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Fasciculations

MedGen UID:
5124
Concept ID:
C0015644
Sign or Symptom
Synonyms: Fasciculation; Muscle fasciculation; Muscle twitch
SNOMED CT: Muscular fasciculation (82470000); Writhing muscles (82470000); Spontaneous contraction of muscle (82470000); Flickering muscles (82470000); Fluttering muscles (82470000); Muscle fasciculation (82470000)
 
HPO: HP:0002380

Definition

Fasciculations are observed as small, local, involuntary muscle contractions (twitching) visible under the skin. Fasciculations result from increased irritability of an axon (which in turn is often a manifestation of disease of a motor neuron). This leads to sporadic discharges of all the muscle fibers controlled by the axon in isolation from other motor units. [from HPO]

Term Hierarchy

Conditions with this feature

Fabry disease
MedGen UID:
8083
Concept ID:
C0002986
Disease or Syndrome
Fabry disease results from deficient activity of the enzyme alpha-galactosidase A (a-Gal A) and progressive lysosomal deposition of globotriaosylceramide (GL-3) in cells throughout the body. The classic form, occurring in males with less than 1% a-Gal A enzyme activity, usually has its onset in childhood or adolescence with periodic crises of severe pain in the extremities (acroparesthesia), the appearance of vascular cutaneous lesions (angiokeratomas), sweating abnormalities (anhidrosis, hypohidrosis, and rarely hyperhidrosis), characteristic corneal and lenticular opacities, and proteinuria. Gradual deterioration of renal function to end-stage renal disease (ESRD) usually occurs in men in the third to fifth decade. In middle age, most males successfully treated for ESRD develop cardiac and/or cerebrovascular disease, a major cause of morbidity and mortality. Heterozygous females typically have milder symptoms at a later age of onset than males. Rarely, they may be relatively asymptomatic throughout a normal life span or may have symptoms as severe as those observed in males with the classic phenotype. In contrast, males with greater than 1% a-Gal A activity may have: (1) a cardiac variant phenotype that usually presents in the sixth to eighth decade with left ventricular hypertrophy, cardiomyopathy and arrhythmia, and proteinuria, but without ESRD; or (2) a renal variant phenotype, associated with ESRD but without the skin lesions or pain; or (3) cerebrovascular disease presenting as stroke or transient ischemic attack.
Azorean disease
MedGen UID:
9841
Concept ID:
C0024408
Disease or Syndrome
Spinocerebellar ataxia type 3 (SCA3), also known as Machado-Joseph disease (MJD), is characterized by progressive cerebellar ataxia and variable findings including a dystonic-rigid syndrome, a parkinsonian syndrome, or a combined syndrome of dystonia and peripheral neuropathy. Neurologic findings tend to evolve as the disease progresses.
Sandhoff disease
MedGen UID:
11313
Concept ID:
C0036161
Disease or Syndrome
Sandhoff disease is a progressive neurodegenerative disorder characterized by an accumulation of GM2 gangliosides, particularly in neurons, and is clinically indistinguishable from Tay-Sachs disease (272800).
Familial hyperkalemic periodic paralysis
MedGen UID:
68665
Concept ID:
C0238357
Disease or Syndrome
Hyperkalemic periodic paralysis is a condition that causes episodes of extreme muscle weakness or paralysis, usually beginning in infancy or early childhood. Most often, these episodes involve a temporary inability to move muscles in the arms and legs. Episodes tend to increase in frequency until mid-adulthood, after which they occur less frequently. Factors that can trigger attacks include rest after exercise, potassium-rich foods such as bananas and potatoes, stress, fatigue, alcohol, pregnancy, exposure to cold temperatures, certain medications, and periods without food (fasting). Muscle strength usually returns to normal between attacks, although many affected people continue to experience mild stiffness (myotonia), particularly in muscles of the face and hands.Most people with hyperkalemic periodic paralysis have increased levels of potassium in their blood (hyperkalemia) during attacks. Hyperkalemia results when the weak or paralyzed muscles release potassium ions into the bloodstream. In other cases, attacks are associated with normal blood potassium levels (normokalemia). Ingesting potassium can trigger attacks in affected individuals, even if blood potassium levels do not go up.
Isaac syndrome
MedGen UID:
116151
Concept ID:
C0242287
Disease or Syndrome
