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Stroke and TIA
Chapter Summary
• Stroke is described as a focal or global dysfunction of cerebral function lasting longer
than 24 hours.
• If symptoms are present for less than 24 hours, the condition is termed ‘transient
ischaemic attack’ (‘TIA’).
• The history and examination will point towards the underlying cause and the territory of
the brain affected.
• Thrombolysis is considered as treatment for ischaemic stroke provided the patient
presents within 4.5 hours of the onset of symptoms.
• Antiplatelet therapy is usually used in patients following a stroke for secondary
prevention.
128
Lumps
21
INTRODUCTION
Lumps and bumps are extremely common presenting
patient complaints. A lump can also be identified by the
clinician on examination. Aetiologically, lumps generally
fall into one of the following categories:
• congenital or acquired
• inflammatory (either acute or chronic)
• traumatic
• neoplastic (primary or secondary and malignant or
benign)
• other (e.g. metabolic, degenerative, hormonal)
A detailed history, examination and subsequent investigations will help in determining the differential diagnosis, and
therefore management for a mass found. Management can
range from simple explanation, reassurance and monitoring
to urgent referral for surgery.
HISTORY AND EXAMINATION FINDINGS
A methodological approach to history taking and examination with particular emphasis on mass inspection is crucial
in determining the potential cause.
It is important to determine where was the lump found.
Common places include the neck, breast, axilla, scrotum
and perianal area, and skin. To a clinician the site will give
important clues regarding the anatomical origin of the lump
and potential underlying disease.
Important questions to ask about the lump include:
• When was the lump first noticed?
• Has it developed with time?
• Is it tender?
• Are there any other lumps or associated symptoms?
It is important to inquire about the patient’s medical
history as previous illness could itself be a cause of lump
development. Ask if there is a history of any other lumps
or a history of trauma and whether there is a history of
foreign travel.
The examination should focus on describing the lump.
It is important to try to establish an anatomical plane of the
swelling as it may be arising from the skin, subcutaneous
tissue, tendon, muscle, bone or internal organ.
Inspection and palpation of the swelling will help further characterize the swelling. These can be remembered
by the S’s:
• Site: should be described anatomically (e.g. lump in
the breast). If it is difficult to ascribe other features,
neighbouring structures should be identified.
• Size: needs to be measured with a diagram recording
the position, dimension and shape.
• Shape: certain lumps can have a characteristic shape
(e.g. two-lobed thyroid).
• Surface: comment on regularity, whether its uniform
or smooth or irregular. Margins of the swelling should
also be characterized as well- or ill-defined, smooth
and regular or irregular.
• Surroundings: examine around the lump, its regional
lymph nodes or, if it is a lymph node, its draining area.
• Structure (consistency): the lump may be solid or
gaseous, soft, fluctuant or firm. Fluid lumps can be
transilluminated, and they are compressible with
displacement of the fluid in two planes.
• Stability: describe if the lump is mobile or fixed to
surrounding/underlying structures.
• Sound: auscultate the swelling looking for bruits or
bowel sounds in a hernia.
• Secretion: look for evidence of discharge or a punctum.
• Sensation: feel the lump for temperature (may be
raised over inflamed lumps), tenderness and pulsation
(distinguish between expansile and transmitted
pulsation).
• Sign of emptying or indentation: examine if the lump
decreases in size or disappears when compressed or
remains indented.
It is extremely important to keep a good record of the examined lump to ensure an appropriate timeline, and monitor
any changes or developments. A diagram should be drawn
of the findings or a picture can be kept in the records with
appropriate patient consent.
HINTS AND TIPS
Remember to always examine the corresponding
area of the patient on the opposite side of the
body.
CLINICAL NOTE
A sebaceous cyst can be differentiated from lipoma
by the presence of a punctum on its surface.
129
Lumps
INVESTIGATIONS
Often diagnosis of a lump can be made clinically and does
not require investigating. When, however, this is not adequate, several tests can be helpful:
• Ultrasound scan or Doppler studies are useful for
fluid-filled lumps or to determine heterogeneity of a
swelling.
