components of the cranial vault - The Complete Academic Support Hub

W H A T Y O U S H O U L D K N O W B E F O R E Y O U S T A R T T H I S C H A P T E R
Can you name the major anatomical structures of the brain, and explain how they relate to function?
Can you identify the components of the cranial vault, and explain how the Monro–Kellie doctrine dictates
management of these components within the skull?
Can you describe how mean arterial pressure inﬂuences cerebral perfusion pressure, and what the signifcance
of this is in relation to control of blood pressure?
Can you describe the inﬂammatory process, and identify the cardinal signs of inﬂammation?
Can you describe the relationship between the vertebral divisions and the spinal cord in relation to function?
K E Y T E R M S
Acquired brain
injury (ABI)
Autonomic
dysreﬂexia
Central cord
syndrome
Cerebral blood
ﬂow (CBF)
Cerebral perfusion
pressure (CPP)
Concussion
Contrecoup
contusion
Conus medullaris
Coup contusion
Diffuse axonal
injury (DAI)
Extradural
haematoma (EDH)
Flaccid paralysis
Intracranial
pressure (ICP)
Mean arterial
pressure (MAP)
Primary brain injury
Secondary brain
injury
Spastic paralysis
Spinal shock
Subdural
haematoma (SDH)
Traumatic brain
injury (TBI)
L E A R N I N G O B J E C T I V E S
After completing this chapter, you should be able to:
1 Compare and contrast the pathophysiology of primary and secondary head injury.
2 Explore the relationship of the Monro–Kellie doctrine to traumatic brain injury.
3 Outline the clinical diagnosis and current management for traumatic brain injury.
4 Outline the pathogenesis of spinal cord injury.
5 Identify the common classifcations of spinal cord injury.
6 Discuss the characteristics of common spinal cord syndromes.
7 Explore the diagnosis and management of spinal cord injury.
8 Examine the common complications associated with spinal cord injury.
Neurotrauma 11
Copyright © Pearson Australia (a division of Pearson Australia Group Pty Ltd) 2019— 9781488617676 — Bullock/Principles of Pathophysiology 2e
Bullock, S, & Hales, M 2018, Principles of Pathophysiology EBook, Pearson Education Australia, Melbourne. Available from: ProQuest Ebook Central. [20 March 2021].
Created from utas on 2021-03-20 18:12:08.
Copyright © 2018. Pearson Education Australia. All rights reserved.
200 P A R T 3 N E R V O U S S Y S T E M P A T H O P H Y S I O L O G Y
INTRODUCTION
A person’s brain is the centre of their existence, and their spinal
cord is a critical element to facilitate interaction and participation
in life. Alterations in brain or cord function can therefore have a
devastating eﬀect on a person’s abilities and their place in society.
This chapter will focus on the eﬀects of brain and spinal
cord injury. Traumatic brain injury (TBI) is often devastating,
yet it may occur along a spectrum from mild to severe in nature.
However, even mild injuries may compromise a person’s
function or independence with changes in memory, cognition,
personality and/or behaviour. Coma and death are signifcant
and severe consequences of TBI. Spinal cord injury can also be
life-shattering and result in profound disability and loss of
independence.
TRAUMATIC BRAIN INJURY (TBI)
Traumatic brain injury (TBI) is characterised by an alteration of
brain function usually caused by an external force. The
mechanism can be divided into primary brain injury, which is
damage occurring at the time of insult as a direct result of tissue
loss due to the trauma, and secondary brain injury, which is
damage occurring post injury because of other extracranial
causes, such as hypoxia, hypotension or hypoglycaemia, or
intracranial causes, such as haemorrhage, swelling or infection.
Primary and secondary brain injury will be discussed in detail
later in this chapter.
Acquired brain injury (ABI) is most commonly associated with
the misuse or abuse of drugs and/or alcohol, or other causative
agents, including infections, strokes, tumours and a large
number of other diseases and disorders. Stroke and CNS
infections are covered in Chapter 9.
A TBI results in damage or alteration in brain function as a
direct result of injury. Causes can include blunt-force trauma,
such as falls, penetrating force where an object such as a knife
enters the cranial vault, and acceleration–deceleration injury,
which often occurs in motor vehicle accidents and sport. In
the latter instance, the injury to the brain occurs when the
brain itself moves backwards and forwards with rapid
succession. TBI can manifest as confusion, alteration in
consciousness level, seizure, coma, autonomic dysfunction
and neurological defcit.
EPIDEMIOLOGY
It is estimated that 10 million new TBIs occur each year
worldwide, and TBI is a leading cause of death and long-term
disability in both industrialised and developing countries.
Incidence of TBI in Australia is reported as 107 per 100 000, but
worldwide rates range from as high as 811 per 100 000 in New
Zealand to as low as 7.3 per 100 000 in Western Europe. In
Australia, there were approximately 23970 hospitalisations for
individuals with intracranial injury between 2014 and 2015, of
which 63% occurred in males (Figure 11.1). Approximately
28% of hospitalisations for intracranial injury occur between the

Male Female

AssignmentTutorOnline

1400
1600
1800
2000
1200
1000
800
600
400
200
0
Number of discharges of people with intracranial injury
1–4
5–9
10–14
15–19
20–24
25–29
30–34
35–39
40–44
45–49
50–54
55–59
60–64
65–69
70–74
75–79
80–84
> 85
Age group at separation
Figure 11.1
Number of hospitalisations for intracranial injury as the principal diagnosis by gender and age, Australia, 2014–15
Source: Based on Australian Institute of Health and Welfare (2017b). © Australian Institute of Health and Welfare 2017.
Copyright © Pearson Australia (a division of Pearson Australia Group Pty Ltd) 2019— 9781488617676 — Bullock/Principles of Pathophysiology 2e
Bullock, S, & Hales, M 2018, Principles of Pathophysiology EBook, Pearson Education Australia, Melbourne. Available from: ProQuest Ebook Central. [20 March 2021].
Created from utas on 2021-03-20 18:12:08.
Copyright © 2018. Pearson Education Australia. All rights reserved.
C H A P T E R 1 1 N E U R O T R A U M A 201
ages of 10 and 29 years old, with the unequal gender
distribution thought to be due to increased risk-taking
behaviour by males. TBIs from falls is the cause of 10% of
admissions of individuals over 85 years of age, and this is the
only age group where female injury rates exceed male rates.
TBI statistics overall are also most likely underestimated, as
many people who sustain a mild head injury may never seek
medical attention.
It is estimated that within the general population
approximately 17% of men and 9% of women have a history of
head injury resulting in loss of consciousness; however,
interestingly, individuals within the correctional system have
significantly higher rates of TBI. Juvenile offenders are
approximately three times more likely to have sustained a
previous head injury, and in some studies between 34% and
82% of inmates have received a previous TBI.
Falls, transportation-related accidents and assaults are
identifed as the top three mechanisms of injury contributing to
TBI. Alcohol use was reported as an important factor in all
cases. Falls caused over 2 in every 5 TBIs.
While the majority (70–80%) of primary head injuries are
classifed as minor, a signifcant proportion of individuals who
sustain minor TBI may continue to experience poor functional
outcomes as a result of secondary brain injury, missed injuries
and existing comorbidities. Of the 20–30% of people who
sustain moderate-to-severe head injury, approximately 10% of
these are dead on arrival at the emergency department, while the
remainder will require admission to an intensive care unit, with
management lasting approximately 7–10 days.
PRIMARY BRAIN INJURY
L E A R N I N G O B J E C T I V E 1
Compare and contrast the pathophysiology of primary
and secondary head injury.
AETIOLOGY AND PATHOPHYSIOLOGY
The primary or acute phase of TBI describes the cellular and
structural injury that occurs as a direct result of the force of the
injury. The severity of the primary injury is determined by the
extent of neuronal and vascular damage. Glial injury and loss of
axonal integrity result in neuronal cellular leakage and alteration
in cell membrane potential. Increased capillary permeability
alters vascular homeostasis, especially in relation to solutes (see
Chapters 1 and 3). The physical mechanisms of TBI can be
classified as impact loading, impulsive loading and static
loading.
Physical mechanisms of traumatic brain injury
Impact loading Impact loading causes TBI through a
combination of contact and inertial forces. It is defned as a
collision of the head with a solid object at a tangible speed. For
example, a motorbike rider is travelling at 110 km/h and is
thrown from the motor bike. The rider’s head strikes the side of
a small car, resulting in TBI. Contact or inertial forces may
strain the brain beyond its structural and mechanical tolerance.
Brain tissue can be deformed by compression forces, which
compress tissue and cause damage. Brain tissue can also be
deformed by stretching or shearing. Shearing distorts tissues by
causing the tissues to slide over each other, resulting in damage.
Impulsive loading Inertial force occurs when the head is set
in motion, leading to acceleration-induced TBI. It is defned as
sudden motion without significant physical contact. As an
example, after failing to stop, a truck collides with the rear of
the station wagon and the impact forces the station wagon and
the driver forward in a sudden motion. Even though the station
wagon driver’s head does not physically strike another object,
the brain moves within the skull as a result of the force of
impulse loading.
Static loading Static loading is rare, and occurs when a
slowly moving object traps the person’s head against a fxed
rigid structure and gradually squeezes the skull, causing
numerous fractures, which may result in deformity of the skull
and brain. It is defned as a loading in which the eﬀect of speed
may not be signifcant. For example, a worker’s head is pinned
and crushed between a very large, slow-moving cylinder and the
cement ﬂoor.
Protective and preventative measures, such as the wearing of
helmets, safety equipment and seatbelts, and anti-speeding
campaigns are regarded as sound risk-mitigation strategies that
can reduce the degree of injury sustained at the time of impact.
However, where a TBI has occurred, the mechanism of injury
can provide the clinician with some degree of insight into the
degree of trauma sustained and the potential site(s) of injury.
Common effects of primary traumatic brain injury
Skull fracture Skull fractures are generally labelled and
categorised according to location, pattern and whether they are
open or closed. Closed fractures do not permit communication
with the outside environment, whereas open fractures do. A
simple fracture is defned as having one bone fragment, while a
compound fracture exists when there are two or more bone
fragments.
Linear fractures A linear fracture is a fracture in the line of the
skull that passes through its entire thickness (see Figure 11.2A).
Linear fractures are generally caused by a signifcant blow to
the head.
Depressed fractures A depressed skull fracture results in
bone fragmentation that causes an actual depression in the
surface of the skull. Depressed skull fractures are generally
the result of a powerful mechanism of injury, and bone
fragments may become embedded in underlying brain tissue
(see Figure 11.2B).
Base of skull fractures Base of skull (BOS) fractures are
fractures that involve the base of skull and cribriform plate (see
Figure 11.2C). The most common BOS fractures involve the
petrous portion of the temporal bone, external auditory canal
and the tympanic membrane. BOS fractures are commonly
associated with the tearing of the dura mater, resulting in
cerebrospinal ﬂuid (CSF) leakage from the ear due to the open
Copyright © Pearson Australia (a division of Pearson Australia Group Pty Ltd) 2019— 9781488617676 — Bullock/Principles of Pathophysiology 2e
Bullock, S, & Hales, M 2018, Principles of Pathophysiology EBook, Pearson Education Australia, Melbourne. Available from: ProQuest Ebook Central. [20 March 2021].
Created from utas on 2021-03-20 18:12:08.
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202 P A R T 3 N E R V O U S S Y S T E M P A T H O P H Y S I O L O G Y
Figure 11.2
Skull fractures
(A) Linear skull fracture. (B) Depressed fracture. (C) Base of skull fracture.
A B C
conduit with the external environment. Periorbital ecchymosis,
also known as raccoon eyes, is a type of intraorbital bleeding
usually seen with cribriform plate fracture (see Figure 11.3).
Battle’s sign (see Figure 11.4), an ecchymosis over the mastoid
process, usually occurs 12–24 hours post injury and also
indicates a BOS fracture.
Concussion A concussion is a transient alteration in cerebral
function without structural defect, which manifests as a loss of
consciousness followed by rapid recovery. Concussion is usually
caused by an acceleration–deceleration force or blunt-force
trauma. The reticular activating system (RAS), which is primarily
responsible for maintaining an alert and conscious state, is
thought be disrupted. The concussed person may provide a
history of unconsciousness or memory loss for the event. The
period of unconsciousness is usually brief. Concussion can also
produce light-headedness, vertigo, headache, nausea, vomiting,
photophobia, tinnitus, fatigue and cognitive dysfunction. For
many people, concussive symptoms may remain three months
post injury, and, for some, symptoms may remain at one year.
Figure 11.3
Racoon eyes, or periorbital ecchymosis
(A) Periorbital ecchymosis with lids almost swollen shut. (B) Periorbital ecchymosis with eyes open and subconjunctival
haemorrhage visable.
Source: (A) Casa nayafana/Shutterstock; (B) ARZTSAMUI/Shutterstock.
A B
Copyright © Pearson Australia (a division of Pearson Australia Group Pty Ltd) 2019— 9781488617676 — Bullock/Principles of Pathophysiology 2e
Bullock, S, & Hales, M 2018, Principles of Pathophysiology EBook, Pearson Education Australia, Melbourne. Available from: ProQuest Ebook Central. [20 March 2021].
Created from utas on 2021-03-20 18:12:08.
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C H A P T E R 1 1 N E U R O T R A U M A 203
Figure 11.4
Battle’s sign
Source: Mediscan/Alamy Stock Photo.
Contrecoup
Coup
1
2
Figure 11.5
Coup and contrecoup contusion
1. Coup contusion—in this example the temporal lobe
injury is sustained from trauma of impacting the
windscreen.
2. Contrecoup contusion—in this example the injury
occurs to the occiptal lobe as a result of the backward
motion of the brain onto the back of the skull.
Source: LeMone & Burke (2008), Figure 44.5, p. 1554.
The term post-concussion syndrome is used to describe
the presence of at least three manifestations (such as
headache, fatigue, irritability, dizziness, impaired memory
and concentration, photophobia, phonophobia or insomnia)
appearing within the week following the concussion. Persistent
post-concussive syndrome (PPCS) is described as the
manifestations continuing for more the three months.
Contusion—coup and contrecoup It must be remembered
that the brain is mobile within the cranial vault and, as a result,
can sustain multiple injuries. Cerebral contusion is bruising to
the brain tissue, resulting in an alteration of neurological
function that includes consciousness level. The most common
locations for cerebral contusions are the frontal and temporal
lobes. Cerebral contusions occur in 20–30% of cases of severe
TBI, and larger contusions can be associated with haematoma
formation. Causes include blunt-force trauma and severe
acceleration–deceleration forces. Coup contusions occur at the site
of impact, and occur because of the generation of negative
pressure when the skull is distorted and then returns to its normal
shape. Contrecoup contusions are similar to coup contusions but
are located opposite the site of impact.
The amount of energy dissipated at the site of direct
impact determines the ensuing contusion. For example, the
energy impact from a small, hard object will dissipate at the
site of impact, resulting in a coup contusion (see Figure 11.5).
In contrast, impact from a larger object causes less injury at
the impact site as energy is dissipated at the beginning or end
of the head motion, leading to a contrecoup contusion (see
Figure 11.5).
Intracranial haemorrhage There are many types of
intracranial haemorrhage. Some are named according to a
description of their anatomical location in relation to the meninges,
such as extradural, subdural and subarachnoid haematomas.
Intracerebral haemorrhages occur within the brain parenchyma.
Intraventricular haemorrhages obviously occur within the
ventricles of the brain. Figure 11.6 explores the common clinical
manifestations and management of intracranial haemorrhage.
Extradural haematoma An extradural haematoma (EDH), also
known as an epidural haematoma, occurs from impact loading to
the skull with associated laceration of the dural arteries or veins.
As a result, blood collects in the potential space (the extradural
space) between the skull and the dura mater (see Figure 11.7).
EDHs are relatively rare, and account for about 2% of all TBIs,
with the most common presentations in people 20–40 years of
age. Typically, EDHs result from blunt-force trauma to the
temporal bone and injury to the underlying middle meningeal
artery. The principal threat to the brain is from the expanding mass
of blood displacing the temporal lobe medially and resulting in
herniation. The classic history for EDH presentation is a brief loss
of consciousness, followed by an increase in conscious state and
then a rapid decline into unconsciousness. The conscious period is
known as the lucent interval, and during this time the person may
appear lethargic, nauseated and confused, and complain of
headache. This clinical pattern occurs in a small number of cases,
as the majority of individuals either never lose consciousness or
never regain consciousness after the initial injury. The mortality
rate for EDH is about 20%, but may be greatly reduced with rapid
surgical evacuation of the haematoma.
Copyright © Pearson Australia (a division of Pearson Australia Group Pty Ltd) 2019— 9781488617676 — Bullock/Principles of Pathophysiology 2e
Bullock, S, & Hales, M 2018, Principles of Pathophysiology EBook, Pearson Education Australia, Melbourne. Available from: ProQuest Ebook Central. [20 March 2021].
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204 P A R T 3 N E R V O U S S Y S T E M P A T H O P H Y S I O L O G Y

