Pathofyziology of nerve system II Intracranial hypertension Epilepsy Pain Intracranial hypertension Epilepsy Pain Intracranial Pressure and Cerebral Perfusion Pressure Brain is enclosed in the skull… … an advantage before trouble occurs… … big problem after trouble occurs. Intracranial pressure (ICP) is pressure inside the skull Intracranial compartments • Brain • Cerebrospinal fluid (CSF) • Blood Cerebral perfusion pressure • The pressure gradient through which blood flows to the brain CPP = MAP - ICP Cerebral perfusion pressure Mean arterial pressure Intracranial pressure http://ars.els-cdn.com Cerebral perfusion pressure CPP = MAP - ICP Cerebral perfusion pressure Mean arterial pressure Intracranial pressure CPP is a crucial parameter determining CBF (cerebral blood flow) normal cerebral perfusion pressure (CPP) = 70-100mmHg safe CPP> 50 mmHg CPP 30-50 mm Hg leads to a reversible functional disorder CPP <30mm Hg leads to irreversible changes https://i.ytimg.com/vi/RAhqTAcdh_4/maxresdefault.jpg Cerebral perfusion pressure CPP = MAP - ICP Cerebral perfusion pressure Mean arterial pressure Intracranial pressure Baroreflex http://www.azkurs.org/chapter-20-blood-vessels--circulation.html Intracranial pressure (ICP)  Normal 7-15mmHg  Tolerable till 25 mmHg  Loss of consciousness 40-50 mmHg  Over 50 mmHg ischemia of brain Fast onsetof ICP (e.g. bleeding) X Slow onset ICP (e.g. Tumor growth) Cerebral perfusion pressure CPP = MAP - ICP Cerebral perfusion pressure Mean arterial pressure Intracranial pressure Causes of Intracranial Hypertension Brain compartment • Edema • Tumor • Hemorrhage • Infection CSF compartment • Hydrocephalus Compartment of blood • Venous sinus thrombosis • Acidosis - ischemia Causes of Intracranial Hypertension Brain Edema Cytotoxic (intracellular) • Na/K ATPase failure • Na or Ca influx • H2O • Mainly occurs in first 24 h. following insult Vazogenic (extracellular) • Damage of endothelial cells and Blood – Brain barrier • Extravasation of proteins and electrolytes into Interstitial space • Mainly occurs at 24 h. after insult and later Interstitial • Obstruction of CSF circulation • Mechanical damage of CSF- brain barrier • Infiltration of CSF into intersticial space Compensation - (slow) increase of ICP • Limitation: of cerebrospinal fluid volume (CSF) and venous reserve https://clinicalgate.com/intracranial-hypertension/ Compensation/de-compensation - (fast) increase of ICP ↑ ICP ↓ CPP ↓ CBF Kompenzace ↑ MAP Nedostatečná Dostatečná IschemieEdém Normalizace CBF CPP = MAP - ICP Cerebral perfusion pressure Mean arterial pressure Intracranial pressure ↑ ICP ↓ CPP ↓ CBF Compensation ↑ MAP Nedostatečná Sufficient IschemieEdém Normalisation of CBF Compensation/de-compensation - (fast) increase of ICP CPP = MAP - ICP Cerebral perfusion pressure Mean arterial pressure Intracranial pressure ↑ ICP ↓ CPP ↓ CBF Compensation ↑ MAP Unsufficient Sufficient IschemiaEdema Normalisation of CBF Compensation/de-compensation - (fast) increase of ICP CPP = MAP - ICP Cerebral perfusion pressure Mean arterial pressure Intracranial pressure Cushing´s triad https://it.pinterest.com/pin/395753885990152490/ Cushing´s triad https://it.pinterest.com/pin/395753885990152490/ Sympathetic activation Cushingova triáda https://it.pinterest.com/pin/395753885990152490/ Unclear mechanism Probably rebound coactivation of parasympathetic system (simultaneous increase of sympathetic tone and parasympathetic tone) Perhaps also pressure on the brain stem Sympathetic activation Sympathetic activation Compression of adjacent tissue Infratentorial lesions • Allvays acute • Risk of brain • stem compression Cerebral herniation • Subfalcine • Transtentorial • Tonsillar • Central Permanent damage of brain Risk of brain stem compression Consequences of Intracranial Hypertension http://slideshare.net http://edutoolanatomy.wikispaces.com Central Herniation Intracranial hypertension Epilepsy Pain Epilepsy One of the most common neurological diseases About 50 million people suffer from epilepsy worldwide Approx. 