Dizziness and Vertigo _________________________________________________________________________
Pathophysiology The vestibular system includes three semicircular canals (or sim- ply “canals”) and two otolith organs (the saccule and utricle). The canals (posterior, lateral, and anterior) are positioned at right angles to each other to detect angular accelerations of the head. The canals are organized as functional pairs (left and right ear) in the same spatial plane; any rotation in that plane excites one pair member and inhibits the other [28; 29]. The canals are filled with endolymph fluid and lined with sensitive hair cells to act like a gyroscope. Motion from head rotation induces endolymph movement in the canal oriented in the spatial plane, which stimulates hair cells, activates the ampulla (the motion sensor) and cupula, and sends sensory output to the brain via the vestibular nerve [15; 28]. The saccule and utricle contain sensory epithelium and func- tion to detect linear or translational acceleration forces (e.g., gravity, accelerating or braking a car) [15]. Hair cells in the sac- cule and utricle are embedded in a matrix of calcium carbonate crystals (otoliths). Deflection of otoliths by gravity stimulates or inhibits neuronal output from the attached hair cells [11]. Otoliths that dislodge and migrate into a canal are called oto- conia. Endolymph fluid is usually non-reactive to gravity, but otoconia moves with gravity, causing inappropriate endolymph motion and hair cell stimulation and false signaling of head motion to the brain [23]. The brain receives and integrates peripheral sensory inputs. A false vestibular input conflicts with inputs from ocular, proprioceptive, and the unaffected vestibular systems. This causes a sensory mismatch in the brain integration, perceived as a spinning sensation (vertigo) normally lasting less than 60 seconds after cessation of head movement and inappropriate endolymph motion [23; 30]. BPPV is subtyped by afflicted canal and mechanism. Posterior canal BPPV (85% to 95%) is the most common. Lateral canal BPPV (5% to 15%) is less common, likely because it self-resolves sooner. Anterior canal BPPV (<1%) is uncommon due to the orientation. Rare variants include multi-canal and bilateral multi-canal BPPV [15; 21]. Otoconia contact abnormally stimulates the cupula, triggering vertigo and nystagmus. BPPV is subtyped as [20; 31]: • Canalithiaisis: Head movements cause free-floating otoconia to stimulate the cupula • Cupulolithiasis: Otoconia attach to the cupula, rendering it hypersensitive to linear acceleration and gravity Canalithiasis is much more common because the otoconia particulate mass required to exceed the symptomatic threshold is much lower than in cupulolithiasis (0.087 ug vs. 0.69 ug) [20; 32].
Recurrence and Cardiovascular Risk Factors Cardiovascular comorbidities are significantly associated with, and potentially important risk factors for, recurrent BPPV. In a nationwide study of 2,682 patients with BPPV (mean age: 59.3 years; 61% female), the prevalence of high blood pressure (55.8%), hypercholesterolemia (38.6%), diabetes (17.7%), and family history of cardiovascular disease (49.4%) were signifi- cantly higher than the national averages [33]. A high percentage of patients had hearing loss (42.9%), tinnitus (41.2%), or both (26.8%). The presence of hypertension, dyslipidemia, and pre- existing cardiovascular comorbidities were significantly related to recurrent BPPV episodes, and the presence of diabetes or thyroid/autoimmune disease was also relevant [33]. VIRAL OR BACTERIAL INFECTIOUS CAUSES Vestibular Neuritis Vestibular neuritis, the second most common cause of vertigo (after BPPV), is a viral or post-viral inflammatory disorder affecting the vestibular portion of the 8th cranial nerve. It most commonly affects persons 30 to 50 years of age, and men and women are equally affected. New cases are more common in the spring and early summer [10; 34]. Histopathologic nerve studies of these patients are consistent with a viral inflamma- tory etiology [15]. Vestibular neuritis is characterized by the sudden, acute onset of severe vertigo, nausea, vomiting, and gait instability without hearing loss, typically preceded by an upper respiratory tract infection [35]. The course and treatment of vestibular neuritis and viral labyrinthitis are similar; in both, the severity of acute vestibular symptoms can raise concerns of a central etiology, and the severity of vertigo, nausea, and vomiting reflects the severity of vestibular asymmetry [7; 15; 34]. Viral Labyrinthitis Labyrinthitis is an inflammatory disorder affecting both the vestibular and cochlear components of the 8th cranial nerve, caused by local or systemic viral or bacterial infection resulting in acute loss of vestibular and hearing function [10]. Viral laby- rinthitis, the most common form of labyrinthitis, often results from varicella zoster, influenza, or herpes simplex-1 infection [35]. Sudden sensorineural hearing loss in the affected ear is due to pan-labyrinthine inflammation affecting the cochlea. The estimated prevalence of sudden sensorineural hearing loss is 1 case in 10,000 persons; up to 40% of these patients have prominent vertigo or disequilibrium symptoms, and up to 15% of patients presenting with positional vertigo have viral labyrinthitis [35].
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