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Richard Davenport
https://t.me/med1917
Hadi Manji
The nervous system
7
Anatomy and physiology 134
The history 134
Common presenting symptoms 134
Past medical history 138
Drug history 138
Family history 138
Social history 138
The physical examination 139
Assessment of conscious level 139
Meningeal irritation 139
Speech 139
Dysphasia 140
Cortical function 140
Cranial nerves 142
Olfactory (I) nerve 142
Optic (II), oculomotor (III), trochlear (IV) and abducens (VI) nerves 144
Trigeminal (V) nerve 144
Facial (VII) nerve 145
The vestibulocochlear (VIII) nerve 148
Glossopharyngeal (IX) and vagus (X) nerves 148
Accessory (XI) nerve 148
Hypoglossal (XII) nerve 149
Motor system 150
Anatomy 150
Stance and gait 151
Inspection and palpation of the muscles 152
Tone 153
Power 154
Deep tendon reflexes 155
Primitive reflexes 158
Coordination 158
Sensory system 159
Anatomy 159
Common presenting symptoms 160
Sensory modalities 161
Peripheral nerves 162
Median nerve 162
Radial nerve 164
Ulnar nerve 164
Common peroneal nerve 164
Lateral cutaneous nerve of the thigh 164
Interpretation of the findings 164
Investigations 165
Initial investigations 165
Specific investigations 165
OSCE example 1: Headache history 167
OSCE example 2: Tremor 167
Integrated examination sequence for the nervous system 168
134 • THE NERVOUS SYSTEM
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Anatomy and physiology
The nervous system consists of the brain and spinal cord (central
nervous system, CNS) and the peripheral nerves (peripheral
nervous system, PNS). The PNS includes the autonomic nervous
system, which is responsible for controlling involuntary functions.
The neuron is the functional unit of the nervous system. Each
neuron has a cell body and axon terminating at a synapse,
supported by astrocytes and microglial cells. Astrocytes provide
the structural framework for the neurons, control their
biochemical environment and form the blood-brain barrier.
Microglial cells are blood-derived mononuclear macrophages
with immune and scavenging functions. In the CNS, oligodendrocytes produce and maintain a myelin sheath around the
axons. In the PNS, myelin is produced by Schwann cells.
The brain consists of two cerebral hemispheres, each with
four lobes (frontal, parietal, tempora l and occipital), the brainstem and the cerebellum. The brainstem comprises the
midbrain, pons and medulla. The cerebellum lies in the posterior
fossa, with two hemispheres and a central vermis attached to
the brainstem by three pairs of cerebellar peduncles. Between
the brain and the skull are three membranous layers called the
meninges: dura mater next to the bone, arachnoid and pia
mater next to the nervous tissue. The subarachnoid space
between the arachnoid and pia is filled with cerebrospinal fluid
(CSF) produced by the choroid plexuses. The t otal volume of
CSF is between 140 and 270 mL, and there is a turnover of the
entire volume three to four times a day; thus, CSF is produced
at a rate of approximately 700 mL/day.
The spinal cord contains afferent and efferent fibres arranged
in discrete bundles (pathways running to and from the brain),
which are responsible for transmitting motor and sensory information. Peripheral nerves have myelinated and unmyelinated
axons. The sensory cell bodies of peripheral nerves are situated
in the dorsal root ganglia. The motor cell bodies are in the
anterior horns of the spinal cord (Fig. 7.1).
The history
For many common neurological symptoms such as headache,
numbness, disturbance/loss of consciousness and memory
loss, the history is the key to diagnosis, as the examination may
be normal. Some symptoms, including loss of consciousness or
amnesia, require an additional witness history; make every effort
to contact such witnesses. Whilst histories can lend themselves
to remote consulting, remote neurological examination is challenging if not impossible. People with communication difficulties
(e.g. due to deafness, spoken language, cognitive impairment, or
non-verbal such as autism) require particularly careful attention to
overcome these barriers.
Remember the two key questions: where (in the nervous
system) is the lesion and what is the lesion?
Neurological symptoms may be difficult for patients to
describe, so clarify exactly what they mean. Words such as
‘blackout’, ‘dizziness’, ‘weakness’ and ‘numbness’ may have
different meanings for different patients, so ensure you understand what the person is describing.
Ask patients what they think or fear might be wrong with them,
as neurological symptoms cause much anxiety. Patients
commonly research their symptoms on the internet; searches on
common benign neurological symptoms, like numbness or
weakness, usually list the most alarming (and unlikely) diagnoses
such as multiple sclerosis, motor neuron disease or brain tumours first, and almost never mention more common conditions
such as carpal tunnel syndrome or functional disorders.
