Pathophysiology of cns
MartaGerasymchuk
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83 slides
May 14, 2013
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About This Presentation
prepared by MD, PhD, Associate Professor. Marta R. Gerasymchuk. Pathophysiology department of Ivano-Frankivsk National Medical University
Slide Content
Pathophysiology of the Pathophysiology of the
nervous system: violation of nervous system: violation of
sensory, motor and trophic sensory, motor and trophic
function.function.
nervous system: violation of nervous system: violation of
sensory, motor and trophic sensory, motor and trophic
function.function.
Actuality of the lectureActuality of the lecture
The nervous system as a main regulatory system of an organism in this or The nervous system as a main regulatory system of an organism in this or
that measure participates in pathogenesis of each diseases. The earliest and that measure participates in pathogenesis of each diseases. The earliest and
obligatory form of participation of the nervous system in pathology is obligatory form of participation of the nervous system in pathology is
defensive and adaptive the response. The protective reflexes (cough, defensive and adaptive the response. The protective reflexes (cough,
vomiting), protective inhibition, response hypotalamo-hypophysial-adrenal vomiting), protective inhibition, response hypotalamo-hypophysial-adrenal
system belong to such responses. system belong to such responses.
At the same time during development of diseases the nervous system At the same time during development of diseases the nervous system
becomes the object of a defeat itself. It is defensive and adaptive the becomes the object of a defeat itself. It is defensive and adaptive the
response of the damaged nervous system are reduced, and it becomes a response of the damaged nervous system are reduced, and it becomes a
source of pathological, harmful to an organism reflexes. Itself graving and source of pathological, harmful to an organism reflexes. Itself graving and
character of violations of nervous activity depend on localization of character of violations of nervous activity depend on localization of
pathological process and appear as a complex of diverse symptoms. pathological process and appear as a complex of diverse symptoms.
Frequently there is a pain, which on the essence is typical pathological Frequently there is a pain, which on the essence is typical pathological
process, but at the same time has signal and adaptive significance. The process, but at the same time has signal and adaptive significance. The
disturbance of nervous activity is always reflected in the function of internal disturbance of nervous activity is always reflected in the function of internal
organs. organs.
The fundamental knowledges of the reasons and mechanisms of disorders The fundamental knowledges of the reasons and mechanisms of disorders
motor, sensitive and trophic functions of the nervous system are necessary for motor, sensitive and trophic functions of the nervous system are necessary for
understanding of pathogenesis nervous diseases, and also many symptoms understanding of pathogenesis nervous diseases, and also many symptoms
of a damage of internal organs.of a damage of internal organs.
The nervous system as a main regulatory system of an organism in this or The nervous system as a main regulatory system of an organism in this or
that measure participates in pathogenesis of each diseases. The earliest and that measure participates in pathogenesis of each diseases. The earliest and
obligatory form of participation of the nervous system in pathology is obligatory form of participation of the nervous system in pathology is
defensive and adaptive the response. The protective reflexes (cough, defensive and adaptive the response. The protective reflexes (cough,
vomiting), protective inhibition, response hypotalamo-hypophysial-adrenal vomiting), protective inhibition, response hypotalamo-hypophysial-adrenal
system belong to such responses. system belong to such responses.
At the same time during development of diseases the nervous system At the same time during development of diseases the nervous system
becomes the object of a defeat itself. It is defensive and adaptive the becomes the object of a defeat itself. It is defensive and adaptive the
response of the damaged nervous system are reduced, and it becomes a response of the damaged nervous system are reduced, and it becomes a
source of pathological, harmful to an organism reflexes. Itself graving and source of pathological, harmful to an organism reflexes. Itself graving and
character of violations of nervous activity depend on localization of character of violations of nervous activity depend on localization of
pathological process and appear as a complex of diverse symptoms. pathological process and appear as a complex of diverse symptoms.
Frequently there is a pain, which on the essence is typical pathological Frequently there is a pain, which on the essence is typical pathological
process, but at the same time has signal and adaptive significance. The process, but at the same time has signal and adaptive significance. The
disturbance of nervous activity is always reflected in the function of internal disturbance of nervous activity is always reflected in the function of internal
organs. organs.
The fundamental knowledges of the reasons and mechanisms of disorders The fundamental knowledges of the reasons and mechanisms of disorders
motor, sensitive and trophic functions of the nervous system are necessary for motor, sensitive and trophic functions of the nervous system are necessary for
understanding of pathogenesis nervous diseases, and also many symptoms understanding of pathogenesis nervous diseases, and also many symptoms
of a damage of internal organs.of a damage of internal organs.
CONTENTCONTENT
•Nervous System: Neurons Nervous System: Neurons
•Division of the Nervous SystemDivision of the Nervous System
•Pain: features of pain as a kind of sensitivity. Pain: features of pain as a kind of sensitivity.
Etiology and pathogenesis of pain.Etiology and pathogenesis of pain.
•Antinociceptive systemsAntinociceptive systems
•Upper Motor NeuronsUpper Motor Neurons and Disorders and Disorders
•Sensory LossSensory Loss
•Spinal Cord InjuriesSpinal Cord Injuries
•DysphasiaDysphasia
•Diseases of the Basal GangliaDiseases of the Basal Ganglia
•Nervous System: Neurons Nervous System: Neurons
•Division of the Nervous SystemDivision of the Nervous System
•Pain: features of pain as a kind of sensitivity. Pain: features of pain as a kind of sensitivity.
Etiology and pathogenesis of pain.Etiology and pathogenesis of pain.
•Antinociceptive systemsAntinociceptive systems
•Upper Motor NeuronsUpper Motor Neurons and Disorders and Disorders
•Sensory LossSensory Loss
•Spinal Cord InjuriesSpinal Cord Injuries
•DysphasiaDysphasia
•Diseases of the Basal GangliaDiseases of the Basal Ganglia
FunctionFunction of neurons of neurons
A). Sensory input A). Sensory input
B). IntegrationB). Integration
C). Response C). Response
A). Sensory input A). Sensory input
B). IntegrationB). Integration
C). Response C). Response
A). Non nervous A). Non nervous or glial cellsor glial cells..
1). Astrocytes1). Astrocytes
2). Microglia2). Microglia
3). Ependymal3). Ependymal
4). Oliodendrocytes4). Oliodendrocytes
5). Satellite cells5). Satellite cells
6). 6). Schwann cellsSchwann cells form myelin sheaths form myelin sheaths
Types of cellsTypes of cells
1). Astrocytes1). Astrocytes
2). Microglia2). Microglia
3). Ependymal3). Ependymal
4). Oliodendrocytes4). Oliodendrocytes
5). Satellite cells5). Satellite cells
6). 6). Schwann cellsSchwann cells form myelin sheaths form myelin sheaths
Types of cellsTypes of cells
Types of Types of
cellscells
B). NeuronsB). Neurons
1). Structure 1). Structure
II). ). cell body cell body oror soma soma -- endoplasmic endoplasmic
reticulum called thereticulum called the nissl body nissl body. .
IIII). ). ProcessesProcesses or or tracts (nerves)tracts (nerves)
a).a). Dendrites: Dendrites: input regioninput region
b).b). Axon:Axon: Carries information away Carries information away
c).c). Synaptic knobsSynaptic knobs or or Axonal Axonal
terminalsterminals.. Releases Releases
neurotransmitters.neurotransmitters.
2). 2). AxonsAxons
a).a). myelin sheathmyelin sheath - - protects and protects and
electrically insulates fibers conduct electrically insulates fibers conduct
nerve impulses faster than nerve impulses faster than
nonmylenated fibers.nonmylenated fibers.
b).b). nodes of Ranvier nodes of Ranvier: :
spaces between the sheathsspaces between the sheaths
The action potential skips to the nodesThe action potential skips to the nodes
cellscells
B). NeuronsB). Neurons
1). Structure 1). Structure
II). ). cell body cell body oror soma soma -- endoplasmic endoplasmic
reticulum called thereticulum called the nissl body nissl body. .
IIII). ). ProcessesProcesses or or tracts (nerves)tracts (nerves)
a).a). Dendrites: Dendrites: input regioninput region
b).b). Axon:Axon: Carries information away Carries information away
c).c). Synaptic knobsSynaptic knobs or or Axonal Axonal
terminalsterminals.. Releases Releases
neurotransmitters.neurotransmitters.
2). 2). AxonsAxons
a).a). myelin sheathmyelin sheath - - protects and protects and
electrically insulates fibers conduct electrically insulates fibers conduct
nerve impulses faster than nerve impulses faster than
nonmylenated fibers.nonmylenated fibers.
b).b). nodes of Ranvier nodes of Ranvier: :
spaces between the sheathsspaces between the sheaths
The action potential skips to the nodesThe action potential skips to the nodes
Nerve ImpulseNerve Impulse
A). TermsA). Terms
1). 1). Resting membrane PotentialResting membrane Potential : :
PolarizedPolarized
2). 2). DepolarizationDepolarization: :
Change in ion concentrationChange in ion concentration
3). 3). Hyperpolarization Hyperpolarization
Change in ion concentration inside Change in ion concentration inside
becomes more negativebecomes more negative
4). 4). Graded Potential Graded Potential
Localized change in ion; subthresholdLocalized change in ion; subthreshold
5). 5). Action Potential Action Potential
Change in ion concentration that Change in ion concentration that
does not decrease over distance.does not decrease over distance.
B). B). Action PotentialAction Potential
Stages of an Action PotentialStages of an Action Potential
polarized resting potentialpolarized resting potential
depolarizes depolarizes
repolarizesrepolarizes
undershoot phaseundershoot phase
UndershooUndershoott : : the K+ channels stay open the K+ channels stay open
once resting potential is reached;once resting potential is reached;
hyperpolarizing the cell.hyperpolarizing the cell.
A). TermsA). Terms
1). 1). Resting membrane PotentialResting membrane Potential : :
PolarizedPolarized
2). 2). DepolarizationDepolarization: :
Change in ion concentrationChange in ion concentration
3). 3). Hyperpolarization Hyperpolarization
Change in ion concentration inside Change in ion concentration inside
becomes more negativebecomes more negative
4). 4). Graded Potential Graded Potential
Localized change in ion; subthresholdLocalized change in ion; subthreshold
5). 5). Action Potential Action Potential
Change in ion concentration that Change in ion concentration that
does not decrease over distance.does not decrease over distance.
B). B). Action PotentialAction Potential
Stages of an Action PotentialStages of an Action Potential
polarized resting potentialpolarized resting potential
depolarizes depolarizes
repolarizesrepolarizes
undershoot phaseundershoot phase
UndershooUndershoott : : the K+ channels stay open the K+ channels stay open
once resting potential is reached;once resting potential is reached;
hyperpolarizing the cell.hyperpolarizing the cell.
Nerve Nerve ImpulseImpulse
C). C). PropagationPropagation
Cannot be depolarized again until the membrane has Cannot be depolarized again until the membrane has
reached resting potential. The action potential moves at a reached resting potential. The action potential moves at a
constant velocity constant velocity
D). D). All or none phenomenonAll or none phenomenon
Not all depolarizations result in action potentialsNot all depolarizations result in action potentials.. The The
depolarization must reach the depolarization must reach the threshold pointthreshold point
E). E). Refractory periodRefractory period
AAbsolute refractory periodbsolute refractory period cannot respond to another cannot respond to another
stimuli. stimuli.
RRelative refractory period elative refractory period -- tthe threshold is higher he threshold is higher
F). Impulse VelocityF). Impulse Velocity
Strong stimuli result in more nerve impulses Not Strong stimuli result in more nerve impulses Not
stronger impulses or fasterstronger impulses or faster
C). C). PropagationPropagation
Cannot be depolarized again until the membrane has Cannot be depolarized again until the membrane has
reached resting potential. The action potential moves at a reached resting potential. The action potential moves at a
constant velocity constant velocity
D). D). All or none phenomenonAll or none phenomenon
Not all depolarizations result in action potentialsNot all depolarizations result in action potentials.. The The
depolarization must reach the depolarization must reach the threshold pointthreshold point
E). E). Refractory periodRefractory period
AAbsolute refractory periodbsolute refractory period cannot respond to another cannot respond to another
stimuli. stimuli.
RRelative refractory period elative refractory period -- tthe threshold is higher he threshold is higher
F). Impulse VelocityF). Impulse Velocity
Strong stimuli result in more nerve impulses Not Strong stimuli result in more nerve impulses Not
stronger impulses or fasterstronger impulses or faster
SynapseSynapse – – junction that carries junction that carries
information between neurons information between neurons
A). TypesA). Types
1). Electrical synapse: ions to cross junction1). Electrical synapse: ions to cross junction
2). Chemical synapse2). Chemical synapse
neurotransmitters neurotransmitters
B). Termination of neurotransmitterB). Termination of neurotransmitter
1). Degradation enzymes1). Degradation enzymes
2). Neurotransmitter reabsorbed2). Neurotransmitter reabsorbed
3). Diffusion of the neurotransmitter 3). Diffusion of the neurotransmitter
Impulse Impulse
releasesreleases Ca++ (in neuron) Ca++ (in neuron)
± neurotransmitter released ± binds to receptors± neurotransmitter released ± binds to receptors ±±
ion channels open on postsynaptic membraneion channels open on postsynaptic membrane
information between neurons information between neurons
A). TypesA). Types
1). Electrical synapse: ions to cross junction1). Electrical synapse: ions to cross junction
2). Chemical synapse2). Chemical synapse
neurotransmitters neurotransmitters
B). Termination of neurotransmitterB). Termination of neurotransmitter
1). Degradation enzymes1). Degradation enzymes
2). Neurotransmitter reabsorbed2). Neurotransmitter reabsorbed
3). Diffusion of the neurotransmitter 3). Diffusion of the neurotransmitter
Impulse Impulse
releasesreleases Ca++ (in neuron) Ca++ (in neuron)
± neurotransmitter released ± binds to receptors± neurotransmitter released ± binds to receptors ±±
ion channels open on postsynaptic membraneion channels open on postsynaptic membrane
A). Excitatory Synapses
neurotransmitters results in the
depolarization of postsynaptic
membrane. Creating localized graded
response.
(dendrites do not have action
potentials)
IF THE GRADED RESPONSE IS
STRONG ENOUGH TO BE CARRIED
TO THE AXON A FULL ACTION
POTENTIAL WILL RESULT
B). Inhibitory Synapses
Binding neurotransmitters reduces
the postsynaptic membranes ability
to create an action potential.
Induces hyperpolarization.
Types of Neurotransmitters
neurotransmitters results in the
depolarization of postsynaptic
membrane. Creating localized graded
response.
(dendrites do not have action
potentials)
IF THE GRADED RESPONSE IS
STRONG ENOUGH TO BE CARRIED
TO THE AXON A FULL ACTION
POTENTIAL WILL RESULT
B). Inhibitory Synapses
Binding neurotransmitters reduces
the postsynaptic membranes ability
to create an action potential.
Induces hyperpolarization.
Types of Neurotransmitters
C. Integration or Summation of Synaptic Events
It takes more than one synaptic event to create
an action potential.
Presynaptic inhibition = excitatory
neurotransmitter by one neuron + inhibitory
neurotransmitter of another neuron
It takes more than one synaptic event to create
an action potential.
Presynaptic inhibition = excitatory
neurotransmitter by one neuron + inhibitory
neurotransmitter of another neuron
Neurotransmitters
A). Acetylcholine (ACh)
B). Biogenic Amines
•1). Dopamine
•2). Norepinephrine
•3). Epinephrine
•4). Serotonin
C). Amino Acids
D). Peptides
•1). endorphins
E). Novel or Miscellaneous
A). Acetylcholine (ACh)
B). Biogenic Amines
•1). Dopamine
•2). Norepinephrine
•3). Epinephrine
•4). Serotonin
C). Amino Acids
D). Peptides
•1). endorphins
E). Novel or Miscellaneous
Division of the Nervous
System
A). Central Nervous
System: (CNS)
• Brain and Spinal Cord
only
B). Peripheral Nervous
System
• Outside CNS
1). Sensory or afferent
division:
• Carries impulses to CNS
2). Motor or efferent
division
• Carries impulses from the
CNS.
I). Somatic Nervous System
• voluntary
II). Autonomic Nervous
System
• involuntary
•a. Parasympathetic
•b. Sympathetic
System
A). Central Nervous
System: (CNS)
• Brain and Spinal Cord
only
B). Peripheral Nervous
System
• Outside CNS
1). Sensory or afferent
division:
• Carries impulses to CNS
2). Motor or efferent
division
• Carries impulses from the
CNS.
I). Somatic Nervous System
• voluntary
II). Autonomic Nervous
System
• involuntary
•a. Parasympathetic
•b. Sympathetic
The Sympathetic The Sympathetic
Nervous SystemNervous System
The The first fibersfirst fibers of the sympathetic nerves, called the of the sympathetic nerves, called the
preganglionic fiberspreganglionic fibers, leave from the thoracic or lumbar , leave from the thoracic or lumbar
regions of the spine. regions of the spine.
Soon after Soon after leaving the spineleaving the spine, a preganglionic fiber , a preganglionic fiber joins joins
other preganglionic fibersother preganglionic fibers to form an to form an autonomic ganglionautonomic ganglion. .
At this point, the At this point, the preganglionic fiber synapsespreganglionic fiber synapses on the on the
second nerve fiber of the systemsecond nerve fiber of the system, the , the postganglionic fiberpostganglionic fiber, ,
and and releases acetylcholinereleases acetylcholine, which causes the , which causes the
postganglionic fiber to fire an postganglionic fiber to fire an action potentialaction potential. .
From the From the autonomic gangliaautonomic ganglia, the postganglionic fiber travels , the postganglionic fiber travels
to its to its target organtarget organ, the muscle or gland. , the muscle or gland.
The The sympathetic postganglionic fibersympathetic postganglionic fiber usually releases the usually releases the
neurotransmitter norepinephrineneurotransmitter norepinephrine. . Target organ receptors for Target organ receptors for
norepinephrinenorepinephrine are called are called adrenergic receptorsadrenergic receptors..
Nervous SystemNervous System
The The first fibersfirst fibers of the sympathetic nerves, called the of the sympathetic nerves, called the
preganglionic fiberspreganglionic fibers, leave from the thoracic or lumbar , leave from the thoracic or lumbar
regions of the spine. regions of the spine.
