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CP3 Medicine > Neurology 2 > Flashcards

Neurology 2 Flashcards

1
Q

What is normal ICP?

A

0-10mmHg

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2
Q

What are the causes of increased ICP?

A

Vasogenic: increased capillary permeability
tumour, trauma, ischaemia, infection

cytotoxic: cell death
interstitial: obstructive hydrocephalus

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3
Q

What are the symptoms of increasing ICP?

A

Headache: dull persisting ache, worse on lying, present on waking, worse by coughing / straining
vomiting
seizures
irritability

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4
Q

What are the signs of increasing ICP?

A

GCS deterioration
progressive dilation of pupil on the affected side
Cushing’s reflex
Cheyne-Stokes respiration

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5
Q

What is the management of increasing ICP?

A

A-E
Elevate the head of the bed to 30-40 degrees
If intubated, hyperventilate to reduce PaCo2
(immediately decreases ICP)

Mannitol: 0.2g/kg 20% IV over 15 minutes
Clinical effect after 20 minutes

Corticosteroid - if oedema around tumour

Fluid restriction

Consider monitoring ICP - surgically implanted extradural catheter

Make diagnosis and treat

controlled hypothermia, CSF drainage and barbiturates

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6
Q

How would you approach a patient with ?spinal cord trauma?

A

A-E
MOI
Physical exam: visual inspection, palpation of vertebral column, neurological assessment

Imaging: AP/lateral C2 open mouth
CT
spine x ray

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7
Q

What are the indications for CT spine?

A

If already having head/other body CT
If X-rays are suspicious
If intubated/rapid diagnosis required

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8
Q

Describe the approach to the unconscious patient?

A

A-E

LOC - needs C-spine stabilisation: collar or sandbags and tape
neurological deterioration: urgent CT head to T4/5 should be performed
If not, x ray of c, t and l-spine

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9
Q

What factors might indicate radiography of c-spine?

A

over 65
paraesthesia in the extremities
dangerous mechanism
5 factors not cleared

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10
Q

What are the 5 factors that clinically Clear the C-spine?

A 
Simple rear end RTA
sitting position in ED
Walking at any time
delayed onset of neck pain 
absence of C-spine tenderness

If none present, radiography is required

If one or more - patient asked to rotate the neck 45 degrees to the left and to the right
If the patient able to do this, C-spine cleared

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11
Q

What bone is injured in base of skull fracture?

A

Temporal bone (75%) - known as posterior fossa fracture

Anterior fossa (25%): occipital, sphenoid and ethmoid bones

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12
Q

What are the signs of posterior fossa base of skull fractures ?

A

Battle’s sign: bruising over the mastoids
CSF otorrhoea
Bleeding of the ear
Conductive deafness: lasts 6-8 weeks
If lasting <3 weeks may be due to haemo-tympanum / mucosal oedema

CN palsies of V, VI and VII
Facial numbness and weakness, lateral rectus palsy

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13
Q

What are the signs of anterior fossa fractures?

A

Raccoon eyes
CSF rhinorrhoea
bleeding from the nose

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14
Q

Which base of skull fractures require referral to neurosurgery?

A

posterior fossa - need referral but often will not require intervention

anterior fossa - urgent referral

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15
Q

What are the complications of base of skull fractures?

A

Intracranial infection (relatively rare)
facial nerve palsy
ossicular chain disruption
carotid injury

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16
Q

How are depressed skull fractures managed?

A

Can be subtle on examination
Impossible to know if there is interruption of the dura without exploration
All compound depressed skull fractures are surgically explored within 12 hours

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17
Q

Describe motor response on GCS

A

motor / 6

6: obeys commands
5: localises to pain
4: withdraws from pain
3: flexor response to pain:
2: extensor response to pain
1: no response

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18
Q

Describe verbal response on GCS?

A

verbal / 5:

5: orientated
4: confused conversation: responds to questions, some disorientation
3: inappropriate speech, random speech, no conversational exchange
2: incomprehensible speech: moaning but no words
1: no speech

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19
Q

Describe eye response on GCS?

A

eye / 4

4: spontaneous eye opening
3: eye opening in response to speech
2: eye opening in response to pain
1: no eye opening

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20
Q

How is GCS classified in terms of injury?

A

13-15: mild injury
9-12: moderate injury
<9: severe injury

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21
Q

What are the neuro differentials for an unconscious patient?

