Catastrophic Neurologic Disorders in the Emergency Department , 2nd Edition

Chapter 4. Spinning

Akin to other equally less precise descriptions, spinning (or the perception of movement) may have different meanings. The sensation of spinning in a patient acutely admitted to the emergency department frequently is due to near fainting, hyperventilation, acute peripheral vestibular disease,1,2,3,4 anxiety, or other disorders outside the purview of acute neurology (Box 4.1). Naturally, it is essential to extrapolate urgent disorders from patients reporting signs such as acute floating, giddiness, wooziness, drunkenness, tilting, and imbalance. Some of these disorders are discussed in more detail in the third section of this book and include vertigo as presenting signs of cerebellar hematoma, acute embolus to the basilar artery, and dissection of the vertebral artery. Other key neurologic signs and neuroimaging features usually point to the diagnosis. The main task is to find convincing arguments for a lesion in the central nervous system as a cause of spinning and certain elements in the history that should point to a lesion of the central vestibular system or cerebellum. When present, they justify an urgent magnetic resonance imaging (MRI) study for which the patient may be transferred to a tertiary center. There are both otologic and neurologic emergencies that need to be considered. Otologic emergencies should be considered because emergent antibiotic or antiviral therapy could minimize longstanding sequelae (see Color Fig. 4.1 in separate color insert). These disorders are summarized in Table 4.1.7

Clinical Assessment

When acute spinning represents vertigo, the history may provide additional clues. Autonomic symptoms such as vomiting, nausea, pallor, and sweating are less pronounced in central lesions but are so common and come in different degrees of severity that they cannot be used as major discriminating factors. Vertigo due to positional change, coughing, sneezing, fluctuating hearing loss, nonpulsatile tinnitus, and hearing loss is more typical of peripheral vestibular disease.8

Oscillopsia is another important sign, in which patients feel images are moving or bouncing. When combined with spontaneous nystagmus and transient vertigo, a peripheral source is likely. Central causes may be strongly considered when oscillopsia is induced by head movement. Lesions in the cerebellum produce a spinning sensation, but more often severe scanning speech and impaired finger-to-nose and heel-knee-shin testing predominate in the clinical picture. Ipsilateral hearing loss points to an occlusion of the anterior inferior cerebellar artery.9 Ipsifacial numbness, hypophonia, and Horner's syndrome localize in the lateral medulla oblongata. Details of these disorders and other cerebrovascular-related occlusions are found in Chapter 15.

Several neurologic signs need careful documentation. The characterization of nystagmus is necessary and an important determinant.10,11 Central nystagmus has a characteristic direction dependence. When present, gaze to where the fast component of nystagmus beats increases the frequency and amplitude in any type of nystagmus. In central causes of nystagmus, gaze away from the direction of the fast component will achieve the opposite effect and may abolish or, in extremes of gaze, reverse the direction of nystagmus. A vertical nystagmus (up- or downbeat) is almost always central but can be drug-induced (particularly opioids).12 Gaze-evoked nystagmus with similar amplitudes in both directions is due to drugs but has been reported in myasthenia gravis, multiple sclerosis, and cerebellar atrophy.10Periodic alternating nystagmus (nystagmus changing in direction) has typically been considered in disease of craniocervical function but can be due to phenytoin intoxication or lithium.13 Common central types of nystagmus are shown in Table 4.2.

Box 4.1. Systemic Illness and Drug-Induced Dizziness

Certain metabolic derangements could produce a profound (and sometimes permanent) effect on the vestibular system. Longstanding juvenile diabetes mellitus, fat emboli, and hyperviscosity syndromes may acutely occlude the common cochlear artery.5 Less clear mechanisms known for acute vertigo arc dialysis, acute anemia, and hypothyroidism; and many of die vasculitic syndromes such as polyarteritis nodosa, Wegener's granulomatosis, Behçet's disease, connective tissue disorders. Vertigo can be a paraneoplastic manifestation. Drugs known to damage the auditory system are aminoglycosides, anti-epileptic drugs, loop diuretics, and cis-platin, Exposure to these drugs may be only brief, and toxic levels are not always required to produce permanent destruction of auditory and vestibular systems.6

