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Neurology SB > Chronic Pain and Head Injury > Flashcards

Chronic Pain and Head Injury Flashcards

1
Q

what is nociceptive pain

A

an appropriate physiological response to painful stimuli via an intact nervous system

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2
Q

what is neuropathic pain

A

an inappropriate response caused by a dysfunction in the nervous system

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3
Q

what is allodynia

A

pain from a stimulus that is not normally painful e.g. cotton wool

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4
Q

what is hyperalgesia

A

more pain than expected from a painful stimulus e.g. pin prick

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5
Q

what are common causes of neuropathic pain

A 
shingles 
surgery
trauma
diabetic neuropathy 
amputation
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6
Q

what is the mode of action of NSAIDS

A

inhibition of COX

prostaglandin synthesis decrease

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7
Q

SE of NSAIDs

A

GI irritation/bleeding
Renal toxicity
Potential drug-drug interactions
CV side effects

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8
Q

SE of opioids

A 
N + V
Constipation 
Dizziness or vertigo 
Dry skin/pruritus 
Drowsiness
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9
Q

SE of TCAs (e.g. amytriptyline)

A 
Constipation
Dry mouth
Drowsiness
Arrhythmia 
Insomnia 
Increased appetite
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10
Q

examples of anticonvulsants

A

carbamazepine
gabapentin
pregabalin

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11
Q

SE of anticonvulsants

A 
sedation
dizziness
ataxia
peripheral oedema
nausea
weight gain
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12
Q

SE of SNRIs

A 
Dry mouth 
Increased sweating 
Loss of appetites
N + V
Constipation
Drowsiness
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13
Q

what are the 3 forms of pain

A

nociceptive (acute) pain
inflammatory (prolonged) pain
pathological (neurogenic) pain

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14
Q

what are the characteristic of pain in the skin

A

Well localised

- Pricking, Stabbing, Burning

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15
Q

what are the characteristic of pain in the muscle

A

Poorly localised

- Aching, Soreness/ tenderness, cramping, stabbing, burning

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16
Q

what are the characteristic of pain in the viscera

A 
Poorly localised (often referred to a somatic structure)
- Dullness, Vagueness, Fullness, Nausea
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17
Q

how is pain relayed in nociceptive pain

A
  • intense stimuli
  • release of neurotransmitters that excite second order neurones in the CNS
  • Depolarization due to noxious stimulus elicits action potentials that propagate to the CNS
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18
Q

what are the first order neurones in nociceptive pain pathway

A

nociceptors

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19
Q

what are the 2 types of fibres in nociceptors

A

Aδ-fibres

C-fibres

20
Q

what are the features of Aδ-fibres

A
  • mechanical/thermal nociceptors
  • thinly myelinated
  • respond to noxious mechanical and thermal stimuli.
  • Mediate ‘first’, or fast, pain
21
Q

what are the features of C fibres

A
  • nociceptors that are unmyelinated
  • respond to all noxious stimuli (i.e. they are polymodal)
  • Mediate ‘second’, or slow, pain
22
Q

are all Aδ-fibres and C-fibres nociceptors

23
Q

where is the major site of protein synthesis on a neurone

24
Q

where is the site of calcium dependent transmitter release

A

central terminal

25
what is the pathway of neurotransmission between the primary afferent and second order neurones
- AP - opening of voltage gated calcium channels - calcium influx - glutamate release - activation of glutamate receptors - Membrane depolarization (e.p.s.p.) - opening of voltage gated sodium channels - AP
26
what are the 2 distinct processes of the nociceptive pathway following tissue damage
- peripheral sensitisation | - central sensitisation
27
what mediates peripheral sensitisation and what does it cause
- nociceptors at the site of injury/tissue inflammation | - primary hyperalgesia
28
what does central sensitisation reflect and what does it cause
- increase in CNS neurone activity and properties | - Causes secondary hyperalgesia and allodynia
29
how does viscerosomatic pain present
sharp | well localised
30
what are the spinal nociceptive tracts
The spinothalamic tract (STT) | The spinoreticular tract (SRT)
31
what is the pathophysiology of what happens after a head injury
- release of excitatory amino acids e.g. glutamate - binding to receptors e.g. NMDA - release of intracellular calcium, cell swelling, activation of apoptosis
32
how does secondary brain injury occur
Loss of blood-brain-barrier, leucocyte infiltration = inflammation Loss of cerebral autoregulation of blood pressure = ischaemia Loss of cerebral autoregulation of blood flow = metabolic de-coupling = more ischaemia and oedema
33
what is the Monro-Kellie hypothesis
skull consists of brain, blood and CSF An increase in volume of one component must produce a decrease in another component otherwise the ICP will rise
34
how is cerebral perfusion pressure calculated
CPP = MAP - ICP Mean arterial pressure Intracranial pressure
35
what has a major influence on CPP
hypotension
36
what is the ideal CPP after head injury
> 60mmHg i.e MAP >80mmHg and ICP <20mmHg
37
what is a normal adults ICP
9-11mmHg
38
what are the 2 types of skull base fractures
anterior cranial fossa fracture posterior cranial fossa fracture
39
what is the physical sign of an anterior cranial fossa fracture
“raccoon” or “panda eyes”
40
what is the physical sign of an posterior cranial fossa fracture or what other type of fracture
“Battle sign” over mastoid area basilar skull fracture
41
what is the definition of a coma
Do not open eyes Do not obey commands Do not speak equates to GCS sum of 8 or less
42
what kills patients with head injuries
hypoxia hypotension raised ICP
43
when should you request CT head scan in trauma
skull fracture GCS < 15 focal neurological signs on anti-coagulants e.g. warfarin
44
what are the types of traumatic intracranial bleeding (going from outside to inside)
``` Extradural haematoma Subdural haematoma Traumatic subarachnoid haemorrhage Intracerebral contusion Intracerebral haematoma Intraventricular haemorrhage ```
45
what is a Decompressive craniectomy
surgical removal of part of the skull to allow a swelling brain room to expand without being squeezed
46
what are late effects of head injury
epilepsy - seen early, in first 2 weeks CSF leak - into nose or middle ear Cognitive problems - post-concussion syndrome
47
what is post-concussion syndrome
poor concentration headache poor memory lethargy

Neurology SB (23 decks)

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