A

Vascular: stroke, shock, haematoma, SAH

Infective / inflammatory: sepsis, meningitis, encephalitis, abscess

Trauma: traumatic brain injury

Autoimmune: brainstem demyelination

Metabolic: hypo/hyper: glycaemia, calcaemia, natraemia
hypo: adrenals, thyroidism
severe uraemia
Wernicke-Korsakoff

Neoplasm: cerebral tumour

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22
Q

How should an unconscious neuro patient be managed?

A 
A-E + 
temperature 
breathe
top to toe examination 
respiration: classical patterns 
Cheyne stokes
kussmaul resp: deep and laboured

Neurological
pupils: classical signs

Ix: bloods and urine tests
imaging: head CT and MRI

LP: if CT excluded mass lesions / raised ICP

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23
Q

What are the classical pupil signs?

A

Unilateral dilated pupil: raised ICP
Bilateral fixed, dilated pupil: sign of brainstem death or deep coma
pinpoint: opiate overdose, pontine lesions interrupting the sympathetic pathway

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24
Q

What is a STROKE?

A

an acute, focal neurological deficit of cerebrovascular origin that persists >24 hours

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25
Q

What is a TIA?

A

An acute, focal neurological deficit of cerebrovascular origin that persists <1 hour without signs of cerebral infarction on MRI scanning

High risk of stroke within 4 weeks of a TIA

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26
Q

What is amaurosis fugax?

A

Sudden, transient loss of vision in one eye
Often occurs with TIAs and cane the first clinical evidence of ICA stenosis
This can also occur due to ocular disease or migraine

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27
Q

What are the irreversible risk factors for ischaemic stroke?

A

age
personal / family history
hyper-coagulable states
atrial fibrillation

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28
Q

What are the reversible risk factors for ischaemic stroke?

A 
Hypertension 
hypercholesterolaemia 
diabetes
smoking
acohol
poor diet
low exercise
increased weight 
use of oestrogen containing oral contraceptives

less commonly: endocarditis, migraine, polycythaemia, APL syndrome, vasculitis, amyloiditis

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29
Q

What are the risk factors for haemorrhagic stroke?

A 
Family history
Uncontrolled hypertension 
Vascular abnormalities (aneurysms, AVMs, HHT) 
Coagulopathies / anticoagulant therapy
Heavy recent alcohol intake
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30
Q

What are the two types of stroke?

A

ISCHAEMIC (85%): arterial embolus from a distant side
arterial thrombosis in atheromatous carotid, vertebral or basilar artery

HAEMORRHAGIC (15%)
SAH: 5%
Intra-cerebral haemorrhage: 10%

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31
Q

What are the three types of cerebral ischaemia?

A

Regional infarction
lacunar infarction
global ischaemia

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32
Q

What is a regional infarction?

A

Thrombosis / embolus in large vessels

usually affects cortical areas

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33
Q

What are lacunar infarctions?

A

microinfarcts: caused by small vessel disease: arteriosclerosis
usually affecting sub-cortical areas e.g. basal ganglia
can be asymptomatic

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34
Q

What is global ischaemia?

A

infarcts at arterial boundary zones due to a global reduction in blood flow due to severe hypotension

‘watershed’ infarction

if severe, can cause cortical laminar necrosis where there is death of the majority of neurones 24 hours after the insult, with patient remaining in a vegetative state

‘post-arrest syndrome’

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35
Q

What are the three zones of cerebral ischaemic damage?

A

Infarct core: tissue almost certain to die
oligaemic periphery: tissue that will survive, due to collateral supply
ischaemic penumbra: tissue in between - can have either outcome

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36
Q

What is malignant MCA syndrome?

A

when large cerebral infarcts cause death by associated tissue oedema, leading to herniation ad brainstem compression

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37
Q

What are the clinical features of ischaemic stroke?

A 
Contralateral limb weakness / hemiplegia 
facial weakness
higher dysfunction 
visual disturbances 
epileptic fit (rare)
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38
Q

What higher dysfunction symptoms can be seen in ischaemic stroke?

A 
Expressive aphasia
Receptive aphasia
Apraxia
Asterognosis 
Agnosia 
Inattention
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39
Q

What are the 4 different types of stroke?

A

TACS: proximal MCA occlusion
PACS: distal MCA or ACA occlusion
LACS: occlusion of a lacunar branch of the MCA
POCS: PCA occlusion

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40
Q

What are the criteria for TACS?