Intracranial haemorrhage

types

Epidural

from
rupture
of

Intraventricular

from
rupture
of

Loop diuretics

Subdural

from
rupture
of

Subarachnoid

from
rupture
of

Intracerebral

from
rupture
of

Superficial arterial
and venous vessels

results

Haemorrhage

between

Haemorrhage

between

Dura mater	Arachnoid mater
results in

Haemorrhage

between

Arachnoid mater	Pia mater
results in

Haemorrhage

within

Brain
tissue

Haemorrhage

within

Cortical
bridging veins

results

results
Veins	Berry aneurysm

Intracerebral
vessels

results

Subependymal
veins

results

Brain
ventricles

Increased intracranial pressure

Bulging fontanelle Behavioural changes Seizures Vomiting
(infant)
ALOC Altered LOC Drowsiness Headache
manage

results in
Dura mater	Epidural space

results
results
Osmotic diuretics Hypothermia Decompressive craniotomy Airway management
BP changes

Antihypertensives	Maintain BP
manage

Management

manages
Figure 11.6
Clinical snapshot: Intracranial haemorrhage
ALOC 5 altered level of consciousness; BP 5 blood pressure.
Copyright © Pearson Australia (a division of Pearson Australia Group Pty Ltd) 2019— 9781488617676 — Bullock/Principles of Pathophysiology 2e
Bullock, S, & Hales, M 2018, Principles of Pathophysiology EBook, Pearson Education Australia, Melbourne. Available from: ProQuest Ebook Central. [20 March 2021].
Created from utas on 2021-03-20 18:12:08.
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C H A P T E R 1 1 N E U R O T R A U M A 205
Subdural haematoma A subdural haematoma (SDH) is usually
caused by the sudden acceleration then deceleration of brain
tissue, with subsequent tearing of the bridging veins. This
results in bleeding between the dura and the arachnoid layers
of the meninges (see Figure 11.7). SDHs are usually venous in
origin and, as a result, blood tends to collect more slowly than in
EDHs. However, SDHs are often associated with other brain
injuries. SDHs account for 30% of severe TBIs, and result in a
high mortality risk (. 50%). SDHs are usually precipitated by
moderate-to-severe blunt trauma to the head and a reduction in
conscious level. SDHs may be classifed as acute, subacute or
chronic depending on presentation. Acute SDH symptoms
generally appear within 14 days post injury. After two weeks
post injury, SDHs are classifed as subacute or chronic.
Intracerebral haematoma An intracerebral haematoma is
associated with haemorrhage in the brain tissue itself (see
Figure 11.7). It may occur at any location in the brain, but the
most common locations are the temporal and frontal lobes. The
mechanisms of injury include penetrating trauma with resultant
laceration, or diﬀuse injury from blunt-force trauma. Oedema
and haemorrhage formation contribute to reduce cerebral blood
flow (CBF) and raise intracranial pressure (ICP). Signs,
symptoms and prognosis are dependent on the location and size
of the bleed.
Subarachnoid haemorrhage A traumatic subarachnoid
haemorrhage (SAH) occurs when vessels in the subarachnoid
space, the space between the arachnoid and pia mater, have been
ruptured as a direct result of trauma (see Figure 11.8).
Subarachnoid haemorrhage is common following major TBI,
and may be associated with other focal injuries, such as contusion
and lacerations. Hydrocephalus and cerebral vasospasm can
develop post injury and can result in increased ICP.
Intraventricular haemorrhage Intraventricular haemorrhage
occurs when subependymal vessels rupture and, although it is
most common in premature babies, it can also occur as a result
of blunt-force trauma. Of the various types of intracranial
haemorrhage, intraventricular haemorrhage is less common
and is associated with signifcant mortality and morbidity. It
most often occurs in conjunction with other types of
intracranial haemorrhage, especially subarachnoid, but it can
also occur in isolation. Intraventricular haemorrhage may
develop in only one or both of the lateral ventricles, but can
also develop in the third and fourth ventricles independently.
Haemorrhage within all ventricles is also possible and presents
a very poor prognosis.
Epidural (extradural)
haematoma
Intracerebral
haematoma
Subdural
haematoma
Skull
Figure 11.7
Three types of haematomas: extradural,
subdural and intracerebral
Source: LeMone & Burke (2008), Figure 44.6,
p. 1557.
Subarachnoid
haemorrhage
Intracerebral
haemorrhage
Figure 11.8
Subarachnoid and intracerebral haemorrhage
Copyright © Pearson Australia (a division of Pearson Australia Group Pty Ltd) 2019— 9781488617676 — Bullock/Principles of Pathophysiology 2e
Bullock, S, & Hales, M 2018, Principles of Pathophysiology EBook, Pearson Education Australia, Melbourne. Available from: ProQuest Ebook Central. [20 March 2021].
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206 P A R T 3 N E R V O U S S Y S T E M P A T H O P H Y S I O L O G Y
Diﬀuse axonal injury Diffuse axonal injury (DAI) is the tearing
or disruption of axonal fbres in the white matter and brain
stem. Generally, DAI is caused by signifcant blunt-force
trauma. This type of injury is commonly seen in people involved
in motor vehicle accidents, falls from great heights, assaults
and infants subjected to abusive head trauma (such as shaken
baby syndrome). During the insult, the brain is subjected to
rotational and shearing forces that stretch and rupture the
axonal network, causing widespread impairment in the cortex
and diencephalon. The axonal network provides the
infrastructure for cognitive ability and supports major structural
and functional processes. Three forms of DAI exist: mild,
moderate and severe.
In mild DAI, post-traumatic coma lasts 6–24 hours and
death is uncommon. Residual cognitive, psychological and
sensory/motor deficits may be ongoing. In moderate DAI,
widespread neurological impairment is found in the cerebral
cortex and diencephalon. Axons are torn and damage occurs in
both cerebral hemispheres. Prolonged coma, lasting for 24 hours
or more, occurs and recovery is incomplete in 93% of people
who survive. Severe DAI is produced by severe axonal
disruption in the cerebral hemispheres, diencephalon and brain
stem, and 30–40% of people those who survive a severe injury
remain at reduced levels of consciousness for prolonged
periods of time.
SECONDARY BRAIN INJURY
AETIOLOGY AND PATHOPHYSIOLOGY
Secondary brain injury occurs when a cascade of metabolic,
cellular and molecular events damage cells that are already
susceptible after the initial injury. In the hours and weeks
following the primary injury, tissue ischaemia associated with
compressive forces, cerebral oedema or vascular injury can
lead to cellular necrosis. Both primary and secondary brain
injury contribute to the development of intracranial
inﬂammation and an alteration in the cerebral autoregulatory
mechanisms.
Secondary brain injury is a complex pathophysiological
process that develops 2–24 hours after the primary injury. The
predominant mechanism of secondary head injury is that
of impaired cerebral oxygenation due to impaired CBF.
Hypotension (defned as systolic blood pressure , 90 mmHg),
hypoxia (oxygen saturation , 90% or PaO2 , 50 mmHg),
hypoglycaemia, hyperpyrexia and hypocapnia (PaCO2 , 30
mmHg) are identifiable symptoms in the development and
exacerbation of secondary head injury. (See Clinical Box 11.1
for some other causes of secondary brain injury.) Unfortunately,
the development of these symptoms can occur during
resuscitation, transportation, and surgical and intensive care unit
intervention. Any evidence of hypotension and hypoxia has a
deleterious eﬀect on the outcome, and contributes to the vicious
cycle of insufcient CBF, which in turn can damage susceptible
neurons and facilitate the development of secondary brain
injury. Figure 11.9 explores the common clinical manifestations
and management of secondary head injuries.
Intracranial inflammation Brain injury promotes an
inﬂammatory response and the release of cytokines, free radicals
and excitatory amino acids. As with any inﬂammatory response,
when capillary permeability is altered and swelling occurs in
this location it involves the blood–brain barrier and glial cells.
Increased blood–brain barrier permeability may render the
brain vulnerable to the eﬀects of pharmacological agents that
under normal circumstances cannot cross into the cerebral
compartment, such as osmotic diuretics. The degree of
inﬂammation is an important consideration in the management
of raised ICP, as the inﬂammatory response may continue for
some time.
L E A R N I N G O B J E C T I V E 2
Explore the relationship of the Monro–Kellie doctrine to traumatic
brain injury.
Pressure–volume relationship and the Monro–Kellie
doctrine Once the fontanelles have fused, usually by 2 years
of age, the brain is enclosed in a rigid vault. Cerebral circulation
is vulnerable to conditions that increase intracranial volume.
Normal intracranial pressure (ICP) is usually less than 15 mmHg
and is determined by the volume of the brain parenchyma
(1300 mL in an adult), CSF (100–150 mL) and intravascular
blood (100–150 mL). The Monro–Kellie doctrine notes that an
increase in volume of any one of the cerebral components will
increase ICP and decrease the volume of other cerebral
components. If this compensatory reduction in volume does not
occur, then ICP will rise, as volume and pressure are inversely
related.
The brain accounts for only 2% of total body weight, but
consumes over 20% of the body’s total oxygen requirements
and 15% of the total cardiac output. The maintenance of cerebral
perfusion is critical. Cerebral perfusion pressure (CPP) is the
difference between outflow and inflow, and is the driving
pressure for cerebral blood ﬂow (CBF). Estimates of CPP assume
CLINICAL BOX 11.1
Causes of secondary brain injury following traumatic
brain injury associated with increased mortality and
morbidity
• Hypoxia • Hyponatraemia
• Hypotension • Hypernatraemia
• Hypocapnia • Infection
• Hypercapnia • Seizure
• Hyperthermia • Delayed haematoma
• Hypoglycaemia • Subarachnoid haemorrhage
• Hyperglycaemia • Vasospasm
• Hyperosmolality • Hydrocephalus
Source: Bersten & Soni (2013), p. 582.
Copyright © Pearson Australia (a division of Pearson Australia Group Pty Ltd) 2019— 9781488617676 — Bullock/Principles of Pathophysiology 2e
Bullock, S, & Hales, M 2018, Principles of Pathophysiology EBook, Pearson Education Australia, Melbourne. Available from: ProQuest Ebook Central. [20 March 2021].
Created from utas on 2021-03-20 18:12:08.
Copyright © 2018. Pearson Education Australia. All rights reserved.
C H A P T E R 1 1 N E U R O T R A U M A 207
Phases

Cognitive
rehabilitation

manages

Cognitive
deficits
Rehabilitation
Pain
management Speech therapy
Assistance with
ADLs
Mental health
support

Management

erebral blood flow
from
Metabolic
dysfunction
Oedema Excitotoxicity
Capillary
permeability
Blood–brain
barrier function
Glutamate
Further neuronal destruction
Motor
deficits
Sensory deficits
or alterations
Communication
deficits
Functional
deficits
Behavioural
deficits
or CO2
Hypotension
or Na+
or Osmolality
Seizure
Hydrocephalus
support
from
manages

Release of inflammatory mediators

Process

Hypoperfusion phase

Hyperaemia phase

Hyperaemia

Vasospasm phase

Vasodilatory metabolites
Microcirculatory resistance

Secondary head injury

Impaired
autoregulation

Ischaemia Intracranial
pressure
Intracellular
influx
of
Sodium Calcium
Membrane
instability
Mitochondrial
calcium
results in