• Excision biopsy for histology.
• Aspiration or fluid for microscopy and culture, and
cytology.
• Fine-needle aspiration is used in solid masses for
cytology.
• Blood tests, including inflammatory markers, are useful
if the lump is thought to be inflammatory.
• CT and MRI scans are extremely useful in
determining the characteristics of a lump,
determining surrounding anatomy or investigating
the presence of other masses.
DIFFERENTIAL DIAGNOSIS
The features of the lump, its anatomical position and its origin will determine the most likely diagnosis of the lump.
Table21.1 describes the most common differential diagno-
ses based on anatomical location.
Localized lymphadenopathy
‘Localized lymphadenopathy’ describes a lymph nodes that
is abnormal in size, consistency or number. As a general
rule, in adults abnormal size is defined as a short axis of the
node of longer than 10 mm. There is a regional variation between lymph nodes, however, and a specific enlarged lymph
node should be investigated based on individual criteria.
Localized lymphadenopathy is most commonly caused
by a local site of infection (e.g. an abscess on the upper limb
will cause localized lymphadenopathy in the same area).
Generalized lymphadenopathy
This is when more than two noncontiguous lymph node
groups are found to be enlarged. Lymph nodes can increase in size depending on age, location and their current
immune activity. Most generalized lymphadenopathy is
caused by benign conditions such as bacterial or viral infections. Lymphoma, malignancy (e.g. acute leukaemia), HIV
infection, tuberculosis (Fig.21.1) or autoimmune disorders
(e.g. systemic lupus erythematosus) can also be the cause.
The history and examination are important in determining the cause. Constitutional symptoms of fever,
night sweats and malaise should always raise suspicion.
Superclavicular and infraclavicular lymph nodes are always
Table21.1 Anatomical distribution of lumps and their
most likely causes
Location Differential diagnosis
Neck lump 1 Anterior triangle:
Breast lumps Simple cysts
Axilla Breast cancer
Groin and
scrotum
Abdomen Enlarged abdominal organs (e.g. liver
Other Epitrochlear lymph nodes: characteristic
• pharyngeal pouch
• thyroid disease
• branchial cyst
• parotid gland swelling
• lymphadenopathy
2 Posterior triangle:
• carotid body tumour
• carotid artery aneurysm
• cystic hygroma
• cervical rib
• lymphadenopathy
3 Midline swelling:
• thyroglossal cyst
• lymphadenopathy
Breast abscess
Fibroadenomata (mobile lump)
Fibroadenosis (lumpy breast)
Fat necrosis
Breast cancer
Metastatic disease
Hidradenitis suppurativa
Sebaceous cyst
Lipoma
Hernias (inguinal or femoral)
Epididymal cyst
Epididymo-orchitis
Hydrocele
Haematocele
Sebaceous cyst
Psoas muscle abscess
Femoral artery aneurysm
Saphena varix
Cancer
or spleen)
Fibroids
Abdominal cancer
Abdominal aortic aneurysm
Pregnancy
of Hodgkin disease
Supraclavicular lymph node (Virchow
node): strongly suggestive of abdominal
malignancy (most likely gastric)
suggestive of malignancy. Firm, nontender nodes increase
the risk of malignancy.
