9/1 Clinical Syndromes of Spinal Cord - DiCicco-Bloom Flashcards Preview

M2 Neuron Brain Behavior > 9/1 Clinical Syndromes of Spinal Cord - DiCicco-Bloom > Flashcards

Flashcards in 9/1 Clinical Syndromes of Spinal Cord - DiCicco-Bloom Deck (14):
1

localization in the spinal cord

 

principles 

[not a good card] 

segmental: trauma, tumors, infl mass, vascular

longitudinal: heritable, metabolic, systemic disease; secondary to segmental

somatotopic organization: dissociated sensory loss, DC vs. ST; sacral sparing

 

extrinsic (extramedullary, extra-axial):

  • hits the roots, causing pain that affects peripheral neurons and LMN
  • later on, get cord compression that affects UMN and long tracts

intrinsic (intramedullary, intra-axial): 

  • painless
  • hits autonomics early
  • see lumbosacral sparing (when in cervical, thoracic)

2

intrinsic vs extrinsic effects on spinal cord

extrinsic (extramedullary, extra-axial):

  • hits the roots, causing pain that affects peripheral neurons and LMN
  • later on, get cord compression that affects UMN and long tracts

intrinsic (intramedullary, intra-axial): 

  • painless
  • hits autonomics early
  • see lumbosacral sparing (when in cervical, thoracic)

3

motor abnormalities

 

LMN vs UMN

LMN :

  • slow rapid alternating movement proportional  to weakness
  • decreased muscle tone
  • absent/hypoactive deep tendon reflexes
  • atrophy
  • fasciculations

UMN : (more behavioral/functional level - "just doesnt work")

  • slow RAM disproportionate to weakness
  • increased muscle tone
  • hypoeractive DTRs
  • Babinski response

4

spinal nerve arrangement (in relation to vertebrae)

31 pairs of spinal nerves (8C, 12T, 5L, 5S, 1Coccygeal)

  • C1-C7 exit ABOVE vertebra of same number
  • C8 exits BELOW C7 vetrabra
  • T1 and below exit BELOW vetrebra of same number

 

spinal cord ends at L1/L2 vertebra in conus medullaris

cauda equina is the continuation

5

natural enlargements of spinal cord

 

why?

limbs need extra innervation, so there are enlargements to accomondate for that

  • cervical enlargement (C5-C8)
  • lumbosacral enlargement (L2-S3)

6

vasculature of spinal cord

anterior spinal artery serves approx 1/3 of cord

7

clinical syndromes

 

complete transection

causes:

1. trauma

2. demyelinating disease (MS; post-inf transverse myelitis)

3. compression by tumor or inflammatory mass

 

  • chronically, hyperactive reflexes (clonus) and increased tone (together = spasticity)
  • over time, flexor spasms (set off by simple cutaneous stim)
  • automatic bladder emptying after it fills
    • sacral lesion? bladder distends and overflows causing emptying/chronic infection

8

clinical syndromes

 

Brown-Sequard syndrome

spinal hemisection

 

1. ipsilateral CST → UMN syndrome

  • weakness of arm/leg
  • mild atrophy
  • hyper-reflexia (clonus of ankle), Babinski sign
  • loss of abdominal and anal wink

2. ipsilateral posterior column sensory loss (position/vibration)

3. contralateral STT sensory loss (pain, temp)

2 + 3 = dissociated sensory loss

4. autonomics: Horner's syndrome (miosis, ptosis, anhydrosis)

5. complete loss of motor and sensory root functions at level of hemisection

  • incl sensation in dermatomal pattern if 2 roots affected, reduced LMN function

9

extramedullary compression

(dorsal root and spreading)

dorsal root compression

  • paresthesia; loss of pain/temp/proprio/vib in the dermatome

dorsal column compression

  • ipsilateral loss of proprio/vibration

corticospinal tract compression

  • ipsilateral UMN signs: increased tone/reflexes

ventral horn compression

  • loss of ipsilateral LMN → segmental muscle weakness

10

central cord syndrome

cavitation near central canal of spinal cord

most commonly from C3 to T4

causes: AVM, trauma, invfection, astrocytic tumor, congenital malformation

small lesion

  • loss of crossing fibers in anterior commissure → cape distribution of lost spinothalamic fibers crossing at ventral commissure (dorsal columns preserved)

large lesion

  • expansion into lateral funiculus interrupting descending CST with UMN syndrome
  • early on, segmental loss of sensory/motor pathways
  • later, all fx below lesion are affected (EXCEPT most periph localized → sacral sparing)

11

ALS

amyotrophic lateral sclerosis

mixed UMN and LMN disorder → progressively spreads both rostrally and caudaly until fatal

 

  • atrophic weakness of hands/forearms
  • spasticity of legs
  • generalized hyperreflexia

initial symptoms: stiffness/weakness, muscle wasting, forearm fasciculations (twitching)

 

ONLY UMN/LMN, no sensory involvement!

12

subacute combined degeneration

causes:

  • vit B12 deficienty (macrocytic anemia)

 

gradual onset with symmetric sensory loss

dorsal columns most affected, then CST

 

*since B12 def also causes peripheral neuropathy, there may be paradoxical combo of extensor plantar reflex (UMN sign) and hypoactive ankle DTR (LMN sign)

13

multiple sclerosis

neuro problems that are diffuse in time/place

 

dorsal column, CST, cerebellar

  • ataxia, dysmetria, nystagmus, dysarthria

14

anterior spinal artery

 

potential for hypoperfusion

hypoperfusion potential high in 6-8 intercostal arteries of thoracic and lumbar region

 

Artery of Adamkiewicz (T12-L2)

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