Author(s): Steven Siano, MD, Lee Shuping, MD, K. Rao Poduri, MD
Originally published: April 12, 2016 Last updated: April 29, 2021
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Disease/ Disorder

Definition

Vertigo is a sensation of rotation or movement of one’s self (subjective vertigo) or of one’s surroundings (objective vertigo) in any plane. Vertigo may result from diseases of the inner ear or from disturbance from the vestibular pathways in the central nervous system.

Dizziness is a non-specific term used by patients to describe symptoms of impaired spatial perception and imbalance.

Disequilibrium is a feeling of unsteadiness or imbalance on standing or walking and may be due to visual or proprioceptive abnormalities.

Etiology

Dizziness may have a multi factorial origin and can be commonly associated with the following disorders: vertigo, disequilibrium, pre-syncope, and non-specific dizziness.

 The focus here is Vertigo.

Vertigo:

  • Benign paroxysmal positional vertigo (BPPV)
  • Vestibular neuritis
  • Meniere’s disease
  • Vestibular migraine
  • Acoustic neuroma
  • Stroke
  • Multiple sclerosis
  • Cervical arthritis

Disequilibrium:

  • Peripheral neuropathy
  • Visual impairment
  • Vestibular dysfunction
  • Neurologic/neuromuscular disease (CVA, Cerebellar disorders, Parkinson’s disease)
  • Arthritis

Pre-syncope:

  • Orthostatic hypotension
  • Cardiomyopathy
  • Aortic Stenosis
  • Arrhythmia
  • Dys-autonomia
  • Post-prandial hypotension
  • Pharmacologic

Non-specific dizziness:

  • Pharmacologic (cardiac, CNS, urologic)
  • Psychological
  • Metabolic (Diabetes Mellitus, Hypothyroid)
  • Infectious
  • Hyperthermia

Epidemiology including risk factors and primary prevention

  • Precise data on the incidence and prevalence of dizziness is largely unknown1, 2. Overall incidence is estimated between 5-15% US population and approaches 40% after the age of 40 3.Dizziness due to vestibular and psychogenic causes constitutes more than 70% of cases. Serious causes are found in a minority of patients and no cause is found in 7% of cases 4.
  • Dizziness is the primary complaint in 43% of emergency department visits every year 5, 6. Acute dizziness is most often caused by benign conditions, such as peripheral vertigo, orthostatic hypotension, and psychogenic disorders, whereas serious neurologic conditions, such as stroke and brain tumors, are rare 7. Cardiovascular disease was found to be the most common major cause of dizziness in older adults in primary care. Twenty five percent of these patients experience an adverse drug effect causing dizziness 8.
  • Otologic disorders account for 30-50% of all identifiable causes of dizziness, followed by syncopal/disequilibrium (25%), psychiatric (15%) and central brainstem vestibular lesions (10%)
  • Stroke accounts for 3-7% among all causes of vertigo 9.
    • The elderly have the highest of central causes of vertigo (20%) and is most often attributable to stroke. The prevalence of dizziness in the older adults (age > 65) ranges from 4-30%. Prevalence increases by 10% for every 5 years of age thereafter.

Risk Factors

  • Age: > 65 years old are at risk due to an increase in medical conditions and their use of medications.
  • Medications:  Anti-seizure medications, anti-hypertensives, anti-depressants, barbiturates, cocaine, diuretics, nitroglycerin, quinine, salicylates, ototoxic drugs, sedatives, and tranquilizers can cause dizziness.
  • A past episode of dizziness may predispose to recurrence
  • History of migraines, CVD/risk, Trauma, Psychosocial stress/depression and exposure to toxins.

