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CHAPTER 13 Nervous and Locomotor Systems
s
)
Transcellular
Receptor mediated
transcytosis, e.g. insulin
Transcellular
A
e.g. albumin
261
• CSF ows from the lateral ventricles to the third ventricle via the interventricular foramina; it then ows to
the fourth ventricle via the cerebral aqueduct. From the
fourth ventricle CSF ows into the subarachnoid space
via the foramen of Luschka (lateral) and the foramen of
Magendie (midline).
• e CSF circulates around the subarachnoid space and
is reabsorbed back into the circulation via the arachnoid
villi; these drain into the venous sinuses.
• e arachnoid villi may become blocked by blood following a subarachnoid haemorrhage and prevent reabsorption of CSF; this results in hydrocephalus.
Capillary
Tight junction
• A small amount of CSF is also absorbed by spinal villi in
the lumbar region.
• CSF has two main functions:
• hydraulic ‘cushion’: serves to protect the brain from
violent movements of the head
• provides a stable ionic environment for cerebral
function.
Blood–Brain Barrier (Fig. 13.2)
• Lipid-soluble molecules are able to pass freely from the
blood into the interstitial space of the brain; however,
ions are unable to pass freely into the brain. is enables
Astrocyte foot proces
lumen
Basement membrane
Fig. 13.2 The blood–brain barrier. (A) Longitudinal section through a capillary in the brain. The capillaries
have tight cell-to-cell junctions and the astrocytes project foot processes to cover the capillary basement
membrane. (B) Transverse section through a capillary in the brain, showing methods of transport across the
blood–brain barrier.
A
dsorptive transcytosis,
B
Astrocyte foot process
Capillary
lumen
Tight junction
Lipid soluble transport, e.g.
CO2, O2, alcohol,
anaesthetic agents
Basement membrane
Carriers (transport proteins
e.g. glucose, amino acids
262
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SECTION II Physiology
the brain to maintain the ionic environment within very
tight limits, thus allowing the optimal environment for
neuronal communication.
• e blood–brain barrier also prevents the release of
neurotransmitters from neurons into the peripheral
circulation.
• e blood–brain barrier is formed by the structure of
the capillaries. Rather than the freely permeable fenestrated capillaries found in other tissues, the cerebral
capillaries have very tight cell-to-cell junctions in the
endothelium. In addition, the end-feet of astrocytes
cover the basement membrane.
• Specic functions provided by the blood–brain barrier are:
• tight junctions restrict penetration of water-soluble
substances
• lipid-soluble molecules such as CO2, O2, hormones,
anaesthetics and alcohol (that’s why we get drunk!)
can pass freely across the barrier via the lipid membranes of the capillary endothelium
• the endothelium contains transport proteins (carri-
ers) for nutrients such as sugars and amino acids
• certain proteins, e.g. insulin and albumin, may be
transported by endocytosis and transcytosis
• an ‘eux pump’ extrudes unwanted lipid soluble
molecules back into the blood.
• e blood–brain barrier is not continuous and in some
areas consists of fenestrated capillaries. ese areas lie in
the midline and include:
• third and fourth ventricles: allow drugs and noxious
chemicals to trigger the chemoreceptor area in the
oor of the fourth ventricle; this in turn triggers the
vomiting centre. In addition angiotensin II passes
to the vasomotor centre in this region to increase
sympathetic outow and causes vasoconstriction of
peripheral vessels
• posterior lobe of pituitary: allows the release of oxy-
tocin and antidiuretic hormone (ADH) into the
circulation
• hypothalamus: this allows the release of releasing or
inhibitory hormones into the portal–hypophyseal
tract.
BRAINSTEM DEATH
• e brainstem provides the capacity for consciousness.
• e cerebral hemispheres provide the content of
consciousness.
• Brainstem death is a condition in which the heart and
lungs function, but there is no cerebral activity.
• It is legally regarded as being equivalent to the more traditional mode of death, i.e. cessation of respiratory and
cardiac activity.
• e diagnosis of brainstem death is important for
several reasons:
• withdrawal of treatment
• assessment for suitability for organ donation.
• e diagnosis of brainstem death must rst satisfy several preconditions and exclusions before the appropriate
tests can be performed.
Preconditions for the Diagnosis of
Brainstem Death
• ere are four preconditions:
• the patient must be in a coma
• there must be a known cause for the patient’s coma
• this cause must be known to be irreversible
• the patient must be dependent on a ventilator.
