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Anterior cranial fossa
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Cranial nerves • 143
Olfactory nerves
(cribriform plate)
Optic nerve (optic canal)
Superior
Mandibular division of trigeminal
Oculomotor nerve
orbital
fissure
(internal acoustic meatus)
Trochlear nerve
Middle cranial fossa
nerve (foramen ovale)
Abducens nerve
(inferior petrosal sinus)
vestibulocochlear nerves
Posterior cranial fossa
Facial and
Ophthalmic division of
trigeminal nerve
(superior orbital fissure)
Maxillary division of
trigeminal nerve
(foramen rotundum)
Trigeminal ganglion in
Meckel's cave
Trigeminal nerve (motor root)
Glossopharyngeal
nerve
Vagus nerve
Spinal accessory
nerve
Hypoglossal nerve
(hypoglossal canal)
(Jugular
foramen)
Fig. 7.5 Base of the cranial cavity. The dura mater, with the cranial nerves and their exits from the skull. On the right side, part of the tentorium cerebelli and
the roof of the trigeminal cave have been removed.
7.4 Summary of the 12 cranial nerves
7
Nerve Examination Abnormalities/symptoms
I Sense of smell, each nostril Anosmia/parosmia
II Visual acuity
III Light and accommodation reflex Impairment or loss
III, IV and VI Eye position and movements Strabismus, diplopia, nystagmus
V Facial sensation
VII Muscles of facial expression
VIII Whisper and tuning fork tests
IX Pharyngeal sensation Not routinely tested
X Palate movements Unilateral or bilateral impairment
XI Trapezius and sternomastoid Weakness of scapular and neck movement
XII Tongue appearance and movement Dysarthria and chewing/swallowing difficulties
Visual fields
Pupil size and shape
Pupil light reflex
Fundoscopy
Corneal refl ex
Muscles of mastication
Jaw jerk
Taste over anterior two-thirds of tongue
Vestibular tests
Partial sight/blindness
Scotoma; hemianopia
Anisocoria
Impairment or loss
Optic disc and retinal changes
Impairment, distortion or loss
Impairment or loss
Weakness of chewing movements
Increase in upper motor neuron lesions
Facial weakness
Ageusia (loss of taste)
Impaired hearing/deafness
Nystagmus and vertigo
144 • THE NERVOUS SYSTEM
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Parosmia is the perception of pleasant odours as unpleasant;
it may occur with head trauma or sinus infection or be an adverse
effect of drugs. Olfactory hallucinations may occur in Alzheimer’s
disease and focal epilepsies. Phantosmia, when patients
describe a persistent smell, often cigarette smoke, is common
and usually benign.
Optic (II), oculomotor (III), trochlear (IV) and
abducens (VI) nerves
See Chapter 8.
Trigeminal (V) nerve
The V nerve conveys sensation from the face, mouth and part of
the dura and provides motor supply to the muscles of
mastication.
Anatomy
The cell bodies of the sensory fibres are located in the trigeminal
(Gasserian) ganglion, which lies in a cavity (Meckel’s cave) in the
petrous temporal dura (see Fig. 7.5). From the trigeminal ganglion, the V nerve passes to the pons. From here, pain and
temperature pathways descend to the C2 segment of the spinal
cord, so ipsilateral facial numbness may occur with cervical cord
lesions.
There are three major branches of V (Fig. 7.6):
• ophthalmic (V
• maxillary (V
• mandibular (V
Fig. 7.6 The sensory distribution of the three divisions of the trigeminal
1 . Ophthalmic division. 2 . Maxillary division. 3 . Mandibular division.
nerve.
): sensory
1
): sensory
2
): sensory and motor.
3
C2
C3
1
2
3
The ophthalmic branch leaves the ganglion and passes forward to the superior orbital fissure via the wall of the cavernous
sinus (see Fig. 8.3). In addition to the skin of the upper nose,
upper eyelid, forehead and scalp, V
eye (cornea and conjunctiva) and the mucous membranes of the
sphenoidal and ethmoid sinuses and upper nasal cavity.
