neurological assessmentv1[25 10_11][1]

Neurological AssessmentJonathan Downham Advanced Nurse Practitioner 2008

Jonathan Downham 2010

Anatomy of Neurological System

The Brain

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.

Division of cerebral cortex.

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 StemMedulla oblongata- controls autonomic functions

•Cardiac •Respiratory•Vomiting•Vasomotor

Pons (bridge)•Arousal•Controlling autonomic functions•Relaying information between the two hemispheres•Sleep.

Ventricles

Blood Supply

Blood-brain barrierProtects 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 BBBPineal 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 upSubfornical 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

ReflexesTapping 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 movementBasal 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 StateAppearance 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

MoodDelusions.

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.

Neurological Examination•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 impairedcontralateral visual/sensory

inattention, defects in written language


•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


•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.


•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.

GaitHemiplegic 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

GaitParkinsonian 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 NervesI- Olfactory- smell- sensoryII- Optic- sight- sensoryIII- Oculomotor- sight- motorIV Troclear- sight- motorV- Trigeminal- face/jaw/cornea- sensory and motorVI- Abducens- eye- motorVII- Facial- sensory and motorVIII- Vestibulocochlear - sensoryIX- Glossopharyngeal- mouth- sensory and motorX- Vagus- speech- sensory and motorXI- Accessory- spinal accessory- motorXII- 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 patientMove each hand separately then togetherAsk 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

Neurological ExaminationTypes 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 squintCover 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 lesionIf 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.

Neurological Examination• 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.


Neurological Examination• 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.



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


Neurological Examination• 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.


Neurological Examination• 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.


Neurological Examination• 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 reinforcement1+ = present but depressed2+ = normal3+ = increased4+ = clonus



• Biceps jerk


Nerve: musculocutaneous nerveRoot: C5, C6


• Triceps jerk


Nerve: radial nerveRoot: C7


• Brachioradialis/Supinator


Nerve: radialRoot: C6


• Knee jerk


Nerve: femoralRoot: L3-L4


• Ankle jerk


Nerve: tibial nerveRoot: 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 movement1 = flicker of muscle when patient tries to move2 = moves, but not against gravity3 = moves against gravity but not against resistance4 = moves against resistance but not to full strength5 = full strength


Neurological Examination• Assessment of power• Shoulder


AbductionMuscle: deltoidNerve: axillary nerveRoot: C5


• Elbow


Extension

Flexion

FlexionMuscle: biceps brachiiNerve: musculocutaneous nerveRoot: C5, C6

ExtensionMuscle: tricepsNerve: radial nerveRoot: C7


• Wrist


Extension

Flexion

ExtensionMuscle: radialis longus, brevis and ulnarisNerve: radial nerveRoot: C7

FlexionMuscle: Flexor carpi radialisNerve: medial nerveRoot: C6,C7

Neurological Examination• Finger


Extension Flexion

Abduction Adduction

Muscle: extensor digitorumNerve: posterior interosseousRoot: C7

Muscle: Flexor digitorum superficialis and profundusNerve: median and ulna Root: C8

Muscle: first dorsal interosseousNerve: ulnarRoot: T1

Muscle: second palmar interoseousNerve: ulnarRoot: T1

Neurological Examination• Hip


Abduction Adduction

Extension Flexion

Muscle: gluteus medius and minimusNerve: superior gluteal nerveRoot: L4,L5

Muscle: adductorsNerve: obturatorRoot: L2, L3

Muscle: iliopsoasNerve: lumbar sacral plexusRoot: L1, L2

Muscle: gluteus maximusNerve: inferior glutealRoot: L5, S1


• Knee


Flexion

Extension

ExtensionMuscle: quadriceps femorisNerve: femoralRoot: L3, L4

FlexionMuscle: hamstringsNerve: sciaticRoot: L5, S1


• Ankle


Dorsiflexion

Plantar flexion

Plantar flexionMuscle: gastrocnemiusNerve: posterior tibialRoot: S1

DorsiflexionMuscle: tibialis anteriorNerve: deep peroneal nerveRoot: 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.


Jonathan Downham 2010Common 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

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 movement.

Multiple SclerosisDemyelination 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 SclerosisClinical 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 GravisAutoimmune disorder•Antibodies directed against post synaptic acetylcholine receptors•Results in weakness and fatigability of skeletal muscle groups.

Symptoms

Ocular- ptosis and diplopiaCranial muscles- weak face and jaw

-dysarthia-dysphonia-dysphagia

Limb weakness -usually proximal-shoulder and hips

Axial weakness -neck and trunk-respiratory muscle

neurological assessmentv1[25 10_11][1]

Health & Medicine

division of cerebral

occipital lobevisual

bloodbrain barrierprotects

cerebral cortexoutermost

area of synapse

voluntary motor control

area postrema

anterior pituitary