20 -NONNEOPLASTIC DISORDERS of SPINE and SPINAL CORD .

Nonneoplastic Disorders of the Spine and Spinal Cord Infection Spondylitis and Diskitis Epidural and Subdural Infections Meningitis, Myelitis, and Cord Abscess Normal Aging and Disk

Nonneoplastic Disorders of the

Spine and Spinal Cord

Infection

Spondylitis and Diskitis

Epidural and Subdural Infections

Meningitis, Myelitis, and Cord Abscess

Normal Aging and Disk Degeneration

Spondylosis, Arthrosis, and Spinal Stenosis

Disk Bulges and Disk Herniation

Normal Postoperative Spine

"Failed Back" Syndromes

Back Pain in Children

Trauma

Mechanisms of Spine Injury

Osseous Spine Injury Patterns

Soft Tissue Injuries

In this chapter we consider benign acquired

disorders of the spine and spinal cord, beginning

with infection and demyelinating diseases and

INFECTION Spondylitis and Diskitis

Early diagnosis is crucial in the management spine infections because delayed treatment can lead to increased morbidity and mortality.1,2 We begin this section by focussing on pyogenic and tuberculous spondylitis and

diskitis, then turn our attention to epidural abscess and

meningitis We conclude by discussing spinal cord

abscesses (see box)

Pyogenic spondylitis Infective spondylitis involves

one or more of the extradural components of the spine It most often affects the vertebral bodies (osteomyelitis), but the posterior elements, intervertebral disks, epidural spaces, and paraspinous soft tissues can also be affected 3

Etiology and pathology A spectrum of bacterial,

fungal, or parasitic organisms can cause infectious

spondylitis Staphylococcus aureus is the most common

pyogenic organism in adults, accounting for approximately

60% of infections; Enterobacter, a frequent genitourinary

pathogen, accounts for 30%.4 Other common organisms include Escherichia coli, Salmonella, Pseudomonas aeruginosa, and Klebsiella pneumoniae 3

Routes of entry are hematogenous spread, coltiguous

C H A P T E R

Children: disk space first, then vertebrae

Adults: subchondral vertebral body, then disk space

Imaging

Plain films normal early in disease course

"Hot" (hyperintense) disk on T2-weighted MR

Disk, adjacent bone often enhance

Soft tissue mass common; ±epidural abscess,

men-ingitis

gens Systemic bacteremia, typically from a

cutane-ous, urinary tract or pulmonary infection, is the most

common source Hematogenous spread typically

oc-curs via arteries; the vertebral veins (Batson's

plexus)

play a comparatively limited role.5 Contiguous

spread from an adjacent soft-tissue infection (e.g.,

paraspinous muscle or retropharyngeal abscess) is

less common Direct contamination from open

wounds, penetrating foreign bodies, diagnostic

pro-cedures, or surgery is rare

In adults, infection begins in the sulochondral

por-tion of the vertebral body, then spreads to the disk

space and further along the vertebral body in a sub-

ligamentous fashion.5 In children, the

intervertebral disk is richly vascularized and may

serve as the initial site, whereas, in adults, disk

infection is invariably caused by direct spread from

contiguous vertebrae or soft tissues.3,4

Incidence, age, and gender Infectious spondylitis

is uncommon, accounting for only 5% of all cases of

pyogenic osteomyelitis Bacterial vertebral

osteomy-elitis typically affects adults in the 6th and 7th

de-cades Immunocompromised patients and drug

abus-ers are at increased risk There has been a major

in-crease in reported incidence of spinal osteomyelitis

in

the last decade.3,6 There is a slight male predomi-

nance.3,4

Location Although pyogenic spondylitis can

oc-cur anywhere, the lumbar spine is the most common

site, followed by the thoracic spine The sacrum and

cervical spine are less commonly involved.4

Clinical presentation and natural history

Symp-toms vary widely Pain and malaise are common

The patient may be either febrile or afebrile The

erythrocyte sedimentation rate and white blood cell

are often mildly elevated.4 Neurologic deficit and signs of cord compression may occur, with infection spread into the epidural space.4

Imaging findings Plain film radiographs are usually

normal for the first 8 to 10 days following symptom onset Abnormalities such as disk-space narrowing and end plate erosions are often subtle and not detected until relatively late in the disease process (Fig 20-1, A) Radionuclide bone scans are sensitive but nonspecific indicators of early disease.6

CT scans may also be normal early in the disease course Disk-space narrowing, cortical bone loss, and paraspinous soft tissue mass can be seen but are usually present only after moderately severe changes have occurred.6

MR findings are characteristic Tl-weighted sequences typically show a narrowed disk space and low signal intensity in the adjacent vertebral bodies that reflects increased extracellular fluid within the marrow.3,6 Subligamentous or epidural soft tissue masses and cortical

bone erosion are common (Fig 20-1, B) Postcontrast

studies show enhancement of the infected disk space and

osteomyelitic bone (Fig 20-1, B) Paraspinous abscess,

epidural extension, and associated meningeal inflammation are easily delineated on these studies (Fig 20-2).1,2

T2-weighted sequences show high signal in the affected disk space and vertebral bodies The "nuclear cleft" that is typically seen as an area of decreased signal intensity in the middle of the disk is effaced.3

Differential diagnosis The differential diagnosis of

pyogenic spondylitis includes granulomatous spondylitis (see subsequent discussion), intervertebral osteochondrosis, calcium pyrophosphate crystal deposition disease, and axial neuroarthropathy In rare circumstances, metastatic disease can cause changes that are virtually identical to those of infection.7 Occasionally, severe degenerative disk disease is accompanied by secondary spine changes that can also simulate infection.3

Granulomatous spondylitis and miscellaneous spondylitides

Etiology and pathology Granulomatous reaction occurs

with a spectrum of bacterial, viral, parasitic, and fungal infections, as well as some tumors, autoimmune diseases, and idiopathic disorders.3 Granulomatous spondylitis is

most commonly caused by Mycobacterium tuberculosis

(Fig 20-3) Other organisms that may be implicated

include bacilli of the Brucella genus, typically B

melitensis (Fig 20-4).8

Fungal spondylitis is uncommon but is increasing with the rising numbers of immunocompromised and debilitated patients.3 Some fungal infections such as blastomycosis and aspergillosis are indistinguishable from tuberculous

822 PART FIVE Spine and Spinal Cord

Fig 20-1 Lateral plain film radiograph (A) and sagittal postcontrast T1-weighted

MR scan (B) in a 44-year-old woman drug abuser show classic findings of

vertebral osteomyelitis The C5-C6 interspace is narrowed, and the end plates of

the vertebral bodies appear irregular (large arrow) The marrow enhances (B, small

arrows), consistent with osteomyelitis Subligamentous prevertebral soft tissue

mass (B, open arrows) and epidural phlegmon (B, curved arrow) are also present

Subluxation secondary to ligamentous laxity is seen

ers such as actinomycosis, cryptococcosis, and

coc-cidiodomycosis cause patchy vertebral body destruction

or sclerosis with relative disk sparing.3

Parasitic spondylitis is rare For example, only 1% of

echinococcus infections involve bone; when they do,

the spine is the common site.3

Incidence, age, and gender Although pulmonary

tuberculosis has decreased, the incidence of bone and

joint tuberculosis remains unchanged.9 Tuberculous

spondylitis now accounts for 6% of new

extrapulmo-nary tuberculosis cases.10

In developing countries, tuberculous spondylitis is a

disease of children, whereas in North America and

Europe it is most prevalent in middle-aged adults The

mean age at diagnosis is between 40 and 45 years

compared with pyogenic osteomyelitis where the peak

incidence is in the sixth to seventh decades.9

Debilitation, immunosuppression, alcoholism, and drug

addiction are predisposing conditions.3 There is no

gender predilection

Location The lower dorsal and lumbar spine are

affected in nearly three quarters of all cases of

tuber-culous spondylitis; the cervical spine is an uncommon

site.11 Nearly 90% of cases have at least two affected

vertebral bodies; 50% have three or more levels

affected.9,11 "Skip" lesions are common.3 Para-

spinous abscesses are present in 55% to 95% of cases.9 Occasionally, tuberculous spondylitis affects only one vertebral body, sparing the adjacent disk Tuberculosis can affect only part of a vertebral body The transverse processes and posterior elements are sometimes also involved.3

