Am Fam Physician. 2023;107(5):514-523
Patient information: See related handout on what could be causing dizziness.
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
| Cause | Clinical description |
|---|---|
| Peripheral | |
| Benign paroxysmal positional vertigo | Disorder of the inner ear characterized by repeated episodes of positional vertigo1 |
| Vestibular neuritis | Spontaneous episodes of vertigo caused by inflammation of the vestibular nerve or labyrinthine organs, usually from a viral infection |
| Meniere disease | Two 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 |
| Central | |
| Vestibular migraine | Spontaneous episodes of vertigo associated with migraine headaches |
| Vertebrobasilar ischemia | Continuous spontaneous episodes of vertigo caused by arterial occlusion or insufficiency affecting the vertebrobasilar system |
| Other | |
| Peripheral | Acute coronary syndrome, anemia, aortic dissection, arrhythmia, behavioral health concerns, ectopic pregnancy, hormonal imbalance, infection, metabolic disorders, otosclerosis, pulmonary embolism, thyroid disease, vasovagal reflex |
| Central | Cerebellopontine 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.5–7 This approach to the patient helps distinguish between benign and serious causes.
History
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
| Syndrome | Duration | Characteristics | Potential etiologies |
|---|---|---|---|
| Episodic vestibular syndrome | |||
| Triggered | Seconds to minutes | Asymptomatic 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 |
| Spontaneous | Minutes to hours | Head motion may worsen symptoms No obvious triggers Symptoms at rest | Cardiac arrhythmias Hypoglycemia Meniere disease Vertebrobasilar transient ischemic attack Vestibular migraine |
| Acute vestibular syndrome | |||
| Traumatic/toxic | Acute, 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 |
| Spontaneous | Acute, multiple episodes | No 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.
| Medication | Causal mechanism |
|---|---|
| Antiarrhythmic, class 1a Antidementia agents Antihistamines (sedating) Antihypertensives Antidepressants (e.g., ketamine [Ketalar])9 Anti-infectives: anti-influenza agents, antifungals, quinolones Antiparkinsonian agents Attention-deficit/hyperactivity disorder agents Digitalis glycosides Dipyridamole Narcotics Nitrates 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 |
| Alcohol Antiseizure medications Benzodiazepines Lithium | Cerebellar toxicity |
| Antidiabetic agents Beta adrenergic blockers | Hypoglycemia |
| Aminoglycosides Antirheumatic agents | Ototoxicity |
| Anticoagulants 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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