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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
Why is a stroke in the vertebrobasilar artery dangerous
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
26
What is a lacunar stroke
1. Small subcortical strokes in structures (e..g midbrain, internal capsule)
27
Clinical presentation of lacunar strokes
1. Unilateral weakness 2. Pure sensory loss 3. Ataxic hemiparesis ONLY ONE IS AFFECTED OF THESE 3
28
What is ataxic hemiparesis
Unilateral debilitating of function weakness
29
Can you distinguish between ischaemic and haemorrhage infarcts of lacunar strokes
NO Patients on oral anticoagulants are assumed to have had a haemorrhage unless proved otehrwise
30
What causes intacerebral haemorrhage (lacunar strokes)
Severe headaches or coma due to raised ICP (blood forming space-occupying lesions)
31
Differential diagnosis of lacunar strokes
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
32
How is a stroke diagnosed
1. URGENT CT head/MRI head before treatment 2. Pulse, BP and ECG 3. FBC
33
Why is an urgent CT head done before treatment
High risk of haemorrhage (low GCS and raised ICP) 2. Need to rule out haemorrhage stroke before starting thrombolysis 3. Infarction is seen as a low density lesion, subtle changes evident within 3 hours 4. In MRI appears hype-intensive within hours of onset
34
Why is pulse, BP and ECG done in strokes
1. AF
35
Why do we need to be careful about treating high BP in stroke
20% fall may compromise cerebral perfusion
36
Role of FBC in bloods for strokes
1. THROMBOCYTOPENIA 2. POLYCYTHAEMIA 3. Blood glucose to rule out hypoglycaemia
37
How is stroke treated
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
38
When is thrombolysis done
4.5 hours max after onset of symptoms
39
Why do we need to rule out a haemorrhage stroke before doing thrombolysis
MAKES THINSG WORSE = death
40
Contraindications of using thrombolysis
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
41
Treatment in haemorrhage strokes
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
42
How to manage risk factors for stroke prevention
1. ASPIRIN + DIPYRIDAMOLE or CLOPIDOGREL 2. SIMVASTATIN 3. WARFARIN or PIXIBAN (oral anticoagulant) 4. RAMIPRIL
43
Define Subarachnoid haemorrhage
Spontaneous bleeding into the subarachnoid space
44
What age do SAH effect
35-65
45
What common rupture leads to subarachnoid haemorrhage
BERRY ANEURYSM
46
Describe how berry aneurysms occur
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
What conditions are berry aneurysms associated with
POLYCYSTIC KIDNEY DISEASE | COARCTATION OF AORTIA
48
Describe how atrioveonus malformations occur
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
Rare conditions that can cause subarachnoid haemorrhages
1. Bleeding disorder 2. Mycotic aneurysms from endocarditis 3. Acute bacterial meningitis 4. Tumours
50
Risk factors for subarachnoid haemorrhages
1. Hypertension 2. known aneurysm 3. Family history 4. Smoking 5. Bleeding disorders 6. Post-menopausal decreased oestrogen
51
What disease can predispose you to aneurysms
1. Polycystic kidney disease 2. Ehlers dans syndrome 3. Coarctation of aorta
52
What is Ehlers Danlos syndrome
Hyper-mobile joints with increased skin elasticity
53
Pathophysiology of subarachnoid haemorrhages
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
Clinical presentation of subarachnoid haemorrhage
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
What is sentinel headache
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
Differential Diagnosis of subarachnoid haemorrhage
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
How to diagnose SAH
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
How is SAH treated
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
When is Endovascular coiling first line treatment for SAH
1. Preferred to surgical clipping since has lower complication rate where possible 2. Promotes thrombosis and ablation of aneurysm
60
Complications of subarachnoid haemorrhage
1. Rebledidng 2. Cerebral ischaemia due to vasospasm - permanent deficit 3. Hydrocephalus due to blockage of arachnoid granulation - lumbar drain 4. Hyponatraemia
61
Define subdural haemorrhage
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
Is SDH treatable
Yes in those whose conscious level fluctuates or having an evolving stroke - anticoagulants
63
In what patients is a subdural haemorrhage common in
Where patient has a small brain (alcoholics or dementia), babies undergoing trauma or elderly in brain atrophy = makes bridging veins more vulnerable
64
IN what age group is chronic subdural haemorrhage common in
