Neuro-Otology: Diagnosis and Management of Neuro-Otological Disorders

Ocular Motor

The first step in assessing ocular motor function is to search for spontaneous involuntary movements of the eyes. The examiner asks the patient to look straight ahead while observing for nystagmus or saccadic intrusions. Nystagmus is characterized by a slow- and fast-phase component and is classified as spontaneous, gaze-evoked, or positional. The direction of nystagmus is conventionally described by the direction of the fast phase, which is the direction it appears to be “beating” toward. Recording whether the nystagmus is vertical, horizontal, torsional, or a mixture of these provides important localizing information. Spontaneous nystagmus can have either a peripheral or central pattern. Although central lesions can mimic a “peripheral” pattern of nystagmus ( ), unusual circumstances are required for peripheral lesions to cause “central” patterns of nystagmus. The peripheral pattern of spontaneous nystagmus is unidirectional: that is, the eyes beat only to one side ( Video 22.1 ). Peripheral spontaneous nystagmus never changes direction. It is usually a horizontal greater than torsional pattern because of the physiology of the asymmetry in firing rates within the peripheral vestibular system whereby the vertical canals cancel each other out. The prominent horizontal component results from the unopposed horizontal canal asymmetry. Other characteristics of peripheral spontaneous nystagmus are suppression with visual fixation, increase in velocity with gaze in the direction of the fast phase, and decrease with gaze in the direction opposite of the fast phase. Some patients are able to suppress this nystagmus so well at the bedside, or have partially recovered from the initiating event, that spontaneous nystagmus may only appear by removing visual fixation. Several simple bedside techniques can be used to remove the patient’s ability to fixate. Frenzel glasses are designed to remove visual fixation by using +30 diopter lenses. An ophthalmoscope can be used to block fixation. While the fundus of one eye is being viewed, the patient is asked to cover the other eye. Probably the simplest technique involves holding a blank sheet of paper close to the patient’s face (so as to block visual fixation) and observing for spontaneous nystagmus from the side.

Video 22.1 Acute Peripheral Vestibular Nystagmus.

Saccadic intrusions are spontaneous, involuntary saccadic movements of the eyes, without the rhythmic fast and slow phases characteristic of nystagmus. Saccades are fast movements of the eyes normally under voluntary control and used to shift gaze from one object to another. Square-wave jerks and saccadic oscillations are the most common types of saccadic intrusions. Square-wave jerks refer to small-amplitude, involuntary saccades that take the eyes off a target, followed after a normal intersaccadic delay (around 200 msec) by a corrective saccade to bring the eyes back to the target. Square-wave jerks can be seen in neurological disorders such as cerebellar ataxia, Huntington disease (HD), or progressive supranuclear palsy (PSP), but they also occur in normal individuals. If the square-wave jerks are persistent or of large amplitude (macro-square wave jerks), pathology is more likely.

Saccadic oscillations refer to back-to-back saccadic movements without the intersaccadic interval characteristic of square-wave jerks, so their appearance is that of an oscillation. When a burst occurs only in the horizontal plane, the term ocular flutter is used ( Video 22.2 ). When vertical and/or torsional components are present, the term opsoclonus (or so-called dancing eyes) is used. The eyes make constant random conjugate saccades of unequal amplitude in all directions. Ocular flutter and opsoclonus are pathological findings typically seen in several different types of CNS diseases involving brainstem–cerebellar pathways. Paraneoplastic disorders should be considered in patients presenting with ocular flutter or opsoclonus.

Video 22.2 Ocular Flutter.

Gaze Testing

The patient should be asked to look to the left, right, up, and down; the examiner looks for gaze-evoked nystagmus in each position ( Video 22.3 ). A few beats of unsustained nystagmus with gaze greater than 30 degrees is called end-gaze nystagmus and variably occurs in normal subjects. Gaze-evoked downbeating nystagmus ( Video 22.4 ), vertical nystagmus that increases on lateral gaze, localizes to the craniocervical junction and midline cerebellum. Gaze testing may also trigger saccadic oscillations (see Video 22.3, Video 22.4 ).

Video 22.3 Gaze-Evoked Nystagmus and Impaired Smooth Pursuit.

Video 22.4 Gaze-Evoked Downbeating Nystagmus.

