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Yr 3 - Core Conditions > Neurology > Flashcards

Neurology Flashcards

1
Q

Define a stroke

A

A clinical syndrome of presumed vascular origin characterised by rapidly developing signs of focal and global disturbance of cerebral functions which lasts longer than 24 h OR leads to death.

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2
Q

What are the 2 main type of stroke?

A
  1. Ischaemic
  2. Haemorrhagic
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3
Q

What is the mechanism behind an ischaemic stroke?

A

Reduction or complete blockage of blood supply to a part of the brain, resulting in tissue hypoperfusion

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4
Q

What is the mechanism behind a haemorrhagic stroke?

A

Occurs 2ary to a rupture of a blood vessel (usually arterioles and small arteries) or rupture of an abnormal vascular structure within the brain.

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5
Q

What are the 5 main causes of an ishcaemic stroke?

A
  1. Embolism
  2. Thrombus
  3. Small vessel disease
  4. Systemic hypoperfusion
  5. Cerebral venous sinus thrombosis
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6
Q

How can a thrombus lead to a stroke?

A

due to rupture of plaque within cerebral vessel

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7
Q

How can an embolus lead to a stroke?

A

causes blockage of cerebral vessel

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8
Q

How can small vessel disease lead to ischaemic stroke? What is the most common cause of this?

A

Chronic hypertension causes changes in the small vessels of the brain - middle layer of the vessel (tunica media) becomes enlarged and causes narrowing/occlusion of the vessels.

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9
Q

How can systemic hypoperfusion lead to stroke?

A

Supply to entire brain is reduced 2ary to systemic hypotension e.g. in cardiac arrest

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10
Q

How can cerebral venous sinus thrombosis lead to stroke?

A

Blood clots form in veins that drain the brain resulting in venous congestion and tissue hypoxia

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11
Q

Is ishcaemic or haemorrhagic stroke more common?

A

Ischaemic (85%)

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12
Q

What are some causes of haemorrhagic stroke?

A

Hypertension

Trauma

Bleeding disorders

Illicit drug use

Vascular malformations

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13
Q

What are the 2 types of haemorrhagic stroke?

A
  1. Intracerebral haemorrhage
  2. Subarachnoid haemorrhage
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14
Q

Location of intracerebral vs subarachnoid haemorrhage

A

Intracerebral → bleeding within brain (intraparenchymal and/or intraventricular)

Subarachnoid → bleeding outside of brain tissue between the pia mater and arachnoid mater

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15
Q

Cause of intracerebral vs subarachnoid haemorrhage?

A

Intracerebral → hypertension

Subarachnoid → rupture of intracranial saccular aneurysm, anticoagulants, arterial dissections

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16
Q

What is a silent stroke?

A

Radiological or pathological evidence of an infarction or haemorrhage not caused by trauma that doesn’t cause any noticeable symptoms

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17
Q

Incidence of strokes in UK per year?

A

130,000 strokes every year in UK – 100,000 first time strokes and 30,000 recurrent events (once a person has had a stroke/TIA, they are at high risk of a further vascular event)

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18
Q

What is the leading cause of death and disability in the UK?

A

Strokes

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19
Q

Risk factors differ slightly for ischaemic vs haemorrhagic stroke. Give some risk factors for each:

A
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20
Q

Is being male a risk factor for haemorrhagic or ischaemic stroke?

A

Haemorrhagic

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21
Q

Are anticoagulants a risk factor for haemorrhagic or ischaemic stroke?

A

Haemorrhagic

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22
Q

Is AF a risk factor for haemorrhagic or ischaemic stroke?

A

Ischaemic

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23
Q

What test is used for the rapid assessment of potential stroke patients?

A

FAST

  • Facial weakness - Can the person smile? Has their face fallen on one side?
  • Arm weakness - Can the person raise both arms and keep them there?
  • Speech problems - Can the person speak clearly and understand what you say? Is their speech slurred?
  • Time to call 999
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24
Q

Describe the scoring steps of the Glasgow Coma Scale

A

Eye opening:

  • 4 - spontaneous
  • 3 - to voice
  • 2 - to pressure
  • 1 - none

Motor response:

  • 6 - obeying commands
  • 5 - localises to pain
  • 4 - normal flexion (withdraws from pain)
  • 3 - abnormal flexion (flexes to pain)
  • 2 - extension (extends to pain)
  • 1 - none

Verbal response:

  • 5 - orientated
  • 4 - confused
  • 3 - inappropriate words
  • 2 - sounds
  • 1 - none

Out of 15, cannot score <3

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25
Q

Give some potential differentials for a stroke

A
  • Hypoglycaemia
  • Drugs & alcohol toxicity
  • Seizure
  • Migraine with aura
  • Demyelination (e.g. multiple sclerosis)
  • Peripheral neuropathies (e.g. Bell’s palsy)
  • Trauma
  • Systemic or local infection e..g sepsis, encephalitis, CNS abscess
  • Tumour
  • Dementia
  • Subdural haematoma
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26
Q

Give some signs and symptoms of a stroke

A

Sudden onset of focal neurological symptoms cannot be explained by another conditions (e.g. hypoglycaemia):

  • Unilateral weakness (arm > leg)
  • Numbness
  • Unilateral sensory loss
  • Speech disturbance - expressive dysphasia
  • Ataxia
  • Dysphagia
  • Reduced level of consciousness e.g. confusion, syncope
  • Pain
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27
Q

Bell’s palsy vs stroke:

A

Bell’s palsy → cannot raise eyebrow (i.e. upper AND lower unilateral facial paralysis)

Stoke → can raise eyebrow

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28
Q

What are some symptoms of a posterior stroke

A
  • Nystagmus
  • Vertigo
  • N&V
  • Head motion intolerance
  • New gait unsteadiness
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29
Q

What is the 1st line (diagnostic) investigation for a stroke?

