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Neuro Flashcards

1
Q

how many people that have a stroke will die within a year?

A

1/4

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2
Q

events that can create stroke inducing cardiac emboli

A

AF

Endocarditis

MI

any arrhythmia really

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3
Q

factors that increase risk of CNS bleeds

A

hypertension

trauma

aneurysm rupture

anticoagulation

thrombolysis

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4
Q

what could cause stroke in younger patients

A

carotid artery dissection - can be spontaneous or from neck trauma

sudden blood pressure drop by >40mmHg which can affect boundary zones between vascular beds

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5
Q

differentials for stroke symptoms

A

head injury

hypo-hyperglycaemia

subdural haemorhage

Wernicke’s/Hepatic encephalopathy

Drug overdose (if comatose)

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6
Q

modifiable risk factors for stroke

A

Hypertension

smoking

alcohol excess

heart diseae

poor DM control

hyperlipidaemia

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7
Q

what is meningism?

A

it is the triad of nuchal rigidity, headache and photophobia

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8
Q

general signs of stroke

A

meningism

severe headache

coma

carotid bruit

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9
Q

non-modifiable risk factors for stroke

A

AF

Past TIA

IHD

Age

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10
Q

what percentage of strokes are cerebral infarcts

A

50%

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11
Q

what are the signs specific to a cerebral infarct

A

hemiparesis

hemiplegia

contralateral sensory loss

limbs are initially flacid but eventually become spastic

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12
Q

what percentage of strokes are in the brainstem

A

25%

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13
Q

what are the signs specific to brainstem infarcts

A

quadriplegia

locked in syndrome

disturbances of gaze and vision

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14
Q

where is a lacunar infarct

A

in the basal ganglia, internal capsule, thalamus and pons

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15
Q

what percentage of strokes are lacunar

A

25%

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16
Q

what are the 5 syndromes of lacunar stroke

A

ataxic hemiparesis

pure motor

pure sensory

sensorimotor

dysarthria/clumsy hand

in all lacunar strokes except thalamic strokes the cognition/consciousness remains intact

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17
Q

6 important points for the acute management of stroke

A
  1. protect the airway
  2. maintain homeostasis (glucose etc)
  3. screen swallow (nil by mouth until this is done)
  4. CT/MRI within 1hr
  5. antiplatelet agents (once haemorrhagic stroke is excluded)
  6. Thrombolysis if haemorrhagic stroke excluded and onset of symptoms was <4.5hrs ago
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18
Q

what agent do you use to thrombolyse stroke patients

A

alteplase

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19
Q

what should you do 24 hrs after you thrombolyse a stroke patient

A

CT head

to identify any bleeds

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20
Q

what are 8 contraindications for thrombolysis of stroke patient

A

haemorrhage on CT

mild/non-disabling deficit

recent surgery or trauma

previous CNS bleed

arteriovenous malformations/aneurysms

if high INR

known clotting disorder

stroke or serious head injury in the last 3 months

HTN above 200 systolic

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21
Q

primary prevention of stroke

A
  • this is before any stroke occurs so it is control of risk factors
    • treat hypertension
    • control DM
    • improve diet to reduce lipids
    • treat cardiac disease
    • quit smoking
    • exercise more
    • lifelong anticoagulation in AF or with prosthetic heart valve
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22
Q

secondary prevention of stroke

A

this is after a stroke or TIA has occured and you want to prevent a second one

  • control the risk factors as with primary prevention
  • anticoagulate after CVA (2 weeks aspirin 300mg and then move onto long term anti-platelets like clopidogrel)
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23
Q
A
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24
Q

what is the CHA2DS2VASc score and what are the components

A
  • it is a score designed to assess the risk of an AF patient for embolic stroke
    • Congestive cardiac failure
    • Hypertension
    • Age (65-74) (2 points)
    • Diabetes
    • Stroke/TI/Thromboembolism previously (2 points)
    • Vasular disease
    • Sex Category (1 point if female)
  • a score of 2 has an anual stroke risk of 2.2. but risk goes up with more points
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25
Q

stroke complications related to immobility

A

pressure sores

aspiration pneumonia

constipation

contractures

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26
Q

are TIAs usually haemorrhagic or embolic

A

usually embolic

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27
Q

what is the definition of TIA

A

incident of neurological ischaemia in which symptoms last less than 24 hours by which time they have completely resolved

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28
Q

why is prompt intervention with TIA so important

A

without intervention more than 1/12 patients will go on to have a stroke within a week

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29
Q

what is amaurosis fugax

A

it is when the retinal artery is occluded

this causes unilateral progressive vision loss

like a curtain descending

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30
Q

what is a crescendo TIA and what does it suggest

A

more than two TIAs in a week and it suggests some intraranial stenosis

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31
Q

what are 4 main causes of TIA

A

Atherothromboembolism (usually from the internal carotid)

cardioembolism (post MI or in AF)

Hyperviscosity

Vasculitis (rare)

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32
Q

what 3 things can cause hyperviscosity

A

polycythaemia

sickle cell

myeloma

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33
Q

differnetials for TIA

A

hypoglycaemia

migraine

focal epilepsy

hyperventilation

retinal bleeds

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34
Q

tests for TIA

A

FBC

U&E

ESR

Glucose

Lipids

CXR

ECG

Carotid doppler (to check for carortid artery stenosis)

Angiography CT

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35
Q

4 principles of treatment for TIA

A

control CVS risk factors

antiplatelet drugs

anticoagulation

carotid endarterectomy

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36
Q

what antiplatelets following TIA

A

aspirin 300mg following TIA for two weeks then switch to clopidogrel

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37
Q

how long is driving prohibited for after TIA

A

1 month at least

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38
Q

carotid endarterectomy

A

only if occlusion is >70% and the operative risk is acceptable

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39
Q

what is the ABCD2 score

A

the ABCD2 score is a tool to stratify which patients are higher risk of having a stroke following TIA

