Neurological Lesions

Question 1

What happens to the sphincter and bladder during storage/filling and voiding?

Answer 1

(1. ) During filling and storage (99%):
- Symp NS causes bladder detrusor relaxation and sphincter contraction
- Bladder fullness increases, messages to the pons and higher centres to consider voiding
- Can be postponed (i.e. guarding reflex) until it is convenient

(2. ) During voiding:
- PMC co-ordinates voiding via parasymp
- causes bladder detrusor contraction and sphincter relaxation at the same time
- promotes micturation, voiding

Question 2

Describe the Nervous Control of bladder and sphincter

Answer 2

1-3 are involuntary control

(1. ) Parasymp & Ach
- Causes bladder detrusor to contract
- Promotes micturition

(2. ) Symp & NA
- hypogastic nerve T11-L2
- Causes bladder detrusor to relax
- Prevents micturition

(3. ) Somatic Nerve & Ach
- pudenadal nerve S2-4
- Pudenadal Stimulation = Sphincter contracts –> storage
- Pudenadal Inhibition = Sphincter relaxes –> micturition

(4. ) Sensory afferent pelvic nerve
- Transmits info to cerebral cortex
- info about urothelium (such as sphincter tone and detrusor contraction) goes to PMC & PAG then cortex.

Question 3

What kind of spinal cord injury would you get if the lesion was ABOVE or BELOW conus medullaris ?

Answer 3

(1. ) Above conus medullaris = Spastic SC injury

(2. ) Below conus medullaris = Flaccid SC injury

Question 4

Spastic Spinal Cord Injury

Answer 4

Injury above conus medullaris

(1. ) Spasticity is a form of muscle overactivity that occurs when communication between brain & SC is disrupted by injury.
(2. ) This may cause pain, fatigue and other problems.
(3. ) Coordination is lost between bladder, pons, sphincter, bladder trying to excrete urine but sphincter is contracting –> inc bladder pressure

(4. ) Key features:
- Reflex bladder contractions
- Detrusor sphincter dyssynergia
- Poorly sustained bladder contraction

Question 5

Flaccid Spinal cord injury

Answer 5

Injury is below conus medullaris

• Damage to S2-4
• Lost reflex bladder contraction
• Lost guarding reflex
• Lost Receptive relaxation

Features

• Areflexic bladder (does not respond to stimuli)
• Stress incontinence
• Risk of poor compliance

Effect

• Potentially unsafe
• detrusor leak point pressure (DLPP), poor compliance

Question 6

Pathophysiology of Autonomic Dysreflexia?

Answer 6

(1. ) Condition that emerges after SC injury above T6 level
(2. ) Leads to an uncoordinated autonomic response
(3. ) Brain is unaware of its disconnection from SC, so will be unaware of noxious stimulis such as UTI, distended/full bladder, or blocking of catheter
(4. ) H/e cutaneous or visceral stimulation below injury can still be stimulated and cause activation of symp NS in reesponse to stimuli. This leads to vasoconstriction and rise BP
(5. ) There is NO normal compensatory parasymp response travelling below injury so vasoconstriction continues leading to HTN.

Question 7

Sx of Autonomic Dysreflexia?

Answer 7

Over-activation of Symp NS

1. severe HTN
2. severe headache
3. Profuse diaphoresis/sweating (above level of injury)
4. Flushing (above level of injury)
5. Dry and pale skin (vasoconstriction below level of injury)
6. Visual disturbances
7. Nasal stuffiness
8. Anxiety or feelings of doom
9. Nausea and vomiting

NOTE: combination of high BP and cerebral vasodilation put pt at high risk for haemorrhagic stroke, this can be life threatening

Question 8

Mx of Autonomic Dysreflexia?

Answer 8

1. Remove painful stimuli e.g.:
   - Drainage: if distended bladder or bowel
   - Removal of indwelling catheter
2. Monitor vital signs
3. HTN corrected
   - use agents that have a rapid onset but short duration of action