Mkgrady8 Neuro 5 Pain

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pain suppresion mechanisms: local

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occurs in dorsal horn; requires inhibitory interneurons; can involve opiate receptors

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GATE CONTROL THEORY OF PAIN

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local manipulation; activation of large diameter afferents (mechanoreceptors) can inhibit activity of small diameter pain transmitting neurons; occurs in dorsal horn; requires inhibitory interneuron; provided stimulus for additional research and discoveries in pain management; basis for counter irritant as analgesics= rubbing a bruise, liniments, transcutaneous electrical nerve stimulation (TENS), acupuncture, etc; non nociceptive stimuli suppresses nociceptive input; recall= large fibers have the lowest threshold

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pain suppression mechanisms: 2 pathways

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modulation by HIGHER BRAIN CENTERS; direct pathway involves STT, SRT, and SMT; indirect pathway has NO STT, SSRT, and SMT involvement; the perception of pain depends on its context and is subject to central modulation; both pathways involve opiopeptides

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pain suppression results upon activation of what

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specific descending pathways projection to the dorsal horn or the spinal trigeminal nucleus resulting in suppression of nociceptive afferent firing, decreased nociceptive afferent signaling to higher pain processing brain centers, and altered behavior (pain decreases)

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descending pain control mechanisms: direct pathway

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collateral or terminal branches of ALS and trigeminal systems activate neurons in PAG; fibers from PAG activate raphe nucleus magnus (RNM) of reticular formation (5HT containing neurons); RNM synapse in spinal cord dorsal horn laminae I, II, and V; to decrease nociceptive afferent firing at the level of the spinal cord; in dorsal horn monoaminergic fibers synapse on interneurons (to excite the internueonrs, interneurons release enkephalins, inhibition of pain transmission neurons); in dorsal horn monoaminergic fibers also may synapse directly on pain transmission fibers (inhibition of impulse transmission)

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descending pain control mechanisms: indirect pathway

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endogenous pain suppression systems activated by non painful conditions i.e. absence of input from STT, SRT, SMT; stress induced analgesia= anticipatory/preparatory/emotional stress (soldiers), physical exertion/exercise (athletes); acupuncture/acupressure; placebo (pain is the brain's interpretation of afferent neural activity and part of this interpretation is expected, a placebo response, regardless of how it is derived is in part manipulation of expectancy); via hypothalamus and limbic system (amygdala); opiate and non opiate mechanisms are involved (e.g. adenosine receptors, endocannabinoids and receptors; e.g. opiate antagonists are ineffective in completely blocking stress induced analgesia)

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descending pain control: key brain regions

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1. SRT and SMT components of ALS; 2. involves activation of inhibitory interneurons; 3. higher brain centers; 4. key brain structures; 5. specific neurotransmitters; information coming from sensory cortex, hypothalamus, limbic system, and other gray regions outside of the sensory cortex can either have a direct effect on neurons that originate in the periaqueductal gray or can bypass and have a direct effect neurons in the locus ceruleus or can bypass and have a direct effect on the reticular formation or can bypass and have a direct effect on location of entry on primary nociceptive neuron to the spine; so these regions can either augment or inhibit the incoming nociceptive pain depending on if they are acting on an inhibitory neuron or not

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summation of pain suppresion pathways: indirect

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somatic sensory cortex to amygdala, midbrain periaqueductal gray, and hypothalamus

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summary of pain suppression pathways: direct

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dorsal horn of spinal cord and spinal nucleus of CN5 to the midbrain periaqueductal gray to the , medullary reticular formation, locus coeruleus, and raphe nuclei all back to the dorsal horn of spinal cord and spinal nucleus of CN5

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2 broad types of headache

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primary= without an underlying cause; secondary= systemic process, underlying pathology

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causes of pathological/secondary HA

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eye disorders, sinusitis, meningitis, temporal arteritis (GCA), posttraumatic head injury, subarachnoid hemorrhage, brain tumor, trigeminal neuralgia, ANALGESIC REBOUND

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HA: high risk factors (for being secondary)

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acutely ill (worse than migraine); abnormal neurological symptoms; papilloedema; nuchal rigidity; abnormal mental status; explosive or sudden onset; WORST HA EVER; significant head trauma; past history of cancer or coagulopathy; new HA in an older pt (50+ yrs)

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HA: diagnostic testing to do

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lumbar puncture; CT or MRI imaging; intraocular pressure; erythrocyte sedimentation rate (ESR); complete blood count (CMC)

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what are the pain sensitive structures of the head