The maxillary branch (V
cavernous sinus to leave the skull by the foramen rotundum. It
contains sensory fibres from the mucous membranes of the
upper mouth, roof of the pharynx, gums, teeth and palate of the
upper jaw and the maxillary, sphenoidal and ethmoid sinuses.
The mandibular branch (V
ovale and supplies the floor of the mouth, sensation (but not
taste) to the anterior two-thirds of the tongue, the gums and
teeth of the lower jaw, mucosa of the cheek and the temporomandibular joint, in addition to the skin of the lower lips and jaw
area, but not the angle of the jaw (see Fig. 7.6).
The motor fibres of V run in the mandibular branch (V
innervate the muscles of mastication: temporalis, masseter and
medial and lateral pterygoids.
) passes from the ganglion via the
2
3
supplies sensation to the
1
) exits the skull via the foramen
) and
3
Examination sequence (Video 9)
Four aspects need to be assessed: sensory, motor and two
reflexes.
Sensory
• Ask the patient to close their eyes and say ‘yes’ each time
they feel a light touch (you use a cotton-wool tip for this test).
Do this in the areas of V
• Repeat using a fresh neurological pin, such as a Neurotip, to
test superficial pain.
• Compare both sides. If you identify an area of reduced
sensation, map it out. Does it conform to the distribution of
the trigeminal nerve or branches? Remember the angle of the
jaw is served by C2 and not the trigeminal nerve, but V
extends towards the vertex (see Fig. 7.6).
• ‘Nasal tickle’ test: use a wisp of cotton wool to ‘tickle’ the
inside of each nostril and ask the patient to compare. The
normal result is an unpleasant sensation easily appreciated
by the patient.
1,V2
and V3.
Motor (signs rare)
• Inspect for wasting of the muscles of mastication (most
apparent in temporalis).
• Ask the patient to clench their teeth; feel the masseters,
estimating their bulk.
• Ask the patient to open their jaw and note any deviation; the
jaw may deviate to the paralysed side due to contraction of
the intact contralateral pterygoid muscle.
Corneal reflex
Routine testing of the corneal reflex is unnecessary but may be
relevant when the history suggests a lesion localising to the
brainstem or cranial nerves V, VI I or VIII. The affer ent l imb i s vi a
the trigeminal nerve, the efferent limb via the facial nerve.
1
Fig. 7.7 Testing the corneal reflex. The cotton-wool wisp should touch the
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cornea overlying the iris, not the conjunctiva, and avoid visual stimulus.
Cranial nerves • 145
7.5 Comparison of bulbar and pseudobulbar palsy
Bulbar palsy Pseudobulbar palsy
Level of motor
Lesion
Speech Dysarthria Dysarthria and dysphonia
Swallowing Dysphagia Dysphagia
Tongue Weak, wasted
Jaw jerk Absent Present/brisk
Emotional lability Absent May be present
Causes Motor neuron
Lower motor
neuron
and
fasciculating
disease
Upper motor neuron
Spastic, slow-moving
Cerebrovascular disease, motor
neuron disease, multiple sclerosis
7
• Explain to the patient what you are going to do and ask them
to remove their contact lenses, if relevant.
• Gently depress the lower eyelid while the patient looks up.
• Lightly touch the lateral edge of the cornea with a wisp of
damp cotton wool (Fig. 7.7).
• Look for both direct and consensual blinking.
Jaw jerk
• Ask the patient to let their mouth hang loosely open.
• Place your forefinger in the midline between lower lip and
chin.
• Percuss your finger gently with the tendon hammer in a
downward direction (Fig. 7.8), noting any reflex closing of the
jaw.
• An absent, or just present, reflex is normal. A brisk jaw jerk
occurs in pseudobulbar palsy (Box 7.5).
Sensory symptoms include facial numbness and pain. Unilateral loss of sensation in one or more branches of the V nerve
may result from direct injury in association with facial fractures
Fig. 7.8 Eliciting the jaw jerk.