Smooth Pursuit

Smooth pursuit refers to the voluntary movement of the eyes used to track a target moving at a low velocity. It functions to keep the moving object on the fovea to maximize vision. Though characteristically a very smooth movement at low frequency and velocity testing, smooth pursuit inevitably breaks down when tested at high frequencies and velocities. Though smooth pursuit often becomes impaired with advanced age, a longitudinal study of healthy elderly individuals found no significant decline in smooth pursuit over 9 years of evaluation ( ). Patients with impaired smooth pursuit require frequent small saccades to keep up with the target; thus the term saccadic pursuit is used to describe this finding. Abnormalities of smooth pursuit occur as the result of disorders throughout the CNS and with tranquilizing medicines, alcohol, inadequate concentration or vision, and fatigue. However, in a cognitively intact individual presenting with dizziness or imbalance symptoms, bilaterally impaired smooth pursuit is highly localizing to the cerebellum. Patients with early or mild cerebellar degenerative disorders may have markedly impaired smooth pursuit with mild or minimal truncal ataxia as the only findings.

Saccades

Saccades are fast eye movements (velocity of this eye movement can be as high as 600 degrees per second) used to quickly bring an object onto the fovea. Saccades are generated by the burst neurons of the pons (horizontal movements) and midbrain (vertical movements). Lesions or degeneration of these regions leads to slowing of saccades, which can also occur with lesions of the ocular motor neurons or extraocular muscles. Severe slowing can be readily appreciated at the bedside by instructing the patient to look back and forth from one object to another. The examiner observes both the velocity of the saccade and the accuracy. Overshooting saccades (missing the target and then needing to correct) indicates a lesion of the cerebellum ( Video 22.5 ). Undershooting saccades are less specific and often occur in normal subjects.

Video 22.5 Hypermetric Saccades.

Optokinetic Nystagmus and Fixation Suppression of the Vestibulo-Ocular Reflex

Optokinetic nystagmus (OKN) and fixation suppression of the VOR suppression can also be tested at the bedside. OKN is a combination of fast (saccadic) and slow (smooth pursuit) movements of eyes and can be observed in normal individuals when, for example, watching a moving train. OKN is maximally stimulated with both foveal and parafoveal stimulation, so the proper laboratory technique for measuring OKN uses a full-field stimulus by having the patient sit stationary while a large rotating pattern moves around them. This test can be approximated at the bedside by moving a striped cloth in front of the patient, though this technique only stimulates the fovea. Patients with disorders causing severe slowing of saccades will not be able to generate OKN, so their eyes will become pinned to one side. VOR suppression can be tested at the bedside using a swivel chair. The patient sits in the chair and extends his or her arm in the “thumbs-up” position out in front. The patient is instructed to focus on the thumb and to allow the extended arm to move with the body so the visual target of the thumb remains directly in front of the patient. The chair is then rotated from side to side. The patient’s eyes should remain locked on the thumb, demonstrating the ability to suppress the VOR stimulated by rotation of the chair. Nystagmus will be observed during the rotation movements in patients with impairment of VOR suppression, which is analogous to impairment of smooth pursuit. Both OKN and VOR suppression can also be helpful when examining patients having difficulty following the instructions for smooth pursuit or saccade testing.

Vestibular Nerve Examination

Often omitted as part of the cranial nerve examination in general neurology texts, important localizing information can be obtained about the functioning of the vestibular nerve at the bedside. A unilateral or bilateral vestibulopathy can be identified using the head-thrust test ( ) ( Fig. 22.3 and Video 22.6 ). To perform the head-thrust test, the physician stands directly in front of the patient, who is seated on the examination table. The patient’s head is held in the examiner’s hands, and the patient is instructed to focus on the examiner’s nose. The head is then quickly moved about 5–10 degrees to one side. In patients with normal vestibular function, the VOR results in movement of the eyes in the direction opposite the head movement. Therefore the patient’s eyes remain on the examiner’s nose after the sudden movement. The test is repeated in the opposite direction. If the examiner observes a corrective saccade bringing the patient’s eyes back to the examiner’s nose after the head thrust, impairment of the VOR in the direction of the head movement is identified. Rotating the head slowly back and forth (the doll’s eye test) also induces compensatory eye movements, but both the visual and vestibular systems are activated by this low-velocity test, so a patient with complete vestibular function loss and normal visual pursuit will have normal-appearing compensatory eye movements on the doll’s eye test. This slow rotation of the head, however, is helpful in a comatose patient who is not able to generate voluntary visual tracking eye movements. Slowly rotating the head can also be a helpful test in patients with impairment of the smooth-pursuit system, because smooth movements of the eyes during slow rotation of the head indicates an intact VOR, whereas continued saccadic movements during slow rotation indicates an accompanying deficit of the VOR ( ).

