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Aims and Objectives Requires some basic knowledge of clinical examinations Clinical examination station (OSCE) One way to prepare: Retrospective approach Neurological examination: 4 cases Cranial nerves will be covered

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  • Requires some basic knowledge of clinical examinations
  • Clinical examination station (OSCE)
  • One way to prepare: ‘Retrospective approach’
  • Neurological examination: 4 cases
  • Cranial nerves will be covered later on in the week
  • Duration: 60 mins

2

Aims and Objectives

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Clinical examination station: how to prepare?

EXAMINATION ROUTINE PRESENTATION VIVA

  • Perform each step of the

routine confidently

  • Pick up on signs
  • Present findings

systematically

  • List appropriate

differentials based on findings

  • Answer questions

systematically

  • Explain your thinking

‘Retrospective approach’

  • 1. Formulate an OSCE Cases List
  • 2. Prepare your ‘VIVA’ for those cases
  • Positive signs of diagnosis
  • ‘Typical’ findings presentation
  • Risk factors
  • Signs of decompensation
  • List of differentials
  • Complications
  • How would you investigate this patient?
  • How would you manage this patient?
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Clinical examination station: how to prepare?

‘Retrospective approach’

  • 3. Finalise your examination routine
  • Each step of the routine
  • Signs you are looking for
  • Your speech
  • 4. Practice your examination routine
  • n friends
  • 5. Go to the wards/clinics looking for

your cases

EXAMINATION ROUTINE PRESENTATION VIVA

  • Perform each step of the

routine confidently

  • Pick up on signs
  • Present findings

systematically

  • List appropriate

differentials based on findings

  • Answer questions

systematically

  • Explain your thinking
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What cases could come up?

1. Hemiplegia/hemiparesis 2. Multiple sclerosis 3. Parkinson’s disease 4. Peripheral neuropathy 5. Myasthenia gravis 6. Motor neuron disease 7. Proximal myopathy

This is not a definitive list

  • But by preparing for these you will be better at:
  • Your exam routine
  • Looking out for important signs
  • Formulating your findings systematically
  • Tackling the VIVA

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Peripheral neurological examination: OSCE Cases list

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I performed a cardiovascular examination on this patient

  • Who has signs suggestive of mitral regurgitation

My main positive findings are: 1. XXX 2. YYY My relevant negative findings are: 1. XXX (Risk factors) 2. YYY (Signs of decompensation) 3. ZZZ (POSSIBLE associated features) Overall, this points towards a diagnosis of mitral regurgitation

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How to present your findings?

If you have an idea, then back yourself from the start. It gets the examiner listening RELEVANT negatives Patients will be STABLE

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Neurological examination: Case 1

Left Right Tone é 7 beats of ankle clonus N Power ~3 in all movements 5/5 Reflexes é N Co-ordination N N Sensation N N

(1)

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Question 1

Which of the below is NOT a feature of an upper motor neuron lesion? A – Fasciculations B – Hoffman’s reflex C – Increased tone D – Weakness E – Spasticity

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Question 1

Fasciculations Hoffman’s reflex Increased tone Weakness Spasticity app.bitemedicine.com Which of the below is NOT a feature of an upper motor neuron lesion?

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Explanations

app.bitemedicine.com Which of the below is NOT a feature of an upper motor neuron lesion? Fasciculations This is a LMN sign which occurs due to muscle denervation causing spontaneous action potentials Hoffman’s reflex Flicking the middle fingernail downward causes thumb flexion. This suggests a UMN lesion Increased tone This is a feature of UMN lesion Weakness Seen in both UMN and LMN disease Spasticity Seen in UMN disease

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Motor pathways (from brain à muscle)

I want to move my R thumb – what happens?

  • Start: UMN start from LEFT primary motor cortex
  • UMN moves downwards
  • At medulla
  • 90% of fibers cross (LATERAL CORTICOSPINAL TRACT)
  • 10% do not cross (ANTERIOR CORTICOSPINAL TRACT)

L R

(2)

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Motor pathways (from brain à muscle)

I want to move my R thumb – what happens?

  • Start: UMN start from LEFT primary motor cortex
  • UMN moves downwards
  • At medulla
  • 90% of fibers cross (LATERAL CORTICOSPINAL TRACT)
  • 10% do not cross (ANTERIOR CORTICOSPINAL TRACT)
  • UMN continues until they reach the correct spinal level
  • Here they synapse with the LMN at the anterior horn of

spinal cord

  • The LMN innervates the responsible skeletal muscles

L R

(2)

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Upper & lower motor neurons

What counts as an upper motor neuron?

