Presentation is loading. Please wait.

Presentation is loading. Please wait.

Pain Theories Specificity –Separate sensory modality Pattern –Different patterns of activity in neural networks Gate-control.

Similar presentations


Presentation on theme: "Pain Theories Specificity –Separate sensory modality Pattern –Different patterns of activity in neural networks Gate-control."— Presentation transcript:

1 Pain Theories Specificity –Separate sensory modality Pattern –Different patterns of activity in neural networks Gate-control

2 Gate Theory of Pain Segmental level gating mechanism Internuncial neurons may modify activity of pain circuits Activated by large diameter (tactile) axons

3 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.

4 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

5 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

6 Pain Perception Provides information on the location, amount and duration of tissue injury Reactions to pain, include; emotion, autonomic, and behavioural responses

7 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

8 Pain Mechanisms and Pathways Receptors Transmission Pathways Endogenous analgesia

9 Receptors Nociceptors

10 Touch receptors Enclosed in end organ nocioceptors

11 Transmission A-delta neurons C-fiber neurons

12 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

13 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

14 C fibres Discharge is slow to develop, but lasts long after the original stimulus is removed Produce dull, aching pain Poorly localised

15 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

16 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

17

18 Primary sensory cortex (discrimination: location and intensity) Limbic cortex* (emotional experience) Sensory association cortex (perception and meaning) Thalamus (sensation) Sensory nuclei Neospinothalamic tract (sharp, bright pain) Paleospinothalamic tract (dull, aching pain) Periaqueductal gray (PAG)* (endogenous analgesic centre) Pontine noradrenergic neurons Medullary raphe nucleus Spinal cord and dorsal horn* Pain modulating circuits Primary touch fibers Nociceptive Stimuli A-delta (fast) C-fiber (slow)

19 Types of Pain Source –cutaneous –deep somatic –visceral –functional or psychogenic Fast Pain Slow Pain Referred Pain

20

21 Types of Pain Acute Pain Chronic Pain

22 Acute Pain Mild to severe Caused by noxious or tissue damaging stimuli Protective or warning system

23 Chronic Pain Mild to severe Lasts longer than 6 months Usually serves no useful purpose Pain is a major focus of care

24 Special Types of Pain Neuropathic Pain Causalgia Neuralgia Phantom Limb Pain

25 Neuropathic Pain Pathologic change or dysfunction of peripheral nerve Tumour infiltration, compression, constriction, damage, side effect of medical treatment or other peripheral nerve disease

26 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

27 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

28 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

29 Headache Migraine Cluster Tension Chronic Daily Headache Temporomandibular Joint Pain

30 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

31 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

32 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

33 Chronic Daily headache 40% of patients in headache clinics Cause unknown

34 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

35 Narcotics and Pain Inhibition Endorphins Morphine Endorphins bind to receptors in brain stem- activate AP’s down the spinal cord. Here they limit A and C fibres by releasing enkephalins

36 Analgesics and Pain Management Types: –Peripheral –Central –Local –Indirect

37 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

38 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

39 Local Analgesics Local Analgesics can be injected into site of injury or applied topically (eg. Novocaine)

40 Indirectly Acting Drugs Affect non-pain conditions such as emotions that can exacerbate pain experience


Download ppt "Pain Theories Specificity –Separate sensory modality Pattern –Different patterns of activity in neural networks Gate-control."

Similar presentations


Ads by Google