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PATHOPHYSIOLOGY LECTURE1&2 (PATHOPHYSIOLOGY OF PAIN 1 (ETIOLOGY OF…

- - - - 1- TRANSDUCTION
        
        Sensitization of pain receptors --> by stimuli.
        
        the activation of these receptors involves release of chemical mediators like;
        
        Bradykinin
        
        Prostaglandins
        
        Substance P
        
        Histamine
        
        CGRP
      - 2- TRANSMISSION
        
        the transmission of the action potential through nerve fibers to the spinal cord.
        
        Aδ and C fibers transmit pain sensation
        Aδ :
        
        Large diameter myelinated
        
        Higher velocity
        
        Conduct fast pain
        
        Sharp or stabbing pain
        
        Well localized
        
        Projects to parietal lobe
        
        (somatosensory cortex)
        
        C:
        
        Small diameter, unmyelinated
        
        Lower velocity
        
        Conduct slow pain
        
        Dull ache or discomfort
        
        Diffuse
        
        Projects to thalamus
        
        (Limbic system)
        
        action potentials generated in the nociceptors ---> transmitted to the dorsal spinal horn through the fibers --> glutamate plays a role in impulse transmission--> the pain fibers cross to the opposite side of the spinal cord--> ascend to the thalamus through the lateral spinothalamic tract --> the thalamus projects to the sensory cortex or limbic system.
      - 3- PERCEPTION
        
        The process makes one aware of pain and is a higher
        cortical function ( when you feel the pain)
        
        Somatosensory cortex Limbic System
        Aδ fibers C fibers
        Discrimination (sharp quality) Perceive dull aching pain
        Precision (location) Diffuse
        Avoidance reflex
        Associated symptoms
        
        WHAT Worsen pain and WHAT not?
        • Relaxation, distraction, meditation may help decrease pain
        • Depression and anxiety may worsen pain
        
        Increased levels of serotonin and / or Norepinephrine can help reduce certain types of pain.
      - 4- MODULATION
        
        when we use medications to reduce pain, when our body try to produce mediators to reduce it too.
  - - - 1-Somatic pain
        
        1- Cutaneous Pain
        
        • Arise from skin & subcutaneous tissues
        • Sharp, usually well localized pain
        • Can be distributed along dermatomes
        • Overlap of dermatomes – unclear boundaries
        • Burning quality
        • Sudden or slow in onset
        
        2- Deep Pain
        
        Originates in deeper structures
        • Muscles, joints, tendons
        • More diffuse
        • Stimuli:
        _ Pressure on bone
        _Muscle ischemia
        _Tissue damage
        • Radiation – knee joint pain can be referred to hip
      - 2- visceral pain
        
        (Splanchnic)
        
        Originates in intestine, gall bladder, uterus, urinary bladder
        • Pain not evoked in all viscera (liver, lungs)
        • Visceral pleura is not sensitive to pain, but – parietal pleura is.
        • Fewer nociceptors compared to cutaneous or somatic structures
        • Etiology: ischemia or distension
        • Diffuse (poorly localized) pain, no sharp or fast pain --> due to lack of Aδ
        • Referred to other locations
        • Continuous or intermiment, colicky in character
        • Associated with autonomic symptoms (e.g. nausea), sweating
        • Pathophysiology:
        • due to secretion of substance P in dorsal horn of spinal cord
        • Activation of nociceptors – pain persist longer
      - 3- referred pain
        
        Pain is perceived at a site distant from the origin but
        innervated by the same spinal nerve segment
        
        1-Convergence
        
        2- Embryological
    - - tissue damage ( nociceptive pain)
        
        useful
        
        can be somatic (localized and throbbing in nature) or visceral ( diffuse, and appear to arise from other structures (referred) or localized)
      - nerve pain ( non-nociceptive pain )
        
        harmful
        
        neuropathic pain
        
        Etiology: Neuronal injury
        • Nerve compression
        • Entrapment
        • Infection
        • Metabolic – diabetes
        • Surgery – Limb amputation
        • Medications – vincristine (anti-cancer drug)
        
        Burning or electrical shock-like sensation
        
        May not always be responsive to opioids
        
        Intractable sensory disturbance
        • Unexplained widespread pain
        
        Sensory deficit (numbness, paresthesia)
        • Provoked by trivial stimulus
        • Spontaneous at times
        • Persistent or intermittent
        