Exclusion Criteria for the Diagnosis of
Brainstem Death
• ere are a number of exclusion criteria:
• no residual drug eects from narcotics, hypnotics, tran-
quillizers, muscle relaxants, alcohol and illicit drugs
• core body temperature must be >35°C
• no circulatory, metabolic or endocrine abnormality
disturbance that may contribute to the coma.
Brainstem Death Tests
• e UK brainstem death criteria tests seven areas. All
must be absent for the diagnosis to be made.
• e tests include:
1. No pupillary response to light, direct or consensual:
this reex involves cranial nerves II and III.
2. Absent corneal reex – normally would result in
blinking; this reex involves cranial nerves V and VII.
3. No motor response in the cranial nerve distribution
to stimuli in any somatic area, e.g. supraorbital or
nailbed pressure leading to a grimace.
4. No gag reex: back of the throat is stimulated with a
catheter; this reex tests cranial nerves IX and X.
5. No cough reex: no response to bronchial stimula-
tion with a suction catheter; this reex tests cranial
nerves IX and X.
6. No vestibulo-ocular reex: head is exed to 30° and
50 mL of ice-cold water is injected over 1 min into
each external auditory meatus; there should be no
eye movements; this reex tests cranial nerves III, VI
and VIII.
7. Apnoea test: the patient is preoxygenated with 100%
O2 for 10 min; PaCO2 is allowed to rise to 5 kPa
(before testing); the patient is disconnected from the
ventilator and O2 is insuated at 6 L/min; PaCO2 is
allowed to rise to 6.5kPa; there should be NO respiratory eort.
CHAPTER 13 Nervous and Locomotor Systems
Decompensation
Intracranial pressure (ICP; mmHg)
Intracranial volume (arbitrary units)
• ere are several other caveats to the brainstem death
tests:
• performed on two occasions
• performed by two doctors
• one must be a consultant
• must be competent in the eld, e.g. ITU or neurology
• must have >5 years’ experience
• must not be part of the transplant team.
• e time of death is legally dened as the time at which
the rst set of brainstem tests were performed.
263
Herniation
100
80
60
40
SPACE-OCCUPYING LESIONS AND RAISED
INTRACRANIAL PRESSURE
• Space-occupying lesions (SOLs) result from a variety of
causes, and may be focal or diuse.
• Focal SOLs include:
• tumour
• aneurysm
• blood or haematoma
• granuloma
• tuberculoma
• cyst
• abscess.
• Diuse SOLs result from either vasodilatation or oedema.
• e consequences of intracranial SOLs include:
• raised intracranial pressure
• intracranial shi and herniation
• hydrocephalus.
Raised Intracranial Pressure (ICP) (Fig. 13.3)
• e skull is a rigid container in which brain, CSF and
blood are the only contents; it therefore follows that
ICP = V
• is formula is the basis for the Monro–Kellie hypothesis, which states that the ICP will increase if the volume
of one component is increased; the increase in ICP can
only be compensated for by a decrease in one or both of
the other components.
• Normal ICP in the supine position is 0–10 mmHg.
• e removal of blood and CSF can accommodate a SOL
of approximately 100–150 mL; aer this compensatory
point the ICP will increase rapidly.
• Raised ICP has a number of consequences:
• hydrocephalus: an increase in ICP may result in
the interruption of CSF ow; this is most commonly seen with posterior fossa lesions leading to
compression of the cerebral aqueduct and fourth
ventricle
• cerebral ischaemia: remember that CPP=MAP −
ICP. Any rise in ICP will eventually exceed autoregulation and lead to cerebral ischaemia
CSF
+ V
Brain
+ V
Blood
20
0
Fig. 13.3 Pressure–volume curve for intracranial
pressure (ICP). The compensatory properties of the
intracranial contents follow a pressure–volume exponential curve. Increased volume of any of the three
components (i.e. brain, CSF, blood) can be accommodated up to a certain point without any change
in intracranial pressure. Once a critical volume is
reached, decompensation occurs, i.e. blood and CSF
have been pushed from the cranial cavity and ICP
increases exponentially to the point of herniation.