Exacerbated by

Hypoxia

Infection
or Glucose
Haemorrhage
Vasospasm

Ventilatory

manages

Maintain BP
Correct fluid
and electrolytes
Antibiotics
Antiseizure meds
Haemostasis
CSF shunt
Nimodipine
Correct BGL
from
manages manages manages manages
manages
manages
manages
manage
manages
manage
manages
manages
Figure 11.9
Clinical snapshot: Secondary head injury
T 5 decreased; c 5 increased; ADLs 5 activities of daily living; BGL 5 blood glucose level; BP 5 blood pressure; CO2 5 carbon dioxide;
CSF 5 cerebrospinal ﬂuid; Na1 5 sodium ion.
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208 P A R T 3 N E R V O U S S Y S T E M P A T H O P H Y S I O L O G Y
that the relevant inﬂow pressure is equivalent to the mean arterial
pressure (MAP) and outﬂow is related to the ICP. The formula for
CPP is:
CPP = MAP – ICP
Therefore, CPP is used as a measure of CBF. Clinical Box 11.2
outlines the defnitions and formulae that relate to cerebral
blood pressure and perfusion.
Similarly, any space-occupying mass, such as a haematoma
or oedema, within the cranial vault can result in the compression
and displacement of the cerebral contents. Initially, circulating
CSF and blood volume (principally venous) are reduced, but as
the mass size is increased, the space-occupying lesion
compresses brain tissue and reduces CBF due to increased ICP.
As ICP rises outside the normal range, autoregulation is lost,
and CBF becomes totally dependent on CPP, which in turn is
dependent on systemic blood pressure. Rapid rises in ICP can
lead to compression of the brain tissue and herniation, where the
brain tissue itself is displaced and moves towards the foramen
magnum. The common phenomenon known as the Cushing
reﬂex—hypertension, bradycardia and irregular respiration—is
a direct result of a rapid rise in ICP.
Under normal circumstances, CBF is maintained by local
microcirculation that results from changes in arterial pressure.
This is termed autoregulation, and ensures that brain tissue is
adequately perfused with oxygen and that wastes are removed.
Autoregulation of CBF has a functional CPP range of
65–150 mmHg; outside of these ranges, autoregulation is
diminished. Under normal circumstances, a pressure–volume
relationship exists in the brain vasculature that maintains CPP
and CBF. The major regulatory mechanisms for maintaining
adequate CBF are the partial pressure of carbon dioxide (PaCO2),
blood pressure and blood pH. Alteration in PaCO2, blood pressure
or blood pH will result in cerebral vasoconstriction or vasodilation.
Hypotension and/or hypoventilation results in an increase in
PaCO2 and a decrease in pH (acidosis); as a consequence, cerebral
vasodilation occurs in an attempt to increase CBF and deliver
more oxygen. Conversely, hypertension, hyperventilation and an
increase in pH (alkalosis) can cause cerebral vasoconstriction and
a reduction in CBF. Hypocapnia is capable of reducing CBF by
4% for each mmHg change in PaCO2.
Elevated intracranial pressure The Monro–Kellie doctrine
provides the framework for understanding the mechanism
behind rising ICP. CBF is dependent on autoregulation and CPP.
Baroreceptors constantly monitor systemic blood pressure and
provide a positive feedback loop. Myogenic regulation of
systemic blood pressure is achieved by vasodilation and
vasoconstriction, thus altering peripheral vascular resistance in
an eﬀort to maintain adequate CPP and blood ﬂow.
Alterations to cerebral perfusion When the homeostatic
autoregulation mechanism is impaired, neuronal damage and
intracranial inﬂammation occur.
The hypoperfusion phase Within the frst 72 hours following
brain injury, CBF is reduced, resulting in cerebral ischaemia.
When autoregulation fails, the degree of CBF is directly
dependent on systemic blood pressure. The maintenance of
systemic blood pressure may require catecholamine infusion
and intravenous ﬂuid administration to support the CPP and
CBF. Insufcient oxygen delivery renders neurons ischaemic
and exacerbates the speed of the inﬂammatory process, which
results in oedema and, in turn, attracts more inﬂammatory
mediators to the injured site. Therefore, oedema and the
alteration in cellular permeability increase ICP further. Increased
ICP reduces CBF, and this establishes a cycle of raised ICP and
reduced CBF. Cerebral hypoperfusion is found in most cases
where the person has sustained a severe head injury and has a
Glasgow coma scale (GCS) score of less than 8.
The hyperaemic phase Improved CBF is the hallmark of the
hyperaemic phase, and is due to somewhat improved
autoregulatory mechanisms. The hyperaemic phase can last for
7–10 days post injury, and will occur in up to 30% of braininjured people. While improved CPP and blood ﬂow is a
positive development, other management challenges can still
exist. Alteration in blood–brain barrier permeability and
intracranial inﬂammation can contribute to cerebral oedema.
CLINICAL BOX 11.2
Important formulae relating to cerebral blood
pressure and perfusion
Cardiac output (CO):
CO 5 HR 3 SV
If CO → , then heart rate (HR) and/or stroke volume (SV) need to → in
order to be able to maintain CO (hence we see the tachycardia).
Blood pressure (BP):
BP 5 PVR 3 CO
In order to maintain blood pressure (BP), the person’s CO will → (as
above) and pulmonary vascular resistance (PVR) will also →
(tachycardia may be seen with poor distal perfusion as → PVR causes
vasoconstriction of peripheral vessels).
Mean arterial pressure (MAP):
MAP 5 1/3 pulse pressure 1 dBP
As MAP is a measurement of BP, we are able to see the effect of → BP
(hypotension) on the brain. (dBP 5 diastolic blood pressure.)
Cerebral perfusion pressure (CPP):
CPP 5 MAP 2 ICP
CPP is reliant on a balance of MAP (systemic BP) and ICP. If MAP is →
(due to → BP) and ICP is →, then autoregulatory mechanisms will try to
→BP and HR in order to improve CO.
This autoregulatory mechanism has a small window of time before it
becomes inactive. It will not work below a CPP of 50 mmHg.
As MAP and BP both → , CPP can only follow this trend. ICP → further,
and systemic BP is not able to generate an MAP that is able to
overcome the ICP and perfuse the brain. As a result of the poor
perfusion, neurons die from hypoxia.
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C H A P T E R 1 1 N E U R O T R A U M A 209
This oedema may be due to vasospasm caused by intracranial
inflammation, or by catecholamine infusion that has been
used to promote and maintain CPPs during the cerebral
hypoperfusion phase.
The vasospastic phase The vasospastic phase is characterised
by cerebral hypoperfusion due to arterial vasospasm, impaired
autoregulation and metabolic dysfunction. Typically, this
pattern of ischaemia is seen in individuals with severe primary
and secondary brain injury and accounts for 10–15% of
injuries. Vasospastic-induced reduction to CBF may persist for
this group.
Excitotoxicity Following TBI, excessive extracellular cerebral
concentrations of excitatory amino acids (EAA), such as
glutamate, develop. In the central nervous system (CNS),
glutamate is the primary excitatory neurotransmitter. However,
excessive levels of glutamate can alter cell permeability and
result in the release of toxic chemicals—excitotoxicity.
Glutamate reacts with sodium and calcium channels, leading to
an inﬂux of these cations. Calcium enters damaged neurons and
causes the axon to swell and burst. Excessive calcium
concentration also activates proteases, such as calpains, which
are especially damaging to nerve cells.
Two important glutamate receptor subtypes are signifcantly
involved in excitotoxic responses. These glutamatergic receptors
are named according to the agonist substances that activate
them: alpha-amino-3-hydroxyl-5-methyl-4-isoxazole-propionic
acid (AMPA) and N-methyl-d-aspartic acid (NMDA). Changes
to the function of both receptor types have been identifed
following modelled TBI studies.
AMPA receptor changes post TBI Post TBI, cells become
more permeable to calcium, a positively charged ion (Ca21).
The increased intracellular concentration of calcium leads to
a loss of cellular function and integrity. The cell membrane can
no longer regulate the inﬂux of calcium, and the cell becomes
overstimulated and swollen due to the increased concentration
of calcium.
NMDA receptor changes post TBI When nitric oxide binds
with intracellular NMDA receptors, a deadly inﬂux of calcium
occurs into the cell. The degree and reactivity of nitric oxide is
very dependent on the activity of the NMDA receptors. Nitric
oxide is more reactive when the NMDA receptor is very active.
With the increased concentration of intracellular calcium,
the cell will relocate some of this calcium to its mitochondria in
an attempt to restore normal calcium concentrations.
Once inside the mitochondria, the increased concentration
of calcium increases the production of reactive oxygen species,
including superoxide anion. This leads to fatal cellular changes,
including lipid peroxidation, a process in which cell membranes
are irreversibly damaged and DNA fragmentation occurs.
CLINICAL MANIFESTATIONS
An individual with TBI can present in various ways. Some
factors that may influence the clinical presentation include
the force and mechanism of the injury, the developmental age
of the skull, and the friability and structure of the vasculature.
A person may initially present with no symptoms but deteriorate
into unconsciousness, or they may become confused and
manifestly neurologically impaired.
Severe TBI is a leading cause of long-term disability in
developed countries, particularly in young adults. Examples of
long-term disability include motor and sensory impairment,
intellectual and cognitive dysfunction, and memory impairment.
The financial, social and emotional costs of TBI care are
enormous. Depression, mood anxieties and psychiatric disorders
can result from TBI, and can hinder recovery, aﬀect relationships
and reduce a person’s quality of life. Depression is a frequent
consequence of TBI, with severe depression more likely in those
people in whom mood and anxiety disorders were present
before the injury. Major depression is associated with reductions
in memory and the inability to perform tasks independently.
Children who have sustained TBI are more likely to have
cognitive and behavioural impairment, especially if support post
injury is poor.
CLINICAL DIAGNOSIS AND MANAGEMENT
L E A R N I N G O B J E C T I V E 3
Outline the clinical diagnosis and current management for traumatic
brain injury.
Diagnosis Concussion and the duration of concussion are
markers for the severity of neurotrauma. Episodes of concussion
and a brief loss of consciousness (, 30 minutes) occur in 60%
of people who have sustained TBI. TBI cases associated with an
intracranial injury (haemorrhage, haematoma) have a higher
mortality rate compared to TBI cases without intracranial injury.
When evaluating an individual with TBI, comprehensive
neurological examination is essential. Assessing and monitoring
a person’s vital signs are essential tools used to ascertain the
person’s current level of neurological function and the potential
for deterioration. Basic vital signs assessments include the GCS
score, heart and respiratory rate and rhythm, blood pressure,
pupil response and motor/sensory response.
The GCS is a quick and easy tool for assessing the severity
of TBI in the pre-hospital and hospital environment. Individuals
are assessed in three areas: eye (E) opening, motor (M) and
verbal (V) response (see Table 11.1). With reference to TBI, a
person with a score between 13 and 15 is classifed as having
a mild TBI. A score of between 9 and 12 may indicate a moderate
TBI. With a score of 8 or less, a severe TBI is indicated. The
lowest score is 3 (E 5 1; V 5 1; M 5 1). The value of the score
is dependent on the absence of systemic alterations, such as
hypotension, hypoxia, hypothermia and hypoglycaemia, as well
as drugs that aﬀect the CNS, such as benzodiazepines and
alcohol. A slightly varied GCS is used for infants (see
Table 11.1). The GCS gives a prognosis for survival rather than
for functional outcome.
Post-traumatic amnesia Post-traumatic amnesia (PTA) refers
to the inability of the brain to form and retain new continuous
day-to-day memory post injury. The duration of PTA is the best
indicator of the extent of cognitive dysfunction following TBI.
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210 P A R T 3 N E R V O U S S Y S T E M P A T H O P H Y S I O L O G Y
Table 11.1 Glasgow coma scale (GCS) for adults and infants
Adults
Eye opening response (E) Best verbal response (V) Best motor response (M)
4 Spontaneously 5 Oriented 6 Obeys command
3 To verbal command 4 Confused 5 Localises to pain
2 To pain 3 Inappropriate words 4 Withdraws to pain
1 Nil 2 Incomprehensible sounds 3 Abnormal ﬂexion to pain
1 Nil 2 Abnormal extension to pain
1 Nil
Infants
Eye opening response (E) Best verbal response Best motor response (M)
4 Spontaneously 5 Coos or babbles 6 Spontaneous or purposeful
3 To speech 4 Irritable 5 Localises to pain
2 To pain 3 Cries to pain 4 Withdraws to pain
1 Nil 2 Moans to pain 3 Abnormal ﬂexion to pain
1 No verbal response 2 Abnormal extension to pain
1 Nil
In Australia, the most common means of assessing PTA is the
Westmead scale (developed by a group at the Westmead Hospital
in Sydney). During hospital assessment and management,
assessment of PTA is often used in conjunction with the GCS in
determining the degree of DAI and TBI severity. Mild TBI cases
are characterised as having a GCS score of 12–15, and a PTA of
less than 24 hours. Moderate cases of TBI are defned as having
a GCS score of 9–11, and a PTA of 1–7 days in duration. Severe
TBI cases are defned as a GCS score of 3–8, and a PTA lasting
more than 4 weeks in duration.
Classifcation of neurotrauma severity
Neurotrauma severity is classifed as follows:
Minimal
• No loss of consciousness, and
• GCS score of 15, and
• Normal alertness and memory, and
• No neurological defcit, and
• No palpable depressed fracture or other sign of skull
fracture.
Mild
• Brief (, 5 minutes) loss of consciousness, or
• Amnesia for the event, or
• GCS score of 14, or
• Impaired alertness or memory, and
• No palpable depressed fracture or other sign of skull
fracture.
Moderate or potentially severe
• Prolonged (. 5 minutes) loss of consciousness, or
• Persistent GCS score of , 14, or
• Focal neurological defcit, or
• Post-traumatic seizure, or
• Intracranial lesion on computed tomographic (CT) scan, or
• Palpable depressed skull fracture.
The assessment of pulse pressure (systolic minus diastolic
blood pressure; see Clinical Box 9.3) is important, as widening
pulse pressure can be a sign of increasing ICP. Pupillary response
can provide insight into some cranial nerve function, and other
cranial nerves can be assessed using various techniques to elicit
reflexes. Other neurological assessments include motor
assessments that test strength and symmetry in both arms and legs.
ICP monitoring devices can be inserted surgically, and this
guides decision-making for interventions and management
plans. Depending on the person’s age and whether their cranial
sutures have closed, normal ICP is 1–10 mmHg. ICP exceeding
15 mmHg represents mild intracranial hypertension, above
20 mmHg is moderately high, and above 40 mmHg is severe. If
a person is sedated and chemically paralysed, conventional
neurological assessments such as the GCS are worthless, yet
ICP monitoring will still provide an indication of CPP and
enable the informed manipulation of interventions to achieve
the most benefcial outcomes.
Other investigations to quantify the extent of a TBI may
include imaging techniques such as CT, X-ray and magnetic
resonance imaging (MRI). Diagnostic imaging permits
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C H A P T E R 1 1 N E U R O T R A U M A 211
assessment of bone, soft tissue and the formation of collections
such as haematoma. Other important evaluations include the
possibility of a brain structure having shifted from midline.
These imaging techniques are also benefcial to monitor the
progression or resolution of trauma on the contents of the cranial
vault. CT and MRI are expensive investigations and may not be
used for all people presenting with head injury. Minor injury
may be assessed with plain skull flms. The mechanism of injury
and clinical presentation will inform the team as to whether
further, more expensive, invasive investigations are required.
Electroencephalography (EEG) may be used to determine
depth of unconsciousness, and predict survival or functional
outcomes following TBI. EEG measures the electrical activity
of the brain. Cerebral perfusion and metabolic activity to
specifc brain areas can be inferred. The beneft of EEG is
improved when used in conjunction with other imaging
techniques and assessment data. EEG can also be useful in
tracking progress to recovery when comparing initial results to
those obtained during rehabilitation.
Other monitoring techniques employed to assess an
individual with TBI may include:
• brain tissue oxygenation (PbrO2; can be achieved with some
ICP catheters)—brain oxygenation can often detect evolving
injury in at-risk tissue
• transcranial Doppler ultrasound (TCD)—another technique
benefcial for its non-invasive capacity to measure ﬂow
velocities in basal cerebral arteries, providing information
about CBF and vasospasm
• cerebral microdialysis—enables assessment of the
extracellular environment surrounding at-risk tissue; this
technique enables evaluation of brain ischaemia markers,
including glutamate, lactate, glucose and glycerol.
Management The management of TBI is dictated by the
severity and expectation of recovery. Principles of management
are focused on stabilising the individual and preventing
secondary neuronal injury. Priorities of care include prevention
of hypoxia and hypotension.
Airway management Individuals with severe TBI (GCS score
# 8) and people with ventilatory compromise should be intubated
and ventilated to maintain optimal oxygenation. The possibility of
spinal cord injury (especially cervical spine) should also be
considered. Ventilation should be titrated to maintain oxygenation
and prevent hypocapnoea. Sedation and chemical paralysis
(neuromuscular blockade) may be necessary to reduce ventilator
dysynchrony and agitation; however, it interferes with neurological
assessment and, if undertaken for long periods, is associated with
complications such as reduced CBF and myopathy.
Blood pressure management Fluid volume management is
important, the goal of which is to maintain adequate hydration
and prevent dehydration or ﬂuid overload, which can exacerbate
the risk of poor outcomes. Beta-blockers may be necessary to
control excessive sympathetic hyperactivity as a result of
cerebral oedema. Vasodilators may be used, but questions remain
about their safety in relation to their potential eﬀect on ICP.
Management of intracranial hypertension Brain oedema can
be managed with the use of osmotic diuretics, such as mannitol,
or loop diuretics, such as frusemide. Reducing cerebral oedema
is important in order to promote adequate CBF. Increasing the
head of the bed by 15–20 degrees is very benefcial in reducing
ICP, but may not be possible for individuals with other
signifcant orthopaedic trauma. Thermoregulation is important,
and fever should be aggressively treated because of its inﬂuence
on metabolic demand. Induced hypothermia may be used to
reduce increased ICP and metabolic demand. However, it is
generally used judiciously because it can also be associated
with significant complications, such as coagulopathy,
immunosuppression and skin necrosis. Anticonvulsant therapy
may be necessary to reduce seizure activity, providing a
beneficial effect on the development of ICP. Surgical
interventions, such as decompressive craniotomy or the
placement of intraventricular drains, may also be necessary in
the control and management of intracranial hypertension.
Interventions to reduce the likelihood of the Valsalva
manoeuvre, such as the administration of stool softeners,
adequate ﬂuid balance and increased fbre, will assist in reducing
strain during defecation. Codeine is benefcial in reducing the
risk of excessive coughing, which is linked to increased
intrathoracic pressures and a subsequent raising of ICP.
Antiemetics should be provided to reduce emesis. It is also
important to remember the benefcial eﬀects of therapeutic
communication, such as an explanation of care to the aﬀected
individual and their loved ones, which can reduce anxietyrelated increased sympathetic nervous system stimulation.
SPINAL CORD INJURY
Spinal cord injury can result in devastating disability. It can
aﬀect people of any age, culture and socioeconomic status,
although there is an inverse relationship between spinal cord
injury and education level.
EPIDEMIOLOGY
There are currently more than 15000 people in Australia with spinal
cord injury. In 2014–15, 238 people were admitted to Australian
hospitals with a principal diagnosis of paraplegia or tetraplegia. In
New Zealand, between 80 and 130 people are diagnosed with spinal
cord injury every year. Most spinal cord injuries are a result of
trafc accidents, with falls the next most common cause. Age has a
signifcant inﬂuence on the mechanism of a person’s injury, with
motor vehicle accidents being the most common in the young, and
falls the most common in the older adult population.
AETIOLOGY AND PATHOPHYSIOLOGY
PRIMARY INJURY
The mechanism of the trauma and the severity of insult will
signifcantly inﬂuence clinical outcomes. Cellular responses
L E A R N I N G O B J E C T I V E 4
Outline the pathogenesis of spinal cord injury.
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212 P A R T 3 N E R V O U S S Y S T E M P A T H O P H Y S I O L O G Y
that occur as a result of damage to the spinal cord also contribute
to these outcomes. At the time of the initial injury (the
mechanisms of which are discussed later in this chapter),
damage to the intramedullary blood vessels will result in
haemorrhage. As there is limited space within the vertebral
canal, this haemorrhage may begin to cause compression of the
cord and the surrounding blood vessels. Vasospasm may also
occur and further impede circulation to the central grey matter,
resulting in worsening ischaemia.
SECONDARY INJURY
In any injury, an inﬂammatory process begins (see Chapter 3)
and triggers a series of biochemical events that may cause
further damage. As with the secondary process in TBI, a release
of inflammatory mediators results in the intracellular
accumulation of calcium, eicosanoid production, the release of
oxygen free radicals, and the release of excitatory
neurotransmitters such as glutamate. Energy depletion also
occurs as energy-dependent processes begin to fail due to
ischaemia (see Chapter 1). The subsequent destruction of
neurons results from the loss of membrane integrity and
cytoskeleton disruption. Further inﬂammatory mediators are
released, increasing oedema and contributing to the loss of
spinal cord blood ﬂow. Axonal degeneration may commence,
and demyelination may also exacerbate the initial damage. The
compression of the aﬀected blood vessels, induced as a result of
the swelling and blood in the confned space or the haemostatic
mechanisms from platelet aggregation and fbrin deposition, can
stem haemorrhage into the area. Pressures distal to the vascular
obstruction increases and causes protein loss into the interstitial
space, further increasing the oedema. Figure 11.10 explores the
common clinical manifestations and management of spinal cord
injury.
Spinal shock Within an hour of spinal cord injury, spinal
shock (also known as spinal cord concussion) may develop.
Spinal shock is the transient loss of all reﬂexive and autonomic
function below the level of cord damage. (Spinal shock diﬀers
from neurogenic shock; see Clinical Box 11.3.) It is thought
to result from an extracellular accumulation of potassium,
which interferes with nerve impulse generation. There is
debate regarding the defnitive resolution of spinal shock,
with some clinicians suggesting resolution as the return of
cutaneous reﬂexes, such as the bulbocavernosus reﬂex, while
others identify the end of spinal shock with the return of deep
tendon reflexes. Compounding this situation, there is a
disparity in spinal shock resolution by several weeks, as
bulbocavernosus reﬂexes may return within a few days of
injury, yet deep tendon reﬂexes will not generally return for
several weeks.
Systemic effects of spinal cord injury Depending on the
vertebral level aﬀected in the insult, sympathetic activity may
be lost below the level of injury, resulting in cardiovascular
eﬀects. Blood pressure falls due to both arterial and venous
dilation, and results in reduced systemic vascular resistance and
reduced venous return. The parasympathetic nervous system is
unopposed and causes decreased heart rate, which further
contributes to the decrease in cardiac output.
Respiratory eﬀects can be seen when cervical spine injuries
(especially in the C3–C5 region) occur. If airway management
is not initiated within minutes of the trauma, apnoea will result
in death or severe brain injury. Lower-level spinal injuries may
preserve diaphragmatic innervation, but the intercostal and
abdominal muscles may be aﬀected and cause reduced tidal
volume and hypoventilation.
The loss of thermoregulation below the level of the lesion is
known as poikilothermia. This is defned as the inability to
maintain a core temperature through sweating, shivering,
vasodilation or vasoconstriction. Without intervention, the body
temperature below the level of injury moves towards ambient
temperature. This is particularly dangerous for individuals with
injury above T1.
A male may experience priapism, which generally resolves
quickly and without intervention. Both men and women may
develop urinary retention and paralytic ileus, which are
evidenced by abdominal distension.
CLASSIFICATION OF SPINAL CORD INJURY
L E A R N I N G O B J E C T I V E 5
Identify the common classifcations of spinal cord injury.
Spinal cord injuries are often classifed into complete spinal
cord injury, where all sensorimotor function beneath the level
of injury is lost, and incomplete spinal cord injury, where some
sensorimotor function remains. However, clinicians prefer not
to use the terms ‘complete’ and ‘incomplete’ in isolation,
because these arbitrary classifcations are often difcult to
apply, some function may be recovered with time and
treatment, and the label itself may erode hope for aﬀected
individuals. The American Spinal Injury Association’s (ASIA)
impairment scale is commonly used to grade severity of
sensorimotor loss, and, although it still uses the terms
‘complete’ and ‘incomplete’, it also uses other parameters to
provide an extended assessment and classifcation of sensory
and motor function (see Figure 11.11).
CLINICAL BOX 11.3
Spinal shock versus neurogenic shock
It is imperative to understand the difference between spinal shock and
neurogenic shock. Spinal shock is when reﬂexes are temporarily lost
below the level of spinal cord injury.
Neurogenic shock is when bradycardia and vasodilation occur,
resulting in a profound hypotension. This occurs because of the loss of
sympathetic nervous system innervation below the level of spinal cord
injury and the unopposed parasympathetic nervous system effects on
heart rate. Neurogenic shock can only occur in individuals with injuries
above the level of T6.
Copyright © Pearson Australia (a division of Pearson Australia Group Pty Ltd) 2019— 9781488617676 — Bullock/Principles of Pathophysiology 2e
Bullock, S, & Hales, M 2018, Principles of Pathophysiology EBook, Pearson Education Australia, Melbourne. Available from: ProQuest Ebook Central. [20 March 2021].
Created from utas on 2021-03-20 18:12:08.
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C H A P T E R 1 1 N E U R O T R A U M A 213