80% of patients live in developing countries (birth trauma, infection) Epilepsy One of the most common neurological diseases About 50 million people suffer from epilepsy worldwide Approx. 80% of patients live in developing countries (birth trauma, infection) • Epileptic seizure • Transient abnormal brain activity causing change Consciousness Perception Behavior Motor functions Sensitivity • The basis is excessive and synchronous neuronal activity Epilepsy One of the most common neurological diseases About 50 million people suffer from epilepsy worldwide Approx. 80% of patients live in developing countries (birth trauma, infection) • Epileptic seizure • Transient abnormal brain activity causing change Consciousness Perception Behavior Motor functions Sensitivity • The basis is excessive and synchronous neuronal activity Parcial Generalized Non-classifiable Epilepsy - Classification • Focal seizures – account for 80% of adult epilepsies - Simple partial seizures - Complex partial seizures - Partial seizures secondarilly generalised • Generalised seizures • Unclassified seizures Seizure terms • Ictal= seizure • Post-ictal= confusion following seizure • Aura= abnormal sensation preceding loc • Automatisms= nonsensical involuntary movements • Tonic= tonic contraction producing extension and arching • Clonic= alternating muscle contraction-relaxation • Complex= consciousness impaired • Simple= consciousness unimpaired • Partial= focal region involved • Generalized= whole brain • Convulsions= shaking • Grand mal and petite mal=“street terms” for convulsive and non-convulsive seizure respectively Causes of epilepsy • Structural changes of the cortex  Focal pathology  Congenital (malformations of the cerebral cortex)  Acquired (tumor, stroke, trauma) Causes of epilepsy • Structural changes of the cortex  Focal pathology  Congenital (malformations of the cerebral cortex)  Acquired (tumor, stroke, trauma) • Metabolic etiology  Congenital metabolic disorders (porphyria, amino acid metabolism disorders)  Obtained (folic acid deficiency, toxonutritive) Causes of epilepsy • Structural changes of the cortex  Focal pathology  Congenital (malformations of the cerebral cortex)  Acquired (tumor, stroke, trauma) • Metabolic etiology  Congenital metabolic disorders (porphyria, amino acid metabolism disorders)  Obtained (folic acid deficiency, toxonutritive) • Infectious etiology  The most common source of epilepsy worldwide  Congenital (Zika virus, cytomegalovirus)  Acquired (HIV, Toxoplasmosis, Malaria) • Autoimmune disorders Causes of epilepsy • Structural changes of the cortex  Focal pathology  Congenital (malformations of the cerebral cortex)  Acquired (tumor, stroke, trauma) • Metabolic etiology  Congenital metabolic disorders (porphyria, amino acid metabolism disorders)  Obtained (folic acid deficiency, toxonutritive) • Infectious etiology  The most common source of epilepsy worldwide  Congenital (Zika virus, cytomegalovirus)  Acquired (HIV, Toxoplasmosis, Malaria) • Autoimmune disorders • Genetic etiology • Great importance is assumed, but the information is sketchy • Unknown etiology Partial epileptic seizures based on a part of the cerebral cortex from one hemisphere, motor manifestations are one-sided Partial epileptic seizures based on a part of the cerebral cortex from one hemisphere, motor manifestations are one-sided • Partial simplex • No presence of consciousness disorder With motor symptoms (muscle twitching) With somatosensitive / sensory manifestations (sensitivity / sensory disorders) With autonomic manifestations (vomiting, sweating, tachycardia) With psychic manifestations (déja vu, hallucinations) Partial epileptic seizures based on a part of the cerebral cortex from one hemisphere, motor manifestations are one-sided • Partial simplex • No presence of consciousness disorder With motor symptoms (muscle twitching) With somatosensitive / sensory manifestations (sensitivity / sensory disorders) With autonomic