Investigations should be directed by the history and ex-
amination, and can include:
• simple blood tests (e.g. full blood count, blood film and
inflammatory markers)
• infection swabs for primary disease site
130
Fig.21.1 Cutaneous tuberculosis. Lumps can be
superficial but can also infiltrate deeper tissues. Reprinted
with permission from Bolognia etal. Dermatology 3rd
edition. (Figure taken from Figure75.15. Scrofuloderma
Dermatology: 2-Volume Set, 3rd Edition Expert Consult
Premium Edition - Enhanced Online Features and Print by
Jean L. Bolognia, Joseph L. Jorizzo and Julie V. Schaffer)
• viral titres (e.g. hepatitis)
• imaging (chest radiograph, ultrasound scans, CT/MRI
scan)
Management is directed by the diagnosis. The most important aspect concentrates on eliminating a serious underlying cause. Patients are advised to monitor the condition
and seek help if symptoms persist or lymph nodes enlarge
or multiply. As a general rule, the presence of any of the
Differential diagnosis
following should raise suspicion for further investigations
or referral:
• presence for more than 6weeks
• lymph nodes greater than 2 cm or increasing in size
• widespread nature
• associated constitutional symptoms or splenomegaly
Treatment is of the underlying condition and determines
the prognosis.
2121
Splenomegaly
The spleen plays an important role in immunity, and acts
as a large lymph node. It has usually reached twice its original size by the time it is palpable. Splenomegaly most commonly presents as left upper quadrant mass, abdominal
pain or early satiety if the spleen compresses the stomach.
The presence of splenomegaly should raise suspicion of
a potentially serious underlying condition and should be investigated. Specific tests to consider include bone marrow,
liver and lymph node biopsy.
The causes of splenomegaly include:
• haematological causes: leukaemia, lymphoma,
haemolytic anaemia, myelofibrosis, polycythaemia
vera;
• infections: tuberculosis, malaria, schistosomiasis, viral
hepatitis, infective endocarditis, leishmaniasis;
• tumours and cysts: abscess, splenic metastases,
haemangioma;
• connective tissue disorder: systemic lupus
erythematous, Felty syndrome;
• congestive splenomegaly: heart failure, cirrhosis, portal
and splenic vein obstruction, Budd–Chiari syndrome.
If massive splenomegaly is present, chronic myeloid leukaemia, myelofibrosis, leishmaniasis and malaria should be
suspected.
Management is with treatment of the underlying condition. Splenectomy can be considered.
Chapter Summary
• Lumps are one of the most common presenting complaints of patients. They can be signs
of local infection or manifest themselves as features of a serious underlying condition.
The most important aspects in determining the origin of a lump and establishing the
differential diagnosis is thorough history taking and clinical examination.
131
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Focal neurological deficits
22
INTRODUCTION
Focal neurological deficits or signs describe an impairment of
the nervous system that affects a specific part of the body. These
can include muscle weakness or abnormal sensation, and can
Table22.1 Differential diagnosis of sensory and/or motor neurological deficits
Site of lesion Examples
Muscle (see
Chapters32–34)
Neuromuscular junction
(see Chapter32)
Peripheral nerves (see
Chapters32–36)
Congenital
Dystrophy: Duchenne, Becker, limb girdle, facioscapulohumeral
Myotonia: myotonic dystrophy, myotonia congenita (Thomsen disease)
Acquired
Drugs: steroids, cholesterol-lowering drugs (statins and fibrates), penicillamine
Endocrine: Cushing syndrome, thyrotoxicosis, hypothyroidism and hyperparathyroidism
Infection: viral (influenza, HIV infection), parasitic (toxoplasmosis, trichinosis) and bacterial
(Borrelia infection, Clostridium perfringens infection)
Inflammation and autoimmune: polymyositis, dermatomyositis and sarcoidosis
Metabolic: periodic paralyses, glycogen storage diseases and mitochondrial myopathy
Toxin: alcohol
Tumour: sarcoma and paraneoplastic syndromes
Myasthenia gravis
Lambert–Eaton myasthenic syndrome
Clostridium botulinum infection (botulism)
Mononeuropathy (only one nerve involved)
Entrapment: carpal tunnel syndrome (median nerve), and meralgia paraesthetica (lateral
cutaneous nerve of thigh)
Stretching: ulnar nerve neuropathy with increased carrying angle
Trauma
Compression: e.g. by tumour, as in neurofibromatosis, or AVM
Infarction: e.g. due to vasculitis
Mononeuritis multiplex/multifocal neuropathy (two or more nerves involved)
Connective tissue disease: PAN, SLE, RA
Infection: leprosy, herpes zoster, HIV infection, Lyme disease
Inflammation: sarcoidosis
Metabolic: DM
Infiltration: amyloidosis
Tumour: infiltration, paraneoplastic syndrome, neurofibromatosis
Polyneuropathy (with symmetrical deficit most marked distally)
result from disease occurring anywhere along the pathway of a
specific nerve or nerves. Many pathological processes can lead
to this presentation. The differential diagnosis is approached
logically according to the likely anatomical site (the level of the
lesion) and the possible causes at that location (Table22.1).