Time relationships
The onset, duration and pattern of symptoms over time often
provide diagnostic clues: for example, in assessing headache
(Box 7.1) or vertigo (see Box 9.3).
Ask:
• When did the symptoms start (or when was the patient last
well)?
• Are they persistent or intermittent?
• If persistent, are they getting better, getting worse or staying
the same?
• If intermittent, how long do they last, and how long does the
patient remain symptom-free in between episodes?
• Was the onset sudden or gradual/evolving?
Precipitating, exacerbating or relieving factors
• What was the patient doing when the symptoms occurred?
• Does anything make the symptoms better or worse, such as
time of day, menstrual cycle, posture or medication?
Associated symptoms
Associated symptoms can aid diagnosis. For example, headache may be associated with nausea, vomiting, photophobia
(aversion to light) and/or phonophobia (aversion to sound) in
migraine; headache with neck stiffness, fever and rash may be
associated with meningitis (see Box 7.1).
Common presenting symptoms
Headache
Headache is the most common neurological symptom and may
be either primary or secondary to other pathology. Primary
(idiopathic) causes are the most common and include:
• migraine
• tension-type headache
• trigeminal autonomic cephalalgias (including cluster
headache)
• primary stabbing, cough, exertional or sex headache
• primary thunderclap headache
• new daily persistent headache.
Central sulcus
c
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The history • 135
Postcentral gyrus
(sensory area)
Parietal lobe
Sensory speech area
(Wernicke's area)
Occipital lobe
Cerebellum
A
Dorsal root entry zone
Dorsal column
Central canal
Ventral grey horn
Rootlets
Dorsal
Ventral
Mixed spinal
nerve
Anterior median
fissure
Posterior median septum
Dorsal intermediate septum
Dorsal grey horn
Lateral column
Ventral column
Spinal ganglion
Pia mater
Arachnoid
mater
Dura mater
Dural root
sleeve
Precentral gyrus
(motor area)
Pons
Medulla oblongata
Frontal lobe
Lateral sulcus (fissure)
Motor speech area
(Broca's area)
Temporal lobe
Presynapti
nerve fibres
Nucleus
Dendrites
Cell body
7
B
Position sense
Vibration sense
1/2 touch
Voluntary
movement
Equilibrium
Pain
Temperature
1/2 touch
C
Fig. 7.1 Anatomy of the central nervous system. A Lateral surface of the brain. B Spinal cord, nerve roots and meninges. C Cross-section of the spinal
D Spinal motor neuron. The terminals of presynaptic neurons form synapses with the cell body and dendrites of the motor neurons.
cord.
Fasciculus gracilis
Voluntary
movement
Anterior (direct)
corticospinal tract
Fasciculus cuneatus
Anterior spinothalamic tract
Lateral (indirect)
corticospinal tract
Posterior spinocerebellar tract
Anterior spinocerebellar tract
Lateral spinothalamic tract
Areas of
extrapyramidal
tracts
Spinal
motor neurone
Axon
Myelin
Node of
Ranvier
Nerve
terminals
D
136 • THE NERVOUS SYSTEM
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7.1 Clinical characteristics of headache syndromes
Onset Duration/periodicity Pain location Associated features
Primary syndromes
Migraine Evolves over
Cluster
headache
Stabbing
headache
Secondary syndromes
Meningitis Usually evolves
Subarachnoid
haemorrhage
Temporal
arteritis
30–120 min
Rapid onset,
often waking
patient from sleep
Abrupt, rarely
from sleep
over a day or two,
can be abrupt
Abrupt,
immediately
maximal, rare
from sleep
Gradual onset of
temple pain and
scalp tenderness
Usually last <24 h, recurrent with
weeks/months symptom-free
30–120 min, 1–4 attacks within 24
h, clusters usually last weeks to
months, with months to years of
remission
Very brief, seconds or less Anywhere over head Common in migraineurs
Depends on cause and treatment,
usually days to weeks
May be fatal at onset, usually days to
weeks
Continuous Temple and scalp Usually in those >55 years; unwell,
Classically unilateral but may be
anywhere including face/neck
Orbital/retro-orbital; always
same side during cluster, may
switch sides between clusters
Global, including neck stiffness Fever, meningism, rash, false
Anywhere, poor localising value 20% isolated headache only; nausea/
Aura (usually visual), nausea/vomiting,
photophobia and phonophobia
Autonomic features, including
conjunctival injection, tearing, nasal
stuffiness, ptosis, miosis, agitation
localising signs, signs of raised
intracranial pressure
vomiting, reduced consciousness,
false localising signs, III nerve palsies
jaw pain on chewing, visual
symptoms, tender temporal arteries,
elevated erythrocyte sedimentation
rate and C-reactive protein
Secondary (or symptomatic) headaches include potentially lifethreatening or disabling causes, such as subarachnoid haemorrhage or temporal arteritis. One of the key history aspects is
rapidity of onset; isolated headache with a truly abrupt onset may
represent a potentially serious cause, such as subarachnoid
haemorrhage or cerebral vein thrombosis, whereas recurrent
headache is much more likely to be migraine, particularly if
associated with other migrainous features (see Box 7.1). Asking
patients what they do when they have a headache can be
instructive. For example, abandoning normal tasks and seeking a
bed in a dark, quiet room suggest migraine, whereas pacing
around the room in an agitated state, or even headbanging,
suggests cluster headache.
