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Danny's Phase 2A Medicine > Neurology > Flashcards

Neurology Flashcards

1
Q

STROKE

What is it?

A

Ischaemic infarction or brain haemorrhage

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2
Q

STROKE

Risk factors?

A
  • HTN
  • DM
  • HD
    -PVD
    Previous TIA
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3
Q

STROKE

Cause?

A
  • Vessel occlusion
  • Cardiac Emboli
    CNS bleeds e.g. aneurysm rupture
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4
Q

STROKE

Number of deaths?

A

1 per 1000 per year

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5
Q

Clinical Presentation of ACA Stroke

A

1) Leg weakness
2) Sensory disturbances in leg
3) incontinence
4) Gait apraxia (can move lying down but cant walk)
5) drowsiness

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6
Q

Clinical Presentation of MCA Stroke

A

1) Contralateral arm+leg weakness
2) Contralateral sensory loss
3) hemianopia
4) Aphasia (language impairment)
5) Dysphagia
6) facial droop

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7
Q

Clinical Presentation of PCA Stroke

A

1) contralateral hemianopia
2) Cortical blindness
3) Visual agnosia (inability to process sensory information)
4) facial blindness
5) Facial droop

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8
Q

Clinical Presentation of Lateral Medullary Infarct occlusion of PICA (brainstem)

A

1) ipsilateral horner’s syndrome
2) Vomiting
3) Vertigo (environment or you are spinning)
4) Cerebellar signs
5) Facial numbness

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9
Q

What is Horner’s syndrome characterised by?

A

classic triad of miosis (ie, constricted pupil), partial ptosis, and loss of hemifacial sweating (ie, anhidrosis).

Miosis
Ptosis
Anhidrosis

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10
Q

STROKE

tests?

A

ACT FAST

  • CT/MRI
  • ECG for MI/AF
  • CXR FOR LVH
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11
Q

STROKE

Posterior circulating stroke features?

A
  • Vomit/vertigo/nausea
  • Dysarthria/ speech impairment
  • motor deficit
  • locked in
  • visual disturbances
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12
Q

STROKE

Acute treatment? within 1 hour

A
  • protect airway

- check pulse, BP, ECG

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13
Q

STROKE

Within 4.5 hours?

A

thrombolysis (IV alteplase)

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14
Q

STROKE

how should a patient by hydrated?

A

IV so no choking.

food assistance and TED stockinga

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15
Q

STROKE

Primary prevention?

A
  • Reduce Risk Factors

statins, smoking, DM, HTN, exercise

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16
Q

STROKE

Secondary prevention

A
  • Antiplatelet (clopidogrel)
    + Aspirin
    + AF/BP treatment
  • Warfarin if cause was AF
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17
Q

TRANSIENT ISCHAEMIC ATTACK (TIA)

Cause?

A

1) microemboli- which then lyse, from atheromas or thrombus

2) Temporary decrease in cerebral perfusion

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18
Q

TRANSIENT ISCHAEMIC ATTACK (TIA)

Risk Factors?

A
  • HTN
  • DM
  • Smoking
  • Hyperlipidaemia
  • Obesity
  • High alcohol
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19
Q

TRANSIENT ISCHAEMIC ATTACK (TIA)

What is the definition?

A
  • Sudden onset focal neurological deficit with symptoms that are maximal at onset and usually resolve within 15 minutes
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20
Q

TRANSIENT ISCHAEMIC ATTACK (TIA)

carotid Symptoms?

A
  • Amaurosis Fugax (emboli in retinal artery)
  • Aphasia (language impairment)
  • Hemiparesis (one side weakness)
  • Hemisensory loss
  • Hemianopia visual loss
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21
Q

TRANSIENT ISCHAEMIC ATTACK (TIA)

Vertebrobasilar symptoms?

A
  • Diplopia (double vision)
  • Vertigo/ vomit
  • Ataxia (lack of voluntary coordination of muscle movements)
  • tetraplegia
  • Hemisensory loss
  • choking and dysarthria (hard to speak)
  • hemianopia visual loss
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22
Q

What is Amaurosis Fugax?

A
  • progressive visual loss in one eye. ‘curtain descending’
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23
Q

TRANSIENT ISCHAEMIC ATTACK (TIA)

Investigation?

A
  • FBC, ESR, Glucose, lipids, U+E

CXR

ECG

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24
Q

What is a ABCD2 score?

A

Determines time frame needed to investigate a stroke (score of 6+ means 35.5% of stroke in next week)

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25
Q

list the different reasons to get a point for the ABCD2 score?