(Continued)
133
Focal neurological deficits
Table22.1 Differential diagnosis of sensory and/or motor neurological deficits—cont’d
Site of lesion Examples
Congenital
Charcot–Marie–Tooth disease (hereditary sensorimotor neuropathy)
Refsum disease
Friedreich ataxia (spinal cord pathology usually coexists)
Acquired
Connective tissue disease: PAN, SLE, RA
Drugs: nitrofurantoin, metronidazole, vinca alkaloids, platinum-containing drugs, isoniazid
Inflammation: AIDP (Guillain–Barré syndrome), CIDP, multifocal motor neuropathy
Metabolic: DM, renal failure (uraemic neuropathy), porphyria
Toxins: alcohol, lead, mercury and arsenic
Tumour: paraneoplastic syndrome and paraproteinaemias
Infiltration: amyloidosis
Vitamin deficiency: thiamine (B1), niacin (B6), B12, folate
Brachial or lumbar plexus Compression: cervical rib, thoracic outlet syndrome
Idiopathic: neuralgic amyotrophy
Metabolic: DM
Trauma: birth injury (Erb and Klumpke palsies) and, classically, motorbike accidents
Tumour: malignant infiltration (e.g. Pancoast tumour)
Spinal nerve root Infection (e.g. pyogenic meningitis, syphilis, CMV infection)
Prolapsed intervertebral disc and spondylosis
Spinal stenosis
Tumour
Vertebral fracture dislocation
Anterior horn cell (see
Chapter32)
Spinal cord
(see Chapter32)
Cerebellum
(see Chapter32)
Motor neurone disease
Spinal muscular atrophy
Poliomyelitis
Degeneration: osteoarthritis (osteophytes may cause spinal stenosis or foraminal stenosis)
Infection: abscess, HIV infection, TB (Pott disease)
Inflammation: MS, sarcoidosis, RA (atlantoaxial subluxation)
Metabolic: Paget disease causing spinal stenosis or compression
Trauma: direct; prolapsed intervertebral disc; radiotherapy
Tumour: metastases, neurofibroma, meningioma, glioma, ependymoma
Vascular: anterior spinal artery occlusion, aortic dissection, aortic aneurysm (emboli), AVM,
vasculitis
Vitamin deficiency: subacute combined degeneration of the spinal cord (vitamin B12)
Other: syringomyelia, spina bifida, motor neurone disease
Congenital
Friedreich ataxia and spinocerebellar ataxias
Ataxia telangiectasia
Acquired
Endocrine: hypothyroidism
134
History and examination findings
Table22.1 Differential diagnosis of sensory and/or motor neurological deficits—cont’d
Site of lesion Examples
Infection: abscess, meningoencephalitis, postinfectious encephalitis
Inflammation: MS
Toxins: alcohol, lead, anticonvulsants
Trauma: ‘punch-drunk’ syndrome
Tumour: metastases, acoustic neuroma, haemangioblastoma (von Hippel–Lindau disease),
Vascular: infarction, haematoma, AVM
Cerebral hemispheres (see
Chapter32)
Hydrocephalus: primary or secondary
Infection: abscess, meningitis, encephalitis; HIV infection (e.g. AIDS dementia complex),
Inflammation: sarcoidosis, SLE, MS
Metabolic: phenylketonuria, Wilson disease (basal ganglia), other inborn errors of
Toxic: alcohol
Trauma: haematoma, diffuse axonal injury
Tumour: primary or secondary
Vascular: infarction, haemorrhage, AVM, aneurysm
Vitamin deficiency: thiamine (B1), niacin (B6), B
AIDP, Acute inflammatory demyelination polyneuropathy; AVM, arteriovenous malformation; CIDP, chronic inflammatory demyelinating
polyneuropathy; CMV, cytomegalovirus; DM, diabetes mellitus; MS, multiple sclerosis; PAN, polyarteritis nodosa; RA, rheumatoid arthritis;
SLE, systemic lupus erythematosus; TB, tuberculosis.