  • Brain
  • Brainstem
  • Injury to white matter of spinal cord up to level of

synapse

So what counts as a lower motor neuron?

  • Injury to the grey matter of spinal cord at level of

synapse (anterior horn)

  • Injury to axons leaving spinal cord

L R

(2)

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UMN vs LMN lesions

Upper motor neuron lesion Lower motor neuron lesion Site Proximal to anterior horn synapse Distal to synapse Tone Spasticity and/or rigidity Pronator drift Flaccid Power Reduced

  • Upper limb: extensors weaker than

flexors

  • Lower limb: flexors weaker than

extensors Reduced Reflexes Hyperreflexia Hyporeflexia Fasciculations Absent Present

  • UMN lesion means the LMN is no longer regulated
  • So LMN response is NOT controlled
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Neurological examination: Case 1

Left Right Tone é 7 beats of ankle clonus N Power ~3 in all movements 5/5 Reflexes é N Co-ordination N N Sensation N N

(1)

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Neurological examination: Case 1 – Hemiplegia

Please present your findings?

I performed a neurological examination on this patient who has signs suggestive of a LEFT HEMIPLEGIA My main positive findings are:

  • On general inspection:
  • Walking frame by bedside
  • Left sided facial droop
  • The left upper limb was flexed
  • Tone appeared to be increased globally on the left side, with a more than 5 beats of ankle clonus
  • Power was moderately reduced (3/5) globally on the left side with suggestion of a pyramidal

pattern of weakness

  • Reflexes were brisk on the left
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Neurological examination: Case 1 – Hemiplegia

Please present your findings?

My relevant negative findings are:

  • No signs of LMN lesion (no muscle wasting, no fasciculations)
  • Sensation was normal in all modalities tested

This points towards an UMN lesion, more specifically a left sided hemiplegia

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Neurological examination: Case 1 – Hemiplegia

Please present your findings?

My relevant negative findings are:

  • No signs of LMN lesion (no muscle wasting, no fasciculations)
  • Sensation was normal in all modalities tested

This points towards an UMN lesion, more specifically a L sided hemiplegia

  • Taking into account the patient’s age, the most likely cause would be a right sided stroke secondary to

thrombosis (most common), embolus, or haemorrhage

  • Other possible causes include:
  • A space-occupying lesion e.g. tumour
  • A demyelinating process
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Neurological examination: Case 1 – Hemiplegia

What are your differentials?

  • Vascular causes
  • Stroke
  • TIA
  • Signs < 24hrs
  • No evidence of acute infarction on brain

imaging

  • Space-occupying lesion
  • Brain
  • Demyelinating conditions e.g. multiple sclerosis
  • Signs disseminated in time & space e.g. sensory,

motor, cerebellar

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Neurological examination: Case 1 – Hemiplegia

This patient has had a stroke, what further examinations could you perform to support this diagnosis?

I noted a left sided facial droop. I would also formally examine the cranial nerves

  • Would expect unilateral facial weakness with relative sparing of frontalis
  • Examine visual fields which may help localise the site of infarct e.g. MCA stroke will give

homonymous hemianopia Assess for cardiovascular risk factors

  • Check radial pulse for AF (embolic stroke)
  • Auscultate for carotid bruits
  • Listen for heart murmurs
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Neurological examination: Case 1 – Hemiplegia

What are the different types of stroke you are aware of?

Strokes can be classified by:

  • Pathophysiology or
  • Location of infarct

(2)

Pathophysiology Location (Bamford Classification) Ischaemic (85%) Total anterior circulation stroke (highest mortality) Haemorrhagic (15%) Partial anterior circulation stroke Posterior circulation stroke Lacunar stroke

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Neurological examination: Case 2

Left Right Tone N N Power 4/5 on distal movements of foot, otherwise normal 4/5 on distal movements of foot, otherwise normal Reflexes N N Co-ordination N N Sensation Sensory loss in diagram Sensory loss in diagram

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Question 2

Diabetes Chronic renal failure Muscular dystrophy Guillain-Barré syndrome Vitamin B12 deficiency app.bitemedicine.com Which of the following is NOT a cause of peripheral neuropathy?

