and Spine Disorders

Ia extradural arachnoid cyst
Ib sacral meningocele IIextradural meningeal cyst containing neural tissue (= Tarlov cyst) IIIintradural arachnoid cyst

Pitfalls of CT myelography / MRI:

(1)   Nonopacification of noncommunicating arachnoid cyst → misidentification as a different type of lesion

(2)   Absence of mass effect on cord → failure to detect additional cysts / small CSF-isointense arachnoid cyst

DDx:   traumatic / lateral thoracic meningoceles

Cx:   spinal cord myelopathy, nerve root radiculopathy

Extradural Arachnoid Cyst

Cause:  congenital / acquired dural defect

Age:     2nd decade of life; M>F

Location:  thoracic (80%) > cervical (15%) > lumbar (5%)spine; extending over 3.7 vertebral bodies

Site:     posteriorly / posterolaterally to cord

√  scalloping of vertebral body

√  thinning / erosion of pedicles

√  widening of interpeduncular distance

Intradural Arachnoid Cyst

Cause:  congenital deficiency within arachnoid (= true arachnoid cyst) / adhesion from prior infection or trauma (= arachnoid loculation)

√  focal displacement and compression of spinal cord

√  widened dorsal subarachnoid space with diminished CSF flow artifact


=  widening of root sheath with arachnoid space occupying > 50% of total transverse diameter of root + sheath together

Cause:   ? congenital / traumatic, arachnoiditis, infection

Pathogenesis:   hydrostatic pressure of CSF

√  scalloping of posterior margins of vertebral bodies

√  myelographic contrast material fills diverticula



1.   True intramedullary AVM

=  nidus of abnormal intermediary arteriovenous structure with multiple shunts

Age:   2nd–3rd decade

Cx:   subarachnoid hemorrhage, paraplegia

Prognosis:   poor (especially in midthoracic location)

2.   Intradural arteriovenous fistula

=  single shunt between one / several medullary arteries + single perimedullary vein

3.   Dural arteriovenous fistula

=  single shunt between meningeal arteries + intradural vein

4.   Metameric angiomatosis


•  occasionally pulsatile soft-tissue swelling

Location:   ramus + posterior body of mandible

√  cystlike due to bone resorption ± calcifications

√  ± multilocular ± bone expansion

√  ± erosive margins

√  angiogram confirms diagnosis

Cx:   Tooth extraction can result in lethal exsanguination!

DDx:   traumatic bone cyst, central giant cell granuloma, ossifying fibroma



=  nontraumatic subluxation / rotational disorder of atlantoaxial joint leading to limited rotation / fixation of neck comprising many different entities

Cause:   idiopathic spontaneous

(a)  increased ligamentous laxity: rheumatoid arthritis, Marfan syndrome, Down syndrome, Morquio syndrome

(b)  congenital abnormality: incomplete odontoid process, incomplete transverse ligament

(c)  infection: sinusitis, otomastoiditis, otitis media, pharyngitis, adenotonsillitis, cervical / retropharyngeal / tonsillar abscess = Grisel syndrome
(= not associated with trauma or bone disease primarily in children) hyperemia + pathologic ligamentous relaxation

Predisposed:   cervical dystonia, post surgery

May be associated with:   ipsilateral contracted SCMM

•  history of insignificant cervical spine trauma / upper respiratory tract infection

•  limited painful neck motion = painful torticollis

•  head held in “cock-robin” position = rotation + flexion + tilt of head contralateral to direction of rotation with inability to turn head that does not resolve within 5–7 days after injury

X-ray (Dx difficult to make):

√  atlanto-odontoid asymmetry (open mouth odontoid view):

√  decrease in atlanto-odontoid space + widening of lateral mass on side ipsilateral to rotation

√  increase in atlanto-odontoid space + narrowing of lateral mass on side contralateral to rotation

√  atlantoaxial asymmetry remains constant with head turned into neutral position

√  posterior arch of C1 not identified in true lateral projection

√  obscuration of craniovertebral junction in true lateral view

CT (dynamic with 3D reconstruction [a] with head in resting position [b] with maximal contralateral rotation):

√  facet displacement in neutral head position

√  asymmetrically fixed C1-C2 rotation

Rotation up to an average of 79° in adult volunteers, loss of contact of articular facets of C1 and C2 during rotation as high as 74–85% in physiologic conditions. Therefore, a diagnosis of subluxation of the atlanto-occipital joint should not be made based solely on the CT appearance of this joint.


√  disruption of alar + transverse ligg.

√  spinal cord compression (rare)


I  < 3 mm anterior displacement of atlas on axis = rotatory fixation within normal range of movement (most common)

Injury:   intact alar + transverse ligaments

√  pivot around dens, NO anterior displacement of atlas

II  3–5 mm anterior displacement of atlas + unilateral displacement of lateral mass of atlas ← restraint by alar lig.

