Neuro: Part 4 Flashcards
Define stroke
Syndrome of RAPID onset of neurological deficit caused by focal, cerebral, spinal or retinal INFARCTION
What characterises the stroke
RAPIDLY DEVELOPING signs of focal or global disturbance of cerebral functions, lasting MORE than 24 hours or leading to death
In what ethnicity are strokes common
Asian and black african population
Risk factors of strokes
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
What contributes to 80% of strokes
Ischaemia and infarction
Where do ischaemias leading to strokes occur
- Small vessel occlusion -> leads to thrombosis
- Cardiac emboli from AF, MI or infective endocarditis
- Large artery stenosis
- Atherothromboembolism (carotid)
- Hypoperfusion, vasculitis, hyperviscocity
- Hypoperfusion (watershed stroke)
How does hypo perfusion lead to a stroke
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
What accounts for 17% of strokes
CNS bleeds due to: Trauma Aneurysm rupture Anticoagulation Thrombolysis Carotid artery dissection Subarachnoid haemorrhage
Most common causes of strokes in young people
- Vasculitis
- Thrombophilia
- Subarachnoid haemorrhage
- Carotid dissection from neck trauma
- Venous sinus thrombosis *RARE)
What is venous sinus thrombosis
- Thrombosis within the intracranial venous sinuses such as the superior saggital sinus or cortical veins
When do venous sinus thrombosis occur
Pregnancy
Hypercoaguable states
Thrombotic disorders
Dehydration or malignancy
Result of venous sinus thrombosis
Increased cranial pressure
Seizures
Cortical infarction
Main causes of thrombosis in the elderly
- Small vessel occlusion = thrombosis in situ
- Atherothromboembolism
- Heart emboli from AF, infective endocarditis or MI
- CNS bleed
- Sudden BP drop by 40mmHg
- Vasculitis
- Venous sinus thrombosis
Pathophysiology of ischaemic strokes
- Thrombus occurs at site of atheromatous plaque in arteries
- Large artery stenosis acts of embolism source than occlusion
- Occlusive vasculopathy due to hypertension causes small infarcts in deep white matter
What is the occlusive vasculopathy in ischaemic stroke called
Lipohyalinosis
What are the small infarcts to the white matter of the brain called
Lacunes
How can long bone fracture cause a cardio0mebolic stroke
Causes a fat embolus to form
Pathophysiology of haemorrhage strokes
Charcot-Bouchard aneurysms occur
Cerebral amyloid antipathy
Space occupying lesions
What are Charcot-Bouchard aneurysms
Hypertension resulting in micro aneurysm rupture
What is cerebral amyloid antipathy
Deposition of amyloid-B in walls of small and medium-sized arteries in normotensive patients - particularly over 60 results load intercerebrayl haemorrhage
In young adults what causes 1/5th of strokes
Carotid/vertebral artery dissection
Clinical presentation of a stroke in anterior cerebral artery
- SUDDEN RAPID ONSET
- ——————– - Leg weakness than arm
- Sensory disturbances in legs
- Gait Apraxia (loss of ability of normal functions in lower limbs)
- Truncal ataxia (patient can’t sit or stand unsupported and fall backwards
- Incontinence
- Drowsiness (also part of consciousness in frontal lobe)
- Akinetic mutism (decrease in spontaneous speech and stuporous state)
Clinical presenttaion in Middle cerebral artery strokes
- Contralateral ARM and LEG weakness
- CONTRALATERAL sensory loss
- Hemianopia
- Aphasia (inability to understand or produce speech)
- Dysphagia
- Facial droop
Clinical presentation of posterior cerebral artery strokes
VISUAL ISSUES:
- CONTRALATERAL HOMONYMOUS HEMIANOPIA (loss of half vision on same side of both eyes)
- Cortical blindness (eye healthy but brain issue causes it)
- Visual agnosia (can’t interpret visual information but can see)
- Prosopagnosia (can’t see faces)
- Colour naming problems
- Unilateral headache!!!!
