Spinal Cord Lesions

Question 1

Summarize Gate control hypothesis

Answer 1

Nonnociceptive afferents (A alpha/beta fibers) close the gate (diminish pain)

Nociceptive C fibers open gate (enhance pain)

Congenital absence of C type fibers results in disinhibition of SG cell and insensitivity to pain. Decrease in C fibers close the gate.
Herpes zoster: causes a transient compromise in nonnociceptive A alpha/beta fibers that open the gate

Question 2

What causes Brown-Sequard syndrome?

Answer 2

Unilateral transverse lesion of hemisection of spinal cord usually due to knife or bullet wound or a tumor such as a meningioma pressing upon the cord
Relatively common trauma

Question 3

What are the signs and symptoms of Brown-Sequard syndrome?

Answer 3

Ipsilateral loss of proprioception and vibratory sensations form body below level of lesion due to interruption of posterior columns
Ipsilateral spastic paralysis below level of lesions due to destruction of descending motor tracts
Contralateral loss of pain and temperature sensations from body 2 sensory dermatomal segments below level of lesion, due to destruction of LSTT

Question 4

How does subacute combined degeneration and pernicious anemia occur?

Answer 4

Atrophy of mucosal lining of stomach results in absence of intrinsic factor, which is required for absorption of vitamin B12.
Vitamin deficiency can result in macrocytic anemia and degeneration of posterior columns and pyramidal tracts along with polyneuropathy

Question 5

What are the signs of subacute combined degeneration?

Answer 5

Numbness and tingling in fingers and toes (“glove and stocking” anesthesia)
Bilateral loss of proprioception and vibratory sensations
Upper motor neuron signs such as spastic paralysis, paresis, hyperreflexia, and Babinski

Question 6

Summarize signs of upper motor neuron vs lower motor neuron paralysis

Answer 6

UMN:
Spastic paralysis
Hypertonia
Hyperreflexia
Disuse atrophy
Babinski sign

LMN:
Flaccid paralysis
Atonia
Areflexia
Fasciculations
Atrophy