Autonomic Nervous System

Lecturer MED-2023 | Date June 30, 2021

Trans by: Cabalza, R. Dela Cruz, K. Palattao

OUTLINE
I. Overview IV. Enteric Nervous
II. ANS Organization System
and Development V. Regulation of Visceral
A. General Features Motor Flow
of Peripheral VI. Control of Sexual
Visceral Motor Organs
Outflow VII. Appendix
B. Development of VIII. References
the ANS
C. Molecular
Mechanism
III. ANS Divisions
A. Sympathetic
division

I. OVERVIEW
 Primary function: regulation of cardiovascular, respiratory,
digestive, urinary, integumentary, and reproductive organs.
 Two major subdivisions: sympathetic and parasympathetic
 Enteric system is sometimes regarded as third subdivision of
ans.
II. ANS Organization and Development

Targets of Visceral Outflow

 ANS provides neural control of smooth muscle, cardiac
muscle, or glandular secretory cells of viscera.

 Sympathetic – global distribution

 Parasympathetic – effector targets in head and body cavities
See appendix. Comparison of effects of sympathetic and
parasympathetic activity on some visceral functions.

A. General Features of Peripheral Visceral Motor Outflow

 Preganglionic neuron
Cell body in brainstem or spinal cord
o
o Thinly myelinated fiber that projects to the
ganglion
 Postganglionic neuron
o Cell body in autonomic ganglia
o Unmyelinated fiber that projects to visceral
effector cells
o Parasympathetic – long preganglionic, short
postganglionic
o Sympathetic – short preganglionic, long
postganglionic
 Going to skeletal muscles, lower motor neurons (specifically
alpha motor neurons) serve as the final common pathway
linking the CNS and skeletal muscle. Similarly, sympathetic
and parasympathetic serve as the final common pathway
linking the CNS to the viscera and lagi silang maqka-pair.
However, unlike the somatic motor system, the autonomic
nervous system is composed of two neurons.
 This is in general, parasympathetic ganglia are in close
proximity with the effector tissue while sympathetic are
located close sa CNS.
 As you can see, the visceral motor neurons are not organized
into discrete motor units like those of the somatic motor
system.
Figure 1. comparison of somatic motor outflow (A). with sympathetic (B). and
parasympathetic outflow (C)
B. Development of the ANS
Preganglionic visceral motor neurons
 Cell bodies are located in nuclei or cell columns embryologically
derived from the visceral efferent cell column. This column
arises from neuroblasts in the basal plate of brainstem and
spinal cord portions of neural tube
Postganglionic visceral motor neurons
 Cell bodies are located in autonomic ganglia.
 Can either be (1) well-defined, encapsulated clusters (e.g.,
superior cervical ganglion) or (2) clusters of somata (e.g.,
nerve plexuses, or in walls and capsules of visceral organs).
 Autonomic ganglion cells – derived from neural crest cells
that migrate during development
 Myenteric and Auerbach plexuses are also derived from
neural crest cells.
Congenital megacolon/ Hirchsprung disease
 Pathophysiology: Failure of enteric neuronal precursor cells
to migrate into the wall of the developing lower gut

Trans # 11 Posterior Fossa Level (Cerebellar, Auditory and Vestibular System) 1 of 13

 III. ANS DIVISION

A. Sympathetic division

Sympathetic Preganglionic Neurons

 Arises from T1-L2 (sometimes C8 and L3)
 Cell bodies located in Rexed lamina VII, primarily in the
intermediolateral nucleus (cell column) of the lateral horn
 Axons exit the spinal cord in the anterior root and enter the
sympathetic trunk via the white communicating ramus.

 Three courses after entering the sympathetic chain

1. Synapse at that level with postganglionic neurons whose
unmyelinated axons join the spinal nerve via a gray
communicating ramus

C. Molecular Mechanism

2. May ascend or descend in the sympathetic chain to

synapse on postganglionic neurons

 Key molecule in development of ANS is NGF (neurotropin

/nerve growth factor)
 Any mutation involving the steps then results problems in
ANS
 Mutation in NGF ( person with hereditary sensory with
autonomic neuropathy type 4)
3. May pass through the chain ganglion as a preganglionic fiber to
form part of splanchnic nerve