Transient loss of consciousness (TLOC)
Syncope is loss of consciousness due to inadequate cerebral
perfusion and is the most common cause of transient loss of
consciousness (TLOC). Vasovagal (or reflex) syncope (fainting) is
the most common type and is precipitated by stimulation of the
parasympathetic nervous system by factors such as pain or
intercurrent illness. Exercise-related syncope, or syncope with no
warning or trigger, suggests a possible cardiac cause. TLOC on
standing is suggestive of orthostatic (postural) hypotension and
may be caused by drugs (antihypertensives or levodopa) or
associated with autonomic neuropathies, which may complicate
conditions such as diabetes.
Seizure
An epileptic seizure is caused by paroxysmal electrical discharges from either the whole brain (generalised seizure) or part
of the brain (focal seizure). A tonic-clonic seizure (convulsion) is
the most common form of generalised seizure and typically follows a stereotyped pattern with early loss of consciousness
associated with body stiffening (tonic phase) succeeded by
rhythmical jerking crescendoing and subsiding over 30 to 120
seconds (clonic phase); this is followed by a period of unresponsiveness (often with heavy breathing, the patient appearing
to be deeply asleep) and finally confusion or amnesia as the
patient reorientates (postictal phase). The history from the patient
and witnesses can help distinguish syncope from epilepsy
(Box 7.2). Focal seizures may or may not involve loss of
awareness (complete loss of consciousness is less typical) and
are characterised by whichever part of the brain is involved: for
example, a focal motor seizure arising from the motor cortex, or
temporal lobe seizures characterised by autonomic and/or psychic symptoms, often associated with automatisms such as lip
smacking or swallowing. Functional dissociative attacks (also
known as non-epileptic or psychogenic attacks, or pseudoseizures) are common and may be difficult to distinguish from
epileptic seizures. These attacks are often more frequent than
epilepsy, sometimes occurring multiple times in a day, and may
last considerably longer, with symptoms waxing and waning.
Other features may include asynchronous movements, pelvic
The history • 137
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7.2 Features that help discriminate vasovagal syncope from epileptic seizure
Feature Vasovagal syncope Seizure
Triggers Typically, pain, illness, emotion Often none (sleep deprivation, alcohol, drugs)
Prodrome Feeling faint/lightheaded, nausea, tinnitus,
Duration of
unconsciousness
Convulsion May occur but usually brief myoclonic jerks Usual, tonic-clonic 1–2 min
Colour Pale/grey Flushed/cyanosed, may be pale
Injuries Uncommon, sometimes biting of tip of tongue Lateral tongue biting, headache, generalised myalgia, back pain (sometimes
Recovery Rapid, no confusion Gradual, over 30 min; patient is often confused, sometimes agitated/aggressive,
vision dimming
<60 s 1–2 min
Focal onset (not always present)
vertebral compression fractures), shoulder fracture/dislocation (rare)
amnesic
7
thrusts, side-to-side rather than flexion/extension movements
and absence of postictal confusion. The widespread availability
of smartphones allows witnesses to film such events, which may
prove invaluable; the availability of secure platforms for families to
upload such videos for viewing is an evolving area (e.g. https://
www.vcreate.tv/).
