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Up to 21% of adults complain of transient dizziness, with 29% complaining of unsteadiness.1 The symptoms may persist and be incapacitating in some patients. Dizziness may mean vertigo, syncope, presyncope, weakness, giddiness, anxiety, or a disturbance in mentation to various patients.

Vertigo is the perception of movement (rotational or otherwise) where no movement exists. Syncope is a transient loss of consciousness that is 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.

The central nervous system (CNS) coordinates and integrates sensory input from the visual, vestibular, and proprioceptive systems. The three streams of information help form an impression of the orientation of the head and body as well as the perception of motion. Vertigo arises from a mismatch of information from two or more of the involved senses, which, in turn, can be caused by dysfunction in the sensory organ or its corresponding pathway.

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 contain sensors that track rotary motion. The presence of embedded otoconia or particles on the cupulae may transform them into linear motion sensors capable of sensing gravity. 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 causes specialized hair cells inside the canals to move, causing afferent vestibular impulses to fire. Sensory input from the vestibular apparatus travels to the nucleus of the eighth cranial nerve (Figure 164-1).

The CNS structures involved in integrating sensory input from all three sensory modalities include the medial longitudinal fasciculus, the red nuclei, the cerebellum, and the parietal lobes and superior temporal gyrus of the cerebral cortex. Connections between these structures and the oculomotor nuclei that drive the vestibulo-ocular reflex (VOR) complete the system. The VOR prevents visual blurring that otherwise would result from head movements and body sway.

Ordinarily, there is balanced input from the vestibular apparatus on both sides of the body. Asymmetric activity may result in vertigo. Causes of asymmetric activity include unilateral lesions of the vestibular apparatus as well as excessive unilateral firing due (for instance) to abnormal motion of the endolymph. Rapid head movements induce vertigo ...

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