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Vertigo

MedGen UID:
53006
Concept ID:
C0042571
Sign or Symptom
Synonyms: Sensation, Spinning; Sensations, Spinning; Spinning Sensation; Spinning Sensations; Subjective Vertigo; Subjective Vertigos; Vertigo, Subjective; Vertigos; Vertigos, Subjective
SNOMED CT: Subjective vertigo (399090003); Vertigo (399153001); Rotation of self (399090003); Feel I'm spinning round (399090003); Rotary vertigo (399153001); Rotatory vertigo (399153001); Vertigo (spinning sensation) (399153001)
 
HPO: HP:0002321

Definition

An abnormal sensation of spinning while the body is actually stationary. [from HPO]

Conditions with this feature

Von Hippel-Lindau syndrome
MedGen UID:
42458
Concept ID:
C0019562
Disease or Syndrome
Von Hippel-Lindau (VHL) syndrome is characterized by hemangioblastomas of the brain, spinal cord, and retina; renal cysts and clear cell renal cell carcinoma; pheochromocytoma, pancreatic cysts, and neuroendocrine tumors; endolymphatic sac tumors; and epididymal and broad ligament cysts. Cerebellar hemangioblastomas may be associated with headache, vomiting, gait disturbances, or ataxia. Spinal hemangioblastomas and related syrinx usually present with pain. Sensory and motor loss may develop with cord compression. Retinal hemangioblastomas may be the initial manifestation of VHL syndrome and can cause vision loss. Renal cell carcinoma occurs in about 70% of individuals with VHL and is the leading cause of mortality. Pheochromocytomas can be asymptomatic but may cause sustained or episodic hypertension. Pancreatic lesions often remain asymptomatic and rarely cause endocrine or exocrine insufficiency. Endolymphatic sac tumors can cause hearing loss of varying severity, which can be a presenting symptom. Cystadenomas of the epididymis are relatively common. They rarely cause problems, unless bilateral, in which case they may result in infertility.
Meniere disease
MedGen UID:
7530
Concept ID:
C0025281
Disease or Syndrome
Meniere disease is a chronic illness characterized by intermittent episodes of vertigo lasting from minutes to hours, with fluctuating sensorineural hearing loss, tinnitus, and aural pressure (Sajjadi and Paparella, 2008).
Neurofibromatosis, type 2
MedGen UID:
18014
Concept ID:
C0027832
Neoplastic Process
Neurofibromatosis 2 (NF2) is characterized by bilateral vestibular schwannomas with associated symptoms of tinnitus, hearing loss, and balance dysfunction. The average age of onset is 18 to 24 years. Almost all affected individuals develop bilateral vestibular schwannomas by age 30 years. Affected individuals may also develop schwannomas of other cranial and peripheral nerves, meningiomas, ependymomas, and, very rarely, astrocytomas. Because NF2 is considered an adult-onset disease, it may be underrecognized in children, in whom skin tumors and ocular findings (retinal hamartoma, thickened optic nerves, cortical wedge cataracts, third cranial nerve palsy) may be the first manifestations. Mononeuropathy that occurs in childhood is an increasingly recognized finding; it frequently presents as a persistent facial palsy or hand/foot drop.
Benign paroxysmal positional vertigo
MedGen UID:
57837
Concept ID:
C0155502
Disease or Syndrome
Benign recurrent vertigo (BRV), also known as benign paroxysmal positional vertigo (BPPV), is a common disorder affecting up to 2% of the adult population. The majority of individuals with chronic recurrent vertigo have no identifiable cause, no progression of the disorder, and no other neurologic or auditory signs. Many families have multiple affected individuals, suggesting familial transmission of the disorder with moderate to high penetrance (summary by Lee et al., 2006).
Familial hypokalemia-hypomagnesemia
MedGen UID:
75681
Concept ID:
C0268450
Disease or Syndrome
Gitelman syndrome is an autosomal recessive renal tubular salt-wasting disorder characterized by hypokalemic metabolic alkalosis with hypomagnesemia and hypocalciuria. It is the most common renal tubular disorder among Caucasians (prevalence of 1 in 40,000). Most patients have onset of symptoms as adults, but some can present in childhood. Clinical features include transient periods of muscle weakness and tetany, abdominal pains, and chondrocalcinosis (summary by Glaudemans et al., 2012). Gitelman syndrome is sometimes referred to as a mild variant of classic Bartter syndrome (607364). For a discussion of genetic heterogeneity of Bartter syndrome, see 607364.
Diabetes-deafness syndrome maternally transmitted
MedGen UID:
90979
Concept ID:
C0342289