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General Viscerotopic organization
 Superior, middle, inferior cervical ganglion – upper
thoracic segment
 Lumbar and sacral ganglia –lower thoracic and upper
lumbar segment. See appendix. Different ganglions and
innervations
Sympathetic Ganglia
 Cell bodies of sympathetic postganglionic neurons are
generally grouped into discrete ganglia: paravertebral ganglia/
sympathetic chain ganglia and prevertebral ganglia
 The sympathetic chain ganglia are connected to spinal nerves
via white and gray communicating rami.
o White Ramus
 Appears white because it contains
myelinated preganglionic fibers
o Gray Ramus
 Appears gray because they are
composed of unmyelinated
postganglionic fibers
 Only spinal nerves T1-L2 have white rami whereas every
spinal nerve is connected to the sympathetic trunk by
gray ramus. (APPENDIX 1)
Sympathetic chain ganglia/ paravertebral ganglia
 Number of ganglia DOES NOT exactly match the number of
spinal nerves .
 In general, there are 3 cervical, 10-11 thoracic, 3-5 lumbar,
and 3-5 sacral sympathetic ganglia on each side, and a single
coccygeal ganglion (ganglion impar)
 Stellate ganglion – Inferior cervical ganglion + first thoracic
ganglion
Superior Cervical Ganglion
 Largest of the paravertebral ganglia/sympathetic chain.
 Innervate blood vessels and cutaneous targets of the face,
scalp, and neck of territories supplied by first four cervical
spinal nerves.
 They are distributed to these targets via
branches of internal and external carotid
nerves.
 Also innervates salivary glands, nasal glands, lacrimal glands,
pupillary dilator muscle and superior & inferior tarsal muscles.
 Clinical application: Interruption of this sympathetic pathway
will result to Horner syndrome
 Miosis
 Ptosis
Trans # 14 Autonomic Nervous System
 Anhidrosis
 Flushing face
Prevertebral Ganglia
 Found in visceral motor plexuses associated with the
abdominal aorta and its major branches, and they receive
input via the splanchnic nerves.
 Celiac ganglion
o Located at the origin of the celiac artery and supplies
postganglionic fibers to the spleen, and to foregut
derivatives (stomach, superior duodenum, liver,
gallbladder, pancreas)
 Aorticorenal ganglion
o Supplies postganglionic fibers to kidneys
Superior Mesenteric ganglion
 Provides postganglionic fibers to midgut derivatives
 Duodenum
 Jejunum and ileum
 Cecum
 Appendix
 Ascending colon
 Proximal 2/3 of transverse colon
Inferior Mesenteric ganglion
 Projects postganglionic fibers to hindgut derivatives
 Distal 1/3 of transverse colon
 Descending colon
 Sigmoid colon
 Rectum
 Urinary bladder
 Urethra
 Reproductive organs
Functional and Chemical Coding
 Sympathetic system acts in a global, nonselective manner
Effects include increases in heart rate, blood
o
pressure, blood flow to skeletal muscles, blood
glucose level, sweating, and pupil diameter
o Concurrently, there are decreases in gut motility,
digestive gland secretion, and blood flow to
abdominal viscera and skin.
 However, in less extreme conditions, there is selective
control.
o Example: cell groups that control vascular tone
 Sympathetic pathways to blood vessels in
the skin are primarily influenced by
temperature
 Sympathetic outflow to vessels in skeletal
muscle responds to changes in BP
signaled by baroreceptors
 ALL preganglionic neurons are cholinergic
o However, some also express one or more
neuropeptides such as substance P and
enkephalins
 Most postganglionic neurons use norepinephrine
o Some are cholinergic (eccrine sweat glands,
arrector pili muscles, arterioles of skeletal muscle)
 Most prevalent among synthetic peptides is neuropeptide Y
which is released along with norepinephrine by
vasoconstrictor postganglionic fibers.
o Stimulation of vascular smooth muscle contraction,
potentiation of epinephrine effects, and paradoxical
inhibition of norepi release.
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Figure 9. Some effector organs of parasympathetic and their neurotransmitters.
All pre-ganglionic neurons used acetylcholine, may ilan na may kasamang isang
neuropeptide such as enkephalin.
RECEPTOR TYPES IN SYMPATHETIC TARGETS
 Epinephrine is a more potent ligand than norepinephrine
 Consequently, epinephrine is administered to counteract
symptoms of anaphylactic shock, including bronchospasm,
edema, congestion of mucous membranes, and cardiovascular
collapse
Table 1. Receptor types, its type of tissue and their Actions
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COMPLEX REGIONAL PAIN SYNDROME
 Complex regional pain syndrome (CRPS) type II/ causalgia
 Syndrome that can results from partial injury to a peripheral
nerve, typically a nerve serving an extremity.
 Signs and symptoms:
 Spontaneous burning pain
 Hypersensitivity of skin
 Pain triggered by loud noises or strong emotions
 Mottling of skin
 Swelling of extremity
 Pathophysiology: Unclear, but one theory is that sympathetic
postganglionic neurons coursing in the injured nerve develop
abnormal connections to nociceptive posterior root
ganglion neurons –> nociceptive neurons become
hypersensitive to adrenergic stimulation
B. PARASYMPATHETIC DIVISION
Preganglionic and Postganglionic Neurons
 More restricted distribution compared to sympathetic NS
 Cell bodies of preganglionic para – located in (1) nuclei that
provide visceral efferent fibers that travel in CN III, VII, IX, and X
or in (2) sacral spinal cord segments
 Parasympathetic = CRANIOSACRAL
 Sympathetic = THORACOLUMBAR
 Cell bodies of postganglionic parasympathetic neurons
supplying cranial structures are located in discrete ganglia.
 Cell bodies of postganglionic para supplying viscera are
scattered within nerve plexuses of the target organ or in the wall
of the gut (terminal or intramural ganglia) where they
intermingle with neurons of enteric NS.
Figure 10. Parasympathetic Outflow Pathways
See Appendix. Table 2.
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 II. Intrinsic Neural Innervation (originates from the wall of the gut)
A. Myenteric Plexus (aka. Auerbach’s Plexus)
FUNCTIONAL AND CHEMICAL CODING 1. Located between the longitudinal and submucosal plexus
 Preganglionic parasympathetic neurons = cholinergic a. Concerned with the contraction of the smooth muscles
 Postganglionic parasympathetic neurons = cholinergic of the gut.
 Preganglionic neurons = nicotinic
 They release acetylcholine which binds to nicotinic receptors
 Postganglionic = muscarinic
 BOTH pre and postganglionic neurons release molecules aside
from acetylcholine (i.e., neuropeptides).

