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Focal neurological deficits
Look at the patient's face for myotonic facies (myotonic
dystrophy), Cushing syndrome (proximal myopathy) or
hypothyroidism (myopathy or cerebellar dysfunction).
Does the patient have neurofibromatosis (spinal cord or
peripheral nerve lesions) or connective tissue disease such
as rheumatoid arthritis (entrapment mononeuropathy,
mononeuritis multiplex or peripheral neuropathy)?
The resultant disability
COMMUNICATION
Often the most important thing for the patient is
what the lesion prevents the patient from doing.
Assess and distinguish impairment, disability and
handicap, and address the problems accordingly.
It is important to distinguish three related concepts: ‘impairment’ refers to a problem of body function or structure
(e.g. right arm weakness following stroke); ‘disability’ refers
to an inability to perform an activity (e.g. cannot write); and
‘handicap’ refers to social function (e.g. cannot work).
Think what tasks the affected part of the body normally
performs and ask the patient to show you how he or she
manages, such as doing up buttons (for peripheral neuropathy), brushing hair or standing up from a chair (for proximal myopathy). Watching the patient walk is an important
part of the examination and can give useful information
(Table22.3).
Table22.3 Abnormalities of gait
Lesion Gait
Hemiplegia Foot is plantar flexed; leg is
stiff and dragged through a
semicircle
Spastic paraplegia Legs stiff; walk in ‘scissor
fashion’, like ‘walking through
mud’
Proximal myopathy Waddling gait; trunk moves to
swing legs forward; difficulty
in climbing stairs or standing
out of a chair
Parkinsonism Stooped posture, hesitation
in starting, shuffling, festinant
(accelerating), difficulty
turning, poor arm swing and
may freeze
Cerebellar dysfunction Broad based, ataxia with a
tendency to fall to the side of
the lesion; unable to perform
tandem gait (heel to toe)
Dorsal column disease Stamping; broad based with
patient looking at the ground
as unable to sense where
foot is; clumsy and slaps feet
to ground
Foot drop Stepping; legs lifted high off
the ground as no dorsiflexion
of the foot
Musculoskeletal disease Limping; patient avoids
weight bearing on affected
side because of pain
Investigations
The history and examination will guide the choice of investigations. The following tests may be useful.
Bedside investigations
Blood tests
• Full blood count and erythrocyte sedimentation
rate: reactive picture in inflammation, infection and
neoplasm; raised mean corpuscular volume in vitamin
B12 deficiency and alcohol abuse.
• Urea and electrolytes: raised urea and creatinine levels
in renal failure, high or low potassium level in periodic
paralyses.
• Serum calcium: raised level in hyperparathyroidism,
sarcoidosis, malignancy.
• Serum glucose: raised level in diabetes mellitus.
• Liver function tests: raised γ-glutamyltransferase
level in alcohol abuse, raised alkaline phosphatase
level in Paget disease and deranged transaminases in
metastases, infection and Wilson disease.
138
• Thyroid function tests: hyperthyroidism or
hypothyroidism.
• Creatine kinase: markedly raised level in muscle
inflammation and muscular dystrophies.
• Autoantibodies: in systemic disease, (e.g. rheumatoid
arthritis, systemic lupus erythematosus and
polyarteritis nodosa) and in many specific neurological
diseases (Table22.4).
• Serology: HIV infection, herpes and syphilis where
appropriate.
• Immunoglobulins: paraproteinaemias.
Cerebrospinal fluid analysis
• A lumbar puncture is often required. The different tests
that can be performed on the cerebrospinal fluid are
outlined in Table22.5.
Imaging
• Plain radiographs of the spinal column may
demonstrate degenerative and destructive bone lesions
and fractures.
History and examination findings
Table22.4 Autoantibodies in specific neurological diseases
Autoantibody target Associated disease
Ganglioside M1 Multifocal motor neuropathy
Ganglioside Q1b Miller Fisher syndrome
Voltage-gated calcium channel LEMS
Voltage-gated potassium channel Autoimmune encephalitis
NMDA receptor Autoimmune encephalitis
Acetylcholine receptor and muscle-specific kinase Myasthenia gravis
Aquaporin 4 Neuromyelitis optica
Hu, Ri, Yo Paraneoplastic neurological syndromes
GAD Stiff person syndrome
GAD, Glutamate decarboxylase; LEMS, Lambert–Eaton myasthenic syndrome; NMDA, N-methyl-d-aspartate.
