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Phase 2 > Neuro Diseases > Flashcards

Neuro Diseases Flashcards

1
Q

Define dementia.

A

A set of symptoms that may include memory loss and difficulties with thinking, problem solving or language. There is a progressive decline in cognitive function with no impairment of cognition

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2
Q

Describe the epidemiology of dementia.

A

10% of people over 65 and 20% of people over 80 have dementia.

Rare below the age of 55

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3
Q

Give 3 causes of dementia.

A
  1. Alzheimer’s disease (65%).
  2. Fronto-temporal.
  3. Vascular.
  4. Lewy bodies.
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4
Q

Frontal and temporal lobe atrophy is seen on an MRI. What kind of dementia is this patient likely to have?

A

Fronto-temporal.

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5
Q

Give 3 symptoms of fronto-temporal dementia.

A
  1. Disinhibition
  2. Personality and behavioural change
  3. Early memory preservation
  4. Progressive aphasia
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6
Q

What is the pathology of frontotemporal dementia

A

Pick bodies

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7
Q

Which disease is fronto-temporal dementia often associated with?

A

Motor neurone disease.

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8
Q

Give 3 functions of the temporal lobe.

A
  1. Hearing.
  2. Language comprehension.
  3. Memory.
  4. Emotion.
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9
Q

What lobe of the brain is affected in Alzheimer’s disease?

A

Medial Temporal lobe atrophy

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10
Q

Give 4 symptoms of Alzheimer’s disease.

A
  1. Global Memory/cognitive decline
  2. Behavioural change
  3. Hallucinations
  4. Delusions
  5. Depression
  6. Visual spatial changes
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11
Q

What is often the first cognitive marker of AD?

A

Short term memory impairment.

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12
Q

Give 2 histological signs of AD.

A
  1. Beta Plaques of amyloid.

2. neurofibrillary tangles §

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13
Q

What are the risk factors for AD

A

ApoE4 allele
Preseniliin 1/2 mutations
Down’s syndrome

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14
Q

What is the treatment for AD

A

Cholinesterase inhibitors (Rivastigmine)

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15
Q

25% of all patients with AD will develop what?

A

Parkinsonism.

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16
Q

What is the pathology of vascular dementia

A

Multiple infarcts or major strokes

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17
Q

What are the symptoms of vascular dementia

A

Sudden onset, stepwise deterioration with patchy deficits

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18
Q

What might you see on MRI for someone with vascular dementia

A

Extensive infarcts or small vessel disease

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19
Q

What is the treatment for vascular dementia

A

Manage predisposing factors

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20
Q

What is the pathology of Lewy body dementia

A

Lewy bodies in the occipital-parietal cortex

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21
Q

What are the symptoms of Lewy body dementia

A

Fluctuating cognitive dysfunction, visual hallucinations and Parkinsonism

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22
Q

What is the treatment for Lewy body dementia

A

Cholinesterase Inhibitors

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23
Q

What are the treatable causes of dementia

A 
Infection (HIV, HSV)
Vascular (Subdural haematoma)
SLE and Sarcoid 
Nutritional (Thiamine deficiency, B12 and folate deficiency)
Hypothyroid 
Hypercalcaemia 
Hydrocephalus
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24
Q

What are the risk factors for dementia

A 
Family history 
Age 
Down's syndrome 
Alcohol, obesity and increased BP 
Hypercholesterolaemia 
Diabetes 
Atherosclerosis 
Depression
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25
Q

What investigations can you do in primary care to determine whether someone might have dementia?

A
  1. Good history of symptoms.
  2. 6CIT.
  3. Blood tests.
    - FBC, LFTs, Thyroid, B12 and folate
  4. Mini mental state exam
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26
Q

What questions are asked in 6CIT?

A
  1. What year is it?
  2. What month is it?
    (Give an address).
  3. Count backwards from 20.
  4. Say the months of the year in reverse.
  5. Repeat the address.
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27
Q

Why might you do a blood test in someone who you suspect has dementia?

A

To look at the vitamin levels that may suggest a reversible cause e.g. dementia due to B12 deficiency.

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28
Q

Dementia: what secondary care investigation could you do to look at brain structure?

A

MRI of the brain.

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29
Q

What secondary care investigation could you do to look at the pathology of dementia?

A

Amyloid and tau histopathology.

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30
Q

What score on the MMSE indicates serious impairment

A

<17

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31
Q

Name the staging system that classifies the degree of pathology in AD.

A

Braak staging.

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32
Q

Describe Braak staging.

A
  • Stage 5/6 - high likelihood of AD.
  • Stage 3/4 - intermediate likelihood.
  • Stage 1/2 - low likelihood.
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33
Q

What is functional memory dysfunction?

A

Acquired dysfunction of memory that significantly affects a person’s professional/private life in the absence of an organic cause.

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34
Q

How could you determine whether someone has functional memory dysfunction or a degenerative disease?

A

When asked the question ‘when was the last time your memory let you down?’, someone with functional memory dysfunction would give a good detailed answer whereas someone with degenerative disease would struggle to answer.

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35
Q

Give 5 ways in which dementia can be prevented.

A
  1. Stop smoking.
  2. Healthy diet.
  3. Regular exercise.
  4. Healthy weight.
  5. Low alcohol intake.
  6. Education decreases the risk
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36
Q

What medication might you give someone with dementia

A
  1. Acetylcholine esterase inhibitors. (Rivastigmine and Donepezil)
  2. Anti-glutamate (Memantine)
  3. Blood pressure control to reduce vascular damage in vascular dementia
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37
Q

Define subarachnoid haemorrhage

A

Spontaneous arterial bleeding into the subarachnoid space (Between arachnoid and Pia)

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38
Q

Describe the epidemiology of subarachnoid haemorrhage

A

35-65 years

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39
Q

What are the causes of subarachnoid haemorrhage

A
  1. Rupture of saccular aneurysms (Berry aneurysms) (80%)

2. Arteriovenous malformations (15%)

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40
Q

Where are berry aneurysms most likely to form

A

Junction between the posterior communicating artery and the internal carotid

Anterior communicating artery and the anterior cerebral artery

Bifurcation of the middle cerebral artery

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41
Q

What diseases are berry aneurysms associated with

A

Adult polycystic kidney disease
Co-arcation of the aorta
Ehlers Danlos Syndrome

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42
Q

What are the risk factors for subarachnoid haemorrhage

A 
Smoking 
Hypertension 
EtOH 
Bleeding diathesis 
Mycotic aneurysms 
Family history 
Disease that predisposes to aneurysms (PCKD, Ehlers Dnalos) 
Cocaine
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43
Q

What are the symptoms of subarachnoid haemorrhage

A

Sudden, severe occipital headache (Thunderclap)
Collapse and vomiting
Meningism (Neck stiffness, N/V, photophobia)
Seizures
Drowsiness and coma

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44
Q

How would you describe the headache associated with sub-arachnoid haemorrhage?

A

Thunderclap headache - maximum severity within seconds.

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45
Q

What are the signs of subarachnoid haemorrhage

A

Kernigs - cant straighten leg past 135 degrees
Retinal or subhyaloid haemorrhage
Focal neuro @ presentation suggest aneurysm location
Brudzinski’s = when neck is flexed, hip and knees flex

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46
Q

What is a sentinel headache

A

6% of patients experience a sentinel headache from small warning bleeding before subarachnoid haemorrhage

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47
Q

What investigations might you carry out in someone with subarachnoid haemorrhage

A
  1. CT - star shaped lesion - blood in sulci
  2. LP - Bloody in early stages and then xanthochromia due to breakdown of bilirubin
  3. Cerebral angiography
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48
Q

How long do you wait for before doing a lumbar puncture in someone with a suspected SAH?

A

If CT-ve and no CIs and At least 12 hours! You need to wait for the Hb to break down and then CSF will become yellow, this is a sign that there is bleeding in the sub-arachnoid space - xanthochromia.

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49
Q

What are the treatment options for someone with subarachnoid haemorrhage

A
  1. Nimodipine for 3wks to decrease cerebral vasospasm
  2. Endovascular coiling to stop rebleed
  3. Bed rest and BP control
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50
Q

What are the complications of subarachnoid haemorrhage

A
  1. Rebleeding
  2. Cerebral ischaemia (Due to vasospasm)
  3. Hydrocephalus (Due to blockage of the arachnoid granulations)
  4. Hyponatraemia
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51
Q

What is the management for unruptured aneurysms

A

Young patients with unruptured aneurysms >7mm in diameter may benefit from surgery

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52
Q

Define stroke.

A

Rapid onset of focal neurological deficit which is the result of a vascular lesion and is associated with infarction of central nervous tissue lasting >24hr

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53
Q

What can cause a stroke?

A

Infarction either due to cerebral ischaemia (80%) or intracerebral haemorrhage (20%)

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54
Q

What are the causes of Ischaemia

A

Atheroma (Large ie MCA or small vessel perforator)

Embolism (Cardiac from AF, endocarditis, MI) (Atherothromboembolism from carotids)

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55
Q

What are the causes of intracerebral haemorrhage

A 
increased BP
Trauma 
Aneurysm rupture 
Anticoagulants 
Thrombolysis 
Carotid artery dissection 
Watershed stroke (Sudden drop in Bp ie Sepsis)
Vasculitis 
Venus sinus thrombosis 
Anti-phospholipid syndrome
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56
Q

Give 5 risk factors for stroke.

A
  1. Hypertension.
  2. Diabetes mellitus.
  3. Cigarette smoking.
  4. Hyperlipidaemia.
  5. Obesity.
  6. Alcohol.
  7. Family history or previous history of TIA
  8. Cardiac (AF, valve disease)
  9. Ethnicity (Increased in blacks and asians)
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57
Q

What investigation could you do to determine whether someone has had a haemorrhagic or an ischaemic stroke?

A

A CT scan of the head.

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58
Q

How might you identify HTN as a risk factor for stroke

A

Retinopathy
Nephropathy
Big heart on CXR

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59
Q

How might you recognise cardiac emboli as a risk factor for stroke

A

ECG to identify AF

Echo to identify septal defects

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60
Q

How might you recognise carotid artery stenosis as a risk factor for stroke

A

Doppler ultrasound with angio

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61
Q

How might you recognise hyper viscosity as a risk factor for stroke

A

Polycythaemia

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62
Q

Give 5 signs of an ACA stroke.

A
  1. Lower limb weakness and loss of sensation to the lower limb.
  2. Gait apraxia (unable to initiate walking).
  3. Incontinence.
  4. Drowsiness.
  5. Decrease in spontaneous speech (Akinetic mutism)
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63
Q

Give 5 signs of a MCA stroke.

A
  1. Contralateral arm and leg weakness and contralateral sensory loss
  2. Hemianopia.
  3. Aphasia.
  4. Dysphasia.
  5. Facial drop.
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64
Q

Give 5 signs of a PCA stroke.