A rare neuromuscular disorder with onset usually in late childhood or early adulthood, characterized by intermittent or continuous widespread involuntary muscle contractions; FASCICULATION; hyporeflexia; MUSCLE CRAMP; MUSCLE WEAKNESS; HYPERHIDROSIS; TACHYCARDIA; and MYOKYMIA. Involvement of pharyngeal or laryngeal muscles may interfere with speech and breathing. The continuous motor activity persists during sleep and general anesthesia (distinguishing this condition from STIFF-PERSON SYNDROME). Familial and acquired (primarily autoimmune) forms have been reported. (From Ann NY Acad Sci 1998 May 13;841:482-496; Adams et al., Principles of Neurology, 6th ed, p1491)
Spinocerebellar ataxia 2
MedGen UID:
155704
Concept ID:
C0752121
Disease or Syndrome
Spinocerebellar ataxia type 2 (SCA2) is characterized by progressive cerebellar ataxia, including nystagmus, slow saccadic eye movements and, in some individuals, ophthalmoparesis or parkinsonism. Pyramidal findings are present; deep tendon reflexes are brisk early on and absent later in the course. Age of onset is typically in the fourth decade with a ten- to 15-year disease duration.
Amyotrophic lateral sclerosis 17
MedGen UID:
373010
Concept ID:
C1836076
Disease or Syndrome
Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease involving both upper motor neurons (UMN) and lower motor neurons (LMN). UMN signs include hyperreflexia, extensor plantar response, increased muscle tone, and weakness in a topographic representation. LMN signs include weakness, muscle wasting, hyporeflexia, muscle cramps, and fasciculations. Initial presentation varies. Affected individuals typically present with either asymmetric focal weakness of the extremities (stumbling or poor handgrip) or bulbar findings (dysarthria, dysphagia). Other findings may include muscle fasciculations, muscle cramps, and labile affect, but not necessarily mood. Regardless of initial symptoms, atrophy and weakness eventually affect other muscles. The mean age of onset is 56 years in individuals with no known family history and 46 years in individuals with more than one affected family member (familial ALS or FALS). Average disease duration is about three years, but it can vary significantly. Death usually results from compromise of the respiratory muscles.
Amyotrophic lateral sclerosis type 8
MedGen UID:
325237
Concept ID:
C1837728
Disease or Syndrome
Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease involving both upper motor neurons (UMN) and lower motor neurons (LMN). UMN signs include hyperreflexia, extensor plantar response, increased muscle tone, and weakness in a topographic representation. LMN signs include weakness, muscle wasting, hyporeflexia, muscle cramps, and fasciculations. Initial presentation varies. Affected individuals typically present with either asymmetric focal weakness of the extremities (stumbling or poor handgrip) or bulbar findings (dysarthria, dysphagia). Other findings may include muscle fasciculations, muscle cramps, and labile affect, but not necessarily mood. Regardless of initial symptoms, atrophy and weakness eventually affect other muscles. The mean age of onset is 56 years in individuals with no known family history and 46 years in individuals with more than one affected family member (familial ALS or FALS). Average disease duration is about three years, but it can vary significantly. Death usually results from compromise of the respiratory muscles.
Bulbo-spinal atrophy X-linked
MedGen UID:
333282
Concept ID:
C1839259
Disease or Syndrome
Spinal and bulbar muscular atrophy (SBMA) is a gradually progressive neuromuscular disorder in which degeneration of lower motor neurons results in muscle weakness, muscle atrophy, and fasciculations. SBMA occurs only in males. Affected individuals often show gynecomastia, testicular atrophy, and reduced fertility as a result of mild androgen insensitivity.
Amyotrophic lateral sclerosis type 6
MedGen UID:
374989
Concept ID:
C1842675
Disease or Syndrome
Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease involving both upper motor neurons (UMN) and lower motor neurons (LMN). UMN signs include hyperreflexia, extensor plantar response, increased muscle tone, and weakness in a topographic representation. LMN signs include weakness, muscle wasting, hyporeflexia, muscle cramps, and fasciculations. Initial presentation varies. Affected individuals typically present with either asymmetric focal weakness of the extremities (stumbling or poor handgrip) or bulbar findings (dysarthria, dysphagia). Other findings may include muscle fasciculations, muscle cramps, and labile affect, but not necessarily mood. Regardless of initial symptoms, atrophy and weakness eventually affect other muscles. The mean age of onset is 56 years in individuals with no known family history and 46 years in individuals with more than one affected family member (familial ALS or FALS). Average disease duration is about three years, but it can vary significantly. Death usually results from compromise of the respiratory muscles.