A

Head CT

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30
Q

In suspected strokes, a head CT should be performed immediately (within 1 hour) for people with which presentations? If none of these criteria are met, when should a CT head be performed?

A
  • Indications for thrombolysis or early anticoagulation treatment
  • On anticoagulation treatment
  • A know bleeding tendency
  • A depressed level of consciousness (GCS <13)
  • Unexplained progressive or fluctuating symptoms
  • Papilloedema, neck stiffness or fever
  • Severe headache at onset of stroke symptoms

If none of the above – scan within 24 hours

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31
Q

What bedside investigations should be done in a suspected stroke?

A
  • 12-lead ECG - rule out arrhythmia (e.g. AF)
  • Blood glucose - rule out hypoglycaemia
  • Hydration status
  • Swallow assessment
  • CVS & focused neuro exam
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32
Q

What lab investigations should be done in a suspected stroke?

A
  • FBC
  • U&Es
  • LFTs
  • Calcium
  • Specific to stroke:
    • Plasma viscosity
    • Cholesterol level
    • CRP
    • Clotting profile
    • HbA1c
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33
Q

What imaging should be considered in stroke?

A
  • CT head
  • CXR
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34
Q

Why can a CXR be beneficial in stroke?

A

look for aspiration pneumonia if stroke has affected swallowing

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35
Q

What management steps should be taken while awaiting confirmation of diagnosis?

A
  • Avoidance of antiplatelet treatment until haemorrhagic stroke has been excluded!
  • Manage ABCDEs and give O2 while waiting
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36
Q

Management of ischaemic stroke?

A
  • Thrombolysis → Alteplase
  • Aspirin 300mg orally (or 600mg PR) ASAP (provided intracranial haemorrhage excluded)
  • Thrombectomy
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37
Q

Should anticoagulants be given in an acute ischaemic stroke?

A

Anticoagulants are not recommended as an alternative to antiplatelet drugs in acute ischaemic stroke in patients who are in sinus rhythm.

However, parenteral anticoagulants may be indicated in patients who are symptomatic of, or at high risk of developing, deep vein thrombosis or pulmonary embolism.

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38
Q

What is the main drug used in thrombolysis?

A

Alteplase

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39
Q

When should alteplase be given in stroke?

A

if within 4.5 hours and intracranial haemorrhage has been excluded (CT head)

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40
Q

Once patient has been moved to stroke unit, further investigations & management plans can be carried out for other risk factors.

How can carotid stenosis be assessed? What is the management?

A
  • Carotid dopplers - only done if fit for interventions
  • Carotid endarterectomy within 2 weeks of neurological event achieves maximum stroke prevention
  • Narrowing (stenosis) of internal carotid artery of 50-99% → refer urgently to vascular surgery
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41
Q

What is a carotid endarterectomy?

A

Carotid endarterectomy is a surgical procedure to remove a build-up of fatty deposits (plaque), which cause narrowing of a carotid artery.

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42
Q

Management of a haemorrhagic stroke?

A
  • Manage on stroke unit
  • Ensure anticoagulants/antiplatelets are stopped
  • Does anticoagulation need reversal?
  • Manage hypertension – target 140-160 mmHg systolic
  • Assess swallow and manage hydration
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43
Q

Circle of willis:

A
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44
Q

Vascular territories:

A
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45
Q

Functional areas of the brain:

A
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46
Q

Visual disturbances:

A
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47
Q

Which visual disturbance will a MCA stroke typically cause?

A

will usually cause contralateral homonymous hemianopia (i.e. left sided MCA will causes right-sided homonymous hemianopia).

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48
Q

Bamford stroke classification:

A
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49
Q

What is a transient ishcaemic attack (TIA)?

A

It is a transient (less than 24 hours, typically 30 minutes) period of neurological dysfunction without evidence of acute infarction.

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50
Q

How does a TIA differ from a stroke (signs & symptoms wise)?

A

Same signs & symptoms BUT completely resolves within 24 hours of onset

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51
Q

Investigations for TIA?

A

Same as stroke

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52
Q

Immediate management for TIA?

A
  • Aspirin 300mg immediately unless contraindicated
    • Give PPI to anyone with dyspepsia associated with aspirin use
  • Specialist assessment
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53
Q

What is a subarachnoid haemorrhage?

A

Bleeding into the subarachnoid space of the brain, located between the arachnoid and pia mater meningeal layers

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54
Q

What are some causes of a SAH?

A
  • Traumatic injury e.g. road traffic collision
  • Ruptured intracranial aneurysm - most common
  • Arteriovenous malformation (AVM)
  • SAH of unknown aetiology
  • Rare disorders
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55
Q

Give some risk factors for a SAH

A
  • Hypertension
  • Smoking
  • Family history
  • Autosomal dominant polycystic kidney disease (ADPKDO)
  • Age >50 y/o
  • Female sex (1.5x)
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56
Q

Prognosis of a SAH?

A
  • Life-threatening conditions which can damage the brain through hypoxia, raised intracranial pressure and direct cranial injury
  • Death rate 40-60%
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57
Q

Potential complications of a SAH?

A

Permanent neurological disabilities, coma, death

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58
Q

What headache is typically described with a SAH?

A

Sudden onset severe headache, reaching maximum intensity within seconds (‘thunderclap headache’).