A

Contralateral hemiplegia and/or sensory loss; must be at least 2 of face/arm/leg involvement

Homonymous hemianopia

Higher dysfunction: dysphasia, decreased level of consciousness, visuo-spatial neglect, asterognosis or apraxia

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41
Q

What are the criteria for PACS?

A

two out of three TACS criteria:
hemiplegia and/or sensory loss
homonymous hemianopia
higher dysfunction

Higher dysfunction alone with vision spared

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42
Q

What are the criteria for LACS?

A

Pure motor symptoms (>2/3 face, arm, leg)
Pure sensory symptoms (>2/3 face, arm, leg)
Pure sensorimotor symptoms (>2 face, arm, leg)
Ataxic hemiparesis

2 of the face/arm/legs
the lenticulate striate vessels are deep vessels, so no higher cortical functions are affected

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43
Q

What are the criteria for POCS?

A

one of

  1. Cranial nerve palsy AND contralateral motor/sensory deficit
  2. Bilateral motor or sensory deficit
  3. Conjugate eye movement problems such as nystagmus or double vision
  4. Cerebellar dysfunction
  5. Isolated homonymous hemianopia
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44
Q

Describe the prognosis for TACS

A

60% die after 1 year
35% are dependent only 5% independent
low recurrence risk

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45
Q

Describe the prognosis for PACS

A

15% die within a year
30% dependent 55% independent
20% recurrence 1 year

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46
Q

Describe the prognosis for LACS

A

10% die within a year
30% dependent, 60% independent
10% recurrent within a year

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47
Q

Describe the prognosis for POCS

A

20% due within a year
30% dependent
50% independent

20% recurrence within a year

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48
Q

History points for stroke

A

Exact time of onset , body parts affected, seizure at onset

PMH: previous stroke / MI , AF, DM, abscess , tumour

DH: warfarin, heparin, OCP

Social: alcohol abuse, smoking, illicit drugs

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49
Q

How would you examine a patient with ?stroke

A

A-E DONT FORGET GLUCOSE!
GCS

NHISS - national institute of health stroke scale
15-item neurologic examination stroke scale, evaluating levels of lots of different neurological deficit

CVS and heart signs

Resp: spo2, RR, crackles

Neurological: UMN/LMN, CNS, cerebellar examination

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50
Q

What investigations would you do for ?stroke

A

Bloods: FBC, U&Es, glucose + HbA1c, lipids, coagulation studies, ESR

Brain imaging - CT to exclude primary intracranial haemorrhage

MRI?

ECG

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51
Q

What are the indications for brain imaging within 1 hour?

A

if considering thrombolysis
if bleeding risk/headache at onset
if decreased consciousness
if neck stiffness

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52
Q

What is the aim of imaging in ?stroke

A

define arterial territory, exclude stroke mimics and determine haemorrhagic vs thrombo-embolic pathology

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53
Q

CT vs MRI for stroke?

A

MRI: gold standard, higher resolution imaging of arterial territories, but less commonly used due to availability

CT: rapid and commonly used, mainly to exclude haemorrhage. Early signs of infarct seen. If visible on CT, lesions will be seen by day 7

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54
Q

what is the acute management of stroke?

A

A-E
Aspirin 300mg STAT

Once haemorrhage excluded on CT, thrombolysis if within 4.5 hours (alteplase)
THrombectomy within 6 hours

Ward management: SALT, physio, OT, nursing, LMWH on day 3 post stroke

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55
Q

Describe the indications and dose of thrombolysis

A

First, check for contra-indications
must have laboratory blood results back and excluded Haemorrhage by imaging

Within 4 hours

Alteplase 0.9mg/kg as per clinical pathway within hospital

10% bolus over 1 minute, remainder over 60 minutes

56
Q

Describe the roles of the MDT in the management of a stroke patient

A

SALT: swallow assessment within 2 hours, also help patients with communication

Physio: relieve spasticity and prevent contractures
Baclofen may be used to relieve spasticity
early mobilisation = vital

OT: limb splinting, ward groups
Nursing: SSKIN bundle, early nutrition required if NBM

57
Q

How is eligibility for thrombolysis assessed in practice?

A

emergency cal - stroke consultant notified

quick, focussed hx ad examination, NIHSS score
assess for contraindications
IV access, baseline bloods
Weight 
Catheterise

URGENT CT and thrombolyse after consultant review

58
Q

How is the patient monitored following thrombolysis?