Video 22.6 Head-Thrust Tests.

Positional Testing

Positional testing can help identify peripheral or central causes of vertigo. The most common positional vertigo, BPPV, is caused by free-floating calcium carbonate debris, usually in the posterior semicircular canal, occasionally in the horizontal canal, or rarely in the anterior canal. The characteristic burst of upbeat torsional nystagmus is triggered in patients with BPPV by a rapid change from the sitting-up position to supine head-hanging left or head-hanging right (the Dix–Hallpike test; Video 22.7 ). When present, the nystagmus is usually only triggered in one of these positions. A burst of nystagmus in the opposite direction (downbeat torsional) occurs when the patient resumes the sitting position since the debris moves in the opposite direction. A repositioning maneuver can be used to move the debris out of the canal. The modified Epley maneuver ( Fig. 22.4 and Video 22.8 ) is more than 80% effective in treating patients with posterior canal BPPV, compared with 10% effectiveness of a sham procedure (Hilton, 2014). The key feature of this maneuver is the roll across in the plane of the posterior canal so that the debris rotates around the posterior canal and out into the utricle. Once the debris enters the utricle, it no longer disrupts semicircular canal function. Recurrences are common, however (see Video 22.7, Video 22.8 ).

Video 22.7 Benign Paroxysmal Positional Vertigo.

Video 22.8 Epley Maneuver.

If the debris is in the horizontal canal, direction-changing horizontal nystagmus is seen. Patients are tested for HC-BPPV by turning the head to each side while lying in the supine position. The nystagmus can be either paroxysmal geotropic (beating toward the ground) or persistent apogeotropic nystagmus (beating away from the ground). In the case of geotropic nystagmus, the debris is in the posterior segment (or “long arm”) of the horizontal canal, whereas the debris is in the anterior segment (or “short arm”) when apogeotropic nystagmus is triggered. When geotropic nystagmus is triggered, the side with the stronger nystagmus is the involved side. However, when apogeotropic nystagmus is observed, the involved side is generally opposite the side of the stronger nystagmus. With the geotropic variant, class I evidence supports treatment with the barbecue maneuver or the Gufoni maneuver ( ). Another maneuver for HC-BPPV is the “forced prolonged position” ( ). In cases of the apogeotropic variant of HC-BPPV, a variation of the Gufoni maneuver or a head-shaking maneuver can effectively treat the condition, though patients may require a second maneuver to clear the debris from the long arm of the horizontal canal (the same maneuver to treat geotropic HC-BPPV; ).

Positional testing can also trigger central types of nystagmus (usually persistent downbeating), which may be the most prominent examination finding in patients with disorders like Chiari malformation or cerebellar ataxia ( ). Central positional nystagmus can also mimic the nystagmus of HC-BPPV. Positional nystagmus may also be prominent in patients with migraine-associated dizziness ( ).

Fistula Testing

In patients reporting sound- or pressure-induced dizziness, a defect of the bony capsule of the labyrinth can be tested for by pressing and releasing the tragus (small flap of cartilage that can be used to occlude the external ear canal) and observing the eyes for brief associated deviations. Pneumatoscopy (introducing air into the external auditory canal through an otoscope) or Valsalva against pitched nostrils or closed glottis can also trigger associated eye movements. The direction of the triggered nystagmus helps identify the location of the fistula.

Gait

Casual gait is examined for initiation, heel strike, stride length, and base width. Patients are then observed during tandem walking and while standing in the Romberg position (with eyes open and closed). A decreased heel strike, stride length, flexed posture, and decreased arm swing suggest Parkinson disease. A wide-based gait with inability to tandem walk is characteristic of truncal ataxia. Patients with acute vestibular loss will veer toward the side of the affected ear for several days after the event. Patients with peripheral neuropathy or bilateral vestibulopathy may be unable to stand in the Romberg position with eyes closed.