paraneoplastic degeneration
Degenerative disease
malaria, rabies, TB, syphilis
metabolism
12
2222
HISTORY AND EXAMINATION
FINDINGS
History
Despite the vast number of potential underlying diseases,
a lesion at a particular point in the pathway between the
brain and muscle or skin will always produce the same clinical signs regardless of the cause. There are five important
aspects to consider in the history.
Pattern of deficit
Table 22.2 summarizes characteristic symptoms and signs
that arise because of a lesion at a specific neurological level. If
the neurological abnormalities do not fit with a single localized lesion, consider multiple sclerosis (MS), motor neurone
disease, paraneoplastic neuropathy, multisystem disorders
(e.g. sarcoidosis or vasculitis) or, rarely, a functional disorder.
Onset
Sudden onset usually indicates a vascular problem such as infarction or haemorrhage. Lesions due to trauma (e.g. enlarging
haematoma), MS, infection (e.g. abscess), acute prolapsed disc
and myelitis can also develop rapidly (e.g. over hours). An insidious onset, over weeks to months, is more typical of cervical
spondylosis, motor neurone disease, neoplasm or myopathy.
Precipitants
Trauma may result in muscular and neurological deficits.
Acute myasthenia can be precipitated by intercurrent illness
(particularly infection) or drugs (aminoglycosides or penicillamine). The incidence of MS relapses may increase in
the postpartum period and during systemic infections, and
symptoms may be exacerbated by exertion, hot weather or a
hot bath (Uhthoff phenomenon).
Progression
Many lesions cause gradually progressive, unremitting
disease, including tumours, motor neurone disease, hereditary ataxias, syringomyelia and degenerative brain
diseases. Intermittent deficits can be due to transient ischaemic attacks, epilepsy, migraine and myasthenia gravis.
MS is characterized by the development of lesions which
are dissociated in time and site. Symptoms and signs due
135
Focal neurological deficits
Table22.2 Symptoms and signs associated with different anatomical lesions
Site of anatomical
lesion Symptoms Specific signs Muscle Reflexes Sensation
Brachial or lumbar
plexus
Anterior spinal root Muscle weakness Wasting
Posterior spinal root Pain in skin and
Anterior horn cell Muscle weakness Wasting
Spinal cord Pain at site of lesion
Cerebellum Unsteadiness
Cerebral hemispheres Determined by
Muscle weakness
Sensory
disturbance
muscle supplied by
that root
worse on coughing,
sneezing, at night
Urinary/bowel
disturbance
Leg weakness
Sensory
disturbance
Tremor
Altered speech
Falls
Poor coordination
site of lesion
Weakness
Seizures
Altered speech
Disturbed higher
functions
Wasting
Normal Reduced or
At level of
Broad-based gait
Falling to side of
lesion
Intention tremor
Past-pointing
dysdiadochokinesis
Nystagmus
Staccato speech
Postural drift
Dysphasia
Dysarthria
Visual disturbance
Fasciculation
Reduced tone
Reduced power
in distribution of
affected nerves
Fasciculation
Reduced tone
Reduced power
in distribution of
affected root
Fasciculation
Reduced tone
Reduced power
in distribution of
affected nerve
lesion: wasting,
fasciculation,
reduced tone,
reduced power
Below lesion:
spasticity,
increased tone,
reduced power
Reduced tone
Normal power
Increased tone
‘Clasp-knife’
rigidity
Wasting only if
disuse
Reduced power
in pyramidal
distribution (flexors
stronger than
extensors in arms,
extensors stronger
than flexors in legs)
Reduced or
absent
Reduced or
absent
absent
Reduced or
absent
At level of lesion:
reduced or
absent
Below lesion:
increased,
Upgoing plantar
response
Pendular Normal
Brisk
Upgoing plantar
response
Deficit in
distribution of
affected nerves
Normal
Deficit in
distribution of
affected root
Normal
Below lesion:
ipsilateral
posterior
column loss
(proprioception,
vibration sense)
contralateral
spinothalamic
loss (pain and
temperature)
Deficit
determined by
site of lesion
136
History and examination findings
Table22.2 Symptoms and signs associated with different anatomical lesions—cont’d
Site of anatomical
lesion Symptoms Specific signs Muscle Reflexes Sensation
Muscle Weakness
Neuromuscular
junction
Peripheral nerve Muscle weakness
LEMS, Lambert–Eaton myasthenic syndrome.
