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VI. HEARING LOSS AND TINNITUS

Hearing loss and tinnitus are best evaluatedby a team that includes both a
neurologist and an ontologist.
A. HEARING LOSS. Clinical and audiometricdata should guide
neuroimaging. The deficit may be (1) sensorineural (SNHL),
conductive (CHL) or mixed; (2) unilateral or bilateral; and (3)
congenital or acuired.
1. Sensorineural hearing loss. Unilateral or asymmetrical SNHL in
adults is best evaluated with MRI. The most common cause is a
vestibular schwannoma (acoustic neuroma). Even small lesions of
the internal auditory canal and cerebellopontine angle are
diagnosed with thin T1, T2 and postcontrast axial and

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Coronal MRI, and the addition of a high-resolutionvolume sequence
labeled FIESTA (fast Imaging Employing Steady sTate Acquisition). MRI
should also evaluate the remainder of the acoustic pathway for possible
ischemic or demyelinaing lesions, particularly the medullary cochlear
nuclear complex (which lesions mimic those caused by vestibular
schwannomas), thalamaus, and temporal lobe.
SNHL in children, unilateral or bilateral, is usually related to
congenital inner ear diseases, requiring high-resolution noncontrast CT as
the initial evaluation to assess the cochlea, vestibule, semicircular canals,
vestibular aqueuct, andendolymphatic duct and sac. Enlarged vestibular
aqueduct syndrome is a common cause of SNHL

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2. conductive hearing loss. CHL is due to disruption of the
mechanical components of the auditory apparatus (small bony
elements surrounded by air ). CHL is therefore best evaluated by
noncontrast high resolution CT. CHL is most commonly due to
temporal bone inflammatory disease, particularly otomastoditis and
otitis media, managed by otolaryngologists. Otosclerosis (also called
otospongiosis) causes both CHL and SNHL (bilateral in 80%) and
tinnitus. It is due to replacement of endochondral bone by spongius
bone at the oval window (fenestral), or the cochlea (restrofenestral).
Other causes for CHL include middle ear cholesteatomas, tumors
(glomus tympanicum), and traumatic ossicular dislocations, all well
evaluated with CT.
B. TINNITUS. Tinnitus (ringing in the ear) may be very disturbing to
patients. It may be pulsatile or nonpulastile. Objective tinnitus,
heard by both the patient and the examiner, commonly leads to
findings. Subjective tinnitus, only heard by the patient, has a low
diagnostic yield.
1. Pulsatile tinnitus. Pulsatile (pulse synchronous) tinnitus is best
evaluated by MRI/MRA, whether or not direct otoscopic examination
shows a retrotympatic mass. A vascular-appearing tympanic
membrane may be associated with arterial (aberranat carotid
artery, carotid stenosis or dissection, petrous carotid artery
aneurysms), venous (dehiscent or high-riding jugular bulb),
inflammatory (cholesterol granuloma, middle ear mastoiditis)
causes or tumors (glomus tympanicum or jugulotympanicum,
meningioma). Tinnitus with a normal otoscopic. Examination should
raise suspicion for a dural arteriovenous fistula (of the sigmoid
sinus or the tentorium); MRI may show suspicious flow voids, MRA
source images transosseous arterial structures, postcontrast MRI
and MRV an occluded dural sinus. Confirmation (and therapy) is
provided via cathere angiography. Other conditions include benign
intracranical hypertension (pseudotumor cerebri), chronic anemia,
and thyrotoxicosis.
2. Nonpulsatile tinnitus. Nonpulsatile tinnitus is most commonly
caused by menieres diseases, which also manifests as episodes of

vertigo and SNHL increasd volumes of endolymph, causing enlarged

endolymphatic spaces have been incriminated. The diagnosis is
clinical, but when indicated, neuroimaging should be done with CT.
Other causes include otosclerosis and middle ear inflammatory
disease, also best studied with CT.