Disease or Syndrome
Maternally inherited diabetes-deafness syndrome (MIDD) is a mitochondrial disorder characterized by onset of sensorineural hearing loss and diabetes in adulthood. Some patients may have additional features observed in mitochondrial disorders, including pigmentary retinopathy, ptosis, cardiomyopathy, myopathy, renal problems, and neuropsychiatric symptoms (Ballinger et al., 1992; Reardon et al., 1992; Guillausseau et al., 2001). The association of diabetes and deafness is observed with Wolfram syndrome (see 222300), Rogers syndrome (249270), and Herrmann syndrome (172500), but all 3 of these disorders have other clinical manifestations.
Hyperimmunoglobulin D with periodic fever
MedGen UID:
140768
Concept ID:
C0398691
Disease or Syndrome
Mevalonate kinase deficiency is a condition characterized by recurrent episodes of fever, which typically begin during infancy. Each episode of fever lasts about 3 to 6 days, and the frequency of the episodes varies among affected individuals. In childhood the fevers seem to be more frequent, occurring as often as 25 times a year, but as the individual gets older the episodes occur less often.\n\nMevalonate kinase deficiency has additional signs and symptoms, and the severity depends on the type of the condition. There are two types of mevalonate kinase deficiency: a less severe type called hyperimmunoglobulinemia D syndrome (HIDS) and a more severe type called mevalonic aciduria (MVA).\n\nDuring episodes of fever, people with HIDS typically have enlargement of the lymph nodes (lymphadenopathy), abdominal pain, joint pain, diarrhea, skin rashes, and headache. Occasionally they will have painful sores called aphthous ulcers around their mouth. In females, these may also occur around the vagina. Rarely, people with HIDS develop a buildup of protein deposits (amyloidosis) in the kidneys that can lead to kidney failure. Fever episodes in individuals with HIDS can be triggered by vaccinations, surgery, injury, or stress. Most people with HIDS have abnormally high levels of immune system proteins called immunoglobulin D (IgD) and immunoglobulin A (IgA) in the blood. It is unclear why some people with HIDS have high levels of IgD and IgA and some do not. Elevated levels of these immunoglobulins do not appear to cause any signs or symptoms. Individuals with HIDS do not have any signs and symptoms of the condition between fever episodes and typically have a normal life expectancy.\n\nPeople with MVA have signs and symptoms of the condition at all times, not just during episodes of fever. Affected children have developmental delay, problems with movement and balance (ataxia), recurrent seizures (epilepsy), progressive problems with vision, and failure to gain weight and grow at the expected rate (failure to thrive). Individuals with MVA typically have an unusually small, elongated head. In childhood or adolescence, affected individuals may develop eye problems such as inflammation of the eye (uveitis), a blue tint in the white part of the eye (blue sclera), an eye disorder called retinitis pigmentosa that causes vision loss, or clouding of the lens of the eye (cataracts). Affected adults may have short stature and may develop muscle weakness (myopathy) later in life. During fever episodes, people with MVA may have an enlarged liver and spleen (hepatosplenomegaly), lymphadenopathy, abdominal pain, diarrhea, and skin rashes. Children with MVA who are severely affected with multiple problems may live only into early childhood; mildly affected individuals may have a normal life expectancy.
Chiari type I malformation
MedGen UID:
196689
Concept ID:
C0750929
Congenital Abnormality
Arnold-Chiari type I malformation refers to a relatively mild degree of herniation of the posteroinferior region of the cerebellum (the cerebellar tonsils) into the cervical canal with little or no displacement of the fourth ventricle. It is characterized by one or both pointed (not rounded) cerebellar tonsils that project 5 mm below the foramen magnum, measured by a line drawn from the basion to the opisthion (McRae Line)
Cholestasis-pigmentary retinopathy-cleft palate syndrome
MedGen UID:
208652
Concept ID:
C0795969
Disease or Syndrome