Focal neurological symptoms due to stroke or
transient ischaemic attack
A stroke is a focal neurological deficit of rapid onset due to a
vascular cause. A transient ischaemic attack (TIA) is the same,
but symptoms resolve within 24 hours. TIAs are an important risk
factor for impending stroke and demand urgent assessment and
treatment. Hemiplegia following middle cerebral artery occlusion
is a typical example, but symptoms are dictated by the vascular
territory involved. Much of the cerebral hemispheres are supplied
by anterior circulation (the anterior and middle cerebral arteries
are derived from the internal carotid artery), while the occipital
lobes and brainstem are supplied by posterior (vertebrobasilar)
circulation (Fig. 7.2).
Anterior cerebral artery
Anterior communicating artery
Internal carotid artery
Circle of Willis
Middle cerebral artery
Posterior
communicating artery
Posterior cerebral artery
Basilar artery
Vertebral artery
Fig. 7.2 The arterial blood supply of the brain (circle of Willis).
A useful and simple clinical system for classifying strokes is
shown in Box 7.3.
Isolated vertigo, amnesia or TLOC are rarely, if ever, due to
stroke. In the Western world about 80% of strokes are ischaemic, the remainder haemorrhagic. Haemorrhagic stroke is much
more frequent in Asian populations. Factors in the history or
examination that increase the likelihood of haemorrhage rather
than ischaemia include the use of anticoagulation, headache,
vomiting, seizures and early reduced consciousness, although
brain imaging is necessary to be definitive. Spinal strokes are
very rare; patients typically present with abrupt bilateral paralysis,
depending on the level of spinal cord affected. Anterior spinal
7.3 Clinical classification of stroke
Total anterior circulation syndrome (TACS)
• Hemiparesis, hemianopia and higher cortical deficit (e.g. dysphasia or
visuospatial loss)
Partial anterior circulation syndrome (PACS)
• Two of the three components of a TACS
• OR isolated higher cortical de ficit
• OR motor/sensory deficit more restricted than LACS (see below)
Posterior circulation syndrome (POCS)
• Ipsilateral cranial nerve palsy with contralateral motor and/or sensory
deficit
• OR bilateral motor and/or sensory deficit
• OR disorder of conjugate eye movement
• OR cerebellar dysfunction without ipsilateral long-tract deficits
• OR isolated homonymous visual field defect
Lacunar syndrome (LACS)
• Pure motor >2 out of 3 of face, arm, leg
• OR pure sensory >2 out of 3 of face, arm, leg
• OR pure sensorimotor >2 out of 3 of face, arm, leg
• OR ataxic hemiparesis
138 • THE NERVOUS SYSTEM
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artery syndrome is most common and causes loss of motor
function and pain/temperature sensation, with relative sparing of
joint position and vibration sensation below the level of the lesion.
Dizziness and vertigo
Patients use ‘dizziness’ to describe many sensations. Recurrent
‘dizzy spells’ affect approximately 30% of those over 65 years
and can be due to postural hypotension, cerebrovascular disease, cardiac arrhythmia or hyperventilation induced by anxiety
and panic. Vertigo (the illusion of movement) specifically indicates
a problem in the vestibular apparatus (peripheral) or, much less
commonly, the brain (central) (see Box 9.3 and p. 201). Identifying a specific cause of dizziness is often challenging but may be
rewarding in some cases, including benign paroxysmal positional
vertigo (BPPV), which is eminently treatable. As a guide, recurrent episodes of vertigo lasting a few seconds are most likely to
be due to BPPV; vertigo lasting hours may be caused by
Ménière’s disease (with associated symptoms including hearing
loss, tinnitus, nausea and vomiting) or migrainous vertigo (with or
without headache); brain stem or cerebellar stroke may also
present with vertigo, often associated with ataxia, diplopia and
other motor or sensory symptoms and is an important diagnosis
not to miss.
Functional neurological symptoms
Many neurological symptoms are not due to organic or structural
disease. These symptoms are often called ‘functional’ but other
(less useful and more pejorative) terms include psychogenic,
hysterical, somatisation or conversion disorders. Presentations
include blindness, tremor, weakness and collapsing attacks, and
patients will often describe numerous other symptoms, with fatigue, lethargy, pain, anxiety and other mood disorders
commonly associated. Diagnosing functional symptoms requires
experience and patience (p. 424). Clues include symptoms not
compatible with disease (such as retained awareness of
convulsing, or being able to walk normally backwards but not
forwards), considerable variability in symptoms (such as intermittent recovery of a hemiparesis), multiple symptoms (often with
numerous previous assessments by other specialties, particularly
gynaecology, gastroenterology, ear, nose and throat and
cardiorespiratory) and multiple unremarkable investigations,
leading to numerous different diagnoses. The size of a patient’s
case notes can sometimes be a clue in itself! Beware of labelling
symptoms as functional simply because they appear odd or
inexplicable, and remember that functional and organic disease
may coexist. Like disease, most functional neurological disorders
follow recognisable patterns, so be cautious when the pattern is
atypical.
