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2 History and examination
Cognition
(AMTS)
AMTS
MMSE
(GPCOG)
(TYM)
CIT)
IVI, ACE
ARB,
DVT,
SLE.
MS,
HIV
B
DM, CKD
CNS
AVM.
AVM
SLE.
AMTS
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If there is any concern about cognition, cognitive testing should be undertaken.
Abbreviated Mental Test Score
The
10
based on
8 Name of current monarch/ prime minister?
10
questions:
1
If the patient is able to repeat an address (eg 42 West Street), then test recall
after the other questions have been completed.
2
Age?
3
Time (to nearest hour)?
4
Year?
5
Can they recognize 2 people by role (eg doctor, nurse, hospital visitor)?
6
Date of birth?
7
Dates of Second World War?
9
Where are you now (which hospital)?
Count backwards from 20 to
Score of 6 or less suggests dementia (chronic) or delirium (acute).
with the more detailed Mini- Mental State Examination (
copyright). Impaired hearing/ deafness, mood disorders, and language barriers may
lead to a falsely positive screen result. Other tools include the General Practitioner
Assessment of Cognition
Cognitive Impairment Test (
Cramp
Painful muscle spasm. Common at night or after heavy exercise, and in patients
with advanced kidney failure, including dialysis. Other possible causes include dystonia (writer’s cramp,
myopathy (McArdle’s,
p
p
692
erately eective for nocturnal cramps.
Drugs with possible causative role in cramp include diuretics (?related to dK+ ),
domperidone, salbutamol/ terbutaline
kaloids, levothyroxine.
Paraesthe siae
‘Pins and needles’, numbness/ tingling. Can be painful/ ‘burn’ (dysaesthesia).
Causes
• Metabolic: dCa
• Vascul ar: arterial emboli, Raynaud’s,
• Antibody mediated: para neopl astic ,
• Infection: Lyme d iseas e, rabi es.
• Brain: th alami c/ parietal lesions.
• Neuropathy:
(glove & stocking, eg
mononeuropathy (
cytoma. If
2
+
(pe riora l), iPaCO2, hypothyroidism, neurotoxins (ask about bite/ sting).
myelitis/
p
496
). If paroxysmal consider migraine, epilepsy, phaeochromo-
wandering co nside r infec tion ( take travel histor y), eg Strongyloides.
Fac i al pa in
causes Migraine, trigeminal, glossopharyngeal neuralgia (p
other pain- sensitive structure in head/ neck. Post- herpetic neuralgia: classically a
burning/ stabbing pain, involves dermatomal areas aected by shingles (
become chronic/ intractable with hyperalgesia/ allodynia of aected skin.
Vascular and non- neurological causes
• Neck— cervical disc pathology.
• Bone/ sinuses— sinusitis, malignancy.
• Eye— glaucoma, iritis, orbital cellulitis, eye strain,
• Te m po r o m a n d i b u l a r j o i n t — arthritis, idiopathic dysfunction (common).
• Tee t h / gums— caries, broken teeth, abscess, malocclusion.
• Ear— otitis media, otitis externa.
• Vascul ar/ vasc ulitis— aneurysm,
3
The
was established in
patients questioned today should be considered. It needs to be a fair and multicultural test of long- term
memory, not knowledge of taught history.
is a commonly used screening tool
3
1.
, the Test Your Memory Test
6
-
.
465
), salt depletion, muscle ischaemia (claudication, DM),
). Quinine bisulfate
, d
, p
500
), cervical rib, carpal tunnel, sciatica, plexopathy/
, giant cell arteritis,
1972
. A contemporary update of this question to an event within the life of
200– 300
- i/
hig h plas ma vis cosity.
, lumbar fracture, peripheral neuropathy
12
mg PO at night may be mod-
celecoxib, lacidipine, ergot al-
correlates
™, subject to strict
, and Six Item
453
), or from any
p
400
61
), may
2 History and examination
Neurological examination of the upper limbs
(UMN)
(LMN)
BOX
C
C
C
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62
The neurological system can be daunting. Learn at the bedside. Practise. Signs may
be equivocal or contrary to expectation. Always consider signs in the context of
the history. Try re- examining as signs may evolve over time. An essential point is to
distinguish whether a lesion is
upper
or lower motor neuron
Infection control means that the handshake is fast becoming a historical method of
greeting. This is a shame, as it may have given vital diagnostic clues: unable to see
hand in neglect/ blindness; unable to lift hand due to weakness; diculty reaching
hand due to tremor or impaired coordination; unable to release hand in myotonia.
