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Fig. 3.4 Right hypoglossal nerve palsy; note the atrophy and
fasciculation of the right side of the tongue.
Visual inspection to assess the bulk of muscles is commonly ignored, and this is an ill- advised omission, as
wasting of muscles can occasionally give immediate
clues to the pathology. Do not say there is no atrophy
unless you have actually looked at all relevant muscle
groups carefully! If necessary, ask the patient to remove
or roll up clothing. Additionally, look for involuntary
movements and fasciculations.
Muscle tone is tested by passively flexing and extending the elbows, the wrists and the hip, knee and ankle
joints, and by pronating and supinating the wrists and
assessing resistance to these movements. Muscles are
hypertonic in Parkinson’s disease, whereas hypotonia
is seen in lower motor neuron or cerebellar damage.
It is important to be able to assess the tone properly, as
sometimes, it can be the only pointer to pathology in an
otherwise normal clinical examination. Muscle tone is
reflected in the intensity of the stretch reflexes.
Power is tested by assessing the strength of a muscle
group across a joint and is graded against resistance
applied by the examiner from 0 to 5 (Table 3.1). There
are several tests for non- organic limb weakness. For
example, if it is suspected that weakness of a leg is nonorganic in origin, the hands of the examiner are placed
below both the patient’s knees, and the patient is asked
to lift the allegedly weak leg. If there is genuine weakness, and the patient is really trying to lift that leg, the
other leg will press down on the bed. If the weakness is
not genuine (e.g. due to somatization of a psychological
problem), the other leg will not move.
Table 3.1 MRC scale for assessment of muscle power
0 = No muscle contraction visible (paralysis)
1 = Muscle contraction visible, but no movement of joint
2 = Joint movement when effects of gravity are eliminated
3 = Movement sufficient to work against gravity
4 = Movement overcomes gravity and resistance
5 = Normal power
Reflexes
Reflexes can be divided into the following types:
• stretch(deeptendon)reflexes
• superficialreflexes,suchastheabdominalreflexand
cremasteric reflex (not usually tested)
• brainstemreflexes:pupillary,cornealandgagreflexes
(mentioned above)
• primitivereflexes:suckreflex,graspreflexand
palmomental reflex (their presence is often a sign of
frontal lobe lesions)
There are five deep tendon reflexes assessed in the
neurological examination: the biceps, brachioradialis, triceps, knee and ankle reflexes. Their intensity can
be graded from 0 to 5, where 0 is areflexia, 1 is sluggish, 2 is normal, 3 is hyperactive, 4 indicates the presence of non- sustained clonus and 5 is sustained clonus;
0, 4 or 5 are considered abnormal. There may also be a
Hoffman’s sign, which is increased rebound responses
of the finger flexors in response to flicking the middle
fingernail downwards (the thumb may also adduct and
flex in response to this). The patient is examined in the
seated or supine position, and the examiner uses a reflex
tendon hammer to tap on the tendon of the muscle being
tested. If reflexes cannot be elicited, reinforcement techniques, such as the Jendrassik manoeuvre (see Chapter
9), may be required. Asymmetrical decrease or loss of
reflexes is due to peripheral nerve damage (radiculopathies, plexopathies or mononeuropathies). Hyperreflexia
is a sign of upper motor neuron damage and is associated with spasticity and a positive Babinski sign. The latter is evaluated by the slow and firm scraping of the sole
of the foot on the lateral side. This should elicit a flexor
plantar response and adduction of the toes. The positive Babinski sign (see Chapter 9) consists of an extensor plantar response of the big toe and abduction of the
other toes. A positive sign is normal in children aged up
to 2 years (prior to independent walking). In adults, it is
indicative of upper motor neuron damage. Occasionally,
an equivocal response is obtained, when no movement of
the big toe can be elicited at all. This can happen in some
people naturally, as well as in some pathological conditions, as in the aftermath of spinal cord injury.
Superficial reflexes such as the abdominal reflex are
normally elicited by lightly drawing a sharp object across
3
CLINICAL ASSESSMENT
59THE NERVOUS SYSTEM
3
the four abdominal quadrants supplying dermatomes
T8–T12 to observe muscle contraction. This response is
impaired if there is an upper motor neuron lesion above
the spinal level tested. However, they are difficult to
elicit in many patients (due to body fat obscuring muscle
contraction) and so are less often tested.