Injury:   transverse ligament

√  center of rotation shifted to one of lateral masses

III  > 5 mm anterior displacement of atlas + anterior displacement of both lateral masses

Injury:   deficiency of both (alar + transverse) ligaments

IV  posterior displacement of atlas on axis (rare)

Injury:   deficiency of both (alar + transverse) ligaments

DDx:   torticollis (atlantoaxial symmetry reverts to normal with head turned into neutral position)

Traumatic Rotatory Subluxation

Cause:   injury of alar ligaments ← flexion + rotation forces

Age:     more prevalent in children than in adults ← mostly flat articular facets allow ample movement in multiple directions


=  most severe nerve injury of extremities

Cause:   severe traction force on upper limb at birth / in traffic accident (motorcycle)

1.   Erb-Duchenne palsy: adduction injury affecting C5-6 ← downward displacement of shoulder

•  paralysis of shoulder muscles + biceps

2.   Klumpke palsy: abduction injury at C7, C8, T1 ← arm stretched over head

•  paralysis of forearm flexors + intrinsic hand muscles

CT myelography (preferred method):

◊  Shoulder artifacts may be problematic at C8–T1 level

√  displacement of spinal cord to contralateral side ← absence of normal nerve root traction on cord

√  pouchlike nerve root sleeve at site of avulsion

√  asymmetric slightly deformed root sleeve + nerve roots

√  obliteration of tip of root sleeve

√  traumatic meningocele

√  contrast extravasation collecting in axilla

√  metrizamide in neural foramina


  ◊  Conventional MR only in 50% accurate!

Pitfalls:      partial root avulsion, intradural fibrosis, traumatic meningocele, movement artifacts (respiration, swallowing, blood flow)

√  focal T2-hyperintense cord changes ← edema of acute phase / myelomalacia in chronic phase

√  focal T2-hypointense cord changes ← hemosiderin

√  enhancement of morphologically normal intradural nerve root / root stump ← functional impairment (mostly preganglionic)

√  abnormal enhancement of paraspinal (multifidus) muscle ← muscle denervation = indirect sign of root avulsion

√  thickening of postganglionic brachial plexus ← edema + fibrosis



=  midline closure defect of neural tube with a spectrum of anomalies including complete / partial agenesis of sacrum + lumbar vertebrae and pelvic deformity

Etiology:   disturbance of caudal mesoderm < 4th week of gestation from toxic / infectious / ischemic insult

Prevalence:   1÷60,000 births; 0.005–0.01% of population; in 0.1–1% of pregnancies in diabetic women; M÷F = 2.7÷1

Predisposed:   infants of diabetic mothers; risk increases 200–400 times in women dependent on insulin

◊  16–22% of children with sacral agenesis have mothers with diabetes mellitus

◊  NOT associated with VATER syndrome!

A.  Musculoskeletal anomalies

@   Lower extremity

•  symptoms from minor muscle weakness to complete sensorimotor paralysis of both lower extremities

√  hip dislocation

√  hypoplasia of lower extremities

√  flexion contractures of lower extremities

√  foot deformities

@   Lumbosacral spine = SACRAL AGENESIS


Type 1 = unilateral partial agenesis localized to sacrum / coccyx
Type 2 = bilateral partial symmetric defects of sacrum + iliosacral articulation
Type 3 = total sacral agenesis + iliolumbar articulation
Type 4 = total sacral agenesis + ilioilial fusion posteriorly

√  nonossification of lower spine

√  fusion of caudal-most 2 or 3 vertebrae

√  spina bifida (lipomyelomeningocele often not in combination with Arnold-Chiari malformation)

√  narrowing of spinal canal rostral to last intact vertebra

√  hypoplastic iliac wings

B.  Spinal cord anomalies

√  characteristic club- / wedge-shaped configuration of conus medullaris (= hypoplasia of distal spinal cord)

√  ± tethered spinal cord

√  ± dural sac stenosis with high termination

√  ± spinal cord lipoma, teratoma, cauda equina cyst

√  ± syrinx

C.  Genitourinary anomalies

•  neurogenic bladder (if > 2 segments are missing)

•  malformed external genitalia

√  ± bilateral renal aplasia with pulmonary hypoplasia and Potter facies

D.  Hindgut anomalies

•  lack of bowel control

√  anal atresia


•  normal / imperforate anus

√  short CRL in 1st trimester ← diabetic embryopathy

√  normal / mildly dilated urinary system

√  normal / increased amniotic fluid

√  2 umbilical arteries

√  2 hypoplastic nonfused lower extremities in a CHARACTERISTIC froglike position

√  fusion of pelvic bones

√  sacral agenesis, absent vertebrae from lower thoracic / upper lumbar spine caudally

N.B.:   brain, proximal spine, and spinal cord are notably spared!


=  fused lower extremities resembling a mermaid (siren)

Cause:  aberrant vessel that shunts blood from the high abdominal aorta to the umbilical cord (steal phenomenon) → severe ischemia of caudal portion of fetus

◊  NOT associated with maternal diabetes mellitus!

•  pulmonary hypoplasia + Potter facies

•  absence of anus; absent genitalia

√  bilateral renal agenesis / dysgenesis (lethal)

√  marked oligohydramnios

√  single aberrant umbilical artery

√  two-vessel umbilical cord

√  single / fused lower extremity often with fewer leg bones than normal

√  sacral agenesis, absent pelvis, lumbosacral “tail”, lumbar rachischisis

Prognosis:  incompatible with life


=  rare benign periapical lesion

Origin:    true neoplasm of cementum

Prevalence:   <1% of all odontogenic tumors

Age:   < 20 years (50%); < 30 years (75%)

Associated with:   erupted permanent tooth (common); near impacted / unerupted tooth (rare)

Location:   mandible (>75%): 90% molar / premolar region

Site:   fusion with root of tooth(s); invasion of root canal / pulp chamber (occasionally)

√  periapical sclerotic sharply marginated round opaque sunburst lesion

√  surrounded by thin halo of low attenuation

Rx:   complete removal of tooth to avoid recurrence

DDx:   condensing osteitis (periodontal ligament space not obscured)