45
Position the patient comfortably, sitting up at
1
Inspection
° and with arms exposed.
• Muscle wasting/ atrophy: especially small muscles of the hand. Is this symmet-
rical/ asymmetrical? Is there compensatory hypertrophy?
• Abnormal posturing/ movement: fasciculation (if suspicion, try gently tapping),
tremor, dystonia, athetosis. Is this localized or general?
2
Ton e
Assesses resistance to stretch. Exclude pain in hands/ arm/ shoulder prior.
Ask patient to, ‘Relax/ go floppy like a rag- doll/ let me take the weight of your
arm/ try not to help me’. Passively flex and extend elbow/ wrist while also pronating and supinating.
Hypertonia is an increase in resistance to passive movement independent of vel-
ocity. Includes
tremor =
rigidity: resistance throughout stretch (‘lead- pipe’). Rigidity plus
'cog- wheel'. Spasticity: velocity- dependent resistance to sudden, pas-
sive movement, faster movement = stronger resistance.
3
Power
Direct patient to follow commands while you stabilize the joint above and resist
movements in order to grade power (see
Te s t l e f t t h en r i g h t b ef o r e m ov i n g t o t h e n e x t p o s i t i o n . F o r m y o t o m es , s e e
• Shoulder abduction ‘Hold your arms out’ (chicken- wing position). ‘Don’t let me
push down’ (at the elbow).
• Elbow flexion/ extension ‘Bend your arms up in front of you’ (boxer- position, fist
facing in). ‘Stop me from pulling your arm out. Now push me away.’
• Wrist fl exion/ extension ‘Make a fist, arms out straight.’ Stabilize the forearm with
one hand and put your other hand under their fist (‘Push my hand to the ground’),
then above (‘Cock wrist up/ stop me pushing your hand down’).
• Hand Oer the patient two fingers and ask them to squeeze.
• Finger abduction ‘Spread your fingers out. Stop me pushing them together.’ Test
‘Muscle weakness grading’, p
like with like: your thumb versus theirs, your little finger versus theirs. ‘Grip a piece
of paper between two fingers.’ Try to pull the paper away using the same grip.
• Thumb abduc tion ‘Point your thumb (at 90°) towards the ceiling’ (palm facing up).
‘Don’t let me push down’ (with thumb, towards palm).
pp
(p
442
443
448– 9
).
).
.
• Biceps
5/ 6. Strike your finger placed over biceps tendon in antecubital fossa.
• Supinator
• Tric ep s
6. Strike your fingers placed on distal radius.
7. Hold wrist on abdomen with elbow at
Test right, then left to compare. If absent, use ‘reinforcement’: ask patient to clench
teeth on a count of three, at which time you strike (Jendrassik manoeuvre).
Describe as absent, hyporeflexia (present only with reinforcement), normal, or
brisk/ hyperreflexia.
4
Reflexes
90
°. Strike above the olecranon.
2 History and examination
C
7
• Pronator drift With arms outstretched (palms up), ask patient to close their eyes
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and watch for maintained supination.
• Finger– nose test Hold your finger an arm’s length in front of patient. ‘Touch your
nose, then my finger. As fast as you can.’ Look for
• Dysdiadochokinesis Ask patient to touch palms together (pronation of forearm),
then turn hand so dorsal side contacts palm (supination of forearm). Ask them to
repeatedly pronate and supinate forearm. Failure to perform rapidly alternating
movements is dysdiadochokinesis.
Ask the patient to close their eyes while stimuli are applied. Test in all derma-
fig
2.28
and p
tomes (
450
it is not predictable.
Palmar
Aspect
C
6
C
8
C
7
Fig 2.
28
Sensory dermatomes of upper limb.
Reproduced from Harrison (ed) Revision Notes for MCEM Part A
• Light touch Use cotton wool. Touch/ dab (don’t stroke or tickle) manubrium first.
‘This is what it should feel like. Say, “Yes” if you feel it again on your arm. Does it feel
the same or dierent?’
• Pain (p in- prick) Repeat using a neurological pin (not hypodermic needle), asking patient
to tell you if it feels sharp. Allow pin to slide between your fingers— do not apply pressure.
• Tem p er a t u re Repeat using alternating hot and cold probes (a tuning fork or test-
tube are also cold). Can the patient tell hot from cold?