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VII. VERTIGO AND ATAXIA
Vertigo and ataxia point to posterior fossa pathology, where CT has
distinct disadvantages over MRI due to significant artifact from bony
structures and poor contrast resolution.
Causes of peripheral vertigo include vestibular schwannomas, viral
labyrinthitis, menieres disease, or perilymphatic fistulae. Central vertigo
may be due to posterior fossa lesions like demyelinating disease, tumors,
strokes, arnold-chisri malformation, and trauma. The preferred
neuroimaging method to investigate vertigo is MRI (vide supra),
appearing as small enhancing masses. Rarely, viral labyrinthitis will show
as bright T signal within the vestibular apparatus indicative of
hemorrhagic products. Even small multiple sclerosis plaques, ischemic
lesions, appear as bright lesions on T2 and FLAIR imaging.
Ataxia is usually meants as cerebellar dysfunction, altought it may
also be sensory or vestibular. Again, MRI is the preferred imaging modality
to study patients with ataxia due to its superiority in demyelinating
disease, ischemia, and tumors. Other causes of ataxia include chronic
ethanol and phenytoin intoxication, a number of degenerative conditions,
paraneoplastic syndromes, all accompanied with cerebellar atrophy, well
demonstrated on sagittal and coronal MRI
VIII. DISTURBANCES OF VISION
The optic pathways and the globe both are exquisitely well evaluated with
MRI, which is the preferred neuroimaging study in patients with signs of
disturbed vision.

A. Visual loss (including amaurosis fugax). Gradual monocular vision

loss is usually
related to ocular pathology like cataract. Sudden unilateral vision
loss most commonly results from diabetic retinophaty, followed by
ocular ischemic syndrome, which may be caused by retinal vein
occlusion, retinal artery occlusion, anterior ischemic optic
neuropathy (AION), an ischemic syndrome of the anterior ciliary
vasculature, and rarely to demyelinating disease of the optic nerve,
well evaluated with pre- and postcontrast MRI. Amaurosis fugax
designates vision loss caused by reduced blood flow to the eye,
heralding a stroke and prompting therapy. The most common causes
of amaurosis fugax is stenotic carotid disease, best evaluated by
MRA ,as duplex ultrasound lacks precision. CTA has increasing
accuracy to study carotid disease, although heavily calcified plaques
remain a major limitation. As mentioned earlier, conventional
angiography remains useful in doubtful situations.
Visual field deficits related to lesions affecting the optic
chiasm, tracts, and radiations should be first studies with contrastenhanced MRI. Lesions affecting the chiasm, like piyuitary
adenomas and suprasellar lesions are particularly well suited for
coronal and sagittal MRI. Most demyelinating and inflmmatory
conditions and tumors involving the postchiasmatic optic pathways
appear bright on T2 and FLAIR
imaging and occipital lobes appear as dark, tortuous flow voids on
T1 and T2 imaging.
B. Impairment of ocular motility. Ocular motility dysfunction most
commonly result from diabetic neuropathy and traumatic lesions of
the orbit or the superior orbital fissure. Traumatic lesions involving
bony structures are best evaluated with thin-cut CT with coronal
recontructions. Nontraumatic pathology may result from a variety
of lesions affecting the oculomotor, trochelar, and abducens nerves
anywhere between their brainstem nuclei and the orbit, where MRI
has far greater superiority; brainstem strokes, demyelinating and
inflammatory lesions, tumors, petrous apex lesions, cavernous sinus
and orbital apex tumors, aneurysms, and inflammatory lesions. A
sudden third cranial nerve palsy

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Suggestive of posterior communicating artery aneurysms may be initially
evaluated with either MRI/MRA or CT/CTA. Extraocular muscle pathology
[evaluated thyroid ophthalmopathy and intracolar inflammatory disease
(pseudotumor) and tumors] is also well evaluated with coronal MRI of the
orbits.
C. Chemosis and proptosis. Carotid-cavernous fistuale (CCFs) are
the most common causes of ophthalmic venous system flow
reversal and engorgement. Direct CCFs are caused by arterial wall
rupture of the intracavernous carotid segment, most commonly from
a traumatic arterial laceration, less commonly from spontaneous
rupture of a small aneurysms, ehlers-danlos syndrome,
fibromuscular dysplasia, or a spontaneous arterial dissection indirect
CCFs are due to spontaneous arteriovenous shunting to the
ophthalmic vein from dural arterial branches of the external carotid
artery in response to yet poorly understood triggering factors, the
most common associations being pregnancy, dehydration, sinus