A
  • Age >60 = 1 point
  • BP >140/90 = 1 point
  • Unilateral weakness = 2 points
  • speech problems + weakness = 1 point
  • Duration >1 hour = 2 points <1 hour = 1 point
  • diabetes = 1 point
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26
Q

What investigations need to be done for a high/low ABCD2 score?

A

high = MRI & carotid doppler ultrasound within 24 hours

low = same but within a week

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27
Q

treatment of TIA?

A
  • control CVS risks
  • Aspirin + Clopidogrel
  • Carotid Endarterectomy if necessary within 2 weeks
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28
Q

SUBARACHNOID HAEMORRHAGE

What is it?

A

spontaneous bleeding in sub-arachnoid space and they account for 5% of all strokes

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29
Q

SUBARACHNOID HAEMORRHAGE

most common causes?

A
  • berry aneurysm rupture 70%
  • arterio-venous malformations 15%
  • idiopathic 15%
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30
Q

Common sites for berry aneurysms?

A

1) bifurcation of middle cerebral
2) Junction of posterior and internal carotid
3) Junction of anterior communicating and anterior cerebral

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31
Q

SUBARACHNOID HAEMORRHAGE

Symptoms?

A
  • sudden onset of worst headache ‘ever’
  • Vomit / nausea
  • loss of conciousness
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32
Q

SUBARACHNOID HAEMORRHAGE

Signs

A
  • Kernig’s (inability to straighten knee when hip flexed 90 degrees)
  • Brudzinski’s- neck stiffness - flex neck and knee+hip flex too
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33
Q

SUBARACHNOID HAEMORRHAGE

Investigations?

A

CT (Blood in sulci)

if negative do LP 12hrs after

blood becomes yellow due to bilirubin and oxyhaemoglobin degradation ( Xanthochromia)

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34
Q

SUBARACHNOID HAEMORRHAGE

Treatment?

A
  • bed rest + supportive care
  • CCB’s and control of HTN

surgeon may be able to coil/ clip aneurysm

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35
Q

What is a subdural haemorrhage?

A

Bleeding from bridging veins between cortex and sinuses (below dura)

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36
Q

What is an extra-dural haemorrhage?

A

tear in dural venous sinus due to fractured temporal/parietal bone

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37
Q

How long do sub/extra dural haemorrhages take to develop? why do they take this long?

A

can take a very long time

1) pressure change is small
2) clot degrades
3) increased osmotic pressure - enlarges due to H20

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38
Q

investigation and treatment of sub/extra dural haemorrhages?

A

clot evacuation
CT shows haematoma

treatment - Surgery

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39
Q

INTRACEREBRAL STROKE

Types? and what is the percentage of intracerebral out of all strokes?

A

Hypertensive
Lobar

15% of all strokes

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40
Q

INTRACEREBRAL STROKE

Clinical features?

A

1) Loss o consciousness
2) Stroke features
3) severe headache

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41
Q

Cause of hypertensive bleed?

A

Charcot-Bouchard aneurysm due to longstanding HTN

Leaking due to microbleeds across the brain = bad prognosis

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42
Q

What are Lobar bleeds associated with?

A

dementia (B-amyloid deposition in vessel walls)

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43
Q

Features and location of hypertensive bleedas?

A

deep and small bleeds in the basal ganglia, pons and cerebellum

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44
Q

INTRACEREBRAL STROKE

Investigations?

A

ABC and CT of head

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45
Q

what is Hydrocephalus?

A

blood in ventricles and clots them off

small vessels become blocked so more ischaemia = immediate neurosurgery

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46
Q

INTRACEREBRAL STROKE

Treatment?

A

BP control

labetolol + GTN spray immediately

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47
Q

EPILEPSY

Different types of seizures?

A 
generalised Tonic-Clonic Seizure 
Absence Seizure
Myotonic/clonic
Akinetic/Atonic
Motor seizure
temporal
Frontal
occipital
parietal
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48
Q

Describe a generalised tonic-clonic seizure

A

1) Period of ridgity (tonic) followed by rhythmical jerks (clonic)
2) Then drowsy/coma for a few minutes

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49
Q

describe an absence seizure

A

Cessation of activity and staring for a few seconds

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50
Q

describe a Clonic seizure

A

Isolated muscle jerking

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51
Q

Describe a Tonic Seizure

A

Stiffness of body

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52
Q

Describe an Atonic Seizure

A

loss of moving = falling and loss of consciousness

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53
Q

What happens if a partial seizure becomes a generalised seizure?