Brucellar spondylitis can be focal or diffuse In cal disease, osteomyelitis is localized to the anterior aspect of an end plate Lower lumbar involvement is common in brucellar spondylitis, whereas tuberculous spondylitis is most common in the lower thoracic and upper lumbar spine.8

fo-Clinical presentation and natural history

Tuber-culous spondylitis is typically more indolent than pyogenic osteomyelitis Onset is often insidious, and symptom duration frequently ranges from months to years.9 Untreated patients develop progressive ver-tebral collapse with anterior wedging and gibbus formation.10

Imaging findings Plain film findings in

tubercu-lous spondylitis include bone destruction in nearly all cases and associated soft tissue masses in most Re-active sclerosis is not a feature on initial presentation

in Caucasian patients but early sclerosis is seen in proximately 50% of non-Caucasian patients Loss of disk height is present in more than three quarters of

ap-Chapter 20 Nonneoplastic Disorders of the Spine and Spinal Cord 823

Fig 20-2 A 65-year-old man with an infected IV site had a 10-day history of fever

and chills followed by an increasing sensory deficit that proceeded to paraplegia A,

Postcontrast sagittal T1-weighted MR scan shows a frank epidural abscess with

enhancing borders (large arrows) and central low density nidus (open arrows) B,

Sagittal T2-weighted sequence shows the abscess (open arrows) Focal high signal

(solid arrows) at the cervicomedullary junction is probably secondary myelitis

Loculated pus was removed at surgery

Fig 20-3 Sagittal (A) and axial (B) contrast-enhanced T1-weighted MR scans

in a 32year-old man with tuberculous discitis, spondylitis, and psoas abscesses

The affected disk and end plates enhance intensely and homogeneously (A,

arrows) Multiloculated psoas abscesses are present (B, arrows)

824 PART FIVE Spine and Spinal Cord

Fig 20-4 Axial CECT scan in a 52-year-old man shows bilateral psoas abscesses (large

arrows) Bone windows (not shown) disclosed osteomyelitis Note irregular anterior,

lateral end plates (small arrows) Brucella abscesses were drained at surgery

patients; vertebral body fusion eventually occurs in most

cases.10

CT scans characteristically show extensive bony

destruction and large paraspinous abscesses that are

relatively disproportionate to the amount of bone

de-struction Epidural extension and subligamentous spread

are also frequently present.3,9

MR scans invariably show loss of cortical definition of

the affected vertebrae However, affected vertebrae are

often at least partially maintained in pyogenic spondylitis

(Fig 20-3, C) T1WI often shows infection spread beneath

the longitudinal ligaments to involve adjacent vertebral

bodies.9 The disks are sometimes relatively spared,

particularly in relationship to the degree of bone

destruction The posterior elements are commonly

involved.9

Differential diagnosis The major differential diagnosis

of tuberculous spondylitis is pyogenic vertebral

osteomyelitis or other spondylitides such as brucellosis,

actinomycosis, and hydatid disease (Fig 20-4) Tumor is

also a diagnostic consideration when a paraspinal mass is

associated with bone destruction.9

EpiduraI and Subdural Infections

Epidural abscess

Etiology and pathology Spinal epidural abscess (SEA)

typically results from direct hematogenous seeding of the

epidural space from a cutaneous, pulmonary, or urinary

tract source.5 Staphylococcus aureus is by far the most

common organism responsible for spine infections of all

types.12

Two basic stages are observed in SEA Initially,

there is thickened inflamed tissue with granulomatous material and imbedded microabscesses This represents

a "phlegmonous" stage (see Fig 20-1, B).13 In the second stage a collection of liquid pus forms a frank abscess

(Fig 20-5, see Fig 20-2).12

Incidence, age, and gender Spinal epidural

ab-scesses are uncommon, representing approximately one case per 10,000 hospital admissions in tertiary in-stitutions.13 However, the incidence of SEA is now increasing significantly.14 All ages are affected; the mean age is 50 to 55 years.14,15 There is a moderate male predominance in reported cases of SEA.12-15

Location All areas of the spine are affected SEAs

are often extensive; in one third of cases the infection extends over more than six vertebral segments.12

Concomitant diskitis or osteomyelitis is seen in 80%.12

Clinical presentation and natural history Fever and

localized tenderness are common early Symptoms but symptoms are often nonspecific.13 Predisposing conditions include diabetes mellitus, intravenous drug abuse, multiple medical illnesses, and trauma.14 If left untreated, severe neurologic deficits, and death may occur.13

Imaging findings Plain spine radiographs may

disclose osteomyelitis and disk space narrowing (see

Fig 20-1, A) Myelography or CT-myelography onstrates an extradural soft tissue mass with blockage of normal CSF flow.14

dem-MR scans typically show an extradural, soft tissue mass that is iso- to hypointense compared to spinal

Chapter 20 Nonneoplastic Disorders of the Spine and Spinal Cord 825

Fig 20-5 A, Sagittal postcontrast T1-weighted MR scans in this 37-year-old

drug abuser show a large, enhancing epidural phlegmon (arrows) Cephalad

extension into the cisterna magna is present B, Axial scans show thin enhancing

rims (arrows) surrounding hypointense fluid collections Phlegmon and frank

abscesses were found at surgery

cord on T1WI and hyperintense on proton densityand

T2-weighted sequences (see Fig 20-2, B).13 Coexisting

low signal changes in adjacent vertebral bodies are

often seen on T1WI with high signal intensity in the

intervertebral disks and vertebral bodies on

T1-weighted sequences.14

Three patterns are observed following contrast

ad-ministration Diffuse homogeneous or slightly

heter-ogeneous enhancement is seen in 70% of cases (see

Fig 20-1, B).14 This most likely represents the phleg-

monous stage of SEA The second most frequent finding is a thick or thin enhancing rim that surrounds

a liquefied low signal pus collection, seen in 40% of

cases (see Fig 20-2, A) This represents a frank

necrotic abscess.14 In some cases, a combination of

both patterns is observed (see Fig 20-5).13

Subdural abscess Spinal subdural abscesses

(SSA) are rare The relative paucity of reported cases

of SSA compared to intracranial subdural abscesses

826 PART FIVE Spine and Spinal Cord

has been ascribed to absence of venous sinuses in the

spine, the wide epidural space acting as a "filter," and

the centripetal direction of spinal blood flow.16

Clinical presentation is nonspecific; symptoms may

mimic those of acute transverse myelitis, spinal epidural

abscess, epidural hematoma, pyogenic spondylitis, and

neoplasm.16 Imaging studies disclose an intraspinal

space-occupying mass, often without features that would

localize the lesion to the subdural compartment.16

Meningitis, Myelitis, and Cord Abscess

Intradural spinal inflammatory disease includes

meningitis and myelitis The diagnosis of uncomplicated

meningitis is typically established by lumbar puncture,

whereas imaging studies may be more helpful in

diagnosis myelitis

Meningitis Spinal meningitis can be caused by

bacterial (pyogenic, granulomatous), fungal, parasitic, or

viral organisms.3 Pyogenic leptomeningitis is the most

common bacterial infection of the spinal axis The

majority of these cases occur as a manifestation of

cerebral meningitis.3

Granulomatous, pyogenic, and aseptic meningitides are

all seen as contrast-enhancing tissue that surrounds the

spinal cord and nerve roots.17 Three patterns are seen,17

as follows:

1 Delicate, smooth, linear enhancement outlining

the cord, nerve roots, or meninges (Fig 20-6)

2 Discrete nodular foci on the surface of these

structures

3 Diffusely thickened soft tissue that appears as

an intradural filling defect

There is no correlation between enhancement pattern

and disease severity or specific responsible organism.18

Myelitis The term myelitis should be restricted to

inflammatory diseases of the spinal cord, whereas

"myelopathy" is a more general term that is applied to

cord dysfunction from noninflammatory sources (e.g.,

spondylitic or compressive myelopathy, radiation

myelopathy).18

Several infectious agents can cause myelitis Viral

infections typically affect the gray matter Herpes,

coxsackie, and polio viruses are the most common

agents, although HIV-related myelitis is increasing in

frequency.18 Epidural abscess and chronic meningeal

infections such as tuberculosis and fungal meningitis

mail also cause a secondary myelitis (see Fig 20-2,

also occur (see subsequent discussion)

Imaging findings are typically nonspecific and

resemble other noninfectious inflammatory and demy-

Fig 20-6 Sagittal postcontrast T1-weighted MR

scan on this 26-year-old woman with low-grade fever following lumbar surgery shows diffusely

thickened, enhancing meninges (arrows) CSF

showed mildly elevated protein, mild pleocytosis, and no organisms Probable aseptic meningitis

elinating disorders (see subsequent discussion) Focal or diffuse increased intramedullary signal on T2weighted

MR scans, with or without mass effect, is typical Enhancement following contrast administration can be seen in some cases.17

Intramedullary abscess In contrast to brain abscess,

frank pyogenic spinal cord abscesses are extremely rare The few reported cases may represent focal venous infarcts that are complicated by bacterial colonization.3

DEMYELINATING DISEASES Multiple Sclerosis

Etiology and pathology The general etiology a

pathology of multiple sclerosis (MS) are detailed in Chapter 17 Spinal cord plaques are an almost universal autopsy finding in patients with MS; in some cases the spinal cord is the earliest affected site.19 Plaques occur preferentially in the dorsolateral cord and do not respect boundaries between specific tracts or between gray and white matter (Fig 20-7).19

Chapter 20 Nonneoplastic Disorders of the Spine and Spinal Cord 827

Fig 20-7 Axial T2-weighted MR scans in a 46-year-old woman with long-standing

multiple sclerosis and cervical myelopathy show multifocal white and gray matter

high signal intensity foci (arrows)

Fig 20-8 This 43-year-old woman with a 3-month

history of optic neuritis and right arm weakness

developed sudden onset of rapidly progressive

sensory deficit and upper extremity weakness Pre-

(A) and postcontrast (B) sagittal T1-weighted MR

scans show diffuse cervical cord enlargement that

extends from C2 to C7 and enhances moderately

(arrows) The patient developed severe bilateral optic

atrophy and quadriparesis Follow-up scans 3 years

later (not shown) demonstrated diffuse cord atrophy

Neuromyelitis optica (Devic syndrome)

828 PART FIVE Spine and Spinal Cord

Incidence, age, and gender MS is a worldwide

disease, although the greatest prevalence is in temperate

zones such as the United States and Canada, Great

Britain, and northern Europe Disease onset is typically

between 15 and 50 years, with a peak in the third and

fourth decades There is a distinct female predominance,

particularly in children and adolescents with MS.20

Location Spinal cord plaques can be found at any

segment In later stages, plaques are evenly distributed;

in early disease there is a distinct predilection for the

cervical spinal cord.19 An MS variant, Devic disease

(also called neuromyelitis optica), is a rapidly

progressive fulminant demyelination that is restricted to

the optic nerves and spinal cord (Fig 20-8).20a

Imaging findings Spinal MR is not required for

confirmation when a definite diagnosis of MS has been

made on clinical grounds However, in patients with

isolated myelopathy and a clinical suspicion of

demyelinating disease, brain MR is recommended as the

first screening imaging study.21 If such patients have a

normal brain scan, MR examination of the spinal cord is

appropriate (Fig 20-8)

The most common finding on T2-weighted MR scans

is one or more elongated, poorly marginated,

hyperintense intramedullary lesions, particularly if focal

or generalized cord atrophy is identified on T1WI.21

Acute demyelinating lesions may have mass effect and

enhance following contrast administration (Figs 20-8

and 20-9).20

Acute Transverse Myelopathy

Acute transverse myelopathy (ATM) is sometimes

termed acute transverse myelitis In its most dramatic

form, ATM is characterized by an acutely developing,

rapidly progressing lesion that affects both halves o the

cord ATM is not actually a true disease but a clinical

syndrome with diverse causes (see box).22

Etiology and pathology Several neuropathological

processes may give rise to ATM Some cases develop

with active infection; others occur as a post infectious

demyelinating disorder (acute disseminated

encephalomyelitis, or ADEM) (Fig 20-10)

Acute Transverse Myelopathy

Incidence, age, and gender The estimated annual

incidence of ATM is approximately one case per million.22 ATM occurs in all age groups There is no gender

predilection

Location Any segment can be affected, although there is a

slight predilection for the thoracic cord.23 Multilevel involvement is typical.22,23

Clinical presentation and natural history In typical

case, there is no prior history of neurologic all normality.22 Time from symptom onset to maximum deficit ranges from less than 1 hour to 17 days.23 Sensory levels are typically in the thoracic region.23 Prognosis in most cases is poor, and severe residual neurologic deficits are common.22

Imaging findings The major role of neuroimaging is to

identify treatable conditions that can mimic ATM These include acute disk herniation, hematoma, epidural abscess, or compression myelopathies.22

During the acute phase, MR scans are normal in approximately half of all ATM cases and nonspecific in the remainder.23 Focal cord enlargement on T1 and poorly delineated hyperintensities on T2weighted scans are the most commonly identified abnormalities (Fig 20-10).22 Enhancement following contrast administration occurs in

some cases

Miscellaneous Myelopathies Radiation myelopathy Radiation myelopathy is a rare but

serious complication of therapeutic irradiation (see box, p

830) The following three criteria for establishing the diagnosis of radiation myelopathy have been established24:

1 The spinal cord must have been included in the radiation field

2 The neurologic deficit must correspond to the cord segment that was irradiated

3 Metastasis or other primary spinal cord lesions

must be ruled out

Four distinct clinical syndromes of radiation myelopathy have been described, of which chronic progressive radiation myelopathy (CPRM) is the most common form identified on imaging studies.24-26

Chapter 20 Nonneoplastic Disorders of the Spine and Spinal Cord 829

Fig 20-9 This 42-year-old man with a 3-month history of lower extremity weakness had

sudden onset of a rapidly ascending sensory level and paralysis A, Sagittal T1-weighted

