anatomy and physiology of reticular formation

1. RETICULAR
FORMATION
BY: DR. HOSEIN NEEMATI
SUPERVISED BY: PROFESSOR SALEHPOUR

2. n
OBJECTIVE
 INTRODUCTION
 LOCATION OF RETICULAR FORMATION
 NUCLEI OF RETICULAR FORMATION(NEUROAL AGGREGATES )
 AFFERENTS AND EFFERENT OF RETICULAR FORMATION
 FUNCTIONS OF RETICULAR FORMATION
 ASCENDING RETICULAR ACTIVATING SYSTEM
 DESCENDING RETICULAR ACTIVATING SYSTEM
 ROLE IN SLEEP AND WAKE FULLNES
 APPLIED PHYSIOLOGY

3. The brainstem contains extensive fields of intermingled
neuronal cell bodies and nerve fibres, which are collectively
termed the reticular formation. The reticular regions are often
regarded as phylogenetically ancient, representing a primitive
nerve network on which more anatomically organized,
functionally selective connections have developed during
evolution

6. Reticular regions tend to be ill-defined collections of neurones with
diffuse connections. Their conduction paths are difficult to define,
often complex and polysynaptic, and they have ascending and
descending components that are crossed, uncrossed and
sometimes bilateral. Their components subserve somatic and
visceral functions.

9. They also include some distinct and important
cell groups, which are distinguished on the
basis of their conections and neurotransmitter
substances. These
Include:
dopaminergic and noradrenergic
neurones (group A)
serotoninergic (group B)
adrenergic (group C)
cholinergic (group Ch)

11. . Some regions contain only small to
intermediate multipolar cells (‘parvocellular’
regions). However, there are a few areas where
these mingle with large multipolar neurones in
‘gigantocellular’ or ‘magnocellular’ nuclei.

13. In general terms, the reticular formation is a continuous core that
traverses the whole brainstem, and is continuous below with the
reticular intermediate spinal grey. It is divisible, on the basis of
cytoarchitectonic, chemoarchitectonic and functional criteria, into
three bilateral longitudinal columns:
median; medial, containing mostly large reticular neurones; and
lateral, containing mostly small to intermediate neurones

16. MEDIAN COLUMNNUCLEI
midlineand occupyinthe median column of reticular nuclei extends
throughout the medulla, pons and midbrain and contains neurones that
are largely aggregated in bilateral, vertical sheets, located immediately
adjacent to the g the paramedian zones. collectively they are called the
nuclei of the raphe, or raphe nuclei. many neurones in raphe nuclei are
serotoninergic and are grouped into nine clusters, b1–9

18. The raphe pallidus nucleus (B1) and associated raphe obscurus nucleus (B2) lie in the upper
two-thirds of the medulla and cross the pontomedullary junction. The raphe magnus nucleus,
corresponding to many B3 neurones, minimally overlaps with B1 and B2, and ascends into
the caudal pons. Above it is the pontine raphe nucleus, which is formed by cell group B5. Also
located in the pons is the central superior raphe nucleus, which contains parts of cell groups
B6 and B8. The dorsal (rostral) raphe nucleus, approximating to cell group B7, extends
through much of the midbrain.

20. 1. Raphe nuclei of medulla:-
• Nucleus raphe obscures
• Nucleus raphe magnus
• Nucleus pallidus.
2. Raphe nuclei of the pontine reticular formation
• Pontine raphe nucleus
• Inferior central nucleus
3. Raphe nuclei of the Midbrain reticular
formation
• Superior central nucleus
• Dorsal Raphe nucleus

22. all raphe nuclei provide descending serotoninergic projecti ons,which
terminate in the brainstem and spinal cord. Brainstem connections are
multiple and complex. For example, the dorsal raphe nucleus, in addition
to sending a large number of fibres to the locus coeruleus, projects to
the dorsal tegmental nucleus and most of the rhombencephalic reticular
formation, together with the central superior, pontine raphe and raphe
magnus nuclei.

26. Raphe-spinal serotoninergic axons originate mainly from
neurons in the raphe magnus, pallidus and obscurus nuclei.
They project as ventral, dorsal and intermediate spinal tracts in
the ventral and lateral funiculi, and terminate respectively in the
ventral horns and laminae I, II and V of the dorsal horns of all
segments, and in the thoracolumbar intermediolateral
sympathetic and sacral parasympathetic preganglionic cell
columns.

27. The dorsal raphe spinal projections function as a pain control
pathway that descends from a mesencephalic pain control centre
located in the periaqueductal grey matter, dorsal raphe and
cuneiform nuclei. The intermediate raphe-spinal projection is
inhibitory and, in part, modulates central sympathetic control of
cardiovascular function. The ventral raphe-spinal system excites
ventral horn cells and could function to enhance motor responses
to nociceptive stimuli.