A

still classes as partial

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54
Q

describe a motor seizure

A

Motor cortex - jerky movements to contralateral limbs of seizure

may be paralysis few hours later

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55
Q

What is the post-ictal state

A

After seizure headache, confusion, myalgia, weakness

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56
Q

Temporal Seizure effects?

A

visual/olfactory hallucinations.
Deja vu
Jemais vu - things feel unfamiliar

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57
Q

Frontal seizure effects?

A

speech/motor movement loss

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58
Q

EPILEPSY

Cause?

A

unknown

flashing lights possibly

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59
Q

EPILEPSY

Signs of EPILEPTIC?

A
  • tongue bite
  • cyanosis
  • incontinence
  • head turn
  • less than 5 min
  • drowsy and muscle pain
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60
Q

EPILEPSY

Signs of Syncope?

A
  • Upright position, sweating and vomit before/after
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61
Q

EPILEPSY

Signs of NON-EPILEPTIC?

A
  • eyes closed
  • talking
  • crying
  • long duration
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62
Q

EPILEPSY

Investigations?

A

MRI and video EEG

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63
Q

EPILEPSY

Treatment of generalised TOnic-clonic?

A

Sodium Valproate or Lamitrigine

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64
Q

EPILEPSY

Treatment of PArtial?

A

Carbomazepine

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65
Q

EPILEPSY

Treatment of Absence?

A

same as GTC + ethosuximide

Sodium valproate or Lamitrigine + ethosuximide

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66
Q

EPILEPSY

treatment of tonic/ Myotonic/ Atonic

A

sodium valproate or Lamitrigine (avoid carbamazepine)

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67
Q

treatment of severe EPILEPSY?

A

surgery 1) lobe removal/ removal of problematic area

2) Vagal Nerve stimulation

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68
Q

How does carbamezapine work?

A

1) Blocks Na+ channels = decreased firing of neurones and glutamate

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69
Q

Side effects of Carbamezapine?

A 
Nausea
vomiting
drowsy 
double vision 
dizziness
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70
Q

how does valproate work?

A

1) Blocks transmembrane Na+ -stabilises neuronal membranes

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71
Q

Side effects of valproate?

A

hepatotoxicity
hair loss
increased appetite

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72
Q

When should you avoid using Valproate?

A

pregnant and hepatic disease patients

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73
Q

DEMENTIA

What is the percentage change of someone to get dementia at the following ages :

> 65
80
100

A

5-10% >65
20%>80
70%>100

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74
Q

DEMENTIA

Aetiology?

A
  • Alzheimer’s (65%)
  • vascular (25%)
  • lewy bodies (15-25%)
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75
Q

DEMENTIA

What is inevitable for someone with Down’s Syndrome?

A

Alzheimer’s disease

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76
Q

DEMENTIA

Clinical Features of Alzheimer’s?

A

1) Decrease in neurone number
2) neurofibrillary tangles
3) accumulation of B-amyloid plaques

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77
Q

DEMENTIA

Symptoms of Alzheimer’s?

A

INITAL = Memory loss over months/years

progressions

1) All aspects of cerebral function
2) Decrease in language
3) Intellect, verbal and memory loss
4) Agnosia (cant recognise things)
5) Visuospacial skills lost

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78
Q

DEMENTIA

General non cognitive symptoms?

A
  • Aggression
  • Depression
  • Hallucinations
  • Agitation
  • Apathy
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79
Q

DEMENTIA

tests?

A

MMSE
CT for young patient
Good history/ timeline required

bloods- FBC, thyroid, LFTs, B12/folate (exclude other causes)

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80
Q

DEMENTIA

treatment?

A
  • Donepazil
  • Rivastigmine
  • SSRI’s (depression)
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81
Q

When is Vascular Dementia common and how is it characterised?

A

Common after strokes

characterised by periods of stability then sharp decline

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82
Q

what is Lewy Body Dementia?

A
  • fluctuating cognition with variation of attention
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83
Q

Clinical features of Lewy Body Dementia?

A
  • Hallucinations
    2) Parkinson’s
    3) Sleep problems
    4) Depression
  • may not have memory loss early on!
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84
Q

MULTIPLE SCLEROSIS

Types?

A
  • relapsing-remitting
  • primary Progressive (no Rx)
  • Secondary progressive
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85
Q

MULTIPLE SCLEROSIS

Epidemiology?

A

1/1000 F:M 3:1

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86
Q

MULTIPLE SCLEROSIS

Risk factors?

