Sensory Flashcards
What is acute pain?
The normal, predicted physiological response to an adverse chemical, thermal, or mechanical stimulus associated with surgery, trauma, and acute illness
Time-limited
Responsive to therapy
What is pain?
An unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage
What is chronic pain?
A pain state which is persistent and in which the cause of the pain cannot always be removed or is difficult to treat
May be associated with a long term incurable or intractable medical condition or disease
What is nociceptive pain?
Arises from the stimulation of specific pain receptors. These receptors can respond to heat, cold, vibration, stretch and chemical stimuli
released from damaged cells
What is neuropathic pain?
Arises from within the peripheral and central nervous system. Specific receptors do not exist here, with pain generated by nerve cell injury
What is wind up?
Frequency dependent increase in excitability due to activity of c fibers
What can be causes of chronic pain?
Badly Managed Acute Pain Emotionally Sensitive Patient Poor Coping Skills Previous Bad Pain Experiences Pain Goes on For Longer Surgical Complications Genetic Predisposition
What model is used to understand chronic pain?
Biopsychosocial model
Name some somatic nociceptive pain conditions
Lower back pain
Myofascial pain
Arthritis
Name some visceral nociceptive pain conditions
Pancreatitis
interstitial cystitis
endometriosis
Functional pain syndrome
Name some neuropathic pain conditions
Post-herpetic neuralgia (shingles) Neuroma Radicular pain (nerve root irritation) CRPS - complex regional pain syndrome Post-amputation pain
Describe malignant pain
80% of cancer patients suffer from pain Psychological component substantial Multiple etiologies Iatrogenic – CT, RT Other psychosocial factors
What are non pharmacological management options for pain?
Exercise
Physiotherapy
What is complementary therapy for pain?
Acupuncture
TENS - transcutaneous electrical nerve stimulation
Describe the WHO analgesia ladder
Mild to moderate pain - non opioids, NSAIDs, aspirin, paracetamol
Moderate to severe pain - mild opioids eg codeine with or without non opioids
Severe pain - strong opioids eg morphine with or without non opioids
What drugs can act as adjuncts to treating pain?
Anticonvulsants - gabapentin, pregabalin
Antidepressants - amytryptaline
Lidocaine
Baclofen, benzodiazepines
What is the gold standard for cancer pain management?
Opioids
Describe why opioids should be used with caution to treat chronic pain
Can do more harm than good
Addictive properties
Side effects - constipation etc
Opioid induced hyperalgesia from high dose chronic use
Should be used only for functional rehabilitation
What invasive procedures can be used in chronic pain?
Injections: needle techniques to reduce pain in muscle, tendons and joints to reduce inflammation around nerves e.g. trigger point injections, joint injections, acupuncture, epidural steroids
Ablative procedures:permanently interrupt nervous system activity. Chemical: alcohol, phenol Physical: radiofrequency denervation, cryoneurolysis. Used mainly in terminal cancer patients
Implants: continuous catheter techniques, peripheral nerve stimulators
neuromodulations e.g. intrathecal drug delivery, spinal cord stimulators
Nerve blocks: Neuroaxial (epidural, intrathecal), Axial (paravertebral, nerve roots), Peripheral (intercostal, suprascapular, ilioinguinal, upper and lower extremity blocks) Autonomic: stellate ganglion, lumbar sympathetic chain
What types of sensory receptor exist?
Free nerve endings - pain and temp
Pacinian corpuscles - mechanoreceptors, deep pressure
Meissner corpuscles - discriminative touch
Muscle spindles - muscle stretch
Merkel cells and disk - light touch
Ruffini ending - touch
What type of adaptation does the discriminative touch modality undergo?
Fast adaptation
What is located in the post central gyrus?
Primary sensory cortex
Receives contralateral sensory input from the body (inc taste)
What is located in the superior parietal lobule?
Integration of sensory inputs, sensory memory, perception of contralateral self & world
What is the internal capsule?
Dense collection of sensory and motor tracts passing to/from the cortex
What is the corona radiata?
White matter sheet that continues ventrally as the internal capsule and dorsally as the semioval center. Contains both descending and ascending axons that carry nearly all of the neural traffic from and to the cerebral cortex
Associated with the corticospinal tract, the corticopontine tract, and the corticobulbar tract
Describe the structure of the internal capsule
Anterior limb – frontopontine, frontothalamic
Genu - bend
Posterior
Retrolenticular
Head, arm, leg, sensory, vision and hearing arranged somatotopically
How many neurons are involved from sensation up to the cortex?
3
1st order - Ascend ipsilaterally to nuclei in the medulla
2nd order - Decussate and ascendto thalamus via a lemniscus
3rd order - Ascend to cortex via internal capsule
How many Rexed lamina are there?
10
What is a funiculi? And how many are there in the spinal cord?
