NEUROLOGICAL EXAMINATION

 Talley’s should be consulted for this section. Not every aspect of the exam is exhausted here.
 The neurological examination is a treasure hunt, to find the chest of gold, which in this case is usually an
ischaemic piece of brain, a bleed, or a SOL. You cannot find the treasure if you aren’t familiar with the landscape
with its roads and ammenities. Learn the anatomy.
 When examining the neurological system, 8 components need to be explored:
1. Higher fx
2. Meningism
3. CN fx
4. Motor fx
5. Sensory fx
6. Co-ordination
7. Gait
8. Parietal fx

HIGHER FX

 Use Folstein’s MMSE to assess cognition:

o Temporal orientation
o Spatial orientation
o Registration
 Words should be unrelated
o Attention & calculation
 Use serial 7s
o Remote memory
o Naming 2 objects
 Point to 2 common objects & ask
the pt to name them
o Repitition
o Following a complex command
 An easier command is “use your
left infex finger to touch your right
ear” as a paper is not always
practical & the pt may be in bed
 Do not act out the command
o Writing a complex sentence
o Reading & obeying
 Do not act out the action!
o Copy two interlocking pentagons
 A point is only awarded if both pentagons are 5 sided, w a diamond shape where they interlock
 For each part, points are allocated according to how well the pt performs
 Max score = 30
 24 – 30 = normal cognition
 20-23 – mild cognitive impairment
 10-19 – moderate cognitive impairment
 0-9 – severe cognitive impairment
MENINGISM

 Ensure that the pt is lying flat, & you have removed the pillow
from beneath the hear
 Signs of Meningism:
o AP neck stiffness. Start by rotating the head laterally
between your hands. Stiffness in this direction too
suggests possible cervical pathology. Then check AP
stiffness by quickly flexing the neck. Feel for resistance &
watch for pain.
o Brudzinski’s sign
 Pain in the neck & flexion of the hips when the examiner
passively flexes the pt’s neck
 Response to alleviate stretch on the irritated meninges
o Kernig’s sign
 Painful spasm of the hamstrimg m when the examiner
extends the leg while the thigh is flexed

CRANIAL NERVE EXAMINATION

 CN I – olfaction; usually omitted

 CN II
o Inspect the pupils
 Size & symmetry
 Asymmetry = anisocoria
o large and & in CN III palsy
o Small & reactive in Horner’s sd
o Light reflex
 Depicted in the image on the R
 Afferent limb = CN II; Efferent = CN III
 Check direct & consensual response
 A n consensual response involves the contralateral
pupil constricting
 If a pupil is not directly constricting, but there is a
consensual response, the pathology is in CNIII
o Marcus Gunn pupil
 Swinging light test
 Move the pen torch rapidly between the pupils, shining the light for 3s in each eye
 This test may detect a relative afferent pupillary defect (RAPD) – caused by damage to
the tract between the optic nerve and optic chiasm (e.g. optic neuritis in multiple
sclerosis)
 It’s also known as a “Marcus-Gunn” pupil
 A RAPD can be detected by paradoxical dilatation of the affected pupil when a light is
shining into it (it should normally constrict)
 This makes use of the consensual response. The affected eye will constrict when the
light is shone in the unaffected eye d/t consensual constriction. When the light leaves
the unaffected eye, that eye will dilate, & so will the affected eye, consensually.
However, when doing the swinging light test, this is paradoxical, as one would expect, if
the affected pupil was normal, to constrict, because the light has moved there.
o Accommodation
 Focus on a distant object then on the examiner’s finger, placed 15cm in front of the eyes
 Observe the pupils, you should see constriction and convergence bilaterally
  “Argyle Robertson”/ “prostitute’s” pupils will not respond to light but will respond to
accommodation. This is highly specific for neurosyphilis. V rare sign these days. May also occur
in diabetic neuropathy.
o Visual acuity
 Technically should be performed using a Snellen chart, 6m away
 Rarely convenient. Ask pt to count fingers, ONE EYE at a time, from the foot of the bed/ 6m
away. If unable to see this, move to a hand waving, then to light shone directly into the eye.
 Should be wearing glasses/ contacts
o Visual fields
 Sit directly facing the patient, approximately 1m away
 Pt covers 1 eye, you cover the opp eye
 Ask the pt to look into your eye & not move their head or eyes during the exam
 Ask the patient to tell you when they can see your fingertip wiggling
 Outstretch your arms, ensuring they are situated at an equal distance between you & the pt
 Position your fingertip at the outer border of one of the quadrants of your visual field. Rpt for
each quadrant & map defect if present
 Repeat the same assessment process on the other eye
 Draw the path of the optic nerve to localise the lesion

