Spinal Cord and Root Disease Flashcards
ALS presentation
weak, wasted muscles, spasticity, fasciculations, extensor plantar responses, hyperreflexia
Pathophys of ALS
motor neuron damage in anterior horns of spinal cord
Presentation of damaged dorsal spinal roots
sensory deficit, areflexia
Presentation of damaged ventral spinal roots
weakness and wasting
NO spasticity or hyperreflexia
Purkinje Cell damage presentation
ataxia without much weakness
What is damaged in a lumbosacral myelomeningocele
dorsal aspect of the spinal column with an attendant outpouching of meninges and neural elements from spinal cord.
Tx options of syrinx
laminectomy, cyst aspiration, marsupialization of cyst, shunt
Spinal Shock progression
Initially: flaccid quadriplegic and areflexia
Within 3d-3wks: hyperreflexia and spasticity (exaggeration of normal stretch reflex in limbs disconnected from upper motor neuron control)
Note: this happens with cerebrocortical injuries too but not exactly the same timeline
Winging of scapula, what nerve and muscle is damaged
long thoracic nerve (C5-7), serratus anterior muscle
Likely trauma mechanism for vertebral body fracture; what about if not related to trauma
extreme flexion, falls while landing upright;
Not related to trauma: malignancy/osteomyelitis
Brown-Sequard syndrome; what’s the pattern of deficit of pain & temperature vs. proprioception in relation to the lesion and what is damaged?
What else is damaged?
spinothalamic damage: pain & temp deficit 1-2 levels below level of lesion on contralateral side
posterior column damage: proprioception loss ipsilateral to lesion
Corticospinal, rubrospinal tracts, motor neurons: ipsilateral motor paralysis
Pathophys of syringomyelic syndrome
lesion of central gray matter (that affect pain and temp fibers that cross at the anterior commissure; tactile sensation spared)
What is tabetic syndrome
damage to proprioceptive & dorsal root fibers, slassically by syphillis
sx: parasthesias, pain, abnormalities of gait, vibration sense issues.
Upper motor neuron damage progression after trauma
- severe quadriparesis
- rapid recovery of motor function
- spastic paralysis
Lower motor neuron damage (anterior horn cell or more distally) progression following a trauma
fasciculations, fibrillations, flaccid paralysis, hyporeflexia