Why is a stroke in the vertebrobasilar artery dangerous
- WIDE REGION SUPPLIED)
- Can get ‘locked in syndrome’
- Motor deficits such as hemiparesis or tetra paresis and facial paralysis
- Dysarthria (unclear speech articulation) and speech impairment
- Vertigo, nausea and vomiting
- Visual disturbances
- Altered consciousness
What is a lacunar stroke
- Small subcortical strokes in structures (e..g midbrain, internal capsule)
Clinical presentation of lacunar strokes
- Unilateral weakness
- Pure sensory loss
- Ataxic hemiparesis
ONLY ONE IS AFFECTED OF THESE 3
What is ataxic hemiparesis
Unilateral debilitating of function weakness
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
What causes intacerebral haemorrhage (lacunar strokes)
Severe headaches or coma due to raised ICP (blood forming space-occupying lesions)
Differential diagnosis of lacunar strokes
- ALWAYS EXCLUDE HYPOGLYCAEMIA as a cause of euro syndromes
- Hypoglycaemia, migraine aura, focal epilepsy
- TIA
- Intracranial lesion (tumour or subdural haematoma)
- Syncope due to arythmie
How is a stroke diagnosed
- URGENT CT head/MRI head before treatment
- Pulse, BP and ECG
- FBC
Why is an urgent CT head done before treatment
High risk of haemorrhage (low GCS and raised ICP)
- Need to rule out haemorrhage stroke before starting thrombolysis
- Infarction is seen as a low density lesion, subtle changes evident within 3 hours
- In MRI appears hype-intensive within hours of onset
Why is pulse, BP and ECG done in strokes
- AF
Why do we need to be careful about treating high BP in stroke
20% fall may compromise cerebral perfusion
Role of FBC in bloods for strokes
- THROMBOCYTOPENIA
- POLYCYTHAEMIA
- Blood glucose to rule out hypoglycaemia
How is stroke treated
- HYDRATION
- Keep O2 sats > 95%
- If ischaemic stroke confirmed by CT proceed to thrombolysis
- IV ALTEPLASE (tissue plasminogen activator)
- CLOPIDOGREL (anti platelet therapy ) lifelong and ASPIRING daily for 2 weeks if thrombolysis is not suitable
- CLOPIDOGREL anyways for antiplatlet therapy
When is thrombolysis done
4.5 hours max after onset of symptoms
Why do we need to rule out a haemorrhage stroke before doing thrombolysis
MAKES THINSG WORSE = death
Contraindications of using thrombolysis
- Recnet surgery in last 3 months
- Recent arterial puncture
- History of active malignancy
- Evidence of brain aneurysm
- Patient on anticoagulation
- Sevre liver disease
- Acute pancreatitis
- Clotting disorder
Treatment in haemorrhage strokes
- Frequent GCS monitoring
- Antiplatelts contraindicated
- BERIPLEX + VIT K to reverse any anticoagulants patient was on (WARFARIN)
- Control hypertension
- Manual decompression of raised ICP or diuretic (MANNITOL)
- Surgery
How to manage risk factors for stroke prevention
- ASPIRIN + DIPYRIDAMOLE or CLOPIDOGREL
- SIMVASTATIN
- WARFARIN or PIXIBAN (oral anticoagulant)
- RAMIPRIL
Define Subarachnoid haemorrhage
Spontaneous bleeding into the subarachnoid space
What age do SAH effect
35-65
What common rupture leads to subarachnoid haemorrhage
BERRY ANEURYSM
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
What conditions are berry aneurysms associated with
POLYCYSTIC KIDNEY DISEASE
COARCTATION OF AORTIA
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
Rare conditions that can cause subarachnoid haemorrhages
- Bleeding disorder
- Mycotic aneurysms from endocarditis
- Acute bacterial meningitis
- Tumours
Risk factors for subarachnoid haemorrhages
- Hypertension
- known aneurysm
- Family history
- Smoking
- Bleeding disorders
- Post-menopausal decreased oestrogen
What disease can predispose you to aneurysms
- Polycystic kidney disease
- Ehlers dans syndrome
- Coarctation of aorta
What is Ehlers Danlos syndrome
Hyper-mobile joints with increased skin elasticity
