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216 PHYSICAL EXAMINATION
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UNIT 2
FIGURE 7.12 Assessment of light touch
Light touch
1. Use a wisp of cotton and apply the stimulus with very light strokes
E
(
Figure7.12). If the skin is calloused, or for thicker skin on the hands and soles,
the stimulus may need to be intensied, although care must be taken not to
stimulate subcutaneous tissues.
2. Begin with distal areas of the consumer’s limbs and move proximally.
3. Test the hand, lower arm, abdomen, foot and leg. Examination of sensation
of the face is discussed in the cranial nerves section.
4. To prevent the consumer from being able to predict the next touch, alter the
rate and rhythm of stimulation. Also, vary the sites of stimulation, keeping
in mind that the right and left sides must be compared.
5. Instruct the consumer to respond by saying ‘now’ or ‘yes’ when the stimulus
is felt, and to identify the area that was stimulated either verbally or by
pointing to it.
Proprioceptive sensation
Motion and position
1. Grasp the consumer’s index nger with your thumb and index nger.
E
Holdthe nger at the sides (parallel to the plane of movement) in order
notto exert upwards or downwards pressure with your ngers and thus
givethe consumer any clues as to which direction the nger is moving.
Theconsumer’s ngers should be relaxed.
2. Have the consumer shut their eyes, and show the consumer what ‘up’ and
‘down’ feel like by moving the nger in those directions.
3. Use gentle, slow and deliberate movements. Begin with larger movements
that become smaller and less perceptible.
4. Instruct the consumer to respond ‘up,’ ‘down,’ or ‘I can’t tell’ after each time
you raise or lower the nger.
5. Repeat this several times. Vary the motion in order not to establish a
predictable pattern.
6. Repeat steps 2–5 with the nger of the consumer’s opposite hand, and then
with the great toes.
7. If there appears to be a decit in motion sense, proceed to the proximal
joints such as wrists or ankles, and repeat the test.
The consumer should be able to correctly identify the changes of position of
N
thebody.
Inability to perceive direction of movement is abnormal.
A
Peripheral neuropathies will interfere with position sense. A lesion of the
P
posterior column will cause an ipsilateral loss of position sense. Lesions of the
sensory cortex, the thalamus, or the connections between them (thalamocortical
connections) may also disrupt position sense.
More detailed assessment such as vibration sense, cortical sensation (such as
stereognosis, graphaesthesia, two-point discrimination and extinction) is usually
undertaken in advanced assessment and can be found in the online content.
Examination of cranial nerves
A complete examination of the 12 cranial nerves is necessary when a baseline
assessment is desired, if a tumour of a specic cranial nerve is suspected, or if
periodic assessment is needed after surgery or radiation treatments. An abbreviated
cranial nerve examination is an integral part of a neurological screening
examination. The screening examination would include cranial nerves II, III, IV
and VI: visual acuity and gross visual elds, fundoscopic examination, pupillary
reactions, and extraocular movements; cranial nerves VII, VIII, IX, X and XII: facial
musculature and expression, gross hearing, voice and inspection of the tongue.
E
ExaminationNNormal ndingsAAbnormal ndingsPPathophysiology
MENTAL STATUS AND NEUROLOGICAL TECHNIQUES 217
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Olfactory nerve (CN I)
1. Ask the consumer to close their eyes.
E
2. Test each side separately by asking the consumer to occlude one nostril by
pressing against it with a nger. Determine whether the nasal passages are
patent by asking the consumer to breathe through rst one nostril and then
through the other while occluding the opposing nostril by pressing against
it with a nger. Assessment of the olfactory nerve may be delayed if the
consumer has a severe cold, allergic rhinitis, nasal packing, had recent oral
surgery, or if nasal steroids have been used for a prolonged period.
3. Ask the consumer to hold the test vial close to the nostril and inhale
deeply in order to cause the odour to surround the mucous membranes and
adequately stimulate the olfactory nerve (
4. Ask the consumer to identify the contents of each vial.
5. Present one odour at a time and alternate them from nostril to nostril. Keep
aromatic substances such as cloves, coffee, orange, peanut butter or chocolate in
closed glass vials until they are presented to the consumer. Avoid using noxious
odours such as alcohol, camphor, ammonia, acetic acid or formaldehyde, which
may stimulate the trigeminal nerve endings in the nasal mucosa.