A
  • Epstein-barr Virus
  • urban western living
  • low vitamin D
  • Female
  • Genetics
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87
Q

MULTIPLE SCLEROSIS

pathology?

A

1) Antigens against CNS made due to exposure to a similar antigen (e.g. EBV)
2) T-lymphocytes cause problems when they cause the blood-brain barrier

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88
Q

MULTIPLE SCLEROSIS

Cause?

A
  • Demyelination of oligodendrocytes and axonal damage
  • Myelin recovers whereas the axons don’t
  • Shorter gaps between the Nodes of Ranvier due to thin myelin = slow conduction
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89
Q

MULTIPLE SCLEROSIS

Where is inflammation likely to be found?

A

Brain = Ventricles

Spinal Cord = Posterior column

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90
Q

MULTIPLE SCLEROSIS

clinical Features?

A

1) Optic neuritis
2) Pain
3) Spasticity
4) paraesthesia (pins and needles)
5) Bladder/sexual dysfunction
6) Nystagmus (involuntary eye movement)
7) vertigo
8) Diplopia (double vision)

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91
Q

MULTIPLE SCLEROSIS

Exacerbating factors?

A
  • STRESS

- HOT TEMP

92
Q

MULTIPLE SCLEROSIS

diagnosis?

A
  • > 2 CNS symptoms disseminated in time and space
  • MRI shows plaques/inflammatory lesions around ventricles

IgG monoclonal bands

93
Q

MULTIPLE SCLEROSIS

Treatment of Acute relapse?

A

Steroids

Vit D and stress free

94
Q

MULTIPLE SCLEROSIS

Treatment?

A

1) Interferon beta (prevents immune activation)
2) glatiramer acetate (similar to myelin)
3) Natalizumab prevents t-lymphocytes crossing blood-brain barrier

95
Q

MULTIPLE SCLEROSIS

Lifestyle adaptations?

A
  • vit D supplements and stress free
96
Q

MULTIPLE SCLEROSIS

medicine for Spasticity?

A

baclofen

97
Q

MULTIPLE SCLEROSIS

medicine for Tremors?

A

Beta blockers

98
Q

MULTIPLE SCLEROSIS

Medicine for incontinence

A

Tolterodine

Oxybutynin

99
Q

PARKINSON’S

Pathology?

A
  • Mitochondrial DNA dysfunction causes degeneration of dopaminergic neurones In the substantia nigra pars compacta
  • Synuclein deposition leads to Lewy bodies and decreased dopamine
100
Q

PARKINSON’S

Aetiology?

A

Mitochondrial DNA dysfunction and oxidation stress

Idiopathic

101
Q

PARKINSON’S

Risk Factor genes?

A

SNCA and PRKN genes

102
Q

PARKINSON’S

Cardinal Triad?

A

1) Tremor
2) Ridgity
3) Bradykinesia

103
Q

PARKINSON’S

Describe the Tremor

A
  • worse at rest
  • ‘pill rolling’ of thumb over fingers
  • asymmetrical and gradual
104
Q

PARKINSON’S

Describe the Ridgity

A
  • Cogwheel ridgity
  • Whole ROM is rigid
  • Felt especially through rapid pronation/supination
105
Q

PARKINSON’S

Describe Bradykinesia>

A
  • slow initiation of movements
  • Shuffle steps
  • Decreased arm swing
  • Freezing at obstacles
  • Slow blinking
106
Q

PARKINSON’S

Postural Effects?

A
  • Shuffle
  • Stoop
  • Decreased arm swing
  • poor balance
107
Q

PARKINSON’S

Non motor effects?

A
  • Depression
  • constipation
  • Micrographia (abnormally small, cramped handwriting)
  • Dementia
108
Q

PARKINSON’S

tests?

A

Ct to exclude other causes

109
Q

PARKINSON’S

treatment?

A

1) Postural Exercises
2) L-Dopa and Carbidopa
3) Dopamine Agonists
4) MAO-B Inhibitors
5) COMT inhibitors

110
Q

Give an example of a Dopamine Agonist

A

Ropinirole

111
Q

Give an example of a MAO-B inhibitor

A

Rasagiline

112
Q

Give an example of a COMT inhibitor

A

Entacapone

113
Q

What is the function of COMT and MAO-B enzymes?

A

convert Dopamine into DOPAC + HVA.