Table22.5 Cerebrospinal fluid analysis and interpretation
Test/Result Interpretation
Microscopy Direct visualization of microorganisms or malignant cells
Culture and sensitivity Infection
PCR Detection of viral RNA or DNA
Low glucose level (<2/3 of blood glucose level) Bacterial/TB/fungal/carcinomatous meningitis
Very high protein level (>2 g/L) GBS, Froin syndrome,a TB/fungal meningitis, Behçet syndrome
High protein level (0.4–2 g/L) Bacterial meningitis, viral encephalitis, cerebral abscess, cerebral
Oligoclonal bands Multiple sclerosis, SLE, neurosyphilis, neurosarcoidosis, Behçet
Neutrophils Bacterial meningitis
Lymphocytes Partially treated bacterial meningitis, viral encephalitis/ meningitis,
Xanthochromia (yellow CSF due to haemoglobin
breakdown); usually by spectrophotometry
a
Raised cerebrospinal fluid protein level and xanthochromia but normal cell count, seen below a block in spinal cord compression.
CNS, Central nervous system; GBS, Guillain–Barré syndrome; PCR: polymerase chain reaction; SLE, systemic lupus erythematosus;
SSPE, subacute sclerosing panencephalitis; TB, tuberculosis.
malignancy
syndrome, SSPE
TB meningitis, CNS vasculitis, Behçet syndrome, HIV-associated,
lymphoma/leukaemia, SLE
Subarachnoid haemorrhage (xanthochromia from 12 hours after
event)
2222
• MRI of the brain and spine is useful in diagnosing and
localizing central lesions. It provides greater anatomical
detail than CT, and contrast medium can be given to
show blood vessels or areas of blood–brain barrier
breakdown.
• CT is useful in the acute setting (e.g. for detecting
haemorrhage) and provides accurate imaging of bony
structures.
Further investigations
• Electromyogram: useful in primary muscle disease
(typical changes in myotonia and myasthenia); it also
shows denervation (but not its cause).
• Nerve conduction studies: can demonstrate peripheral
neuropathies and the site and type of individual nerve
lesions.
• Evoked potentials: visual evoked potentials
demonstrate previous retrobulbar neuritis in MS.
Auditory and somatosensory evoked potential tests
may also be performed to look for lesions in these
pathways.
• Biopsy: consider if the diagnosis is in doubt despite
the history, examination and noninvasive procedures.
Muscle, nerve and brain biopsies can be performed to
give a definitive histological diagnosis.
139
Focal neurological deficits
Chapter Summary
• Focal neurological deficits are a manifestation of disease somewhere along the pathway
of the nerve supply to the tissues.
• The history and examination will help determine the site of the lesion.
• Stroke is the most common cause of focal neurological deficits in the elderly.
• MRI is a more sensitive diagnostic modality in neurological disease than CT.
140
Dizziness and vertigo
23
INTRODUCTION
‘Dizziness’ is a nonspecific term that describes disorientation or unsteadiness. Vertigo is the illusion of movement,
usually rotation but also swaying or tilting, of a patient or
their surroundings. This is often accompanied by nausea,
vomiting and postural instability. It results from disease either in the labyrinth of the inner ear (the most common
cause) or in cranial nerve VIII or its connections in the
brainstem, including the cerebellum.
The differential diagnosis in the patient with vertigo
includes labyrinth disorders, cranial nerve VIII disease or
brainstem lesions, and is summarized in Table23.1. Rarely,
vertigo can be a feature of temporal lobe disease (e.g. temporal lobe epilepsy).
The differential diagnosis of dizziness is summarized in
Table23.2.
