Spinal Cord Flashcards
1
Q
Compression of the spinal cord from outside in will first affect which tract?
A
Spinothalamic
- pain/temp
- will give a sensory level
2
Q
Where is T4/T10?
What touches T2 in the chest?
A
- T4 = nipple
- T10 = umbilicus
- C4 touches T2; C5-8 and T1 are pulled out in the arm
3
Q
Tract of urinary control from cortex to spine
A
- Frontal lobe: micturition inhibiting center; motor sphincter control
- Deep brain: basal ganglia, pontine micturition center, cerebellar vermis
- Spine: sacral motor nuclei (sphincteromotor nucleus, AHCs, PSNS nuclei), sympathetics from T11-L1
- Urethral and bladder afferents/efferents are at S2-S4
4
Q
Acute vs. Chronic bladder dysfunction
A
Acute = urinary retention Chronic = spastic bladder, urinary frequency
5
Q
When a patient has a myelopathy what do you do?
A
- if acute/subacute: consider it a neurologic emergency
- take a good history, ask where it hurts/palpate, check for fever, do neuro exam (including motor, sensory, reflexes, and gait)
- get imaging (MRI) - looking for compression, masses, structural abnormalities
- if MRI is negative, do LP
- if acute/subacute, tx is usually steroids; if chronic tx will be directed toward the underlying cause
6
Q
Progression of an epidural lesion
A
- Occurs over hours to days
A. first CST/motor sx - even if not weak will see hyperreflexia, +Babinski, and difficulty walking; sensory loss at the level 2/2 DRG compression; urinary urgency (common and they may leave it out)
B. motor - legs get spastic and weak; sensory sx are worse with contralat. numbness and ipsilat epicritic loss; definite sphincter dysfunction
C. flaccid muscles, areflexic; complete sensory level to all modalities; if acute then spinal cord shock is likely
7
Q
Types of extradural myelopathies
A
- disc disease (w/ edema)
- mets
- abscess
- also: hemangioma, hemorrhage, other cancer, etc.
8
Q
Types of intradural, extramedullary myelopathies
A
- nerve sheath tumors (Schwannoma/neurofibroma)
- meningioma
- also: tumor seeding (CNS tumors), cauda equina lesions, cyst, clot, etc.
9
Q
Types of intramedullary myelopathies
A
- syringomyelia
- tumor (ependymoma, glioma, hemangioblastoma)
- myelitis
- also: edema, lipoma, abscess, hematoma, mets, etc.
10
Q
Spinal cord trauma
A
- acute spinal cord compression, with hematoma and/or infarct, maybe cord transection
- IV methylprednisolone for 24hrs
11
Q
Causes of spinal cord dysfunction in patients with cancer
A
- epidural cord compression (tumor [gets in vert, weakens, expands], abscess, hematoma)
- intramedullary processes (mets, abscess, hematoma, syrinx)
- other myelopathies (rad/chemo, paraneoplastic)
- neoplastic meningitis
- spinal arachnoiditis
- *BLT with KP
12
Q
Most metastatic cancer begins in ____. Most spinal abscesses begin in ____.
A
vertebral body disc space (MCC is S. aureus)
13
Q
Pott’s disease
A
TB of the spine
- osteomyelitis of vertebral bodies
- will see paraspinous abscess and bony destruction on imaging
- can cause kyphosis
- stain CSF for tubercle bacilli
14
Q
Where does spinal meningioma occur?
A
Intradural, extramedullary
- common in thoracic spine
- classic pt is a middle aged woman
15
Q
Progression of a Central Cord lesion
A
Compressing the spine from inside to out
A. begins with pain; anterior white commissure is involved early so loss of pain/temp bilaterally
B. severe loss of pain/temp; post columns spared until late (called “dissociated sensory level”); afferent reflex arc is compressed, reflexes lost; CST involvement means spastic paraparesis, +Babinski
C. symptoms worsen; sacral sparing because these fibers are most lateral; may involve face if high enough to hit sensory nuc of CN5
16
Q
Anterior spinal cord syndrome
A
- supplies the anterior 2/3 of the spinal cord (1 ant : 2 post arteries)
- if occluded will cause dissociated sensory level (won’t touch dorsal columns) and arm > leg paralysis/paresis (ant–>post goes arm/trunk/leg in CST)
17
Q
What does spinal cord shock look like?
A
- acute myelopathy
- flaccidity
- complete sensory level to all modalities
- urinary retention (if full bladder, likely distended abdomen)
18
Q
Subacute combined degeneration of the spinal cord
A
- from B12 deficiency/pernicious anemia
- causes bilateral lesions in dorsal columns and CSTs in spine
- therefore spastic weakness of LEs and decreased vibration/proprioception sense; +Romberg sign
19
Q
HTLV-1
A
- causes HAM (HTLV1 associated myelopathy)
- pt gets paraparesis, CNS is infiltrated by monocytes; axons are demyelinated and degenerate (CST > PCs)
- CSF shows oligoclonal bands and increased IgG
20
Q
Vacuolar myelopathy
A
- neuro complication of HIV
- progressive spastic paraparesis
- vacuolation and myelin pallor in PC/LC)
- looks like B12 deficiency
21
Q
Tabes dorsalis
A
- ‘wasting away’ of dorsal columns
- complication of neurosyphilis
- +Romberg sign
22
Q
What is MS?