Past medical history
Symptoms that the patient has forgotten about or overlooked
may be important; for example, a history of previous visual loss
(optic neuritis) in someone presenting with numbness suggests
multiple sclerosis. Birth history and development may be significant, as in epilepsy. Contact parents or family doctors to obtain
such information. If considering a vascular cause of neurological
symptoms, ask about important risk factors, such as other
vascular diseases, hypertension, family history and smoking.
Drug history
Always enquire about drugs, including prescribed, over-thecounter, complementary and recreational/illegal ones, as they
can give rise to many neurological symptoms (for example,
phenytoin toxicity causing ataxia; excessive intake of analgesia
causing medication overuse headache). Recent vaccinations
may be relevant when faced with rapidly progressive weakness
(Guillain-Barré syndrome) or cerebral venous thrombosis
(COVID-19 vaccinations). The absence of vaccinations (e.g. polio
or measles) may be overlooked initially but may provide crucial
clues for diagnosis.
Family history
Obtain a family history for at least first-degree relatives: parents,
siblings and children. In some communities, parental consanguinity is common, increasing the risk of autosomal recessive
conditions, so you may need to enquire sensitively about this.
Some neurological disorders are caused by single-gene defects,
such as myotonic dystrophy or Huntington’s disease. Others
have important polygenic influences, as in multiple sclerosis or
migraine. Some conditions have a variety of inheritance patterns;
for example, Charcot-Marie-Tooth disease may be autosomal
dominant, autosomal recessive or X-linked. Mitochondria
uniquely have their own DNA, and abnormalities in this DNA can
cause a range of disorders (such as diabetes, short stature and
deafness) that manifest in many different systems and may cause
common neurological syndromes such as migraine or epilepsy.
Some diseases, such as Parkinson’s or motor neuron disease,
may be either due to single-gene disorders or sporadic.
Social history
Social circumstances are relevant. How are patients coping with
their symptoms? Are they able to work and drive? What are their
support circumstances, and are these adequate?
Alcohol is the most common neurological toxin and damages
both the CNS (ataxia, seizures, dementia) and the PNS (neuropathy). Poor diet with vitamin deficiency may compound these
problems and is relevant in areas affected by famine, alcoholism
or dietary exclusion. Vegetarians may be susceptible to vitamin
B
deficiency. Recreational drugs may affect the nervous sys-
12
tem; for example, nitrous oxide inhalation causes subacute
combined degeneration of the cord due to dysfunction of the
vitamin B
contributes to vascular and malignant disease. Always consider
sexually transmitted or blood-borne infection, such as human
immunodeficiency virus (HIV) or syphilis, as both can cause a
wide range of neurological symptoms and are treatable. A travel
pathway, cocaine can cause seizures and smoking
12
history may give clues to the underlying diagnosis, such as Lyme
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disease (facial palsy), neurocysticercosis (brain lesions and epilepsy) or malaria (coma). Post-viral syndromes, including postCOVID-19, may cause persistent and disabling symptoms in a
minority.
Occupational history
Occupational factors are relevant to several neurological disorders. For example, toxic peripheral neuropathy, due to exposure
to heavy or organic metals like lead, causes motor neuropathy;
manganese causes Parkinsonism. Some neurological diagnoses
may adversely affect a patient’s occupation, such as epilepsy in
anyone who needs to drive or operate dangerous machinery. For
patients with cognitive disorders, particularly dementias, it may
be necessary to advise on whether to stop working.
The physical examination
Although history-taking can be undertaken remotely, a neurological examination ideally requires direct patient contact.
Neurological assessment begins with your first contact with the
patient and continues during the history. Note facial expression,
demeanour, dress, posture, gait and speech. Mental state examination (p. 368) and general examination (p. 385) are integral
parts of the neurological examination.
Assessment of conscious level
Consciousness has two main components:
• The state of consciousness depends largely on the integrity of
the ascending reticular activating system, which extends from
the brainstem to the thalamus.
• The content of consciousness refers to how aware the person is and depends on the cerebral cortex, the thalamus and
their connections.
Do not use ill-defined terms such as stuporose or obtunded.
