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Y4 OSCE Prep > Neurology Examination > Flashcards

Neurology Examination Flashcards

1
Q

How would you structure an examintion of a patient with PD?

A

Assess for:
postural instability
tremor
rigidity
bradykinesia

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2
Q

How should you assess tremor in a PD patient?

A

Observe (frequency, asymmetry, pill rolling?), then observe with arms outstretched
Finger-nose test: assess for intention tremor , assess for lack of coordination (MSA)
At the same time do dysdiadochokinesia test (MSA)

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3
Q

How should you assess rigidity in a PD patient?

A

tone examination of upper limbs – do slowly then quickly - spastic tone will loosen in quicker movement
then repeat tone exam while getting them to wave the other arm up and down)

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4
Q

How should you assess bradykinesia in a PD patient?

A

Piano fingers and pincer tap motion (In PD would be arrhythmic)
Foot tap (in PD would be arrhythmic)
Assess writing – micrographia and Archimedes spiral

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5
Q

How should you assess the face in a PD patient?

A

Bradykinesia facial manifestations: mask- like facies, drooling, decreased eye blinking
Assess eye movements : progressive supranuclear palsy will cause difficulty in looking down and MSA will cause nystagmus

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6
Q

How should you assess walking in a PD patient?

A

Observe for any instability when standing from sitting + offer lying and standing bp
Observe for struggling to initiate movement, shuffling gait, pedestal turning
Observe for stooped posture

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7
Q

What would be your expected findings for a patient with PD?

A

4-6 Hz asymmetrical pill rolling tremor
Cogwheel rigidity
Evidence of bradykinesia in the hands and on the face
Postural instability and stooped posture, as well as difficulty initiating movement and a shuffling gait
Normal eye movements (rules out PSN)
No nystagmus and no cerebellar signs (rules out MSA)

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8
Q

What are your ddx for a patient with PD?

A

Vascular Parkinsonism
Drug induced Parkinsonsim
Parkinson’s + : PSP, MSA

Other causes of tremor:
benign essential tremor, hyperthyroidism, anxiety

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9
Q

How would you investigate a patient with PD?

A

referral to neurology as it is a clinical diagnosis
can do lying and standing bp for autonomic involvement
could consider SPECT scan to rule out other causes

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10
Q

How would you manage a patient with PD?

A

if the motor symptoms are affecting the patient’s quality of life:levodopa
if the motor symptoms are not affecting the patient’s quality of life: dopamine agonist (bromocriptine, cabergoline), levodopa or monoamine oxidase B (MAO-B) inhibitor (selegiline)

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11
Q

Side effects of levodopa?

A

dry mouth, anorexia, palpitations, postural hypotension, psychosis

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12
Q

Side effects of dopamine agonists?

A

impulse control disorders and excessive daytime somnolence

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13
Q

What would you assess for on observation of the bedspace for a cerebellar disorder?

A

Walking aids:cerebellar disease often causes issues with balance (ataxia), resulting in patients using walking aids to steady themselves.
Hearing aids:hearing loss can be associated with pathology that may impact the cerebellum (e.g. acoustic neuroma causing local cerebellar compression).

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14
Q

How would you examine a patient with a cerbellar disorder?

A

assess gait
assess speech
eye movements
hand movements
upper limb, lower limb

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15
Q

How would you assess gait in a patient with a cerebellar disorder?

A

Ask them to walk and turn to assess for ataxia
Tandem (heel-toe) walking
Romberg’s Test

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16
Q

How would you assess speech in a patient with a cerebellar disorder?

A

Ask the patient to repeat “British constitution” and “Baby hippopotamus”

Ataxic dysarthria can present in several ways:
Scanning speech (also known as staccato speech):words are broken down into separate syllables, often separated by pauses and spoken with varying volume

Slurred speech

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17
Q

How should you asssess eye movements in soemone with a cerebellar disorder?

A

Nystagmus - specify direction (as it moves towards the lesion in cerebellar disease) and also whether it is present in vertical or horizontal gaze
Assess for intranuclear ophthalmoplegia – put up two fingers and ask them to quickly look between
Impaired smooth pursuit (eye movements are jerky when following your finger)
Dysmetric saccades (ask them to look at your hand and then back at your nose, in cerebellar lesions, there will often be overshoot)

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18
Q

How would you assess hand movements and the upper limb in someone with a cerebellar disorder?

A

Assess hand movements:
* Finger-to-nose test – assess for dysmetria and intention tremor, suggest ipsilateral cerebellar pathology
* Test for Dysdiadochokinesia
*
Assess the upper limb:
* Assess pronator drift and the rebound phenomenon (exaggerated suggests spasticity, absence suggests cerebellar disease)
* Assess tone

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19
Q

How would you assess the lower limb in someone with a cerebellar disorder?

A

Assess tone
Heel-shin test
Assess joint position sense (sensory ataxia)

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20
Q

DDx for a cerebellar disorder?