A
  1. Contralateral homonymous hemianopia
  2. Cortical blindness.
  3. Visual agnosia.
  4. Prosopagnosia.
  5. Dyslexia, anomic aphasia
  6. Unilateral headache.
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65
Q

What is visual agnosia?

A

An inability to recognise or interpret visual information.

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66
Q

What is prosopagnosia?

A

An inability to recognise a familiar face.

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67
Q

A patient presents with upper limb weakness and loss of sensory sensation to the upper limb. They also have aphasia and facial drop. Which artery is likely to have been occluded?

A

The middle cerebral artery.

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68
Q

A patient presents with lower limb weakness and loss of sensory sensation to the lower limb. They also have incontinence, drowsiness and gait apraxia. Which artery is likely to have been occluded?

A

The anterior cerebral artery.

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69
Q

A patient presents with a contralateral homonymous hemianopia. They are also unable to recognise familiar faces and complain of a headache on one side of their head. Which artery is likely to have been occluded?

A

The posterior cerebral artery.

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70
Q

What is a lacunar stroke

A

Small infarcts around the basal ganglia, internal capsule, thalamus and pons

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71
Q

What are the symptoms of a lacunar stroke

A

Higher cortical dysfunction
Homonymous hemianopia
Drowsiness
Brainstem signs

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72
Q

What is the treatment for an ischaemic stroke?

A

Thrombolysis e.g. alteplase - IV infusion to break up the clot.

Aspirin 300mg PO once haemorrhagic stroke excluded

May coil bleeding aneurysms

Decompressive hemicraniotomy for some forms of MCA

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73
Q

When is thrombylosis and appropriate treatment for stroke

A

If pt between 18-80 and <4.5 hours since onset of symptoms

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74
Q

What non pharmacological treatment options are there for people after a stroke?

A
  1. Specialised stroke units.
  2. Swallowing and feeding help.
  3. Physiotherapy.
  4. Home modifications.
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75
Q

What are the secondary preventative measures for strokes

A

Statin
Aspirin and clopidogrel
Warfarin instead of aspirin or clopidogrel if cardioembolic stroke

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76
Q

Define TIA

A

Sudden onset focal neurology lasting <24hr due to temporary occlusion of part of the cerebral circulation

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77
Q

What are the signs of a TIA

A

Symptoms are brief and location dependent

If Carotid

  • Amaurosis Fugax - retinal artery occlusion leading to vision loss like a descending curtain due to reduction in retinal, ophthalmic or cilliary blood flow leading to temporal retinal hypoxia
  • Aphasias, hemiparesis and hemisensory loss

If vertebrobasilar
- Double vision, Vomiting, vertigo, ataxia, hemisensory losss, hemianopia vision loss, Loss of consciousness

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78
Q

What are the causes of TIA

A

Atherothromboembolism from carotids
Cardioembolism (Post MI, AF, valve disease)
Hyperviscosity (Polycythaemia and Sickle cell disease)

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79
Q

What are the signs of the causes of TIA

A

Carotid Bruit
Increased BP
Heart murmur (Suggestive of valve disease)
AF

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80
Q

What investigations might you carry out in someone with suspected TIA

A 
Bloods
 - FBC for polycythaemia 
 - U and E 
 - ESR 
CXR
ECG 
Echo 
Carotid doppler and angiography
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81
Q

What is it essential to do in someone who has had a TIA?

A

Assess their risk of having a stroke in the next 7 days - ABCD2 score.

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82
Q

What is the ABCD2 score?

A

It is used in patients who have had TIA’s to assess their risk of stroke in the next 7 days.

  • Age > 60.
  • BP > 140/90mmHg.
  • Clinical features: unilateral weakness, speech disturbance.
  • Duration? >1hr or 10-59min
  • Diabetes?
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83
Q

What is the management of someone with TIA

A
  1. Antiplatelet therapy/anticoagulants (Aspirin and clopidogrel
  2. Cardiac risk factor control (Statin, ACE-I, Exercise, decrease salt)
  3. Assess subsequent stroke risk (ABCD2 score)
  4. Specialist referral to TIA clinic
    >4 = referral within 24hr
    <4 = referral within 1wk
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84
Q

Define and describe the pathophysiology of subdural haemorrhage

A

Bleeding from bridging veins between the cortex and venous sinuses (Sagittal sinus) which creates a haematoma between dura and arachnoid leading to increased ICP and shifting of midline structures away from clot

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85
Q

What are the causes of subdural haemorrhage

A

Often due to minor trauma that occurred a long time ago - especially deceleration injuries

Latent period after the head injury. 8-10 weeks later the clot starts to break down and there is a massive increase in oncotic pressure, water is sucked up into the haematoma -> signs and symptoms develop. There is a gradual rise in ICP.

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86
Q

Name 3 groups of people who are at increased risk of a sub-dural haematoma.

A
  1. Elderly people due to brain atrophy
  2. Alcoholics and epileptics (More likely to fall)
  3. Shaken babies.
  4. People on anticoagulants
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87
Q

Why are elderly people and alcoholics at increased risk of a sub-dural haematoma?

A

Both of these groups have cerebral atrophy which leads to an increased tension on cerebral veins.

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88
Q

What are the symptoms of subdural haemorrhage

A 
Headache 
Fluctuating consciousness
Sleepiness/drowsiness
Gradual physical and mental slowing 
Unsteadiness
Confusion and personality changes
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89
Q

What are the signs of a subdural haemorrhage

A

increased ICP leads to tentorial herniation and coning where the brain herniates through the foramen magnum

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90
Q

What are the investigations for someone with suspected subdural haemorrhage

A

Crescenteric haematoma over one hemisphere
Midline shift
Clot goes from white to grey over time

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91
Q

What is the management for someone with subdural haemorrhage

A

Irrigation and evacuation via burr hole craniostomy
Craniotomy
Address causes of trauma
Mannitol to decrease ICP

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92
Q

Give 3 differences in the presentation of a patient with a subdural haemorrhage in comparison to an extradural haemorrhage.

A
  1. Time frame: extra-dural symptoms are more acute.
  2. GCS: sub-dural GCS will fluctuate whereas GCS will drop suddenly in someone with an extra-dural haematoma.
  3. CT: extra-dural haematoma will have a rounder more contained appearance.
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93
Q

Define extradural haemorrhage

A

Often due to fracture of the temporal or parietal bone leading to laceration of the middle meningeal artery and vein resulting in blood between the bone and dura

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94
Q

When should you suspect extradural haemorrhage

A

Suspect if after head injury GCS falls, is slow to improve or there is a lucid interval

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95
Q

Describe the presentation of extradural haemorrhage

A

Lucid interval - deterioration of GCS after head injury that causes no loss of consciousness

Increased ICP leading to

  • Headache
  • Vomiting and nausea
  • Confusion –> COma
  • Fits/Seizures
  • Ipsilateral blown pupil

Brainstem compression

  • Deep irregular breathing
  • Death by cardiorespiratory arrest
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96
Q

What tests would you do in someone with suspected extra-dural haemorrhage

A

Lens-shaped haematoma and
Skull frature on CT

LP contra-indicated

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97
Q

What is the management of extradural haemorrhage

A

Neuroprotective ventilation
Mannitol to decrease ICP
Craniectomy for clot evacuation and vessel ligation

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98
Q

Will GCS drop rapidly or slowly in someone with an extra-dural haematoma?

A

GCS will drop suddenly - there is a rapid deterioration in consciousness with focal neurological signs.

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99
Q

A 60-year-old man has just had surgery on his carotids and is complaining of difficulty speaking and swallowing. OE his tongue is deviated to the right. Which nerve has most likely been damaged during the operation?

A

Right hypoglossal.

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100
Q

What is meningitis

A

Inflammation of the meninges (usually the inner meninges = leptomeninges)

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101
Q

What are the risk factors for meningitis

A 
Intrathecal drug administration 
Immunocompromised 
Elderly and pregnant 
Crowding 
Endocarditis 
DM 
IVDU
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102
Q

What are the meningitic symptoms of meningitis

A 
Headache and fever 
Neck stiffness 
 - Kernigs 
 - Brudzinskis
Photophobia 
Nausea and vomiting
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103
Q

What are the neurological symptoms of meningitis

A

Decreasing GCS –> Coma
Seizures
Focal neuro ie. CN palsies
Increased ICP = Papilloedema, irritaility, drowsiness and decreased pulse

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104
Q

What are the symptoms of septic meningitis

A

Fever
Decreased BP and increased HR
Purpuric rash = petechial non blanching
DIC

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105
Q

Name the viral causes of meningitis

A

Enteroviruses (Coxsackie and echovirus
HSV2
CMV
VZV

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106
Q

What are the bacterial causes of meningitis

A

Neisseria meningitidis

Streptococci Pneumonia

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107
Q

Name 3 organisms that can cause meningitis in adults.

A
  1. N.meningitidis (g-ve diplococci).
  2. S.pneumoniae (g+ve cocci chain).
  3. Listeria monocytogenes (g+ve bacilli).
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108
Q

Name 3 organisms that can cause meningitis in children.

A
  1. E.coli (g-ve bacilli).
  2. Group B streptococci e.g. s.agalactiae.
  3. Listeria monocytogenes.
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109
Q

Name a fungi that causes meningitis

A

Cryptococcus

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110
Q

How would you describe the rash that is characteristic of meningitis?

A

Non-blanching petechial rash.

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111
Q

What investigations might you do in someone who you suspect has meningitis.

A
  1. Blood cultures.
  2. Bloods: FBC, U+E, CRP, serum glucose, lactate.
  3. Lumbar puncture.
  4. CT head.
  5. Throat swabs.
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112
Q

What antibiotic is commonly given for the treatment of meningitis?

A

Cefotaxime.

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113
Q

What is the treatment of meningitis?

A

Cefotaxime.
+ amoxicillin if L.monocytogenes infection.
+ steroids to reduce inflammation in S.pneumoniae infection.

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114
Q

What is the treatment if viral meningitis is suspected

A

Aciclovir

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115
Q

What are the contraindications for LP

A 
Thrombocytopaenia 
Lateness 
Pressures (Increased ICP)
Unstable (Cardio and resp)
Coagulation disorder 
Infection at LP site 
Neurology
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116
Q

CSF from an LP of someone with bacterial meningitis will show what

A

Be turbid, contain PMNs and have increased protein and low glucose

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117
Q

CSF from an LP of someone with TB meningitis will show what

A

Fibrin Web

Lymphocytic/mononuclear with massive increase in protein

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118
Q

CSF from an LP of someone with Viral meningitis will show what

A

Clear
Lymphocytic and mononuclear
Mild increase in protein

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119
Q

When is a child vaccinated against meningitis C?

A

At 12 weeks and 1 year.

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120
Q

When is a child vaccinated against meningitis ACWY?