• brain shi and herniation: as ICP increases the risk
of herniation increases; this occurs at specic sites
(Fig. 13.4):
• transtentorial: the lesion lies within one hemi-
sphere; leads to herniation of the medial part of
the temporal lobe over the tentorium cerebelli
• tonsillar: caused by a lesion in the posterior fossa;
.
the lowest part of the cerebellum pushes down into
the foramen magnum and compresses the medulla
• subfalcial: caused by a lesion in one hemisphere;
leads to the herniation of the cingulate gyrus
under the falx cerebri
• diencephalic: generalized brain swelling; leads to
the midbrain herniating through the tentorium;
this is termed coning
• systemic eects: the systemic eects of raised ICP
are thought to occur due to autonomic imbalance,
hypothalamic overactivity (due to compression) and
ischaemia of the vasomotor area; the eects include:
• Cushing’s response: ↓ respiratory rate, bradycar-
dia and hypertension
• neurogenic pulmonary oedema
• Cushing’s ulcers
• preterminal events include bilateral pupil con-
striction followed by dilation, tachycardia, ↓
respiratory rate, and hypotension.
264
Parahippocampal
Cingulate
f
foramen magnum
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SECTION II Physiology
Lateral
ventricle
gyrus
Skull
Dura
Tentorium
cerebelli
Midbrain
Pons
Cerebellum
gyrus
Medulla
Falx cerebri
Sub-falcine
herniation
Expanding
lesion
Collapse o
ventricle
Transtentorial
herniation
Cerebellar tonsil
herniation into
Fig. 13.4 Diagram illustrating the possible consequences of an expanding lesion, i.e. haematoma, on one side
of the brain. Diencephalic herniation is caused by generalized brain swelling.
• e clinical manifestations of raised ICP include:
• e clinical manifestations of cerebral herniation include:
• headache
• nausea and vomiting
• papilloedema
• decreased conscious level.
• oculomotor nerve compression: ipsilateral pupil
dilation (transtentorial)
• cerebral peduncles: contralateral hemiparesis
(transtentorial)
• posterior cerebral artery: cortical blindness
(transtentorial)
• cerebral aqueduct: hydrocephalus (transtentorial)
• compression of cardio/respiratory centres in the
medulla: death (tonsillar)
• reticular activating system: coma (all types)
• anterior cerebral artery: infarction (subfalcial)
• distortion of the midbrain and tearing of vessels:
death (all types).
• e symptoms can include:
• clouding of consciousness
• restlessness
• abnormalities of perception
• incoherent speech
• agitation
• violence
• pulling out lines, catheters, drains, etc.
• ere are numerous factors that predispose to or cause
post-operative confusion; these include:
• dehydration
• electrolyte abnormalities
• hypoxia
• infection
• drugs
• uraemia
• hypoglycaemia
• pre-existing psychiatric disorder or dementia
• alcohol and drug withdrawal (particularly in young
patients)
Post-Operative Confusion
• One of the commonest complications occurring in
elderly patients.
• urinary retention
• pain and anxiety
• cerebrovascular accident (CVA)
CHAPTER 13 Nervous and Locomotor Systems
membrane
Membrane potential (mV)
stimulus
Time (ms)
Membrane permeability
265
• head injury (especially in trauma patients)
• sleep deprivation
• ITU syndrome: pain, fear and sleep deprivation can
lead to visual and auditory hallucinations and inability to dierentiate reality from fantasy.
• Post-operative confusion is an important complication
with many serious underlying causes; a full management plan must be formulated and the cause sought.
Appropriate management should include:
• history and examination
• FBC, U&E, LFT, glucose, ABG
• ECG
• sepsis screen: blood cultures, chest X-ray, sputum,
midstream urine, wound swab.
• If a specic cause is found then this must be corrected,
e.g. hypoxia, urinary retention; however, non-specic
treatment may include:
• eliminate drugs likely to cause or increase the confu-
sional state
• presence of nursing sta in a well-lit environment
• low-dose sedation, e.g. haloperidol
• physical restraint – only if patient at risk of harming
self or others.
PERIPHERAL NERVOUS SYSTEM (PNS)
Conduction and Transmission
Action Potentials (Fig. 13.5)
• Action potentials are the method by which nerves send
information; they are electrical signals and are described
as ‘all-or-nothing’.
• Axons have a resting membrane potential with respect to the
extracellular environment; this is approximately −70 mV.
