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Am Fam Physician. 2023;107(5):514-523

Patient information: See related handout on what could be causing dizziness.

This clinical content conforms to AAFP criteria for CME.

Author disclosure: No relevant financial relationships.

Dizziness is a common but often diagnostically difficult condition. Clinicians should focus on the timing of the events and triggers of dizziness to develop a differential diagnosis because it is difficult for patients to provide quality reports of their symptoms. The differential diagnosis is broad and includes peripheral and central causes. Peripheral etiologies can cause significant morbidity but are generally less concerning, whereas central etiologies are more urgent. The physical examination may include orthostatic blood pressure measurement, a full cardiac and neurologic examination, assessment for nystagmus, the Dix-Hallpike maneuver (for patients with triggered dizziness), and the HINTS (head-impulse, nystagmus, test of skew) examination when indicated. Laboratory testing and imaging are usually not required but can be helpful. The treatment for dizziness is dependent on the etiology of the symptoms. Canalith repositioning procedures (e.g., Epley maneuver) are the most helpful in treating benign paroxysmal positional vertigo. Vestibular rehabilitation is helpful in treating many peripheral and central etiologies. Other etiologies of dizziness require specific treatment to address the cause. Pharmacologic intervention is limited because it often affects the ability of the central nervous system to compensate for dizziness.

Family physicians commonly evaluate dizziness.1 Patients' descriptions of their symptoms are unreliable for establishing a diagnosis.2 The differential diagnosis can range from straightforward and self-limiting conditions to more serious conditions requiring further workup (Table 11,3). Physicians are encouraged to use a systematic approach to dizziness to diagnose and treat patients safely.4

Clinical recommendations Evidence rating Comments
The physical examination in patients with dizziness should include orthostatic blood pressure measurement, nystagmus assessment, and the Dix-Hallpike maneuver for triggered vertigo.8,11 C Expert opinion and consensus guideline in the absence of clinical trial
The HINTS (head-impulse, nystagmus, test of skew) examination can help differentiate a peripheral from a central cause of vestibular neuritis.8,15,16 C Expert opinion and consensus guideline in the absence of clinical trial
Magnetic resonance imaging of the head and auditory canal can be helpful in patients with hearing loss and peripheral dizziness, in addition to patients with concerns for central causes of dizziness.18 C Expert opinion and consensus guideline in the absence of clinical trial
Repositioning maneuvers are helpful in treating benign paroxysmal positional vertigo.19,20 A Evidence-based guideline and systematic review of randomized controlled trials with patient-oriented evidence
Benign paroxysmal positional vertigo should not routinely be treated with vestibular suppressant medications such as antihistamines or benzodiazepines.11 C Expert opinion/clinical review
Clinicians should order an audiogram when assessing a patient for Meniere disease.3 C Expert opinion and consensus guideline in the absence of clinical trial
Vestibular migraine should be considered in patients who present with at least five episodes of vestibular symptoms and a history of migraine.33 C Expert opinion/clinical review
CauseClinical description
Benign paroxysmal positional vertigoDisorder of the inner ear characterized by repeated episodes of positional vertigo1
Vestibular neuritisSpontaneous episodes of vertigo caused by inflammation of the vestibular nerve or labyrinthine organs, usually from a viral infection
Meniere diseaseTwo or more episodes of vertigo lasting 20 minutes to 12 hours (definite) or up to 24 hours (probable) and fluctuating or nonfluctuating sensorineural hearing loss, tinnitus, or pressure in the affected ear3
Vestibular migraineSpontaneous episodes of vertigo associated with migraine headaches
Vertebrobasilar ischemiaContinuous spontaneous episodes of vertigo caused by arterial occlusion or insufficiency affecting the vertebrobasilar system
PeripheralAcute coronary syndrome, anemia, aortic dissection, arrhythmia, behavioral health concerns, ectopic pregnancy, hormonal imbalance, infection, metabolic disorders, otosclerosis, pulmonary embolism, thyroid disease, vasovagal reflex
CentralCerebellopontine angle tumors, craniocervical dissection, encephalitis, intracranial hemorrhage, meningitis, multiple sclerosis, seizures

General Approach

Vertigo is a sensation of distorted self-motion when no self-motion is occurring. Dizziness is a sensation of disturbed or impaired spatial orientation without a false or distorted sense of motion.5 These symptoms are vague, presenting a diagnostic dilemma. Using the TiTrATE (timing of the symptoms, triggers that provoke the symptom, and targeted examination) mnemonic can help focus the assessment.57 This approach to the patient helps distinguish between benign and serious causes.