Release of inflammatory mediators

results in

Spinal cord injury

Mechanical ventilation	Chest physio therapy
manage

Primary injury

from

Management

Trauma
Compression
results in Ischaemia

Secondary injury

Intracellular accumulation of calcium ions	Oedema results in
More inflammatory mediators

Release of Failure of energydependent processes
Oxygen free Ischaemia
radicals
Glutamate

Loss of function below lesion

interferes with

Ventilatory function Upper limb function Posture/stabilisation Lower limb function

Continence
manages
manages

Other
conditions

Equipment modification	Hand orthoses
manage

Chest or head strap	Physio therapy
manage

Mobilisation devices	Wheel chair
manage

Bowel/
bladder
program

Exercise

reduces

Osteoporosis

Heterotopic
ossification

Pressure areas

Autonomic
dysreflexia

Pressure
area care Hypervigilance
for
Figure 11.10
Clinical snapshot: Spinal cord injury
Copyright © Pearson Australia (a division of Pearson Australia Group Pty Ltd) 2019— 9781488617676 — Bullock/Principles of Pathophysiology 2e
Bullock, S, & Hales, M 2018, Principles of Pathophysiology EBook, Pearson Education Australia, Melbourne. Available from: ProQuest Ebook Central. [20 March 2021].
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214 P A R T 3 N E R V O U S S Y S T E M P A T H O P H Y S I O L O G Y
S3
S2
L5
S1
L5
L4
L3
L2
L1
T12
T11
T10
T9
T8
T7
T6
T5
T4
T3
C4
C3
C2
T2
C5
T1
C6
Palm
S4-5
• Key Sensory
Points
C2
C3
C4
Dorsum
C6
C8
C7
C5
C6
C7
C8
T1
L2
L3
L4
L5
S1
MOTOR
KEY MUSCLES
SENSORY
KEY SENSORY POINTS
Light Touch (LTR) Pin Prick (PPR)
(VAC) Voluntary Anal Contraction
(Yes/No)
Comments (Non-key Muscle? Reason for NT? Pain?):
NEUROLOGICAL
LEVELS
Steps 1-5 for classification
as on reverse
1. SENSORY
2. MOTOR
R L 3. NEUROLOGICAL
LEVEL OF INJURY
(NLI)
4. COMPLETE OR INCOMPLETE?
Incomplete = Any sensory or motor function in S4-5
5. ASIA IMPAIRMENT SCALE (AIS)
(In complete injuries only)
ZONE OF PARTIAL
PRESERVATION
Most caudal level with any innervation
SENSORY
MOTOR
R L
This form may be copied freely but should not be altered without permission from the American Spinal Injury Association. REV 11/15
RIGHT
UER
(Upper Extremity Right)
T2
T3
T4
T5
T6
T7
T8
T9
T10
T11
T12
L1
LER
(Lower Extremity Right)
S2
S3
S4-5
MOTOR
KEY MUSCLES
SENSORY
KEY SENSORY POINTS
Light Touch (LTL) Pin Prick (PPL) LEFT
UEL
(Upper Extremity Left)
T2
T3
T4
T5
T6
T7
T8
T9
T10
T11
T12
L1
LEL
(Lower Extremity Left)
S2
S3
S4-5
Elbow flexors
Wrist extensors
Elbow extensors
Finger flexors
Finger abductors (little finger)
Hip flexors
Knee extensors
Ankle dorsiflexors
Long toe extensors
Ankle plantar flexors
C2
C3
C4
C2
C3
C4
(DAP) Deep Anal Pressure
(Yes/No)
UEL = UEMS TOTAL
(25) (25) (50)
UER +
MOTOR SUBSCORES
MAX
LER + LEL = LEMS TOTAL
MAX (25) (25) (50)
LTR + LTL = LT TOTAL
MAX (56) (56) (112)
SENSORY SUBSCORES
MAX
PPR + PPL = PP TOTAL
(56) (56) (112)
4 = active movement, against some resistance
5 = active movement, against full resistance
5* = normal corrected for pain/disuse
NT = not testable
MOTOR
(SCORING ON REVERSE SIDE)
0 = total paralysis
1 = palpable or visible contraction
2 = active movement, gravity eliminated
3 = active movement, against gravity
RIGHT TOTALS
(MAXIMUM)
C5
C6
C7
C8
T1
L2
L3
L4
L5
S1
LEFT TOTALS
(MAXIMUM)
SENSORY
(SCORING ON REVERSE SIDE)
0 = absent
1= altered
2 = normal
NT = not testable
INTERNATIONAL STANDARDS FOR NEUROLOGICAL
CLASSIFICATION OF SPINAL CORD INJURY
(ISNCSCI)
Patient Name__________________________________ Date/Time of Exam __________________________
Examiner Name _______________________________ Signature _________________________________
Elbow flexors
Wrist extensors
Elbow extensors
Finger flexors
Finger abductors (little finger)
Hip flexors
Knee extensors
Ankle dorsiflexors
Long toe extensors
Ankle plantar flexors
Figure 11.11
ASIA impairment scale
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C H A P T E R 1 1 N E U R O T R A U M A 215
ASIA Impairment Scale (AIS)
The following order is recommended for determining the classification of
individuals with SCI.
1. Determine sensory levels for right and left sides.
The sensory level is the most caudal, intact dermatome for both pin prick and
light touch sensation.
2. Determine motor levels for right and left sides.
Defined by the lowest key muscle function that has a grade of at least 3 (on
supine testing), providing the key muscle functions represented by segments
above that level are judged to be intact (graded as a 5).
Note: in regions where there is no myotome to test, the motor level is
presumed to be the same as the sensory level, if testable motor function above
that level is also normal.
3. Determine the neurological level of injury (NLI)
This refers to the most caudal segment of the cord with intact sensation and
antigravity (3 or more) muscle function strength, provided that there is normal
(intact) sensory and motor function rostrally respectively.
The NLI is the most cephalad of the sensory and motor levels determined in
steps 1 and 2.
4. Determine whether the injury is Complete or Incomplete.
(i.e. absence or presence of sacral sparing)
If voluntary anal contraction = No AND all S4-5 sensory scores = 0
AND deep anal pressure = No, then injury is Complete.
Otherwise, injury is Incomplete.
5. Determine ASIA Impairment Scale (AIS) Grade:
Is injury Complete? If YES, AIS=A and can record
Is injury Motor Complete? If YES, AIS=B
(No=voluntary anal contraction OR motor function
more than three levels below the motor level on a
given side, if the patient has sensory incomplete
classification)
Are at least half (half or more) of the key muscles below the
neurological level of injury graded 3 or better?
If sensation and motor function is normal in all segments, AIS=E
Note: AIS E is used in follow-up testing when an individual with a documented
SCI has recovered normal function. If at initial testing no deficits are found, the
individual is neurologically intact; the ASIA Impairment Scale does not apply.
AIS=C
NO
NO
NO YES
AIS=D
Movement Root level
Shoulder: Flexion, extension, abduction, adduction, internal C5
and external rotation
Elbow: Supination
Elbow: Pronation C6
Wrist: Flexion
Finger: Flexion at proximal joint, extension. C7
Thumb: Flexion, extension and abduction in plane of thumb
Finger: Flexion at MCP joint C8
Thumb: Opposition, adduction and abduction perpendicular
to palm