(particularly V
drome. Lesions in the caver nous sinus often cause loss of the
corneal r efl ex and V
nerves III, IV and VI may also be involved (see Fig. 8.3). Trigeminal neuralgia causes severe, lancinating pain, typically in
the distribution of V
zoster virus (chickenpox) can affect any sensory nerve, but
typically either V
zoster ophtha lmicus (affecting V
threatening complications. Hutchinson’s sign, vesicles on the
side or tip of the nose, may be present.
Clinically significant weakness of the muscles of mastication is
unusual but may occur in myasthenia gravis, with fatigable
chewing. Claudication (i.e. pain on chewing) of these muscles
can occur in temporal arteritis.
), local invasion by cancer or Sjögren’ ssyn-
2
or V2cutaneous sensor y loss. Cranial
1
or V3. Reactivation of herpes varicella
2
orathoracicdermatome(Fig. 7.9). In herpes
1
), there is a risk of sight-
1
Facial (VII) nerve
The facial nerve supplies the muscles of facial expression (frontalis, orbicularis oculi, buccinators, orbicularis oris and platysma)
and carries parasympathetic fibres to the lacrimal, submandibular and sublingual salivary glands (via nervus intermedius). It
receives taste sensation from the anterior two-thirds of the
tongue (via the chorda tympani; Fig. 7.10).
Anatomy
From its motor nucleus in the lower pons, fibres of the VII nerve
pass back to loop around the VI nerve nucleus before emerging
from the lateral pontomedullary junction in close association with
the VIII nerve (Fig. 7.11); together they enter the internal acoustic
meatus (see Fig. 7.5). At the lateral end of the meatus, the VII
nerve continues in the facial canal within the temporal bone,
exiting the skull via the stylomastoid foramen. Passing through
the parotid gland, it gives off its terminal branches. In its course in
the facial canal, it gives off branches to the stapedius muscle and
its parasympathetic fibres as well as being joined by the taste
fibres of the chorda tympani (see Fig. 7.10).
A
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CB
D
Fig. 7.9 Herpes zoster. A The ophthalmic division of the left trigeminal (V) nerve is involved. B The maxillary division of the left V nerve. C Cervical spinal
root left C4.
Anterior two-thirds
Submandibular
D Thoracic spinal root right T5.
Lacrimal gland
Mucous mambranes
of nasal and oral
cavities
of the tongue
Sublingual
gland
gland
Palate
Pterygopalatine
ganglion
Geniculate ganglion
Chorda
tympani
To facial muscles
Superior salivatory
nucleus
Abducens nucleus
Fourth ventricle
Facial nucleus
Nucleus solitarius
Stylomastoid foramen
To stapedius
muscle
Submandibular ganglion
= Motor fibres
= Sensory
= Parasympathetic
Fig. 7.10 Component fibres of the facial nerve and their peripheral distribution.
Fig. 7.11 Lesions of the pons. Lesions at (1) may result in ipsilateral VI and
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VII nerve palsies and contralateral hemiplegia. At (2) ipsilateral cerebellar signs
and impaired sensation on the ipsilateral side of the face and on the
contralateral side of the body may occur.
Examination sequence (Video 10)
Examination is usually confined to motor function; taste is rarely
tested.
Motor function
• Inspect the face for asymmetry or differences in blinking or
eye closure on one side. Note that minor facial asymmetry is
common and rarely pathological.
• Watch for spontaneous or involuntary movement such as
blepharospasm, hemifacial spasm or aberrant innervation
after facial nerve palsy.
• For the following actions it is often easiest to demonstrate the
actions yourself and ask the patient to copy you, observing
for any asymmetry.
Cranial nerves • 147
• Ask the patient to raise their eyebrows and observe for
symmetrical wrinkling of the forehead (frontalis muscle).
• Ask the patient to screw their eyes tightly shut and resist you
opening them (orbicularis oculi).
• Ask the patient to bare their teeth (orbicularis oris).
• Ask the patient to blow out their cheeks with their mouth
closed (buccinators and orbicularis oris).
