Physiology II Exam 2 - Spring 2023

Exam 2 Info

What does sympathetic control?

“Fight or Flight”

What does parasympathetic control?

“Rest and Digest”

Autonomic Nervous System General Features?

Involuntary

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Visceral

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Moter/efferent control

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If the somatic motor system influences skeletal muscle… what does the autonomic nervous system influence?

Visceral Motor Effectors

Smooth Muscle

Within vasculature

(vascular smooth muscle)

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Within walls of GI tract

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Sphincters (GI and GU)

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Within walls of bladder

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Within eye:

Iris (dilates and constrict pupil)

Ciliary (near/far accommodation)

Visceral Motor Effectors

Heart

Cardiac muscle in walls of ventricles and atria

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SA and AV nodes

Visceral Motor Effectors

Glandular

Sweat glands

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Salivary glands

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Pancreas

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Stomach

Visceral Motor Effectors

Miscellaneous

Adipose Tissue

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Liver

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Kidney

Autonomic Nervous System

Anatomical Features:

2 peripheral neuron system

Synapse on autonomic ganglia

Each neuron is differentiated by term:

*Pre-ganglionic (before ganglion)*

*Post-ganglionic (after the ganglion)* - goes to the target organ

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Central Nervous System

*Know this chart*

Control of Local Blood Flow: Sympathetics

Flow of Capillary Beds:

Precapillary sphincters restrict flow to capillary beds

Able to control the amount of blood within local capillary circulation (mesenteric circulation)

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Diameter of Arterioles:

Vasoconstriction → decreased blood flow (ex. vasoconstriction of arterioles supplying GIT during times of stress/anger)

Vasodilation → increased blood flow (ex. vasodilation of arterioles supplying skeletal muscle during exercise)

Diameter of Arterioles

Image

*See Image*

Flow to Capillary Bed

Image

*See Image*

Neurotransmitter and Receptors Intro

Each division of the autonomic nervous system has its own set of neurotransmitters and receptors

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The unique function of each division is directly related to these

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The function depends entirely on which receptors are present on which organs/tissues

Neurotransmitters and Receptors Continued…

Norepinephrine

NE

Sympathetic Post-ganglionic

*neurotransmitter released at target organ*

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Acetylcholine

ACh

Pre-ganglionic (sympathetic and parasympathetic)

Parasympathetic post-ganglionic

Receptor Chart Image

*See Image*

Receptors of Effector Organs

*Intro*

Adrenergic - NE

Sympathetic

Alpha-1

Alpha-2

Beta-1

Beta-2

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Cholinergic - ACh

Parasympathetic

Muscarinic

Receptor *EXCEPTION*

Sympathetic fibers going to sweat glands use the neurotransmitter ACh

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Receptor is Muscarinic

Receptor Chart

*See Image*

Receptors Made Easy

In the *parasympathetic division*, effector organs have *muscarinic receptors*

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In the sympathetic division there are multiple receptor types in effector organs including the four adrenoreceptors (alpha-1-2, beta 1-2); and in tissues with sympathetic cholinergic innervation, there are muscarinic receptors.

Alpha Receptors Made Easy

“Among the sympathetic adrenoreceptors, receptor type is related to function.”

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The alpha-1: increases smooth muscle activity

Receptors cause contraction of smooth muscle such as vascular smooth muscle, gastrointestinal, and urethral sphincters, pilomotor muscles, and in the radial muscle of the iris.

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The alpha-2 receptors are rare. The main function is quite different than other receptors. Present on *autonomic nerve terminals and in GI tract*, these receptors inhibit activity of both sympathetic and parasympathetic pathways.

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All other receptors are on the tissue itself, these are on post ganglionic neurons

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The alpha-2 receptors are rare. There are 2 types

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Autoreceptors: Located on sympathetic post-ganglionic neurons.