6. Allow enough time to pass between presentation of vials to prevent
confusion of the olfactory system.
7. Record the number of substances tested and the number of times the
consumer was able to correctly identify the contents.
8. Note whether a difference between the right and the left sides was apparent.
The consumer should be able to distinguish and identify the odours with
N
eachnostril.
Anosmia, the loss of the sense of smell, is abnormal.
A
Total loss of the sense of smell may be caused by trauma to the cribriform plate,
P
sinusitis, colds or heavy smoking. Unilateral anosmia may be the result of an
intracranial neoplasm, such as a meningioma of the sphenoid ridge compressing
the olfactory tract or bulb.
Figure 7.13).
FIGURE 7.13 Assessment of CN I
CHAPTER 7
Optic nerve (CN II)
Visual acuity
E N A P
See Chapter 10.
Visual elds
E N A P
See Chapter 10.
Fundoscopic examination
E N A P
See Chapter 10.
Oculomotor nerve (CN III)
Cardinal elds of gaze
E N A P
See Chapter 10.
Eyelid elevation
E N A P
See Chapter 10.
Pupil reactions (direct, consensual, accommodation)
E N A P
See Chapter 10.
Trochlear nerve (CN IV)
Cardinal elds of gaze
E N A P
See Chapter 10.
E
ExaminationNNormal ndingsAAbnormal ndingsPPathophysiology
218 PHYSICAL EXAMINATION
A. Temporalis muscles
B. Masseter muscles
Ophthalmic
Maxillary
Mandibular
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UNIT 2
FIGURE 7.14 Assessment of the motor
component of CN V
FIGURE 7.15 Assessment of the sensory
component of CN V: Light touch
FIGURE 7.16 Assessment of the sensory
component of CN V and motor component
of CN VII: Corneal reex
Trigeminal nerve (CN V)
Motor component
1. Instruct the consumer to clench the jaw.
E
2. Palpate the contraction of the temporalis (Figure 7.14A) and masseter (Figure 7.14B)
muscles on each side of the face by feeling for contraction of the muscles with
the nger pads of the rst three ngers.
3. Ask the consumer to move the jaw from side to side against resistance from
your hand. Feel for weakness on one side or the other as the consumer
pushes against resistance.
4. Test the muscles of mastication by having the consumer bite down with
the molars on each side of a tongue blade and comparing the depth of the
impressions made by the teeth. If you can pull the tongue blade out while
the consumer is biting on it, there is weakness of the muscles of mastication.
5. Observe for fasciculation and note the bulk, contour and tone of the muscles
of mastication.
Sensory component
1. Instruct the consumer to close their eyes.
E
2. Test light touch by using a cotton wisp to lightly stroke the consumer’s face
in each area of the sensory distribution of the trigeminal nerve (
3. Instruct the consumer to respond by saying ‘now’ each time the touch of the
cotton wisp is felt.
4. Test and compare both sides of the face.
5. To assess supercial pain sensation, use a sterile needle. Before testing,
show the consumer how the sharpness of the needle feels compared to the
dullness of the opposite, blunt end. Testing with the blunt end will give some
reliability to the assessment.
a. Instruct the consumer to respond by saying ‘sharp’ or ‘dull’ when each
sensation is felt.
b. Irregularly alternate the sharp and dull ends, and again test each
distribution area of the trigeminal nerve on both sides of the face.
6. Test temperature sensation if other abnormalities have been detected.
Usevials of hot and cold water.
a. Touch the vials to each dermatomal distribution area, alternating hot
andcold.
b. The consumer should respond by saying ‘hot’ or ‘cold’.