To treat Parkinson’s we need as much dopamine as possible therefore these enzymes need to be inhibited

114
Q

BRAIN TUMOURS

Name some different types and their percentage of occurrence

A

Primary Malignant (35%)
Benign (15%)
Metastases (50%)

115
Q

BRAIN TUMOURS

Of Primary malignant BT’s, how many are Astrocytomas and how many are oligodendrogliomas?

A

Astrocytomas (90%)

oligodendrogliomas (5%)

116
Q

BRAIN TUMOURS

a brain tumour will cause an increased intra-cranial pressure, what effects would this pressure increase have

A

Headache + confusion

headache worsens: 1) Morning 2) leaning forward
3) cough/straining

117
Q

BRAIN TUMOURS

Pathology of an increased ICP

A

1) brain displaced downwards
2) Pressure on brainstem
3) drowsiness and respiratory depression

118
Q

BRAIN TUMOURS

Clinical presentation? (apart from raised ICP)

A
  • neurological deficit (depending where the tumour is)

- focal epilepsy (need a CT to exclude a tumour if someone has a new seizure)

119
Q

BRAIN TUMOURS

Tests?

A

CT/MRI and PET scan

120
Q

BRAIN TUMOURS

Treat?

A

Surgery/radiotherapy

121
Q

BRAIN TUMOURS

what is given for rapid relief of symptoms?

A

IV Dexamethasone

122
Q

What does Dexamethasone do?

A

reduce cerebral oedema

123
Q

Where the most common sites of Mets to the brain?

A
  • lung
  • breast
  • colon
  • skin
  • kidney
124
Q

BRAIN TUMOURS

Any associated mutations?

A

50% of tumours have methylated MGMT mutation

125
Q

BRAIN TUMOURS

What does having a methylated MGMT mutation mean?

A

Sensitive to Temozolomide so a better prognosis

126
Q

BRAIN TUMOURS

What may mean a good prognosis for someone with a brain tumour?

A
  • under 50
    IDH mutation
    MGMT mutation
127
Q

What may mean a bad prognosis for someone with a brain tumour?

A
  • over 50

- no IDH or MGMT mutation

128
Q

What is Kernig’s and brudzinski’s signs?

A
  • Kernig’s (inability to straighten knee when hip flexed 90 degrees)
  • Brudzinski’s- neck stiffness - flex neck and knee+hip flex too
129
Q

MENINGITIS

cause?

A

Meningococcus or Pneumococcus

immunocompromised = Cryptococcus

Unvaccinated = H.influenzae

Elderly = S.pneumoniae

130
Q

MENINGITIS

Early Clinical Features?

A

1) Headache
2) Fever
3) kernig’s sign
4) brudzinksi’s sign

131
Q

MENINGITIS

later Clinical Features?

A
  • Decreased consciousness
  • Stiff neck
  • Photophobia
  • Non-blanching petechial rash
  • Seizures
132
Q

MENINGITIS

Investigations?

A

1) Blood cultures
2) Lumbar Puncture
3) IV cefotaxime
4) Head CT
5) Bacterial + viral throat swabs
6) PCR for meningococcus and Pneumococcus

133
Q

MENINGITIS

When should you not do a lumbar puncture

A

When there is a risk of cerebral coning

134
Q

MENINGITIS

When should a CT be done first?

A

If raised ICP

135
Q

MENINGITIS

How would bacterial lumbar puncture look?

A
  • cloudy
  • high neutrophils
  • low CSF
  • high protein
136
Q

MENINGITIS

How would a viral Lumbar Puncture look?

A
  • Clear
  • high lymphocytes
  • normal CSF
  • Normal to high protein
137
Q

MENINGITIS

Which is more serious bacterial or viral?

A

bacterial, there is also no rash with viral

138
Q

MENINGITIS

treat?

A

IMMEDIATELY = IV Cefotaxime and ampicillin

also IV Dexamethasone

139
Q

ENCEPHALITIS

What is it?

A

Inflammation of brain parenchyma

140
Q

ENCEPHALITIS

Clinical features?

A
  • Altered mental state
  • motor and sensory deficits

1) fever
2) headache
3) loss of consciousness
4) lethargy PROGRESSES into seizures

141
Q

ENCEPHALITIS

Cause?

A

Usually virally by Herpes Simplex Virus

immunocompromised are at risk

142
Q

ENCEPHALITIS

investigation|?

A

1st- CT

2nd- LP for viral findings

143
Q

ENCEPHALITIS

Treatment?

A

IV acyclovir IMMEDIATELY

144
Q

What is Shingles?