• As stimuli attempt to activate an action potential the
membrane potential is decreased towards a ‘threshold’;
stimuli below this threshold will not result in an action
potential and are described as subthreshold. If the stimulus is large enough to decrease the membrane potential above the threshold then this will result in an action
potential.
• e action potential, once initiated, begins with a rapid
depolarization and a reversal of the membrane potential to around 50 mV; this occurs in a few tenths of a
millisecond.
• Following depolarization is repolarization: this is where
the cell returns to the normal resting membrane potential; the repolarization may initially be more negative
than the resting potential – hyperpolarization.
• During the action potential the cell has an ‘absolute’
refractory period in which no further action potential
can be generated. During repolarization then a ‘relative’ refractory period exists; an action potential can be
stimulated but will need a stimulus of greater magnitude than the initial stimulus.
• Action potentials self-propagate: once the cell is stimulated, the signal will propagate along all cells.
• e intra- and extracellular concentrations of Na+ and
K+ dier:
• Na+ concentration is greater extracellularly and thus
tends to diuse into the cell, both along this concentration gradient and due to the negative membrane
potential
• K+ has a greater concentration intracellularly and
thus tends to diuse out of the cell.
• e change in permeability of the cell to Na+ and K+
during an action potential is due to conformational
changes in voltage-controlled ion channels by the initial
stimulus depolarizing the cell membrane.
Fig. 13.5 (A) Graph illustrating the theory of the ‘all-or-nothing’ response to electrical stimuli. (B) The ion
flows responsible for depolarization and repolarization of a nerve. (From McGeown JG. Physiology, 2nd edn.
Churchill Livingstone, Edinburgh, 2002, with permission.)
+50
Depolarisation
0
–70
Subthreshold
stimulus
A
0
Suprathreshold
5
Repolarisation
Threshold
Time (ms)
Resting
potential
Na
or conductance (arbitrary units)
0
B
0
Depolarisation
K
24
Repolarisation
266
Action potential jumps from node to node
Myelin sheath
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SECTION II Physiology
• e initial depolarization is due to the rapid inux of
Na+ as the Na+ channel opens; at the same time the K+
channel also opens and K+ is released into the extracellular environment.
• e Na+ channel activates much faster than the K+
channel. is explains the rapid inux of Na+; the channel also closes much faster; the K+ channel remains
open over a longer period than the Na+ channel and is
responsible for repolarization as K+ is released and the
membrane potential falls back to its negative value.
Propagation of Action Potentials
• e action potential results in the inside of the cell being
positive in respect to the extracellular environment; this
is the opposite of the normal negative resting membrane
potential; as a result, the action potential travels from
positive to negative.
• e action potential is unidirectional and sets up local
currents that result in the propagation of the action
potential across the whole membrane; the action potential is unidirectional due to the refractory nature of the
membrane, preventing further depolarization.
• e conduction velocity of action potentials is determined by two factors:
• axon diameter: the greater the diameter the higher
the conduction velocity; this eect is due to the
increase in myelin causing a decrease in electrical
resistance
• myelination: myelinated cells have a much faster
conduction velocity in comparison with unmyelinated cells (50–100 m/s vs 1 m/s); this eect is due to
the gaps between the myelin sheath that surrounds
nerves. ese gaps are called the nodes of Ranvier.
Action potentials are generated only at these points
as the myelin acts to insulate the intervening sections; thus, the action potential jumps between the
gaps. is is referred to as saltatory conduction
(Fig. 13.6).
A classication of nerve bres is shown in Table 13.1.
Synaptic Transmission
• When an action potential reaches the end of an axon it
must be transmitted to the next adjacent nerve; the gap
between neurons is known as the synapse.
• Transmission of the signal relies on the release of neurotransmitters; these then aect the adjacent nerve
chemically to initiate another action potential.
• e action potential travels along the presynaptic nerve.
e axon terminates in an expanded end; this is called
the terminal bouton.
• Inside the bouton are numerous membrane-bound vesicles containing neurotransmitters.
Axon
Node of Ranvier
Transverse
section
Schwann cell
Schwann cell membrane
forms myelin sheath
Axon
Fig. 13.6 Action potential conduction in a myelinated nerve fibre (saltatory conduction). (From McGeown JG.