A
- chronic inflammatory disease of CNS involving destruction of myelin, their axons, and the neurons
- plaques form (inflammation and sclerosis) where the myelin was
- get mulstiple episodes of loss of neuro function (relapse) separated by time and space (areas of function)
- overall progressive disability - each time you relapse it recovers but not as well
- dx: MRI finds plaques within white matter; CSF will have inflammatory profile with high IgG and oligoclonal bands; no NTs
23
Q
Uhthoff’s phenomenon
A
- MS symptoms that worsen in the heat or an increase in body temp
- occurs because of poor electrical conduction along demyelinated axons
- don’t put the patient in a hot bath anymore, they’ll get paralyzed and stop breathing
24
Q
MS Plaques on MRI and pathology
A
- MRI will find the plaques which are diagnostic of MS
- if new plaques, they will be gadolinium-enhancing and hyperintense; this represents active inflammation and breakdown of BBB that allows gadolinium to illuminate the white matter (in brain and/or spinal cord)
- in brain they are periventricular or juxtacortical
- @ edge is robust inflammatory response: monocytes, T cells, B cells, and MPs - but NOT NTs
25
Visual evoked response (aka VEP)
- also called P100 because it normally takes 100msec for light to reach V1 from retina
- in MS may see normal P100 on one side, abnormal/delayed on the other side
26
Pathogenesis of MS
- immune-mediated disease of CNS: LCs penetrate BBB, release cytokines, AI attack on myelin antigens
- etiology unknown, perhaps 2-hit style
- TH1 cells get into BBB, stimulate B cells to make Abs, and MPs to eat myelin; TH2 cells reduce the process a little
27
Relapsing/Remitting vs. Primary Progressive MS
- relapsing remits - exacerbations, then complete or incomplete recovery; slow inconsistent disability accumulates; F>M, 85% of MS cases
- PPMS is a steady progression without relapses; F=M; develop spastic paresis over years, weakness, also sensory disturbance and urinary sx - from CST damage
- if RRMS turns into progressive, then it's call secondary progressive MS
28
Natural history of MS
- avg age of onset 15-45yr
- mortality after about 25yr
- 50% of pts need walking aid w/in 15yr of dx
- average relapse is 1 per yr; fewer over time
- 25% of pts never lose ADLs
29
MS Diagnosis
- clinical signs/sx (subacute onset): MC are optic neuritis, myelitis, CN issues (3/5/7/8/etc), cerebellar ataxia
- MRI: gadolinium enhanced are best for evaluating progression
- LP: look for elevated MBP, oligoclonal banding
- VEP
30
Clinically isolated syndrome
- a clinical episode that suggests a first relapse in a patient with MS
- can manifest as optic neuritis, internuclear ophthalmoplegia, partial transverse myelitis
- lasts at least 24hr, around age 20-45
- w/o evidence of infection, fever, or encephalopathy
31
How to diagnose MS?
- a clinical diagnosis: need 2 attacks, symptomatically distinct, at 2 different times
- 2 distinct clinically isolated syndromes will qualify; or an MRI with a gad-enhancing plus a non-gad-enhancing lesion in different brain regions
- only 1 attack--> you have Monosymptomatic MS (aka CIS); w/o MRI lesion 20% chance of MS in 14yr; if >1 lesion ~90% chance
- to dx, r/o conditions that mimic MS (stroke, vasculitis, Lyme, HIV, HTLV-1, B12 def, structural lesions, etc.)
32
Treatment for MS
- steroids to help acute attacks
| - immune modulating drugs (IFN, mabs, etc.)
33
Transverse myelitis
- acute neuro condition (usually asymmetric) reflecting focal inflammation of the spinal cord
- well-defined sensory level; may have motor/sensory/sphincter disturbances
- hyperintense on T2 weighted MRI; acutely gad-enhancing
- no evidence of spinal cord compression, no back pain, may be the first sign of MS (30% chance)
- treat with IV steroids
34
Neuromyelitis Optica (NMO)
- a disorder of inflammation and demyelination of both the optic nerve and spinal cord
- central spinal MRI lesion (gad-enhancing) in 3/more VB segments
- test positive for aquaporin-4 Abs ("NMO IgG") - this is ab-mediated demyelination, axonal injury, and necrosis
- path: demyelination of gray/white matter with eosinophils; infiltration by MPs; thick hyalinized vessels with complement deposition
- tx: aggressive immunosuppression
35
Internuclear ophthalmoplegia (INO)
- dysconjugate lateral gaze that results in the affected eye being unable to adduct
- results from damage to MLF; seen in MS