manifestations (vomiting, sweating, tachycardia) With psychic manifestations (déja vu, hallucinations) • Partial with complex symptomatology • Failure of consciousness/perception, often occurrence of automatisms (chewing, licking) Partial epileptic seizures based on a part of the cerebral cortex from one hemisphere, motor manifestations are one-sided • Partial simplex • No presence of consciousness disorder With motor symptoms (muscle twitching) With somatosensitive / sensory manifestations (sensitivity / sensory disorders) With autonomic manifestations (vomiting, sweating, tachycardia) With psychic manifestations (déja vu, hallucinations) • Partial with complex symptomatology • Failure of consciousness/perception, often occurrence of automatisms (chewing, licking) • Partial to generalized • arise as partial and then spread throughout the brain Generalized epileptic seizures Involvement of both hemispheres, often impaired consciousness, motor manifestations bilateral Generalized epileptic seizures Involvement of both hemispheres, often impaired consciousness, motor manifestations bilateral  Absence (petit mal; loss of postural tone, patient not responding, mild tonic or clonic manifestations may follow) Generalized epileptic seizures Involvement of both hemispheres, often impaired consciousness, motor manifestations bilateral  Absence (petit mal; loss of postural tone, patient not responding, mild tonic or clonic manifestations may follow)  Myoclonic (sudden short twitchs in series or isolated; many myoclons have no epileptic origin)  Clonic (amplitude increases and frequency decreases during seizure) Generalized epileptic seizures Involvement of both hemispheres, often impaired consciousness, motor manifestations bilateral  Absence (petit mal; loss of postural tone, patient not responding, mild tonic or clonic manifestations may follow)  Myoclonic (sudden short twitchs in series or isolated; many myoclons have no epileptic origin)  Clonic (amplitude increases and frequency decreases during seizure)  Tonic (solid fixing contraction)  Tonic-clonic (grand mal; loss of consciousness, followed by a tonic phase translating into a clonic phase affecting the muscles of whole body including facial muscles, possible breathing disorders, autonomic manifestations, confusion after acquiring consciousness, exhaustion) Generalized epileptic seizures Involvement of both hemispheres, often impaired consciousness, motor manifestations bilateral  Absence (petit mal; loss of postural tone, patient not responding, mild tonic or clonic manifestations may follow)  Myoclonic (sudden short twitchs in series or isolated; many myoclons have no epileptic origin)  Clonic (amplitude increases and frequency decreases during seizure)  Tonic (solid fixing contraction)  Tonic-clonic (grand mal; loss of consciousness, followed by a tonic phase translating into a clonic phase affecting the muscles of whole body including facial muscles, possible breathing disorders, autonomic manifestations, confusion after acquiring consciousness, exhaustion)  Atonic (sudden drop in muscle tone leading to fall) Motor Tonic-clonic Other motor Non-Motor (Absence) Unknown Onset Motor Non-Motor focal to bilateral tonic-clonic Generalized OnsetFocal Onset Motor Tonic-clonic Other motor Non-Motor ILAE 2017 Classification of Seizure Types Basic Version 1 Unclassified 2 1 Definitions, other seizure types and descriptors are listed in the accompanying paper & glossary of terms 2 Due to inadequate information or inability to place in other categories Aware Impaired Awareness From Fisher et al. Instruction manual for the ILAE 2017 operational classification of seizure types. Epilepsia doi: 10.1111/epi.13671 Motor tonic-clonic clonic tonic myoclonic myoclonic-tonic-clonic myoclonic-atonic atonic epileptic spasms2 Non-Motor (absence) typical atypical myoclonic eyelid myoclonia Unknown Onset Motor Onset automatisms atonic2 clonic epileptic spasms2 hyperkinetic myoclonic tonic Non-Motor Onset autonomic behavior arrest cognitive emotional sensory focal to bilateral tonic-clonic Generalized OnsetFocal Onset Aware Impaired Awareness Motor tonic-clonic epileptic spasms Non-Motor behavior arrest ILAE 2017 Classification of Seizure Types Expanded Version1 Unclassified3 1 Definitions, other seizure types and descriptors are listed in the accompanying paper and glossary of terms. 