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59
Q

Symptoms of a SAH?

A
  • Thunderclap headache (establish time to max intensity)
  • N&V
  • Photophobia
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60
Q

A reduced level of consciousness may be present with a SAH. Why?

A

can occur 2ary to raised intracranial pressure

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61
Q

Neck stiffness may be present with a SAH. Why?

A

2ary to meningeal infection

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62
Q

What is Kernig’s test? Purpose?

A

A test used in physical examination to look for evidence of irritation of the meninges.

The inability to extend the knee due to pain when the patient is supine, and the hip and knee are flexed to 90 degrees

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63
Q

What is a positive Kernig’s sign caused by?

A

A positive Kernig’s sign is caused by irritation of motor nerve roots passing through inflamed meninges as they are under tension.

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64
Q

What conditions may a positive Kernig’s sign be seen in?

A
  • Meningits - bacterial, viral
  • SAH
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65
Q

What imaging should be done in a suspected SAH?

A
  • CT head scan
  • CT angiogram
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66
Q

When would a lumbar puncture be indicated in SAH?

A

only necessary if SAH is suspected but CT scan does NOT show any evidence of bleeding or raised intracranial pressure

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67
Q

Management of SAH?

A

ABCDE Assessment:

  • Airway – patients with reduced level of consciousness are at risk of occluding their airway (may require intubation)
  • Breathing – record RR and SpO2
  • Circulation:
    • Record BP and pulse
    • May require IV fluids to maintain BP
    • May require electrolyte replacement (hyponatraemia common in SAH)
    • Calcium channel blockers (e.g. nimodipine) must be given to reduced cerebral artery spasm and 2ary cerebral ischaemia
  • Disability:
    • Assess GCS – if <8, requires anaesthetic input
    • Invasive ICP monitory if GCS deteriorates
  • Exposure - assess for trauma
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68
Q

Define peripheral neuropathy

A

A general term for any disorder affecting the peripheral nerves

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69
Q

Motor vs sensory peripheral neuropathy?

A

Motor → Damage to the peripheral nerves responsible for motor functions (e.g. foot drop) - a solely motor neuropathy is relatively uncommon

Sensory → Damage to the peripheral nerves responsible for causing symptoms of weakness, numbness, and pain.

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70
Q

What is the prototypical example of a solely motor neuropathy?

A

Progressive muscular atrophy (the LMN variant of motor neuron disease).

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71
Q

Give some causes of motor peripheral neuropathy

A
  • Guillain Barre syndrome
  • Hereditary motor neuropathies
  • Acute intermittent porphyria
  • Lead poisoning
  • Paraneoplastic syndrome
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72
Q

What are causes of sensory peripheral neuropathy (ABCDE)?

A
  • Alcohol toxicity
  • B12/folate deficiency
  • Chronic renal disease
  • Diabetes mellitus (T1 & T2)
  • Everything else e.g. vasculitis, paraneoplastic, viral infection
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73
Q

In what distribution does sensory peripheral neuropathy typically present?

A

Glove and stocking → with foot involvement preceding hand involvement

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74
Q

How common are peripheral neuropathies in the UK?

A

Almost 1 in 10 people aged 55 or over in UK

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75
Q

Mononeuropathy vs polyneuropathy?

A

Mononeuropathy refers to damage of a single nerve, whereas polyneuropathy refers to damage of multiple nerves

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76
Q

Is mono or polyneuropathy more common?

A

Poly

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77
Q

What is the most common cause of peripheral neuropathy in the UK?

A

Diabetes

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78
Q

What is the most common mononeuropathy?

A

Carpal tunnel syndrome

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79
Q

What is the most common cause of mononeuropathies?

A

Physical injury/trauma is most common cause e.g. repetitive movements

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80
Q

What causes carpal tunnel syndrome?

A

It results from pressure on the median nerve, which passes through the carpal tunnel.

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81
Q

How does carpal tunnel syndrome present?

A

Numbness, tingling, unusual sensations, pain in first 3 fingers on thumb side, worse at night, difficulty performing actions, weakness.

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82
Q

Presentation of carpal tunnel syndrome vs ulnar nerve palsy?

A

Carpal → pain in first 3 fingers on thumb side

Ulnar → numbness in 4th and 5th digit

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83
Q

Fracture of the humerus can lead to palsy of which nerve?

A

Radial

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84
Q

What is the classic presentation of peroneal nerve palsy?

A

Foot drop

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85
Q

Give the 4 most common causes of polyneuropathy

A
  1. Diabetes
  2. Alcohol
  3. Poor nutrition (B12/folate)
  4. Guillain-Barre syndrome
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86
Q

Complications of peripheral neuropathy?

A
  • Foot ulcers
  • Gangrene
  • Hypertension
  • Arrhythmias
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87
Q

Prognosis of peripheral neuropathy?

A
  • Curative treatment often rare
  • Often progressive
  • Prognosis dependent on underlying cause & which nerves are damaged
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88
Q

What are the 3 categories of the PNS?

A
  1. Motor
  2. Sensory
  3. Autonomic
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89
Q

Do symptoms of peripheral neuropathy usually begin in the hands or feet?

A

Feet

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90
Q

Describe the presentation of symptoms of motor peripheral neuropathy (i.e. proximal or distal, extensor or flexor)?

A

Distal weakness of muscles

Typically involves extensor groups rather than flexor groups of muscles (think foot drop).

