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Pendular nystagmus

MedGen UID:
78770
Concept ID:
C0271388
Disease or Syndrome
Synonyms: Nystagmus, Pendular; Pendular Nystagmus
SNOMED CT: Pendular nystagmus (35743001)
 
HPO: HP:0012043

Definition

Rhythmic, involuntary sinusoidal oscillations of one or both eyes. The waveform of pendular nystagmus may occur in any direction. [from HPO]

Conditions with this feature

Alexander disease
MedGen UID:
78724
Concept ID:
C0270726
Disease or Syndrome
Alexander disease, a progressive disorder of cerebral white matter caused by a heterozygous GFAP pathogenic variant, comprises a continuous clinical spectrum most recognizable in infants and children and a range of nonspecific neurologic manifestations in adults. This chapter discusses the spectrum of Alexander disease as four forms: neonatal, infantile, juvenile, and adult. The neonatal form begins in the first 30 days after birth with neurologic findings (e.g., hypotonia, hyperexcitability, myoclonus) and/or gastrointestinal manifestations (e.g., gastroesophageal reflux, vomiting, failure to thrive), followed by severe developmental delay and regression, seizures, megalencephaly, and typically death within two years. The infantile form is characterized by variable developmental issues: initially some have delayed or plateauing of acquisition of new skills, followed in some by a loss of gross and fine motor skills and language during in the first decade or in others a slow disease course that spans decades. Seizures, often triggered by illness, may be less frequent/severe than in the neonatal form. The juvenile form typically presents in childhood or adolescence with clinical and imaging features that overlap with the other forms. Manifestations in early childhood are milder than those in the infantile form (e.g., mild language delay may be the only developmental abnormality or, with language acquisition, hypophonia or nasal speech may alter the voice, often prior to appearance of other neurologic features). Vomiting and failure to thrive as well as scoliosis and autonomic dysfunction are common. The adult form is typically characterized by bulbar or pseudobulbar findings (palatal myoclonus, dysphagia, dysphonia, dysarthria or slurred speech), motor/gait abnormalities with pyramidal tract signs (spasticity, hyperreflexia, positive Babinski sign), or cerebellar abnormalities (ataxia, nystagmus, or dysmetria). Others may have hemiparesis or hemiplegia with a relapsing/remitting course or slowly progressive quadriparesis or quadriplegia. Other neurologic features can include sleep apnea, diplopia or disorders of extraocular motility, and autonomic dysfunction.
Cone monochromatism
MedGen UID:
87386
Concept ID:
C0339537
Congenital Abnormality
Blue cone (OPN1SW; 613522) monochromatism is a rare X-linked congenital stationary cone dysfunction syndrome characterized by the absence of functional long wavelength-sensitive and medium wavelength-sensitive cones in the retina. Color discrimination is severely impaired from birth, and vision is derived from the remaining preserved blue (S) cones and rod photoreceptors. BCM typically presents with reduced visual acuity, pendular nystagmus, and photophobia. Patients often have myopia (review by Gardner et al., 2009). There is evidence for progression of disease in some BCM families (Nathans et al., 1989; Ayyagari et al., 2000; Michaelides et al., 2005).
Nystagmus 1, congenital, X-linked
MedGen UID:
333352
Concept ID:
C1839580
Disease or Syndrome
FRMD7-related infantile nystagmus (FIN) is characterized by either the onset of horizontal, conjugate, gaze-dependent nystagmus in the first six months of life or periodic alternating nystagmus (with cyclical changes of nystagmus direction) of infantile onset. Binocular vision and color vision are normal and visual acuity is typically better than 6/12. An abnormal head posture is seen in approximately 15% of affected individuals. The eyes are structurally normal and electrophysiologic studies (e.g., visual evoked potential, electroretinogram) are normal. Affected females report slightly better visual acuity than affected males; however, no differences between males and females in the amplitude, frequency, and waveform of nystagmus are observed.
Leber congenital amaurosis 6
MedGen UID:
344245
Concept ID:
C1854260
Congenital Abnormality
Leber congenital amaurosis comprises a group of early-onset childhood retinal dystrophies characterized by vision loss, nystagmus, and severe retinal dysfunction. Patients usually present at birth with profound vision loss and pendular nystagmus. Electroretinogram (ERG) responses are usually nonrecordable. Other clinical findings may include high hypermetropia, photodysphoria, oculodigital sign, keratoconus, cataracts, and a variable appearance to the fundus (summary by Chung and Traboulsi, 2009). For a general description and a discussion of genetic heterogeneity of LCA, see 204000.
Pyruvate dehydrogenase E2 deficiency
MedGen UID:
343386
Concept ID:
C1855565
Disease or Syndrome
Pyruvate dehydrogenase deficiency is characterized by the buildup of a chemical called lactic acid in the body and a variety of neurological problems. Signs and symptoms of this condition usually first appear shortly after birth, and they can vary widely among affected individuals. The most common feature is a potentially life-threatening buildup of lactic acid (lactic acidosis), which can cause nausea, vomiting, severe breathing problems, and an abnormal heartbeat. People with pyruvate dehydrogenase deficiency usually have neurological problems as well. Most have delayed development of mental abilities and motor skills such as sitting and walking. Other neurological problems can include intellectual disability, seizures, weak muscle tone (hypotonia), poor coordination, and difficulty walking. Some affected individuals have abnormal brain structures, such as underdevelopment of the tissue connecting the left and right halves of the brain (corpus callosum), wasting away (atrophy) of the exterior part of the brain known as the cerebral cortex, or patches of damaged tissue (lesions) on some parts of the brain. Because of the severe health effects, many individuals with pyruvate dehydrogenase deficiency do not survive past childhood, although some may live into adolescence or adulthood.
Achromatopsia 2
MedGen UID:
387867
Concept ID:
C1857618
Disease or Syndrome
Achromatopsia is characterized by reduced visual acuity, pendular nystagmus, increased sensitivity to light (photophobia), a small central scotoma, eccentric fixation, and reduced or complete loss of color discrimination. All individuals with achromatopsia (achromats) have impaired color discrimination along all three axes of color vision corresponding to the three cone classes: the protan or long-wavelength-sensitive cone axis (red), the deutan or middle-wavelength-sensitive cone axis (green), and the tritan or short-wavelength-sensitive cone axis (blue). Most individuals have complete achromatopsia, with total lack of function of all three types of cones. Rarely, individuals have incomplete achromatopsia, in which one or more cone types may be partially functioning. The manifestations are similar to those of individuals with complete achromatopsia, but generally less severe. Hyperopia is common in achromatopsia. Nystagmus develops during the first few weeks after birth followed by increased sensitivity to bright light. Best visual acuity varies with severity of the disease; it is 20/200 or less in complete achromatopsia and may be as high as 20/80 in incomplete achromatopsia. Visual acuity is usually stable over time; both nystagmus and sensitivity to bright light may improve slightly. Although the fundus is usually normal, macular changes (which may show early signs of progression) and vessel narrowing may be present in some affected individuals. Defects in the macula are visible on optical coherence tomography.
Leber congenital amaurosis 4
MedGen UID:
346808
Concept ID:
C1858386
Disease or Syndrome
Autosomal recessive childhood-onset severe retinal dystrophy is a heterogeneous group of disorders affecting rod and cone photoreceptors simultaneously. The most severe cases are termed Leber congenital amaurosis (LCA), whereas the less aggressive forms are usually considered juvenile retinitis pigmentosa (Gu et al., 1997). Various intermediate phenotypes between LCA and retinitis pigmentosa are known and are sometimes described as 'early-onset severe rod-cone dystrophy' or 'early-onset retinal degeneration' (Booij et al., 2005). For a general phenotypic description and a discussion of genetic heterogeneity of Leber congenital amaurosis, see LCA1 (204000); for retinitis pigmentosa, see 268000; for cone-rod dystrophy, see 120970.
Pierpont syndrome
MedGen UID:
356049
Concept ID:
C1865644
Disease or Syndrome
Pierpont syndrome (PRPTS) is a multiple congenital anomaly syndrome associated with learning disability. Key features include distinctive facial characteristics, especially when smiling, plantar fat pads, and other limb anomalies (summary by Burkitt Wright et al., 2011).
Persistent hyperplastic primary vitreous, autosomal recessive
MedGen UID:
370100
Concept ID:
C1969783
Disease or Syndrome
Persistent hyperplastic primary vitreous (PHPV), also termed 'persistent fetal vasculature,' is a developmental malformation of the eye in which the primary vitreous fails to regress in utero, resulting in the presence of a retrolental fibrovascular membrane with persistence of the posterior portion of the tunica vasculosa lentis and hyaloid artery. This abnormality is usually unilateral and associated with microphthalmia, cataract, glaucoma, and congenital retinal nonattachment (see Haddad et al., 1978; Khaliq et al., 2001; Prasov et al., 2012). PHPV shares phenotypic overlap with Norrie disease (310600). Genetic Heterogeneity of Persistent Hyperplastic Primary Vitreous A dominant form of PHPV has been described (PHPVAD; 611308).
Chromosome 2q31.1 duplication syndrome
MedGen UID:
462290
Concept ID:
C3150940
Disease or Syndrome
A rare, genetic, chromosomal anomaly syndrome resulting from partial duplication of the long arm of chromosome 2 characterized by congenital pendular nystagmus associated with bilateral cutaneous syndactyly between the third and fourth fingers.
Leber congenital amaurosis 7
MedGen UID:
462542
Concept ID:
C3151192
Disease or Syndrome