*Inhibits release of NE (conserves NE), not present in adrenal medulla*

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Heteroreceptors: Located on parasympathetic post-ganglionic neurons

*Inhibits release of ACh (indirectly inhibits GI activity)*

Beta Receptors Made Easy

Beta-1:

Activity of heart - All functions of the heart

Increase metabolism - Receptors are involved in homeostatic functions such as, lipolysis, renin secretion

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Beta-2:

Decrease smooth muscle activity

Receptors cause relaxation of smooth muscle in bronchioles, wall of the bladder, and wall of the GIT

*+relaxation of vascular smooth muscle supplying skeletal muscle*

Inhibits urine

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Sympathetic Nervous System

“Fight or Flight”

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Originates from lateral gray horn from T1-L2

*Peripheral components of sympathetic nervous system*

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Called thoracodorsal due to origin from thoracic and upper lumbar spine

Sympathetic Anatomy

Pre-ganglionic fibers (short) originate in lateral gray horn of spinal cord between T1-L2

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Fibers will travel to synapse on post-ganglionic fibers in one of many sympathetic ganglia

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Sympathetic Ganglia

Near the spinal cord

*Paravertebral (sympathetic chain)* - located further from the spine, supply cast area from head down to feet

*Prevertebral* - Located right next to spine, supply visceral organs (celiac, superior mesenteric, inferior mesenteric)

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Pre-ganglionic fibers can synapse at the same segmental level, or ascend/descend to another level before synapsing on ganglion

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Reflects the diffuseness of sympathetic function

Sympathetic Ganglia: Adrenal Medulla

Adrenal Medulla: Unique “specialized ganglion”

One autonomic fiber travels directly to adrenal medulla

Activates and releases into blood:

*Epinephrine (80%)* - aka adrenaline, preferentially activates Beta-2 receptors

*Norepinephrine (20%)*

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Sympathetic NS maintains vascular tons, the apha-1 receptors maintain that tone. If you lesson the constricting signal, the vasculature will dilate.

Sympathetic Anatomy

Post-ganglionic fibers (long) travel from ganglia to effector organ

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Synapse on effector organ is a diffuse branching varicosity - *Not as specific of a synapse, like a vine growing up a tree, very widespread, wide effect*

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Sympathetic ganglia: Near the spinal cord

Sympathetic Nervous System

Mobilizes for activity

*Danger, Stress, Fear*

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How exactly does it accomplish this?

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What needs to happen physiologically, when you are in danger?

How is blood pressure raised?

Sympathetic activity causes:

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Norepinephrine to be released at post-ganglionic synapse

Heart: Beta-1 adrenergic receptors are stimulated by NE

= Cardiac muscle in ventricles increase contractile force.

*Minimal effect*

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Norepinephrine (NE) to be released at post-ganglionic synapse

Vascular smooth muscle: Alpha-1 adrenergic receptors are stimulated by NE

= Smooth muscle constricts in walls of arterioles.

*Much more notable effect*

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How is heart rate raised?

Sympathetic activity causes:

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Norepinephrine (NE) to be released at post-ganglionic synapse

SA & AV nodes: Beta-1 adrenergic receptors are stimulated by NE

= Increased set rate of depolarization.

How is skeletal muscle blood flow increased?

Sympathetic activity causes:

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Vascular smooth muscle and within skeletal muscles: Beta-2 adrenergic receptors are stimulated by NE

= Increased blood flow to skeletal muscles

How is blood glucose increased?

Sympathetic activity causes:

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Liver: Beta-2 adrenergic receptors are stimulated by NE

= Increased Gluconeogenesis and Glycogenolysis

How is respiration increased?

Sympathetic activity causes:

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Smooth muscle of Bronchioles: Beta-2 adrenergic receptors are stimulated by NE

= Dilation of bronchioles increases amount of O2/CO2 exchange

*Causes relaxation of muscle = dilation*

How is GIT activity decreased?

We need glucose to got to more important things, so this is stopped

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Sympathetic activity causes:

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GI Smooth Muscle: Beta-2 adrenergic receptors are stimulated by NE - Muscles are slowed

*In Walls*

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GI Sphincters: Alpha-1 adrenergic receptors are stimulated by NE - sphincters are activated to decrease the overall GIT activity

*In Walls*

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GI Smooth Muscle Sphincters: Decreased peristalsis and sphincters close

= Net decrease in GIT activity and digestion

*Thus chronic stress causes GIT issues, especially constipation*

What is super important to keep fluid balance and blood pressure?

Kidneys!

How is urine formation decreased?