In a unilateral lower motor neuron VII nerve lesion, there is
weakness of both upper and lower facial muscles. Bell’spalsyis
the term used to describe an idiopathic acute lower motor neuron
VII nerve paralysis, often preceded by mastoid pain. It may be
associated with impairment of taste and hyperacusis (high-pitched
sounds appearing unpleasantly louder than normal). Bell’sphenomenon occurs when a patient closes their eyes: as eye closure
is incomplete, the globe can be seen to roll upwards to avoid
corneal exposure (Fig. 7.12A). Ramsay Hunt syndrome occurs in
herpes zoster infection of the geniculate (facial) ganglion. This
produces a severe lower motor neuron facial palsy, ipsilateral loss
of taste and buccal ulceration, and a painful vesicular eruption in
the external auditory meatus. Other causes of a lower motor
neuron VII lesion include cerebellopontine angle tumours (including
acoustic neuroma), trauma and parotid tumours. Synkinesis
(involuntary muscle contraction accompanying a voluntary movement: most commonly, twitching of the corner of the mouth with
ipsilateral blinking) is a sign of aberrant reinnervation and may be
seen in recovering lower motor neuron VII lesions.
In unilateral VII nerve upper motor neuron lesions, weakness is
marked in the lower facial muscles with relative sparing of the
upper face. This is because there is bilateral cortical innervation
of the upper facial muscles. The nasolabial fold may be flattened
and the corner of the mouth drooped, but eye closure is usually
preserved (see Fig. 7.12B). Hemifacial spasm presents with
synchronised twitching of the ipsilateral eye and mouth.
Bilateral facial palsies are less common but occasionally occur,
as in Guillain–Barré syndrome, sarcoidosis or infection such as
Lyme disease, HIV or leprosy. Facial weakness, especially with
respect to eye closure, can also be found in some congenital
myopathies (facioscapulohumeral or myotonic dystrophies).
7
Loss of frontal
wrinkling
Bell’s phenomenon
Loss of
nasolabial fold
Mouth deviates
to normal side
A
Fig. 7.12 Types of facial weakness. A Right facial weakness due to right lower motor neurone lesion. B Right facial weakness due to left upper motor
neurone lesion.
Preserved function
in upper face
Loss of
nasolabial fold
Mouth deviates
to normal side
B
148 • THE NERVOUS SYSTEM
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Distinct from VII nerve palsies, Parkinson’s disease can cause
loss of spontaneous facial movements, including a slowed blink
rate, and involuntary facial movements (levodopa-induced dyskinesias) may complicate advanced disease.
Involuntary emotional movements, such as spontaneous
smiling, have different pathways and may be preserved in the
presence of paresis.
The vestibulocochlear (VIII) nerve
See page 194.
Glossopharyngeal (IX) and vagus (X) nerves
The IX and X nerves have an intimate anatomical relationship.
Both contain sensory, motor and autonomic components. The
glossopharyngeal (IX) nerve mainly carries sensation from the
pharynx and tonsils, and sensation and taste from the posterior
one-third of the tongue. The IX nerve also supplies the carotid
chemoreceptors. The vagus (X) nerve carries important sensory
information but also innervates upper pharyngeal and laryngeal
muscles. The main functions of IX and X that can be tested
clinically are swallowing, phonation/articulation and sensation
from the pharynx/larynx. In the thorax and abdomen, the vagus
(X) nerve receives sensory fibres from the lungs and carries
parasympathetic fibres to the lungs, heart and abdominal
viscera.
Glossopharyngeal
Sensory to pharynx
Motor to stylopharyngeus
Taste from posterior one-third
of tongue
Pharyngeal nerve
Elevators of palate and
closure of nasopharynx
Peristaltic movement of
constrictor muscles
(superior middle
and inferior)
Superior laryngeal
nerve
Internal
External
PONS
IX
Vagus
nerve
MEDULLA
X
XI
Jugular
foramen
Spinal part of
accessory nerve
Motor to sternomastoid and
trapezius muscles
Recurrent laryngeal
nerve
Motor to all the
intrinsic muscles
of the larynx
XI
Fig. 7.13 The lower cranial nerves: glossopharyngeal (IX), vagus
(X) and accessory (XI).