• Vibration Use a
128
Hz tuning fork. Confirm the patient can feel buzzing at a reference point (vertex of head/ manubrium). Test for the start and end of vibration sensation (to distinguish from pressure, stop it with your fingers) at most distal bony
prominence. Move proximally to next most distal bony prominence until vibration is
correctly identified.
• Proprioception With the patient’s eyes closed, hold the distal phalanx of the big
finger at the sides, not on top/ below. Flex and extend the joint explaining, ‘This is
up’, and, ‘This is down’. Repeat movements stopping at intervals to ask whether the
fingertip is up or down. If impaired, test at the next most distal joint.
Top tips
• Use the tendon hammer like a pendulum, let it drop, don’t grip it too tightly.
• Ensure you are testing light touch, not stroke sensation.
5
Coordination
intention tremor and past pointing.
6
Sensation
), comparing left with right. Alter the rate of touch so
C
4
C
5
T
3
T
2
T
1
(
2011
), with permission from Oxford University Press.
C
4
T
3
Dorsal
Aspect
T
2
C
5
T
1
C
6
C
8
63
2 History and examination
Neurological examination of the lower limbs
S
L
L
UMN
UMN
BOX
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64
If the patient is able, begin your examination with gait analysis. Gait analysis (p
may give more clinical information than any other test. If they aren’t able to walk,
start with them lying down, legs fully exposed.
1
Ask patient to walk a few metres, turn, and walk back to you. Note walking
Gait
Gait and inspection
aids, symmetry, size of paces, arm swing. Look for abnormalities of gait cycle (eg
abnormalities in toe- o or heel- strike). Ask patient to ‘walk heel- to- toe as if on a
tightrope’ to exaggerate instability. Ask patient to walk on tiptoes (
cnemius lesion), then on heels (
be reduced by joint pathology. Exclude pain (
weakness. Unequal wear on the sole of the shoe may suggest an abnormal gait.
• Trendelenburg gait: unilateral weakness of hip abductor, eg superior gluteal
5
lesion.
nerve/
• Waddling/ myopathic gait: inability to stabilize pelvis due to bilateral hip ab-
ductor weakness (eg muscular dystrophy). Pelvis tilts to non- weight- bearing
leg with each step leading to a waddle.
• Hemiplegic (diplegic) gait: foot (feet) in extension (
circumverted/ swung round to move forward.
• Neuropathic gait: weak foot dorsiflexion leads to a high step to avoid toe drag.
• Parkinsonian gait: slow initiation, stooped posture, small and shuing steps,
turning ‘en bloc’ (head, trunk, and pelvis turn together like a statue).
• Choreiform gait: irregular, jerky, involuntary movements in arms and legs (eg
basal ganglia disorder).
• Ataxic gait: wi de - based irregular steps, lateral veering/ falling, truncal instability.
Romberg’s test Ask patient to stand unaided with arms by sides and close their
4,5
lesion, foot drop). Range of movement may
antalgic gait) before you diagnose
lesion) need to be
eyes (be ready to support). If they sway/ lose balance the test is positive and indicates posterior column disease (proprioception- related disease).
Inspect Abnormal posturing, muscle wasting, fasciculation, deformities of the
foot, eg pes cavus (Friedreich’s ataxia, Charcot– Marie– Tooth disease). Is one leg
smaller than the other (old polio, infantile hemiplegia)?
2
Ton e
Assesses resistance to stretch. Exclude pain prior. Ask patient to, ‘Relax/ go floppy
like a rag- doll/ let me take the weight of your leg/ try not to help me’. Roll knee
from side to side to passively internally/ externally rotate leg. Put your hand behind
the knee and raise it quickly. If the heel lifts away from the bed, tone is increased.
Clonus Plantar- flex foot then quickly dorsiflex and hold. More than 3 ‘beats’ of
plantar flexion is abnormal. Rapid downward movement of patella may elicit
patella clonus. Hypertonia and clonus suggest an
lesion.
1
or gastro-
463
)
Direct patient to follow commands while you resist movements in order to
grade power (see
fore moving to the next position. For myotomes see
• Hip flexion/ extension ‘Keep your leg straight and lift it up. Don’t let me push it
down.’ Then position hand under thigh. ‘Now push my hand into the bed.’
• Hip abduction Position hands on outer thigh: ‘Push your leg out to the side.’
• Hip adduction Position hand on inner thighs: ‘Push your legs together.’
• Knee flexion/ extension ‘Bend your knee and bring your heel to your bottom.