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91
Q

Describe the presentation of symptoms of sensory peripheral neuropathy

A
  • Gradual onset of distal dysesthesia, pain and numbness in hands or feet → ‘Glove and stocking pattern’ is characteristic
  • Sharp, stabbing, throbbing or burning
  • Distal loss of pin, temperature and vibration perception
  • Loss of proprioception
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92
Q

Describe ‘glove and stocking pattern’

A

The distal portions of the nerves are affected first (pattern occurs due to length of axon)

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93
Q

Describe the presentation of symptoms of autonomic peripheral neuropathy

A
  • Orthostasis / posutral hypotension
  • Impotence in males
  • Gastroparesis
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94
Q

Describe the signs present in sensory peripheral neuropathy

A
  • Distal loss of pin, temperature and vibration perception
  • Loss of proprioception
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95
Q

Describe the signs present in motor peripheral neuropathy

A

Note - this is a LMN disease:

  • Muscle wasting
  • Fasciculations
  • Tremors
  • Reduced muscle tone (hypotonia)
  • Distal weakness in peripheral neuropathy
  • Hyporeflexia or areflexia e.g. absent ankle jerks
  • Wasting and fasciculation of muscles
  • Hypomimia (Parkinson’s)
  • Ophthalmoplegia (MS, myasthenia gravis)
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96
Q

Describe the signs present in autonomic peripheral neuropathy

A
  • Orthostatic hypotension
  • Sweating problems
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97
Q

What bedside investigations should be conducted in peripheral neuropathy?

A
  • Obs
  • Urinalysis
  • Blood glucose
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98
Q

What lab investigations should be conducted in peripheral neuropathy?

A

FBC, B12, TFTs, ANA & rheumatoid factor, HbA1c, cholesterol, ESR & CRP

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99
Q

Why may a CXR be indicated in peripheral neuropathy?

A

For asymptomatic lung cancer that can cause a purely sensory neuropathy.

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100
Q

What type of peripheral neuropathy would asymptomatic lung cancer present as?

A

Purely sensory

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101
Q

Nerve conduction studies that can be carried out in peripheral neuropathy. What would show in demyelinating neuropathies vs axonal neuropathies?

A

Demyelinating → slower conduction velocities or even conduction block

Axonal → reduced amplitude of compound motor or sensory nerve action potentials

102
Q

What is the pharmacological management for peripheral neuropathies?

A
  • Corticosteroids
  • Immunosuppressants
103
Q

What is Guillain-Barre syndrome?

A

An ascending inflammatory demyelinating polyneuropathy.

104
Q

Causes of Guillain-Barre?

A
  • Typically 1-3 weeks after infection (e.g. Campylobacter, mycoplasma, EBV).
  • 40% of cases are idiopathic
105
Q

Presentation of Guillain-Barre?

A
  • Progressive ascending symmetrical limb weakness (affecting the lower limbs first)
    • Paraesthesia may precede the onset of motor symptoms
  • Respiratory muscles can be affected in severe cases
  • LMN signs in lower limbs:
    • Hypotonia
    • Flaccid paralysis
    • Areflexia
106
Q

How do seizures differ from epilepsy?

A

Seizures are individual** occurrences of abnormal electrical activity in the brain. Epilepsy is a **chronic neurological disorder that causes repeated seizure activity.

107
Q

What is a seizure?

A

Seizures are transient episodes abnormal electrical activity in the brain.

108
Q

How does a generalised seizure differ from a focal seizure?

A

Generalised → Affecting entire brain

Focal → Involving subsection of brain

109
Q

What are the subtypes of generalised seizures?

A
  • Tonic
  • Tonic-clonic
  • Atonic
  • Myoclonic
  • Absence
110
Q

What is the most common type of generalised seizure?

A

Tonic clonic → most common where patient falls to ground stiff (tonic phase) followed by series of rhythmic jerks (clonic phase)

111
Q

What is ‘2ary generalisation’ of a seizure?

A

Starts focal → localises to entire brain

112
Q

How are focal seizures classified?

A

Subclassified on clinical features (part of brain they involve)

113
Q

How long do generalised tonic clonic seizures last?

A

Sudden onset, typically lasts <5 minutes

114
Q

Give some features of a tonic clonic seizure (during and after)

A
  • Loss of consciousness and tonic (muscle tensing) and clonic (muscle jerking) movements
  • During:
    • Lateral tongue biting
    • Urinary incontinence
  • After:
    • Post-ictal confusion (though may recall onset, especially if 2ary generalised)
    • May be left with residual focal neurological deficit (Todd’s Paresis)
115
Q

What is Todd’s Paresis?

A

Todd’s paralysis is a neurological condition experienced by individuals with epilepsy, in which a seizure is followed by a brief period of temporary paralysis

116
Q

Who are absence seizures most common in?

A

Children (but 90% will grow out of them)

117
Q

How do absence seizures present?

A
  • Patient becomes blank, stares into space and then abruptly returns to normal
  • During episode, they are unaware of surroundings and won’t respond
  • Typically last only 10-20 seconds
118
Q

Differentials of a seizure?

A
  • Syncope (vasovagal, arrhythmogenic)
  • Pseudoseizures
119
Q

Define epilepsy

A

An umbrella term for a condition where there is a tendency to have seizures. A diagnosis of epilepsy is made by a specialist based on the characteristics of the seizure episodes.

120
Q

What is the main investigation used to diagnose epilepsy?

A

Electroencephalogram (EEG)

121
Q

What does an EEG do?

A

n this test, electrodes are attached to your scalp with a paste-like substance or cap. The electrodes record the electrical activity of your brain.

122
Q

What other investigations should be done in epilepsy to rule out other pathologies?