A

At age 14.

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121
Q

At what vertebral level would you do a lumbar puncture?

A

L4/5.

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122
Q

Give 4 potential adverse effects of doing a lumbar puncture.

A
  1. Headache.
  2. Damage to spinal cord.
  3. Paraesthesia.
  4. CSF leak.
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123
Q

When is a child vaccinated against meningitis B?

A

At 8 weeks and 16 weeks.

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124
Q

You see a patient who you suspect has meningitis. It is noted that they have raised ICP. Would you do a lumbar puncture?

A

NO! You would not do a lumbar puncture in someone with raised ICP due to the risk of coning.

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125
Q

Give 4 signs of raised intra-cranial pressure.

A
  1. Papilloedema.
  2. Focal neurological signs.
  3. Loss of consciousness.
  4. New onset seizures.
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126
Q

Define encephalitis

A

Inflammation of brain parenchyma

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127
Q

What are the symptoms of encephalitis

A 
Infectious prodrome (Fever, rash, cold sores, conjunctivitis, meningeal signs)
Behaviour and personality change 
Decreasing GCS and coma 
Fever 
Headache 
Seizures 
Hx of travel or animal bite
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128
Q

What are the causes of encephalitis

A

Viral

  • HSV1/2
  • CMV, EBV, VZV
  • HIV

Non Viral

  • Any bacterial meningitis
  • TB
  • Malaria
  • Lyme disease
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129
Q

What investigations would you carry out in someone with suspected encephalitis

A

Bloods (Cultures, viral PCR, malaria film)
Contrast CT (Focal bilateral temporal involvement)
LP (Increased protein, lymphocytes and PCR)
EEG

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130
Q

What is the treatment for encephalitis?

A

Acyclovir.

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131
Q

Encephalitis without the fever is what

A

Encephalopathy

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132
Q

In what group of people is encephalitis common?

A

The immunocompromised.

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133
Q

A lumbar puncture is done and a CSF sample is obtained from someone who is suspected to have encephalitis. Describe what the lymphocyte, protein and glucose levels would be like in someone with encephalitis.

A
  • Lymphocytosis (raised lymphocytes).
  • Raised protein.
  • Normal glucose.
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134
Q

Give 4 symptoms of rabies.

A
  1. Fever.
  2. Anxiety.
  3. Confusion.
  4. Hydrophobia.
  5. Hyperactivity.
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135
Q

Name the organism responsible for causing tetanus.

A

Clostridium tetani (gram positive anaerobe).

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136
Q

Give 3 symptoms of tetanus.

A
  1. Trismus (lockjaw).
  2. Sustained muscle contraction.
  3. Facial muscle involvement.
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137
Q

Name the organism responsible for causing botulism.

A

Clostridium botulinum.

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138
Q

Give 3 symptoms of botulism.

A
  1. Diplopia (double vision).
  2. Dysphagia.
  3. Peripheral weakness.
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139
Q

Define epilepsy

A

Recurrent tendency to spontaneous, intermittent, abnormal electrical activity in part of the brain that manifests as seizures

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140
Q

Define seizure.

A

A convulsion caused by paroxysmal discharge of cerebral neurones.
Abnormal and excessive excitability of neurones.

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141
Q

Give 5 causes of transient loss of consciousness.

A
  1. Syncope.
  2. Epileptic seizures.
  3. Non-epileptic seizures.
  4. Intoxication e.g. alcohol.
  5. Ketoacidosis/hypoglycaemia.
  6. Trauma.
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142
Q

Give 5 causes of epilepsy.

A 
2/3 are idiopathic 
Congenital (Tuberous sclerosis)
Acquired (Vascular CVA, SLE
Non epileptic (EtOH, Opiates,)
Increased ICP
Infection (Meningitis, encephalitis)
Eclampsia
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143
Q

Define aura

A

A simple partial seizure which may proceed other manifestations experienced as epigastric rising, deja vu, automatisms, smells, lights and sounds

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144
Q

What is a partial (focal) seizure

A

Features referable to one hemisphere, often associated with structural brain abnormality

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145
Q

What is a primary generalised seizure

A

No warning/aura

Discharge throughout both hemispheres w/o localising features and loss of consciousness

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146
Q

What is a simple seizure

A

Awareness unimpaired

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147
Q

What is a complex seizure

A

Awareness impaired

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148
Q

What is a secondary generalised

A

Focal seizure = generalised

Aura –> tonic clonic

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149
Q

Describe the presenting features of simple partial seizures

A

Doesn’t affect consciousness or memory

Focal motor, sensory, autonomic and psychic symptoms

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150
Q

Describe the presenting features of complex partial seizures

A

Aura
Autonomic (Change in skin colour, temperature, palpitations)
Awareness lost (Motor arrest and motionless stare)
Automatisms (Lip-smacking, fumbling, chewing, swallowing)
Amnesia

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151
Q

Describe the presenting features of absence (Petit Mal) seizures

A

Often seen in childhood - child ceases activity, daydreaming and stares - stop talking mid sentence then carries on where left off

Abrupt onset and offset 
Short <10sec
Eyes (Blank stare and glazed)
Normal intelligence,
Clonus or automatisms 
EEG: 3Hz spike and wave 
Stimulated by hyperventilation and photics
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152
Q

Describe the presenting features of tonic clonic seizures (Grand Mal)

A

Loss of consciousness
Tonic = limbs stiffen and person falls to floor if standing
Clonic = Rhythmic jerking of limbs (Contract and relax)
Incontinence
Tongue biting
Post-ictal confusion and drowsiness

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153
Q

Describe myoclonic seizures presenting features

A

Sudden jerk of limb, face or trunk and stiffening

Movement cessation/falling + convulsants

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154
Q

Describe the presenting features of atonic seizures

A

Sudden loss of muscle tone –> Fall forwards

No loss of consciousness

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155
Q

Describe the presenting features of tonic seizures

A

Increase in muscle tone + stiffening causing patient to fall backwards

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156
Q

What features localise a seizure to the temporal lobe

A

Automatisms (Lip smacking, chewing, fumbling)
Deja vu
Delusional behaviour
Abdominal rising/N and V
Emotional disturbance - terror, panic, anger
astes and smells

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157
Q

What features localise a seizure to frontal lobe

A

Motor features: Arrest, Jacksonian march, Todd’s palsy

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158
Q

What features localise a seizure to the parietal lobe

A

Sensory disturbance = tingling and numbness

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159
Q

What features localise a seizure to the occipital lobe

A

Visual phonomenon = spots, lines and flashes

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160
Q

What investigations would you cary out in someone with epilepsy

A

Basic blood products (FBC, U + E’s and glucose)
Urine toxicology
ECG
EEG - helps classification and prognosis
Neuroimaging = MRI

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161
Q

What are the treatments for tonic clonic seizures

A

Valproate and lamotrigine

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162
Q

What are the treatments for absence seizures

A

Valproate and lamotrigine

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163
Q

What are the treatments for tonic, atonic and myoclonic seizures

A

Valproate and levetiracetam

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164
Q

What is the treatment for a focal or 2 generation seizure

A

Lamotrigine nd CBZ

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165
Q

What treatments are used in acute seizure management

A

Diazepam and lorazepam

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166
Q

What are the surgical treatment options for epilepsy

A

Neurosurgical resection

Vagal nerve stimulation can decrease seizure frequency

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167
Q

What are the side effects of lamotrigine

A

Skin rash associated with hypersensitivity, fever
Diplopia and blurred vision
Vomiting

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168
Q

What are the side effects of valproate

A 
Appetite = increase wt 
Liver failure 
Pancreatitis 
Reversible hair loss 
Oedema 
Ataxia 
Teratogenicity 
Encephalopathy
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169
Q

What are the side effects of carbamazepine

A 
Leukoapenia 
Skin rashes 
Diplopia, blurred vision 
SIADH
Impaired balance
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170
Q

What are the side effects of phenytoin

A 
Ginigival hypertrophy 
Hirstuism 
Cerebellar syndrome 
Peripheral sensory neuropathy 
Diplopia 
Tremr
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171
Q

Which anti-epileptics should pregnant women avoid

A

Avoid valproate and take lamotrigine instead

CBZ and PHE are enzyme inducers so reduce the effectiveness of OCP

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172
Q

What is the mode of action of lamotrigine and carbamazepine

A

Inhibit pre-synaptic Na+ so prevents axonal firing

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173
Q

What is the mode of action of sodium valproate

A

Inhibits voltage gated Na+

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174
Q

Give 5 signs of an epileptic seizure.

A
  1. 30-120s in duration.
  2. ‘Positive’ symptoms e.g. tingling and movement.
  3. Tongue biting.
  4. Head turning.
  5. Muscle pain.
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175
Q

Define syncope.

A

Insufficient blood or oxygen supply to the brain causes paroxysmal changes in behaviour, sensation and cognitive processes.

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176
Q

Give 5 signs that a transient loss of consciousness is due to syncope.

A
  1. Situational.
  2. 5-30s in duration.
  3. Sweating.
  4. Nausea.
  5. Pallor.
  6. Dehydration.
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177
Q

Give a definition for a non-epileptic seizure.

A

Mental processes associated with psychological distress cause paroxysmal changes in behaviour, sensation and cognitive processes.

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178
Q

Give 5 signs of a non-epileptic seizure.

A
  1. Situational.
  2. 1-20 minutes in duration (longer than epileptic).
  3. Eyes closed.
  4. Crying or speaking.
  5. Pelvic thrusting.
  6. History of psychiatric illness.
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179
Q

Which is likely to last for longer, an epileptic or a non-epileptic seizure?

A

A non-epileptic seizure can last from 1-20 minutes whereas an epileptic seizure lasts for 30-120 seconds.

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180
Q

A patient complains of having a seizure. An eye-witness account tells you that the patient had their eyes closed, was speaking and there was waxing/waning/pelvic thrusting. They say the seizure lasted for about 5 minutes. Is this likely to be an epileptic or a non-epileptic seizure?

A

This is likely to be a non-epileptic seizure.

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181
Q

A patient complains of having a seizure. An eye-witness account tells you that the patient was moving their head and biting their tongue. They say the seizure lasted for just under a minute. Is this likely to be an epileptic or a non-epileptic seizure?

A

This is likely to be an epileptic seizure.

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182
Q

A patient complains of having a ‘black out’. They tell you that before the ‘black out’ they felt nauseous and were sweating. They tell you that their friends all said they looked very pale. Is this likely to be due to a problem with blood circulation or a disturbance of brain function?

A

This is likely to be due to a blood circulation problem e.g. syncope.

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183
Q

What 2 categories can epileptic seizures be broadly divided into?

A
  1. Focal epilepsy - only one portion of the brain is involved.
  2. Generalised epilepsy - the whole brain is affected.
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184
Q

Give 3 examples of focal epileptic seizures.