Anatomy
Both nerves arise as several roots from the lateral medulla and
leave the skull together via the jugular foramen (see Fig. 7.5). The
IX nerve passes down and forward to supply the stylopharyngeus muscle, the mucosa of the pharynx, the tonsils and the
posterior one-third of the tongue, and sends parasympathetic
fibres to the parotid gland. The X nerve courses down in the
carotid sheath into the thorax, giving off several branches,
including pharyngeal and recurrent laryngeal branches, which
provide motor supply to the pharyngeal, soft palate and laryngeal
muscles. The main nuclei of these nerves in the medulla are the
nucleus ambiguus (motor), the dorsal motor vagal nucleus
(parasympathetic) and the solitary nucleus (visceral sensation;
Fig. 7.13).
Examination sequence (Videos 11 and 11A)
• Assess the patient’s speech for dysarthria or dysphonia (p.
211).
• Ask them to say ‘Ah’. Look at the movements of the palate
and uvula using a torch. Normally, both sides of the palate
elevate symmetrically and the uvula remains in the midline.
• Ask the patient to puff out their cheeks with their lips tightly
closed. Listen for air escaping from the nose. For the cheeks
to puff out, the palate must elevate and occlude the nasopharynx. If palatal movement is weak, air will escape audibly
through the nose.
• Ask the patient to cough; assess the strength of the cough.
• Testing pharyngeal sensation and the gag re flex is unpleasant
and has poor predictive value for aspiration. Instead, and in
fully conscious patients only, use the swallow test. Administer
3 teaspoons of water and observe for absent swallow, cough
or delayed cough or change in voice quality after each
teaspoon. If there are no problems, observe again while the
patient swallows a glass of water.
Isolated unilateral IX nerve lesions are rare. Unilateral X nerve
damage leads to ipsilateral reduced elevation of the soft palate,
which may cause deviation of the uvula (away from the side of
the lesion) when the patient says ‘Ah’. Unilateral lesions of IX and
X are most commonly caused by strokes, skull-base fractures or
tumours. Damage to the recurrent laryngeal branch of the X
nerve due to lung cancer, thyroid surgery, mediastinal tumours
and aortic arch aneurysms causes dysphonia and a ‘bovine’
cough. Bilateral X nerve lesions cause dysphagia and dysarthria,
and may be due to lesions at the upper (pseudobulbar palsy) or
lower (bulbar palsy) motor neuron levels (see Box 7.5). Less
severe cases can result in nasal regurgitation of fluids and nasal
air escape when the cheeks are puffed out (dysarthria and nasal
escape are often evident during history taking). Always consider
myasthenia gravis in patients with symptoms of bulbar
dysfunction, even if the examination seems normal.
Accessory (XI) nerve
The accessory nerve has two components:
• a cranial part closely related to the vagus (X) nerve
Cranial nerves • 149
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• a spinal part that provides fi bres to the upper t rapezius
muscles, responsible for elevating (shrugging) the shoulders and elevating the arm above the horizontal, and the
sternomastoid muscle s that control head turning and neck
flexion.
The spinal component is discussed here.
Anatomy
The spinal nuclei arise from the anterior horn cells of C1–5. Fibres
emerge from the spinal cord, ascend through the foramen
magnum and exit via the jugular foramen (see Fig. 7.5), passing
posteriorly.
Examination sequence (Video 11B)
• Face the patient and inspect the sternomastoid muscles for
wasting or hypertrophy; palpate them to assess their bulk.
• Stand behind the patient to inspect the trapezius muscle for
wasting or asymmetry.
• Ask the patient to shrug their shoulders, then apply down-
ward pressure with your hands to assess the power.
• Test power in the left sternomastoid by asking the patient
to turn their head to the right while you provide resistance
with your hand placed on the right side of the patient’s
chin. Reverse the procedure to check the right
sternomastoid.
• Test both sternocleidomastoid muscles simultaneously by
asking the patient to flex their neck. Apply your palm to the
forehead as resistance.