Leber congenital amaurosis comprises a group of early-onset childhood retinal dystrophies characterized by vision loss, nystagmus, and severe retinal dysfunction. Patients usually present at birth with profound vision loss and pendular nystagmus. Electroretinogram (ERG) responses are usually nonrecordable. Other clinical findings may include high hypermetropia, photodysphoria, oculodigital sign, keratoconus, cataracts, and a variable appearance to the fundus (summary by Chung and Traboulsi, 2009). For a general description and a discussion of genetic heterogeneity of LCA, see 204000.
Jalili syndrome
MedGen UID:
501210
Concept ID:
C3495589
Disease or Syndrome
Jalili syndrome is an autosomal recessive disorder consisting of cone-rod dystrophy and amelogenesis imperfecta. Significant visual impairment with nystagmus and photophobia is present from infancy or early childhood and progresses with age. Enamel of primary and secondary dentitions is grossly abnormal and prone to rapid posteruptive failure, in part reflecting hypomineralization (summary by Parry et al., 2009).
Peroxisome biogenesis disorder 5A (Zellweger)
MedGen UID:
766854
Concept ID:
C3553940
Disease or Syndrome
The peroxisomal biogenesis disorder (PBD) Zellweger syndrome (ZS) is an autosomal recessive multiple congenital anomaly syndrome. Affected children present in the newborn period with profound hypotonia, seizures, and inability to feed. Characteristic craniofacial anomalies, eye abnormalities, neuronal migration defects, hepatomegaly, and chondrodysplasia punctata are present. Children with this condition do not show any significant development and usually die in the first year of life (summary by Steinberg et al., 2006). For a complete phenotypic description and a discussion of genetic heterogeneity of Zellweger syndrome, see 214100. Individuals with PBDs of complementation group 5 (CG5, equivalent to CG10 and CGF) have mutations in the PEX2 gene. For information on the history of PBD complementation groups, see 214100.
Microphthalmia, isolated, with coloboma 9
MedGen UID:
767506
Concept ID:
C3554592
Disease or Syndrome
MCOPCB9 is characterized by microphthalmia and coloboma (Aldahmesh et al., 2012). MCOPS15 is characterized by microphthalmia and/or coloboma, with developmental delay in which speech appears to be more severely affected than motor abilities. Additional ocular anomalies that have been observed include ptosis, keyhole-shaped pupils, microcornea, sclerocornea, and anterior segment dysgenesis (Chassaing et al., 2016; Stephen et al., 2018; Singh et al., 2019). For a discussion of genetic heterogeneity of colobomatous microphthalmia, see MCOPCB1 (300345). For a discussion of genetic heterogeneity of syndromic microphthalmia, see MCOPS1 (309800).
X-linked colobomatous microphthalmia-microcephaly-intellectual disability-short stature syndrome
MedGen UID:
813072
Concept ID:
C3806742
Disease or Syndrome
X-linked colobomatous microphthalmia-microcephaly-intellectual disability-short stature syndrome is a rare syndromic microphthalmia disorder characterized by microphthalmia with coloboma (which may involve the iris, cilary body, choroid, retina and/or optic nerve), microcephaly, short stature and intellectual disability. Other eye abnormalities such as pendular nystagmus, esotropia and ptosis may also be present. Additional associated abnormalities include kyphoscoliosis, anteverted pinnae with minimal convolutions, diastema of the incisors and congenital pes varus.
Hermansky-Pudlak syndrome 8
MedGen UID:
854728
Concept ID:
C3888026
Disease or Syndrome
Hermansky-Pudlak syndrome (HPS) is characterized by oculocutaneous albinism, a bleeding diathesis, and, in some individuals, pulmonary fibrosis, granulomatous colitis, or immunodeficiency. Ocular findings include reduced iris pigment with iris transillumination, reduced retinal pigment, foveal hypoplasia with significant reduction in visual acuity (usually in the range of 20/50 to 20/400), nystagmus, and increased crossing of the optic nerve fibers. Hair color ranges from white to brown; skin color ranges from white to olive and is usually a shade lighter than that of other family members. The bleeding diathesis can result in variable bruising, epistaxis, gingival bleeding, postpartum hemorrhage, colonic bleeding, and prolonged bleeding with menses or after tooth extraction, circumcision, and other surgeries. Pulmonary fibrosis, a restrictive lung disease, typically causes symptoms in the early thirties and can progress to death within a decade. Granulomatous colitis is severe in about 15% of affected individuals. Neutropenia and/or immune defects occur primarily in individuals with pathogenic variants in AP3B1 and AP3D1.
Hypomyelinating leukodystrophy 9
MedGen UID:
863760
Concept ID:
C4015323
Disease or Syndrome
Hypomyelinating leukodystrophy-9 is an autosomal recessive neurologic disorder characterized by onset of delayed psychomotor development, spasticity, and nystagmus in the first year of life. Additional neurologic features such as ataxia and abnormal movements may also occur. Brain imaging shows diffuse hypomyelination affecting all regions of the brain (summary by Wolf et al., 2014). For a general phenotypic description and a discussion of genetic heterogeneity of HLD, see 312080.