infections. Contrast-enhanced CT and MRI show dilated ophthalmic

vein and cavernous sinus in direct CCFs. Indirect CCFs may be much
more subtle, sometimes only suspected on the the basis of small
vermicular flow voids around a dural sinus. Catheter angiography is
diagnostic and provides the route for transvascular therapy.
IX. TRAUMA
CT is the frontline neuroimaging modality in trauma because it is fast,
delivers a negligible radiation dose, and has superior accuracy in
detecting acute intracranial blood. High-resolution, fast CT scanners
are routinely installed within emergency departments. Skull films no
longer have a role in assesing patients with significant head trauma,
with the possible rare exception of linear skull fractures not well seen
on scout or axial CT images. CT is done liberally in trauma patients,
including those without neurological signs, despite a low yield; it is
cost-effective compared to admission and observation.
A. Closed head injury. Except in the infratemporal and subfrontl
regions, and the posterior fossa, CT is superior in detecting even
very subtle blood collections. CT is interior to MRI in the detection of
diffuse axonal injury (DAI). CT imaging parameters in trauma should
include a narrow window (for acute blood), an intermediate window
(for subacute blood), and a wide (bone) window. Acute blood may be
present in the form of intracerebral (contusion), epidural, or
subdural hematomas and subarachoid hemorraghe (SAH). Fractures
are well evaluated on bone windows and from coronal dan sagittal
recontruction images. Patients with acute trauma and favorable
initial coma scores usually fare well and do not require extensive
follow-up imaging. In patients with moderate or severe trauma, or
low initial glasgow coma scores (CGS), sequential CTs allow
extension of initial hemorraghe, re-hemorraghe, cerebral edema,
herniation, response to external ventricular drainage, and
intracranial pressure monitors. A shift of the midline structures
(measured at the level of the septum pellucidum) greater than 10
mm has poor prognostic value. Diffuse cerebral edema, more
common in younger patients causes effacement of CSF spaces and
may to medical attention several days or weeks after head trauma,
with worsenng be isodense on CT, and therefore difficult to see. MRI
is superior to evaluate both extraaxial collections with standard T1
and T2 sequences, and the presence of blood products in the brain
parenchyma with gradient echo sequences.
B. Penetrating head injury. CT is the modality of choice in patients
with penetrating head injuries. Metallic objects (shrapnel) and glass

appear hyperdense on CT whereas wood objects appear hypodense

(air-containing). CT permitsan excellent evaluation of the extent of
bone damage, and that of the underlying parenchyma, including
hematomas, edema, infarction, and herniation.

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C. Cervical spine injury. Plain x-rays remain the first-line imaging
method in ptients with cervical spine trauma and should include at
least anteroposterior, lateral, and open-mouth (odontoid) views.
Cervical spine CT with fast scanners offers submillimeter resolution
allowing detection of the slightest fractures. MRI is the preferred
method to evaluate spinal cord contusions, which appear bright on
T2 and short tau inversion recovery (STIR) pulse sequences, and
dark on gradient echo sequences due to the magnetic susceptibility
effect of acute blood.

