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Medicine Year 2 2 > 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

Aetiology?

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
  • distance from equator
  • 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

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
  • melanoma
  • colorectal
  • 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

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 limb weakness, starting from the legs upwards and affecting proximal muscles the most

217
Q

GUILLAIN-BARRE SYNDROME

Cause?

A

Infective triggers 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

Nerve conduction studies shows decreased motor conduction

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

Medicine Year 2 2 (15 decks)

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