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40
Q

what does a score of 4 or more in ABCD2 mean

A

it means they are high risk for a stroke and need asssessment by a specialist within 24hrs

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41
Q

what does a score of 6 or more in ABCD2 mean

A

it means that they are 35.5% likely to have a stroke in the next week

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42
Q

factors not on ABCD2 but that will increase risk of stroke following TIA

A

AF

>1 TIA in a week

TIA while anticoagulated

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43
Q

what is the incidence of subarachnoid hemorrhage

A

9/100,000/yr

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44
Q

what is the typical age range for a subarachnoid haemorrhage

A

35-65

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45
Q

symptoms of subarachnoid haemorrhage

A

thunderclap headache

sudden onset

vomiting

collapse

seizures

coma often follows

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46
Q

What is strongly contraindicated in a EDH

A

LUMBAR PUNCTURE

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47
Q

signs of sub arachnoid haemorrhage

A

neck stiffness

kernig’s sign

focal neurology (may indicate site)

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48
Q

what is kernig’s sign

A

A sign indicating the presence of meningitis (inflammation of the meninges covering the brain and spinal cord). The test for Kernig sign is done by having the person lie flat on the back, flex the thigh so that it is at a right angle to the trunk, and completely extend the leg at the knee joint. If the leg cannot be completely extended due to pain, this is Kernig sign.

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49
Q

what are the causes of subarachnoid haemorrhage

A
  • rupture of berry aneurysm (80%)
  • encephalitis
  • vasculitis
  • tumour with invading blood vessels
  • idiopathic
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50
Q

common sites of berry aneurysm rupture

A

junction of posterior communicating artery with internal carotid or aterior cerebral

bifurcation of the middle cerebral artery

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51
Q

8 risk factors for subarachnoid haemorrhage

A

previous aneurysmal SAH

smoking

alcohol misuse

bleeding disorders

family history

PKD

aortic coarctation

Ehlers Danlos Syndrome

hypertension

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52
Q

5 differentials of SAH

A

meningitis

migraine

intracerebral bleed

cortical vein thrombosis

dissection of carotid or vertebral artery

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53
Q

what is the treatment for rising ICP

A

IV mannitol

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54
Q

tests for suspected SAH

A

urgent CT detects >95% of SAH within the first 24hrs

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55
Q

what to do if the CT is negative but the history is convincing for SAH

A

consider a lumbar puncture if there is no CI

this should be done 12hrs after headache onset to allow breakdown of the RBCs

therefore the positive sign is yellow CSF due to bilirubin

not red which could be confused with blood from traumatic LP

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56
Q

management for SAH

A
  • refer all proven SAH to neurosurgery immediately
  • CNS exam often
    • GCS, repeat CT, EWS
  • maintain cerebral perfusion
    • hydration and BP
  • nimodipine
    • CCB that reduces vasospasm
  • surgery
    • surgical clipping of aneurysm
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57
Q

complications from SAH

A

re-bleeding is the most common cause of death

cerebral ischaemia due to vasospasm can cause permanent CNS deficit and is the commonest cause of morbidity

hydrocephalus due to blockage of arachnoid granulations

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58
Q

describe the mortality of SAH patients based on their signs

A
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59
Q

where does the bleeding come from in subdural haematoma

A

from bridging veins that connect the dural venous sinuses and the cortex

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60
Q

what happens in subdural haematoma

A
  • bridging veins are vulnerable to deceleration injury
  • this results in accumulating haematoma between the dura and the arachnoid
  • this gradually raises the ICP
  • this can lead to coning
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61
Q

what kind of event causes a subdural

A
  • they are mostly from trauma
    • trauma is often forgotten because it was so minor
    • trauma can have been up to 9 months ago
  • can occur without trauma
    • in the case of low ICP the brain shrinks and bridging veins are vulnerable
      • elderly patients and alcoholics with atrophy
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62
Q

three populations who are vulnerable to SDH

A

alcoholics

elderly

those on anticoagulant drugs

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63
Q

symptoms of a subdural haematoma

A
  • fluctuating consciousness
  • insidious intellectual or physical slowing
  • sleepiness
  • headache
  • personality change
  • unsteadiness
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64
Q

signs of SDH

A

rising ICP

seizures

localising neurological symptoms can occur amonth after injury

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65
Q

differentials for SDH

A

stroke

dementia

CNS masses

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66
Q

imaging for SDH

A

CT/MRI shows clot with or without a midline shift

crescent shaped collection of blood over one hemisphere (differentiates from extradural)

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67
Q

management of SDH

A
  • reverse any clotting abnormalities urgently
  • generally, lots over 19mm with 5mm midline shift need evacuating
    • craniotomy or
    • burr hole washout
  • address the cause of the trauma
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68
Q

what natural history should make you think of extradural haematoma

A

beware any loss of consciousness following any head injury that initially caused no loss of consciousness

or

after an initial drowsiness following an injury seems to have resolved

lucid interval pattern is typical of extradural bleeds

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69
Q

what typically causes an extradural haemorrhage

A

suspect after any traumatic skull fracture

often it’s a fractured temporal or parietal bone causing a laceration of the middle meningeal artery and/or vein

any tear in a dural venous sinus will also cause an extradural bleed

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70
Q

8 clinical features of EDH

A
  • lucid interval
    • hrs-days
  • lowering GCS
  • incresing ICP
  • increasingly severe headache
  • vomiting
  • confusion
  • seizures
  • hemiparesis
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71
Q

how do symptoms and signs of EDH progress if the bleeding continues

A

ipsilateral pupil may dilate

coma deepens

bilateral limb weakness develops

breathing may become deep and irregular (indicates brainstem compression)