A
  • ECG (e.g. AF)
  • MRI brain (tumours)
  • Blood electrolytes: Na, K, Ca, Mg
  • Blood glucose (rule out hypoglycaemia, diabetes)
  • Blood cultures, urine cultures, lumbar puncture (meningitis, sepsis, encephalitis)
123
Q

What is the 1st line drug choice for tonic clonic seizures?

A

Sodium valproate

124
Q

What is the 2nd line drug choice for tonic clonic seizures?

A

Lamotrigine or carbamazepine

125
Q

What is the 1st line drug choice for focal seizures?

A

Lamotrigine or carbamazepine (opposite of tonic clonic)

126
Q

What is the 2nd line drug choice for focal seizures?

A

Sodium valproate (or levetiracetam)

127
Q

What is the 1st line drug choice for absence seizures?

A

Sodium valproate (or ethosuximide)

128
Q

Which 2 anti-epileptics should be monitored carefully due to their interactions with other drugs?

A

Phenytoin and carbamazepine (inducers of the P450)

129
Q

Are anti-epileptics safe during pregnancy?

A

No - teratogenic (lamotrigine is a good choice for women of childbearing age)

130
Q

Define status epilepticus

A

A seizure lasting >5 minutes or multiple seizures within a 5-minute period with incomplete resolution.

131
Q

Complications of status epilepticus

A

Medical emergency, may lead to permanent brain damage or death.

132
Q

Management of patients with status epilepticus?

A

ABCDE approach

  • A – Secure airway
  • B:
    • Check O2 sats  give high-concentration O2
    • Check respiratory function (RR etc)
    • ABG
  • C:
    • Assess cardiac function
    • Gain IV access (insert cannula)
    • Routine venous bloods: FBC, U&Es, LFTs, CRP, calcium and magnesium, clotting
  • D:
    • Check blood glucose levels
    • Gain IV access (inset cannula)
    • IV lorazepam → repeated after 10 minutes if seizure continues
  • If seizure persists, the final step is infusion of IV phenobarbital or phenytoin:
    • Intubation required
    • Transfer to intensive care
133
Q

What drug should be given in status epilepticus?

A

IV lorazepam

134
Q

Define Parkinsonism

A

Umbrella term for the clinical syndrome involving bradykinesia with at least one of the following: rigidity, tremor, and postural instability.

135
Q

What are the differentials for parkinsonism?

A
  • Idiopathic Parkinson’s disease (this is the prototypical) parkinsonian syndrome
  • Multiple system atrophy (MSA)
  • Dementia with Lewy Bodies:
  • Progressive supranuclear palsy (PSP)
  • Vascular Parkinsonism
  • Drugs
  • Wilson’s disease
136
Q

How could vascular parkinsonism differ from Parkinson’s disease?

A

Vascular tends to be tremor negative and localised to lower limbs

137
Q

Which drugs can lead to parkinsonism?

A

Antipsychotics and metoclopramide (dopamine antagonist)

138
Q

What class of drug is metoclopramide?

A

Antiemetic → Dopamine antagonist

139
Q

What is the most common neurodegenerative condition in the UK?

A

Alzheimer’s

140
Q

What is the pathophysiology of Parkinson’s disease?

A

Progressive loss of dopaminergic neurons in the substantia nigra of the basal ganglia → the fall in dopamine levels results in symptoms.

141
Q

What is the function of basal ganglia structures?

A

.Basal ganglia structures are responsible for coordinating habitual movements (e.g. walking, looking around), controlling voluntary movements and learning specific movement patterns.

142
Q

What is the function of dopamine?

A

Dopamine is a neurotransmitter produced by the substantia nigra which transmits signal from the substantia nigra to other parts of the basal ganglia via the nigrostriatal pathways (these pathways control smooth, purposeful movement)

143
Q

What are the 3 cardinal features of Parkinson’s dsiease?

A
  1. Resting tremor
  2. Rigidity
  3. Bradykinesia
  4. (postural instability)
144
Q

How is the tremor seen in Parkinson’s often described as?

A

‘Pill rolling tremor’ – looks like patient is rolling a pill between their fingertips and thumb

145
Q

Is a pill rolling tremor more pronounced on rest or movement?

A

More pronounced when resting and improves on voluntary movement

Tremor worsened if patient is distracted (e.g. asking patient to do a task with the other hand)

146
Q

Is the tremor seen in Parkinson’s disease symmetrical or asymmetrical?

A

Asymmetrical (can help differentiate from other forms of Parkinsonism)

147
Q

Frequency of Parkinson’s disease tremor?

A

Occur at frequency of 4-6 Hz (occurs 4-6 times a second)

148
Q

What 2 types of rigidity can be seen in Parkinson’s disease?

A
  1. Lead pipe
  2. Cog-wheel
149
Q

Describe cogwheel rigidity

A

If you take their hand and passively flex and extend their arm at the elbow, you will feel a tension in their arm that gives way to movements in small increments (like little jerks) → i.e. jerky movement

150
Q

Describe lead pipe rigidity

A

stiffness continues throughout the movement

151
Q

What is cogwheel rigidity caused by?

A

tremor superimposed on hypertonia

152
Q

Give some presentations of bradykinesia in Parkinson’s disease

A
  • Slowness in initiation of voluntary movement
  • Reduction in speed during repetitive actions
  • Shuffling gate – small steps when walking
  • Difficulty turning, have to take lots of little steps
  • Reduced facial movements and expressions (hypomimia)
  • Handwriting gets smaller and smaller (classic presenting complaint in exams)
153
Q

How may postural instability in Parkinson’s disease present?