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skin, subq tissue, muscles, arteries, and periosteum of the skull; tissues of the eye, ear, nasal, and sinus cavities; intracranial venous sinuses and their tributary veins; parts of the dura at the base of the brain and the arteries within the dura mater and pia arachnoid; distension, contraction, or dilation of extracranial or intracranial arteries; BRAIN PARNCHYMA LACKS PAIN FIBERS; the trigeminal and the first 3 cervical nerves govern all these and REMEMBER THAT ALL BRANCHES OF CN5 HAVE MENINGIAL BRANCHES

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what are the 3 groups of primary headache disorders

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migraine, cluster, tension; they can all be chronic and long term or just episodic

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important concept: when acute forms of primary HA become chronic

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become a type of pathological pain; a form of synaptic plasticity (these changes can happen quickly of more slowly (activity dependent)); brain suppression pain mechanisms stop working because over activity of nociceptice afferents leads to synaptic plasticity

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2 main types of migraine HA

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with or without aura

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diagnostic criteria of episodic migraine (without aura)

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lasts 4-72 hrs; at least 5 HA attacks; has 2 of the following characteristics= unilateral pain localized to temple/orbital region, pulsating pain, moderate to severe pain intensity, aggravated by routine physical activity; one of the following symptoms must be present= nausea/vomiting, photophobia/phonophobia

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diagnostic criteria of episodic migraine (with aura)

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same pain/duration etc as for migraine without aura; aura= recurrent disorder manifesting in attacks of reversible, focal, neurological symptoms that usually develop gradually over 5-20 mins and last for less than 60 mins

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what is the aura

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complex of neurological symptoms that occur before or at the onset of migraine NA; visual auras are the most common= photopsia, scotomas, fortification spectrum (what else can cause similar visual disturbances? detached retinas); sensory aura is next common= tingling; motor weakness and aphasia are the least common and can present with + and/or - features and usually mixed; auras can be present without HA

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pathophysiology theory of migraine HA

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complex neurovascular disorder= problems with neural innervation of cranial circulation; involves abnormal pain processing pathways and structures; disturbances in other multi sensory pathways; genetic predisposition

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A 19 y/o female student at TTU presents to youroffice complaining about recurring leg pain. She is on the cross country team and runs about 100 miles per week. She says that a team mate is currently goingto PT for similar complaints and receiving transcutaneous electrical nervestimulation (TENS). What structures arethe TENS unit activating? a. alpha motor neurons b. C nerve fibers c. Abeta nerve fibers d. Dorsal root ganglia

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C Abeta nerve fibers

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blood vessels in the supratentorial dura mater: relation to HA

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vasodilation of meningeal blood vessels activates CN5; antidromic release of vasoactive peptides from nociceptive (C fiber) dendrites causes even more dilation of blood vessels; so this feeds on itself; TRIGEMINOVASCULAR REFLEX

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peripheral sensitization

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CN5 afferents release calcitonin gene related peptide (CGRP) as peripheral nerve endings; CGRP is the most potent vasodilator known; feed forward system of more vasodilation, more activation of CN5, and more release of CGRP; (this is the same as the last slide except it specifies CGRP); ANY ACTIVATION OF CN5 LEADS TO THE RELEASE OF VASOACTIVE PEPTIDES FROM NERVE TERMINALS (DENDRITES) of C fibers which causes a larger generator potential of free nerve endings, results in an increased number of action potentials along the primary afferent as well as recruitment of more afferents firing (aka peripheral sensitization)

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acute treatment of HA

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triptans are DOC and they are agonists of 5-HT1 receptors (serotonin receptors); KNOW SUMATRIPTAN WHICH IS A TRIPTAN

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how do triptans work

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5HT receptors are located on cerebral and coronary blood vessels (BV); when activated result in constriction of cerebral and coronary BVs= 5HT1B, D are on meningeal BN, agonists will result in BV constriction, stop vasodilation and prevent trigeminovascular reflex (promote normalization of afferent signaling)

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potential problem of triptans

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constriction of coronary BVs; different subtype of 5HT receptor on HEALTHY coronary arteries= 5HT2 receptors are on coronary arteries, 5HT2>>>>5HT1B on coronary arteries; so do not give IV (potential to cause coronary vasospasm) and so not give to pts with coronary artery disease or hypercholesterolemia/hyperlipidemia (coronary arteries with atherosclerotic plaques have a greater number of 5HT1B receptors than healthy coronary arteries)