MR scan shows enlargement of the midthoracic spinal cord (arrows) B, Sagittal

T2-weighted scan shows intramedullary high signal (arrows) C, T1WI following contrast

administration shows patchy enhancement (arrows) Biopsy for possible spinal cord

neo-plasm disclosed multiple sclerosis

Fig 20-10 This 16-year-old girl had a two-week history of right arm and leg

numbness and tingling following a flulike illness Sagittal T1- (A) and proton

density-weighted (B) MR scans show enlargement of the upper cervical cord (A,

arrows) with high signal intensity on PDWI (B, arrows) Acute transverse

myelopathy

830 PART FIVE Spine and Spinal Cord

Most cases of CPRM are seen following radiotherapy

of nasopharyngeal carcinomas The most commonly

affected area is therefore the cervical spinal cord The

latent period between termination of irradiation and

symptom onset varies from 3 to 40 months, although

most cases occur between 9 and 20 months.25

Imaging findings vary When MR scans are obtained

more than 3 years after symptom onset, cord atrophy

without abnormal signal intensity is seen.26 Scans

performed within 8 months of symptom onset typically

disclose long-segment hyperintensity on

Miscellaneous Myelopathies

Etiology Congenital spinocerebellar degeneration syndromes

(e.g., Friedrich ataxia)

Radiation

AIDS

Compression (HNP, spinal stenosis, tumor)

Vascular malformations

Toxic/metabolic (alcoholism, vitamin B12 deficiency)

T2WI, with or without associated cord swelling an enhancement following contrast administration (Fig 20-11).26

AIDS-related myelopathy AIDS-related myelopathy is

probably related to direct injury of neurons by the HIV virus, although secondary demyelination of the posterior and lateral columns also occurs.18

Compressive myelopathy Some investigators have

described intramedullary high signal intensity foci on proton density- or T2-weighted MR scans in cases of moderate to marked spinal stenosis (see Fig 20-31, D).27 This can occur secondary to degenerative disk disease or spondyloarthropathy and is probably related to focal cord ischemia Some cases resolve following decompressive surgery.27 Serotonergic mechanisms have been implicated in the deleterious secondary events accompanying spinal cord compression injury.28

Miscellaneous causes of compressive myelopathy include mass effect from primary or secondary spine tumors or other epidural lesions such as epidural abscess.18 The myelopathy frequently associated with vascular malformations and fistulae is probably produced by venous congestion combined with direct compression from dilated spinal veins.29

Degenerative and toxic myelopathies Miscellaneous

causes of spinal cord dysfunction include the inherited and acquired degenerative disorders such

as Friedreich ataxia and other spinocerebellar degen- erations, amyotrophic lateral sclerosis, toxic disease (e.g., chronic alcoholism), and metabolic disorders (e.g., vitamin B12 deficiency).18

VASCULAR DISEASES Normal Vascular Anatomy

A brief description of normal functional anatomy is necessary before delineating the various vascular diseases

that involve the spine and spinal cord (see box, p 831)

Spinal arteries The spinal cord blood supply consists of

one anterior and two posterior spinal arteries At the lower cervical cord and upper two thoracic segments, the anterior spinal artery (ASA) is supplied by two to four anterior radicular arteries that arise from the vertebral, deep cervical, superior intercostal, and ascending cervical arteries Radicular arteries are less prominent in the midthoracic cord The thoracolumbar region is supplied by the ASA, also known as the artery of Adamkiewicz (Fig 20-12) The cauda equina is supplied by lower lumbar, iliolumbar, and lateral sacral arteries.30

Via centrifugal branches from deep penetrating arteries

Fig 20-11 This patient had onset of bilateral upper

extremity weakness 3 months following radiation

therapy A, Postcontrast sagittal T1-weighted MR

scan shows cord enhancement (arrows) B, Sagittal

T2WI shows diffuse cord swelling and intramedullary

high signal intensity (arrows) that extends cephalad

to the medulla (curved arrow) Presumed radiation

myelopathy Note high signal in vertebral bodies

caused by fatty marrow replacement

Chapter 20 Nonneoplastic Disorders of the Spine and Spinal Cord 831

Vascular Disease of the Spinal Cord

Aneurysm, AVM, infarct much less common than

in brain

Aneurysm extremely rare except with AVM Infarct 2o to atherosclerosis, aortic dissection, disk herniation, trauma, hypertension, etc

Venous infarct (?Foix-Alajouanine syndrome)

Spinal cord vascular supply

One anterior, two posterior spinal arteries Anterior spinal artery (Adamkiewicz) supplies 70% of cord

Many end arteries, comparative few collaterals

"Watershed zone" at periphery of central gray matter

blood supply, including the corticospinal tracts all

the gray matter (except for the posterior horns).31

Within the cord interior there are no anastomoses,

and these central penetrating vessels are essentially

end arteries.31

The posterior aspect of the spinal cord is

sur-rounded by an arterial network that forms a plexus

dominated by the two posterior spinal arteries

(PSAs) The PSAs supply approximately 30% of the

cord, including the posterior horns, posterior

col-umns, and a peripheral rim of white matter.31 They

do this in a centripetal fashion via numerous

periph-eral perforating arteries that are richly

interconnected by anastomotic channels The spinal

cord "watershed zone" is located along the periphery

of the gray matter at the border between these

centrifugal (ASA) and centripetal (PSA)

circulations.31

Fig 20-12 Normal anatomy of the anterior spinal artery A, Spinal cord in situ with

dura reflected shows the anterior spinal artery and its major branches (arrows) B,

Selective angiogram of the left T10 segmental artery shows the characteristic

"hairpin" turn of the anterior spinal artery (of Adamkiewicz) C, Anatomic drawing

shows spinal cord vascular supply

832 PART FIVE Spine and Spinal Cord

The lateral aspect of the spinal cord is supplied by an

arterial network located between the anterior and posterior

nerve roots It typically has numerous axial dorsoventral

anastomoses.32

Extradural venous spaces and spinal veins

Extradural venous spaces An extensive network of

anastomosing, interconnecting, extradural venous channels

extends from the skull base to the sacrum The anterior

longitudinal venous plexus is particularly prominent in the

upper cervical and lumbar regions (see Chapter 19).32,33

Basivertebral venous plexuses drain the vertebral bodies,

and radicular veins accompany nerve roots as they exit the

neural foramina.34

Spinal veins Spinal venous drainage occurs via intrinsic

and extrinsic venous systems The intrinsic venous system is

composed of numerous sulcal and axial veins that form a

network that interconnects with numerous vertical and

transmedullary anastomotic channels The extrinsic system

is formed by a pial venous network that collects the intrinsic

perforators, longitudinal collector veins that lie anterior and

posterior to the cord, and radicular veins.32

Aneurysms

Etiology and pathology Spinal aneurysms (SAs) are

localized, saccular dilatations of spine or spinal cord

arteries They are usually, but not invariably, associated

with intramedullary spinal cord arteriovenous

malformations (AVMs).35

Incidence, age, and gender Compared to their

in-tracranial counterparts, isolated SAs are extremely rare.36a

SAs have been identified in 20% of patients with

intramedullary AVMs Patients are typically between the

ages of 10 and 40 years; the mean age is 18.5 years There is

no gender predilection.35

Location The intramedullary AVMs associated with

SAs are equally divided between the cervical and thoracic

spinal cord SAs are almost always located on one of the

main high-flow vessels feeding the AVM; nearly 70% are

found on the anterior spinal artery.35 In contrast to

intracranial aneurysms, SAs do not usually occur at

bifurcation points.36a

Clinical presentation Symptoms are due to SAH in

85% of cases and progressive neurologic deficits in 15%

Recurrent hemorrhage is common in untreated cases.35

Imaging Angiography is the definitive imaging study

Diagnostic criteria for SA include (1) visualization of an

arterial vessel outpouching during the initial arterial phase

and (2) selective injections with

multiple views to rule out dilated vessels or overlapping loops that might mimic aneurysm.35