A

patient closely monitored over 24 hours via cardiac monitor and has specific observations completed on STOC (stroke thrombolysis observation chart).

if patient develops a severe headache, acute HTN, n+V they get an emergency CT

59
Q

What therapeutic interventions should be avoided following thrombolysis?

A

avoid: catheterisation during infusion
avoid aspirin or heparin for 24 hours
avoid NG tube insertion for 24 hours

60
Q

What is the management of stroke if thrombolysis is contra-indicated?

A

300mg Aspirin STAT

Manage conservatively on ward

61
Q

What is the secondary prevention management of stroke?

A

Antihypertensive therapy:
anti platelet: 300mg aspirin od for 2 weeks and clopidogrel 75mg after

atorvastatin 80mg offer from 48 hours post-stroke regardless of cholesterol levels

identify and tackle lifestyle factors:
stop smoking and excess alcohol, regular exercise, cardio protective diet
manage other co-morbidities: good AF control / anticoagulation, good diabetes control + carotid USS

62
Q

What are the driving regulations post-stroke?

A

normal license: must not drive for 4 weeks post-stroke

after this, they may return if clinical improvement is ok without notifying DVLA

63
Q

Describe the post-stroke complications

A 
Malignant MCA syndrome
DVT / pulmonary embolism 
Aspiration and hydrostatic pneumonia 
pressure sores 
depression 
seizures
incontinence
post-stroke pain - worsens outcome, multi-factorial in nature (central, muscular etc) 
often requires pain team input
64
Q

What is malignant MCA syndrome?

A

Rapid neurological deterioration due to the effects of cerebral oedema following middle cerebral artery territory stroke

high morbidity / mortality, occurring mainly in patients <60

65
Q

What is the presentation of malignant MCA syndrome?

A

Increasing agitation / restlessness
reducing GCS
haemodynamic / thermal instability
signs of raised ICP

66
Q

What is the management of malignant MCA syndrome?

A

decompressive hemicraniectomy
if CT/MRI shows an infarct of at least 50% of the MCA territory, in a patient <60 with any decrease in gcs, NICE recommend immediate referral for decompressive hemicraniectomy

67
Q

What are the high risk features of a TIA?

A

Recurrent TIAs within a short period of time
AF or TIA whilst anticoagulated
ABCD2 score 4+

68
Q

What are the ABCD2 criteria ?

A

AGE: >60 = 1 point
BLOOD PRESSURE: >140/90 = 1 point
CLINICAL FEATURES: unilateral weakness = 2 points
speech disturbance without weakness = 1 point
DURATION of symptoms: 60+ mins = 2 points
10-59 minutes = 1 point
DIABETES: 1 point if pre-existing

69
Q

What is the management if high risk features are present?

A 
300mg aspirin (unless contraindicated) 
if currently taking low-dose aspirin, continue current dose
arrange referral to a specialist clinic within 24 hours 
advise patients not to drive until seen by specialist

Secondary prevention: Atorvastatin 80mg

If low risk, mx = the same but referral to specialist is less urgent; within 1 week

70
Q

How are these patients managed in specialist clinic?

A

carotid artery doppler to assess for carotid artery stenosis
if >50%, carotid endarterectomy should be offered

71
Q

What are the benefits of carotid endarterectomy?

A

reduces risk of further stroke / TIA by 75%
risk of procedure related stroke and mortality risks also
an alternative is percutaneous luminal angioplasty +/- stunting

72
Q

What are the risk factors for venous sinus thrombosis?

A

Pro-thrombotic risk factor (85%) - OCP, pregnancy, malignancy, genetic thrombophilia

head injury
recent LP
Infection

73
Q

Describe the pathology of venous sinus thrombosis?

A

Venous infarction leads to vascular congestion
eventually there is haemorrhagic necrosis

split into cortical and dural venous thrombosis

74
Q

Describe the signs of cortical venous thrombosis?

A 
Headache: may be thunderclap 
focal signs
seizures
fever
encephalopathy
75
Q

What are the signs of dural venous sinus thrombosis?

A 
cavernous sinus thrombosis:
ocular pain, worse on movement 
Proptosis and chemises 
ophthalmoplegia 
papilloedema 
fever

saggital and lateral sinus thrombosis: signs of raised ICP, headache, vomiting, fever, papilloedema, seizures

76
Q

What are the investigations and findings for venous sinus thrombosis?