Soon after Soon after leaving the spineleaving the spine, a preganglionic fiber , a preganglionic fiber joins joins
other preganglionic fibersother preganglionic fibers to form an to form an autonomic ganglionautonomic ganglion. .
At this point, the At this point, the preganglionic fiber synapsespreganglionic fiber synapses on the on the
second nerve fiber of the systemsecond nerve fiber of the system, the , the postganglionic fiberpostganglionic fiber, ,
and and releases acetylcholinereleases acetylcholine, which causes the , which causes the
postganglionic fiber to fire an postganglionic fiber to fire an action potentialaction potential. .
From the From the autonomic gangliaautonomic ganglia, the postganglionic fiber travels , the postganglionic fiber travels
to its to its target organtarget organ, the muscle or gland. , the muscle or gland.
The The sympathetic postganglionic fibersympathetic postganglionic fiber usually releases the usually releases the
neurotransmitter norepinephrineneurotransmitter norepinephrine. . Target organ receptors for Target organ receptors for
norepinephrinenorepinephrine are called are called adrenergic receptorsadrenergic receptors..
The Parasympathetic Nervous SystemThe Parasympathetic Nervous System
The fibers of the parasympathetic nervous systemThe fibers of the parasympathetic nervous system (PNS) (PNS)
leave the brain in the cranial nervesleave the brain in the cranial nerves or or leave the spinal cord leave the spinal cord
from the sacral areafrom the sacral area. .
The The preganglionic fiberpreganglionic fiber of the of the PNSPNS is typically long and travels is typically long and travels
to an autonomic ganglionto an autonomic ganglion located located near the target organnear the target organ. .
Preganglionic parasympathetic nervesPreganglionic parasympathetic nerves release release acetylcholineacetylcholine
that that then stimulates the postganglionic fiberthen stimulates the postganglionic fiber. .
The The parasympathetic postganglionic fiberparasympathetic postganglionic fiber then travels a short then travels a short
distance distance to its target tissueto its target tissue, a , a muscle or a glandmuscle or a gland. This nerve . This nerve
also releases acetylcholinealso releases acetylcholine. .
Preganglionic acetylcholine receptorsPreganglionic acetylcholine receptors for sympathetic and for sympathetic and
parasympathetic fibersparasympathetic fibers are called are called nicotinic receptorsnicotinic receptors. .
Postganglionic acetylcholine receptorsPostganglionic acetylcholine receptors are called are called muscarinic muscarinic
receptorsreceptors. These names relate to the experimental . These names relate to the experimental
stimulation of the receptors by stimulation of the receptors by nicotinenicotine and and muscarinemuscarine (a (a
mushroom poison). mushroom poison).
The fibers of the parasympathetic nervous systemThe fibers of the parasympathetic nervous system (PNS) (PNS)
leave the brain in the cranial nervesleave the brain in the cranial nerves or or leave the spinal cord leave the spinal cord
from the sacral areafrom the sacral area. .
The The preganglionic fiberpreganglionic fiber of the of the PNSPNS is typically long and travels is typically long and travels
to an autonomic ganglionto an autonomic ganglion located located near the target organnear the target organ. .
Preganglionic parasympathetic nervesPreganglionic parasympathetic nerves release release acetylcholineacetylcholine
that that then stimulates the postganglionic fiberthen stimulates the postganglionic fiber. .
The The parasympathetic postganglionic fiberparasympathetic postganglionic fiber then travels a short then travels a short
distance distance to its target tissueto its target tissue, a , a muscle or a glandmuscle or a gland. This nerve . This nerve
also releases acetylcholinealso releases acetylcholine. .
Preganglionic acetylcholine receptorsPreganglionic acetylcholine receptors for sympathetic and for sympathetic and
parasympathetic fibersparasympathetic fibers are called are called nicotinic receptorsnicotinic receptors. .
Postganglionic acetylcholine receptorsPostganglionic acetylcholine receptors are called are called muscarinic muscarinic
receptorsreceptors. These names relate to the experimental . These names relate to the experimental
stimulation of the receptors by stimulation of the receptors by nicotinenicotine and and muscarinemuscarine (a (a
mushroom poison). mushroom poison).
Functions of the Sympathetic and Functions of the Sympathetic and
Parasympathetic NervesParasympathetic Nerves
The The sympathetic nervous systemsympathetic nervous system innervates the innervates the heartheart, ,
causing an causing an increase in heart rateincrease in heart rate and and strength of contractionstrength of contraction. .
Sympathetic nervesSympathetic nerves innervate innervate all large and small arteriesall large and small arteries
and and veinsveins, causing , causing constriction of all vessels constriction of all vessels except the except the
arterioles supplying skeletal musclearterioles supplying skeletal muscle. .
Sympathetic nervesSympathetic nerves innervate the innervate the smooth muscle of the smooth muscle of the
gutgut, causing , causing decreased motilitydecreased motility, and the , and the smooth muscle of smooth muscle of
the respiratory tractthe respiratory tract, causing , causing bronchial relaxationbronchial relaxation and and
decreased bronchial secretionsdecreased bronchial secretions. .
Sympathetic stimulationSympathetic stimulation affects the affects the liverliver, , stimulates stimulates
secretions of the secretions of the sweat glandssweat glands, and is responsible for , and is responsible for
ejaculation during male orgasmejaculation during male orgasm..
Parasympathetic fibersParasympathetic fibers innervate the innervate the heartheart, , slowing the slowing the
heart rateheart rate, and the , and the gutgut, causing , causing increased motilityincreased motility. .
Parasympathetic nervesParasympathetic nerves innervate innervate bronchial smooth bronchial smooth
musclemuscle, causing , causing airway constrictionairway constriction, and the , and the genitourinary genitourinary
tracttract, causing , causing erection in the maleerection in the male..
Parasympathetic NervesParasympathetic Nerves
The The sympathetic nervous systemsympathetic nervous system innervates the innervates the heartheart, ,
causing an causing an increase in heart rateincrease in heart rate and and strength of contractionstrength of contraction. .
Sympathetic nervesSympathetic nerves innervate innervate all large and small arteriesall large and small arteries
and and veinsveins, causing , causing constriction of all vessels constriction of all vessels except the except the
arterioles supplying skeletal musclearterioles supplying skeletal muscle. .
Sympathetic nervesSympathetic nerves innervate the innervate the smooth muscle of the smooth muscle of the
gutgut, causing , causing decreased motilitydecreased motility, and the , and the smooth muscle of smooth muscle of
the respiratory tractthe respiratory tract, causing , causing bronchial relaxationbronchial relaxation and and
decreased bronchial secretionsdecreased bronchial secretions. .
Sympathetic stimulationSympathetic stimulation affects the affects the liverliver, , stimulates stimulates
secretions of the secretions of the sweat glandssweat glands, and is responsible for , and is responsible for
ejaculation during male orgasmejaculation during male orgasm..
Parasympathetic fibersParasympathetic fibers innervate the innervate the heartheart, , slowing the slowing the
heart rateheart rate, and the , and the gutgut, causing , causing increased motilityincreased motility. .
Parasympathetic nervesParasympathetic nerves innervate innervate bronchial smooth bronchial smooth
musclemuscle, causing , causing airway constrictionairway constriction, and the , and the genitourinary genitourinary
tracttract, causing , causing erection in the maleerection in the male..
The Autonomic Nervous System
Structure Sympathetic StimulationParasympathetic Stimulation
Iris (eye muscle) Pupil dilation Pupil constriction
Salivary Glands Saliva production reduced Saliva production increased
Oral/Nasal Mucosa Mucus production reduced Mucus production increased
Heart Heart rate and force increased Heart rate and force decreased
Lung Bronchial muscle relaxed Bronchial muscle contracted
Stomach Peristalsis reduced Gastric juice secreted; motility
increased
Small Intestine Motility reduced Digestion increased
Large Intestine Motility reduced Secretions and motility increased
Liver Increased conversion of glycogen
to glucose
---
Kidney Decreased urine secretion Increased urine secretion
Adrenal medulla Norepinephrine and epinephrine
secreted
---
Bladder Wall relaxed Sphincter closed Wall contracted Sphincter relaxed
Structure Sympathetic StimulationParasympathetic Stimulation
Iris (eye muscle) Pupil dilation Pupil constriction
Salivary Glands Saliva production reduced Saliva production increased
Oral/Nasal Mucosa Mucus production reduced Mucus production increased
Heart Heart rate and force increased Heart rate and force decreased
Lung Bronchial muscle relaxed Bronchial muscle contracted
Stomach Peristalsis reduced Gastric juice secreted; motility
increased
Small Intestine Motility reduced Digestion increased
Large Intestine Motility reduced Secretions and motility increased
Liver Increased conversion of glycogen
to glucose
---
Kidney Decreased urine secretion Increased urine secretion
Adrenal medulla Norepinephrine and epinephrine
secreted
---
Bladder Wall relaxed Sphincter closed Wall contracted Sphincter relaxed
THE SOMATOSENSORY SYSTEMTHE SOMATOSENSORY SYSTEM
■ ■ The somatosensory system relays information to theThe somatosensory system relays information to the
CNS about four major body sensations: CNS about four major body sensations:
touch, touch,
temperature,temperature,
pain, pain,
body positionbody position. .
Stimulation of receptorsStimulation of receptors on regions of the body wall is on regions of the body wall is
required torequired to initiate the sensory response.initiate the sensory response.
■ ■ The system is organized into The system is organized into dermatomesdermatomes, with each, with each
segment supplied by a segment supplied by a single dorsal root ganglionsingle dorsal root ganglion that that
sequentially relays the sensory information tosequentially relays the sensory information to the the
spinal cord, the thalamus, and the sensoryspinal cord, the thalamus, and the sensory cortexcortex..
■ ■ Two pathwaysTwo pathways carry sensory information throughcarry sensory information through the the
CNSCNS. The . The discriminative pathwaydiscriminative pathway crosses in the crosses in the
medulla and relays touch and body position. Themedulla and relays touch and body position. The
anterolateral pathwayanterolateral pathway crosses in the spinal cord crosses in the spinal cord and and
relays temperature and pain sensation fromrelays temperature and pain sensation from the the
opposite side of the body.opposite side of the body.
■ ■ The somatosensory system relays information to theThe somatosensory system relays information to the
CNS about four major body sensations: CNS about four major body sensations:
touch, touch,
temperature,temperature,
pain, pain,
body positionbody position. .
Stimulation of receptorsStimulation of receptors on regions of the body wall is on regions of the body wall is
required torequired to initiate the sensory response.initiate the sensory response.
■ ■ The system is organized into The system is organized into dermatomesdermatomes, with each, with each
segment supplied by a segment supplied by a single dorsal root ganglionsingle dorsal root ganglion that that
sequentially relays the sensory information tosequentially relays the sensory information to the the
spinal cord, the thalamus, and the sensoryspinal cord, the thalamus, and the sensory cortexcortex..
■ ■ Two pathwaysTwo pathways carry sensory information throughcarry sensory information through the the
CNSCNS. The . The discriminative pathwaydiscriminative pathway crosses in the crosses in the
medulla and relays touch and body position. Themedulla and relays touch and body position. The
anterolateral pathwayanterolateral pathway crosses in the spinal cord crosses in the spinal cord and and
relays temperature and pain sensation fromrelays temperature and pain sensation from the the
opposite side of the body.opposite side of the body.
The Sensory Unit
The somatosensory experience arises from
information provided by a variety of receptors
distributed throughout the body.
There are four major modalities of sensory
experience:
(1) discriminative touch, which is required to
identify the size and shape of objects and their
movement across the skin;
(2) temperature sensation;
(3) sense of movement of the limbs and joints
of the body;
(4) nociception or pain sense.
The somatosensory experience arises from
information provided by a variety of receptors
distributed throughout the body.
There are four major modalities of sensory
experience:
(1) discriminative touch, which is required to
identify the size and shape of objects and their
movement across the skin;
(2) temperature sensation;
(3) sense of movement of the limbs and joints
of the body;
(4) nociception or pain sense.
Kinds of SensitivityKinds of Sensitivity
1. 1. PainfulPainful
2. 2. TemperatureTemperature
3. 3. TactileTactile
4. 4. ProprioceptiveProprioceptive
1. 1. PainfulPainful
2. 2. TemperatureTemperature
3. 3. TactileTactile
4. 4. ProprioceptiveProprioceptive
DEFINITION OF PAINDEFINITION OF PAIN
PAINPAIN – – it is typical pathological processit is typical pathological process, ,
whichwhich was generated during evolutionwas generated during evolution andand
which arise owing to action on an organism which arise owing to action on an organism
painfulpainful ( (nociceptivenociceptive) ) irritantirritant oror weakeningweakening
ofof antipainful antipainful ((antinociceptiveantinociceptive) ) systemsystem
PainPain is an “unpleasant sensory and is an “unpleasant sensory and
emotional experience associatedemotional experience associated with with
potential tissue damage, or described in potential tissue damage, or described in
terms ofterms of such damage.”such damage.”
PAINPAIN – – it is typical pathological processit is typical pathological process, ,
whichwhich was generated during evolutionwas generated during evolution andand
which arise owing to action on an organism which arise owing to action on an organism
painfulpainful ( (nociceptivenociceptive) ) irritantirritant oror weakeningweakening
ofof antipainful antipainful ((antinociceptiveantinociceptive) ) systemsystem
PainPain is an “unpleasant sensory and is an “unpleasant sensory and
emotional experience associatedemotional experience associated with with
potential tissue damage, or described in potential tissue damage, or described in
terms ofterms of such damage.”such damage.”
CLASSIFICATION OF
PAIN
•Physiological pain
•Pathological pain
•Acute pain
•Chronical pain
MEDIATORS OF MEDIATORS OF
PAINPAIN
•Substanse Р
•Glutamic acid
•Cholecystokinin
•Neurotensin
PAIN
•Physiological pain
•Pathological pain
•Acute pain
•Chronical pain
MEDIATORS OF MEDIATORS OF
PAINPAIN
•Substanse Р
•Glutamic acid
•Cholecystokinin
•Neurotensin
TYPES OF PAINTYPES OF PAIN
Pain can be classified according to
location,
site of referral, and
duration.
Cutaneous pain is a sharp, burning pain that has its
origin in the skin or subcutaneous tissues.
Deep pain is a more diffuse and throbbing pain that
originates in structures such as the muscles, bones,
and tendons and radiates to the surrounding
tissues.
Visceral pain is a diffuse and poorly defined pain
that results from stretching, distention, or ischemia
of tissues in a body organ.
Referred pain is pain that originates at a visceral site
but is perceived as originating in part of the body
wall that is innervated by neurons entering the same
segment of the nervous system.
Acute pain usually results from tissue damage and
is characterized by autonomic nervous system
responses.
Chronic pain is persistent pain that is accompanied
by loss of appetite, sleep disturbances, depression,
and other debilitating responses.
Pain can be classified according to
location,
site of referral, and
duration.
Cutaneous pain is a sharp, burning pain that has its
origin in the skin or subcutaneous tissues.
Deep pain is a more diffuse and throbbing pain that
originates in structures such as the muscles, bones,
and tendons and radiates to the surrounding
tissues.
Visceral pain is a diffuse and poorly defined pain
that results from stretching, distention, or ischemia
of tissues in a body organ.
Referred pain is pain that originates at a visceral site
but is perceived as originating in part of the body
wall that is innervated by neurons entering the same
segment of the nervous system.
Acute pain usually results from tissue damage and
is characterized by autonomic nervous system
responses.
Chronic pain is persistent pain that is accompanied
by loss of appetite, sleep disturbances, depression,
and other debilitating responses.
PAIN SENSATION
■ Pain is both a protective and an unpleasant physical and emotionally
disturbing sensation originating in pain receptors that respond to a
number of stimuli that threaten tissue integrity.
■ There are two pathways for pain transmission:
• The fast pathway for sharply discriminated pain that moves directly
from the receptor to the spinal cord using myelinated Aδ fibers and from
the spinal cord to the thalamus using the neospinothalamic tract
• The slow pathway for continuously conducted pain that is transmitted
to the spinal cord using unmyelinated C fibers and from the spinal cord
to the thalamus using the more circuitous and slower-conducting
paleospinothalamic tract.
■ The central processing of pain information includes transmission to the
somatosensory cortex, where pain information is perceived and
interpreted; the limbic system, where the emotional components of pain
are experienced; and to brain stem centers, where autonomic nervous
system responses are recruited.
■ Modulation of the pain experience occurs by way of the endogenous
analgesic center in the midbrain, the pontine noradrenergic neurons,
and the nucleus raphe magnus in the medulla, which sends inhibitory
signals to dorsal horn neurons in the spinal cord.
■ Pain is both a protective and an unpleasant physical and emotionally
disturbing sensation originating in pain receptors that respond to a
number of stimuli that threaten tissue integrity.
■ There are two pathways for pain transmission:
• The fast pathway for sharply discriminated pain that moves directly
from the receptor to the spinal cord using myelinated Aδ fibers and from
the spinal cord to the thalamus using the neospinothalamic tract
• The slow pathway for continuously conducted pain that is transmitted
to the spinal cord using unmyelinated C fibers and from the spinal cord
to the thalamus using the more circuitous and slower-conducting
paleospinothalamic tract.
■ The central processing of pain information includes transmission to the
somatosensory cortex, where pain information is perceived and
interpreted; the limbic system, where the emotional components of pain
are experienced; and to brain stem centers, where autonomic nervous
system responses are recruited.
■ Modulation of the pain experience occurs by way of the endogenous
analgesic center in the midbrain, the pontine noradrenergic neurons,
and the nucleus raphe magnus in the medulla, which sends inhibitory
signals to dorsal horn neurons in the spinal cord.
Classical and non-Classical and non-
classical views of pain classical views of pain
transmission and pain transmission and pain
modulationmodulation (a). (a).
Classical pain Classical pain
transmission transmission
pathwaypathway. .
(b):(b): Normal painNormal pain. .
Under basal Under basal
conditions, pain is not conditions, pain is not
modulated by glia. modulated by glia.
(c)(c) Pain facilitation:Pain facilitation:
classical view. In classical view. In
response to intense response to intense
and/or prolonged and/or prolonged
barrages of incoming barrages of incoming
“pain” signals, the “pain” signals, the
PTNs become PTNs become
sensitized and over-sensitized and over-
respond to subsequent respond to subsequent
incoming signals incoming signals
(d)(d) Pain Pain
facilitation:facilitation: new new
view. Here, glial view. Here, glial
activation is activation is
conceptualized as a conceptualized as a
driving force for driving force for
creating and creating and
maintaining pain maintaining pain
facilitation. facilitation.
