SPINE cystic Flashcards

1
Q

Entity. Definition. Clinical presentation.

A

Arachnoid cyst.

Intraspinal extramedulary loculated CSF collection.

Asymptomatic .
When symptomatic: Pain, paraparesis, paresthesia
Worsening neurologic deficits: suspect enlarging cyst

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2
Q

Arachnoid cyst: classification

A

Nabors classification of spinal MC
Type I: Extradural MC without spinal nerve root fibers
IA: Extradural arachnoid cyst
IB: Sacral meningocele
Type II: Extradural MC with spinal nerve root fibers (Tarlov Cyst, spinal nerve root diverticulum)
Type III: Intradural arachnoid MC

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3
Q

Arachnoid cyst:
Associations, complications

A

Associations: Multiple arachnoid cyst associated with **adult polycystic kidney disease. **

Complications: worsening neurologic deficits.

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4
Q

Arachnoid cyst:
Morphology. Dx.

A

Morphology:
-Nonenhancing extramedullary loculated CSF intensity collection displacing cord or nerve roots
-Well circumbscribed, oval, elongated
-Location: intraspinal, extramedullary, extra or intradural. 80% thoracic > 15% C > 5% L

Primary:
Extradural: Posterior or posterolateral lower thoracic spine
Intradural: Dorsal midthoracic spine
Anterior location uncommon
Secondary (trauma, instrumentation, subarachnoid haemorrhage):
Non specific location.

-Both connects to arachnoid space throught neck.
-Extradural meningeal cyst (MC) may extend through enlarged neural foramina: dumbbell lesion
-Cap sign: Extradural MC outlined by rostral and caudal epidural fat
-Bony remodelling/expansion: posterior vertebra scalloping, thinned pedicles, widened interpedicular distance.

Dx:
-MR heavily T2 + C+.
-Delayed imaging on postmyelography CT to allow filling of cyst, and demonstrate communication between extradural MC and subarachnoid space.

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5
Q

Etiology. Definition

A

Idiopatic Spinal cord Herniation.

Focal anterior displacement of cord through ventral side of the dura, causing herniation and S-shaped thinned cord, and expansion of dorsal subarachnoid space.

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6
Q

Entity. Definition. Presentation.

A

Def: Smooth remodeling of posterior vertebral body, expansion of osseous spinal canal, ± kyphoscoliosis
Pedicular attenuation, widened interpediculate distance, erosion of anterior and posterior elements
Patulous, expansile dural sac enlargement

Presentation: back pain ± radiculopathy

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7
Q

Dural Ectasia: Associations.

A

Associations:
-NF1, connective tissue (Marfan, Ehlers Danlos) idiopatic.
-lateral thoracic or lumbar meningocele, anterior sacral meningocele, kyphoscoliosis, joint hypermobility, lens abnormalities, aneurysm, arterial dissection, and peripheral or central neoplasms

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8
Q

Dural Ectasia:
Morphology. DD

A

Morphology:
-Smooth, C-shaped scalloping of posterior vertebral bodies with patulous dural sac
-Lumbar > cervical, thoracic

Recommendation: Important to determine underlying disorder for treatment planning, genetic counseling, and determining prognosis

DD:
-Extradural arachnoid cyst
-Congenital vertebral displasia, mucopolysaccaridosis, OI.
-Spinal tumor (astrocytoma, ependymoma, nerve sheath tumor) or syrinx
-**Cauda equina síndrome of anylosing spondylitis (Imaging and clinical stigmata of ankylosing spondylitis typically present)

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9
Q

Etiology. Definitions. Clinical presentations

A

Hydrosyingomyelia

-Hydromyelia: cystic central canal dilatation (>2mm). Lines by ependymal cell.
-Syringomyelia: cystic spinal cord cavity, not contiguous with central cord cana. Not lined by -ependymal cell.
-Syringobulbia: Brainstem syrinx extension
-Syringocephaly: Brain/cerebral peduncle syrinx extension

Epidemio: late adolescence/early adulthood. M = F.
-Primary: young patients. ↑ prevalence with **basilar invagination, Chiari 1 **or 2 malformation
-Secondary: any age. 25% of spinal cord injury.