32. Principally, the mesencephalic serotoninergic raphe system is reciprocally
interconnected rostrally with the limbic system, septum, prefrontal cortex and
hypothalamus. Efferents ascend and form a large ventral and a diminutive dorsal
pathway.

34. Somatic motor control - Some motor neurons send their axons to the reticular
formation nuclei, giving rise to the reticulospinal tracts of the spinal cord. These
tracts play a large role in maintaining tone, balance, and posture, especially during
movement. The reticular formation also relays eye and ear signals to
the cerebellum so that visual, auditory, and vestibular stimuli can be integrated in
motor coordination. Other motor nuclei include gaze centers, which enable the
eyes to track and fixate objects, and central pattern generators, which produce
rhythmic signals to the muscles of breathing and swallowing

35. Habituation – This is a process in which the brain learns to ignore repetitive,
meaningless stimuli w This is a process in which the brain learns to ignore repetitive,
meaningless stimuli while remaining sensitive to others. A good example of this is a
person who can sleep through loud traffic in a large city, but is awakened promptly due
to the sound of an alarm or crying baby. Reticular formation nuclei that modulate activity
of the cerebral cortex are part of the reticular activating systemperson who can sleep
through loud traffic in a large city, but is awakened promptly due to the sound of an alarm
or crying baby. Reticular formation nuclei that modulate activity of the cerebral cortex are
part of the reticular activating system.[2][
HABITUATION

37. MEDIAL COLUMN OF
RETICULARNUCLEI
THE MEDIAL COLUMN OF RETICULAR NUCLEI IS
COMPOSED PREDOMINANTLY OF NEURONES OF
MEDIUM SIZE, ALTHOUGH VERY LARGE NEURONES ARE
FOUND IN SOME REGIONS, AND MOST HAVE
PROCESSES ORIENTATED IN THE TRANSVERSE PLANE.
IN THE LOWER MEDULLA THE COLUMN IS INDISTINCT,
AND IS PERHAPS REPRESENTED BY A THIN LAMINA
LATERAL TO THE RAPHE NUCLEI.

39. MEDIAL COLUMN OF RETICULAR
NUCLEI
Pons
 Oral pontine reticular formation
 Caudal pontine reticular formation
 Reticulotegmental area
Medulla
 Reticularis gigantocellularis

41. Afferent components to the medial reticular nuclear
1.spinoreticular projection
2.spinal trigeminal fibers
3. spinal vestibular fiber
4.spinal cochlear fibres.

42. RETICULOSPINAL TRACT
Pontine(lateral) rticulospinal tract.origin from oral
and
caudal pontine reticular formation
Medullary(medial)reticulospinal tract. Origin from
medullary reticular formation
Terminate in venteral spinal cord

45. Function
1. Integrates information from the motor systems to coordinate
automatic movements of locomotion and posture
2. Facilitates and inhibits voluntary movement; influences
muscle tone
3. Mediates autonomic functions
4. Modulates pain impulses

46.  The MRST is responsible for exciting anti-gravity, extensor muscles. The
fibers of this tract arise from the caudal pontine reticular nucleus and the oral
pontine reticular nucleus and project to the lamina VII and lamina VIII of the
spinal cord
 The LRST is responsible for inhibiting excitatory axial extensor muscles of
movement. The fibers of this tract arise from the medullary reticular
formation, mostly from the gigantocellular nucleus, and descend the length of
the spinal cord in the anterior part of the lateral column. The tract terminates
in lamina VII mostly with some fibers terminating in lamina IX of the spinal
cord.

47. Lesions to the cortico-reticulospinal system can result in decreased
postural control and reduced selectivity of postural control.
If the excitatory fibres in the reticular formation have a leison this can
result in hypotonia by the loss of descending excitatatory impulses to
the spinal cord. Conversly in the inhibitory fibres are disrupted in the
reticular formation this could result in hypertonia (spasticity) As the
lateral reticulospinal's is involved in inhibition, if this pathway is disruped
it can result in spasticity . In addition due to the lack of descending
inhibition, the medial reticulospinal tract would then maintain spasticity
in the musculatur

50. DECORTICAT POSTURING
• Decorticate posturing is also called decorticate
response, decorticate rigidity, flexor posturing, Patients with
decorticate posturing present with the arms flexed, or bent inward on
the chest, the hands are clenched into fists, and the legs extended
and feet turned inward. A person displaying decorticate posturing in
response to pain gets a score of three in the motor section of
the Glasgow Coma Scale

