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Neurophysiology > Lecture 23- Spinal injury > Flashcards

Lecture 23- Spinal injury Flashcards

1
Q

What are the disturbances that arise from spinal cord injury (SCI)?

A
  • Loss of ability to control bowel function
  • Paradoxical nocturnal hypertension resulting in nocturnal diuresis
  • Hypotensive episodes on moving to an upright position
  • Paroxysmal hypertensive episodes (blood pressure goes up instead of down, large excursions of blood pressure that cannot be control)
  • Autonomic Dysreflexia
  • Persistent, abnormal and recurrent urinary tract infection
  • Loss of urinary continence
  • Loss of sexual function
  • (Sleep apnea and disturbed sleep)
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2
Q

What is the main cause of morbidity in people with SCIs?

A

-Autonomic dysfunctions represent the primary causes of morbidity and mortality following SCI

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3
Q

Where are the autonomic control centres and what happens when SCI occurs?

A
  • in the spinal cord are disconnected from the medulla, pons and cortex
  • most of the injuries around the neck
  • young men, drive too fast etc. 18-25
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4
Q

How common is bowel dysfunction following and SCI?

A
  • 86% of people with SCI have problems with bowel control
  • The daily problem has two parts:
  • The bowel cannot be emptied at will – the person is constipated

And

  • If there are feces in the bowel they can and will be released spontaneously -they cannot control when the bowl is emptied and then overflows and is released spontaneously
  • If the bowel could be emptied in the morning the patient could go about daily life without there being a reservoir of feces threatening to be released
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5
Q

What are the defecation circuits?

A
  • you can control defecation consciously through cortical control
  • lower brain stem
  • two pathways= inhibiting and facilitating pathways= similar to bladder control
  • these pathways impinge on the defecation centre lumbarsacral spinal region L5-S2
  • few people have injuries at that levels so most people have that damaged
  • ghrelin receptors function there -then through pelvic nerves and into the enetric reflex pathways
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6
Q

What is ghrelin?

A
  • Ghrelin is a 28 Amino-acid Octanoylated peptide
  • The largest source of Ghrelin is the stomach
  • Plasma ghrelin increases with time after a meal and drops quickly after meal ingestion
  • Its best established roles are stimulation of eating and promotion of growth hormone release
  • It has been recently discovered that ghrelin activates some autonomic preganglionic neurons
  • Ghrelin receptor agonists stimulate the spinal cord defecation centre
  • it is a hormone
  • stimulates apetite, hunger hormone= more of it= hungry
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7
Q

What is the effect of the ghrelin receptor agonist, CP464709, on fecal pellet output in the conscious rat?

A

-put ghrelin in and makes them shit

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8
Q

Does the ghrelin receptor agonist act in the central nervous system?

A
  • The ghrelin receptor agonist acts in the central nervous system
  • Effect of cutting the spinal nerves between the lumbo-sacral cord and the colorectum on the effect of the ghrelin receptor agonist
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9
Q

What prevents the effect of ghrelin agonist?

A

-Effect of the ghrelin receptor agonist is prevented by blocking autonomic ganglia with hexamethonium (C6)

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10
Q

Where are the ghrelin receptors located?

A
  • in the interomediolateral column
  • in the interomediolateral column that is where the Grelin receptors are
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11
Q

What are the sites of ghrelin agonist activity?

A

-

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12
Q

How do you prove the theoretical principle?

A
  • create SCI in rats and test the effects
  • Conclusion: The spinal lesion removed autonomic descending inputs to vasoconstrictor pathways
  • confirmation of lesion effect: cardiovascular changes after SCI
  • The spinal lesion removed autonomic descending inputs to vasoconstrictor pathways
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13
Q

Is the ghrelin receptor agonist effective after CSI in the rat?

A

-yes

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14
Q

What is the human trial with ghrelin?

A
  • Following animal proof of principle
  • The Human Trial: Conducted at Austin Health Open label, ascending dose trial to determine safety and drug handling/ availability in people living with SCI, compared to uninjured controls
  • Limited dose range and confined to paraplegics to assure safety
  • 6 people with SCI, 10 uninjured controls
  • Pharmacokinetic profile – 30 min to 12 h. Follow up at 4 weeks
  • Monitor blood pressure, heart rate, temperature, fecal output
  • 12 lead ECG
  • Full blood and urine analysis
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15
Q

How did the human trial go?

