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
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