Physiology, 2nd edn. Churchill Livingstone, Edinburgh, 2002, with permission.)
nucleus
Axon
membrane
CHAPTER 13 Nervous and Locomotor Systems
267
TABLE 13.1 Different Types of Nerve
Fibre, Showing Functions, Conduction
Velocities and Diameters
Conduction
Type Function
Aα
Aβ
Aγ
Aδ
B Autonomic 10 3
C Pain 1 0.5–1
Motor
proprioception
Touch and
pressure
Muscle spindles 30 3–6
Pain,
temperature
and touch
Velocity (m/s)
100 15–20
50 5–10
20 2–5
Diameter
(µm)
• e transmission of the action potential occurs by:
• the action potential depolarizes the presynaptic
membrane by opening voltage-gated Ca2+ channels
• Ca2+ enters the axon down an electrochemical and
concentration gradient
• the increase in Ca2+ results in the vesicles fusing
with the presynaptic membrane and releasing neurotransmitters into the synaptic cle
• the neurotransmitters then bind with receptors on
the post-synaptic membrane
• binding of neurotransmitters initiates secondary
signals within the cell and opens ion channels, thus
generating a depolarizing current
• the transmitter is released from the receptor and is
broken down by specic breakdown pathways.
Neurotransmitters
• Neurotransmitters are chemicals that are responsible for
the transmission of action potentials across the synapse.
• e main neurotransmitters include:
• acetylcholine (ACh): this is an excitatory transmit-
ter; it is present in the brain, spinal cord, autonomic
nerves and the PNS. It is broken down to acetate and
choline by the enzyme acetylcholinesterase
• amines: this group includes catecholamines (adrena-
line, noradrenaline, and dopamine), 5-hydroxytryptamine (serotonin) and histamine. e catecholamines
are formed from the amino acid tyrosine. Two
enzymes degrade catecholamines: monoamine oxidase breaks down transmitter taken up by the presynaptic neuron; and catechol-O-methyl transferase
breaks down catecholamines taken up by the postsynaptic neuron
• amino acids: several amino acids act as neurotransmitters; these include:
• glycine: inhibitory
• glutamate: excitatory or inhibitory (can be con-
verted to GABA)
• aspartate: excitatory
• peptides: examples of peptide transmitters include:
• substance P: involved in the transmission of pain
sensation
• endorphins: inhibit pain pathways.
Pain and Sensation
• Pain is dened as an unpleasant sensory and emotional
experience associated with actual or potential tissue
damage.
• Pain can be classied into:
• nociceptive: somatic and visceral
• referred
• neuropathic
• psychogenic.
• Nociceptive and referred pain are the commonest types
of pain encountered in the surgical patient.
• Somatic pain is dened as pain that originates from the
skin, muscles, bones and joints; it tends to be sharp in
nature and is well localized.
• Visceral pain is due to ischaemia, inammation and
stretching or contraction (colic) of smooth muscle in
hollow viscera; it is poorly localized.
• Referred pain occurs when damage to an internal organ
is associated with pain in a particular skin region; this
occurs as the organ in question shares the same dermatomal innervation as the region the pain is felt. Examples
of referred pain include:
• MI and angina: pain may be referred to the neck, jaw,
shoulder and le arm
• spleen: haemoperitoneum leads to le-sided diaphrag-
matic irritation and le shoulder tip pain (Kehr’s sign)
• appendix: central abdominal pain in the T10 der-
matome is the initial sign until peritoneal irritation
localizes the pain to the right iliac fossa
• gall bladder: cholecystitis can lead to irritation of the
right hemidiaphragm and right shoulder tip pain
(Boas’ sign).
• Pain can also be classied according to the speed of
onset; so-tissue injury is associated with a sudden
sharp pain that lasts for a few seconds and is followed by
a longer-lasting dull throbbing pain. Peripheral nerves
dier in their diameter and conduction velocity; this
explains the dierent pain sensations:
• Aδ bres: these are myelinated nerves; as a result,
they have a high conduction speed and diameter.
ey are responsible for the sharp initial pain
268
Descending inputs
Pons
brain
afferent
= Opioid receptors
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SECTION II Physiology
Periaqueductal
grey matter
and
raphe magnus
mid-
Nucleus
Serotonin
+
Enkephalin-releasing
hormone
Locus
coeruleus
-
Noradrenaline
(Norepinephrine)
Relay neurone
Fig. 13.7 Descending inputs modulating pain sensation.
• C bres: these are unmyelinated nerves and thus
have a smaller diameter and lower conduction velocity. ey are responsible for the longer-lasting dull
pain.