A
  • Poor balance
  • Difficulty going from sitting to standing
  • Gait
  • Frequent falls
154
Q

Some other motor signs of Parkinson’s disease:

A
  • Reduced blink rate
  • Hypomimia (expressionless face)
  • Hypophonia (quiet speech)
  • Drooling
  • Micrographia (reduction in size of handwriting) – draw out spiral and ask them to draw one next to it
  • Reduced arm swing
  • Festination – tendency to pick up speed as patient travels in a particular direction (resulting in shuffling gait)
  • Freezing (e.g. when walking through a doorway)
155
Q

Some non-motor signs of Parkinson’s disease:

A
  • Depression
  • Sleep disturbance and insomnia
  • Loss of sense of smell (anosmia)
  • Cognitive impairment and memory problems
  • Hallucinations
  • Falls
156
Q

Some autonomic signs of Parkinson’s disease:

A
  • Weight loss
  • Dysphagia
  • Constipation
  • Orthostatic hypotension
  • Drooling
157
Q

A common exam task challenges you to distinguish between the tremor of Parkinson’s disease and a benign essential tremor:

A
158
Q

Parkinson’s tremor vs benign essential tremor → symmetry

A

P → asymmetrical

BET → symmetrical

159
Q

Parkinson’s tremor vs benign essential tremor → frequency

A

P → 4-6 Hz

BET → 5-8Hz

160
Q

Parkinson’s tremor vs benign essential tremor → affected by rest

A

P → worse at rest

BET → improves at rest

161
Q

Parkinson’s tremor vs benign essential tremor → intentional movement

A

P → improves

BET → worse

162
Q

Parkinson’s tremor vs benign essential tremor → alcohol

A

P → no change with alcohol

BET → improves with alcohol

163
Q

How does alcohol affect a benign essential tremor?

A

Improves it

164
Q

Diagnosis of Parkinson’s disease?

A

Clinical diagnosis using UK Parkinson’s disease brain bank criteria:

  • Bradykinesia plus at least one of:
    • Rigidity
    • Tremor
    • Postural instability
165
Q

What is the 1st line pharmacological treatment for Parkinson’s disease?

A

Levodopa

166
Q

What 2 drugs can levodopa often given alongside?

A
  1. Carbidopa (co-careldopa = levodopa + carbidopa)
  2. Benserazide (co-benyldopa = levodopa + benserazide)
167
Q

Why is levodopa given alongside carbadopa or benserazide?

A

These drugs are peripheral decarboxylase inhibitors i.e. stop levodopa being broken down in the body before it gets the chance to enter the brain

168
Q

What is the main side effect of levodopa?

A

Dyskinesia

169
Q

Define meningitis

A

Inflammation of the meninges.

170
Q

Define meningococcus

A

Neisseria meningitidis bacteria.

171
Q

Define meningococcal septicaemia

A

When Neisseria meningitidis bacterial infection is in the bloodstream (this causes classic ‘non-blanching’ rash).

172
Q

Define meningococcal meningitis

A

When Neisseria meningitidis bacteria infect the meninges and the CSF.

173
Q

Meningitis can be infective or non-infective. What are some causes of non-infective meningitis?

A
  • Malignancy (leukaemia, lymphoma, other tumours)
  • Chemical meningitis
  • Drugs (NSAIDs, trimethoprim)
  • Sarcoidosis
  • SLE
  • Behcet’s disease
174
Q

What is the most common cause of meningitis?

A

Viral → enteroviruses

175
Q

What are the 2 most common cause of bacterial meningitis in adults and children?

A
  1. Streptococcus pneumoniae
  2. Neisseria meningitidis
176
Q

What is the most common cause of bacterial meningitis in neonates?

A

Group B Strep (streptococcus agalactiae)

177
Q

how is group B strep usually contracted by neonates?

A

usually contracted during birth from GBS bacteria that can live harmlessly in vagina

178
Q

Who does listeria monocytogenes usually cause bacterial meningitis in?

A

often in patients at extremes of age

179
Q

Give some examples of enteroviruses

A

Echoviruses, Coxsackie viruses A and B, poliovirus

180
Q

What is the most common cause of viral meningitis?

A

Enteroviruses

181
Q

Give some other causes of viral meningitis

A
  • HSV2 (more associated with meningitis)
  • HSV1 (more associated with meningoencephalitis/encephalitis particularly affecting the temporal lobes)
  • Paramyxovirus – can be a complication of mumps infection
  • Measles and rubella viruses – can cause meningoencephalitis
  • Varicella Zoster virus – can be a complication of chickenpox
  • Rabies virus
  • Arboviruses
182
Q

What is the most common cause of fungal meningitis?

A

Cryptococcus neoformans

183
Q

Presentation of meningitis in children/adults?

A
  • Headache
  • N&V
  • Fever
  • Photophobia
  • Neck stiffness
  • Non-blanching rash → seen in meningococcal septicaemia
  • Focal neurology
  • Seizures
184
Q

Presentation of meningitis in neonates?

A

Presentation can be non-specific:

  • Hypotonia
  • Poor feeding
  • Lethargy
  • Hypothermia
  • Bulging fontanelle
185
Q

Immediate management of viral meningitis?

A

IV aciclovir

186
Q

Immediate management of bacterial meningitis?

A

IV ceftriaxone 2x daily

+ IV amoxicillin in young/old patients → to better cover listeria

187
Q

Investigations that can be done in meningitis?