Classical and non-Classical and non-
classical views of pain classical views of pain
transmission and pain transmission and pain
modulationmodulation (a). (a).
Classical pain Classical pain
transmission transmission
pathwaypathway. .
(b):(b): Normal painNormal pain. .
Under basal Under basal
conditions, pain is not conditions, pain is not
modulated by glia. modulated by glia.
(c)(c) Pain facilitation:Pain facilitation:
classical view. In classical view. In
response to intense response to intense
and/or prolonged and/or prolonged
barrages of incoming barrages of incoming
“pain” signals, the “pain” signals, the
PTNs become PTNs become
sensitized and over-sensitized and over-
respond to subsequent respond to subsequent
incoming signals incoming signals
(d)(d) Pain Pain
facilitation:facilitation: new new
view. Here, glial view. Here, glial
activation is activation is
conceptualized as a conceptualized as a
driving force for driving force for
creating and creating and
maintaining pain maintaining pain
facilitation. facilitation.
Pain TheoriesPain Theories
Traditionally, two theories have been offered to explain Traditionally, two theories have been offered to explain
thethe physiologic basis for the pain experience. physiologic basis for the pain experience.
The The firstfirst, , specificityspecificity theorytheory, regards pain as a separate , regards pain as a separate
sensory modality evoked bysensory modality evoked by the activity of specific the activity of specific
receptors that transmit information toreceptors that transmit information to pain centers or pain centers or
regions in the forebrain where pain is experienced.regions in the forebrain where pain is experienced.
The The secondsecond theory includes a group of theories theory includes a group of theories
collectivelycollectively referred to as referred to as pattern theorypattern theory. It proposes that . It proposes that
pain receptorspain receptors share endings or pathways with other share endings or pathways with other
sensory modalitiessensory modalities but that different patterns of activity
(i.e., spatial or temporal) of the same neurons can be
used to signal painful and nonpainful stimuli.
For example, light touch applied to the skin would
produce the sensation of touch through low-frequency
firing of the receptor; intense pressure would produce
pain through high-frequency firing of the same receptor.
Traditionally, two theories have been offered to explain Traditionally, two theories have been offered to explain
thethe physiologic basis for the pain experience. physiologic basis for the pain experience.
The The firstfirst, , specificityspecificity theorytheory, regards pain as a separate , regards pain as a separate
sensory modality evoked bysensory modality evoked by the activity of specific the activity of specific
receptors that transmit information toreceptors that transmit information to pain centers or pain centers or
regions in the forebrain where pain is experienced.regions in the forebrain where pain is experienced.
The The secondsecond theory includes a group of theories theory includes a group of theories
collectivelycollectively referred to as referred to as pattern theorypattern theory. It proposes that . It proposes that
pain receptorspain receptors share endings or pathways with other share endings or pathways with other
sensory modalitiessensory modalities but that different patterns of activity
(i.e., spatial or temporal) of the same neurons can be
used to signal painful and nonpainful stimuli.
For example, light touch applied to the skin would
produce the sensation of touch through low-frequency
firing of the receptor; intense pressure would produce
pain through high-frequency firing of the same receptor.
Gate control theoryGate control theory
AA modification of specificity theory, was modification of specificity theory, was proposed proposed
by Melzack and Wall in 1965 to meet the by Melzack and Wall in 1965 to meet the
challengeschallenges presented by the pattern theories. presented by the pattern theories.
This theory postulated theThis theory postulated the presence of neural presence of neural
gating mechanisms at the gating mechanisms at the segmental spinalsegmental spinal cord cord
level to account for interactions between pain and level to account for interactions between pain and
othersensory modalitiesothersensory modalities. .
According to the According to the gate control theorygate control theory, the , the
internuncialinternuncial neuronsneurons involved in the gating involved in the gating
mechanism mechanism are activatedare activated by large-diameter, faster-by large-diameter, faster-
propagating fibers that carry tactilepropagating fibers that carry tactile informationinformation. The . The
simultaneous firing of the large-diametersimultaneous firing of the large-diameter touch touch
fibersfibers has the has the potential for blocking the potential for blocking the
transmission oftransmission of impulsesimpulses from the from the small-diameter small-diameter
myelinated and unmyelinatedmyelinated and unmyelinated pain fiberspain fibers..
AA modification of specificity theory, was modification of specificity theory, was proposed proposed
by Melzack and Wall in 1965 to meet the by Melzack and Wall in 1965 to meet the
challengeschallenges presented by the pattern theories. presented by the pattern theories.
This theory postulated theThis theory postulated the presence of neural presence of neural
gating mechanisms at the gating mechanisms at the segmental spinalsegmental spinal cord cord
level to account for interactions between pain and level to account for interactions between pain and
othersensory modalitiesothersensory modalities. .
According to the According to the gate control theorygate control theory, the , the
internuncialinternuncial neuronsneurons involved in the gating involved in the gating
mechanism mechanism are activatedare activated by large-diameter, faster-by large-diameter, faster-
propagating fibers that carry tactilepropagating fibers that carry tactile informationinformation. The . The
simultaneous firing of the large-diametersimultaneous firing of the large-diameter touch touch
fibersfibers has the has the potential for blocking the potential for blocking the
transmission oftransmission of impulsesimpulses from the from the small-diameter small-diameter
myelinated and unmyelinatedmyelinated and unmyelinated pain fiberspain fibers..
NNeuromatrix euromatrix TTheoryheory
More recently, Melzack has developed the neuromatrix theory to
address further the brain’s role in pain as well as the multiple
dimensions and determinants of pain. This theory is particularly useful
in understanding chronic pain and phantom limb pain, in which
there is not a simple one-to-one relationship between tissue injury and
pain experience.
The neuromatrix theory proposes that the brain contains a widely
distributed neural network, called the body-self neuromatrix, that
contains somatosensory, limbic, and thalamocortical componentssomatosensory, limbic, and thalamocortical components.
Genetic and sensory influences determine the synaptic
architecture of an individual’s neuromatrix that integrates multiple
sources of input and evokes the sensory, affective, and cognitive
dimensions of pain experience and behavior.
These multiple input sources include:
somatosensory;
other sensory impulses affecting interpretation of the situation;
inputs from the brain addressing such things as attention, expectation,
culture, and personality;
intrinsic neural inhibitory modulation;
various components of stress-regulation systems.
More recently, Melzack has developed the neuromatrix theory to
address further the brain’s role in pain as well as the multiple
dimensions and determinants of pain. This theory is particularly useful
in understanding chronic pain and phantom limb pain, in which
there is not a simple one-to-one relationship between tissue injury and
pain experience.
The neuromatrix theory proposes that the brain contains a widely
distributed neural network, called the body-self neuromatrix, that
contains somatosensory, limbic, and thalamocortical componentssomatosensory, limbic, and thalamocortical components.
Genetic and sensory influences determine the synaptic
architecture of an individual’s neuromatrix that integrates multiple
sources of input and evokes the sensory, affective, and cognitive
dimensions of pain experience and behavior.
These multiple input sources include:
somatosensory;
other sensory impulses affecting interpretation of the situation;
inputs from the brain addressing such things as attention, expectation,
culture, and personality;
intrinsic neural inhibitory modulation;
various components of stress-regulation systems.
PAIN
•Damage to these pathways produces a deficit
in pain and temperature discrimination and
may also produce abnormal painful
sensations (dysesthesias) usually in the
area of sensory loss. Such pain is termed
neuropathic pain and often has a strange
burning, tingling, or electric shocklike quality.
It may arise from several mechanisms.
•Damaged peripheral nerve fibers become
highly mechanosensitive and may fire
spontaneously without known stimulation.
They also develop sensitivity to
norepinephrine released from sympathetic
postganglionic neurons.
•Electrical impulses may spread abnormally
from one fiber to another (ephaptic
conduction), enhancing the spontaneous
firing of multiple fibers.
•Neuropeptides released by injured nerves
may recruit an inflammatory reaction that
stimulates pain. In the dorsal horn,
denervated spinal neurons may become
spontaneously active.
•In the brain and spinal cord, synaptic
reorganization occurs in response to injury
and may lower the threshold for pain. In
addition, inhibition of pathways that modulate
transmission of sensory information in the
spinal cord and brainstem may promote
neuropathic pain.
•Damage to these pathways produces a deficit
in pain and temperature discrimination and
may also produce abnormal painful
sensations (dysesthesias) usually in the
area of sensory loss. Such pain is termed
neuropathic pain and often has a strange
burning, tingling, or electric shocklike quality.
It may arise from several mechanisms.
•Damaged peripheral nerve fibers become
highly mechanosensitive and may fire
spontaneously without known stimulation.
They also develop sensitivity to
norepinephrine released from sympathetic
postganglionic neurons.
•Electrical impulses may spread abnormally
from one fiber to another (ephaptic
conduction), enhancing the spontaneous
firing of multiple fibers.
•Neuropeptides released by injured nerves
may recruit an inflammatory reaction that
stimulates pain. In the dorsal horn,
denervated spinal neurons may become
spontaneously active.
•In the brain and spinal cord, synaptic
reorganization occurs in response to injury
and may lower the threshold for pain. In
addition, inhibition of pathways that modulate
transmission of sensory information in the
spinal cord and brainstem may promote
neuropathic pain.
PainPain
Free nerve endingsFree nerve endings of unmyelinated of unmyelinated
C fibers and small-diameter myelinated C fibers and small-diameter myelinated
AAδδ fibers in the skin convey sensory fibers in the skin convey sensory
information in response to information in response to chemical, chemical,
thermal, and mechanical stimulithermal, and mechanical stimuli. .
Intense stimulationIntense stimulation of these nerve of these nerve
endings endings evokes the sensation of painevokes the sensation of pain. .
In contrast to skin, most deep tissues In contrast to skin, most deep tissues
are relatively insensitive to chemical or are relatively insensitive to chemical or
noxious stimuli. noxious stimuli.
However, inflammatory conditions can However, inflammatory conditions can
sensitize sensory afferents from deep sensitize sensory afferents from deep
tissues to evoke pain on mechanical tissues to evoke pain on mechanical
stimulation. This sensitization appears stimulation. This sensitization appears
to be to be mediated bymediated by bradykinin, bradykinin,
prostaglandins, and leukotrienesprostaglandins, and leukotrienes
released during the inflammatory released during the inflammatory
response. response.
Information from Information from primary afferent fibersprimary afferent fibers
is relayed is relayed via sensory gangliavia sensory ganglia to the to the
dorsal horn of the spinal corddorsal horn of the spinal cord and then and then
to the to the contralateral spinothalamic tractcontralateral spinothalamic tract, ,
which connects to which connects to thalamic neuronsthalamic neurons
that project to the that project to the somatosensory somatosensory
cortexcortex..
Free nerve endingsFree nerve endings of unmyelinated of unmyelinated
C fibers and small-diameter myelinated C fibers and small-diameter myelinated
AAδδ fibers in the skin convey sensory fibers in the skin convey sensory
information in response to information in response to chemical, chemical,
thermal, and mechanical stimulithermal, and mechanical stimuli. .
Intense stimulationIntense stimulation of these nerve of these nerve
endings endings evokes the sensation of painevokes the sensation of pain. .
In contrast to skin, most deep tissues In contrast to skin, most deep tissues
are relatively insensitive to chemical or are relatively insensitive to chemical or
noxious stimuli. noxious stimuli.
However, inflammatory conditions can However, inflammatory conditions can
sensitize sensory afferents from deep sensitize sensory afferents from deep
tissues to evoke pain on mechanical tissues to evoke pain on mechanical
stimulation. This sensitization appears stimulation. This sensitization appears
to be to be mediated bymediated by bradykinin, bradykinin,
prostaglandins, and leukotrienesprostaglandins, and leukotrienes
released during the inflammatory released during the inflammatory
response. response.
Information from Information from primary afferent fibersprimary afferent fibers
is relayed is relayed via sensory gangliavia sensory ganglia to the to the
dorsal horn of the spinal corddorsal horn of the spinal cord and then and then
to the to the contralateral spinothalamic tractcontralateral spinothalamic tract, ,
which connects to which connects to thalamic neuronsthalamic neurons
that project to the that project to the somatosensory somatosensory
cortexcortex..
Primary pain pathways
NociceptiveNociceptive
stimulistimuli
Somesthetic association cortexSomesthetic association cortex
(perception and meaning)(perception and meaning)
Limbic cortexLimbic cortex
(emotional experience)(emotional experience)
PontinePontine
noradrenergic neuronsnoradrenergic neurons
Primary somesthetic cortexPrimary somesthetic cortex
(discrimination: location and intensity)(discrimination: location and intensity)
Medullary raphe nucleusMedullary raphe nucleus
Thalamus (sensation)Thalamus (sensation)
Somesthetic nucleiSomesthetic nuclei
Spinal cord and dorsal hornSpinal cord and dorsal horn
pain modulating circuitspain modulating circuits
Periaqueductal gray (PAG)Periaqueductal gray (PAG)
(endogenous analgesic center)(endogenous analgesic center)
Medullary NRMMedullary NRM
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Primary touch fibers
A-delta
(fast)
C-fiber
(slow)
NociceptiveNociceptive
stimulistimuli
Somesthetic association cortexSomesthetic association cortex
(perception and meaning)(perception and meaning)
Limbic cortexLimbic cortex
(emotional experience)(emotional experience)
PontinePontine
noradrenergic neuronsnoradrenergic neurons
Primary somesthetic cortexPrimary somesthetic cortex
(discrimination: location and intensity)(discrimination: location and intensity)
Medullary raphe nucleusMedullary raphe nucleus
Thalamus (sensation)Thalamus (sensation)
Somesthetic nucleiSomesthetic nuclei
Spinal cord and dorsal hornSpinal cord and dorsal horn
pain modulating circuitspain modulating circuits
Periaqueductal gray (PAG)Periaqueductal gray (PAG)
(endogenous analgesic center)(endogenous analgesic center)
Medullary NRMMedullary NRM
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(fast)
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(slow)
Characteristics of Characteristics of
Acute and Chronic PainAcute and Chronic Pain
Characteristic Acute Pain Chronic Pain
Onset Recent Continuous or intermittent
Duration Short duration (<6 months) 6 months or more
Autonomic responses
Consistent with sympathetic fight-
orflight response*
Increased heart rate
Increased stroke volume
Increased blood pressure
Increased pupillary dilation
Increased muscle tension
Decreased gut motility
Decreased salivary flow (dry mouth)
Absence of autonomic
responses
Psychological
component
Associated anxiety
Increased irritability
Associated depression
Somatic preoccupation
Withdrawal from outside
interests
Decreased strength of
relationships
Other types of
response
Decreased sleep
Decreased libido
Appetite changes
Acute and Chronic PainAcute and Chronic Pain
Characteristic Acute Pain Chronic Pain
Onset Recent Continuous or intermittent
Duration Short duration (<6 months) 6 months or more
Autonomic responses
Consistent with sympathetic fight-
orflight response*
Increased heart rate
Increased stroke volume
Increased blood pressure
Increased pupillary dilation
Increased muscle tension
Decreased gut motility
Decreased salivary flow (dry mouth)
Absence of autonomic
responses
Psychological
component
Associated anxiety
Increased irritability
Associated depression
Somatic preoccupation
Withdrawal from outside
interests
Decreased strength of
relationships
Other types of
response
Decreased sleep
Decreased libido
Appetite changes
Pain Threshold and Tolerance
Cando Baseline Dolorimeter
Pain threshold and tolerance affect an
individual’s response to a painful stimulus.
Although the terms often are used
interchangeably, pain threshold and pain
tolerance have distinct meanings. Pain
threshold is closely associated with tissue
damage and the point at which a stimulus is
perceived as painful.
Pain tolerance relates more to the total pain
experience; it is defined as the maximum
intensity or duration of pain that a person is
willing to endure before the person wants
something done about the pain.
Psychological, familial, cultural, and
environmental factors significantly influence
the amount of pain a person is willing to
tolerate. The threshold to pain is fairly uniform
from one person to another, whereas pain
tolerance is extremely variable. Separation
and identification of the role of each of
these two aspects of pain continue to pose
fundamental problems for the pain
management team and for pain researchers.
Cando Baseline Dolorimeter
Pain threshold and tolerance affect an
individual’s response to a painful stimulus.
Although the terms often are used
interchangeably, pain threshold and pain
tolerance have distinct meanings. Pain
threshold is closely associated with tissue
damage and the point at which a stimulus is
perceived as painful.
Pain tolerance relates more to the total pain
experience; it is defined as the maximum
intensity or duration of pain that a person is
willing to endure before the person wants
something done about the pain.
Psychological, familial, cultural, and
environmental factors significantly influence
the amount of pain a person is willing to
tolerate. The threshold to pain is fairly uniform
from one person to another, whereas pain
tolerance is extremely variable. Separation
and identification of the role of each of
these two aspects of pain continue to pose
fundamental problems for the pain
management team and for pain researchers.
Alterations in Pain Sensitivity
Hypersensitivity (i.e., hyperesthesia) or increased painfulness (i.e.,
hyperalgesia)
Primary hyperalgesia occurs at the site of injury.
Secondary hyperalgesia occurs in nearby uninjured tissue.
Hyperpathia is a syndrome in which the sensory threshold is raised,
but when it is reached, continued stimulation, especially if repetitive,
results in a prolonged and unpleasant experience. This pain can be
explosive and radiates through a peripheral nerve distribution. It is
associated with pathologic changes in peripheral nerves, such as
localized ischemia.
Spontaneous, unpleasant sensations called paresthesias occur with
more severe irritation (e.g., the pins-and-needles sensation that
follows temporary compression of a peripheral nerve).
The general term dysesthesia is given to distortions (usually
unpleasant) of somesthetic sensation that typically accompany partial
loss of sensory innervation.
Hypersensitivity (i.e., hyperesthesia) or increased painfulness (i.e.,
hyperalgesia)
Primary hyperalgesia occurs at the site of injury.
Secondary hyperalgesia occurs in nearby uninjured tissue.