7. Because sensation to the cornea is supplied by the trigeminal nerve, test the
corneal reex (the motor component is CN VII). The corneal reex should
not be routinely assessed in conscious consumers, unless there is a clinical
suspicion of trauma to CN V or CN VII.
a. Ask the consumer to open their eyes and look away from you.
b. Approach the consumer out of the line of vision to eliminate the
blinkreex. You can stabilise the consumer’s chin with your hand if
itismoving.
c. Lightly stroke the cornea with a slightly moistened cotton wisp (to avoid
irritating the cornea) (
Figure 7.16). Avoid stroking just the sclera or the
lashes of the eye. An alternative technique is to instil normal saline eye
drops instead of a light stroke of a cotton wisp.
d. Observe for bilateral blinking of the eyes.
e. Repeat on the opposite eye.
Figure 7.15).
E
ExaminationNNormal ndingsAAbnormal ndingsPPathophysiology
MENTAL STATUS AND NEUROLOGICAL TECHNIQUES 219
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The temporalis and masseter muscles should be equally strong on palpation.
N
Thejaw should not deviate and should be equally strong during side-to-side
movement against resistance. The volume and bulk of the muscles should be
bilaterally equal. Sensation to light touch, supercial pain and temperature
should be present on the sensory distribution areas of the trigeminal nerve.
Thecorneal reex should cause bilateral blinking of eyes.
Lesions of the trigeminal nerve may give rise to either reduced sensory
A
perception or to facial pain, both of which are abnormal.
Aneurysms of the internal carotid artery next to the cavernous sinus may give
P
rise to severe pain in the ophthalmic or mandibular distribution of the
trigeminal nerve due to the pressure of the aneurysm on the nerve. Neoplasms
that compress the gasserian ganglion or root, such as meningiomas, pituitary
adenomas and malignant tumours of the nasopharynx, may cause facial pain
and impairment of sensation. Head injuries, especially basilar skull fractures,
may give rise to facial anaesthesia and paralysis of the muscles of mastication.
Trigeminal neuralgia (tic douloureux), characterised by brief, paroxysmal,
A
unilateral facial pain along the distribution of the trigeminal nerve, is abnormal.
The pain can be provoked by touch or movement of the face, such as in tooth
brushing, yawning, chewing or talking. There is no associated motor weakness.
Trigeminal neuralgia may occur in consumers with multiple sclerosis due to
P
demyelination of the root of CN V. The consumer with a posterior fossa tumour
may have trigeminal neuralgia. In most cases, there is no aetiology found.
Postherpetic neuralgia is found most often in the elderly. The pain is continuous
A
and is described as a constant, burning ache with occasional stabbing pains. The
stabbing pain may begin spontaneously or may be provoked by touch. The pain
is unilateral and tends to follow the distribution of the ophthalmic distribution
of the trigeminal nerve. It is abnormal.
Herpes zoster involvement of the trigeminal nerve causes postherpetic neuralgia.
P
Inammatory lesions are found throughout the trigeminal pathways.
Tetanus is characterised by tonic spasms interfering with the muscles that open
A
the jaw (trismus).
Dysphagia and spasms of the pharyngeal muscles are also
observed in tetanus. Tetanus is abnormal.
Motor root involvement of the trigeminal nerve causes the spasm of the
P
masseter muscles.
CHAPTER 7
Abducens nerve (CN VI)
Cardinal elds of gaze
E N A P
See Chapter 10.
Facial nerve (CN VII)
Motor component
1. Observe the consumer’s facial expressions for symmetry and mobility
E
throughout the examination.
2. Note any asymmetry of the face, such as wrinkles or lack of wrinkles on one
side of the face or one-sided blinking.
3. Test muscle contraction by asking the consumer to:
a. frown
b. raise their eyebrows
c. wrinkle their forehead while looking up
d. close their eyes lightly and then keep them closed against your resistance
(Figure 7.17)
e. smile, show teeth, purse lips, and whistle
f. puff out the cheeks against the resistance of your hands.
E
ExaminationNNormal ndingsAAbnormal ndingsPPathophysiology
FIGURE 7.17 Assessment of the motor
component of CN VII: Opening the
consumer’s eyes against resistance
220 PHYSICAL EXAMINATION
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UNIT 2
4. Observe for symmetry of facial muscles and for weakness during the
E
abovemanoeuvres.