=  nonneoplastic benign hamartoma associated with tooth apex

Histo:   proliferation of connective tissue within periodontal membrane

Age:   4th–5th decade; in woman: black / Asian descent

•  asymptomatic / dull ache

Associated with:   vital nonrestored tooth + intact lamina dura

Location:   mandible >> maxilla

Site:   usually apex of vital tooth

√  one / more, closely apposed / confluent, round / ovoid lucent lesion with varying amounts of opacity:

√  initially lytic lesion

√  later mixed lysis + sclerosis with varying amounts of opacity; little expansion

√  calcifies centrally with time

√  periapical sclerotic sharply marginated area NOT fused to tooth

√  ± low-attenuation halo

√  adjacent lesions may coalesce

Cementoblastoma and cemento-osseous dysplasia are both periapical sclerotic sharply marginated lesions with low-attenuation halo.

DDx:  (1)   Cementoblastoma (in child + young adult, fuses directly to tooth root)

(2)   Cemento-osseous dysplasia (common in black woman + woman of Asian descent during 4th / 5th decade of life, does not fuse to tooth root)

Periapical Cemento-osseous Dysplasia

Site:     anterior mandible between mandibular canine teeth involving one / a few teeth

√  often multicentric

DDx:  ossifying fibroma, fibrous dysplasia, Paget disease

Focal Cemento-osseous Dysplasia

Site:     posterior mandible involving molar teeth

√  no extension into adjacent bone

√  no cortical expansion

DDx:  periapical periodontitis, ossifying fibroma

Florid Cemento-osseous Dysplasia

=  diffuse form of periapical cemento-osseous dysplasia

Location:   involving ≥ 2 jaw quadrants / entire mandible

May be complicated by:   osteomyelitis with drainage of necrotic bone debris into oral cavity


=  single lesion of altered vascular + reactive response within bone

Age:   < 30 years (75%); in girls + young women

•  painless swelling, tenderness on palpation

Location:   mandible÷maxilla = 2÷1

Site:   anterior to 1st molar (= deciduous teeth); propensity for crossing midline (especially in maxilla)

√  small unilocular area of lucency (early)

√  multilocular honeycomb with wispy internal septa (later)

√  expansion of bone + erosion / remodeling of cortex

√  displacement of teeth + root resorption

√  usually well-defined border

DDx:   brown tumor of HPT (histologically similar)


=  2nd most common nonlymphoproliferative primary malignant tumor of spine in adults

Peak age:   30 and 70 years; M÷F = 2÷1 to 4÷1

Location:   thoracic + lumbar spine > sacrum

Site:   posterior element (40%), vertebral body (15%), both (45%)

√  large calcified mass with bone destruction

√  ± true ossification ← residual osteochondroma


√  low attenuation of nonmineralized portion of tumor

√  chondroid matrix mineralization


√  nonmineralized portion of tumor = high water content:

√  low to intermediate SI on T1WI

√  very high signal intensity on T2WI

√  rings and arcs enhancement pattern ← lobulated growth

√  extension through intervertebral disk (in 35%)

Rx:   en bloc resection


Prevalence:   1÷2,000,000; 2–4% of all primary malignant bone tumors; 1% of all CNS tumors

◊  2nd most common primary malignant tumor of spine in adults after lymphoproliferative neoplasms! Highly malignant in children.

Etiology:   originates from embryonic remnants of notochord / ectopic cordal foci between Rathke pouch + coccyx (notochord appears between 4th and 7th week of embryonic life and forms nucleus pulposus)

Mean age:   50 (range, 30–70) years; peak in 5th decade; M÷F = 2÷1

Path:   lobulated tumor with fluid, gelatinous mucoid substance, recent + old hemorrhage, necrotic areas, occasionally calcifications + sequestered bone fragments contained within pseudocapsule

Histo:   [physallis, Greek = bladder, bubble; phoros = bearing]

(1)  typical chordoma: cords + clusters of physaliferous cells (PAS-positive stain) in a lobular arrangement with a large bubblelike multivacuolated cytoplasm containing intracytoplasmic mucous droplets; abundant extracellular mucus deposition + areas of hemorrhage

(2)  chondroid chordoma: cartilage instead of mucinous differentiation of extracellular matrix

Location:   (a)   50–60% in sacrum (sacrococcygeal chordoma)

(b)  30–35% in clivus (sphenooccipital chordoma)

(c)  15% in vertebrae (vertebral chordoma): cervical > thoracic / lumbar spine; vertebral body with sparing of posterior elements

(d)  other sites (5%) in mandible, maxilla, scapula

Site:   midline / paramedian

√  amorphous calcification (50–75%)

√  heterogeneous enhancement


√  low-attenuation within soft-tissue mass ← myxoid-type tissue

√  higher attenuation fibrous pseudocapsule

MR (modality of choice):

√  low to intermediate intensity on T1WI, occasionally hyperintense ← high protein content:

√  heterogeneous internal texture ← calcification, necrosis, gelatinous mucoid collections

√  very high SI on T2WI ← physaliferous cells similar to nucleus pulposus with high water content


√  prominent vascular stain


√  cold lesion on bone scan

√  no uptake on gallium scan

Metastases (in 5–43%) to:   liver, lung, regional lymph nodes, peritoneum, skin (late), heart

Prognosis:   poor in spite of low grade + slow growth; almost 100% recurrence rate despite radical surgery

DDx:   giant notochordal rest (nonprogressive indistinct lesion, normal bone / variable degree of sclerosis, no soft-tissue involvement)

Intracranial Chordoma (35%)

=  locally invasive + destructive lesion of clivus

Location:   infrasellar midline

√  mass of usually T1 hypointensity + T2 signal hyperintensity

√  hypointense intratumoral septations

√  foci of T1 signal hyperintensity within tumor / periphery ← residual ossified fragments / tumor calcifications, / small collections of proteinaceous fluid / hemorrhage

√  posterior extension indenting pons

DDx:  cartilaginous tumor (more lateral location, at petrooccipital synchondrosis, curvilinear calcifications)

Sacrococcygeal Chordoma (50–70%)

=  large destructive sacral mass with 2ndary soft-tissue extension

◊  Most common primary sacral tumor after giant cell tumor!