Isolated XI nerve lesions are uncommon, but the nerve may be
damaged during surgery in the posterior triangle of the neck,
penetrating injuries or tumour invasion. Wasting of the upper fibres of trapezius may be associated with displacement (‘winging’) of the upper vertebral border of the scapula away from the
spine, while the lower border is displaced towards it. Wasting
and weakness of the sternomastoids are characteristic of myotonic dystrophy. Weakness of neck flexion or extension, the latter
causing head drop, may occur in myasthenia gravis, motor
neuron disease, myotonic dystrophy and some myopathies.
Dystonic head postures causing antecollis (neck flexed), retrocollis (neck extended) or torticollis (neck twisted to one side) are
not associated with weakness.
Examination sequence (Video 11C)
• Ask the patient to open their mouth. Look at the tongue at
rest for wasting, fasciculation or involuntary movement.
• Ask the patient to put out their tongue. Look for deviation or
involuntary movement.
• Ask the patient to move their tongue quickly from side to side.
• Test power by asking the patient to press their tongue
against the inside of each cheek in turn while you press from
the outside with your finger.
• Assess speech by asking the patient to say ‘yellow lorry.’
• Assess swallowing with a water swallow test (p. 148).
Unilateral lower motor XII nerve lesions lead to tongue wasting
on the affected side and deviation to that side on protrusion
(Fig. 7.14). Bilateral lower motor neuron damage results in global
wasting; the tongue appears thin and shrunken and fasciculation
may be evident. Normal rippling or undulating movements may
be mistaken for fasciculation, especially if the tongue is protruded; these usually settle when the tongue is at rest in the
mouth. When associated with lesions of the IX, X and XI nerves,
typically in motor neuron disease, these features are termed
bulbar palsy (see Box 7.5).
Unilateral upper motor XII nerve lesions are uncommon;
bilateral lesions lead to a tongue with increased tone (spastic),
and the patient has difficulty flicking the tongue from side to side.
Bilateral upper motor lesions of the IX–XII nerves are called
pseudobulbar palsy (see Box 7.5). Tremor of the resting or
protruded tongue may occur in Parkinson’s disease, although
jaw tremor is more common. Other orolingual dyskinesias
(involuntary movements of the mouth and tongue) are often
drug-induced and include tardive dyskinesias due to
neuroleptics.
7
Hypoglossal (XII) nerve
The XII nerve innervates the tongue muscles; the nucleus lies in
the dorsal medulla beneath the floor of the fourth ventricle.
Anatomy
The nerve emerges anteriorly and exits the skull in the h ypoglossal canal, passing to the root of the tongue (see Fig. 7.5).
Fig. 7.14 Left hypoglossal nerve lesion. From Epstein O, Perkin GD, de
Bono DP, et al. Clinical Examination. 2nd ed. London: Mosby; 1997.
150 • THE NERVOUS SYSTEM
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Motor system (Videos 12 and 13)
Anatomy
The principal motor pathway has CNS (corticospinal or pyramidal
tract: upper motor neuron) and PNS (anterior horn cell: lower
motor neuron) components (Fig. 7.15). Other parts of the nervous system, such as the basal ganglia and cerebellum, have
important modulating effects on movement. It is important to
distinguish upper from lower motor neuron signs to help localise
the lesion (Box 7.6).
7.6 Features of motor neuron lesions
Upper motor
neuron lesion
Inspection Usually normal (may be
Tone Increased with clonus Normal or decreased, no
Weakness Preferentially affects
Deep tendon
reflexes
Plantar response Extensor (Babinski sign) Flexor
disuse wasting in
longstanding lesions)
extensors in arms,
flexors in leg
Increased Decreased/absent
Lower motor
neuron lesion
Muscle wasting,
fasciculations
clonus
Usually more focal, in
distribution of nerve root
or peripheral nerve
Upper motor neuron lesions
If the lesion affects the CNS pathways, the lower motor neurons
are under the uninhibited influence of the spinal reflex. The motor
units then have an exaggerated response to stretch with
increased tone (spasticity), clonus and brisk reflexes. There is
weakness but not wasting (although atrophy may develop with
longstanding lesions). Primitive reflexes, such as the plantar
extensor response (Babinski sign), may be present.
Fig. 7.15 Principal motor pathways.