o Fundoscopy
 CN III, IV, VI
o Ptosis
 If unilat
 Horner’s sd
 CN III (Levator palpebrae) defect
 If bilat
 MG
o Note resting strabismus (strabismus in the primary position)
 Below shows the primary strabismus that will occur w a R sided lesion of the CN III, IV & VI,
respectively:

o Eye movements
 Ask the pt to report diploplia (& to describe it) when performing this
 Hold your finger about 30cm directly in front of the patient’s eyes
 Ask pt to focus on it
 Look at the eyes in the primary position for any deviation or abnormal movements
 Occular bobbing
o Rare sign of rapid downward movement of both eyes, followed by a slow return
of the eyes to the midline position
o The offending lesion is usually in the pons, secondary to infarction/
haemorrhage
 Ask the patient to keep their head still and follow your finger with their eyes.
 Move your finger the H shape
 Observe for restriction of eye movement & nystagmus
 CN V
o Sensory exam
 Demonstrate on stermun
 Ask pt to report a difference in sensation btw 2 sides
 When testing pain, alternate sharp & dull & assess the ability to distinguish
 Test light touch & pinprick
 Forehead – ophthalmic branch (V1)
 Cheek – maxillary branch (V2)
 Jaw – mandibular branch (V3)
o Motor exam
 Mm of mastication
 Ask the patient to clench their teeth whilst you feel the bulk of masseter and temporalis
bilaterally
 Ask the patient to open their mouth whilst you apply resistance under the jaw – note
any deviation (jaw will deviate to side of lesion)
o Jaw jerk (afferent CN V, efferent CN V)
 Ask patient to open mouth loosely
 Place your finger horizontally across the chin
 Tap your finger with a patella hammer
 N = slight closure of the jaw
 Abn = brisk complete closure of the jaw – UMN lesion
 o Corneal reflex (afferent CN V, efferent CN VII)
 Explain procedure
 Depress lower eyelid
 Ask patient to look upwards
 Touch edge of cornea using a wisp of cotton wool
 Normal response = Direct and consensual blinking
 CN VII
o Usually only the motor component is tested
o Inspect the face
 Asymmetry
 Drooping of the corner of the mouth
 Loss of nasolabial folds
o Ask to perform actions
 Raised eyebrows – frontalis m
 NB – look for sparing or affectation of the frontalis m
o Remember, all cranial nerves receive bilateral UMN innervation, except the
lower portion of the facial nerve nucleus. For this reason, UMN lesions affecting
CNs usually do not translate into a fxal deficit, except for lower facial weakness
(ie frontalis +/- orbicularis oculi sparing). If the frontalis m is also weak, it is
probably a LMN lesion
 Closed eyes - orbicularis occuli - assess symmetrical burial of eyelashes. Ask to resist you
opening eyes
 This m is often also bilaterally innervated ; affectation may suggest LMN lesion.
 If v weak, the pt will not be able to close that eye at all. Ask about dry eyes when
awakening.
 Blown out cheeks – buccinators
 Smiling – orbicularis oris
o Closed lips – “close your lips tight and don’t let me open them” – check each side, assess power
 CN VIII
o Gross hearing testing
 Ask the patient if they have noticed a change in their hearing recently.
 Assess each ear individually, standing behind the patient.
 Explain to the patient that you’re going to say a word/ number and you’d like them to repeat it
back to you.
 With your mouth approximately 15cm from the ear, whisper a number or word.
 Mask the ear not being tested by rubbing the tragus.
 Ask the patient to repeat the number or word back to you.
 If the patient repeats the correct word or number, repeat the test at an arm’s length from the
ear (normal hearing allows whispers to be perceived at 60cm).
 Assess the other ear in the same way.
o Rinne’s test
 Place vibrating 512 Hz tuning fork on the mastoid process
 Ask the patient if they are able to hear it (bone conduction)
 If they are able to hear it, ask them to let you know when they can no longer hear it
 Once the patient is unable to hear the sound via the mastoid process move the tuning fork to
2cm from the external auditory meatus
 Ask the patient if they are able to hear the tuning fork air conduction)
 If able to hear the tuning fork via air conduction (after they were no longer able to hear via bone
conduction) it suggests their air conduction is better than bone conduction (Rinne’s +ve), which
is NORMAL. (confusing concept, because usually a +ve sign indicates pathology)
 Neural deafness = Air conduction > Bone conduction (both air and bone conduction reduced
equally)
 Conductive deafness = Bone conduction > Air conduction (Rinne’s –ve)
o Weber’s test
 Place a vibrating 512 Hz tuning fork on midline of forehead
 Ask where the sound is loudest
 N – sound is heard equally in both ears
 Neural deafness – sound is heard louder on the side of the intact ear
 Conductive deafness – sound is heard louder on the side of the affected ear
 CN IX, X
o Inspect palate & uvula
 Symmetry – note any obvious deviation of the uvula
 Ask patient to say “ahhhh” – observe uvula moving upwards – any deviation? (deviation away
from side of lesion)
 Gag reflex (afferent IX, efferent X) – usually omitted
o Swallow – ask patient to take a sip of water – note any coughing / delayed swallow
 CN XI
o Strapezius weakness
 Turn ahead against resistance – weakness pushing to the R = L sided lesion & visa versa
o Trapezius
 Assess weakness when shrugging against resistance
 CN XII
o Inspect tongue for wasting & fasciculations at rest
o Ask patient to protrude tongue – any deviation? (deviates towards side of lesion)
o Place your finger on the patient’s cheek and ask to push their tongue against it – assess power
BULBAR PALSY VS PSEUDOBULBAR PALSY