Patho-anatomy/physiology

  • Dependent on the underlying specific cause of dizziness.
  • Dizziness is a sensation of postural instability. Cerebral cortex and cerebellum integrate sensory information obtained from the visual, auditory, vestibular and proprioceptive systems to maintain balance and equilibrium through appropriately coordinated motor responses 10. Disturbance in any of these individual components or the pathways that connect them may result in dizziness. The differential diagnosis of vertigo includes both peripheral vestibular causes (i.e., those originating in the peripheral nervous system) and, central vestibular causes (i.e., those originating in the central nervous system).
  • Blood perfusion to the brainstem, cerebellum and inner ear arise from the vertebra-basilar system.  Those who present with nausea and vomiting with vertigo and nystagmus may be presenting with symptoms of stroke in the posterior fossa from arterial occlusion or rupture of the vertebro-basilar system. However, the signs and symptoms as a manifestation of stroke associated with dizziness and vertigo may vary depending on the affected vascular territory. In the emergency room, presentation with acute onset central vertigo (a subtype of dizziness) should include stroke or transient ischemic attacks in their differential. Due to the overlapping of symptoms, it is hard to differentiate between vascular vertigo and other causes of vertigo . The most common causes of vertigo are benign paroxysmal positional vertigo (BPPV) and Meniere disease; both of them are inner ear disorders, while other causes of vertigo are central vestibular lesions such as cerebrovascular disease and acoustic neuroma are also to be kept in the differential.
  • Dizziness may be of cardiovascular origin. State of consciousness is maintained by adequate cerebral blood flow. Cardiac syncope results from inadequate effective cardiac output and may be due to serious underlying structural heart disease or arrhythmia. Arrhythmias are the most frequent causes of syncope and dizziness. Syncope from arrhythmia results from ventricular tachycardia, which accounts for 11% of all cases of syncope11 Vasovagal syncope can be caused by acute stress or fear and is also seen in anxiety, panic, and major depressive disorders.

Disease progression including natural history, disease phases or stages, disease trajectory (clinical features and presentation over time)

Depends on the etiology and its progression that is responsible for dizziness.

New onset/Acute
Acute unilateral injury to peripheral or central vestibular structures present as acute vestibular syndrome consisting of severe vertigo, nausea and vomiting, spontaneous nystagmus, and postural instability12 .

Healthy young people usually have a benign and self-limited course with acute vertigo. Persons with risk factors for stroke who do not have the typical findings of spontaneous nystagmus and postural instability should be evaluated promptly for a cerebellar stroke with imaging.

Sub-acute
N/A

Chronic/Stable:
Up to 30% of patients who experience episodic balance problems develop persistent unsteadiness or dizziness. Treatment consists of pharmacotherapy, vestibular and balance rehabilitation therapy (VBRT) as mentioned below. VBRT is an excellent habituation/desensitization program for chronic dizziness. In addition, cognitive-behavioral therapy may be helpful for dizziness due to anxiety or depression 13.

Pre-terminal
About 3% to 5% of American adults have recurrent bouts of dizziness and 1% have complains of persistent dizziness.

Specific Secondary or Associated conditions and complications

Secondary conditions: Age, migraine, hyperlipidemia hypertension, and stroke were independently associated with BPPV14.

Complications: Dizziness can interfere with driving, work, and lifestyle. Dizziness is incapacitating and leads to decreased productivity, clinical depression, and falls with injuries including hip fractures.

Essentials of Assessment

History

Interview should be focused on patients’ description of symptoms and/or sensations experienced, and should include time course, provoking and aggravating factors, recent trauma, as well as associated symptoms. Additional history should include prescribed medications, alcohol and caffeine consumption, and recreational drug use.

Common descriptions include by category 5

  • Vertigo: sensation of motion, “spinning”, “whirling” or “tilting”.
  • Disequilibrium: sensation of “imbalance” or “wobbly”
  • Pre-syncope: sensation of “passing out”, “blacking out” or “losing consciousness”
  • Non-specific dizziness: vague symptoms of “lightheadedness”, “giddy”, “faint” or “disconnected with environment”.

Physical Examination

Initial focus should include a comprehensive neurologic and cardiopulmonary examination, followed by supplemental testing used to provoke patient symptoms. This should include manual muscle testing, cranial nerve examination, spontaneous and gaze-evoked nystagmus, bedside vestibulo-ocular reflex assessment, positional testing, and gait and balance testing.

Clinical Functional Assessment: mobility, self-care cognition/behavior/affective state

A thorough history should include how patients’ symptoms impact mobility and ADLs. Additional information should be gathered on previous diagnoses of mood or psychiatric disorders as and present affective state. While no specific functional assessment has been shown to assist in the underlying diagnosis for dizziness, gait and balance testing should be standard for all examinations and will ultimately help the physiatrist generate a plan which best targets the patients ‘concerns.

Laboratory studies

Laboratory studies, including hormone and metabolic panels, are very low yield in diagnosing the cause of dizziness. In one meta-analysis, 0.6% (26 of 4,538) of patients had laboratory abnormalities 5.

Lab work with hemoglobin/hematocrit, Glucose, Electrolytes, BUN, Folic acid Vitamin B12 and Thyrotropin should be performed in all cases with chronic dizziness and Tilt table test for patients with syncope or postural hypotension. For vestibular disorders, electro-nystagmography, rotational testing and dynamic Post urography are helpful.  If arrhythmias are suspected, EKG, Holter and event monitoring ECHO and carotid Doppler should be done 10.