Pontocerebellar hypoplasia type 1
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. In PCH type 2 (see PCH2A, 277470), there is progressive microcephaly from birth combined with extrapyramidal dyskinesias. PCH3 (608027) is characterized by hypotonia, hyperreflexia, microcephaly, optic atrophy, and seizures. PCH4 (225753) is characterized by hypertonia, joint contractures, olivopontocerebellar hypoplasia, and early death. Patients with PCH5 (610204) have cerebellar hypoplasia apparent in the second trimester and show seizures. PCH6 (611523) is associated with mitochondrial respiratory chain defects (summary by Graham et al., 2010). Also see PCH7 (614969), PCH8 (614961), PCH9 (615809), and PCH10 (615803). 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); 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); and PCH10 (615803), caused by mutation in the CLP1 gene (608757).
Spinocerebellar ataxia autosomal recessive 4
MedGen UID:
335442
Concept ID:
C1846492
Disease or Syndrome
Charcot-Marie-Tooth disease type 2F
MedGen UID:
335784
Concept ID:
C1847823
Disease or Syndrome
Charcot-Marie-Tooth hereditary neuropathy type 2 (CMT2) is an axonal (non-demyelinating) peripheral neuropathy characterized by distal muscle weakness and atrophy, mild sensory loss, and normal or near-normal nerve conduction velocities. CMT2 is clinically similar to CMT1, although typically less severe. Peripheral nerves are not enlarged or hypertrophic. The subtypes of CMT2 are similar clinically and distinguished only by molecular genetic findings.
Spinal muscular atrophy Ryukyuan type
MedGen UID:
376517
Concept ID:
C1849102
Disease or Syndrome
Erythrokeratodermia with ataxia
MedGen UID:
338703
Concept ID:
C1851481
Disease or Syndrome
Spinocerebellar ataxia-34 is an autosomal dominant neurocutaneous disorder characterized by onset of erythremia and hyperkeratosis in early childhood, followed by slowly progressive cerebellar ataxia manifesting in the fourth or fifth decade of life. Skin lesions tend to improve with age, and cognition is preserved (summary by Cadieux-Dion et al., 2014). For a general discussion of autosomal dominant spinocerebellar ataxia, see SCA1 (164400).
Neutral lipid storage disease with myopathy
MedGen UID:
339913
Concept ID:
C1853136
Disease or Syndrome
Neutral lipid storage disease with myopathy is an autosomal recessive muscle disorder characterized by adult onset of slowly progressive proximal muscle weakness affecting the upper and lower limbs and associated with increased serum creatine kinase; distal muscle weakness may also occur. About half of patients develop cardiomyopathy later in the disease course. Other variable features include diabetes mellitus, hepatic steatosis, hypertriglyceridemia, and possibly sensorineural hearing loss. Leukocytes and muscle cells show cytoplasmic accumulation of triglycerides (summary by Reilich et al., 2011). Neutral lipid storage disease with myopathy belongs to a group of disorders termed neutral lipid storage disorders (NLSDs). These disorders are characterized by the presence of triglyceride-containing cytoplasmic droplets in leukocytes and in other tissues, including bone marrow, skin, and muscle. Chanarin-Dorfman syndrome (CDS; 275630) is defined as NLSD with ichthyosis (NLSDI). Patients with NLSDM present with myopathy but without ichthyosis (summary by Fischer et al., 2007).
Neuropathy, hereditary motor and sensory, Okinawa type
MedGen UID:
346886
Concept ID:
C1858338
Disease or Syndrome
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; 105400) (summary by Ishiura et al., 2012).
Ataxia with fasciculations
MedGen UID:
400052
Concept ID:
C1862440
Disease or Syndrome
Amyotrophic lateral sclerosis type 1
MedGen UID:
400169
Concept ID:
C1862939
Disease or Syndrome
Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease involving both upper motor neurons (UMN) and lower motor neurons (LMN). UMN signs include hyperreflexia, extensor plantar response, increased muscle tone, and weakness in a topographic representation. LMN signs include weakness, muscle wasting, hyporeflexia, muscle cramps, and fasciculations. Initial presentation varies. Affected individuals typically present with either asymmetric focal weakness of the extremities (stumbling or poor handgrip) or bulbar findings (dysarthria, dysphagia). Other findings may include muscle fasciculations, muscle cramps, and labile affect, but not necessarily mood. Regardless of initial symptoms, atrophy and weakness eventually affect other muscles. The mean age of onset is 56 years in individuals with no known family history and 46 years in individuals with more than one affected family member (familial ALS or FALS). Average disease duration is about three years, but it can vary significantly. Death usually results from compromise of the respiratory muscles.