MED12-related disorders include the phenotypes of FG syndrome type 1 (FGS1), Lujan syndrome (LS), X-linked Ohdo syndrome (XLOS), Hardikar syndrome (HS), and nonspecific intellectual disability (NSID). FGS1 and LS share the clinical findings of cognitive impairment, hypotonia, and abnormalities of the corpus callosum. FGS1 is further characterized by absolute or relative macrocephaly, tall forehead, downslanted palpebral fissures, small and simple ears, constipation and/or anal anomalies, broad thumbs and halluces, and characteristic behavior. LS is further characterized by large head, tall thin body habitus, long thin face, prominent nasal bridge, high narrow palate, and short philtrum. Carrier females in families with FGS1 and LS are typically unaffected. XLOS is characterized by intellectual disability, blepharophimosis, and facial coarsening. HS has been described in females with cleft lip and/or cleft palate, biliary and liver anomalies, intestinal malrotation, pigmentary retinopathy, and coarctation of the aorta. Developmental and cognitive concerns have not been reported in females with HS. Pathogenic variants in MED12 have been reported in an increasing number of males and females with NSID, with affected individuals often having clinical features identified in other MED12-related disorders.
Episodic ataxia type 1
MedGen UID:
318554
Concept ID:
C1719788
Disease or Syndrome
Episodic ataxia type 1 (EA1) is a potassium channelopathy characterized by constant myokymia and dramatic episodes of spastic contractions of the skeletal muscles of the head, arms, and legs with loss of both motor coordination and balance. During attacks individuals may experience a number of variable symptoms including vertigo, blurred vision, diplopia, nausea, headache, diaphoresis, clumsiness, stiffening of the body, dysarthric speech, and difficulty in breathing, among others. EA1 may be associated with epilepsy. Other possible associations include delayed motor development, cognitive disability, choreoathetosis, and carpal spasm. Usually, onset is in childhood or early adolescence.
Episodic ataxia type 2
MedGen UID:
314039
Concept ID:
C1720416
Disease or Syndrome
Episodic ataxia is a genetically heterogeneous neurologic condition characterized by spells of incoordination and imbalance, often associated with progressive ataxia. Episodic ataxia type 2 is the most common form of EA (Jen et al., 2007). For a discussion of genetic heterogeneity of episodic ataxia, see EA1 (160120).
Autosomal dominant nonsyndromic hearing loss 9
MedGen UID:
371327
Concept ID:
C1832425
Disease or Syndrome
DFNA9 is an autosomal dominant adult-onset form of progressive sensorineural hearing loss associated with variable vestibular dysfunction (summary by Robertson et al., 2006).
Autosomal dominant nonsyndromic hearing loss 11
MedGen UID:
331297
Concept ID:
C1832475
Disease or Syndrome
Autosomal dominant deafness-11 is a nonsyndromic form of progressive neurosensory hearing loss with postlingual onset. Some affected individuals have mild vestibular symptoms (summary by Sun et al., 2011).
Hypertrophic cardiomyopathy 10
MedGen UID:
331754
Concept ID:
C1834460
Disease or Syndrome
Any hypertrophic cardiomyopathy in which the cause of the disease is a mutation in the MYL2 gene.
Syncope, familial vasovagal
MedGen UID:
373086
Concept ID:
C1836438
Disease or Syndrome
Vasovagal syncope (VVS) is an exaggerated tendency toward the common faint caused by a sudden and profound hypotension with or without bradycardia. Several lines of evidence indicate central and peripheral abnormalities of sympathetic function. Newton et al. (2005) stated that a definitive diagnosis of VVS is made only when a patient has reproduction of symptoms in association with hypotension or bradycardia. The head up tilt (HUT) test is the investigation carried out to induce these hemodynamic changes (Parry and Kenny, 1999). This disorder may be the same as Streeten-type orthostatic hypotensive disorder (143850).
Alpha-N-acetylgalactosaminidase deficiency type 2
MedGen UID:
324539
Concept ID:
C1836522
Disease or Syndrome
Alpha-N-acetylgalactosaminidase (NAGA) deficiency is a very rare lysosomal storage disorder with atypical features. It is clinically heterogeneous with 3 main phenotypes: type I is an infantile-onset neuroaxonal dystrophy (609241); type II, also known as Kanzaki disease, is an adult-onset disorder characterized by angiokeratoma corporis diffusum and mild intellectual impairment; and type III is an intermediate disorder (see 609241) with mild to moderate neurologic manifestations (Desnick and Schindler, 2001).
Autosomal recessive nonsyndromic hearing loss 2
MedGen UID:
325485
Concept ID:
C1838701
Disease or Syndrome
Any autosomal recessive nonsyndromic deafness in which the cause of the disease is a mutation in the MYO7A gene.
Episodic ataxia type 3
MedGen UID:
376220
Concept ID:
C1847839
Disease or Syndrome
