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Year 2 > Neuro: Part 4 > Flashcards

Neuro: Part 4 Flashcards

1
Q

Define stroke

A

Syndrome of RAPID onset of neurological deficit caused by focal, cerebral, spinal or retinal INFARCTION

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2
Q

What characterises the stroke

A

RAPIDLY DEVELOPING signs of focal or global disturbance of cerebral functions, lasting MORE than 24 hours or leading to death

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3
Q

In what ethnicity are strokes common

A

Asian and black african population

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4
Q

Risk factors of strokes

A 
Male
Black or asian
Hypertension 
Past TIA
Smoking 
Diabetes Mellitus
Increasing Age
Heart Disease (valvular, ischaemic)
Alcohol
Polycythaemia, thrombophilia
AF - stasis of blood in poorly contracted atria = thrombus formation 
Hypercholesterolaemia
Vasculitis
Infective endocarditis
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5
Q

What contributes to 80% of strokes

A

Ischaemia and infarction

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6
Q

Where do ischaemias leading to strokes occur

A
  1. Small vessel occlusion -> leads to thrombosis
  2. Cardiac emboli from AF, MI or infective endocarditis
  3. Large artery stenosis
  4. Atherothromboembolism (carotid)
  5. Hypoperfusion, vasculitis, hyperviscocity
  6. Hypoperfusion (watershed stroke)
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7
Q

How does hypo perfusion lead to a stroke

A

Sudden drop in BP by more than 40mmHg = low cerebral blood flow = global ischaemia leading to ‘watershed infarcts’ in vulnerable areas of the cortex between boundaries of different arterial territories - sepsis

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8
Q

What accounts for 17% of strokes

A 
CNS bleeds due to:
Trauma
Aneurysm rupture
Anticoagulation 
Thrombolysis
Carotid artery dissection 
Subarachnoid haemorrhage
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9
Q

Most common causes of strokes in young people

A
  1. Vasculitis
  2. Thrombophilia
  3. Subarachnoid haemorrhage
  4. Carotid dissection from neck trauma
  5. Venous sinus thrombosis *RARE)
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10
Q

What is venous sinus thrombosis

A
  1. Thrombosis within the intracranial venous sinuses such as the superior saggital sinus or cortical veins
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11
Q

When do venous sinus thrombosis occur

A

Pregnancy
Hypercoaguable states
Thrombotic disorders
Dehydration or malignancy

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12
Q

Result of venous sinus thrombosis

A

Increased cranial pressure
Seizures
Cortical infarction

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13
Q

Main causes of thrombosis in the elderly

A
  1. Small vessel occlusion = thrombosis in situ
  2. Atherothromboembolism
  3. Heart emboli from AF, infective endocarditis or MI
  4. CNS bleed
  5. Sudden BP drop by 40mmHg
  6. Vasculitis
  7. Venous sinus thrombosis
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14
Q

Pathophysiology of ischaemic strokes

A
  1. Thrombus occurs at site of atheromatous plaque in arteries
  2. Large artery stenosis acts of embolism source than occlusion
  3. Occlusive vasculopathy due to hypertension causes small infarcts in deep white matter
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15
Q

What is the occlusive vasculopathy in ischaemic stroke called

A

Lipohyalinosis

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16
Q

What are the small infarcts to the white matter of the brain called

A

Lacunes

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17
Q

How can long bone fracture cause a cardio0mebolic stroke

A

Causes a fat embolus to form

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18
Q

Pathophysiology of haemorrhage strokes

A

Charcot-Bouchard aneurysms occur

Cerebral amyloid antipathy

Space occupying lesions

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19
Q

What are Charcot-Bouchard aneurysms

A

Hypertension resulting in micro aneurysm rupture

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20
Q

What is cerebral amyloid antipathy

A

Deposition of amyloid-B in walls of small and medium-sized arteries in normotensive patients - particularly over 60 results load intercerebrayl haemorrhage

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21
Q

In young adults what causes 1/5th of strokes

A

Carotid/vertebral artery dissection

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22
Q

Clinical presentation of a stroke in anterior cerebral artery

A
  1. SUDDEN RAPID ONSET
    - ——————–
  2. Leg weakness than arm
  3. Sensory disturbances in legs
  4. Gait Apraxia (loss of ability of normal functions in lower limbs)
  5. Truncal ataxia (patient can’t sit or stand unsupported and fall backwards
  6. Incontinence
  7. Drowsiness (also part of consciousness in frontal lobe)
  8. Akinetic mutism (decrease in spontaneous speech and stuporous state)
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23
Q

