2.

Investigate different types of spinal injuries and the signs and

symptoms of injury in scenario as well as the consequences in
dermatome and myotome mapping.
 
Spinal Shock - following a spinal cord injury (SCI) is a specific term that relates to the
loss of all neurological activity below the level of injury. This includes motor, sensory,
reflex and autonomic function. It lasts roughly 30-60 minutes but can last up to 6
weeks post injury.
 
 There is complete loss of motor and sensory function below the level of the
lesion.
 Characterised by a combination of autonomic dysfunction and below level of
lesion: flaccid paralysis, atonia, areflexia.
 
Four Phases
 Areflexia
 Initial reflex return
 Hyperreflexia
 Hyperreflexia - spasticity
 
Phase 0-1d Areflexia/Hyporeflexia Characterized by a complete loss - or
1 weakening - of all reflexes below the SCI.
This phase lasts for a day. The neurons
involves in various reflex arcs normally
receive a basal level of excitatory
stimulation from the brain. After an SCI,
these cells lose this input, and the neurons
involved become hyperpolarised and
therefore less responsive to stimuli.
Phase 1-3d Initial Reflex Returns Occurs over the next two days, and is
2 characterised by the return of some, but not
all, reflexes below the SCI. The first reflexes
to reappear are polysynaptic in nature, such
as the BULBOCAVERNOSUS REFLEX - a
postsynaptic reflex that is useful in testing
for spinal shock (involves internal/external
anal sphincter contraction in response to
squeezing the glans penis or clitoris).
 
Reflexes return due to the hypersensitivity
of reflex muscles following denervation -
more receptors for neurotransmitters are
expressed and muscles therefore are easier
to stimulate. Restoration of reflexes is from
polysynaptic to monosynaptic.
Phase 1-4w Hyperreflexia (initial). Abnormally strong reflexes usually with
3 Axon-supported minimal stimulation. Interneurons and lower
 synapse growth motor neurons below the SCI begin
sprouting, attempting to re-establish
synapses. The first synapses to form are
from shorter axons, usually from
interneurons.
Phase 1- Hyperreflexia and Takes longer since synapse formation is
4 12m Spasticity soma-mediated (takes longer for axonal
transport to push growth factors and
proteins from soma to end of axon).
 
Autonomic Effects
 In spinal cord injuries above T6, neurogenic shock may occur, from the loss of
autonomic innervation from the brain.
 
Babinski Reflex (plantar reflex) - one of the first reflexes to return as spinal shock
subsides. The return of reflexes marks the end of spinal shock.
 
 As reflex function returns, spastic paraplegia or quadriplegia develops with
hyperreflexia (overreactive reflexes). This is due to sprouting of the lower motor
neurones, that are constantly trying to regrow.
 
Neurogenic Shock
 Shock caused by loss of brainstem and higher centre control of the
sympathetic nervous system.
 Hypotension, vasodilation, bradycardia (due to reduced venous return).
 Loss of impulses from the thermoregulatory centre in brain prevents ability to
sweat below level of injury.
 
 

 
 
Spinal Cord Injury can result from:
 Trauma: contusion or penetration/transection of neural tissue
 Compression - tumour; haematoma or bony encroachment
 
Major mechanisms of injury are:
 Hyperflexion
 Hyperextension
 Compression
Secondary effects of SCI include oedema, inflammatory/immune processes,RRRR.
 
Consequences of Spinal cord Injury at different segmental levels
Respiration
C3, C4, C5
 Phrenic nerve - innervates the diaphragm
 Section above this level results in disconnection of all the motor neurones
innervating the respiratory muscles from the respiratory centres in the hind and
midbrain.
 Breathing caeses and patient dies if artificial ventilation is not administered
 
C6,C7
 Innervates intercostal muscles
 Severing the spinal cord below the origin of the phrenic but above thoracic at
C6 and C7 segments cause disconnection of the motor neurones that innervate
the intercostals.
 
 Severing the spinal cord below the origin of phrenic but above thoracic at the
C6 and C7 segments cause disconnection of motor neurons that innervate the
intercostal muscles
 
 Breathing remains intact due to diaphragm
 Paradoxical breathing (chest moves out upon expiration and in upon
inspiration) is present.
 Thorax is sucked in during inspiration instead of expanding by contraction of
external intercostals.
 
Limb Movements
 Patients need constant monitoring and prophylaxis - increased risk of
pressure sores and DVT
 Loss of function depends on spinal lesion
 
 Complete --> complete functional loss below level of injury (no sensation or
voluntary movement and both sides equally affected).
 
 Incomplete --> Partial functional loss (can move one limb more than the other
or have some sensation in a paralysed limb).
 
 Reappearance of any sensation or voluntary movement below
segmental level would indicate cord injury is incomplete.
 
