Neurological Assessment Guide

Neurological Assessment
Jonathan Downham Advanced Nurse Practitioner 2008
Jonathan Downham 2010

Anatomy of Neurological System

Cerebrum
•Cerebral cortex
•Basal ganglia
•Limbic system

Cerebral cortex
•Outermost to the cerebrum
•Plays a key role in:
•Memory
•Attention
•Awareness
•Thought
•Language
•Consciousness
•Movement
•Folded- grooves called
sulci

Cerebral cortex- motor areas
Primary motor cortex-
•Executes voluntary
movements
Supplementary motor
areas and premotor
cortex-
•Select voluntary
movements

Cerebral cortex- sensory areas
Post central gyrus-
•Receives the bulk of
sensory inputs

Basal Ganglia
•Striatum
•Caudate
•Putamen
•Damage to striatum- Huntingtons
disease
•Globus pallidus
•Substantia Nigra
•Degeneration of dopamine
producing cells- Parkinsons.
•Subthalmic nucleus
Associated with a variety of functions
including-
•Vountary motor control
•Learning
•Eye movements
•Emotions

Limbic system
•Hippocampal circuit-
•Receives information
form medial temporal
lobe associated with
learning and memory.
•Amygdala-
•Processing of
emotional responses.

Frontal lobe-
•Primary motor cortex- muscle
movement
•Preparation of movement and
control of posture
•Broca’s area- the ‘how’ of
speech
•Pre-frontal cortex- rich in
connections from other areas.
Plan behavior, control emotional
state.
Parietal lobe-
•Inputs into here build up a picture of
how the body is positioned.
•Left hemisphere represents only
right side.
•Right hemisphere represents all of
left and some of right.
•Right sided lesions will produce
more severe effects on the
processing of left half of space.
•Neglect
Temporal lobe-
•Language comprehension and
response- Wernickes area
•Visual object recognition
•Learning and memory.
Occipital lobe-
•Visual cortex.

Cerebellum
Involved in-
•Control of axial muscles
(balance)
•Coordination of head and
eye movements
•Control of postural muscle
tone and movement
execution
•Controls precision in rapid
and dextrous movements

Brain Stem
Medulla oblongata- controls
autonomic functions
•Cardiac
•Respiratory
•Vomiting
•Vasomotor
Pons (bridge)
•Arousal
•Controlling autonomic
functions
•Relaying information
between the two
hemispheres
•Sleep.

Blood-brain barrier
Protects the brain from
"foreign substances" in the
blood that may injure the brain.
Protects the brain from
hormones and
neurotransmitters in the rest
of the body.
Maintains a constant
environment for the brain.

‘Holes’ in the BBB
Pineal body: Secretes melatonin and neuroactive peptides. Associated
with circadian rhythms.
Neurohypophysis (posterior pituitary): Releases neurohormones like
oxytocin and vasopressin into the blood.
Area postrema: "Vomiting center": when a toxic substance enters the
bloodstream it will get to the area postrema and may cause the animal to
throw up
Subfornical organ: Important for the regulation of body fluids.
Vascular organ of the lamina terminalis: A chemosensory area that
detects peptides and other molecules.
Median eminence: Regulates anterior pituitary through release of
neurohormones

•Collect information from
surrounding cells and conduct to
cell body.
•Principal role is to increase the
potential for synapses
•Output is all or none impulse
•Travels down the axon

•An electrical insulator
•Depolarisation only occurs
at the nodes of ranvier
•Conduction in mylelinated
neurons is approx 6 times
faster.
•Area of synapse.

Synapse and neurotransmitters.
1. Action potential
arrives at terminal
bouton.
2. Depolarisation
opens voltage gated
channels
3. Calcium ions enter
bouton
4. This liberates
vesicles
5. Which then fuse
with synaptic
membrane releasing
their contents
6. Neurotransmitter binds
to receptors on the other
side.

Autonomic nervous system
• Controls in voluntary internal processes e.g.-
– Digestion
– Regulation of blood flow
• Acts mainly on-
– Heart
– Smooth muscle
– Metabolic processes
– Glandular structures.

Autonomic nervous system
• Central control primarily by the hypothalamus
– Gains information from various sources e.g.
• Water status
• Pain
– Output in the form of
• Hormonal (via pituitary gland)
• Neural.
– Structures in the medulla also play a role and
communicate with the hypothalamus

Oculomotor nerve III
Facial nerve VII and
glossopharyngeal nerve IX

Spinal Cord
Spinothalamic tracts
•Carry conscious pain, temperature, crude touch, and pressure.
•Lateral and an anterior tract.
•Terminate in the areas of the cerebral cortex which perceive these sensations.