Bulbar palsy Pseudobulbar palsy

Pathogenesis LMN lesion in the medulla (CN IX – XII) Bilateral UMN lesions above the mid-pons,
affecting the corticobulbar tracts.
Causes  Brainstem glioma  Bilateral strokes
 Brainstem strokes  Multiple Sclerosis
 GBS  Bilateral Metastases
 Myasthenia Gravis  Motor Neurone Disease (MND)
 Polymyositis
 Dystrophia Myotonica
Signs  Dysarthria
 Dysphagia
 Nasal Regurgitation
 Flaccid, wasted, fasciculating tongue  Small, spastic, immobile tongue
 Present/absent jaw jerk  Brisk jaw jerk
 Absent gag reflex  Brisk gag reflex in later stages
 Not emotionally labile  Emotional lability

MOTOR EXAMINATION

 Inspection
o Wasting/ hypertrophy
o Involuntary movements
Tremor Rhythmic oscillations caused by intermittent muscle contractions.
Tics Paroxysmal, stereotyped muscle contractions, commonly suppressible, might be simple
(single muscle group)/ complex. Temporarily suppressible.
Myoclonus Shock-like, arrhythmic twitches. Not suppressible.
Chorea Dance-like, unpatterned movements, often approximate a purpose (e.g. Adjusting
clothes, checking a watch). Often rapid & may involve proximal/ distal m groups.
Athetosis Writhing movements, mostly of arms & hands. Often slow
Dystonia Sustained/ repetitious muscular contractions, often produces abnormal posture.
Hemiballismus Wild, large-amplitude, flinging movements on one side of body, commonly affecting
proximal limb muscles but can also affect the trunk.
o Fasciculations
o Posture
 Classic spastic posturing post CVA:
o UL: arm flexion & adduction, forearm flexion & pronation, wrist & finger flexion
o LL: thigh flexion, adduction & internal rotation, leg extension, foot equinovarus
 Tone
o Thambisa!
o Always support the arm both proximal & distal to the joint you are testing
o UL:
 Move the wrist through its full range of motion
 Pronate and supinate the forearm – feel for any spasticity (pronator catch – remember that in
UMN lesions, the pronator has inc tone)
 Flex and extend the elbow joint – in an UMN, pyramidal lesion, there will be a bicep catch
(because this m has inc tone)
 Flex/extend/abduct/adduct the shoulder joint
o LL:
 Leg roll
 Roll the patient’s leg and watch the foot – it should flop independently of the leg
 If the foot moves w the leg, en block, it is hypertonic
 Obviously make sure you’re watching the foot when you do this
 Leg lift
 Briskly lift leg off the bed at the knee joint – the heel should remain in contact with the
bed
 If hypertonic, the quadriceps catch will cause the leg to remain extended, & the foot will
leave the bed
 Ankle clonus – explain what you will be doing
 Position the patient’s leg so that the knee and ankle are slightly flexed, supporting the
leg with your hand under their knee, so they can relax.
 Rapidly dorsiflex and partially evert the foot
 Keep the foot in this position – don’t just let go
 Clonus is felt as rhythmical beats of dorsiflexion/plantarflexion (>5 is abnormal)
 Knee clonus
 With the leg extended, cup the patella and rapidly push it inferiorly to stretch the
quadriceps m. hold in this position & feel for rhythmical spasm of the quadriceps m
 Clonus is a sign of significant spasticity
o Classify as eutonic/ hypotonic (LMN lesion/ cerebral/ spinal shock)/ hypertonic (UMN lesion)
o If hypertonic, classify as:
 Spastic – pyramidal lesion
 Velocity dependent – usually more hypertonic when moving the limb quickly
 There is flexor-extensor discordance – in the UL, this is demonstrated by inc tone in the