5. Note any abnormal movements such as tremors, tics, grimaces or immobility.
Normal ndings of the motor portion of the facial nerve include symmetry
N
between the right and the left sides of the face as well as between the upper
andlower portions of the face at rest and while executing facial movements.
There should be an absence of abnormal muscle movement.
Bell’s palsy (idiopathic facial palsy), characterised by complete accid paralysis
A
of the facial muscles on the involved side, is abnormal. The affected side of the
face is smooth, the eye cannot close, the eyebrow droops, the labiofacial fold is
gone, and the mouth may droop. Loss of the sensation of taste in the anterior
two-thirds of the tongue may occur.
Bell’s palsy is caused by damage to the facial nerve. It is a lower motor neurone
P
paralysis because the damage occurs along the facial nerve from its origin
toitsperiphery.
Supranuclear facial palsy is characterised by paralysis in the lower one-third to
A
two-thirds of the face; the upper portion of the face is spared. The nasolabial
foldis at, and the eye on the affected side can close, although may be weaker.
The consumer may be unable to keep the eye closed against resistance applied
by the nurse. The muscles of the upper portion of the face remain intact.
Supranuclear facial palsy is abnormal.
Supranuclear facial palsy is due to an upper motor neurone lesion of the
P
facialnerve.
Sensory component
1. Sensory examination of the facial nerve is limited to testing taste.
E
Theportions of the tongue that are tested are:
a. the tip of the tongue for sweet and salty tastes
b. along the borders and at the tip for sour taste
c. the back of the tongue and the soft palate for bitter taste.
2. Test both sides of the tongue with each solution.
3. The consumer’s tongue should protrude during the entire assessment of
taste, and talking is not allowed. In order for the consumer to identify the
substance, the words sweet, salty, bitter and sour should be written on a
cardso that the consumer can point to what is tasted. Be sure the consumer
does not see which solution is being tested.
4. Cotton swabs may be used as applicators, using a different one for
eachsolution.
5. Dip the cotton swab into the solution being tested and place it on the
appropriate part of the tongue.
6. Instruct the consumer to point to the word that best describes the
tasteperception.
7. Instruct the consumer to rinse the mouth with water before the next
solutionis tested.
8. Repeat steps 5–7 until each solution has been tested on both sides of
thetongue.
Normal sensation would be accurate perceptions of sweet, sour, salty and
N
bittertastes.
Ageusia (loss of taste) and hypogeusia (diminution of taste) are abnormal.
A
Age, excessive smoking, extreme dryness of the oral mucosa, colds, medications,
P
lesions of the medulla oblongata and lesions of the parietal lobe may cause
alterations in the sense of taste.
E
ExaminationNNormal ndingsAAbnormal ndingsPPathophysiology
MENTAL STATUS AND NEUROLOGICAL TECHNIQUES 221
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Acoustic nerve (CN VIII)
Cochlear division
Hearing
E N A P
See Chapter 11.
Weber and Rinne tests
E N A P
See Chapter 11.
Vestibular division
The vestibular division of CN VIII assesses for vertigo.
1. During the history, ask the consumer if vertigo is experienced.
E
2. Note any evidence of equilibrium disturbances. Refer to the section on
cerebellar examination.
3. Note the presence of nystagmus.
N
Vertigo is not normally present.
Vertigo describes an uncomfortable sensation of movement of the environment
A
or the movement of self within a stationary environment; it is often
accompanied by nausea, vomiting and nystagmus.
Vertigo is caused by a disorder of the labyrinth or the vestibular nerve. Causative
P
factors may include migraine headache, which causes a disruption in the supply
of the internal auditory artery. Tumours of the cerebellopontine angle may cause
vertigo by compressing the vestibular nerve. Head injuries that involve the
labyrinth may cause vertigo. Blockage of the Eustachian tube during ascent in
anaeroplane may lead to vertigo.
Ménière’s disease, characterised by vertigo that lasts for minutes or hours,
A
low-pitched roaring tinnitus, progressive hearing loss, nausea and vomiting,
isabnormal. The consumer also experiences pressure in the ear.