Finger: Abduction of the index finger	T1
Hip: Adduction	L2
Hip: External rotation	L3
Hip: Extension, abduction, internal rotation Knee: Flexion Ankle: Inversion and eversion Toe: MP and IP extension Hallux and Toe: DIP and PIP flexion and abduction	L4
L5
Hallux: Adduction	S1

A = Complete. No sensory or motor function is preserved in
the sacral segments S4-5.
B = Sensory Incomplete. Sensory but not motor function
is preserved below the neurological level and includes the sacral
segments S4-5 (light touch or pin prick at S4-5 or deep anal
pressure) AND no motor function is preserved more than three
levels below the motor level on either side of the body.
C = Motor Incomplete. Motor function is preserved at the
most caudal sacral segments for voluntary anal contraction (VAC)
OR the patient meets the criteria for sensory incomplete status
(sensory function preserved at the most caudal sacral segments
(S4-S5) by LT, PP or DAP), and has some sparing of motor
function more than three levels below the ipsilateral motor level
on either side of the body.
(This includes key or non-key muscle functions to determine
motor incomplete status.) For AIS C – less than half of key
muscle functions below the single NLI have a muscle grade ≥ 3.
D = Motor Incomplete. Motor incomplete status as defined
above, with at least half (half or more) of key muscle functions
below the single NLI having a muscle grade ≥ 3.
E = Normal. If sensation and motor function as tested with
the ISNCSCI are graded as normal in all segments, and the
patient had prior deficits, then the AIS grade is E. Someone
without an initial SCI does not receive an AIS grade.
Using ND: To document the sensory, motor and NLI levels,
the ASIA Impairment Scale grade, and/or the zone of partial
preservation (ZPP) when they are unable to be determined
based on the examination results.
INTERNATIONAL STANDARDS FOR NEUROLOGICAL
CLASSIFICATION OF SPINAL CORD INJURY
ZPP (lowest dermatome or myotome
on each side with some preservation)
Muscle Function Grading
0 = total paralysis
1 = palpable or visible contraction
2 = active movement, full range of motion (ROM) with gravity eliminated
3 = active movement, full ROM against gravity
4 = active movement, full ROM against gravity and moderate resistance in a muscle
specific position
5 = (normal) active movement, full ROM against gravity and full resistance in a
functional muscle position expected from an otherwise unimpaired person
5* = (normal) active movement, full ROM against gravity and sufficient resistance to
be considered normal if identified inhibiting factors (i.e. pain, disuse) were not present
NT = not testable (i.e. due to immobilization, severe pain such that the patient
cannot be graded, amputation of limb, or contracture of > 50% of the normal ROM)
Sensory Grading
0 = Absent
1 = Altered, either decreased/impaired sensation or hypersensitivity
2 = Normal
NT = Not testable
When to Test Non-Key Muscles:
more than 3 levels below the motor level on each side should be tested to
most accurately classify the injury (dierentiate between AIS B and C).
Figure 11.11
ASIA impairment scale (continued)
Source: American Spinal Injury Association: International Standards for Neurological Classifcation of Spinal Cord Injury, revised 2011; Atlanta, GA. Reprinted 2011.
Copyright © Pearson Australia (a division of Pearson Australia Group Pty Ltd) 2019— 9781488617676 — Bullock/Principles of Pathophysiology 2e
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216 P A R T 3 N E R V O U S S Y S T E M P A T H O P H Y S I O L O G Y
Spinal injuries are commonly classifed according to three
criteria: the vertebral level, the degree and the mechanism
aﬀected.
Vertebral level The classifcation based on ‘vertebral level’
refers to the anatomical location, occurring within the cervical,
thoracic, lumbar or sacral vertebrae (see Figure 11.12). The
higher the injury, the greater the level of disability experienced.
It is important to understand that there is a slight diﬀerence
between motor and sensory innervation. So, depending on the
vertebral level and degree of injury, the person may experience
a motor impairment, but still have some sensation above
that level.
In relation to motor function, injuries including C3–C5 will
dictate the degree of ventilatory support required by the injured
individual. The nerves in this region are responsible of the
innervation of the diaphragm, and trauma to this area can result
in significant reliance on mechanical ventilation. Injuries
including C5–C7 will interfere with arm movement and
strength, as nerves in this region are responsible for innervating
elbow and wrist movement. Injuries to the thoracic spine will
generally inﬂuence the ability to maintain posture and support
breathing, as intercostal innervation arises from nerves in this
area. Lumbar spine injuries can inﬂuence hip, knee and ankle
movement. Lower limb strength, and bowel and bladder function
are also controlled by nerves in the lumbosacral regions.
Degree The classifcation based on ‘degree’ refers to the
terms ‘complete’ and ‘incomplete’. As previously discussed,
these two terms are only of some benefit when further
clarifcation can be made. The defnition of complete loss of all
movement and sensation beneath the level of injury is dependent
on time. It takes several weeks before swelling (known as spinal
shock; discussed earlier in this chapter) reduces. When this
occurs, some function above the initial level of injury may begin
to return.
Mechanism The classification based on ‘mechanism’ is
important, and may inform to some extent the clinical outcomes
and recovery expectations. Common mechanisms that result in
spinal cord injury are flexion, flexion–extension, rotation,
compression and hyperextension (see Figure 11.13).
Flexion and ﬂexion–extension are commonly caused by
acceleration–deceleration situations, such as a car accident.
Rotation injuries occur commonly in the cervical spine, and
may result from diving accidents. Compression can occur as a
Cervical

Thoracic
Lumbar
Sacral
12
Anterior
C2
C3
Trigeminal
nerve
C4
T2
T3
T4
T5
T6
T7
T9
C5
T1
T8
T10
T11
T12
L1
S2
L1 S3
L2
L3
L4
L5
S1
C6
C6
C7 C8
T1
T2

C2
C3
C4
T4
T5
T6
T7
T9
T10
T12
T2
T11
T3
T8

S2
S3
S1

C4
L1
L2
L3
L5
S1
C6
C7
C8
T1
T2
C5
L4
L1
L2
L4
S4
S5
Posterior
L3
C4
C5
Figure 11.12
Classifcation of spinal cord injury
based on ‘vertebral level’,
demonstrating areas of muscular
innervation related to spinal nerve
Copyright © Pearson Australia (a division of Pearson Australia Group Pty Ltd) 2019— 9781488617676 — Bullock/Principles of Pathophysiology 2e
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C H A P T E R 1 1 N E U R O T R A U M A 217
result of the primary injury, but may also be caused by secondary
swelling, ruptured intervertebral discs, and pressure from a
tumour, or as a result of chronic disease, such as a spondylopathy.
Hyperextension may occur as a result of falling forward and
striking the head, face or chin on a step or other structure, which
allows the occipital region of the skull to move forcefully
towards the back.
Other descriptive terms used in the classification of
spinal cord injury Other common terminology used in the
description of spinal cord injury includes laceration, transection,
contusion, compression, distraction and concussion.
Laceration The spinal cord may be partly damaged by a rip
or tear from vertebral fractures that have become displaced in
the trauma, or by external causes such as a knife or a bullet. A
laceration will result in permanent injury, and can be associated
with oedema and further cord compression.
Transection The true defnition of ‘transection’ is when the
spinal cord is completely severed. This may occur as a result
of penetrating trauma or from fragments of fractured vertebrae.
Complete transection is less common. Clinicians may also use
the terminology ‘partial transection’ when they are referring to a
large laceration (e.g. half the spinal cord).
Contusion Spinal contusion can be caused by falls or acceleration–deceleration injuries. The vessels supplying the spinal
cord rupture and a haemorrhage occurs in the spinal cord and
the meninges.
Compression Spinal compression occurs as a result of crushing or distorting the spinal cord within the vertebral canal. Cord
compression can occur as a result of the primary injury from
fragments of fractured vertebrae, or ruptured or dislocated intervertebral disc, and from any number of other non-trauma causes,
such as an abscess or a tumour. Cord compression also often
occurs as a secondary injury as a result of the inﬂammatory process and haemorrhage from the primary trauma.
Distraction Distraction is the process of pulling the spinal
cord apart. This often occurs as a result of a lap seatbelt and
acceleration–deceleration incidents, when motion thrusts the top
and bottom half of the body forward with excessive force, but a
portion of the thoracolumbar vertebrae is restrained by the lap
seatbelt, resulting in a stretching of the soft tissue structures and
spinal cord in these areas.
Concussion Spinal concussion can be caused by a violent blow.
There may or may not be vertebral damage; however, there is
no apparent damage to the cord. Neurologically there are motor and sensory defcits and spinal shock may occur; however,
the defcits subside in a very short period of time (maybe even
hours). Most often, there are no residual neurological defcits
once recovered.
Complete spinal cord injury Although less common,
complete spinal cord injury results in a total absence of function
beneath the level of the injury, in the absence of spinal shock. In
this type of injury, there is little or no prospect of regaining
function (without signifcant advances in current research).
Complete spinal cord injury tends to occur more in the thoracic
and lumbar regions, as the relative dimension of the vertebral
foramen (the canal for the spinal cord) to the spinal cord width
is smaller. As seen in Figure 11.14, the vertebral canal varies in
A B
C D
Figure 11.13
Common mechanisms of spinal injury
(A) Flexion and ﬂexion–extension injury.
(B) Rotation injury.
(C) Compression injury.
(D) Hyperextension injury.
Source: Concept adapted from Ebnezer
& John (2003), Essentials of orthopaedics for
physiotherapists. New Dehli, India: Jaypee Brothers
Medical Publishers, Figure 14.5, p. 176.
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218 P A R T 3 N E R V O U S S Y S T E M P A T H O P H Y S I O L O G Y
size, depending on the vertebral region. A small canal aﬀords
less area for mechanical stress and post-injury swelling, and can
affect the extent of the damage. Chronic disease can also
inﬂuence the size of the canal. Vertebral canal stenosis can cause
or contribute to spinal cord injury, as can dislocation of the
intervertebral discs.
CLINICAL MANIFESTATIONS
As previously discussed, complete spinal injury will result in
the loss of all sensory and motor function beneath the level of
the injury. Along with the symmetrical sensorimotor defcits
dictated by the aﬀected region or vertebral level, systemic
eﬀects may also occur (as discussed above).
INCOMPLETE SPINAL CORD INJURY
It is more common for individuals to experience an incomplete
spinal cord injury. Once spinal shock has reduced, the function
regained will be dependent on the area of cord damaged. The
spinal cord is arranged into both ascending and descending
tracts that are located in diﬀerent regions within the spinal cord
(see Figure 11.15). The affected regions will influence the
severity of the motor and sensory defcit, and each person will
experience gain or retain diﬀerent function.
The ascending tracts are sensory tracts, and tend to have the
prefx spino- and a sufx pertaining to where the fbres frst
synapse. An example of this is the anterior spinocerebellar
tract. This tract is located anteriorly and synapses in the
cerebellum. Sensory tracts transmit sensory information from
proprioceptors, and cutaneous and visceral receptors.
Information such as temperature, pressure, pain and the relative
location of body parts is relayed through these fbres.
The descending tracts are motor tracts and tend to have a
prefx that denotes the brain region from which the fbres begin
and the suffix -spinal. An example of this is the anterior
corticospinal tract. This tract is also located anteriorly and
carries information from the cerebral cortex. These tracts control
visceral and somatic motor activity.
L E A R N I N G O B J E C T I V E 6
Discuss the characteristics of common spinal cord syndromes.
Several diﬀerent types of injuries can occur. Some more
common injuries can be classifed as anterior cord syndrome,
central cord syndrome, Brown-Séquard syndrome and cauda
equina syndrome.
Anterior cord syndrome Anterior cord syndrome is
commonly caused by mechanical events, such as trauma or disc
herniation, but can also be caused by vascular events. The front
of the spinal cord is aﬀected and, therefore, the individual will
often lose distal motor function and some sensory function,
such as pain and temperature sensation (see Figure 11.16).
Unconscious proprioception (proprioception associated with
posture) is also lost. Individuals with anterior cord syndrome
may retain the sense of vibration, pressure and light touch. They
will usually retain conscious proprioception (proprioception of
limbs, and joint position and range).

