the occipital lobes and brainstem are supplied by the posterior
(vertebrobasilar) circulation (Fig. 7.2).
A useful and simple clinical system for classifying stroke is
Isolated vertigo, amnesia or TLOC are rarely, if ever, due
to stroke. In industrialised countries about 80% of strokes are
ischaemic, the remainder haemorrhagic. Factors in the history or
examination that increase the likelihood of haemorrhage rather
Fig. 7.2 The arterial blood supply of the brain (circle of Willis).
7.3 Clinical classification of stroke
Total anterior circulation syndrome (TACS)
• Hemiparesis, hemianopia and higher cortical deficit (e.g. dysphasia
Partial anterior circulation syndrome (PACS)
• Two of the three components of a TACS
• OR isolated higher cortical deficit
• OR motor/sensory deficit more restricted than LACS (see below)
Posterior circulation syndrome (POCS)
• Ipsilateral cranial nerve palsy with contralateral motor and/or
• 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
• 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
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. 320) and general examination (p. 20) are integral
parts of the neurological examination.
Consciousness has two main components:
• The state of consciousness depends largely on 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 conscious level.
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 urinary tract infection or pneumonia. Conversely, 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.
• Position the patient supine with no pillow.
• Expose and fully extend both of the patient’s legs.
• Place your hands on either side of the patient’s head,
• Flex the patient’s head gently until their chin touches their
• 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 spasm in the neck muscles.
• Flexion of the hips and knees in response to neck flexion
• Flex one of the patient’s legs to 90 degrees at both the
hip and the knee, with your left hand placed over the
• Extend the knee while the hip is maintained in flexion.
Look at the other leg for any reflex flexion. Kernig’s sign is
positive when extension is resisted by spasm in the
hamstrings. Kernig’s sign is absent with local causes of
neck stiffness, such as cervical spine disease or raised
can give rise to many neurological symptoms (for example,
phenytoin toxicity causing ataxia; excessive intake of simple
analgesia causing medication overuse headache; use of cocaine
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. Many 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 that manifest in many
different systems (such as diabetes, short stature and deafness),
and may cause common neurological syndromes such as migraine
or epilepsy. Some diseases, such as Parkinson’s or motor
neurone disease, may be either due to single-gene disorders
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 and
alcoholism or dietary exclusion. Vegetarians may be susceptible
to vitamin B12 deficiency. Recreational drugs may affect the
nervous system; for example, nitrous oxide inhalation causes
subacute combined degeneration of the cord due to dysfunction
of the vitamin B12 pathway, and smoking 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 history may
give clues to the underlying diagnosis, such as Lyme disease
(facial palsy), neurocysticercosis (brain lesions and epilepsy) or
Occupational factors are relevant to several neurological disorders.
For example, toxic peripheral neuropathy, due to exposure to
heavy or organic metals like lead, causes a motor neuropathy;
manganese causes Parkinsonism. Some neurological diagnoses
may adversely affect 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 • 125
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)
Dysphasia is a 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.
The language areas are located in the dominant cerebral
hemisphere, which is the left in almost all right-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
regions of the parietal lobe are involved in understanding written
The arcuate fasciculus connects Broca’s and Wernicke’s areas.
• During spontaneous speech, listen to the fluency and
appropriateness of the content, particularly paraphasias
(incorrect words) and neologisms (nonsense or
• Show the patient a common object, such as a coin or
• 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
• Ask the patient to read a passage from a newspaper.
• Ask the patient to write a sentence; examine the
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
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
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
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
Dysarthria refers to slurred or ‘strangulated’ speech caused by
articulation problems due to a motor deficit.
Dysphonia describes loss of volume caused by laryngeal
• Listen to the patient’s spontaneous speech, noting
• 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
• Ask the patient to count to 30 to assess fatigue.
• Ask the patient to cough and to say ‘Ah’; observe the soft
Disturbed articulation (dysarthria) may result from localised
lesions of the tongue, lips or mouth, ill-fitting dentures or
neurological dysfunction. This may be due to pathology anywhere
in the upper and lower motor neurones, cerebellum, extrapyramidal
system, or nerve, muscle or neuromuscular junction.
Bilateral upper motor neurone lesions of the corticobulbar tracts
cause a pseudobulbar dysarthria, characterised by a 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 (see Box 7.5 later) results from bilateral lower motor
neurone 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.
Cerebellar dysarthria may be slow and slurred, similar to alcohol
intoxication. Myasthenia gravis causes fatiguing speech, becoming
increasing nasal, and may disappear altogether. Parkinsonism may
cause dysarthria and dysphonia, with a low-volume, monotonous
voice, words running into each other (festination of speech), and
Fig. 7.3 Testing for meningeal irritation: Kernig’s sign.
cortical function can be difficult and time-consuming but is essential
in patients with cognitive symptoms. There are various tools, all
primarily developed as screening and assessment tools for dementia.
For the bedside the Mini-Mental State Examination (MMSE) and
Montreal Cognitive Assessment (MoCA) are quick to administer,
while the Addenbrooke’s Cognitive Examination is more detailed
but takes longer. None of these bedside tests is a substitute for
detailed neuropsychological assessment. The assessment of
cognitive function is covered in more detail on page 323.
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
M a s t i c a t i o n S a l i v a t i o n V o c a l i s a t i o n
B Fig. 7.4 Cortical function. A Features of localised cerebral
lesions. B Somatotopic homunculus.
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 (Ch. 8) and the VIII nerve
to hearing and balance (Ch. 9).
The olfactory nerve conveys the sense of smell.
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 neurones, which
project centrally via the olfactory tract to the medial temporal
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
The posterior part of the frontal lobe is the motor strip (precentral
gyrus), which controls voluntary movement. The motor strip
is organised somatotopically (Fig. 7.4B). The area anterior
to the precentral gyrus is concerned with personality, social
behaviour, emotions, cognition and expressive language, and
contains the frontal eye fields and cortical centre for micturition
Frontal lobe damage may cause:
• personality and behaviour changes, such as apathy or
• loss of emotional responsiveness, or emotional lability
• cognitive impairments, such as memory, attention and
• dysphasia (dominant hemisphere)
• conjugate gaze deviation to the side of the lesion
• primitive reflexes, such as grasp
• focal motor seizures (motor strip).
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
Temporal lobe dysfunction may cause:
• focal seizures with psychic symptoms
• contralateral upper quadrantanopia (see Fig. 8.5(4))
• receptive dysphasia (dominant hemisphere).
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
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).
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)
7.4 Summary of the 12 cranial nerves
Nerve Examination Abnormalities/symptoms
Optic disc and retinal changes
Strabismus, diplopia, nystagmus
Impairment, distortion or loss
Increase in upper motor neurone
IX Pharyngeal sensation Not routinely tested
X Palate movements Unilateral or bilateral impairment
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
There are three major branches of V (Fig. 7.6):
• mandibular (V3): sensory and motor.
Fig. 7.6 The sensory distribution of the three divisions of the
trigeminal nerve. 1, Ophthalmic division. 2, Maxillary division.
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