Hyperpathia is a syndrome in which the sensory threshold is raised,
but when it is reached, continued stimulation, especially if repetitive,
results in a prolonged and unpleasant experience. This pain can be
explosive and radiates through a peripheral nerve distribution. It is
associated with pathologic changes in peripheral nerves, such as
localized ischemia.
Spontaneous, unpleasant sensations called paresthesias occur with
more severe irritation (e.g., the pins-and-needles sensation that
follows temporary compression of a peripheral nerve).
The general term dysesthesia is given to distortions (usually
unpleasant) of somesthetic sensation that typically accompany partial
loss of sensory innervation.
Alterations in Pain Sensitivity
•Severe pathologic processes can result in reduced or lost
tactile (e.g., hypoesthesia, anesthesia), temperature (e.g.,
hypothermia, athermia), and pain sensation (i.e.,
hypalgesia).
•Analgesia is the absence of pain on noxious stimulation or
the relief of pain without loss of consciousness. The inability to
sense pain may result in trauma, infection, and even loss of a
body part or parts. Inherited insensitivity to pain may take the
form of congenital indifference or congenital insensitivity to
pain.
•Allodynia (Greek allo, “other,” and odynia, “painful”) is the
term used for the puzzling phenomenon of pain that follows a
non-noxious stimulus to apparently normal skin. This term is
intended to refer to instances in which otherwise normal
tissues may be abnormally innervated or may be referral sites
for other loci that give rise to pain with non-noxious stimuli.
•Trigger points are highly localized points on the skin or
mucous membrane that can produce immediate intense pain
at that site or elsewhere when stimulated by light tactile
stimulation.
•Severe pathologic processes can result in reduced or lost
tactile (e.g., hypoesthesia, anesthesia), temperature (e.g.,
hypothermia, athermia), and pain sensation (i.e.,
hypalgesia).
•Analgesia is the absence of pain on noxious stimulation or
the relief of pain without loss of consciousness. The inability to
sense pain may result in trauma, infection, and even loss of a
body part or parts. Inherited insensitivity to pain may take the
form of congenital indifference or congenital insensitivity to
pain.
•Allodynia (Greek allo, “other,” and odynia, “painful”) is the
term used for the puzzling phenomenon of pain that follows a
non-noxious stimulus to apparently normal skin. This term is
intended to refer to instances in which otherwise normal
tissues may be abnormally innervated or may be referral sites
for other loci that give rise to pain with non-noxious stimuli.
•Trigger points are highly localized points on the skin or
mucous membrane that can produce immediate intense pain
at that site or elsewhere when stimulated by light tactile
stimulation.
CHRONICAL PAINFUL
SYNDROMES
Phantom pain
Causalgia
Neuralgia
Eccentric pain
Projectional pain
SYNDROMES
Phantom pain
Causalgia
Neuralgia
Eccentric pain
Projectional pain
NeuralgiaNeuralgia
NeuralgiaNeuralgia is characterized by severe, brief, is characterized by severe, brief,
often repetitive attacksoften repetitive attacks of lightning-like or of lightning-like or
throbbing pain. It occurs along the distributionthrobbing pain. It occurs along the distribution of of
a spinal or cranial nerve and usually is a spinal or cranial nerve and usually is
precipitatedprecipitated by stimulation of the cutaneous by stimulation of the cutaneous
region supplied by that nerve.region supplied by that nerve.
Trigeminal Neuralgia.Trigeminal Neuralgia.
Trigeminal neuralgia, or Trigeminal neuralgia, or tic tic
douloureuxdouloureux,, is one of the is one of the
most common and severe most common and severe
neuralgias. It is manifestedneuralgias. It is manifested
by by facial ticsfacial tics or or grimacesgrimaces
and characterized by and characterized by
stabbing,stabbing, paroxysmal paroxysmal
attacks of pain that usually attacks of pain that usually
are limited to the unilateralare limited to the unilateral
sensory distribution of one sensory distribution of one
or more branches of theor more branches of the
trigeminal nerve, most trigeminal nerve, most
often the maxillary or often the maxillary or
mandibular divisions.mandibular divisions.
NeuralgiaNeuralgia is characterized by severe, brief, is characterized by severe, brief,
often repetitive attacksoften repetitive attacks of lightning-like or of lightning-like or
throbbing pain. It occurs along the distributionthrobbing pain. It occurs along the distribution of of
a spinal or cranial nerve and usually is a spinal or cranial nerve and usually is
precipitatedprecipitated by stimulation of the cutaneous by stimulation of the cutaneous
region supplied by that nerve.region supplied by that nerve.
Trigeminal Neuralgia.Trigeminal Neuralgia.
Trigeminal neuralgia, or Trigeminal neuralgia, or tic tic
douloureuxdouloureux,, is one of the is one of the
most common and severe most common and severe
neuralgias. It is manifestedneuralgias. It is manifested
by by facial ticsfacial tics or or grimacesgrimaces
and characterized by and characterized by
stabbing,stabbing, paroxysmal paroxysmal
attacks of pain that usually attacks of pain that usually
are limited to the unilateralare limited to the unilateral
sensory distribution of one sensory distribution of one
or more branches of theor more branches of the
trigeminal nerve, most trigeminal nerve, most
often the maxillary or often the maxillary or
mandibular divisions.mandibular divisions.
Postherpetic Neuralgia.Postherpetic Neuralgia.
Postherpetic pain is pain Postherpetic pain is pain
that persiststhat persists as a as a
complication of herpes complication of herpes
zoster or shingles. It zoster or shingles. It
describes thedescribes the presence of presence of
pain more than 1 month pain more than 1 month
after the onset of the after the onset of the
acuteacute attack. attack.
Postherpetic neuralgiaPostherpetic neuralgia
develops in from 10% to develops in from 10% to
70% of70% of patients with patients with
shingles; the risk shingles; the risk
increases with age. increases with age.
The pain ofThe pain of postherpetic postherpetic
neuralgia occurs in the neuralgia occurs in the
areas of innervation of areas of innervation of
thethe infected gangliainfected ganglia. .
During the acute attack of During the acute attack of
herpes zosterherpes zoster, the, the
reactivated virus travels reactivated virus travels
from the ganglia to the from the ganglia to the
skin of the correspondingskin of the corresponding
dermatomes, causing dermatomes, causing
localized vesicular localized vesicular
eruptioneruption and hyperpathia and hyperpathia
((i.e.i.e., abnormally , abnormally
exaggerated subjective exaggerated subjective
responseresponse to pain). to pain).
Postherpetic pain is pain Postherpetic pain is pain
that persiststhat persists as a as a
complication of herpes complication of herpes
zoster or shingles. It zoster or shingles. It
describes thedescribes the presence of presence of
pain more than 1 month pain more than 1 month
after the onset of the after the onset of the
acuteacute attack. attack.
Postherpetic neuralgiaPostherpetic neuralgia
develops in from 10% to develops in from 10% to
70% of70% of patients with patients with
shingles; the risk shingles; the risk
increases with age. increases with age.
The pain ofThe pain of postherpetic postherpetic
neuralgia occurs in the neuralgia occurs in the
areas of innervation of areas of innervation of
thethe infected gangliainfected ganglia. .
During the acute attack of During the acute attack of
herpes zosterherpes zoster, the, the
reactivated virus travels reactivated virus travels
from the ganglia to the from the ganglia to the
skin of the correspondingskin of the corresponding
dermatomes, causing dermatomes, causing
localized vesicular localized vesicular
eruptioneruption and hyperpathia and hyperpathia
((i.e.i.e., abnormally , abnormally
exaggerated subjective exaggerated subjective
responseresponse to pain). to pain).
Postherpetic Neuralgia
Phantom Limb Pain
•Phantom limb pain, a type of
neurologic pain, follows
amputation of a limb or part of a
limb. As many as 70% of those
who under amputation
experience phantom pain.
•The pain often begins as
sensations of tingling, heat and
cold, or heaviness, followed by
burning, cramping, or shooting
pain. It may disappear
spontaneously or persist for
many years. One of the more
troublesome aspects of phantom
pain is that the person may
experience painful sensations
that were present before the
amputation, such as that of a
painful ulcer or bunion.
•Phantom limb pain, a type of
neurologic pain, follows
amputation of a limb or part of a
limb. As many as 70% of those
who under amputation
experience phantom pain.
•The pain often begins as
sensations of tingling, heat and
cold, or heaviness, followed by
burning, cramping, or shooting
pain. It may disappear
spontaneously or persist for
many years. One of the more
troublesome aspects of phantom
pain is that the person may
experience painful sensations
that were present before the
amputation, such as that of a
painful ulcer or bunion.
•Several theories have been proposed as to the causes of phantom pain.
•One theory is that the end of a regenerating nerve becomes trapped in the scar
tissue of the amputation site. It is known that when a peripheral nerve is cut, the scar
tissue that forms becomes a barrier to regenerating outgrowth of the axon. The
growing axon often becomes trapped in the scar tissue, forming a tangled growth
(i.e., neuroma) of smalldiameter axons, including primary nociceptive afferents and
sympathetic efferents. It has been proposed that these afferents show increased
sensitivity to innocuous mechanical stimuli and to sympathetic activity and circulating
catecholamines.
•A related theory moves the source of phantom limb pain to the spinal cord,
suggesting that the pain is caused by the spontaneous firing of spinal cord neurons
that have lost their normal sensory input from the body. In this case, a closed
self-exciting neuronal loop in the posterior horn of the spinal cord is postulated to
send impulses to the brain, resulting in pain. Even the slightest irritation to the
amputated limb area can initiate this cycle.
•Other theories propose that the phantom limb pain may arise in the brain. In one
hypothesis, the pain is caused by changes in the flow of signals through
somatosensory areas of the brain.
•Treatment of
phantom limb pain
has been
accomplished by the
use of sympathetic
blocks, TENS of the
large myelinated
afferents innervating
the area, hypnosis,
and relaxation
training.
•One theory is that the end of a regenerating nerve becomes trapped in the scar
tissue of the amputation site. It is known that when a peripheral nerve is cut, the scar
tissue that forms becomes a barrier to regenerating outgrowth of the axon. The
growing axon often becomes trapped in the scar tissue, forming a tangled growth
(i.e., neuroma) of smalldiameter axons, including primary nociceptive afferents and
sympathetic efferents. It has been proposed that these afferents show increased
sensitivity to innocuous mechanical stimuli and to sympathetic activity and circulating
catecholamines.
•A related theory moves the source of phantom limb pain to the spinal cord,
suggesting that the pain is caused by the spontaneous firing of spinal cord neurons
that have lost their normal sensory input from the body. In this case, a closed
self-exciting neuronal loop in the posterior horn of the spinal cord is postulated to
send impulses to the brain, resulting in pain. Even the slightest irritation to the
amputated limb area can initiate this cycle.
•Other theories propose that the phantom limb pain may arise in the brain. In one
hypothesis, the pain is caused by changes in the flow of signals through
somatosensory areas of the brain.
•Treatment of
phantom limb pain
has been
accomplished by the
use of sympathetic
blocks, TENS of the
large myelinated
afferents innervating
the area, hypnosis,
and relaxation
training.
Antinociceptive systemsAntinociceptive systems
NeuronalNeuronal opiate systemopiate system – – metmet- - and leuencephalinand leuencephalin
NeuronalNeuronal unopiate systemunopiate system – – noradrenalinnoradrenalin, , serotoninserotonin, ,
dopaminedopamine
HormonalHormonal opiate systemopiate system – – hormoneshormones of of
adenohypophysisadenohypophysis
HormonalHormonal unopiate systemunopiate system – – vasopressinvasopressin
NeuronalNeuronal opiate systemopiate system – – metmet- - and leuencephalinand leuencephalin
NeuronalNeuronal unopiate systemunopiate system – – noradrenalinnoradrenalin, , serotoninserotonin, ,
dopaminedopamine
HormonalHormonal opiate systemopiate system – – hormoneshormones of of
adenohypophysisadenohypophysis
HormonalHormonal unopiate systemunopiate system – – vasopressinvasopressin
Hormonal unopiate systemHormonal unopiate system
1. 1. Adrenocorticotropic hormoneAdrenocorticotropic hormone
2. 2. MelanostimulatingMelanostimulating hormoneshormones
3. 3. β β --LipotropicLipotropic hormonehormone
4. 4. LargeLarge endorphinesendorphines::
kitorphinkitorphin
ββ--kosomorphinkosomorphin
dinorphindinorphin
1. 1. Adrenocorticotropic hormoneAdrenocorticotropic hormone
2. 2. MelanostimulatingMelanostimulating hormoneshormones
3. 3. β β --LipotropicLipotropic hormonehormone
4. 4. LargeLarge endorphinesendorphines::
kitorphinkitorphin
ββ--kosomorphinkosomorphin
dinorphindinorphin
1.1.Opening of abscessOpening of abscess
2.2.Reposition ofReposition of
fragmentsfragments
3.3.Splintation of extremitySplintation of extremity
4.4.Section of scarsSection of scars
5.5.DesympathizationDesympathization
6.6.GangliectomyGangliectomy
1.1.AcupunctureAcupuncture
2.2.ElectroacupunctureElectroacupuncture
3.3.LaseropunctureLaseropuncture
4.4.ElectrostimulationElectrostimulation
5.5.ElectrophoresisElectrophoresis
6.6.UltrasoundUltrasound
7.7.Magnetico-laserMagnetico-laser therapytherapy
8.8.MassageMassage
9.9.Manual Manual therapytherapy
METHODS OF METHODS OF
ANAESTIZATIONANAESTIZATION
PsycologicalPsycological
PhysicalPhysical
PharmacologicalPharmacological
SurgicalSurgical
NeurosurgicalNeurosurgical
1. 1. ConversationConversation
2. 2. RelaxationRelaxation
3. 3. HypnosisHypnosis
4. 4. AutotrainingAutotraining
5. 5. CorrectCorrect stereotypestereotype of motionof motion
6. 6. Self-removel of painSelf-removel of pain
2.2.Reposition ofReposition of
fragmentsfragments
3.3.Splintation of extremitySplintation of extremity
4.4.Section of scarsSection of scars
5.5.DesympathizationDesympathization
6.6.GangliectomyGangliectomy
1.1.AcupunctureAcupuncture
2.2.ElectroacupunctureElectroacupuncture
3.3.LaseropunctureLaseropuncture
4.4.ElectrostimulationElectrostimulation
5.5.ElectrophoresisElectrophoresis
6.6.UltrasoundUltrasound
7.7.Magnetico-laserMagnetico-laser therapytherapy
8.8.MassageMassage
9.9.Manual Manual therapytherapy
METHODS OF METHODS OF
ANAESTIZATIONANAESTIZATION
PsycologicalPsycological
PhysicalPhysical
PharmacologicalPharmacological
SurgicalSurgical
NeurosurgicalNeurosurgical
1. 1. ConversationConversation
2. 2. RelaxationRelaxation
3. 3. HypnosisHypnosis
4. 4. AutotrainingAutotraining
5. 5. CorrectCorrect stereotypestereotype of motionof motion
6. 6. Self-removel of painSelf-removel of pain
Upper Motor NeuronsUpper Motor Neurons
Planned movements and those guided by sensory,
visual, or auditory stimuli are preceded by
discharges from prefrontal, somatosensory, visual,
or auditory cortices, which are then followed by
motor cortex pyramidal cell discharges that occur
several milliseconds before the onset of movement
AnatomyAnatomy
The The motor cortexmotor cortex is the is the
region from which region from which
movements can be elicited movements can be elicited
by electrical stimuli (Figure). by electrical stimuli (Figure).
This includes:
the primary motor area
(Brodmann area 4),
premotor cortex (area 6),
supplementary motor
cortex (medial portions of
6),
primary sensory cortex
(areas 3, 1, and 2).
In the motor cortex, groups
of neurons are organized in
vertical columns, and
discrete groups control
contraction of individual
muscles.
Planned movements and those guided by sensory,
visual, or auditory stimuli are preceded by
discharges from prefrontal, somatosensory, visual,
or auditory cortices, which are then followed by
motor cortex pyramidal cell discharges that occur
several milliseconds before the onset of movement
AnatomyAnatomy
The The motor cortexmotor cortex is the is the
region from which region from which
movements can be elicited movements can be elicited
by electrical stimuli (Figure). by electrical stimuli (Figure).
This includes:
the primary motor area
(Brodmann area 4),
premotor cortex (area 6),
supplementary motor
cortex (medial portions of
6),
primary sensory cortex
(areas 3, 1, and 2).
In the motor cortex, groups
of neurons are organized in
vertical columns, and
discrete groups control
contraction of individual
muscles.
►Cortical motor neuronsCortical motor neurons contribute axons that contribute axons that
converge in the corona radiata and descend in the converge in the corona radiata and descend in the
posterior limb of the internal capsule, cerebral posterior limb of the internal capsule, cerebral
peduncles, ventral pons, and medullapeduncles, ventral pons, and medulla. These fibers . These fibers
constitute the constitute the corticospinalcorticospinal and and corticobulbar corticobulbar
tractstracts and together are and together are known as known as upper motor upper motor
neuron fibersneuron fibers. As they descend through the . As they descend through the
diencephalon and brainstem, fibers separate to diencephalon and brainstem, fibers separate to
innervate extrapyramidal and cranial nerve motor innervate extrapyramidal and cranial nerve motor
nuclei. The lower brainstem motor neurons receive nuclei. The lower brainstem motor neurons receive
input from crossed and uncrossed corticobulbar input from crossed and uncrossed corticobulbar
fibers, although neurons that innervate lower facial fibers, although neurons that innervate lower facial
muscles receive primarily crossed fibers.muscles receive primarily crossed fibers.
►In the ventral medullaIn the ventral medulla, the remaining corticospinal , the remaining corticospinal
fibers course in a tract that is pyramidal in shape in fibers course in a tract that is pyramidal in shape in
cross section—thus, the name cross section—thus, the name pyramidal tractpyramidal tract.. At At
the the lower end of the medullalower end of the medulla, most fibers , most fibers
decussate, although the proportion of crossed and decussate, although the proportion of crossed and
uncrossed fibers varies somewhat between uncrossed fibers varies somewhat between
individuals. The bulk of these fibers descend as the individuals. The bulk of these fibers descend as the
lateral corticospinal tractlateral corticospinal tract of the spinal cord. of the spinal cord.