Pathophysiology of subarachnoid haemorrhages
- 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
Clinical presentation of subarachnoid haemorrhage
- Sudden onset of severe OCCIPITAL headache (thunder clap headache)
- Vomtiing, collapse, seizures, coma
- Depressed level of consciousness
- Drowsiness lasting for days
- Neck stiffness
- Kerning’s sign (unable to extend patients leg at the knee when thigh is flexed)
- Brudzinski’s sign (when patents neck is flexed by doctor, patient will flex their hip and knee)
- Retinal and vitreous bleeds
- Papilloedema - dilated optic disc
- Vision loss or diplopia (double vision)
- 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 - Marked increase in BP as a reflex to following haemorrhage
- Sentinel headache
What is sentinel headache
- Patient may EARLIER have experience a sentinel headache, due to a small WARNING LEAK of the offending aneurysm (6%)
Ask about this in history
Differential Diagnosis of subarachnoid haemorrhage
- MUST be differentiated from MIGRAINE: short time to maximal headache intensity and the presence of neck stiffness usually indicate SAH
- Primary care only 25% of those with severe, sudden thunderclap headache have SAH
- In 50-60%, no cause if found in headache
- Meningitis
- Intracerebral bleeds
- Cortical vein thrombosis
How to diagnose SAH
- ABG: excludes hypoxia
- Head CT (GOLD STANDARD DIAGNOSTIC)
- CT angiography if aneurysm confirmed to see extent
- 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
How is SAH treated
- REFER TO NEUROSURGEON IMMEDIATELY
- Maintain cerebral perfusion by keeping hydrated (IV fluid) and aim for BP < 160mmHg
- IV/ORAL NIMODIPINE (Calcium channel blocker to reduce vasospasm)
- Endovascular coiling
- Surgery: Intracranial stents and ballon remodelling for wide-necked aneurysm
When is Endovascular coiling first line treatment for SAH
- Preferred to surgical clipping since has lower complication rate where possible
- Promotes thrombosis and ablation of aneurysm
Complications of subarachnoid haemorrhage
- Rebledidng
- Cerebral ischaemia due to vasospasm - permanent deficit
- Hydrocephalus due to blockage of arachnoid granulation - lumbar drain
- Hyponatraemia
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
Is SDH treatable
Yes in those whose conscious level fluctuates or having an evolving stroke - anticoagulants
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
IN what age group is chronic subdural haemorrhage common in
Elderly and those on anticoagulants
Describe the pathophysiology of a subdural haemorrhage
- Trauma due to deceleration (violent injury) or dural metastases results in bridging veins bleeding between cortex and venous sinuses
- Bleeding forms haematoma between dura and arachnoid = reduced pressure + bleeding stops
- 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
What is the big dangerous problem with subdural haemorrhages
It shifts midline structures away from side of the clot = tectorial erniation and coning
What is coning
Brain herniates through foramen magnum
risk factors for subdural haemorrhage
- Traumatic head injury
- Cerebral atrophy = veins more vulnerable
- Alcoholism
- Anticoagulation
- Physical abuse to infant
Clinical presentation of a subdural haematoma
- FLUCTUATING LEVEL OF CONSCIOUSNESS
- Sleepiness
- Headache
- Personality chang e
- Unsteadiness
- Signs of raised ICP
- Focal neurology (hemiparesis or sensory loss)
- Seizures
- Coma and coning
What are the typical signs of increased intracranial pressure
- HEADACHE
- VOMITING
- NAUSEA
- SEIZURES
- RAISED BP
Differential diagnosis of subdural haemorrhage
- Stroke
- Dementia
- CNS masses
- SAH
- Extradural haemorrhage
Diagnostics of Subdural haemorrhage
- CT HEAD