(particularly
climbing stairs,
getting out of chair)
Pain (inflammation)
Diplopia
Dysphagia
Altered voice
Proximal muscle
weakness
Sensory
disturbance
May be purely
sensory, purely
motor or mixed
Myotonia
in myotonia
dystrophica
Calf
pseudohypertrophy
and Gowers sign in
Duchenne muscular
dystrophy
Fatigable
weakness with
repetition in
myasthenia gravis
Increasing strength
with repetition in
LEMS
Mononeuropathy
and mononeuritis
multiplex – signs
in distribution of
affected nerves
Polyneuropathy –
signs symmetrical
and distal (glove
and stocking)
Wasting (usually
proximal)
Tone normal or
reduced
Power reduced
Wasting only if
severe
Tone normal
Power alters with
repetition
Wasting
Fasciculation
Reduced tone
Reduced power
Usually normal;
reduced or absent
in severe muscle
disease only
Downgoing plantar
response
Normal Normal
Reduced or absent Deficit of all
Normal
modalities (glove
and stocking
distribution)
2222
to trauma or vascular events may slowly abate with time or
remain static following the initial event.
Evidence of cause
The following factors provide evidence of a cause:
• family history: e.g. hereditary ataxias, phenylketonuria,
neurofibromatosis;
• drug history: e.g. phenytoin (cerebellar signs), vinca
alkaloids and platinum-containing drugs (peripheral
neuropathy), penicillamine (myasthenia gravis);
• dietary history: intake of vitamins B1, B6 and B12 and
folate;
• alcohol history;
• preexisting illness: e.g. diabetes, hypertension
(cerebrovascular disease), rheumatoid arthritis,
tuberculosis or malignancy;
• history of trauma;
• associated features: e.g. swinging pyrexia and rigors
(abscess), vasculitic symptoms (connective tissue
disease), anorexia and weight loss (malignancy),
symptoms of hypothyroidism or hyperthyroidism;
• travel history (exposure to infections, e.g. Lyme
disease) and risk factors for HIV infection.
Examination
Perform a full neurological examination (see Chapter2).
The clinical examination should aim to answer three
questions. Firstly, where is the anatomical site of the lesion
or lesions? Secondly, is there anything to suggest the underlying pathological process? Finally, what disability does the
patient have because of the neurological deficit?
The anatomical site of the lesion
From the moment you meet the patient, observe the patient
carefully. How does the patient shake your hand? Can the
patient lift their arm up? Can they let go of your hand (myotonia)? Watch how the patient undresses or gets on to the
bed. A severe deficit will often become apparent before you
start the examination.
Table22.2 should help you identify where the anatomical
lesion is likely to be, based on the neurological signs present.
The underlying cause
Once the site of the lesion has been identified, think of the
differential diagnosis as outlined at the beginning of this
chapter.
137