Don’t let me pull it away.’ ‘Now kick out/ push me away.’
• Ankle plantar flexion Position hand on sole of foot. ‘Push your foot down/ push
my hand.’
• Ankle dorsiflexion Position hand on dorsum of foot. ‘Lift your foot so your toes
point to the ceiling. Don’t let me push your foot down.’
3
Power
‘Muscle weakness grading’, p
443
). Test left then right be-
pp
450–1
.
2 History and examination
4
, S1, S2. Run an orange stick up the lateral sole of the foot in the
L
5
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Reflexes
Test right, then left to compare.
• Knee L3,4
. Bend knee, take w eight of le g. Str ike pa tella t endon , just below p atell a.
• Ankle L5
, S1
. Bend knee, then move it laterally. Hold and dorsiflex the foot, then
strike the Achilles tendon. If hip pain or limited mobility, dorsiflex the foot with a
straight leg and position hand on sole. Strike your hand, feeling for an ankle jerk.
• Plantar refl exes L5
direction of the big toe. As you approach the base of the toes move medially. Plantar
flexion of the great toe is normal. Dorsiflexion (positive
(in adults).
Heel– shin test
Babinski sign) is abnormal
5
Coordination
Using your finger on the patient’s shin to demonstrate, instruct patient
to, ‘Put your (left/ right) heel just below your (right/ left) knee. Run your heel smoothly
down your shin. Lift it up and place it back on your knee. Now run it down again.’
Foot tap test Place your palms just below the patient’s feet. Ask them to tap your
palms with their left foot only, right foot only, both feet together, and both feet
interchangeably.
6
Sensation
Ask the patient to close their eyes while stimuli are applied. Test in all derma-
fig
2.29
and p
450
tomes (
), comparing left with right. Alter the rate of touch so
it is not predictable.
T
T
12
10
T
11
L
1
L
2
L
3
S
4
S
L
L
3
2
3
S
5
S
2
65
L
4
L
L
4
L
5
• Light touch As upper limbs (p63).
• Pain (pi n- prick) As upper limbs (p63).
• Tem p er a t u re As upper limbs (p63).
• Vibration As upper limbs (p63).
• Joint position sense With the patient’s eyes closed, hold the distal phalanx of the
5
S
1
big toe at the sides, not on top/ below. Flex and extend the joint explaining, ‘This is
up’, and, ‘This is down’. Repeat movements stopping at intervals to ask whether the
toe tip is up or down. If impaired, test at the next most distal joint.
Top tips
• If you are limited for time, gait is the most useful test to start with.
• Make sure you test each muscle group individually by stabilizing above the joint
you are testing.
S
1
Fig 2.
29
Sensory derma-
tomes of lower limb.
Reproduced from Harrison
5
L
4
(ed) Revision Notes for
L
MCEM Part A (
permission from Oxford
2011
), with
University Press.
2 History and examination
Cranial nerve examination
I
II
OHCS
III
VII
UMN
LMN
VIII
IX
IX
X
XI
XII
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66
Olfactory nerve
Ask if they have noticed a change in sense of taste/ smell. Test familiar smells, eg
coee at each nostril (test nostrils separately, exclude occlusion of the nostril).
Optic nerve
• Acuity Test each eye separately. Correction with glasses/ pin- hole. Use Snellen chart
inside front cover).
(
• Visual fields Compare with your s (confrontation ): ask the p atient to look at your eye/
nose and ask them to indicate when they see finger movement (or count your fingers)
in each outer quadrant of the visual field. Or test formally via perimetry.
• Pupils Size, shape, symmetry. Reaction to light (fig
sponds to light) and consensual (opposite pupil responds). Swinging light test for
relative afferent pupillary defect detects asymmetrical disease: light shone into the
normal eye causes bilateral pupillary constriction. When light is moved to the abnormal eye, both pupils paradoxically dilate as consensual pupillary relaxation in the
normal eye dominates.
arm’s length, then move it towards their nose. Pupils constrict on near gaze.
• Ophthalmoscopy Darken the room. Warn the patient you need to get close to their
face. Optic disc (pale? swollen?). Follow vessels from disc to view each quadrant. If
the view is obscured, look for a cataract. View the fovea by asking the patient to look
directly at the light. See
Oculomotor nerve, IV Trochlear nerve, VI Abducens nerve
Gently stabilize the patient’s head. Ask them to look at your finger as you trace a
Nystagmus is an involuntary, repetitive, to– fro movement of the eyes.