The main pathological nding is distension of the endolymphatic system, with
P
degenerative changes in the organ of Corti.
CHAPTER 7
Glossopharyngeal and vagus nerves (CN IX and CN X)
The glossopharyngeal and vagus nerves are tested together because of their overlap
in function.
1. Examine soft palate and uvula movement and gag reex as described
E
inChapter 11.
2. Assess the consumer’s quality of speech for a nasal quality or hoarseness. Ask
the consumer to produce guttural and palatal sounds, such as k, q, ch, b and d.
3. Assess the consumer’s ability to swallow a small amount of water. Observe
for regurgitation of uids through the nose. If the consumer is unable to
swallow, observe how oral secretions are handled.
4. The sensory examination of the glossopharyngeal and vagus nerves is limited
to taste on the posterior one-third of the tongue. This examination was
previously discussed in the section on CN VII.
Refer to Chapter 11 for normal soft palate and uvula movement and gag
N
reexndings. The speech is clear, without hoarseness or a nasal quality.
Theconsumer is able to swallow water or oral secretions easily. Taste (sweet,
salty, sour and bitter) is intact in the posterior one-third of the tongue.
Unilateral lowering and attening of the palatine arch; weakness of the soft
A
palate; deviation of the uvula to the normal side; mild dysphagia, regurgitation
of uids, and nasal quality of the voice; loss of taste in the posterior one-third of
the tongue; and hemianaesthesia of the palate and pharynx, are abnormal.
Unilateral glossopharyngeal and vagal paralysis, such as with trauma or skull
P
fractures at the base of the skull, will cause these symptoms.
E
ExaminationNNormal ndingsAAbnormal ndingsPPathophysiology
222 PHYSICAL EXAMINATION
A. Strength of sternocleidomastoid muscle
B. Strength of trapezius muscle
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UNIT 2
FIGURE 7.18 Assessment of CN XI
Marked nasal quality of the voice, difculty with guttural and palatal sounds,
A
severe dysphagia with liquids, and inability of the palate to elevate on
phonation, are abnormal.
Bilateral vagus nerve paralysis will cause these more marked symptoms, and
P
often occurs simultaneously with signs and symptoms of other lower brain stem
cranial nerve dysfunctions, such as in progressive bulbar palsy in amyotrophic
lateral sclerosis (ALS).
Spinal accessory nerve (CN XI)
1. Place the consumer in a seated or a supine position. Inspect the
E
sternocleidomastoid muscles for contour, volume and fasciculation.
2. Place your right hand on the left side of the consumer’s face. Instruct
theconsumer to turn the head sideways against the resistance of your
hand(
Figure 7.18A).
3. Use the other hand to palpate the sternocleidomastoid muscle for strength
ofcontraction. Inspect the muscle for contraction.
4. Repeat steps 2 and 3 in the opposite direction. Compare the strength of the
two sides.
5. To assess the function of the trapezius muscle, stand behind the consumer
and inspect the shoulders and scapula for symmetry of contour. Note any
atrophy or fasciculation.
6. Place your hands on top of the consumer’s shoulders and instruct the
consumer to raise the shoulders against the downwards resistance of your
hands (
7. Observe the movements and palpate the contraction of the trapezius
muscles. Compare the strength of the two sides.
The consumer should be able to turn their head against resistance with a
N
smooth, strong and symmetrical motion. The consumer should also demonstrate
the ability to shrug the shoulders against resistance with strong, symmetrical
movement of the trapezius muscles.
Inability to turn the head towards the paralysed side, and a at, noncontracting
A
muscle on that side are abnormal ndings. The contralateral sternocleidomastoid
muscle may be contracted.
These ndings are the result of unilateral paralysis of the sternocleidomastoid
P
muscle due to trauma, tumours, or infection affecting the spinal accessory nerve.
The inability of the consumer to elevate one shoulder, asymmetrical drooping
A
ofthe shoulder and scapula, and a depressed outline of the neck are abnormal
ndings. The involved shoulder may also show atrophy and fasciculation of
themuscles.