►Different groups of Different groups of neurons in the cortex control neurons in the cortex control
muscle groupsmuscle groups of the contralateral face, arm, and of the contralateral face, arm, and
legleg. Neurons near the ventral end of the central . Neurons near the ventral end of the central
sulcus control muscles of the face, whereas sulcus control muscles of the face, whereas
neurons on the medial surface of the hemisphere neurons on the medial surface of the hemisphere
control leg muscles. Because the control leg muscles. Because the movements of the movements of the
face, tongue, and hand are complex in humans, a face, tongue, and hand are complex in humans, a
large share of the motor cortex is devoted to their large share of the motor cortex is devoted to their
controlcontrol. A . A somatotopic organization somatotopic organization is also apparent is also apparent
in the in the lateral corticospinal tract lateral corticospinal tract of the cervical of the cervical
cord, where fibers to motor neurons that control leg cord, where fibers to motor neurons that control leg
muscles lie laterally and fibers to cervical motor muscles lie laterally and fibers to cervical motor
neurons lie medially.neurons lie medially.
converge in the corona radiata and descend in the converge in the corona radiata and descend in the
posterior limb of the internal capsule, cerebral posterior limb of the internal capsule, cerebral
peduncles, ventral pons, and medullapeduncles, ventral pons, and medulla. These fibers . These fibers
constitute the constitute the corticospinalcorticospinal and and corticobulbar corticobulbar
tractstracts and together are and together are known as known as upper motor upper motor
neuron fibersneuron fibers. As they descend through the . As they descend through the
diencephalon and brainstem, fibers separate to diencephalon and brainstem, fibers separate to
innervate extrapyramidal and cranial nerve motor innervate extrapyramidal and cranial nerve motor
nuclei. The lower brainstem motor neurons receive nuclei. The lower brainstem motor neurons receive
input from crossed and uncrossed corticobulbar input from crossed and uncrossed corticobulbar
fibers, although neurons that innervate lower facial fibers, although neurons that innervate lower facial
muscles receive primarily crossed fibers.muscles receive primarily crossed fibers.
►In the ventral medullaIn the ventral medulla, the remaining corticospinal , the remaining corticospinal
fibers course in a tract that is pyramidal in shape in fibers course in a tract that is pyramidal in shape in
cross section—thus, the name cross section—thus, the name pyramidal tractpyramidal tract.. At At
the the lower end of the medullalower end of the medulla, most fibers , most fibers
decussate, although the proportion of crossed and decussate, although the proportion of crossed and
uncrossed fibers varies somewhat between uncrossed fibers varies somewhat between
individuals. The bulk of these fibers descend as the individuals. The bulk of these fibers descend as the
lateral corticospinal tractlateral corticospinal tract of the spinal cord. of the spinal cord.
►Different groups of Different groups of neurons in the cortex control neurons in the cortex control
muscle groupsmuscle groups of the contralateral face, arm, and of the contralateral face, arm, and
legleg. Neurons near the ventral end of the central . Neurons near the ventral end of the central
sulcus control muscles of the face, whereas sulcus control muscles of the face, whereas
neurons on the medial surface of the hemisphere neurons on the medial surface of the hemisphere
control leg muscles. Because the control leg muscles. Because the movements of the movements of the
face, tongue, and hand are complex in humans, a face, tongue, and hand are complex in humans, a
large share of the motor cortex is devoted to their large share of the motor cortex is devoted to their
controlcontrol. A . A somatotopic organization somatotopic organization is also apparent is also apparent
in the in the lateral corticospinal tract lateral corticospinal tract of the cervical of the cervical
cord, where fibers to motor neurons that control leg cord, where fibers to motor neurons that control leg
muscles lie laterally and fibers to cervical motor muscles lie laterally and fibers to cervical motor
neurons lie medially.neurons lie medially.
Upper and Lower motoneurons innervate the skeletal
muscles and are essential for motor function.
•Amyotrophic lateral sclerosis (ALS), fatal combined degeneration of
motoneurons and motor fiber tracts (i.e. combined gray and white matter disease).
Motoneurons of entire neuraxis! ALS - most devastating neurodegenerative
disease of aging CNS that so resembles Alzheimer and Parkinson diseases.
muscles and are essential for motor function.
•Amyotrophic lateral sclerosis (ALS), fatal combined degeneration of
motoneurons and motor fiber tracts (i.e. combined gray and white matter disease).
Motoneurons of entire neuraxis! ALS - most devastating neurodegenerative
disease of aging CNS that so resembles Alzheimer and Parkinson diseases.
Upper and Lower motoneurons innervate the skeletal
muscles and are essential for motor function.
•Amyotrophic lateral sclerosis (ALS), also known as Lou
Gehrig’s disease after the famous New York Yankees
baseball player, is a devastating neurologic disorder that
selectively affects motor function. ALS is primarily a disorder
of middle to late adulthood, affecting persons between 55
and 60 years of age, with men developing the disease nearly
twice as often as women.
ETIOPATHOPHYSIOLOGY, PATHOLOGY
•Neuron degeneration, atrophy, and loss → glial replacement.
No inflammation! Degeneration of motoneurons:
•1. Motor cortex (pyramidal cells in precentral cortex) → loss
of large myelinated fibers in anterior & lateral spinal
columns (gliotic sclerosis of lateral columns = LATERAL
SCLEROSIS)
N.B. posterior columns are usually spared in SALS. N.B. posterior columns are usually spared in SALS.
•2. Brain stem - lower nuclei are more often / more
extensively involved than upper nuclei (e.g. oculomotor
nuclei loss is modest and rarely demonstrable clinically,
whereas hypoglossal nuclei are prominently degenerated).
•3. Spinal anterior horns → loss of myelinated fibers in
anterior root →muscle denervation atrophy
(AMYOTROPHY); reinnervation is possible (but much less
extensive as in poliomyelitis, peripheral neuropathy).
muscles and are essential for motor function.
•Amyotrophic lateral sclerosis (ALS), also known as Lou
Gehrig’s disease after the famous New York Yankees
baseball player, is a devastating neurologic disorder that
selectively affects motor function. ALS is primarily a disorder
of middle to late adulthood, affecting persons between 55
and 60 years of age, with men developing the disease nearly
twice as often as women.
ETIOPATHOPHYSIOLOGY, PATHOLOGY
•Neuron degeneration, atrophy, and loss → glial replacement.
No inflammation! Degeneration of motoneurons:
•1. Motor cortex (pyramidal cells in precentral cortex) → loss
of large myelinated fibers in anterior & lateral spinal
columns (gliotic sclerosis of lateral columns = LATERAL
SCLEROSIS)
N.B. posterior columns are usually spared in SALS. N.B. posterior columns are usually spared in SALS.
•2. Brain stem - lower nuclei are more often / more
extensively involved than upper nuclei (e.g. oculomotor
nuclei loss is modest and rarely demonstrable clinically,
whereas hypoglossal nuclei are prominently degenerated).
•3. Spinal anterior horns → loss of myelinated fibers in
anterior root →muscle denervation atrophy
(AMYOTROPHY); reinnervation is possible (but much less
extensive as in poliomyelitis, peripheral neuropathy).
Amyotrophic lateral sclerosisAmyotrophic lateral sclerosis
Cytoplasmic ultrastructural abnormalities (cytoskeleton is affected Cytoplasmic ultrastructural abnormalities (cytoskeleton is affected
early!):early!):
1) in proximal motor axons - strongly argentophilic 1) in proximal motor axons - strongly argentophilic SPHEROIDS SPHEROIDS
(accumulated (accumulated neurofilament bundlesneurofilament bundles that may contain other cytoplasmic that may contain other cytoplasmic
structures, such as mitochondria). structures, such as mitochondria).
some patients have mutations in some patients have mutations in neurofilament heavy chain subunit neurofilament heavy chain subunit
(22q).(22q).
abnormal neurofilaments interfere with axonal transport, resulting in abnormal neurofilaments interfere with axonal transport, resulting in
failure to maintain axonal structure and transport of macromolecules failure to maintain axonal structure and transport of macromolecules
such as neurotrophic factors required for motor neuron survival. such as neurotrophic factors required for motor neuron survival.
2) 2) Bunina bodies Bunina bodies - tiny round eosinophilic structures. - tiny round eosinophilic structures.
3) 3) Lewy body-like eosinophilic inclusions Lewy body-like eosinophilic inclusions (immunoreactive to (immunoreactive to
neurofilaments, ubiquitin neurofilaments, ubiquitin ((marker for degenerationmarker for degeneration)), and gene encoding , and gene encoding
Cu/Zn superoxide dismutase [SOD1]). Cu/Zn superoxide dismutase [SOD1]).
Number of abnormalities in Number of abnormalities in GLUTAMATEGLUTAMATE metabolism have been metabolism have been
identified in ALS (incl. alterations in tissue glutamate levels, transporter identified in ALS (incl. alterations in tissue glutamate levels, transporter
proteins, postsynaptic receptors) - primary or secondary events? proteins, postsynaptic receptors) - primary or secondary events?
60% patients have 60% patients have large decrease in GLUTAMATE TRANSPORT large decrease in GLUTAMATE TRANSPORT
activity*activity* in motor cortex and spinal cord (but not in other regions of in motor cortex and spinal cord (but not in other regions of
central nervous system) → ↑ extracellular levels of glutamate → central nervous system) → ↑ extracellular levels of glutamate →
excitotoxicity. excitotoxicity.
*loss of astrocytic *loss of astrocytic glutamate transporter protein EAAT2glutamate transporter protein EAAT2 (due to defect in (due to defect in
mRNA splicing). mRNA splicing).
Cytoplasmic ultrastructural abnormalities (cytoskeleton is affected Cytoplasmic ultrastructural abnormalities (cytoskeleton is affected
early!):early!):
1) in proximal motor axons - strongly argentophilic 1) in proximal motor axons - strongly argentophilic SPHEROIDS SPHEROIDS
(accumulated (accumulated neurofilament bundlesneurofilament bundles that may contain other cytoplasmic that may contain other cytoplasmic
structures, such as mitochondria). structures, such as mitochondria).
some patients have mutations in some patients have mutations in neurofilament heavy chain subunit neurofilament heavy chain subunit
(22q).(22q).
abnormal neurofilaments interfere with axonal transport, resulting in abnormal neurofilaments interfere with axonal transport, resulting in
failure to maintain axonal structure and transport of macromolecules failure to maintain axonal structure and transport of macromolecules
such as neurotrophic factors required for motor neuron survival. such as neurotrophic factors required for motor neuron survival.
2) 2) Bunina bodies Bunina bodies - tiny round eosinophilic structures. - tiny round eosinophilic structures.
3) 3) Lewy body-like eosinophilic inclusions Lewy body-like eosinophilic inclusions (immunoreactive to (immunoreactive to
neurofilaments, ubiquitin neurofilaments, ubiquitin ((marker for degenerationmarker for degeneration)), and gene encoding , and gene encoding
Cu/Zn superoxide dismutase [SOD1]). Cu/Zn superoxide dismutase [SOD1]).
Number of abnormalities in Number of abnormalities in GLUTAMATEGLUTAMATE metabolism have been metabolism have been
identified in ALS (incl. alterations in tissue glutamate levels, transporter identified in ALS (incl. alterations in tissue glutamate levels, transporter
proteins, postsynaptic receptors) - primary or secondary events? proteins, postsynaptic receptors) - primary or secondary events?
60% patients have 60% patients have large decrease in GLUTAMATE TRANSPORT large decrease in GLUTAMATE TRANSPORT
activity*activity* in motor cortex and spinal cord (but not in other regions of in motor cortex and spinal cord (but not in other regions of
central nervous system) → ↑ extracellular levels of glutamate → central nervous system) → ↑ extracellular levels of glutamate →
excitotoxicity. excitotoxicity.
*loss of astrocytic *loss of astrocytic glutamate transporter protein EAAT2glutamate transporter protein EAAT2 (due to defect in (due to defect in
mRNA splicing). mRNA splicing).
DemyelinationDemyelination
In In myelinated nervesmyelinated nerves, the axon between two nodes of Ranvier (internodal , the axon between two nodes of Ranvier (internodal
segment) is surrounded by a segment) is surrounded by a myelin sheathmyelin sheath. This is a precondition for . This is a precondition for
saltatory conduction of the action potentials, i.e., the “jumping” propagation saltatory conduction of the action potentials, i.e., the “jumping” propagation
of excitation from one nodal constriction (R1) to the next (R2). The of excitation from one nodal constriction (R1) to the next (R2). The
internodal segment itself cannot generate an action potential, i.e., internodal segment itself cannot generate an action potential, i.e.,
depolarization of the second node (R2) is completely dependent on the depolarization of the second node (R2) is completely dependent on the
current from the first node (R1). However, the current is usually so strong current from the first node (R1). However, the current is usually so strong
that it can even jump across the nodes. that it can even jump across the nodes.
Nevertheless, on the way along the internodal segment the amplitude of the Nevertheless, on the way along the internodal segment the amplitude of the
current will diminish. First of all, the membrane in the internodal segment current will diminish. First of all, the membrane in the internodal segment
must change its polarity, i.e., the must change its polarity, i.e., the membrane capacitance membrane capacitance must be must be
discharged, for which a current is needed. Secondly, current can also discharged, for which a current is needed. Secondly, current can also
escape through individual escape through individual ionic channels ionic channels in the axonal membrane (orange in the axonal membrane (orange
arrow). However, myelination of the internodal segment causes the arrow). However, myelination of the internodal segment causes the
membrane resistance (Rm) to be elevated and the capacity (Cm) of the membrane resistance (Rm) to be elevated and the capacity (Cm) of the
membrane condensor to be reduced.membrane condensor to be reduced.
The The resistance resistance of the axonal membrane of the internodal segment is very of the axonal membrane of the internodal segment is very
high because of the low density of ionic channels there. Furthermore, the high because of the low density of ionic channels there. Furthermore, the
perimembranous space is insulated by a layer of fat from the free perimembranous space is insulated by a layer of fat from the free
extracellular space. The low extracellular space. The low capacitance capacitance of the condensor is due to the of the condensor is due to the
large distance between the interior of the axon and the free extracellular large distance between the interior of the axon and the free extracellular
space as well as the low polarity of the fatty material in the space between space as well as the low polarity of the fatty material in the space between
them.them.
In In myelinated nervesmyelinated nerves, the axon between two nodes of Ranvier (internodal , the axon between two nodes of Ranvier (internodal
segment) is surrounded by a segment) is surrounded by a myelin sheathmyelin sheath. This is a precondition for . This is a precondition for
saltatory conduction of the action potentials, i.e., the “jumping” propagation saltatory conduction of the action potentials, i.e., the “jumping” propagation
of excitation from one nodal constriction (R1) to the next (R2). The of excitation from one nodal constriction (R1) to the next (R2). The
internodal segment itself cannot generate an action potential, i.e., internodal segment itself cannot generate an action potential, i.e.,
depolarization of the second node (R2) is completely dependent on the depolarization of the second node (R2) is completely dependent on the
current from the first node (R1). However, the current is usually so strong current from the first node (R1). However, the current is usually so strong
that it can even jump across the nodes. that it can even jump across the nodes.
Nevertheless, on the way along the internodal segment the amplitude of the Nevertheless, on the way along the internodal segment the amplitude of the
current will diminish. First of all, the membrane in the internodal segment current will diminish. First of all, the membrane in the internodal segment
must change its polarity, i.e., the must change its polarity, i.e., the membrane capacitance membrane capacitance must be must be
discharged, for which a current is needed. Secondly, current can also discharged, for which a current is needed. Secondly, current can also
escape through individual escape through individual ionic channels ionic channels in the axonal membrane (orange in the axonal membrane (orange
arrow). However, myelination of the internodal segment causes the arrow). However, myelination of the internodal segment causes the
membrane resistance (Rm) to be elevated and the capacity (Cm) of the membrane resistance (Rm) to be elevated and the capacity (Cm) of the
membrane condensor to be reduced.membrane condensor to be reduced.
The The resistance resistance of the axonal membrane of the internodal segment is very of the axonal membrane of the internodal segment is very
high because of the low density of ionic channels there. Furthermore, the high because of the low density of ionic channels there. Furthermore, the
perimembranous space is insulated by a layer of fat from the free perimembranous space is insulated by a layer of fat from the free
extracellular space. The low extracellular space. The low capacitance capacitance of the condensor is due to the of the condensor is due to the
large distance between the interior of the axon and the free extracellular large distance between the interior of the axon and the free extracellular
space as well as the low polarity of the fatty material in the space between space as well as the low polarity of the fatty material in the space between
them.them.
Demyelination Demyelination can be can be
caused by degenerative, caused by degenerative,
toxic, or inflammatory toxic, or inflammatory
damage to the nerves, damage to the nerves,
or by a deficiency of or by a deficiency of
vitamins B6 or B12. vitamins B6 or B12.
If this happens, Rm will If this happens, Rm will
be reduced and Cm be reduced and Cm
raised in the internodal raised in the internodal
segment. segment.
As a result, more current As a result, more current
will be required to will be required to
change the polarity of change the polarity of
the internodal segment the internodal segment
and, through opening up and, through opening up
the ionic channels, large the ionic channels, large
losses of current may losses of current may
occur.occur.
caused by degenerative, caused by degenerative,
toxic, or inflammatory toxic, or inflammatory
damage to the nerves, damage to the nerves,
or by a deficiency of or by a deficiency of
vitamins B6 or B12. vitamins B6 or B12.
If this happens, Rm will If this happens, Rm will
be reduced and Cm be reduced and Cm
raised in the internodal raised in the internodal
segment. segment.
As a result, more current As a result, more current
will be required to will be required to
change the polarity of change the polarity of
the internodal segment the internodal segment
and, through opening up and, through opening up
the ionic channels, large the ionic channels, large
losses of current may losses of current may
occur.occur.
Multiple SclerosisMultiple Sclerosis
•Multiple sclerosis (MS), a demyelinating disease of the CNS, is a major cause of
neurologic disability among young and middleaged adults. Approximately two thirds
of persons with MS experience their first symptoms between 20 and 40 years of age.
In approximately 80% of the cases, the disease is characterized by exacerbations
and remissions over many years in several different sites in the CNS.
•Initially, there is normal or nearnormal neurologic function between exacerbations. As
the disease progresses, there is less improvement between exacerbations and
increasing neurologic dysfunction.