Vascular Malformations

Vascular malformations of the spine and s cord are uncommon lesions Most are arteriovenous malformations (AVMs) or arteriovenous fistulae (AVFs) Cavernous angiomas and capillary telangiectasias are less common; venous angiomas are rarely, if ever,

encountered

Arteriovenous malformations and arteriovenous fistulae

Pathology and classification AVMs have a true

nidus of pathological vessels interposed between larged feeding arteries and draining veins 37 AVFs drain directly into enlarged venous outflow tracts.38

en-Spinal AVMs have been subdivided into four general categories: Type I is a dural arteriovenous fistula Type I AVMs are primarily found in the dorsal aspect of the lower thoracic cord and conus medullaris Most type I AVMs consist of a single transdural arterial feeder that drains into an intradural arterialized vein The draining vein often extends over multiple segments.39 Type I AVMs typically affect men between their fifth and eighth decades.38 Nearly 60% are spontaneous, whereas approximately 40% are caused by trauma.40 Progressive neurologic deterioration, probably caused by chronic venous hypertension, is typical.39

Type II AVMs, so-called glomus malformations, are intramedullary AVMs in which a localized compact vascular plexus is supplied by multiple feeders from the anterior or posterior spinal arteries Type II AVMs drain into a tortuous, arterialized venous plexus that surrounds the spinal cord These AVMs are usually located dorsally

in the cervicomedullary region.38 Most occur in younger patients with acute onset of neurologic symptoms secondary to intramedullary hemorrhage.38

Type III AVMs, the so-called juvenile type, are large, complex vascular masses that involve the cord and often have extramedullary or even extraspinal extension Multiple arterial feeders from several different vertebral levels are common

Type IV AVMs are intradural extramedullary riovenous fistulas These lesions are fed by the anterior spinal artery and lie completely outside the spinal cord and pia mater There is no intervening small vessel network, and the fistula drains directly into an enlarged venous outflow tract of variable size Most type IV AVMs are anterior to the spinal cord and are fed by the anterior spinal artery Most occur near the conus medullaris Type IV AVMs occur in patients between their third and sixth decades Progressive neurologic deficits are typical.38

arte-Chapter 20 Nonneoplastic Disorders of the Spine and Spinal' Cord 833

Fig 20-13 Gross pathology (A), myelography (B), and angiography (C) of spinal cord

AVM (arrows) Note the enlarged anterior spinal artery (arrowheads) (A, Courtesy

Roy College of Surgeons of England, Slide Atlas of Pathology, Gower Medical

Publishing, 1988.)

Incidence, age, and gender AVMs are the most

common spinal vascular anomaly, accounting for between

3% and 11% of spinal space-occupying lesions.41 Age at

symptom onset and gender vary with AVM type (see

previous discussion) The most common AVM is type 1,

i.e., dural arteriovenous fistula Type III, or juvenile,

AVMs are rare

Location Location varies with specific AVM type (see

previous discussion) The thoracolumbar area is the most

common location overall and the site of slightly over half

of AVMs (Fig 20-13, A); 40% of AVMs occur in the

cervical spinal cord.37

Clinical presentation and natural history Clinical

presentation and natural history also vary with AVM type

Paresis, sensory changes, bowel and bladder dysfunction,

and impotence are common symptoms Hemorrhage is

seen in approximately 50% of cases.37 Venous

hypertension may be important in the development of cord

symptoms.41a

Imaging findings Myelography may show filling

defects caused by the enlarged vessels (Fig 20-13, B)

Cord atrophy is common

MR imaging may show foci of high-velocity signal loss

within the enlarged vessels (Fig 20-14) The cord is

sometimes atrophic, and high signal intensity is often

observed on T2-weighted scans.42 Hemorrhagic residua

may be present AVM "mimics" are caused by dephasing

from turbulent CSF flow or CSF flow-

Fig 20-14 Sagittal T2-weighted MR scans of the

cervical (A) and thoracic (B) regions show multifocal

areas of highvelocity signal loss (flow voids) dorsal

to the spinal cord caused by an AVM Note thoracic cord atrophy and myelomalacia, seen as

intramedullary hyperintensity in B (Courtesy W.T.C

Yuh.)

834 PART FIVE Spine and Spinal Cord

Fig 20-15 Axial T2-weighted MR scan shows

discrete regions of high-velocity signal loss (arrows),

caused by CSF flow artifacts The patient was

neurologically normal

ing at different rates within functionally separate

compartments created by the dentate ligaments and

septum posticum around the thoracic spinal cord (Fig

20-15)

Spinal angiography is the definitive diagnostic

procedure for the evaluation of spinal AVMs (see Fig

20-13, C) Initial global (intraaortic) injection is

fol-lowed by selective catheterization of the appropriate

vessels to assess site and feeding pedicles, flow pattern,

venous drainage, and hemodynamic effects (e.g.,

vascular steal).40

Cavernous angiomas

Pathology Spinal cord cavernous angiomas are

similar to intracranial cavernous angiomas Grossly,

these lesions are typically soft, spongy,

well-circumscribed dark red or reddish-brown masses

Mi-croscopically, cavernous angiomas consist of

blood-filled endothelial-lined spaces lined by thickened,

hy-alinized walls that lack elastic fibers and smooth

muscle.43 Localized hemorrhages of different ages may

be present Calcification is rare.44

Incidence, age, and gender Spinal cord cavernous

malformations are extremely rare They typically

be-come symptomatic between the third and sixth decades

There is a 2:1 female predominance.44

Location One large series reports the thoracic cord

as the site of slightly more than half of cavernous

angiomas, with the cervical cord the next most common

location.43 Multiple lesions occur but are uncommon.44

Clinical presentation and natural history

Intra-Fig 20-16 Sagittal T1-weighted MR scan in a

patient with lower extremity weakness shows a

hypointense conus lesion (black arrow) surrounding

a tiny high signal focus (white arrow) Presumed

cavernous angioma

medullary spinal cord cavernous angiomas usually cause sensorimotor symptoms with progressive pain-ful paraparesis Clinical course varies from slowly progressive symptoms to acute quadriplegia.44

Imaging Spinal angiography is typically normal

Findings on MR scans include residua of subacute and chronic hemorrhage characterized by mixed high- and low-signal components The typical appearance is

a small high signal focus on both T1- and T2-weighted or gradient-refocussed scans (Fig 20-16) If a typical spinal cord lesion is identified on MR scans, the brain should be studied using gradient-refocussed sequences to screen for asymptomatic intracranial lesions.45

Capillary telangiectasias and venous tions Capillary telangiectasias of the pons, medulla,

malforma-and spinal cord are often found incidentally at topsy but are rarely identified on imaging studies Venous malformations are also common brain anom-alies but are rarely, if ever, observed in the spinal cord

au-Infarction Arterial infarction

Etiology and pathology The blood supply to the

Chapter 20 Nonneoplastic Disorders of the Spine and Spinal Cord 835

Fig 20-17 An adolescent had sudden onset of lower extremity paraplegia following

vig-orous exercise A, Sagittal T1-weighted MR scan shows distal cord enlargement (arrows)