Imaging

Imaging is not beneficial unless an underlying neurologic abnormality is suspected5.

Supplemental assessment tools

  • Dix-Hallpike maneuver, a test for BPPV – involves rapidly moving the patient from a sitting position to “head hanging,” where the patient’s head is at least 10 degrees below horizontal. Onset of vertigo and nystagmus indicating a positive test
  • Orthostatic blood pressure
  • Otoscopy
  • Cervical active and passive range of motion
  • Romberg test
  • Hyperventilation
  • Caloric testing
  • Standardized psychological testing
  • CV testing: EKG /Holter, ECHO, carotid Doppler
  • Vision and Hearing testing

Early prediction of outcomes

Predictors of outcome are dependent on underlying cause for dizziness. Most causes of dizziness are benign and up 30% resolve spontaneously by two-weeks of symptom onset and up to 50% resolve by one-year15. The absence of early activity and/or rehabilitation may prolong recovery,

Environmental

N/A

Social role and social support system

For most causes of dizziness, the role of social supports is undetermined. In psychogenic or undetermined etiologies however, social and psychiatric support may have more of a definitive role in recovery, though this has not been studied.

Professional issues

Diagnosing dizziness is challenging, as it is a non-specific symptom associated with numerous possible underlying etiologies. A careful history and physical examination will usually point to the probable cause. Cardiovascular, neurologic, and laboratory testing should be guided by the clinical evaluation.

There are no established guidelines for when to make specialist referrals, when to do imaging studies, or when to make activity and/or rehabilitation recommendations. Multifactorial interventions will help chronic dizziness and assist in day to day functioning and quality of life.

Rehab Management and Treatments

Available or Current treatment Guidelines

  • Medical management of dizziness depends on its cause 16.
    • Dizziness from medication use responds to withdrawal or dose adjustments of the offending agent.
    • Vestibular suppressants, anticholinergics, antihistamines, benzodiazepines, calcium channel antagonists, sodium intake, beta-blockers, neurotransmitter pro-drugs and dopamine receptor antagonists give symptomatic relief of acute dizziness.
    • Compression stockings or abdominal binders may help with orthostasis
  • Rehabilitation program consists of 17,18
    • Investigation and Diagnosis
    • Rehabilitation Plan:
      • Correction of remediable problems such as hypotension, vascular disease should be addressed with appropriate measures. Consider referral to cardiology vs endocrinology, depending on clinical picture and description of symptoms.
      • Medications for vertigo and related disorders, such as prochlorperazine, promethazine, ondansetron, cyclizine or metoclopramide orally, intramuscularly or as a suppository are used as needed.  Diazepam reduces neural activity by CNS suppression and is an anxiolytic drug. Consider baseline EKG given the potential medication action on QTc19.
      • Specific exercise program: such as vestibular rehabilitation with exercises designed to provoke dizziness by repeating movements until not tolerated wherein the dizziness becomes worse; however, over weeks to months, the dizziness improves from central adaptation. This approach helps patients with peripheral and central vestibular dizziness.  Gait and balance exercises are part and parcel of the exercise program.
      • Visual rehabilitation to address visual tracking deficits, convergence/divergence disorders, and hyper sympathetic response to visual stimuli may be effective in treatment of visually mediated disequilibrium 20, 21.
      • Education on fall prevention and environmental safety with stair railings, grab bars, railings for toilet seats and removing the tethers are an important part of management of dizziness.
      • General fitness program
      • Realistic patient & family social and occupational goals

Different disease stages

New onset/Acute: The majority of causes of acute dizziness are due to vestibular dysfunction. For these cases, pharmacologic and surgical interventions are rarely curative. Medical management often serves to suppress secondary symptoms rather than to treat the underlying cause. There is strong evidence to suggest that vestibular rehabilitation in combination with physical/repositioning maneuvers (Canalith repositioning procedure) may resolve symptoms and improve function18.For most all other causes of dizziness the role of rehabilitation is unclear and medical management is aimed at treatment of the underlying cause.

Vestibular dysfunction: NA

Acute stage: Medication management is often used with the aim to suppress the vestibular system and treat associated symptoms such as nausea. Surgery is of little role in the acute setting. There is strong evidence to support vestibular rehabilitation in combination with physical maneuvers to treat symptoms and aid in longer-term functional recovery. There is moderate evidence that these effects may be maintained post-intervention.22

Sub-acute stage: There is no evidence detailing appropriate management for sub-acute dizziness, though it may be surmised that management would likely mirror that for chronic dizziness.