Coordination and balance
Good coordination of movement reflects the coopera-
CLINICAL ASSESSMENT
tion of separate groups of muscles. Ataxia (poor coordination) can be sensory, caused by dysfunction of the
afferent connections from muscles and joints within the
nerve or spinal cord dorsal columns, or motor, caused
by damage to the cerebellum. This can result in truncal
ataxia of the proximal muscles when the midline cerebellum is affected or appendicular ataxia of the limbs when
the cerebellar hemispheres are affected. The integrity of
cerebellar function, and that of several other components
of the motor system, is evaluated using coordination
tests. For the upper limb, these include the finger- nose
test (where the patient is asked to alternately touch their
own nose and the examiner’s fingertip as fast as possible) and rapid supination and pronation of the hand.
The inability to execute rapid pronation/supination is
termed dysdiadochokinesia and is a sign of cerebellar
ataxia. For the lower limb, tests include the heel- kneeshin test (where the patient is asked to draw the heel of
the contralateral leg up and down the lower limb of the
ipsilateral leg), the heel- to- toe test (pigeon- toe walking
in a straight line without losing balance) and Romberg’s
test. In this last test, the patient stands upright, feet
together, hands by their side, with their eyes open and
then closed. The clinician observes any signs of sway and
loss of balance—termed a positive Romberg sign—which
is worse with the eyes shut, indicating a sensory ataxia
(and issues with the spinal cord dorsal columns). The test
is based on the idea that a person needs two of the following three senses to maintain balance while standing:
proprioception (the ability to know one’s body position
in space), vestibular function (the ability to know one’s
head position in space) and vision (used to monitor and
adjust body position). A patient who has a problem with
proprioception can still maintain balance by relying on
vestibular function and vision. Romberg’s test is used to
differentiate between sensory and motor ataxia, the latter
of which is caused by cerebellar dysfunction.
Gait
The examination of gait involves an assessment of the
patient’s ability to rise from a chair, posture and postural
stability and ambulation. Difficulty in rising from a chair
may reflect the weakness of muscles or basal ganglia disease. The posture of the patient is also pathognomonic
for certain diseases. For example, Parkinson’s disease
patients have a stooped posture, whereas patients with
progressive supranuclear palsy may have a rigid, hypererect posture.
During assessment of ambulation the examiner assesses
speed, length of stride and ability to turn; leg circumduction (by abducting the hip and thigh in order to clear the
foot above the ground during the swing phase of gait),
stiffness, knee bending, arm swing and deviation from a
straight line while walking are also noted. Patients with
Parkinson’s disease have a shuffling, festinating (i.e. rapid
and increasingly accelerating) gait, experience difficulty in stopping at will and also have a decreased arm
swing. Patients with progressive supranuclear palsy
may present with a wide- based stride and slowing of
ambulation. To detect subtle movement abnormalities,
a forced gait test (walking on heels, tiptoes, inside/outside of the foot only, hopping or climbing stairs) can be
performed.
For assessment of postural stability, the patient is
asked to stand with the feet next to each other. Patients
with cerebellar disease or labyrinthine problems may not
be able to stand without separating the feet. The clinician may also perform the Romberg test, during which
the patient is asked to stand still and close their eyes.
Wide oscillations and a loss of equilibrium may reflect
damage to the posterior columns. Truncal ataxia can also
be assessed and is seen as an inability of the patient to
walk in a straight line when asked to perform the heelto- toe task, in which they must place the heel of one foot
in direct contact with the toe of the other foot. The gait
in cerebellar truncal ataxia is ‘drunken’. A waddling gait
(like that of a duck) is due to proximal muscular weakness and is seen in muscular dystrophies and myopathies. It is important to remember, however, that the
commonest disorders of gait in the general population
are due to local musculoskeletal pathology in the limbs,
for example, arthritis of the hips, and it is important to
exclude this.
Sensory examination
This part of the examination evaluates the response to
painful stimuli, temperature and light touch, and also
vibration and joint position sense. It is important to
note that sensory changes may be milder and more difficult to detect than motor or reflex changes and depend
on the patient’s willingness or ability to express what
they are feeling. Consequently, it can often be the hardest part of the examination to interpret with certainty.
As in the cranial nerves and motor examination, it is
important to compare both sides of the body (always
with the patient’s eyes closed) using each test before
deciding whether the results are abnormal or normal.
