U11C4 Spinal Cord Injury Flashcards

1
Q

UMN vs LMN lesions

A

Lesions in the cervical and thoracic spine -> UMN
Lesions in lumbar spine -> LMN
Lesion in conus -> UMN and LMN

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2
Q

What does lesions in the cervical, thoracic and lumbar cord result in?

A

Lesion in the cervical cord -> arms and legs
Lesions in thoracic cord -> legs
Lesions anywhere -> bladder and bowel symptoms

Lesions in cervical/thoracic spinal cord:
- Pyramidal weakness of arms and legs (cervical) or legs (thoracic)
- Spasticity
- Brisk reflexes, upgoing (extensor) plantar reflexes
- Sensory level
- Sphincter involvement

Lesions in lumbar spine (cauda equina):
- Flaccid weakness
- Normal reduced/tone
- Reduced or absent reflexes
- Patchy leg sensory reduction
- Sphincter involvement (reduced anal tone)

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3
Q

What are the functions of the spinal cord?

A
  • Sensory information from the body to the brain (afferent)
  • Motor control from brain to body (efferent)
  • Includes bladder, bowel and sexual function
  • Autonomic function from brain to body
  • Spinal reflexes
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4
Q

Where are the spinal tracts located on a transverse cross section of the spine?

A
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5
Q

What are the 2 main sensory inputs?

A
  • The dorsal column (proprioception and vibration) ascends in the DORSAL (posterior) part of the spinal cord and crosses over in the MEDULLA (after the spinal cord)
  • The spinothalamic tract crosses over immediately in the SPINAL CORD and ascend in the LATERAL part of the spinal cord
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6
Q

Where do motor tracts cross over and descend?

A

in the MEDULLA (before reaching the spinal cord) and descend mainly in the LATERAL spinal cord

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7
Q

How would transverse myelitis of the thoracic spine present? What is it and treatment?

A

Sub acute history of progressive bilateral lower limb weakness. Ascending numbness and pins and needles spread up legs to level of umbilicus. Urinary urgency and frequency. Tone- spastic lower limbs with ankle clonus. Gait- circumduction of hips, stiff. Co-ordination- normal. UMN signs.

  • inflammation of the spinal cord
  • treatment is high dose steroids
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8
Q

How does prolapsed disc causing compressive lesion present?

A

Sudden onset lumbar back pain after lifting heavy table. Bilateral lower limb weakness. Bilateral buttock and lower limb sensory disturbance. Urinary hesitancy and reduced sensation when voiding. Tone and co-ordination normal.

  • Lesion is in the lumbar spine
  • LMN and neurosurgical emergency
  • Urinary symptoms- When the bladder stretches, it reflexively contracts (spinal reflex). This is mediated by autonomic fibres running in the pelvic nerves, emerging from S2-4. This reflex is inhibited by fibres running from the pons, down the spinal cord (higher control)
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9
Q

How does an anterior spinal stroke present?

A

Old man develops back pain then sudden onset weakness in both legs. Reduced sensation to lower abdomen. Urinary retention. Tone- reduced in lower limbs. Gait- unable to walk.

  • lesion in the anterior part of the thoracic spinal cord due to anterior spinal artery stroke
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10
Q

How does transverse myelitis of the right half of the cervical spine present?

A

Sub acute history of weakness of right leg then arm. Similar length history of numbness of left arm and leg. Urinary urgency. Tone- increase tone in right upper and lower limbs. Gait- circumduction of left hip

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11
Q

How would subacute combined degeneration of the cord (secondary to vitamin B12 deficiency) present? What is the treatment?

A

6 month history of weakness and numbness in lower limbs. Very unsteady on feet, especially at night. No urinary symptoms. Alcohol dependent. Tone- normal. Romberg’s positive. Gait- ataxic. Co-ordination- poor heel-shin test.

  • Lesion is in posterolateral spinal cord
  • Treatment is B12 replacement
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12
Q

How would syringomyelia present?

A

Two year history of progressive numbness in her hands, arms and shoulders. She had an accidental burn to the hand that she had not noticed. Longstanding headaches on coughing. Tone- normal.

  • Lesion is in the central cervical spinal cord
  • Central lesion affects crossing spinothalamic
  • Causes can be congenital, trauma or malignancy
  • Treatment is conservative and neurosurgical
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13
Q

How are spinal cord injuries managed?

A
  • Acute management depends on aetiology e.g. neurosurgical stabilisation of fracture, immunosuppression for inflammation
  • Generic management post injury:
  • Spasticity – anti-spasticity medication eg baclofen, botulinum toxin
  • Pain – neuropathic pain medication, nerve root blocks
  • Bladder dysfunction – B&B team, bladder relaxant medication, ISC, botulinum toxin
    Bowel – laxatives, bowel irrigation
  • Skin – nursing care, specialist mattresses
  • Respiratory function (esp high cervical) – respiratory support
  • Autonomic dysreflexia
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14
Q

What is the pathway of the motor tracts?

A

MOTOR: From skeletal muscle -> synapses in ventral horn -> to lateral corticospinal tract -> DECUSSATES (switches side) -> passes through medullary pyramids -> passes through crus cerebri -> thalamus -> motor cortex

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15
Q

What is the pathway of the somatosensrory tracts?