Clinical presenttaion in Middle cerebral artery strokes

A
  1. Contralateral ARM and LEG weakness
  2. CONTRALATERAL sensory loss
  3. Hemianopia
  4. Aphasia (inability to understand or produce speech)
  5. Dysphagia
  6. Facial droop
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24
Q

Clinical presentation of posterior cerebral artery strokes

A

VISUAL ISSUES:

  1. CONTRALATERAL HOMONYMOUS HEMIANOPIA (loss of half vision on same side of both eyes)
  2. Cortical blindness (eye healthy but brain issue causes it)
  3. Visual agnosia (can’t interpret visual information but can see)
  4. Prosopagnosia (can’t see faces)
  5. Colour naming problems
  6. Unilateral headache!!!!
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25
Q

Why is a stroke in the vertebrobasilar artery dangerous

A
  1. WIDE REGION SUPPLIED)
  2. Can get ‘locked in syndrome’
  3. Motor deficits such as hemiparesis or tetra paresis and facial paralysis
  4. Dysarthria (unclear speech articulation) and speech impairment
  5. Vertigo, nausea and vomiting
  6. Visual disturbances
  7. Altered consciousness
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26
Q

What is a lacunar stroke

A
  1. Small subcortical strokes in structures (e..g midbrain, internal capsule)
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27
Q

Clinical presentation of lacunar strokes

A
  1. Unilateral weakness
  2. Pure sensory loss
  3. Ataxic hemiparesis

ONLY ONE IS AFFECTED OF THESE 3

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28
Q

What is ataxic hemiparesis

A

Unilateral debilitating of function weakness

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29
Q

Can you distinguish between ischaemic and haemorrhage infarcts of lacunar strokes

A

NO

Patients on oral anticoagulants are assumed to have had a haemorrhage unless proved otehrwise

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30
Q

What causes intacerebral haemorrhage (lacunar strokes)

A

Severe headaches or coma due to raised ICP (blood forming space-occupying lesions)

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31
Q

Differential diagnosis of lacunar strokes

A
  1. ALWAYS EXCLUDE HYPOGLYCAEMIA as a cause of euro syndromes
  2. Hypoglycaemia, migraine aura, focal epilepsy
  3. TIA
  4. Intracranial lesion (tumour or subdural haematoma)
  5. Syncope due to arythmie
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32
Q

How is a stroke diagnosed

A
  1. URGENT CT head/MRI head before treatment
  2. Pulse, BP and ECG
  3. FBC
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33
Q

Why is an urgent CT head done before treatment

A

High risk of haemorrhage (low GCS and raised ICP)

  1. Need to rule out haemorrhage stroke before starting thrombolysis
  2. Infarction is seen as a low density lesion, subtle changes evident within 3 hours
  3. In MRI appears hype-intensive within hours of onset
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34
Q

Why is pulse, BP and ECG done in strokes

A
  1. AF
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35
Q

Why do we need to be careful about treating high BP in stroke

A

20% fall may compromise cerebral perfusion

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36
Q

Role of FBC in bloods for strokes

A
  1. THROMBOCYTOPENIA
  2. POLYCYTHAEMIA
  3. Blood glucose to rule out hypoglycaemia
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37
Q

How is stroke treated

A
  1. HYDRATION
  2. Keep O2 sats > 95%
  3. If ischaemic stroke confirmed by CT proceed to thrombolysis
  4. IV ALTEPLASE (tissue plasminogen activator)
  5. CLOPIDOGREL (anti platelet therapy ) lifelong and ASPIRING daily for 2 weeks if thrombolysis is not suitable
  6. CLOPIDOGREL anyways for antiplatlet therapy
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38
Q

When is thrombolysis done

A

4.5 hours max after onset of symptoms

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39
Q

Why do we need to rule out a haemorrhage stroke before doing thrombolysis

A

MAKES THINSG WORSE = death

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40
Q

Contraindications of using thrombolysis

A
  1. Recnet surgery in last 3 months
  2. Recent arterial puncture
  3. History of active malignancy
  4. Evidence of brain aneurysm
  5. Patient on anticoagulation
  6. Sevre liver disease
  7. Acute pancreatitis
  8. Clotting disorder
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41
Q