Familial infantile bilateral striatal necrosis
MedGen UID:
1672478
Concept ID:
C4087174
Disease or Syndrome
Bilateral striatal necrosis (BSN) encompasses a heterogeneous group of neurologic disorders with different causation. Familial infantile striatal degeneration is rare and can be inherited as an autosomal recessive or mitochondrial (see 500003) disorder. The familial form has an insidious onset and a slowly progressive course; the sporadic form is associated with acute systemic illness. Many features of BSN overlap with Leigh syndrome (see 256000) and certain metabolic disorders, including glutaric acidemia I (231670) and methylmalonic aciduria (251000). See also Aicardi-Goutieres syndrome (225750) (Mito et al., 1986; De Meirleir et al., 1995). Genetic Heterogeneity of Striatonigral Degeneration Childhood-onset striatonigral degeneration (617054) is caused by mutation in the VAC14 gene (604632) on chromosome 16q22. See also adult-onset autosomal dominant striatal degeneration (ADSD; 609161), caused by mutation in the PDE8B gene (603390) on chromosome 5q13, and early-onset dystonia-37 with striatal lesions (DYT37; 620427), caused by mutation in the NUP54 gene (607607) on chromosome 4q21.
Leukodystrophy, hypomyelinating, 16
MedGen UID:
1631337
Concept ID:
C4693779
Disease or Syndrome
Hypomyelinating leukodystrophy-16 is an autosomal dominant neurologic disorder characterized by onset of hypotonia, nystagmus, and mildly delayed motor development in infancy. Affected individuals have motor disabilities, including ataxic or broad-based gait, hyperreflexia, intention tremor, dysmetria, and a mild pyramidal syndrome. Some patients have cognitive impairment, whereas others may have normal cognition or mild intellectual disability with speech difficulties. Brain imaging typically shows hypomyelination, leukodystrophy, and thin corpus callosum (summary by Simons et al., 2017). For a general phenotypic description and a discussion of genetic heterogeneity of hypomyelinating leukodystrophy, see 312080.
Cataract 48
MedGen UID:
1684457
Concept ID:
C5193082
Disease or Syndrome
Cataract-48 (CTRCT48) is characterized by infantile or early-childhood cataracts and visual impairment (Ansar et al., 2018).
Hypotonia, hypoventilation, impaired intellectual development, dysautonomia, epilepsy, and eye abnormalities
MedGen UID:
1672905
Concept ID:
C5193124
Disease or Syndrome
Hypotonia, hypoventilation, impaired intellectual development, dysautonomia, epilepsy, and eye abnormalities (HIDEA) is an autosomal recessive neurodevelopmental syndrome characterized by global developmental delay, poor or absent speech, hypotonia, variable ocular movement and visual abnormalities, and respiratory difficulties, including hypoventilation, and sleep apnea. Patients may have significant breathing problems during respiratory infections that may lead to early death (summary by Rahikkala et al., 2019).
Leukodystrophy, hypomyelinating, 19, transient infantile
MedGen UID:
1684698
Concept ID:
C5231463
Disease or Syndrome
Transient infantile hypomyelinating leukodystrophy-19 (HLD19) is a disorder characterized by onset of transient neurologic abnormalities in early infancy, with resolution within the first or second decades. Affected individuals typically present in the newborn period or in early infancy with nystagmus and motor deficits associated with marked hypomyelination on brain imaging. Both neurologic impairment and abnormal brain imaging spontaneously resolve during childhood. Most patients have normal cognition and can attend regular schools, although some may have persistent neurologic deficits, such as gait ataxia, speech pronunciation defects, and/or mild cognitive impairment (summary by Yan et al., 2019). For a discussion of genetic heterogeneity of HLD, see 312080.
Microcephaly, developmental delay, and brittle hair syndrome
MedGen UID:
1718781
Concept ID:
C5394425
Disease or Syndrome
Microcephaly, developmental delay, and brittle hair syndrome (MDBH) is a multisystem disorder with clinical variability. Affected individuals show cognitive and motor disabilities, as well as some degree of fine, brittle hair with microscopic shaft abnormalities. Other shared features include failure to thrive in early childhood and short stature, with some patients exhibiting feeding difficulties and hepatic steatosis (Kuo et al., 2019).
Mitochondrial complex 2 deficiency, nuclear type 3
MedGen UID:
1751884
Concept ID:
C5436934
Disease or Syndrome
Mitochondrial complex II deficiency nuclear type 3 (MC2DN3) is an autosomal recessive multisystemic metabolic disorder with a highly variable phenotype. Some patients may have an encephalomyopathic picture with episodic developmental regression, loss of motor skills, hypotonia, ataxia, dystonia, and seizures or myoclonus. Other patients present in infancy with hypertrophic cardiomyopathy, which may be fatal. Laboratory studies show increased serum lactate and mitochondrial complex II deficiency in muscle and fibroblasts (summary by Jackson et al., 2014 and Alston et al., 2015). For a discussion of genetic heterogeneity of MC2DN, see MC2DN1 (252011).