Clinical:
-Cloak-like pain and temperature/sensory loss with preservation of position sense, proprioception, light touch.
-Upper extremity weakness, gait instability
-Cranial neuropathy (2° to syringobulbia)

Clinical profile:
-Symmetrically enlarged central cavity asymptomatic or presents with nonspecific neurologic signs (spasticity, weakness, segmental pain)
-Paracentral cavitation associated with combination of long tract and segmental signs referable to level, side, and quadrant of spinal cord cavitation

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10
Q

Hydrosyringomyelia:
Causes/Associations

A

90% congenital (primary): **Chiari malformation (1** > 2) myelomeningocele or other spinal dysraphism, tethered cord, arachnoid adhesions, congenital scoliosis, spinal cord injury, Klippel Feil, DW, MMC

10% acquired (secondary): post-trauma, post-infectious, post-inflammatory, and intramedullary tumors (particularly ependymomas and hemangioblastomas). 


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11
Q

Hydrosyringomyelia:
Morphology, Dx.

A

Expanded spinal cord (intramedullary) due to dilated, beaded, or sacculated cystic cavity.
Bony remodeling: Normal or canal enlargement, vertebral scalloping (severe, longstanding syrinx)
-Hydromyelia: Central canal patency** > 2mm.** Can communicate or not with 4th ventricle.
-Syringomyelia: Paracentral/ exccentric spinal cord cavitation, adjacent gliotic parenchyma.
Noncontiguous with central cana (can extend into anterior commissure, posterior horn)

Dx:Longitudinally oriented CSF-filled cavity ± surrounding gliosis, myelomalacia

Best clue: MR
T1: Hypointense spinal cord cleft
T2: Hyperintense intramedullary cavity ± adjacent gliosis, myelomalacia
± arachnoidal adhesions, cord tethering, or edema
C+: Nonenhancing cavity (enhancement suggests inflammatory or neoplastic lesion)
Myelography: Delayed syrinx contrast uptake

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12
Q

Entity, def, clinica

A

PERINEURAL CYST
Def: Dilatation of arachnoid and dura of spinal posterior nerve root sheath, containing nerve fibers
Type II of Nabors classification.

Epidemio: 30-40yo.
Clinical: Majority asymptomatic: > 80%
Symptoms may worsen with postural changes, Valsalva maneuvers
Cyst rupture → spontaneous intracranial hypotension
Symptoms simulate disc herniation and spinal stenosis

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13
Q

Perineural cyst,
Morphology, dx

A

Morphology:
Occur anywhere along spine.
Most common lumbar spine and sacrum
S2 and S3 nerve roots most commonly **involved
Thin-walled, cystic mass. Follow CSF signal. No enhancement
± neural foraminal widening (
bone remodeling)**

Dx: CSF-intensity mass enlarging neural foramen or sacral canal.
Administer gadolinium to exclude solid mass if signal intensity not definitely cystic
Delayed CT (30-60 minutes) after intrathecal contrast injection to visualize filling of perineural cyst

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14
Q

Etiology. definition. Clinical presentation

A

Spinal cord infarct.

Def: Cord infarction 2° to vessel occlusion (radicular artery)

Clinical: >50yo. M=F
-Abrupt-onset. Rapid progression; maximum deficit within hours
-Anterior spinal syndrome: Paralysis, pain, and temperature sensation loss, bladder and bowel dysfunction
-Posterior SCI: Loss of vibration sense, proprioception

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15
Q

Spinal cord infarction:
Path/etiology
Associations

A

Up to 50%: idiopathic, of unknown etiology.
-Majority of known causes: related to aortic pathology (atherosclerosis, aneurysm, surgery): impairment of anterior spinal artery is most common.
-Septicemia; systemic hypotension
-Blunt trauma with dissection
-Fibrocartilaginous embolism
-vasculitis.
-Iatrogenic; transforaminal steroid injection, selective root block

Associations: Look for associated **vertebral body infarctions **as confirmatory evidence of cord ischemia in aortic disease

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16
Q

Spinal cord infarct,
Morph, dx.

A

Morphology:
-Central hyperintensity on T2WI, which involves central gray matter = anterior horn, more variable involvement of cord periphery (entire cross section area)
-Cord size: Slight cord expansion in acute phase. Thinning if chronic.
-Location: distal thoracic cord (arterial border zone)
-Size: usually** > 1 vertebal body**.