‘H- shape’.
A few beats of nystagmus may be physiological, especially at extremes of gaze.
• IIIrd nerve palsy: eye looks down and out. Ptosis, large pupil if external parasympa-
thetic fibres compressed/ damaged.
• IVth nerve palsy: diplopia on looking down and in (often noticed on descending stairs),
head tilt (ocular torticollis) compensates.
• VIth nerve palsy: impa ired la teral m ovemen t/ lateral diplopia.
V Trigeminal nerve
• Sensory Check sensation (usually light touch) in all three divisions of the nerve (oph-
thalmic = forehead, mandibular = cheek, mandibular = jaw). Corneal reflex may be
lost first: approach the eye from the side (outside line of vision) and lightly touch a thin
strand of clean cotton to the cornea. Observe for blinking and tearing.
• Motor ‘Open your mouth’ and jaw deviates to the side of lesion. Palpate muscles of
mastication (temporalis, masseter, pterygoids) as patient clenches teeth.
Facial nerve
‘Raise your eyebrows’, ‘Close your eyes tightly’, ‘Show me your teeth’, ‘Pu out your
cheeks’. Weakness leads to facial droop.
the face (cortical innervation to upper face is bilateral).
side of face. Test taste (anterior two- thirds of tongue) with salt/ sweet solutions.
Vestibulocochlear nerve
Test hearing: ask to repeat a number whispered in each ear while you block the
Balance/ vertigo (p
other.
Glossopharyngeal nerve, X Vagus nerve
The palate should move symmetrically on saying ‘Ah’. 10th nerve lesions cause
paralysis of the palate. The asymmetric lift of the uvula means that it will point
away from the lesion, towards the normal side.
of the soft palate with an orange stick. The aerent arm of the reflex involves
the eerent arm involves
Accessory nerve
‘Shrug your shoulders’ against resistance. ‘Turn your head’ against resistance.
Hypoglossal nerve
‘Stick out your tongue.’ The tongue deviates to the side of the lesion.
2.30
) should be direct (pupil re-
Accommodation: as k the pati ent to fo cus o n you r fin ger/ pen at
p
327
. Slit lamp examination is superior.
lesions aect the lower two- thirds of
lesions aect all of one
458
). Weber’s and Rinne’s tests (p
459
).
Gag reflex: gently touch the back
.
;
2 History and examination
Causes of cranial nerve lesions
DM
SLE
DM, MS
MS
ICP
VIII
III
ICP
VI MS,
ICP
VII LMN
OHCS
UMN CVA
VIII
CVA
IX, X, XI
XII
TB,
VIII
V, VI, IX
III, IV, V
OHCS
IX, X, XI:
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Where is the lesion? Think systematically: in brainstem (eg MS), pressing on the
brainstem (eg tumour), at the neuromuscular junction (eg myasthenia), or in the
muscles (eg a dystrophy)? Cranial nerves may be aected singly or in groups. Any
cranial nerve may be aected by
p
552
),
(p
552
(
the lower cranial nerves one by one. Causes of cranial nerve lesions include:
• I Trauma , respi ratory tract i nfect ion, m ening itis, fron tal lo be tum our.
• II (A lso s ee p66.) Monocular blindness: l esio ns of one eye/ optic nerve, eg MS, giant
cell arteritis.
multiplex, eg
), syphilis. Chronic meningitis (malignant, TB, or fungal) can pick o
Bilateral blindness: a ny ca us e o f m ul ti fo ca l n eu ro pa th y/ mononeuritis
, neurosyphilis, rarely methanol. Bitemporal hemianopia:
compression of optic chiasm, eg pituitary adenoma, craniopharyngioma, internal
carotid artery aneurysm (
the visual field, contralateral to the lesion) due to lesions beyond the chiasm, eg
stroke, abscess, tumour.
tral vision, relative aerent papillary defect, disc swelling (papillitis) due to, eg
, syphilis, collagen vascular disorders. Ischaemic papillopathy (swelling of
optic disc due to stenosis of the posterior ciliary artery) due to, eg giant cell ar-
Papilloedema (fig
teritis.
scess, encephalitis, hydrocephalus, idiopathic intracranial hypertension); rarer is
a retro- orbital lesion (eg cavernous sinus thrombosis,
frontal tumours, Friedreich’s ataxia, retinitis pigmentosa, syphilis, glaucoma,
Leber’s optic atrophy, chronic optic nerve compression.
nystagmus often vestibular (acute = nystagmus away from lesion, chronic = towards lesion), or cerebellar (nystagmus towards the aected side). Nystagmus
in abduction: consider internuclear ophthalmoplegia (
plus deafness/ tinnitus:
nystagmus with head position: benign positional vertigo (
tagmus: lesion in midbrain/ base of the
amen magnum lesion.