Monomelic amyotrophy
MedGen UID:
356265
Concept ID:
C1865384
Disease or Syndrome
Monomelic amyotrophy, also known as Hirayama disease, is characterized by insidious onset of weakness and wasting of the muscles of the hand and forearm. It is usually unilateral, but can be bilateral. It occurs most commonly as a sporadic condition, is most common in young men, and follows a relatively benign course after a few years of progression (Nalini et al., 2004; Misra et al., 2005).
Amyotrophic lateral sclerosis type 5
MedGen UID:
356388
Concept ID:
C1865864
Disease or Syndrome
Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease involving both upper motor neurons (UMN) and lower motor neurons (LMN). UMN signs include hyperreflexia, extensor plantar response, increased muscle tone, and weakness in a topographic representation. LMN signs include weakness, muscle wasting, hyporeflexia, muscle cramps, and fasciculations. Initial presentation varies. Affected individuals typically present with either asymmetric focal weakness of the extremities (stumbling or poor handgrip) or bulbar findings (dysarthria, dysphagia). Other findings may include muscle fasciculations, muscle cramps, and labile affect, but not necessarily mood. Regardless of initial symptoms, atrophy and weakness eventually affect other muscles. The mean age of onset is 56 years in individuals with no known family history and 46 years in individuals with more than one affected family member (familial ALS or FALS). Average disease duration is about three years, but it can vary significantly. Death usually results from compromise of the respiratory muscles.
Spinocerebellar ataxia with rigidity and peripheral neuropathy
MedGen UID:
401079
Concept ID:
C1866770
Disease or Syndrome
Adult proximal spinal muscular atrophy, autosomal dominant
MedGen UID:
357133
Concept ID:
C1866777
Disease or Syndrome
Spinal muscular atrophy is characterized by degeneration of the anterior horn cells in the spinal cord, leading to symmetric muscle weakness and wasting. See also autosomal recessive adult-onset proximal spinal muscular atrophy (SMA4; 271150), caused by defect in the SMN1 gene (600354), and autosomal dominant childhood-onset proximal SMA (158600).
Ataxia, spastic, 2, autosomal recessive
MedGen UID:
370750
Concept ID:
C1969796
Disease or Syndrome
Autosomal recessive spastic ataxia is a neurologic disorder characterized by onset in the first 2 decades of cerebellar ataxia, dysarthria, and variable spasticity of the lower limbs. Cognition is not affected (summary by Dor et al., 2014). For a discussion of genetic heterogeneity of spastic ataxia, see SPAX1 (108600).
Combined saposin deficiency
MedGen UID:
382151
Concept ID:
C2673635
Disease or Syndrome
Spinocerebellar ataxia, autosomal recessive 10
MedGen UID:
462348
Concept ID:
C3150998
Disease or Syndrome
Autosomal recessive spinocerebellar ataxia-10 is an autosomal recessive neurodegenerative disorder with onset in the teenage or young adult years of gait and limb ataxia, dysarthria, and nystagmus associated with marked cerebellar atrophy on brain imaging (summary by Vermeer et al., 2010). Some patients have low levels of coenzyme Q10 (CoQ10) in muscle and may show some clinical improvement with CoQ10 treatment (Balreira et al., 2014).
Amyotrophic lateral sclerosis 14, with or without frontotemporal dementia
MedGen UID:
462753
Concept ID:
C3151403
Disease or Syndrome
Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease involving both upper motor neurons (UMN) and lower motor neurons (LMN). UMN signs include hyperreflexia, extensor plantar response, increased muscle tone, and weakness in a topographic representation. LMN signs include weakness, muscle wasting, hyporeflexia, muscle cramps, and fasciculations. Initial presentation varies. Affected individuals typically present with either asymmetric focal weakness of the extremities (stumbling or poor handgrip) or bulbar findings (dysarthria, dysphagia). Other findings may include muscle fasciculations, muscle cramps, and labile affect, but not necessarily mood. Regardless of initial symptoms, atrophy and weakness eventually affect other muscles. The mean age of onset is 56 years in individuals with no known family history and 46 years in individuals with more than one affected family member (familial ALS or FALS). Average disease duration is about three years, but it can vary significantly. Death usually results from compromise of the respiratory muscles.