52. There are two parts to decorticate posturing.
•The first is the disinhibition of the red nucleus with facilitation of
the rubrospinal tract. The rubrospinal tract facilitates motor
neurons in the cervical spinal cord supplying the flexor muscles of
the upper extremities. The rubrospinal tract and medullary
reticulospinal tract biased flexion outweighs the medial and lateral
vestibulospinal and pontine reticulospinal tract biased extension in
the upper extremities.
•The second component of decorticate posturing is the disruption
of the lateral corticospinal tract which facilitates motor neurons in
the lower spinal cord supplying flexor muscles of the lower
extremities. Since the corticospinal tract is interrupted, the pontine
reticulospinal and the medial and lateral vestibulospinal biased
extension tracts greatly overwhelm the medullary reticulospinal
biased flexion tract.

53. The effects on these two tracts
(corticospinal and rubrospinal) by
lesions above the red nucleus is
what leads to the characteristic
flexion posturing of the upper
extremities and extensor posturing
of the lower extremities

54. Decorticate posturing indicates
that there may be damage to
areas including the cerebral
hemispheres, the internal
capsule, and the thalamus. It
may also indicate damage to
the midbrain.

55. DECEREBRATE POSTURE
• Decerebrate posturing is also called decerebrate
response, decerebrate rigidity, or extensor posturing. It describes
the involuntary extension of the upper extremities in response to
external stimuli. In decerebrate posturing, the head is arched back,
the arms are extended by the sides, and the legs are extended. A
hallmark of decerebrate posturing is extended elbows The arms and
legs are extended and rotated internally. The patient is rigid, with the
teeth clenched. The signs can be on just one side of the body or on
both sides, and it may be just in the arms and may be intermittent.

56. A person displaying decerebrate posturing in response to pain gets
a score of two in the motor section of the Glasgow Coma Scale (for
adults)
Decerebrate posturing indicates brain stem damage, specifically
damage below the level of the red nucleus It is exhibited by people
with lesions or compression in the midbrain and lesions in
the cerebellum Decerebrate posturing is commonly seen
in pontine strokes.

58. . Spinoreticular fibres
 part of the anterolateral system, arise from neurones in the
intermediate grey matter of the spinal cord.
 They decussate in the ventral white commissure, ascend
in the ventrolateral funiculus,
 terminate not only at all levels of the medial column of
reticular nuclei but also in the intralaminar nuclei of the
thalamus.

60. . Information is sent from there to the intradmedian
nucleus of the thalamic intralaminar nuclei. The
thalamic intralaminar nuclei project diffusely to entire
cerebral cortex where pain reaches conscious level
and promotes behavioral arousal.It is believed that
spinoreticular tract projects to neurons having a large
receptive fields that may cover wide areas of the body
and play a role in the memory and in the affective
(emotional) component of pain

61. Efferents from the medial column of reticular nuclei
project through a multisynaptic pathway within the
column to the thalamus.
Areas of maximal termination of spinoreticular fibres also
project directly to the intralaminar thalamic nuclei.
The multisynaptic pathway is integrated into the lateral
column of reticular nuclei with cholinergic neurones in
the lateral pontine tegmentum.
The intralaminar thalamic nuclei project directly to the
striatum and neocortex.

63. LATERAL COLUMN OF RETICULAR
FORMATION NUCLEOS
MIDBRAIN
CUNEIFORM AND SUBCONEIFORM
NUCLOS
PONS
RETICULLARIS PARVOCELLULARIS
PARABRACHIAL PEDUNCULOPONTINE
LOCUS COERULEUS
MEDULLA
RETICULLARIS PARVOCELLULARIS
RETICULLARIS LATERALIS

64. The lateral column of reticular nuclei contains six nuclear groups, which
include the parvocellular reticular area; superficial ventrolateral reticular area;
lateral pontine tegmental noradrenergic cell groups A1, A2 and A4 to A7 (A3
is absent in primates); adrenergic cell groups C1 and C2; and cholinergic cell
groups Ch5 and Ch6. The column descends through the lower two-thirds of
the lateral pontine tegmentum and upper medulla, where it lies between the
gigantocellular nucleus medially and the sensory trigeminal nuclei laterally. It
continues caudally and expands to form most of the reticular formation
lateral to the raphe nuclei. It abuts the superficial ventrolateral reticular area,
nucleus solitarius, nucleus ambiguus and vagal nucleus, where it contains the
adrenergic cell group C2 and the noradrenergic group A2.

