Vertigo: What You Need to Know for Clinical Practice and the Boards

Introduction

Vertigo is a sensation of spinning, either of the patient or of his or her environment.

There are four types of vertigo that you must consider in a patient who complains of a spinning sensation:

• Toxic vertigo
• Central nervous system vertigo
• Peripheral nervous system vertigo
• Hematologic vertigo (hyperviscosity syndrome)

Toxic Vertigo

Salicylates and anticonvulsants, particularly phenytoin, are classic causes of toxic vertigo. The hallmark of salicylate toxicity is metabolic acidosis with concomitant respiratory alkalosis.  (A classic case of salicylate poisoning is broken down here. Know it cold before sitting for any standardized test in general medicine!). The hallmark of phenytoin toxicity is nystagmus, with other signs and symptoms of sedative intoxication such as slurred speech and ataxia.

Other important vestibulotoxins include the aminoglycosides and quinine (tonic water!).

Central Vertigo

” Central vertigo results from dysfunction of the vestibular portion of the eight cranial nerve, vestibular nuclei [in the brain stem], and their connections.” Bhidayasiri (2005).

If the patient has no cerebellar signs (intention tremor, dysmetria, dysdiadochokinesia, gait ataxia, ataxic dysarthria) and the only neurological issue is vertigo, then chances are slim to none that he or she has central vertigo secondary to a stroke. The brainstem is packed with extremely critical microscopic neurocircuitry. It is extremely unlikely that a stroke would knock out the vestibular branch of the vestibulocochlear nerve (CN VIII) only, without leaving any other signs or symptoms of cranial nerve abnormalities.

In any event, the most common causes of central vertigo are:

• Posterior circulation syndromes: These patient’s have brainstem and cerebellum issues (vertigo, diplopia and ataxia). Never miss lateral medullary syndrome, which is also known as Wallenberg syndrome or posterior inferior cerebellar artery (PICA) syndrome. These patients present with vertigo, oropharyngeal dysphasia, dysarthria, and limb ataxia. They can also develop airway compromise and aspiration pneumonia secondary to inability to clear secretions. So if you come across a drooling patient, either in real life or on the Boards, who has complex constellation of neurological finding, but has no limb weakness or altered mental status, then the most likely diagnosis is Wallenberg syndrome. Institute intensive care-level monitoring and order a modified barium swallow if necessary. A chest radiograph will sometimes show opacifications that are consistent aspiration pneumonia or pneumonitis.
• Vestibular schwannoma (acoustic neuroma): look for unilateral acute or subacute sensorineural hearing loss, most especially in patients with café-au-lait spots or cutaneous neurofibromas. The Weber test will lateralize to the “good ear.” If you don’t have a tuning fork, just ask the patient to hum. The patient will hear it better in the good ear. The Rinne test will show air conduction better than bone conduction. (Air conduction better than bone conduction is seen in patients with sensorineural hearing loss and in normal patients because the normal function of the middle ear apparatus is to amplify sound). In any event, when you’re done fiddling around with the tuning fork, get  a brain MRI with gadolinium.
• Multiple sclerosis: look for non-toxic acute optic neuritis (painful, unilateral, with visual disturbances), internuclear ophthalmoplegia (on horizontal gaze, there is weak or failed adduction of the eye that should adduct, along with horizontal jerk nystagmus of the abducting eye), with and other relapsing and remitting neurological signs and symptoms. These patient’s need funduscopy to look for optic nerve swelling and an MRI of the brain and spinal cord to look for plaques (“Dawson fingers“). Cerebrospinal fluid may show a mild lymphocytosis with elevated total protein. Cerebrospinal fluid electrophoresis often shows oligoclonal bands of gammaglobulin.

Peripheral Vertigo

“Peripheral vertigo is caused by dysfunction of the vestibular end organs, including semicircular canals, utricle, and saccule.” Bhidayasiri (2005). The most common cause of peripheral vertigo are:

• Benign paroxysmal positional vertigo (BPPV): this is, by far, the most common cause of vertigo. These patient present with a sudden onset of vertigo, often associated with a sudden head movement, such as rolling around in bed. Try to induce it with the Dix-Hallpike maneuver (video here). Peripheral vertigo will result in delayed onset (3-40 seconds) horizontal or rotary nystagmus that stops within 30 seconds and is fatigable. Central vertigo is immediate, persistent and vertical.
• Vestibular neuritis: these patients present with sustained vertigo, nausea, vomiting, without hearing loss or tinnitus, the onset of which is not associated with sudden head movements. These patients are unable to maintain gaze fixation with head thrust testing (video here).
• Ménière disease: the tipoff for this is episodic, progressively worsening vertigo with hearing loss and tinnitus. These patients need an audiogram.

Hematologic vertigo

Hyperviscosity syndrome is sometimes seen in patients with hematological malignancies, classically Waldenström macroglobulinemia. These patients present with vertigo, blurry vision, and mucosal bleeding. The macroglobulin responsible for hyperviscosity in Waldenström macroglobulinemia is IgM (mnemonic: “W” is an upside down “M”). Formal diagnosis requires serum protein electrophoresis with immunofixation and serum viscosity, but the fastest way to make the diagnosis of hyperviscosity syndrome is with funduscopy. This will sometimes show retinal venous engorgement with sausage-like beading of the retinal veins.