A A A D D D D
A	D spino	orsal columns o reticular tract
spino
spino
spin
l spino

A
D
D D

A A D D A	spin
A D D
D D A D
al

Ascending tracts
(sensory)
Descending tracts
(motor)
Posterior cerebellar tract Lateral thalamic tract Anterior cerebellar tract Anterior thalamic tract and lateraLateral cortico tract spinal
Anterior reticulo tract spinal
Anterior cortico tract spinal
Lateral reticulo tract spinal
Tecto tract spinal
Lateral reticulo tract spinal
Vestibulo tract Figure 11.15
Ascending and
descending spinal cord
tracts
The blue areas of this
diagram denote
ascending tracts, and
the red areas denote
descending tracts.
Figure 11.14 A B C
Vertebral foramen of various
vertebrae
(A) Cervical vertebra.
(B) Thoracic vertebra.
(C) Lumbar vertebra.
Source: © Sciencopia.
Copyright © Pearson Australia (a division of Pearson Australia Group Pty Ltd) 2019— 9781488617676 — Bullock/Principles of Pathophysiology 2e
Bullock, S, & Hales, M 2018, Principles of Pathophysiology EBook, Pearson Education Australia, Melbourne. Available from: ProQuest Ebook Central. [20 March 2021].
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C H A P T E R 1 1 N E U R O T R A U M A 219
Central cord syndrome Central cord syndrome is commonly
caused by hyperextension in the cervical spine, causing contusion
to the centre of the spinal cord. Depending on the size of the lesion,
the individual will generally experience signifcant upper extremity
weakness and even greater distal motor loss. Temperature and pain
sensation is generally lost, yet proprioception and sensation of
vibration is generally preserved (see Figure 11.17). If the damage
is severe, the aﬀected person may have ﬂaccid paralysis in the upper
limbs and spastic paralysis in the lower limbs. The individual will
commonly retain perianal sensation and preserved voluntary anal
tone, resulting in faecal continence.
Brown-Séquard syndrome Brown-Séquard syndrome is
commonly caused by penetrating injuries. Transection occurs
across half a section of the spinal cord (hemi-section). There is
complete loss of motor function on the aﬀected side (ipsilateral)
A
A
A
A
D
D
D
D
AA

D	DAD
D D

AA
D
D DA D D
Variable
loss of motor function
Variable
loss of temperature, pain sensation
and unconscious proprioception
Conscious
proprioception
preserved
Anterior cord lesion
Most often cervical
Figure 11.16
Anterior cord syndrome
A
A
D
D
D
D D
A
A
D
D
D D
Temperature and pain
sensation generally lost
Central cord lesion
Proprioception and vibration
generally preserved
Worse upper
extremity
weakness
(if severe—
flaccid
paralysis)
Most often cervical
Greater distal
motor loss
(If severe—
spastic paralysis in
lower limbs)
D
A A
A
D
D
A
D
A
D
A
Figure 11.17
Central cord syndrome
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220 P A R T 3 N E R V O U S S Y S T E M P A T H O P H Y S I O L O G Y
but not on the unaﬀected side (contralateral) (see Figure 11.18).
Proprioception is lost on the ipsilateral side but not the contralateral
side, and other sensory activities, such as pain and temperature, are
lost on the contralateral side but not on the ipsilateral side.
Cauda equina syndrome Cauda equina syndrome is
commonly caused by compression or trauma affecting the
lumbosacral nerve roots beneath the conus medullaris (beneath
the spinal cord). There are various causes of cauda equina
syndrome, including trauma, tumour or, most commonly,
intervertebral disc herniation or rupture (see Figure 11.19).
Neurological defcit may be either unilateral or bilateral, but is
most often unilateral and asymmetric. Motor defcits include
lower extremity weakness and reduced or absent reflexes.
A
A
A
A
D
D
D
D
A
A
D
D
A
D
D D
AA
D
D DA D D
Contralateral
Loss of
pain and
temperature
sensation
Ipsilateral
Ipsilateral
Loss of motor
function
Loss of
proprioception
Figure 11.18 Transection across half of spinal cord
Brown-Séquard syndrome
Nerve roots
(cauda equina)
in dural sac
Annulus fibrosus
Nucleus pulposus
Lumbar vertebrae
Spinal nerve root
Compressed
nerve roots
within narrowed
spinal canal
Lumbar disc
prolapse
Inverterbral
disc
Variable
deficits
sensorimotor
Often bladder and bowel
dysfunction from
deficits
sensorimotor
Figure 11.19
Cauda equina syndrome
Source: © Sciencopia.
Copyright © Pearson Australia (a division of Pearson Australia Group Pty Ltd) 2019— 9781488617676 — Bullock/Principles of Pathophysiology 2e
Bullock, S, & Hales, M 2018, Principles of Pathophysiology EBook, Pearson Education Australia, Melbourne. Available from: ProQuest Ebook Central. [20 March 2021].
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C H A P T E R 1 1 N E U R O T R A U M A 221
Urinary incontinence and constipation or urinary retention are
common, and result from both motor and sensory deficits.
Lower back and sciatic pain are common.
DIAGNOSIS AND MANAGEMENT
L E A R N I N G O B J E C T I V E 7
Explore the diagnosis and management of spinal cord injury.
Initial assessment of neurological function will generally have
occurred pre-hospital and, most often, spinal immobilisation
will have been applied. Basic life support measures may need to
be initiated. If the injury is high in the cervical region, airway
support will be required and manual ventilation may also be
necessary. Circulatory support may be required for either
neurogenic or hypovolaemic shock. Spinal cord injuries are
often experienced in the context of multitrauma, so circulatory
and orthopaedic stabilisation is necessary before transport.
DIAGNOSIS
In the emergency department, a full primary and secondary
assessment should be undertaken, followed by a further, more
comprehensive neurological assessment. Motor function is
evaluated through muscle strength and rectal tone. Limb muscle
strength is graded on a six-point scale, with a score of 0 the
most severe loss and a score of 5 representing no loss of motor
function:
0—Total paralysis, no movement
1—Slight contraction assessed visually or by palpation (but
no movement)
2—Active movement (no movement against gravity)
3—Active movement (against gravity)
4—Active movement (against some resistance)
5—Active movement (against strong resistance)
Sensory assessment should be evaluated using light touch
and pin-prick responses over dermatomes on both sides of the
bodies. Dermatomes are areas of skin supplied by a spinal
nerve; when assessed, they provide an accurate map of sensory
function and defcit (see Figure 11.20).
Reﬂexes should also be tested. Serial assessments of motor
and sensory function can provide an insight into the progression
of neurological damage or recovery. Figure 11.21 demonstrates
the spinal nerves associated with some reﬂexes that can be
tested. Reﬂexes are graded on a fve-point system.
0—No response
11—Sluggish
21—Normal
31—Brisk
41—Clonus
Imaging studies are important in the diagnosis and
quantifcation of spinal cord injury severity. There is debate
regarding the best method of spinal cord assessment that is
Anterior
C2
C3
Trigeminal
nerve
C4
T2
T3
T4
T5
T6
T7
T9
C5
T1
T8
T10
T11
T12
L1
S2

S3
L2
L3
L4
L5
S1
C6
C7
C8
T1
T2
C4
C5

C2
C3
C4
T4
T5
T6
T7
T9
T10
T12
T2
T11
T3
T8

S2
S3
S1

C4
L1
L2
L3
L5
S1
C6
C7
C8
T1
T2
C5
L4
L1
L2
L4
S4
S5
Posterior
L3
Figure 11.20
Dermatomes
sufficiently capable of demonstrating injury but does not
contribute to an unnecessary financial burden. Health care
institutions and medical professionals have their own procedures
and protocols to assess spinal cord injury, depending on the
mechanism of injury, the symptomology of the aﬀected individual
and numerous other factors. Depending on the circumstances and
clinical presentation, investigations may include imaging such as
X-ray, CT or even MRI (see Figure 11.22). MRI is far superior to
other imaging techniques for the diagnosis of spinal cord injury.
However, the cost is prohibitive, and the use of the resource is
unnecessary for a signifcant percentage of individuals who
present following minor trauma.
MANAGEMENT
Management of airway, breathing and circulation is the priority
in the treatment of spinal cord injuries. Injuries above C5 may
require airway support, and mechanical ventilation will be
required if hypoventilation or apnoea develops. Intubation is
complicated by the necessity to maintain immobilisation in a
Copyright © Pearson Australia (a division of Pearson Australia Group Pty Ltd) 2019— 9781488617676 — Bullock/Principles of Pathophysiology 2e
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222 P A R T 3 N E R V O U S S Y S T E M P A T H O P H Y S I O L O G Y
Anterior
C2
C3
Trigeminal
nerve
C4
T2
T3
T4
T5
T6
T7
T9
C5
T1
T8
T10
T11
T12
L1
S2

S3
L2
L3
L4
L5
S1
C6
C7
C8
T1
T2
Achilles reflex
(S1 and S2)
Pectoralis reflex (C5–T1)
Pronater
reflex
(C6–C7)
Upper abdominal reflex (T8–T9)
Mid-abdominal reflex (T9–T10)
Lower abdominal reflex (T11–T12)
Quadriceps reflex (L2–L4)
Cremasteric reflex (L1–L2) and
Superficial anal reflex (L1–L2)
Patellar reflex
(L3–L4)
Hamstring reflex (L4–S2)
L1
L2
L3
L5
S2
S3
L4
S1
S4
S5
Posterior
Brachioradialis
reflex (C6–C7)
Adductor reflex (L2–L4)
Plantar reflex (L4–S2)
Bicep reflex
(C5–C6)
C2
C3
C4
T4
T5
T6
T7
T9
T10
T12
T2 C4
T11
S1
C6
C7
C8
T1
T2
C5
T3
T8
L1
L2
L4
L3
Figure 11.21
Spinal nerves and their
associated reﬂexes
Figure 11.22
Comparison of three different imaging modalities on the same individual with C5–C6 subluxation
(A) Neck X-ray.
(B) Multi-detector computed tomography (MDCT scan).
(C) Magnetic resonance imaging (MRI). Note the signifcant beneft of the MRI scan in contrast to the neck X-ray.
Source: Beattie & Choi (2006). © EB Medicine, LLC.
A B C
neutral position, as well as when maxillofacial injuries have
occurred as a result of the original trauma. Circulatory support
may be necessary in the context of neurogenic shock resulting
in hypotension and bradycardia, or from hypovolaemic shock
because of significant blood loss from the trauma. Fluid
resuscitation with colloid or crystalloid solutions, or blood, may
be necessary to establish haemodynamic stability.
Following management of respiratory and cardiovascular
issues, an orthosis or rigid collar can be applied to achieve
immobilisation, or surgical reduction can provide stabilisation
and alignment of vertebrae (see Figure 11.23).
The debate of whether to administer high-dose
corticosteroids has been resolved. For many years,
methylprednisolone was administered post spinal trauma in
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C H A P T E R 1 1 N E U R O T R A U M A 223
order to attenuate neuroinflammatory processes causing
secondary damage, despite limited, quality evidence supporting
the eﬀects. However, recently, literature reviews and further
research indicate that the risks associated with
immunosuppression, metabolic, pulmonary, adrenal and
haematological complications far outweigh the possible limited
and unproven functional gains.
Pain management is essential, especially in individuals with
motor defcits but intact sensation. Narcotic analgesics may be
required initially. Administration of an antiemetic agent is
advisable to reduce the risk of airway compromise or aspiration
from vomiting, especially in the context of the emetic properties
of narcotic therapy. A nasogastric tube should be inserted if the
person is intubated, and it may also be needed in a non-intubated
individual to ensure gastric decompression and to manage
gastric stasis if it develops.
Other medications that may be required include an
anticoagulant to reduce the risk of deep vein thrombosis, and
antibiotics to prevent infection if any open fractures or
lacerations occurred as a result of the initial injury.
A urinary catheter will probably be required to manage a
neurogenic bladder, but it will also be benefcial to monitor
accurate urine output and reduce the risk of movement that may
have been necessary to assist with urinary elimination.
Pressure area care is essential to reduce the risk of decubitus
ulcers, which can form very rapidly during immobilisation.
Removal of the transport backboard should be undertaken as
soon as possible. Pressure-relieving equipment should be used,
and care should be taken to protect skin integrity. This task
becomes easier following spinal stabilisation.
Spinal cord injury may result in significant disability
requiring months in hospital and even more time in rehabilitation.
Psychological support is paramount to ensuring progress, and
assistance from other people with spinal cord injuries may help
the person embrace the potential of succeeding in life after a
spinal cord injury.
COMPLICATIONS OF SPINAL CORD INJURY
L E A R N I N G O B J E C T I V E 8
Examine the common complications associated with spinal
cord injury.
Even after the acute trauma has been managed and rehabilitation
has begun, many issues may complicate the health of a person
with a spinal cord injury. Examples include: the need for
ventilatory support; the preservation of skin integrity; the
management of urinary and faecal continence; the prevention of
heterotopic ossifcation, osteoporosis and spasticity; and, for
individuals with injuries at T6 or above, the assessment and
management of autonomic dysreﬂexia.
VENTILATORY SUPPORT
As previously mentioned, individuals with high cervical
injuries may be left with the need for permanent ventilatory
support from a mechanical ventilator. Not long after the initial
injury, a tracheostomy will be surgically fashioned to facilitate
a more appropriate and efcient method of ventilation. If a fully
ventilated person is to be discharged home, signifcant support
and education will be required. Carers will need to be taught
about how to care for a ventilated individual, how to reduce the
risk of barotrauma, how to suction the affected person’s
oropharynx and trachea to clear secretions, how to assess for
the development of infections and, most importantly, how to
ensure that adequate ventilation is occurring for the apnoeic
individual at all times. A fully ventilator-dependent person will
die in minutes if the ventilator circuit disconnects or becomes
obstructed and there is nobody present to correct the problem.
Figure 11.23
Halo-cervical orthosis
Used to stabilise injury yet permit the
individual to mobilise or begin rehabilitation
earlier, rather than being confned to bed.
The halo can reduce complications
associated with total immobility.
‘Halo ring’ head
section pins are
screwed into skull
Moulded body
cast with padding
liner applied to torso
Metal bars frame a
structure specific to
the individual
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224 P A R T 3 N E R V O U S S Y S T E M P A T H O P H Y S I O L O G Y
Ventilatory-associated pneumonia is a concern for
individuals who are dependent on mechanical ventilation.
Because of the need for artifcial airway placement, respiratory
defences are bypassed. The anatomical barriers of nasal hair and
the nasal turbinates, reﬂexive defences such as the cough, gag
and sneeze reflexes, particle filtration and the mucociliary
transport system are all aﬀected. Pneumonia not only increases
the risk of systemic infection but also the development of
atelectasis, which will further complicate ventilation and
oxygenation. Appropriate hand hygiene, pulmonary hygiene
and maintenance of adequate health will assist in preventing
ventilator-associated pneumonia.
SKIN INTEGRITY
Prolonged immobilisation and insensate areas (i.e. areas without
sensation) signifcantly increase the risk of decubitus ulcers.
However, many interventions can be undertaken to reduce this
risk. It is important to maintain good hygiene, especially in
perineal areas. Individuals will most likely need education to
promote urinary and faecal continence. Techniques should be
employed to reduce the risk of friction when positioning and
turning. Pressure-relieving techniques and devices should be used
to reduce the risk of prolonged immobilisation. It is important that
surfaces and material in contact with insensate areas are ﬂat and
free from buttons, plastic or other material that may apply pressure
and compromise skin integrity. Maintaining adequate nutrition is
also imperative to promote skin integrity and wound healing.
CONTINENCE
Individuals with spinal cord injury can develop neurogenic
bowel and neurogenic bladder.
Neurogenic bowel One of the determining factors for bowel
continence is whether the individual develops a spastic
(reﬂexic) or a ﬂaccid (areﬂexic) bowel. A spastic bowel is when
the gastrointestinal muscles still have tone, and the reﬂex to
and from the spinal cord (beneath the level of injury) enables
peristalsis and anal sphincter tone. This will occur in cervical
or thoracic spine injuries. There may be no sensory perception
of a faecal mass in the anus, but through bowel training and
regular elimination patterns continence can be achieved. A
ﬂaccid bowel results in poor or no gastrointestinal muscle tone.
Injuries to the lumbar or sacral spine will result in an areﬂexic
bowel. Decreased peristalsis and decreased anal sphincter tone
may result in an increased risk of constipation or faecal
incontinence. Bowel management programs can assist to some
degree.
Neurogenic bladder There are several types of bladder
complications from spinal cord injury, and, although they can be
subdivided by cause, spinal cord bladder impairment can be
generally classified as storage failure or voiding failure.
Figure 11.24 demonstrates the causes of urinary continence
impairment in spinal cord injury. The management options for a
neurogenic bladder include intermittent or indwelling
catheterisation, reﬂex voiding and the use of alpha-adrenergic
blockers. Some surgical options include urethral stents,
transurethral sphyncterotomy, bladder augmentation, electrical
stimulation or urinary diversion.
OSTEOPOROSIS
Loss of bone density in an individual with spinal cord injury
occurs as a result of changes in bone metabolism due to
immobilisation and decreased weight bearing. Although both