A
  1. Simple partial seizures with consciousness.
  2. Complex partial seizures without consciousness.
  3. Secondary generalised seizures.
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185
Q

Give 3 examples of generalised epileptic seizures.

A
  1. Absence seizures.
  2. Myoclonic seizures.
  3. Generalised tonic clonic seizures.
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186
Q

Describe a generalised tonic clonic seizure.

A

Sudden onset rigid tonic phase followed by a convulsion (clonic phase) in which the muscles jerk rhythmically.
The episode lasts up to 120s and is associated with tongue biting and incontinence.

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187
Q

Give 2 features of absence seizures.

A
  1. Commonly present in childhood.

2. Child ceases activity and stares for a few seconds.

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188
Q

Describe a myoclonic seizure.

A

Isolated muscle jerking.

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189
Q

What is the treatment for focal epileptic seizures?

A

Carbamazepine.

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190
Q

What is the treatment for generalised epileptic seizures?

A

Sodium valporate.

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191
Q

What is the major side effect of sodium valporate?

A

It is teratogenic!

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192
Q

Give 4 potential side effects of AED’s e.g. sodium valporate and carbamazepine.

A
  1. Cognitive disturbances.
  2. Heart disease.
  3. Drug interactions.
  4. Teratogenic.
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193
Q

What is status epilepticus

A

Seizure lasting >30min or repeated seizures w/o intervening consciousness

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194
Q

What is the management for status epilepticus

A

Lorazepam
Phenytoin
Diazepam
Dexamethasone

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195
Q

What are the causes of Parkinsonism

A 
Parkinson's disease
Infection (Syphilis, HIV, CJD)
Vascular = multiple infarcts 
Drugs = antipsychotics
Genetic = Wilson's disease
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196
Q

What are the three cardinal signs of parkinsonisms

A

Tremor
- worse @ rest, exacerbated by distraction, 4-6hz, pill rolling
Rigidity
- Increase tone in all muscle groups = lead pipe rigidity
- Rigidity + tremor = cog-wheel rigidity
Bradykinesia
- Slow initiation of movement and reduction of amplitude and speed of repetition
- Expressionless face
- Monotonous voice
- Micrografia
Gait
- Decreased arm swing
- Festinance (Short, shuffling steps with flexed trunk)
- Freezing esp in doorways
- Decreased blinking

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197
Q

What is dopamine produced from?

A

Tyrosine -> L-dopa -> dopamine.

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198
Q

Describe the pathophysiology of parkinson’s disease.

A

There is a loss of dopamine producing neurones in the pars compacta region of the substantia nigra.

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199
Q

Where does the substantia nigra project to?

A

The striatum.

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200
Q

Describe the epidemiology of PD

A

Mean onset 65 years

2% prevalence

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201
Q

Describe the pathophysiology of PD

A

Destruction of dopaminergic neurones in the pars compacta of substantia migrant
B-amyloid plaques
Neurofibrillary tangles: Hyperphosphorlated tau

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202
Q

Describe the clinical features of PD

A

Asymmetric onset - side of onset remains worse

Tremor = increased by stress and decreased by sleep
Rigidity
Akinesia = Slow initiation, micrographia, monotonous voice
Postural instability = stooped gait
Postural hypotension and autonomic dysfunction
Psychosis = visual hallucinations
Sleep disorders
Depression/Dementia

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203
Q

Describe the autonomic dysfunction in PD

A 
Postural hypotension 
Constipation 
Hypersalviation 
Urgency, frequency and nocturia 
ED 
Hyperhiridrosis
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204
Q

Describe the symptoms of parkinson’s disease.

A
  1. Bradykinesia - problems with doing up buttons, writing smaller, small steps/shuffling, walking slowly, reduced arm swing.
  2. Rigidity - pain, problems turning in bed.
  3. Resting tremor.
  4. Postural instability.
  5. Depression, psychiatric problems, dementia.
205
Q

You ask a patient who you suspect might have PD to walk up and down the corridor so that you can assess their gait. What features would be suggestive of PD?

A
  • Stooped posture.
  • Asymmetrical arm swing.
  • Small steps.
  • Shuffling.
206
Q

What are the investigations for someone with suspected PD

A

DaTSCAN

MRI and PET scan

207
Q

What is the non medical management of PD

A

Physio

Depression screening

208
Q

What is the management of PD in young individuals

A

Dopamine agonists (Ropinirole, pramipexole)
MOA-B inhibitors (Rasagiline and selegiline)
L-DOPA

209
Q

What is the management of PD in the biologically frail

A

L-DOPA

MAO-B inhibitors (MAO-B normally breaks down dopamine)

210
Q

What other therapies can be used in the treatment of PD

A 
COMT inhibitor (Tolcapone and entacapone)
Apomorphine (Potent Dopamine agonist)
Amantidine (Weak dopamine agonist)
Atypical antipsychotics 
SSRIs 
Anticholingergics
211
Q

What are the surgical managements for PD

A

Deep brain stimulation - stimulates the sub thalamic nucleus

212
Q

What are the side effects of L-DOPA

A 
Dyskinesia (Impairment of voluntary movement)
On-Off phenomena = motor fluctuations 
Psychosis 
Mouth dryness 
Insomnia 
Nausea and vomiting 
Excessive daytime sleepiness
213
Q

Define multiple sclerosis

A

A chronic inflammatory autoimmune T cell mediated condition of the CNS characterised by multiple plaques of demyelination disseminated in Time and space

214
Q

Describe the epidemiology of MS.

A
  • Presents between 20-40 y/o.
  • Females > males.
  • Rare in the tropics.
215
Q

Describe the aetiology of MS.

A
  • Environment e.g. EBV infection is shown to be associated.
  • Genetic predisposition (HLA-DRB1
  • Chance
    Vitamin D, smoking and obesity .
216
Q

Briefly describe the pathophysiology of MS.

A

Genetic susceptibility + environmental trigger -> T cell activation -> B cell and macrophage activation -> inflammation and destruction of oligodendrocytes, demyelination and axon destruction.

217
Q

What is the hallmark of MS

A

Plaques of demyelination

218
Q

Where would MS plaques be seen histologically?

A 
Optic nerves 
Spinal cord 
Cerebral hemispheres 
Medulla and pons 
Cerebellar white matter
219
Q

Does myelin regenerate in someone with MS?

A

Yes but it is much thinner which causes inefficient nerve conduction.

220
Q

Describe the classification of MS

A

Relapsing remitting
Secondary progressive
Primary progressive
Progressive relapsing

221
Q

Give 3 major features of an MS plaque.

A
  1. Inflammation.
  2. Demyelination.
  3. Axon loss.
222
Q

Describe the relapsing/remitting course of MS.

A

The patient has random attacks over a number of years. Between attacks there is no disease progression. = accumulating disability

223
Q

Describe the chronic progressive course of MS.

A

Slow decline in neurological functions from the onset.

224
Q

What can exacerbate the symptoms of MS?

A

Heat - typically a warm shower.

Symptoms can be relieved by cool temperatures.

225
Q

Describe the presentation of multiple sclerosis

A

Tingling/numbness
Eye = optic neuritis
Ataxia
Motor = spastic paraparesis

226
Q

What are the sensory features of MS

A

Dys/paraethesia
Decrease in vibration sense
Trigeminal neuralgia
Lhermitte’s sign (Neck flexion –> Electric shocks in trunk and limbs)

227
Q

What are the eye features of MS

A

Diplopia
Visual phenomenon
Optic neuritis
Nystagmus

228
Q

What are the GI features of MS

A

Swallowing disorders

Constipation

229
Q

What are the motor features of MS

A

Spastic weakness

Transverse myelitis

230
Q

What are the cerebellum features of MS

A

Trunk and limb ataxia
Scanning dysarthria
Falls

231
Q

What are the sexual/GU features of MS

A 
ED, anorgasmia 
Retention 
Incontinence 
Sexual dysfunction 
Urinary frequency and urgency
232
Q

Give 5 signs of MS.

A
  1. Spasticity.
  2. Nystagmus and double vision.
  3. Optic neuritis: impaired vision and pain.
  4. Weakness.
  5. Sensory symptoms.
  6. Paraesthesia.
  7. Bladder and sexual dysfunction.
233
Q

Give 3 atypical symptoms of MS e.g. if a patient presents with these they are unlikely to have MS

A
  1. Aphasia.
  2. Hemianopia.
  3. Muscle wasting.
234
Q

What is the diagnostic criteria for MS?

A
  1. > 2 CNS lesions disseminated in time and space.

2. Exclusion of conditions that may give a similar clinical presentation.

235
Q

Name 3 conditions in the differential diagnosis of MS.

A
  1. SLE.
  2. Sjögren’s.
  3. AIDS.
236
Q

What investigations might you do in someone to see if they have MS?

A
  1. MRI of brain and spinal cord - lesions may be seen around ventricles.
  2. Lumbar puncture - CSF.
  3. Abs = Anti-MBP, NMO-IgG
237
Q

What might electrophoresis of CSF show for someone with MS?

A

Oligoclonal IgG bands.

238
Q

What is the drug management of someone having an acute MS attack

A

Methylprednisolone

239
Q

Describe the drug management to prevent MS relapse

A

Beta interferon (Anti-inflammatory)
Natalizumab
Alemtuzumab

240
Q

What are the symptomatic treatments for mS

A 
Fatigue = modafenil 
Depression = SSRI (Citalopram)
Pain = amitriptyline, gabapentin
Spasticity = Baclofen, physio
Urgency/frequency = Oxybutynin
ED = Sildenafil 
Tremor = clonazepam
241
Q

Describe the non-pharmacological treatment for MS.

A
  1. Psychological therapies and counselling.
  2. Speech therapists.
  3. Physiotherapy and occupational therapy.
242
Q

What are the symptoms of spinal cord compression

A

Deep local stabbing pain
Stabbing radicular pain in a dermatomal distribution and LMN weakness @ lesion level
Progressive UMN weakness and sensory loss below the lesion
Bladder hesitancy, frequency and painless retention
Faecal incontinence or constipation

243
Q

What are the signs of spinal cord compression

A

Shooting radicularpain @ level, anaesthesia below
LMN signs @ level
UMN signs below level

244
Q

What are the causes of spinal cord compression

A 
Trauma 
Infection 
secondary to malignancy of breast, thyroid, bronchus and kidneys and prostate 
Disc prolapse 
Haematoma 
Intrinsic cord tumour 
Myeloma 
Disc herniation
245
Q

What investigations would you carry out in someone with suspected spinal cord compression

A

MRI

CXR

246
Q

What is the treatment for someone with spinal cord compression

A

Neurosurgical emergency
Dexamethasone
Chemo, radio and decompressive laminectomy
Surgical decompression

247
Q

What is the differential diagnosis for spinal cord compression

A 
Transverse myelitis 
MS 
Cord vasculitis 
Spinal artery thrombosis 
Aortic dissection
248
Q

Briefly describe the pathophysiology of cauda equina syndrome.

