Radiology Spine Flashcards
Ankylosing spondylitis
spondyloarthropathy. chronic, multisystem inflm disorder primarily in sacroiliac joints (SI) and axial skeleton. HLA-B27
clinical presentation:
1) insidious onset of low back pain and stiffness
2) spontaneous remision and exacerbation
3) onset sx< 40yo
4) present sx >3mo
5) sx worse in morning or with inactivity
6) improve after exercise
skeletal ankylosing spondylitis
sacroilitis and spondylitis. spondylodiscitis, enthesitis, arthritis of hips and shoulder. osteoporosis and vertebral fractures, pseudoarthrosis
extraskeletal ankylosing spondylitis
anterior uveitis, enteric mucosal lesions, lungs, incr CVD, atlantoaxial J subluxation and SC compression, cauda equina syndrome, IgA nephropathy and amyloidosis
ankylosing spondylitis dx
bamboo spine due to vertebral fusion by marginal syndesmophwytes. MRI or CT of Si J, spin, peripheral J may reveal early sacroilitis erosions.
ankylosing spondylitis tx
symtomatic: pain ctrl with NSAIDs, selective COX2, DMARDs, anti-TNF inhibitor, pamidronate, thalidomide, exercise, physical therapy. surgical- stability fracture and prevent neuro deficit
ASA infarction presentation
acute motor paralysis (usually bilateral), loss of complete P/T. sparing of proprioception nd vibratory. hypotension, sexual dysfunction or bowel and bladder dysfunction, compromise respiration if lesion is in rostral cervical cord
ASA infarct neuro exam
vary with portion of cord affected. deficit below lvl of lesion. LMN sign, UMN sings. lower extremity affected more than upper. bilateral P/T loss.
asa infarction radiology
restricted diffusion on DWI. abn signal in vertebral body. min enhancement unlike spinal tumor. snake eye appearance of corticospinal tracts
ASA infarction tx
sx care of bladder, bowel, skin. maybe high dose corticosteroid or anticoag
anterior horn cellitis
MRI show swelling of T2 - owl’s eyes bc involve central gray matter. bilateral LE weakness and areflexia
B12 myelopathy
-neuro dysfunc in peripheral and optic N, posteiror and lateral columns of SC. Present with cold numbness, tingling in tips of toes and then fingers- ascending paresthesias. limb weakness and ataxia if untx.
neuro exam: impair vibration and J-position sense with progresses over time to loss of light touch, pin-prick, and T. leg affected bf arm. positive romberg. absent ankle jerk with relative hyperreflexia at knees. dx: MRI spine may reveal T2/FLAIR hyper intensity in posterior column. tx: parenteral or oral cobalamin
HIV vacuolar myelopathy
late stages of HIV, low CD4, vacuolation of lateral and posterior columns. resemble myelopathy of B12 def.
Clinical: gradual progression of painless leg weakness, stiffness, sensory loss, imbalance, sphincter dysfunction
neuro: slowly progressive spastic paraparesis with rare involvement of upper extremities, hypereflexia, pos babinski, sensory ataxia, bladder and bowel incontinence.
dx studies: T2 weighted MRI- symmetric non-enhancing hyperintesnsities, tx: supportive care- anti spasticity agent, manage sphincter dysfunc , rehab
spinal AVM
dural, intradural or intrameddular. dev in embryogenesis.
present: progressive back pain, sensory loss, weakness over mo-y. if hemorrhage- acute severe back pain, weakness, or paralysis. numbness with discrete sensory lvl. urinary/fecal incontinence.
neuro exam: bruit over SC. UMN signs, spastic paraparesis or quadriparesis, loss of P/T caudal to lesion
imaging: MRI = first line. digital subtraction angiography is gol standard.
tx: surgical ligation or resection, endovascular emboliation, spinal radiation, or combo
spinal cavernomas cause and clinical presentation
sinusoidal vascular channels lined with endothelium, surrounded by hemosiderin stained glotic rim of tissue. rare
clical:
1) progressive-slow dev of chronic myelopathy due to micohemorrhages or enlarged cavernoma –> mass effect.
2) acute- in hemorrhage, severe back pain, weakness or paralysis, numbeness, hyperreflexa, urinary/fecal incontinence.