A

reactivation of dormant Herpes zoster virus in dorsal root ganglion

145
Q

Features of Shingles?

A

dermatome distribution of pain and a rash (papules and vesicles)

146
Q

Treatment of shingles?

A

PO Acyclovir

147
Q

Headache red flags?

A

1) papilloedema (optic disc swelling that is caused by increased intracranial pressure)
2) seizure
3) Cancer history

148
Q

Urgent referrals for headache?

A
  • suspected Meningitis
  • thunderclap headache
  • Red eye (glaucoma)
149
Q

What is Aura?

A

Patient knows about a seizure e.g. strange feeling in gut

150
Q

Migraine Diagnostic Criteria without Aura?

A

1) >5 attacks
2) they last 4-72 hours
3) Nausea/Vomiting
4) unilateral/Pulsating
5) aggravated by movement

151
Q

20% of migraines have aura, what may this be?

A

1) Flashing lights (visual)
2) tingling (sensory)
3) Dysphagia (speech)

152
Q

Partial triggers of headaches? (50%)

A 
Chocolate
Hangovers
Orgasm
Cheese
Oral contraceptives
Lie ins
Alcohol
Tumult (loud noise)
Exercise
153
Q

abortive treatment of headaches?

A

NSAIDs/paracetamol

+ PO rizatriptan (migraines)

154
Q

Preventative treatment for migraines?

A

1st- propranolol or amitriptyline or topiramate

2nd- valproate/Botulinum toxin type A

155
Q

How do migraines happen?

A

1) changes in brainstem blood flow = unstable trigeminal nuclei
2) Inflammatory mediators released
3) These impact on trigeminal nerve nucleus

156
Q

MOTOR NEURONE DISEASE

characteristics?

A
  • Relentless and unexplained destruction of:
  • UMN
  • anterior horn cells
    cranial nerve nuclei
157
Q

MOTOR NEURONE DISEASE

what does it never affect?

A
  • Sensory
  • Ocular movement (eye)
  • sphincters
158
Q

MOTOR NEURONE DISEASE

What will most people die of if they have MND within 3 years?

A

Respiratory failure - bulbar palsy / pneumonia

159
Q

MOTOR NEURONE DISEASE

Cause?

A

oxidative stress and free radicals

160
Q

What is Oxidative stress

A

Oxidative stress is essentially an imbalance between the production of free radicals and the ability of the body to counteract or detoxify their harmful effects through neutralization by antioxidants

161
Q

MOTOR NEURONE DISEASE

Clinical features of Amyotrophic lateral Sclerosis (50%)

A
  • Lateral corticospinal tracts and anterior horn cells affected;
    1) Progressive spastic tetraplegia
    2) Split hand sign; thumb side of hand appears separated due to excessive wasting (thenar muscles disproportionately wasted as compared to the hypothenar muscles)
162
Q

MOTOR NEURONE DISEASE

what does Progressive muscle Atrophy affect (10%)

A
  • LMN lesion
  • distal 1st to be affected
  • NO UMN signs
163
Q

MOTOR NEURONE DISEASE

what does Progressive Bulbar Palsy affect (10%)

A

Cn 9-12 affected

LMN lesion of:
tongue (fasciculations)
speech - dysarthria
swallowing dysphagia

164
Q

MOTOR NEURONE DISEASE

give examples of UMN signs?

A
  • Spasticity
  • brisk reflexes
  • Upgoing plantars (Babinski reflex)

SEE TABLE IN NOTES

165
Q

What is the Babinski reflex?

A

when the sole of the foot is stimulated with a blunt instrument. The reflex can take one of two forms. In normal adults, the plantar reflex causes a downward response of the hallux. An upward response of the hallux is known as the Babinski response

166
Q

MOTOR NEURONE DISEASE

LMN signs?

A
  • Wasting
  • tongue fasciculations
  • abdo,back,thigh fasciculations

SEE TABLE IN NOTES

167
Q

MOTOR NEURONE DISEASE

Investigations?

A

1) EMG - shows muscle degeneration (electromyography)

2) MRI + LP (exclude inflammatory types)

168
Q

MOTOR NEURONE DISEASE

treatment?

Drug
dysphagia
Resp failure
Drooling
spasticity
A 
1) Riluzole (blocks Na+ channels = less glutamate)
PEG feeding - Dysphagia
ventilatory support -resp failure
amitriptyline - Drooling
Baclofen - spasticity
169
Q

MYASTHENIA GRAVIS

Epidemiology?