Spinal Cord
Spinocerebellar tract
•Carries unconscious proprioception (muscle sense) to the cerebellum
•The fibres either do not cross, or cross and re-cross so that they innervate the
cerebellum on the same side.

Spinal Cord
Fasciculus Gracilis and Fasciculus Cuneatus (Dorsal column)
•Carry discriminative touch (the gracilis) and conscious proprioception (the cuneatus).
•The Fibres of these tracts go first to the medulla where they synapse and cross.
•Then through a pathway called the medial lemniscus they pass to the thalamus.
•Then on to the cerebral cortex for perception.

Spinal Cord
Corticospinal tract (Pyramidal tract)
The corticospinal tract originates in the cerebral cortex where voluntary motor control is
localized. There are two branches, the lateral and the anterior.
The lateral crosses in the medulla in an area known due to its appearance as the
pyramids. Controls the precise movements of the limbs
The anterior does not cross. Control the less precise movements of the limbs These
fibres are called "upper motor neurons" and they synapse with "lower" motor neurons in
the cord which lead to the skeletal muscles.

Motor Control
• 3 types of movement
– Reflex responses
• Involuntary responses
– Rhythmic motor patterns- e.g. Walking
• Largely autonomic but require voluntary control to
start/stop
– Voluntary movements
• Goal directed, learned and improve with practice.

Motor Control
• Sensation
– Feedback control
• Sense of proprioception gives us information about the
position of our bodies.
• Patients who have lost this due to large fibre sensory
neuropathy do not know where there limbs are in
space unless they can see them
– Feedforward control
• Information is used to derive advanced information
and direct the movement toward a predicted position
e.g. picking up a drink.

Motor Control
• Upper motor neuron

Motor Control
• Lower motor neuron
– Alpha motor neurons
• Production of force by
skeletal muscle
– Gamma motor neurons
• Cause contraction of
spindle fibres
– Innervation ratio
• High ratio- coarse
movements
• Low ratio- fine
movements

Motor Control
•Muscle fibres made up of
cylindrical structures called
myofibrils
•Action potentials sweep
down the sarcolemma
•When action potential
arrives at t tubule it
unblocks voltage gated
channel
•This allows outflow of
calcium into myofibril
cytosol
•This calcium is needed for
myofibril contraction.

Motor control
•Myofibrils divided by series of Z lines
•Myosin- thick filaments
•Actin- thin filaments
•Ratchet action along muscle fibre between two filaments
•At rest attachment sites are covered with troponin
•Calcium binds to troponin allowing contraction- needs ATP
•Relaxation occurs when calcium is removed by sarcoplasmic reticulum- needs
ATP

Reflexes
Tapping patella tendon
can indicate if L2 and L3
are intact.
May also indicate if spinal
motor neurons are
receiving an abnormal
drive from higher centres.
In upper motor neuron
lesions there is a loss of
descending inhibition-
therefore brisk reflexes.

Tone
• This is the continuous and passive partial
contraction of the muscles
• It helps maintain posture.
• Produced by tonic firing of spinal motor
neurons.
• Set by stretch receptors and higher centres via
the spinal cord.

Control of movement
•Body needs to know where it is before it
moves.
•Gathers this form somatosensory,
proprioceptive and sensory data
•Goes to posterior parietal cortex.
•This is connected with anterior frontal
lobe (pre frontal areas)- abstract thought,
decision making, consequences of
actions.
•Both send axons that converge on
cortical area 6
•Planning and execution of movement
•Motor cortex area 4 controls muscle
movement.

Control of movement
Basal Ganglia
•Selection of movement
•Ensuring appropriate
movements are made-
important in fine
movement and walking
•Control of saccadic
movement of eyes (very
fast jumps)
•Memory relating to body
position

Control of movement
Cerebellum
•Receives info from vestibular
nuclei- head position
•Involved in control of balance,
and coordination of head and
eye movements
•Controls postural muscle
control and movement
execution
•Precision in rapid and
dextrous movements

Vision
•Visual field is the area which can be seen
with both eyes looking directly ahead.
•Hemispheres process information from only
the contralateral side of the axis
•Each hemifield is constructed from both
retinae
•E.g. Right visual hemisphere is processed in
the left visual cortex....
•...but is constructed from temporal (outside)
portion of the left retinae....
•....and nasal (inside) portion of the right eye.
•So nasal fibres cross over whilst temporal
fibres do not.