A
  • Blood tests:
    • FBC
    • U&Es
    • Clotting
    • Glucose
  • ABG
  • Blood cultures
  • CT head
  • Lumbar puncture
188
Q

CSF features in bacterial vs viral meningitis → appearance

A

Bacterial → cloudy

Viral → clear

189
Q

CSF features in bacterial vs viral meningitis → protein

A

Bacterial → high

Viral → mildy raised or normal

190
Q

CSF features in bacterial vs viral meningitis → glucose

A

Bacteria → low

Viral → normal

191
Q

CSF features in bacterial vs viral meningitis → WCC

A

Bacteria → high (neutrophils)

Viral → high (lymphocytes)

192
Q

CSF features in bacterial vs viral meningitis → culture

A

Bacterial → bacteria

Viral → negative

193
Q

What is the key complication of meningitis?

A

Hearing loss

194
Q

What can be given to to reduce frequency and severity of hearing loss and neuro damage?

A

Steroids (dexamethasone)

195
Q

Other complications of meningitis:

A
  • Seizures and epilepsy
  • Cognitive impairment and learning disability
  • Memory loss
  • Focal neurological deficits e.g. limb weakness or spasticity
  • Septic shock
  • Disseminated intravascular coagulation
  • Syndrome of inappropriate antidiuretic hormone secretion (SIADH)
  • Death
196
Q

Define encephalitis

A

A histological diagnosis characterised by inflammation of the ‘encephalon’ (or brain parenchyma)

197
Q

Who is encephalitis most commonly seen in?

A

Bimodal age distribution seen – highest incidence in those <1 y/o and >65 y/o

198
Q

What is the most common cause of encephalitis?

A

Viral - HSV1

199
Q

Presentation of encephalitis?

A
  • Altered mental state (encephalopathy)
  • High fevers
  • New onset seizures
  • Flu-like prodromal illness
200
Q

Main investigation for encephalitis?

A

MRI head

201
Q

Management for viral encephalitis?

A

IV aciclovir

202
Q

What is the most common type of headache?

A

Tension headache

203
Q

What 2 signs i giant cell arteritis associated with (as well as headache)?

A
  1. Temporary monocular blindness
  2. Temporal tenderness
204
Q

When taking a headache history, what red flags should you ask about?

A
  • Neck stiffness, photophobia, fever → meningitis
  • Occipital headache of sudden onset, reaching max intensity within 5 mins → subarachnoid haemorrhage
  • Dizziness → stroke
  • Recent head trauma → subdural haemorrhage
  • Posture dependent - e.g. worse lying down → raised ICP
  • Headache worse on coughing → raised ICP
  • Vomiting → raised ICP
  • Pregnancy → pre-eclampsia
  • Sleep disturbance
  • Tenderness in temporal region & jaw claudication → giant cell arteritis
205
Q

why is fundoscopy an essential part of a headache assessment?

A

Look for papilloedema

206
Q

What does papilloedema indicate?

A

Raised ICP which can be due to brain tumour, benign intracranial hypertension, intracranial bleed

207
Q

How does a tension headache present?

A

Mild ache across the forehead and in a band-like pattern around the head.

This may be due to muscle ache in the frontalis, temporalis and occipitalis muscles (i.e. tenderness of the scalp muscles)

208
Q

Are there any visual changes with a tension headache?

A

NO

209
Q

Triggers for a tension headache?

A
  • Stress
  • Depression
  • Alcohol
  • Skipping meals
  • Dehydration
210
Q

Management of a tension headache?

A
  • Reassurance
  • Basic analgesia
  • Relaxation techniques
  • Hot towels to local area
211
Q

What is a 2ary headache?

A

Give a similar presentation to a tension headache but with a clear cause:

  • Underlying medical condition e.g. infection, obstructive sleep apnoea, pre-eclampsia
  • Alcohol
  • Head injury
  • Carbon monoxide poisoning
212
Q

Define sinusitis

A

A headache associated with inflammation in the ethmoidal, maxillary, frontal, or sphenoidal sinuses.

213
Q

Presentation of sinusitis?

A
  • Headache
  • Facial pain behind the nose, forehead, and eyes
  • Tenderness over the affected sinus
  • Usually resolves within 2-3 weeks
214
Q

Is most sinusitis viral or bacterial?

A

Viral

215
Q

Management of sinusitis?

A
  • Nasal irrigation with saline
  • Prolonged symptoms can be treated with nasal steroid spray
  • Abx sometimes required
216
Q

What is an analgesic headache?

A

Headache caused by long-term analgesia use

217
Q

Presentation of an analgesic headache?

A

Similar non-specific features to a tension headache, these are 2ary to continuous or excessive use of analgesia.

218
Q

management of analgesic headache

A

Withdrawal of analgesia (challenging in patients with chronic pain and those who believe analgesia is necessary to treat the headache).

219
Q

What does a hormonal headache tend to be related to?

A

Low oestrogen

220
Q

When does a hormonal headache typically come on?

A
  • 2 days before and first 3 days pf menstrual period
  • Around menopause
  • Pregnancy
221
Q

When does a hormonal headache in pregnancy typically come on? How can this be differentiated from a headache related to pre-eclampsia?

A
  • Hormonal headache - Worse in first few weeks and improves in last 6 months
  • Headaches in 2<u>nd</u> half of pregnancy should prompt investigation for pre-eclampsia
222
Q

Management for hormonal headache?

A

Oral contraceptive pill

223
Q

What is cervical spondylosis?

A

Common condition caused by degenerative changes in the cervical spine.

224
Q

Presentation of cervical spondylosis?

A
  • Neck pain, usually made worse by movement
  • Headache
225
Q

What is important to exclude before a diagnosis of cervical spondylosis?