Sympathetic activity causes:

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Kidney: Beta-1 adrenergic receptors are stimulated by NE

Increased renin secretion (RAAS)

= increase in NA+ resorption by kidney

= decreased urine formation (osmosis)

*Also: decreased blood flow to kidney*

How is far vision improved?

Accommodation

Accommodation

Ciliary Muscle of Eye:

Sympathetic stimulation - relaxes ciliary muscle, puts increased tension on lens, flattens lens for far vision

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Sympathetic activity causes:

Ciliary muscle of eye: Beta-2 adrenergic receptors are stimulated by NE

Relaxation of ciliary muscle, increased flatness of lens

= decreases refractive power of eye

How is pupillary diameter increased? - Mydriasis

Radial muscle of Iris:

Sympathetic stimulation: Alpha-1

Contraction leads to dilation of pupil

Increases light available to retina

Parasympathetic Nervous System

aka Craniosacral

“Rest and Digest”

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Originated from cranial nerves:

3, 7, 9, 10

Sacral nerves: S2-S4 (at cord level, not spinal level)

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Called Cranio-sacral due to origin from cranial nerves and sacral nerves.

Parasympathetic Anatomy

Pre-ganglionic fibers (long) originate in cranial nerves or sacral nerves S2-S4

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Fibers will travel long distances to synapse on post-ganglionic fibers in parasympathetic ganglion located near or inside effector organ

Parasympathetic Nervous System

Controls the body’s desire to conserve energy and digest

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How exactly does it accomplish this?

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What needs to happen physiologically, when you rest verses when you are in danger?

Physiological Processes

Maintains resting:

Heart rate

Respiration

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Increases GI activity

Increases secretion from accessory digestive organs/glands

*saliva, gastric acid, pancreatic enzymes*

Increases lacrimal secretions

Improves near vision (accommodation) & constricts pupil

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How is heart rate managed?

Parasympathetic activity causes:

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Acetylcholine (ACh) to be released at post-ganglionic synapse

Heart: Muscarinic receptors are stimulated by ACh

= SA & AV nodes decrease rate of depolarization - up to resting heart rate

= Cardiac muscle in atria decreases contractile force

How is respiration managed?

Parasympathetic activity causes:

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Acetylcholine (ACh) to be released at post-ganglionic synapse

Lungs: Muscarinic receptors are stimulated by ACh

= Constriction of smooth muscle of bronchioles.

How is GIT activity increased?

Parasympathetic activity causes:

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Acetylcholine (ACh) to be released at post-ganglionic synapse

Smooth muscle in walls of GIT: Muscarinic receptors are stimulated by ACh

= Increased activity of smooth muscle peristalsis

What is Peristalsis?

Circular and longitudinal layers of smooth muscle alternating contractions to propel food.

How is GI activity increased?

Parasympathetic activity causes:

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Acetylcholine (ACh) to be released at post-ganglionic synapse

Sphincters of GIT: Muscarinic receptors are stimulated by ACh

= Relaxation of smooth muscle sphincters

How is digestion increased?

Parasympathetic activity causes:

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Salivary glands, pancreas, stomach: Muscarinic receptors are stimulated by ACh

= Increased rate of digestive enzyme secretions from accessory digestive organs

How is urination increased?

aka micturation

Parasympathetic activity causes:

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Detruser Muscle of Bladder: Muscarinic receptors are stimulated by ACh

*detruiser the juicer*

Internal Urethral Sphincter: Muscarinic receptors are stimulated by ACh

*not under voluntary control, we will also relax in response to parasympathetic activity*

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= Urination is not exclusively controlled by the voluntary external urethral sphincter.

How is near vision improved? → Accommodation

Parasympathetic activity causes:

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Ciliary Muscle of Eye: Muscarinic receptors are stimulated by ACh

Contraction of ciliary muscle

increased roundness of lens

= Increases refractive power of eye → improves near vision

Accommodation

Default is distance vision

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Accommodation allows for near vision

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Far vision: Refracted mostly by cornea

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Near vision: increases refraction needed by lens

Increases lens thickness = increased refraction

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*Our default is distance vision, when we need to see close, accommodation occurs for that to happen*

How is pupillary diameter decreased? → Miosis

Circular sphincter muscle of Iris:

Parasympathetic stimulation →

Contraction leads to constriction of pupil

Makes less light available to retina

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*What mediates response to constrict in the eye? → Parasympathetic*

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This is helpful to remember for people with headaches!