Use the Glasgow Coma Scale (see Box 18.5), a reliable and
reproducible tool, to record consciousness level.
Meningeal irritation
Meningism (inflammation or irritation of the meninges) can lead to
increased resistance to passive flexion of the neck (neck stiffness) or the extended leg (Kernig’s sign). Patients may lie with
flexed hips to ease their symptoms. Meningism suggests infection (meningitis) or blood within the subarachnoid space (subarachnoid haemorrhage) but can occur with non-neurological
infections, such as a urinary tract infection or pneumonia.
Conversely, the absence of meningism does not exclude pathology within the subarachnoid space. In meningitis, neck
stiffness has relatively low sensitivity but higher specificity. The
absence of all three signs of fever, neck stiffness and altered
mental state virtually eliminates the diagnosis of meningitis in
immunocompetent individuals.
The physical examination • 139
7
Fig. 7.3 Testing for meningeal irritation: Kernig’s sign.
Examination sequence (Video 7)
• Position the patient supine with no pillow.
• Expose and fully extend both of the patient’s legs.
Neck stiffness
• Place your hands on either side of the patient’s head, sup-
porting the occiput.
• Flex the patient’s head gently until their chin touches their
chest.
• Ask the patient to hold that position for 10 seconds. If neck
stiffness is present, the neck cannot be passively flexed and
you may feel a spasm in the neck muscles.
• Flexion of the hips and knees in response to neck flexion is
Brudzinski’s sign.
Kernig’s sign
• Flex one of the patient’s legs to 90 degrees at both the hip
and the knee, with your left hand placed over the medial
hamstrings (Fig. 7.3).
• Extend t he knee while the hip is maintained in flexion. Look
at the other leg for any reflex flexion. Kernig’ssignis
positive when extension is resisted by spasms in the
hamstrings. Kernig’ssignisabsentwithlocalcausesof
neck stiffness, such as cervical spine disease or raised
intracranial pressure.
Speech
Dysarthria refers to altered or abnormal speech caused by
articulation problems due to a motor deficit. Dysphonia describes the loss of volume caused by laryngeal disorders. Both
affect speech only, whereas dysphasia may affect other language functions (e.g. reading or writing).
140 • THE NERVOUS SYSTEM
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Examination sequence (Video 8)
• Listen to the patient’s spontaneous speech, noting volume,
rhythm and clarity.
• Ask the patient to repeat phrases such as ‘yellow lorry’ to test
lingual (tongue) sounds and ‘baby hippopotamus’ for labial
(lip) sounds, then a tongue twister such as ‘The Leith police
dismisseth us.’
• Ask the patient to count to 30 to assess fatigue.
• Ask the patient to cough and to say ‘ah’; observe the soft
palate rising bilaterally.
Disturbed articulation (dysarthria) may result from localised
lesions of the tongue, lips or mouth, ill-fitting dentures or
neurological dysfunction such as bulbar palsy or cerebellar
disease.
Pseudobulbar versus bulbar palsies (see Box 7.5): bilateral
upper motor neuron lesions of the corticobulbar tracts cause a
pseudobulbar dysarthria, characterised by slow, harsh, strangulated speech with difficulty pronouncing consonants and may
be accompanied by a brisk jaw jerk and emotional lability. The
tongue is contracted and stiff. Bulbar palsy results from bilateral
lower motor neuron lesions affecting the same group of cranial
nerves (IX, X, XI, XII). The nature of the speech disturbance is
determined by the specific nerves and muscles involved.
Weakness of the tongue results in difficulty with lingual sounds,
while palatal weakness gives a nasal quality to the speech. Other
lower motor neuron signs such as a wasted, fibrillating tongue
may be seen.
Cerebellar dysarthria is slow and slurred, similar to alcohol
intoxication. Myasthenia gravis causes fatiguing speech that
becomes increasingly nasal and may disappear altogether.
Parkinsonism may cause dysarthria and dysphonia, with a lowvolume, monotonous voice, words running into each other
(festination of speech) and marked stuttering/hesitation.
Dysphonia usually results from either vocal cord pathology, as
in laryngitis, or damage to the vagal (X) nerve supply to the vocal
cords (recurrent laryngeal nerve). Inability to abduct one of the
vocal cords leads to a ‘bovine’ (and ineffective) cough.
Dysphasia
regions of the parietal lobe are involved in understanding written
language and numbers.
The arcuate fasciculus connects Broca’s and Wernicke’s
areas.