•Multiple sclerosis (MS), a demyelinating disease of the CNS, is a major cause of
neurologic disability among young and middleaged adults. Approximately two thirds
of persons with MS experience their first symptoms between 20 and 40 years of age.
In approximately 80% of the cases, the disease is characterized by exacerbations
and remissions over many years in several different sites in the CNS.
•Initially, there is normal or nearnormal neurologic function between exacerbations. As
the disease progresses, there is less improvement between exacerbations and
increasing neurologic dysfunction.
Huntington's diseaseHuntington's disease
Huntington's diseaseHuntington's disease is inherited as an is inherited as an
autosomal dominant disorder. autosomal dominant disorder.
When disease onset occurs later in life, When disease onset occurs later in life,
patients develop involuntary, rapid, jerky patients develop involuntary, rapid, jerky
movements (movements (choreachorea) and slow writhing ) and slow writhing
movements of the proximal limbs and trunk movements of the proximal limbs and trunk
((athetosisathetosis). ).
When disease onset occurs earlier in life, When disease onset occurs earlier in life,
patients develop signs of parkinsonism with patients develop signs of parkinsonism with
tremor (cogwheeling) and stiffness. The tremor (cogwheeling) and stiffness. The
spiny spiny GABAergic neuronsGABAergic neurons of the striatum of the striatum
preferentially degenerate, resulting in a net preferentially degenerate, resulting in a net
decrease in GABAergic output from the decrease in GABAergic output from the
striatum. This contributes to the striatum. This contributes to the
development of chorea and athetosis. development of chorea and athetosis.
DopamineDopamine antagonists, which block antagonists, which block
inhibition of remaining striatal neurons by inhibition of remaining striatal neurons by
dopaminergic striatal fibers, reduce the dopaminergic striatal fibers, reduce the
involuntary movements. Neurons in deep involuntary movements. Neurons in deep
layers of the cerebral cortex also layers of the cerebral cortex also
degenerate early in the disease, and later degenerate early in the disease, and later
this extends to other brain regions, including this extends to other brain regions, including
the hippocampus and hypothalamus. the hippocampus and hypothalamus.
Thus, the disease is characterized by Thus, the disease is characterized by
cognitive defects and psychiatric cognitive defects and psychiatric
disturbances in addition to the movement disturbances in addition to the movement
disorder.disorder.
Huntington's diseaseHuntington's disease is inherited as an is inherited as an
autosomal dominant disorder. autosomal dominant disorder.
When disease onset occurs later in life, When disease onset occurs later in life,
patients develop involuntary, rapid, jerky patients develop involuntary, rapid, jerky
movements (movements (choreachorea) and slow writhing ) and slow writhing
movements of the proximal limbs and trunk movements of the proximal limbs and trunk
((athetosisathetosis). ).
When disease onset occurs earlier in life, When disease onset occurs earlier in life,
patients develop signs of parkinsonism with patients develop signs of parkinsonism with
tremor (cogwheeling) and stiffness. The tremor (cogwheeling) and stiffness. The
spiny spiny GABAergic neuronsGABAergic neurons of the striatum of the striatum
preferentially degenerate, resulting in a net preferentially degenerate, resulting in a net
decrease in GABAergic output from the decrease in GABAergic output from the
striatum. This contributes to the striatum. This contributes to the
development of chorea and athetosis. development of chorea and athetosis.
DopamineDopamine antagonists, which block antagonists, which block
inhibition of remaining striatal neurons by inhibition of remaining striatal neurons by
dopaminergic striatal fibers, reduce the dopaminergic striatal fibers, reduce the
involuntary movements. Neurons in deep involuntary movements. Neurons in deep
layers of the cerebral cortex also layers of the cerebral cortex also
degenerate early in the disease, and later degenerate early in the disease, and later
this extends to other brain regions, including this extends to other brain regions, including
the hippocampus and hypothalamus. the hippocampus and hypothalamus.
Thus, the disease is characterized by Thus, the disease is characterized by
cognitive defects and psychiatric cognitive defects and psychiatric
disturbances in addition to the movement disturbances in addition to the movement
disorder.disorder.
HUNTINGTON DISEASEHUNTINGTON DISEASE
Classical familial, Classical familial,
genetic diseasegenetic disease
Progressive Progressive
motor loss and motor loss and
dementiadementia
““chorea”, i.e. chorea”, i.e.
“jerky” “jerky”
movementsmovements
Progressive, fatalProgressive, fatal
Atrophy of basal Atrophy of basal
ganglia, i.e., ganglia, i.e.,
corpus striatumcorpus striatum Cortical (basal ganglia) atrophyCortical (basal ganglia) atrophy
Ventricular enlargementVentricular enlargement
Classical familial, Classical familial,
genetic diseasegenetic disease
Progressive Progressive
motor loss and motor loss and
dementiadementia
““chorea”, i.e. chorea”, i.e.
“jerky” “jerky”
movementsmovements
Progressive, fatalProgressive, fatal
Atrophy of basal Atrophy of basal
ganglia, i.e., ganglia, i.e.,
corpus striatumcorpus striatum Cortical (basal ganglia) atrophyCortical (basal ganglia) atrophy
Ventricular enlargementVentricular enlargement
CNS DEGENERATIVE DISEASESCNS DEGENERATIVE DISEASES
•SPINOCEREBELLAR SPINOCEREBELLAR
DEGENERATIONS DEGENERATIONS
(ATAXIAS)(ATAXIAS)
–Spinocerebellar ataxiasSpinocerebellar ataxias
–Friedrich AtaxiaFriedrich Ataxia
–Ataxia-TelangiectasiaAtaxia-Telangiectasia
•SPINOCEREBELLAR SPINOCEREBELLAR
DEGENERATIONS DEGENERATIONS
(ATAXIAS)(ATAXIAS)
–Spinocerebellar ataxiasSpinocerebellar ataxias
–Friedrich AtaxiaFriedrich Ataxia
–Ataxia-TelangiectasiaAtaxia-Telangiectasia
SPINOCEREBELLAR DEGENERATIONSSPINOCEREBELLAR DEGENERATIONS
Cerebellar cortexCerebellar cortex
Spinal cordSpinal cord
Peripheral nervesPeripheral nerves
FEATURES:FEATURES:
•ATAXIAATAXIA (loss of extremity muscle (loss of extremity muscle
coordination)coordination)
•SPASTICITYSPASTICITY
•NEUROPATHIESNEUROPATHIES
Cerebellar cortexCerebellar cortex
Spinal cordSpinal cord
Peripheral nervesPeripheral nerves
FEATURES:FEATURES:
•ATAXIAATAXIA (loss of extremity muscle (loss of extremity muscle
coordination)coordination)
•SPASTICITYSPASTICITY
•NEUROPATHIESNEUROPATHIES
ACQUIRED ACQUIRED
TOXIC/METABOLICTOXIC/METABOLIC
CNS DISEASESCNS DISEASES
VitaminVitamin B1B1 deficiency (Wernicke-Korsakoff)deficiency (Wernicke-Korsakoff)
Vitamin Vitamin B12 B12 deficiency (vibratory sense)deficiency (vibratory sense)
Diabetes Diabetes Increased/Decreased GLUCOSEIncreased/Decreased GLUCOSE
Hepatic FailureHepatic Failure (NH4+)(NH4+)
CO CO (Cortex, hippocampus, Purkinje cells)(Cortex, hippocampus, Purkinje cells)
CH3-OHCH3-OH, Methanol (Retinal ganglion cells), Methanol (Retinal ganglion cells)
CH3-CH2-OH CH3-CH2-OH (acute/chronic, direct/nutrit’l)(acute/chronic, direct/nutrit’l)
RadiationRadiation (Brain MOST resistant to Rad. Rx.)(Brain MOST resistant to Rad. Rx.)
Chemo Chemo (Methotrexate + Radiation)(Methotrexate + Radiation)
TOXIC/METABOLICTOXIC/METABOLIC
CNS DISEASESCNS DISEASES
VitaminVitamin B1B1 deficiency (Wernicke-Korsakoff)deficiency (Wernicke-Korsakoff)
Vitamin Vitamin B12 B12 deficiency (vibratory sense)deficiency (vibratory sense)
Diabetes Diabetes Increased/Decreased GLUCOSEIncreased/Decreased GLUCOSE
Hepatic FailureHepatic Failure (NH4+)(NH4+)
CO CO (Cortex, hippocampus, Purkinje cells)(Cortex, hippocampus, Purkinje cells)
CH3-OHCH3-OH, Methanol (Retinal ganglion cells), Methanol (Retinal ganglion cells)
CH3-CH2-OH CH3-CH2-OH (acute/chronic, direct/nutrit’l)(acute/chronic, direct/nutrit’l)
RadiationRadiation (Brain MOST resistant to Rad. Rx.)(Brain MOST resistant to Rad. Rx.)
Chemo Chemo (Methotrexate + Radiation)(Methotrexate + Radiation)
Discriminative SensationDiscriminative Sensation
Primary sensory cortex provides Primary sensory cortex provides
awareness of somatosensory information awareness of somatosensory information
and the ability to make sensory and the ability to make sensory
discriminations. discriminations.
Touch, pain, temperature, and vibration Touch, pain, temperature, and vibration
sense are considered the primary sense are considered the primary
modalities of sensation and are relatively modalities of sensation and are relatively
preserved in patients with damage to preserved in patients with damage to
sensory cortex or its projections from the sensory cortex or its projections from the
thalamus. thalamus.
In contrast, complex tasks that require In contrast, complex tasks that require
integration of multiple somatosensory integration of multiple somatosensory
stimuli and of somatosensory stimuli with stimuli and of somatosensory stimuli with
auditory or visual information are impaired. auditory or visual information are impaired.
These include the ability to distinguish These include the ability to distinguish two two
pointspoints from one when touched on the skin from one when touched on the skin
((two-point discriminationtwo-point discrimination), localize tactile ), localize tactile
stimuli, perceive the position of body parts stimuli, perceive the position of body parts
in space, recognize letters or numbers in space, recognize letters or numbers
drawn on the skin (drawn on the skin (graphesthesiagraphesthesia), and ), and
identify objects by their shape, size, and identify objects by their shape, size, and
texture (texture (stereognosisstereognosis).).
Primary sensory cortex provides Primary sensory cortex provides
awareness of somatosensory information awareness of somatosensory information
and the ability to make sensory and the ability to make sensory
discriminations. discriminations.
Touch, pain, temperature, and vibration Touch, pain, temperature, and vibration
sense are considered the primary sense are considered the primary
modalities of sensation and are relatively modalities of sensation and are relatively
preserved in patients with damage to preserved in patients with damage to
sensory cortex or its projections from the sensory cortex or its projections from the
thalamus. thalamus.
In contrast, complex tasks that require In contrast, complex tasks that require
integration of multiple somatosensory integration of multiple somatosensory
stimuli and of somatosensory stimuli with stimuli and of somatosensory stimuli with
auditory or visual information are impaired. auditory or visual information are impaired.
These include the ability to distinguish These include the ability to distinguish two two
pointspoints from one when touched on the skin from one when touched on the skin
((two-point discriminationtwo-point discrimination), localize tactile ), localize tactile
stimuli, perceive the position of body parts stimuli, perceive the position of body parts
in space, recognize letters or numbers in space, recognize letters or numbers
drawn on the skin (drawn on the skin (graphesthesiagraphesthesia), and ), and
identify objects by their shape, size, and identify objects by their shape, size, and
texture (texture (stereognosisstereognosis).).
Anatomy of Sensory LossAnatomy of Sensory Loss
The patterns of sensory loss often indicate
the level of nervous system involvement.
Symmetric distal sensory loss in the limbs,
affecting the legs more than the arms,
usually signifies a generalized disorder of
multiple peripheral nerves
(polyneuropathy).
Sensory symptoms and deficits may be
restricted to the distribution of a single
peripheral nerve (mononeuropathy) or
two or more peripheral nerves
(mononeuropathy multiplex).
Symptoms limited to a dermatome indicate
a spinal root lesion (radiculopathy).
The patterns of sensory loss often indicate
the level of nervous system involvement.
Symmetric distal sensory loss in the limbs,
affecting the legs more than the arms,
usually signifies a generalized disorder of
multiple peripheral nerves
(polyneuropathy).
Sensory symptoms and deficits may be
restricted to the distribution of a single
peripheral nerve (mononeuropathy) or
two or more peripheral nerves
(mononeuropathy multiplex).
Symptoms limited to a dermatome indicate
a spinal root lesion (radiculopathy).
Alterations in Motor Responses and Alterations in Motor Responses and
MovementMovement
Abnormal motor responses include inappropriate or absent Abnormal motor responses include inappropriate or absent
movements in response to painful stimuli. Brainstem reflexes movements in response to painful stimuli. Brainstem reflexes
such as sucking and grasping responses will occur if higher such as sucking and grasping responses will occur if higher
brain centers have been damaged. brain centers have been damaged.
Flexion and rigidity of limbs also are motor responses indicative Flexion and rigidity of limbs also are motor responses indicative
of brain damage. of brain damage.
Muscle conditionsMuscle conditions that indicate abnormal brain function include that indicate abnormal brain function include
hyperkinesia hyperkinesia ((excessive muscle movementsexcessive muscle movements), ), hypokinesiahypokinesia
((decreased muscle movementsdecreased muscle movements), ), paresis paresis ((muscle weaknessmuscle weakness), ),
and and paralysisparalysis ( (loss of motor functionloss of motor function). ).
Specific loss of cerebral cortex functioning, but no loss of Specific loss of cerebral cortex functioning, but no loss of
brainstem function, results in a particular body posture called brainstem function, results in a particular body posture called
flexor posturingflexor posturing. .
Flexor posturingFlexor posturing is characterized by flexion of the upper is characterized by flexion of the upper
extremities at the elbows and external rotation and extension of extremities at the elbows and external rotation and extension of
the lower extremities. This posture the lower extremities. This posture may be unilateral or may be unilateral or
bilateralbilateral. Extensor posturing occurs with severe injury to higher . Extensor posturing occurs with severe injury to higher
brain centers and the brainstem and is characterized by brain centers and the brainstem and is characterized by rigid rigid
extension of the limbs and neckextension of the limbs and neck..
MovementMovement
Abnormal motor responses include inappropriate or absent Abnormal motor responses include inappropriate or absent
movements in response to painful stimuli. Brainstem reflexes movements in response to painful stimuli. Brainstem reflexes
such as sucking and grasping responses will occur if higher such as sucking and grasping responses will occur if higher
brain centers have been damaged. brain centers have been damaged.
Flexion and rigidity of limbs also are motor responses indicative Flexion and rigidity of limbs also are motor responses indicative
of brain damage. of brain damage.
Muscle conditionsMuscle conditions that indicate abnormal brain function include that indicate abnormal brain function include
hyperkinesia hyperkinesia ((excessive muscle movementsexcessive muscle movements), ), hypokinesiahypokinesia
((decreased muscle movementsdecreased muscle movements), ), paresis paresis ((muscle weaknessmuscle weakness), ),
and and paralysisparalysis ( (loss of motor functionloss of motor function). ).
Specific loss of cerebral cortex functioning, but no loss of Specific loss of cerebral cortex functioning, but no loss of
brainstem function, results in a particular body posture called brainstem function, results in a particular body posture called
flexor posturingflexor posturing. .
Flexor posturingFlexor posturing is characterized by flexion of the upper is characterized by flexion of the upper
extremities at the elbows and external rotation and extension of extremities at the elbows and external rotation and extension of
the lower extremities. This posture the lower extremities. This posture may be unilateral or may be unilateral or
bilateralbilateral. Extensor posturing occurs with severe injury to higher . Extensor posturing occurs with severe injury to higher
brain centers and the brainstem and is characterized by brain centers and the brainstem and is characterized by rigid rigid
extension of the limbs and neckextension of the limbs and neck..
Brown-Séquard syndrome
•In the spinal cord, segregation of fiber tracts and the
somatotopic arrangement of fibers give rise to distinct
patterns of sensory loss. Loss of pain and
temperature sensation on one side of the body
and of proprioception on the opposite side occurs
with lesions that involve one half of the cord on the
side of the proprioceptive deficit (Brown-Séquard
syndrome).
•Compression of the upper spinal cord causes loss of
pain, temperature, and touch sensation first in
the legs, because the leg spinothalamic fibers are
most superficial. More severe cord compression
compromises fibers from the trunk. In patients with
spinal cord compression, the lesion is often above
the highest dermatome involved in the deficit. Thus,
radiographic studies should be tailored to visualize
the cord at and above the level of the sensory deficit
detected on examination.
•Intrinsic cord lesions that involve the central portions
of the cord often impair pain and temperature
sensation at the level of the lesion because the fibers
crossing the anterior commissure and entering the
spinothalamic tracts are most centrally situated.
Thus, enlargement of the central cervical canal in
syringomyelia typically causes loss of pain and
temperature sensation across the shoulders and
upper arms.
•In the spinal cord, segregation of fiber tracts and the
somatotopic arrangement of fibers give rise to distinct
patterns of sensory loss. Loss of pain and
temperature sensation on one side of the body
and of proprioception on the opposite side occurs
with lesions that involve one half of the cord on the
side of the proprioceptive deficit (Brown-Séquard
syndrome).
•Compression of the upper spinal cord causes loss of
pain, temperature, and touch sensation first in
the legs, because the leg spinothalamic fibers are
most superficial. More severe cord compression
compromises fibers from the trunk. In patients with
spinal cord compression, the lesion is often above
the highest dermatome involved in the deficit. Thus,
radiographic studies should be tailored to visualize
the cord at and above the level of the sensory deficit
detected on examination.
•Intrinsic cord lesions that involve the central portions
of the cord often impair pain and temperature
sensation at the level of the lesion because the fibers
crossing the anterior commissure and entering the
spinothalamic tracts are most centrally situated.
Thus, enlargement of the central cervical canal in
syringomyelia typically causes loss of pain and
temperature sensation across the shoulders and
upper arms.