•
Pupil sparing = parasympathetic fibres unaected (‘medical’), eg DM, giant
cell arteritis, syphilis. With dilated pupil = external compression of parasympathetic fibres (‘surgical’): i
occupying lesion, posterior communicating artery aneurysm (
• IV Usu ally d ue to traum a when occurs in iso lation .
• V Tr ig em in al ne ur al gi a ( p
•
•
•
•
•
p
459
neuroma (
small pupils ± qu adrip aresi s).
media, skull fracture, cerebellopontine angle tumour, eg acoustic neuroma, malignant parotid tumour.
(p
acoustic neuroma, brainstem
).
Wer nick e’s e nce phal opa thy, fals e lo cal izin g si gn in i
Bell’s palsy (p
458
, p
498
459
) Noise damage, Paget’s disease, Ménière’s disease, herpes zoster,
Trau ma , br ai ns te m l e si on s, ne c k t um ou rs .
Syringomyelia, tumour, stroke, bulbar palsy, trauma,
Groups of c rani al ne rves
•
, then
•
perior orbital fissure lesion (Tolosa– Hunt syndrome,
•
• : myasthenia gravis, muscular dystrophy, myotonic dystrophy, mononeuritis
multiplex (
, and X: cere bello ponti ne ang le path ology, eg aco ustic neurom a.
(ophthalmic division), VI: cavernous sinus pathology, eg thrombosis, su-
jug ular foram en les ion.
p
496
).
Top tips
• Partial visual field loss is due to neurological disease. Monocular/ binocular
blindness is most commonly a disease of the eye, eg cataracts, retinopathy.
• Papill itis = unilateral optic disc swelling. Papilloedema = bilateral. Check both eyes!
, stroke, MS, cancer, sarcoidosis, vasculitis
fig
10.3
, p
447
). Homonymous hemianopia (aects half
Optic neuritis causes pain on moving eye, loss of cen-
12.21
, p
558
) most commonly due to i
(tumour, ab-
p
478
). Optic atrophy: MS,
Nystagmus: horizontal
p69, fig
2.31
th nerve lesion, barotrauma, Ménière’s (p
4
th ventricle. Downbeat nystagmus: for-
). Nystagmus
458
p
458
). Upbeat nys-
). Variable
Pupil abnormalities: s ee p68.
(uncal herniation through the tentorium), eg space-
453
), herpes zoster, nasopharyngeal cancer, acoustic
), Ramsay Hunt syndrome (p
p
814
).
, pontine stroke (fixed
499
,
p
856
), polio, otitis
, tumour.
, drugs (eg aminoglycosides).
pol io.
p
858
).
67
2 History and examination
Cranial nerve lesions of the eye
CNIII
ICP
CNII
CNIII
B
HSV
HIV
B
Pre-tectal nucleus
To occip
ital cortex
Reflex constriction
CNIII
C
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68
Pupillary abnormalities
• Symmetry: equal and circular?
• Dilated or constricted?
• React to light, directly and consensually?
• Constrict normally on convergence/ accommodation?
Irregular pupils
Anterior uveitis (iritis), trauma, syphilis.
Dilated pupils
Confirm pathological dilatation (not pathological constriction in the other eye).
Dilated pupil occurs with external compression of
(p
814
due to: i
) (uncal herniation through the tentorium), space- occupying
(parasympathetic fibres)
lesion, posterior communicating artery aneurysm. Also mydriatic drugs.
Constricted pupils
Sympathetic nerve damage (Horner’s, p48, and ptosis, p69), opiates, miotics
(pilocarpine drops for glaucoma), pontine damage.
Unequal pupils (anisocoria)
Unilateral lesion, mydriatic/ miotic medication, eye surgery, syphilis, Holmes– Adie
pupil. Some inequality may be normal.
Light reaction
Both pupils should constrict, one by a direct and the other by a consensual light
fig
2.30
reflex (
the message passes up the optic nerve (
thence to the
one eye causes only contralateral constriction, the defect is ‘eerent’, as the aerent
pathways from the retina being stimulated must be intact =
). The lesion site is deduced by knowing the pathway: from the retina
nuclei on both sides producing pupillary constriction. If a light in
) to the superior colliculus (midbrain) and
Marcus Gunn sign.