Examination sequence
• During spontaneous speech, listen to the fluency and
appropriateness of the content, particularly paraphasias
(incorrect words) and neologisms (nonsense or meaningless
new words).
• Show the patient a common object, such as a coin or pen,
and ask them to name it.
• Give a simple three-stage command, such as ‘Pick up this
piece of paper, fold it in half and place it under the book.’
• Ask the patient to repeat a simple sentence, such as ‘Today
is Tuesday.’
• Ask the patient to read a passage from a newspaper.
• Ask the patient to write a sentence; examine the handwriting.
Expressive (motor) dysphasia results from damage to Broca’s
area. It is characterised by reduced verbal output with non-fluent
speech and errors of grammar and syntax. Comprehension is
intact.
Receptive (sensory) dysphasia occurs due to dysfunction in
Wernicke’s area. There is poor comprehension, and although
speech is fluent, it may be meaningless and contain paraphasias
and neologisms.
Global dysphasia is a combination of expressive and receptive
difficulties caused by involvement of both areas.
Dysphasia (a focal sign) is frequently misdiagnosed as confusion (non-focal). Always consider dysphasia before assuming
confusion, as this fundamentally alters the differential diagnosis
and management.
Dominant parietal lobe lesions affecting the supramarginal
gyrus may cause dyslexia (difficulty comprehending written language), dyscalculia (problems with simple addition and subtraction) and dysgraphia (impairment of writing). Gerstmann’s
syndrome is the combination of dysgraphia, dyscalculia, finger
agnosia (inability to recognise the fingers) and inability to distinguish left from right. It localises to the left parietal lobe in the
region of the angular gyrus.
Dysphasia is a central disturbance of language resulting in abnormalities of speech production and/or understanding. It may
involve other language symptoms, such as writing and/or
reading problems, unlike dysarthria and dysphonia.
Anatomy
The language areas are located in the dominant cerebral hemisphere, which is the left in almost all right-handed people and
most left-handed people.
Broca’s area (inferior frontal region) is concerned with word
production and language expression.
Wernicke’s area (superior posterior temporal lobe) is the
principal area for comprehension of spoken language. Adjacent
Cortical function
Thinking, emotions, language, behaviour, planning and initiation
of movements and perception of sensory information are functions of the cerebral cortex and are central to awareness of, and
interaction with, the environment. Certain cortical areas are
associated with specific functions, so particular patterns of
dysfunction can help localise the site of pathology (Fig. 7.4A).
Assessment of higher cortical function can be difficult and timeconsuming but is essential in patients with cognitive symptoms.
There are various tools, primarily developed as screening and
assessment tools for dementia. At the bedside, the Montreal
Cognitive Assessment (MoCA; https://www.mocatest.org) may
be used to detect mild cognitive impairment, while the 4AT
2 Parietal lobe
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Dominant side
FUNCTION
Calculation
Language
Planned movement
Appreciation of size,
shape, weight
and texture
1 Frontal lobe
FUNCTION
Personality
Emotional response
Social behaviour
LESIONS
Disinhibition
Lack of initiative
Antisocial behaviour
Impaired memory
Incontinence
Grasp reflexes
Anosmia
4 Temporal lobe
Dominant side
FUNCTION
Auditory perception
Speech, language
Verbal memory
Smell
A
LESIONS
Dyscalculia
Dysphasia
Dyslexia
Apraxia
Agnosia
Homonymous hemianopia
1
LESIONS
Dysphasia
Dyslexia
Poor memory
Complex hallucinations
(smell, sound, vision)
Homonymous hemianopia
Non-dominant side
FUNCTION
Spatial orientation
Constructional skills
4
Non-dominant side
FUNCTION
Auditory perception
Music, tone sequences
Non-verbal memory
(faces, shapes, music)
Smell
The physical examination • 141
LESIONS
Neglect of non-dominant side
Spatial disorientation
Constructional apraxia
Dressing apraxia
Homonymous hemianopia
3 Occipital lobe
FUNCTION
Analysis of vision
2
LESIONS
Homonymous hemianopia
7
Hemianopic scotomas
Visual agnosia
Impaired face recognition
3
(prosopagnosia)
Visual hallucinations
(lights, lines and zigzags)
LESIONS
Poor non-verbal memory
Loss of musical skills
Complex hallucinations
Homonymous hemianopia
Trunk
Hip
Knee
Ankle
Toes
Shoulder
B
Fig. 7.4 Cortical function. A Features of localised cerebral lesions. B Somatotopic homunculus.