SPINAL CORD INJURIESSPINAL CORD INJURIES
CAUSES:CAUSES:
TRAUMATRAUMA
FALLSFALLS
GSWGSW
TUMORSTUMORS
TYPES:TYPES:
CONCUSSIONCONCUSSION
COMPRESSIONCOMPRESSION
CONTUSION & CONTUSION &
TRANSECTIONTRANSECTION
LACERATIONLACERATION
HEMORRHAGEHEMORRHAGE
(HEMATOMYALIA)(HEMATOMYALIA)
COMPRESSION OF COMPRESSION OF
BLOOD SUPPLY TO BLOOD SUPPLY TO
THE CORDTHE CORD
CAUSES:CAUSES:
TRAUMATRAUMA
FALLSFALLS
GSWGSW
TUMORSTUMORS
TYPES:TYPES:
CONCUSSIONCONCUSSION
COMPRESSIONCOMPRESSION
CONTUSION & CONTUSION &
TRANSECTIONTRANSECTION
LACERATIONLACERATION
HEMORRHAGEHEMORRHAGE
(HEMATOMYALIA)(HEMATOMYALIA)
COMPRESSION OF COMPRESSION OF
BLOOD SUPPLY TO BLOOD SUPPLY TO
THE CORDTHE CORD
Injury
Level
Segmental Sensorimotor Function Dressing, Eating Elimination Mobility
C1 Little or no sensation or control of head and
neck; no diaphragm control; requires
Continuous ventilation
Dependent Dependent Limited. Voice or sip-n-puff
controlled electric wheelchair
C2 to
C3
Head and neck sensation; some neck
control. Independent of mechanical
ventilation for short periods
Dependent Dependent Same as for C1
C4 Good head and neck sensation and motor
control; some shoulder elevation;
diaphragm movement
Dependent; may be
able to eat with
adaptive sling
Dependent Limited to voice, mouth, head,
chin, or shoulder-controlled
electric wheelchair
C5 Full head and neck control; shoulder
strength; elbow flexion
Independent with
assistance
Maximal assistanceElectric or modified manual
wheel chair, needs transfer
assistance
C6 Fully innervated shoulder; wrist extension
or dorsiflexion
Independent or with
minimal assistance
Independent or with
minimal assistance
Independent in transfers and
wheelchair
C7 to
C8
Full elbow extension; wrist plantar flexion;
some finger control
Independent Independent Independent; manual
wheelchair
T1 to
T5
Full hand and finger control; use of
intercostal and thoracic muscles
Independent Independent Independent; manual
wheelchair
T6 to
T10
Abdominal muscle control, partial to good
balance with trunk muscles
Independent Independent Independent; manual
wheelchair
T11 to
L5
Hip flexors, hip abductors (L1–3); knee
extension (L2–4); knee flexion and ankle
dorsiflexion (L4–5)
Independent Independent Short distance to full
ambulation with assistance
S1 to
S5
Full leg, foot, and ankle control;
innervation of perineal muscles for
bowel, bladder, and sexual function
(S2–4)
Independent Normal to impaired
bowel and bladder
function
Ambulate independently with or
without assistance
Functional Abilities by Level of Cord InjuryFunctional Abilities by Level of Cord Injury
Level
Segmental Sensorimotor Function Dressing, Eating Elimination Mobility
C1 Little or no sensation or control of head and
neck; no diaphragm control; requires
Continuous ventilation
Dependent Dependent Limited. Voice or sip-n-puff
controlled electric wheelchair
C2 to
C3
Head and neck sensation; some neck
control. Independent of mechanical
ventilation for short periods
Dependent Dependent Same as for C1
C4 Good head and neck sensation and motor
control; some shoulder elevation;
diaphragm movement
Dependent; may be
able to eat with
adaptive sling
Dependent Limited to voice, mouth, head,
chin, or shoulder-controlled
electric wheelchair
C5 Full head and neck control; shoulder
strength; elbow flexion
Independent with
assistance
Maximal assistanceElectric or modified manual
wheel chair, needs transfer
assistance
C6 Fully innervated shoulder; wrist extension
or dorsiflexion
Independent or with
minimal assistance
Independent or with
minimal assistance
Independent in transfers and
wheelchair
C7 to
C8
Full elbow extension; wrist plantar flexion;
some finger control
Independent Independent Independent; manual
wheelchair
T1 to
T5
Full hand and finger control; use of
intercostal and thoracic muscles
Independent Independent Independent; manual
wheelchair
T6 to
T10
Abdominal muscle control, partial to good
balance with trunk muscles
Independent Independent Independent; manual
wheelchair
T11 to
L5
Hip flexors, hip abductors (L1–3); knee
extension (L2–4); knee flexion and ankle
dorsiflexion (L4–5)
Independent Independent Short distance to full
ambulation with assistance
S1 to
S5
Full leg, foot, and ankle control;
innervation of perineal muscles for
bowel, bladder, and sexual function
(S2–4)
Independent Normal to impaired
bowel and bladder
function
Ambulate independently with or
without assistance
Functional Abilities by Level of Cord InjuryFunctional Abilities by Level of Cord Injury
CLINICAL EFFECTS OF SCICLINICAL EFFECTS OF SCI
•SPINAL SHOCK
•REFLEX ACTIVITY
•WHIPLASH INJURY
•HERNIATED NUCLEUS PULPOSUS
•SPINAL SHOCK
•REFLEX ACTIVITY
•WHIPLASH INJURY
•HERNIATED NUCLEUS PULPOSUS
•IMMEDIATE FLACCID PARALYSIS & SENSORY LOSS
BELOW THE LEVEL OF LESION
•PRIAPISM
•BULBOCAVERNOUS REFLEX IS LOST BUT REUTRNS
AFTER A FEW HRS
•OTHER REFLEXES REMAIN ABSENT
•3-6 WKS
AUTONOMIC DISTURBANCES:AUTONOMIC DISTURBANCES:
•SWEATING IS ABOLISHED
BELOW THE LEVEL OF INJURY
•URINE & FECES RETAINED
•GASTRIC ATONY
•ORTHOSTATIC HYPOTENSION
•SLOW, & STEADY PULSE
BELOW THE LEVEL OF LESION
•PRIAPISM
•BULBOCAVERNOUS REFLEX IS LOST BUT REUTRNS
AFTER A FEW HRS
•OTHER REFLEXES REMAIN ABSENT
•3-6 WKS
AUTONOMIC DISTURBANCES:AUTONOMIC DISTURBANCES:
•SWEATING IS ABOLISHED
BELOW THE LEVEL OF INJURY
•URINE & FECES RETAINED
•GASTRIC ATONY
•ORTHOSTATIC HYPOTENSION
•SLOW, & STEADY PULSE
REFLEX ACTIVITY
•REPLACE SPINAL SHOCK AFTER 2-3
WEEKS IF LUMBO-SACRAL SEGMENTS
ARE UNDAMAGED
•OCCURS IN ACUTE SPINAL INJURY,
NOT IN PROGRESSIVE ONES
•AUTOMATIC BLADDER; REFLEX
SWEATING & DEFECATION
•FIRST SIGN OF WEARING OFF:
–CONTRACTION OF HAMSTRING
–FLEXION/ EXTENSION OF TOES WITH
PLANTAR STIMULATION
•REPLACE SPINAL SHOCK AFTER 2-3
WEEKS IF LUMBO-SACRAL SEGMENTS
ARE UNDAMAGED
•OCCURS IN ACUTE SPINAL INJURY,
NOT IN PROGRESSIVE ONES
•AUTOMATIC BLADDER; REFLEX
SWEATING & DEFECATION
•FIRST SIGN OF WEARING OFF:
–CONTRACTION OF HAMSTRING
–FLEXION/ EXTENSION OF TOES WITH
PLANTAR STIMULATION
ParalysisParalysis
ParalysisParalysis is the loss of sensory and voluntary motor is the loss of sensory and voluntary motor
function. With spinal cord transection, paralysis is function. With spinal cord transection, paralysis is
permanent. permanent.
Paralysis Paralysis of the of the upper and lower extremitiesupper and lower extremities occurs with occurs with
transection of the cord at level C6 or higher and is called transection of the cord at level C6 or higher and is called
quadriplegiaquadriplegia. .
ParalysisParalysis of the lower half of the body occurs with of the lower half of the body occurs with
transection of the cord below C6 and is called transection of the cord below C6 and is called
paraplegiaparaplegia. .
If only one half of the cord is transectedIf only one half of the cord is transected, , hemiparalysishemiparalysis
may occur. may occur.
Permanent paralysisPermanent paralysis may occur even when the cord is may occur even when the cord is
not transected, as a result of the destruction of the not transected, as a result of the destruction of the
nerves following cord nerves following cord hemorrhage and swellinghemorrhage and swelling. .
In addition, demyelination of the axons in the cord can In addition, demyelination of the axons in the cord can
lead to clinically complete lesions, even though the lead to clinically complete lesions, even though the
spinal cord may not be transected. spinal cord may not be transected.
DemyelinationDemyelination of the axons most likely occurs as part of of the axons most likely occurs as part of
the inflammatory response to cord injury.the inflammatory response to cord injury.
ParalysisParalysis is the loss of sensory and voluntary motor is the loss of sensory and voluntary motor
function. With spinal cord transection, paralysis is function. With spinal cord transection, paralysis is
permanent. permanent.
Paralysis Paralysis of the of the upper and lower extremitiesupper and lower extremities occurs with occurs with
transection of the cord at level C6 or higher and is called transection of the cord at level C6 or higher and is called
quadriplegiaquadriplegia. .
ParalysisParalysis of the lower half of the body occurs with of the lower half of the body occurs with
transection of the cord below C6 and is called transection of the cord below C6 and is called
paraplegiaparaplegia. .
If only one half of the cord is transectedIf only one half of the cord is transected, , hemiparalysishemiparalysis
may occur. may occur.
Permanent paralysisPermanent paralysis may occur even when the cord is may occur even when the cord is
not transected, as a result of the destruction of the not transected, as a result of the destruction of the
nerves following cord nerves following cord hemorrhage and swellinghemorrhage and swelling. .
In addition, demyelination of the axons in the cord can In addition, demyelination of the axons in the cord can
lead to clinically complete lesions, even though the lead to clinically complete lesions, even though the
spinal cord may not be transected. spinal cord may not be transected.
DemyelinationDemyelination of the axons most likely occurs as part of of the axons most likely occurs as part of
the inflammatory response to cord injury.the inflammatory response to cord injury.
Clinical
Manifestations
of Paralysis
•Loss of sensation,
motor control, and
reflexes below the
level of injury, and
up to two levels
above, will occur.
Body temperature
will reflect ambient
temperature, and
blood pressure will
be reduced.
•The pulse rate is
often normal, with
low blood pressure.
Manifestations
of Paralysis
•Loss of sensation,
motor control, and
reflexes below the
level of injury, and
up to two levels
above, will occur.
Body temperature
will reflect ambient
temperature, and
blood pressure will
be reduced.
•The pulse rate is
often normal, with
low blood pressure.
Complications
•If damage and swelling around the cord is in the
cervical spine (down to approximately C5),
respirations may cease because of compression of
the phrenic nerve, which exits between C3 and C5
and controls the movement of the diaphragm.
•Autonomic hyper-reflexia is characterized by high
blood pressure with bradycardia (low heart rate),
and sweating and flushing of the skin on the face
and upper torso.
•In the past, individuals suffering from a C2 or higher
transection invariably died as a result of respiratory
arrest. Although this is still true for many, recent
advances in treatment modalities and better
emergency rescue service responses have resulted
in the survival of many individuals with high cord
transection.
•A severe spinal cord injury affects virtually all
systems of the body to some degree. Commonly,
urinary tract and kidney infections, skin breakdown
and the development of pressure ulcers, and muscle
atrophy occur. Depression, marital and family
stress, loss of income, and large medical expenses
are some of the psychosocial complications.
•If damage and swelling around the cord is in the
cervical spine (down to approximately C5),
respirations may cease because of compression of
the phrenic nerve, which exits between C3 and C5
and controls the movement of the diaphragm.
•Autonomic hyper-reflexia is characterized by high
blood pressure with bradycardia (low heart rate),
and sweating and flushing of the skin on the face
and upper torso.
•In the past, individuals suffering from a C2 or higher
transection invariably died as a result of respiratory
arrest. Although this is still true for many, recent
advances in treatment modalities and better
emergency rescue service responses have resulted
in the survival of many individuals with high cord
transection.
•A severe spinal cord injury affects virtually all
systems of the body to some degree. Commonly,
urinary tract and kidney infections, skin breakdown
and the development of pressure ulcers, and muscle
atrophy occur. Depression, marital and family
stress, loss of income, and large medical expenses
are some of the psychosocial complications.
DysphasiaDysphasia
Dysphasia is impairment of language comprehension or production. is impairment of language comprehension or production.
Aphasia is total loss of language comprehension or production. Aphasia is total loss of language comprehension or production.
Dysphasia usually results from cerebral hypoxia, which is often Dysphasia usually results from cerebral hypoxia, which is often
associated with a stroke but can result from trauma or infection. Brain associated with a stroke but can result from trauma or infection. Brain
damage leading to dysphasia usually involves the left cerebral damage leading to dysphasia usually involves the left cerebral
hemisphere.hemisphere.
Broca's dysphasia results from damage to Broca's area in the frontal results from damage to Broca's area in the frontal
lobe. Persons with Broca's dysphasia will understand language, but lobe. Persons with Broca's dysphasia will understand language, but
their ability to meaningfully express words in speech or writing will be their ability to meaningfully express words in speech or writing will be
impaired. This is called expressive dysphasia.impaired. This is called expressive dysphasia.
Wernicke's dysphasia results from damage to Wernicke's area in the results from damage to Wernicke's area in the
left temporal lobe. With Wernicke's dysphasia, verbal expression of left temporal lobe. With Wernicke's dysphasia, verbal expression of
language is intact, but meaningful understanding of spoken or written language is intact, but meaningful understanding of spoken or written
words is impaired. This is called receptive dysphasia.words is impaired. This is called receptive dysphasia.
Agnosia is the failure to recognize an object because of the inability is the failure to recognize an object because of the inability
to make sense of incoming sensory stimuli. Agnosia may be visual, to make sense of incoming sensory stimuli. Agnosia may be visual,
auditory, tactile, or related to taste or smell. Agnosia develops from auditory, tactile, or related to taste or smell. Agnosia develops from
damage to a particular primary or associative sensory area in the damage to a particular primary or associative sensory area in the
cerebral cortex.cerebral cortex.
Dysphasia is impairment of language comprehension or production. is impairment of language comprehension or production.
Aphasia is total loss of language comprehension or production. Aphasia is total loss of language comprehension or production.
Dysphasia usually results from cerebral hypoxia, which is often Dysphasia usually results from cerebral hypoxia, which is often
associated with a stroke but can result from trauma or infection. Brain associated with a stroke but can result from trauma or infection. Brain
damage leading to dysphasia usually involves the left cerebral damage leading to dysphasia usually involves the left cerebral
hemisphere.hemisphere.
Broca's dysphasia results from damage to Broca's area in the frontal results from damage to Broca's area in the frontal
lobe. Persons with Broca's dysphasia will understand language, but lobe. Persons with Broca's dysphasia will understand language, but
their ability to meaningfully express words in speech or writing will be their ability to meaningfully express words in speech or writing will be
impaired. This is called expressive dysphasia.impaired. This is called expressive dysphasia.
Wernicke's dysphasia results from damage to Wernicke's area in the results from damage to Wernicke's area in the
left temporal lobe. With Wernicke's dysphasia, verbal expression of left temporal lobe. With Wernicke's dysphasia, verbal expression of
language is intact, but meaningful understanding of spoken or written language is intact, but meaningful understanding of spoken or written
words is impaired. This is called receptive dysphasia.words is impaired. This is called receptive dysphasia.
Agnosia is the failure to recognize an object because of the inability is the failure to recognize an object because of the inability
to make sense of incoming sensory stimuli. Agnosia may be visual, to make sense of incoming sensory stimuli. Agnosia may be visual,
auditory, tactile, or related to taste or smell. Agnosia develops from auditory, tactile, or related to taste or smell. Agnosia develops from
damage to a particular primary or associative sensory area in the damage to a particular primary or associative sensory area in the
cerebral cortex.cerebral cortex.
Alterations in Pupil Responses
•The ability of our eyes to dilate or
constrict, rapidly and equally,
depends on an intact brainstem.
•Cerebral hypoxia and many drugs
change pupil size and reactivity.
Therefore, pupil size and reactivity
offer valuable information concerning
brain integrity and function.
•Important pupil changes seen with
brain damage are pinpoint pupils
seen with opiate (heroin) overdose
and bilaterally fixed and dilated pupils
usually seen with severe hypoxia.
•Fixed pupils are typically seen with
barbiturate overdose.
•Brainstem injury presents with pupils
fixed bilaterally in the midposition.
•The ability of our eyes to dilate or
constrict, rapidly and equally,
depends on an intact brainstem.
•Cerebral hypoxia and many drugs
change pupil size and reactivity.
Therefore, pupil size and reactivity
offer valuable information concerning
brain integrity and function.
•Important pupil changes seen with
brain damage are pinpoint pupils
seen with opiate (heroin) overdose
and bilaterally fixed and dilated pupils
usually seen with severe hypoxia.
•Fixed pupils are typically seen with
barbiturate overdose.
•Brainstem injury presents with pupils
fixed bilaterally in the midposition.
DISORDERS OF THE RETINAL
BLOOD SUPPLY
■ The blood supply for the
retina is derived from
the central retinal
artery, which supplies
blood flow for the
entire inside of the
retina, and from
vessels in the choroid,
which supply the rods
and cones.
■ Central retinal occlusion
interrupts blood flow to
the inner retina and
results in unilateral
blindness.
■ The retinopathies,
which are disorders of
the retinal vessels,
interrupt blood flow to
the visual receptors,
leading to visual
impairment.
■ Retinal detachment
separates the visual
receptors from the
choroid, which
provides their major
blood supply.
Fundus of the eye
as seen in retinal
examination with an
ophthalmoscope:
(left) normal
fundus; (middle)
diabetic retinopathy
—combination of
microaneurysms,
deep hemorrhages,
and hard exudates
of background
retinopathy; (right)
hypertensive
retinopathy with
purulent exudates.
Some exudates are
scattered, while
others radiate from
the fovea to form a
macular star.
BLOOD SUPPLY
■ The blood supply for the
retina is derived from
the central retinal
artery, which supplies
blood flow for the
entire inside of the
retina, and from
vessels in the choroid,
which supply the rods
and cones.
■ Central retinal occlusion
interrupts blood flow to
the inner retina and
results in unilateral
blindness.
■ The retinopathies,
which are disorders of
the retinal vessels,
interrupt blood flow to
the visual receptors,
leading to visual
impairment.