A very rare form of hereditary episodic ataxia with characteristics of vestibular ataxia, vertigo, tinnitus and interictal myokymia.
Episodic ataxia type 4
MedGen UID:
376222
Concept ID:
C1847843
Disease or Syndrome
A very rare form of hereditary episodic ataxia with characteristics of late-onset episodic ataxia, recurrent attacks of vertigo and diplopia.
Migraine, familial hemiplegic, 2
MedGen UID:
355962
Concept ID:
C1865322
Disease or Syndrome
Familial hemiplegic migraine (FHM) falls within the category of migraine with aura. In migraine with aura (including FHM) the neurologic symptoms of aura are unequivocally localizable to the cerebral cortex or brain stem and include visual disturbance (most common), sensory loss (e.g., numbness or paresthesias of the face or an extremity), and dysphasia (difficulty with speech). FHM must include motor involvement, such as hemiparesis (weakness of an extremity). Hemiparesis occurs with at least one other symptom during FHM aura. Neurologic deficits with FHM attacks can be prolonged for hours to days and may outlast the associated migrainous headache. FHM is often earlier in onset than typical migraine, frequently beginning in the first or second decade; the frequency of attacks tends to decrease with age. Approximately 40%-50% of families with CACNA1A-FHM have cerebellar signs ranging from nystagmus to progressive, usually late-onset mild ataxia.
Episodic ataxia type 5
MedGen UID:
356142
Concept ID:
C1866039
Disease or Syndrome
An extremely rare form of hereditary episodic ataxia with characteristics of recurrent episodes of vertigo and ataxia lasting several hours.
Episodic ataxia type 6
MedGen UID:
390739
Concept ID:
C2675211
Disease or Syndrome
An exceedingly rare form of hereditary episodic ataxia with varying degrees of ataxia and associated findings including slurred speech, headache, confusion and hemiplegia.
Episodic ataxia type 7
MedGen UID:
383209
Concept ID:
C2677843
Disease or Syndrome
Episodic ataxia is a group of related conditions that affect the nervous system and cause problems with movement and coordination. People with episodic ataxia have episodes of poor coordination and balance (ataxia). During these episodes, many people also experience dizziness (vertigo), nausea and vomiting, migraines, blurred or double vision, slurred speech, and ringing in the ears (tinnitus). Seizures, muscle weakness, and paralysis that affect one side of the body (hemiplegia) may also occur during these episodes. \n\nResearchers have identified at least 11 types of episodic ataxia, distinguished by their pattern of signs and symptoms, age of onset, length of episodes, and genetic cause.\n\nAdditionally, a muscle abnormality called myokymia or an eye abnormality called nystagmus can occur during or between episodes. Myokymia causes muscle cramping; stiffness; or continuous, fine muscle twitching that appears as rippling under the skin. Nystagmus refers to rapid, involuntary eye movements.\n\nEpisodes of ataxia and other symptoms can begin anytime from early childhood to adulthood. They can be triggered by environmental factors such as stress, caffeine, alcohol, certain medications, physical activity, and illness. The duration of episodes may vary from seconds to days, and the frequency ranges from several episodes per day to one or two every few months. Between episodes, affected individuals may have no signs or symptoms. However, some continue to experience ataxia, which may worsen over time.\n\nSome children with episodic ataxia have delayed development of speech or motor skills, such as standing and walking. They may also have learning difficulties.
Renal hypomagnesemia 6
MedGen UID:
462645
Concept ID:
C3151295
Disease or Syndrome
Craniofacial anomalies and anterior segment dysgenesis syndrome
MedGen UID:
481729
Concept ID:
C3280099
Disease or Syndrome
Childhood encephalopathy due to thiamine pyrophosphokinase deficiency
MedGen UID:
482496
Concept ID:
C3280866
Disease or Syndrome
Thiamine metabolism dysfunction syndrome-5 (THMD5) is an autosomal recessive metabolic disorder due to an inborn error of thiamine metabolism. The phenotype is highly variable, but in general, affected individuals have onset in early childhood of acute encephalopathic episodes associated with increased serum and CSF lactate. These episodes result in progressive neurologic dysfunction manifest as gait disturbances, ataxia, dystonia, and spasticity, which in some cases may result in loss of ability to walk. Cognitive function is usually preserved, although mildly delayed development has been reported. These episodes are usually associated with infection and metabolic decompensation. Some patients may have recovery of some neurologic deficits (Mayr et al., 2011). For a discussion of genetic heterogeneity of disorders due to thiamine metabolism dysfunction, see THMD1 (249270).