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Explanations

app.bitemedicine.com Which of following is NOT a cause of peripheral neuropathy? Diabetes A common cause Chronic renal failure Uraemia can cause a neuropathy Muscular dystrophy This is a muscle pathology, not a nerve pathology Guillain-Barré syndrome Causes a neuropathy, typically post infection Vitamin B12 deficiency Can cause a neuropathy

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Sensory pathways (from skin à brain)

2 main pathways

  • Dorsal column (medial lemniscus)
  • Touch
  • Vibration
  • Proprioception
  • Anterolateral spinothalamic tract
  • Pain
  • Temperature
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Neurological examination: Case 2 – Peripheral neuropathy

Please present your findings?

I performed a peripheral neurological examination on this patient, who has signs of a PREDOMINANTLY SENSORY PERIPHERAL NEUROPATHY My main positive findings are:

  • Power was moderately reduced in distal movements (4/5)
  • There was a glove and stocking distribution of sensory loss affecting both the dorsal

column and spinothalamic tracts

  • The sensory loss was more marked in the lower limbs
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Neurological examination: Case 2 – Peripheral neuropathy

Please present your findings?

My relevant negative findings are:

  • Normal tone, reflexes and co-ordination

This points towards a predominantly sensory peripheral neuropathy

  • The cause of the peripheral neuropathy is unclear. Absence of any signs of:
  • Diabetes (finger prick marks)
  • Chronic alcoholism (distended abdomen, jaundice, spider telangiectasia)
  • Charcot Marie Tooth (young, pes cavus, inverted champagne bottle appearance of the

lower limbs)

  • Make other differentials less likely
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Neurological examination: Case 2 – Peripheral neuropathy

What are the possible causes of a peripheral neuropathy

Causes of predominantly sensory neuropathy - ABCDE

  • Alcohol & diabetes = most common
  • Vit B12 deficiency
  • Chronic renal failure and cancer (paraneoplastic)
  • Drugs e.g. isoniazid, vincristine
  • Every vasculitides (e.g. SLE) and Everything else (e.g. paraneoplastic)

Causes of predominantly motor neuropathy

  • Charcot-Marie Tooth (hereditary sensory and motor neuropathy)
  • Guillain-Barré syndrome (if in the acute setting)
  • Chronic inflammatory demyelinating polyneuropathy (more chronic)

(3)

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Neurological examination: Case 2 – Peripheral neuropathy

How would you investigate this patient?

Bedside

  • Blood glucose
  • Urine dip (glycosuria)

Bloods

  • DM: fasting glucose, HbA1c
  • Alcohol: FBC, LFTs, clotting, vitamin B12 and folate
  • Chronic renal failure: U&E
  • Vitamin deficiency: B12, folate
  • Vasculitis: ESR, autoantibody screen
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Neurological examination: Case 2 – Peripheral neuropathy

How would you investigate this patient?

Imaging

  • X-ray or CT imaging: paraneoplastic

Special

  • Nerve conduction studies
  • Genetic: PMP22 gene in CMT
  • Antibodies in paraneoplastic syndromes: anti-hu, anti-Yo
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Neurological examination: Case 3

Left Right Tone é 7 beats ankle clonus é 7 beats ankle clonus Power 3/5 in all movements 3/5 in all movements Reflexes é é Co-ordination Impaired heel-shin coordination Impaired heel- shin coordination Sensation Impaired proprioception and light touch Impaired proprioception and light touch Age: 30 Gender: female

(1)

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Question 3

Lhermitte’s sign Internuclear ophthalmoplegia Dysdiadochokinesia Fasciculations Retrobulbar optic neuritis app.bitemedicine.com Which of the following is NOT a sign seen in multiple sclerosis?

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Explanations

app.bitemedicine.com Which of following is NOT a sign seen in multiple sclerosis? Lhermitte’s sign Cervical neck flexion triggers an electric shock sensation down the spine Internuclear ophthalmoplegia Occurs due to demyelination of the medial longitudinal fasciculus (see later) Dysdiadochokinesia Cerebellar demyelination is possible in MS Fasciculations MS affects the CNS and therefore will not cause LMN pathology Retrobulbar optic neuritis MS commonly affects the optic nerve

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Neurological examination: Case 3 – Multiple sclerosis

Please present your findings?

