Vertigo: When Should I Be Concerned?

Vertigo or “dizziness” is such a nonspecific and vague symptom and can denote anything from an existing cardiovascular issue (global cerebral hypoperfusion, or reduction of blood flow to the brain), to a spatially disorienting imbalance caused by vestibular dysfunction (i.e., inner or middle ear inflection), to a stroke in the posterior circulation (brainstem region). In rare cases the etiology is psychogenic. Bone fide vertigo may be defined as the sensation of spinning, tilting, or any whirling movement that disorients and discombobulates an individual, but the word itself can also be used more loosely in a colloquial sense when referring to clumsiness, confusion, lightheadedness, and incoordination and physical awkwardness precipitated by a clouded sensorium and an altered mental status.

When a patient presents with a symptom picture punctuated by vertigo, the doctor’s task is to determine whether the cause is neurologic or systemic. Prudent clinical reasoning is profoundly contingent upon open disclosure but above all specific and accurate descriptions of the dizziness itself. What are some of its qualitative aspects? With respect to chronicity is it acute or chronic, continuous or episodic? Are there specific proprioceptive or environmental triggers? Is it orthostatic, or elicited by rapid and jerky movements of the head? Answers to these help in creating and narrowing down a list of differential diagnoses and in parsing out the most likely from the least likely. Lamentably, when it comes to the reliability of patient reporting, clinical research has demonstrated that subjective characterizations and descriptions of dizziness correlate poorly with the underlying etiology. Put differently laypersons are not very adept at describing the “quality” of their dizziness, making the clinician’s task of determining whether the phenomenon is genuine room-spinning vertigo or not dismally impossible. Perhaps the best subjective report is one offering explicit information about chronicity (i.e., acute or chronic, continuous or episodic), severity (mild, moderate, or severe), existing triggers and exacerbations/alleviations, and the symptom-cluster more generally (i.e., what other symptoms are present, save for dizziness).   

The most common cause of recurrent vertigo in the populace is benign paroxysmal positional vertigo (BPPV) which is triggered when an individual’s neck is extended as to peer upwards, or alternatively when the individual is rolling around in bed or getting in and out of bed. Despite being common, the diagnosis is sometimes missed by family physicians. Episodes are transient and may be accompanied by gait disturbances, unsteadiness, or nauseating pangs, however the vertigo may also occur in isolation. One specific position is symptomatic and foreshadows the dizziness by 5-10 seconds, and in what may seem counterintuitive and bizarre, is the same position that must be assumed numerous times for the symptom to abate. As the name implies the condition is benign and caused by free-floating calcium carbonate particles that dislodge from the otolith membrane and proceed to enter the semicircular canals, either floating in the endolymph or meshing against the cupola. Neurologists use bedside repositioning maneuvers like the Epley maneuver to eject the debris back into the vestibule, the inner ear’s central chamber, and thus reinstate equilibrium.

Episodes of recurrent spontaneous dizziness–spinning, tilting, or rocking in quality–and lasting minutes to several hours is a hallmark feature of Ménière’s disease, a condition caused by idiopathic development of burgeoning inner ear pressure [called endolymphatic hydrops]. While the disorder is unilateral and affects only one ear, bilateral presentations do exist. Prevalence is higher in the 20s-50s age range. The inaugural and inchoate phase of the disorder may involve only isolated vertigo, however with the passage of time an array of other symptoms, for instance nausea and vomiting, tinnitus, and a sensation of fullness in the ear, may develop and predominate during an attack. Inevitably, progressive hearing loss develops and lingers between attacks. There’s some nosological inter-variability in the context of disease progression, with many patients going into remission while others progressively worsen over the years as to adversely impact their quality of life.

Patients presenting for neuro-otological examination during a vertiginous attack will present with spontaneous peripheral/horizontal nystagmus [involuntary rhythmic oscillation of the eyes] which initially beats towards the affected ear [called the “irritative” phase] before reversing and beating towards the unaffected ear [called the “paretic” phase] as the acute symptoms of dizziness subside. The consensus among medical professionals is that direction-changing nystagmus is a phenomenon unique to Ménière’s and effectively pathognomonic of the condition. Audiometry will reveal low-frequency hearing loss for the affected ear when the disease is present and vestibular issues–typically veering to the left or right on an Unterberger test–amidst the throes of a vertiginous attack. Moreover, clinicians often find that the video head impulse test (VHIT), a clinical assessment of the vestibulo-ocular reflex, is normal with no catchup saccade required to keep the eyes anchored to a specific point in the visual field as the head turns. The panoply of diagnostic tests aids in clarifying a diagnosis made on clinical grounds, and treatment is noninvasive and focused on the implementation of an aggressive low-sodium diet and the prescription of a diuretic to reduce symptom triggers. Debilitating and intractable permutations necessitate intratympanic steroid injections with gentamycin, and in some cases, surgical resection of the inner ear–a labyrinthectomy–or endolymphatic sac decompression which involves subtraction of a bone segment adjacent to an endolymphatic sac is executed for symptomatic relief. 