Urinary continence issues in spinal cord injury

from

Failure to
store

Failure to
empty

External sphincter

Hyperreflexive

Detrusor muscle

Hyperreflexive

Areflexive

Impaired
coordination

C2–S1
lesions

Lumbosacral
lesions

Lesions below
S2

Simultaneous contraction of
detrusor and external sphincter

Lesions above
S1

Overflow
incontinence Obstruction

External sphincter

Figure 11.24
Causes of urinary
continence issues in
spinal cord injury
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C H A P T E R 1 1 N E U R O T R A U M A 225
osteoclast and osteoblast activity increase after spinal cord
injury, osteoclast activity exceeds osteoblast activity. Chronic
increases in the parathyroid hormone occur, and result in further
demineralisation of non-weight-bearing bone. The risk of
osteoporosis can be reduced within weeks of injury through the
use of supported weight-bearing exercises, functional electrical
stimulation, and the administration of bisphosphonate drugs.
Newly injured individuals will benefit greatly from these
prophylactic measures. However, it is not yet possible to
improve bone density in demineralised bone associated with
chronic osteoporosis from spinal cord injury, so the management
of fractures will still be necessary. Osteoporosis is discussed in
detail in Chapter 42.
NEUROGENIC HETEROTOPIC OSSIFICATION
Following spinal cord injury, individuals may develop
heterotopic ossifcation, which is the growth of bone in the
connective tissue near a joint below the level of injury. Although
heterotopic ossifcation can occur anywhere, common sites of
heterotopic ossifcation include the ﬂexor and adductor areas of
the hip, the medial–collateral ligament in the knees, and
sometimes in the shoulders and elbows. The mechanism is not
well understood, but it is known that deposition of calcium
phosphate occurs in aﬀected muscle, which begins to ossify
over time by replacement with hydroxyapatite crystals.
Individuals with heterotopic ossifcation may present with periarticular inﬂammation or a reduced range of motion. Severe
cases may result in ankylosis of peripheral joints. Frequent and
regular passive range-of-motion exercises are the best way to
prevent heterotopic ossification. Treatment may consist of
attempting to block ectopic bone deposition through the
administration of bisphosphonates, which are known to play an
important role in calcium–phosphate metabolism. Surgical
resection of the ossification can result in significant
complications, such as infection, excessive bleeding, potential
postoperative fracture of severely osteoporotic bone, and
recurrence. Surgical resection may beneft individuals whose
ossifcation interferes with positioning to reduce pressure area
or muscle spasm.
SPASTICITY AND MUSCLE SPASMS
Muscle spasms below the level of spinal cord injury occur as a
result of uninhibited spinal reflexes. Motor reflexes from
noxious stimuli, such as stretching, pressure and inﬂammation,
trigger a muscle contraction, which, in an individual with an
intact spine, would be blocked by a descending inhibited signal.
In an individual with spinal cord injury, structural damage to the
cord prevents an inhibitory signal and a spasm occurs. There are
some benefts of muscle spasm, so it is generally not treated
unless it interferes with activities of daily living. Spasms can
also, to a small extent, decrease disuse osteoporosis, because a
limb in spasm applies some stress to the bone, which may retard
osteoclast and stimulate osteoblast activity. In addition, the
muscle contraction occurring in a spasm provides a small
amount of work to the muscle groups involved, which may
reduce the speed of disuse atrophy development.
The presence of spasm and spasticity in an individual with
insensate areas can signify a problem that needs to be found and
rectifed (e.g. infection or malpositioning).
Management options include the use of medications such as
the muscle relaxant baclofen. Baclofen is a gamma-aminobutyric
acid (GABA) derivative that acts on the presynaptic GABA
receptors to inhibit excitatory neurotransmitters (glutamate
and aspartic acid), reducing reflex activity. This drug can
be administered systemically or via an intrathecal pump.
Muscle relaxants such as benzodiazepines may also be used.
Therapeutic botulinum toxin may be used to reduce tone and
spasticity for three to four months. Severe spasticity may
be managed by an aggressive surgical intervention called a
radiofrequency rhizotomy, which destroys the nerve innervating
the aﬀected joints.
AUTONOMIC DYSREFLEXIA
Autonomic dysreﬂexia is a medical emergency that can occur in
individuals with a spinal cord injury at T6 or higher. An
exaggerated and uninhibited autonomic nervous system
response to a noxious stimulus beneath the spinal cord lesion
results in a reﬂex sympathetic outﬂow, causing vasoconstriction.
The profound vasoconstriction causes severe hypertension and
results in a reﬂexive parasympathetic nervous system response
causing bradycardia (see Figure 11.25).
Immediate identification of the noxious stimulus is
imperative. The most common causes of autonomic dysreﬂexia
include irritation or obstruction in the bladder or bowel, a
pressure area or wound infection, or fracture beneath the spinal
cord lesion. Once the cause has been identifed, immediate
interventions to rectify the problem should be undertaken. If the
individual has a urinary catheter, it should be checked for kinks,
obstructions or infections. The catheter may need to be ﬂushed
or replaced, and antibiotics commenced. Faecal impaction can
cause autonomic dysreﬂexia. The use of enemas or manual
evacuation may be necessary to resolve the issue. Checking for
creases, buttons or other materials that could cause pressure
areas is important, and the assessment of skin integrity may
reveal a pressure area. Repositioning and relief from the
causative agent may begin to resolve the situation.
The most critical observation in autonomic dysreﬂexia is
blood pressure. Profound hypertension may exceed a systolic
volume of 250 mmHg and signifcantly increase the risk of
haemorrhage from vessel failure in the brain, kidney or eyes, or
may result in myocardial infarction or seizure. Antihypertensive
drugs may be required immediately, especially if there is some
difculty in isolating the cause. Due to the life-threatening
potential of autonomic dysreﬂexia, prevention is a priority.
Bowel and bladder management programs, appropriate and
frequent pressure area care, and hypervigilence for events or
phenomena that may cause autonomic dysreﬂexia should be
undertaken to ensure that it does not develop.
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226 P A R T 3 N E R V O U S S Y S T E M P A T H O P H Y S I O L O G Y

Noxious stimuli	sensed by
beneath lesion

Nociceptors

relayed by

Spinothalamic tract
(up spinal cord)

blocked by

Lesion at T6
or above

results
in

Reflex SNS response

causing

Vasoconstriction

results
in

Piloerection

Hypertension

sensed
by

Pallor

Baroreceptors

relayed via

Bladder
irritation,
infection or
obstruction

Bowel
irritation
or faecal
impaction

Fracture

Pressure
area or
wound
infection

beneath lesion

CN IX

beneath lesion
Bradycardia Headache
above lesion
x
Spinal cord injury
at T6 or above
Diaphoresis
Headache
Diaphoresis
above lesion

Vasodilation

Flushed skin
Pallor
Piloerection
Bradycardia
Hypertension
Flushed skin

PSNS response	results in	CN X via
results in

Medulla
oblongata

Figure 11.25
Autonomic dysreﬂexia
CN 5 cranial nerve; PSNS 5 parasympathetic nervous system; SNS 5 sympathetic nervous system.
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C H A P T E R 1 1 N E U R O T R A U M A 227
CHILDREN AND ADOLESCENTS
• If a child develops a spinal cord injury before the adolescent growth spurt, they are most likely to
develop scoliosis.
• Babies and young children have a large head-to-body ratio and relatively weak cervical musculature,
which increases the risk of cervical spine injuries because of a higher fulcrum of motion. (A baby’s
head is approximately 25% of their body mass, whereas an adult’s head is approximately 10% of
their body mass.)
• Children under 8 years of age are most at risk of developing spinal cord injury without radiographic
abnormality, because of immature bone and lax ligaments, which permit excessive compression or
distraction of the spinal cord.
OLDER ADULTS
• Older adults over 65 years of age are at an increased risk of cervical spine injury from falls and
osteoporotic changes contributing to spinal cord injury.
• Many spinal cord injuries in older adults result in central cord syndrome due to falls, resulting in
neck hyperextension.
LIFESPAN
ISSUES
INDIGENOUS HEALTH FAST FACTS AND CULTURAL CONSIDERATIONS
FAST FACTS
Aboriginal and Torres Strait Islander women are 21 times more likely than non-Indigenous Australian women to experience a TBI
from assault.
Aboriginal and Torres Strait Islander peoples are admitted with injuries to their head and neck 2.4 times more often than non-Indigenous
Australians. Statistics on spinal cord injuries in Aboriginal and Torres Strait Islander peoples are diffcult to locate; however, anecdotal
evidence suggests that Indigenous Australians are over-represented in relation to admission for secondary complications.
Ma ˉori are 3–4 times more likely than European New Zealanders to experience TBI from assault.
Pacifc Islander people are 1.4 times more likely than European New Zealanders to experience TBI.
Ma ˉori are 1.5 times more likely than European New Zealanders to experience spinal cord injury.
Pacifc Islander people are 2.4 times more likely than European New Zealanders to experience spinal cord injury.
CULTURAL CONSIDERATIONS
Apart from the mobility and access diffculties experienced by all individuals with brain or spinal injury, which are often exacerbated in rural
and regional areas, Aboriginal and Torres Strait Islander peoples experience additional challenges.
A particular diffculty exists in the cultural limitations of the psychometric tools used to assess intellectual function and behavioural changes
following TBI. Many neuropsychological testing tools have signifcant limitations or are inappropriate in the assessment of Aboriginal and
Torres Strait Islander peoples. The tests are often culturally defcient, undertaken in English, and rely on written responses and the need to
answer many questions. Most psychometric instruments have not been validated for their use in Indigenous Australian populations. Health
care professionals need to understand that in some cultures it is rude to ask numerous questions, maintain eye contact or even discuss some
issues if the assessor is of a different gender. Reliance on unmodifed tests that do not take into account a person’s history, culture, language,
customs or life experiences will result in inaccurate measurement. Choice of assessment tools such as the Kimberley Indigenous Cognitive
Assessment (KICA-Cog), the Westmead Post Traumatic Amnesia Test, or Cogstate are likely to be the most appropriate.
Source: Extracted from Australian Aphasia Rehabilitation Pathway (2014); Australian Institute of Health and Welfare (2017a); Dudgeon et al. (2014); Dudley et al. (2014); Jagnoor & Cameron
(2014); Lagolago et al. (2015); van den Heuvel et al. (2017).
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228 P A R T 3 N E R V O U S S Y S T E M P A T H O P H Y S I O L O G Y
K E Y C L I N I C A L I S S U E S
• Airway management is imperative for an individual with either traumatic
brain injury or spinal cord injury. The mechanism causing the injury may
also result in anatomical deformity, and airway obstruction or oxygenation
and ventilation may be compromised because of a neurological cause.
• Airway management using airway devices and manual or mechanical
ventilation may be necessary to support oxygenation and ventilation in
an individual with neurotrauma.
• When undertaking airway management in an individual with an altered
level of consciousness or trauma, always consider the probability of
cervical spine damage.
• Cardiovascular instability is common in traumatic brain injury as a
result of raised intracranial pressure. It is also common in spinal cord
injury because of neurogenic shock or even hypovolaemic shock from
the soft tissue or orthopaedic damage that caused the spinal trauma.
• Depending on the cause, fluid volume support, vasopressors or
inotropes may be required to manage hypotension in individuals with
neurotrauma. Hypotension will interfere with cerebral perfusion
pressure, and can exacerbate the damage in traumatic brain injury and
spinal cord injury.
• Profound hypertension may occur in the context of raised intracranial
pressure or in spinal cord injury in the context of autonomic dysreflexia.
Beta-blockers or nitrates may be required to manage hypertension to
prevent a cerebrovascular accident.
• The Glasgow coma scale is important in the initial and continuing
assessment of an individual who has experienced neurotrauma.
• Individuals with spinal cord injury may have a disparity in motor and
sensory function. Never assume that paralysis means that the individual
cannot feel the area involved. Both motor and sensory assessments are
necessary to gauge the exact deficits occurring. Assessments should
also be repeated as necessary to monitor clinical changes.
• Many complications associated with spinal cord injury are preventable.
Maintenance of skin integrity is achieved with good pressure area care
and hygiene; continence issues can be managed with bowel and
bladder programs; and osteoporosis, spasticity and muscle spasm can
be assisted with range-of-movement and weight-bearing exercises.
• Individuals and carers of people with spinal cord injury above T6 must be
hypervigilant for the life-threatening development of autonomic dysreflexia.
Severe headache, flushed skin and profound sweating above the lesion,
coupled with pallor and piloerection below the injury, are classic signs.
Assessment to determine the cause must be undertaken immediately.
C H A P T E R R E V I E W
• Traumatic brain injury (TBI) is caused by traumatic forces that are
applied to the skull and brain. The mechanisms of injury include blunt
and penetrating force trauma and acceleration–deceleration injuries.
• TBI results in an alteration in brain function evidenced by cognitive
dysfunction and alteration in conscious level.
• The demographic trend for TBI demonstrates that males are more than
twice as likely as females to suffer death and disability from TBI.
• Adults over 75 years of age have the highest rate of TBI-related
hospitalisation and death.
• Falls, transportation (motor vehicle accidents) and assault are the
primary precipitating factors in TBI death and disability.
• The Glasgow coma scale and post-traumatic amnesia tools are
used to assess functionality and cognitive impairment.
• Primary brain injury occurs at the time of impact, whereas
secondary brain injury occurs post injury.
• Cerebral blood flow (CBF) relies on adequate cerebral perfusion
pressure (CPP) and is closely autoregulated.
• Autoregulation of CBF occurs with a CPP of 50–150 mmHg. Outside
this range, autoregulation is lost and CBF is dependent upon systemic
blood pressure.
• The Monro–Kellie doctrine provides the framework for
understanding the mechanism involved in rising intracranial
pressure (ICP). Cerebral components include cerebral spinal fluid
(CSF), blood and brain tissue. An increase in one component will
elevate pressure and decrease the volume of the other components.
Any space-occupying mass, such as a haematoma or oedema, has the
potential to also increase ICP.
• Compliance of brain tissue is poor and, if compensatory reduction in
volume does not occur, then ICP will rise, as pressure and volume are
inversely related. Compression and displacement of cerebral contents
can occur due to raised ICP.
• As ICP rises, autoregulation is lost and CBF is reduced. Ischaemia and
infarction of cerebral tissue ensues.
• Concussion is a transient alteration in cerebral structure, and is thought
to be due to disruption of the reticular activating system (RAS).
• Contusion is bruising to brain tissue and can include coup and
contrecoup injuries.
• Brain haemorrhage can include extradural, subdural, intracerebral
and subarachnoid haemorrhage.
• Diffuse axonal injury is caused by significant blunt-force trauma,
and results in the tearing of axonal fibres in the white matter and the
brain stem.
• Secondary brain injury develops post injury. Inflammation, elevated
ICP, ischaemia and excitotoxicity are all mechanisms of injury.
• Primary spinal cord injury occurs directly to the tissue at the time
of the initial injury and cannot be reversed.
• Secondary spinal cord injury occurs as a result of haemorrhage,
oedema and ischaemia, and results in further destruction of neurons.
• Spinal shock is a transient loss of reflexive and autonomic function
below the spinal cord lesion and resolves in days to weeks.
• Spinal cord injuries can be classified in a number of different ways,
including by vertebral level, degree or mechanism.
• Complete spinal cord injuries result in total loss of all function
beneath the lesion, and are less common than incomplete spinal cord
injuries.
• Many common incomplete spinal cord injuries can be classed into
spinal syndromes, such as anterior cord syndrome, central cord
syndrome, Brown-Séquard syndrome and cauda equina syndrome.
• Spinal cord injuries can result in significant and various
complications, such as the need for ventilatory assistance, breaks in
skin integrity, issues with maintaining continence, the development of
osteoporosis, neurogenic heterotopic ossification, muscle spasms and
spasticity.
• Autonomic dysreflexia is a complex, life-threatening complication of
spinal cord injury above the level of T6. It results in severe hypertension
and bradycardia because of the failure of the autonomic nervous
system control as a result of a spinal cord lesion.
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Bullock, S, & Hales, M 2018, Principles of Pathophysiology EBook, Pearson Education Australia, Melbourne. Available from: ProQuest Ebook Central. [20 March 2021].
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C H A P T E R 1 1 N E U R O T R A U M A 229
R E V I E W Q U E S T I O N S
1 Compare and contrast the major characteristics of primary and
secondary brain injury.
2 What are the mechanisms of injury that cause primary and secondary
brain injury?
3 From an epidemiological perspective, who is most at risk of sustaining
a TBI?
4 A person has fallen from a horse. His conscious level is reduced, and
he withdraws, grunts and opens his eyes to pain. What is his Glasgow
coma scale (GCS) score?
5 Differentiate between extradural and subdural haematomas. Why are
older adults more at risk of suffering subdural haematomas?
6 Outline normal brain physiology, and utilise the terms CBF, CPP, MAP
and ICP in your answer.
7 How does the Monro–Kellie doctrine help to explain the Cushing reflex?
8 Compare and contrast coup and contrecoup contusion injuries.
9 If a person has a blood pressure of 90/45 mmHg, what is their MAP?
Is this sufficient to maintain CBF?
10 Jane is a 35-year-old woman who has been injured while playing
hockey. The hockey ball has struck the right temporal region of her
skull. She has had a period of brief unconsciousness and now is
conscious. Her GCS score is 14 (E 5 4, V5 4, M 5 6), blood pressure
(BP) is 140/90 mmHg, and heart rate (HR) is 110 beats per minute
(bpm) (sinus tachycardia). She does not want an ambulance to attend
or to go to hospital. She convinces her friends to take her home. What
injuries could Jane have sustained, and what are the risks in nonassessment and treatment?
11 A short period of time has passed and Jane is now very unwell. She
has a GCS score of 7 (E 5 2, V 5 2, M 5 3), BP of 95/45 mmHg and
HR of 160 bpm (sinus tachycardia). Explain how rising intracranial
pressure reduces cerebral blood flow, and relate this to Jane’s case.
12 With relation to spinal cord injury, define:
a spinal shock