2 These could be focal or generalized, with or without alteration of awareness 3 Due to inadequate information or inability to place in other categories From Fisher et al. Instruction manual for the ILAE 2017 operational classification of seizure types. Epilepsia doi: 10.1111/epi.13671 Status epilepticus A protracted seizure Life-threatening condition Status epilepticus A protracted seizure Life-threatening condition Grand mal - a seizure longer than 15 minutes (Grand mal usually resolve spontaneously over 5-10 minutes)  Petit mal - hours to days (can be difficult to diagnose) • Untreated status epilepticus leads to energy collapse, brain edema and death • The possibility of failure of basic vital functions due to CNS disruption Intracranial hypertension Epilepsy Pain Free nerve endings • Unsialized nerve endings • Polymodal • Nociception • Thermoreception • Mechanoreception • A delta fibers • C fibers http://www.slideshare.net/CsillaEgri/presentations Nociceptors • Free nerve endings responding to very intense stimuli • The nature of the stimulus - Mechnaical Big pressure Sharp object - Thermal Upper limit approx. 45 dg. Celsius Lower limit - variable - Chemical pH Inflammatory mediators, etc. Nociceptors • Free nerve endings responding to very intense stimuli • The nature of the stimulus - Mechnaical Big pressure Sharp object - Thermal Upper limit approx. 45 st. Celsius Lower limit - variable - Chemical pH Inflammatory mediators, etc. Nerve fibers http://www.slideshare.net/CsillaEgri/presentations Reception component • algoreceptors, nociceptors are free nerve endings (specialized chemoreceptors) • localization: skin, tendon shrouds, ligaments, muscles, hollow organs • receptors do not adapt, density fluctuates: fingertips> dentin> back skin> not in parenchyma of liver, spleen, lung, brain, cartilage • the force of irritation translates into the pulse frequency in the periphery • nociceptive fibers may be irritated throughout their course Termoreceptors • Free nerve endings sensitive to heat • TRP channels (transient receptor potential) • Each TRP channel subtype is sensitive to a particular temperature and chemical substance http://www.slideshare.net/CsillaEgri/presentations Termoreceptors • Temperature perception is determined by the activity ratio of different thermoreceptors http://www.slideshare.net/CsillaEgri/presentations Conduction of painful sensations • 2 types of fibers - form half of all back spinal cord fibers 1. strong myelinated fibers, type Aδ - superficial pain, respond to strong mechanical stimuli 2. thin non-myelinated fibers of type C - deep pain, polymodal: mechanically, chemically, by heat, by cold, by anoxia • bradykinin • potassium release from damaged cells • Histamine • Serotonin • drop of pH in the tissue • calcitonin gene related peptide, vasointestinal peptide, ATP https://www.slideshare.net/muhammadakhan754365/pain-anatomy-and-physiology Mechanism of algoreceptors activation Tissue damage Cell membrane damage and activation of phospholipase A Release of arachidonic acid via cyklooxygenase arises prostaglandin E2 enhanced the effect of mediators on algorithms Inflammatory reaction with hyperemia histamine and bradykinin substance P First neuron fibers • switched in the posterior spinal horn in ncl. proprius the synapse mediator is substance P • substance P is the second peripheral nociceptive sensitizer • substantia gelatinosa Rolandi - an inhibitory region in the posterior spinal horns → mediator - enkephalin • back horn area is damped from CNS → tractus reticulospinalis https://www.researchgate.net/figure/Nociception-Normal-pain-signalling-in-the-body-is- transmitted-to-the-spinal-cord-dorsal_fig1_316130682 