A

Paraneoplastic syndrome
Abscess/atrophy
Stroke/sclerosis (multiple sclerosis)
Trauma
Raised ICP
Infection
Ethanol and poisons
Spinocerebellar ataxia (progressive degenerative genetic disease)

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21
Q

Investigation of choice for a cerebellar disorder?

A

MRI

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22
Q

How would you inspect a patient with peripheral neuropathy?

A

Colour: Peripheral cyanosis/ pallor, haemosiderin staining
Breaks in skin barrier: Venous or arterial ulcers, gangrene
Missing limbs/ digits:amputation due to critical ischaemia
Joint deformity : e.g. Charcot arthropathy (progressive degenerationof aweight-bearing jointdue toperipheral neuropathy)
Scars, Hair loss

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23
Q

How would you examine a patient with peripheral neuropathy?

A

start by testing sensation

if glove and stocking distribution begin by working from foot upwards
soft touch , then fine touch

then repeat in dermatomal distribution

then test joint position sense and vibration sense
then test reflexes

then test tone, power and coordination

24
Q

What factors are thought to be protective against developing PD?

A

smoking
caffeine
aerobic exercise

25
Q

What factors are thought to increase risk of developing PD?

A

Family history
- particularly evident if onset of disease is in people less than 50-years-old

Previous head injury

26
Q

Describe the tremor seen in PD

A

‘Pill-rolling’ resting tremor, 4-6 hertz frequency

Usually unilateral or worse on one side than another

Exacerbated by rest, and improves when a person engages in purposeful actions

Exaggerated when the other hand is being used to do something else (can ask someone to mime painting a fence)

27
Q

How does muscle rigidity in PD manifest for the patient?

A

muscular stiffness, stooped posture, and reduced arm swing when walking

28
Q

What non-motor sxs may a patient with PD experience?

A

Depression
Sleep disturbance and insomnia
Loss of the sense of smell (anosmia)
Cognitive impairment and memory problems

29
Q

How may Parkinson’s Disease be investigated and diagnosed?

A

Usually a clinical diagnosis: UK Parkinson’s Disease Society Brain Bank Clinical Diagnostic Criteria

Investigations to differentiate from other disorders:

Single photon emission computed tomography (SPECT) to distinguish Parkinson’s disease from an essential tremor and Parkinsonism

Structural MRI to exclude structural abnormalities as the cause of the symptoms

30
Q

What is the diagnostic criteria for PD?

A

Presence of bradykinesia plus at least one of the following:
* Muscular rigidity
* Resting tremor (4-6 Hz frequency)
* Postural instability (not caused by a visual, vestibular, cerebellar or proprioceptive dysfunction)

31
Q

What are the similarities and differences between Multiple System Atrophy and PD?

A

Similarities:
Both may initially present with Parkinsonian features
Both may respond to levodopa therapy
Both have an element of autonomic dysfunction (although more pronounced in MSA)

Differences:
In MSA, there is usually cerebellar involvement, which is part of the exclusion criteria for Parkinson’s disease
Cognition is well preserved in MSA

32
Q

How can drug-induced Parkinsonism be differentiated from PD?

A

Can be distinguished via a thorough medication history

Other movement disorders also caused by these drugs can help differentiate, such as akathisia, tardive dyskinesia and acute dystonia

Usually causes symmetrical symptoms (PD is asymmetrical)

33
Q

How can vascular Parkinsonism be differentiated from PD?

A

Usually can be identified via a thorough history and radiological findings
Probably step-wise progression rather than continuous

34
Q

What may cause secondary Parkinsonism?

A

Drug induced: Anti-psychotics and anti-emetic drugs which act via dopaminergic antagonism

Vascular: due to multiple infarcts affecting the basal ganglia

35
Q

What is the main side effect of prolonged use of dopamine agonists?

A

Pulmonary fibrosis

36
Q

What can be used to manage dyskinesia associated with levodopa?

A

Amantadine - a glutamate antagonist

37
Q

What can be used as an adjuvant to medical therapy for PD?

A

Deep brain stimulation- if sxs not controlled by medication

Physio
Speech therapy
Occupational therapy

38
Q

What antibodies are usually found in patients with myasthenia?

A

Acetylcholine receptor (AChR) antibodies

39
Q

How can you elicit fatiguability in the muscles when examining for myasthenia gravis?

A

Repeated blinking will exacerbate ptosis
Prolonged upward gazing will exacerbate diplopia on further testing
Repeated abduction of one arm 20 times will result in unilateral weakness when comparing both sides

40
Q

What should you look for on examination of Myasthenia gravis?

A

Check for a thymectomy scar
Test the forced vital capacity (FVC)

41
Q

How can Myasthenia gravis be investigated?

A

Antibody testing:
AChR antibodies (around 85%)
MuSK antibodies (less than 10%)
LRP4 antibodies (less than 5%)

A CT or MRI of the thymus gland is used to look for a thymoma.