I performed a neurological examination on this patient who has signs suggestive of MULTIPLE SCLEROSIS My main positive findings are:

  • On general inspection:
  • A walking aid by the bedside
  • A suprapubic catheter implying urinary incontinence
  • Tone appeared to be increased bilaterally with >5 beats of ankle clonus
  • Power was reduced globally bilaterally
  • Coordination was impaired as shown by impaired heel-shin coordination. This could be due to

weakness or cerebellar damage

  • Sensation showed dorsal column pathology with:
  • Impaired fine touch &
  • Impaired proprioception
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Neurological examination: Case 3 – Multiple sclerosis

Please present your findings?

My relevant negative findings are:

  • Normal pain sensation

This points towards a CNS demyelinating condition

  • Taking into account the patient’s age & gender, the most likely diagnosis would be

MULTIPLE SCLEROSIS

  • Other possible causes could include:
  • Neuromyelitis optica (Devic’s disease)
  • Transverse myelitis
  • Vit B12 deficiency with subacute combined degeneration of the cord
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Neurological examination: Case 3 – Multiple sclerosis

What are your differentials?

1. Multiple sclerosis

  • Characterised by multiple lesions in the CNS
  • Disseminated in time & space

2. Transverse myelitis

  • ACUTE inflammation of spinal cord
  • Motor weakness, sensory loss, autonomic dysfunction

3. Neuromyelitis optica (Devic’s disease)

  • ACUTE presentation of:
  • Optic neuritis + transverse myelitis
  • 4. Subacute combined degeneration of the cord
  • Due to Vit B12 deficiency
  • Neurological signs (typically brisk knee jerk and absent ankle jerk), glossitis, pallor (anaemia)
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Neurological examination: Case 3 – Multiple sclerosis

What are the signs associated with multiple sclerosis?

Multiple sclerosis is an inflammatory condition of the CNS characterised by multiple lesions disseminated in time & space as defined by the McDonald criteria Sensory

  • Loss of proprioception & fine touch (dorsal column)
  • Lhermitte’s sign (cervical cord)
  • Neck flexion causes electric shock sensation down the spine

Motor

  • Weakness

Cerebellar

  • DANISH

Autonomic signs

  • Urinary and/or fecal incontinence

Eye signs

  • Optic neuritis (optic nerve)
  • Internuclear ophthalmoplegia (Medial longitudinal fasciculus affected)

(4)

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Neurological examination: Case 3 – Multiple sclerosis

What are the different types of multiple sclerosis

  • 1. RELAPSING-REMITTING
  • Most common
  • Involves acute episodes with no disease

progression between attacks

  • 2. SECONDARY PROGRESSIVE

Starts as RR but transforms into a progressive course without acute relapses

  • 3. PRIMARY PROGRESSIVE

Symptoms gradually progress from initial onset without acute episodes or periods of remission

  • 4. PROGRESSIVE RELAPSING

Progressive disease with occasional acute episodes

(5)

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Neurological examination: Case 4 – Multiple sclerosis

How would manage this patient?

MDT approach: GP, neurology, physiotherapy, occupational therapy Conservative

  • Make patient aware of local & national support groups
  • Physiotherapy
  • Supportive: baclofen (spasticity), analgesia (neuropathic pain), catheter

Medical

  • Flare: glucocorticoids e.g. IV methylprednisolone
  • Maintenance: DMARDs e.g. interferon beta and alemtuzumab
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Neurological examination: Case 4

Left Right Tone é Lead-pipe Normal Power 5/5 5/5 Reflexes N N Co-ordination N N Sensation N N Left sided resting tremor

(6)

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Question 4

Myerson’s sign Ataxic gait Reduced facial expression Bradykinesia Cog wheeling app.bitemedicine.com Which of following is NOT a sign seen in Parkinsonism?

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Explanations

app.bitemedicine.com Which of following is NOT a sign seen in Parkinsonism? Myerson’s sign Glabellar tap does not result in attenuated blink response (see later) Ataxic gait Cerebellar pathology is not common unless the patient has a Parkinson plus syndrome Reduced facial expression Hypomimia is a sign of PD Bradykinesia A common sign in PD Cogwheeling A common sign in PD and caused by rigidity

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Neuro examination: Case 4 – Parkinson’s disease

Please present your findings?

I performed a neurological examination on this patient who has signs suggestive of PARKINSON’S DISEASE My main positive findings are:

  • On general inspection:
  • A pill roll tremor in the R hand
  • On assessment of gait:
  • Difficulty in initiating gait
  • Festinating gait (short shuffling steps)
  • Reduced arm swing
  • A tendency to stoop forward
  • Turning en bloc (multiple steps to turn around)
  • Tone appeared to be increased with lead pipe rigidity
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Neurological examination: Case 4 – Parkinson’s disease

Please present your findings?