Timing (i.e., onset, duration, and evolution of the dizziness) can help distinguish between episodic and continuous dizziness. Episodic vestibular syndromes are clinical syndromes of transient vertigo, dizziness, or unsteadiness lasting seconds to hours. Acute vestibular syndromes are acute-onset, continuous vertigo, dizziness, or unsteadiness lasting days to weeks. Table 2 describes vestibular presentations of dizziness.5,7 Figure 1 can help in the assessment of dizziness.8

SyndromeDurationCharacteristicsPotential etiologies
Episodic vestibular syndrome
TriggeredSeconds to minutesAsymptomatic at rest
Physical examination (Dix-Hallpike) can be helpful in assessment
Symptoms triggered by head motion or change in body position
Benign paroxysmal positional vertigo
Orthostatic hypotension
SpontaneousMinutes to hoursHead motion may worsen symptoms
No obvious triggers
Symptoms at rest
Cardiac arrhythmias
Meniere disease
Vertebrobasilar transient ischemic attack
Vestibular migraine
Acute vestibular syndrome
Traumatic/toxicAcute, typically one episode
Resolves over days to weeks once exposure is stopped
Onset of symptoms in relation to exposure
Physical examination less helpful due to temporal relationship to exposure
Drug intoxication
Head trauma
Medication adverse effects
SpontaneousAcute, multiple episodesNo obvious traumatic events or toxic exposures
Physical examination (HINTS [head-impulse, nystagmus, test of skew]) can distinguish between central and peripheral etiologies
Brain stem or cerebellar stroke
Listeria encephalitis
Thiamine deficiency
Vestibular neuritis

After establishing timing, clinicians should determine if the symptoms are triggered or spontaneous. Triggers are actions, movements, or situations that provoke the onset of dizziness in patients with intermittent symptoms, but they do not differentiate peripheral from central etiologies.6 Episodic vestibular syndromes can be triggered or spontaneous. For example, patients with benign paroxysmal positional vertigo are often triggered by changes in their position. Patients with orthostatic hypotension may describe symptoms when triggered by moving from a sitting or supine to a standing position. Meniere disease is an example of episodic vestibular syndrome that is spontaneous but not triggered.3 Vestibular migraine is another example of spontaneous episodic vestibular syndrome and manifests as vertigo in patients with a history of migraines.7 Panic attacks can present as spontaneous episodic vestibular syndrome.

Acute vestibular syndrome can also be characterized as triggered or spontaneous. Triggered acute vestibular syndrome is usually caused by toxins, such as medications, or trauma. A medication and toxic exposure history can aid in diagnosis. Table 3 lists medications and substances associated with dizziness.8,9 Traumatic brain injury, tympanic membrane rupture, whiplash, skull fracture, vertebral artery dissection, and other trauma can trigger acute vestibular syndrome.10 Etiologies for spontaneous acute vestibular syndrome include vestibular neuritis, transient ischemic attack, or stroke, which can be determined through a physical examination, laboratory tests, and imaging.

MedicationCausal mechanism
Antiarrhythmic, class 1a
Antidementia agents
Antihistamines (sedating)
Antidepressants (e.g., ketamine [Ketalar])9
Anti-infectives: anti-influenza agents, antifungals, quinolones
Antiparkinsonian agents
Attention-deficit/hyperactivity disorder agents
Digitalis glycosides
Phosphodiesterase type 5 inhibitors
Skeletal muscle relaxants
Sodium-glucose cotransporter-2 inhibitors
Urinary anticholinergics
Cardiac effects: hypotension, other arrhythmias, postural hypotension, torsades de pointes
Skeletal muscle relaxants
Urinary anticholinergics and gastrointestinal antispasmodics
Central anticholinergic effects
Antiseizure medications
Cerebellar toxicity
Antidiabetic agents
Beta adrenergic blockers
Antirheumatic agents
Antithyroid agents
Bleeding complications (anticoagulants), bone marrow suppression (antithyroid agents)

Physical Examination

Patients with triggered episodic vestibular syndrome can be further evaluated with the Dix-Hallpike maneuver and orthostatic vitals.8,11 Orthostatic hypotension is a sustained reduction in systolic blood pressure of at least 20 mm Hg or a diastolic blood pressure reduction of 10 mm Hg within three minutes of standing from a supine or sitting position.12 The Dix-Hallpike maneuver can diagnose benign paroxysmal positional vertigo1 (Figure 213). Transient upbeat-torsional nystagmus during the maneuver suggests benign paroxysmal positional vertigo, especially in the absence of spontaneous or gaze-evoked nystagmus.2 This examination should be performed only when patients have triggered episodic vestibular syndrome. However, a negative result on the Dix-Hallpike maneuver does not eliminate benign paroxysmal positional vertigo if the timing and triggers are consistent with that diagnosis.14

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