66. The lateral paragigantocellular nucleus lies at the rostral pole of the
diffuse superficial ventrolateral reticular area (at the level of the facial
nucleus). The zone extends caudally as the nucleus retroambiguus and
descends into the spinal cord. It contains noradrenergic cell groups A1, A2,
A4 and A5 and the adrenergic cell group C1.
 The ventrolateral reticular area is involved in cardiovascular, respiratory, vasoreceptor
and chemoreceptor reflexes and in the modulation of nociception.
 The A2 or noradrenergic dorsal medullary cell group lies in the nucleus of the tractus
solitarius,vagal nucleus and adjoining parvocellular reticular area
 Adrenergic group C1 lies rostral to the A2 cell group. Noradrenergic cell group A4
extends into the lateral pontine tegmentum, along the subependymal surface of the
superior Cerebellar peduncle
 Noradrenergic group A5 forms part of the paragigantocellular
nucleus in the caudolateral pontine tegmentum

68. The lateral pontine tegmental reticular grey matter is related to the
superior cerebellar peduncle and forms the medial and lateral
parabrachial nuclei and the ventral Kölliker-Fuse nucleus, a pneumotaxic
centre.
The locus coeruleus (noradrenergic cell group A6), area subcoeruleus,
noradrenergic cell group A7 and cholinergic group Ch5 in the
pedunculopontine tegmental
nucleus are all located in the lateral pontine and mesencephalic
tegmental reticular zones.

70. Cell group A6 contains all the noradrenergic cells in
the central region of the locus coeruleus. Group A6
has ventral (nucleus subcoeruleus), rostral and
caudolateral extensions; the last merges with the A4
group.
The locus coeruleus probably functions as an
attention centre,focusing neural functions on
prevailing needs.
The noradrenergic A7 group occupies the
rostroventral part of the pontine tegmentum
The A7, A5, A1 complex is also connected
by noradrenergic cell clusters with group A2
caudally and with group A6 rostrally.

72. The A5 and A7 groups lie mainly within the medial
parabrachial
and Kölliker-Fuse nuclei.
Reticular neurones in the lateral pontine tegmental
reticular area, like those of the ventrolateral zone,
function to regulate respiratory,
cardiovascular and gastrointestinal activity.
Two micturition centres are located in the dorsomedial
and ventrolateral parts of the lateral pontinetegmentum.

73. In the human brain, the parabrachial area, also known as
the parabrachial complex and parabrachial nucleus, is a
horseshoe-shaped strip of gray matter comprising
 the subparabrachial nucleus(Kölliker-Fuse nucleuS)
 the lateral parabrachial nucleus
 the medial parabrachial nucleus.
It is located at the junction of the midbrain and Pons in
the lateral reticular formation, rostral to the parvocellular
reticular nucleus near the superior cerebellar peduncle
PARABRACHIAL COMPLEX

74. The respiratory centers are divided into four major groups:
medulla
 dorsal respiratory group
 ventral respiratory group.
pons
 pneumotaxic center also known as the pontine respiratory
group
 apneustic center.

76. Inspiratory center (Dorsal respiratory group)
•Location: Dorsal portion of medulla
•Nucleus: Nucleus tractus solitaries
Expiratory center (Ventral respiratory group)
•Location: Antero- lateral part of medulla, about 5 mm
anterior and lateral to dorsal respiratory group
•Nucleus: Nucleus ambiguus and nucleus retro
ambiguus.
•Function: It generally causes expiration but can cause
either expiration or inspiration depending upon which
neuron in the group is stimulated. It sends inhibitory
impulse to the apneustic center

77. Pneumotaxic center
•Location: Pons (upper part )
•Nucleus: Nucleus parabrachialis
•Function: It controls both rate and pattern of breathing. Limit
inspiration.
Apneustic center
•Location: Pons (lower part)
•Functions:
a.It discharges stimulatory impulse to the inspiratory center causing
inspiration.
b.It receives inhibitory impulse from pneumotaxic center and from
stretch receptor of lung.
c.It discharges inhibitory impulse to expiratory center

80. The automatic central control of
respiration may be influenced and
temporarily overridden by volitional
control from the cerebral cortex
(motor area , area 4,6) for a variety of
activities, such as speech, singing,
laughing, intentional and
psychogenic alterations of
respiration, and breath holding

85. Central chemoreceptors
Central chemoreceptors, located
primarily within the ventrolateral surface
of medulla, respond to changes in brain
extracellular fluid [H1] concentration.
Other receptors have been recently
identified in the brainstem,
hypothalamus, and the cerebellum.
These receptors are effectively CO2
receptors because central [H1]
concentrations are directly dependent on
central PCO2 levels.