Vision
• Attention-
– Active pursuit of a focus from sensory information
in order to process it further.
– Pre attentive process is a rapid scanning of a
scene.
– The attentive process focuses on specific features
of a scene.

Vision
• Perception
– Making sense of what is seen.
– Organising visual information into objects and
background and then identifying those objects.
– Relies on comparison with memories of objects
– Occurs in visual association cortex.

Vision
• Eye movements-
• Stabilisation-
– Vestibulo-ocular- uses vestibular input to hold
retinal image stable during brief or rapid head
movement.
– Optokinetic- uses visual input to hold the retinal
image stable during sustained or slow head
rotation

Vision
• Keep fovea on target
– Saccade
• Very fast
• Guided by current tasks
• Horizontal saccadic
movements generated in
the pontine reticular
formation
• Vertical movements in the
midbrain.

Vision
• Keep fovea on target
– Smooth pursuit
• Controlled by visual and frontal corticol areas.
– Vergence
• Adjusts the eyes for differing image distances.
• Controlled by midbrain neurons.
– Smooth pursuit and saccadic eye movements
can combine e.g. When looking out of a train
window.

Vision
• Agnosia-
– Patients cannot recognise and name objects from visual
examination.
– They may still be able to describe physical characteristics
of the object.
– Failure of the higher processes of perception
• Neglect-
– A deficit in attention and awareness to one side of space.
– Commonly related to damage in the tempero-parietal
junction and posterior parietal cortex.

Hearing
•Once they leave the cochlear
nucleus most of the axons cross
over to the other side of the
brain.
•Because of the bilateral
projections to the auditory cortex
damage to one side of the
central auditory pathway will not
result in deafness in one ear.
Brodmans area/ Wernickes area

Hearing
•Pinna of outer ear crucial in
localising sound.
•Sound waves enter the ear either
directly or are reflected.
•Reflected sounds are slightly
delayed in hitting the tympanic
membrane.
•Differences in time delay are
used to determine the sounds
position.

Hearing
•Two types of hearing loss
•Conductive-
•Caused by failure of sound to reach the inner
ear.
•Sensorineural-
•Caused by failure at the level of the cochlea
or more centrally.

Somatosensation
• Receptors are formed by peripheral
terminations of axons of dorsal root ganglions.
• Types-
– Mechanoreceptors- pick up changes in pressure
(touch), or movement
– Nociceptors- respond to pain
– Thermoceptors- temperature.

Somatosensation
• Fibres signalling modalities of touch travel up
the dorsal column pathway.
• Fibres signalling thermal and pain information
travel in the spinothalmic tract.

Somatosensation
•The region of
the skin
inervated by a
dorsal root is
called a
dermatome.

Neurological Examination
•Nervous system
•Headache
•Blackout
•Fits
•Muscle weakness
•Altered sensation
•Change in vision
•Dizziness
•Tremors

A neurological examination is composed of
the following areas:
• Mental status and speech
• Gait
• Cranial nerves
• Motor system
• Sensory system
• Reflexes.

Mental State
Appearance and behaviour-
•Signs of self neglect (depression, dementia,
alcoholism).
•Anxiety- restless, fidgety.
•Appropriate behaviour- overfamiliar and
disinhibited, or unresponsive with little emotional
response
•Rapid mood changes
•Appropriate concern shown about symptoms

Mental State
Appearance and behaviour-
•Signs of self neglect (depression, dementia,
alcoholism).
•Anxiety- restless, fidgety.
•Appropriate behaviour- overfamiliar and
disinhibited, or unresponsive with little emotional
response
•Rapid mood changes
•Appropriate concern shown about symptoms
Mood
Delusions.

Higher Function
• Attention and orientation
• Memory
• Calculation
• Abstract thought
• Spatial perception
• Visual and body perception
• Apraxia

Higher Function
• Attention and orientation
– Orientation
• Time
• Place
• Person
– Attention
• Ask patient to repeat some numbers back to you
• Easier if it is a number familiar to you
• Make the numbers longer, then ask them to repeat
backwards.

Higher Function
• Memory
– Immediate recall and attention
• Ask patient to remember an address
• Or “One thing a nation must have to become rich and
great is a large secure supply of wood.”- Babcocks
sentence.
– Short term memory
• After about 5 minutes ask the patient to recall the
address you gave them.
– Long term memory
• Try to pick an appropriate event that you think the
patient should be able to recall.