b
c
d

neurogenic shock
transection
compression injury

13 What is the difference between complete and incomplete spinal
injuries?
14 What is the difference between all of the different types of spinal cord
syndrome in incomplete spinal injury?
15 What complications can occur as a result of spinal cord injury? Explain
the mechanism.
16 What are the signs and symptoms of autonomic dysreflexia? How
should it be managed?
H E A LT H P R O F E S S I O N A L C O N N E C T I O N S
Midwives Midwives must be able to identify neonatal spinal cord injury. Although rare, neonatal spinal cord injury can occur as a result of
delivery, or it may occur in utero. Intrapartum manipulation, such as traction or rotation, increases the risk of spinal cord injury; however, spinal
cord injury may also occur as a result of situations causing cord compression or ischaemia. In-utero malposition, vascular insults and prenatal
ischaemia can result in cord injury. Post-delivery procedures, such as lumbar puncture, umbilical arterial cannulation and the placement of a
central venous catheter, have also, on rare occasions, resulted in spinal cord injury. If assessment of a newborn indicates respiratory
compromise and profound hypotonia, spinal cord injury should be considered.
Physiotherapists Physiotherapists provide critical support to individuals following traumatic brain injury or spinal cord injury. Signifcant
rehabilitation programs must be designed to facilitate maximum function. Programs are generally several months in duration and focus on
specifc goals, depending on the predicted function. In caring for an individual with spinal cord injury, there are two distinct phases in therapy
plans. Initially, in the acute stages, management of respiratory function, positioning, stretching and range-of-movement exercises are a priority.
Depending on the level of injury, a physiotherapist may assist individuals with breathing and coughing techniques, as well as with pulmonary
hygiene, such as suctioning. Maintenance of joint range of movement with passive exercises for paralysed limbs and active exercises for nonparalysed limbs will also form an important component of the role of a physiotherapist in the acute stages of spinal injury. As the rehabilitation
commences—a less acute phase—the focus is on increasing sitting endurance, strengthening active muscles groups and working towards
achieving some degree of functional mobility, depending on the level of injury. Also, as physiotherapists spend so much time with individuals
who have experienced spinal cord injury, it is imperative to understand the causes and management of autonomic dysreﬂexia.
Nutritionists/Dieticians Because individuals with spinal cord injury have a lower resting metabolic rate and often reduced activity levels,
their energy requirements are lower than in active, able-bodied individuals. Obesity can become a problem and complicate physiotherapy,
transfers and activities of daily living. Considerations of activity factor should be made in the estimation of caloric intake requirements. The
activity factor may differ depending on the vertebral level of the lesion, because this can inﬂuence the activity level. Vertebral level will also
inﬂuence gastric emptying and bowel motility. Important nutrition and dietary considerations for individuals with spinal cord injury must include
bowel function. An increase in fbre and adequate hydration are necessary to reduce the risk of constipation. Excessive consumption of
caffeine, fruit and spicy foods may result in diarrhoea. Cardiovascular disease is common in people with spinal cord injury, so common sense
and healthy eating, avoiding foods high in fat, salt and sugar, will be benefcial. It is important to ensure adequate protein, vitamins and
minerals to facilitate wound healing, especially in the context of pressure area sores. Avoidance of carbonated drinks and citrus juices can
reduce the risk of urinary tract infection, as they can inﬂuence urinary pH to become too alkaline.
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Bullock, S, & Hales, M 2018, Principles of Pathophysiology EBook, Pearson Education Australia, Melbourne. Available from: ProQuest Ebook Central. [20 March 2021].
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230 P A R T 3 N E R V O U S S Y S T E M P A T H O P H Y S I O L O G Y
Occupational therapists Occupational therapists are responsible for maximising an individual’s capacity to perform activities of daily
living. A critical factor in understanding the potential function of an individual with spinal cord injury is to recognise the defcits caused by
injuries at specifc vertebral levels. It is also important to be cognisant of the remaining motor and sensory function following the trauma, as
this will inﬂuence an individual’s capacity to perform certain tasks. Occupational therapists are also responsible for designing and often
constructing splints to maintain optimal function. Organisation of adaptive equipment, such as devices to assist with mobility, eating, grooming
or writing, will be necessary and dictated by the functional capacity of the injured individual.
C A S E S T U DY
Ms Tonya Walton was a passenger in a motor vehicle accident where the 25-year-old male driver died. She is 29 years of age (UR number 276984) and
was brought in by the paramedics with a Glasgow coma scale (GCS) score recorded as E 5 2, V 5 3, M 5 6. All of the occupants of the car tested positive
for drugs and alcohol. Ms Walton was not wearing a seatbelt, and hit her forehead on the windscreen during the accident. Although she had no skull
fracture, she developed a subdural haematoma and had a craniotomy five days ago. Apart from some minor skin abrasions, Ms Walton had no other
injuries. Upon return to the ward after two days in intensive care,her GCS score was recorded as E54, V54, M56. She demonstrated moderate weakness
in her right grip but equal strength in her legs.
At the start of this shift, her blood pressure was 140/100 mmHg, her pain was recorded as 2/10 (headache) and her GCS score was recorded as E 5 4,
V 5 5, M 5 6. Her other neurological assessments included slight weakness in her right hand and normal strength in both legs. Her pupils were equal and
reacting to light. She had both direct and consensual reactions. Her most recent observations (5 minutes ago) are as follows:
Temperature Heart rate Respiration rate Blood pressure SpO2
36.5°C 84 18 175⁄115 98% (RA*)
*RA 5 room air.
Her pain is 7/10 (headache) and her GCS score is E 5 4, V 5 4, M 5 6. Her other neurological assessments include moderate weakness in her right hand
and normal strength in both legs. Her pupils are equal and reacting to light, but sluggish. This morning’s pathology results are as follows.
HAEMATOLOGY
Patient location: Ward 3 UR: 276984
Consultant: Smith NAME: Walton
Given name: Tonya Sex: F
DOB: 08/05/XX Age: 29
Time collected 08:30

Date collected Year	XX/XX XXXX
Lab #	2345434

Copyright © Pearson Australia (a division of Pearson Australia Group Pty Ltd) 2019— 9781488617676 — Bullock/Principles of Pathophysiology 2e
Bullock, S, & Hales, M 2018, Principles of Pathophysiology EBook, Pearson Education Australia, Melbourne. Available from: ProQuest Ebook Central. [20 March 2021].
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C H A P T E R 1 1 N E U R O T R A U M A 231
FULL BLOOD COUNT UNITS REFERENCE RANGE
Haemoglobin 132 g/L 115–160
White cell count 5.3 3 109/L 4.0–11.0
Platelets 204 3 109/L 140–400
Haematocrit 0.44 0.33–0.47
Red cell count 4.12 3 109/L 3.80–5.20
Reticulocyte count 1.5 % 0.2–2.0%
MCV 89 fL 80–100
Neutrophils 3.12 3 109/L 2.00–8.00
Lymphocytes 3.13 3 109/L 1.00–4.00
Monocytes 0.28 3 109/L 0.10–1.00
Eosinophils 0.29 3 109/L , 0.60
Basophils 0.08 3 109/L , 0.20
ESR 9 mm/h , 12
COAGULATION PROFILE
aPTT 32 secs 24–40
PT 15 secs 11–17
BIOCHEMISTRY
Patient location: Ward 3 UR: 276984
Consultant: Smith NAME: Walton
Given name: Tonya Sex: F
DOB: 08/05/XX Age: 29
Time collected 08:30

Date collected Year	XX/XX XXXX
Lab #	345655

ELECTROLYTES UNITS REFERENCE RANGE
Sodium 138 mmol/L 135–145
Potassium 4.4 mmol/L 3.5–5.0
Chloride 102 mmol/L 96–109
Bicarbonate 24 mmol/L 22–26
Glucose 5.8 mmol/L 3.5–6.0
Copyright © Pearson Australia (a division of Pearson Australia Group Pty Ltd) 2019— 9781488617676 — Bullock/Principles of Pathophysiology 2e
Bullock, S, & Hales, M 2018, Principles of Pathophysiology EBook, Pearson Education Australia, Melbourne. Available from: ProQuest Ebook Central. [20 March 2021].
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232 P A R T 3 N E R V O U S S Y S T E M P A T H O P H Y S I O L O G Y
C R I T I C A L T H I N K I N G
1 Considering Ms Walton’s demographic information and the cause of her injury, how does this compare with the epidemiology of traumatic brain injury?
2 What was Miss Walton’s initial GCS score? What type of traumatic brain injury does this signify? What is the significance of the initial GCS score in
relation to potential neurological outcome?
3 Consider Ms Walton’s most recent observations. What neurological changes has she experienced? Make a list of all of the significant observations.
4 What could be causing this change in neurological status? Observe the pathology results. Are these of any benefit in determining what might be
occurring? (Hint: Is there any significance in observing the coagulation profile? Can it add any important information to the clinical picture?)
5 What interventions are required to assist Ms Walton immediately? What are the immediate dangers in relation to Ms Walton’s change in neurological
status? If her neurological status deteriorates further, what new dangers may present?
6 Review Ms Walton’s most recent GCS score. What parameter suggests that assessment might be becoming complicated? (Hint: Think ‘V’.) What other
assessments can be used in evaluating an individual’s neurological status?
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Copyright © Pearson Australia (a division of Pearson Australia Group Pty Ltd) 2019— 9781488617676 — Bullock/Principles of Pathophysiology 2e
Bullock, S, & Hales, M 2018, Principles of Pathophysiology EBook, Pearson Education Australia, Melbourne. Available from: ProQuest Ebook Central. [20 March 2021].
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