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72
Q

differentials of EDH

A

epilepsy

carotid dissection

stroke

TIA

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73
Q

tests for suspected SDH

A
  • CT head
    • egg shaped bleed
  • Skull x ray
    • check for fracture lines crossing middle meningeal artery
  • REMEMBER THAT A LUMBAR PUNCTURE IS CONTRAINDICATED
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74
Q

What is the management of EDH

A

urgent transfer to neurosurgery for clot evacuation and ligation of bleeding vessel

care of the airway

if ICP is high then IV mannitol

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75
Q

prognosis for EDH and indicators

A

excellent if prompt diagnosis and management

poor if coma, pupil abnormalities or decerebrate rigidity are present pre-op

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76
Q

what is the definition of epilepsy

A

this is the recurrent tendancy to spontaneous intermittent abnormal electrical activity in the brain manifesting in seizures

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77
Q

how do you know if a blackout is epilepsy or syncope

A

Syncope is a temporary loss of consciousness usually related to insufficient blood flow to the brain

epilepsy is an electrical disturbance of brain function

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78
Q

what is the definition of epileptic seizure

A

paroxysmal event in which changes of behaviour, sensation or cognitive decline are processes that are caused by excessive hypersynchronous neuronal discharges in the brain

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79
Q

how long does an epileptic seizure last generally

A

30-120 seconds

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80
Q

how long can a post ictal state last, when does it happen and how is it characterised

A
  • 5-30 minutes after the seizure
  • characterised by:
    • drowsiness
    • confusion
    • nausea
    • hypertension
    • headache
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81
Q

what would an epileptic prodrome look like

A

it can last for hours or days before the seizure and it is a change in mood or behaviour

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82
Q

what portion of epileptic seizures are idiopathic

A

2/3

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83
Q

name three structural causes of epilepsy

A

cortical scarring due to a historic head injury

stroke

vascular malformation

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84
Q

what must an epilepsy history include

A

a detailed description from a witness of the seizure

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85
Q

broadly what are the two different types of seizures and what are the differences between them

A
  • Focal seizures (AKA partial seizures)
    • affects particular part of the body depending on the neurological origin of the seizure
  • Generalised seizures
    • originate from widespread electrical discharge that can’t be localised
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86
Q

what are the three types of focal seizure and very briefly what are the differences

A
  • without impairment of consciousness
    • and no post-ictal symptoms
  • with impairment of consciousness
    • consciousness may be impaired at time of seizure or after an aura
    • and there are commonly post-ictal seizures
  • evolving to a bilateral convulsing seizure
    • typically progresses to a convulsive generalised seizure
    • this occurs in 2/3 patients with partial seizures
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87
Q

what are the four types of generalised seizures and briefly describe each of them

A
  • absence seizures
    • brief pauses <10s - suddenly stops talking mid sentence before carrying on where left off
    • commonly presents in childhood
  • tonic clonic seizure
    • there’s loss of consciousness
    • limbs stiffen then jerk
    • commonly post ictal confusion and drowsiness
  • myoclonic seizures
    • sudden jerk of face, limb or trunk
    • might be suddenly thrown to ground or have sudden disobedient limb.
    • ‘plate throwing epilepsy’
  • atonic seizures
    • no loss of consciousness
    • sudden loss of muscle tone causing a fall
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88
Q

how many types of epilepsy are there and what is classification based on

A
  • there are over 40 types
  • classification is based on
    • seizure type
    • EEG findings
    • other features
    • age of onset
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89
Q

what is a provoked seizure

A

most people will have a seizure if provoked but this is not epilepsy

3-10% of provoked seizures recur

whereas 30-50% of unprovoked seizures occur

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90
Q

examples of seizure provocation

A
  • anoxic seizures following syncope
  • trauma
  • haemorrhage
  • alcohol or benzodiazepine withdrawal
  • infection
  • drugs (cocaine)
  • metabolite imbalance
    • glucose
    • sodium
    • calcium
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91
Q

Investigations of Epilepsy

A
  • look for a provoking cause
    • check metabolite levels
      • hyper or hypoglycaemia
      • hyper or hyponatraemia
      • hypocalcaemia
      • uremia
    • Drug levels (are they compliant with their anti-epileptic)
    • LP if infetion is suspected
  • consider an EEG
  • MRI to look for structural lesions
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92
Q

what type of activity should an epileptic patient not undertake

A

driving

swimming

heights

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93
Q

epilepsy and driving

A

the patient MUST contact the DVLA and not drive until they have been seizure free for >1yr

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94
Q

1st line medical treatment for focal seizures

A

carbamazepine or Lamotrigine

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95
Q

1st line medical treatment for generalised tonic-clonic seizures

A

sodium valproate or Lamotrigine

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96
Q

1st line treatment for absence seizures

A

sodium valproate

2nd line is Lamotrigine

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97
Q

1st line medical treatment for myoclonic seizures

A

sodium valproate

2nd line is levetiracetam

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98
Q

what drug might worsen myoclonic seizures

A

carbamazepine

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99
Q

what is the first line medical treatment for atonic seizures

A

sodium valproate or lamotrigine

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100
Q

surgery for epilepsy?