Bundles of more than 1 tract 3 Dorsal Lateral Ventral
What sensory modalities are carried in the dorsal funiculus?
Fine touch and proprioception from lower body
What modality tracts are carried in the lateral funiculus?
Motor supply to ipsilateral body
What sensory modalities are carried in the ventral funiculus?
Pain and temperature
What sensory modalities are carried by the dorsal column tracts?
Discriminative touch, vibration & conscious proprioception
What are the two parts of the dorsal column tracts?
Fasciculus cuneatus - above ~T6
Fasciculus gracilis - below ~T6
Describe the path that the dorsal columns follow
1st order neurons pass into dorsal cord and ascends ipsilaterally to lower medulla where they synapse with 2nd order neuron at nucleus cuneatus or gracilis
2nd order neurons decussate and ascend to ventral posterior nucleus of thalamus & synapse with 3rd order neurons
3rd order neurons travel to primary sensory cortex
What sensory dysfunction can tertiary syphilis result in?
Tabes dorsalis
Destruction of dorsal columns
What does dorsal column damage cause?
Loss of fine touch, vibration and conscious proprioception below level of lesion ispilateral in cord damage
Sensory ataxia – leads to positive Romberg sign (requires vision to stand steady) & stamping gait
Pseudoathetosis – writhing of digits, hands and feet
What sensory modalities are carried by the spinothalamic tract?
Pain, temperature and simple tactile sensation
Describe the pathway of the spinothalamic tract
1st order neurons ascend 1-2 vertebral level in dorsal grey matter before synapsing with 2nd order neurons which decussate via the anterior white commissure
2nd order neurons ascend spinothalamic tract to ventral posterior lateral nucleus of thalamus via spinal lemniscus and synapse with 3rd order neurons
3rd order neurons travel to primary sensory cortex
What is the trigeminal lemniscus?
Carries pain and temperature sensation from to the ventral posterior medial nucleus of the thalamus
What disorder can lead to disruption of the spinothalamic tract?
Syringomyelia - cavitation/expansion of central canal in cervical region Pain and temperature sensation lost in arms and top of chest
What is sacral sparing?
An expanding ventral grey matter tumour can knock out all contralateral pain & temperature sensation except sacral region due to somatotopic organisation of spinothalamic tract
What sensory modalities are carried in the spinocerebellar tract?
Unconscious proprioception to the ipsilateral cerebellum
Dorsal spinocerebellar tract - Muscle spindles, few Golgi tendon organs
Ventral spinocerebellar tract - Golgi tendon organs
Describe the pathway followed by the dorsal spinocerebellar tracts
Lower limb - Clarke’s dorsal nucleus, Sits between C8-L3 1st & 2nd order dorsal spinocerebellar neurons synapse here! Damaged in Freidrich’s ataxia. 2nd order neuron ascends ipsilaterally and passes directly to cerebellum
Upper limb - muscle spindle information passes through the cuneocerebellar tract (runs with fasciculus cuneatus). 1st order neuron ascends to medulla then synapses with 2nd order which goes to cerebellum
Describe the pathway followed by the ventral spinocerebellar tracts
Lower limb - 1st order neuron synapses with 2nd order which then decussates and ascends contralaterally before decussating again and entering cerebellum
Upper limb - Golgi tendon information passes through the rostral spinocerebellar tract. 1st order neurons synapse with second order which then enter the cerebellum ipsilateral
What information is carried by the ventral spinocerebellar tract?
Stretch of the tendon at the muscle tendon interface of the lower limb
What do pure lesions of the spinocerebellar tract cause?
Ataxia / malcoordination of motor action
Wide-based gait
Symptoms normally masked by motor weakness/paralysis
Describe the route of cranial nerve sensory nuclei
Send neurons along a route similar to sensory neurons of the body
Most sensory fibres decussate on route to contralateral thalamus
Fibres run from thalamus to primary sensory cortex
Most nociception from CN VII, IX, X passes via CN V’s sensory nucleus
Describe where trigeminal touch sensation fibres pass
contralateral thalamus via the trigeminal lemniscus
1st order trigeminal nerve sensory neurons synapse in CN V nucleus
2nd order neurons ascend in trigeminal lemniscus to ventral posterior medial nucleus of the thalamus
3rd order neurons pass to primary sensory cortex
What sensory losses would result from a brainstem lesion?
Ipsilateral facial
Contralateral body
What are the thalami?
organised collection of nuclei of sensory, visual, auditory and motor-associated functions
Where do muscle spindle sensory fibres run?
Dorsal column & spinocerebellar pathways
Which afferent neurons carry sensation from muscle spindles?
1a afferents
What is nociceptive pain sensed by?
Free ending on C- and Aδ- fibres
Describe the gate control theory of pain
Input from pain fibres activates 2nd order cells and inhibit local interneurons in substantia gelatinosa
Pain signal travels onwards
Mechanical stimulation activates inhibitory interneurons
Reduces pain transmission by inhibiting 2nd order cells
Descending control can also increase activity of these interneurons
Where are the main output to descending tracts from higher pain centres?
