Chronic Pain and Head Injury Flashcards
what is nociceptive pain
an appropriate physiological response to painful stimuli via an intact nervous system
what is neuropathic pain
an inappropriate response caused by a dysfunction in the nervous system
what is allodynia
pain from a stimulus that is not normally painful e.g. cotton wool
what is hyperalgesia
more pain than expected from a painful stimulus e.g. pin prick
what are common causes of neuropathic pain
shingles surgery trauma diabetic neuropathy amputation
what is the mode of action of NSAIDS
inhibition of COX
prostaglandin synthesis decrease
SE of NSAIDs
GI irritation/bleeding
Renal toxicity
Potential drug-drug interactions
CV side effects
SE of opioids
N + V Constipation Dizziness or vertigo Dry skin/pruritus Drowsiness
SE of TCAs (e.g. amytriptyline)
Constipation Dry mouth Drowsiness Arrhythmia Insomnia Increased appetite
examples of anticonvulsants
carbamazepine
gabapentin
pregabalin
SE of anticonvulsants
sedation dizziness ataxia peripheral oedema nausea weight gain
SE of SNRIs
Dry mouth Increased sweating Loss of appetites N + V Constipation Drowsiness
what are the 3 forms of pain
nociceptive (acute) pain
inflammatory (prolonged) pain
pathological (neurogenic) pain
what are the characteristic of pain in the skin
Well localised
- Pricking, Stabbing, Burning
what are the characteristic of pain in the muscle
Poorly localised
- Aching, Soreness/ tenderness, cramping, stabbing, burning
what are the characteristic of pain in the viscera
Poorly localised (often referred to a somatic structure) - Dullness, Vagueness, Fullness, Nausea
how is pain relayed in nociceptive pain
- 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
what are the first order neurones in nociceptive pain pathway
nociceptors
what are the 2 types of fibres in nociceptors
Aδ-fibres
C-fibres
what are the features of Aδ-fibres
- mechanical/thermal nociceptors
- thinly myelinated
- respond to noxious mechanical and thermal stimuli.
- Mediate ‘first’, or fast, pain
what are the features of C fibres
- nociceptors that are unmyelinated
- respond to all noxious stimuli (i.e. they are polymodal)
- Mediate ‘second’, or slow, pain
are all Aδ-fibres and C-fibres nociceptors
No
where is the major site of protein synthesis on a neurone
soma
where is the site of calcium dependent transmitter release
central terminal
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
what are the 2 distinct processes of the nociceptive pathway following tissue damage
- peripheral sensitisation
- central sensitisation
what mediates peripheral sensitisation and what does it cause
- nociceptors at the site of injury/tissue inflammation
- primary hyperalgesia
what does central sensitisation reflect and what does it cause
- increase in CNS neurone activity and properties
- Causes secondary hyperalgesia and allodynia
how does viscerosomatic pain present
sharp
well localised
what are the spinal nociceptive tracts
The spinothalamic tract (STT)
The spinoreticular tract (SRT)
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
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
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
how is cerebral perfusion pressure calculated
CPP = MAP - ICP
Mean arterial pressure
Intracranial pressure
what has a major influence on CPP
hypotension
what is the ideal CPP after head injury
> 60mmHg
i.e MAP >80mmHg and ICP <20mmHg
what is a normal adults ICP
9-11mmHg
what are the 2 types of skull base fractures
anterior cranial fossa fracture
posterior cranial fossa fracture
what is the physical sign of an anterior cranial fossa fracture
“raccoon” or “panda eyes”
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
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
what kills patients with head injuries
hypoxia
hypotension
raised ICP
when should you request CT head scan in trauma
skull fracture
GCS < 15
focal neurological signs
on anti-coagulants e.g. warfarin
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
what is a Decompressive craniectomy
surgical removal of part of the skull to allow a swelling brain room to expand without being squeezed
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
what is post-concussion syndrome
poor concentration
headache
poor memory
lethargy