Auditory Examination

The bedside examination of the auditory system begins with otoscopy. The tympanic membrane is normally translucent; changes in color indicate middle ear disease or tympanosclerosis, a semicircular crescent or horseshoe-shaped white plaque within the tympanic membrane. Tympanosclerosis is rarely associated with hearing loss but is an important clue to past infections. The area just superior to the lateral process of the malleus should be carefully inspected for evidence of a retraction pocket or cholesteatoma. Findings on otoscopy are usually not associated with causes of dizziness because the visualized abnormalities typically do not involve the inner ear.

Finger rubs at different intensities and distances from the ear are a rapid, reliable, and valid screening test for hearing loss in the frequency range of speech ( ). If a patient can hear a faint finger rub stimulus at a distance of 70 cm (approximately one arm’s length) from one ear, then a hearing loss on that side—defined by a gold-standard audiogram threshold of greater than 25 dB at 1000, 2000, and 4000 Hz—is highly unlikely. On the other hand, if a patient cannot hear a strong finger rub stimulus at 70 cm, hearing loss on that side is highly likely. The whisper test can also be used to assess hearing at the bedside ( ). For this test, the examiner stands behind the patient to prevent lip reading and occludes and masks the nontest ear, using a finger to rub and close the external auditory canal. The examiner then whispers a set of three to six random numbers and letters. Overall, the patient is considered to have passed the screening test if they repeat at least 50% of the letters and numbers correctly. The Weber and Rinne tests are commonly used bedside tuning fork tests. To perform these, a tuning fork (256 Hz or 512 Hz) is gently struck on a hard rubber pad, the elbow, or the knee about two-thirds of the way along the tine. To conduct the Weber test, the base of the vibrating fork is placed on the vertex (top or crown of the head), bridge of the nose, upper incisors, or forehead. The patient is asked if the sound is heard and whether it is heard in the middle of the head or in both ears equally, toward the left, or toward the right. In a patient with normal hearing, the tone is heard centrally. In asymmetrical or a unilateral hearing impairment, the tone lateralizes to one side. Lateralization indicates an element of conductive impairment in the ear in which the sound localizes, a sensorineural impairment in the contralateral ear, or both. The Rinne test compares the patient’s hearing by air conduction with that by bone conduction. The fork is first held against the mastoid process until the sound fades. It is then placed 1 inch from the ear. Normal subjects can hear the fork about twice as long by air as by bone conduction. If bone is greater than air conduction, a conductive hearing loss is suggested.

Acute Unilateral Vestibulopathy (Vestibular Neuritis)

A common presentation to the ED or outpatient clinic is the rapid onset of severe vertigo, nausea, vomiting, and imbalance. The symptoms gradually resolve over days to weeks, but about 20% of patients report some dizziness even 12 months later (Shupak, 2008). The typical etiology of this disorder is vestibular neuritis, which is presumed to be viral because the course is generally benign and self-limited, similar to Bell palsy. Small histopathological studies support the etiology of a viral cause. However, ischemia or demyelination can also cause an acute unilateral vestibulopathy. The key to identifying an acute unilateral vestibulopathy is recognizing the peripheral vestibular pattern of nystagmus and identifying a positive head-thrust test in the setting of a rapid onset of vertigo without other neurological symptoms. The course of vestibular neuritis is self-limited, and the mainstay of treatment is symptomatic. A course of corticosteroids might improve recovery of the caloric response but symptomatic and functional outcomes were not clinically different ( ). Vestibular physical therapy—delivered with in person sessions or even home training—can help patients compensate for the vestibular lesion (Hillier et al., 2011).

Benign Paroxysmal Positional Vertigo

BPPV has a lifetime cumulative incidence of nearly 10% (von Brevern, 2005). Patients typically experience brief episodes of vertigo when getting in and out of bed, turning in bed, bending down and straightening up, or extending the head back to look up. As noted earlier, the condition is caused when calcium carbonate debris dislodged from the otoconial membrane inadvertently enters a semicircular canal. The debris can be free-floating within the affected canal (canalithiasis) or stuck against the cupula (cupulolithiasis). Though the positional attacks are the hallmark feature, some BPPV patients also report constant mild unsteadiness (Von Brevern, 2015). The gold standard test is the Dix-Hallpike test with the positive finding being the hallmark triggered and transient upbeat-torsional nystagmus. Repositioning maneuvers are highly effective in removing the debris from the canal, though recurrence is common (see Fig. 22.4 ; ). Once the debris is out of the canal, patients are instructed to avoid extreme head positions to prevent the debris from re-entering the canal. Patients can also be taught to perform a repositioning maneuver, should they have a recurrence of the positional vertigo.