A

Spinal compression at or distal to the L1 nerve root disrupts sensation and movement. It is a surgical emergency.

249
Q

Give 5 signs of cauda equina syndrome.

A
  1. Bilateral sciatica (pain radiates down the leg to the foot).
  2. Saddle anaesthesia.
  3. Bladder/bowel dysfunction.
  4. Erectile dysfunction.
  5. Variable leg weakness.
250
Q

What investigation might you do to see if someone has cauda equina syndrome?

A

MRI of spine.

251
Q

What is the management for someone with cauda equina

A

Neurosurgical emergency
Dexamethasone
Chemo, radio and decompressive laminectomy
Surgical decompression

252
Q

Define Guillain barre syndrome

A

Acute inflammatory demyelinating ascending polyneuropathy affecting PNS Schwann cells following upper respiratory tract or GI infection

253
Q

What are the causes of Guillain barre syndrome

A

Post infection
Bacterial = C.jejuni, mycoplasma
Viral = CMV, EBV, HSV, HIV

254
Q

What are the symptoms of Guillain barre syndrome

A 
Symmetrical ascending flaccid weakness/paralysis 
LMN signs (Areflexia and fasciculations)
Back pain 
Arrhythmias 
Labile BP
Sweating 
Urinary retention
255
Q

What investigations would you conduct in someone with Guillain barre syndrome

A

Serology for anti-ganglioside Abs
Evidence of infection ie stool samples
Slow conduction velocities on nerve conduction studies
CSF protein >5,5g/L

256
Q

What is the management for Guillain barre syndrome

A

IVIg

Plasma exchange

257
Q

What are the 4 stages of a seizure?

A
  1. Prodromal - often emotional signs.
  2. Aura.
  3. Ictal.
  4. Post-ictal - often drowsy and confused.
258
Q

Define MND

A

Cluster of degenerative disease characterised by axonal degeneration of neurones in the motor cortex, CN nuclei and anterior horn

259
Q

Which neurones are affected in MND

A

UM and LM neurones

260
Q

Do you get sensory loss and sphincter disturbance in MND

A

NO!!!!

261
Q

Are eye movements affected in MND

A

NO!!!

262
Q

Describe the epidemiology of MND

A

M>F
Median age @ onset = 60 years
Often fatal in 2-4yrs

263
Q

What are the causes of MND

A

Unknown

10% familial = SOD1 mutation

264
Q

What are the investigations for someone with suspected MND

A

Brain/cord MRI
LP
EMG - shows denervation

265
Q

What are the features of MND

A 
UMN = Spasticity, increased reflexes, increased planters, muscle weakness, upper limb (Extensors weaker than flexors)
Lower limb (Flexors weaker than extensors)

LMN = wasting, fasciculation of tongue/abdo/thigh, muscular atrophy

Speech or swallowing impairment
Fronto-temporal dementia

266
Q

What is the medical management of MND

A

Riluzole - antiglutamatergic that prolongs life by 3months

267
Q

What are the side effects of MND

A

Vomiting
Increased pulse
Headache
Vertigo

268
Q

What is the supportive treatment for MND

A 
Dribbling = propantheline or amytryptyline 
Dysphagia = Nasogastric tube or PEG 
Respiratory failure = NIV 
Pain = analgesic ladder 
Spasticity = Baclofen, botulinum
269
Q

What is the classification of MND

A

Amyotrophic lateral sclerosis
Progressive bulbar palsy
Progressive muscular atrophy
Primary lateral sclerosis

270
Q

What are the symptoms of ALS

A

Loss of motor neurones in the cortex and anterior horn –> UMN signs and LMN wasting + fasciculation

271
Q

What are the genetic causes of ALS

A

SOD1, TDP-43, C9ORF72, FUS

272
Q

What are the symptoms of progressive bulbar palsy

A 
Only affects CN9-12 --> bulbar palsy 
LMN only = dysphagia and dysarthria 
Flaccid, fasciculation tongue 
Quiet or nasal speech 
Normal/absent jaw reflex
loss of gag reflex
273
Q

What are the symptoms of progressive muscular atrophy

A

Anterior horn lesion –> LMN signs only

Distal to proximal

274
Q

What are the symptoms of primary lateral sclerosis

A

Loss of Betz cells in motor cortex leading to mainly UMN signs
Marked spastic leg weakness and pseudobulbar palsy

275
Q

What is pseudo bulbar palsy

A

Bilateral lesions above the mid pons leading to UMN lesions of swallowing and talking

276
Q

What are the signs of pseudo bulbar palsy

A

Spastic tongue
Slow tongue movements
Brisk jaw jerk reflex
Emotional incontinence

277
Q

What are the causes of pseudo bulbar palsy

A

MS
MND
Stroke

278
Q

What are the causes of bulbar palsy

A

MND
Guillain barre
Central pontine myelitis

279
Q

Give 3 things that modulate LMN action potential transmission to effectors.

A
  1. Cerebellum.
  2. Basal ganglia.
  3. Sensory feedback.
280
Q

Where are LMN’s located?

A

LMN cell bodies are found in the spinal cord or in the cranial nerve nuclei in the brainstem.

281
Q

Give 5 potential sites of damage along the ‘final common pathway’.

A
  1. Cranial nerve nuclei.
  2. Motor neurones.
  3. Spinal ventral roots.
  4. Peripheral nerves.
  5. NMJ.
  6. Muscles.
282
Q

Give 3 diseases that are associated with motor neurone damage.

A
  1. Motor neurone disease.
  2. Spinal atrophy.
  3. Poliomyelitis.
  4. Spinal cord compression.
283
Q

Give 3 pathologies that are associated with ventral spinal root damage.

A
  1. Tumours.
  2. Prolapsed intervertebral discs.
  3. Cervical/lumbar spondylosis (wear and tear).
284
Q

What investigations could you do to see if someone has damage to their LMN’s?

A
  1. EMG.
  2. MRI.
  3. Muscle enzymes.
  4. Lumbar puncture -> CSF.
285
Q

What are muscle spindles innervated by?

A

Gamma motor neurones.

286
Q

What is the function of muscle spindles?

A

Muscle spindles control muscle tone and tell you how much a muscle is stretched.

287
Q

Describe the pyramidal pattern of weakness in the upper limb.

A

Flexors are stronger than extensors.

288
Q

Describe the pyramidal pattern of weakness in the lower limb.

A

Extensors are stronger than flexors.

289
Q

Give 4 potential sites of UMN damage.

A
  1. Motor cortex lesions.
  2. Internal capsule.
  3. Brainstem.
  4. Spinal cord.
290
Q

Give 3 clinical patterns of motor neurone disease.

A
  1. Muscular atrophy: anterior horn cell lesion - LMN. Fasciculations, weakness, wasting.
  2. Amyotrophic lateral sclerosis: loss of neurones in the motor cortex and the anterior horn of the spinal cord - LMN and UMN signs -> progressive spastic tetra-paresis.
  3. Progressive bulbar palsy: destruction of Cn 9-12.
291
Q

Progressive bulbar palsy is a clinical pattern of MND. What symptoms might someone present with?

A
  1. Dysarthria (slurred speech).
  2. Dysphagia.
  3. Wasting and fascitulations of the tongue.
292
Q

What is the long term consequence of amyotrophic lateral sclerosis?

A

Progressive spastic tetraparesis.

293
Q

What is the treatment for motor neurone disease?

A
  • Riluzole - inhibits glutamate release and slows disease progression.
  • Ventilatory support.
  • Feeding by a PEG.
294
Q

MND: give 3 limb onset symptoms.

A
  1. Weakness.
  2. Clumsiness.
  3. Wasting of muscles.
  4. Foot drop.
  5. Tripping.
295
Q

MND: give 3 bulbar onset symptoms.

A
  1. Dysarthria.
  2. Slurred speech.
  3. Dysphagia.
  4. Wasting and fasciculation of the tongue.
296
Q

MND: give 3 respiratory onset symptoms.

A
  1. Dyspnoea.
  2. Orthopnoea.
  3. Poor sleep.
297
Q

Describe the pathophysiology of myasthenia gravis

A

Autoimmune disease mediated by antibodies against nicotinic ACh receptors which interferes with neuromuscular transmission via depletion of working post synaptic receptor sites

298
Q

What is the presentation of myasthenia gravis

A

Increasing muscular fatigue
Extra-ocular= bilateral ptosis and diplopia
Bulbar = voice deteriorates on counting to 50
Face = myasthenia snarl on attempting to smile
Neck = head droop
Limb = asymmetric, proximal weakness
Normal tendon reflexes but may be fatiguable
Weakness worsened by pregnancy, infection and emotion

299
Q

What investigations would you carry out in someone with suspected myasthenia gravis

A

Tensilon test = give edrophonium which is a cholinesterase enzyme in the NMJ that breaks down ACh - +ve if power improves within 1min

Anti-AChR Abs 
MuSK Abs 
EMG = decreased response to a train of Impulses 
Decreased respiratory function 
Thymus CT 
TFT's
300
Q

What is myasthenia gravis associated with in <50yrs

A

More common in women and associated with AI disease (DM, RA, graves) and thymus hyperplasia

301
Q

What is myasthenia gravis associated with in >50yrs

A

More common in men and associated with thymic atrophy or thymic tumour

302
Q

What auto antibodies might be present in someone with myasthenia gravis?

A
  1. Anti-AChR antibodies.

2. Antibodies against tyrosine kinase - anti-MuSK antibodies

303
Q

What is the treatment for myasthenia gravis

A

Anticholinesterases (Pyridostigmine)
Prednisolone
Thyrectomy

304
Q

What are the cholinergic SE of anticholinesterases

A 
Salivation 
Lacrimation 
diarrhoea 
Sweating 
Vomiting 
Miosis
305
Q

What are the potential complications of myasthenia gravis

A

Myasthenic Crisis
- Weakness of respiratory muscles during relapse
- Monitor FVC
Treat with plasmapheresis or IVIg

306
Q

Describe the pathophysiology of Lambert Eaton myasthenic gravis

A

Antibodies to VGCC which decreases the influx of Ca2+ during presynaptic excitation leading to decreases presynaptic ACh vesicle fusion

307
Q

What are the causes of Lambert Eaton myasthenic Gravis

A

Paraneoplastic from small cell lung carcinoma

Autoimmune

308
Q

What is the presentation of Lambert Eaton Myasthenic Gravis

A 
Same as myasthenia gravis as well as 
Leg weakness 
Autonomic and areflexia 
Movement improves symptoms 
Small response to edrophonium
309
Q

What is the management of Lambert Eaton Myasthenic syndrome

A

IVIg

310
Q

Define essential tremor

A

Characterised by a fine tremor affecting all the voluntary muscles most notably the hands but also other areas include head, jaw and vocal tremor

311
Q

What are the features of essential tremor

A 
Fine tremor 
Symmetrical 
More prominent on voluntary movement 
Worse when tired, stressed or after caffeine 
Improved by alcohol 
Absent during sleep
312
Q

What is the treatment for essential tremor

A 
Beta blockers (Propranolol)
Primidone (Barbiturate anti-epileptic medicine)
Gabapentin
313
Q

Describe the inheritance pattern seen in huntington’s disease.