Professional guidelines

PubMed

Pascual-Camps I, Barranco-Gonzalez H, Aviñó-Martínez J, Silva E, Harto-Castaño M
J Pediatr Ophthalmol Strabismus 2018 Mar 1;55(2):85-92. Epub 2017 Dec 19 doi: 10.3928/01913913-20171117-01. PMID: 29257187
Straube A, Bronstein A, Straumann D; European Federation of Neurologic Societies
Eur J Neurol 2012 Jan;19(1):6-14. Epub 2011 Sep 12 doi: 10.1111/j.1468-1331.2011.03503.x. PMID: 21906211
Tilikete C, Vighetto A
Curr Opin Neurol 2011 Feb;24(1):38-43. doi: 10.1097/WCO.0b013e328341e3b5. PMID: 21102332

Recent clinical studies

Etiology

Rowe FJ, Hanna K, Evans JR, Noonan CP, Garcia-Finana M, Dodridge CS, Howard C, Jarvis KA, MacDiarmid SL, Maan T, North L, Rodgers H
Cochrane Database Syst Rev 2018 Mar 5;3(3):CD011290. doi: 10.1002/14651858.CD011290.pub2. PMID: 29505103Free PMC Article
Jang L, Borruat FX
Eur Neurol 2014;72(3-4):144-9. Epub 2014 Aug 16 doi: 10.1159/000360531. PMID: 25139385
Tilikete C, Jasse L, Pelisson D, Vukusic S, Durand-Dubief F, Urquizar C, Vighetto A
Neurology 2011 May 10;76(19):1650-7. doi: 10.1212/WNL.0b013e318219fa9c. PMID: 21555732
Leigh RJ, Khanna S
Semin Ophthalmol 2006 Apr-Jun;21(2):83-6. doi: 10.1080/08820530600613985. PMID: 16702074
Zee DS
Am J Otol 1985 Nov;Suppl:30-4. PMID: 3878088