Chronic stage: Treatment consists of pharmacotherapy, vestibular and balance rehabilitation therapy (VBRT) (an exercise program performed at home by patients supervised by physical therapists), including the Epley maneuver (which involves sequential movement of the head into four positions, staying in each position for roughly 30 seconds) targeting visual dysfunction may be utilized at this point.

It is an excellent habituation/desensitization program for chronic dizziness. In addition, Cognitive-behavioral therapy may be helpful for dizziness due to anxiety and depression. 13

As with the acute stage, pharmacologic interventions play a limited role in the management of dizziness. Medication management is implemented to suppress symptoms and is not curative. 22 Vestibular rehabilitation is a non-invasive curative therapy shown to improve subjective measures of dizziness, balance, and gait performance, as well as, activities of daily living, and visual impairments (Cochrane review). Such rehabilitation therapies have been found to be superior to medication management in terms of improving symptoms. 22

Conditions such as superior canal dehiscence can be amenable to surgical intervention and should be managed by otolaryngology.23

Coordination of care:

Patient, family, and the treating team of physiatrists, Otolaryngologists, cardiologists, neuro-ophthalmologists, optometrists, endocrinologists and neurologists may play a role in team effort to manage dizziness

Patient and family education

Patients and family should be educated to be aware that dizziness can lead to loss of balance and falls with injuries. They should be advised to make their homes fall-proof by removing tripping hazards such as loose rugs, and long electrical cords. Emphasize to move slowly and avoid driving when they feel dizzy.

Management of treatment outcomes: including those that are impairment-based, activity participation-based and environmentally-based

  • Correction and amelioration of co-morbid conditions, polypharmacy, treating and avoidance of dehydration especially in the older adults.
  • Physical therapy for balance exercises, gait training and vestibular rehabilitation
  • Provision of gait aides such as canes and walkers for safe gait

Translation into practice: practice “pearls”/performance improvement in practice(PIPs) changes in clinical practice behaviors and skills)

Clinical Pearl: Head Impulse Test (HIT) (where in the examiner abruptly accelerates and then decelerates the head, moving the head in rapidly at high speed and then stopping it) is the most sensitive and specific bedside test for distinguishing central from peripheral causes in the acute vestibular syndrome when other focal neurologic or otologic findings are lacking 24 .

Gaps in the Evidence- Based Knowledge

The Canalith repositioning procedure (CRP) has been demonstrated to be very effective in the treatment of benign paroxysmal positional vertigo (BPPV); however, there is still some controversy concerning the necessity of treatment. Some physicians believe that dizziness is often benign and self-limited and hence no therapy is required.

The utilization of visual based therapies, especially in the setting of traumatic brain injury show promise, though larger scale research needs to be completed. This lack of population based evidence causes some physicians to discourage its utility in treatment of post-TBI disequilibrium.

Cutting Edge/ Emerging and Unique Concepts and Practice

Effectiveness of conventional versus virtual reality-based balance exercises with Nintendo Wii Fit Plus in vestibular rehabilitation for unilateral peripheral vestibular was studied and is found not to be superior to conventional vestibular rehabilitation but thought to provide a more enjoyable method of retraining after balance peripheral vestibular loss. 25