Higher Function
• Calculation
– Serial sevens
• Ask patient to take seven from a hundred then seven
from what remains and so on.
• Doubling threes.
• Abstract thought- frontal lobe function
– Explain well known proverbs (glasshouses, rolling
stone etc)
– Difference between a pair of objects e.g. Skirt and
trousers.

Higher Function
• Spatial perception (tests parietal and occipital
lobe function
– Clock face- ask patient to draw a clock face and fill
in numbers. Then ask him to draw a particular
time.
– Five pointed star – ask them to draw a five
pointed star
– Half clock missing- visual inattention
– Unable to draw- constructional apraxia

Higher Function
• Visual and body perception- parietal and
occipital lesions
– Abnormalities of perception of sensation despite
normal sensory perceptions are called agnosias.
– Facial recognition- ask patient to identify famous
faces (prosopagnosia)

Higher Function
– Body perception
• Patient ignores one side and is unable to find his hand
if asked
• Does not recognise his hand if shown it
(asomatagnosia)
• Unaware of weakness of affected side (anosagnosia)
• Ask patient to show you his index ginger, ring finger
etc. (finger agnosia)
• Ask patient to touch his right ear with his left index
finger (left/right agnosia)

Higher Function
– Sensory agnosia
• Pt closes eyes. Place familiar object in hand and ask
what it is (astereognosis)
• Write a letter/number on his hand and ask what it is
(agraphaesthesia)
• Apraxia
– Ask the patient to perform an imaginary task
• Unable to initiate even though understands- ideational
apraxia
• Performs but makes errors- ideomotor apraxia

• Speech
• Aphasia
• Dysphonia
• Disturbance of voice production.
May reflect abnormality of the
nerve supply via the vagus.
• Dysarthria
• Motor disorder. Can reflect
difficulties at different levels.

• Aphasia- absence of speech
• Wernicke’s aphasia-
• Poor comprehension,
fluent, (receptive) but
often meaningless
• Broca’s aphasia
• Preserved
comprehension, non
fluent (expressive)
speech
• Global aphasia
• Difficulty understanding
and speaking.

•Test speech
•Aphasia
•Listen to patients speech, fluency and contents
•Assess their comprehension by giving simple commands
•Assess their ability to name objects
•Assess their ability to repeat sentences, (No ifs, ands or
buts).
Type Lesion Speech fluency Speech content Comprehension Association
Expressive Broca's area non-fluent normal normal
telegrammatic speech,
dysarthia
Receptive Wernicke's area fluent impaired impaired neologisms, excessive speech
Conductive Arcuate Fasiculus fluent normal normal
impaired function in
repetitive tasks
Global Parietal lobe/ dominant hemisphere non-fluent impaired impaired
contralateral visual/sensory
inattention, defects in
written language

•Test speech
•Dysphonia
•In dysphonia speech volume is reduced and voice
sounds husky.
•May be due to recurrent laryngeal nerve
weakness.
•May have bovine like cough- cough lacks
explosive start- ? vocal cord palsy.
•Ask patient to say ‘eeee’- if weakens may indicate
myasthenia

•Test speech
•Dysarthia
•Ask the patient to repeat ‘British Constitution’,
‘West Register Street’, and ‘baby hippopotaumus’
•Cerebellar dysarthia- slurred speech. (?MS)
•Extrapyramidal dsyarthia- soft and monotonous
(Parkinsons)
•Pseudobulbar dysarthia- high pitched with
strangled quality
•Bulbar dysarthia- speech has a nasal quality.

•Test speech
•Dysarthia
•Lower motor neuron dysarthia-
•Palatal- nasal speech as with bad cold- X
cranial nerve
•Tongue – distorted speech, letters t,s and
d- XII cranial nerve
•Facial- difficulty with b,p,m and w- VII
cranial nerve

Gait
• Ask patient to walk up and down the room
• Observe
– Posture
– Pattern of arm and leg movements
• If gait appears normal ask them to walk heel
to toe.

Gait
Hemiplegic gait
•Ipsilateral arm held flexed and
adducted
•Ipsilateral leg held extended
•Pts tilt pelvis forward to swing
affected leg around
Spastic gait
•Pts walk in small steps
•Legs are held in adduction with
knees touching each other
•Gives the gait a scissored quality

Gait
Parkinsonian gait
•Slow and shuffling
•Small stride length
•Reduced arm swinging
•Flexed posture
Footdrop gait
•Pts over flex the
knee and hip
•Gives a high
stepping quality
Cerebellar ataxic gait
•Pts walk on a wide base
•Often unsteady
•Stagger to affected side if
unilateral lesions
•Stagger backwards if bilateral
lesions
•Appear drunk
Romberg test
•Ask patient to stand with feet
together
•Pts with cerebellar or vestibular
lesions are ataxic with eyes open
•Pts with proprioceptive sensory
loss may be ataxic when they close
their eyes.