RECEPTORS TYPES IN PARASYMPATHETIC TARGETS

 Nicotinic receptors are limited to skeletal muscle, and
cholinergic synapses in autonomic ganglia and CNS
 Muscarinic receptors – involved in response of smooth muscle,
cardiac muscle and glandular cells to acetylcholine
 M1 – parasympathetic stimulation of gastric acid secretion
 M2 – parasympathetic depression of heart rate
See Appendix. Table 3.
IV. ENTERIC NERVOUS SYSTEM
 a.k.a. Intrinsic Nervous System
 There is a HIGH DEGREE OF AUTONOMY of digestive
functions.
 BASIS: The wall of the gut (from the esophagus to anus) is
equipped with an elaborate intrinsic network of neurons
 ENTERIC NERVOUS SYSTEM or INTRINSIC NERVOUS Figure 13. Myenteric Plexus
SYSTEM
 referred to by some authorities as the THIRD DIVISION of
the AUTONOMIC NERVOUS SYSTEM.
INNERVATIONS OF THE GASTROINTESTINAL SYSTEM B. Submucosal Plexus (aka. Meissner’s plexus)
I. Extrinsic Neural Innervation 1. Lies in the submucosa
A. Parasympathetic Innervation a. Concerned on the glandular functions in the gut

Figure 11. Parasympathetic Innervation

B. Sympathetic Innervation

Figure 13. Submucosal Plexus

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 A. INTRINSIC INNERVATIONS OF THE
GASTROINTESTINAL SYSTEM
1. Afferent Neurons PERISTALTIC REFLEX
 Also referred to as SENSORY NEURONS  The presence of ingested material in the intestine evokes
 FUNCTIONS: waves of contraction and relaxation that slowly propel the
 Mechanoreceptors – very responsive to stimuli like touch, material toward the anus.
pressure, stretching and gravity
 Chemoreceptors – very responsive to changes in pH, or in Presence of a stimulus: food bolus
level of certain substances like O2 and CO2
 Nociceptors – can initiate actual or potential tissue
damage
- can be activated by several types of stimuli
Receptor activation: intrinsic mechanoreceptive sensory neurons
within the target tissue. E.g., extremes of
temperature, too much strain, stretch or too
much chemical changes that can cause tissue
damage like during local inflammatory  These sensory neurons activate populations of excitatory and
processes. inhibitory INTERNEURONS in the myenteric plexus.
2. Interneurons
1. Excitatory Interneurons
 Provides connection between afferent and efferent neurons
 FUNCTIONS:  Activate EXCITATORY MOTOR NEURONS UPSTREAM from
 Excitatory the bolus.
 Inhibitory  EFFECT: CONTRACTION UPSTREAM FROM THE BOLUS
 Orally projecting  Activate INHIBITORY MOTOR NEURONS DOWNSTREAM
 Caudally projecting from the bolus.
3. Efferent Neurons  EFFECT: RELAXATION DOWNSTREAM FROM THE
 Also referred to as MOTOR NEURONS BOLUS
 FUNCTIONS: 2. Inhibitory Interneurons
 Secretomotor  Inhibit EXCITATORY MOTOR NEURONS DOWNSTREAM
 Excitatory Muscle Motor  EFFECT: RELAXATION DOWNSTREAM FROM THE
 Inhibitory Muscle Motor BOLUS

