Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

OS9.2 - Neuro > Spinal Cord > Flashcards

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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Acute vs. Chronic bladder dysfunction

A 
Acute = urinary retention
Chronic = spastic bladder, urinary frequency
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Types of extradural myelopathies

A
  • disc disease (w/ edema)
  • mets
  • abscess
  • also: hemangioma, hemorrhage, other cancer, etc.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Types of intramedullary myelopathies

A
  • syringomyelia
  • tumor (ependymoma, glioma, hemangioblastoma)
  • myelitis
  • also: edema, lipoma, abscess, hematoma, mets, etc.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Spinal cord trauma

A
  • acute spinal cord compression, with hematoma and/or infarct, maybe cord transection
  • IV methylprednisolone for 24hrs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Most metastatic cancer begins in ____. Most spinal abscesses begin in ____.

A 
vertebral body
disc space (MCC is S. aureus)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Where does spinal meningioma occur?

A

Intradural, extramedullary

  • common in thoracic spine
  • classic pt is a middle aged woman
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
Q

Visual evoked response (aka VEP)

A
  • 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
Q

Pathogenesis of MS

A
  • 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
Q

Relapsing/Remitting vs. Primary Progressive MS

A
  • 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
Q

Natural history of MS

A
  • 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
Q

MS Diagnosis

A
  • 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
Q

Clinically isolated syndrome

A
  • 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
Q

How to diagnose MS?

A
  • 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
Q

Treatment for MS

A
  • steroids to help acute attacks

- immune modulating drugs (IFN, mabs, etc.)

33
Q

Transverse myelitis

A
  • 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
Q

Neuromyelitis Optica (NMO)

A
  • 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
Q

Internuclear ophthalmoplegia (INO)

A
  • dysconjugate lateral gaze that results in the affected eye being unable to adduct
  • results from damage to MLF; seen in MS

OS9.2 - Neuro (10 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions