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107 Cards in this Set

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Early management of spinal cord injury aims to:
Minimise secondary spinal cord damage

Prevent complications from altered physiological functioning that follows SCI
Tetraplegia = ?
Aka. Quadriplesia.
impairment of motor and sensory function involving the upper limbs, trunk and lower limbs due to damage to the cervical spinal cord

i.e. T1 or above
Paraplegia = ?
impairment of trunk and/or lower limb muscle function as a result of damage to the thoracic cord, lumbar cord or nerve roots within the spinal canal

i.e. T2 or below
Spinal level of injury = ?
lowermost neurologically intact segment with normal motor and sensory function
Complete v. incomplete spinal injury
Complete = no voluntary motor or sensory function is preserved more than 3 segments below the level of the injury and in particular the lowest sacral segments; this includes impairment of autonomic function with loss of bladder and bowel control

Incomplete = some preservation of voluntary motor and/or sensory function, including sacral sensory sparing
Spinal shock = ?
What may be masked by spinal shock?
a state of diminished excitability of the isolated spinal cord that commonly follows acute spinal injury

state in which there is loss of sensory and motor function below the level of spinal cord injury and is marked by absence of somatic and autonomic reflexes (flaccidity) below the level of cord injury

may mask associated hypovolaemic shock associated with injuries to long bones, pelvis, abdomen and chest
Spinal cord injury above T6 --> ?
substantial loss of sympathetic vascular tone with resultant hypotension
Spinal shock may make it difficult to accurately define what ?
Both the degree of underlying pathology in the spinal cord and the prognosis for recovery during the first few days to weeks
Management of structural spinal injury. Why repeat assessments?
Radiological assessment of spinal stability and degree of spinal canal encroachment
Repeated clinical assessments early after injury provide evidence of change in neurological status which may influence surgical management
Low cervical and high thoracic injuries may be associated with…
respiratory insufficiency from paralysis of intercostal and abdominal muscles; the diaphragm then becomes the only muscle of active inspiration apart from the accessory muscles
What becomes severely impaired when mm. of forced expiration paralysed?
The ability to cough effectively
High cervical cord injury involving phrenic n.--> ?
diaphragmatic paralysis requiring mechanical ventilation
How can thoracic injuries be associated with respiratory impairment?
Thoracic injuries may also be associated with respiratory impairment chest injuries such as haemothorax.
Paralytic ileus = ?
Sufficient intestinal paralysis that prohibits the passage of food through the intestine leading to intestinal blockage.
Usually present after early injury and requires naso-gastric aspiration
Risk factors for thromboembolism after spinal cord injury
How reduce incidence?
Bed rest

Reduce incidence by both pharmacological prophylaxis and mechanical measures

[from pop med lecture - give DVT prophylaxis for ~6 months whilst in spinal unit - once leave hospital they do NOT continue with prophylaxis - their risk is only slightly higher than general popn]
How should one position paralysed limbs and why?
In a way that prevents muscle shortening, to reduce the severity of spasticity and prevent the development of contractures.
What happens to the paralysed bladder following spinal shock? What must be avoided?
The paralysed bladder remains flaccid for some time following spinal shock and over-distension of the bladder must be avoided through catheterisation
Stress ulceration can be reduced by ?
Proton pump inhibitors
When does spinal shock typically occur?
following traumatic spinal cord injury but can also occur following inflammation or interruption to the blood supply of the spinal cord
Flaccidity= ?
absence of somatic and autonomic reflexes
Spinal shock more prominent in which situations?
more prominent following relatively abrupt spinal cord lesions, such as the spinal cord injury that occurs in a diving, football or MVA
Spinal shock less likely to occur in which situations?
less likely to occur with slowly evolving disorders, such as chronic spinal cord compression, due to cervical myelopathy or tumour
When might a patient with multiple sclerosis develop spinal shock?
Spinal shock more likely with acutely developing 'transverse myelitis'.
What changes ass'd with LOSS of REFLEX activity do you see in spinal shock? (3)
1. Lose somatic reflexes --> loss of deep tendon reflexes and a flaccid paralysis of the affected limbs

2.loss of reflex activity in viscera so that the bladder and bowel lose their tone and become flaccid

3. loss of autonomic reflexes - major disturbance in CV system (above T6 substantial loss of sympathetic vascular tone)
T/F: Spinal shock --> increase in reflex activity
FALSE!!! decrease
What happens to bladder and bowel in spinal shock?
Loss of reflex activity in viscera so that the bladder and bowel lose their tone and become flaccid.

This may result in complete absence of bowel activity (paralytic ileus) and bladder tone (bladder distension).
What is required to diagnose spinal shock?
Areflexic acute flaccid paralysis
T/F: Spinal shock is a neurovascular condition
False. It is a NEURAL condition.
Can you lose cardiovascular control in spinal shock? Why?
Yes - because you can lose autonomic reflexes.

This doesn't happen in all patients.
Above what spinal level do you get substantial loss of sympathetic tone?


Decreased vascular resistance --> pooling in extremities --> dramatic fall in BP (potentially with bradycardia because of impaired sympathetic innervation and preserved vagal innervation)
Spinal v. hypovolaemic shock
SPINAL - skin remains warm and dry, blood volume remains the same

HYPOVOLAEMIC - skin is cold and clammy, blood volume decreases, normal reflex activity to increase HR and peripherally vasoconstrict
Management of spinal v. hypovolaemic shock
Do NOT treat spinal shock with FLUIDS. If severe can treat with inotropes (s.a. dopamine)

This is the normal treatment for hypovol. shock
T/F: if recognised fall in BP is not hypovolaemic shock, can leave it untreated
TRUE! unless severe then treat with inotropes
Do you treat spinal shock with fluid replacement? Why?
NO!! - can lead to fluid overload and further problems
How long can spinal shock last?
several hours to 4 weeks
What happens to reflexes following period of spinal shock?


Can lead to increased tone and hyperreflexia of the limbs and bladder if they are below the lesion

If lesion above T6 - can lead to autonomic dysreflexia
Spinal cord surrounded by which 3 layers of connective tissue?

These are collectively known as what?
Pia mater
Arachnoid mater
Dura mater

Collectively known as MENINGES
What is the filum terminale?
fibrous band of pia mater that anchors the spinal cord to the sacrum and coccyx below
Two enlargements of spinal cord. Where are they exactly? Why?
Cervical enlargement (C1-6)
Lumbar enlargement (T12-L1)

Because large number of neurons innervating the limbs
Segments of the spinal cord:
31 in total:

8 cervical
12 thoracic
5 lumbar
5 sacral
1 coccygeal
Spinal cord extends from where to where?
Vertebral levels C1 to approx L1/L2
Sacral spinal segments lie opposite which vertebrae?
lower thoracic
Where is csf?
Subarachnoid space (between arachnoid and pia)
To which vertebral level do dura and arachnoid continue?
What exists below vertebral level L2?
Spinal cord has ended.

Have large subarachnoid space which contains CSF and lumbar, sacral and coccygeal, dorsal and ventral roots
Where would you needle puncture to sample CSF?
BELOW L1/2 so as to not damage spinal cord. Subarachnoid space exists to S2 so you would sample at approx L4/5
Where in the spinal cord are neurons found?
Cell bodies found in H-shaped central mass (the grey matter)
What is contained in dorsal horn?
Primary somatic and visceral afferent (sensory) neurons
What is contained in ventral horn?
Large alpha MNs
Small gamma MNs
Interneurons (lots!)
What is contained in intermediate grey?
Autonomic pre-ganglionic neurons (in two major groups - intermediolateral and intermediomedial)
Autonomic pre-ganglionic fibres in the SPINAL CORD:

Where are the sympathetic ?
Where are the parasympathetic?
Sympathetic - from C8 to L1

Parasympathetic - S2 to S4
What laminae found in dorsal horn?

What laminae found in ventral horn?

What laminae found in intermediate grey?

[6, 7, 10]
What is white matter in spinal cord?

How is it divided?
The axons that pass to and from the grey matter.

Lies peripherally to the grey matter.

White because of myelin sheath

Divided into columns (or funiculi) - dorsal, ventral, lateral
In which lamina are somatic motoneurons located?
Rexed lamina IX (9)
What is contained in the 2 different columns of motoneurons?

Do both columns traverse the entire length of spinal cord??
MEDIAL: [length of SC]
MNs innervating AXIAL muscles of body

LATERAL: [only in cervical/lumbar enlargements]
MNs innervating UPPER and LOWER LIMB muscles

[memory tool - Lateral Limbs]
Upper vs. lower motor neurons?
UMN = cells of origin of motor pathway

LMN = Cells in the VENTRAL HORN
Damage to ventral horn somatic motor neurons results in: (4)
1. paralysis (absence of movement)
2. wasting of denervated muscles
3. absence of muscle tone (flaccidity)
4. absence of reflexes (areflexia)
Damage to descending motor pathways results in:

What is not present?
Paralysis or paresis present (weakness of movement)

do NOT have muscle wasting

have NORMAL or INCREASED muscle tone (spasticity)

INTACT or ENHANCED reflexes (hyperreflexia)
T/F: using UMN symptoms can help identify level(s) of segmental damage
FALSE - use LMN symptoms
Does damage to the spinal cord involving both grey and white matter give UMN or LMN symptoms?
BOTH !!!
The damage to the white matter gives UMN symptoms
The damage to the grey matter gives LMN symptoms
What would you see with grey matter damage?
"LMN symptoms"
Wasting, areflexia
What would you see with white matter damage?
"UMN symptoms"
Spasticity, hyperreflexia
Where is the main primary afferent (dorsal root) spinal entry zone
medial edge of the dorsal horn
From where to myelinated primary afferents come?
encapsulated somatic receptors
Where do myelinated primary afferents lie in relation to unmyelinated primary afferents?
myelinated lie MEDIAL to unmyelinated

[memory tool - Myelinated lie Medial]
Diameter of myelinated and unmyelinated primary afferents?
myelinated = large
unmyelinated = small
central processing of primary afferent input involves three main channels of communication:
[list 3]
1. Reflex channels
2. cerebellar channels.
3. Lemniscal channels
[[[[up to 'somatosensory organisation' in Spinal cord structure and function: longitudinal organisation]]]
How many synapses in;
(A) stretch reflex arc
(B) flexor reflect
(A) ONE (monosynaptic)
(B) MANY (polysynaptic)
How is the integration of activity across a large no. of spinal segments achieved?

When might this occur?
Intersegmental fibres (propriospinal fibres) of spinal interneurons

As during the flexor reflex, when multiple muscle groups need to be activated
how do deep tissues (muscles, tendons, joints) of the LOWER LIMB communicate with the cerebellum?
Dorsal spinocerebellar tract neurons receive primary afferent proprioceptive input from the lower limb and 'relay' it to the ipsilateral cerebellum
how do deep tissues (muscles, tendons, joints) of the UPPER LIMB communicate with the cerebellum?
External cuneate nucleus of the caudal medulla sends proprioceptive information from the upper limb to the cerebellum
Are we consciously aware of any of the proprioceptive info that reaches the cerebellum ?
What and where are the dorsal column nuclei ?
Cuneate (upper limb) and gracile (lower limb) nuclei

In the medulla
What are the 2 major "lemniscal channels"
Dorsal column tract
Spinothalamic tract
Info carried in the spinothalamic tract allows us to perceive and localise what?
Pain, temperature, light touch
Give the 3 general principles of lemniscal systems
1. 1st order neurons - cell bodies are found in the periphery

2. no primary afferent fibres project directly to thalamus (i.e. at least 1 synapse before thalamus)