Peak age:  40–60 years; M÷F = 2–3÷1

Path:  slow-growing tumor → large size at presentation

•  clinically indolent and subtle; rectal bleeding (42%)

•  low back pain (70%); sciatica + weakness in hip / lower limbs ← sacral root compression

•  constipation, frequency, urgency, straining on micturition ← compression by tumor

•  autonomic dysfunction → urinary / fecal incontinence

•  palpable sacral mass on digital examination (17%)

Location:  predominantly in 4th + 5th sacral segment

√  presacral mass with average size of 10 cm extending superiorly + inferiorly; rarely posterior location

√  displacement of rectum + bladder

√  solid tumor with cystic areas (in 50%)

√  amorphous peripheral calcifications (15–89%)

√  secondary bone sclerosis in tumor periphery (50%)

√  honeycomb pattern with trabeculations (10–15%)

√  may cross sacroiliac joint


√  osteolytic midline mass in sacrum + coccyx associated with soft-tissue mass and calcifications

CT (useful for defining extent of bone involvement):

√  bone destruction associated with lobulated midline soft-tissue mass

√  areas of low attenuation within mass ← high water content of myxoid properties


√  hypo- / isointense mass relative to muscle on T1WI:

√  intrinsic hyperintense areas on T1WI ← hemorrhage or myxoid / mucinous collections

√  hyperintense mass similar to nucleus pulposus on T2WI ← high water content:

√  dividing septa + hemosiderin of low signal intensity

√  heterogeneous often moderate enhancement

The combination of high T2 signal intensity in a lobulated sacral mass that contains areas of hemorrhage and calcification is strongly suggestive of a chordoma!

Prognosis:  7–10 years average survival; 50–74% 5-year survival rate (in adulthood); 52–64% 10-year survival; 52% 20-year survival

Dx:     fine-needle aspiration biopsy

Rx:     radical surgical excision (most critical); radiation therapy; 70% rate of local recurrence after excision


›  Primary neural tumor: schwannoma, neurofibroma, meningioma, myxopapillary ependymoma (from within spinal canal, more intense enhancement)

›  Primary bone tumor:

(1)  Giant cell tumor (2nd most common primary, upper sacrum, may be eccentric, ± extension across SI joint, low-to-intermediate T2 intensity ± fluid-fluid levels)

(2)  Chondrosarcoma (off midline from sacroiliac joint space cartilage, heterogeneous T2 SI, no hemorrhage)

(3)  Aneurysmal bone cyst

(4)  Osteoblastoma

(5)  Lymphoma

›  Metastasis, plasmacytoma

›  Soft-tissue neoplasm: atypical hemangioma, prostatic carcinoma, osteosarcoma, osteomyelitis

Sphenooccipital Chordoma (15–35%)

Age:     younger patient (peak age of 20–40 years); M÷F – 1÷1

•  orbitofrontal headache

•  visual disturbances, ptosis

•  6th nerve palsy / paraplegia

Location:   clivus, sphenooccipital synchondrosis

√  bone destruction (in 90%): clivus > sella > petrous bone > orbit > floor of middle cranial fossa > jugular fossa > atlas > foramen magnum

√  reactive bone sclerosis (rare)

√  calcifications / residual bone trabeculae (20–70%)

√  soft-tissue extension into nasopharynx (common), into sphenoid + ethmoid sinuses (occasionally), may reach nasal cavity + maxillary antrum

√  variable degree of enhancement


√  large intraosseous mass extending into prepontine cistern, sphenoid sinus, middle cranial fossa, nasopharynx

√  posterior displacement of brainstem

√  usually hypo- / isointense to brain / occasionally inhomogeneously hyperintense on T1WI

√  hyperintense on T2WI

√  ± CHARACTERISTIC honeycomb enhancement pattern

Prognosis:  4–5 years average survival

DDx:  meningioma, metastasis, plasmacytoma, giant cell tumor, sphenoid sinus cyst, nasopharyngeal carcinoma, chondrosarcoma

Vertebral / Spinal Chordoma (15–20%)

◊  More aggressive than sacral / cranial chordomas

Age:     younger patient; M÷F = 2÷1

•  low back pain + radiculopathy + retention of urine

Location:   cervical (8% – particularly C2), thoracic spine (4%), lumbar spine (3%)

Site:     midline centra sparing posterior elements; arising in perivertebral musculature (uncommon)

√  destructive expansile lesion of vertebral body:

√  + epidural soft-tissue mass of collar button / mushroom / dumbbell shape over several segments

√  often incomplete sparing of disk spaces to involve adjacent bodies (10–14%) simulating infection