A

if there is a single, known epileptogenic focus then it can work

an example would be a tumour

carries risk of causing focal neurological defect

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101
Q

what is sudden unexpected death in epilepsy

A

this is more common in uncontrolled epilepsy

this may be related to nocturnal seizure-associated apnoea or systole

17% of epilepsy deaths are due to SUDEP

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102
Q

how much higher is mortality in epileptic population than in gen pop

A

3x higher

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103
Q

how many epilepsy related deaths are there in the UK every year

A

>700

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104
Q

three considerations for epilepsy in pregnancy

A

there’s a 5% risk of fetal abnormalities

sodium valproate is teratogenic so transition to other drugs is required

most AEDs are present in breast milk but lamotrigine is thought not to be harmful to infants

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105
Q

how long does syncope last and how long is recovery from syncope

A

lasts 5-30 seconds

recovery within 30s

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106
Q

what are non-epileptic seizures

A

these are psychogenic and situational

suspect if there’s gradual onset, prolonged duration and abrupt termination

also characteristic are closed eyes that are resistant to opening

can coexist with true epilepsy

patient may have history of mental illness

CNS exam, MRI, CT and EEG are all normal

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107
Q

What is status epilepticus

A
  • seizure lasting more than 30moinutes without intervening consciousness
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108
Q

what are the risks with status epilepticus

A

mortality

permanent brain damage

likelihood of both increase with the length of the attack

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109
Q

management of convulsive status epilepticus

A

secure airway and get anaesthetist support

oxygen

IV bolus of lorazepam to stop seizure

assess metabolite and drug levels

correct hypotension

correct metabolite levels

if seizures continue start phenytoin infusion

if seizure lasts more than 60-90mins anaesthetist may consider propofol infusion for paralysis

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110
Q

what is the mean age of onset of parkinson’s

A

60

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111
Q

what is the prevalence of parkinson’s at 85-95 years

A

3.5%

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112
Q

what is parkinsonism

A
  • triad of
    • resting tremor (‘pill rolling’)
    • hypertonia
    • bradykinesia - slow initiation of movement
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113
Q

what are two key features of parkinson’s seen on examination

A
  • cogwheel rigidity
    • caused by rigidity and tremor together
  • micrographia
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114
Q

what is the pathogenesis of parkinsons

A

loss of dopaminerfic neurons in the substantia nigra

this is associated with formation of lewy bodies in the basal ganglia, brain stem and cortex

most cases are sporadic but there are some genetic loci implicated in familial cases

115
Q

clinical features of parkinson’s

10 things

A
  • the parkinsonism triad
  • micrographia
  • non motor symptoms
    • autonomic disfunction
      • constipation
      • dribbling
      • urinary frequency/urgency
    • sleep disturbance
    • reduced sense of smell
  • neuropsychiatric complications
    • depression
    • dementia
    • psychosis
  • it is invariably worse on one side - if symmetrical then look for other causes
116
Q

diagnosis of parkinson’s

A

it is clinical and based on the triad

if there is a good response to dopaminergic therapy then this is supportive of the diagnosis

MRI to exclude structural pathology

117
Q

what is a non-pharmacological option for treatment of parkinson’s

A

deep brain stimulation

118
Q

when should you start pharmacological treatment for parkinson’s

A

when over 70 or when symptoms of parkinson’s are seriously interfering with life

this is because efficacy decreases with time and SEs get worse with time

119
Q

what are the 4 types of pharmacological treatment for parkinson’s

A

levodopa

dopamine agonists

mono amine oxidase B inhibitors (MAO-B)

COMT inhibitors

120
Q

what is the most important pharmacological treatment of parkinson’s

describe how it is given and with what

A

levodopa

it is given with a dopa-decarboxylase inhibitor (carbidopa) in a combined drug called co-careldopa or co-beneldopa

carbidopa helps the dopa not be metabolised before it reaches the brain

121
Q

what are the side effects of levodopa treatment

A

dyskinesia

dystonia

psychosis

hallucinations

nausea

vomiting

122
Q

what is an example of a dopamine agonist used for parkinson’s and why might they be used

A

ropinirole

can delay starting levodopa

123
Q

what is an example of a MAO-B, why might they be used and how do they work

A

selegiline

they are an alternative to dopamine agonists early in PD

they prevent the breakdown of dopamine

124
Q

what is an example of a COMT inhibitor, how does it work and what is a risk

A

tolcapone

stops the breakdown of levodopa

is hepatotoxic so close monitoring of LFTs is important

125
Q

what is the most common type of headache

A

tension headache

126
Q

if someone says it’s the first headache of this type that they’ve ever had and it’s the worst headache ever what should you be worried about

127
Q

if someone complains of unilateral headache and eye pain what is it

A

a cluster headache or alternatively acute glaucoma

128
Q

if a headache is initiated by a cough or is worse in the morning or on bending over what does it indicate

A

that it’s related to high ICP

129
Q

if there’s persisting headache with scalp tenderness in the over 50s what should you suspect

A

giant cell arteritis

130
Q

if there’s headache with fever or neck stiffness what should you be concerned about

A

meningitis

131
Q

two vital questions on taking a history of new headache

A

travel? malatia

pregnant? pre-eclampsia - especially if proteinuria and HTN

132
Q

are cluster headaches more common in men or women

133
Q

what is one modifiable risk factor for cluster headaches

134
Q

clinical presentation of cluster headache

A
  • rapid onset excruciating pain around one eye
  • eye can become watery and bloodshot with lid swelling and lacrimation
  • facial flushing
  • pain is strictly unilateral and always affets the same side
  • lasts from 15-180 minutes
  • occurs once or twice a day and is often nocturnal
  • clusters are 4-6 weeks and followed by periods of months to years between clusters
  • sometimes it can be chronic and not episodic
135
Q

treatment for acute attack of cluster headache

A

100% oxygen via non-rebreathe mask

SC sumatriptan

136
Q

prevention of cluster headaches

A

avoid triggers like alcohol

verapamil might help (CCB)

