Transcript Pain bare
Pain Theories • Specificity – Separate sensory modality • Pattern – Different patterns of activity in neural networks • Gate-control Gate Theory of Pain • Segmental level gating mechanism • Internuncial neurons may modify activity of pain circuits • Activated by large diameter (tactile) axons Three Factors Involved in Opening and Closing the Gate • The amount of activity in the pain fibers. • The amount of activity in other peripheral fibers • Messages that descend from the brain. Conditions that Open the Gate • Physical conditions – Extent of injury – Inappropriate activity level • Emotional conditions – Anxiety or worry – Tension – Depression • Mental Conditions – Focusing on pain – Boredom Conditions That Close the Gate • Physical conditions – Medications – Counter stimulation (e.g., heat, massage) • Emotional conditions – Positive emotions – Relaxation, Rest • Mental conditions – Intense concentration or distraction – Involvement and interest in life activities Pain Perception • Provides information on the location, amount and duration of tissue injury • Reactions to pain, include; emotion, autonomic, and behavioural responses Pain Perception • Autonomic sympathetic response • Emotional response- fear, anger, anxiety, panic, depression • Behavioural response- spinal cord reflexes to pull tissue away, immobilising wound, coping • Pain informs of danger- attempt to remove stimulus, seek help Pain Mechanisms and Pathways • • • • Receptors Transmission Pathways Endogenous analgesia Receptors • Nociceptors nocioceptors Touch receptors Enclosed in end organ Transmission • A-delta neurons • C-fiber neurons A fibres • myelinated-conduct AP’s fast • found in skin, mucous membranes • fire immediately on stimulation, stop when stimulus removed • produce sharp pain (eg. getting injection), well localised C fibres • unmyelinated-slower • found in same areas as type A, and in organs, skeletal muscle, tendon • Tend to be stimulated by substances (bradykinin, serotonin, histamine, potassium) released from damaged tissues C fibres • Discharge is slow to develop, but lasts long after the original stimulus is removed • Produce dull, aching pain • Poorly localised Pathways • Pain fibers synapse in the dorsal horn. • Neurons may carry impulse to ventral root to initiate spinal reflexes • And/or, impulses proceed up the spinothalamic tract to the medulla and thalamus Pain and the CNS • fibres synapse in SC; travel up spinothalamic tracts and activate the following regions of brain: – – – – Sensory cortex Reticular activating system Hypothalamus Limbic system Sensory association cortex (perception and meaning) Primary sensory cortex (discrimination: location and intensity) Thalamus (sensation) Limbic cortex* (emotional experience) A-delta (fast) C-fiber (slow) Paleospinothalamic tract (dull, aching pain) Nociceptive Stimuli Neospinothalamic tract (sharp, bright pain) Sensory nuclei Periaqueductal gray (PAG)* (endogenous analgesic centre) Pontine noradrenergic neurons Medullary raphe nucleus Spinal cord and dorsal horn* Pain modulating circuits Primary touch fibers Types of Pain • Source – – – – cutaneous deep somatic visceral functional or psychogenic • Fast Pain • Slow Pain • Referred Pain Types of Pain • Acute Pain • Chronic Pain Acute Pain • Mild to severe • Caused by noxious or tissue damaging stimuli • Protective or warning system Chronic Pain • • • • Mild to severe Lasts longer than 6 months Usually serves no useful purpose Pain is a major focus of care Special Types of Pain • • • • Neuropathic Pain Causalgia Neuralgia Phantom Limb Pain Neuropathic Pain • Pathologic change or dysfunction of peripheral nerve • Tumour infiltration, compression, constriction, damage, side effect of medical treatment or other peripheral nerve disease Causalgia • Extremely painful • Follows sudden and violent deformation of peripheral nerves of limbs • Nerve typically damaged, but not severed • Pain characteristically burning, easily excitable and excruciating Neuralgia • Severe, brief, often repetitive attacks of lightening-like or throbbing pain • Occurs along distribution of a spinal or cranial nerve • Usually precipitated by stimulation of cutaneous region supplied by nerve • Trigeminal neuralgia one of most common and severe Phantom Limb Pain • Up to 70% of amputees • Often begins as sensations of tingling, heat and cold, or heaviness, followed by burning, cramping, or shooting pain • May experience painful sensations that were present before amputation Headache • • • • • Migraine Cluster Tension Chronic Daily Headache Temporomandibular Joint Pain Migraine • Females = 2 x males • With aura (15%) or without • Without aura is an idiopathic, recurring disorder that lasts 1 – 3 days • Unilateral, pulsating, moderate to severe aggravated by normal physical activity • Associated with nausea, photophobia and phonophobia Cluster • Affect ore males than females • Tend to occur nightly over weeks or months with long remission period • Typically severe, unrelenting, unilateral pain • Most commonly around the eye • Pain radiates to ipsilateral trigeminal nerve Tension • Most common, slightly more common in women • Dull aching diffuse, nondescript headaches not associated with vomiting nor worsened by activity • May be associated with disorders of the pericranial or scalp muscles Chronic Daily headache • 40% of patients in headache clinics • Cause unknown Temporomandibular Joint Pain • Common • Usually due to imbalance in joint movement because of bruxism or joint problems • Almost always referred and commonly presents as facial muscle pain, headache, neckache or earache • Aggravated by jaw action Narcotics and Pain Inhibition • Endorphins • Morphine • Endorphins bind to receptors in brain stemactivate AP’s down the spinal cord. Here they limit A and C fibres by releasing enkephalins Analgesics and Pain Management • Types: – – – – Peripheral Central Local Indirect Peripheral Analgesics • Act by blocking the production of substances produced in the inflammatory response (eg prostaglandins or bradykinins) which stimulate pain receptors • eg Aspirin; NSAID’s, Tylenol Central Analgesics • Narcotics - already mentioned • There are different types of endorphin receptors in CNS, each narcotic analgesic acts on a different type of receptor • eg. codeine, morphine, methadone, oxycodone • May produce respiratory depression Local Analgesics • Local Analgesics can be injected into site of injury or applied topically (eg. Novocaine) Indirectly Acting Drugs • Affect non-pain conditions such as emotions that can exacerbate pain experience