Nociception is tested through applying pinprick stimuli
to the skin. Temperature perception is tested using a
cold object (e.g. the side of a tuning fork) but is less often
tested than the pinprick sensation. These are rarely tested
together because if one is present, almost invariably so is
the other. Vibration is tested by placing a vibrating tuning fork on the bony prominences of the various joints
tested. Light touch is assessed by dabbing (static touch)
60 SYSTEMS OF THE BODY
3
or stroking (dynamic touch) a twist of cotton wool on
the skin of the patient and asking them to say when and
where they feel the stimulus.
During examination, comparisons of the two sides,
and proximal to distal, are made in order to identify the
site of the lesion. When a sensory deficit is suspected or
identified, the examiner must determine its modality
and map its distribution on a sensory examination chart
to see if it matches that found with lesions of the peripheral nerve, spinal nerve, spinal cord, posterior fossa or
supratentorial region. For example, decreased response
to pinprick on one half of the body is due to a lesion in
the contralateral ascending pathways or the cerebral
hemisphere. If the deficit is mainly distal and bilateral
(e.g. ‘stocking’ or ‘glove’ distribution of a deficit), the
cause may be a peripheral neuropathy. It is also important to note that considerable individual variation occurs
in the segmental or radicular (dermatome) innervation
patterns and therefore also in the anatomical location of
dysfunction.
Cortical function
Tests assessing sensory cortical function depend on
the integrity of the pathways to the brain; if they are
damaged, then these tests should not be performed.
Certain sensory and higher mental functions require
specific intact cortical lobes. Spatial awareness/perception (parietal lobe) can be assessed by examining sensory input and spatial limb position with a variety of
tests. Stereognosis (the ability to identify objects using
only tactile sensation) is assessed by asking the patient
to identify common objects, such as a key or money,
by touch alone. Graphesthesia (the ability to recognise
any symbols drawn on the skin) loss is tested by using
numbers or letters drawn on the skin, which the patient
should identify by touch alone. Assessing the patient’s
ability to perform simple mathematical calculations, such
as addition or subtraction, examines calculating skills,
while asking a patient to copy a drawing of a symmetrical object, such as a clock, examines sensory neglect. All
of these tests assess parietal lobe function. Damage to the
parietal lobe (in particular, to the non- dominant parietal
lobe) gives rise to various types of apraxia, that is, the
inability to execute movements or tasks. Constructional
apraxia—failure to build, draw or comprehend the spatial relationships of objects—can be identified by asking a patient to copy a construction made with building
blocks, whereas ideomotor apraxia—failure to make
movements upon a verbal command—can be identified
by asking a patient to mimic getting dressed or copying
arm movements made by the examiner.
Higher mental skills, such as reasoning, working
memory, abstract thought and the organization and
reorganization of information, are functions of the frontal lobes; damage to these results in characteristic deficits. These abilities can be assessed using the following
tests. Reasoning and abstract thought can be assessed by
asking the patient to explain the meaning of idioms in
their own words, for example, ‘people who live in glass
houses shouldn’t throw stones’, or ‘there’s no smoke
without fire’ or identifying similarities between pairs of
objects, for example, cats and dogs.
Working (short- term) memory is assessed by examining digit span recall. This involves paying attention to
and verbally recalling the order of two series of numbers that are presented to the patient to view, and then
removed. If all are correctly recalled, another (longer)
series of numbers is used, and the test repeated. If these
are all correctly recalled, the test is repeated until the
subject makes an error on a trial at a given list length.
Digit span corresponds to the length of the longest list
for which the patient was correct in both trials. Normal
short- term memory span is between five and nine items.
People normally show greater recall of numbers at the
beginning of the list, as they are rehearsed more often,
and good recall of numbers at the end of the list, as they
have the least time to decay from memory; numbers in
the middle of the list are the ones most likely to be forgotten. Recent memory can also be tested by asking a
patient to recall a list of items presented to them 3–5 minutes previously.
The Wisconsin card sorting test is a sensitive test of
executive function, involved in processes such as rule
changing or set shifting. The cards given to the patient
have symbols on them that differ in number, shape and
colour, and the examiner chooses a category for sorting the cards, such as by colour, shape or number. The
patient must then sort the pack of cards by placing each
card, in turn, under an appropriate stimulus card based
upon a rule that the examiner has generated (colour,
shape or number). After the patient places each card on
top of an appropriate stimulus card, the examiner says
‘correct’ or ‘incorrect’, depending upon whether their
rule is being obeyed. For example, if the rule is shape, for
example, a circle, when the subject places a single cross
on top of a single circle (working on a number rule), then
they are wrong. The subject should continue placing the
cards on top of the appropriate stimulus card until 10
successive correct placings have been scored. When this
has been achieved, the sorting rule is changed. Scoring is
performed in two ways: categories achieved within the
number of cards given and perseverative errors. The former is the number of changes of criterion and the latter
is the number of errors caused by the subject continuing
to choose a discontinued criterion. Damage to the frontal cortex gives rise to errors of these types, and the effect
is particularly severe if the dorsolateral frontal cortex is
damaged.