■ Retinal detachment
separates the visual
receptors from the
choroid, which
provides their major
blood supply.
Fundus of the eye
as seen in retinal
examination with an
ophthalmoscope:
(left) normal
fundus; (middle)
diabetic retinopathy
—combination of
microaneurysms,
deep hemorrhages,
and hard exudates
of background
retinopathy; (right)
hypertensive
retinopathy with
purulent exudates.
Some exudates are
scattered, while
others radiate from
the fovea to form a
macular star.
DISORDERS OF DISORDERS OF
THE MIDDLE EARTHE MIDDLE EAR
■ The middle ear is a small air-filled
compartment in the temporal bone.
It is separated from the outer ear
by the tympanic membrane,
contains tiny bony ossicles that aid
in the amplification and
transmission of sound to the inner
ear, and is ventilated by the
eustachian tube, which is
connected to the nasopharynx.
■ ■ The eustachian tube, which is lined with a mucousThe eustachian tube, which is lined with a mucous membrane that is membrane that is
continuous with the nasopharynx,continuous with the nasopharynx, provides a passageway for provides a passageway for
pathogens to enter thepathogens to enter the middle ear.middle ear.
■ ■ Otitis media (OM) refers to inflammation of the middleOtitis media (OM) refers to inflammation of the middle ear, usually ear, usually
associated with an acute infectionassociated with an acute infection (acute OM) or an accumulation of (acute OM) or an accumulation of
fluid (OME). Itfluid (OME). It commonly is associated with disorders of eustachiancommonly is associated with disorders of eustachian
tube function.tube function.
■ ■ Impaired conduction of sound waves and hearingImpaired conduction of sound waves and hearing loss occur when the loss occur when the
tympanic membrane has beentympanic membrane has been perforated; air in the middle ear has perforated; air in the middle ear has
been replacedbeen replaced with fluid (OME); or the function of the bonywith fluid (OME); or the function of the bony ossicles has ossicles has
been impaired (otosclerosis).been impaired (otosclerosis).
THE MIDDLE EARTHE MIDDLE EAR
■ The middle ear is a small air-filled
compartment in the temporal bone.
It is separated from the outer ear
by the tympanic membrane,
contains tiny bony ossicles that aid
in the amplification and
transmission of sound to the inner
ear, and is ventilated by the
eustachian tube, which is
connected to the nasopharynx.
■ ■ The eustachian tube, which is lined with a mucousThe eustachian tube, which is lined with a mucous membrane that is membrane that is
continuous with the nasopharynx,continuous with the nasopharynx, provides a passageway for provides a passageway for
pathogens to enter thepathogens to enter the middle ear.middle ear.
■ ■ Otitis media (OM) refers to inflammation of the middleOtitis media (OM) refers to inflammation of the middle ear, usually ear, usually
associated with an acute infectionassociated with an acute infection (acute OM) or an accumulation of (acute OM) or an accumulation of
fluid (OME). Itfluid (OME). It commonly is associated with disorders of eustachiancommonly is associated with disorders of eustachian
tube function.tube function.
■ ■ Impaired conduction of sound waves and hearingImpaired conduction of sound waves and hearing loss occur when the loss occur when the
tympanic membrane has beentympanic membrane has been perforated; air in the middle ear has perforated; air in the middle ear has
been replacedbeen replaced with fluid (OME); or the function of the bonywith fluid (OME); or the function of the bony ossicles has ossicles has
been impaired (otosclerosis).been impaired (otosclerosis).
HEARING LOSS
■ Hearing loss represents
impairment of the ability
to detect and perceive
sound.
■ Conductive hearing loss is
caused by disorders in
which auditory stimuli are
not transmitted through
the structures of the outer
and middle ears to the
sensory receptors in the
inner ear.
■ Sensorineural hearing
loss is caused by
disorders that affect the
inner ear, auditory nerve,
or auditory pathways.
■ Hearing loss represents
impairment of the ability
to detect and perceive
sound.
■ Conductive hearing loss is
caused by disorders in
which auditory stimuli are
not transmitted through
the structures of the outer
and middle ears to the
sensory receptors in the
inner ear.
■ Sensorineural hearing
loss is caused by
disorders that affect the
inner ear, auditory nerve,
or auditory pathways.
Diseases of the Basal GangliaDiseases of the Basal Ganglia
The basal ganglia are The basal ganglia are
made up of:made up of:
– – the the corpus striatumcorpus striatum
(consisting of the (consisting of the caudate caudate
nucleus nucleus and the and the
putamenputamen););
– – the inner and outer the inner and outer
globus pallidusglobus pallidus
(pallidum, consisting of an (pallidum, consisting of an
internal and an external internal and an external
part);part);
– – the the subthalamic subthalamic
nucleusnucleus; and; and
– – the the substantia nigrasubstantia nigra
(pars reticulata [p. r.] and (pars reticulata [p. r.] and
pars compacta [p. c.]).pars compacta [p. c.]).
Their Their functionfunction is mainly is mainly
to control movement in to control movement in
conjunction with the conjunction with the
cerebellum,motor cortex, cerebellum,motor cortex,
corticospinal tracts, and corticospinal tracts, and
motor nuclei in the brain motor nuclei in the brain
stem. stem.
The basal ganglia are The basal ganglia are
made up of:made up of:
– – the the corpus striatumcorpus striatum
(consisting of the (consisting of the caudate caudate
nucleus nucleus and the and the
putamenputamen););
– – the inner and outer the inner and outer
globus pallidusglobus pallidus
(pallidum, consisting of an (pallidum, consisting of an
internal and an external internal and an external
part);part);
– – the the subthalamic subthalamic
nucleusnucleus; and; and
– – the the substantia nigrasubstantia nigra
(pars reticulata [p. r.] and (pars reticulata [p. r.] and
pars compacta [p. c.]).pars compacta [p. c.]).
Their Their functionfunction is mainly is mainly
to control movement in to control movement in
conjunction with the conjunction with the
cerebellum,motor cortex, cerebellum,motor cortex,
corticospinal tracts, and corticospinal tracts, and
motor nuclei in the brain motor nuclei in the brain
stem. stem.
Parkinson’s Disease
Parkinson’s disease is a disease Parkinson’s disease is a disease
of the substantia nigra (p. c.) of the substantia nigra (p. c.)
which via dopaminergic tracts which via dopaminergic tracts
influences GABAergic cells in the influences GABAergic cells in the
corpus striatum. The corpus striatum. The cause cause is is
frequently a frequently a hereditary disposition hereditary disposition
that in middle to old age leads to that in middle to old age leads to
degeneration of dopaminergic degeneration of dopaminergic
neurons in the substantia nigra. neurons in the substantia nigra.
Further causes are Further causes are trauma trauma (e.g., (e.g.,
in boxers), in boxers), inflammation inflammation
(encephalitis), (encephalitis), impaired circulation impaired circulation
(atherosclerosis), (atherosclerosis), tumors tumors and and
poisoning poisoning (especially by CO, (especially by CO,
manganese, and 1-methyl-4-manganese, and 1-methyl-4-
phenyl-1,2,3,6-tetrahydropyridine phenyl-1,2,3,6-tetrahydropyridine
[MPTP], which was once used as [MPTP], which was once used as
a substitute for heroin). The cell a substitute for heroin). The cell
destruction probably occurs partly destruction probably occurs partly
by apoptosis; superoxides are by apoptosis; superoxides are
thought to play a causal role. For thought to play a causal role. For
symptoms to occur, over 70% of symptoms to occur, over 70% of
neurons in the substantia nigra (p. neurons in the substantia nigra (p.
c.) must have been destroyed.c.) must have been destroyed.
The loss of cells in the substantia The loss of cells in the substantia
nigra (p. c.) decreases the nigra (p. c.) decreases the
corresponding corresponding dopaminergic dopaminergic
innervation innervation of the striatum.of the striatum.
Parkinson’s disease is a disease Parkinson’s disease is a disease
of the substantia nigra (p. c.) of the substantia nigra (p. c.)
which via dopaminergic tracts which via dopaminergic tracts
influences GABAergic cells in the influences GABAergic cells in the
corpus striatum. The corpus striatum. The cause cause is is
frequently a frequently a hereditary disposition hereditary disposition
that in middle to old age leads to that in middle to old age leads to
degeneration of dopaminergic degeneration of dopaminergic
neurons in the substantia nigra. neurons in the substantia nigra.
Further causes are Further causes are trauma trauma (e.g., (e.g.,
in boxers), in boxers), inflammation inflammation
(encephalitis), (encephalitis), impaired circulation impaired circulation
(atherosclerosis), (atherosclerosis), tumors tumors and and
poisoning poisoning (especially by CO, (especially by CO,
manganese, and 1-methyl-4-manganese, and 1-methyl-4-
phenyl-1,2,3,6-tetrahydropyridine phenyl-1,2,3,6-tetrahydropyridine
[MPTP], which was once used as [MPTP], which was once used as
a substitute for heroin). The cell a substitute for heroin). The cell
destruction probably occurs partly destruction probably occurs partly
by apoptosis; superoxides are by apoptosis; superoxides are
thought to play a causal role. For thought to play a causal role. For
symptoms to occur, over 70% of symptoms to occur, over 70% of
neurons in the substantia nigra (p. neurons in the substantia nigra (p.
c.) must have been destroyed.c.) must have been destroyed.
The loss of cells in the substantia The loss of cells in the substantia
nigra (p. c.) decreases the nigra (p. c.) decreases the
corresponding corresponding dopaminergic dopaminergic
innervation innervation of the striatum.of the striatum.
Literature:Literature:
1.1.General and clinical pathophysiology / Edited by Anatoliy V. Kubyshkin – Vinnytsia: General and clinical pathophysiology / Edited by Anatoliy V. Kubyshkin – Vinnytsia:
Nova Knuha Publishers – 2011. – P.Nova Knuha Publishers – 2011. – P.627627––663838..
2.2.Russell J. Greene. Pathology and Therapeutics for Pharmacists. A basis for clinical Russell J. Greene. Pathology and Therapeutics for Pharmacists. A basis for clinical
pharmacy practice / Russell J. Greene, Norman D. Harris // Published by the pharmacy practice / Russell J. Greene, Norman D. Harris // Published by the
Pharmaceutical Press An imprint of RPS Publishing 1 Lambeth High Street, London Pharmaceutical Press An imprint of RPS Publishing 1 Lambeth High Street, London
SE1 7JN, UK 100 South Atkinson Road, Suite 200, Greyslake, IL 60030-7820, 3rd SE1 7JN, UK 100 South Atkinson Road, Suite 200, Greyslake, IL 60030-7820, 3rd
edition, USA. – 2008. – Chapter 7. – P. 455–512.edition, USA. – 2008. – Chapter 7. – P. 455–512.
3.3.Essentials of Pathophysiology: Concepts of Altered Health States (Lippincott Williams & Essentials of Pathophysiology: Concepts of Altered Health States (Lippincott Williams &
Wilkins), Trade paperback (2003) Wilkins), Trade paperback (2003) / / Carol Mattson Porth, Kathryn J. Gaspard. –Chapters Carol Mattson Porth, Kathryn J. Gaspard. –Chapters
36, 38-40. – P. 637–363, 456–777. 36, 38-40. – P. 637–363, 456–777.
4.4.Symeonova N.K. Pathophysiology / N.K. Symeonova // Kyiv, AUS medicine Publishing. Symeonova N.K. Pathophysiology / N.K. Symeonova // Kyiv, AUS medicine Publishing.
– 2010. – P. 512–531. – 2010. – P. 512–531.
5.5.Gozhenko A.I. General and clinical pathophysiology / A.I. Gozhenko, I.P. Gurcalova // Gozhenko A.I. General and clinical pathophysiology / A.I. Gozhenko, I.P. Gurcalova //
Study guide for medical students and practitioners. Study guide for medical students and practitioners. Edited by prof. Zaporozan, OSMU. – Edited by prof. Zaporozan, OSMU. –
Odessa. – 2005. – P. 2Odessa. – 2005. – P. 29292––307307. .
6.6.Silbernagl S. Color Atlas of Pathophysiology / S. Silbernagl, F. Lang // Thieme. Silbernagl S. Color Atlas of Pathophysiology / S. Silbernagl, F. Lang // Thieme.
Stuttgart. New York. – 2000. – P. 298–331. Stuttgart. New York. – 2000. – P. 298–331.
7.7.Corwin Elizabeth J. Handbook of Pathophysiology / Corwin Elizabeth J. – 3th edition. Corwin Elizabeth J. Handbook of Pathophysiology / Corwin Elizabeth J. – 3th edition.
Copyright ВCopyright В. . – Lippincott Williams & Wilkins – 2008. – – Lippincott Williams & Wilkins – 2008. – Chapter 8. – P. 185–202, 208–Chapter 8. – P. 185–202, 208–
209, 220–224.209, 220–224.
8.8.Robbins and Cotran Pathologic Basis of Disease 8th edition./ Kumar, Abbas, Fauto. – Robbins and Cotran Pathologic Basis of Disease 8th edition./ Kumar, Abbas, Fauto. –
2007. – Chapter 2007. – Chapter 2323. – P. . – P. 881–902881–902..
9.9.Copstead Lee-Ellen C. Pathophysiology / Lee-Ellen C. Copstead, Jacquelyn L. Copstead Lee-Ellen C. Pathophysiology / Lee-Ellen C. Copstead, Jacquelyn L.
Banasik // Elsevier Inc, 4th edition. – 2010. – P. 998–1034, 1086–1123.Banasik // Elsevier Inc, 4th edition. – 2010. – P. 998–1034, 1086–1123.
10.10. Pathophysiology, Concepts of Altered Health States, Carol Mattson Porth, Glenn Pathophysiology, Concepts of Altered Health States, Carol Mattson Porth, Glenn
Matfin. Matfin. –– New York, Milwaukee. New York, Milwaukee. –– 2009. 2009. –– P. P. 1181–1299 1181–1299..
1.1.General and clinical pathophysiology / Edited by Anatoliy V. Kubyshkin – Vinnytsia: General and clinical pathophysiology / Edited by Anatoliy V. Kubyshkin – Vinnytsia:
Nova Knuha Publishers – 2011. – P.Nova Knuha Publishers – 2011. – P.627627––663838..
2.2.Russell J. Greene. Pathology and Therapeutics for Pharmacists. A basis for clinical Russell J. Greene. Pathology and Therapeutics for Pharmacists. A basis for clinical
pharmacy practice / Russell J. Greene, Norman D. Harris // Published by the pharmacy practice / Russell J. Greene, Norman D. Harris // Published by the
Pharmaceutical Press An imprint of RPS Publishing 1 Lambeth High Street, London Pharmaceutical Press An imprint of RPS Publishing 1 Lambeth High Street, London
SE1 7JN, UK 100 South Atkinson Road, Suite 200, Greyslake, IL 60030-7820, 3rd SE1 7JN, UK 100 South Atkinson Road, Suite 200, Greyslake, IL 60030-7820, 3rd
edition, USA. – 2008. – Chapter 7. – P. 455–512.edition, USA. – 2008. – Chapter 7. – P. 455–512.
3.3.Essentials of Pathophysiology: Concepts of Altered Health States (Lippincott Williams & Essentials of Pathophysiology: Concepts of Altered Health States (Lippincott Williams &
Wilkins), Trade paperback (2003) Wilkins), Trade paperback (2003) / / Carol Mattson Porth, Kathryn J. Gaspard. –Chapters Carol Mattson Porth, Kathryn J. Gaspard. –Chapters
36, 38-40. – P. 637–363, 456–777. 36, 38-40. – P. 637–363, 456–777.
4.4.Symeonova N.K. Pathophysiology / N.K. Symeonova // Kyiv, AUS medicine Publishing. Symeonova N.K. Pathophysiology / N.K. Symeonova // Kyiv, AUS medicine Publishing.
– 2010. – P. 512–531. – 2010. – P. 512–531.
5.5.Gozhenko A.I. General and clinical pathophysiology / A.I. Gozhenko, I.P. Gurcalova // Gozhenko A.I. General and clinical pathophysiology / A.I. Gozhenko, I.P. Gurcalova //
Study guide for medical students and practitioners. Study guide for medical students and practitioners. Edited by prof. Zaporozan, OSMU. – Edited by prof. Zaporozan, OSMU. –
Odessa. – 2005. – P. 2Odessa. – 2005. – P. 29292––307307. .
6.6.Silbernagl S. Color Atlas of Pathophysiology / S. Silbernagl, F. Lang // Thieme. Silbernagl S. Color Atlas of Pathophysiology / S. Silbernagl, F. Lang // Thieme.
Stuttgart. New York. – 2000. – P. 298–331. Stuttgart. New York. – 2000. – P. 298–331.
7.7.Corwin Elizabeth J. Handbook of Pathophysiology / Corwin Elizabeth J. – 3th edition. Corwin Elizabeth J. Handbook of Pathophysiology / Corwin Elizabeth J. – 3th edition.
Copyright ВCopyright В. . – Lippincott Williams & Wilkins – 2008. – – Lippincott Williams & Wilkins – 2008. – Chapter 8. – P. 185–202, 208–Chapter 8. – P. 185–202, 208–
209, 220–224.209, 220–224.
8.8.Robbins and Cotran Pathologic Basis of Disease 8th edition./ Kumar, Abbas, Fauto. – Robbins and Cotran Pathologic Basis of Disease 8th edition./ Kumar, Abbas, Fauto. –
2007. – Chapter 2007. – Chapter 2323. – P. . – P. 881–902881–902..
9.9.Copstead Lee-Ellen C. Pathophysiology / Lee-Ellen C. Copstead, Jacquelyn L. Copstead Lee-Ellen C. Pathophysiology / Lee-Ellen C. Copstead, Jacquelyn L.
Banasik // Elsevier Inc, 4th edition. – 2010. – P. 998–1034, 1086–1123.Banasik // Elsevier Inc, 4th edition. – 2010. – P. 998–1034, 1086–1123.
10.10. Pathophysiology, Concepts of Altered Health States, Carol Mattson Porth, Glenn Pathophysiology, Concepts of Altered Health States, Carol Mattson Porth, Glenn
Matfin. Matfin. –– New York, Milwaukee. New York, Milwaukee. –– 2009. 2009. –– P. P. 1181–1299 1181–1299..
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