The Cranial Nerves.
Once On October The
Tenth, All Five Virgins Gave
Victor A Hug.
Some say marry money but my
brother says big brains matters
most

The Cranial Nerves
I- Olfactory- smell- sensory
II- Optic- sight- sensory
III- Oculomotor- sight- motor
IV Troclear- sight- motor
V- Trigeminal- face/jaw/cornea- sensory and motor
VI- Abducens- eye- motor
VII- Facial- sensory and motor
VIII- Vestibulocochlear - sensory
IX- Glossopharyngeal- mouth- sensory and motor
X- Vagus- speech- sensory and motor
XI- Accessory- spinal accessory- motor
XII- Hypoglossal- speech and tongue- motor
Once On October The
Tenth, All Five Virgins Gave
Victor A Hug.
Some say marry money but my
brother says big brains matters
most.

I- Olfactory nerve-
•Not tested routinely.
•May only wish to test if the patient
complains of being unable to smell.
•This should then be tested by asking
patient to close his eyes and one nostril
and then exposing him to an aroma.
•Bilateral loss of sense of smell is often
associated with loss of sense of taste

II- Optic Nerve
•Visual Acuity
•Visual Fields
•Fundi

Visual Acuity
•Test with Snellen chart
•Hold chart about 20
feet away.
•Test both eyes getting
patient to cover each
eye in turn.
•Ask patient to read
smallest line possible

Visual Acuity
•Correctable reduced acuity =
ocular defect
•Un-correctable reduced acuity =
•Corneal lesion
•Cataract
•Macular degeneration
•Retinal heamorrhage
•Optic neuropathy
•Bilateral occipital lesions

Visual fields-
Check for visual inattention-
Hold hands stretched out halfway between
you and patient
Move each hand separately then together
Ask patient to indicate which moved.
•Tested using confrontation
•Sit at same level as patient.
•Ask them to cover one eye
•You cover opposite eye.
•Bring finger into view from all
angles.
•Patient to say when he sees it.

Fundi-
•Using ophthalmoscope
•Lower lights
•Start at +20 setting
•Hold scope in left hand to
left eye when looking at
patients left
•Patient to focus on spot
on wall behind you.
•Swap for other side.

Cotton wool spots
result from occlusion
of retinal pre-capillary
arterioles supplying
the nerve fibre layer
with concomitant
swelling of local nerve
fibre axons.
Flame-shaped
heamorrhage in
association with severe
hypertension
Papilloedema from
malignant hypertension.
There is blurring of the
borders of the optic disk
with hemorrhages

Types of eye movement
•Saccadic (Frontal Lobe)
•Rapid movement of one point of fixation to another
•Pursuit eye movement (Occipital Lobe)
•Slow eye movement used to maintain fixation on a moving
object
•Vestibular-positional eye movements (Cerebellar vestibular nuclei)
•Eye movements which compensate for movement of the head to
maintain fixation
•Convergence (Mid-brain)
•Movements that maintain fixation as an object is brought closer
to the face.

III (oculomotor), IV (trochlear), and VI (abducens)
Look at eyelids for
ptosis and symmetry
•Common causes
•Congenital
•Horners syndrome
•III nerve palsy
•Myasthenia gravis

Test the pupillary
reflex by shining a
light on the pupil.
Look at both direct
and consensual
response

Observe the patient
following a target up
and down and to
either side.
Perform cover test, looking for
squint
Cover left eye, then uncover
rapidly and cover right eye. Look
to see if left eye has to correct to
look back at your eye

V- Trigeminal
Split into three
divisions

V- Trigeminal
Sensory- test the sensation over the three distributions
of the nerve using cotton wool and pin.
Corneal reflex- lightly touch the cornea with damp
cotton wool. Patient should blink
•Afferent defect (Vth cranial nerve defect) results in
depression or absence of direct and consensual reflex
•Efferent defect(VIIth cranial nerve defect) results in
impairment or defect on affected side.
Motor- test jaw opening against resistance.