Treatment in haemorrhage strokes

A
  1. Frequent GCS monitoring
  2. Antiplatelts contraindicated
  3. BERIPLEX + VIT K to reverse any anticoagulants patient was on (WARFARIN)
  4. Control hypertension
  5. Manual decompression of raised ICP or diuretic (MANNITOL)
  6. Surgery
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42
Q

How to manage risk factors for stroke prevention

A
  1. ASPIRIN + DIPYRIDAMOLE or CLOPIDOGREL
  2. SIMVASTATIN
  3. WARFARIN or PIXIBAN (oral anticoagulant)
  4. RAMIPRIL
43
Q

Define Subarachnoid haemorrhage

A

Spontaneous bleeding into the subarachnoid space

44
Q

What age do SAH effect

A

35-65

45
Q

What common rupture leads to subarachnoid haemorrhage

A

BERRY ANEURYSM

46
Q

Describe how berry aneurysms occur

A

Rupture of the junction of the posterior communicating artery with the internal carotid or of the anterior communicating artery with the anterior cerebral artery

47
Q

What conditions are berry aneurysms associated with

A

POLYCYSTIC KIDNEY DISEASE

COARCTATION OF AORTIA

48
Q

Describe how atrioveonus malformations occur

A

Vascular developmental malformation often with a fistula between arterial and venous systems causing high flow though the AVM and high-pressure arterialisation of draining veins

49
Q

Rare conditions that can cause subarachnoid haemorrhages

A
  1. Bleeding disorder
  2. Mycotic aneurysms from endocarditis
  3. Acute bacterial meningitis
  4. Tumours
50
Q

Risk factors for subarachnoid haemorrhages

A
  1. Hypertension
  2. known aneurysm
  3. Family history
  4. Smoking
  5. Bleeding disorders
  6. Post-menopausal decreased oestrogen
51
Q

What disease can predispose you to aneurysms

A
  1. Polycystic kidney disease
  2. Ehlers dans syndrome
  3. Coarctation of aorta
52
Q

What is Ehlers Danlos syndrome

A

Hyper-mobile joints with increased skin elasticity

53
Q

Pathophysiology of subarachnoid haemorrhages

A
  1. Ruptures aneurysm lead stop tissue ischaemia as well as rapid raised ICP as blood acts like a space-occupying lesion, puts pressure on the brain resulting in deficits
54
Q

Clinical presentation of subarachnoid haemorrhage

A
  1. Sudden onset of severe OCCIPITAL headache (thunder clap headache)
  2. Vomtiing, collapse, seizures, coma
  3. Depressed level of consciousness
  4. Drowsiness lasting for days
  5. Neck stiffness
  6. Kerning’s sign (unable to extend patients leg at the knee when thigh is flexed)
  7. Brudzinski’s sign (when patents neck is flexed by doctor, patient will flex their hip and knee)
  8. Retinal and vitreous bleeds
  9. Papilloedema - dilated optic disc
  10. Vision loss or diplopia (double vision)
  11. Focal neurology at presentation may suggest site of aneurysm:
    Fixed Dilated Pupils - signs of CN3 palsy caused by pressure on CN3 seen in posterior communicating artery aneurysm
  12. Marked increase in BP as a reflex to following haemorrhage
  13. Sentinel headache
55
Q

What is sentinel headache

A
  1. Patient may EARLIER have experience a sentinel headache, due to a small WARNING LEAK of the offending aneurysm (6%)
    Ask about this in history
56
Q

Differential Diagnosis of subarachnoid haemorrhage

A
  1. MUST be differentiated from MIGRAINE: short time to maximal headache intensity and the presence of neck stiffness usually indicate SAH
  2. Primary care only 25% of those with severe, sudden thunderclap headache have SAH
  3. In 50-60%, no cause if found in headache
  4. Meningitis
  5. Intracerebral bleeds
  6. Cortical vein thrombosis
57
Q

How to diagnose SAH

A
  1. ABG: excludes hypoxia
  2. Head CT (GOLD STANDARD DIAGNOSTIC)
  3. CT angiography if aneurysm confirmed to see extent
  4. Lumbar Puncture:
    CT normal but SAH still suspected
    CSF in SAH in uniformly bloody early on and becomes Xanthochromic (yellow) after several hours due to breakdown of bilirubin
    Xanthrochromia = SAH
58
Q