Diagnosis

Rucker JC
Continuum (Minneap Minn) 2019 Oct;25(5):1376-1400. doi: 10.1212/CON.0000000000000772. PMID: 31584542
Pascual-Camps I, Barranco-Gonzalez H, Aviñó-Martínez J, Silva E, Harto-Castaño M
J Pediatr Ophthalmol Strabismus 2018 Mar 1;55(2):85-92. Epub 2017 Dec 19 doi: 10.3928/01913913-20171117-01. PMID: 29257187
Kang S, Shaikh AG
J Neurol Sci 2017 Apr 15;375:8-17. Epub 2017 Jan 10 doi: 10.1016/j.jns.2017.01.033. PMID: 28320194Free PMC Article
Thurtell MJ, Leigh RJ
Handb Clin Neurol 2011;102:333-78. doi: 10.1016/B978-0-444-52903-9.00019-4. PMID: 21601073
Tilikete C, Vighetto A
Curr Opin Neurol 2011 Feb;24(1):38-43. doi: 10.1097/WCO.0b013e328341e3b5. PMID: 21102332

Therapy

Fiani B, Runnels J, Sarhadi K, Sarno E, Kondilis A
Acta Neurol Belg 2021 Oct;121(5):1111-1116. Epub 2021 Jul 20 doi: 10.1007/s13760-021-01761-8. PMID: 34286476
Nerrant E, Abouaf L, Pollet-Villard F, Vie AL, Vukusic S, Berthiller J, Colombet B, Vighetto A, Tilikete C
J Neuroophthalmol 2020 Jun;40(2):198-206. doi: 10.1097/WNO.0000000000000807. PMID: 31169568
Mehta AR, Kennard C
Pract Neurol 2012 Jun;12(3):147-53. doi: 10.1136/practneurol-2011-000181. PMID: 22661344
McLean RJ, Gottlob I
Expert Opin Pharmacother 2009 Aug;10(11):1805-16. doi: 10.1517/14656560902978446. PMID: 19601699
Straube A
Curr Opin Neurol 2005 Feb;18(1):11-4. doi: 10.1097/00019052-200502000-00004. PMID: 15655396

Prognosis

Talsma HE, Kruijt CC, de Wit GC, Zwerver SHL, van Genderen MM
Invest Ophthalmol Vis Sci 2023 Dec 1;64(15):30. doi: 10.1167/iovs.64.15.30. PMID: 38133506Free PMC Article
Nerrant E, Tilikete C
J Neuroophthalmol 2017 Sep;37(3):332-340. doi: 10.1097/WNO.0000000000000507. PMID: 28410279
Tusa RJ
Semin Ophthalmol 1999 Jun;14(2):65-73. doi: 10.3109/08820539909056066. PMID: 10758214
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Arch Neurol 1975 Mar;32(3):191-4. doi: 10.1001/archneur.1975.00490450071010. PMID: 1119962

Clinical prediction guides

Talsma HE, Kruijt CC, de Wit GC, Zwerver SHL, van Genderen MM
Invest Ophthalmol Vis Sci 2023 Dec 1;64(15):30. doi: 10.1167/iovs.64.15.30. PMID: 38133506Free PMC Article
Kerkeni H, Brügger D, Mantokoudis G, Abegg M, Zee DS
Am J Case Rep 2022 Jul 3;23:e935148. doi: 10.12659/AJCR.935148. PMID: 35780294Free PMC Article
Nerrant E, Abouaf L, Pollet-Villard F, Vie AL, Vukusic S, Berthiller J, Colombet B, Vighetto A, Tilikete C
J Neuroophthalmol 2020 Jun;40(2):198-206. doi: 10.1097/WNO.0000000000000807. PMID: 31169568
Tilikete C, Jasse L, Pelisson D, Vukusic S, Durand-Dubief F, Urquizar C, Vighetto A
Neurology 2011 May 10;76(19):1650-7. doi: 10.1212/WNL.0b013e318219fa9c. PMID: 21555732
Lopez LI, Bronstein AM, Gresty MA, Du Boulay EP, Rudge P
Brain 1996 Apr;119 ( Pt 2):465-72. doi: 10.1093/brain/119.2.465. PMID: 8800942

Recent systematic reviews

Rowe FJ, Hanna K, Evans JR, Noonan CP, Garcia-Finana M, Dodridge CS, Howard C, Jarvis KA, MacDiarmid SL, Maan T, North L, Rodgers H
Cochrane Database Syst Rev 2018 Mar 5;3(3):CD011290. doi: 10.1002/14651858.CD011290.pub2. PMID: 29505103Free PMC Article
Mohamed W, Neil E, Kupsky WJ, Juhász C, Mittal S, Santhakumar S
J Neurol Sci 2011 Sep 15;308(1-2):1-8. Epub 2011 Jun 22 doi: 10.1016/j.jns.2011.05.029. PMID: 21696776

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