Table23.1 Differential diagnosis of vertigo (see Chapter32)
Location of lesion Examples
Labyrinth Middle ear disease (e.g. otitis media)
Ménière disease
BPPV
Labyrinthitis
Traumatic vertigo
Perilymphatic fistula
Cranial nerve VIII Vestibular neuronitis
Acoustic neuroma
Ramsay Hunt syndrome: herpes zoster of the geniculate ganglion
Ototoxic drugs: aminoglycosides such as gentamicin
Petrous temporal bone disease (e.g. Paget disease)
Brainstem/cerebellum Vertebrobasilar ischaemia: ΤΊΑ, posterior circulation stroke (including lateral medullary
syndrome), rotational ischaemia
Multiple sclerosis: demyelination
Migraine
Encephalitis
Tumour
Alcohol abuse
Episodic ataxia (inherited autosomal dominant disorders)
Syringobulbia
BPPV, Benign paroxysmal positional vertigo; TIA, transient ischaemic attack.
Table23.2 Differential diagnosis of dizziness without
true vertigo
Causes Further information
Low cardiac output See Chapter27
Nonspecific dizziness –
often due to a psychiatric
disorder (e.g. anxiety)
Anaemia See Chapter36
Hypoglycaemia See Chapter33
Postural hypotension See Chapter27
Visual disturbance See Crash Course:
Cerebrovascular disease See Chapter32
Pyrexia See Chapter37
See Crash Course:
Psychiatry
Neurology
141
Dizziness and vertigo
COMMUNICATION
When a patient presents with ‘vertigo’ or
‘dizziness’, it is vital to establish whether true
vertigo is present or not, as these symptoms result
from different diseases.
History
The history is the basis of diagnosis in vertigo. It is important to elicit the time course of the vertigo and the likely site
of the lesion by asking about other auditory and neurological symptoms. Typical features of specific diseases are
shown in Table23.3.
COMMUNICATION
It is important to bear in mind that occasionally
patients with vestibular dysfunction will not
report vertigo, and that patients with presyncope
Onset and pattern of vertigo
The following should be established:
• Onset: peripheral lesions generally cause acute
occasionally report a mild spinning sensation.
Table23.3 Characteristic features of conditions causing vertigo
Disease Cause Length of vertigo
Ménière disease Excess
Vestibular
neuronitis
BPPV Debris within the
Perilymphatic
fistula
Vertebrobasilar
insufficiency
Acoustic
neuroma
Central lesions Tumour
BPPV, Benign paroxysmal positional vertigo.
endolymphatic
fluid (hydrops)
Possibly viral Days to weeks
semicircular canals
Can follow head
injury and
vestibular
neuronitis
Rupture of round
window
membrane
Often due to
barotrauma
Can be
spontaneous
Compression of
vertebral arteries
by osteophytic
cervical vertebrae
Schwannoma of
vestibular nerve
Demyelination
Vascular migraine
20 min to 24 h
Often preceded by
sensation of fullness
in the ear
Explosive onset
Less than 1 min
Precipitated by
changes in head
position
Frequent, shortlasting episodes,
persisting for months
to years
Seconds
Precipitated by neck
extension or rotation
Gradual onset
Progressive
Dependent on
underlying disease
Aural
symptoms
Fluctuating
but progressive
sensorineural
deafness
Tinnitus
None None Spontaneously resolves
None None Episodic attacks
Deafness and
tinnitus
None Dysarthria
Unilateral
deafness and
tinnitus
Often spared Usually present
HISTORY AND EXAMINATION FINDINGS
severe symptoms; central lesions tend to be of
gradual onset with less severe vertigo, unless caused
by ischaemia.
Neurological
symptoms Natural history
None Episodic, unilateral at
None Often resolves with bed
Diplopia
Visual loss
Syncope
Cranial nerve V
and VII palsies
Ipsilateral
cerebellar signs
and dependent
on site of
lesion
first becomes bilateral in
25%–45%
Frequency diminishes
with duration
in weeks
Spontaneous resolution
over weeks to months,
but may recur after a
symptom-free period
rest
Can be surgically
repaired
Episodic attacks
Symptoms progress until
surgical removal
Tumour/demyelination:
symptoms progress
until underlying is cause
treated
142
History and examination findings
2323
• Duration and recurrence: is it a single episode (e.g.
ischaemia or migraine) or recurring (e.g. benign
paroxysmal positional vertigo (BPPV))? Are the attacks
brief (seconds to minutes) or prolonged (hours to days)?