Abnormalities of speech and language may interfere
significantly with history taking and with the ability of
the patient to perform parts of the rest of the examination; therefore the assessment of any impairments is
often performed at the beginning of the clinical examination. The clinician may detect aphasia (i.e. disorders of
understanding and expression), dysphonia (disturbance
CLINICAL ASSESSMENT
61THE NERVOUS SYSTEM
3
of voice production) or dysarthria (problems with the
articulation of words). Damage to Broca’s area produces
difficulties with verbal output, but not with comprehension, whereas damage to Wernicke’s area does not affect
verbal output: the subject is normally fluent, but the
comprehension of language is impaired, and they may
talk rapidly, producing jumbled speech that resembles a
‘word salad’.
People with diminished levels of consciousness are
assessed using the Glasgow Coma Scale, which ranges
CLINICAL ASSESSMENT
from a minimum score of 3 to a maximum of 15 (see
Table 11.7). The three parameters assessed are the verbal,
eye- opening and motor responses. A score of 8 indicates
coma, 8–12 indicates a severe head injury and 12 indicates a mild head injury.
The neurologist’s approach to the examination of cortical function reflects the attempt to diagnose an organic
(physical) disease of the brain that may disrupt mental
functions, whereas in psychiatry, the clinician may be
more interested in dysfunctional brain syndromes that
may not be associated with organic disease.
Other investigations
In addition to the clinical examination, other diagnostic
techniques may be employed to help identify or confirm
the cause of the problem. These include haematological,
microbiological, biochemical, immunological, neurophysiological and medical imaging. Some are outlined
below.
Nervous system imaging
Radiography
X- ray contrast images are produced by the differential
absorption of X- rays as they pass through air, water, fat
and mineral components of the body. Structures such as
the brain and spinal cord are mostly water and so are
largely invisible on the image, whereas bone has a high
calcium content and so absorbs much X- ray energy.
Radiographic analysis can reveal bony fractures (skull
or spine) or misalignment, tumours and metastatic processes, general alterations in the skull, inflammatory
processes, vascular abnormalities (aneurysms or malformations) or degenerative processes (e.g. calcification of
intervertebral discs).
Computed tomography
During computed tomography (CT), a beam of X- rays
scans the head or spine in a series of successive planes,
and the differential absorption of the rays by the tissue
is reflected in an image of the structures scanned. Images
are obtained in the coronal or axial plane. CT is used in
the diagnosis of brain infarcts and haemorrhages, fractures, hydrocephalus, cerebral atrophy and tumours. For
skull analysis, CT has superseded X- rays for most pur-
poses. It is relatively insensitive to spinal cord pathology,
although it can detect herniated discs and bony fractures.
An additional injection of contrast medium can help display the vascular system and identify aneurysms and
arteriovenous malformations. CT or magnetic resonance
imaging (MRI) can be used interchangeably in some indications. However, there are instances when one or the
other technique is preferable. For example, CT is valuable in the evaluation of intracranial abnormalities in
patients with craniocerebral trauma. Skull X- ray examination is more accurate for fractures of the cranial vault,
whereas CT is preferable for fractures of the base of the
skull. In particular, the acutely injured patient may not
be amenable to a complex MRI scan. A CT scan (under
10 seconds) is also shorter than an MRI scan (5–10 minutes), which is an important factor. Acute haemorrhage
is also better demonstrated by CT than by MRI analysis.
In contrast, MRI is preferable for evaluation of patients
in a subacute phase of injury or with chronic injury. For
example, 48 hours after haemorrhage, even small collections of blood in subdural locations can be imaged by
MRI, although they are not visible by CT. Herniation of
discs, which ultimately results in compression of nerve
roots, can also be rapidly imaged by CT.