The edrophonium test can be helpful where there is doubt about the diagnosis

42
Q

How can Myasthenia Gravis be managed?

A

Long acting acetylcholinesterase inhibitor (Pyridostigime) that prolongs the action of ACh and improves symptoms

Immunosuppression (e.g., prednisolone or azathioprine) suppresses the production of antibodies

Thymectomy can improve symptoms, even in patients without a thymoma

Rituximab (a monoclonal antibody against B cells) is considered where other treatments fail

43
Q

How can diabetic neuropathy be managed?

A

first-line treatment: amitriptyline, duloxetine, gabapentin or pregabalin

tramadol may be used as ‘rescue therapy’ for exacerbations of neuropathic pain

pain management clinics may be useful in patients with resistant problems

44
Q

Give some causes of peripheral neuropathy with predominately motor loss

A

Guillain-Barre syndrome
Charcot-Marie-Tooth
diphtheria
porphyria
lead poisoning
chronic inflammatory demyelinating polyneuropathy (CIDP)

45
Q

Give some causes of peripheral neuropathy with predominately sensory loss

A

diabetes
alcoholism
vitamin B12 deficiency
amyloidosis
uraemia
leprosy

46
Q

How does B12 deficiency cause peripheral neuropathy?

A

subacute combined degeneration of spinal cord
dorsal column usually affected first (joint position, vibration) prior to distal paraesthesia

47
Q

What is Charcot-Marie Tooth Disease?

A

the most common hereditary peripheral neuropathy

usually autosomal dominant, results in predominantly motor loss

sxs usually start to appear before the age of 10 but can be delayed until 40 or later

48
Q

Give some causes of peripheral neuropathy

A

A – Alcohol
B – B12 deficiency
C – Cancer (e.g., myeloma) and Chronic kidney disease
D – Diabetes and Drugs (e.g., isoniazid, amiodarone, leflunomide and cisplatin)
E – Every vasculitis

49
Q

What features does Charcot-Marie Tooth present with?

A

Distal muscle weakness and atrophy
There may be a history of frequently sprained ankles
Foot drop (due to weakness of ankle dorsiflexion)
High-arched feet (pes cavus)
Hammer toes
Hyporeflexia
Stork leg deformity

50
Q

How can Charcot-Marie Tooth disease be managed?

A

there is no cure

Analgesia for neuropathic pain (e.g., amitriptyline)
Physiotherapy to maintain muscle strength and joint range of motion
Occupational therapy
Podiatry input for insoles and orthoses to improve symptoms
Orthopaedic surgery for severe joint deformities

51
Q

Bell’s palsy may be defined as an acute, unilateral, idiopathic, facial nerve paralysis.

Who does it most commonly present in?

A

peak incidence is 20-40 years and the condition is more common in pregnant women

52
Q

What features does Bell’s palsy present with?

A

lower motor neuron facial nerve palsy → forehead affected (in contrast, an upper motor neuron lesion ‘spares’ the upper face)

patients may also notice:
post-auricular pain (may precede paralysis)
altered taste
dry eyes
hyperacusis

53
Q

How can Bell’s palsy be managed?

A

commence on a course of prednisolone (if present within 72 hours of onset) and give eye care advice

Eye care is important in Bell’s palsy - drops, lubricants and night time taping should be considered to prevent exposure keratopathy

54
Q

How should Bell’s palsy be followed up?

A

if the paralysis shows no sign of improvement after 3 weeks, refer urgently to ENT

most people with Bell’s palsy make a full recovery within 3-4 months

if untreated around 15% of patients have permanent moderate to severe weakness

55
Q

Give some lower motor neurone causes of facial nerve palsy

A

Bell’s palsy
Ramsay-Hunt syndrome (due to herpes zoster)
acoustic neuroma
parotid tumours
HIV
diabetes mellitus

56
Q

How should you examine a patient with suspected Bell’s palsy?

A

Start by testing the facial nerve (CN7):
* ask to raise their eyebrows, screw their eyelids tightly shut and resist opening, smile, and blow air into their cheeks and resist it being pushed out
* ask if they have noticed any change in their taste

Test trigeminal nerve (CN5)
* Test sensation in all three divisions
* Ask to clench teeth and palpate temporalis and masseter muscle
* Ask to move the jaw from side to side

Test Vestibulocochlear (CN8)
* Before you start ask if they have noticed any new rashes around their ear and show that you are looking at the peri-auricular region
* Whisper a number in each ear with other ear covered and ask them to repeat
* Carry out Weber and Rinne’s tests
* Say that you would also like to perform otoscopy (if they have any ear pain)

Check eyes
* Quickly do pupillary responses and eye movements
* Ask if there has been any change in vision and dry eyes

Assess gait - balance issues and weakness

57
Q

How would you investigate a patient with peripheral neuropathy?

A

FBC, U&Es, LFTs (alcohol) B12, folate
blood glucose, Hba1c
Nerve conduction studies
Medication review

Y4 OSCE Prep (20 decks)

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