A

CT: often normal
LP: raised ICP
MRI angiography: may be required for diagnosis

SUSPECT if thunderclap headache and raised ICP with no signs of meningitis and no changes on CT

77
Q

What percentage of strokes are haemorrhagic?

A

15%
10% intra-cerebral haemorrhage
5% SAH

78
Q

What is the cause of deep intra-cerebral haemorrhage?

A

Rupture of micro-aneurysms and degeneration of small deep penetrating arteries

Occur in sub-cortical areas

79
Q

Who gets lobar intra-cerebral haemorrhage?

A

occurs in normotensive individuals >60 in the cerebral cortex

can be (rarely) caused by cerebral amyloid angiopathy

80
Q

What is the presentation of intra-cerebral haemorrhage?

A

As per haemorrhagic stroke

81
Q

What ix should be done for intra-cerebral haemorrhage?

A

CT - haemorrhage seen immediately

MRI: very reliable after 2 hours from symptom onset

82
Q

What is the management of intra-cerebral haemorrhage?

A

CT head immediately
FBC and clotting
ADMIT
Surgical tx discussed and ICU for ventilation

reverse anticoagulation
Lower BP to <140/90 in 1 hour: IV betalol but avoid hypotension

Neurosurgical intervention may be required: if deepening coma and coning

83
Q

What is the presentation of SAH?

A

Thunderclap headache - develops over seconds, usually in times of transient hypertension like exercise or sex

vomiting: comes on after developing the headache
Photophobia
increasing drowsiness / coma
focal signs may point to location of lesion

84
Q

What are the examination findings of SAH?

A

Neck stiffness

Positive Kernig’s sign: takes 6 hours to develop
Papilloedema: may be present, along with retinal haemorrhages

patient may earlier have experienced a sentinel headache due to a small warning leak from the offending aneurysm.

85
Q

What are the predisposing abnormalities for SAH?

A

Berry aneurysm: 70%
arteriovenous malformations: 10%
no lesion found: 20%

86
Q

Where do berry aneurysms form?

A

Circle of Willis and adjacent arteries:
Anterior communicating artery - most common
posterior communicating artery: at bifurcation from ICA
Middle cerebral artery: at the bifurcation / trifurcation

87
Q

What are the risk factors for berry aneurysms?

A 
polycystic kidney disease
FH
smoking
HTN
Ehlers-Danlos / Marfans
88
Q

What are arteriovenous malformations?

A

congenital collection of abnormal arteries / veins
Tendency to rebleed if symptomatic once

10% will rebleed annually
can also cause epilepsy, often focal

89
Q

What are the complications of SAH?

A

Death - 30% will die immediately

Rebleed: aneurysms - if vasospasm is sufficient, a clot can form but this rebleeds in 3-4 days
AVM: rebleed in years

Hydrocephalus: due to fibrosis in the CSF pathways
Cerebral vasospasm: can be severe, leading to delayed ischaemic change

90
Q

What investigations should be done for SAH?

A

Bloods: FBC, U+E, LFT, ESR, clotting
CT: initial investigation of choice
LP: if CT normal - >12h after symptom onset. CSF will be xanthochromic, visual inspection enough for diagnosis

CT/MRI angiography in all patients fit for surgery

91
Q

What is the management of SAH?

A 
4 weeks bed rest - HTN control 
nimodipine - prevent vasospasm, reduce mortality 
IV fluids: prevent vasospasm
analgesia, anti-emetics 
stool softeners to prevent straining 
discuss with neurology
?Surgical intervention
92
Q

What neurosurgical interventions might be done for SAH?

A

‘coiling’ - inserting a catheter into the arterial system (taking an “endovascular approach”), placing platinum coils into the aneurysm and sealing it off from the artery.

neurosurgical clipping

93
Q

What is subdural haematoma?

A

collection of blood in the subdural space following rupture of a vein, usually following a head injury, although can occur spontaneously

94
Q

What is the cause of acute subdural haematoma?

A

Severe acceleration-deceleration head injury, often with co-existing brain damage

95
Q

Describe the typical patient with acute subdural haematoma

A

young - come into hospital with a dilated pupil and no lucid interval before decreased GCS

96
Q

What is the management of acute subdural haematoma?

A

Craniotomy and early evacuation of the Clot
often seriously ill even with early intervention

need ICU admission with intracranial pressure monitoring

97
Q

What are the causes of subacute subdural haematoma?