Combined oxidative phosphorylation deficiency 6
MedGen UID:
463103
Concept ID:
C3151753
Disease or Syndrome
Charcot-Marie-Tooth disease type 2P
MedGen UID:
482427
Concept ID:
C3280797
Disease or Syndrome
Charcot-Marie-Tooth hereditary neuropathy type 2 (CMT2) is an axonal (non-demyelinating) peripheral neuropathy characterized by distal muscle weakness and atrophy, mild sensory loss, and normal or near-normal nerve conduction velocities. CMT2 is clinically similar to CMT1, although typically less severe. Peripheral nerves are not enlarged or hypertrophic. The subtypes of CMT2 are similar clinically and distinguished only by molecular genetic findings.
Amyotrophic lateral sclerosis 18
MedGen UID:
766633
Concept ID:
C3553719
Disease or Syndrome
Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease involving both upper motor neurons (UMN) and lower motor neurons (LMN). UMN signs include hyperreflexia, extensor plantar response, increased muscle tone, and weakness in a topographic representation. LMN signs include weakness, muscle wasting, hyporeflexia, muscle cramps, and fasciculations. Initial presentation varies. Affected individuals typically present with either asymmetric focal weakness of the extremities (stumbling or poor handgrip) or bulbar findings (dysarthria, dysphagia). Other findings may include muscle fasciculations, muscle cramps, and labile affect, but not necessarily mood. Regardless of initial symptoms, atrophy and weakness eventually affect other muscles. The mean age of onset is 56 years in individuals with no known family history and 46 years in individuals with more than one affected family member (familial ALS or FALS). Average disease duration is about three years, but it can vary significantly. Death usually results from compromise of the respiratory muscles.
Spinal muscular atrophy, jokela type
MedGen UID:
767312
Concept ID:
C3554398
Disease or Syndrome
The Jokela type of spinal muscular atrophy (SMAJ) is an autosomal dominant lower motor neuron disorder characterized by adult-onset of muscle cramps and fasciculations affecting the proximal and distal muscles of the upper and lower limbs. The disorder is slowly progressive, resulting in weakness and mild muscle atrophy later in life (summary by Jokela et al., 2011).
Distal hereditary motor neuronopathy 2D
MedGen UID:
777992
Concept ID:
C3711384
Disease or Syndrome
Distal hereditary motor neuronopathy type IID is an autosomal dominant neurologic disorder characterized by onset of slowly progressive distal lower limb weakness and atrophy between the second and fourth decades of life. Weakness usually begins in the calf muscles and later involves more proximal muscles. The severity is variable, and some patients have difficulty walking or running. Most also have upper limb involvement, particularly of the triceps and intrinsic hand muscles. Some patients may lose independent ambulation later in the disease course. Sensory impairment is typically not present, and cognition and bulbar function are normal (summary by Sumner et al., 2013). For a general phenotypic description and a discussion of genetic heterogeneity of distal HMN (dHMN), see HMN type I (HMN1; 182960).
Spinal muscular atrophy, lower extremity predominant 2, autosomal dominant
MedGen UID:
815379
Concept ID:
C3809049
Disease or Syndrome
SMALED2 is an autosomal dominant form of spinal muscular atrophy characterized by early-childhood onset of muscle weakness and atrophy predominantly affecting the proximal and distal muscles of the lower extremity, although some patients may show upper extremity involvement. The disorder results in delayed walking, waddling gait, difficulty walking, and loss of distal reflexes. Some patients may have foot deformities or hyperlordosis, and some show mild upper motor signs, such as spasticity. Sensation, bulbar function, and cognitive function are preserved. The disorder shows very slow progression throughout life (summary by Oates et al., 2013). For discussion of genetic heterogeneity of lower extremity-predominant spinal muscular atrophy, see SMALED1 (158600).
CHARCOT-MARIE-TOOTH DISEASE, AXONAL, TYPE 2Z
MedGen UID:
907298
Concept ID:
C4225243
Disease or Syndrome
FRONTOTEMPORAL DEMENTIA AND/OR AMYOTROPHIC LATERAL SCLEROSIS 4
MedGen UID:
902979
Concept ID:
C4225325
Disease or Syndrome
FRONTOTEMPORAL DEMENTIA AND/OR AMYOTROPHIC LATERAL SCLEROSIS 3
MedGen UID:
897127
Concept ID:
C4225326
Disease or Syndrome