B, Sagittal T2WI shows high signal intensity (arrows) C, Postcontrast T1WI shows patchy

enhancement CSF studies were normal Presumed cord infarct (Courtesy D Mendelsohn.)

tudinal arterial trunks: a single anterior spinal artery

and paired posterior spinal arteries (see previous

discussion).46 Collateral flow is comparatively limited,

and any pathologic process that interferes with this

crucial blood supply may result in ischemia or

infarc-tion.46

Spontaneous anterior spinal cord infarction

pri-marily affects individuals with severe atherosclerotic

disease or aortic dissection Other reported etiologies

include syphilis, vasculitis, fibrocartilagenous emboli

from disk herniation, cervical subluxation,

hypoten-sion, hematologic disorders, pregnancy, diabetes,

thrombophlebitis, trauma, and tuberculosis.47,48

Incidence, age, and gender Spinal cord infarction

is extremely rare Patient age in reported cases ranges

from 15 to 75 years.47

Location Most cord infarcts occur at the upper

thoracic region or thoracolumbar junction The extent

of involvement ranges from a single segment to

multiple levels.46

Clinical presentation and natural history Clinical

symptoms vary The classic ASA infarct presents with sudden onset of flaccid para- or quadriparesis with or without burning and lancinating pain Dissociated

sensory loss with preserved touch, vibration, and position

sense is common.49

Imaging T1-weighted MR scans in acute cord

in-farction may demonstrate an enlarged cord (Fig 20-17,

A) Central or anterior intramedullary high signal is

typically present on T2WI (Fig 20-17, B) Enhancement following contrast may be initially absent but occurs a few days to a few weeks following symptom onset (Fig 20-17, C).48-50 Follow-up scans may show focal cord atrophy with myelomalacia and residual high signal intensity on T2WI.50

Venous infarction Little is known about venous

ischemia, infarction and their potential relationships to myelopathy.50a The disorder called Foix-Alajouanine

syndrome, also known as subacute necrotic myelitis,

836 PART FIVE Spine and Spinal Cord

Fig 20-18 A 78-year-old man had a 2-year history of slowly progressive lower

extrem-ity weakness with sudden onset of paraplegia Coronal (A) and axial (B) T1-weighted

MR scans show intra- and extramedullary high signal foci (arrows) mixed with

hypoin-tense areas Surgery disclosed multiple thrombosed thick-walled veins draining a able AVM Possible Foix-Alajouanine syndrome

prob-may be secondary to venous stagnation, thrombosis, and

infarction.32 Pathologic studies in these cases show

enlarged, thick-walled tortuous veins that are often

thrombosed Coagulative necrosis that involves both

gray and white matter is typical.51 MR studies suggest a

vascular malformation with serpentine filling defects,

thrombosed vessels, and cord edema (Fig 20-18)

DEGENERATIVE DISEASES

The widespread prevalence of patients with back and

neck pain makes the spine one of the most frequently

requested neuroirnaging examinations Patients with

low-back pain have a significant impact on health care

costs, particularly in the United States.52 Some authors

estimate that up to 80% of all adults have low-back pain

at some time in their lives and that a herniated nucleus

pulposus is the cause in only a small percentage of these

cases.53

In this section we discuss the pathology and imaging

of degenerative spine disease We begin with a

discussion of normal age-related changes in the

in-tervertebral disks and vertebral bodies We then

de-lineate the spectrum of disk herniations, facet arthroses

and spinal stenosis, and the spectrum of imaging

findings in the post-operative spine, including the called "failed back" syndromes We conclude our dis-

so-cussion by briefly considering back pain in children

Normal Aging and Disk Degeneration

Normal aging is a complex physiologic process that encompasses various degrees of gross anatomic and biochemical changes in the entire diskovertebral complex.54 Whether a distinction can or should be made between normal aging and disk degeneration is controversial.54-56 What is clear is that age-related changes in the MR appearance of both the intervertebral disks and vertebral bodies normally occur in asymptomatic individuals.54,55,57-60

Normal disc microarchitecture and MR signal intensity Sharpey's fibers and the outer anular rings

consist of well-organized collagen fibrils with low signal intensity on both T1- and T2-weighted sequences.61 The central disk contains two basic tissues: wispy fibrocartilage from the inner anulus and the gelatinous matrix of the nucleus pulposus These two disk regions are inseparable on routine spin-echo MR scans; both have high signal intensity on T2WI After childhood, an intranuclear "cleft" composed of

Chapter 20 Nonneoplastic Disorders of the Spine and Spinal Cord 837

Fig 20-19 Sagittal T2-weighted MR scans in this 38-year-old man show normal

high signal intensity in the upper three intervertebral disks Note the low signal

intranuclear “cleft” (B, single arrows) The L4-L5 and L5-S1 disks are

comparatively hypointense, indicating increasing collagen content and decreasing disk hydration The L4-L5 disk is bulging and has a small high signal

intensity focus in the posterior anulus (A, arrow), consistent with circumferential anular tear There is a small central L5-S1 HNP (B, double arrows)

fibrous transformation of the previously gel-like matrix

is seen on T2WI (see Chapter 19).61

Normal disk aging Both morphologic and

chemical changes occur in the intervertebral disks with

al development and aging These are in turn red by

changes on MR scans, particularly T2-weighted

sequences

In children, a transition occurs between the

imma-ture nucleus pulposus seen in newborns and the adult

configuration In the newborn, the nucleus pulposus is

fibrocartilaginous with little fiber evident on gross

anatomic sections The nucleus appears grossly

homogeneous except for a small primitive notochordal

remnant.58,62

During the first and second decades of life, fibrous

tissue initially develops near the dorsal or ventral

margin of the nucleus pulposus and spreads toward the

center The notochordal remnants are obliterated, and

the distinction between nucleus pulposus and anulus

fibrosus is gradually lost In adults, especially after age

30, there is an indistinct boundary between the nucleus

pulposus and inner anulus fibrosus.58

Physiologic a g in the nucleus pulposus is related to

specific chemical changes in the intervertebral disk

These are a decrease in water-binding, ca-

pacity, disintegration of large molecular proteoglycans, and increase in collagen content.63

In the first decade of life, the nucleus pulposus contains 85% to 88% water, and the anulus fibrosus contains 75% In adulthood, the water content of both is about 70%.55 With aging, the collagen content of the anulus increases from 20% of dry weight to over 25% The total proteoglycan content of the nucleus decreases with age as the disk becomes more fibrous.55

MR imaging of disk aging Intervertebral disk signal

intensity on MR scans is related to the water content of the nucleus pulposus and fibrocartilage of the inner anulus.55 In the neonate and young child, the nucleus has a very high signal intensity on T2-weighted images and is sharply demarcated from the anulus.62 With maturation, this demarcation is gradually lost as the nucleus and the inner anulus become more fibrous.55 Both the nucleus and inner anulus have high signal intensity on T2WI, but the outer anulus is hypointense

at all ages.55 A fibrous plate also develops in the disk equator This is seen on T2-weighted MR scans as a central transverse band of reduced signal intensity in the nucleus pulposus (Fig 20-19).58

838 PART FIVE Spine and Spinal Cord

Fig 20-20 Pathology of radial anular (type II) tear of

the anulus fibrosis Vascularized tear (arrows)

extends through the outer anulus into the nucleus

pulposus (Courtesy G Momberger.)