How is SAH treated

A
  1. REFER TO NEUROSURGEON IMMEDIATELY
  2. Maintain cerebral perfusion by keeping hydrated (IV fluid) and aim for BP < 160mmHg
  3. IV/ORAL NIMODIPINE (Calcium channel blocker to reduce vasospasm)
  4. Endovascular coiling
  5. Surgery: Intracranial stents and ballon remodelling for wide-necked aneurysm
59
Q

When is Endovascular coiling first line treatment for SAH

A
  1. Preferred to surgical clipping since has lower complication rate where possible
  2. Promotes thrombosis and ablation of aneurysm
60
Q

Complications of subarachnoid haemorrhage

A
  1. Rebledidng
  2. Cerebral ischaemia due to vasospasm - permanent deficit
  3. Hydrocephalus due to blockage of arachnoid granulation - lumbar drain
  4. Hyponatraemia
61
Q

Define subdural haemorrhage

A

Caused by the accumulation of blood in the subdural space (between arachnoid and dura mater) following rupture of a bridging vein between cortex and the venous sinus

62
Q

Is SDH treatable

A

Yes in those whose conscious level fluctuates or having an evolving stroke - anticoagulants

63
Q

In what patients is a subdural haemorrhage common in

A

Where patient has a small brain (alcoholics or dementia), babies undergoing trauma or elderly in brain atrophy = makes bridging veins more vulnerable

64
Q

IN what age group is chronic subdural haemorrhage common in

A

Elderly and those on anticoagulants

65
Q

Describe the pathophysiology of a subdural haemorrhage

A
  1. Trauma due to deceleration (violent injury) or dural metastases results in bridging veins bleeding between cortex and venous sinuses
  2. Bleeding forms haematoma between dura and arachnoid = reduced pressure + bleeding stops
  3. Weeks later, haematoma autolysis due to increase in oncotic and osmotic pressure, water is sucked into haematoma resulting in it enlarging
    INCREASE IN INTRACRANIAL PRESSURE
66
Q

What is the big dangerous problem with subdural haemorrhages

A

It shifts midline structures away from side of the clot = tectorial erniation and coning

67
Q

What is coning

A

Brain herniates through foramen magnum

68
Q

risk factors for subdural haemorrhage

A
  1. Traumatic head injury
  2. Cerebral atrophy = veins more vulnerable
  3. Alcoholism
  4. Anticoagulation
  5. Physical abuse to infant
69
Q

Clinical presentation of a subdural haematoma

A
  1. FLUCTUATING LEVEL OF CONSCIOUSNESS
  2. Sleepiness
  3. Headache
  4. Personality chang e
  5. Unsteadiness
  6. Signs of raised ICP
  7. Focal neurology (hemiparesis or sensory loss)
  8. Seizures
  9. Coma and coning
70
Q

What are the typical signs of increased intracranial pressure

A
  1. HEADACHE
  2. VOMITING
  3. NAUSEA
  4. SEIZURES
  5. RAISED BP
71
Q

Differential diagnosis of subdural haemorrhage

A
  1. Stroke
  2. Dementia
  3. CNS masses
  4. SAH
  5. Extradural haemorrhage
72
Q

Diagnostics of Subdural haemorrhage

A
  1. CT HEAD

2. MRI HEAD

73
Q

What would CT head show in subdural haemorrhage

A
  1. Diffuse spreading, hyper dense CRESCENT SHAPED collection of blood over 1 hemisphere (differentiates it from extradural haemorrhage)
  2. Shifting of midline structures
74
Q

What would an MRI head dhow for Subdural haemorrhage

A

Subacute haematomas and smaller haematomas

75
Q

What do we need to look out for in CT heads for subdural haemorrhage

A
  1. As clot ages, protein degradation causes brain to isodense (same colour as the brain) and hypodense
76
Q

How is subdural haemorrhage treated

A
  1. ABC, prioritise HEAD CT
  2. Stablisise patient
  3. Refer to neurosurgeons
  4. Address cause of trauma (fall due to cataract or arrhythmia)
  5. IV MANNITOL to reduce ICP
77
Q

When do we suspect EXTRADURAL HAEMORRHAGE

A

After head injury, conscious level falls and is slow to improve

78
Q

What is an EXTRADURAL HAEMORRHAGE

A

Collection of blood between dura mater and bone caused by head injury

79
Q

What usually causes an extradural haemorrhage

A

Due to traumatic head injury = fracture in temporal or parietal bone causing laceration of middle meningeal artery