Magnetic resonance imaging
MRI generates signals that are due to the interaction of
hydrogen ions (essentially components of the water
in the nervous tissue) with magnetic fields; it does not
involve the use of X- rays. Initially, protons are oriented
in a strong magnetic field, and they are subsequently
excited using a lateral magnetic pulse. During relaxation
they emit signals that can be decoded and transformed
into an image that reflects anatomical structures as a
function of their water content. Because grey matter contains more water than white matter, a clear difference
between the two tissue types is readily seen. Two types
of image are obtained: T1- weighted and T2- weighted
images (Fig. 3.5). T1- weighted images show details of the
anatomy, whereas T2- weighted images highlight areas
of increased signal density or pathology. Table 3.2 sum-
marises signal differences between T1- and T2- weighted
images.
An easy way to differentiate between MRI and CT
scans of the head is that bone appears white with CT
and dark with MRI. Areas that are white or bright
with CT are called high- density areas, whereas with
MRI they are called high- signal areas. Gadolinium can
be used as a contrast agent in MRI. Variations in MRI
analysis include fluid- attenuated inversion recovery
(FLAIR) and diffusion- weighted imaging (DWI); both
are used for detecting areas of small lesions in acute
ischaemic stroke. Although more cumbersome, MRI
analysis has an advantage over the quicker CT scan.
It is particularly good for seeing regions of demyelination in the central nervous system. For example, in
multiple sclerosis, a normal CT scan may be obtained,
whereas the MR image in the same patient will be
62 SYSTEMS OF THE BODY
T1 T2
Fig. 3.5 Comparison of T1- and T2- weighted axial magnetic resonance images. The lipid component of the brain is bright in a T1- weighted
image, so myelin gives a bright signal. Water (and hence cerebrospinal fluid- filled spaces) appears dark on T1- weighted images but bright on T2weighted images.
3
CLINICAL ASSESSMENT
Table 3.2 Differential signal characteristics of T1- weighted and
T2 - weighted brain magnetic resonance images
T1 T2
Cerebrospinal Black White
Fat White White
Cortical bone Black Black
White matter Light grey Dark grey
Grey matter Dark grey Light grey
grossly abnormal (e.g. T2- weighted images would show
areas of increased signal intensity corresponding to
plaques). MRI also gives better definition and sensitivity in tumour detection. MRI has become a procedure of
choice for the evaluation of spinal abnormalities. MRI
provides clear images of the spinal cord and roots and
disc spaces and helps in the definitive diagnosis in cases
of spinal cord compression, syringomyelia or tumours.
A practical limitation of MRI is that, since its strong
magnetic field tends to shift any ferromagnetic objects,
it can only be used safely in the absence of metal
implants (e.g. metal plates), defibrillators and pacemakers. In addition, since the MRI machine is like a tube
in which the patient has to lie still for long periods for
the scan, it is not suitable for claustrophobic patients or
people who are not very cooperative, such as children
or confused patients or people in a lot of pain.
Functional MRI (fMRI) is a variation of the technique
that is predominantly used as an experimental research
technique. It allows the correlation of anatomical location and function without injection of additional substances or tracers. In the brain, blood perfusion is related
to neural activity; thus fMRI (like positron emission
tomography [PET]) can be used to explore the activities
of various brain regions when subjects perform specific
tasks or are exposed to specific stimuli.
Diffusion tensor imaging (DTI) is a refinement of MRI
based on mathematical algorithms that estimate water
molecule diffusion in particular directions in the generated image. DTI provides a quantitative analysis of the
magnitude and directionality of water molecules. It is
now possible to use this to visualise, in three dimensions,
specific white matter tracts in the brain, as axon bundles
travelling in a particular direction constrain water molecule diffusion in a single direction; this is called tractography. It can identify major CNS tracts such as the corpus
callosum or corticospinal tracts etc. and is used for presurgical operation planning, assessing white matter
changes induced by tumours, microstructural alteration
of white matter by diseases such as Alzheimer’s disease
(dysconnectivity and impact of plaque formation) or
traumatic brain injury or investigating the anatomy of
the developing brain.
Positron emission tomography and single photon
emission tomography
PET is based on the use of compounds labelled with
radioisotopes that emit positrons. There are 15O- labelled
63THE NERVOUS SYSTEM
3
compounds that can be used to monitor cerebral blood
flow and its fluctuations during cerebral activity. PET
has a lower spatial and temporal resolution than fMRI.
PET analysis using 18F- fluorodeoxygluose can be used to
gather information about cerebral glucose metabolism.