 OVERALL EFFECT: Propulsion of the bolus toward the anus

INTERSTITIAL CELLS OF CAJAL (ICC)
through this combination of constriction of the segment
above the bolus and relaxation of the intestinal segment
 Smooth muscle-like cells. below the bolus.
 Have extensive connections both with each other and with
conventional smooth muscle cells, which are themselves
electrically coupled.
 FUNCTIONS:
 Initiate rhythmic electrical activity (analogous to the
pacemaker cells of the heart).
Generate and propagate slow waves of depolarization in the
smooth muscle layers of the gut wall, which are translated by the
enteric nervous system into FUNCTIONALLY useful waves of
contraction

Figure 15. Peristaltic Reflex

Figure 14. Interstitial Cell of Cajal
This picture shows the neural pathways mediating the peristaltic reflex.
Distention of the intestinal lumen by a bolus of ingested material activates
an elaborate intrinsic network that includes sensory neurons, motor
neurons, and several types of interneurons. THE RESULT is contraction of
circular smooth muscle upstream from the bolus and relaxation of circular
smooth muscle downstream from the bolus so that it is propelled toward
the anus.

Trans # 14 Autonomic Nervous System 6 of 13

 D. VASOCONSTRICTOR SYMPATHETIC FIBERS directly
REFLEX-MEDIATED SECRETION
innervate blood vessels of the GI tract.

E. OTHER SYMPATHETIC FIBERS innervate glandular

PRESENCE OF A STIMULUS
↓ Enteroendocrine cells (monitor the chemical composition
of luminal contents) in the lining epithelium respond to
contents in the lumen
RECEPTOR ACTIVATION
↓ Chemoreceptive Sensory Neurons
ACTIVATION OF SECRETOMOTOR PATHWAYS
structures in the wall of the gut
GASTRIAC RECEPTIVE RELAXATION REFLEX
C. REFLEXES
 Distention of the stomach results in relaxation of the smooth
muscle in the stomach; this allows filling of the stomach to occur
without an increase in intraluminal pressure.

↓ EFFECT: Secretions by glandular cells

B. EXTRINSIC REGULATION
OF THE GASTROINTESTINAL SYSTEM
1. Parasympathetic Input
 Generally, for enhancement
 Serves to conserve energy and to assimilate sources energy
for the body
2. Sympathetic Input
 Generally inhibitory
 Mainly concerned in preparing the body to respond to certain
emergency

PARASYMPATHETIC INNERVATION
I. COMPONENTS
A. Vagus Nerve
1. 10th cranial nerve (Cranial Part)
2. Medulla Oblongata
3. Innervates the esophagus, stomach, gallbladder, Figure 16. Gastriac Receptive Relaxation Reflex
pancreas, first part of the intestine, cecum, and the
proximal part of the colon. DEFECATION REFLEX
B. Pelvic Nerves  The defecation reflex involves the evacuation of fecal material
1. Sacral Part from the rectum in response to stimulation of afferent nerves in
2. Innervate the distal part of the colon and the anorectal the distal bowel.
region.  The intrinsic defecation reflex.
The parasympathetic defecation reflex
II. TYPICAL ORGANIZATION
A. PREGANGLIONIC NERVE CELL BODIES
1. Brainstem (Vagus)
2. Spinal Cord (Pelvic) - S2-S4
B. AXONS from these PREGANGLIONIC NEURONS run in
the nerves to the gut.
C. POSTGANGLIONIC NEURONS
1. Enteric neurons in the gut wall.
D. SYNAPSE
1. Obligatory Nicotinic Synapse
2. ACETYLCHOLINE released from nerve terminal
acting at NICOTINIC RECEPTORS localized on the
postganglionic neuron, which is an INTRINSIC
NEURON.