3. Highly organised topographically - somatotopic localisation and modality specificity provide the basis for the discriminative quality of our conscious perception of somatosensation
Spinothalamic tract:
primary afferents synapse on second order neurons in which laminae
I (1) or V (5)
How far do 2nd order neurons ascend before they cross the spinal cord to join the spinothalamic tract?
ascend not more than 1 or 2 segments and cross to the opposite side to enter the 'spinothalamic tract'
Where is the spinothalamic tract?
within the ventral (anterior) part of the lateral column

i.e. forms part of anterolateral system
information carried within the gracile and cuneate tracts provides the basis for our ability to perceive what..?
Somatosensory: limb position and complex tactile sensations (e.g., weight, texture, shape)
Dorsal column tract:
Where do the primary afferents synapse?
primary afferent info enters dorsal column and ascends ipsialterally up the SC to terminate on 2nd order neurons in the MEDULLA (dorsal column nuclei)
How might psychological and emotional reactions to SCI be exaggerated?
premorbid psychiatric illness
risk taking behaviour
drug and alcohol abuse
Autonomic instability (dysreflexia) commonly affects individuals with SCI at or above which spinal level?
What are some important things SCI patients need to be educated about?
bladder and bowel management, autonomic dysreflexia, skin care and sexuality
aims of SCI rehabilitation
maximise independence, assist psychological adjustment and reintegrate the individual into the community and workplace
Poor adjustment to spinal cord injury ass'd with..[3]
chronic pain
Good outcome of SCI adjustment ass'd with ... [6]
young age
female sex
higher education level
ability to relate well
confidence in one's mastery over environment
ability to have indulged in risk taking behaviour
Data in US shows what differences in marriage and divorce rates SCI patients vs. matched controls?
fewer marriages and more divorces
How have previously common renal complications been reduced?
improved management of bladder dysfunction and monitoring of urological function
How can a Pt with SCI improve their mobility and function?
Physical strengthening
development of modified techniques/new skills
provision of specialised equipment
what are important considerations in helping individuals to rebuild their lives after SCI [5]
Premorbid lifestyle and interests

educational background

work history

social support

economic circumstances
Define nociceptive pain
Pain that arises from actual or threatened damage to non-neural tissue (i.e. somatic or visceral structures) and is due to the activation of intact nociceptors
Clinical point of view - 3 main types of pain
non-cancer chronic
Define acute pain. Give e.g.'s
present for relatively short period of time (mins-weeks)

e.g. pain following injury or surgery or acute disease processes such as appendicitis or renal calculi
Define chronic pain
Longer than 3 mo
Define neuropathic pain
Pain caused by a lesion or disease of the somatosensory nervous system
Does our psychological state impact on the way we perceive pain? Give e.gs
YES! Our psychological state makes a huge contribution to our experience of pain.

E.g. sporting activities or in battle, people may display little awareness of pain despite major injuries ..

or if someone is super anxious - can increase pain perception
what factors need to be considered in a pain assessment? [2]
1. what structures may be involved and what is the pathology that may be generating the pain

2. what psychosocial factors may be operating that modify the way that the person both feels and expresses their pain
How is a pain assessment carried out?
1. Accurate history - focus on location and characteristics

2. Determine psychosocial contributors - personality, mood, social environment

3. Careful physical exmanination

4. Further Ix if req'd
In what type of pain are psychosocial factors more likely to contribute ?
How is acute nociceptive pain treated?
Try to treat the underlying disease causing the pain and give basic analgesics until healing has occured:
- Oral analgesics / anti-inflamms / opiates
- PCA / epidural anaesthesia if req'd
Does neuropathic pain respond to analgesia? what may it respond to? why?
Doesn't respond to simple analgesics, rarely responds to strong opioids.

may respond to other "adjuvant" medications such as anticonvulsants and antidepressants because of their effects on other receptors involved in pain transmission
What are some non-pharmacological interventions for chronic pain?
Why do them ?
stimulation techniques, physiotherapy, exercise, relaxation techniques and psychological approaches

may help to either reduce pain directly or to manage pain and reduce its impact on the person's life