        WHAT ARE THE CAUSES OF THE TRANSMISSION OF NEURONAL PAIN?
        1- Increased activity of sodium channels
        2- Decreased levels of serotonin and NE (in inhibitory pathways)
        3-Increased activity of NMDA receptors due to glutamate activation
        
        CLASSIFICATION OF NEUROPATHIC PAIN:
        
        single area - nerve entrapment or - nerve compression or - neuralgia
        
        1- trigeminal neuralgia
        
        Common and severe neuralgia
        
        Clinical features
        
        Unilateral
        • Trigeminal nerve distribution (5th cranial nerve)
        • Facial tics or spasms
        • Intermittent
        • Excruciating stabbing pain
        
        • Provoked by:
        1-Movement
        2-Light touch
        3-Eating
        
        2- post herpetic neuralgia
        
        caused by Varicella-Zoster virus – chicken pox --> virus remains latent in sensory ganglia
        
        Reactivation due to decrease in immunity
        
        Virus travels to skin
        
        unilateral
        
        Clinical features:
        • Vesicular eruptions
        • Constant burning, aching, throbbing pain
        • Intermittent stabbing or shooting pain
        • Wind, clothing evoke pain – allodynia
        • Interferes with sleep and basic activities
        
        3- post traumatic neuralgia
        
        wide area
        
        1- diabetes
        
        is a complication of both type I and II diabetes that occurs about 10 years after the onset of diabetes
        • Peripheral sensory neuropathy is common
        • Pathophysiology: osmotic toxicity due to sorbitol
        
        Clinical features:
        • Bilateral, symmetric, peripheral glove and stocking distribution
        • Decreased perception of vibration, pain and temperature more in legs than hands
        • Paresthesias (altered sensation) – tingling and itching
        • Neuropathic pain, numbness, decreased tactile sensation
        • May also cause neuropathic ulcers in foot due to decreased
        perfusion and repeated trauma due to decreased sensation
        
        2- hypothyroidism
        
        3- Neurotoxic drugs
        
        Vincristine --> used to treat cancer (chemotherapy)
        
        4- alcohol
        
        multisymptom/ multisystem
        
        complex regional pain syndrome
        
        characterized by autonomic and vasomotor instability
        • Initiating traumatic event
        • Continuing pain
        • Allodynia – perception of pain from a non-painful stimuli
        • Hyperalgesia – pain disproportionate to the inciting injury
        • Changes in skin blood flow
        • Abnormal sensorimotor activity in the area of pain
        
        PATHOPHYSIOLOGY:
        
        Clinical features
        • Pain - severe burning pain with or without deep ache
        • Provoked by minimal movement or touch
        • Increases with repeated stimulation
        • Persists even after the stimulation has stopped
        • Emotional changes can provoke pain
        • Dystrophic or atrophic changes to skin, soft tissue,
        bone such as rubor / pallor; sweating / dryness
        • Edema
        • Patchy osteoporosis
        
        can be spontaneous ( continuous or intermittent) - provoked (allodynia " mechanical" or hyperalgesia " thermal")
    - - Acute
      - chronic
- - - - 1- migraine
        
        recurrent episodes of headache, most often unilateral
        
        associated with visual or sensory symptoms— collectively known as an aura—that arise most often before the headache but that may occur during or afterward
        
        affect women more than men
        
        Positive family history
        • Brain sensitive to environmental and sensory stimuli
        • This is further exaggerated in women during menstrual period
        
        WHAT TRIGGERS MIGRAINE? ( ETIOLOGY)
        
        Bright lights
        • Sounds
        • Hunger
        • Excess stress
        
        Hormones (menses)
        • Lack of sleep
        • Alcohol
        • Chocolate
        • Monosodium glutamate
        • Estrogen
        
        PATHOPHYSIOLOGY :
        1) Vasodilation of intracranial blood vessels
        2) Trigeminal nucleus activation
        3) Serotonin (5-HT) theory --> decreased levels of it
        4) Dopamine theory--> dose not cause pain, it cause symptoms such as nausea and vomiting
        5) Role of estrogen --> increased levels of estrogen
        
        CLASSIFICATION OF MIGRAINE
        
        1- without aura
        
        2- with aura ( classic migraine)
        
        CLINICAL PRESENTATION
      - 2- tension type headache TTH
      - 3- cluster headache
      - chronic daily headache
    - - 1- cranial neuralgia
      - 2- facial pain
    - - Trauma
        
        Vascular
        
        Non-vascular intracranial
        
        Substance abuse / withdrawal
        
        Infection
        
        Homeostasis
        
        Psychiatric
        
        Facial (ENT)