18 Central Vertigo and Disequilibrium Vertigo or disequilibrium associated with central lesions or as a symptom of known diagnoses is well established and easy to ascertain, control, or manage. The real dilemmas occur when the vertigo is acute and ascribed to a peripheral etiology rather than a life-threatening central bleed/stroke. However, the money spent in evaluating every patient with an acute vertiginous attack is staggering. This chapter assesses various methods of differentiating the central from the peripheral in a cost-effective manner so that not every acute vertiginous attack receives an MRI, vascular studies, cardiac tests, laboratory analysis, and hospital admission. Because peripheral causes of vertigo are so much more common and can be determined with some degree of certainty with bedside tests and laboratory analysis, they should be considered first if the patient exhibits no other overt central neurologic pathology/symptoms. Thus, physicians need to understand the complexities of these conditions and be well versed in the head thrust test, vestibulo-ocular reflex (VOR), nystagmus, and benign paroxysmal positional vertigo (BPPV).1,2 In the classic paper by Fisher,3 written almost 50 years ago, the notion that acute vertigo could have a central cause was described. Since then, other papers have demonstrated the severity of some of the consequences, such as death. With the advent of MRI, we now know that smaller central bleeds can be the root cause of an acute vertiginous attack. The problem is whether the acute vertigo is really due to the pathology on the scan, since the age of the lesion is typically not able to be determined. This section predicates that the patient has no focal neurologic signs/symptoms that would negate a peripheral cause. In those cases where the patient does exhibit these signs/symptoms (such as dysarthria, unilateral weakness or numbness, disorientation), diffusion-weighted MRI (MRI-DWI) with and without contrast is indicated. History is also extremely important. Whether the episode is a constant one lasting days to weeks to months versus multiple small spells of vertigo associated with movements that then subside when not moving is important. Thus, history as well as bedside evaluation is extremely useful in pinpointing a peripheral versus central cause. The examination should include testing for dysmetria and truncal ataxia, both key central pathology findings. However, it is eye movement, nystagmus, that can be very revealing of central or peripheral etiologies. Some of the more common central findings include bidirectional nystagmus, gaze-evoked nystagmus in the vertical or horizontal plane, inability to suppress the vertical ocular reflex (VOR), rebound nystagmus, and abnormal saccades or smooth pursuit testing. It is the smooth pursuit and positional testing that prove to be the more difficult. Bedside testing of smooth pursuit is performed with the patient following the examiner’s finger or a high-contrast focal point, such as a penlight, which the examiner moves back and forth. This test does require adequate vision and therefore it may be difficult in some elderly patients, especially those with cataracts. Normal patients can easily track the moving source in a fluid motion, while central lesions induce a jerky path of following, often termed a saccadic pursuit pattern. In addition, testing for suppression of the VOR can be done by having the patient extend his arm out and hold up his thumb. While the patient fixates on the thumb, the chair is rotated back and forth. The slow visual tracking system should be able to suppress the VOR, and if it cannot, then a central pathology is indicated. Abnormal smooth pursuits can be associated with any central pathology but in patients with acute vertigo, the most common etiology is a midline cerebellar lesion. The only time that abnormal smooth pursuit is found with a peripheral etiology is in acute labyrinthitis, when the patient has high-velocity nystagmus. In this case, the smooth pursuit may be abnormal in the direction of the fast phase. Positional testing can also reveal central pathology. In BPPV, the typical nystagmus is in the horizontal-rotary direction and is fatiguable. Central findings typically include nonfatiguable nystagmus, the vertical or downbeating nystagmus (although superior canal otoliths can cause a downbeat nystagmus), and inability to cure the problem with typical bedside maneuvers. The most common central lesions in these instances involve the cerebellum’s flocculonodular lobe and include Chiari malformation, tumor, or a cerebellar degenerative process. Recent papers suggest a new test may be important in places like the emergency department for assessing central versus peripheral pathology in acute vertigo.4,5,6,7 The test is known as HINTS, and it is a battery of three tests of oculomotor physiology performed at the bedside. HINTS stands for h ead i mpulse test, n ystagmus, t est of s
Introduction
Diagnostic Evaluation of the Acute Vertiginous Attack
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