• Aggravating features: is there a relation to specific
positions or movements? Is it worse on coughing/
sneezing?
CLINICAL NOTES
VESTIBULAR NEURONITIS AND VESTIBULAR
LABYRINTHITIS
Vestibular neuronitis is dysfunction of the branch
of the nerve responsible for balance, resulting in
dizziness or vertigo without change in hearing.
Vestibular labyrinthitis occurs when both branches
of cranial nerve VIII are affected, resulting in
hearing changes as well as dizziness or vertigo.
Aural symptoms
The presence of aural symptoms suggests that the lesion is
peripheral, involving the labyrinth or cranial nerve VIII:
• deafness (fluctuating or progressive);
• tinnitus;
• ear discharge or pain;
• a sensation of ear ‘fullness’ (Ménière disease).
Neurological symptoms
The following symptoms suggest a central lesion or acoustic
neuroma:
• other cranial nerve involvement: facial weakness, facial
paraesthesia, visual disturbance, dysarthria, dysphagia;
• seizures;
• weakness, paraesthesia, ataxia.
CLINICAL NOTE
HISTORY ASPECTS SUGGESTING AN
UNDERLYING CAUSE
• Recent upper respiratory tract infection or ear
• Head trauma or recent labyrinthitis: benign
paroxysmal positional vertigo.
• Direct ear trauma or previous ontological
surgery: perilymphatic fistula.
• Drug history (e.g. aminoglycosides, furosemide,
antipsychotics, anticonvulsants).
• Alcohol history: acute intoxication may cause
vertigo.
• Recent flying or diving (e.g. barotrauma –
perilymphatic fistula).
• Associated headache with photophobia or
phonophobia: migrainous vertigo.
• Medical history: risk factors for vascular disease
(ischaemia), multiple sclerosis, migraine.
• Family history of vertigo: inherited episodic
ataxia (channelopathies).
Examination
Full neurological examination, ear examination and eye
examination should be performed (see Chapter2). The following specific abnormalities should be looked for carefully:
• Nystagmus: observe the direction of slow and
fast phases, and whether they change direction or
amplitude with direction of gaze. Are there features of a
peripheral or central cause (see Chapter2)?
• Dix–Hallpike manoeuvre: the patient's neck is extended
and the head is turned to one side; the patient is then
lowered quickly to a supine position. Reproduction
of symptoms of vertigo and horizontal and torsional
nystagmus indicate a positive test result. The test is
around 80% sensitive for detection of BPPV.
• Romberg test: the patient stands erect with the feet
together and arms outstretched. The patient is then
asked to close the eyes. Inability to maintain balance
represents a positive test result and indicates a vestibular
(labyrinthine) or sensory (proprioceptive) dysfunction.
Patients usually fall to the side of the lesion.
• Head impulse test: the patient is asked to fix the gaze
on a target; the head is then quickly turned through
20 degrees horizontally. Abnormal corrective eye
movements indicate a positive test result and suggest a
peripheral lesion.
• Focal neurological signs: if present, these suggest a central
lesion, acoustic neuroma or Ramsay Hunt syndrome.
• Eyes: papilloedema (tumour with raised intracranial
pressure), optic atrophy (demyelination) and
ophthalmoplegia (cranial nerve defect, demyelination).
• Ears: otoscopy may reveal otitis media or a herpetic rash.
• Neck movements: are they limited or do they provoke
the symptoms? Rarely, cervical spondylosis can cause
‘rotational vertebrobasilar ischaemia’ on head turning.
Fig.23.1 summarizes the examination approach.
HINTS AND TIPS
Remember benign paroxysmal positional vertigo is
diagnosed with the Dix–Hallpike manoeuvre and is
treated with the Epley manoeuvre.
143
Dizziness and vertigo
Focal neurology
tests (see Chapter 2)
Eyes
— Nystagmus
— Papilloedema
— Optic atrophy
— Ophthalmoplegia
Neck
— Movements
(limited?
provoke
symptoms?)