86. Peripheral chemoreceptors include the carotid bodies
and the aortic bodies.
The carotid bodies, located bilaterally at the bifurcation
of the internal and external carotid arteries, are the
primary peripheral monitors.
They are highly vascular structures that monitor the
status of blood about to be delivered to the brain and
provide afferent input to the medulla through the 9th
cranial nerve.
The carotid bodies respond mainly to PaO2, but also to
changes in PaCO2 and pH.
PERIPHERAL
CHEMORECEPTORS

87. Descending motoneurons include two anatomically
separate groups:
• The corticospinal and corticobulbar tracts for the
volitional control of respiration and
• The reticulospinal tracts for the automatic control of
respiration .

92. The Pontine micturition center (PMC, also known
as Barrington's nucleus) is a collection of neuronal cell
bodies located in the rostral pons in the brainstem involved in
the supraspinal regulation of micturition. When activated, the
PMC relaxes the urethral sphincter allowing for micturition to
occur. The PMC coordinates with other brain centers,
including the medial frontal cortex, insular
cortex, hypothalamus and periaqueductal gray (PAG). The
PAG acts as a relay station for ascending bladder information
from the spinal cord and incoming signals from higher brain
areas.
MICTURATION CENTER

93. •Normal voiding occurs in response to afferent signals of the bladder filling, and it is
controlled by nervous system of the brain and spinal cord.
•CNS and PNS coordinate the activity of the detrusor smooth muscle and urethral
sphincter muscle.
•The S2–S4 spinal cord constitute primary parasympathetic micturition center that
innervate the bladder as well as the distal urethral sphincter (striated sphincter).
•Above the sacral segments, the thoracolumbar segments (T11-L2) provide the
sympathetic outflow from the spinal cord to the bladder and the proximal urethral
sphincter.
•Above the spinal cord is an important control center in the pons where it directly
excites bladder neurons and inhibits the urethral sphincter, thus resulting
coordination of the bladder contraction and sphincter relaxation at the same time to
empty the urine.
•The cerebral cortex appears to be involved in inhibiting lower centers of
micturition.
•Primary neurologic control of the bladder and urethral sphincters depends on
multiple levels of the nervous system, especially the sacral segments and the pons

94. Peripheral innervation:
 The lower urinary tract is innervated by three
principal sets of peripheral nerves involving
the parasympathetic, sympathetic, and somatic
nervous systems from 3 major nerves, namely
the pelvic, hypogastric and pudendal nerves,
respectively.
 These nerves contain afferent (sensory) as
well as efferent (motor) axons.
 Parasympathetic and sympathetic nervous
systems form pelvic plexus at the lateral side
of the rectum before reaching bladder and
sphincter.

95. oParasympathetic nerves:
emerge from the S2-4 (parasympathetic
nucleus; intermediolateral column of gray
matter)
exciting the bladder and relax the urethra

96. oSympathetic pathways:
originate from the T11-L2 (sympathetic nucleus;
intermediolateral column of graymatter)
inhibiting the bladder body and excite the bladder
base and proximal urethral sphincter

97. oSacral somatic pathways:
emerge from the S2-4 (Onuf’s nucleus; ventral
horn)
form pudendal nerve, providing an innervation to
the striated urethral sphincter.
Pudendal nerves from S2-4 excite the distal striated
urethral sphincter.

99. Sympathetic postganglionic nerves — for
example, the hypogastric nerve — release
noradrenaline, which activates β adrenergic
inhibitory receptors in the detrusor muscle
to relax the bladder, α-adrenergic
excitatory receptors in the urethra and the
bladder neck, and α- and β-adrenergic
receptors in bladder ganglia

101. The micturition reflex is a bladder-to-bladder contraction reflex for which the
reflex center is located in the rostral pontine tegmentum (pontine micturition
center: PMC). There are two afferent pathways from the bladder to the brain. One
is the dorsal system and the other is the spinothalamic tract. Afferents to the PMC
ascend in the spinotegmental tract, which run through the lateral funiculus of the
spinal cord. The efferent pathway from the PMC also runs through the lateral
funiculus of the spinal cord to inhibit the thoracolumbar sympathetic nucleus and
the sacral pudendal nerve nucleus,

102. There are two centers that inhibit micturition in the
pons, which are the pontine urine storage center and
the rostral pontine reticular formation. In the
lumbosacral cord, excitatory glutamatergic and
inhibitory glycinergic/GABAergic neurons influence
both the afferent and efferent limbs of the micturition
reflex. The activity of these neurons is affected by the
pontine activity. There are various excitatory and
inhibitory areas co-existing in the brain, but the brain
has an overall inhibitory effect on micturition, and thus
maintains continence. For micturition to occur, the
cerebrum must abate its inhibitory influence on the
PMC

103. PONTINE MICTURITION CENTERS (Barrington's nucleus):
– pontomesencephalic reticular formation micturition center
(located in the locus ceruleus, pontomesencephalic gray
matter, and nucleus tegmentolateralis dorsalis). – collection of
cell bodies located in the rostral pons in the brainstem
involved in the supraspinal regulation of micturition (urination).
– The PMC makes connections with other brain centers to
control micturition, including the medial frontal cortex, insular
cortex, hypothalamus and periaqueductal gray (PAG). – The
PAG in particular acts a relay station for ascending bladder
information from the spinal cord and incoming signals from
higher brain areas.