A

AD inheritance.

314
Q

In huntington’s disease, what area of the basal ganglia and what neurotransmitter are affected?

A
  • Striatum (caudate nucleus).

- GABA.

315
Q

What triplet code is repeated in Huntington’s disease?

A

CAG triplet repeat in the HTT gene on chromosome 4

>39 repeats = HD.

316
Q

Describe the pathology of Huntington’s disease

A

Progressive cerebral atrophy with loss of neurones in the caudate nucleus and putamen of basal ganglia resulting in decreased ACh and GABA synthesis in the striatum

GABA is main inhibitory NT so loss of these neurones will result in decreased inhibition of dopamine release and therefore excessive thalamic stimulation and excessive movements

317
Q

What are the cardinal features of Huntingtons disease

A
  1. Chorea
  2. Dementia
  3. Psychiatric problems
  4. Positive family history
318
Q

Define chorea

A

Continous flow of jerky, semi-purposeful movement flitting from one part of the body to another (Fidgity, cant sit still, patient often not aware of abnormal movements)

319
Q

What are the psychiatric problems associated with Huntington’s

A

Personality changes
Depression
Psychosis

320
Q

What tests might you do one someone with suspected Huntington’s disease

A

Genetic testing showing CAG repeats over 35

CT/MRI showing caudate nucleus atrophy and increased size of the frontal horns of lateral ventricles

321
Q

What is the treatment for Huntington’s disease

A

Chorea = Neuroleptic ie. sulpiride
Depression = SSRI
Psychosis - Neuroleptic ie haloperidol
Aggression = risperidone

322
Q

What is the epidemiology of brain tumours

A

Incidence of glioma increases with age
In adults the majority are supratentorial
In children, the majority occur in posterior fossa

323
Q

Describe the pathophysiology of brain tumours

A

Tumour acts as space occupying lesion which increases ICP

Tumour initially small and there are no symptoms because brain is initially compliant and removes CSF from the ventricles in order to offset the increased pressure

Once the increasing CSF cannot be relocated there is sharp rise in ICP resulting in symptoms

Rising pressure results in midline shift of the brain and herniation through the foramen Magnum

324
Q

From what cell do primary brain tumours originate?

A

Glial cells:

  • Astrocytoma (90%).
  • Oligodendroglioma (<5%).
325
Q

Which primary brain tumour do you associate with genetic defects in chromosomes in 1 and 19?

A

Oligodendroglioma.

326
Q

Name some primary brain tumours

A

Glioma
Meningioma (Arise from arachnoid matter and push into brain)
Vestibular schwanoma (Solid tumours from Schwann cells)
Medulloblastoma
Ependymoma (Arise from ependymal cells)

327
Q

What are the two pathways that lead to malignant glioma

A

Common pathway

Less common pathway

328
Q

Describe the common pathway to GBM.

A

Esp those in 50-60yrs
Initial genetic error of glucose glycolysis -> Isocitrate Dehydrogenase 1 mutation -> excessive build up of 2-hydroxyglutarate -> genetic instability in glial cells triggered and inappropriate mitosis

329
Q

Describe the less common pathway

A

More common in those over 50-60

No IDH-1 mutation and instead a catastrophic genetic mutation

330
Q

Where might secondary brain tumours arise from?

A
  1. Lung (NSCC).
  2. Breast.
  3. Malignant melanoma.
  4. Kidney.
  5. Thyroid
  6. Prostate
331
Q

Describe the WHO glioma grading.

A
  1. Grade 1: Pilocytic Astrocytoma = benign paediatric tumour.
  2. Grade 2: pre-malignant tumour.
  3. Grade 3: ‘anaplastic astrocytoma’ - cancer.
  4. Grade 4: glioblastoma multiforme (GBM).
332
Q

What are the 3 cardinal presenting symptoms of brain tumours?

A
  1. Raised ICP.
  2. Progressive neurological deficit.
  3. Epilepsy.
333
Q

Give 3 symptoms of raised ICP.

A
  1. Headache (Worse in morn, and increased by coughing, straining and leaning forward)
  2. Drowsiness.
  3. +/- vomiting.
  4. Papilloedema
334
Q

You ask a patient with a brain tumour about any factors that aggravate their headache. What might they say?

A
  1. Worst first thing in the morning.

2. Worst when coughing, straining or bending forward.

335
Q

What is the cardinal physical sign of raised ICP?

A

Papilloedema.

Due to obstruction of venous return from the retina.

336
Q

What is the differential diagnosis for space occupying lesions

A 
Aneurysm 
Abscess 
Cyst 
Haemorrhage 
Idiopathic inter cranial hypertension
337
Q

What investigations would you do in someone with suspected brain tumour

A

CT/MRI
Biopsy via skull burr hole to determine cancer grade
LP is CONTRAINDICATED when there is possibility of a mass lesion since withdrawing CSF may provoke immediate coning

338
Q

Describe the treatment of brain tumours

A

Surgical debulking or complete resection
Radiotherapy
Chemotherapy (Temozolomide)
Dexamethasone

339
Q

Describe tumour resistance to temozolomide

A

Prodrug activated by HCl that crosses the BBB, methylates guanine in DNA making replication impossible at base site but process can be reversed by methyl guanine methyl transferase (MGMT) = tumour resistance to temozolomide)

340
Q

Give 5 good prognostic factors for GBM.

A
  1. <45 y/o.
  2. Aggressive surgical therapy.
  3. Good performance post surgery.
  4. Secondary GBM.
  5. MGMT ‘mutant’ - will respond well to chemo.
341
Q

Give 5 poor prognostic factors for GBM.

A
  1. > 50 y/o.
  2. Poor neurological function after surgery.
  3. Non-radical surgery treatment.
  4. Primary GBM.
  5. MGMT ‘wild type’ - no response to chemo.
342
Q

Give 3 causes of grade 2 glioma deterioration.

A
  1. Tumour transformation to a malignant phenotype.
  2. Progressive mass effect due to slow growth.
  3. Progressive neurological deficit from functional brain destruction.
343
Q

Give 3 features of oligodendroglioma’s.

A
  1. Genetic defects in chromosomes 1 and 19.
  2. All IDH1 mutation positive.
  3. Chemo sensitive.
  4. 10-15 year survival.
344
Q

What is a medulloblastoma

A

Primitive small blue cell tumour of the cerebellum seen in children which is highly malignant but responds to excision, radiotherapy and chemo

345
Q

Define weakness.

A

Impaired ability to move a body part in response to will.

346
Q

Define paralysis.

A

The ability to move a body part in response to will is completely lost.

347
Q

Define ataxia.

A

Willed movements are clumsy and uncontrolled.

348
Q

Define involuntary movements.

A

Spontaneous movement independent of will.

349
Q

Define apraxia.

A

The ability to carry out familiar purposeful movements is lost in the absence of paralysis or other sensory or motor impairments.

350
Q

What is the function of the cerebellum?

A

The cerebellum is responsible for precise control, fine adjustment and co-ordination of motor activity based on continual sensory feedback. The cerebellum decides HOW you do something. It computes motor error, adjusts commands and projects this information back to the motor cortex.

351
Q

What are the 3 layers of the cerebellum?

A
  • Molecular layer.
  • Purkinje layer.
  • Granular layer.
352
Q

What are the symptoms of cerebellar ataxia

A 
Slurring of speech 
Swallowing difficulties 
Oscillopsia 
Clumsiness 
Tremor 
Loss of precision movement and motor skills 
Unsteadiness when walking 
Stumbles and falls 
Cognitive problems
353
Q

What would you see on examination of someone with cerebellar ataxia

A 
Gait 
Limb ataxia 
Eye movements 
Speech 
Sensory ataxia
354
Q

What are the signs of cerebellar ataxia

A 
Nystagmus 
Dysarthria 
Action tremor 
Dysdiodochokinaesia 
Truncal ataxia 
Limb ataxia 
Gait ataxia
355
Q

How can the severity of ataxia be classified?

A
  • Mild: patient is independent or requires 1 walking aid.
  • Moderate: patient requires 2 walking aids.
  • Severe: patient is wheelchair dependent.
    SARA scale can also be used, looks at gait, stance, sitting and speech.
356
Q

What investigations might you do in someone who is presenting with signs of cerebellar dysfunction?

A

MRI - will show cerebellar atrophy and will exclude other causes e.g. CV, tumour, hydrocephalus.

357
Q

Give an example of an AR inherited cerebellar ataxia.

A

Friedreich’s ataxia (FA) - presents early in childhood. Motor and sensory problems. Patients are at increased risk of diabetes/CV problems.

358
Q

Give an example of an AD inherited cerebellar ataxia.

A

Spino-cerebellar ataxia 6 (SCA6) and episodic ataxia (presents with difficulty focusing and migraines).

359
Q

Give 4 causes of acquired cerebellar ataxia.

A
  1. Toxic e.g. alcohol, lithium, phenytoin
  2. Idiopathic.
  3. Neurodegenerative.
  4. Immune mediated.
360
Q

Give 3 examples of immune mediated cerebellar ataxia.

A
  1. Post-infection cerebellitis.
  2. Gluten ataxia.
  3. Para-neoplastic cerebellar degeneration (secondary from lung or breast, look for a tumour on MRI. Rapid onset).
  4. Primary autoimmune cerebellar ataxia.
361
Q

What is the cause of chronic traumatic encephalopathy?

A

Often seen following repetitive mild traumatic brain injury.

362
Q

Give 3 initial symptoms of chronic traumatic encephalopathy.

A
  1. Irritable.
  2. Impulsive.
  3. Aggressive.
  4. Depressed.
363
Q

Give 3 later symptoms of chronic traumatic encephalopathy.

A
  1. Dementia.
  2. Gait and speech problems.
  3. PD symptoms.
364
Q

Give 3 signs of chronic traumatic encephalopathy.

A
  1. Atrophy of deep brain structures.
  2. Enlarged ventricles.
  3. Tau deposited in sulci.
365
Q

If a patient has aphasia what region in the brain has been affected?

A

Broca’s area.

366
Q

If a patient has receptive dysphasia what region in the brain has been affected?

A

Wernicke’s area.

367
Q

What proportion of strokes are due to intracerebral haemorrhages?

A

10-15%.

368
Q

Give 2 primary causes of intra-cerebral haemorrhage.