flexors – bicep & pronator teres; in the LL, inc tone in the extensors – quadriceps catch
 Rigid – extrapyramidal lesion
 Velocity independent - it feels the same if you move the limb fast or slowly.
 Termed lead pipe rigidity
 Equal flexor & extensor hypertonia
 Power
o Test fx in all planes of motion for each joint. Know which spinal level supplies the mm responsible for the
movement (myotomes). Support the joint being tested proximally & distally.
o UL
 Shoulders
 ABduction (C5); ADduction (C6/7)
 Elbow
 Flexion (C5/6), Extension (C7)
 Wrist (exclude gravity)
 Extension (C6), Flexion (C6/7)
 Fingers
 Finger extension, flexion, abduction, adduction
 o LL
 Hip
 Flexion (L1/2), Extension (L5/S1), ABduction (L4/5), ADduction (L2/3)
 Knee
 Flexion (S1), Extension (L3/4)
 Ankle
 Dorsiflexion (L4), Plantarflexion (S1/2), Inversion (L4), Eversion (L5/S1)
 Big toe
 Extension (L5)
o Grade
Grade Description
0 No evidence of any m contraction
1 Flicker of movement seen
2 Joint can move if gravity is excluded
3 Joint can move against gravity – this is a useful way to describe the power of a completely
uncooperative it. “all limbs are moving against gravity, power can be assumed to be at least
grade 3 in most m groups”
4 Some weakness against resistance
5 N power – good resistance
 NB: one must always fully describe the distribution of power loss as its precise character points
to the cause
 Is it proximal/ distal? Extensor more than flexor? Upper limb more than lower limb? Dense?
Fatigable? Radicular weakness? Mononeuropathic weakness? Hemiparesis? Hemiplegia?
Paraparesis? Paraplegia?
o Pronator drift
 During a pronator-drift test, a patient is asked to hold
arms outstretched w palms facing upward
 Eyes are closed in order to accentuate the response, because without vision, the patient must
rely on proprioception alone to maintain the position of the arms.
 In the presence of UMN lesion, the supinator mm in the UL are weaker than the pronator mm,
and as a result, the arm drifts downward & the palm turns toward the floor
 Reflexes
o Can use accentuating manoeuvres like teeth clench if pt is unable to relax
o UL
 DTR
 Biceps reflex (C5/6) – relax arms on the pts sides, slightly flexed
 Triceps reflex (C7) – place forearm rested at 90º flexion
 Supinator reflex (C6)
 Hoffman’s reflex = UMN lesion on the contralat side
 loosely hold the middle finger & flick the fingernail downward, allowing the middle
finger to flick upward reflexively. A positive response is seen when there is flexion &
adduction of the thumb on the same hand.
o LL
 DTR
 Knee jerk (L3/4) – support the knee in a semi flexed position
 Ankle jerk (L5/S1) – bend the knee slightly & dorsiflex the ankle
 Plantar reflex (S1)
 +ve Babinski = UMN lesion on the contralat side
o Using a blunt object, stroke the lat part of sole, from the heel up towards the
toes, then turn to stroke medially towards the big toe
 o The characteristic response is:
 dorsiflexion of the big toe, which precedes all other movements
 Followed by fanning out & extension of the o toes,
 Dorsiflexion of the ankle &
 Flexion of the hip & knee joint
 This response represents 'positive' Babinski sign. There is no such thing
as a 'negative' Babinski sign.
o Note: some pts will be sensitive under the foot & pull away or make bizarre
movements that make interpretation of the sign difficult. In this case, you may
gently stroke the lat aspect of the foot upwards OR you may run your knuckles
down the pt’s shin. Where manoeuvres will illicit the same sign.

