJ, Delgado Kloos C
Artif Intell Med 2021 Feb;112:102007. Epub 2021 Jan 5 doi: 10.1016/j.artmed.2020.102007. PMID: 33581827
Zheng X, Wei W, Liu P, Wu C, Lu L, Tang C
Neurol Neurochir Pol 2020;54(6):561-567. Epub 2020 Oct 13 doi: 10.5603/PJNNS.a2020.0079. PMID: 33047784

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