137
Q

what is the M:F for migraines

138
Q

what % of people suffer with migraines

139
Q

which artery territory stroke do you sometimes get akinetic muteness

and what is it

A

ACA

motor components not that affected but they can’t talk and they’re almost unconscious with it

140
Q

8 ACA territory stroke symptoms

A
  • Leg Weakness
  • Sensory disturbance in the legs (homonculi)
  • Gait Apraxia
  • Truncal Ataxia
  • Incontinence
  • Drowsiness
  • Akinetic Mutism
  • Decrease in spontaneous speech
  • Stuporus state
141
Q

6 MCA stroke symptoms

A
  • Contralateral arm and leg weakness
  • Contralateral sensory loss
  • Hemianopia
  • Aphasia
  • Dysphasia
  • Facial Droop
142
Q

PCA stroke symptoms

A
  • Contralateral homonymous hemianopia
  • cortical blindness with bilateral involvement of the occipital lobe branches
  • visual agnosia
  • Can’t interpret visual information, but can see
  • Prosopagnosia
  • dyslexia, Anomic aphasia, colour naming and discrimination problems
  • Headaches unilateral
143
Q

as strokes get older how does there appearance change on CT

A

the infarcted area gets darker

144
Q

what is MCA syndrome stroke

A

this is where the mca stroke is so big that all the oedema causes compression of the rest of the brain

it can lead to herniation and is very dangerous

145
Q

what is almost never a feature of ischaemic stroke and what is the exception

A

bad headache

the exception is in posterior cerebral artery strokes

146
Q

posterior circulation strokes symptoms

A
  • Motor deficits such as hemiparesis or tetraparesis and facial paresis
  • Dysarthria and speech impairment
  • Vertigo, nausea, and vomiting
  • Visual disturbances
  • Altered consciousness
147
Q

what part of the brain will be affected by posterior circulation strokes

A

the brainstem

can be devastating and has high mortality

148
Q

why can you detect change so quickly with MRI

A

MRI gives basically a map of water content of tissue

water changes in the brain happen rapidly in response to injury so you can sometimes see change within minutes

149
Q

what are warning syndromes

A

small infarcts in the small cerebral arteries

in people who are vasculopaths

they have transient motor symptoms that go away and come back repeatedly before persisting

warning syndrome occurs over a couple of days - ‘very odd and looks like a seizure’

it’s less self contained than a TIA

150
Q

when would clot retrieval be indicated in stroke patients

A

this only works for clots in larger arteries

151
Q

what does the modified rankin scale assess

A

the degree of disability or dependence in the daily activities of people who experience stroke

0-5

5 being worst, 0 being no symptoms

152
Q

characteristic CT signs for ruptured berry aneurysm on circle of willis

A

spider sign

153
Q

what are the classic presentations of migraines

A
  • visual or other aura lasting 15-30 minutes followed by 1hr unilateral throbbing headache
  • isolated aura with no headache
  • episodic severe headache without aura - may be premenstrual usually unilateral with nausea, vomiting and photophobia/phonophobia
  • maybe allodynia where all stimuli cause pain even brushing hair/wearing glasses
154
Q

what is an aura

A
  • Visual: chaotic melting and jumbling of lines and dots, with or without hemianopia
  • Somatosensory: paraesthesia spreading from fingers to face
  • Motor: dysarthria and ataxia
  • Speech: dysphasia and paraphasia
155
Q

how frequently do people with migraines have triggers

156
Q

what are the triggers for migraines

A
  • CHOCOLATE
    • Chocolate
    • Hangovers
    • Orgasms
    • Cheese/caffeine
    • Oral contraceptive
    • Lie ins
    • Travel
    • Exercise
157
Q

what two things are associated with migraine

A

family history and obesity

158
Q

diagnosis of migraines

A

clinical and is based on the history

  • the diagnostic criteria if there aer no aura are
    • >5 headaches lasting 4-72hrs with nausea/vomiting or photo/phonophobia
    • AND any 2 of:
      • unilateral
      • pulsating
      • impairs or is worsened by usual activity
159
Q

6 differentials for migraine

A

Cluster headaches

high BP

intracranial pathology

sinusitis

otitis media

TIA can mimic migraine aura

160
Q

last resort treatment for chronic migraine

A

12 weekly botulinum toxin type A injections

161
Q

prophylactic treatment for migraines

how much can it reduce attack frequency in patients

A

propanolol

this can achieve 50% reduction in attack frequency in most patients

162
Q

treatment during a migraine attack

A

triptans combined with either NSAIDs or paracetamol

anti-emetics for nausea

163
Q

when would a triptan be contraindicated

A

IHD, Coronary spasm and uncontrolled HTN

164
Q

non-pharma treatment for migraines

A

acupuncture

avoid identified triggers

ensure that it’s not analgesic rebound headache

165
Q

what are worsening headaches in pregnancy associated with

A

pre-eclampsia

166
Q

what percentage of MS patients develop progressive disability

167
Q

what is the concordance in identical twins of MS

168
Q

what is the geographical distribution of MS

A

there is increasing incidence at latitude

adult migrants take their risk with them

children migrants acquire the risk of the region in which they settle

169
Q

what is the mean age of onset of MS

170
Q

what is the M:F

171
Q

what is the presentation of MS

A

~20% of people present with unilateral optic neuritis (pain on moving the eye ± vision loss)

corticospinal tract and bladder invovlement are also common

symptoms may worsen the heat

can be sensory, motor, sexual/GU, GI, Eye, cerebellar and the presentation depends on site of the lesion