106. Storage reflexes
During filling, there is low-level activity from bladder
afferent fibers signaling distension via the pelvic nerve,
which in turn stimulates sympathetic outflow to the
bladder neck and wall via the hypogastric nerve. This
sympathetic stimulation relaxes the detrusor and
contracts the bladder neck at the internal sphincter.
Afferent pelvic nerve impulses also stimulate the
pudendal (somatic) outflow to the external sphincter
causing contraction and maintenance of continence

107. Voiding reflexes.
Upon initiation of micturition, there is high-intensity
afferent activity signaling wall tension, which activates
the brainstem pontine micturition center.
Spinobulbospinal reflex can be seen as an ascending
signal from afferent pelvic nerve stimulation (left side),
which passes through the periaqueductal gray matter
before reaching the pontine micturition center and
descending to elicit parasympathetic contraction of the
detrusor, and somatic relaxation via the pudendal nerve

109. . • The somatic storage reflex or the pelvic-to-pudendal or
guarding reflex is initiated when one laughs, sneezes, or
coughs, which causes increased bladder pressure.
Glutamate is the primary excitatory transmitter for the
reflex. Glutamate activates NMDA and AMPA receptors
which produce action potentials. These action potentials
activate the release of acetylcholine causing the
rhabdosphincter muscle fibers to contract.

110. HIGHER CENTERS • CORTICAL CENTERS
 Situated in • Medial frontal lobe • Cingulate gyrus • Corpus
collosum • cortical input is inhibitory on micturition reflexes.
 Subcortical centers: – thalamic nuclei – limbic system, –
Red nucleus – Substantia nigra – Hypothalamus –
Subthalamic nucleus. • Cerebellum : – anterior vermis of
the cerebellum – fastigial nucleus are concerned with
micturition

113. SPINAL REFLEX ARC •
AFFERENT ARC: – Sensation of stretch arising from
bladder wall travels through the parasympathetic nerves
to the center for micturition • DETRUSOR CENTER OR
SACRAL PARASYMPATHETIC NUCLEUS – sacral
segments S2,S4 of the spinal cord.
•
EFFERENT ARC (PARASYMPATHATIC) – travels
through the pelvic nerves to the pelvic plexus; short
postganglionic fibers travel from the plexus to the detrusor
muscle

114. Parasympathetic postganglionic nerves release both
cholinergic (acetylcholine, ACh) and non-adrenergic,
non-cholinergic transmitters. Cholinergic transmission
is the major excitatory mechanism in the human
bladder . It results in detrusor contraction and
consequent urinary flow and is mediated principally
by the M3 muscarinic receptor, although bladder
smooth muscle also expresses M2 receptors5.
Muscarinic receptors are also present on
parasympathetic nerve terminals at the neuromuscular
junction and in the parasympathetic ganglia .

115. Somatic cholinergic motor nerves that supply
the striated muscles of the external urethral
sphincter arise in S2–S4 motor neurons in
Onuf's nucleus and reach the periphery through
the pudendal nerves . A medially placed motor
nucleus at the same spinal level supplies axons
that innervate the pelvic floor musculature

116. The somatic motor neurons that
innervate the external urethral sphincter
are located in the ventral horn (lamina
IX) in Onuf's nucleus, have a similar
arrangement of transverse dendrites
and have an extensive system of
longitudinal dendrites that travel within
Onuf's nucleus

117. In the brain, many neuron populations are involved in
the control of the bladder, the urethra and the urethral
sphincter. Some, such as the serotonergic neurons of
the medullary raphe nuclei, the noradrenergic
neurons of the locus coeruleus and the
noradrenergic A5 cell group in the brain stem, are
non-specific ‘level-setting’ mechanisms with diffuse
spinal projections . Others are specific for
micturition: these include the neurons of Barrington's
nucleus (also called the pontine micturition centre
(PMC)) and those of the periaqueductal grey (PAG),
cell groups in the caudal and preoptic hypothalamus,
and the neurons of several parts of the cerebral

118. The neural pathways that control lower-urinary-
tract function are organized as simple on–off
switching circuits that maintain a reciprocal
relationship between the urinary bladder and
the urethral outlet. Storage reflexes are
activated during bladder filling and are
organized primarily in the spinal cord, whereas
voiding is mediated by reflex mechanisms that
are organized in the brain

119. Micturition Reflex
Referring again to Figure 26–7, one can see that as the
bladder fills, many superimposed micturition contraction
begin to appear, as shown by the dashed spikes.They
are the result of a stretch reflex initiated by sensory
stretch receptors in the bladder wall, especially by the
receptors in the posterior urethra when this area begins
to fill with urine at the higher bladder pressures. Sensory
signals from the bladder stretch receptors are conducted
to the sacral segments of the cord through the pelvic
nerves and then reflexively back
again to the bladder through the parasympathetic nerve
fibers by way of these same nerves.