References

  1. Petrucci, Anna Grazia, Alessandro De Stefano, and Francesco Dispenza. “Epidemiology of Dizziness.” Textbook of Vertigo: Diagnosis and Management 2013: 26-37
  2. Neuhauser HK, Lempert T. Vertigo: epidemiologic aspects. Semin Neurol. 2009, 29 (5): 473–81.
  3. Kerber KA, Meurer WJ, West BT, Fendrick AM. Dizziness presentations in U.S. emergency departments, 1995-2004. Acad Emerg Med. Aug 2008; 15(8):744-50.
  4. H.K. Neuhauser, Chapter 5 – The epidemiology of dizziness and vertigo, Editor(s): Joseph M. Furman, Thomas Lempert, Handbook of Clinical Neurology, Elsevier, Volume 137, 2016, Pages 67-82, ISSN 0072-9752, ISBN 9780444634375, https://doi.org/10.1016/B978-0-444-63437-5.00005.
  5. Post R, Dickerson, LM. Dizziness: A Diagnostic Approach. Am Fam Physician. 2010; 82(4):361-368.
  6. Ali S. Saber Tehrani et. Al. Rising Annual Costs of Dizziness Presentations to U.S. Emergency Departments, Academic Emergency Medicine;  Acad Emerg Med, 20, 7, 1069-6563 https://doi.org/10.1111/acem.12168;  2013
  7. Navi B, Kamel H, Shah MP, et al. Rate and predictors of serious neurologic causes of dizziness in the emergency department. Mayo Clin Proc 2012; 87:1080-10888.
  8.  Maarsingh, OR, Dros, J , F G, Henk Weert, V,  Van der Windt DA.,  Riet, GT  and Van der Horst HE. 1Department of Family Practice and EMGO Institute for Health and Care Research, VU University Medical Center, Amsterdam, The Netherlands Causes of Persistent Dizziness in Elderly Patients in Primary Care. Ann Fam Med. 2010; 8(3): 196–205.9.
  9.  Della-Morte D and Rundek T. Dizziness and vertigo. Front Neurol Neurosci. Feb 14, 2012; 30:22-5. Epub.
  10. Nanda, A, and Tinetti, ME. “Chronic dizziness and vertigo.” Geriatric Medicine. Springer New York, 2003: 995-1008.
  11. W Arthur, G C Kaye. The pathophysiology of common causes of syncope Review. Postgrad Med J 2000; 76:750-753.
  12.  Hotson J R and. Baloh, RW. Acute Vestibular Syndrome. N Engl J Med September 3, 1998; 339: 680-685.
  13. Martin, KA, Staab, JP. Strategies for managing patients with chronic subjective dizziness, Current Psychiatry July 2012; Vol. 11, No. 07: 45-6.
  14. Von Brevern  M,  Radtke A,  Lezius F, Ziese T, Lempert T,  Neuhauser H.  Epidemiology of benign paroxysmal positional vertigo: a population based study Neurol Neurosurg Psychiatry 2007; 78: 710-715.
  15.  Wilhelmsen K, Ljunggren A, Goplen F, Eide GE, Nordahl SH. Long-term symptoms in dizzy patients examined in a university clinic. BMC Ear Nose Throat Disord. 2009; (9): 2.
  16. Hain TC, Uddin M. Pharmacological treatment of vertigo. CNS Drugs. 2003; 17(2):85-100.
  17. Luxon, LM. Evaluation and Management of the Dizzy Patient. JNeurol Neurosurgery Psychiatry, 2004:75(Supp. IV); 45-52.
  18. Kerber KA, Baloh RW. The evaluation of a patient with dizziness. Neurol Clin Pract 2011; 1:24.
  19.  Farzam K, Tivakaran VS. QT Prolonging Drugs. [Updated 2020 Nov 27]. In: StatPearls Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-.
  20. Ciuffreda KJ, Rutner D, Kapoor N, Suchoff IB, Craig S, Han ME. Vision therapy for oculomotor dysfunctions in acquired brain injury: a retrospective analysis. Optometry. 2008 Jan;79(1):18-22. doi: 10.1016/j.optm.2007.10.004. PMID: 18156092.
  21. Thiagarajan P, Ciuffreda KJ, Capo-Aponte JE, Ludlam DP, Kapoor N. Oculomotor neurorehabilitation for reading in mild traumatic brain injury (mTBI): an integrative approach. NeuroRehabilitation. 2014;34(1):129-46. doi: 10.3233/NRE-131025. PMID: 24284470.
  22. Hillier SL, McDonnell M: Vestibular rehabilitation for unilateral peripheral vestibular dysfunction. Cochrane database of systematic reviews 2011, (2).
  23. Minor LB, Solomon D, Zinreich J, Zee DS. Sound- and/or pressure-induced vertigo due to bone dehiscence of the superior semicircular canal. Archives of Otolaryngology—Head & Neck Surgery 1998;124: 249–258.
  24. Eggers, S DZ  Bundrick, J and  Litin, SC.  Clinical Pearls in Neurology Mayo Clin Proc. 2012 Mar; 87(3): 280–285.
  25.  Meldrum D, Herdman S, Vance R, Murray D, Malone K, Duffy D, Glennon A, McConn-Walsh R. Effectiveness of conventional versus virtual reality-based balance exercises in vestibular rehabilitation for unilateral peripheral vestibular loss: results of a randomized controlled trial. Arch Phys Med Rehabil. 2015 Apr 1. pii: S0003-9993(15)00289-0. doi: 10.1016/j.apmr.2015.02.032. [Epub ahead of print]

Original Version of the Topic

K. Rao Poduri, MD, David Essaff, MD. Dizziness. 4/12/2016

Author Disclosures:

Steven Siano, MD
Nothing to Disclose

Lee Shuping, MD
Nothing to Disclose

K. Rao Poduri, MD
Nothing to Disclose