Grades of DTRs
0 Absent
1+ Reduced
2+ Normal
3+ Brisk
4+ Brisk w clonus
Always compare to the reflex on the contralat side. Brisk reflexes = UMN lesion; reduced reflexes = LMN lesion OR
early UMN lesion, ie cerebral/ spinal shock.
SENSORY EXAMINATION
 C4 - Over the acromioclavicular joint.
 Dermatomes  C5 - On the lateral (radial) side of
the antecubital fossa, just proximally to the
elbow.
 C6 - On the dorsal surface of the proximal
phalanx of the thumb.
 C7 - On the dorsal surface of the proximal
phalanx of the middle finger.
 C8 - On the dorsal surface of the proximal
phalanx of the little finger.
 T1 - On the medial (ulnar) side of
the antecubital fossa
 T4 – nipple line
 T5 – 9 – on trunk, btw nipple line & umbilicus
 T10 – umbilicus
 L2 - On the anterior medial thigh
 L3 – medial aspect of knee
 L4 - Over ant knee & medial malleolus.
 L5 - On the dorsum of the foot at the
third metatarsophalangeal joint.
 S1 - On the lateral aspect of the calcaneus.
 S2 - At the midpoint of the popliteal fossa.
 S3 - Over the tuberosity of the
ischium or infragluteal fold
 S4 & S5 - In the perianal area

 Light tough – dorsal column medial lemniscus (DCML) pw

o Use a whisp of cotton wool to assess light tough, w eyes of pt closed
o If you identify/ suspect a peripheral neuropathy, test in the glove & stocking pattern
o Ask if it feels the same bilaterally
 Pain – pinprick sensation – spinothalamic
o Alternate sharp & dull & assess the ability of the pt to detect the specific sharp sensation. If there is loss
of pain sensation, the pressure will still be felt, but the pt will not be able to interpret the sharpness. Ie.
The pt might say it feels dull, when it is sharp.
 Vibration – DCML
o Use a 128hz vibrating tuning fork. Pt should report when the vibration stops. Start distally, move
proximally over bony prominences.
 Proprioception
o Move the distal phalanges & assess whether the pt can assess whether it is being moved up/ down.
Proximally if abnormalities are found.
CO-ORDINATION EXAMINATION