Elbow
Wrist
Hand
Little
Ring
Middle
Swallowing
Index
Thumb
Tongue
M
Neck
Brow
s
a
Eye
t
Face
Jaw
c
i
a
Lips
t
n
o
i
t
a
s
i
l
a
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i
V
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S
142 • THE NERVOUS SYSTEM
https://t.me/med1917
(the4AT.com) is a very useful rapid clinical test for delirium. None
of these bedside tests is a substitute for detailed neuropsychological assessment. The assessment of cognitive function is
covered in more detail on page 372.
Frontal lobe
The posterior part of the frontal lobe is the motor strip (precentral gyrus), which controls v oluntar y movement. The motor
strip is organised somatotopically (Fig. 7.4B). The area anterior
to the precentral gyr us is concern ed with person ality, social
behaviour, emotions, cogniti on and expressive langua ge, and
contains the frontal eye fields and cort ical centr e for micturit ion
(Fig. 7.4A).
Frontal lobe damage may cause:
• personality and behaviour changes, such as apathy or
disinhibition
• loss of emotional responsiveness, or emotional lability
• cognitive impairments, such as memory, attention and
concentration
• dysphasia (dominant hemisphere)
• conjugate gaze deviation to the side of the lesion
• urinary incontinence
• primitive reflexes, such as grasp
• focal motor seizures (motor strip).
Temporal lobe
The temporal lobe contains the primary auditory cortex, Wernicke’s area and parts of the limbic system. The latter is crucially
important in memory, emotion and smell appreciation. The
temporal lobe also contains the lower fibres of the optic radiation
and the area of auditory perception.
Temporal lobe dysfunction may cause:
• Memory impairment
• Focal seizures with psychic symptoms
• Contralateral upper quadrantanopia (see Fig. 8.5[4])
• Receptive dysphasia (dominant hemisphere).
Parietal lobe
The postcentral gyrus (sensory strip) is the most anterior part of
the parietal lobe and is the principal destination of conscious
sensations. The upper fibres of the optic radiation pass through
it. The dominant hemisphere contains aspects of language
function, and the non-dominant lobe is concerned with spatial
awareness.
Features of parietal lobe dysfunction include:
• cortical sensory impairments
• contralateral lower quadrantanopia (see Fig. 8.5[5])
• dyslexia, dyscalculia, dysgraphia
• apraxia (an inability to carry out complex tasks despite having
an intact sensory and motor system)
• focal sensory seizures (postcentral gyrus)
• visuospatial disturbance (non-dominant parietal lobe).
Occipital lobe
The occipital lobe blends with the temporal and parietal lobes
and forms the posterior part of the cerebral cortex. Its main
function is analysis of visual information.
Occipital lobe damage may cause:
• visual field defects: hemianopia (loss of part of a visual field) or
scotoma (blind spot) (see Fig. 8.5[6])
• visual agnosia: the inability to recognise visual stimuli
• disturbances of visual perception, such as macropsia (seeing
things larger) or micropsia (seeing things smaller)
• visual hallucinations.
Cranial nerves
The 12 pairs of cranial nerves (with the exception of the olfactory
[I] pair) arise from the brainstem (Fig. 7.5 and Box 7.4). Cranial
nerves II, III, IV and VI relate to the eye (see Chapter 8) and the VIII
nerve to hearing and balance (see Chapter 9 ).
Olfactory (I) nerve
The olfactory nerve conveys the sense of smell.
Anatomy
Bipolar cells in the olfactory bulb form olfactory filaments with
small receptors projecting through the cribriform plate high in the
nasal cavity. These cells synapse with second-order neurons,
which project centrally via the olfactory tract to the medial temporal lobe and amygdala.
Examination sequence
Bedside testing of smell is of limited clinical value and rarely
performed, although objective ‘scratch and sniff’ test cards, such
as the University of Pennsylvania Smell Identification Test
(UPSIT), are available. You can ask patients if they think their
sense of smell is normal, although self-reporting can be surprisingly inaccurate.
Hyposmia or anosmia (reduction or loss of the sense of
smell) may result from upper respiratory infection (for example
with the Sars-CoV-2 virus), sinus disease, damage to the olfactory filaments after head injury or inf ection, local
compression (by olfactory groove meningi oma, for example,
see Fig. 7.29C) or invasion by basal skull tumours. Disturbance of smell may also occur very early in Parkinson’ sand
Alzheimer’s diseases. Patients often note hypogeusia/ageusia
(altered taste) with anosmia too, as taste is crucially influenced
by the sense of smell.
ALGrawany
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