Lateral geniculate body
Edinger-Westphal nucleus
Midbrain
Ciliary ganglion
Holmes– Adie (myotonic) pupil
The aected pupil is moderately dilated and poorly/ non- reactive to light. It is slowly
reactive to accommodation; wait and watch: it may eventually constrict more than
a normal pupil. It is often associated with diminished or absent ankle and knee
reflexes, in which case the
dental finding. Rare causes: Lyme disease, syphilis, parvovirus
Argyll Robertson pupil
The pupil is constricted and unreactive to light, but reacts to accommodation.
Occurs in late neurosyphilis. Hypothesized due to rostral midbrain pathology affecting eerent pupillary fibres on the dorsal aspect of the Edinger– Westphal nucleus (part of the light reflex) while sparing more ventral fibres associated with
the accommodation. Mimicked (pseudo- Argyll Robertson pupils) by: Lyme disease,
, zoster, DM, sarcoidosis, MS, paraneoplastic, d
hyporeflexia, impaired upward gaze, convergence retraction nystagmus,
Hutchinson pupil
This is the sequence of events resulting from rapidly rising unilateral intracranial
pressure (eg intracerebral haemorrhage). The pupil on the side of the lesion first
constricts then widely dilates. The other pupil then goes through the same sequence
See p
814
.
Fig 2.
30
Light reflex. Action potentials
go along the optic nerve (red), traverse
Chiasm
the optic chiasm, pass synapses at the
pre- tectal nucleus, en route to Edinger–
Westphal nuclei of
to both iri ses ’ ci lia ry m usc les (so both pupils
constrict) via ciliary ganglion (also relays
Light
accommodation and corneal sensation,
and gets sympathetic roots from
carrying fibres to dilate pupil).
. These send fibres
8– T2,
Holmes– Adie syndrome is present. Usually a benign inci-
19
,
, autoimmunity.
, Parinaud’s syndrome (pupillary
12
p
694
).
2 History and examination
III, IV
HIV
Ptosis
CNIII
CNIII
CNIII
T
CNS
OHCS
ESR
MS.
OHCS
OHCS
TIA
HIV
SLE
DM
CNS
TIA (
https://t.me/med1917
Drooping of the upper eyelid. Best observed with patient sitting up. Causes
1
lesions. Oculomotor nerve (
vator palpebrae). Lesions therefore cause unilateral complete ptosis. Look for
other evidence of a
of the eye, dilated pupil unreactive to light or accommodation. If eye pain, suspect infiltration (eg lymphoma, sarcoidosis). If i
infection (tick bite?).
2
Sympathetic lesions. Nerves from the cervical sympathetic chain innervate the su-
perior tarsal muscle with lesions leading to a milder ptosis. Usually unilateral par-
tial p to s i s , w h i c h m a y b e ov e r c o m e b y l o o k i n g up .
ptosis + m iosi s (c onst ric ted pupi l), + a nhid ros is (l ack of sw eat ing) , + enophthalmos
) innervates main muscle concerned (le-
lesion: ophthalmoplegia with ‘down and out’ deviation
° or dconsciousness, suspect
Horner’s syndrome (fig
(sinking of eye). Causes: usually malignancy/ trauma along nerve path, ie midbrain,
brainstem, upper spinal cord, neck, lung apex (Pancoast’s tumour), orbit.
3
Myopathy, eg dystrophia myotonica, myasthenia gravis. Usually bilateral par-
tial ptosis.
4
Congenital. Usually partial and without other
signs.
Internuclear ophthalmoplegia
To p r o d u c e s y n c h r o n o u s e y e m o v e ments, cranial nerves
, and VI
communicate through the medial
longitudinal fasciculus in midbrain
fig
2.31
). In internuclear ophthal-
(
moplegia a lesion disrupts communication causing:
• Weakness of the ipsilateral eye in
adduction.
• Nystagmus of the contralateral
eye in abduction.
There may be incomplete or slow
abduction of the ipsilateral eye
during lateral gaze. Convergence
is preserved.
Causes MS, vascular. Rare:
syphilis, Lyme disease, brainstem
tumour, phenothiazine toxicity.
,
Fig 2.
31
Internuclear ophthalmoplegia.