122. Once a micturition reflex begins, it is “self-
regenerative.”
That is, initial contraction of the bladder activates
the stretch receptors to cause a greater increase
in sensory impulses to the bladder and posterior
urethra, which causes a further increase in reflex
contraction of the bladder; thus, the cycle is repeated
again and again until the bladder has reached a strong
degree of contraction
. Then, after a few seconds to
more than a minute, the self-regenerative reflex begins
to fatigue and the regenerative cycle of the micturition
reflex ceases, permitting the bladder to relax.

123. When the bladder is only partially filled, these
micturition
contractions usually relax spontaneously after
a fraction of a minute, the detrusor muscles stop
contracting,
and pressure falls back to the baseline. As the
bladder continues to fill, the micturition reflexes
become more frequent and cause greater contractions
of the detrusor muscle.

124. Facilitation or Inhibition of Micturition
by the Brain
The micturition reflex is a completely autonomic
spinal cord reflex, but it can be inhibited or facilitated
by centers in the brain.
These centers include
 strong facilitative and inhibitory centers in the
brain stem, located mainly in the pons, and
 several centers located in the cerebral cortex that
are mainly inhibitory but can become excitatory.

125. The micturition reflex is the basic cause of micturition, but
the higher centers normally exert final control of
micturition as follows:
1. The higher centers keep the micturition reflex partially
inhibited, except when micturition is desired.
2. The higher centers can prevent micturition, even if the
micturition reflex occurs, by continual tonic contraction of
the external bladder sphincter until a convenient time
presents itself.
3. When it is time to urinate, the cortical centers can
facilitate the sacral micturition centers to help initiate a
micturition reflex and at the same time inhibit the external
urinary sphincter so that urination can occur.

126. Voluntary urination is usually initiated in the following
way: First, a person voluntarily contracts his or her
abdominal muscles, which increases the pressure in
the bladder and allows extra urine to enter the
bladder neck and posterior urethra under pressure,
thus stretching their walls. This stimulates the stretch
receptors, which excites the micturition reflex and
simultaneously inhibits the external urethral
sphincter.
Ordinarily, all the urine will be emptied, with rarely
more than 5 to 10 milliliters left in the bladder.

131. Abnormalities of Micturition
Atonic Bladder Caused by Destruction of Sensory Nerve Fibers.
Micturition reflex contraction cannot occur if the
sensory nerve fibers from the bladder to the spinal cord
are destroyed, thereby preventing transmission of
stretch signals from the bladder.When this
happens, a
person loses bladder control, despite intact
efferent
fibers from the cord to the bladder and despite
intact
neurogenic connections within the brain. Instead
of
emptying periodically, the bladder fills to capacity
and overflows a few drops at a time through the

132. A common cause of atonic bladder is
crush injury to the sacral region of the
spinal cord. Certain diseases can also
cause damage to the dorsal root nerve
fibers that enter the spinal cord. For
example, syphilis can cause
constrictive fibrosis around the dorsal
root nerve fibers, destroying them. This
condition is called tabes dorsalis, and
the resulting bladder condition is called
tabetic bladder.

133. Automatic Bladder Caused by Spinal Cord Damage Above the Sacral
Region. If the spinal cord is damaged above the
sacral region but the sacral cord segments are still intact, typical
micturition reflexes can still occur. However, they are no longer
controlled by the brain. During the first few days to several weeks after
the damage to the
cord has occurred, the micturition reflexes are suppressed
because of the state of “spinal shock” caused by the sudden loss of
facilitative impulses from the brain
stem and cerebrum. However, if the bladder is emptied periodically by
catheterization to prevent bladder injury caused by overstretching of
the bladder, the excitability of the micturition reflex gradually increases
until typical micturition reflexes return; then, periodic (but
unannounced) bladder emptying occurs. Some patients can still
control urination in this condition by stimulating the skin (scratching or