— Cranial nerve palsies
— Cerebellar signs
— Gait
— Limb weakness/
abnormal sensation
Ears
— Otitis media
— Herpetic infection
— Deafness
— Rinne and Weber
Blood pressure
— Postural
hypotension
General
—Dix–Hallpike
manoeuvre
— Gait
• Imaging: MRI should be performed if a central lesion
or acoustic neuroma is suspected. See Box23.1 for
other indications.
• Audiometry: this will help distinguish between
conductive and sensorineural deafness.
• Caloric tests: normally, running cold and then warm
water into the external auditory meatus causes
nystagmus with the fast phase away and towards,
respectively; where there is disease in the ipsilateral
labyrinth, cranial nerve VIII or brainstem, this normal
response will be reduced or absent.
• Electronystagmography: a more accurate assessment of
the presence and type of nystagmus.
BOX23.1 INDICATIONS FOR BRAIN IMAGING
IN ACUTE VERTIGO
Fig.23.1 Examining the patient with vertigo.
Investigations
• Simple tests include routine observations (including
lying and standing blood pressure to investigate
postural hypotension), blood glucose and ECG.
Routine blood tests may reveal infection or evidence of
other underlying disease.
Chapter Summary
• Vertigo can be of peripheral (vestibular labyrinth, semicircular canals, vestibular nerve) or
central (cerebral cortex, brainstem, cerebellum) origin.
• Peripheral vertigo is the most common type.
• Benign paroxysmal positional vertigo is the most common disease that leads to vertigo.
• New-onset headache (raises possibility of
haemorrhage)
• Intact head impulse tests (increased likelihood
of central lesion)
• Other cranial nerve symptoms/signs suggesting
a central cause
• Nystagmus with features of a central lesion
• Acute deafness (raises the possibility of
labyrinthine stroke)
N.B. The presence of significant cardiovascular risk factors
should increase the suspicion of a vascular event.
144
Back pain and joint pain
24
INTRODUCTION
Back pain and joint disease are common problems. Back pain,
in particular, affects up to two-thirds of adults at some point in
their life and, as such a common presenting complaint, places a
considerable burden on health services. Both complaints often
present together and can be unspecific and benign but also can
manifest themselves through significant underlying disease.
HISTORY AND EXAMINATION FINDINGS
Different types of joint and back pain have many features in
common, and examination will provide further additional
important clues to the cause.
History
When you are exploring the presenting complaint and determining the characteristics of the pain, remember to consider:
• Site (e.g. level of spine, specific joints) and radiation of pain.
• Time course, including speed of onset, progression and
variation over the day (e.g. worse in the morning with
inflammatory arthritis). Is the pain present at night?
• Character (e.g. shooting, arthritis or arthralgia) and
severity (what is the loss of function and is it affecting
the patient’s daily activity?)
• Joint swelling and stiffness. The pattern of distribution
and joint deformity (symmetrical or asymmetrical,
monoarthritis or polyarthritis).
• Aggravating and relieving features (e.g. pain due to disc
prolapse may be worsened on leaning forward; pain
due to neoplasia is often unremitting).
Ask about associated features:
• Weakness and sensory loss: can this be localized to a
single myotome/dermatome (e.g. disc prolapse) or is it
more generalized (e.g. cauda equina syndrome)?
• Incontinence (cauda equina syndrome).
• Fever (infection, lymphoma).
• Weight loss (inflammatory disease, neoplasia, chronic
infection).
• Pseudoclaudication: leg pain on walking (indicative of
spinal stenosis).
• Systemic features (e.g. anaemia, rashes, eye disease,
involvement of other systems (e.g. respiratory,
gastrointestinal systems)).
• Depression, anxiety and psychosocial factors (Table24.1).
Other important points to consider include:
• age (Table24.2);
• history of trauma;
• medical history: immune compromise, recent or
chronic infection, cancer;
• previous or current medication (e.g. gout precipitated
by thiazide and loop diuretics);
• family history: inflammatory arthritis;
• social history: smoking, alcohol, occupation, sport.
CLINICAL NOTES
Remember that with inflammatory causes the pain
is worse first thing in the morning, is associated with
stiffness, and abates after 30–60 min of movement
(e.g. rheumatoid arthritis). Conversely, mechanical
back pain and degenerative arthritis (e.g. osteoarthritis)
are often worse with movement and abate at rest.
