Lecture 43: Injuries of the Spinal Cord Flashcards
Injuries of the _______ are the most frequent traumatic injuries of CNS
Injuries of the spinal cord are the most frequent traumatic injuries of CNS (Brain is proected by the skull, the spinal cord is more vulnerable)
Describe the effects of a hemisection of the l_eft spinal cord_ at the Th8 level.
For example, after hemisection of the left spinal cord at the Th8 level:
- Motor deficits
- Monoplegia (no voluntary motor functions) of left leg: loss of synaptic inputs to motoneurons from corticospinal tract and rubrospinal tract
- Hyperactive reflexes in left leg (increased stretch reflexes & clonus, Babinski reflex): increased excitability of motoneurons due to imbalance of synaptic inputs from reticulospinal and vestibulospinal tracts
- Sensory deficits
- Loss of pain and temperature sensation below Th8 on the right side. (Note that spinothalamic tract is crossed at the segmental level).
- Fine tactile perception and proprioception lost below Th8 on the left side (ipsilateral to the lesion). (Note the dorsal columns remain ipsilateral throughout their course in spinal cord)
What happens in Acute Complete Transections of the Spinal Cord (Spinal Shock)
- Period of areflexia (spinal shock) lasting 1-3 days due to loss of excitatory inputs from descending tracts (reticulospinal and vestibulospinal tracts):
E.g. after complete lesion at T8 level (below cervical enlargement of spinal cord):
- Paraplegia (flaccid paralysis in both legs)
- *Total anaesthesia below T8 (all conscious sensation lost)
- *Areflexia below T8 (no muscle reflexes, e.g. no tendon reflexes, plantar responses silent)
- *Blood vessels dilated so hot surface temperature (moderate BP↓; or much bigger BP↓ in quadriplegic patients)
- Rostral ventrolateral medulla (RVL) stimulates pre-sympathetic neurons (PSNs) to eventually induce vasoconstriction (figure left)
- PSNs are mainly in thoracic levels, so higher thoracic lesions have higher drop in BP, vice versa.
- *Thermal sweating absent so dry skin (due to lesion of autonomic nervous system)
- Bladder and bowels atonic: bladder distends with urinary overflow
- Dysfunction of sexual organs
What is a spinal shock?
Spinal shock is a combination of areflexia/hyporeflexia and autonomic dysfunction that accompanies spinal cord injury.
The initial hyporeflexia presents as a loss of both cutaneous and deep tendon reflexes below the level of injury accompanied by loss of sympathetic outflow, resulting in hypotension and bradycardia.
Describe the effects of Complete Transection of the Spinal Cord (spinal shock) at the T8 level (below cergical enlargement of the spinal cord)
Period of areflexia (spinal shock) lasting 1-3 days due to loss of excitatory inputs from descending tracts (reticulospinal and vestibulospinal tracts):
E.g. after complete lesion at T8 level (below cervical enlargement of spinal cord):
- Paraplegia (flaccid paralysis in both legs)
- *Total anaesthesia below T8 (all conscious sensation lost)
- *Areflexia below T8 (no muscle reflexes, e.g. no tendon reflexes, plantar responses silent)
- *Blood vessels dilated so hot surface temperature (moderate BP↓; or much bigger BP↓ in quadriplegic patients)
- Rostral ventrolateral medulla (RVL) stimulates pre-sympathetic neurons (PSNs) to eventually induce vasoconstriction (figure left)
- PSNs are mainly in thoracic levels, so higher thoracic lesions have higher drop in BP, vice versa.
- *Therma_l sweating absent_ so dry skin (due to lesion of autonomic nervous system)
- Bladder and bowels atonic: bladder distends with urinary overflow
- Dysfunction of sexual organs
Describe the recovery after acute, complete spinal cord lesion (spinal shock)
- Recovery (partial) and additional symptoms several weeks after injury:
* Muscle tone ↑ (but voluntary movements of legs remain absent)
- Hyperactive muscle stretch reflexes (spasticity and ‘clonus’)
- Spontaneous reflex emptying of bladder and rectum
- BP↑ but unstable (‘autonomic dysreflexia’; more pronounced in quadriplegics)
- If you measure BP it is unpredictable.
