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INTRODUCTION AND EPIDEMIOLOGY

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Dizziness is a common complaint in patients >40 years old, leading to roughly 10 million visits to ambulatory care settings and 25% of ED visits.1 Dizziness can lead to falls in elderly patients. The symptoms may persist and be incapacitating. Patients may use various terms for the complaint: dizziness may mean vertigo, syncope, presyncope, weakness, giddiness, anxiety, or a disturbance in mentation.

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Vertigo is the perception of movement (rotational or otherwise) where no movement exists. Syncope is a transient loss of consciousness accompanied by loss of postural tone with spontaneous recovery. Near-syncope is light-headedness with concern for an impending loss of consciousness. Psychiatric dizziness is defined as a sensation of dizziness not related to vestibular dysfunction that occurs exclusively in combination with other symptoms as part of a recognized psychiatric symptom cluster.2 Disequilibrium refers to a feeling of unsteadiness, imbalance, or a sensation of "floating" while walking.

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Acute vestibular syndrome is a symptom complex consisting of vertigo, nausea and vomiting, intolerance to head motion, spontaneous nystagmus, unsteady gait, and postural instability caused by injury to peripheral or central vestibular structures. To be called acute vestibular syndrome, the associated vertigo must persist for at least 24 hours, thus excluding causes of transient vertigo such as benign paroxysmal positional vertigo (BPPV). Acute vestibular syndrome may be peripheral or central in origin. Clinical findings that distinguish central from peripheral causes include focal neurologic deficits such as hemiparesis, hemisensory loss, or gaze palsy. The most common peripheral cause of acute vestibular syndrome is vestibular neuronitis. The most common central cause is ischemic stroke of the posterior fossa (brainstem or cerebellar), followed by demyelination. There is growing evidence that a significant number of patients with central acute vestibular syndrome are misdiagnosed in the ED. A systematic review estimated that roughly 25% of patients presenting with acute vestibular syndrome have had a stroke.3

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The time-honored paradigm of evaluating dizziness is based largely on the patient's subjective description. More recently, objective bedside physical examination has emerged as a more reliable way of arriving at the correct diagnosis.4

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PATHOPHYSIOLOGY

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The CNS coordinates and integrates sensory input from the visual, vestibular, and proprioceptive systems. Vertigo arises from a mismatch of information from two or more of the involved senses, caused by dysfunction in the sensory organ or its corresponding pathway.

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Visual inputs provide spatial orientation. Proprioceptors help relate body movements and indicate the position of the head relative to that of the body. The vestibular system (via the otoliths) establishes the body's orientation with respect to gravity. The cupulae's sensors track rotary motion. The three semicircular canals sense orientation to movement and head tilts and are filled with a fluid called endolymph. The endolymphatic sac produces glycoproteins that create an osmotic sink necessary to maintain flow. The movement of fluid in the semicircular canals ...

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