Recent clinical studies

Etiology

Zhang Z, Zhang DS, Sui W, Liu XH, Zhang L, Sun JH
Int J Clin Pharmacol Ther 2016 Jun;54(6):426-32. doi: 10.5414/CP202531. PMID: 27087153
Takamatsu N, Nodera H, Mori A, Maruyama-Saladini K, Osaki Y, Shimatani Y, Oda M, Izumi Y, Kaji R
J Med Invest 2016;63(1-2):49-53. doi: 10.2152/jmi.63.49. PMID: 27040052
Sleutjes BT, Montfoort I, van Doorn PA, Visser GH, Blok JH
Clin Neurophysiol 2015 Jul;126(7):1440-5. Epub 2014 Oct 30 doi: 10.1016/j.clinph.2014.10.145. PMID: 25468238
Krämer HH, Vlazak A, Döring K, Tanislav C, Allendörfer J, Kaps M
Clin Neurophysiol 2014 Dec;125(12):2441-5. Epub 2014 Apr 26 doi: 10.1016/j.clinph.2014.04.009. PMID: 24875234
Fatemeh H, Mojgan R
Acta Anaesthesiol Taiwan 2010 Mar;48(1):28-32. doi: 10.1016/S1875-4597(10)60006-9. PMID: 20434110

Diagnosis

Takamatsu N, Nodera H, Mori A, Maruyama-Saladini K, Osaki Y, Shimatani Y, Oda M, Izumi Y, Kaji R
J Med Invest 2016;63(1-2):49-53. doi: 10.2152/jmi.63.49. PMID: 27040052
Sleutjes BT, Montfoort I, van Doorn PA, Visser GH, Blok JH
Clin Neurophysiol 2015 Jul;126(7):1440-5. Epub 2014 Oct 30 doi: 10.1016/j.clinph.2014.10.145. PMID: 25468238
Krämer HH, Vlazak A, Döring K, Tanislav C, Allendörfer J, Kaps M
Clin Neurophysiol 2014 Dec;125(12):2441-5. Epub 2014 Apr 26 doi: 10.1016/j.clinph.2014.04.009. PMID: 24875234
Kleine BU, Boekestein WA, Arts IM, Zwarts MJ, Schelhaas HJ, Stegeman DF
Clin Neurophysiol 2012 Feb;123(2):399-405. Epub 2011 Aug 4 doi: 10.1016/j.clinph.2011.06.032. PMID: 21820354
Mills KR
Brain 2010 Nov;133(11):3458-69. Epub 2010 Oct 19 doi: 10.1093/brain/awq290. PMID: 20959307