2.18
69
, p48) =
Visual loss
Get ophthalmology help. See
Consider:
• Red eye: glaucoma, uveitis (p
• Pain: giant cell arteritis— temporal headache, jaw claudication, scalp tender-
urgent steroids (p
ness, i
• Cloudy cornea: corneal ulcer (
• Flashes/ floaters:
• Visual field defect: cerebrovascular disease, space- occupying lesion, glaucoma,
emboli (examine for valvular heart disease/ carotid bruit).
• Relevant history: trauma, migraine, hypertension, MS, diabetes, connective
tissue disease, hyperlipidaemia.
• Systemic disease:
, migraine, retinal detachment.
retinitis,
Sudden Acu te gl auco ma, r etinal d etac hmen t, vi treo us ha emorrha ge (e g pro lifera-
retinopathy), central retinal artery/ vein occlusion, optic neuritis (eg MS),
tive
lesions (eg
migraine,
temporal arteritis, drugs (eg quinine/ methanol), pituitary apoplexy.
Gradual Optic atrophy, chronic glaucoma, cataracts, macular degeneration, toxic
amblyopia.
pp
344– 63
.
559
).
554
). Also optic neuritis, eg
p
334
), glaucoma (
, sarcoidosis.
p
331
).
amaurosis fugax), stroke, space- occupying lesion),
2 History and examination
SLE
HRT
DASHING
ALGrawany
https://t.me/med1917
Higher mental function
70
Higher mental functions include language, memory, thinking, attention, abstraction,
and perception. In order to assess:
• Reassure: ‘I know this may be dicult...’
• Engage in conversation. Ask open questions that require more than yes or no to
answer. This tests fluency, reception, understanding, and allows assessment of
articulation.
• Assess for dysphasia: ‘What is this?’ while pointing to, eg pen (nominal dysphasia).
• Test for conduction dysphasia and dysarthria: Ask patient to repeat complex words,
eg ‘British constitution’, ‘baby hippopotamus’.
• Assess movement (and comprehension) using complex instructions that require move-
ment across the midline, eg ‘Make a fist with your right hand, then extend your right
index finger, then touch your left ear’.
Assessment will be aected by hearing loss, visual loss, and cognitive impairment.
Movement
Movement disorders
• Athetosis: slow sinuous writhing movements, present at rest. Due to a lesion in
the putamen.
tive loss.
• Chorea: a flow of jerky movements, flitting from one limb to another (each
seemingly a fragment of a normal movement). Meaning = dance (hence ‘choreography’). The early stages of chorea may be detected by feeling fluctuations
in muscle tension while the patient grips your finger. Causes: basal ganglia lesion (stroke, Huntington’s
(p
neuroacanthocytosis (acanthocytes in peripheral blood, chorea, orofacial dyskinesia, axonal neuropathy); hyperthyroidism (
ceptives/
• Hemiballismus: uncontrolled unilateral flailing movements of proximal limb
joints. Due to contralateral subthalamic lesions (
Dyspraxia
Poor performance of complex movements despite ability to do each individual
component. Test by asking the patient to copy unfamiliar hand positions, or
mime an object’s use, eg a comb.
• Dressing dyspraxia: the patient is unsure of the orientation of clothes. Test by
pulling the sleeve of a sweater inside- out before asking the patient to put it on
(mostly non- dominant hemisphere lesions).
• Constructional dyspraxia: diculty in assembling or drawing objects, eg a
five- pointed star (non- dominant hemisphere lesions, hepatic encephalopathy).
• Gait dyspraxia: diculty performing the complex movement of walking (bilat-
eral frontal lesions, posterior temporal region lesions, and hydrocephalus).
Cerebellar disease
Think
Dysdiadochokinesis Ataxia Slurred speech
Hypotonia and reduced power Intention tremor Nystagmus
Gait: broad based
Examination:
Speech: slurred/ ataxic/ staccato.
Eye movements: nystagmus.
Tone and power: hypotonia and reduced power.
Coordination: coordination tests for dysdiadochokinesis (p63, p65, p
Gait: broad based, patients fall to the side of the lesion. Romberg’s test is negative.
Pseudoathetosis: athetoid movements due to severe propriocep-
p
464
552
); Wilson’s disease (p
, chlorpromazine, cocaine— ‘crack dancing’). See p
:
); Sydenham’s chorea (St Vitus’ dance) (p
281
); neonatal kernicterus; polycythaemia (p
p
212
); drugs (levodopa, oral contra-
p
464
).
464
.
495
146
);
362
);
).
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