Spinal Cord Lesions Flashcards
Sensory Disruptions
Loss of epicritic sensation ⇒ loss of 2 point discrimination
Loss of sense of limb position
Loss of protopathic sensations ⇒ loss of sense of temperature
Analgesia ⇒ loss of sense of pain
Anaesthesia ⇒ total loss of sensation
Paresthesias ⇒ unusual sensation
Hyperalgesia ⇒ incresed sensitivity and pain
Cutaneous hallucinations ⇒ sensation without external stimuli
Loss of stereognosis ⇒ inability to recognize objects by touch
Motor Disruptions
Motor symptoms more complex than sensory losses.
Must consider types of paralysis, reflexes, muscle use patterns, and voluntary abilities.
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Altered muscle tone
- Increased tone ⇒ spastic symptoms
- Decreased tone ⇒ flaccid symptoms
- Paresis or paralysis ⇒ weakness or lost voluntary control
- Lost reflex responses
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Overactive reflex responses
- overly strong knee jerk
- out of context flexion withdrawal
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Unusual reflex responses
- Babinski, grasp, routing
- Oscillation or clonus
- Spasms or involuntary flexions
- Fasciculations ⇒ motor units contract individually and sporadically
- Flaccid paralysis
- Spastic paralysis
- Ataxia
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Rigidity
- Inability to initiate movement and active contractions
- Involuntary contractions ⇒ cogwheel rigidity, lead pipe rigidity
- Apraxia ⇒ inability to perform a task without loss of muscle control, sensation, or coordination
Peripheral Nerve Lesion
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Sensory signs:
- Complete sensation loss over a large area not tied to dermatomes.
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Motor signs:
- Flaccid paralysis of muscles supplied.
- Do not respect myotome boundaries.
Symptoms are not segmental.
May gradually improve as PNS regenerates.
Dorsal Root Lesion
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Sensory signs
- Complete pain/temperature sensation loss of associated dermatomes.
- Partial areflexia of associated myotomes.
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Motor signs ⇒ can mimic some symptoms of LMN lesion
- Loss of reflexes in myotome
- Voluntary contraction normal
- Pain and temperature loss is more prominent and detectable than fine touch loss
- Due to broader overlap of medial division dermatomes compared to lateral division fields on the skin
- Homonymous Ia reflexes of myotome are lost
- Heteronymous reflexes from other muscles outside myotome & FRA responses from innervated segments may persist
- Ventral roots are intact so voluntary contractiosn are preserved
Dorsal Horn Lesion
Ipsilateral loss of pain and temperature sensation in associated dermatomes.
If medial division fibers spared ⇒ no loss of fine touch or proprioception.
- Dorsal horn lesions destroy the cells receiving afferent input
- May spare the dorsal roots (i.e. cells contributing to STT)
- Afferents may bypass injured area in Lissauer’s tract or dorsal columns
- Dermatome extent of symptoms may be less than extend of damage
Ventral Root Lesion
Loss of any response in myotome.
Flaccid paralysis.
- Complete loss of reflexes, tone, and voluntary control
- Some regrowth into periphery may be possible
Ventral Horn Lesion
Motor signs:
Fasciculations if damage is progressive.
Loss of any response in myotome if damage is complete.
Flaccid paralysis.
- Anterior horn cells are killed
- Motor neurons die causing motor unit fasciculations
- Affected myotomes weaken then flaccid
- Reflexes cannot be initiated because motor innervation of muscle is gone
Dorsal Columns Lesion
Ipsilateral loss of proprioceptive and epicritic sensation at and below the lesion.
Pain and temperature sensation spared.
- Gray matter is spared.
- Fine touch and proprioceptive afferents below the lesion unable to reach gracile or cuneate relay nuclei
Anterolateral system (STT) lesion
Contralateral loss of pain and temperature sensation starting 1 level below the lesion.
Proprioceptive and fine touch sensation spared.
- Spinothalamic tract (STT) cut
- STT fibers originate contralaterally
- Dorsal columns and gray matter spaced
- Due to Lissauer’s tract, symptoms begin about a segment below site of damage ⇒ level of symptom is “dropped” lower
Anterior White Commissure Lesion
Bilateral loss of spinothalamic and ventral spinocerebellar axons in affected segments.
Loss of pain and temperature sensation.
Ataxia.
Reflexes of affected segments spared while motor pools unaffected.
- Anterior white commissure carries STT and VSCT fibers across midline.
- Pathway damaged in affected segments.
- If lesion enlarges medially, lateral motor pools will be damaged as well
Dorsal spinocerebellar tract (DSCT)
&
Ventral spinocerebellar tract (VSCT)
Lesions
Ataxic symptoms.
Poor joint coordination.
Wide ataxic walking gait.
- DSCT and VSCT deliver information for coordination to the cerebellum.
- Damage causes loss or degradation of cerebellar mediated motor control
Lateral Funiculus Lesion
Ipsilateral loss of fractionated voluntary movement below lesion.
Spastic paralysis due to loss of mixed reticulospinal pathways.
Ipsilateral babinski sign or grasp reflex below lesion.
- LCST and medullary pathways (MRST) intermingled in lateral funiculus
- loss of voluntary contraction of muscles
- altered reflex responses
- some medullary effects are usually present with spinal lesions
- Reflex tone is affected below the lesion
- Some inhibited reflexes are released from CST inhibition
Clonus
Clasp-Knife Response
Following UMN lesion, inhibitory control over GTO reflex lost.
Local reflex circuit becomes more excitable.
Clasp-knife response observed.
LCST Lesion
Location of lesion along tract affects laterality of symptoms:
Lesion above decussation ⇒ contralateral symptoms.
Below decussation ⇒ ipsilateral symptoms.