Conduction of painful sensations Aδ fibers – from the skin, well localized pain, so-called primary pain → tractus spinothalamicus - 3 neuronal phylogenetically newer pathway C fibers – poorly localized, secondary pain from deeper parts of the skin and deeper lokalised organs → tractus spinoretikulothalamicus – an older polysynaptic system, impulses are transmitted to higher centers through short axon pathways vegetative response: change in pressure, tachypnea, mydriasis, sweating, increased muscle tone,… Somatosensory pathways • Three systems • (Archispinothalamic) • Interconnection of adjacent segments (tr. Spinospinalis) • Paleospinothalamic • tr. Spinoreticularis, tr. Spinotectalis… • Neospinothalamic • tr. Spinothalamicus • Dorsal column system • tr. Spinobulbaris 55 Somatosensory pathways • Three systems • (Archispinothalamic) • Interconnection of adjacent segments (tr. Spinospinalis) • Paleospinothalamic • tr. Spinoreticularis, tr. Spinotectalis… • Neospinothalamic • tr. Spinothalamicus • Dorsal column system • tr. Spinobulbaris 56 Somatosensory pathways • Paleospinothalamic • Low resolution – dull, diffuse pain („slow pain“) • Neospinothalamic • High resolution – sharp, localized pain („fast pain“), temperature • Low resolution – touch • Dorsal column system • High resolution – touch, proprioception 57 Somatosensory pathways • Paleospinothalamic • Low resolution – dull, diffuse pain („slow pain“) • Neospinothalamic • High resolution – sharp, localized pain („fast pain“), temperature • Low resolution – touch • Dorsal column system • High resolution – touch, proprioception 58 Somatosenzory pathways http://neuroscience.uth.tmc.edu/s2/chapter02.html Paleospinothalamic system • Tr. Spinoreticularis, spinotectalis… 60 Paleospinothalamic system • Tr. Spinoreticularis, spinotectalis… • Evolved before neocortex 61 Paleospinothalamic system • Tr. Spinoreticularis, spinotectalis… • Evolved before neocortex • The primary connection to the subcortical structures 62 Paleospinothalamic system • Tr. Spinoreticularis, spinotectalis… • Evolved before neocortex • The primary connection to the subcortical structures • Basic defensive reactions and reflexes - vegetative response, reflex locomotion - opto-acoustic reflexes etc. 63 Paleospinothalamic system • Tr. Spinoreticularis, spinotectalis… • Evolved before neocortex • The primary connection to the subcortical structures • Basic defensive reactions and reflexes - vegetative response, reflex locomotion - opto-acoustic reflexes etc. • Secondarily connected to cortex (after its evolution; tr. Spinoreticulo-thalamicus), but this system has a small resolutions – dull diffuse pain 64 Paleospinothalamic system • Tr. Spinoreticularis, spinotectalis… • Evolved before neocortex • The primary connection to the subcortical structures • Basic defensive reactions and reflexes - vegetative response, reflex locomotion - opto-acoustic reflexes etc. • Secondarily connected to cortex (after its evolution; tr. Spinoreticulo-thalamicus), but this system has a small resolutions – dull diffuse pain • This tract is not designed for „such a powerful processor as neocortex“ 65 Paleospinothalamic system • Tr. Spinoreticularis, spinotectalis… • Evolved before neocortex • The primary connection to the subcortical structures • Basic defensive reactions and reflexes - vegetative response, reflex locomotion - opto-acoustic reflexes etc. • Secondarily connected to cortex (after its evolution; tr. Spinoreticulo-thalamicus), but this system has a small resolutions – dull diffuse pain • This tract is not designed for „such a powerful processor as neocortex“ • Approximately half of the fibers cross the midline 66 http://neuroscience.uth.tmc.edu Neospinothalamic system • Tr. Spinothalamicus 68 Neospinothalamic system • Tr. Spinothalamicus • Younger structure primarily connected to neocortex • „High capacity/resolution“ 69 Neospinothalamic system • Tr. Spinothalamicus • Younger structure