Meniere Disease

Meniere disease is characterized by recurrent attacks of vertigo associated with auditory symptoms (hearing loss, tinnitus, aural fullness) during attacks. Over time, progressive hearing loss develops. Attacks are variable in duration, most lasting longer than 20 minutes, and are associated with severe nausea and vomiting. The course of the disorder is also highly variable. For some patients, the attacks are infrequent and decrease over time, but for others they can become debilitating. Occasionally, auditory symptoms are not appreciated by the patients or identified by interictal audiograms early in the disorder, but inevitably patients with Meniere disease develop these features, usually within the first year. Thus the term vestibular Meniere disease , previously used for patients with recurrent episodes of vertigo but no hearing loss, is no longer used. Though usually a disorder involving only one ear, Meniere disease becomes bilateral in about one-third of patients.

Endolymphatic hydrops, or expansion of the endolymph relative to the perilymph, is regarded as the etiology, though the underlying cause is unclear. In addition, the characteristic histopathological changes of endolymphatic hydrops have been identified in temporal bone specimens of patients with no clinical history of Meniere disease ( ). Some patients with well-documented Meniere disease experience abrupt episodes of falling to the ground, without loss of consciousness or associated neurological symptoms. Patients often report the sensation of being pushed or thrown to the ground. The falls are hard and often result in fractures or other injuries. These episodes have been called otolithic catastrophes of Tumarkin because of the suspicion that they represent acute stimulation of the otoliths. The bedside interictal examination of patients with Meniere disease may identify asymmetrical hearing, but the head-thrust test is usually normal. Treatment is initially directed toward an aggressive low-salt diet and diuretics, though the evidence for these treatments is poor. Intratympanic gentamicin injections can be effective and are minimally invasive. Sectioning of the vestibular nerve and destruction of the labyrinth are other procedures ( ). Autoimmune inner-ear disease presents as a fulminate variant of Meniere disease. Another variant is so-called delayed endolymphatic hydrops. Patients with this disorder report recurrent episodes of severe vertigo without auditory symptoms developing years after a severe unilateral hearing loss caused by a viral or bacterial infection.

Vestibular Paroxysmia

Vestibular paroxysmia is characterized by brief (seconds to minutes) episodes of vertigo, occurring suddenly without any apparent trigger (Strupp, 2016). The disorder may be analogous to hemifacial spasm and trigeminal neuralgia, which are felt to be due to spontaneous discharges from a partially damaged nerve. In patients with vestibular paroxysmia, unilateral dysfunction can sometimes be identified on vestibular or auditory testing. Like the analogous disorders, it is conceivable that a normal vessel could be compressing the cranial nerve, and surgical removal of the vessel might seem to be a treatment option. However, many asymptomatic subjects have a normal vessel lying on the eighth nerve (usually the anterior inferior cerebellar artery), and most vestibular paroxysmia patients have a favorable course with conservative or medication management (Strupp, 2016), so the decision to operate in this delicate region is rarely indicated. Medications associated with a reduction in episodes include carbamazepine, oxcarbazepine, and gabapentin (Strupp, 2016).

Vestibular Fistulae

Superior canal dehiscence was first described in 1998 ( ). As the name implies, dehiscence of the bone overlying the superior canal results in a fistula between the superior canal and the middle cranial fossa. Normally the semicircular canals are enclosed by the rigid bony capsule, so these vestibular structures are unaffected by sound pressure changes. The oval and round windows direct the forces associated with sound waves into the cochlea and along the spiral basilar membrane. A break in the bony capsule of the semicircular canals can redirect some of the sound or pressure to the semicircular canals, causing vestibular activation, a phenomenon known as Tullio phenomenon . Prior to the discovery of SCD, fistulas were known to occur with rupture of the oval or round window or erosion into the horizontal semicircular canal from chronic infection. Pressure changes generated by increasing intracranial pressure (ICP; Valsalva against closed glottis) or increasing middle ear pressure (Valsalva against pinched nostrils or compression of the tragus) triggers brief nystagmus in the plane of the affected canal. Surgically repairing the defect can be attempted if the patient is debilitated by the symptoms, but most patients do well with conservative management (Ward, 2017). A study looking at long-term outcome after SCD surgical treatment had a low follow-up rate (43%; 93/218) but reported trends in improved audio-vestibular symptoms that were greatest for autophony, pulsatile tinnitus, audible body sounds, and sensitivity to loud sounds, and least for dizziness (Alkhafaii, 2017). Patients with SCD may have hypersensitivity to bone-conducted sound and bone-conduction thresholds on the audiogram lower than the normal 0 dB hearing levels, even though air conduction thresholds remain normal ( ).