A
  • Summary: No adverse effects
  • Body Temperature and pulse rate -No changes
  • Electrocardiogram: No events
  • Blood: No evidence of any changes in blood cells, blood chemistry or liver function
  • Urine: No changes
  • Physical examination: No change
  • Defecation Time to defecation after capromorelin: 89 +/- 32 min (mean, standard deviation)
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16
Q

What are the cardiovascular issues in SCIs?

A
  • Circulatory disorders account for 40% of deaths in SCI
  • Nocturnal hypertension
  • Postural hypotension
  • Autonomic dysreflexia
  • Premature cardiovascular disease
  • Renal dysfunction
  • Many SCI patients experience paradoxical nocturnal hypertension and suffer from postural hypotension on rising. Nocturnal hypertension causes nocturnal diuresis. Instead of passing
17
Q

What is blood pressure like in an SCI person?

A
  • in a normal person the blood pressure drops at night but with SCI the sleep activated pathways are not there so the blood pressure goes up when they go to sleep = autostatic hypertension
  • Severe hypotensive maladjustment on rising in SCI
  • in normal person the barorceptors drive the pathways to constrict the blood veins and blood pressure is maintained = this makes them pee much more during the night
18
Q

What is autonomic dysreflexia?

A
  • Dysreflexia in spinal cord injury: Exaggerated Psuedo-affective reflex (Autonomic Dysreflexia)
  • eg. go on a nail= pressure goes up but then down regulated
19
Q

What are the circuits for dysreflexia?

A

-autostatic hypotension= lowering of blood pressure when stand up

20
Q

Summary cardiovascular:

A
  • Many people living with SCI have reversed diurnal variation of blood pressure & also have nocturnal diuresis
  • Pharmacological reduction of nocturnal blood pressure reduces the nocturnal diuresis and stops fainting in the morning
  • Orthostatic blood pressure changes in autonomic dysfunction are probably caused by volume depletion
  • Paradoxical blood pressure changes may be linked to poor sleep and sleep apnea
  • People with SCI suffer from exaggerated, dangerous phasic blood pressure increase, autonomic dysreflexia
21
Q

What are the causes of rehospitalisation after spinal cord injury?

A

-

22
Q

How is the bladder affected by the SCI?

A
  • The barrier function of the urothelium is impaired following spinal cord injury in a rat model
  • the bladder becomes leaky after SCI
  • disrupts the lining of the bladder, not clear why and how but is autonomically innervated
  • above injury= rise in blood flow if injured, and flare response but this is lost below the injury site
23
Q

What helps with the epithelial damage to the bladder post SCI?

A
  • Autonomic (efferent) blockade reduces damage to the urothelium
  • Hexamethonium relieves
  • Ablating the peptidergic afferent fibres with capsaicin exacerbates damage to the urothelium
24
Q

How is blood flow connected to the bladder issues post SCI?

A

-Axon reflex evoked vasodilation is reduced below the lesion in SCI subjects: Poor blood flow control could contribute to problems

25
Q

Conclusions:

A
  • Injury to the spinal cord causes autonomic dysfunction because the spinal autonomic reflex centres are disconnected from the medulla, pons and cerebral cortex
  • We now have clues to solving: • Loss of ability to control bowel function • Paradoxical nocturnal hypertension resulting in nocturnal diuresis • Hypotensive episodes on moving to an upright position
  • More work is required to deal with • Paroxysmal hypertensive episodes – Autonomic Dysreflexia • Persistent, abnormal and recurrent urinary tract infection • Loss of urinary continence • Loss of sexual function
26
Q

What are the purposes of the ANS?

A
  • The ANS adjusts the activities of organs and tissues that are not under overt voluntary control so that they operate at levels most favorable to the states of the body and environment.
  • The idea that the sympathetic and parasympathetic divisions are somehow in opposition to each other is not true.
  • More closely aligned with reality is the concept that there exist function-specific autonomic pathways, that are (largely) independently involved in control of specific organs and tissues
  • The ANS has associated afferent neurons, e.g. baroreceptor afferents

Neurophysiology (33 decks)

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