VII- Facial
•Patient to look up- note any loss of
wrinkling
•Patient to close eyes. Try to gently
pull them open.
•Ask patient to bare teeth. Look for
any asymmetry.
•Ask patient to blow out cheeks
Look for asymmetry of nasolabial folds and position of two corners of mouth.
If weakness detected then if confined to lower part of face- UMN lesion
If both upper and lower them LMN lesion

VIII- Vestibulocochlear nerve
•Whispered voice test-
•Stand behind patient with mouth about 15cm
from ear to be tested
•Mask hearing in other ear by rubbing tragus
•Ask patient to repeat what you say.
•Move away to arms length. If patient can hear
whispered voice from here then hearing is said to
be normal.

• Webers test
– Place fork in
middle of
forehead
– Ask patient where
they hear sound.
– Normally this
would be equally
in both ears or in
the middle.
– Note to which
side it lateralises.

• Rinne’s test
– Place the vibrating
forks base against
the mastoid
process
– Then place the fork
at the external
auditory meatus
and ask which is
louder.
– Air conduction
should be better
than bone
conduction
Sensorineural deafness i.e. Air condction better
than bone conduction;
•Lesion of the cochlea e.g. Menieres
disease
•Lesion in the nerve

• IX and X- Glossopharyngeal and Vagus
– Ask patient to say ‘aah’ and observe for palatal
movement. Make sure it is bilateral.
– Observe uvula. Should stay central.
• Moves to one side- upper or lower motor lesion of vagus on the
other side
• Does not move on saying aah- bilateral palatal muscle paresis
– Only test gag reflex if thought necessary.
– Listen for dysphonia (altered voice production) or
a bovine like cough.

• XI and XII- accessory and hypoglossal
– Force chin down against resistance of your hand
– Turn the chin to one side against resistance
– Ask patient to stick out their tongue
• Observe for any fasiculations or wasting
• Note any deviation to one side or the other.

• XI and XII- accessory and hypoglossal
– Small tongue
• With fasiculations-bilateral lower motor neurone disease, motor
neuron disease
• With reduced speed of movement- bilateral upper motor neurone
disease
– Tongue deviates to one side
• With unilateral wasting and fasiculation- unilateral lower motor
neurone disease
• With normal bulk- unilateral upper motor neurone disease
– Tongue moves in and out on protrusion (trombone
tremor)
• Cerebellar disease. Jonathan Downham 2010

• Motor system
– Inspection
– Palpation
– Assessment of muscular tone
– Assessment of tendon reflexes
– Assessment of power
– Assessment of coordination
– Assessment of gait.

• Upper motor neurone
disease affects those
motor neurons which
originate in the motor
region of the cerebral
cortex.
• Lower motor neurone
disease affects those
motor neurons
connecting the
brainstem and spinal
cord to muscle fibres.

• Five patterns of muscular weakness-
Upper motor neurone (UMN)
•Increased tone
•Increased reflexes
•Pyramidal pattern of weakness
•Weak extensors in the arm
•Weak flexors in the leg
Lower motor
neurone (LMN)
•Wasting
•Fasiculation
•Decreased tone
•Absent reflexes
Muscle disease
•Wasting
•Decreased tone
•Impaired or absent reflexes
Neuromuscular Junction
•Fatiguable weakness
•Normal or decreased tone
•Normal reflexes
Functional weakness
•Normal tone
•Normal reflexes
•No wasting
•Erratic power

• Inspection
– Posture
– Gait
– Coordination
– Wasting
– Fasciculation
– Tremors
• Physiological
• Essential
• Action
• Intention

• Palpation
– Complete exposure of the patient. Maintain
dignity
– Look for:
• Asymmetry
• Deformities
• Wasting
• Fasiculation
– Palpate muscles to feel their bulk.

• Tone
– Upper limb
• Hold patients hand as if shaking hands. Support elbow and put
through a range of movements
– Lower limb
• Roll leg from side to side then briskly lift knee into flexed position
– Decreased tone- heel does not lift off the bed
– Knee clonus
• With leg extended sharply push patella with thumb and forefinger
– Ankle clonus
• Support patients leg with knee and ankle in 90 degree flexion.
Quickly dorsiflex and evert the ankle.

• Tone:
– Resistance felt by the examiner when moving a joint
passively through its range of movement.
• Flaccidity
– May occur in LMN disease. Often associated with muscle
wasting.
• Spasticity
• Velocity dependant resistance to passive movements
• A feature of UMN disease
• Accompanied by weakness, hyper-reflexia, an extensor
plantar response and sometimes clonus.
• Rigidity
• Sustained resistance throughout the range of movement
• Most easily detected when the limb is moved slowly
• Clonus
• Rhythmic contractions evoked by sudden stretch of muscles
• When sustained indicates UMN damage.