Other Peripheral Disorders

There are many other peripheral vestibular causes of vertigo, but most are uncommon. Vertigo often follows a blow to the head, even without a corresponding temporal bone fracture. This so-called labyrinthine concussion results from the susceptibility of the delicate structures of the inner ear to blunt trauma. Vestibular ototoxicity, usually from gentamicin, can cause a vestibulopathy that is usually bilateral but rarely can be unilateral ( ). A bilateral vestibulopathy can also occur from an immune-mediated disorder (e.g., autoimmune inner-ear disease, Cogan syndrome), infectious process (e.g., meningitis, syphilitic labyrinthitis), structural lesion (bilateral acoustic neuroma), or a genetic disorder (e.g., neurodegenerative or isolated vestibular). The bilateral vestibular loss often goes unrecognized because the vestibular symptoms can be overshadowed by auditory or other symptoms. Although the most prominent vestibular symptoms of bilateral vestibulopathy are oscillopsia and imbalance, some nonspecific dizziness and vertigo attacks may occur as well. Vestibular schwannomas typically present with slowly progressive unilateral hearing loss, but rarely vertigo can occur. Because the tumor growth is slow, the vestibulopathy is compensated by the CNS. Finally, any disorder affecting the skull base, such as sarcoidosis, lymphoma, bacterial and fungal infections, or carcinomatous meningitis, can cause either unilateral or bilateral peripheral vestibular symptoms.

Brainstem or Cerebellar Ischemia/Infarction

Ischemia affecting vestibular pathways within the brainstem or cerebellum often causes vertigo. Brainstem ischemia is normally accompanied by other neurological signs and symptoms, because motor and sensory pathways are in close proximity to vestibular pathways. Vertigo is the most common symptom with Wallenberg syndrome, infarction in the lateral medulla in the territory of the posterior inferior cerebellar artery (PICA), but other neurological symptoms and signs (e.g., diplopia, facial numbness, Horner syndrome) are typically present. Ischemia of the cerebellum can cause vertigo as the most prominent or only symptom, and a common dilemma is whether the patient with acute-onset vertigo needs a magnetic resonance imaging (MRA) scan to rule out cerebellar infarction. Computed tomography (CT) scans of the posterior fossa are not a sensitive test for acute ischemic stroke ( ). Abnormal ocular motor findings in patients with brainstem or cerebellar strokes include (1) spontaneous nystagmus that is purely vertical or torsional, (2) direction-changing gaze-evoked nystagmus (patient looks to the left and has left-beating nystagmus, looks to the right, and has right-beating nystagmus), (3) impairment of smooth pursuit, and (4) overshooting saccades. Central causes of nystagmus can sometimes closely mimic the peripheral vestibular pattern of spontaneous nystagmus ( ). In these cases, a negative head-thrust test (i.e., no corrective saccade) or a skew deviation could be the key indicators of a central rather than a peripheral vestibular lesion ( ). Cardiovascular risk factors are also independent predictors of stroke in dizziness patients (Kerber, 2015) and therefore should be considered in evaluation and management plans.

Multiple Sclerosis

Dizziness is a common symptom in patients with multiple sclerosis (MS). Vertigo is the initial symptom in about 5% of patients with MS. A typical MS attack has a gradual onset, reaching its peak within a few days. Milder spontaneous episodes of vertigo, not characteristic of a new attack, and positional vertigo lasting seconds are also common in MS patients. Nearly all varieties of central spontaneous and positional nystagmus occur with MS, and occasionally patients show typical peripheral vestibular nystagmus when the lesion affects the root entry zone of the vestibular nerve. MRI of the brain identifies white matter lesions in about 95% of MS patients, although similar lesions are sometimes seen in patients without the clinical criteria for the diagnosis of MS.