Catecholaminergic polymorphic ventricular tachycardia 4
MedGen UID:
766961
Concept ID:
C3554047
Disease or Syndrome
Catecholaminergic polymorphic ventricular tachycardia (CPVT) is characterized by episodic syncope occurring during exercise or acute emotion. The underlying cause of these episodes is the onset of fast ventricular tachycardia (bidirectional or polymorphic). Spontaneous recovery may occur when these arrhythmias self-terminate. In other instances, ventricular tachycardia may degenerate into ventricular fibrillation and cause sudden death if cardiopulmonary resuscitation is not readily available. The mean onset of symptoms (usually a syncopal episode) is between age seven and 12 years; onset as late as the fourth decade of life has been reported. If untreated, CPVT is highly lethal, as approximately 30% of affected individuals experience at least one cardiac arrest and up to 80% have one or more syncopal spells. Sudden death may be the first manifestation of the disease.
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.
Primary familial polycythemia due to EPO receptor mutation
MedGen UID:
1641215
Concept ID:
C4551637
Disease or Syndrome
Primary familial and congenital polycythemia (PFCP) is characterized by isolated erythrocytosis in an individual with a normal-sized spleen and absence of disorders causing secondary erythrocytosis. Clinical manifestations relate to the erythrocytosis and can include plethora, the hyperviscosity syndrome (headache, dizziness, fatigue, lassitude, visual and auditory disturbances, paresthesia, myalgia), altered mental status caused by hypoperfusion and local hypoxia, and arterial and/or venous thromboembolic events. Although the majority of individuals with PFCP have only mild manifestations of hyperviscosity such as dizziness or headache, some affected individuals have had severe and even fatal complications including arterial hypertension, intracerebral hemorrhage, deep vein thrombosis, coronary disease, and myocardial infarction. To date 116 affected individuals from 24 families have been reported.
GCGR-related hyperglucagonemia
MedGen UID:
1677024
Concept ID:
C4763635
Disease or Syndrome
Mahvash disease (MVAH) is an autosomal recessive disorder caused by inactivating mutations in the glucagon receptor, leading to alpha-cell hyperplasia of the pancreas, hyperglucagonemia without glucagonoma syndrome, and occasional hypoglycemia. The disease may lead to glucagonomas and/or primitive neuroectodermal tumors (PNETs).
Episodic ataxia, type 9
MedGen UID:
1714171
Concept ID:
C5394520
Disease or Syndrome
Episodic ataxia type 9 (EA9) is a neurologic disorder characterized by onset of ataxic episodes in the first years of life. Features may include difficulty walking, dizziness, slurred speech, headache, vomiting, and pain. The ataxic episodes vary in frequency and duration; most tend to occur every few weeks or months and last minutes to hours. Prior to the EA, most patients have neonatal- or infantile-onset tonic or generalized tonic-clonic (GTC) seizures that may be severe and refractory to medication, but remit later in infancy or early childhood, either spontaneously or concurrently with medication. Some patients have mildly delayed development with speech delay and/or autistic features or mildly impaired intellectual development. However, others show normal psychomotor development. Treatment of the ataxic episodes with acetazolamide is effective in about 50% of patients (summary by Schwarz et al., 2019). For a phenotypic description and discussion of genetic heterogeneity of episodic ataxia, see EA1 (160120).
Neurodegeneration with ataxia and late-onset optic atrophy
MedGen UID:
1779901
Concept ID:
C5543254
Disease or Syndrome
Neurodegeneration with ataxia and late-onset optic atrophy (NDAXOA) is an autosomal dominant disorder with somewhat variable manifestations. Most affected individuals present in mid-adulthood with slowly progressive cerebellar and gait ataxia, optic atrophy, and myopathy or myalgia. Some patients may have a childhood history of neurologic features, including limited extraocular movements. Additional features can include cardiomyopathy, psychiatric disturbances, and peripheral sensory impairment (summary by Taylor et al., 1996 and Courage et al., 2017).