Autonomic Control Centers → CNS Discussed more with Exam 3, but know this info…

Hypothalamus →

Temperature Regulation

Thirst

Food Intake

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Brain Stem →

Micturition Center

Pneumotaxic Center (respiratory inhibition)

Vasomotor Center

Respiratory Center

Swallowing, coughing, vomiting

Case #1 → Patient with motion sickness is treated with a muscarinic receptor antagonist. What are pros and cons?

Pros →

Effectively treats motion sickness

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Cons →

What would you expect side effects to be?

Dry mouth, dilation of pupils, increased heart rate, difficulty voiding urine, constipation

Case #2 → Horner Syndrome… what is it and what symptoms would you expect?

Loss of sympathetic tone to 1/2 of face

*What provides sympathetic tone to the face? T1 (technically T1-L2)*

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What symptoms would you expect?

Drooping eyelid to 1/2 of face → Superior tarsal muscle is actually under autonomic control (ptosis of the lid)

Lack of sweating to 1/2 of face

Constriction of pupil to 1 eye

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Case #3 → Pheochromocytoma

Tumor of Adrenal Medulla

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What symptoms would you expect?

Panic attacks, racing heart, increased blood pressure, throbbing headaches, cold hands, cold feet, feeling hot, nausea, vomiting

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*They’re not being chased by a tiger, but they feel like they are. Just massive, constant, adrenaline response*

Vasovagal Syncope

Increase in parasympathetic tone in response to increase in sympathetic tone

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Triggers:

Sight of blood, fear, injury, heat

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Symptoms:

Decreased heart rate, decreased blood pressure, lightheaded, vision problems, warm sensation

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Rule out serious cardiac pathology!

via EKG, Echo

All reflexes (visceral and somatic) need what?

Receptor

Sensory Nerve

CNS Center

Efferent Nerve

Effector

Somatic Reflex vs Visceral Reflex

Somatic Reflexes:

Receptors are somatic sensory nerve endings

*nociceptors, muscle spindles, golgi tendon organs*

Effectors are skeletal muscles

Protective in nature

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Visceral Reflexes:

Receptors are in visceral organs & mediated by autonomic nerves

Effectors are smooth muscle, cardiac muscle, glands

Regulatory in nature (help maintain homeostasis)

Autonomic (Visceral) Reflexes

Occur in smooth muscle (vascular & GI), cardiac muscle, & glands

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Baroreceptor Reflex

Pupillary Light Reflex

Vagovagal Reflex

Blushing

Salivary

Autonomic (Visceral) Reflexes → Blood Pressure

Baroreceptor Reflex → Sensory Component

Mechanoreceptors (Baroreceptos) detect changed in blood pressure

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Frequency of firing (strength) is:

Enhanced with increased pressure/stretch = stimulates signal to decrease BP

Decreased with decreased pressure/stretch = stimulates signal to increase BP

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Carotid Sinus →

Innervated by carotid sinus nerve → glossopharyngeal nerve → nucleus of solitary tract (medulla)

Transduce pressures between \~50 - 180 mm Hg

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Aortic Arch →

Innervated by Vagus Nerve → nucleus of solitary tract (medulla)

Autonomic (Visceral) Reflexes → Blood Pressure

Baroreceptor Reflex → Motor Component: Sympathetics

In self-defence → Karate chop thing stimulates this(video)

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When blood pressure INCREASES: Sympathetics

When blood pressure increases, sympathetics will reduce rate of firing

Origin of signal = vasomotor (vasoconstrictor) center in medulla

*decrease rate of firing - signal sent from medulla to spinal cord where sympathetic fibers originate*

Same pathway: only difference is reduced rate of firing

Result is reduced vasoconstrictor activity to lower BP

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When blood pressure DROPS: Sympathetics will act to increase BP

Origin of signal = Vasomotor (vasoconstrictor) center in medulla

*Increase rate of firing - signal sent from medulla to spinal cord where sympathetic fibers originate*

Origin of preganglionic fibers = Intermediolateral gray column from T1-L2

Destination of postganglionic fibers = smooth muscle of arterioles

*Case vasoconstriction via Alpha-1 adrenergic receptors*

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Autonomic (Visceral) Reflexes → Blood Pressure

Orthostatic Hypotension

Diminished ability to vasoconstrict when patient takes upright position/stands up after sitting/laying down.