A

UPPER LIMB – Fasciculus cuneatus -> synapses in nucleus cuneatus -> DECUSSATES -> passes through medial leminiscal tracts -> synapses in VPL nucleus in thalamus -> somatosensory cortex
LOWER LIMB -Fasciculus gracilis-> synapses in nucleus gracilis -> DECUSSATES -> passes through medialleminiscaltracts -> synapses in VPL nucleus in thalamus -> somatosensory cortex

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16
Q

Partial vs complete lesion consequence

A

Partial lesion left side: Loss of motor and sensory on the same side (left) but pain and temp are lost on the other side (right)
Complete: loss of everything

17
Q

What is the pain perception tracts?

A

Ascending pain pathway: Damaged tissue releases prostaglandins which stimulate sensory nerve fibres and transmit this stimulus to an electrical stimulus in a process known as transduction.
This first order neuron then travels in the dorsal horn in the spinal cord and synapses with a 2nd order neuron. The neurotransmitter released between the 1st and 2nd order neuron here is substance p.
The 2nd order neuron then decussates and travels to the brain where it synapses with a 3rd order neuron in the thalamus.
The 3rd-order neuron then travels to a specific part of the somatosensory cortex in the post-central gyrus which correlates with the location in the body in which the stimulus originated.

Descending pain pathway: When not inhibited neurons from the periaqueductal grey matter will travel down to the nucleus raphe magnus and synapse with a second order neuron.
The 2nd order neuron is a serotonin noradrenergic neuron which travels to the dorsal horn of the spinal cord.
This 2nd order neuron then works to control pain signals travelling to the brain via interacting with the synapse between the 1st and 2nd order neuron of the corticospinal tract

18
Q

What are the diagnostic tests for a spinal cord injury?

A
  • Myelogram- X-ray after dye is injected
  • Somatosensory evoked potential (SSEP)- tests if nerve signals can pass through the spinal cord
  • MRI
  • CT- interpedicular widening with retropulsion of bony fragments
  • Neurological exam
  • Abdominal exam
19
Q

What is the frailty scale?

A
  • CFS is used in patients over 65 to screen for frailty
  • A score from 1 (very fit) to 9 (terminally ill) is given based on the descriptions and pictures
  • Score 5 often referral to geriatric or frailty specialists.
  • The Clinical Frailty Scale focuses on items that can be observed without specialist training, including mobility,balance, use ofwalking aids, and the abilities to eat, dress, shop, cook, and bank.
  • Scoring should match the description, and should not be based solely on the pictures that accompany each level. Visual subjective tool
  • It provides a standardised way of healthcare workers to communicate a person’s frailty status
20
Q

What is neurogenic shock? How is it identified and treat?

A
  • SC injury (fractures or dislocations) affecting cervical and upper thoracic segments which disrupts descending sympathetic tracts → shuts down NS so loss of innervation to BV
  • Increase in vascular capacity as loss of vasomotor tone throughout the body resulting in dilation of BV → neurogenic shock
  • Consequence in arteries = shock as there is decreased oxygen delivery to the organs – hypoperfusion
  • In veins = pooling of blood in veins, affecting CO of heart as less venous return
  • By not maintaining vascular tone, effectively shutting down CV system
21
Q

How does a spinal cord lesion impact the micturition reflex?

A
  • Controlled by autonomic NS and is inhibited or facilitated by higher centres in the brain. Pons contains the micturition centre
  • When our bladder is empty:
  • Dominated by sympathetic NS - relax detrusor muscle and voluntary action to contract the external sphincter
  • Parasympathetic NS is inhibited by higher brain centres
  • Allows for urine retention
  • When our bladder is full:
  • Dominated by parasympathetic NS - inhibition by pons micturition centre is relieved
  • Higher brain centre will still control voluntary action of external sphincter so we are not voiding urine whenever
  • If the injury is above the sacral region, spinal reflexes do begin to return after shock has worn off. Pons cannot signal to inhibit parasympathetic NS so cannot control bladder emptying – this leads to bladder spasming
  • Injuries at the site of the sacral region, spinal reflexes have been severed and this will lead to urinary retention as bladder will keep filling up and relaxing
22
Q

What are hospital acquired infections?

A
23
Q

What are the causes and risk factors of UTIs?

A
24
Q

What are the clinical findings of UTIs and LUTIs?

A
25
Q

What are the diagnostic tests for a UTI?

A
26
Q

What is the treatment and management for a spinal cord injury?

A
  • Immobilisation with collars and boards
  • Thoracolumbar-lumbar sacral orthosis
  • Neurological decompression
  • Spinal fusion
  • Spinal fixation
27
Q

Why is creatinine clearance and serum gentamicin measured whilst taking gentamicin

A
28
Q

What is the corticospinal tract?

A
  • Motor commands
  • Upper motor axons (from UMNs in layer 5 – neocortex has 6 layers – of M1)
  • ~85% of axons decussate at the caudal medulla (pyramidal decussation)
  • Project through the lateral funiculus
29
Q

What is the dorsal column medial lemiscus (DCML) tract?

A
  • Touch and proprioceptive info
  • DC projects to dorsal column nuclei (cuneate and gracile)
  • DCN neurons decussate and project through medialleminiscusto thalamus
  • Information interpreted in S1
30
Q

What is the spinothalamic tract?

A
  • Pain and temperature info
  • Immediate synaptic connection to 2nd order neuron (substantia
    gelatinosa and/or nucleus proprius and/or layer 5)
  • Projection neuron decussates at that level
  • Thalamus to S1