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summary: migraine HA

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acute migraine very complex disease caused by many things; more prevalent in women than in men; severe unilateral head pain; can present with or without auras; DOC for treatment are the 5HT1 agonists= triptans, contraindicated in pts with CAD, high cholesterol and high blood lipids, will cause vasospasm

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tension type HA: 3 types

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infrequent episodic (acute), frequent episodic, and chronic

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diagnostic criteria for tension type HA (TTHA)

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lasts 30 mins-7 days; has 2 of the following criteria= bilateral location, pressing non pulsating quality, mild or moderate intensity, NOT aggravated by routine physical activity; both of the following= no nausea or vomiting, may have photophobia or phonophobia; at least 10 episodes < 1 day/mo/yr

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acute treatment of TTHA

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analgesics and antipyretics; NSAIDs; lifestyle changes; focus on teaching pt how to gain control over striated muscles

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summary: TTHA

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bilateral, diffuse, moderate pain; least studies of all HA disorder; bc involves/includes abnormal function of striated muscles, other non drug therapies work well; high comorbidity with depression and anxiety, drugs for these CNS disorders may help

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cluster HA: diagnostic criteria

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type of trigeminal autonomic cephalgia; severe to very severe unilateral orbital, supraorbital, and or temporal pain lasting 15-180 mins if untreated; max pain reached quickly (within 15 mins); HA is accompanies by at least one of the following (all ipsilateral) (these are autonomic symptoms)= conjunctival injection and/or lacrimation, nasal congestion and/or rhinorrhea, eyelid edema, forehead and facial sweating, miosis and/or ptosis, sense of restlessness or agitation; at least 2 cluster periods lasting 7-365 days and separated by pain free remission periods of >1 month

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cluster HA: summary

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more prevalent in men than women; unilateral, orbital/supraorbital location of intense severe pain; short lived (180 mins but reaches a crescendo within 15 mins); associated with ipsilateral to pain are autonomic sx; occurs at same time of day or night; occur in groups or clusters of at least 5

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cause of cluster headache

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poorly understood; needs to explain 3 distinguishing features= trigeminal distribution of the pain, ipsilateral cranial autonomic features, circadian pattern of attacks; possibly hypothalamus issue

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why do you think it could be the hypothalamus

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contains cells that regulate autonomic functinos and nuclei that serve as the major circadian pacemaker in mammals (suprachiasmatic nucleus); the biologic clock is serotonergically modulated and is connected anatomically to the eye; PET has confirmed highly specific activation of hypothalamic grey matter and more grey matter

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summary of pathogenesis of cluster HA

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incompletely understood; CN5 not necessary for some chronic forms of the disease; inflammation of the cavernous sinus walls? maybe; involvement of the sphenopalatine ganglion; definite hypothalamic involvement

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acute treatment of cluster HA

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oxygen and sumatriptan (abortive); corticosteroids, calcium channel blockers, and antiepileptics (preventative)

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alternative treatments for chronic cluster HA which is refractory to all other meds

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hypothalamic deep brain stimulation; occipital nerve stimulation; high frequency stimulation of the sphenopalatine ganglion (blocks cranial parasympathetic outflow)

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medication overuse HA: caused by what, treatment

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all DOC used in the acute treatment of primary HA can result in MOH; HA ceases when drug treatment ceases; technically a secondary HA (HA is caused by prolonged drug use); how long is long enough to cause MOH= depending on the drug between 10-15 days; so in a HEALTHY individual TAKING SUMATRIPTAN AS PRESCRIBED IS SAFE but MOH can result due to it being used EXCESSIVELY in a SUSCEPTIBLE PT

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A 27 y/o female pt presents to her PCP. Sx included severe, pulsating right temporalpain, photophobia, and vomiting. Sxlasted 6-8 hrs. The severity of the HAand sx are severe enough that she cannot go to work and all aspects of normal dailyactivities are affected. The MOA for theDOC to alleviate her sx? a. histamine antagonist b. histamine agonist c. serotonin agonist d. serotonin antagonist e. glutamate antagonist

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C; this is a migraine; DOC is sumatriptan

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the fast component of pain

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injury to the skin or superficial tissues; pain is well defined, localized, and of short duration; ex injuries that produce cutaneous pain include paper cuts, minor (first degree) burns, and lacerations; mediated by A delta fibers and free nerve endings and the STT

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slow component of pain

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pain is dull, poorly localized pain of longer duration than cutaneous pain; ex include sprained ankle and broken bones; mediated by C nerve fibers and free nerve endings and the SMT, SRT, and collaterals off the STT