A
  1. Hypertension -> Berry or Charcot-Bouchard aneurysms -> rupture.
  2. Lobar (amyloid angiopathy).
369
Q

Give 5 secondary causes of intra-cerebral haemorrhage.

A
  1. Tumour.
  2. Arterio-venous malformations (AVM).
  3. Cerebral aneurysm.
  4. Anticoagulants e.g. warfarin.
  5. Haemorrhagic transformation infarct.
370
Q

Give 3 potential complications of Charcot-Bouchard aneurysms.

A
  1. Rupture (haemorrhage).
  2. Thrombosis.
  3. Leakage (microbleeds).
371
Q

What is the likely cause of bleeds in the basal ganglia, pons and/or cerebellum?

A

Hypertension.

372
Q

Describe the treatment for anti-coagulant related intra-cerebral haemorrhage.

A

Check warfarin INR and consider reversal with vitamin K.

If low platelets, platelet transfusion.

373
Q

What are the two types of trauma

A

Primary = immediate biophysical forces of trauma

Secondary = presenting sometime after the traumatic event

374
Q

What can be the affect of non missile trauma to the scalp?

A

Contusions and lacerations.

375
Q

What can be the affect of non missile trauma to the skull?

A

Fracture.

376
Q

Give 2 risks associated with skull fracture.

A
  1. Haematoma.

2. Infection.

377
Q

What can be the affect of non missile trauma to the meninges?

A

Haemorrhage and infection (due to skull fracture).

378
Q

What can be the affect of non missile trauma to the brain?

A

Contusions, lacerations, haemorrhage and infection (due to skull fracture).

379
Q

Describe the aetiology of diffuse traumatic axonal injury.

A

Acceleration/deceleration -> shearing rotational forces -> axons tear.

380
Q

Give a sign of diffuse vascular injury due to non missile trauma.

A

Multiple petechial haemorrhages.

381
Q

What is more severe: diffuse traumatic axonal injury or diffuse vascular injury?

A

Diffuse vascular injury is MUCH more severe. It can result in near immediate death.

382
Q

Describe the mechanism behind acceleration/deceleration damage.

A

A force to the head can cause differential brain movements -> shearing, traction and compressive stresses -> risk of axon tear and blood vessel damage.

383
Q

What is contusion?

A

Superficial ‘bruises’ of the brain.

384
Q

What is laceration?

A

When a contusion is severe enough to tear the pia mater.

385
Q

What are the causes of brain swelling

A

Congestive brain swelling due to vasodilation and increased cerebral blood volume

Vasogenic oedema due to extravasation of oedema fluid from damaged blood vessels

Cytotoxic oedema due to increased water content of neurones and glia

386
Q

Give an example of a primary headache.

A
  1. Migraine.
  2. Tension headache.
  3. Cluster headache.

No underlying cause

387
Q

Give an example of a secondary headache.

A
  1. Meningitis.
  2. Subarachnoid haemorrhage.
  3. Giant cell arteritis.
  4. Medication overuse headache.
  5. Idiopathic intracranial hypertension
388
Q

Give 6 questions that are important to ask when taking a history of headache.

A
  1. Time: onset, duration, frequency, pattern.
  2. Pain: severity, quality, site and spread.
  3. Associated symptoms e.g. nausea, vomiting, photophobia, phonophobia.
  4. Triggers/aggravating/relieving factors.
  5. Response to attack: is medication useful?
  6. What are symptoms like between attacks?
389
Q

Give 5 red flags for suspected brain tumour in a patient presenting with a headache.

A
  1. New onset headache and history of cancer.
  2. Cluster headache.
  3. Seizure.
  4. Significantly altered consciousness, memory, confusion.
  5. Papilloedema (swollen optic disc).
  6. Other abnormal neuro exam.
390
Q

What are the red flags for a secondary headache

A 
HIV or immunosuppressed 
Fever 
Seizure and new headache 
Thunderclap headache 
Suspected meningitis 
Suspected encephalitis 
Acute glaucoma 
Headache and focal neurology
391
Q

Give 3 activities that can trigger trigeminal neuralgia.

A
  1. Washing your face.
  2. Eating.
  3. Shaving.
  4. Talking.
392
Q

Define migraine

A

Recurrent headaches for 4-72hours involving aura and GI disturbances

Episodic cerebral oedema and dilation of the cerebral vessels

393
Q

Describe the pathophysiology of Migraine

A

Vascular = cerebrovascular constriction leading to aura and dilatation leading to headache

Brain = spreading cortical depression

Inflammation = activation of CN V nerve terminals in meninges and cerebral vessels

394
Q

How long do migraine attacks tend to last for?

A

Between 4 and 72 hours.

395
Q

Give 5 triggers of migraine.

A
  1. Cheese.
  2. OCP.
  3. Alcohol.
  4. Caffeine.
  5. Anxiety.
  6. Travel.
  7. Exercise.
396
Q

Describe the epidemiology of migraine

A

More common in women below 40

Most common cause of episodic headache

397
Q

What are the headache symptoms in migraine

A

Aura lasting 15-30min then unilateral, throbbing headache
Phono/photophobia
N/v
Allodynia

398
Q

Describe the pain of a migraine.

A
  1. Unilateral.
  2. Throbbing.
  3. Moderate/severe pain.
  4. Aggravated by physical activity.
399
Q

Would a patient with migraine experience any other symptoms?

A

Photophobia and/or phonophobia are common complaints. May have nausea but not vomiting.

400
Q

Describe the diagnosis of migraine without aura.

A

> 5 attacks lasting between 4 and 72 hours with nausea/vomiting or photophobia/phonophobia. And >2 of:

  • Unilateral pain.
  • Throbbing pain.
  • Pain aggravated by physical activity.
  • Moderate/severe pain.
  • Nausea
  • Photo/phonophobia
401
Q

Describe the clinical presentation of prodrome

A

Precede migraine by hrs and days
Yawning
Food cravings
Changes in sleep, appetite and mood

402
Q

What would a patient experiencing migraine with aura complain of?

A
  • Visual disturbances e.g. flashing lights, zig-zag lines, Scotomas, shimmering,
  • Sensory disturbances e.g. tingling in hands and feet.
  • Language aura (Dysphasia and paraphasia)
  • motor aura (Dysarthria, ataxia, hemiparesis)
403
Q

How can migraines be subdivided?

A
  1. Episodic with (20%)/without (80%) aura.

2. Chronic migraine.

404
Q

What is the differential diagnosis of migraine

A

CLuster/tension headache
Cervical spondylosis
HTN
Epilepsy

405
Q

What is the acute treatment of migraine

A

Paracetamol
NSAID
Rizatriptan (Sumitriptan = 5HT1B/D agonist)
Ergotamine (5-HT agonist)

406
Q

What are the prophylactic treatments for migraine

A

Propranolol and topiramate
Valproate, pizotifen, gabapentin
Amitriptyline and acupuncture

407
Q

Describe the epidemiology of cluster headache

A

More common in male smokers between 20-40yrs

408
Q

What are the symptoms of a cluster headache

A

Rapid onset severe pain around behind one eye (unilateral)

Red, watery eye, nasal congestion, lacrimation, rhinorrhoea, mitosis and ptosis

409
Q

How long do cluster headaches last

A

15min-3hrs 1-2x/day

410
Q

Name a type of headache that is accompanied with cranial autonomic features.

A

Cluster headache.

411
Q

Describe the classification of cluster headache

A

Episodic = >2 cluster periods lasting 7 days to a year separated by pain free periods lasting > 1 month

Chronic = Attacks occurs for more than one year without remission or with remission lasting <1 month

412
Q

What is the management for acute cluster headache

A

15mins 100% 15L oxygen and triptan (Selective serotonin 5-HT agonist)

413
Q

What is the preventative management for a cluster headache

A

Avoid triggers, short term corticosteroids, verapamil and lithium

414
Q

What is the most common type of primary headache?

A

Tension headache.

415
Q

How long do tension headaches usually last for?

A

From 30 minutes to 7 days.

416
Q

Describe the classification of tension headaches

A 
Episodic = <15days/month
Chronic = >15 days a month for at least 3 months
417
Q

Describe the pain of a tension headache.

A
  1. Bilateral.
  2. Pressing/tight (Non pulsating)
  3. Mild/moderate pain.
  4. Not aggravated by physical activty.
418
Q

Would a patient with a tension headache experience any other symptoms?

A

No!

Nausea, vomiting, photo/phonophobia would not be associated.

419
Q

What is the treatment for tension headache

A

Reassurance and lifestyle = regular exercise and avoidance of triggers
Stress relief
Aspirin, paracetamol, NSAIDs but no opioids

420
Q

What is the most common type of secondary headache?

A

Medication overuse headache.

421
Q

What is the diagnostic criteria for medication overuse headache?

A
  1. Headache present for >15 days/month.
  2. Regular use for >3 months of >1 symptomatic treatment drugs.
  3. Headache has developed or markedly worsened during drug use.
422
Q

What are the common causes of drug overuse headaches

A

Opioids, mixed analgesics (Co-codamol), ergotamine and triptans

423
Q

What is the management of drug overuse headaches

A

Remove analgesia, aspirin/naproxen

424
Q

Define trigeminal neuralgia

A

Paroxysms of uniletal intense stabbing pain in the trigeminal distribution precipitate by innocuous stimuli

425
Q

What are the triggers for trimgeminal neuralgia

A

Washing, shaving, eating, talking

426
Q

What are the secondary causes of trigeminal neuralgia

A

Compression of CN, MS, Zoster, Chiari malformation

427
Q

What is the diagnostic criteria for trigeminal neuralgia

A

• At least three attacks unilateral facial pain fulfilling the following
o Occurring in one or more distributions of the trigeminal nerve with no radiation beyond the trigeminal distribution
o Pain has at least three of the following four characteristics
 Reoccurring in paroxysmal attacks from a fraction of a second to 2 minutes
 Severe intensity
 Electric shock like, shooting, stabbing, sharp
 Precipitated by innoculous stimuli to the affected side of the face
o No clinical evident neurological deficit

428
Q

Describe the pain of trigeminal neuralgia.

A
  1. Unilateral face pain.
  2. Pain commonly in V3 distribution.
  3. Very severe.
  4. Electric shock like/shooting/sharp.
429
Q

How long does the pain associated with trigeminal neuralgia usually last for?

A

A few seconds.

430
Q

What is the treatment for trigeminal neuralgia

A

Anticonvulsant (Carbamazepine, lamotrigine, gabapentin)

If drugs fail then microvascular decompression may be required

431
Q

What features might be present in the history of a headache that make you suspect meningitis?