A

40-60s, mainly women

170
Q

MYASTHENIA GRAVIS

Pathology>

A
  • Autoimmune disease mediated by A-bodies to nicotinic ACh receptors
  • both T/B cells involved
  • Depletion of Post-synaptic receptors
171
Q

MYASTHENIA GRAVIS

Associations?

A

50 years - Thymic hyperplasia / atrophic / tumour

172
Q

MYASTHENIA GRAVIS

Clinical Features?

A

Fatigability of muscle on sustained activity that gets better with rest

Ocular muscles affected 1st then moves down

speech
chewing
swallowing
breathing

173
Q

MYASTHENIA GRAVIS

Specific features?

A
  • ptosis (eye-lid droop)
  • diplopia (double - vision)
  • Voice fade
174
Q

MYASTHENIA GRAVIS

Diagnostic test?

A

ask patient to hold up arms and they will fall

175
Q

MYASTHENIA GRAVIS

Scientific investigations?

A
  • Autoantibodies to AChR in 90% of cases
  • Autoantibodies to MuSK
  • CT of thymus
  • See if ptosis improves by 2mm when ice applied for >2 mins
176
Q

MYASTHENIA GRAVIS

treatment?

A

1st - symptom control - Pyridostigmine (anticholinesterase)

2nd - Steroids (prednisolone)

3rd- thymectomy

177
Q

TENSION HEADACHES

Cause?

A

Depression and anxiety

178
Q

TENSION HEADACHES

Diagnostic Criteria?

A

1) >10
2) Last 30 mins - 7 days
3) 2 of: bilateral pain, pressing/tightening
4) mild/moderate
5) Not triggered by exercise

179
Q

TENSION HEADACHES

treat?

A

paracetamol/NSAIDs - not overusing analgesia

180
Q

CLUSTER HEADACHES

Diagnostic Criteria

A

1) >5
2) Severe
3) unilateral
4) temporal/orbital pain
5) 15-180 mins
6) Restlessness and agitation
7) Occurs every other day, as many as 8 each day

181
Q

CLUSTER HEADACHES

Acute Treatment?

A

100%O2 for 15 mins

Subcutaneous Sumatriptan

182
Q

TRIGEMINAL NEURALGIA

What is it?

A

Compression on trigeminal root e.g. aneurysm or tumour

183
Q

TRIGEMINAL NEURALGIA

Diagnostic criteria

A
  • Severe, stabbing pain lasting seconds-mins

- Precipitated by stimuli to the face

184
Q

TRIGEMINAL NEURALGIA

Treat?

A

carbamazepine

185
Q

CAUDA EQUINA SYNDROME

Where does the spinal cord end

A

L1/L2

186
Q

CAUDA EQUINA SYNDROME

cause?

A

Lumbar disc prolapse - L4-L5 and L5-S1

187
Q

CAUDA EQUINA SYNDROME

associated with?

A

bladder and bowel dysfunction

and perianal numbness (saddle paraesthesia)

188
Q

CAUDA EQUINA SYNDROME

Signs?

A

1) back pain
2) leg weakness
3) Numbness
4) decreased reflexes

189
Q

CAUDA EQUINA SYNDROME

treat?

A

MRI of spine and surgical decompression

190
Q

NEUROPATHIES

Cause?

A

acute compression and entrapment

191
Q

NEUROPATHIES

Common mononeuropathies?

A

median
ulnar
common peroneal
radial- (wrist drop)

192
Q

POLYNEUROPATHIES

Sensory Symptoms?

A
  • Pins and needles
  • Numbness
  • Pain in extremities
  • Tingling
    ‘glove and stocking’ - numbness in distal areas (hands and feet)
193
Q

POLYNEUROPATHIES

Motor symptoms?

A

weakness

194
Q

POLYNEUROPATHIES

Autonomic Symptoms?

A
  • Postural Hypotension
  • erectile dysfunction
  • Sweating
  • diarrhoea
195
Q

POLYNEUROPATHIES

Causes?

A 
Diabetes
Alcohol
Vit B12 deficiency
Infections (Guillain-Barre)
Drugs (isoniazid)
196
Q

POLYNEUROPATHIES

treatment?

A
  • weak opiates
  • SSRI’s/TCAs
  • treat cause
  • Physiotherapy
197
Q

CARE OF UNCONCIOUS PATIENT

What are the severity ranges on the Glasgow coma score?

A

mild >13
moderate 9-12
severe <8

198
Q

CARE OF UNCONCIOUS PATIENT

What cant they do?