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visceral pain

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originates from body organs visceral nociceptors are located within body organs and internal cavities; pain usually more aching and of a longer duration than somatic pain; pain is extremely difficult to localize, and several injuries to visceral tissue exhibit referred pain where the sensation is localized to an area completely unrelated to the site of injury; ex myocardial ischemia where the sensation can occur in the upper chest as a restricted feeling or as an ache in the left shoulder, arm or even hand; ex is phantom limb pain where a sensation of pain from a limb that one no longer has or no longer gets physical signals from (a sign of synaptic plasticity)

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inflammatory processes can lead to

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peripheral sensitization (damaged nerves can also lead to peripheral sensitization)

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neuropathic pain: what is it, what causes it

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occurs as a result of injury or disease to the nerve tissue itself; include changes in receptors and axons; disrupts the ability of the sensory nerves to transmit correct info to the thalamus and hence the brain interprets painful stimuli even though there is no obvious or documented physiologic cause for the pain; included the malfunction of descending pain control mechanisms; mechanisms= inhibitory interneurons gone or no longer inhibitory, or loss of descending control, or sprouting of C fibers in spinal cord, or extension of interneuron dendrites into additional spinal cord laminae (allows for convergence which is recruitment of polysynaptic interconnections that strengthen signal)

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chronic migraine (without aura) diagnostic criteria

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if HA occurence is > 15 day/month for >3 months in the absence of med overuse HA; TAKE HOME MESSAGE IS INCREASED FREQUENCY; this type of HA has a strict menstrual relationship

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etiology of chronic migraine HA

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based on PERIPHERAL SENSITIZATION turning into CENTRAL SENSITIZATION (it is at the level of the nucleus caudalis that central sensitization occurs); maybe over excitation of peripheral synapses/primary afferents; maybe change in receptors; maybe change in primary afferents; maybe convergence; maybe alternations in descending pain suppression mechanisms involves abnormal pain processing pathways and structures or disturbances in other multi sensory pathways

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in brainstem CN5 afferents release what

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CGRP onto second order neurons; CGRP facilitates pain transmission by lowering threshold to fire AP

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convergence theory

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includes activation of greater occipital nerve= psinal nerve from dorsal rami of cervical spinal nerve 2, receives afferents from posterior scalp and neck muscles; excessive nociceptor afferent stimulation leads to central sensitization at C2 level of SC; direct connection/synapse into TNC= lissauer's tract and tract running through substantia gelatinosa

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central sensitization theory of pain

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migraine triggers cause excitation of cortical neurons; results in inhibition of periaqueductal grey (PAG) and nucleus raphe magnus (NRM); normal firing of the PAG and NRM results in dampening/deceasing pain input at the level of the spinal cord and TNC; if inhibited then this disinhibition would result in more incoming afferents signaling at the level of the TNC; same principle applies to incoming afferents in spinal cord; SO MIGRAINE IS A DYSFUNCTION OF SENSORY MODULATORY NETWORKS RESULTING IN ABNORMAL PROCESSING OF NORMAL NEURAL TRAFFIC

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migraine: a disease of allostatic load

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1. brain responds to stressful events by activating hormonal and neural mediators that lead to modifying behaviors to adapt to these stressors 2. these responses and/or modifying behaviors maintain physiological stability or allostasis 3. WHEN THESE STRESSORS ARE FREQUENT OR SEVERE ALLOSTATIC responses are DYSREGULATED AND MALADAPTIVE AND ALLOSTATIC load develops 4. ALLOSTATIC LOAN CAN ALTER BRAIN FUNCTION BY ALTERING BRAIN NETWORKS 5. this can lead to further abnormal response to stressors increased ALLOSTATIC LOAD becoming a feed forward cycle of abnormal brain rewiring and function

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prophylactic treatment: who can take them, why are they taken

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these drugs are indicated in pts who have severe disabling migraines, cannot take vasoconstrictors, refractory to acute treatment; taken daily to prevent the occurrence of chronic headache to decrease frequency, decrease severity, increase effectiveness of abortive meds when headaches do occur, change chronic back to episodic, prevent chronic from developing

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what are the prophylactic treatments

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beta blockers; antiepileptic drugs (remember not to give these to pregnant women because it decreases folate levels (spina bifida)); BOTOX; but these aren't very efficacious

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diagnostic criteria for TTHA

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at least 10 episodes >15 days/month for >3 months; can evolve over time from episodic tension type HA or de novo; hard to distinguish from chronic migraine

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TTHA and MOH

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chronic tension type HA is less often associated with med overuse; however episodic tension type HA has commonly become a chronic HA through overuse of analgesics (NSAIDS)