Dx:
-MR with contrast + diffusion
Classic imaging appearance: T2 hyperintensity involving anterior horn cells: central owl’s eye pattern
Well defined transition zone: suggestive of vascular territory
T1: slight cord expansion in acute phase. Atrophy in chronic phase. Haemorrhagic convertion (hyper), rare.
DW: restriction.
MRA: assess etiology of vascular origin.
-CTA: underlying aortic disease, dural a-v fistula. (Not directly useful for identifying anterior spinal artery since lack of visualization of ASA does not prove diagnosis)

17
Q

Spinal cord infract
Name 3 DD

A

-MS (Peripheral location, < 2 segments)

-Transverse myelitis (known causes such as MS, ADEM, idiopatic. Central with > 2/3 cross sectional. 3/4 segments)

-ADEM (child/young adult. Brain affected more than cord)

-Neuromyelitis optica (> 3 vertebral body segments)

-Type 1 dural fistula (cord expansion and edema. Enlarged serpentine pial veins and cord surface)
Spinal cord neoplasm (enhancement)

-Radiation myelopathy (history)

-Parasitic/bascterial infection (focal enhancement)

18
Q

Entity. Definition. Clinical presentation

A

Spinal subdural haemorrhage.

Def: Hemorrhage into spinal subarachnoid space from variety of etiologies

Clinical: Bimodal persentation: adult > children
-Acute back or radicular pain ± signs of cord compression (numbness, weakness, paraplegia, fecal and urinary incontinence)
-Spinal SAH characterized by sudden headache, acute sciatic pain, xanthochromic CSF, meningeal irritation, sensory deficit or paralysis

19
Q

Spinal subdural haemorrhage,
Path, Associations, Complications.

A

Path:
Cause nearly always secondary: Spontaneous RARE (Need to exclude pathologic cause)
**Trauma (> 50%) **MVA, post operative, LP.
Aneurysmal subarachnoid hemorrhage (SAH) with spinal extension
Spinal arteriovenous malformations (Mainly types II, III, IVc, conus malformations)
Tumor (spinal ependymoma)
Anticoagulant therapy
Infection (pneumococcal meningitis, herpes)
Systemic disease (LES, polyarteritis nodosa)
Spinal artery aneurysm (rare)

20
Q

Subarachnoid haemorrhage,
Morpth, Dx

A

Morphology:
**Fluid-fluid level **within thecal sac/ cauda equina.
Intrathecal location. L > T > C

Dx:
-MR: Best tool: T1, T2, Contrast, Gre.
T1, T2: Variable intensity depending on stage of blood breakdown and by-products
Gre: due to blood products.
C+: may enhance due to secondary inflammatory reaction.
Dynamic-enhanced MRA useful as screen for spinal vascular malformation
-CTA: usefull for underlying vascular malformations.
-Angio: conventional for spinal vascular malformation.

21
Q

Etiology. Definition. Clinical presentation.

A

Epidural spinal haemorrhage.

Rare but can cause severe morbidity considered surgical emergencies.

Def: Accumulation of hemorrhage between dura and spine not caused by significant trauma or iatrogenic procedures

Epidemio: Bimodal: Childhood and 5th and 6th decade. M > F.
Clinical:
Acute onset of neck, back pain
Progressive paraparesis
Bladder or bowel dysfunction

22
Q

Spinal epidural haemorrhage,
Path, Assoc, Complications

A

Path:
Causes:
Idiopathic: 40-50%
Minor trauma: Rupture of valveless epidural venous plexus
Transient **venous hypertension **(Valsalva, sneezing, coughing)
Disc herniation: 78% lumbar. Rupture of adjacent epidural veins.
Anticoagulation or coagulopathy
Vascular anomaly
No genetic associations

Associations: Disc herniation. AV malformation.

Complications: postoperative recovery depends on severity and duration of **neurologic deficit. **

23
Q

Spinal Epidural Haemorrhage,
Morphology. Dx

A

Morphology:
**Extradural **T1-hyperintense Lentiform or biconvex fluid collection
Outlined by dorsal epidural fat cranially and rostrally
Multilevel > single level
**Thoracic, lumbar **> cervical (more common in children)
Dorsal > ventral > circumferential
Variable cord compression.