Autonomic (Visceral) Reflexes → Digestion

Control of GI Activity

Extrinsic (autonomic nervous system)

*Nerves that innervate have cell bodies outside gut wall*

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Intrinsic (enteric nervous system)

*Nerves that innervate have cell bodies inside gut wall*

Submucosal & Myenteric Plexuses contained here.

Autonomic (Visceral) Reflexes → Digestion

Vagovagal GI Reflex → Sensory Component

Parasympathetic Innervation:

Vagus nerve innervated esophagus, stomach, gallbladder, pancreas, & intestines (ending at proximal colon)

*stretch detected in stomach*

Pelvic/sacral nerves S2-S3 innervate the distal colon and anorectal region

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Sympathetic Innervation:

Afferents from prevertebral ganglia (celiac, superior an inferior mesenteric)

These follow similar course as spinal somatic sensory neurons

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Sensory fibers return to nucleus of solitary tract (Vagus)

Synapse in interneuron

Interneuron communicated with efferent fibers (vagus)

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Autonomic (Visceral) Reflexes → Digestion

Vagovagal GI Reflex → Motor Component

Efferent fibers from vagus (dorsal vagal complex) return to GIT

Stomach relaxes to accommodate large amounts of food in response to stretch stimulus

Parietal cels in stomach release gastric acid

Efferent fibers also communicate with enteric nervous system to regulate peristalsis throughout entire GIT

Autonomic (Visceral) Reflexes → Eyes

Pupillary Light Reflexes

Diameter of pupil reacts to amount of light hitting retina

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Large stimulation of retinal ganglia cells results in pupil constriction (miosis)

*decreased light hitting retina*

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Minimal stimulation of retinal ganglia cells results in pupil dilation (mydriasis)

*increased available light for retina*

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Autonomic (Visceral) Reflexes → Eyes

Pupillary Light Reflexes → Sensory Component

Retinal ganglia cells (optic nerve) return to pretectal region of midbrain

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Bright light stimulates parasympathetic pathway

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Low light stimulates sympathetic pathway

Autonomic (Visceral) Reflexes → Eyes

Pupillary Light Reflexes → Motor Component

*Parasympathetics*

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Bright light

Efferent fiber from pretectal region of midbrain communicated with Edinger Westphal Nucleus (CN3)

Edinger Westphal nucleus is origin of parasympathetic fibers of oculomotor nerve

Efferent fibers of CN3 cause pupillary constriction (stimulates circular sphincter muscle of iris)

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*Sympathetics*

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Low light

Efferent fiber from pretectal region of midbrain communicated with sympathetic preganglionic fibers in upper thoracics

Sympathetic pre-ganglionic fibers synapse in superior cervical ganglion

Post ganglionic fibers cause pupillary dilation (stimulates radial dilator) muscle of Iris

Layers of Motor Control

Voluntary Actions →

Conscious control by higher brain centers (primary motor cortex)

*Fine detailed movement especially in hands/finger and facial muscles*

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Involuntary/Subconscious Action →

Learned patterns of movement controlled by basal nuclei (ganglia)

Maintenance of posture and muscle tone by extrapyramidal tracts and muscle spindles

Involuntary reflexes coordinated by the spinal cord

Coordinated actions that are reliant in the sensory/motor integration of the cerebellum

Primary Motor Cortex

Origin of the Corticospinal (pyramidal) Tracts

Direct pathway to spinal cord

Produces voluntary movements of skeletal muscle

“Upper Motor Neurons” → first neuron in motor pathway

Brain Stem Nuclei

Origin of the Extrapyramidal Tracts

Indirect.reflexive

Postural

Cerebellum

Coordinates smooth motor activity

Basal Nuclei

Coordinates the inhibition/activation of motor cortex

Pre-Motor & Supplementary Motor Cortex

Prepares patterns of movement for the primary motor cortex

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Receives information from basal nuclei and cerebellum vis thalamus

