B7.015 Selective Vulnerability from the Spinal Cord Flashcards
UMN damage symptoms
increased muscle tone
no atrophy
hyperreflexia
pathological reflexes present
LMN damage symptoms
decreased muscle tone
atrophy
hyporeflexia
pathological reflexes absent
reflex grading scale
0: no reflex
1: reflex only with reinforcement
2: reflex without reinforcement
3: reflex spreads to other muscles
4: clonus
+ if high amplitude
- if low amplitude
normal plantar response
toes down (flexion)
abnormal plantar response
Babinski sign
toes up and fanned
exaggerated withdrawal response
use of Babinski sign in UMN damage
moderate sensitivity (60-70% have it with an UMN injury) high specificity
what type of midline structural lesion would cause bilateral arm and leg weakness
high cervical spinal cord lesion
why should you consider midline lesions first
typically more dangerous and require more urgent therapy
dorsal horn
sensory
ventral horn
motor
what is present in the central gray matter
sensory dorsal cells
motor ventral cells
what is present in the peripheral white matter
intersegmental communications
“long tracts”
why do cervical and lumbar sections of the spinal cord have large ventral horns?
innervate limbs which require more motor control than the abdominal area (thoracic cord)
why is there a 3rd small out pouching between the dorsal and ventral horns in the thoracic cord
region where the sympathetic neurons exit the cord
orientation of lateral corticospinal tract in the cord
on lateral side of the cord, between dorsal and ventral horns
leg nerves lateral
arm nerves medial
2 neurons of the corticospinal tract
UMN
LMN
3 neurons of the DCML system
- dorsal root ganglion
- nucleus gracilis or cuneatus (corticomedullary junction)
- thalamus
orientation of the DCML system in the cord
on dorsal side in between the 2 dorsal horns
wedge shaped area
acute B1 deficiency
Wernicke Korsakoff
targets: mamillary bodies, medial dorsal nucleus of the thalamus, peri aqueductal structures
chronic B1 deficiency
dry beriberi
targets: peripheral nerves
B3 deficiency
pellagra
targets: cerebrum (dementia)
B6 deficiency
pyridoxine deficiency
may be caused by isoniazid
targets: peripheral nerves
B12 of Cu deficiency
subacute combined degeneration
targets: posterior columns, corticospinal tract
vitamin E deficiency
vitamin E deficiency
due to fat malabsorption
targets: neuropathy, retinopathy, spinocerebellar tracts
indications of Cu or B12 deficiency
macrocytic anemia bariatric surgery (impairs absorption) zinc supplementations (competes with Cu for absorption)
treatment of Cu deficiency
stop zinc supplements
copper replacement
-IV infusion
-oral
why do we see consistent patterns of structural selective vulnerability
shared anatomy
- proximity
- blood supply
why do we see consistent patterns of toxic metabolic selective vulnerability
shared physiology
- toxin sensitivity
- metabolic insult insensitivity
3 neurons of ALS system
- dorsal root ganglion
- dorsal horn
- thalamus
orientation of ALS system in the spinal cord
anterior section slightly lateral to the anterior horns
deficits with hemi-section loss of the thoracic spinal cord
contralateral pain and temp loss
ipsilateral proprioceptive loss
ipsilateral weakness
C5 weakness
deltoid
infraspinatus
biceps
C5 reflex
biceps
pectoralis
C6 weakness
wrist extensors
biceps
C6 reflex
biceps
brachioradialis
C7 weakness
triceps
C7 reflex
triceps
L4 weakness
iliopsoas
quads
L4 reflex
patellar tendon (knee jerk)
L5 weakness
foot dorsiflexion
big toe extension
foot eversion, inversion
L5 reflex
none
S1 weakness
foot plantar flexion
S1 reflex
Achilles tendon (ankle jerk)
cervical mantle
area where C5-T1 dermatomes get pulled out into arms and the neck to check jumps from C4 to T2
levels of pain and temp loss in relation to a lesion
several levels below (travel up a few levels before decussation)
areas affected by posterior spinal artery infarction
bilateral proprioceptive loss
areas affected by anterior spinal artery infarction
bilateral pain and temperature loss and weakness
deficits seen in cervical central cord syndrome
pain and temp loss in upper extremities only (suspended loss)
NO proprioceptive loss
LMN loss in upper extremities
UMN loss in lower extremities
deficits seen in external compressive lesion of cervical spinal cord
usually corticospinal tract damage
- selectively vulnerable for an unknown reason
- bilateral spasticity and mild weakness without sensory change
causes of subacute combined degeneration
B12 def
Cu def
Friedrich’s ataxia (also have spinocerebellar involvement)
deficits seen in subacute combined degeneration
corticospinal and DCML only
bilateral, symmetric proprioceptive loss and weakness
(pain and temp is fine)
deficits seen in primary lateral sclerosis
corticospinal tract only
UMN weakness alone
-bilateral symmetric weakness
deficits seen in amyotrophic lateral sclerosis
corticospinal and anterior horn cell involvement
UMN and LMN weakness
conditions that cause anterior horn cell deficits
spinal muscular atrophy
poliomyelitis
deficits seen with anterior horn cell damage
LMN weakness alone
bilateral, symmetric
conditions that cause posterior column deficits
Tabes dorsalis (tertiary syphilis) B6 intoxication paraneoplastic (sensory neuropathy)
deficits seen with posterior column damage
bilateral, symmetric proprioceptive loss
conditions that can cause multifocal deficits
transverse myelitis
multiple sclerosis