134. Uninhibited Neurogenic Bladder Caused by Lack
of Inhibitory Signals from the Brain. Another
abnormality of micturition is the so-called
uninhibited neurogenic bladder,
which results in frequent and relatively
uncontrolled micturition.This condition derives
from partial damage in the spinal cord or the brain
stem that interrupts most
of the inhibitory signals.Therefore, facilitative
impulses passing continually down the cord keep
the sacral centers so excitable that even a small
quantity of urine elicits an uncontrollable
micturition reflex, thereby promoting frequent

135. Spinal Shock
After SCI, initially there is flaccid muscle paralysis and absent
somatic activity, as well as suppressed autonomic activity below
the area of th lesion. The bladder is acontractile and areflexic.
The bladder neck is generally closed and competent. Sphincter ton will be
mainteined Because of the preservation of external
sphincter tone, urinary incontinence is usually secondaty to poor
emptying and overflow incontinence. Patients will have urinaty
retention during the period of spinal shock and require either
intermittent or continuous catheterization to empty the bladder.
Involuntary voiding between intermittent catheterizations indicates
the return of reflex bladder activity. Spinal shock generally
lasts 6 to 12 weeks but may continue as long as 1 to 2 month years.
SPINAL SHOCK

136. Locus coeruleus

137. The locus coeruleus is located in the posterior area of the
rostral pons in the lateral floor of the fourth ventricle. It is
composed of mostly medium-size neurons. Melanin granules
inside the neurons of the LC contribute to its blue color. Thus, it
is also known as the nucleus pigmentosus pontis, meaning
"heavily pigmented nucleus of the pons.

138. The locus coeruleus (LC) is the major noradrenergic nucleus of the brain,
giving rise to fibres innervating extensive areas throughout the neuraxis.
Recent advances in neuroscience have resulted in the unravelling of the
neuronal circuits controlling a number of physiological functions in which the
LC plays a central role. Two such functions are the regulation of arousal and
autonomic activity, which are inseparably linked largely via the involvement of
the LC. The LC is a major wakefulness-promoting nucleus, resulting from
dense excitatory projections to the majority of the cerebral cortex, cholinergic
neurones of the basal forebrain, cortically-projecting neurones of the thalamus,
serotoninergic neurones of the dorsal raphe and cholinergic neurones of the
pedunculopontine and laterodorsal tegmental nucleus, and substantial inhibitory
projections to sleep-promoting GABAergic neurones of the basal forebrain and
ventrolateral preoptic area. Activation of the LC thus results in the
enhancement of alertness through the innervation of these varied nuclei

140. The importance of the LC in controlling autonomic function
results from both direct projections to the spinal cord and
projections to autonomic nuclei including the dorsal motor
nucleus of the vagus, the nucleus ambiguus, the
rostroventrolateral medulla, the Edinger-Westphal nucleus,
the caudal raphe, the salivatory nuclei, the paraventricular
nucleus, and the amygdala. LC activation produces an
increase in sympathetic activity and a decrease in
parasympathetic activity via these projections. Alterations
in LC activity therefore result in complex patterns of
neuronal activity throughout the brain, observed as
changes in measures of arousal and autonomic function

142. Noradrenergic receptors on follower cells receiving an afferent input
from the LC can be generally classified as α1-, α2- or β-adrenoceptors.
Activation of α1-adrenoceptors by noradrenaline generally leads to
excitation of the follower cells and there is some evidence that β-
adrenoceptors are also excitatory . In contrast, activation of α2-
adrenoceptors leads to inhibition of the follower cells , and also of the
noradrenergic neurones themselves (“autoreceptors”). The
consequences of autoreceptors activation can be detected as changes in
the firing rate of LC neurones and in the release of noradrenaline. α2 –
Adrenoceptors are widely distributed in the brain and there are
regional differences in their role in modulating noradrenaline releas

144. The reticular activating system (RAS),
or extrathalamic control modulatory
system, is a set of connected nuclei in
the brains of vertebrates that is responsible
for regulating wakefulness and sleep-wake
transitions. As its name implies, its most
influential component is the reticular
formation
RETICULAR ACTIVAYING SYSTEM

145. Anatomical components
The RAS is composed of several neuronal circuits connecting the brainstem to
the cortex. These pathways originate in the upper brainstem reticular core and
project through synaptic relays in the rostral intralaminar and thalamic nuclei to
the cerebral cortex As a result, individuals with bilateral lesions of thalamic
intralaminar nuclei are lethargic or somnolent.Several areas traditionally
included in the RAS are:
 Midbrain Reticular Formation
 Mesencephalic Nucleus (in Midbrain)
 Thalamic Intralaminar nucleus (centromedian nucleus)
 Dorsal Hypothalamus
 Tegmentum
The RAS consists of evolutionarily ancient areas of the brain, which are crucial
to survival and protected during adverse periods. As a result, the RAS still
functions during inhibitory