TRAUMA TO TEMPLE

80
Q

In wat age group are extradural haemorrhages common

A

Young adults

81
Q

Clinical presentation of extradural haemorrhages

A
  1. Head injury
  2. BRIEF post-traumatic loss of consciousness or initial drowsiness
  3. LUCID interval - period of time between traumatic brian injury and decrease in consciousness
  4. ICP symptoms
  5. Signs of brainstem depression
  6. Decreased GCS and coning
  7. Death due to respiratory arrest
  8. Hemiparesis with abnormally fast reflexes
  • ——LATE SIGNS——
    8. Bradycardia
    9. Raised BP
82
Q

What are signs of brainstem depending

A
  1. Pupil dilatation
  2. bilateral limb weakness
  3. Breathing is deep and irregular
83
Q

Differential diagnosis of Extradural haemorrhage

A
  1. Epilepsy
  2. Carotid dissection
  3. CO poisoning
    ^^
    —– lucid period—-
  4. Subdural haematoma
  5. Subarachnoid haemorrhage
  6. Meningitis
84
Q

Diagnostics of extradural haemorrhage

A
  1. CT HEAD

2. SKULL X-ray

85
Q

What would CT head dhow in extradural haemorrhage

A
  1. HYPERDENSE HAEMATOMA that is biconvex/lemon shaped next to skull
  2. Blood forms more rounded than subdural haematoma
86
Q

Skull X-ray in extradural haemorrhage

A

Normal or shows fracture lines crossing course of middle meningeal artery

87
Q

Treatment of extradural haemorrhage

A
  1. ABCDE emergency management
  2. IV MANNITOL if increased ICP
  3. Clot evacuation + ligation of bleeding vessel - neurosurgery
  4. Maintain airway via intubation and ventilation
88
Q

Define epilepsy

A

Recurrent tendency to spontaneous, intermittent, abnormal electrical activity in part of the brain, manifesting in seizures

An ongoing liability to recurrent epileptic seizures

89
Q

Define an epileptic seizure

A

Paroxysmal/unprovoked event in which changes of behaviour, sensation or cognitive processes are caused by excessive, hyper synchronous neuronal discharges in the brain

90
Q

What is the motor sign of electrical discharges in the brain

A

CONVULSIONS

91
Q

What abnormal metabolic circumstances cause seizures

A

Hypoxia

Low Na

92
Q

At what ages can epilepsy occur

A

Before 20

After 60

93
Q

How long do seizures last

A

30-120 seconds

94
Q

What causes epilepsy

A 
Idiopathic (2/3 of cases)
Cortical scarring due to head injury 
Space-occupying lesion 
Tumour
Tuberous sclerosis
Alzheimer's or Dementia
Alcohol withdrawal
95
Q

Risk factors of epilepsy

A
  1. FAMILY HISTORY
  2. Premature born babies who are small for age
  3. Abnormal blood vessels in brain
  4. Alzheimer’s or dementia
  5. Use of drugs (cocaine)
  6. Stroke/brian tumour/infection
96
Q

Describe the elements of a seizure

A
  1. PRODROME
  2. AURA
  3. POST-itically
97
Q

What is prodrome

A

Duration: lasting hours or days and doesn’t always resulting seizure
2. Not part of the seizure - changes in mood or behaviour

98
Q

What is Aura

A

Seizure Where patient is aware and may precede seizure

  1. Strange feeling in gut
  2. Deja vu
  3. Strange smells
  4. Flashing lights
  5. Partial seizure often but not necessarily from temporal lobe
99
Q

Post-itically seuizure

A
  1. Headache, confusion, myalgia and sore tongue
  2. temporary weakness after focal seizure in motor cortex - TODD’s PALSY
  3. Dysphagia following seizure in temporal lobe
100
Q

What can seizures be classified into

A
  1. Primary generalised

2. Partial/focal seizures

101
Q

What are primary generlaised

A

RARER:
1. Simultaneous onset of electrical discharge through the whole cortex with no localising features to one hemisphere

ALWAYS ASSOCIATED with loss of consciousness or awareness

102
Q

Pharmacology of Carbamazepine, Lamotrigine

A
  1. Inhibit voltage gated sodium channels on pre-synaptic membrane - stops it from getting excited
103
Q

Pharmacology of prcegablin and gabapentin

A
  1. Inhibit voltage gated calcium channels on pre-synaptic membrane

Year 2 (155 decks)

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