Vertigo in a hypertensive patient

Vertigo as a presenting complaint can be challenging diagnostically, but not when approached in a systematic, rational way. We discussed a case of a hypertensive patient of Western African origin who presented with vertigo, ultimately found to have a cerebellar stroke.

This case highlights a few key principles in the approach to vertigo:

1) Verify that this is truly vertigo - ie a sensation of oneself or the room spinning, as compared to presyncope or lightheadedness. The diagnostic approach for these 2 entities can be quite different.

2) Once you have decided that this is vertigo, decide whether it is of central (ie CNS) or peripheral (ie vestibular) etiology.

First, let's discuss what the central and peripheral causes are:

Peripheral

Benign positional paroxysmal

vertigo (transient, positional, caused by otoliths)

Ménière’s disease (recurrent vertigo, aural fullness, tinnitus, nausea, vomiting)

Acute labyrinthitis (typically viral)

Acute vestibular neuronitis (inflammation of the nerve, typically viral)

Cholesteatoma

Herpes zoster oticus (Ramsay Hunt syndrome)

Medication-related

Central

Cerebellopontine angle tumor

Cerebrovascular disease (TIA, Stroke, hemorrhage)

Migraine

Multiple sclerosis

Medication-related

There are several key features on history that can help differentiate between peripheral and central causes, in over 75% of cases.

Central:

• Longer duration of symptoms without relief
• Less severe nausea and vomiting
• More likely purely horizontal, rotatory, or vertical nystagmus that is not alleviated by fixing on an object
• Sudden only if cerebrovascular in nature
• Associated neurological symptoms/findings
• Cardiovascular risk factors
• Short latency after performing Dix-Hallpike before nystagmus

Peripheral

• Rotatory illusions
• Much more likely to have nausea and vomiting
• Nystagmus is often both horizontal and rotational, improving with fixing gaze, and usually triggered by some provoking factor (ie position)
• Often sudden onset
• Often associated with other symptoms: tinnitus, ear pain/fullness, hearing loss, recent viral illness
• Long latency after performing Dix-Hallpike before nystagmus

Physical examination should pay special attention to a full neurological examination (including gait), H&N examination looking at the tympanic membranes, orthostatic vitals, and performing a Dix-Hallpike Maneuver.

See here for a great review.

Lastly, it is important to note that this man was of Western African origin and quite young. Studies have shown that s

mall-vessel cerebrovascular disease and vascular-related cognitive impairment are more prevalent in hypertensive subjects of black African origin compared with Caucasians. This particular study found that

African-Caribbean subjects were typically 4 years younger but had been hypertensive for 3 years longer than Caucasians. They found that mean 24-hour BP was more poorly controlled in African-Caribbean patients and that ethnicity was independently related to

increased hypertensive white matter damage and executive cognitive dysfunction. Another study estimated that the higher BP in hypertensive black patients (as compared to Caucasions) results in 5480 more deaths due to heart disease and 2190 more deaths due to strokes in the US. It is important for us to consider why these differences in both risk factors and outcomes exist - access to healthcare and socioeconomic status being important factors. Interestingly, you may have seen in the news recently - the Annals of Internal Medicine published on culturally-appropriate storytelling (ie African-American patients describing their experiences with hypertension) as an intervention to lower BP - with fascinating results! See here.