Hypothalamus, periaqueductal gray and brainstem nuclei
Descending inhibition travels to ANS and spinal lamina in dorsolateral
funiculus where 5HT and NA dominant
What drugs are used to treat neuropathic pain?
Tricyclic antidepressants and anti epileptic drugs
Gabapentin+Amitriptyline in combo
Carbemazepine alone - never in combo
How many subclasses of NSAIDs are there?
6
Describe the mechanism of action of NSAIDs as painkillers
Cyclooxygenases break down arachidonic acid to give prostaglandins
NSAIDs Block production of prostaglandins by inhibiting COX enzymes
Three forms of COX: COX 1 – Normal cell function, COX 2 - Inflammation, COX 3 - Fever
How do prostaglandins lead to increased pain?
Act on prostaglandin receptor which is GPCR which leads to opening of voltage gated Na channels and therefore increased depolarisation of nociceptors
What are clinical uses of NSAIDs?
Anti-inflammation Anti-pyretic Analgesic Anti-coagulant May delay healing, not used post operatively, post partum
Describe some commonly used NSAIDs
Aspirin (CV drug)
Ibuprofen (weak action)
Naproxen (strong, low side-effects)
Diclofenac (similar to Naproxen, CV problems)
Indomethacin (strong, high side effects)
COX-2 Inhibitors: Celecoxib, Etoricoxib, Parecoxib (similar to naproxen, lower GI effects)
Paracetamol - antipyretic as COX 3i
List some common side effects of NSAIDs
GI problems: vomitting, nausea, diarrhoea, bleeding/ulceration
CV incidents: thrombosis
Headache: drug induced headache
Dizziness, Insomnia, Nervousness, Depression, Vertigo,
Tinnitus: sign of toxic state, reduce dose quickly
Photosensitivity, Renal Impairment, Hypertension
Hypersensitivity: skin rashes and eruptions, angioedema,
bronchospasm
Reye’s syndrome in under 16s - fatty deposits in liver and brain
Which drugs can interact with NSAIDs?
Avoid concomitant use of oral NSAIDs
Antidepressants: increased risk of bleeding with SSRIs (e.g. fluoxetine, paroxetine) and venlafaxine
Increased risk of nephrotoxicity with ACE inhibitors and diuretics and also with drugs used for arthritic/skin conditions, e.g. ciclosporin
NSAID can enhance the anti-coagulant effects of many drugs used for CV disorders (e.g. warfarins, heparins and can antagonise the hypotensive effects, e.g when used with alpha and beta-blockers and nitrates
What is salicylism?
Salicylate toxicity may occur with high dose acute or chronic ingestion of NSAIDs (1% mortalilty)
Severe toxicity:
Auditory (ototoxicity, tinnitus, deafness)
Pulmonary (apnoea, aspiration pneumonitis, pulmonary oedema,
alkylosis, respiratory arrest)
Cardiovascular (tachycardia,hypotension, asystole, dysrhythmias)
CNS (depression, seizure, encephalopathy, delirium, hallucinations)
GI (pancreatitis, hepatitis (rare in acute cases))
Renal Failure
Coma
Chronic intoxication where plasma levels > 300mg/kg: Fluid replacement, Haemodialysis, Activated charcoal, Lorazepam/diazepam i.v. for seizures
What are the 4 main groups of synthetic derivatives of opioids?
Phenylpiperidine series (e.g. pethidine) Methadone series (e.g. dextropropoxyphene) Benzomorphan series (e.g. cyclazocine) Thebaine derivatives (e.g. buprenorphine)
What are pure agonist opioids?
Full agonist activity, may have strong (e.g. morphine, diamorphine,
tramadol) or weak activity (e.g. codeine, dihydrocodeine)
What are partial opioid agonists?
Can be used for addiction rehabilitation
e.g. nalorphine, pentazocine, buprenorphine
What are opioid antagonists?
Used in overdose
e.g.naloxone, naltrexone
What are clinical uses of opioids?
Analgesia – chronic and acute
Anaesthesia (Alfentanil, Fentanil, Remifentanil)
Antitussive (Phlocodine, Dextromethorphan)
Antidiarrhoeal (codeine, loperamide)
Coronary Care (pre-surgical, surgical and post)
Cancer Care (Morphine, Diamorphine, Oxycodone)
Where are sites of opioid action?
Peri aqueductal gray
Nucleus Raphe Paragigantocellularis in medulla
Dorsal horn
Periphery
Describe the mechanism for opioid drugs
Decrease neuronal transmission by:
Decreasing opening of voltage gated calcium channels
Decreasing Ca2+ release from intracellular stores
Increasing K+ outflow via KATP and KIR channels
Decreasing exocytosis