Peripheral vestibular and congenital nystagmus can be markedly muted by visual fixation of the patient.14 Nystagmus can be observed with eye closure, but it is easier to examine the eye with the ophthalmoscope covering the opposite eye. This maneuver eliminates fixation and brings on alternating drift and correcting jerks of the retina as a manifestation of the nystagmus. Frenzel glasses (30 plus lenses) also eliminate fixation, and both eyes can be observed due to the great magnification (Frenzel glasses are rarely available in emergency rooms and require ear, nose, and throat consultation). Positional nystagmus can be documented after a rapid change from sitting to head hanging over the examination table, turning the head sideways. A torsional and vertical nystagmus appears after 10 seconds' delay and produces a vertiginous sensation that fades away with repeated testing. Both delay and fatigability are characteristic of this positional nystagmus. This maneuver (Dix-Hallpike) is helpful to bring on a vestibular lesion mostly due to canalithiasis. Its absence may suggest a central cause.

Vestibulospinal reflexes (i.e., neuronal connections from labyrinths and vestibular neurons to anterior horn cells) are tested by past-pointing, the Romberg test, and tandem walking. Past-pointing is tested by having the patient touch the hand of the examiner with an extended arm, close his or her eyes, point up, and try to touch the examiner's hand again in a repeated to and fro movement but with eyes closed. Past-pointing occurs toward the damaged side. Abnormalities of the past-pointing test may not be replicated by the more traditional finger-to-nose test because joint and muscle proprioception during this coordinated movement may compensate. Another technique is vertical writing with eyes closed. This test identifies unilateral vestibular dysfunction, but this may occur in both peripheral and central causes.15

Table 4.1. Vertigo and Otologic Emergencies




Herpes zoster oticus

Ear lobe vesicles, hearing loss, facial palsy

Acyclovir 1 g/day for 10 days

Bacterial labyrinthitis

Acute deafness, prior cholesteatoma, meningitis

Surgical management or specific antibiotics

Malignant external otitis (Pseudomonas aeruginosa)

Extreme ear pain, facial palsy (may be multiple cranial nerves)

Ciprofloxacin or gentamicin

Perilymph fistula

Tinnitus, hearing loss, position vertigo, prior strain or Valsalva or barotrauma

Conservative first, then surgery

Labyrinth hemorrhage

Nausea, vomiting, hearing loss, trauma

Correct underlying coagulopathy

Data from Cummings et al.7

Table 4.2. Nystagmus in Acute Lesions of the Central Vestibular System





Increasing amplitude with downgaze

Cervicomedullary junction


Increasing amplitude with upgaze

Dorsal medulla oblongata


With continuous lateral position, reversal or disappearance




Brain stem

Ocular bobbing

Downward jerk with slow return to midposition


Static posture is tested by Romberg's test. Standing with feet close together and eyes closed can be maintained for 30 seconds in normal individuals less than 70 years old.7 Crossing the arms against the chest adds a touch of difficulty and may bring on more subtle swaying. Tandem gait walking (10 steps) evaluates vestibular function when done with eyes closed and cerebellar function with eyes opened. Dysbalance due to acute vermian or cerebellar hemisphere lesion can be dramatic because patients are unable to sit steady or unable to stand unassisted.

Line of Action

A few patients presenting with spinning will have an emergent neurologic disorder. In many, an acute nonviral labyrinthitis can be diagnosed or drug toxicity has emerged.5,6 As mentioned before, a full-scale neurologic evaluation should proceed only after otologic emergencies have been considered and rejected as possible explanations. The signs and symptoms that point to a central cause of vertigo and warrant urgent MRI and magnetic resonance angiography are summarized in Figure 4.2. This will image the posterior fossa structures and flow interruptions in the vertebrobasilar circulation. Cerebrospinal fluid examination could document elevated immunoglobulin G synthesis and oligoclonal bands supporting a first bout of multiple sclerosis or pleocytosis with a wide range of diagnostic possibilities, including meningeal carcinomatosis and major central nervous system infections (see Chapter 18).

Figure 4.2 Critical steps in vertigo evaluation due to central nervous system cause. MRA, magnetic resonance angiography.


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14. Leigh RJ, Zee DS: The Neurology of Eye Movements, 3rd ed. New York: Oxford University Press, 1999.

15. Fukuda T: Vertical writing with eyes covered: a new test of vestibulospinal reaction. Ada Otolaryngol 50:26, 1959.