Forbes – Lesion Localization – NS Exam 2







Tracts Tested Clincally:
o Dorsal Column-medial lemniscal
o Spinothalamic
o Corticospinal/ Corticobulbar = Pyramidal System
Degeneration: the portion of axon separated from cell body will die.
o Ascending Tracts degenerate above lesion
o Descending Tracts degenerate  below lesion
Regeneration basically doesn’t occur in CNS = permanent disruption of normal function below the lesion.
Sensory testing
o Modalities: discriminative touch, proprioception, vibration, pain, temp
o ID of Ascending Tracts: DCML or ST
o Test dermatomal lvl of deficits
 Sensory level (this is key localizing features)
o Key dermatomes (spinal cord segments) :
 T4 – nipple
 T10- umbilicus
 L5 – front of leg
 Overlap bxt nerve roots & dermatomes
 each dermatome served by 3 adjacent nerve roots – need to cut these to get complete
anesthesia w/in one dermatome
 severing single root  minimal loss of sensation in most dermatomes
Motor testing
o Upper Motor Neuron
 What tracts? Where in tract?
o Lower Motor Neuron – check dermatomes – spinal cord segments:
 C5 = deltoid
 C6= Biceps
 C7= Triceps
 C8= digits
 L4= quadriceps
 S1= plantar flexion
Refex Testing Assesses both: motor and sensory
o assesses afferent and efferent part of reflex arc
o State of control by descending tracts
 corticospinal
 Reticol & Vestibulospinal
o Specific Segments
o Reflex tests:
 Biceps  C6
 Triceps  C7
 Brachioradialis  C6
 Quadriceps  L4
 Gastroc  S1
Spinal Cord Transection
o Spinal Shock – acute phase
 All functions below lvl of lesion immediately depressed
 Lasts days – weeks – months
 Cause:
 Loss of ascending tract info
 Sudden loss of descending tract influence
 Loss of excitatory or facilitatory influence predominates during spinal shock.
o


Gradual recovery of reflexes after spinal shock
 Reflex apparatus is still intact so LMNs still get input
 Modulation or regulation from descending tracts is gone
 Loss of inhibitory influence comes to predominate (maybe b/c):
 Vacant synaptic sites on LMNs  occupied by new nerve sprouts from primary afferents
– so that a sensory stimulus would have greater effect on LMN
 Denervation hypersensitivity leads to increased responsiveness of LMNs to
neurotransmitter
 Progressive return of reflex activity – from Fitz.
o Residual (Chronic) Dysfunction:
1.) UMN deficits below the level of the lesion
a.) Spastic paresis/paralysis
b.) Marked muscle tone
c.) Hyperactive deep tendon reflexes
d.) Diaphragmatic palsy if lesion above C4/5
e.) Horner’s syndrome if damage above T2
2.) LMN deficits at the level of the lesion
a.) Flaccid paresis/paralysis
b.) Reduced muscle tone
c.) Hypoactive deep tendon reflexes
d.) Neurogenic atrophy
e.) Fibrillation
With a cord lesion at cervical levels:
o UMN deficits in legs
o LMN deficits in arms
With a cord lesion at lumbar levels:
o Both UMN & LMN deficits in legs
o LMN deficits predominate since the reflex arc is disrupted.