• Deep tendon reflexes
– Using tendon hammer allow weight of tendon
hammer to determine strength of blow
– Abnormally brisk reflexes are generally a sign of upper
motor neurone disease
– Diminished or absent reflexes are signs of lower
motor neurone disease
– If no response try reinforcement methods
• For upper reflexes ask patient to clench teeth
• For lower reflexes ask them to hook their fingers together
then try to separate.

• Reflexes can be graded-
0 = absent
+/- = present but only with reinforcement
1+ = present but depressed
2+ = normal
3+ = increased
4+ = clonus

• Biceps jerk
Nerve: musculocutaneous nerve
Root: C5, C6

• Triceps jerk
Nerve: radial nerve
Root: C7

• Brachioradialis/Supinator
Nerve: radial
Root: C6

• Knee jerk
Nerve: femoral
Root: L3-L4

• Ankle jerk
Nerve: tibial nerve
Root: S1-S2

• Plantar reflex
A normal reflex is for the patient
to have plantar flexion of all his
toes.
A completely abnormal reflex is
indicated if there is-
• dorsiflexion (turning upward)
of the big toes,
•fanning of all toes,
•turning upward of the ankle,
• or flexion (bending) of the
knee and hip.

• Power can be graded-
0 = no movement
1 = flicker of muscle when patient tries to move
2 = moves, but not against gravity
3 = moves against gravity but not against resistance
4 = moves against resistance but not to full strength
5 = full strength

• Assessment of power
• Shoulder
Abduction Muscle: deltoid
Nerve: axillary nerve
Root: C5

• Elbow
Extension
Flexion
Flexion
Muscle: biceps brachii
Nerve: musculocutaneous nerve
Root: C5, C6
Extension
Muscle: triceps
Nerve: radial nerve
Root: C7

• Wrist
Extension
Flexion
Extension
Muscle: radialis longus, brevis and
ulnaris
Nerve: radial nerve
Root: C7
Flexion
Muscle: Flexor carpi radialis
Nerve: medial nerve
Root: C6,C7

• Finger
Extension Flexion
Abduction Adduction
Muscle: extensor digitorum
Nerve: posterior interosseous
Root: C7
Muscle: Flexor digitorum superficialis and
profundus
Nerve: median and ulna
Root: C8
Muscle: first dorsal interosseous
Nerve: ulnar
Root: T1
Muscle: second palmar interoseous
Nerve: ulnar
Root: T1

• Hip
Abduction Adduction
Extension Flexion
Muscle: gluteus medius and minimus
Nerve: superior gluteal nerve
Root: L4,L5
Muscle: adductors
Nerve: obturator
Root: L2, L3
Muscle: iliopsoas
Nerve: lumbar sacral plexus
Root: L1, L2
Muscle: gluteus maximus
Nerve: inferior gluteal
Root: L5, S1

• Knee
Flexion
Extension
Extension
Muscle: quadriceps femoris
Nerve: femoral
Root: L3, L4
Flexion
Muscle: hamstrings
Nerve: sciatic
Root: L5, S1

• Ankle
Dorsiflexion
Plantar flexion
Plantar flexion
Muscle: gastrocnemius
Nerve: posterior tibial
Root: S1
Dorsiflexion
Muscle: tibialis anterior
Nerve: deep peroneal nerve
Root: L4, L5

• Assessment of coordination
– Rebound phenomenon
– Finger-nose test
– Heel-shin test
– Rapid alternating movements

Sensory examination
•Light touch
•Dab with cotton
wool
•Pain
•Check patient can
identify stimulus as
sharp.

Common peroneal nerve Femoral nerve
Lateral cutaneous nerve

Vibration sense
•Place tuning fork on sternum and ask if he can feel
it
•Patient then closes eyes
•Place on distal joint and ask if he feels it.
•If not move up to next proximal joint
•Compare left with right
Joint position sense
•Move the distal interphalangeal joint of the index
finger/toe by the sides
•With patients eyes closed ask them if the joint is
moving up or down.