172
Q

Tests for MS

A
  • MRI - sensitive but not specific
    • but it’s the most useful since we can use it to exclude other causes of pathology
  • CSF
    • looking for oligoclonal bands of IgG that are not present in serum
  • Evoked potentials
    • you would see visual, auditory or somatosensory delays
173
Q

diagnosis of MS

A
  • this is made using the McDonald criteria
  • if the presentation is dead on then it may be enough to diagnose clinically
  • if there are fewer attacks and fewer clinical lesions then it’s likely the diagnosis needs to be confirmed with MRI, CSF and Evoked Potentials
174
Q

progression of MS

A
  • most patients follow relapsing remitting course followed by secondary progressive disease
  • 10% of patients have absence of relapses and this is called primary progressive MS
  • small minority of patients experience no progressive disablement at all
175
Q

what are poor prognostic signs in MS

A

older men

motor signs at onset

many early relapses

many MRI lesions

176
Q

what are 4 principles of managing MS

A

lifestyle advice

monoclonal antibodies

treating relapses

treating symptom control

177
Q

lifestyle advice for MS

A

regular exercise

stopping smoking

avoiding stress

178
Q

Monoclonal antibodies for MS

A

alemtuzumab (anti T-Cell)

179
Q

treating relapses in MS

A

methylprednisolone shortens acute relapses but must be used less than 2x a year due to SE

180
Q

treating symptom control in MS

use 4 main symptoms

A
  • spasticity
    • baclofen or gabopentin
  • tremor
    • Botulinum toxin A injections every 12 weeks
  • urinary urgency/frequency
    • potential for self-catheterisation
  • fatigue
    • CBT
    • exercise
181
Q

what is the prevalence of MND

A

6/100,000 people

182
Q

what is the M:F of motor neuron disease

183
Q

what can distinguish MND from MS and polyneuropathies?

A

in MND there is no sphincter loss and no sensory loss

184
Q

what distinguishes MND from myasthenia gravis

A

MND never affects eye movements

185
Q

what are the four clinical patterns of MND and which is the most common

A
  • Amyotrophic lateral sclerosis (ALS) 80%
  • Progressive bulbar palsy 10-20%
  • Progressive muscular atrophy
  • Primary lateral sclerosis
186
Q

what happens in progressive bulbar palsy

A

this only affects cranial nerves IX-XII and is a disease of these nuclei

LMN lesion of the tongue causes flaccid fasciculation of tongue (like a sack of worms)

speech can be quiet, horse or nasal

187
Q

where are neurons lost in ALS

A

motor cortex and the anterior horn of the cord so this combines UMN and LMN symptoms

188
Q

what is median age of onset in MND

189
Q

presentation of MND

A
  • stumbling spastic gait
  • foot drop
  • weak grip
  • shoulder abduction is hard (hair washing)
  • UMN signs
    • spasticity
    • brisk reflexes
    • upward plantars
  • LMN signs
    • wasting
    • fasciculation
    • areflexia
190
Q

what is the prognosis of MND

A

poor

half of patients survive less than 3 years post diagnosis

involve palliative care from diagnosis

191
Q

Members of the MDT for MND

A

neurologist

palliative nurse

hospice

physio

speech therapist

dietician

social services

192
Q

what is the only medicine shown to improve survival in MND and what does it do

A

riluzole

it is an inhibitor of glutamate

193
Q

symptomatic treatment of MND - 3

A
  • excess saliva
    • positioning
    • oral care
    • suctioning
    • botulinum toxin A may help
  • dysphagia
    • blend food
    • gastrostomy
  • communicative difficulty
    • augmentative and alternative communication equipment
194
Q

4 non-infective causes of meningitis

A
  • paraneoplastic
  • drug side effects
  • autoimmune
    • vasculitis
    • SLE
195
Q

10 clinical features of meningitis: divide into early and late

A
  • Early
    • headache
    • fever
    • leg pain
    • cold hands and feet
    • abnormal skin colour
  • Late
    • meningism
    • kernig’s sign
    • seizures
    • Petychial rash (non-blanching could be only 1 or 2 spots)
    • shock
196
Q

what is the mortality of bacterial meningitis when treated

197
Q

what percentage of patients have permanent effects from bacterial meningitis

198
Q

4 potential complications from bacterial meningitis

A

amputation

hearing loss

seizures

brain damage

199
Q

what is the immediate treatment for suspected bacterial meningitis

A

IM benzylpenicillin

200
Q

Management of suspected meningitis

A

Ix and Mx proceed in parallel

take blood cultures

begin empirical Abx early with ceftriaxone (can cros BBB)

if they are immunocompromised or >60 give amoxicillin too

give dexamethasone - steroid - helps reduce incidence of neuro sequelae

201
Q

when is a definitive diagnosis of meningitis given

A
  • later when a lumbar puncture is done - wait until patient is stable
  • Lumbar puncture
    • microscopy
    • gram stain
    • culture
    • viral PCR
202
Q

in suspected meningitis if the gram stain is -ve diplococci what is the causative organism likely to be

A

neisseria meningitidis

203
Q

in suspected meningitis if the gram stain is +ve diplococci what is the causative organism likely to be

A

strep pneumoniae

204
Q

what would the CIs for LP be in Meningitis

A

any evidence of shock

petychial rash

raised ICP

abnormal clotting

205
Q

Gram -ve rods that can cause meningitis

A

Haemophilus influenzae B

E.coli

206
Q

Gram positive rods that can cause meningitis

207
Q

gram +ve cocci that can cause meningitis

A

group B strep

208
Q

3 viruses that can cause meningitis

A

enterovirus

herpes simplex virus

varicella zoster virus

209
Q

5 differential diagnoses of meningitis

A

migraine

flu or other viral illness

sinusitis

brain abscess

malaria

210
Q

Public health for meningitis

A

if it’s neisseria meningitis then close contacts need to be notified immediately

they have a 1/300 chance of developing meninigits

they should be given Abx prophylactically

reduces risk and prevents onward transmission

211
Q

abx prophylaxis for meningitis high risk

A

ciprofloxacin or rifampicin

212
Q

6 signs and symptoms of encephalitis

A

bizarre behaviour or confusion

falling GCS

fever

headache

focal neuro signs

seizures

213
Q

causes of encephalitis

A
  • it is usually viral
    • mainly HSV
    • varicella zoster
    • west nile (ask about travel)
  • Non-viral causes
    • any bacterial meningitis
    • autoimmune or paraneoplastic
214
Q