- Flexor (withdrawal) reflex on noxious stimulation recover (after several months)
- Extensor plantar (Babinski) reflex (dorsiflexion= abnormal)
- Paresthesia (abnormal sensations from the affected areas, e.g. a burning pain in the abdomen) due to the reorganization of synapses in sensory pathways
What is responsible for the (partial) recovery in the Acute, Complete, Spinal Cord Lesion
- ‘Sprouting’ of axon terminals and formation of new synapses (re=programming of remaining axon connections, known as synaptic plasticity)
- Denervation supersensitivity (fewer synaptic inputs induce ↑ receptor expression on post-synaptic membrane in order to sensitize to remaining neurotransmitters)
Describe Respitaroy and Monot Management of Quadriplegic patients
Quadriplegic patients
- Artificial ventilation (such as _breathing pacemaker_s by placing stimulating electrodes on phrenic nerves, only possible if lesion above phrenic nucleus) (figure left)
Note that spinal level innervating diaphragm are from C3/4/5 (intercostal muscles are innervated from ventral horn of thoracic region), which can be the site of lesion in quadriplegic patient, therefore they cannot breathe.
A breathing pacemaker controls activity in the diaphragm muscle, the primary muscle of breathing. Electrodes implanted around the nerves to the diaphragm (phrenic nerves), or placed directly into the muscle cause an inspiratory (inhalation) event to occur.
What are Breathing Pacemakers?
A breathing pacemaker controls activity in the diaphragm muscle, the primary muscle of breathing.
Electrodes implanted around the nerves to the diaphragm (phrenic nerves), or placed directly into the muscle cause an inspiratory (inhalation) event to occur.
An external transmitter sends a signal through the implanted electrodes causing the diaphragm to contract.
The contraction mimics the activity that occurs with normal breathing. Exhalation occurs passively in response to the inhaled air.
Describe the Motor Managment of Paraplegic Patients
Paraplegic patients
- ‘Parastep‘: microcomputer-controlled system for evoking coordinated muscle contraction that enables a paraplegic to stand up and walk
- Rex Bionics (robotic ‘exoskeleton’): a pair of robotic legs that enables a paraplegic to stand up, walk, move sideways, turn around, go up and down steps etc**.
- ‘__ReWalk‘: a much lighter exoskeleton with easier navigation manufactured in Israel
Describe how Peripheral nerve grafted to the brain provides a permissive environment for axon regeneration.
Peripheral nerve grafts to the brain (CNS) provides a permissive environment (due to Schwann cells) for axon regeneration.
(CNS nerve cells cannot regenerate because of different glial cells - CNS has oligodendrocites
Experiment on rats
1) Cut optic nerves (CNS) in rats (so they became blind)
2) A graft was made by a piece peripheral nerve from the eye to the Superior colliculus to encourage regeneration
3) the experimenters put in an recording microelectrode into the superior colliculus
4) When he presented the rats with flashes of light, after time, he saw action potentials in the recording.
Describe some Regeneration that can occur in the spinal cord (in experimental animals)
- Nerve grafts (as in the rat study)
- Neutralising antibodies to a growth-inhibiting myelin-associated glycoprotein (MAG) and ‘NOGO-A’ secreted by oligodendrocytes (as opposite to functions of Schwann cells)
- Tissue bridges with peripheral nerves (nerve grafts), Schwann cells, or olfactory ‘ensheathing glia’ cells (risk of inflammation and gliosis
- Cell transplant with: (1) embryonic stem cells; (2) bone marrow stem cell transplants
Why can’t nerves in the CNS regenerate like PNS?
Growth-inhibiting myelin-associated glycoprotein (MAG) and ‘NOGO-A’ is secreted by oligodendrocytes