3) episodic: hemorrhage resolves and rebleed occur.
SC cavernous malformtation (SCCMs) neuro exam, imaging, tx
neuro: incr tone and hyperreflexia caudal to lesion, spastic paraparesis or quadriparesis base on location .sensory and t loss caudal.
imaging: popcorn -gradient echo.
tx: resction
episdural metastasis
mostly from breast, lung or prostate ca. SC compression most often at thoracic lvl. clinical presentation- pain- progressive racial referred or radicular. later with myelopathy
neuro exam: spastic paraparesis, loss of sensation to all modalities, UPM signs, loss of rectal sphincter tone.
dx: MRI, leptomeningeal enhancement and intramedulary tumor. if unknown primary lesion then biopsy.
tx: high dose IV corticosteroids, radiotherapy, decompressive surgery
nerve sheath tumor
25% of tumor arising in intradural, extra medullary space. ex schwannomas
Etiology: sporatic (50s-70s( or inherited - NF1 or NF2
patho: derive from schwann cells or perineurial cell soft PNS.
clinical presentaiton: slow growing. often simp, can cause back or radicular pain. worse at night or in morning,resolve during day.
neuro: spastic paraparesis, diminished sensory below lesion, UMN signs, loss of bowel/bladder sphincter tone.
dx: MRI spine+ gado. majority enhance diffusely. heterogenous enhancement if intramural cyst or necrosis present
tx: gross total resection- goldstanard. no chemo/rad
syringomyelia: etiology, presenation
fluid filled cavity within SC
etiology: chiari I or II. tethered cords (congital or acquired), spinal archnoiditis, trauma, SC tumor, VP shunt, idiopathic
clinical presentation: dissociated sensory loss: no P/T. has light touch, proprioception, vibratory sensation. often cape like distribution over shoulder and back. pain frequently felt in neck and shoulders. as central lesion enlarge, weakness in more distal M follow by proximal, an atrophic areflexic paralysis dev due to disruption of centrally situated anterior horn GM. bladder dysfunc and urinary retention
syringomyelia neuro exam, dx, tx
neuro: cape - lose P/T. motor: UMN- bilateral motor paresis, upper?lower. LMN- atrophic, arefexic paralysis at site of lesion
dx: MRI spine show dilated cavity with same intensity as CSF on T2. no gad.
tx: vary based on etiology.
syringobulbia
syrinx rupture –> brainstem. cause direct entry of CSF into brainstem
clinical: early sign and sx of CN 10-12- dysphonia, dysarthria, dysphagia, palatal and tongue weakness. pt also complain of HA, vertigo, diplopia, tinnitus.
Neurology exam: CN def, nystagmus, weakness, hyperreflexia, scoliosis,
tx: surgical with sub occipital craniotomy or craniovertebral decompression. monitor for hydrocephalus prior to surgery
syringobulbia
when syrinx rupture extends into brainstem causing direct entry of CSF into brainstem
syringobulbia clinic
early: lower cranial N dysfunc (10-12)- dysphonia, dysarthria, dysphagia, palatal and tongue weakness. sometimes HA, vertigo diplopia, tinnitus
neuro exam: CN deficit, nystagmus, weakness, hyperreflexia, scoliosis
syringobulbia tx
surgical-suboccipital craniotomy or craniovertebral decompression. monitor for hydrocephalus prior to surgery
cervical spondylotic myelopathy (CSM) clinical
most common SC D in elderly (>55). clinical: insidious onset of neck, sub scapular, should pain radiating to arm uni or bilateral. clumsy, weak, numb, or tingling hands. weak or stiff leg. stiff neck. gait prob. bladder dysfunc.