I. COMPONENTS
A. Cell bodies in the thoracolumbar spinal cord
B. PREVERTEBRAL GANGLIA
1. Celiac
2. Superior Mesenteric Ganglia
3. Inferior Mesenteric Ganglia

II. TYPICAL ORGANIZATION

A. POSTGANGLIONIC NEURONS IN THE GANGLIA
whose fibers leave the ganglia and reach the end organ
along major blood vessels and their branches.
B. PARAVERTEBRAL (CHAIN) GANGLIA seen in
C. sympathetic innervation of other organ systems.
Figure 17. Neural Control of Defecation

Trans # 14 Autonomic Nervous System 7 of 13

ENTEROGASTRIC REFLEX
 A nervous reflex whereby stretching of the wall of the
duodenum results in inhibition of gastric motility and reduced
rate of emptying of the stomach.
 It is a feedback mechanism to regulate the rate at which
partially digested food (chyme) leaves the stomach and enters
the small intestine.
 Receptors in the duodenal wall detect distension of the
duodenum caused by the presence of chyme and also raised
acidity (i.e. low pH) of the duodenal contents due to excess
gastric acid. They send signals via the parasympathetic nervous
system, causing reflex inhibition of stomach-wall muscles
responsible for the stomach emptying.
Figure 18. Enterogastric Reflex
GASTROCOLIC REFLEXES
 A physiological reflex that controls the motility of the lower
gastrointestinal tract following a meal. As a result of the
gastrocolic reflex, the colon has increased motility in response
to the stretch of the stomach with the ingestion of food.
 The gastrocolic reflex allows room for the consumption of more
food via control over peristalsis and movement of ingested food
distally toward the rectum.
GASTROILEAL REFLEXES
 It works with the gastrocolic reflex to stimulate the urge to
defecate.
 This urge is stimulated by the opening of the ileocecal valve and
the movement of the digested contents from the ileum of the
small intestine into the colon for compaction.
D. CLINCAL CORRELATIONS
Irritable Bowel Syndrome
 The gastrocolic reflex has correlations with the pathogenesis of
irritable bowel syndrome.
 The act of food consumption can provoke an overreaction of the
gastrocolic response due to heightened visceral sensitivity seen
in IBS patients, resulting in abdominal pain, constipation,
diarrhea, bloating, and tenesmus.
Hirschsprung Disease
 Hirschsprung disease (HSCR) is a birth defect. This disorder is
characterized by the absence of particular nerve cells
(ganglions) in a segment of the bowel in an infant.
 The absence of ganglion cells causes the muscles in the
bowels to lose their ability to move stool through the intestine
(peristalsis).
Trans # 14 Autonomic Nervous System
V.REGULATION OF VISCERAL MOTOR OUTFLOW
A. CARDIOVASCULAR SYSTEM
Baroreceptor Reflex
 Functions as a buffer to maintain blood pressure during sudden
changes in posture.
 STIMULUS: Sudden change in position
 RECEPTOR ACTIVATION: Mechanoreceptors in the carotid
and aortic sinuses
 SENSORY NEURONS: Primary Visceral Sensory Neurons of
the Glossopharyngeal and Vagus Nerves convey signals to the
SOLITARY NUCLEUS
 PROJECTIONS OF THE SOLITARY NEURONS influence the
tonic activity of PARASYMPATHETIC (VAGAL) OUTPUT to the
HEART and SYMPATHETIC OUTPUT to the HEART AND
PERIPHERAL BLOOD VESSELS.
 So the stimulus here is the sudden change in position. For
example: a patient from reclining position suddenly got up, so
what happens next there will be receptor activation,
mechanoreceptors are sensitive to sudden changes in
gravitational pull, mechanoreceptors in the carotid and aortic
sinuses are activated. Next are the sensory neurons especially
the primary visceral sensory neurons of the Glossopharyngeal
and Vagus nerve convey signals to the solitary nucleus then
projection of the solitary neurons influence the tonic activity of
parasympathetic (vagal) output to the heart and sympathetic
output to the heart and peripheral blood vessels.
 So the main purpose of this is kapag kasi biglang tumayo yung
tao, may sudden pulling of blood sa lower areas of the body
resulting in deprivation of blood to the brain and other vital
organs, so the purpose of the baroreceptor is to maintain
normal circulation despite the position change.
 Rapid reduction in a baroreceptor discharge resulting in a
DECREASE in signals from the solitary nucleus to two
brainstem targets:
 VAGAL PREGANGLIONIC PARASYMPATHETIC NEURONS
that suppress heart rate and cardiac output, receive an
excitatory drive from neurons of the solitary nucleus.
 EFFECT: Increased heart rate and cardiac output.
 VASOPRESSOR NEURONS in the Rostral Ventrolateral