√  exophytic anterior soft-tissue mass

√  expansion into neural foramen mimicking nerve sheath tumor

√  solitary midline spinal mass

√  sclerosis / “ivory vertebra” in 43–62%

√  total destruction of vertebra, initially without collapse

√  amorphous peripheral calcifications in 40%

Cx:     complete spinal block

Prognosis:  4–5 years average survival

DDx:  metastasis, primary bone tumor, primary soft-tissue tumor, neuroma, meningioma


=  reactive osteitis surrounding apex of tooth with pulpitis / pulpal necrosis

Associated with:   carious tooth

√  periapical inflammatory lesion: granuloma / cyst / abscess

√  periapical poorly marginated nonexpansile sclerosis


=  characterized by egress of CSF from intracranial cavity through abnormal communication between subarachnoid space and pneumatized structure within skull base (= osteodural defect)




(a)  traumatic (80–90% of all cases)

◊  2% of all head injuries develop CSF fistula

(b)  nontraumatic:

›  infection

›  tumor (esp. those arising from pituitary gland)

(c)  spontaneous: idiopathic intracranial hypertension

•  rhinorrhea / otorrhea (may be exacerbated by Valsalva maneuver)

•  “serous otitis media” with conductive / sensory hearing loss

•  presence of β-2 transferrin (= polypeptide specific for CSF) / β-trace protein


(a)  invasive techniques (time-consuming, poorly tolerated)

1.   Radionuclide cisternography

2.   CT cisternography

◊  Contraindicated in active meningitis / elevated intracranial pressure!


›  requires poorly tolerated lumbar puncture

›  time-consuming

›  slight risk of complications (low-tension headache, infection, bleeding at puncture site)

›  hypersensitivity reaction to contrast

›  high dose of radiation

›  requires active CSF leak

(b)  noninvasive techniques (best used in combination)

1.   Multidetector CT (92% sensitive, 100% specific)

√  bone defect / dehiscence at skull base

√  adjacent prominent arachnoid granulations

√  air-fluid level / opacification of contiguous sinus / middle ear / mastoid

√  pneumocephalus

√  lobular / nondependent area of soft-tissue opacification (meningocele, meningoencephalocele)

DDx:   mucosal reaction, cholesteatoma, granulation tissue, cholesterin granuloma

2.   MR cisternography (87–100% sensitive, 57–100% specific, 78–89% accurate)

√  hyperintense CSF fistulous tract

√  CSF collection = meningocele

DDx:   inflammatory paranasal secretions

√  extradural brain = meningoencephalocele

√  secondary gliosis of herniated brain

√  dural enhancement in stalk of meningoencephalocele

Spontaneous CSF Fistula

Location:  cribriform plate along course of anterior ethmoid artery (most common), lateral lamella, perisellar region (sphenoid roof > floor of sella > posterior wall), lateral recess of sphenoid, tegmen tympani, tegmen mastoideum, skull base foramina

Traumatic CSF Fistula

•  traumatic leak: usually unilateral; onset within 48 hours after trauma, usually scanty; resolves in 1 week

•  nontraumatic leak: profuse flow; may persist for years

•  anosmia (in 78% of trauma cases)

Location:  fractures through frontoethmoidal complex + middle cranial fossa (most commonly)

Cx:   (1)   meningitis / encephalitis / brain abscess (in 25–50% of untreated cases)

(2)  pneumocephalus


=  triad of anorectal malformation + sacrococcygeal osseous defect + presacral mass (= ASP triad)

=  rare syndrome characterized by autosomal dominant genetic inheritance (in > 50%)

Path:   presacral mass consists of teratoma, anterior sacral meningocele > dermoid cyst, hamartoma, enteric duplication cyst

Age:   < 16 years at diagnosis (in 80%)

•  constipation


◊  Therapeutic decision-making should be based on clinical assessment alone!

◊  There are no prognostic indicators on images in patients with acute lumbar radiculopathy!

◊  35% of individuals without back trouble have abnormal findings (HNP, disk bulging, facet degeneration, spinal stenosis)

◊  Imaging is only justified in patients for whom surgery is considered!


loss of disk height leads to stress on facet joints + uncovertebral joints (= uncinate process), exaggerated joint motion with misalignment (= rostrocaudal subluxation) of facet joints, spine instability with arthritis, capsular hypertrophy, hypertrophy of posterior ligaments, facet fracture

Plain film:

√  intervertebral osteochondrosis = disease of nucleus pulposus (= desiccation = loss of disk water):

√  narrowing of disk space

√  vacuum disk phenomenon

√  disk calcification

√  bone sclerosis of adjacent vertebral bodies

√  spondylosis deformans = degeneration of the outer fibers of the annulus fibrosus:

√  endplate osteophytosis growing initially horizontally and then vertically several millimeters from diskovertebral junction ← displacement of nucleus pulposus in anterior + anterolateral direction producing traction on osseous attachment of annulus fibrosus [= fibers of Sharpey])

√  enlargement of uncinate processes

√  osteoarthritis = degenerative disease of synovium-lined apophyseal / costovertebral joints:

√  degenerative spondylolisthesis

√  cartilaginous node = intraosseous disk herniation


√  delineation of thecal sac, spinal cord, exiting nerve roots

CT (accuracy > 90%):

√  facet joint disease (marginal sclerosis, joint narrowing, cyst formation, bony overgrowth)

√  uncovertebral joint disease of cervical spine (osteophytes project into lateral spinal canal + neuroforamen)


√  scalloping of cord (T2WI FSE / GRE images):

√  anterior encroachment by disk / spondylosis

√  posterior encroachment by ligamentum flavum hypertrophy

√  loss of disk signal ← desiccation ←decrease in water-binding proteoglycans + increase in collagen within nucleus pulposus) on T2WI