• Pain transmission can be divided into:
• transduction
• transmission
• modulation
• perception.
• Transduction involves the production of electrical
impulses; following tissue damage there is the release
of inammatory substances, i.e. prostaglandins, histamine, serotonin, bradykinin and substance P. ese substances lead to electrical impulses that are transmitted
along sensory nerves.
• Transmission of pain sensation is along Aδ and C bres
to the spinal cord; here they synapse in lamina I and III
in the dorsal horn.
• e sensation of pain is then transmitted along the spinal cord where it is modulated before nally being perceived in the sensory areas of the brain.
• Modulation of pain involves the ‘gate control theory’
of Melzack and Wall: this theory proposes that pain
impulses received in the dorsal horn can be modulated
by other descending spinal inputs. ese include inhibitory inputs from the periaqueductal grey matter and
nucleus raphe magnus (both releasing serotonin) and
-
Pain sensation
º
I
neuron
the locus coeruleus (releases noradrenaline) (Fig. 13.7).
In addition there is the release of the naturally occurring
enkephalins and endorphins.
Drug Modulation of Pain
• ere are numerous forms of analgesia used in current
surgical practice; each acts on dierent elements in the
chain of pain sensation.
• e provision of analgesia is particularly useful in the surgical patient; the eects of inadequate analgesia include:
• respiratory:
• ↑ chest wall splinting
• ↓ tidal volume
• ↓ vital capacity
• ↓ functional residual capacity (FRC)
• diculty coughing and retention of secretions,
leading to atelectasis and pneumonia
• cardiovascular:
• pain increases BP and heart rate, thus placing
increased strain on the heart
• immobilization and increased risk of thromboembolism
• ileus
• urinary retention
• stress response
• psychological stress.
• Transduction: drugs like paracetamol and NSAIDs
inhibit prostaglandin production. Prostaglandins are
CHAPTER 13 Nervous and Locomotor Systems
269
involved in sensitizing nociceptive receptors in injured
tissues to the eects of nociceptive compounds such as
bradykinin and substance P.
• Transmission: Aδ and C bres are involved in the transmission of pain sensation. Local anaesthetics can be
used to prevent the conduction of action potentials in
these nerve bres. Aβ bres are involved in inhibiting
transmission to higher centres; stimulation can thus
provide analgesia. is is the basis for TENS (transcutaneous electrical nerve stimulator) machines.
• Modulation: opioids are potent analgesics. ey produce their eect by combining with opioid receptors in
the spinal cord and higher centres. e analgesic eect
of opioids is due to:
• combining with receptors in higher centres such as
the periaqueductal grey matter and nucleus raphe
magnus; here they stimulate descending inhibitory
inputs to pain perception
• binding to opioid receptors in the dorsal horn and
inhibiting pain transmission; this action is believed
to be related to hyperpolarizing the cell and thus
decreasing the chance of propagating the pain
impulse
• inhibiting the release of substance P.
• Perception: pain perception can be inuenced by factors
such as fear, anxiety, depression, and activation of the
‘ght or ight’ mechanism.
AUTONOMIC NERVOUS SYSTEM
(ANS) (Fig. 13.8)
• e autonomic nervous system is involved in the control
of visceral organs, smooth muscle and secretory glands.
• It is principally involved in maintaining the internal
environment by regulating cardiac, respiratory and
digestive functions.
• e eerent neurons of the ANS have a two-neuron
arrangement. is diers from somatic nerves. e cell
body of the rst neuron lies in the brainstem or spinal
cord (preganglionic); the second neuron is located in the
periphery in an autonomic ganglion (post-ganglionic).
• e ANS can be divided into two specic functional
groups:
• sympathetic
• parasympathetic.
Sympathetic Nervous System
• Sympathetic neurons:
• located in the thoracic and upper 2–3 lumbar seg-
ments of the spinal cord
• preganglionic neurons lie in the lateral horn of the
spinal grey matter
• preganglionic axons leave via the ventral root of the
spine to join the spinal nerve (see Chapter 4)
• post-ganglionic neurons have their cell bodies either
in the sympathetic chain (see Chapter 4) or in a
named plexus along the aorta, i.e. coeliac, superior
and inferior mesenteric.