Dx: Biconvex epidural mass hyperintense on T1WI and T2WI with hypointense foci highly suggestive of spinal epidural hematoma
-MR: best
T1WI acute: < 48 hours. Isointense > hypo-/hyperintense
T1WI subacute and chronic. Hyperintense > isointense
T2WI heterogeneously hyperintense
Gre: Hyperintense with prominent hypointense deoxyhemoglobin
C+: Focal enhancement in acute SSEDH represents active extravasation of contrast-enhanced blood
Peripheral enhancement due to adjacent dural hyperemia
+/- cord edema
Myelography: block of CSF.

24
Q

Etiology. Definition. Clinical presentation.

A

Spinal cavernous malformation.

Def: Vascular lesion with lobulated, thin, sinusoidal vascular channels, and no interspersed neural tissue

Epidemio: 3rd to 6th decade of life. M = F. 10-30% multiple, familial
Clinical: Sensorimotor deficits, progressive paraparesis
Broad range of dynamic behavior (may progress, enlarge, or regress): 4 clinical patterns (similar to MS) (profile: young adult with sudden paraplegia):
-Multiple episodes of neurologic deterioration, intermittent recovery
-Slowly progressive neurologic decline
-Sudden symptom onset with rapid decline (hours to days)
-Mild symptoms with acute onset, gradual decline (weeks to months)

25
Q

Spinal cavernous malformation,
Path, Assoc

A

Path: Angiogenically immature lesions with endothelial proliferation, increased neoangiogenesis
Discrete, lobulated blue-reddish brown (mulberry-like) nodule
Vascular spaces with single layer of endothelial cells
No intervening neural tissue between vascular spaces.
Pseudocapsule (gliotic, hemosiderin-stained cord)
Ca⁺⁺ are rare (common in brain CMs)

-Multiple (familial) CM syndrome (20%). Rare. AD. Loss-of-function mutations in 1 of 3 genes
At high risk for hemorrhage and** formation of new lesions,** infratentorial location, lower age at clinical presentation
12% of spinal CM patients have familial variety/ 10-30% multiple, familial

26
Q

Spinal cavernous malformation,
Morphology, Dx

A

Morphology:
Locules of blood with **fluid-fluid levels, popcorn appearance, surrounded by very T2-hypointense rim (hemosiderin)
Spinal cord uncommon site: 3-5% of all cavernous malformations (CMs)
Round, heterogeneous signal abnormality, well-defined margins
Location:
thoracic (50%), Cervical (40%) **(lumbar and conus uncommon)

Dx: Heterogeneous mass (locules of blood with popcorn appearance) surrounded by dark rim (hemosiderin)
NECT: often normal. Cord may appear widened.
CECT: faint enhancement (rare)
MR: T1: Heterogeneity due to blood products of varying ages
Typical speckled popcorn heterogeneous signal
T2: Heterogeneous, hemosiderin rim
no edema unless recent hemorrhage
T2 GRE: Prominent blooming due to susceptibility effects
C+ absent or minimal
Angiography: typically negative.

Recommendation: **MR of brain w/SWI to identify supratentorial lesion. Use GRE.
**

27
Q

Bow Hunter Syndrome?

A

Def: Vertebrobasilar insufficiency secondary to mechanical positional occlusion/stenosis of vertebral artery during head rotation.

Clinical: Vertebrobasilar insufficiency:
Motor or sensory deficits, ataxia, diplopia, dysarthria, dysmetria, vertigo, visual field deficit, cranial nerve dysfunction, syncope

Path:
-Vertebral artery at C1-C2 particularly prone to mechanical compression
-Hypoplasia or stenosis of contralateral vertebral artery predisposes patients to vertebrobasilar ischemic attacks during head rotation

Associations:
May occur anywhere along vertebral course related to spondylosis, atlantoaxial instability, hypertrophy of atlantooccipital membranes, paravertebral muscle fascial bands

Prognosis/Treatment: conservative (restriction of head motion) vs surgical treatment.

Morphology/Dx:
Occlusion or stenosis of vessel with head positional dependence based on ultrasound, MRA, CTA, or catheter angiography
Best tool: angiography.
-Along course of vertebral artery, typically at C1-C2 junction
- Stenosis or occlusion of vertebral artery with head position change
-Hypoplasia or stenosis of contralateral vertebral artery predisposes patients to vertebrobasilar ischemic attacks during head rotation