Dizziness and Vertigo _________________________________________________________________________
Acoustic Neuroma (Vestibular Schwannoma or Schwann Cell Tumors) Acoustic neuromas are tumors of the vestibular portion of the 8th cranial nerve, diagnosed in roughly 3,000 cases annually. Acoustic neuromas can expand and compress surrounding structures along the brainstem, potentially leading to sensori- neural hearing loss and vertiginous symptoms [19; 59]. DEMYELINATING AND NEURODEGENERATIVE DISORDERS Multiple Sclerosis Multiple sclerosis (MS), an idiopathic demyelinating disorder of the central nervous system (CNS), is considered an autoim- mune disease most likely caused by an autoantigen to a myelin protein [47]. Data from a study published in 2019 indicate that the estimated prevalence of MS is 363 cases per 100,000 individuals in the United States, and it affects three times as many women than men [60]. CNS demyelinization usually occurs in the white matter, where plaque formation disrupts signal conduction and leads to symptoms [47]. Demyelinating plaques that develop in central vestibular pathways may cause recurrent episodes of vestibular symptoms, especially during illness and with heat exposure (Uhthoff phenomenon). The plaques may be visible on MRI [18; 19]. Vertigo is the presenting symptom at onset in 5% of MS cases, and more than 50% of patients present with vertigo at some point in the disease course. MS can mimic an 8th cranial nerve lesion when plaque develops in the entry of the nerve root in the brainstem to produce vertigo and horizontal nystagmus [47]. MS may present with dizziness, vertigo, or imbalance, especially with brainstem or cerebellum lesions that affect the vestibular system; these lesions may also result in nystagmus, ataxia, slurred speech, and diplopia. Despite the increased risk of CNS vertigo in patients with MS, non-MS (peripheral and central) causes (e.g., BPPV, vestibular migraine) can co-occur [15]. Parkinson Disease and Parkinson-Plus Syndromes Dizziness may be a manifestation of many neurodegenerative disorders. At presentation, patients with Parkinson disease may describe the shuffling or festinating gait as being “dizzy” or “off balance.” Medications such as levodopa or dopamine agonists (e.g., pramipexole, ropinirole) may cause orthostatic hypotension, and hence presyncopal dizziness [18]. The Parkinson-plus syndromes (e.g., multiple system atrophy, dementia with Lewy bodies) often cause many symptoms that are construed as “dizziness.” Multiple system atrophy causes dysautonomia (causing orthostatic presyncope or syncope), vertigo, nystagmus (causing oscillopsia), and/or cerebellar findings (leading to gait ataxia). Progressive supranuclear palsy often presents with falls and complaints of imbalance; loss of downgaze often causes imbalance when descending stairs [18].
Cerebellar Vertigo Syndromes Neurodegenerative and hereditary diseases of the cerebellum often lead to postural vertigo, gait disorders with ataxia, and cerebellar oculomotor disorders such as saccadic dysmetria, gaze saccades, gaze nystagmus, and downbeat nystagmus [61]. Episodic ataxia type 2 is a rare but important disorder to identify because the random attacks of vertigo, ataxic gait, and slurred speech lasting minutes to days often respond dramati- cally to acetazolamide. The onset of recurrent episodes may occur in childhood or early adulthood, but the condition is often undiagnosed into late adulthood. This disorder is due to a voltage-sensitive calcium channel mutation [15]. PERSISTENT POSTURAL PERCEPTUAL DIZZINESS Persistent postural perceptual dizziness (PPPD) develops when a precipitating condition (typically an acute vestibular event, vestibular migraine, panic attacks, or anxiety with prominent dizziness) occurs in individuals with a maladaptive behavioral response to the acute symptoms [62]. In this way, PPPD is a new diagnostic entity that bridges previous knowledge gaps by connecting persistent non-vertiginous dizziness, perceptual hypersensitivity, and chronic anxiety [15; 62]. PPPD may be a highly prevalent cause of chronic non-vertigi- nous dizziness. The population and primary care prevalence is not yet known, but the female-to-male ratio is 5:1. PPPD symptoms are often worsened by sleep deprivation and stress but not by head motion to the degree seen with most vestibular disorders [15; 62]. The central etiology relates to behavioral factors, neurotrans- mitter function, and other probable CNS mechanisms [15]. Brain imaging of patients with PPPD shows reduced connectiv- ity in multisensory vestibular processing and spatial cognition, with increased connectivity between visual and emotional processing. Dizziness burden, anxiety, and depression correlate with connectivity in clinically relevant brain regions [63]. PPPD may linger following minor head injury and become entwined with other symptoms of post-concussive syndrome [15]. MAL DE DÉBARQUEMENT SYNDROME A transient experience of “sea legs” after returning to land from riding on a boat is not uncommon, but in mal de débarque- ment syndrome it persists for weeks, months, or years. Mal de débarquement syndrome is an uncommon vestibular disorder in which a sense of rocking first appears soon after disembark- ing and is most common in women. Travel by aircraft or auto- mobile can also trigger the persistent unsteadiness. Symptoms typically abate during passive motion (e.g., a boat or car ride) but resume when motion ceases. The cause is unknown, but it may be a disorder of the vestibular velocity storage mechanism with a limited adaptive ability [15; 62].
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