A

May occur spontaneously or after minor trauma
risk factors:
elderly - cortical atrophy stretches brittle veins
alcohol abuse: clotting is reduced
other coagulopathies

98
Q

What are the s/s of subacute subdural haematoma?

A 
raised ICP signs: 
headache
drowsiness
confusion 
focal neurological signs

eventually stupor and coma due to coning

99
Q

What imaging modality should be used for subdural haematoma?

What changes are seen?

A

CT
acute: classical crescenteric shape with increased density (white) conforming to the contour of the skull
may be accompanying midline shift and compression of the ventricles

Chronic subdural haematoma: blood becomes more radiolucent (dark) and assumes a lentiform shape similar to that of an extradural haematoma

100
Q

What patients get extradural haematoma?

A

young patients following minor assault or sporting injury

blow = to Side of head, enough to cause a fracture and associated tearing of the middle meningeal artery

Blood accumulates rapidly over minutes to hours in the extradural space

101
Q

What is the presentation of extradural haematoma?

A

brief duration of unconsciousness and then a lucid recovery period

progressive hemiparesis and stupor develops due to transtentorial coning.

Ipsilateral dilated pupil, then bilateral fixed dilated pupils

untreated –> hemiplegia and respiratory arrest

102
Q

What investigations are done for extradural haematoma?

A

CT: characteristic lentiform shape

midline shift and compression of the ventricles as it enlarges

103
Q

What is the management of extradural haematoma?

A

Urgent neurosurgical referral
Burr holes to release pressure
Prognosis very good if this is performed early

104
Q

What are the primary headache disorders?

A

Tension headache
migraine
cluster headache

105
Q

What are the secondary headache syndromes?

A 
raised ICP
Idiopathic intracranial hypertension
hypertension 
meningeal irritation (SAH/meningitis) 
post-traumatic
GCA
Sinusitis
Metabolic disturbance 
Drugs: nitrates, vasoactive agents
106
Q

What are the causes of facial pain?

A

Trigeminal neuralgia
Postherpetic neuralgia
Atypical facial pain

107
Q

What is a tension headache?

A

Continuous, severe pressure, felt bilaterally over the vertex, occiput and eyes
can be ‘band like’ but not pulsating

108
Q

Who gets tension headaches? When do they occur?

A

anyone - but most common in middle aged women

every day and can persist for many months/years

109
Q

What is the management of tension headaches?

A

Reassurance
Standard analgesics:
If episodic: paracetamol and aspirin/NSAID (warn about overuse)

If medications 2+ times/week - preventative:
low dose amitryptiline
75mg initially, and treated upwards if partial response

chronic tension headache - reassurance, relaxation and addressing underlying stressors important

110
Q

What is a cluster headache?

A

short lived: 30-120 min episodes of sever unilateral pain, typically centred on one eye
comes on very suddenly, often waking a patient from sleep

May get red eye, eye/nose watering, ptosis, vomiting on affected side

May get an aura beforehand

111
Q

When do cluster headaches come on? frequency?

A

May occur several times / day and are recurrent for several weeks or months before the disorder remits

112
Q

What are the precipitants of cluster headache?

A

males > females
Alcohol = common precipitant
strong smells, exercise

113
Q

What is the management of cluster headache?

A

exclude secondary causes and other causes of eye pain
e.g. ACAG

Subcutaneous triptan: sumatriptan 6mg
High flow oxygen

oral triptan/analgesia not effective for acute attack.

prophylactic treatment is with alcohol avoidance and verapamil, lithium or prednisolone

114
Q

What are the causes / triggers of migraine?

A

? who knows!! onset in puberty

menstruation, OCP use, physical exercise, food (cheese, chocolate, red wine), alcohol, emotional states.

Vasodilatation after a period of vasoconstriction (aura phase) is thought to correlate with the onset of the headache.

115
Q

What are the subsets of migraine?

A

Migraine without aura
Migraine with aura
Silent migraine (migraine with aura but without a headache)
Hemiplegic migraine

116
Q

How does a classical migraine with aura present?

A

Starts with a sense of ill health followed by visual aura in the field of vision opposite to the side of the succeeding headache. Sensory aura less common

THEN: throbbing headache with anorexia, nausea, vomiting and photophobia.
Headache begins locally and spreads bilaterally, aggravated by movement an can last several hours/days

117
Q

What is the presentation of a migraine without aura?

