9/1 Clinical Syndromes of Spinal Cord - DiCicco-Bloom Flashcards
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)
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)
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
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
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)
vasculature of spinal cord
anterior spinal artery serves approx 1/3 of cord
clinical syndromes
complete transection
causes:
- trauma
- demyelinating disease (MS; post-inf transverse myelitis)
- 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
clinical syndromes
Brown-Sequard syndrome
spinal hemisection
- ipsilateral CST → UMN syndrome
- weakness of arm/leg
- mild atrophy
- hyper-reflexia (clonus of ankle), Babinski sign
- loss of abdominal and anal wink
- ipsilateral posterior column sensory loss (position/vibration)
-
contralateral STT sensory loss (pain, temp)
* 2 + 3 = dissociated sensory loss* - autonomics: Horner’s syndrome (miosis, ptosis, anhydrosis)
-
complete loss of motor and sensory root functions at level of hemisection
* incl sensation in dermatomal pattern if 2 roots affected, reduced LMN function
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
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)
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!
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)
multiple sclerosis
neuro problems that are diffuse in time/place
dorsal column, CST, cerebellar
- ataxia, dysmetria, nystagmus, dysarthria
anterior spinal artery
potential for hypoperfusion
hypoperfusion potential high in 6-8 intercostal arteries of thoracic and lumbar region
Artery of Adamkiewicz (T12-L2)