PET analysis can also be used to follow the deposition
of amyloid in the brain of individuals with Alzheimer’s
disease, using ligands such as 18F- florbetapir or
18
F- florbetaben. Single photon emission computed
tomography (SPECT) uses a similar principle to PET. The
CLINICAL ASSESSMENT
radioisotopes have a longer half- life than those used in
PET and emit single photons. It is a less costly technique,
but the resolution is significantly lower. Specific SPECT
ligands could be used to detect, for example, neurodegenerative processes. In Parkinson’s disease, a disease
characterised by loss of dopaminergic innervation, a DaT
scan can be carried out for diagnostic purposes using
SPECT and the tracer ioflupane (
of the dopamine transporter (uptake transporter) on
dopaminergic fibres. Various PET or SPECT ligands for
the translocator protein (TSPO), expressed by activated
microglia, can be used to detect neuroinflammation.
Angiography
Angiography consists of the injection of contrast medium
into the circulation, usually through a catheter placed in
the femoral artery. It helps in the visualization of vascular abnormalities, aneurysms and the blood supply to
tumours. This method has been superseded by magnetic
resonance angiography, which provides detailed information on vascular anatomy and blood flow without
need for the use of contrast medium, although this can
be given intravenously if required.
Doppler/duplex scanning
This technique uses ultrasound imaging of the carotid
arteries of the neck. It can reveal arterial stenosis and the
characteristics of blood flow through arteries. This is a
useful, non- invasive screening method in the investigation
of cerebrovascular accidents or transient ischaemic attacks.
Electrical activity
Electroencephalography
Electroencephalography (EEG) recordings are used to
globally characterize the electrical activity of the brain.
The activity is recorded using scalp electrodes placed
equidistantly on the head. A normal EEG recording is
characterized by well- defined rhythms that have specific
frequencies that vary with the level of patient alertness.
Abnormal or asymmetric waveforms are indicative of
pathology. EEG is used primarily in the diagnosis of epilepsy, as the analysis of the traces can help identify the
seizure locus and, in some cases, the type of epilepsy.
EEG is also useful in ventilated unconscious patients to
detect seizures, as in these patients there may not be any
123
I), which is a marker
external evidence of seizure activity. It is also occasionally used to confirm brain death, as it can show whether
the electrical activity of the brain has ceased or not. EEG
can be used in combination with MRI.
Event- related potentials
Changes in EEG recordings can occur in response to
stimuli. These are called event- related potentials (ERPs).
ERPs are evoked in the primary cortical regions that
correspond to the type of stimuli used (e.g. cutaneous
stimulation triggers ERPs in the somatosensory cortex).
As an example, visual ERPs can be used to assess the
integrity of the visual system and detect demyelination
in the optic pathways. Auditory ERPs are less sensitive
than visual ERPs but can detect the presence of acoustic neuromas. Somatosensory ERPs test the integrity of
somatosensory pathways and are sensitive in detecting,
for example, the demyelination associated with multiple
sclerosis. Evoked potentials can be distinguished from
background noise and spontaneous activity with the use
of signal- averaging techniques.
Electromyography and nerve conduction tests
These procedures are used in the diagnosis of muscular
and peripheral nerve disorders. In electromyography
(EMG), spontaneous, voluntary and electrically stimulated muscle activity is recorded, using intramuscular
needles or surface electrodes. This technique can detect
fibrillations or fasciculations. The latter are due to spontaneous motor unit discharges in degenerating nerve
fibres causing irregular flickering over the surface of the
affected muscle. The former arise when muscle fibres are
denervated and are due to the spontaneous and simultaneous discharges of muscle fibres in response to release
of acetylcholine from degenerating motor fibres; they are
not visible to the naked eye.
Nerve conduction velocity assessment is based on
electrical stimulation of a nerve; the rate of action potential propagation along the nerve and the amplitude and
time of the response are measured. Motor nerve, sensory
nerve and mixed nerve conduction studies can be performed. Conduction studies are performed in patients
with suspected peripheral nerve damage, such as carpal tunnel syndrome (where the median nerve is compressed in the carpal tunnel) or diabetic neuropathy.
Cerebrospinal fluid examination
Cerebrospinal (CSF) examination is a procedure commonly used for the diagnosis of infection in the nervous
system, multiple sclerosis or other neuroimmunological disorders, as well as to identify bleeding into the subarachnoid space. The CSF is sampled using a lumbar
puncture procedure (see Box 4.2). In general, a CT scan or
fundoscopy should be performed before a lumbar puncture to rule out raised intracranial pressure. CSF pressure
is measured, and fluid is withdrawn for analysis.