A

Classical visual/sensory aura = absent, however patients may feel non-specifically unwell prior to onset of headache

118
Q

What is the management of migraine (non-pharm)

A

Examine to rule out other differentials: focal neurology, raised ICP, meningism, temporal arteritis, retinal haemorrhage

headache diary: assess frequency, severity of attacks, precipitants and exacerbating/relieving factors

avoidance of external triggers

119
Q

What is the pharmacological management of migraine?

A

In acute attack: oral NSAID or paracetamol + anti-emetic (metoclopramide)

offer oral triptan (sumatriptan 50mg) if attacks severe to take ASAP at start of attack.

don’t use opioids.

follow up - if they don’t respond to triptan, might not be migraine

120
Q

What is the preventative treatment of migraine?

A

If >2 / month
Topiramate / propranolol first line - prop in child bearing age

amitryptiline / anti-convulsants if these aren’t successful or tolerated

121
Q

How are menstrual related migraines managed?

A

Mefanamic acid from first day of Menses throughout menstruation, or triptans starting 2 Days before expected menses

COCP avoided in women with migraine with aura, however, contraceptive methods that prevent menstruation can be tried

slight increased stroke risk in those on COCP greater if migraine sufferers

122
Q

Who is most likely to suffer with idiopathic intracranial hypertension?

A

young, obese women

123
Q

What are the s/s of idiopathic intracranial hypertension?

A

Raised ICP symptoms but no mass lesion on imaging
thought to be a disorder of CSF resorption
most common presentation is visual disturbance (diplopia, obscurations and headaches)
Sometimes associated with pulsatile tinnitus and a 6th nerve palsy

bilateral papilloedema

124
Q

What is the management of idiopathic intracranial HTN?

A

weight loss
trial of corticosteroids
surgical shunt

125
Q

What is the cause of trigeminal neuralgia?

A

Compression/pathology (MS) of the trigeminal nerve root

126
Q

What are the symptoms of trigeminal neuralgia?

A

Agonising sharp pain over the distribution of the facial nerve on one side, lasting only seconds, with sensory trigger

127
Q

What is the management of trigeminal neuralgia?

A

simple analgesics ineffective;

carbamazepine offers good symptom control

Referral

128
Q

What is atypical facial pain?

A

Episodic aching in non-anatomical distributions of head/neck

commonly associated with depression/anxiety, and may respond to anti-depressants

129
Q

What is hydrocephalus?

A

Excessive CSF within the cranium

High CSF pressure leads to dilatation of the lateral ventricles +/- dilation of the 3rd / 4th ventricles

130
Q

What are the causes of non-communicating hydrocephalus and communicating?

A

Non-communicating = most common type, due to blockage of the CSF pathway from the ventricles to sub-arachnoid space

Communicating hydrocephalus = due to impairment of CSF reabsorption at the arachnoid villi along the dural venous sinuses
usually precipitated by infection or SAH

Rarely, hydrocephalus can be due to excess CSF production

131
Q

Who is most likely to develop hydrocephalus?

A

Patients with congenital malformations
e.g. stenosis of the aqueduct of sylvius

posterior fossa/brainstem tumours
post-brain insult
SAH/head injury/meningitis

132
Q

What are the clinical features of hydrocephalus?

A 
Headache 
vomiting 
papilloedema 
cognitive impairment
ataxia 
bilateral pyramidal signs
133
Q

What are the investigations of hydrocephalus

A

CT - assess signs of ventricles

MRI if suspecting malformations/tumours

134
Q

What is the medical management of hydrocephalus?

A

Medical - reduce CSF secretion / increase absorption
(delay surgical management)
acetazolamide, alone or in combination with furosemide

135
Q

What is the surgical management of hydrocephalus?

A

Ventriculo-atrial or ventricle-peritoneal shunting for progressive symptoms
valves open at certain pressures to release CSF

Endoscopic third ventriculostomy is an alternative procedure, appropriate for obstructive hydrocephalus

neurosurgical removal of tumours if appropriate

136
Q

What is normal pressure hydrocephalus?

A

Syndrome of enlarged lateral ventricles, usually in the elderly, associated with a classic triad: dementia, desperate no signs of cortical atrophy on CT
Urinary incontinence
Apraxic gait
whacky wobbly weeing

Isolated CSF measurements normal, but continuous monitoring may show intermittent periods of raised pressure

137
Q

What is the management of normal pressure hydrocephalus?

A

Some patients respond to ventriculoperitoneal shunting, only indicated if they respond to trials of lumbar drainage

CP3 Medicine (19 decks)

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