Medulla (RVLM). Neurons in this region have intrinsic
pacemaker features and receive inhibitory inputs from the
solitary nucleus. When these RVLM neurons are released from
the inhibitory drive of solitary neurons, the result is increased
sympathetic outflow.
 EFFECT: Increased cardiac output Increased resistance in
vascular beds of skeletal muscle and abdominal visceral
organs but not of the skin, heart, and brain.
 OVERALL EFFECT: When a person moves from a reclining to
a standing posture, the resultant pooling of blood in the lower
half of the body is quickly countered by increased vascular tone
and increased cardiac output.
Figure 19. Baroreceptor Reflex
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 So when we are in a reclined position, there is a baroreceptor
input in solitary nucleus which is excitatory, so what happens
first is it stimulates the vagal motor nucleus. The function of the
vagal motor nucleus is it suppresess the heart rate and cardiac
output. Another input in the solitary nucleus is it also
suppresses vasopressor medullary neurons whic facilitate
sympathetetic preganglionic outflow. Pag naiinhibit sila na-
fafacilitate yung sympathetic preganglionic outflow which results
in increase heart rate and cardiac output, also increase in tone
of vessels in skeletal muscles.
Clinical Correlations: Orthostatic Hypotension
 A severe drop in blood pressure when the patient assumes an
upright position.
 Without the baroreceptor reflex, movement to a standing
position results in dizziness or fainting (reflex syncope) because
of decreased blood flow to the brain.
 This manifestation of orthostatic hypotension is a serious
consequence of many forms of autonomic dysfunction,
including familial dysautonomia (FD; hereditary sensory and
autonomic neuropathy, or HSAN, type III), and multiple system
atrophy (MSA).
 The pathophysiology of FD is a loss of visceral afferent fibers
resulting in inadequate baroreceptor input, whereas MSA is a
progressive neurodegenerative condition characterized by a
loss of neurons from the intermediolateral cell column.
Chemoreceptor Reflex
 Maintains homeostasis of blood gas composition by adjusting
respiration, cardiac output, and peripheral blood flow.
 STIMULUS:Decreased partial pressure of oxygen (PO2) and
increased partial pressure of carbon dioxide (PCO2)
 RECEPTORS: Chemoreceptors in the carotid and aortic bodies
 SENSORY NEURONS: Glossopharyngeal and Vagal Afferents
that terminate in the Solitary Nucleus
 OVERALL EFFECTS: These changes result in a decreased
blood flow to skeletal muscles and viscera, whereas blood flow
to the brain is maintained. Thus proportionately more
oxygenated blood is available to the brain than to skeletal
muscle and viscera. The resulting conservation of oxygen
preserves vital functioning of the CNS.
 So here very vital ang CNS and other organs, instead of
spending oxygenated blood to to other parts of the body this will
divert more oxygenated blood to the brain and other vital organs
so that function will be maintained.
B. URINARY BLADDER AND MICTURITION
 Micturition (emptying of the urinary bladder) is brought about by
contraction of smooth muscle of the bladder wall (DETRUSOR
MUSCLE) and relaxation of smooth muscle of the INTERNAL
URETHRAL SPHINCTER and of skeletal muscle of the
EXTERNAL URETHRAL SPHINCTER
 PARASYMPATHETIC OUTFLOW
 PREGANGLIONIC NEURONS: Sacral Spinal Cord
 POSTGANGLIONIC NEURONS: Bladder Wall
 EFFECTS: Contraction of the detrusor and inhibition of the
internal sphincter
 SYMPATHETIC INNERVATION
 EFFECTS: Inhibitory on both detrusor and the
parasympathetic postganglionic neurons in the bladder wall.
 EXTERNAL URINARY SPHINCTER
 Subject to both reflex and voluntary control.
 Supplied by ALPHA MOTOR NEURONS IN SPINAL CORD
SEGMENTS S3 AND S4.
 During periods of urine storage, activity of bladder afferent
neurons is low.
 The low activity of the sensory neurons results in:
(1) low activity of parasympathetic excitatory innervation to the
detrusor and inhibitory innervation of the internal sphincter,
Trans # 14 Autonomic Nervous System
(2) tonic activity of sympathetic neurons that inhibit both the
parasympathetic ganglion cells in the bladder wall and the
detrusor muscle directly, and
(3) tonic activity of sacral somatic motor neurons mediating
constriction of the external sphincter.
 As urine accumulates, pressure on the bladder wall activates
tension receptors until bladder afferent activity rises to a
threshold level.
 This increased activity of bladder afferents induces micturition