primarily connected to neocortex • „High capacity/resolution“ • Detail information about pain stimuli (sharp, localized pain) • Information about temperature 70 Neospinothalamic system • Tr. Spinothalamicus • Younger structure primarily connected to neocortex • „High capacity/resolution“ • Detail information about pain stimuli (sharp, localized pain) • Information about temperature • Crude touch sensation 71 Neospinothalamic system • Tr. Spinothalamicus • Younger structure primarily connected to neocortex • „High capacity/resolution“ • Detail information about pain stimuli (sharp, localized pain) • Information about temperature • Crude touch sensation • The fibers cross midline at the level of entry segment 72 http://neuroscience.uth.tmc.edu Dorsal column system • Tr. Spinobulbaris 74 Dorsal column system • Tr. Spinobulbaris • The youngest system • High capacity 75 Dorsal column system • Tr. Spinobulbaris • The youngest system • High capacity • Tactile sensation • Vibration • Proprioception 76 Dorsal column system • Tr. Spinobulbaris • The youngest system • High capacity • Tactile sensation • Vibration • Proprioception • Fine motor control • Better object recognition • Adaptive value 77 Dorsal column system • Tr. Spinobulbaris • The youngest system • High capacity • Tactile sensation • Vibration • Proprioception • Fine motor control • Better object recognition • Adaptive value • The fibers cross midline at the level of medulla oblongata 78 http://neuroscience.uth.tmc.edu Gate theory • Melzack and Wall 1965 • Stimulation of A fibers – closes • Stimulation of C fibers – opens • substantia gelatinosa Rolandi neurons with inhibitory function modulate the input of pulses from A and C fibers into T effector neurons • T cells are actively inhibited by substantia gelatinosa neurons at rest • the resulting impression is determined by the ratio of nociceptive, modulating and feedback mechanisms Gate theory • mechanisms: 1. substantia gelatinosa Rolandi 2. descendent inhibitory system • descendent inhibitory system : a/ opioid system: comes from the cortex, thalamus, limbic-hypothalamic structures periakveductal gray and reticular formation b/ adrenergic system: from locus coeruleus c/ serotoninergic system: comes from the nuclei of the brain stem (nucleus raphae magnus, nucleus reticularis gigantocelularis) Pain modulation on the spinal level Gate control theory of pain https://en.wikipedia.org/wiki/Gate_control_theory 82 Algogenní efekt Analgetický efekt substance P, neurokiny, neurotenzin, neuropeptid Y endorfiny, enkefaliny, dynorfiny noradrenalin noradrenalin serotonin serotonin GABA GABA serin, glycin, glutamát somatostatin N-metyl-D-aspartát, NO kalcitonin prostaglandiny a další Processing of painful information neocortex - cognitive processing limbic system - affective processing hypothalamus - release of hormones, endorphins brain stem - control of breathing and circulation, reticular activation system spinal cord - motor and sympathetic reflexes http://neuroscience.uth.tmc.edu Thalamus a neocortex • Almost all the afferent information gated in the thalamus • Olfaction is an exception • Bilateral connections between neocortex and thalamus http://www.slideshare.net/drpsdeb/presentations 87 Neokortex http://www.shadmehrlab.org/Courses/physfound_files/wang_5.pdfhttp://www.slideshare.net/drpsdeb/presentations Pain• Distressing feeling associated with real or potential tissue damage • Sensor x psychological component • Physiological x pathological pain • Acute (up to 6months) x chronic (more than 6 months) https://www.cheatography.com/uploads/davidpol_1460561912_Pain_Scale__Arvin61r58.png89 Descendent pathways modulating pain • Somatosemcoric cortex • Hypotalamus • Periaquaeductal gray • Nuclei raphe 90 Bolest Fyziologická • Aktivace nociceptorů • Informace o (potenciálním) nebezpečí/poškození Patologická • Není vázána na nociceptory • Poškození struktur zapojenných do vedení nebo zpracování bolestivého podnětu • Nerv (neuropatie) • Plexus (plexopatie) • Kořen (radikulopatie) • Míšní dráha (myelopatie) • Mozek (např. thalamus) • Mechanismus • Např. tlak, krvácení, metabolické postižení Akutní • Do 6 měsíců • Většinou odeznění po odstranění příčiny • Vegetativní odpověď – Aktivace sympatiku • Psychologická komponenta – Úzkost Chronická • Nad 6 měsíců • Obtížně léčitelná • Vegetativní odpověď chybí • Psychologická komponenta – Deprese, podráždění Bolest Fyziologická • Aktivace nociceptorů • Informace o (potenciálním) nebezpečí/poškození Patologická • Není vázána na nociceptory • Poškození struktur zapojenných do vedení nebo zpracování bolestivého podnětu • Nerv (neuropatie) • Plexus (plexopatie) • Kořen (radikulopatie) • Míšní dráha (myelopatie) • Mozek (např. thalamus) • Mechanismus • Např. tlak, krvácení, metabolické postižení Akutní • Do 6 měsíců • Většinou odeznění po odstranění příčiny • Vegetativní odpověď – Aktivace sympatiku • Psychologická komponenta – Úzkost Chronická • Nad 6 měsíců • Obtížně léčitelná • Vegetativní odpověď chybí • Psychologická komponenta – Deprese, podráždění Visceral organ pain • it is transmitted to typical skin ranges → Head zones corresponding to the projection of the affected organ → localy observed increased sensitivity to other modalities and enhancement of vegetative symptoms : vasomotor, sudomotor, dermographism + increased muscle tone to defense musculaire Referred pain http://www.slideshare.net/drpsdeb/presentations 94 Dermatomy http://www.slideshare.net/drpsdeb/presentations Dermatomy http://www.slideshare.net/drpsdeb/presentations http://www.slideshare.net/CsillaEgri/presentations Special types of pain • neuralgia sharp, seizure, affects peripheral or cranial nerves (often trigeminus, facialis) → after traumatic injury, oppression, viral disease, mainly herpetic, metabolic (DM) • pain in chronic compression of peripheral nerves and nerve roots intervertebral disk hernia, nerve depression in bone channel → pain + paraesthesia, mechanoreceptors (tactile) are discontinued from long term pressure action, painful afferentation remains intact • → burning pain Phantom pain http://www.slideshare.net/drpsdeb/presentations Special types of pain • phantom pain after limb amputation, after losing other parts of the body, after tooth extraction → the impression of the presence of a removed body part, a smaller percentage (about 30%) of pain (patients with long-term pain before amputation) → substantia gelatinosa deaferentation or brain irritation Special types of pain • ischemic pain it is a result of a defect in blood flow to the myocardium, smooth or skeletal muscle → release of substance P, histamine, serotonin, potassium from cells, ↓ pH migraine pain migraine is characterized by pulsating, predominantly unilateral headaches typically lasting 4-72 hours with nausea, eventual vomiting, photophobia and phonophobia, suffering from 12% of the adult population Migraine • the spread of blood flow down the cortex is secondary to decreased neuronal function (metabolic depression) epiphenomenon of so-called Lea's cortical depression spontaneous electrical activity Depression begins at the occipital pole and spreads forward on the lateral, medial and ventral sides of the brain a transient ionic and metabolic disturbance at the front of the wave that triggers changes in blood flow and focal symptoms vessel blood flow decreases by 20-30%, usually for 2-6 hours Migraine • the so-called trigeminovascular system mediates pain perception when depolarizing the fibers of the trigeminovascular system, substance P is released from the nerve endings into the wall of the cerebral vessels and also transmits nociceptive signals to the CNS Substance P potentiates pain mechanisms by increasing vascular permeability, degranulates mast cells with subsequent release of histamine, serotonin, and dopamine, and stimulates prostaglandin synthesis. → These substances surround the artery with painful sterile inflammation. Trigeminal system http://www.slideshare.net/drpsdeb/presentations 103 Thanks