• Spinal nerves are connected to the sympathetic chain by
two small branches: the lateral white ramus communicantes (myelinated), and the medial grey ramus com-
• e sympathetic innervation of the head and neck is via
preganglionic neurons synapsing with post-ganglionic
bodies within the sympathetic chain; the post-ganglionic
neurons then leave via the grey rami communicantes to
join the spinal nerve.
• e sympathetic innervation of the abdominal and
pelvic organs diers from that of the head and neck.
Preganglionic neurons pass straight through the sympathetic chain to their individual plexuses and synapse
with post-ganglionic cell bodies within the plexus.
• e neurotransmitter of the sympathetic nervous system is noradrenaline (except sweat glands; these are
innervated by cholinergic bres).
Parasympathetic Nervous System
• Preganglionic neurons lie in cranial nerve nuclei within
the brainstem; the parasympathetic output is derived
from the oculomotor, facial, glossopharyngeal and
vagus nerves; this provides innervation to the head,
neck, thorax and abdomen.
• e pelvic viscera are innervated by preganglionic neurons derived from the S2–4 spinal roots.
• e parasympathetic nervous system feeds into ve
ganglia before being distributed to the structures it
innervates; these ganglia are:
• oculomotor (III) nerve → ciliary ganglion
• facial (VI) nerve → sphenopalatine ganglion and
submandibular ganglion
• glossopharyngeal (IX) nerve → otic ganglion
• S2–4 → pelvic splanchnic nerve → pelvic ganglion.
• e cell bodies of post-ganglionic neurons lie in ganglia that are found in close proximity to the organ they
innervate; an example would be the enteric nervous
system (see Chapter 10). Here neurons contribute to
two plexuses, the myenteric and submucosal. ese are
found within the bowel wall itself.
• e neurotransmitter of the parasympathetic nervous
system is acetylcholine.
Functions of the Autonomic Nervous System
• e eects of the autonomic nervous system are summarized below.
270
Spinal
Spinal
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cord
A
SECTION II Physiology
Sympathetic
chain
Superior cervical ganglion
Cervicothoracic ganglion
Coeliac
ganglion
Renal
ganglion
Pelvic ganglion
Head and neck
Dilator pupillae
Blood vessels
Sweat glands
Muscles of hairs
Respiratory tract
Cardiac branches
Oesophagus
Gut from
stomach to colon
Liver, biliary tract
Pancreas
Kidney, ureter
Bladder
Hind gut
Reproductive tract
Ciliary muscle
Sphincter pupillae
Lacrimal gland
Nasal glands
Submandibular gland
Sublingual gland
Parotid gland
Oesophagus
Cardiac branches
Respiratory tract
Gut from stomach
to colon
Liver, biliary system
Pancreas
Bladder
Urethra
Hind gut
Uterus, uterine tubes
Erectile tissue
B
1
Oculomotor nerve
2
3
pharyngeal
Glosso
4
Pelvic splanchnic
5
Facial nerve
nerve
Vagus nerve
nerve
cord
S2
S3
S4
Fig. 13.8 (A) Layout of the sympathetic nervous system. (B) The parasympathetic nervous system: 1 = ciliary
ganglion, 2 = sphenopalative ganglion, 3 = submandibular ganglion, 4 = otic ganglion, 5 = pelvic ganglion.
• Sympathetic system:
• dilates pupils
• reduces salivary secretions
• reduces lacrimal secretions
• increases heart rate (tachycardia)
• increases the contractility of the heart
• bronchodilation
• decreases GI motility
• increases sweat gland secretion
• contraction of erector pili muscles in the skin.
• Parasympathetic system:
• constricts pupils
• increases salivary secretion
• increases lacrimal secretion
• decreases heart rate (bradycardia)
• decreases the contractility of the heart
• bronchoconstriction
• increases GI motility.
LOCOMOTOR SYSTEM
Skeletal Muscle Physiology
Structure of Skeletal Muscle
• Muscles are composed of a number of muscle bres;
these are grouped together to form bundles called
fasciculi.
• e muscle bres are composed of numerous lamentous bundles called myobrils.
• e myobrils contain the contractile proteins actin
and myosin; under a microscope muscle has a striated
appearance due to the arrangement of actin and myosin:
• the dark bands or A bands are composed of the
thicker myosin laments
• the light bands or I bands are composed of the thin-
ner actin laments
• the I band is divided by the Z line; the space between
Z lines is called a sarcomere
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