Neurologic Manifestations of Benign Positional Vertigo Clinical Presentation

Benign paroxysmal positional vertigo typically has a sudden onset. Many patients wake up with it, noticing the vertigo while trying to sit up suddenly. Thereafter, propensity for positional vertigo may extend for days to weeks and occasionally to months or years. In many, the symptoms periodically clear and then recur.

The severity covers a wide spectrum. In extreme cases, the slightest head movement may be associated with nausea and vomiting. In other cases, despite significant nystagmus, the patient seems relatively unfazed.

People who have benign paroxysmal positional vertigo do not usually feel dizzy all the time. Severe dizziness occurs when head movements trigger the attack. At rest and between episodes, patients usually have few or no symptoms.

However, some patients complain of an incessant foggy or cloudy sensorium.

Classic benign paroxysmal positional vertigo usually is triggered by the sudden action of moving from the erect position to the supine position while angling the head 45 degrees toward the side of the affected ear. Merely being in the provocative position is not enough to trigger an attack. The head must actually move to the offending position. After reaching the provocative position, the person experiences a lag period of a few seconds before the vertigo strikes again.

When benign paroxysmal positional vertigo is triggered, patients feel as though they are suddenly thrown into a rolling spin, toppling toward the side of the affected ear. The symptoms start very suddenly and usually dissipate within 20-30 seconds. This sensation is triggered again upon sitting erect; however, the direction of the nystagmus is reversed.

The physical examination findings in patients afflicted with benign paroxysmal positional vertigo are generally unremarkable. With one exception, the Dix-Hallpike maneuver, the entire neuro-otologic examination findings may be normal. However, the presence of neuro-otologic findings does not preclude the diagnosis of benign paroxysmal positional vertigo.

The Dix-Hallpike maneuver is the standard clinical test for benign paroxysmal positional vertigo. The finding of classic rotatory nystagmus with latency and limited duration is considered pathognomonic. A negative test is meaningless except to indicate that active canalithiasis is not present at that moment.

This test is done by moving the patient rapidly from a sitting to a supine position with the head turned 45 degrees to the right. After waiting for about 20–30 seconds, the patient is returned to the sitting position. If no nystagmus is seen, the procedure is then repeated on the left side.

Dix-Hallpike tips:

• Do not turn head to 90 degrees as it can produce an illusion of bilateral involvement.

• Tailor the briskness of the test to the individual patient. Sudden vigorous movements may be harmful to older patients with frail necks. Severely affected individuals can be tested slowly.

• The Epley modification, performed from behind the patient, is easier; the outer canthus can be pulled superolaterally to visualize the eyeball rotation.

• In typical nystagmus, axis is near the undermost canthus. Minimize suppression by directing the patient's gaze to the anticipated axis of rotation.

• Classic posterior semicircular canal benign paroxysmal positional vertigo produces geotropic rotatory nystagmus. The top pole of the eyes rotates toward the undermost (ie, affected) ear.

• Purely horizontal nystagmus would indicate horizontal canal involvement.

• Sustained or nonfatiguing nystagmus might indicate cupulolithiasis rather than canalithiasis.

One of the most common causes of benign paroxysmal positional vertigo is head trauma. Although the true mechanisms are not exactly certain, the concussive forces presumably cause particles that reside in the vestibule to become displaced to the canal. Other factors that predispose individuals to benign paroxysmal positional vertigo include inactivity, acute alcoholism, major surgery, and CNS disease.

Many patients have concomitant ear pathology, which underscores the importance of a complete neuro-otologic examination.

The frequencies of various causes are as follows:

• 39% idiopathic

• 21% trauma

• 29% ear diseases

• 9% chronic otitis media

• 7% vestibular neuronitis

• 7% Ménière disease

• 4% otosclerosis

• 2% sudden sensorineural hearing loss

• 11% CNS disease

• 9% vertebrobasilar insufficiency

• 2% acoustic neuroma

• 2% cervical vertigo