Spinal Cord

Houses descending tracts:

Pyramidal

Extrapyramidal

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Serves to relay signal to lower motor neuron

Located in the anterior gray horn

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Reflexes → Pre-programmed responses

Primary Motor Cortex

Located in the precentral gyrus of the frontal lobe (Brodmann’s area 4)

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Mapped in a similar fashion as the primary somatosensory cortex

→ Topographical representation is seen in the motor homunculus

→ 1/2 of the primary motor cortex is devoted to muscles controlling the hands and muscles of speech

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3 Categories →

Functional Motor Cortex - Somatotopic Mapping - Motor Homunculus

Primary Motor Cortex

Output cells are called pyramidal cells

→ Very large neurons

→ Make up corticospinal (pyramidal) tract

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50-100 pyramidal cells needed to cause excitation of muscle

Importantly: Electrical stimulation will result in muscle contraction

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Surgical removal = loss of discrete control of movement in distal extremities (especially the hands)

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Gross (without fine control) movement is spared even without primary motor cortex

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Underscores complexity of motor control

→ Approx. 30% of Corticospinal tract fibers originate in pre/supplementary motor cortex

→ Approx. 40% of Corticospinal tract fibers originate in Primary Sensory Cortex

Primary motor Cortex - Main Output

Corticospinal (Pyramidal) Tracts → Key focus of output vis primary motor cortex

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Giant Bets Cells → LMN lesions

Very large myelinated fibers (70m/sec transmission)

3% of fibers in Corticospinal (pyramidal) tracts

97% of fibers contribute to “background tonic signals”

Primary Motor Cortex - Additional Output

In addition to pyramidal tracts:

→ Corticobulbar (cranial nerves)

→ Inferior olivary (to cerebellum)

→ Extrapyramidal tracts (below)

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Primary motor cortex outputs to extrapyramidal (brain stem) nuclei

→ Rubrospinal (brainstem - posture)

→ Pontine-reticulospinal (brainstem - posture)

→ Medullary-reticulospinal (brainstem-posture)

→ Vestibulospinal (brainstem-posture)

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Discussed later in the section

Incoming Sensory Pathways To Motor Cortex

Subcortical fibers from:

→ Adjacent areas of the cortex

→ Somatic sensory areas (via Thalamus)

→ Visual & Auditory cortex (via Thalamus)

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Subcortical fibers from:

→ Opposite hemisphere which pass through corpus collosum

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*Most of sensory motor is processed in cerebellum*

Incoming Sensory Pathways to Motor Cortex

Nuclei of Thalamus coordinate function between motor cortex, basal ganglia, and cerebellum

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Fibers come from the intralaminar nuclei of Thalamus (control level of excitability of the motor cortex), some of these may be pain fibers

Motor Cortex and Conscious Control

The motor cortex is the focus for the start point of voluntary motor control pathways

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The corticospinal (pyramidal) tract is the major pathway for controlled/precise output from the motor cortex

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Corticospinal (pyramidal) tracts must pass from the cortex, all the way to the ventral gray horn of the cord within the white matter. Let’s look at the path that these tracts take…

*See Image*

Premotor and Supplementary Motor Cortex

Premotor Area:

Guided more by external stimuli (sensory)

→ Mirror neurons (mimicking movement)

*Like a dad doing it and the son mimicking. It happens, not as well*

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Topographical organization similar to primary motor cortex

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Work in concert with other motor areas.

Supplementary Motor Area

Learning and planning (mental rehearsal)

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Topographically organized

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Functions in concert with premotor area to provide positional movement for the body.

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It provides the background for fine motor control of the arms and hands by primary motor cortex

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Motor Cortex

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Supplementary vs Premotor Areas

Case of a stroke victim

→ Could not smile evenly when asked

*Supplemental area damaged*

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→ But - Could smile when told a joke

*Premotor area intact*

Specialized Areas of Motor Cortex

Broca’s Area →

Motor area, producing sounds that will become words

Damage causes impaired *motor* production of speech

Closely associated area controls appropriate respiratory function for speech.

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*Spastic paralysis is hallmark of UMN lesion → Holding arm*

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Eye Fixation and Head Rotation Area →

For coordinated head and eye movements

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Hand Skills Area →

Can move hands, but struggles with intentional movements, figuring out how to do what they are trying to/asked to do.