Professional guidelines

PubMed

Chandrasekhar SS, Tsai Do BS, Schwartz SR, Bontempo LJ, Faucett EA, Finestone SA, Hollingsworth DB, Kelley DM, Kmucha ST, Moonis G, Poling GL, Roberts JK, Stachler RJ, Zeitler DM, Corrigan MD, Nnacheta LC, Satterfield L
Otolaryngol Head Neck Surg 2019 Aug;161(1_suppl):S1-S45. doi: 10.1177/0194599819859885. PMID: 31369359
Magnan J, Özgirgin ON, Trabalzini F, Lacour M, Escamez AL, Magnusson M, Güneri EA, Guyot JP, Nuti D, Mandalà M
J Int Adv Otol 2018 Aug;14(2):317-321. doi: 10.5152/iao.2018.140818. PMID: 30256205Free PMC Article
Bhattacharyya N, Gubbels SP, Schwartz SR, Edlow JA, El-Kashlan H, Fife T, Holmberg JM, Mahoney K, Hollingsworth DB, Roberts R, Seidman MD, Steiner RW, Do BT, Voelker CC, Waguespack RW, Corrigan MD
Otolaryngol Head Neck Surg 2017 Mar;156(3_suppl):S1-S47. doi: 10.1177/0194599816689667. PMID: 28248609

Recent clinical studies

Etiology

Kim JS, Newman-Toker DE, Kerber KA, Jahn K, Bertholon P, Waterston J, Lee H, Bisdorff A, Strupp M
J Vestib Res 2022;32(3):205-222. doi: 10.3233/VES-210169. PMID: 35367974Free PMC Article
Zwergal A, Feil K, Schniepp R, Strupp M
Semin Neurol 2020 Feb;40(1):87-96. Epub 2019 Dec 30 doi: 10.1055/s-0039-3400315. PMID: 31887755
Alyono JC
Otolaryngol Clin North Am 2018 Aug;51(4):725-740. Epub 2018 May 24 doi: 10.1016/j.otc.2018.03.003. PMID: 29803531
Choi JY, Lee SH, Kim JS
Curr Opin Neurol 2018 Feb;31(1):81-89. doi: 10.1097/WCO.0000000000000511. PMID: 29084063
Neuhauser HK
Handb Clin Neurol 2016;137:67-82. doi: 10.1016/B978-0-444-63437-5.00005-4. PMID: 27638063

Diagnosis

Kim HJ, Park J, Kim JS
J Neurol 2021 May;268(5):1995-2000. Epub 2020 Nov 24 doi: 10.1007/s00415-020-10314-7. PMID: 33231724Free PMC Article
Omron R
Emerg Med Clin North Am 2019 Feb;37(1):11-28. doi: 10.1016/j.emc.2018.09.004. PMID: 30454774
Choi JY, Lee SH, Kim JS
Curr Opin Neurol 2018 Feb;31(1):81-89. doi: 10.1097/WCO.0000000000000511. PMID: 29084063
Dommaraju S, Perera E
Aust Fam Physician 2016 Apr;45(4):190-4. PMID: 27052132
Li Y, Peng B
Pain Physician 2015 Jul-Aug;18(4):E583-95. PMID: 26218949

Therapy

Rhee TG, Shim SR, Forester BP, Nierenberg AA, McIntyre RS, Papakostas GI, Krystal JH, Sanacora G, Wilkinson ST
JAMA Psychiatry 2022 Dec 1;79(12):1162-1172. doi: 10.1001/jamapsychiatry.2022.3352. PMID: 36260324Free PMC Article
Lima TM, Visacri MB, Aguiar PM
Eur J Clin Pharmacol 2022 Mar;78(3):311-338. Epub 2021 Oct 27 doi: 10.1007/s00228-021-03216-8. PMID: 34705064
Strupp M, Dlugaiczyk J, Ertl-Wagner BB, Rujescu D, Westhofen M, Dieterich M
Dtsch Arztebl Int 2020 Apr 24;117(17):300-310. doi: 10.3238/arztebl.2020.0300. PMID: 32530417Free PMC Article
Onakpoya IJ, Thomas ET, Lee JJ, Goldacre B, Heneghan CJ
BMJ Open 2019 Jan 21;9(1):e023600. doi: 10.1136/bmjopen-2018-023600. PMID: 30670513Free PMC Article
Murdin L, Hussain K, Schilder AG
Cochrane Database Syst Rev 2016 Jun 21;2016(6):CD010696. doi: 10.1002/14651858.CD010696.pub2. PMID: 27327415Free PMC Article