Unilateral paralysis of the trapezius muscle may be suspected, usually due to
P
trauma, tumours or infection.
For information on torticollis, see Chapter 9.
A P
Figure 7.18B). This can be performed in front of or behind the consumer.
Hypoglossal nerve (CN XII)
1. See Chapter 11 for assessment of tongue movement.
E
2. Assess lingual sounds by asking the consumer to say ‘la la la’.
N
See Chapter 11 for normal tongue movements. Lingual speech is clear.
Inability or difculty in producing lingual sounds is abnormal. The speech
A
sounds lispy and clumsy.
Lesions of the hypoglossal nerve will cause difculty in pronunciation of
P
lingualsounds.
E
ExaminationNNormal ndingsAAbnormal ndingsPPathophysiology
MENTAL STATUS AND NEUROLOGICAL TECHNIQUES 223
A. Decerebrate rigidity (abnormal extension)
B. Decorticate rigidity (abnormal flexion)
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Examination of motor system
E N A P
For
see Chapter 16. See the following for additional abnormal ndings
andpathophysiology.
Extrapyramidal rigidity is evident when resistance is present during passive
A
movement of the muscles in all directions and lasts throughout the entire range
of motion. It may involve both exor and extensor muscles and is abnormal.
Extrapyramidal rigidity is due to lesions located in the basal ganglia.
P
Decerebrate rigidity (decerebration) is characterised by rigidity and sustained
A
contraction of the extensor muscles and is abnormal. The arms are adducted,
extended and hyperpronated. The legs are stify extended and the feet are
plantar exed (
clenched (opisthotonos).
Decerebration may be found in unconscious consumers with deep, bilateral
P
diencephalic injury that progresses to midbrain dysfunction. Decerebrate rigidity
may also occur due to midbrain and pontine damage, which occurs with
compression of these structures due to expanding cerebellar or posterior fossa
lesions. Severe metabolic disorders that depress diencephalic and forebrain
function may also cause decerebration.
Decorticate rigidity (decortication) is characterised by hyperexion of
A
thearms (exion of the arm, wrist and ngers, adduction of the arms),
hyperextension and internal rotation of the legs, and plantar exion (
It is abnormal.
Decorticate rigidity is found in unconscious consumers with cerebral hemisphere
P
lesions that interfere with the corticospinal tract.
on muscle size, tone, strength and involuntary movements
Figure 7.19A). The back and neck may be arched and the teeth
Figure 7.19B).
CHAPTER 7
FIGURE 7.19 Motor system dysfunction
Pronator drift
1. Have the consumer extend the arms out in front with palms up for 20 seconds.
E
2. Observe for downwards drifting of an arm.
N
There should be no downwards drifting of an arm.
Downwards drifting of an arm is abnormal.
A
Downwards drifting of an arm may indicate hemiparesis, such as in stroke.
P
Examination of cerebellar function (coordination and gait)
Motor coordination refers to smooth, precise and harmonious muscular activity.
Movement requires the coordination of many muscle groups. Coordination is
an integrated process involving complicated neural integration of the motor and
premotor cortex, basal ganglia, cerebellum, vestibular system, posterior columns
and peripheral nerves.
E
ExaminationNNormal ndingsAAbnormal ndingsPPathophysiology
224 PHYSICAL EXAMINATION
A. Supination
B. Pronation
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UNIT 2
FIGURE 7.20 Assessment of coordination:
Fingertip-to-nose touch
Equilibratory coordination refers to maintenance of an upright stance and
depends on the vestibular, cerebellar and proprioceptive systems. Nonequilibratory
coordination refers to smaller movements of the extremities and involves the
cerebellar and proprioceptive mechanisms.
Incoordination is categorised into three different types of syndromes: cerebellar,
vestibular and posterior column syndromes. Incoordination is not considered to be
secondary to involuntary movements, paresis or alterations of muscle tone.
Gait refers to the consumer’s manner of walking.
Coordination
1. Instruct the consumer to sit comfortably facing you, with eyes open and
E
arms outstretched. Ensure that consumers who wear corrective lenses
(glasses or contacts) are wearing them prior to assessing their coordination.