A

other causes of neck pain e.g. inflammation, malignancy, infection, spinal cord, or nerve root lesions.

226
Q

Give some differentials of a headache

A
  • Tension headaches
  • Migraines
  • Cluster headaches
  • Sinusitis
  • Giant cell arteritis:
    • Associated with temporary monocular blindness and temporal tenderness
    • Treat with high-dose steroids
  • Glaucoma
  • Intracranial haemorrhage
  • Subarachnoid haemorrhage
  • Hormonal headache
  • Trigeminal neuralgia
  • Meningitis
  • Encephalitis
  • Analgesic headache
  • Cervical spondylosis
  • Raised intracranial pressure (brain tumours)
227
Q

What is trigeminal neuralgia thought to be caused by?

A

Compression of nerve

228
Q

Triggers for trigeminal neuralgia?

A

Cold weather, spicy food, caffeine, citrus fruits, eating, talking, touching the face

229
Q

Are the majority of trigeminal neuralgia cases unilateral or bilateral?

A

Unilateral (90%)

230
Q

Which neurodegenerative disease can be associated with trigeminal neuralgia?

A

Multiple sclerosis → Around 5-10% of people with multiple sclerosis have trigeminal neuralgia

231
Q

Presentation of trigeminal neuralgia?

A
  • Intense facial pain that comes on spontaneously in the trigeminal nerve distribution → often described as an electricity-like shooting pain
  • Lasts anywhere between a few seconds to hours
232
Q

1st line treatment for trigeminal neuralgia?

A

carbamazepine

(then potentially surgery to decompress or intentionally damage the trigeminal nerve)

233
Q

What red flags can be seen in a headache history in the context of raised intracranial pressure (ICP)?

A
  • Worse in morning
  • Worse on bending over
  • Improves after vomiting and lying down
  • Neurological deficits → due to compression of cranial structures by a space-occupying lesion (tumour, haemorrhage)
234
Q

1ary investigation in raised ICP?

A

CT head

235
Q

What is a migraine?

A

Complex neurological condition that causes headaches and other associated symptoms. They occur in ‘attacks’ that often follow a typical pattern.

236
Q

4 types of migraines:

A
  • Migraine without aura
  • Migraine with aura
  • Silent migraine (migraine with aura but without a headache)
  • Hemiplegic migraine
237
Q

Triggers for migraines?

A
  • Stress
  • Bright lights
  • Strong smells
  • Certain foods e.g. chocolate, cheese, caffeine
  • Dehydration
  • Menstruation
  • Abnormal sleep patterns
  • Trauma
  • Oral contraceptives
238
Q

Are migraines unilateral or bilateral?

A

Unilateral

239
Q

Presentation of a migraine?

A
  • Unilateral, throbbing headache
  • Headache symptoms:
    • Last between 4-72 hours
    • Moderate to severe intensity
    • Pounding or throbbing in nature
    • Usually unilateral but can be bilateral
    • Photophobia
    • Phonophobia – discomfort with loud noises
    • With or without aura
    • N&V
240
Q

If an aura is not present, what criteria is required to diagnose a migraine?

A
  • At least 5 headaches lasting 4-72 hours with;
  • N/V or photo/phonophobia AND 2 of;
    • Unilateral headache
    • Pulsating character
    • Impaired or worsened by daily activities
241
Q

What is an aura? Give some examples

A

This is the term used to describe the visual changes associated with migraines. There can be multiple types:

  • Sparks in vision
  • Blurring vision
  • Lines across vision
  • Loss of different visual fields
242
Q

Management of migraines?

A
  • Dark, quiet room & sleep
  • Paracetamol
  • Triptans (e.g. sumatriptan)
  • NSAIDs
  • Antiemetics (if vomiting occurs) → metoclopramide is most effective in migraines
  • Prophylaxis:
    • Propranolol
    • Topiramate (teratogenic)
    • Amitriptyline
243
Q

What class of drug are triptans?

A

5HT receptor agonists (serotonin receptor agoinsts)

244
Q

Indications for triptans?

A

Migraines

245
Q

Which antiemetic is most effective in migraines?

A

Metoclopramide

246
Q

Which medications can be used in the prophylaxis of migraines?

A
  • Propanolol
  • Topiramate
247
Q

What criteria makes up the definition of a total anterior circulation stroke?

A

All 3 of:

  1. Contralateral homonymous hemianopia
  2. Contralateral limb weakness
  3. Higher cerebral dysfunction e.g. dysphasia
248
Q

What criteria makes up the definition of a partial anterior circulation stroke?

A

2 out of 3 of:

  1. Contralateral homonymous hemianopia
  2. Contralateral limb weakness
  3. Higher cerebral dysfunction e.g. dysphasia
249
Q

What criteria makes up the definition of a posterior anterior circulation stroke?

A

At least 1 of:

  1. Cranial nerve palsy and contralateral/sensory deficit
  2. Bilateral motor/sensory deficit
  3. Conjugate eye movement disorder (gaze palsy)
  4. Cerebellar symptoms (vertigo, nystagmus, ataxia)
  5. Isolated homonymous hemianopia
250
Q

What criteria makes up the definition of a lacunar stroke?

A

1 of the following:

  1. Pure sensory
  2. Pure motor
  3. Sensori-motor
  4. Ataxic hemiparesis)

(no loss of higher cerebral function)

251
Q

What symptom has to be present for a diagnosis of Parkinson’s to be made?

A

Bradykinesia

Yr 3 - Core Conditions (33 decks)

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