64 SYSTEMS OF THE BODY
3
The normal volume of CSF is approximately 150
mL, and this is recycled approximately every 8 hours.
Maximum lumbar CSF pressure is 180–190 mmH2O. An
increase indicates infection, increased CSF production
or decreased resorption or the presence of a tumour. The
normal concentration of glucose in the CSF is approximately 50–80 mg/dL (2.8–4.4 mmol/L). In conditions
such as diabetes mellitus, it is greatly elevated (>200 mg/
dL or 11.3 mmol/L). A low glucose concentration may
reflect infection or meningeal inflammatory processes
(see Table 12.5). The latter may also be suggested by the
presence of polymorphonuclear leukocytes in the CSF.
Numbers of mononuclear cells are increased in chronic
inflammation. Analysis of the protein types present in
the CSF can demonstrate the presence of specific antibodies in multiple sclerosis patients. The CSF can also be
analysed serologically in the diagnosis of syphilis. The
presence of red blood cells or xanthochromia (a yellow
discolouration indicating the presence of bilirubin) in the
CSF often indicates subarachnoid haemorrhage.
General comments
In order to make a diagnosis when a lesion or dysfunction in the nervous system occurs, clinicians use certain
theoretical constructs. This is particularly the case in
neurology and is reflected in this overview of how the
clinical examination proceeds in a logical and orderly
fashion through the complexities of the nervous system.
Constructs and models are helpful, even if the constructs
themselves are changed by the rapidly advancing pace of
knowledge in neuroscience. The following are examples
of such simple constructs: (1) the hierarchical organization
of the nervous system (with higher functions represented
rostrally and lower functions represented caudally), (2)
the cerebral localization of function, (3) the topographical representation of body parts and (4) the dominance of
one hemisphere. It is important to remember at all times
that such constructs are only tools and the real world of
neurology and psychiatry far exceeds any simple models of nervous system function. In practice, the neurological examination is rarely performed in its entirety.
Importantly, impairment in one part of the examination
may affect a patient’s ability to perform other parts of the
examination; this is especially true if there is cognitive
impairment, as this will impair the motor and sensory
examination. Thus the practitioner must appropriately
modify the testing based on the patient’s limitations. With
experience, the practitioner learns to perform a screening
examination of the most important elements, and then
focuses on the most relevant in further detail.
CLINICAL ASSESSMENT
65THE NERVOUS SYSTEM
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THE SPINAL CORD
Chapter summary
1. The spinal cord is located between the cervical C1 and lumbar L1– 2
vertebral levels; below this vertebral level only spinal roots are
found, and they are known as the cauda equina.
2. The spinal cord is composed of white and grey matter. The white
matter contains axons of ascending and descending pathways, to
and from the brain, each of which has a specific location and carries
specific information. Most of the pathways decussate at some point
in the CNS, and it is important to know these decussation sites, as
they are associated with particular neurological deficits.
3. The blood supply of the spinal cord is derived from two posterior
and one anterior spinal arteries that originate from the vertebral
artery circulation in the brainstem.
4. The three main sensory pathways that convey the sensory modalities
of discriminative touch, pain, temperature, and balance (unconscious
proprioception) are, the dorsal column medial lemniscus and the
spinothalamic and spinocerebellar tracts, respectively. Each is
associated with particular peripheral receptors and relay through
specific brainstem, thalamic, and cerebellar nuclei to terminate in
the cerebral or cerebellar cortex.
4
5. Damage to the spinal cord can cause loss of all functions below the lesion
level, either immediately if the cord is completely transected, or within
a few hours secondary to oedema, even if the lesion is incomplete.
Following traumatic injury, there are two phases: spinal shock with
complete areflexia, flaccid paralysis, atonic bowel and bladder function,
and loss of vasomotor control, followed 1–2 weeks later (as the shock
resolves) by hyperreflexia, hypertonia, limb spasticity, Babinski sign,
autonomic hyperactivity (vascular and sweating) and impaired bladder
and bowel functions (e.g. urge incontinence, automatic emptying).
Certain symptoms are associated with distinct spinal cord syndromes.