Lower motor neuron lesions
Motor fibres, together with input from other systems involved in
the control of movement, including extrapyramidal, cerebellar,
vestibular and proprioceptive afferents, converge on the cell
bodies of lower motor neurons in the anterior horn of the grey
matter in the spinal cord (see Fig. 7.15).
The group of muscle fibres innervated by a single anterior horn
cell forms a ‘motor unit.’ A lower motor neuron lesion causes
weakness and wasting in these muscle fibres, reduced tone
(flaccidity), fasciculation and reduced or absent reflexes.
Basal ganglia lesions
The basal ganglia are connected structures within the cerebral
hemispheres and brainstem (Fig. 7.16). They include the caudate
nucleus and putamen (collectively known as the striatum), globus
pallidus, thalamus, subthalamic nucleus and substantia nigra (the
latter in the brainstem). The basal ganglia receive much information from the cortex and are involved in regulating many activities, principally control of movement, but are also involved in
eye movement, behaviour and executive function control. Disorders of the basal ganglia may cause reduced movement
(typically Parkinsonism; p. 151) or, less commonly, excessive
movement such as ballism or tics (p. 153).
Assess the motor system using the following method:
• assessing stance and gait
• inspecting and palpating muscles
Motor system • 151
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A
B
Thalamus
Fig. 7.16 Basal ganglia. A Anatomical location. B Coronal view.
• assessing tone
• testing movement and power
• examining reflexes
• testing coordination.
Stance and gait
Stance and gait depend on intact visual, vestibular, sensory,
corticospinal, extrapyramidal and cerebellar pathways, together
with functioning lower motor neurons and spinal reflexes. Nonneurological gait disorders are discussed on page 152. Certain
abnormal gait patterns are recognisable, suggesting diagnoses
(Box 7.7 and Fig. 7.17).
Examination sequence
Stance
• Ask the patient to stand with their (preferably bare) feet
together and eyes open.
• Swaying, lurching or an inability to stand with the feet
together and eyes open suggests cerebellar ataxia.
• Ask the patient to close their eyes (Romberg’s test) but be
prepared to steady/catch them. Repeated falling is a positive
result. Swaying is common and should not be misinterpreted.
• The ‘pull test’ assesses postural stability. Ask the patient to
stand with their feet slightly apart. Inform them that you are
Caudate
nucleus
Putamen
Thalamus
Amygdala
Caudate
nucleus
Putamen
Globus pallidus
externa (GPe)
Globus pallidus
interna (GPi)
Subthalamic nucleus (STN)
Substantia nigra (SN)
Striatum
7.7 Common gait abnormalities
Gait
disturbance Description Causes
Parkinsonian Stooped posture
Gait apraxia Small, shuffling steps (marche a
Spastic Stiff ‘walking-through-mud’ or
Myopathic Waddling (proximal weakness)
Foot drop Foot slapping Neuropathies
Central ataxia Wide-based, ‘drunken’
Sensory
ataxia
Functional Variable, often bizarre,
© Crown Copyright.
going to push them forwards or pull them backwards. They
should maintain their position if possible. Standing behind the
patient, deliver a brisk push forwards or pull backwards. You
must be ready to catch them if they are unable to maintain
their balance. If in doubt, have an assistant standing in front of
the patient.
Shuffling(reducedstridelength)
Loss of arm swing
Postural instability
Freezing
petits pas)
Difficulty in starting to walk/
freezing
Better ‘cycling’ on bed than
walking
scissors gait
Bilateral Trendelenburg signs
Tandem gait poor
Wide-based
Positive Romberg sign
inconsistent
Knees flexed, buckling
Dragging immobile leg behind
Parkinson’s disease
and other
Parkinsonian
syndromes
`
Cerebrovascular
disease
Hydrocephalus
Spinal cord lesions
Muscular dystrophies
and acquired
myopathies
Common peroneal
nerve palsy
L5 radiculopathy
Cerebellar disease
Neuropathies
Spinal cord disorders
Functional
neurological
disorders
Gait
• Look at the patient’s shoes for abnormal wear patterns.