CLINICAL NOTE
Chronic arthritis and the associated reduction in
function can lead to feelings of helplessness and
depression. Assessment of these features is an
important part of the history taking in patients with
arthritis.
Table24.1 Yellow flags: factors associated with the
development of chronic pain
Factor Associations
Physical/pain
related
Psychological Anxiety, depression, emotional
Social Lack of education
Behavioural Smoking, poor coping skills,
Occupational Highly physical employment,
Other Involvement in litigation
Obesity, older age, increased severity
of pain, disability, neurological
involvement, previous episode of pain
distress, somatization
avoidance of activity because of fear
of pain, prior inactivity
dissatisfaction with job, lack of
employer flexibility in type of work done
145
Back pain and joint pain
CLINICAL NOTE
Causes of joint pain can be remembered by
the mnemonic ‘SOFTER TISSUE’: sepsis,
osteoarthritis, fractures, tendon/muscle,
epiphyseal, referred, tumour, ischaemia,
seropositive arthritides, seronegative arthritides,
urate, extraarticular rheumatism (e.g.
polymyalgia).
Examination
Examination should start with the affected area of the
joint or spine and subsequently be directed by the history. Given a variety of joints can be affected, to make
the task easier the general principle of LOOK, FEEL,
MOVE can be applied to ensure a complete examination
is performed:
• Look: obvious deformities, joint alignment, postural
abnormality (kyphosis, scoliosis), swelling or redness,
rashes, masses.
• Feel: assess the area for tenderness, inflammation
(swelling, heat) and crepitus (joint degeneration).
Evaluate any masses fully.
• Move: is there a reduced range of movement or pain on
movement? Is the joint stiff?
Table24.2 Red flags for back and joint pain
Factor Associations
Age >55 or <20years Neoplasia more common in
Thoracic pain Neoplastic disease
Nocturnal, constant pain Malignancy
History of trauma Vertebral fractures
Systemic symptoms (e.g.
weight loss, rashes)
Immunosuppression or
history of malignant
disease
Prolonged steroid use Predisposes to
Neurological symptoms,
including sphincter
dysfunction
the elderly and inflammatory
disease more common in
the young
Inflammatory, infectious or
neoplastic disease
Infectious disease,
neoplasm
osteoporosis and
pathological fractures
Cauda equine, nerve
root disease, spinal cord
compression
Always remember to assess at least the joint above and the
joint below the joint being examined and offer a neurological examination. If particular symptoms occur, examine
the systems involved (rectal examination to exclude cauda
equine, respiratory examination for lung fibrosis, etc.)
Specific examination findings in the most common joint
diseases can be found in Table24.3.
Table24.3 Specific examination findings in common joint diseases
Joint disease Systemic features Local features
Rheumatoid
arthritis
Osteoarthritis Most commonly asymmetrical and
Ankylosing
spondylitis
Septic arthritis Systemic compromise: fever and rigours;
DIP, Distal interphalangeal; FABER, flexion, abduction, and external rotation; MCP, metacarpophalangeal; PIP, proximal interphalangeal.
Symmetrical deforming arthropathy
Cervical spine disease
Anaemia
Eye disease (keratoconjunctivitis sicca,
keratitis, scleromalacia perforans)
affecting large weight-bearing joints
Most commonly affects spine and sacroiliac
joints
Reduced chest expansion and lung
fibrosis
Aortic regurgitation due to aortitis
Eye iritis
tachycardia; tachypnoea; hypotension
Swelling of PIP and MCP joints
Wasting of small hand muscles
Extensor tendons nodules
Ulnar deviation of fingers (subluxation of MCP joints)
Swan-neck finger deformity (hyperextension of PIP joints
and flexion of MCP and DIP joints)
Boutonniere finger deformity (flexion of PIP joints and
extension of MCP and DIP joints)
Z-thumb
Trigger fingers
Heberden nodes (swelling of DIP joints)
Bouchard nodes (swelling of PIP joints)
Subluxation of first carpometacarpal joint (square hand)
Question mark posture (loss of lumbar lordosis and fixed
kyphosis)
Limited range of movement in the whole spine but
especially in cervical and lumbar regions (Schober test)
Tender sacroiliac joints (positive results of Gaenslen and
FABER tests)
Monoarthritis with swollen, red, hot and extremely
tender joint
146
Investigations
2424
COMMUNICATION
Be aware that when you are introducing yourself to
the patient with rheumatoid arthritis, shaking hands
may be painful for the patient.