 Remember: nystagmus is a sign of incoordination. So in a pt unable to perform these complex tests, one should
at least assess for nystagmus
o Nystagmus is normal in the extremes of gaze. Do not assess for gaze-evoked nystagmus beyond 30◦ &
150◦
o The fast component dictates the direction of nystagmus. Eg “horizontal, right beating nystagmus”. The
direction is towards the side of the lesion.
 Truncal ataxia
o This is usually a sign of a lesion in the vermis/ flocculonodular lobe.
o Ask pt to sit uo, and cross his/ her arms in front of his/ her chest. The pt w truncal ataxia will fall.
o This pt will not be able to stand w/out falling
 Dysmetria & intention tremor
o Dysmetria = a lack of coordination of movement typified by the undershoot/ overshoot of intended
position w the hand, arm, leg/ eye.
o Intention tremor = broad, coarse, & low frequency (below 5 Hz) tremor. The amplitude increases as an
extremity approaches the endpoint of deliberate & visually guided movement.
o Both are signs of ataxia, pointing to an ipsilat cerebellar lesion.
o Finger-nose test
 Note – the accuracy of this test is compromised by weakness in the tested limb
 Position your finger so that the patient has to fully outstretch their arm to reach it. The action
should be repeated repetitively & as fast as possible.
 Ensure that the pt is not fixating his elbow on the bed. The elbow should be lifted from the bed,
free in the air.
o Heel-shin test
 Note – the accuracy of this test is compromised by weakness in the tested limb
 Dysdiadokokinesia
o impaired ability to perform rapid, alternating movements.
o Sign of ataxia, pointing to an ipsilat cerebellar lesion.
 Ataxic gait
o Broad based. The pt will fall to the side of the cerebellar lesion.
o Impaired tandem walking.
 Romberg’s sign
o Note: this is not a sign of incoordination, but a sign of loss of proprioception
o The pt stands upright w hands to the side & eyes open. Eyes are subsequently closed. The pt w loss of
proprioception will lose balance when closing eyes.
GAIT

 Ask the patient to walk a few metres then to quickly turn around & return.
 Assess posture, arm swing, stride length, base, speed, symmetry, balance & how many steps it takes to turn
around.
Gait abnormalities
Type of gait Description
Ataxic Broad based & unbalanced. Impaired tandem gait. If cerebellar in origin, will fall to the
side of the lesion. If proprioception loss, will intently watch feet to find balance. The
normal individual only uses +/- 2 steps to turn around. The ataxic individual will take
many steps to turn around.
Spastic hemiperesis Circumduction of an extended lower limb (swings around in an arch w each step), w
the foot in equinovarus, & the arm adducted w the forearm flexed & pronated, & the
wrist & fingers flexed (can be bilat if there is a bilat UMN lesion)
Spastic paraparesis Same leg posture & circumduction described above, but both legs are involved & there
is arm sparing.
Parkansonian/ Small, shuffling steps, w a forwardly displaced centre of gravity (stooped forward).
shuffling Appears rushed (festinating). Pt may freeze. One may notice a classic pill-rolling
tremor.
Waddling Legs are lifted off the ground w the aid of a tilting trunk. Caused by proximal myopathy.
Steppage/ high Caused by foot frop d/t tibialis ant dysfx. Usually a deep peroneal n problem. Heel
stepping walking will be impaired.

PARIETAL LOBE FX
Dominant lobe dysfx Non-dominant lobe dysfx
 Aphasia  Visual-spatial disorientation
 Gerstmann’s Syndrome o Hemineglect
o It consists of 4 components: o Dressing apraxia
 Agraphia or dysgraphia o Constructional apraxia
 Acalculia or dyscalculia
 Finger agnosia
 Left-right disorientation
 Both dominant & non-dominant lesions
o Cortical sensory loss
o Sensory inattention
o Astereognosis
o Agraphasthesia
o Proprioceptive loss
o Two-point discrimination loss
o Inferior homonymous quadrantinopia
o Loss of Optokinetic Nystagmus
o Visual inattention

 Speech d/os
o NB: not all speech disorders imply parietal lesions, but they are all discussed here. In reality, the
speech of a patient is obviously assessed throughout the interview & examination.
o Types of speech disorders:
 Dysphasia – parietal lesions
 Dysarthria – problem w articulation. Can involve motor dysfx of any part that controls
articulation, from the larynx, to the soft palate, to the tongue
 Dysphonia – usually a recurrent laryngeal n lesion
 Mutism
 o Dysphasia/ aphasia
 Impairment of language caused by CNS pathology
 Remember the ffw areas, involved in language:
 Broca’s Area: Inferior frontal gyrus – “motor
language” of dominant lobe
 Wernicke’s Area: Posterior third of superior
temporal gyrus & Supramarginal and Angular Gyri in
parietal lobe – “receptive language” of dominant
lobe
 Arcuate fasciculus connects Wernicke’s to Broca’s
Areas