Fig 20-21 Imaging findings of anular tears are shown on the MR scans of this 38-year-old man with

low back pain and no previous surgery A, Sagittal

T1-weighted scan shows normal disk heights and slight posterior bulging of the L4-L5 and L5-S1

intervertebral disks (arrows) B, Sagittal T2WI shows

these disks are comparatively hypointense Small high signal foci are seen in the outer anulus of both

disks (arrows) C, Postcontrast T1WI shows these

areas enhance (arrows), probably due to vascularized

granulation tissue in the anular tears D, Sagittal,

cryornicrotome section demonstrates age-related degenerative changes in the vertebral bodies and intervertebral disks Note loss of height and posterior bulging of the L4-L5 and L5-S1 disks There is also fatty marrow replacement adjacent to both de-generated disks, seen here as yellow deposits

replacing the red marrow (D, Courtesy V

Haughton.)

Chapter 20 Nonneoplastic Disorders of the Spine and Spinal Cord 839

Both aging and degeneration affect disk signal

intensity.55 These are clearly not independent variables, and

distinguishing between the two is sometimes difficult.54

Diminishing signal intensity or T2WI reflects increasing

collagen content (Fig 20 19).58 This occurs both with

maturation and degeneration

Anular tears Tears of the anulus fibrosis also occur

with aging Three distinct types have been described

Concentric (type 1) tears are caused by delamination of

longitudinal anular fibers Radial (type II) tears involve all

layers of the anulus from the nucleus to the disk surface

(Fig 20-20) Trans verse (type III) tears involve the

insertion of Sharpey fibers into the ring apophysis.62

Transverse and concentric anular tears are common in

adult disks whether or not degenerative changes are present

in the nucleus pulposus These tears are probably incidental

findings.59,62 The significance of radial anular (type II) tears

is controversial some authors have implicated these tears

with accelerated disk degeneration.55,61

The most common imaging finding with anular tear is

high signal intensity on T2-weighted MR scan (Fig 20-21,

B; see Fig 20-19) Enhancing foci on post contrast

T1-weighted sequences are sometimes identified (Fig

20-21, C)

Disk degeneration Disk degeneration, defined as

diminished signal on T2-weighted MR scans combined with loss of disk space height, is common in asymptomatic

patients (see box, p 840) Early disk degeneration may also

occur without a loss in disk height or signal intensity on T2WI.61 Another sign of disk degeneration is intradiskal gas (vacuum disk phenomenon) This is seen on CT scans as extremely low density collections within the disk itself.62 Degeneration or bulging of at least one lumbar disk is seen

in 35% of patients between 20 and 39 years of age and in virtually all patients over 60 years of age.56

Vertebral body and marrow space changes with aging With maturation, there is gradual conversion of red (hemopoietically active) marrow to yellow (inactive)

marrow (see Chapter 19) Further changes in the vertebral

body marrow occur with disk degeneration; signal intensity changes in the marrow adjacent to the vertebral end plates

is a common observation on MR scans (Fig 20-21, D) Two types of marrow changes are associated with degenerative disk disease In the so-called type 1 change, there is decreased signal intensity on T1- and increased signal intensity on T2-weighted scans Histopathologic examination in these cases shows disruption and fissuring

of end plates and vascularized fibrous tissue In the so-called type 2 change, increased signal intensity is present

on T1-weighted

Fig 20-22 Sagittal T1- (A) and T2-weighted (B) MR scans in a 56-year-old

woman with low back pain show multiple dessicated disks Note high signal

intensity in the subchondral marrow around the L5-S1 interspace (A, large

arrows) The marrow signal is mildly hyperintense on T2WI (B, large arrows)

These so-called type II changes represent fatty replacement of vascular marrow (compare with Fig 20-21, D) There is also a focus of dense bony sclerosis that

is low signal on both sequences (curved arrows)

840 PART FIVE Spine and Spinal Cord

Fig 20-23 Focal fatty marrow replacement is illustrated on these two scans A,

Sagittal T1WI in this 63-year-old man shows multiple round "hot spots" (high

signal intensity foci) in the vertebral bodies (arrows) B, Repeat scan with fat suppression shows the high signal foci are now low signal (arrows) C, Sagittal

T1-weighted scan in a 73-year-old woman with osteoporosis shows very patchy fatty marrow replacement There was no evidence of systemic disease or malignancy

scans with isointense or slightly increased signal on

T2-weighted sequences Type 2 changes represent fatty

marrow replacement (Figs 20-22 and 20-23).60

Marrow changes are sometimes more focal and can

resemble vertebral body hemangiomas on T1WI (Fig

20-23, A); fat suppression sequences are helpful in

distinguishing these two entities (Fig 20-23, B)

Oc-casionally, fatty marrow replacement is diffusely patchy,

resulting in mottled, inhomogeneousappearing vertebral

bodies (Fig 20-23, C) If dense vertebral sclerosis

occurs in response to degeneration of an adjacent

intervertebral disk, the affected subchondral marrow is

low signal on both T1- and T2-weighted scans

Spondylosis, Arthrosis, and Spinal Stenosis

Spondylosis

Etiology and pathology The primary pathologic

finding in spondylosis is osteophytosis Osteophytes are

bony excrescences that originate near the margin of

vertebral bodies or facet joints.64

Vertebral body osteophytes probably result from

weakening of anular fibers with disk bulging and

traction on Sharpey fibers Osteophytes typically

de-velop where these fibers attach to the vertebral body,

usually several millimeters from the diskovertebral

Incidence, age, and gender Spondylosis and

osteophytosis increase with advancing age The prevalence of osteophytes in patients 50 years of age

or older is estimated at 60% to 80% Men are more frequently affected than women; individuals engaged in occupations that require heavy physical labor are more often affected.65 Schmorl's nodes are seen in up to 75% of the normal population.64

Location Although any spinal segment can be

in-volved, the lumbar and cervical areas are the most common sites, whereas the thoracic spine is often less frequently and less severely involved In the cervical spine the levels that are most frequently affected by both disk herniation and chronic spondylosis are C6-C7 (60% to 75%) and C5-C6 (20% to 30%).66 In the

Chapter 20 Nonneoplastic Disorders of the Spine and Spinal Cord 841

Fig 20-24 Degenerative spondylosis A, Axial post-myelogram CT scan shows low

density in the intervertebral disk (vacuum disk phenomenon) (open arrows), marginal osteophytes (small arrows), and bulging disk (arrowheads) Asymmetric protrusion of

disk material to the right, extending into the neural foramen and extraforaminal soft

tissues (curved arrows), represents a moderate-size disk herniation B, Coronal

T1-weighted MR scan in another case shows thinned L4-L5 disk space (small black

arrows), lateral osteophytes (large arrow), and degenerative marrow changes (open arrows) Some lateral subluxation of L4 on L5 is present Note the right L4 nerve root (arrowheads) draped over the osteophyte

lumbar spine, L4-L5 and L5-S1 are the most

com-monly and most severely affected sites Multilevel

disease is common in both the cervical and lumbar

regions

Imaging findings Imaging findings in spondylosis

include Schmorl's nodes, osteophytes, and end plate

sclerosis (Fig 20-24) Schmorl's nodes are seen on CT

scans as end-plate sclerotic areas surrounding

lucen-cies that represent interbody herniation of disk

ma-terial

Vertebral body osteophytes are bony spurs or ledges

that originate several millimeters from the

dis-kovertebral junction and extend first in a horizontal

and then in a vertical direction (Figs 20-24, B, and

20-25, A).65 Facet osteophytes are seen on axial

im-ages as mushroom-like facet overgrowths with

sub-chondral sclerosis Sagittal scans through the neural

foramina show posterosuperior bony narrowing, often

combined with ligamentum flavum laxity that further

narrows the foramen (Fig 20-25, B)