My relevant negative findings are:

  • Normal power, reflexes, co-ordination & sensation

This points towards Parkinsonism.

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Neurological examination: Case 4 – Parkinson’s disease

Please present your findings?

My relevant negative findings are:

  • Normal power, reflexes, co-ordination & sensation

This points towards Parkinsonism.

  • Taking into account the patient’s age the most likely cause is Parkinson’s disease
  • Other causes to consider include:
  • Parkinson plus syndromes such as multi-system atrophy
  • Drug induced parkinsonism
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Neurological examination: Case 4 – Parkinson’s disease

What are the 3 classical signs of Parkinsonism?

  • Bradykinesia
  • Tremor
  • Rigidity
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Neurological examination: Case 4 – Parkinson’s disease

This patient has Parkinson’s disease. What are the other types of Parkinsonism?

Parkinson’s disease

  • Usually asymmetrical signs

Parkinson plus syndrome (usually symmetrical signs) Lewy body dementia

  • Dementia precedes parkinsonism features

Drug-induced Parkinsonism

  • Anti-psychotics e.g. chlorpromazine, metoclopramide

Multiple system atrophy Progressive supranuclear palsy Corticobasal degeneration Postural hypotension Cerebellar syndrome Vertical gaze palsy Apraxia Alien hand

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Neurological examination: Case 4 – Parkinson’s disease

What special tests can you perform to support your diagnosis of Parkinson’s disease?

Check for bradykinesia

  • Ask patient to touch their fingers to their thumb as fast as they can

Test handwriting

  • Ask the patient to draw e.g. spirals
  • Micrographia

Glabellar tap (repetitive tap on forehead)

  • Normal: blinks in response to 1st few taps
  • Parkinson’s disease: blinking persists (Myerson’s sign)

Normal Parkinson’s disease

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Neurological examination: Case 4 – Parkinson’s disease

How would manage this patient?

MDT approach: GP, neurology, physiotherapy, occupational therapy Conservative

  • Make patient aware of local & national support groups e.g. Parkinson’s UK

Medical

  • L-DOPA with a peripheral dopa decarboxylase inhibitor
  • Dopamine agonists e.g. ropinirole
  • MAO-B inhibitor e.g. selegiline
  • COMT inhibitors e.g. entacapone

Surgery (rare)

  • Deep brain stimulation e.g. subthalamic nucleus
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Top decile question

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Recap

‘Retrospective approach’

  • 1. Formulate an OSCE Cases List
  • 2. Prepare your ‘VIVA’ for those cases
  • Positive signs of diagnosis
  • ‘Typical’ findings presentation
  • Risk factors
  • Signs of decompensation
  • List of differentials
  • Complications
  • How would you investigate this patient?
  • How would you manage this patient?
  • 3. Finalise your examination routine
  • Each step of the routine
  • Signs you are looking for
  • Your speech

EXAMINATION ROUTINE PRESENTATION VIVA

  • Perform each step of the

routine confidently

  • Pick up on signs
  • Present findings

systematically

  • List appropriate

differentials based on findings

  • Answer questions

systematically

  • Explain your thinking
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SLIDE 52
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SLIDE 53
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References

  • 1. rawpixel.com / CC0
  • 2. OpenStax College / CC BY (https://creativecommons.org/licenses/by/3.0)
  • 3. Benefros at English Wikipedia / CC BY-SA (http://creativecommons.org/licenses/by-sa/3.0/)
  • 4. Samir at the English language Wikipedia / CC BY-SA (http://creativecommons.org/licenses/by-sa/3.0/)
  • 5. GetThePapersGetThePapers at English Wikipedia / Public domain
  • 6. {{PD-US}} Sir_William_Richard_Gowers_Parkinson_Disease_sketch_1886.jpg: Sir William Richard Gowersderivative

work: Beao / Public domain

All other images were acquired under the basic license from Shutterstock or made by BiteMedicine and not suitable for redistribution

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Further information

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Presenter’s contact details

  • Instagram: @arun.kiru
  • Youtube: Arun Kiru
  • Twitter: @ArunKirupakaran
  • Email: arunkiru@doctors.org.uk