A
  1. Pyrexia.
  2. Photophobia.
  3. Neck stiffness.
  4. Non-blanching purpura rash.
432
Q

What are the symptoms of a SAH headache

A

Thunderclap headache has maximum severity within seconds

433
Q

What are the characteristics of a headache resulting from raised intracranial pressure

A

Worse in the morning, when stooping, with visual probs, obese women

a. Worse on waking
b. Worse on coughing, sneezing and straining
c. Postural, worse lying down
d. Nausea and vomiting
e. Papilloedema – may be absent if acute

434
Q

What is giant cell arteritis

A

Systemic immune mediated vasculitis affecting medium to large size arteries of aorta and its extra cranial branches

435
Q

What condition is giant cell arteritis associated with

A

Polymyalgia rheumatica

436
Q

What is the epidemiology of giant cell arteritis

A

Primarily over 50 and more common in females

437
Q

What are the symptoms f the headache in giant cell arteritis

A

Unilateral temple/scalp pain and tenderness
Thickened pulseless temporal artery
Jaw claudication, amaurosis fuax and sudden blindness

438
Q

What is the treatment for giant cell arteritis

A

High dose prednisolone

439
Q

What muscle is essential for correcting the extorsion action of lateral rectus when walking downstairs?

A

Super oblique (Cn 4 innervation).

440
Q

What muscle needs to be working in order to test the action of superior and inferior rectus?

A

Lateral rectus.

441
Q

Superior and inferior oblique can never have isolated action. How can they be tested?

A

Position the eye so that superior and inferior recti are giving maximal rotation and look for complete correction.

442
Q

What is a UMN?

A

A neurone that is located entirely in the CNS. Its cell body is located in the primary motor cortex.

443
Q

Give 4 signs of UMN weakness.

A
  1. Spasticity.
  2. Increased muscle tone.
  3. Hyper-reflexia.
  4. Minimal muscle atrophy.
444
Q

Give 3 causes of UMN weakness.

A
  1. MS.
  2. Brain tumour.
  3. Stroke.
445
Q

What is a LMN?

A

A neurone that carries signals to effectors. The cell body is located in the brain stem or spinal cord.

446
Q

Give 5 signs of LMN weakness.

A
  1. Flaccid.
  2. Reduced muscle tone.
  3. Hypo-reflexia.
  4. Muscle atrophy.
  5. Fasciculations.
447
Q

Name 6 mechanisms that can cause nerve malfunction

A
  1. Demyelination
  2. Axonal degeneration
  3. Compression
  4. Infarction
  5. Infiltration
  6. Infarction
  7. Wallerian Degeneration
448
Q

What is a peripheral neuropathy

A

Disorder of the peripheral nervous system

449
Q

Which are the large myelinated fibres

A 
Aa = proprioception 
Ab = light touch, pressure and vibration
450
Q

Which are the small myelinated fibres

A

Adelta = myelinated= pain and cold sensations

C fibres = unmyelinated = pain and warm sensations

451
Q

Define mononeuropathy

A

Lesions of individual peripheral or cranial nerves

452
Q

What are the causes of mononeuropathy

A

Trauma, entrapment (Tumour)

453
Q

Define mononeuritis multiplex

A

2 or more peripheral nerves affected

454
Q

What are the causes of a mono neuritis multiplex (Remember WAARDS PLC)

A 
Wegners 
AIDs 
AMyloid 
RA
DM
Sarcoidosis 
PAN 
Leprosy 
Carcinomatosis
455
Q

Median nerve neuropathy C6-T1 occurs where and what is the cause

A

Wrist/carpal tunnel or trauma

456
Q

What are the motor features of carpal tunnel

A

LLOAF muscles dysfunction

Thenar wasting

457
Q

What are the LLOAF muscles

A

2 lumbricals
Opponens pollicis
Abductor pollicis brevis
Flexor pollicis brevis

458
Q

What are the sensory losses with carpal tunnel

A

Radial 3 and half fingers and palm
Aching pain in hand
Decreased 2 point discrimination

459
Q

What tests can you use to diagnose carpal tunnel

A

Phalen’s test

Tinel’s test

460
Q

What is phalen’s test

A

1 min maximal wrist flexion = symptoms

461
Q

What is tinel’s test

A

Tapping over nerve at wrist induces tingling

462
Q

What is the management of carpal tunnel

A

Splinting
Local steroid injection
Decompression surgery

463
Q

What is the cause of Ulnar C7-t1 mononeuropathy

A

Elbow trauama

464
Q

What are the motor features of ulnar mononeuropathy

A

Partial claw hand
Hypothenar wasting
Weakness and wasting of 1st dorsal interosseous

465
Q

What are the sensory loss features seen in ulnar

A

Ulnar 1 and half fingers

466
Q

What are the locations of radial C5-T1 mononeuropathy

A

Wrist
Humerus
Axilla

467
Q

Wha are the motor features of radial mononeurppathy

A

Finger drop
Wrist drop
Tricep paralysis

468
Q

What sensory loss occurs in radial mononeuropathy

A

Dorsal thumb root (Snuff box)

469
Q

What is the cause of brachial plexus mononeuropathy

A

Trauma

Radiotherapy (Eg breast)

470
Q

What are the motor features of a brachial plexus mononeurpathy

A 
C5-6 = Erb'spalsy = waiter's tip 
C8-T1 = Klumpke's = claw hand
471
Q

What are the sensory losses associated with brachial plexus mononeuropathy

A

C5-6 dermatome

C8-T1 dermatome

472
Q

What are the causes of phrenic nerve (C3-5) mononeuropathy

A

Neoplastic (Lung carcinoma, myeloma, thymoma)
Mechanical (Cervical spondylosis, big left atrium)
Infective (Zoster, HIV, Lyme, TB)

473
Q

What are the motor features of a phrenic nerve mononeuropathy

A

Orthopnoea and raised hemidiaphragm

474
Q

What is the cause of a lateral cutaneous nerve of the thigh (L2-3) mononeuropathy

A

Entrapment under inguinal ligament

475
Q

What is the sensory loss associated with lateral cutaneous nerve of the thigh mononeuopathy

A

Meralgia parasthetica - anterolateral burning thigh pain

476
Q

What is the cause of a sciatic nerve (L4-S3) mononeuropathy

A

Pelvic tumours

Pelvic or femur fracture

477
Q

What are the motor features of sciatic mononeuropathy

A

Hamstring

All muscles belo the knee = foot drop

478
Q

What are the causes of a common peroneal nerve (L4-S1) mononeuropathy

A

Fibular head trauma, sitting crossed legged

479
Q

What are the motor features of common peroneal nerve mononeuropathy

A

Foot drop

Weak ankle dorsiflexion and eversion

480
Q

What are the motor features of tibial mononeuropathy (L4-S3)

A

Cant plantar flex –> Cant stand on tip toe
Foot inversion
Toe flexion

481
Q

Define polyneuropathy

A

Generalised disorders of peripheral or cranial nerves

482
Q

Describe the distribution of polyneuropathies

A

Symmetrical and widespread

483
Q

What are the characteristics signs of polyneuropathy

A

Distal weakness and sensory loss (Glove and stocking)

484
Q

What is the classification of poly neuropathies

A 
Time course (Acute or chronic)
Function (Motor, sensory, autonomic, mixed)
Patho: Demyelination, axonal degeneration or both
485
Q

What are the metabolic causes of polyneuropathy (PN)

A

DM
Renal failure
Hypothyroid
decreased B1 or B12

486
Q

What are the inflammatory causes of PN

A

Guillain barre

Sarcoidosis

487
Q

What are the vasculitis cause of PN

A

Polyarteritis nodosa
RA
Wegner;s

488
Q

What are the infective causes of PN

A

HIV
Sphillis
Leprosy
Lyme

489
Q

What are the toxic causes of PN

A

Lead and arsenic

490
Q

What are the drug causes of PN

A

Isoniazid
EtOH
Phenytoin
Vincristine

491
Q

Describe the history taking for pN

A

Time course
Precise symptoms
Associated events (D and V = GBS)
Travel, EtOH and drugs

492
Q

What are the main causes of sensory neuropathy

A

Alcohol
B12
DM
Vasculitis

493
Q

What are the general features of sensory neuropathies

A

Glove and stocking distribution with length dependent
Deep tendon reflexes may be decreased
Signs of trauma or joint deformity

494
Q

What are the main causes of motor neuropathy

A

Guillain barre
Paraneoplasstic
Lead poisoning

495
Q

What are the features of motor neuropathy

A

Weakness, clumsiness of hands and difficulty walking
LMN signs
CN signs = diplopia, dysarthria, dysphagia
Difficulty breathing

496
Q

What are the causes of autonomic neuropathy

A

DM
HIV
SLE
Guillain Barre

497
Q

What are the features of an autonomic neuropathy

A

Sympathetic = postural hypotension, ED, Ejaculatory failure and decreased sweating

Parasympathetic = Constipation, nocturnal diarrhoea, urinary retention and Horner’s syndrome

498
Q
  1. A 72 year old patient with a 15 year history of diabetes complains of burning sensation and tingling in his both feet for 3 years. Over the last 12 months the symptoms have progressed up to the level of the knees.
    On examination he has reduced tendon reflexes in the upper limbs and the knees and absent tendon reflexes in the ankles. He has reduced vibration sensation up to the knees.

What’s the diagnosis?

A

Peripheral neuropathy of axonal type (length dependent)

499
Q
  1. A 32 year old woman with a 5 day history of progressive distal and proximal weakness and tingling in both upper and lower limbs.
    On examination she has absent tendon reflexes.
    Her medical history is unremarkable, however she reports D&V about 3 weeks ago.
    What’s the diagnosis?
A

Acute polyneuropathy – Guillain Barre syndrome

500
Q
  1. A 52 year old man reports patchy sensory loss and complains of poor balance, symptoms which are getting gradually worse.
    Ten year earlier he was diagnosed with coeliac disease.
    On examination he has mild sensory ataxia, reduced reflexes and patchy loss of pinprick and vibration sensation.
    What is the most likely diagnosis?
A

Sensory ganglionopathy

501
Q

What nerve is affected in carpal tunnel syndrome?

A

median nerve

502
Q

Give 3 risk factors for carpal tunnel syndrome.

A
  1. Pregnancy.
  2. Obesity.
  3. RA.
  4. Hypothyroidism.
  5. Acromegaly.
503
Q

Define spondyloisthesis.

A

Slippage of vertebra over the one below.

504
Q

Define spondylosis.

A

Degenerative disc disease.

505
Q

Define myelopathy.

A

Spinal cord disease; UMN problem. Surgery is often indicated to prevent deterioration.

506
Q

Define radiculopathy.

A

Spinal nerve root disease; LMN problem.

507
Q

Is myelopathy or radiculopathy an UMN problem?

A

Myelopathy is a spinal cord disease and therefore is an UMN problem.

508
Q

Is myelopathy or radiculopathy a LMN problem?

A

Radiculopathy is a spinal nerve root disease and therefore is a LMN problem.

Phase 2 (16 decks)

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