2. Ask the consumer to rst touch the index nger to the nose, then to
alternate rapidly with the index nger of the opposite hand.
3. With their eyes closed, have the consumer continue to rapidly touch the
nose with alternate index ngers (
4. With their eyes open, ask the consumer to again touch nger to nose.
Next,ask the consumer to touch your index nger, which is held about
45cm away from the consumer.
5. Change the position of your nger as the consumer rapidly repeats the
manoeuvre with one nger.
6. Repeat steps 4 and 5 with the other hand.
7. Observe for intention tremor or overshoot or undershoot of the
consumer’snger.
8. To assess rapid alternating movements, ask the consumer to rapidly
alternate patting their knees, rst with the palms and then alternating
palms with the backs of the hands (rapid supinating [see
pronating [see
Figure 7.21B] of the hands).
9. Ask the consumer to repeatedly touch the thumb to each of the ngers of
the hand in rapid succession from index to the fth nger, and back.
Figure 7.20).
Figure 7.21A] and
FIGURE 7.21 Assessment of coordination: Rapid alternating hand movements
FIGURE 7.22 Assessment of coordination:
Heel slide
10. Repeat step 9 with the other hand.
E
11. Observe coordination and the ability of the consumer to perform these in
rapid sequence.
12. With the consumer in a seated or supine position, ask the consumer to place
the heel just below the knee on the shin of the opposite leg and to slide it
down to the foot (Figure 7.22).
13. Repeat with the opposite foot.
E
ExaminationNNormal ndingsAAbnormal ndingsPPathophysiology
MENTAL STATUS AND NEUROLOGICAL TECHNIQUES 225
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15. Ask the consumer to draw a circle or a gure 8 with a foot either on the
E
ground or in the air (
Figure 7.23).
16. Repeat with the other foot.
17. Observe for coordination and regularity of the gure.
18. Test the lower extremities for rapid alternating movement by asking the
consumer to rapidly extend the ankle (‘tap your foot’) or to rapidly ex and
extend the toes of one foot.
19. Repeat with the opposite foot.
20. Note rate, rhythm, smoothness and accuracy of the movements.
The consumer is able to rapidly alternate touching nger to nose and moving
N
nger from nose to your nger in a coordinated fashion. The consumer is able
toperform alternating movements in a purposeful, rapid, coordinated manner.
The consumer demonstrates the ability to purposefully and smoothly run heel
down shin with equal coordination in both feet and to draw a gure 8 or circles
with the foot.
Dyssynergy, the lack of coordinated action of the muscle groups, is abnormal.
A
FIGURE 7.23 Assessment of coordination:
Figure 8
The consumer is unable to carry out smooth, coordinated movements.
Theconsumer’s movements appear jerky, irregular and uncoordinated.
Dysmetria, impaired judgement of distance, range, speed and force of
movement, is abnormal. The consumer misjudges distance and overshoots.
Dysdiadochokinesia, the inability to perform rapid alternating movements,
P
isabnormal. The consumer is unable to abruptly stop one movement and begin
another opposite movement.
Cerebellar disease causes all of these abnormal ndings.
CHAPTER 7
Gait
E N A P
See Chapter 16 for assessment of gait.
EVALUATION OF HEALTH ASSESSMENT AND PHYSICAL
EXAMINATION FINDINGS
In the evaluation phase of a health assessment, the focus is on ensuring the data
gathered is complete, accurate and documented appropriately. (See case study as
an example of the focused assessment, and Chapter 22 for a comprehensive health
assessment.) In evaluating the data you should:
> draw on your critical thinking and problem-solving skills to make sound
clinicaldecisions
> act on abnormal data (include communicating ndings to other
health professionals)
> ensure documentation reects the outcomes of the clinical decisions/actions
taken. (Refer to Chapter 3, which discusses in detail why documentation is so
important and how this may be undertaken in different health settings.)
The case study that follows steps you through this process.
E
ExaminationNNormal ndingsAAbnormal ndingsPPathophysiology
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