A

1) gag
2) Circulating depression
3) cant maintain airway
4) No protection

199
Q

CARE OF UNCONCIOUS PATIENT

1st line treatment?

A

basic life support

200
Q

CARE OF UNCONCIOUS PATIENT

Acute life support is made up of?

A

1) Intubation
2) IV fluids
3) Drugs to maintain circulation
4) venous access

201
Q

CARE OF UNCONCIOUS PATIENT

Intensive care?

A

same as acute ,life support +:

  • catheter
  • tracheal suction
  • nutrition
  • pressure sore prevention
202
Q

GIANT CELL ARTERITIS

who is it common in?

A

elderly

203
Q

GIANT CELL ARTERITIS

Symptoms?

A

1) Scalp tenderness
2) headache
3) Amaurosis Fugax (blind in 1 eye)

204
Q

GIANT CELL ARTERITIS

Extracranial symptoms?

A

1) Dyspnoea
2) Morning stiffness
3) Unequal weak pulses

205
Q

GIANT CELL ARTERITIS

Investigations?

A

RAISED- ESR, CRP, platelets, Alkaline phosphate

  • low Hb
  • temporal Artery Biopsy
206
Q

GIANT CELL ARTERITIS

treatment?

A

immediate prednisolone

delay the risk of irreversible bilateral vision loss

207
Q

HUNTINGTON’S

Features of Huntington’s?

A
  • Chorea (involuntary movements)
  • personality change
  • ## Dementia
208
Q

HUNTINGTON’S

what is it and what are its genetic components

A

-Incurable neurodegenerative disorder

  • Autosomal dominant
  • expansion of CAG repeat on chromosome 4 that produces mutant Huntington protein
209
Q

HUNTINGTON’S

How does someone die of Huntington’s?

A

loss of basal ganglia neurones/ GABA/ ACh until death

210
Q

SPINAL CORD COMPRESSION

Aetiology?

A
  • Secondary malignancy in spine from (breast, kidney, lung, prostate, thyroid)

BKLPT

211
Q

SPINAL CORD COMPRESSION

features?

A

weak legs
sensory loss
spinal pain
arm weakness often less severe

212
Q

SPINAL CORD COMPRESSION

Signs?

A

Look for motor sensory and reflexes

1) normal above the lesion
2) LMN signs at the level of the lesion
3) UMN signs below the level of the lesion

213
Q

SPINAL CORD COMPRESSION

Investigations?

A

Instant MRI
screening bloods and biopsy
CXR to check for lung malignancy

214
Q

SPINAL CORD COMPRESSION

Treatment?

A

Malignant = IV Dexamethasone while waiting for Chemo/Radio

215
Q

GUILLAIN-BARRE SYNDROME

What is it?

A

Acute inflammatory demyelinating polyneuropathy

216
Q

GUILLAIN-BARRE SYNDROME

key clinical feature?

A

Progressive symmetrical ascending weakness (starting at the feet and moving up the body)

Reduced reflexes

There may be peripheral loss of sensation or neuropathic pain

It may progress to the cranial nerves and cause facial nerve weakness

217
Q

GUILLAIN-BARRE SYNDROME

Cause?

A

Infective triggers (commonly post campylobacter gastroenteritis or EBV/CMV) cause antibodies to attack nerves

218
Q

GUILLAIN-BARRE SYNDROME

How may death occur?

A

autonomic neuropathy = cardiac arrest

219
Q

GUILLAIN-BARRE SYNDROME

Investigation?

A

1) lumbar puncture
- rise in protein with a normal white blood cell count (albuminocytologic dissociation) - found in 66%

2) nerve conduction studies may be performed
- decreased motor nerve conduction velocity (due to demyelination)

  • prolonged distal motor latency
  • increased F wave latency
220
Q

GUILLAIN-BARRE SYNDROME

treatment?

A

IV immunoglobulins for 5 days and plasma exchange

221
Q

What is Hydrocephalus?

A

abnormal build up of CSF (cerebrospinal fluid) in the cavities (ventricles) of the brain. The build-up is often caused by an obstruction that prevents proper fluid drainage

222
Q

What does interferon beta do?

A

prevents immune activation1) Interferon beta (prevents immune activation

223
Q

What is glatiramer acetate similar to?

A

Myelin

224
Q

what does Natalizumab do?

A

prevent t-lymphocytes crossing the blood-brain barrier

225
Q

classic triad of Meningitis?

A
  • Photosensitivity
  • Stiff neck
  • Headache

Danny's Phase 2A Medicine (15 decks)

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