Elderly and those on anticoagulants
65
Describe the pathophysiology of a subdural haemorrhage
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
What is the big dangerous problem with subdural haemorrhages
It shifts midline structures away from side of the clot = tectorial erniation and coning
67
What is coning
Brain herniates through foramen magnum
68
risk factors for subdural haemorrhage
1. Traumatic head injury 2. Cerebral atrophy = veins more vulnerable 3. Alcoholism 4. Anticoagulation 5. Physical abuse to infant
69
Clinical presentation of a subdural haematoma
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
What are the typical signs of increased intracranial pressure
1. HEADACHE 2. VOMITING 3. NAUSEA 4. SEIZURES 5. RAISED BP
71
Differential diagnosis of subdural haemorrhage
1. Stroke 2. Dementia 3. CNS masses 4. SAH 5. Extradural haemorrhage
72
Diagnostics of Subdural haemorrhage
1. CT HEAD | 2. MRI HEAD
73
What would CT head show in subdural haemorrhage
1. Diffuse spreading, hyper dense CRESCENT SHAPED collection of blood over 1 hemisphere (differentiates it from extradural haemorrhage) 2. Shifting of midline structures
74
What would an MRI head dhow for Subdural haemorrhage
Subacute haematomas and smaller haematomas
75
What do we need to look out for in CT heads for subdural haemorrhage
1. As clot ages, protein degradation causes brain to isodense (same colour as the brain) and hypodense
76
How is subdural haemorrhage treated
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
When do we suspect EXTRADURAL HAEMORRHAGE
After head injury, conscious level falls and is slow to improve
78
What is an EXTRADURAL HAEMORRHAGE
Collection of blood between dura mater and bone caused by head injury
79
What usually causes an extradural haemorrhage
Due to traumatic head injury = fracture in temporal or parietal bone causing laceration of middle meningeal artery TRAUMA TO TEMPLE
80
In wat age group are extradural haemorrhages common
Young adults
81
Clinical presentation of extradural haemorrhages
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
What are signs of brainstem depending
1. Pupil dilatation 2. bilateral limb weakness 3. Breathing is deep and irregular
83
Differential diagnosis of Extradural haemorrhage
1. Epilepsy 2. Carotid dissection 3. CO poisoning ^^ ----- lucid period---- 4. Subdural haematoma 2. Subarachnoid haemorrhage 3. Meningitis
84
Diagnostics of extradural haemorrhage
1. CT HEAD | 2. SKULL X-ray
85
What would CT head dhow in extradural haemorrhage
1. HYPERDENSE HAEMATOMA that is biconvex/lemon shaped next to skull 2. Blood forms more rounded than subdural haematoma
86
Skull X-ray in extradural haemorrhage
Normal or shows fracture lines crossing course of middle meningeal artery
87
Treatment of extradural haemorrhage
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
Define epilepsy
Recurrent tendency to spontaneous, intermittent, abnormal electrical activity in part of the brain, manifesting in seizures An ongoing liability to recurrent epileptic seizures
89
Define an epileptic seizure
Paroxysmal/unprovoked event in which changes of behaviour, sensation or cognitive processes are caused by excessive, hyper synchronous neuronal discharges in the brain
90
What is the motor sign of electrical discharges in the brain
CONVULSIONS
91
What abnormal metabolic circumstances cause seizures
Hypoxia | Low Na
92
At what ages can epilepsy occur
Before 20 | After 60
93
How long do seizures last
30-120 seconds
94
What causes epilepsy
``` Idiopathic (2/3 of cases) Cortical scarring due to head injury Space-occupying lesion Tumour Tuberous sclerosis Alzheimer's or Dementia Alcohol withdrawal ```
95
Risk factors of epilepsy
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
Describe the elements of a seizure
1. PRODROME 2. AURA 3. POST-itically
97
What is prodrome
Duration: lasting hours or days and doesn't always resulting seizure 2. Not part of the seizure - changes in mood or behaviour
98
What is Aura
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
Post-itically seuizure
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
What can seizures be classified into
1. Primary generalised | 2. Partial/focal seizures
101
What are primary generlaised
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
Pharmacology of Carbamazepine, Lamotrigine
1. Inhibit voltage gated sodium channels on pre-synaptic membrane - stops it from getting excited
103
Pharmacology of prcegablin and gabapentin
1. Inhibit voltage gated calcium channels on pre-synaptic membrane

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