What is the mortality of untreated viral encephalitis

215
Q

Ix of suspected encephalitis

A
  • MRI head
    • is there meningeal involvement? meningoencephalitis
  • LP and viral PCR
216
Q

encephalitis management

A
  • start IV acyclovir within 30 minutes of patient arriving as empirical treatment for HSV
  • supportive therapy in ICU if necessary
  • symptomatic treatment like phenytoin for seizures
217
Q

what is the name of the bacteria that causes tetanus

A

clostridium tetani

218
Q

tetanus presentation - 9 things

A
  • trismus - lockjaw
  • risus sardonicus - grin of hypertonic facial muscles
  • respiratory compromise
  • generalised spasms
  • pain
  • hypertension
  • tachycardia
  • arrhythmia
  • fever
219
Q

how many people does rabies kill every year

A

35-50 thousand globally

220
Q

what is the incubation period of rabies

A

min two weeks - max years

221
Q

what is the prodromal presentation of rabies - 6 things

A

headache

malaise

odd behaviour

agitation

fever

paraesthesia at bite site

222
Q

what are the two forms of rabies disease

A

furious rabies

paralytic rabies

223
Q

what are some features of furious rabies

A

hyperactivity and terror (e.g. hydrophobicity)

224
Q

what happens in paralytic rabies

A

flaccid paralysis of bitten limb –> coma –> death

225
Q

treatment following bite

A

wash wound for more than 15 minutes with soap and water

post exposure prophylaxis with vaccine and rabies Ig

226
Q

what is the incubation period of varicella zoster virus

227
Q

what does VZV do once it is in the body

A

infiltrates the respiratory mucosa

replicates in lymph nodes

disseminates to the skin forming virus containing vesicles which are chickn pox

remains in sensory nerve roots

reactivation (shingles) is dermatomal

228
Q

chicken pox prodrome

A

lasts 1-2 days

fever

malaise

headache

abdo pain

229
Q

what type of rash from chicken pox and how long does it last

A

pruritic

macular before becoming vesicular

lasts around 48hrs

230
Q

when are you contageous with chicken pox

A

1-2 days pre rash and 5 days post rash

231
Q

what is the presentation of shingles

A

macular rash becoming vesicular in dermatomal distribution

disseminated infection in the immunosuppressed

infectious until scabs appear

232
Q

treatment for shingles

what if pregnant

A

ora acyclovir for uncomplicated chicken pox/shingles in adults

needs to be taken within 48hrs of onset of rash

IV acyclovir if pregnant

233
Q

what is a coup and a centre coup

A

coup is a brain bruise at the site of impact

centre coup is the one at the opposite side of the impact

234
Q

what is diffuse axonal injury following head injury and what are the consequences

A

this is a clinicopathological syndrome of widespread axonal damage (including to the brainstem)

it usually involves acceleration and deceleration of head

mild –> recovery of consciousness ± long term deficit

severe –> unconscious from impact and may remain so or conscious with severe disability

235
Q

initial features of chronic traumatic encephalopathy

5 things

A
  • irritability
  • impulsivity
  • aggression
  • depression
  • memory loss
    *
236
Q

later features of Chronic Traumatic Encephalopathy

A

dementia

gait and speech problems

parkinsonism

237
Q

clinical findings in chronic traumatic encephalopathy

3 things

A
  • Atrophy of many nuceli
  • Enlarged ventricles with a fenestrated cavum septum
  • Tau positive neurofibrillary astrocytic tangles
238
Q

in general what do you treat seizures with in the acute setting

A

lorazepam ± phenytoin

239
Q

what is giant cell arteritis

A
  • aka temporal arteritis
  • granulomatous arteritis of the aorta and larger vessels like the extracranial branches of the carotid arteries
240
Q

which arteries does giant cell arteritis typically affect

A

temporal

opthalmic

facial

occipital

carotid

241
Q

what is the M:F of giant cell arteritis and at what age does it affect

A

M:F is 1:2

consider it in those over 50

incidence increases with age

242
Q

how does temporal arteritis present?

A

headache

jaw claudication

scalp tendernes

non-specific malaise

acute blindness in one eye

ESR may be raised

243
Q

what is it when arteritis presents with acute blindness in one eye

A

this is irreversible blindness

it’s called arteric ischaemic optic neuropathy (AION)

urgent medical emergency to prevent blindness in the other eye

244
Q

diagnosis of temporal arteritis

A

temporal artey biopsy is the goldstandard

you will see necrotising arteritis

245
Q

what is AION

A

arteric ischaemic optic neuropathy

this is sudden painless monocular visual loss

the optic disk becomes swollen and pale with haemorrhages at the margin

this is diagnostic of GCA since you don’t see these changes elsewhere

246
Q

treatment for temporal arteritis

A

prompt corticosteroids like prednisolone

normally a dramatic response in 48hrs

guide treatment using CRP and ESR

247
Q

what are the autoantibodies against in myasthenia gravis and which immune cells are implicated

A

the antibodies are against nicotinic acetylcholine receptors on the post synaptic side of the neuromuscular junction

both T and B cells are involved

248
Q

muscle groups affected by myasthenia gravis in order of most commonly affected to least