Benign recurrent vertigo is also a symptom of vestibular migraine and, depending on the idiosyncratic symptom picture, can be difficult to differentiate from Ménière’s disease, especially when aspects of the patient’s medical history are ambiguous and the typical headache and focal neurological signs spearheading the throes of an acute migraine attack are absent. With vestibular migraine, the duration of recurrent vertigo can vary considerably and last anywhere from several minutes to days on end. Qualitative aspects of vertigo may be different in a patient with vestibular migraine as well; chronic motion sensitivity spawning carsickness and seasickness is common along with hypersensitivity to other sensory stimuli. Moreover, premonitory migraine symptoms like scintillating scotoma or somatosensory auras may be present whereas symptoms like low-frequency hearing loss, tinnitus, and the sensation of aural fullness which assail Ménière’s disease patients are notably absent.

In contradistinction to the direction-changing peripheral nystagmus seen during acute Ménière’s disease attacks, patients with vestibular migraine may present to the clinic with horizontal, vertical, or torsional nystagmus during or between attacks–their nystagmus tends to be more ‘versatile.’ Widely regarded by clinicians as a deceptive chameleon with an uncanny ability to masquerade as another disease or disorder, vestibular migraine should be suspected when recurrent episodes of dizziness dominate the clinical picture without any sign of progressive low-frequency hearing loss. The neurological exam, the VHIT, and the audiogram are all normal when vestibular migraine is the veridical diagnosis, and the acute or prophylactic treatments are the same as those deployed for conventional migraine disorders.  

An analogous and common condition involving the rapid onset of debilitating vertigo in concert with imbalance and nausea and vomiting lasting 24 hours or longer is an acute vestibular syndrome, otherwise known as vestibular neuritis. Unlike labyrinthitis, hearing acuity in vestibular neuritis remains normal with no accompanying tinnitus or sensation of aural fullness while the vertigo is present at rest and exacerbated by abrupt head movements. Similarly, focal neurological symptoms like weakness, numbness, diplopia, or dysarthria are absent. Widely regarded as neurological sequelae of a viral illness, the condition tends to be a once-in-a-lifetime event with recurrence being extremely rare.

Diagnosis of acute vestibular neuritis is made on clinical grounds during an attack and its chief cardinal signs are: (1) peripheral or unidirectional horizontal and rotatory nystagmus which suppresses in illumination and is fast-beating with the eyes turned away from the affected ear, (2) an absence of skew deviation, or no vertical misalignment of the eyes which is usually a telltale sign of CNS pathologies, and (3) an inability to maintain fixation on a particular visual-spatial location when the examining doctor turns the patient’s head towards the affected ear, necessitating a corrective saccade to reconnect with the visual target. The latter is called a positive head impulse test. Vestibular neuritis is treated with a brief course of corticosteroids while adjuvant physical therapy is used for compensation of disequilibrium, the sensation of tilting or veering to one side commonly associated with the condition.

When any of the said cardinal features–positive head impulse test, unidirectional peripheral nystagmus, and absence of vertical eye skew–are not met, then cerebellar or brainstem lesion should be suspected. Stroke is the chief differential diagnosis in a symptom picture where vestibular neuritis is strongly suspected but not confirmed. Lamentably, there is no specific examination to parse out an infarction in the posterior circulation [cerebellar or brainstem stroke] from other neurological conditions, and to further compound matters lesions in this part of the brain may or may not manifest classical stroke symptoms and signs like ataxia, dysdiadochokinesia, central direction-changing nystagmus, and so forth. In fact, some cerebellar and brainstem strokes may present with isolated spontaneous vertigo and nothing else. If there are serious concerns for a central vestibular lesion predicated on the aforementioned “red flags,” the patient should present to the ED for neuroimaging.