INVESTIGATIONS
Investigations should be requested according to clinical suspicion elucidated by the history and examination. A list of
investigations that can aid in diagnosis when you are considering joint and back pain follows.
Bedside investigations
Blood tests
• Full blood count: anaemia; raised white cell count in
infection and occasionally in rheumatoid arthritis
(RA), leucopenia and thrombocytopenia in systemic
lupus erythematosus (SLE), neutropenia in Felty
syndrome.
• Erythrocyte sedimentation rate and C-reactive protein:
nonspecific markers of inflammation but may be useful
in detecting inflammatory arthritis.
• Renal function, liver function, calcium, parathyroid
hormone, vitamin D, urate, myeloma screen: may
be useful depending on the suspected underlying
disease.
• Autoantibody screen:
○ Rheumatoid factor: positive in about 80% of
patients with RA. May also be positive in SLE,
mixed connective tissue diseases, scleroderma and
Sjögren syndrome.
○ Antinuclear antibodies: positive in RA and SLE.
○ Anti-double-stranded DNA antibodies: high titres
in SLE.
○ Other autoantibodies according to clinical
suspicion.
• Viral serology: if a viral cause for the arthropathy
is suspected (e.g. rubella, mumps, infectious
mononucleosis, Coxsackie virus and hepatitis B virus).
Joint aspiration is necessary when you are excluding septic
arthritis and diagnosing crystal arthropathy. If septic arthritis is suspected, joint aspiration should be performed before
layed. Analysis of aspirate should cover:
• Appearance: purulence indicates infection, frank blood
indicates haemarthrosis or traumatic tap.
• Microscopy and culture for bacteria, polarized
light microscopy for crystals: monosodium urate
indicates gout, calcium pyrophosphate indicates
pseudogout.
• White cell count: high in inflammatory arthropathies.
• Culture: specific for potential organisms, their
resistance and their sensitivity.
COMMON PITFALLS
In pseudogout, crystals are positively birefringent
in plane-polarized light. Remember this by the P’s
(positive, plane, polarized). In gout, the crystals are
negatively birefringent.
Imaging
Imaging can be very useful when you are considering joint
disease and back pain. Plain radiographs are readily available and can show specific features characteristic of disease
(Table24.4).
MRI is now widely used to provide images of soft tissue
injury, including ligaments, muscle and intervertebral discs,
inflammatory processes such as osteomyelitis and malignancy. It is also a first-line imaging method when spinal
cord compression or cauda equina is suspected.
CT is used to assess bones and joints, and can be a
good method to further delineate fracture. Other imaging
methods to consider include more invasive methods such
Table24.4 Plain radiographic findings in common joint
diseases
Disease Plain radiograph findings
Rheumatoid
arthritis
Osteoarthritis Loss of joint space, marginal
Gout Soft tissue swelling and punched-
Ankylosing
spondylitis
Back pain Spine and pelvis X-ray is useful for
A joint X-ray will show soft
tissue thickening, juxtaarticular
osteoporosis, loss of joint space,
bony erosions and subluxation
Chest imaging may show pleural
effusion, pulmonary fibrosis,
rheumatoid nodules and rheumatoid
pneumoconiosis (Caplan syndrome)
osteophytes, subchondral sclerosis
and cysts are visible on X-ray
out lesions in juxtaarticular bone are
common findings in gout
Sacroiliac joint and spine radiograph
shows ‘bamboo spine’ (squaring
of the vertebrae and obliteration of
sacroiliac joints)
detecting fractures (traumatic and
compression fractures), disc space
narrowing, degenerative change,
spondylolisthesis, and changes of
inflammatory disease (e.g. sacroiliitis,
squaring of the vertebrae)
147