A

extraocular

bulbar (swallowing/chewing)

face

neck

limb girdle

Evil Boys Find No Love

249
Q

4 signs of myasthenia gravis

A

ptosis

diplopia

myasthenic snarl on smiling

voice fades on counting to 50 (dysphonia)

250
Q

8 things that can make myasthenia gravis symptoms worse

A

pregnancy

infection

over treatment

change of climate

emotion

exercise

beta blockers

opiates

251
Q

associations between myasthenia gravis and other diseases

A

RA and SLE

women under 50 it’s associated with thymic hyperplasia

men over 50 it’s associated with thymic atrophy and thymic tumour

252
Q

Ix of myasthenia gravis

A
  • raised anti-AChR antibodies present in 90%
  • If anti AChR abs are -ve then look for anti-MuSK (muscle specific tyrosine kinase)
  • neat test for clinic: ptosis improves by >2mm after ice application to eyelid for more than 2mins (NOT DIAGNOSTIC)
253
Q

treatment for myasthenia gravis

A
  • anticholinestarase e.g. pyridostigmine
    • has cholinergic side effects
  • immunosuppression
    • treat relapses with prednisolone
254
Q

what is myasthenic crisis and how do you treat it

A
  • it is life threatening weakness of resp muscles during a relapse
  • difficult to differentiate from cholinergic crisis (which you can get from over treatment)
  • monitor their FVC
  • ventilate if necessary
  • treat with plasmapheresis (removes AChR antibodies in blood)
  • identify and treat the trigger of the relapse
255
Q

what is the incidence of GBS

A

1-2/100,000 per year

256
Q

how does GBS present

A

a few weeks after an infeciton a symmetrial ascending muscle weakness starts

257
Q

5 triggers for GBS

A

campylobacter jejuni

CMV

Mycoplasma

HIV

EBV

258
Q

what about GBS is unusual for neuropathies

A

proximal muscles may be more affected than distal

259
Q

treatment for GBS

A

ventilate if necessary

IV Ig

plasma exchange

steroids have no role

260
Q

prognosis for GBS

A

Good

~85% make a full or nearly full recovery

10% are unable to walk alone at 1 yr

mortality is 10%

262
Q

what mode of inheritance is huntington’s

A

AD inheritance

263
Q

what are the symptoms of huntington’s chorea

A
  • early
    • irritability
    • depression
    • incoordination
  • progresses to
    • chorea
    • death
    • seizures
    • death within 15 years of diagnosis
264
Q

what is the genetic basis of Huntington’s

A

expansion of CAG repeats on chromosome 4

number of repeats correlates with severity of disease

<26 repeats is normal

>40 is full penetrance

265
Q

triggers for trigeminal neuralgia

A

washing affected area

shaving

eating

talking

266
Q

symptoms of trigeminal neuralgia

A

paroxysmal intense stabbing pain that lasts seconds in the trigeminal nerve distribution

it is unilateral

typically affects mandibular or maxillary divisions

267
Q

who is most affected by trigeminal neuralgia

A

generally it’s men >50

268
Q

causes of trigeminal neuralgia

A
  • compression of the trigeminal root by:
    • aneurysmal intercrania vessels
    • tumour
    • MS
    • skull base malformations
269
Q

Ix

A

MRI needed to exclude dangerous secondary causes

270
Q

Treatment for trigeminal neuralgia

A
  • anti-convilsant medication
    • carbamazepine
    • phenytoin
    • Lamotrigine
271
Q

what percentage of people over 80 have dementia

272
Q

initial Ix of dementia

A

AMTS

MSE to identify anxiety, depression or hallucinations

273
Q

name 4 types of dementia

A

alzheimers

vascular dementia

lewy body dementia

fronto-temporal dementia

274
Q

what percentage of dementia is vascular dementia

275
Q

what is vascular dementia

A

it is the cumulative effect of many small strokes

it has a sudden onset and a stepwise deterioration

look for signs of arteriopathy (HTN, past strokes, focal CNS signs)

276
Q

what is lewy body dementia

A

there’s fluctuating congnitive impairment

they have detailed visual hallucinations

later they get parkinsonism

histology is characterised by lewy bodies in the brainstem and neocortex

277
Q

fronto-temporal dementia

A

frontal and temporal atrophy with loss of >70% of spindle neurons

executive impairment

behavioural/personality change

disinhibition

hyperorality

emotional unconcern

episodic memory and spatial orientation are preserved until later stages

278
Q

7 clinical features of alzheimers

A
  • impairment of
    • visuo-spatial skill
    • memory verbal abilities
    • executive function
  • anosogosia
    • lack of insight
  • irritability
  • mood disturbance
  • psychosis
  • agnosia
279
Q

most vulnerable parts of the brain in alzheimers

A

hippocampus

amygdala

temporal neocortex

subcortical nuclei

280
Q

three risk factors for alzheimers

A
  • 1st degree relative with AD
  • down’s syndrome
    • inevitable
  • homozygosity for ApoE allele E4 on chr 19
    • increases risk x12
281
Q

what is mean survival from diagnosis of unequivocal alzheimer’s symptoms

282
Q

what is the management of Alzheimers

A
  • acetylcholinesterase inhibitors like donepezil
    • these can cause heart block and peptic ulcer disease
    • discontinue if no improvement
    • do not use in mild disease
  • BP control
283
Q

what occurs on a cellular and molecular level in alzheimers

A
  • accumulation of beta-amyloid peptide
  • results in
    • neuronal damage
    • neurofibrillary tangles
    • more amyloid plaques
    • loss of Ach

formative 3b (18 decks)

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