Medical Excellence- Issue 1

cutoffs should be adjusted based on baseline blood pressure [77]. However, the orthostasis can be delayed (onset >10 min), and the duration of monitoring remains controversial [78–80]. Emergency physicians are familiar with the most common causes of acute orthostasis such as medications and hypovolemia. Strong bedside predictors of moderate blood loss are postural dizziness so severe as to prevent standing or a postural pulse in- crement >30 beats per min, but the sensitivity of these findings is only 22% [81]. Furthermore, the benign postural orthostatic tachycardia syndrome (POTS) produces similar clinical findings [82]. The absence of tachycardia or even relative bradycardia can occur with intraperitoneal blood such as ruptured ectopic preg- nancy [83]. Benign paroxysmal positional vertigo produces dizziness upon arising in 58% [68], which can mimic orthostatic hypo- tension [84], and often goes undiagnosed in the elderly [25, 85]. Alternatively, orthostatic hypotension may be incidental and misleading, especially in older patients taking antihypertensive medications [86]. In patients with postural symptoms, BPPV and orthostatic hypotension can usually be differentiated by con- sidering other positional triggers such as rolling over in bed or reclining, both of which are common in BPPV but should not occur with orthostatic hypotension. Benign paroxysmal positional vertigo notwithstanding, or- thostatic dizziness and orthostatic hypotension are not always related [74, 87]. Orthostatic dizziness without systemic orthos- tatic hypotension has been reported with hemodynamic TIA due to vascular stenosis [88] and in patients with intracranial hypo- tension [89]. Neurological evaluation is probably indicated for patients with reproducible and sustained orthostatic dizziness but no demonstrable hypotension. Spontaneous Episodic Vestibular Syndrome (s-EVS) The s-EVS is marked by recurrent, spontaneous episodic dizzi- ness that ranges in duration from seconds to days but usually lasts minutes to hours. Most patients are therefore asymptomatic at the time of clinical assessment, and if they are, one cannot provoke an episode at the bedside (because it is not “trigger- able”), so the evaluation relies almost entirely on history. The most common benign cause is vestibular migraine [90–92] fol- lowed by Ménière’s disease [91]. The most common dangerous cause is vertebrobasilar TIA [93]. Other causes of the s-EVS include reflex (e.g., vasovagal) syncope [94] and panic attacks [95]. Uncommon dangerous causes of s-EVS are cardiovascu- lar (cardiac arrhythmia, unstable angina pectoris, pulmonary embolus), endocrine (hypoglycemia, neurohumoral neoplasms), or toxic (intermittent carbon monoxide exposure). Diagnosis is not difficult when cases are typical. Unfortunately, classical fea- tures such as frank loss of consciousness in reflex syncope [96], headache in vestibular migraine [97], and fear in panic attacks [98] are frequently absent. Atypical case presentations probably contribute to diagnostic confusion in patients with transient neurological attacks [99]. Definite vestibular migraine diagnosis requires recurrent attacks with vestibular symptoms, a history of migraine accord- ing to the International Classification of Headache Disorders, and migraine symptoms during at least half of the attacks [91]. Attack duration in vestibular migraine ranges from seconds to days [91]. Headache is often absent with the attack; when head- ache does occur, it may begin before, during, or after the dizzi- ness and may differ from the patient’s other “typical” migraine headaches [91, 100]. Nausea, vomiting, photophobia, phono- phobia, and visual auras may accompany vestibular migraine. Hearing loss or tinnitus sometimes occurs [101], creating some overlap between vestibular migraine and Ménière’s disease [102]. If present, nystagmus can be of a peripheral, central, or mixed type [100]. The diagnosis is normally made based purely on clin- ical history and the exclusion of alternative causes [91]. Patients with Ménière’s disease classically present with epi- sodic vertigo accompanied by unilateral tinnitus and aural full- ness, often with reversible sensorineural hearing loss. Episodes typically last minutes to hours. Only one in four initially present with the complete symptom triad [103], and non-vertiginous dizziness is common [104]. Definite Ménière’s disease requires at least two spontaneous episodes of vertigo lasting at least 20 min, audiometrically documented hearing loss (at least once, whether Table 6: Characteristics of patients with t-EVS that suggest a central mimic (CPPV) rather than typical BPPV. 1. Presence of symptoms or signs that are NOT seen in BPPV (a) Headache (b) Diplopia (c) Abnormal cranial nerve or cerebellar function 2. Presence of nystagmus without dizziness 3. Atypical nystagmus characteristics (a) Down-beating nystagmus a (b) Nystagmus that beats in different directions on repeat testing 4. Poor response to therapeutic maneuvers (a) Unable to cure patient with typical canalith repositioning maneuver (b) Frequent recurrent symptoms a Down-beating nystagmus can be seen with anterior canal BPPV. However because BPPV of this canal is rare and because down-beating nystagmus is also seen with central causes, it is safer for emergency physicians to consider this finding to be always worrisome prompting imaging, consultation, and/or referral 10  |  Issue-1 MEDICAL EXCELLENCE