CSM neuro exam
Motor: weakness or atrophy of UE. LMN finding in myotomal distribution. abysm lower extremity weakness and spasticity (UMN findings)
sensory: variable, asym. dermatomal or sensory lvl
reflexes: hyperreflexia, ankle clonus, babinski sign, hoffman’s sign
gait- spastic, scissoring quality,
lhermitt’e sign: electric shock like sensation down center of back following neck flexion
CSM dx, tx
MRI or CT. tx: surgical- decompression of SC when frank myelopathy occurs. med- noninvasive therapy- cervical immobilization (color or neck brace), cervical traction, skull traction and physical therapy
cervical spondylitic myelopathy path
path: antibody to aqauporin 4 (NMO IgG) ch in capillaries of brainstem and cerebellum
cervical spondylitic myelopathy presenation
sx of para or quadiplegia, sensory loss and sphincter paralysis (acute myelitis) and visual loss (optic neuritis)
cervical spondylitic myelopathy neuro exam + dx
neuro: persistent and profound flaccidity of legs (arms if cervical lesion), areflexia, atonality of bladder
CSF analysis: few-100s of mononuclear cell. incr protein, no oligoclonal bands
imaging: MRI-T2 signal changes and gado enhancement of cord. cord swelling may be present in acute to subacute period. longitudinally extensive lesion that occupy several spinal seg. atrophy of involved set of cord
cervical spondylitic myelopathy tx
high dose corticosteroid, plasma exchange to remove NMO ab, cyclophosphamide to prevent relapses
spinal neurocysticercosis, patho, presenation
rare. seed in subarachnoid space.
present: asym. if grow, compress SC- late insidious onset of black/radicular pain with progressive weakness and myelopathy
spinal neurocysticercosis neuro exam +dx
motor- spastic paraparesis
sensory- sensory lvl- decr sensation below lesion
reflexes- hyperreflexic, toes upgoing
bowel, bladder: loss of sphincter tone
T1- cyst wall is isointense to CSF
T2- incr signal intesnisty in cyst. pericystic edema in SC parenchyma. occasionally scolex visualized as a mural nodule
spinal neurocysticercosis tx
praziquantel or albendazole and steroids. surgical decompression and excision of lesions in setting of clinical deterioration
demyelinating disease of the spine presentation
presentation: numbness that spreads over 1 or both sides of the body from sacral set to ft, anterior thighs and up over trunk.
variable and usually asx weakness and then paralysis of the legs.
-sphincter dysfunc- late complication
demyelinating disease of spine dx, tx
CSF- mild or normal lymphocytosis. oligoclonal bands (sometimes absent on 1st attack)
MRI T2- abn. gado enchancement. w/wo cord expansion
tx: high dose corticosteroid, plasma exchange, IVIG
cauda equina syndrome (CES) caused by…
mass from conus modulars or film terminal consistent with ependymoma
narrowing of SC that compress N root below termination of SC.
CES present
localized low back pain w/wo unilateral or bilateral sciatica (radicular pain); pain may be completely absent
-bowel and bladder dysfunc (urinary manifestation begin with retention then overflow incontinence) constipation
weakness of legs
saddle anesthesia
sexual dysfunc- impotence (less common)
CES neuro exam
motor- asym paraplegia, hypotonia, rare fasiculations, atrophy with chronic lesions
sensory- saddle hypoesthesia or anesthesia, lower extremity sensory loss is asx (may be unilateral) in specific dermatomes; no sensory dissociation
reflexes- absent or diminished knee or ankle jerks and diminished bulbocavernous reflex
loss of anal sphincter tone and anal wink
CES dx
L spin with gad.
EDX- EMG of lower extremities and bilateral external anal sphincter M- acute denervation; NCS of pudendal N may rule out more distal peripheral nerve lesions
lumbar puncture- r/o inflm diseases
CES tx
urgent surgical decompression in <6hr from injury
medical therapy- antibiotics for infection, steroids for inflm conditions. no proven medical tx, direct at cause
PT, OT
spinal lipoma patho, etio
intradural fatty accumulation. mostly in T-spine in adult and C-spine in kids. dorsal midline of SC–> flatten cord ventrally
20s-30s
spinal lipoma presentation
slow growing, mass effect. numbness or spastic weakness in extremities, back pain, radicular pain uncommon
spinal lipoma neuro exam
motor- splastic paraparesis
sensory- sensory lvl with decr sensation below lesion
reflexes- hyperreflexic toes upgoing
bowel/bladder- loss of sphincter tone
neuroimaging spinal lipoma
CT- homogenous low attenuation, wo solid of enhancing component
MRI- sharply circumscribed mass largely conform to dura but distorting cord. follow fat signal on all seq. t1-hyper, T2-hypo, no enhancement on T1 post
spinal lipoma tx
decompression with biopsy or subtotal resection
pott’s spine.
osteomyelitis +arthritis. usually affect >1 vertebra.
