Aims and Objectives

• Requires some basic knowledge of clinical examinations

• Clinical examination station (OSCE) • One way to prepare: ‘Retrospective approach’ • : 4 cases • Cranial nerves will be covered later on in the week

• Duration: 60 mins

2 Clinical examination station: how to prepare?

‘Retrospective approach’ EXAMINATION • Perform each step of the 1. Formulate an OSCE Cases List ROUTINE routine confidently • Pick up on signs 2. Prepare your ‘VIVA’ for those cases • Positive signs of diagnosis PRESENTATION • Present findings • ‘Typical’ findings presentation systematically • Risk factors • List appropriate • Signs of decompensation differentials based on findings • List of differentials • Complications VIVA • Answer questions systematically • How would you investigate this patient? • Explain your thinking • How would you manage this patient?

3 Clinical examination station: how to prepare?

‘Retrospective approach’ EXAMINATION • Perform each step of the 3. Finalise your examination routine ROUTINE routine confidently • Each step of the routine • Pick up on signs • Signs you are looking for • Your speech PRESENTATION • Present findings systematically 4. Practice your examination routine • List appropriate on friends differentials based on findings

5. Go to the wards/clinics looking for VIVA • Answer questions your cases systematically • Explain your thinking

4 Peripheral neurological examination: OSCE Cases list

What cases could come up? 1. Hemiplegia/ 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 5 How to present your findings?

I performed a cardiovascular examination on this patient If you have an idea, then • Who has signs suggestive of mitral regurgitation back yourself from the start. It gets the examiner listening My main positive findings are: 1. XXX 2. YYY

My relevant negative findings are: RELEVANT negatives 1. XXX (Risk factors) 2. YYY (Signs of decompensation) 3. ZZZ (POSSIBLE associated features)

Overall, this points towards a diagnosis of mitral regurgitation Patients will be STABLE

6 Neurological examination: Case 1 Left Right

Tone é N 7 beats of ankle (1) clonus Power ~3 in all 5/5 movements Reflexes é N

Co-ordination N N

Sensation N N

7 Question 1

Which of the below is NOT a feature of an upper motor neuron lesion?

A – B – Hoffman’s reflex C – Increased tone D – Weakness E – Spasticity

8 Question 1

Which of the below is NOT a feature of an upper motor neuron lesion?

Fasciculations

Hoffman’s reflex

Increased tone

Weakness

Spasticity

app.bitemedicine.com 9 Explanations

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

app.bitemedicine.com 10 Motor pathways (from brain à muscle) R L

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)

(2)

11 Motor pathways (from brain à muscle) R L

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

(2)

12 Upper & lower motor neurons R L

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

(2)

13 UMN vs LMN lesions

• UMN lesion means the LMN is no longer regulated • So LMN response is NOT controlled

Upper motor neuron lesion Lower motor neuron lesion Site Proximal to anterior horn synapse Distal to synapse Tone Spasticity and/or rigidity Flaccid Pronator drift Power Reduced Reduced • Upper limb: extensors weaker than flexors • Lower limb: flexors weaker than extensors Reflexes Hyporeflexia

Fasciculations Absent Present 14 Neurological examination: Case 1 Left Right

Tone é N 7 beats of ankle (1) clonus Power ~3 in all 5/5 movements Reflexes é N

Co-ordination N N

Sensation N N

15 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 16 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

17 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

18 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

19

• Ejection systolic murmur with radiation to carotids

3. Tricuspid regurgitation • Pansystolic murmur 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

20 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

Pathophysiology Location (Bamford Classification) (2) Ischaemic (85%) Total anterior circulation stroke (highest mortality) Haemorrhagic (15%) Partial anterior circulation stroke Posterior circulation stroke

Lacunar stroke

21 Neurological examination: Case Left Right 2 Tone N N

Power 4/5 on distal 4/5 on distal movements of movements of foot, otherwise foot, otherwise normal normal Reflexes N N

Co-ordination N N

Sensation Sensory loss in Sensory loss in diagram diagram

22 Question 2

Which of the following is NOT a cause of peripheral neuropathy?

Diabetes

Chronic renal failure

Muscular dystrophy

Guillain-Barré syndrome

Vitamin B12 deficiency

app.bitemedicine.com 23 Explanations

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

app.bitemedicine.com 24 Sensory pathways (from skin à brain)

2 main pathways

• Dorsal column (medial lemniscus) • Touch • Vibration • Proprioception

• Anterolateral spinothalamic tract • Pain • Temperature

25 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

26 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

27 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) (3) • Guillain-Barré syndrome (if in the acute setting) • Chronic inflammatory demyelinating polyneuropathy (more chronic)

28 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

29 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

30 Neurological examination:

CaseAge: 30 3 Left Right Gender: female Tone é é

7 beats ankle 7 beats ankle clonus clonus Power 3/5 in all 3/5 in all movements movements

Reflexes é é

(1) Co-ordination Impaired heel-shin Impaired heel- coordination shin coordination

Sensation Impaired Impaired proprioception and proprioception light touch and light touch

31 Question 3

Which of the following is NOT a sign seen in multiple sclerosis?

Lhermitte’s sign

Internuclear ophthalmoplegia

Dysdiadochokinesia

Fasciculations

Retrobulbar optic neuritis

app.bitemedicine.com 32 Explanations

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

app.bitemedicine.com 33 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 34 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

35 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)36 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) (4) • Internuclear ophthalmoplegia (Medial longitudinal fasciculus affected)

37 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)

38 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

39 Neurological examination: Case 4 Left Right

Tone é Lead-pipe Normal

Power 5/5 5/5

Reflexes N N Left sided resting Co-ordination N N

Sensation N N

(6) 40 Question 4

Which of following is NOT a sign seen in Parkinsonism?

Myerson’s sign

Ataxic gait

Reduced facial expression

Bradykinesia

Cog wheeling

app.bitemedicine.com 41 Explanations

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

app.bitemedicine.com 42 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 43 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.

44 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

45 Neurological examination: Case 4 – Parkinson’s disease What are the 3 classical signs of Parkinsonism?

• Bradykinesia • Tremor • Rigidity

46 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)

Multiple system atrophy Progressive supranuclear Corticobasal degeneration palsy

Postural hypotension Vertical gaze palsy Apraxia

Cerebellar syndrome Alien hand

Lewy body dementia • Dementia precedes parkinsonism features

Drug-induced Parkinsonism 47 • Anti-psychotics e.g. chlorpromazine, metoclopramide 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 Parkinson’s disease • Normal: blinks in response to 1st few taps • Parkinson’s disease: blinking persists (Myerson’s sign)

48 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

49 Top decile question

50 Recap ‘Retrospective approach’

1. Formulate an OSCE Cases List • Perform each step of the EXAMINATION 2. Prepare your ‘VIVA’ for those cases routine confidently ROUTINE • Pick up on signs • Positive signs of diagnosis • ‘Typical’ findings presentation • Risk factors • Present findings • Signs of decompensation PRESENTATION systematically • List appropriate • List of differentials differentials based on • Complications findings • How would you investigate this patient? • Answer questions • How would you manage this patient? VIVA systematically 3. Finalise your examination routine • Explain your thinking • Each step of the routine • Signs you are looking for • Your speech

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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

54 Further information

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