√  annular tear:

(1)  concentric tear – separation of annular lamellae

(2)  transverse tear

(3)  radial tear – crossing multiple annular lamellae with greater vertical dimension + more limited horizontal extent

•  diskogenic pain

◊  does NOT imply disk herniation

√  gap near middle of annulus

Modified Dallas Diskogram Classification




contrast confined within nucleus pulposus


contrast extends to inner third of annulus


contrast extends to middle third of annulus


outer third of annulus + < 30° of circumference


outer third of annulus + > 30° of circumference


extension of contrast beyond annulus

√  cleft of high SI in a normally hypointense outer annulus on T2WI

√  contrast enhancement ← granulation tissue / hyperemia / inflammation

√  reduction in disk height (late):

√  Schmorl’s node

√  moderate linear uniform enhancement on T1WI

√  vacuum phenomenon with low signal on T1WI

√  endplate + marrow changes (Modic & DeRoos):

=  linear signal alterations paralleling adjacent endplates

(a)  Type 1 (4%) = edema pattern

Cause:   replacement of bone marrow with hyperemic fibrovascular tissue + edema ← acute disk degeneration

√  hypointense on T1WI + hyperintense on T2WI

√  contrast-enhancement of marrow

(b)  Type 2 (16%) = fatty marrow pattern

Cause:   replacement of bone marrow with fat ← chronic disk degeneration

√  hyperintense marrow signal on T1WI

√  iso- to mildly hyperintense on T2WI

√  hypointense on STIR

(c)  Type 3 = bony sclerosis pattern

Cause:   replacement of bone marrow with sclerotic bone ← chronic disk degeneration after a few years

√  hypointense marrow signal on T1WI + T2WI

√  juxtaarticular synovial cyst in posterolateral spinal canal (most frequently at L4-5):

√  smooth well-defined extradural mass adjacent to facet joint

√  variable signal pattern ← serous, mucinous, gelatinous fluid components, air, hemorrhage

√  contrast-enhancing hypointense perimeter ← fibrous capsule with calcium + hemosiderin


SPECT imaging of vertebrae can aid in localizing increased uptake to vertebral bodies, posterior elements, etc.

√  eccentrically placed increased uptake on either side of an intervertebral space (osteophytes, diskogenic sclerosis)

Sequelae:    (1)  Disk bulging

(2)  Disk herniation

(3)  Spinal stenosis

(4)  Facet joint disease

(5)  Instability

√  dynamic slip > 3 mm on flexion-extension

√  static slip > 4.5 mm

√  traction spurs

√  vacuum phenomenon

DDx:   Idiopathic segmental sclerosis of vertebral body (middle-aged / young patient, hemispherical sclerosis in anteroinferior aspect of lower lumbar vertebrae with small osteolytic focus, only slight narrowing of intervertebral disk; unknown cause)

Bulging Disk = Disk Bulge

=  concentric smooth expansion of softened disk material beyond the confines of endplates with disk extension outward involving > 50% of disk circumference

Cause:  weakened and lengthened but intact annulus fibrosus + posterior longitudinal ligament

Age:     common finding in individuals > 40 years of age

Location:   L4-5, L5-S1, C5-6, C6-7

√  rounded symmetric defect localized to disk space level

√  smooth concave indentation of anterior thecal sac

√  encroachment on inferior portion of neuroforamen

√  accentuated by upright myelography


√  nucleus pulposus hypointense on T1WI + hyperintense on T2WI ← desiccation (= water loss through degeneration + fibrosis)

Herniation of Nucleus Pulposus

=  HNP = protrusion of disk material > 3 mm beyond margins of adjacent vertebral endplates involving < 50% of disk circumference

Cause:  rupture of annulus fibrosus with disk material confined within posterior longitudinal ligament

◊  21% of an asymptomatic population has a herniated disk!

•  local somatic spinal pain = sharp / aching, deep, localized

•  centrifugal radiating pain = sharp, well-circumscribed, superficial, “electric,” confined to dermatome

•  centrifugal referred pain = dull, ill-defined, deep or superficial, aching or boring, confined to somatome (= dermatome + myotome + sclerotome)


(a)  posterolateral (49%) = weakest point along posterolateral margin of disk at lateral recess of spinal canal

◊  The posterior longitudinal ligament is tightly adherent to posterior central margins of disk!

(b)  posterocentral (8%)

(c)  bilateral (to both sides of posterior ligament)

(d)  lateral / foraminal (< 10%)

(e)  extraforaminal = anterior (commonly overlooked) (29%)

(f)  intraosseous / vertical = Schmorl node (14%)


√  sharply angular indentation on lateral aspect of thecal sac with extension above / below level of disk space (ipsilateral oblique projection best view)

√  asymmetry of posterior disk margin

√  double contour ← superimposed normal + abnormal side (horizontal beam lateral view)

√  narrowing of intervertebral disk space (most commonly a sign of disk degeneration)

√  deviation of nerve root / root sleeve

√  enlargement of nerve root (“trumpet” sign) ← edema

√  amputated / truncated nerve root (= nonfilling of root sleeve)


√  herniated disk material of low SI displaces the posterior longitudinal ligament and epidural fat of relative high SI on T1WI

√  “squeezed toothpaste” effect = hourglass appearance of herniated disk at posterior disk margin on sagittal image