Therapy

Zhang Z, Zhang DS, Sui W, Liu XH, Zhang L, Sun JH
Int J Clin Pharmacol Ther 2016 Jun;54(6):426-32. doi: 10.5414/CP202531. PMID: 27087153
Yun MJ, Kim YH, Go YK, Shin JE, Ryu CG, Kim W, Paik NJ, Han MK, Do SH, Jung WS
Yonsei Med J 2010 Jul;51(4):585-9. doi: 10.3349/ymj.2010.51.4.585. PMID: 20499427Free PMC Article
Fatemeh H, Mojgan R
Acta Anaesthesiol Taiwan 2010 Mar;48(1):28-32. doi: 10.1016/S1875-4597(10)60006-9. PMID: 20434110
Fermont J, Arts IM, Overeem S, Kleine BU, Schelhaas HJ, Zwarts MJ
Amyotroph Lateral Scler 2010;11(1-2):181-6. doi: 10.3109/17482960903062137. PMID: 19533451
Forcelini CM, Rotta FT, Posenato N, Rovani JS, Crusius PS, Mallmann AB, Seibert CA, Crusius MU, Carazzo C, Crusius CU, Goellner E, Ragnini J, Wayhs SY
Arq Neuropsiquiatr 2007 Dec;65(4A):1015-7. PMID: 18094867

Prognosis

Tremolizzo L, Susani E, Aliprandi A, Salmaggi A, Ferrarese C, Appollonio I
Amyotroph Lateral Scler Frontotemporal Degener 2014 Dec;15(7-8):546-50. Epub 2014 May 27 doi: 10.3109/21678421.2014.913636. PMID: 24863345
Grizelj R, Vuković J
J Pediatr 2013 Nov;163(5):1526.e1. Epub 2013 Jul 1 doi: 10.1016/j.jpeds.2013.05.030. PMID: 23809046
Beckmann YY, Ciftçi Y, Seçil Y, Eren S
Crit Care Med 2010 Dec;38(12):2377-8. doi: 10.1097/CCM.0b013e3181fa0458. PMID: 20890193
Mateen FJ, Sorenson EJ, Daube JR
Amyotroph Lateral Scler 2008 Apr;9(2):120-1. doi: 10.1080/17482960701855864. PMID: 18428004
Kleine BU, Stegeman DF, Schelhaas HJ, Zwarts MJ
Neurology 2008 Jan 29;70(5):353-9. doi: 10.1212/01.wnl.0000300559.14806.2a. PMID: 18227416

Clinical prediction guides

Takamatsu N, Nodera H, Mori A, Maruyama-Saladini K, Osaki Y, Shimatani Y, Oda M, Izumi Y, Kaji R
J Med Invest 2016;63(1-2):49-53. doi: 10.2152/jmi.63.49. PMID: 27040052
de Carvalho M, Swash M
Clin Neurophysiol 2016 Jan;127(1):870-3. Epub 2015 Feb 19 doi: 10.1016/j.clinph.2015.02.004. PMID: 25754259
Krämer HH, Vlazak A, Döring K, Tanislav C, Allendörfer J, Kaps M
Clin Neurophysiol 2014 Dec;125(12):2441-5. Epub 2014 Apr 26 doi: 10.1016/j.clinph.2014.04.009. PMID: 24875234
Tremolizzo L, Susani E, Aliprandi A, Salmaggi A, Ferrarese C, Appollonio I
Amyotroph Lateral Scler Frontotemporal Degener 2014 Dec;15(7-8):546-50. Epub 2014 May 27 doi: 10.3109/21678421.2014.913636. PMID: 24863345
Yun MJ, Kim YH, Go YK, Shin JE, Ryu CG, Kim W, Paik NJ, Han MK, Do SH, Jung WS
Yonsei Med J 2010 Jul;51(4):585-9. doi: 10.3349/ymj.2010.51.4.585. PMID: 20499427Free PMC Article

Recent systematic reviews

Finsterer J, Soraru G
J Mol Neurosci 2016 Mar;58(3):321-9. Epub 2015 Oct 19 doi: 10.1007/s12031-015-0663-x. PMID: 26482145
Bunnell A, Ney J, Gellhorn A, Hough CL
Muscle Nerve 2015 Nov;52(5):701-8. Epub 2015 Sep 21 doi: 10.1002/mus.24728. PMID: 26044880Free PMC Article
Costa J, Graça P, Evangelista T, de Carvalho M
Clin Neurophysiol 2005 Dec;116(12):2847-52. Epub 2005 Oct 25 doi: 10.1016/j.clinph.2005.07.016. PMID: 16256429
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