D. Vascular injury. Blunt injury to the neck may result in traumatic

arterial dissections, pseudo-aneurysms or acute occlusions. In stable
patients, MRA or CTA are excellent imaging methods. Unstable
patients may go directly to angiography, particularly if endovascular
management is contemplated. Penetrating injuries may result in
similar lesions, in addition to significant bleeding from both arterial
and venous (jugular vein) injuries. CTA is the imaging method of
choice in these patients because current fast scanners allow
evaluation of large anatomical areas with high-resolution and
limited-contrast administration. Unstable patients may also require
emergency angiography and possibly lifesaving endovascular
occlusion of a bleeding artery (however, often without the benefit of
a preliminary balloon test occlusion).
X.NECK PAIN AND CERVICAL RADICULOPATHY
Cervical spondylosis is the most common cause of neck pain and
cervical radiculopathy, and its incidence increases with age. It is
characterized by hypertrophic arthropathy of the facet joints,
osteophyte formation at the disk margins, and progressive
intervertebral disk degeneration and herniation. All these changes
result in central canal and neural foraminal stenoses, with resulting
restriction of the spinal cord and the nerve roots. In younger patients,
sudden disc herniation may cause acute symptoms. Other causes of
cervical pain and radiculopathy include syringomyelia with or without
chiari malformation, benign tumors of the spinal canal or the neural
foramina like schwannomas and meningiomas, demyelinating disease
(fig. 32.8), and posttraumatic myelomalacia. MRI is the preferred
method to image these patients because it allows superior evaluation
of the cervicomedullary junction, the cord, the spinal canal, and the
neural foramina. CT myelography may be useful in patients with
cervical spondylosis and contraindications or intolerance to MRI.
XI.BACK PAIN
Low back pain is n extremely common complain, expressed at least
once by 85% of the population.
A. General causes and evaluation. Most causes of transient low
back pain are benign and related to degenerative diseae, muscle
strain, mild trauma, excess weight, and poor posture. In addition,
increasing perception in both the medical community and the public
is that imaging for back pain is grossly overused. Imaging is ony
recommended for back pain associated with certain findings, like
radiculopathy or lower motor neuron deficit, sudden onset, older

age, signs of systemic infedtion, known or suspected malignancy,

and trauma. MRI is the preferred study in these cases. The
relationship between persistent back pain (including radicular pain)
and instability is increasingly appreciated. Instability may be defined
as loss of stiffness of a segment of the spine, subjecting it to
abnormal displacement during physiological movements. Plain xrays of the spine, in neutral position, flexion and extension are the
most widely used screening method, and allow identification of
patients who are likely to benefit from corrective surgery, that is,
those wth spondylolisthesis and lumbar intervertebral instability. CT
is useful in many to provide further detail. CT myelography and MRI
have similar merits in the presurgical evaluation of spinal stenosis.

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B. Lumbar radiculopathy (sciatica). Lumbar radiculopathy is pain
that originates along the course of the sciatic nerve, which runs
from the lumbar spine tu the posterior thigh. Lumbar disc
herniation, the most common cause of sciatica, is a break in the
annulus fibrosus with subsequent displacement of nucleus pulposus,
cartilage, or bone byond the disc space. Other causes of sciatica
include degenerative disease (including synovial cysts) and spinal

stenosis, tumors (primary and metastatic), infections (osteomyelitis,

abscess), and hematomas (epidural, subdural, psoas). MRI is the
study of choice for the initial evaluation of lumbar radiculopathy,
because it demonstrates the lower cord, cauda equina, nerve roots,
bony elements, and discs with exquisite contrast in multiple planes.
Contrast enhancement offers superiority in evaluating infections and
tumors. Disc herniations are extremely well evaluated with MRI,
although CT myelography has excellent accuracy as well. MRI is
inferior to CT in spondylolysis and spondylolisthesis.
C. Failed back syndrome. Following lumbar disc surgery, recurrent or
residual pain is an often-encountered problem, termed failed back
or failed back surgery syndrome, reported in up to 40% of
postoperative patients. Distinguishing between recurrent (or
residual) disc and scar tissue is very important because surgery is
indicated for recurrent disc but not for scar tissue. Postcontrast MRI
is the study of choice, showing showing soft tissue adjacent to the
affected nerve root with significant enhancement in granulation
tissue, but not in disc. Although these findings are usually reliable,
disc material may indeed enhance slightly due to inflammatory
changes early after surgery (and up to several months), and scar
tissue may not enhance much. Recurrent pain following lumbar disc
suegery has other causes, like arachnoiditis, mechanical instability,
and epidural fibrosis, which are sometimes difficult to sort out.