√  asymmetry of posterior disk margin on axial image

Cx:   (1)   spinal stenosis mild = < ⅓
moderate = ⅓ to ⅔
severe = > ⅔

(2)  neuroforaminal stenosis


conservative therapy reduces size of herniation by

0–50% in 11% of patients,
50–75% in 36% of patients,
75–100% in 46% of patients

(secondary to growth of granulation tissue)

Broad-based Disk Protrusion

√  triangular shape of herniation with a base wider than the radius of its depth

√  25–50% of disk circumference

Focal Disk Protrusion

√  triangular shape of herniation with a base wider than the radius of its depth

√  < 25% of disk circumference

Disk Extrusion

=  prominent focal extension of disk material through the annulus with only an isthmus of connection to parent disk through intact / ruptured posterior longitudinal ligament

√  mushroom-shaped herniation with base narrower than the radius of its depth

√  “toothpaste” sign

Disk Sequestration


=  complete separation of disk material from parent disk with rupture through posterior longitudinal ligament into epidural space

◊  Missed free fragments are a common cause of failed back surgery!

√  migration superiorly / inferiorly away from disk space with compression of nerve root above / below level of disk herniation

√  disk material > 9 mm away from intervertebral disk space = NO continuity

√  soft-tissue density with higher value than thecal sac

DDx:   (1)   Postoperative scarring (retraction of thecal sac to side of surgery)

(2)  Epidural tumor

(3)  Tarlov cyst (dilated nerve root sleeve)

(4)  Conjoined nerve root (2 nerve roots arising from thecal sac simultaneously representing mass in ventrolateral aspect of spinal canal; normal variant in 1–3% of population)

Free Fragment Migration

=  separated disk material travels above / below intervertebral disk space

√  ± continuity

Cervical Disk Herniation

Peak age:   3rd–4th decade

•  neck stiffness, muscle splinting; dermatomic sensory loss

•  weakness + muscle atrophy; reflex loss

Sites:  C6-7 (69%); C5-6 (19%); C7-T1 (10%); C4-5 (2%)


(1)  compression of exiting nerve roots with pain radiating to shoulder, arm, hand

(2)  cord compression (spinal stenosis + massive disk rupture)

Thoracic Disk Herniation

Prevalence:   1% of all disk herniations

Sites:  T11-12

√  calcification of disk fragments + parent disk (frequent)

Lumbar Disk Herniation

•  sciatica =

(1)  Stiffness in back

(2)  Pain radiating down to thigh / calf / foot

(3)  Paresthesia / weakness / reflex changes

•  pain exaggerated by coughing, sneezing, physical activity + worse while sitting / straightening of leg

Sites:  L4-5 (35%) > L5/S1 (27%) > L3-4 (19%) > L2-3 (14%) > L1-2 (5%)


=  SPLIT CORD = MYELOSCHISIS [diastema, Greek = slit, cleft]

=  sagittal division of spinal cord into two hemicords, each containing a central canal, one dorsal horn + one ventral horn

Etiology:   congenital malformation as a result of adhesions between ectoderm and endoderm; M÷F = 1÷3


(a)  2 hemicords each covered by layer of pia within single subarachnoid space + dural sac (60%); not accompanied by bony spur / fibrous band

(b)  2 hemicords each with its own pial, subarachnoidal + dural sheath (40%); accompanied by fibrous band (in 25%), cartilaginous / bony spurs (in 75%)

Associated with:   myelomeningocele

•  hypertrichosis, nevus, lipoma, dimple, hemangioma overlying the spine (26–81%)

•  muscle wasting, ankle weakness in one leg; clubfoot (50%)

Location:   lower thoracic / upper lumbar > upper thoracic > cervical spine

√  sagittal cleft in spinal cord resulting in 2 asymmetric hemicords which usually reunite caudal to cleft

√  occasionally 2 coni medullaris

√  eccentric central canal within both hemicords

√  bony spur through center of spinal canal arising from posterior aspect of centra (< 50%)

√  thickened filum terminale > 2 mm (> 50%)

√  tethered cord (> 50%)

√  low conus medullaris below L2 level (> 75%)

√  defect in thecal sac on myelogram

@   Vertebrae

√  congenital scoliosis (50–75%)

◊  5% of patients with congenital scoliosis have diastematomyelia

√  spina bifida over multiple levels

√  anteroposterior narrowing of vertebral bodies

√  widening of interpediculate distance

√  narrowed disk space with hemivertebra, butterfly vertebra, block vertebra

√  fusion + thickening of adjacent laminae (90%)

(a)  fusion to ipsilateral lamina at adjacent levels

(b)  diagonal fusion to contralateral adjacent lamina = intersegmental laminar fusion

Cx:   progressive spinal cord dysfunction


◊  Most common pediatric spine problem!


(1)  Bloodborne bacterial invasion of vertebrae infecting disk via communicating vessels through endplate

◊  Vertebral osteomyelitis + diskitis may be the same entity!