• Perform a timed get-up-and-go test (see Fig. 17.4)
• Note stride length, arm swing, steadiness (including turning),
limping or other difficulties.
• Look for abnormal movements that may be accentuated by
walking, such as tremor (in Parkinson’s disease) or dystonic
movements.
• Listen for the slapping sound of a foot-drop gait.
• Ask the patient to walk first on their tiptoes, then heels. Ankle
dorsiflexion weakness (foot drop) is much more common
than plantar flexion weakness and makes walking on the
heels difficult or impossible.
• Ask the patient to walk heel to toe in a straight line (tandem
gait). This emphasises gait ataxia and may be the only
abnormal finding in midline cerebellar (vermis) lesions.
7
A
152 • THE NERVOUS SYSTEM
https://t.me/med1917
Spastic hemiparesis
One arm held immobile and
close to the side with elbow,
wrist and fingers flexed
Leg extended with plantar
flexion of the foot
On walking, the foot is
dragged, scraping the toe
in a circle (circumduction)
Caused by upper motor
neurone lesion, e.g. stroke
Fig. 7.17 Abnormalities of gait.
Unsteadiness on standing with the eyes open is common in
cerebellar disorders. Instability that only occurs, or is markedly
worse, on eye closure (Romberg sign) indicates proprioceptive
sensory loss (sensory ataxia) or bilateral vestibular failure. Cerebellar ataxia is not usually associated with a positive Romberg
test.
Hemiplegic gait (unilateral upper motor neuron lesion) is
characterised by extension at the hip, knee and ankle and circumduction at the hip such that the foot on the affected side is
plantar flexed and describes a semicircle as the patient walks.
The upper limb may be flexed (see Fig. 7.17A).
Bilateral upper motor neuron damage causes a scissor-like
gait due to spasticity. Cerebellar dysfunction leads to a broadbased, unsteady (ataxic) gait, which usually makes walking
heel to toe impossible. In Parkinsonism, initiation of walking may
be delayed; the steps are short and shuffling with loss/reduction
of arm swing (see Fig. 7.17D). A tremor may become more
apparent. The stooped posture and impairment of postural reflexes can result in a festinant (rapid, short-stepped, hurrying)
gait. As a doorway or other obstacle approaches, the patient
may freeze. Turning involves many short steps, with the risk of
falls. Postural instability on the pull test, especially backwards,
occurs in Parkinsonian syndromes. Proximal muscle weakness
B Steppage gait
Foot is dragged or lifted high
and slapped on to the floor
Unable to walk on the heels
Caused by foot drop owing to
lower motor neurone lesion
C Sensory or cerebellar ataxia
Gait is unsteady and wide-
based. Feet are thrown forward
and outward and brought down
on the heels
In sensory ataxia, patients watch
the ground. With their eyes
closed, they cannot stand
steadily (positive Romberg sign)
In cerebellar ataxia, turns are
difficult and patients cannot
stand steadily with feet together
whether eyes are open or
closed
Caused by polyneuropathy or
posterior column damage, e.g.
syphilis
may lead to a waddling gait with bilateral Trendelenburg signs
(see p. 296 and Fig. 13.38). Bizarre gaits, such as when patients
drag a leg behind them, are often functional but some diseases,
including Huntington’s disease, produce unusual and chaotic
gaits.
D Parkinsonian gait
Posture is stooped with head
and neck forwards
Arms are flexed at elbows and
wrists. Little arm swing
Steps are short and shuffling
and patient is slow in getting
started (festinant gait)
Caused by lesions in the basal
ganglia
Inspection and palpation of the muscles
Examination sequence
• Completely expose the patient while maintaining their comfort
and dignity.
• Look for asymmetry, inspecting both proximally and distally.
Note deformities, such as flexion deformities or pes cavus
(high foot arches).
• Inspect for wasting or hypertrophy, fasciculation and invol-
untary movement.
Muscle bulk
Lower motor neuron lesions may cause muscle wasting. This is
not seen in acute upper motor neuron lesions, although disuse
atrophy may develop with longstanding lesions. A motor neuron
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