 Bedside tests include:

 Assessment of fluency
o Fluent = >60 words/min
o Non-fluent = <50words/min (50-60 is a grey area)
 Assessment of repetition
 Assessment of reading & writing
 Naming objects
 Classification:
 Previously termed expressive & receptive aphasia. This has been replaced w “fluent
& non-fluent aphasia”

Fluent aphasia Non-fluent aphasia

Description >60 words/min <50 words/min
Causes Wernicke’s dysphasia Broca’s dysphasia
 Most disabling  70% of all dysphasias
 May superficially appear normal, w good  Usually 5-10 words/min
grammar & annotation, but on careful  Usually assoc w a R heliparesis
consideration, there is excessive output  Will be able to follow commands –
(logorrhoea) of speech, void of meaning ie receptive language is intact
 Often misdiagnosed as psych, because of  Pt is frustrated that he cannot get
excessive & illogical speech the words out
 Cannot follow commands  Can read but cannot write
 Cannot repeat Global dysphasia
 Cannot read/ write  Cannot understand commands
Conduction aphasia  Cannot read or write
 Intact comprehension & language  Usually a large stroke. Hemiparesis,
production hemisensory loss, homonomous
 Impaired ability to repeat hemianopia
Transc cortical sensory (TCS) Transcortical motor (TCM)
 Repetition preserved  Similar to Broca’s but speech
 Often have echolalia improves w repetition. Lesion is
 Lesion of the posterior portion of the supero-ant to broca’s area
borderzone region affecting parietal lobe
 Classically caused by ICA stenosis
 Tests of both lobes
o Tests of cortical sensation loss
 NB – to perform this test, the pt must have intact light touch, pinprick & T sensation
 Sensory inattention
o Pt closes eyes. Touch arms & ask pt to say whether L/R. at some point, touch
both arms at the same time. The pt will only perceive that one arm is being
touched. He will not say “both”.
 Astereognosis
o Inability to recognise a familiar object by feel
o Place something in hand, like a pen/ keys and ask what it is
 Agraphaesthesia
o Unable to interpret numbers / letters formed in the pt’s palm by the examiner’s
finger, using pressure
 2 point discrimination
o Loss of ability to perceive 2 separate points applied to the fingertip
o A n individual can interpret 2 separate points placed 2-8cm apart on the
fingertips
o Loss of opticokinetic nystagmus
 N individuals will have nystagmus when a patterned object is rotated
infront of the pt’s eyes when the pt is asked to focus on it. Formally, a
striped drum is used. This is not readily available. One may use a tape
measure.
 This can be elicited by running a tape measure in front of the pt’s eyes
 If nystagmus does not occur, it is a sign of parietal dysfx
o Visual inattention
 This may only be performed if there are intact visual fields
 Place two fingers in the extremes of visual fields. Wiggle one at a time, asking pt “L/R?”
 Then wiggle both simultaneously. The pt will not interpret that both are moving. Same
as sensory inattention.
 Tests of dominant lobe
o Dysphasias – described above
o Acalculia – cannot perform simple calculations
o Finger agnosia – cannot identify which fingers are which on a hand. If he/ she is
asked to draw a hand, will look something like this:
o L-R disorientation
 Tests of the non-dominant lobe
o Hemineglect
 Indicidual will neglect left side of body grooming, will not eat off left side of plate, will not read
the left side of words, will not draw the left side of pictures
o Dressing apraxia
 Take off the pt’s hospital down. Turn one sleeve inside out without the pt seeing. Give it back.
The pt will not be able to put it back on as the inside out sleeve will confuse him/ her.
o Constructional apraxia
 Inability of patients to copy drawings accurately/ to construct three-dimensional objects