4
Introduction
Spinal cord injury (SCI), whether through disease
or trauma, can lead to a devastating loss of function
below the level of injury and adversely affects several
body systems. Moreover, because of the poor regenerative capacity of the central nervous system (CNS),
THE SPINAL CORD
patients suffer from lifelong disability that may range
from partial loss of function to complete quadriplegia and artificial ventilation. In the UK there are more
than 40,000 people suffering from traumatic SCI, with
approximately 1200 new cases every year. Worldwide,
27 million people have SCI with 250,000 new cases each
year. It is estimated that as a function of the severity of
injury, each SCI case costs somewhere between £0.5 and
1.9 million in lifetime support and care. At least onethird to one- half of these patients are readmitted to hospital after the initial trauma.
Neurological assessment of patients with spinal cord
damage requires an understanding of several concepts:
the basic organization of the spinal cord, the relationships between the main nervous pathways that relay
sensory and motor information to and from the brain,
and the ability to correlate radiological evidence of injury
to the vertebral column with different segmental levels of
the spinal cord.
The aim of this chapter is to describe the organization of the spinal cord, the positions and functions of the
various relay pathways that reside within it, and then to
describe how these are affected in SCI.
Gross anatomy of the spinal cord and vertebral column
The spinal cord connects the brain to the peripheral
nervous system (PNS). It is located within the vertebral
canal, which provides structural protection, and is held
in place by spinal roots and denticulate ligaments (Fig.
4.1). The adult spinal cord is approximately 18 inches
(46 cm) long and extends from the foramen magnum to
the level of the L2 vertebra. This is not so at birth, when
it extends much lower (to the L3 vertebral level), but
because the vertebral column grows faster than the cord,
it leaves the cord positioned progressively higher up in
the spinal canal. This means that different spinal cord
levels can be related to specific vertebral levels (Table
4.1). The spinal cord tapers off at its caudal end to form
the conus medullaris, and beyond this point, the spinal
canal is filled only with spinal roots descending caudally
to find their intervertebral foramen. In the sacral region
these fan out, resembling a horse’s tail, and this is termed
the cauda equina (see Fig. 4.1).
The spinal cord and spinal roots are covered by the
meninges and further protection is provided by the presence of cerebrospinal fluid (CSF), which surrounds the
cord in the subarachnoid space. The pia mater is thin and
difficult to identify as a discrete membrane, except as the
denticulate ligaments along the sides of the spinal cord.
The denticulate ligaments attach the surface of the cord
to the dura mater to stabilize the cord within the vertebral canal. The lowest level at which they are observed is
the L1 lumbar root level. The filum terminale is an extension of the pia mater that is attached to the coccygeal
segments, whose function is to suspend the cord in the
CSF (like the denticulate ligaments). The arachnoid and
dura mater extend beyond the L2 level to the level of the
S2 vertebra. Thus, if a sample of CSF is needed, a lumbar
puncture needle can be inserted below the level of the L2
vertebra without fear of damaging the spinal cord (Box
4.2). Spinal dorsal roots attach to the cord, and the pos-
terolateral sulcus and ventral roots exit the cord at the
anterolateral sulcus (Fig. 4.3).
The diameter of the spinal cord is not uniform along
its length (Fig. 4.3). At the cervical and lumbar levels, the
spinal cord locally enlarges to accommodate the increased
sensorimotor connections involved with the limbs, via
the cervical and lumbar enlargements. The cervical spinal cord is also largest because it carries tract fibres from
lower body levels that are ascending to higher levels. The
thoracic region is small because the input is only from
Box
Case history
4.1
Humpty Dumpty sat on a wall, and Humpty Dumpty had a
great fall. He presents 2 weeks later, complaining of weak
legs and unsteadiness of gait. He says that he was unable
to walk the day after he fell, but progressively recovered
movement later that week. Neurological examination
reveals that he has muscle weakness and brisk reflexes
in his right leg compared to the left leg, and there is a
Babinski sign in the right foot. Abdominal and cremasteric reflexes are absent on the right side, and there is no
voluntary movement of the right leg. There is loss of joint
position sense in the right leg, as he has inability to sense
movement of his toes either up or down, and there is loss
of responses to light touch and vibration on the right leg,
extending up as far as the belly button. In addition, there
is a loss of temperature and pin- prick sensation in the left
leg, which extends up the left side to his belly button. He is
immediately sent for X- rays and further neurological tests
at the local hospital.
This case gives rise to the following questions:
1. What is the location and organization of the sensory
tracts in the spinal cord?
2. What is the location and organization of the motor
tracts in the spinal cord?
3. What is the clinical significance of a Babinski sign?
4. Why are there dissociated sensory losses in both legs?
5. Where is the lesion?
68
SYSTEMS OF THE BODY