Prognosis

Kanyılmaz T, Topuz O, Ardıç FN, Alkan H, Öztekin SNS, Topuz B, Ardıç F
Braz J Otorhinolaryngol 2022 Nov-Dec;88 Suppl 3(Suppl 3):S41-S49. Epub 2021 Oct 26 doi: 10.1016/j.bjorl.2021.08.010. PMID: 34799265Free PMC Article
Lou Y, Cai M, Xu L, Wang Y, Zhuang L, Liu X
Am J Otolaryngol 2020 May-Jun;41(3):102412. Epub 2020 Feb 4 doi: 10.1016/j.amjoto.2020.102412. PMID: 32057490
Adrion C, Fischer CS, Wagner J, Gürkov R, Mansmann U, Strupp M; BEMED Study Group
BMJ 2016 Jan 21;352:h6816. doi: 10.1136/bmj.h6816. PMID: 26797774Free PMC Article
James AL, Thorp MA
BMJ Clin Evid 2007 Mar 1;2007 PMID: 19454061Free PMC Article
Leliever WC, Barber HO
Laryngoscope 1981 Jan;91(1):1-6. doi: 10.1288/00005537-198101000-00001. PMID: 6969834

Clinical prediction guides

Uz U, Uz D, Akdal G, Çelik O
J Int Adv Otol 2019 Dec;15(3):420-424. doi: 10.5152/iao.2019.6483. PMID: 31846923Free PMC Article
Kattah JC
Stroke Vasc Neurol 2018 Dec;3(4):190-196. Epub 2018 Jun 23 doi: 10.1136/svn-2018-000160. PMID: 30637123Free PMC Article
Strupp M, Lopez-Escamez JA, Kim JS, Straumann D, Jen JC, Carey J, Bisdorff A, Brandt T
J Vestib Res 2016;26(5-6):409-415. doi: 10.3233/VES-160589. PMID: 28262641Free PMC Article
Neuhauser HK
Handb Clin Neurol 2016;137:67-82. doi: 10.1016/B978-0-444-63437-5.00005-4. PMID: 27638063
Kuhn M, Heman-Ackah SE, Shaikh JA, Roehm PC
Trends Amplif 2011 Sep;15(3):91-105. Epub 2011 May 22 doi: 10.1177/1084713811408349. PMID: 21606048Free PMC Article

Recent systematic reviews

Rhee TG, Shim SR, Forester BP, Nierenberg AA, McIntyre RS, Papakostas GI, Krystal JH, Sanacora G, Wilkinson ST
JAMA Psychiatry 2022 Dec 1;79(12):1162-1172. doi: 10.1001/jamapsychiatry.2022.3352. PMID: 36260324Free PMC Article
Jafari Z, Kolb BE, Mohajerani MH
Can J Neurol Sci 2022 Mar;49(2):184-195. Epub 2021 Apr 12 doi: 10.1017/cjn.2021.63. PMID: 33843530Free PMC Article
Fancello V, Hatzopoulos S, Corazzi V, Bianchini C, Skarżyńska MB, Pelucchi S, Skarżyński PH, Ciorba A
Int J Immunopathol Pharmacol 2021 Jan-Dec;35:20587384211027373. doi: 10.1177/20587384211027373. PMID: 34142589Free PMC Article
Murdin L, Hussain K, Schilder AG
Cochrane Database Syst Rev 2016 Jun 21;2016(6):CD010696. doi: 10.1002/14651858.CD010696.pub2. PMID: 27327415Free PMC Article
Tassinari M, Mandrioli D, Gaggioli N, Roberti di Sarsina P
Audiol Neurootol 2015;20(3):153-65. Epub 2015 Mar 31 doi: 10.1159/000375393. PMID: 25832807

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