85%- in thoracolumbar.
etio- 2nd to extraspinal source –> progressive bone destruction leading to anterior vertebral body collapse and kyphosis (gibbous deformity), cold abscess formation, SC narrowing (by abscesses, granulation tissue, direct dural invasion), leading to SC compression and neuro deficits
pott’s clinical
varies based on stage, site affected, presence of complications (neuro deficit, abscess or sinus tracts)
- constitutional sx (fever, wt loss, night sweat)
- spinal or radicular back pain (earliest and most common sx)
- rare dysphagic, stridor, torticollis, hoarseness (due to lower cervical spine disease)
- focal weakness and sensory abn
- bladder and bowel dysfunction
potts disease neuro exam
varies based on lvl of SC or nerve root compression
- kyphosis deformity
-local pain in affected are of spine associated with muscle spasm and rigidity
motor- progressive para/quadriparesis
sensory- impaired sensation below lvl of lesion
reflexes- hyperreflexia with ankle clonus and upping toes
pott’s dx
lab- ppd, ESR, microbiology
imaging- MRI with gad- evaluate disk space infection and osteomyelitis.. demonstrate extension of disease into soft tissue and spread of TB debris under anterior and posterior longitudinal ligaments.
CT- define shape and calcification of soft tissue abscesses
histo- exudative granulation tissue with interspersed abscesses –> caveating necrosis
pott’s tx
RIPE. 6-12mo. decompressive surgery if acute neuro deterioration, spinal deformity with instability, R to drug, paravertebral abscess or non-diagnostic bx
spinal cord contusion- patho
most common cord injury. bruised cord –> inflm, bleeding from vessels. temporary -1-2d incomplete or complete debilitation of SC
spinal cord contusion presentation
varying degree of sx associated with location and severity.
weakness, numbness, tingling below lesion, bladder and bowel dysfunc
spinal cord contusion neuro exam
varies with level and portion of cord affected. deficit below lvl of lesion
LMN- acutely due to spinal shock- flaccid paraparesis or quadriparesis
UMN- over d-wks. spastic paraparesis or quadriparesis
sensory decr.
loss of anal sphincter tone
spinal cord contusion dx, tx
mri- T2/FLAIR signal change- cord edema
tx- supportive care, spine immobilization, collar or brace, high dose corticosteroid, mechanical ventilation, bladder catheter, feeding tube, physical therapy
spinal meningiomas etio, path
most common intramural, extra medullary tumor. 25-46% of primary spinal neoplasm. 4:1 W/M. middle age. 80% in T spine, 15% c spine, arise from arachnoid cap cells of arachnoid villi in meninges
spinal meningiomas- present
slow growing tumor, often asx. if big –> back or radicular pain –> weakness+/- sensory change with sphincter disturbance- late finding
spinal meningiomas neuro exam, dx
motor- spastic paraparesis sensory- sensory lvl decr below lesion reflex- UMN loss of sphincter tone MRI spine with gad- isodense to spinal cord on T1 and T2 with intense enhancement post contrast
spinal meningioma tx
high dose corticosteroid if SC compression, surgical resection + rad if malig=rare
neuroenteric cyst, etio, patho
rare lesion of SC. heterotypic endodermal tissue. 90% in intramural/extramedullary.