(2)  Invasive procedure / trauma: surgery, diskography, myelography, chemonucleolysis

(3)  Extension of adjacent infection


(a)  pyogenic: Staphylococcus aureus (> 50%), gram-negative rods (in IV drug abusers / immunocompromised patients)

(b)  nonpyogenic: tuberculosis, coccidioidomycosis

◊  TB has a propensity to extend beneath longitudinal ligaments with involvement of multiple vertebral levels

Pathogenesis:   infection starts in disk (still vascularized in children) / in anterior inferior corner of vertebral body (in adults) with spread across disk to adjacent vertebral endplate

Age peaks:   6 months to 4 years; 10–14 years; 6th–7th decade

•  over 2–4 weeks gradually progressing irritability, malaise, low-grade fever; refusal to bear weight; myelopathy

•  neck / back / referred hip pain, limp, focal tenderness

•  elevated sedimentation rate, WBC count often normal

•  positive blood culture (in 58%)

Location:   L3-4, L4-5, unusual above T9

Distribution:   2 adjacent vertebrae + intervening disk

Plain film (positive 2–4 weeks after onset of symptoms):

√  decrease in disk space height (earliest sign) = intraosseous herniation of nucleus pulposus into vertebral body through weakened endplate

√  indistinctness of adjacent endplates with destruction

√  endplate sclerosis (during healing phase beginning anywhere from 8 weeks to 8 months after onset)

√  bone fusion (after 6 months to 2 years)

CT (SAG / COR reformatted images more sensitive!):

√  early loss of disk height

√  endplate irregularities ← destruction

√  vertebral body collapse

√  paravertebral inflammatory mass / abscess

√  epidural soft-tissue extension with deformity of thecal sac

MR (preferred modality; 93% sensitive, 97% specific, 95% accurate):

◊  Very sensitive modality early on in disease process!

√  ↓ marrow intensity on T1WI in 2 contiguous vertebrae

√  signal intensity of disk decreased on T1WI + increased on T2WI compared to skeletal muscle

◊  Fluid-sensitive sequence with fat suppression!

√  progressive destruction of vertebral body

√  in early stage preserved disk height with variable intensity on T2WI (often increased)

√  in later stages loss of disk height with increased intensity on T2WI (= intradiskal fluid)


√  focal enhancement of involved disk + adjacent vertebral endplates ± bone marrow

NUC (41% sensitive, 93% specific, 68% accurate on 99mTc-MDP + 99mTc WBC scans):

√  positive before radiographs

√  increased uptake in vertebral endplate adjacent to disk

√  bone scan usually positive in adjacent vertebrae (until age 20) ← vascular supply via endplates; may be negative after age 20

Dx:   needle biopsy (77% positive) before IV antibiotics

Cx:    (1)  epidural / paravertebral abscess ← extension of infection

(2)  kyphosis

Rx:   immobilization in body cast for ~ 4 weeks

DDx:   neoplastic disease (no breach of endplate, disk space often intact)

Postoperative Diskitis

Frequency:   0.75–2.8%

Organism:  Staphylococcus aureus; many times no organism recovered

•  severe recurrent back pain 7–28 days after surgery accompanied by decreased back motion, muscle spasm, positive straight leg raising test

•  fever (33%), wound infection (8%)

•  persistently elevated / increasing ESR


√  decreased SI within disk + adjacent vertebral body marrow on T1WI

√  increased SI in disk + adjacent marrow on T2WI often with obliteration of intranuclear cleft

√  contrast-enhancement of vertebral bone marrow ± disk space

DDx:  degenerative disk disease type I (no gadolinium-enhancement of disk)

Pyogenic Spondylodiskitis


Pathophysiology:   infection of anterior vertebral body (2° to rich blood supply) → extension into disk → extension into neighboring vertebra

Predisposed:   diabetes mellitus, immunocompromised, IV drug abuse

Location:   lumbar > thoracic > cervical spine

•  insidious back pain, fever, chills, night sweats

•  elevated ESR, elevated C-reactive protein, ±leukocytosis

DDx:  (1)   Dialysis-associated spondyloarthropathy (intradiskal fluid + enhancement uncommon, NO epidural / paraspinal abscess)

(2)  Degenerative disk disease (hypointense T1 and hyperintense T2 endplate changes flanking a degenerated disk ± enhancement, NO fluidlike disk signal intensity, disk vacuum phenomenon)



Atlantooccipital Dislocation


=  disruption of tectorial membrane + paired alar ligaments resulting in grossly unstable injury

◊  Diagnosis difficult to make and easy to overlook at whole-body CT!

Cause:  rapid deceleration with either hyperextension or hyperflexion → in up to ⅓ of high-velocity injuries

Age:     in adults much less common than in children ← larger size of head relative to body, increased laxity of ligaments, shallow horizontally oriented occipitoatlantoaxial joint, hypoplastic occipital condyles

May be associated with:   occipital condyle fracture

•  neurologic symptoms: range from respiratory arrest with quadriplegia to normal neurologic exam

•  discomfort, stiffness

Direction of dislocation / subluxation: anteriorly, posteriorly, superiorly (vertical = life-threatening)

Lateral radiograph:

√  Powers ratio (assessment for anterior subluxation) = BC÷OA ratio > 1 = ratio of distance between basion + spinolaminar line of C1 and distance between posterior cortex of anterior tubercle of C1 + opisthion (74% sensitive)

√  basion-dens interval (BD) > 12 mm on X-ray / 9.5 mm on CT without traction placed on head / neck

√  basion-axial interval > 12 mm anterior / > 4 mm posterior to posterior axial line (PAL)

√  atlanto-dental interval > 3 mm (man) / > 2.5 mm (woman):

√  “V sign” = cranially divergent predental lines ← transverse ligament injury

√  atlanto-occipital interval > 4 mm

√  atlanto-axial interval > 2.6–4 mm

√  > 10 mm soft-tissue swelling anterior to C2 + pathologic convexity of soft tissues (80%)

CT (≤ 1.25 mm thick sections, superior to radiographs):

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Jun 29, 2017 | Posted by in GENERAL RADIOLOGY | Comments Off on and Spine Disorders
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