Parkinson’s Disease.
• Caused by cell death in the
substantia nigra
– Basal ganglia normally exert an inhibitory
response on various muscles.
– This prevents them becoming active at
inappropriate times.
– When an action is required dopamine
reduces this inhibition.
– So low levels of dopamine function demand
greater exertions for any given movement
http://www.nice.org.uk/nicemedia/live/10984/30087/30087.pdf

Parkinson’s Disease.
• Hypokinesia-
– Poverty of movement e.g. Lack of blinking, expressionless
face.
• Bradykinesia-
– Slowness of movement. Initially manifests as problems
with performing fine motor movements.
• Akinesisa-
– Difficulty initiating and termination movements
• Rigidity-
– Caused by increased muscle tone. Can be uniform (lead
pipe) or ratchety (cogwheel).
• Rest Tremor-
– Maximal when limb is at rest, disappearing with voluntary

Multiple Sclerosis
Demyelination affecting white matter tracts in the central
nervous system
• relapsing-remitting: clearly defined disease relapses with full recovery or with
sequelae and residual deficit upon recovery; periods between relapses
characterised by a lack of disease progression. About 80% have relapsing-remitting
disease at onset
● secondary progressive: initial relapsing-remitting course followed by progression
with or without occasional relapses, minor remissions and plateaux. About 50% of
people with relapsing-remitting MS develop secondary progressive MS during the
first 10 years of their illness
● primary progressive: disease progression from onset with occasional plateaus and
temporary minor improvements allowed. About 10–15 % have primary
progressive disease at onset.
Marked variability in disease progression.

Multiple Sclerosis
• Areas of demyelination are found in the white
matter of the brain and spinal cord.
• There is a particular predilection for lesions in
certain areas-
– Periventricular areas of the cerebral hemispheres
– Corpus callosum
– Brainstem
– Cervical cord
– Optic nerves

Multiple Sclerosis
Clinical features
Optic and retrobulbar neuritis
•Subacute visual loss
•Usually unilateral
•Central scotoma
•Pain on movement
•Afferent pupillary defect
Both pupils dilate when
swung to the affected eye
Brainstem presentation
•Diplopia- failure of adduction of
the eye
•Nystagmus-due to cerebellar
disease
•Vertigo
•Dysartia
•Facial numbness
•Dysphagia
•Ataxia
•Hemisensory or patchy sensory
changes in the limbs.
Spinal cord lesion
•Spastic paraparesis
•Tetraparesis
•Tonic spasms
•Difficulty walking
•Sensory loss

MS- diagnostic tools
• Evoked potential studies
– Visual
– Somatosensory
– Brainstem auditory evoked potentials
• CSF sampling
– Presence of oligoclonal bands
• MRI scan

MS- Treatment
• Treatment for MS can be split into three main
categories:
– treatment for relapses of MS symptoms (steroids)
• Methylprednislone- reduce immune response and swelling around
nerves
– treatment for specific MS symptoms
• Visual problems- gabapentin
• Muscles spasms/neuropathic pain-
physio/gabapentin/carbemazapine
• Mobility problems- mainly muscular-physio and drugs as above
• Depression- anti-depressants
• Bladder problems- over active bladder needs anti-cholinergics-
oxybutynin or tolterodine

MS- Treatment
– treatment to slow the progression of MS (disease-
modifying medicines)
• Interferon beta 1a and 1b
• Glatiarmer
• Natalizumab

Stroke (CVA)
Middle Cerebral Artery Occlusion
•Most commonly artery involved in stroke.
•Supplies motor and sensory cortices
•Comprehension (Wernickes) and expression
(Brocas)
•These areas are found in the dominant hemisphere
•So an occlusion in the left cerebral artery will affect
speech production in right handed individuals
•Contralateral hemiplegia
•Contralateral corticol
hemisensory loss
•Dominant hemisphere
aphasia
•Non dominant
hemisphere neglect
•Contralateral hemianopia

Stroke (CVA)
Anterior Cerebral Artery Occlusion
•Occlusion proximal to anterior communication
artery normally well tolerated because of cross flow
•Distal occlusion causes
•Contralateral weakness
•Corticol sensory loss in the leg
•Incontinence is often present
•Contralateral grasp

Stroke (CVA)
Posterior Cerebral Artery Occlusion
•Effect of occlusion depends on site
•Proximal occlusion- III nerve palsy,
contralateral hemiplgia, thalamic syndrome,
chorea
•Corticol vessel occlusion- hemianopia with
macular sparing
•Bilateral occlusion- corticol blindness- pt is
blind but lacks insight and often denies it.

Myasthenia Gravis
Autoimmune disorder
•Antibodies directed against post
synaptic acetylcholine receptors
•Results in weakness and fatigability of
skeletal muscle groups.
Symptoms
Ocular- ptosis and diplopia
Cranial muscles- weak face and jaw
-dysarthia
-dysphonia
-dysphagia
Limb weakness -usually proximal-
shoulder and hips
Axial weakness -neck and trunk
-respiratory muscle

Neurological Assessment Guide

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Neurological Assessment Guide

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