etio- persistence of neuroenteric canal prevent proper sep of endoderm and notochord –> congenital cyst define by presence of mucus secreting epithelium ~ GI tract
neuroenteric cyst clinical
progressive focal pain at lvl of lesion, radicular pain and paresthesias, fluctuating myelopathic signs
bladder and bowel dysfunc - based on location
neuro enteric cyst neuro exam
motor- fluctuating unilateral or bilateral spastic paraparesis/ quariparesis
sensory- sensory lvl may be present
reflexes- fluctuating UMN
neuroenteric cyst imaing
MRI + gado- delineate cyst form and relationship to surrounding neural structures
non contrast enhacing lesion that are isoentense on T1 and hyper on T2
CT- detect osseous malformation
CT myelogram- positive meniscus sign (partial dye obstruction with intramural/extramedullary cyst and complete contrast obstruction with intramural/intramedullary cyst
neuroenteric cyst tx
surgery-total resection. partial-> recur+ arachnoiditis
cervical disk herniation, patho, presentation, dx, tx
radiculopathy- mechanical compression or irritation of N as it exist spine. most in C/L spine due to motility of neck and lower back
causes- disk herniation, osteophyte from osteoarthritis, thickening of surrounding lig
numbness, tingling, weakness, M atrophy. decr reflexes.local or radicular pain
dx: MRI or CT spine. EDX - to determine exact root involved
tx- bed rest, PT, NSAIDS, M relaxants. steroid for severe pain
surgery if refractory to medical management
copper deficiency myelopathy
etio, presnt, neuro, dx, tx
acquired, non-compressive myelopathy. mimic subacute deign due to it B12 def.
etio- impair absorption- gastric surgery, zinc overload, malabsorption syndrome
present- progressive spastic ataciv gait with proprioceptive deficits due to polyneuropathy
neuro: UMN, sensory ataxia due to impaired vibration and J-position sense, pos romberg, wide based ataxic and spastic gait
dx- MRI T2 hyper in dorsal midline C or T spine
low serum copper and ceruloplasmin lvl
tx- copper supplement
spinal epidural hematoma (SEDH) patho
usually in thoracolumbar. peridural venous plexus > arterial sources. expansion limited to few vertebrae lvl
SEDH presentation
sudden, severe focal neck or back pain with delayed radicular pain. weakness, numbness, tingling below lvl of lesion. bladder and/or bowel dysfunc.
Neuro: LMN acutely (spinal shock) –> UMN para or qudriparesis. sensory lvl with radicular paresthesias.
SEDH dx, tx
dx- MRI- location/extent. show biconvex. taper superior and inferiorly
functional study SSEP use for monitor or prognostication following surgery
tx- surgical intervesion 36-48hr with decompressive laminectomy and hematoma removal
conservative tx when neuro deficit improve in early phase or with coexistence of coagulopathy
spinal epidural abscess (SEA)
infection what spread over verbal lvl and expand threatening SC or cauda equine directly by mechanical compression and indirectly by vascular compromise. most in T spine
taph aureas- most common
SEA present
triad- fever, back pain, neuro deficit
stage 1) focal pain at level 2) radicular pain + paresthesias, 3) M/S/ B/B dysfunc 4) paralysis
neuro- tenderness to palpation. LMN acute –> UMN. senosry lvl with radicular paresthesias.
SEA dx, tx
lab- culture, CBC, ESR, leukocytosis in 2/3 pt.
MRI with gado, LP- CI if suspect unless need to exclude meningitis
tx- emergency decompression + drainage. antibiotic against MRSA. penicillin, 3rd gen cephalosporin, amino glycoside.
alantoaxial instability (AAI)
excessive mvt at junction btw C1, C2 due to bony or ligamentous abn. occipital pain, vertigo, brainstem sign, lower CN palsy, myelopathy. sudeck sign- displacement of spine of axis in direction of head tilt
plain radiograph or CT
no tx for asx, cervical stabilization if sx
synovial cyst
facet J dty causing degeneration or herniation of synovial fluid through tears in J capsule
most at L4/5 due to mobility causing spinal instability.
presentation dep on size, site, relationship to adj structures. most radicular or back pain, neurogenic claudication, or caudal equip syndrome. myelopathy if C/T spine
neuro mild weakness to myelopathy (UMN)
hypo on T1, hyper T2
tx: conservative -bred rest, NSAID, PT, bracing, transcutaneous electrical stimulation, epidural or intra-articular steroid injection and cyst aspiration
surgical- facetectomy with laminectomy
burst fracture
14% of spinal injury. in high energy trauma. most in thoracolumbar J. present with moderate to severe back pain exacerbated by mvt. numbness, tingling, weakness. B/B dysfunc if SC involved.
CT > plain raiography
MRI- soft tissue injury
tx- conservative management with brace and pain management if no neuro deficit. decompression, stabization and fusion for unstable fracture with neuro deficit