Differential diagnosis Osteophytes should be

dis-tinguished from syndesmophytes Syndesmophytes

are slender, vertically oriented ligamentous calcifications and osseous excrescences that extend from the margin of one vertebral body to another.65 Syndesmophytes are often associated with facet joint ankylosis and are one of the imaging hallmarks of ankylosing spondylitis.64 Osteophytes should also be distinguished from the sweeping, asymmetric lateral bony excrescences of psoriasis and Reiter syndrome and the flowing ossifications of diffuse idiopathic skeletal hyperostosis (DISH).65

Arthrosis, facet joint disease, and synovial cysts

Etiology and pathology The articular processes of the

spine form synovium-lined articulations, the apophyseal joints (see Chapter 19) Osteoarthritis is seen pathologically as fibrillation and erosion of articular cartilage, partial or complete denudation of the cartilagenous surface, and new bone formation.65

Juxta-articular cysts, also known as "synovial cysts" or

"ganglion cysts," sometimes form next to degenerated facet joints (Table 20-1).67 Cyst contents range from serous or mucinous fluid to semisolid ge-

842 PART FIVE Spine and Spinal Cord

Fig 20-25 A, Axial post-myelogram CT scan shows left lateral

recess narrowing (curved arrow) secondary to vertebral body osteophyte (small arrows) Note partially calcified (double

arrows), broadbased disk bulge (open arrows) B, Sagittal

T1-weighted MR scan in another patient shows normal L3-L4

and L4-L5 neural foramina (curved arrows) Facet arthrosis and lax ligamentum flavum (small arrows) narrows the L5-S1 neural foramen and mildly compresses the exiting L5 root (large

arrow)

Fig 20-26 A, Axial post-myelogram CT scan shows eburnation (small arrows) and

cystic changes (open arrows) around both articular facet joints Ligamenturn flavum degeneration and laxity narrows the canal posteriorly (arrowheads), whereas

spondylolisthesis with disk bulge (curved arrows) narrows the canal anteriorly B,

Axial T2-weighted MR scan in another patient shows severe facet arthrosis with

"mushroom"-shaped facet spurs (curved arrow) The neural foramen (large arrow) is markedly narrowed by the facet arthrosis and a lateral disk herniation (small arrows)

Chapter 20 Nonneoplastic Disorders of the Spine and Spinal Cord 843

Table 20-1 Spine Cysts

with contents rhagic

Arachnoid cyst Thoracic spine, dor- Rare Arachnoid- Canal ±expanded, If cyst communicates

Extradural sal to cord; usu- lined pedicles thinned; with thecal sac,

Intradural ally single =CSF density/ only finding on

signal; may be se- CT-myelogram is vere cord cord compression, compression anterior displace-

ment

Arachnoid Root sleeve dilata- Very Dura + arach- Bulbous dilations of

pouch/ tion; often multi- common noid root sleeve; can

diverticulum ple mimic HNP, tu-

mor; fill with in trathecal contrast injection; do not enhance after I.V

contrast

Meningocele

Lateral All levels; thoracic Common with Dura + arach- CSF-filled outpouch- Kyphoscoliosis, other

most common NF-1, Mar- noid ing; posterior ver- signs of NF-1 often

scalloping, larged neural fo-ramina

en-Intraosseous Sacrum Uncommon Arachnoid Scalloped sacrum;

cyst similar to CSF

Traumatic Cervical most com- Uncommon Not lined by "Empty root sleeve" Intraspinal cyst can

pseudome- mon meninges secondary to root occur, cause mass

ningocele avulsion effect

Perineural Root sleeve at dor- Uncommon Nerve fibers, May look like nerve

cyst ("Tarlov" sal root ganglion ganglion root tumor

or "Rexed" cells in cyst

Incidence and age Facet degeneration begins in the first 2

decades of life.66 Facet arthrosis (apophyseal joint

osteoarthritis) is seen in the majority of adults and is

virtually universal in patients over 60 years of age.65,66,70

Location The middle and lower cervical spine and the

lower lumbar spine are most commonly affected; facet

disease is uncommon in the thoracic region.64 The lower

lumbosacral spine is the most common site for synovial

cysts; the cervical region is an uncommon location.67

Imaging Imaging findings of facet arthrosis on plain film

and NECT scans include joint space narrowing, bone

eburnation, and osteophytosis (Fig

20-26, A).65 Sagittal and thin-section axial MR scans are particularly helpful in delineating the effect of facet

hypertrophy on the neural foramina (see Fig 20-26, B; Fig 20-25, B).71,72

Juxtaarticular cysts display a spectrum of imaging findings Cyst density on NECT scans varies from hypo- to hyperdense compared to the adjacent ligamentum flavum (Figs 20-27 and 20-28) Signal on MR scans is also variable Some cystic contents resemble CSF, whereas others may be high signal or show hemorrhagic residua and

fluid-fluid levels (Figs 20-29, A and B) 68,69,73 Some synovial cysts also have a solid component; both the solid component and cyst capsule may enhance following contrast administration.74

Occasionally, synovial cysts erode bone or present

844 PART FIVE Spine and Spinal Cord

Fig 20-27 A, Anatomic drawing illustrates a synovial cyst (curved arrow) Note

posterolateral compression of the thecal sac (small arrows) B, Axial NECT scan shows a slightly hyperdense mass adjacent to the left facet joint (arrows) C, CT scan

obtained following contrast injection into the facet joint shows the mass (arrows) fills

with contrast, indicating the cyst communicates with the joint space Synovial cyst was removed at laminectomy

as a neural foraminal lesion and resemble an epidural

or nerve root tumor (Fig 20-28).75 Therefore the

ma-jor differential diagnosis of lumbar synovial cyst is a

large migrated free disk fragment and cystic nerve

root tumor.76

Chapter 20 Nonneoplastic Disorders of the Spine and Spinal Cord 845

Spinal stenosis

Etiology and pathology Spinal stenosis can be

congenital, acquired, or result from a combination of congenital abnormalities with superimposed degenerative

changes (see box).64

Congenital stenosis occurs with short pedicle dromes Here, the pedicles typically are thick and reduced

syn-in anteroposterior diameter Msyn-inimal disk bulges or spondylotic changes superimposed on a congenitally small canal can produce severe neurologic deficits (Fig 20-30) Other congenital spinal stenoses occur with achondroplasia and inherited metabolic disorders such as Morquio syndrome.64

Spinal Stenosis

Spondylolysis with spondylolisthesis

Miscellaneous

Ligamentous ossification/calcification (e.g., OPLL) Epidural lipomatosis

Fig 20-28 Axial post-myelogram CT scan shows

severe degenerative facet disease with "mushroom cap"

arthrosis (curved arrow) Vertebral body and facet

osteophytes (small arrows) narrow the neural foramen

Ligamenturn flavum ossification is present

(arrowheads), contributing to the canal and neural

foraminal stenosis A low density soft tissue mass

occupies the neural foramen and compresses the thecal

sac (open arrows) A large juxtaarticular (synovial) cyst

was removed at surgery

Fig 20-29 Axial T1- (A) and T2-weighted (B) scans show severe facet arthrosis

(curved arrows) and a mixed signal juxtaarticular cyst (small arrows) Hemorrhagic

synovial cyst was removed at surgery