by way of both spinal and brainstem reflexes that result in
inhibition of sympathetic outflow, activation of parasympathetic
outflow, and inhibition of somatic motor neurons supplying the
external sphincter muscle.
***see appendix. Innervation of the Urinary Bladder
C. REFLEX
Storage Reflex
 At low levels of bladder filling, low-frequency firing of bladder
afferents initiates reflexes that promote urine storage → Lumbar
sympathetic neurons and motoneurons of the Onuf nucleus are
activated → Relaxation of the bladder detrusor muscle and
contraction of the bladder neck and external sphincter muscles
 Parasympathetic neurons are inhibited
Micturition Reflex
 Bladder filling reaches a threshold volume (approximately 300
mL)→ High frequency firing of bladder afferents triggers the
micturition reflex → Activation of the sacral parasympathetic
neurons → Stimulates contraction of the bladder detrusor
muscle
 Sympathetic neurons and somatic motor neurons are inhibited,
thus relaxing the bladder neck and external sphincter muscles
***see Appendix. Neural Control of Micturition
Figure 20. Normal Micturition Pathway
It involves a supraspinal pathway, it is coordinated by pontine micturition center
which is located in the dorsal pons. This center is activated through the
periaqueductal gray matter by high frequency bladder afferent discharges.
For example: there will be a detected high frequency bladder afferent discharges
'pag naabot yung threshold na 300mL, it will communicate with the
periaqueductal gray matter which in turn coordinate with the pontine micturition
center. Through the projections to the sacral spinal cord, the pontine micturition
center promotes coordinated activation of the sacral parasympathetic neurons
which innervates the bladder detrusor and sphincter muscle. We also see
segmental control, for example may bladder afferent discharges ulit, dito sa level
kaya na macontrol kaso ang problem dito kailangan pa rin under control ng
pontine micturition center, kasi may times na 'di coordinated yung sa detrusor at
external sphincter, so tataas yung pressure sa bladder.Meron ding medial frontal
cortex control, reason why we have voluntary control of our micturition reflex,
whenever the situation is not proper for us to urinate.
Voluntary Control of Micturition
 Under the activity of the pontine micturition center (reflex)
 May be transiently inhibited by input from the medial frontal lobe,
possibly through a relay in the medial hypothalamus and
periaqueductal grayà the basis for voluntary control of
micturition
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Segmental Micturition Reflex
 Poorly coordinated, and sometimes the bladder detrusor and
external sphincter muscles contract at the same time.
 Neurogenic bladder – develops as a result of disturbances at
different levels of the system for bladder control
3 manifestations of Neurogenic Bladder
1. urinary incontinence
2. urinary urgency
3. urinary retention
D. CLINICAL CORRELATIONS
Un-inhibited Bladder
 LESION: the inhibitory connections between the medial aspect
of the frontal lobes and the pontine micturition center.
 MANIFESTATIONS: Patients have urinary urgency and
incontinence.
 Because the connections between the pontine micturition center
and the spinal cord are intact, the reflex arc is preserved,
bladder size is normal, and urine is not retained.
 The anal reflex, which indicates the integrity of the sacral spinal
cord and cauda equina, is also preserved.
 Common in the elderly but is also a manifestation of dementia,
hydrocephalus, and Parkinson disease
Spastic Bladder
 LESIONS: Interrupt the connections between the pontine
micturition center and the sacral spinal cord.
 MANIFESTATIONS: Patients have urinary frequency and
incontinence.
 Sacral micturition reflex is preserved, but because of the lack of
pontine control, there is detrusor-sphincter dyssynergia.
 Contractions of the bladder detrusor and external sphincter
muscles are not coordinated.
 This increases the intravesical pressure during micturition
(because the action of the bladder
 Detrusor muscle is opposed by that of the external sphincter
muscle).
 This leads to hypertrophy of the bladder wall and reduction of
bladder volume and compliance.
 Urinary retention occurs eventually and, together with increased
intravesical pressure, predisposes to hydronephrosis, urinary
tract infection, and renal failure.
 Occurs with midline or bilateral lesions of the cervical or
thoracic spinal cord, as may occur with traumatic injury or