Spinal lesion
 High cervical segments - quadriplegia
 C5 - control of shoulder and biceps but no wrist or hand control
 C6 - wrist control but no hand control
 C7 and T1 - straighten arms but may have problems with dexterity of hands
and fingers
 
T1-T8:
 Paraplegia with hands not affected
 Poor control of trunks as abdominal muscles are affected
 Balance while sitting is still very good
 
Lumbar and sacral regions:
 Decreased control of hip flexors and legs
 
 
Bladder Control

 A spinal cord injury at almost every part of the cord will result in loss of
bladder control, this is because the micturition centre is at S2-S4 while in period
of spinal shock.
 
Return of Reflexes Following Spinal Cord Injury
Some reflexes never return and if they do, they adopt a more primitive form.
 
Somatic Reflexes
 Never regains voluntary control of skeletal musculature
 Reflex activity gradually recovers (together with autonomic activity)
  Flexor reflexes return first - ankle, knee and hip in sequence
 Extensor reflex return about 6 months after transection - tend to be
exaggerated leading to spastic paralysis
 Final stage is of predominant extensor activity with extensor spaces -
hyperreflexia (abnormally strong reflexes produced with minimal stimulation)
 
Plantar Reflex
 Maintains a standing position
 Tested by babinski response (adult responds with plantar flexion). This helps
test for the damage of pyramidal tracts in adults.
 
Results:
 Negative babinski - plantar flexion
 Positive babinski - dorsiflexion of great toe
 
After transection, Babinski response is lost with other reflexes and when it reappears
it assumes the abnormal form --> sign the spinal shock is wearing off.
 
Autonomic Reflexes
 Trivial stimulus to groin or sole of feet leads to exaggerated spinal reflex with
responses of flexion of leg, defaecation, micturition and erection in males.
 
Primitive control of autonomic function by spinal mechanisms is re-established but
blood pressure continues to remain more unstable than in normal person. Blood
pressure rises with filling of bladder due to stretch receptor bombardment.
 
Change of posture from lying to standing causes venous pooling in legs and leads to
reduced venous return --> blood pressure falls and subject may faint (orthostatic
hypotension)
 
Reflex Arc

 
 
 
Describe the difference between Lower Motor Neurone and Upper Motor
Neurone Lesions.
 

UMN vs LMN
 UMN are neurones located in brain or brainstem and the body is located in
the primary motor cortex. Axon of this neurone travels down spinal cord and will
activate a neurone in the ventral horn.
 LMN are the neurones located in the ventral horn of spinal cord. Axons travel
peripherally to innervate muscle.
UMN
Hypertonicity, Hyperreflexia, Spasticity
(tightness of muscle)
 
UMN regulates a LMN so that means if
there is damage the LMN is not
regulated properly so the LMN can be
inappropriately active. This means it
causes increased muscle tone.
 
Hyperreflexia - If we try elicit a reflex we
will get a large contraction of muscle and
large kicking out of leg. This is because
UMN regulates LMN and if we lose the
regulation the LMN is able to send out
larger impulses to the muscle.
Disuse atrophy - the muscle begins to
waste due to a disuse. Because there is
no control from the higher CNS (brain),
the muscle cannot be controlled or used.
The muscle becomes atrophied due to
disuse.
 
No fasciculations - no involuntary muscle
twitching
Positive Babinski Sign - points toes
upwards and fans toes out.
LMN
Hypo
 
Hypotonicity, Hyporeflexia,
Flaccidity
 
LMN innervates skeletal muscle. If there
is damage to LMN or axon the LMN
loses ability to innervate skeletal
muscle. If we try to elicit a reflex, the
muscle will have a decreased/no reflex
and it will be looser
Denervation atrophy - if we cut of the
nervous system input (the direct
connection of LMN to skeletal muscle)
we completely cut off the nervous
system input.
 
Fasciculations - involuntary muscle
contractions. This is because if there is
damage to LMN or axon you will get
random or inappropriate contractions of
that muscle
Negative Babinski Sign - points there
toes downwards
Ascending and Descending Pathways
Descending Pathways: Motor
 Axons of UMN either project to the cranial nerve nuclei or to the motor nuclei
in the spinal cord
 
Corticospinal
 Begins in cerebral cortex (basalis pedunculi)
 85% cross over just below medulla at the pyramidal decussate - lateral
pathway - controls limbs and digits
 15% don’t cross and form the anterior pathway and decussate at the level of
spinal nerve where they exit
 Controls trunk, shoulder and neck.
 
 
 Spinal cord injuries above the level of decussation will cause deficits on the
contralateral side.
 Lesions below will result in deficits on the ipsilateral side.
 
Ascending/Sensory Pathways
DCML
 Injury to spinal cord, the sensory loss will be ipsilateral because the
decussation occurs in the medulla
 
Spinothalamic
 Injury to certain side of spinal cord will cause sensory loss to be contralateral