Damage causes motor apraxia - the inability to perform fine hand movements if the hand skills area is damaged.

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Fluent Aphasia → speech is effortless, but meaning is impaired. Issue is not in motor area

Likely writing is impaired too, but not sure on that.

Wernicke’s Area (NOT in Motor Cortex)

Damage causes →

Decreases speech comprehension

Incorrect choice of words

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Could have fluent aphasia

Outgoing Cortical Motor Signals

*Remember motor cortex stimulates and inhibits*

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Direct pathway (Pyramidal) →

Corticospinal tract

For discrete detailed movement

Modulate (inhibit) unintended movement

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Indirect pathway (Extrapyramidal) →

Signals to basal ganglia, cerebellum, brainstem nuclei

Modulate (inhibit) unintended movement

Corticospinal (Pyramidal) Tracts

Descending Projection Fibers

→ Going from motor cortex, through internal capsule, down through pyramids, down the cord

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Extend from topographical region associated with each particular muscle/group (motor homunculus)

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Pass by the basal nuclei and thalamus (within posterior limb of internal capsule)

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Extend through brain stem (cerebral peduncles) & cross (decussation of pyramids)

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*Point where tracts cross marks the point where the spinal cord begins and medulla ends*

Corticospinal (Pyramidal) Tracts

Lateral Corticospinal →

*Main One*

1st Order/Upper Motor Neuron

Appendicular muscle control - limbs

Eventually synapses with 2nd order neuron that controls appendicular muscles (muscles that we have fine control over)

All fibers cross

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Ventral Corticospinal →

1st Order/Upper Motor Neuron

Axial muscle control - End in mid thoracics

Eventually synapses with 2nd order neuron that controls axial muscles (muscles that we have gross control over)

Approx. 50% of fibers cross.

Motor Cortex - Effect on All Descending Tracts

Primary Motor Cortex →

*Stimulatory Function*

Should normally activate corticospinal tracts

Damage results in loss of voluntary movement

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Primary motor Cortex →

*Inhibitory Function*

Should normally modulate (inhibit) unintended movement

Damage results in loss of inhibition of unintended movement

*When it can’t inhibit, we get things like spastic paralysis*

Lesions of the Motor Cortex - Effect on Pyramidal Tracts

Loss of voluntary control and loss of inhibition

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Result is *Spastic Paralysis*

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Note on Stroke

Immediate Effect → Weakness

Thus we look for FAST

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Over Time → Spasticity is long term effect

Outgoing Cortical Motor Signals

Direct Pathway (Pyramidal)

→ Corticospinal tract

→ For discrete detailed movement

→ Modulate (Inhibit) unintended movement

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Indirect Pathway (not synapsing on LMN → Skeletal Muscle)

→ To Brainstem Nuclei (Extrapyramidal)

→ To Basal Ganglia, Cerebellum

→ Modulate (inhibit) unintended movement

Brainstem: Extrapyramidal Control of Motor Function by the Brainstem

Posture:

→ Gross Extensors

→ Gross Flexors

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Contains centers for repetitive movement and equilibrium (CN 8 plays role in equilibrium)

Orientation of the Pontine and Medullary Reticular Nuclei

*See Image*

Brainstem → Extrapyramidal Control of Motor Function by the Brainstem

Vestibular Nuclei & Tracts - Anti-gravity/extensors (uncrossed)

Pontine-reticular Nuclei and Tract - Anti-gravity/extensors (Bilateral)

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Red Nuclei & Rubrospinal Tract - Anti-extensors (flexor dominant) -- Crosses

Medullary-reticular Nuclei & Tract - Anti-extensors (flexor dominant) -- Bilateral

Vestibular and Pontine Reticular Nuclei

Powerful Excitatory/Anti-Gravity Tone

→ High degree of natural excitability

→ When unopposed, they produce extension

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Centers for control of extensors/antigravity muscle activity

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Involved in activating and sending signals down cord via:

→ Lateral Vestibulospinal Tract - descends ipsilaterally

→ Pontine-reticulospinal Tract (medial reticulospinal) - descends bilaterally