multiple sclerosis.
Flaccid Bladder
 Occurs with midline or bilateral lesions of the segmental reflex
arc at the sacral level of the spinal cord or its afferents or
efferents in the cauda equine.
 In the absence of the micturition reflex, the bladder becomes
distended with urine and hypotonic
 Because of concomitant weakness of the external sphincter
muscle, the bladder empties partially (overflow incontinence)
but only infrequently
 Patient has urinary retention, typically with a postvoid residual
volume larger than 100 mL
 Involvement of the cauda equina and sacral cord is manifested
by perianal anesthesia and absence of the anal reflex
***see appendix. Clinical Correlations Summary
VI.CONTROL OF SEXUAL ORGANS
Hypothalamus
 Receives input from the cerebral cortex and circulating sex
hormones (estrogens and testosterone)
 Has a critical role in the regulation of sexual and reproductive
behavior
 Autonomic output
 Men: for penile erection and ejaculation
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 Women: for engorgement of the clitoris and vaginal
lubrication
 Sacral parasympathetic output
 For reflex penile erection
 Mediated primarily by nitric oxide
 Lumbar sympathetic output
 Mediated by α1-adrenergic receptors,
 For contraction of the vas deferens, which is required for
ejaculation
 May also contribute to emotionally triggered erection in
patients with spinal cord injury
 When sympathetic input is excessive, however, it elicits
vasoconstriction of erectile tissue and prevents penile erection
Generalized Autonomic Failure
 Pathophysiology
 Postganglionic (efferent) autonomic failure due to deposition
of a-synuclein in the ganglia and peripheral autonomic
nerves
 Dysfunction or loss of peripheral sympathetic nerves leads to
impaired production of catecholamines such as
norepinephrine
 Clinical Manifestations
 The hallmark of generalized autonomic failure is neurogenic
orthostatic hypotension
 The dysfunction can be widespread leading to genitourinary,
bowel, thermoregulatory, and systemic manifestations
 Genitourinary dysfunction
 Urinary frequency and urgency and in more severe cases,
urinary retention and incontinence may occur
 Erectile dysfunction in males
 Genitourinary symptoms are caused by sacral
parasympathetic failure
 Gastrointestinal symptoms
 Constipation due to dysfunction of the ENS or the vagal
innervation of the GIT
 Thermoregulation
 Anhidrosis due to sympathetic cholinergic impairment
 Compensatory hyperhidrosis
 Orthostatic Hypotension
 Most common presenting symptom
 Normally, it is accompanied by compensatory increase in
sympathetic outflow via baroreflex but in autonomic failure,
there is an inadequate sympathetic response due to
peripheral cardiac and vasomotor denervation
 Neurologic Symptoms
 Mild, generalized bradykinesia with reduced blink rate
 Gait may be subtly normal with slowing and reduced arm
swing
**see appendix. Generalized Autonomic Failure
Autonomic Hyperactivity
 Characterized by overactivity of the sympathetic nervous
system due to the excessive response of adrenal medulla and
sympathetic ganglia
 Clinical Manifestations
 Sympathetic hyperactivity manifests with hypertension,
tachyarrhythmias, hyperhidrosis, peripheral vasoconstriction,
and hyperthermia or hypothermia.
 Massive sympathoexcitation can lead to intracranial
hemorrhage, vasogenic brain edema, congestive heart
failure, apical ballooning (Takotsubo) syndrome, and
neurogenic pulmonary edema.
 Less commonly, autonomic hyperactivity also involves the
parasympathetic system and manifests primarily with
bradyarrhythmia or even syncope
 Causes
 Head trauma, hypoxic brain injury, subarachnoid
hemorrhage, autonomic dysreflexia in spinal cord injury,
Guillain-Barré syndrome,and iatrogenic disorders such as
neuroleptic malignant syndrome and serotonin syndrome
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 VII. APPENDIX
APPENDIX 1

Table 2. Peripheral Pathways of Parasympathetic Outflow

Trans # 14 Autonomic Nervous System 11 of 13

Table 3. Comparison of the Sympathetic and Parasympathetic Division of
Autonomic Outflow

Innervation of the urinary bladder.

Neural Control of Micturition

Trans # 14 Autonomic Nervous System 12 of 13

Clinical Correlations Summary

Generalized Autonomic Failure

VIII. REFERENCES
 Reporter’s PPT and Lecture
 Benarroch, E. E., Daube, J. R., Flemming, K. D., &
Westmoreland,
B. F. (2008). Mayo clinic medical Neurosciences. Organized by
Neurologic Systems and Levels.

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