2. MRI HEAD
What would CT head show in subdural haemorrhage
- Diffuse spreading, hyper dense CRESCENT SHAPED collection of blood over 1 hemisphere (differentiates it from extradural haemorrhage)
- Shifting of midline structures
What would an MRI head dhow for Subdural haemorrhage
Subacute haematomas and smaller haematomas
What do we need to look out for in CT heads for subdural haemorrhage
- As clot ages, protein degradation causes brain to isodense (same colour as the brain) and hypodense
How is subdural haemorrhage treated
- ABC, prioritise HEAD CT
- Stablisise patient
- Refer to neurosurgeons
- Address cause of trauma (fall due to cataract or arrhythmia)
- IV MANNITOL to reduce ICP
When do we suspect EXTRADURAL HAEMORRHAGE
After head injury, conscious level falls and is slow to improve
What is an EXTRADURAL HAEMORRHAGE
Collection of blood between dura mater and bone caused by head injury
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
In wat age group are extradural haemorrhages common
Young adults
Clinical presentation of extradural haemorrhages
- Head injury
- BRIEF post-traumatic loss of consciousness or initial drowsiness
- LUCID interval - period of time between traumatic brian injury and decrease in consciousness
- ICP symptoms
- Signs of brainstem depression
- Decreased GCS and coning
- Death due to respiratory arrest
- Hemiparesis with abnormally fast reflexes
- ——LATE SIGNS——
8. Bradycardia
9. Raised BP
What are signs of brainstem depending
- Pupil dilatation
- bilateral limb weakness
- Breathing is deep and irregular
Differential diagnosis of Extradural haemorrhage
- Epilepsy
- Carotid dissection
- CO poisoning
^^
—– lucid period—- - Subdural haematoma
- Subarachnoid haemorrhage
- Meningitis
Diagnostics of extradural haemorrhage
- CT HEAD
2. SKULL X-ray
What would CT head dhow in extradural haemorrhage
- HYPERDENSE HAEMATOMA that is biconvex/lemon shaped next to skull
- Blood forms more rounded than subdural haematoma
Skull X-ray in extradural haemorrhage
Normal or shows fracture lines crossing course of middle meningeal artery
Treatment of extradural haemorrhage
- ABCDE emergency management
- IV MANNITOL if increased ICP
- Clot evacuation + ligation of bleeding vessel - neurosurgery
- Maintain airway via intubation and ventilation
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
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
What is the motor sign of electrical discharges in the brain
CONVULSIONS
What abnormal metabolic circumstances cause seizures
Hypoxia
Low Na
At what ages can epilepsy occur
Before 20
After 60
How long do seizures last
30-120 seconds
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
Risk factors of epilepsy
- FAMILY HISTORY
- Premature born babies who are small for age
- Abnormal blood vessels in brain
- Alzheimer’s or dementia
- Use of drugs (cocaine)
- Stroke/brian tumour/infection
Describe the elements of a seizure
- PRODROME
- AURA
- POST-itically
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
What is Aura
Seizure Where patient is aware and may precede seizure
- Strange feeling in gut
- Deja vu
- Strange smells
- Flashing lights
- Partial seizure often but not necessarily from temporal lobe
Post-itically seuizure
- Headache, confusion, myalgia and sore tongue
- temporary weakness after focal seizure in motor cortex - TODD’s PALSY
- Dysphagia following seizure in temporal lobe
What can seizures be classified into
- Primary generalised
2. Partial/focal seizures
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
Pharmacology of Carbamazepine, Lamotrigine
- Inhibit voltage gated sodium channels on pre-synaptic membrane - stops it from getting excited
Pharmacology of prcegablin and gabapentin
- Inhibit voltage gated calcium channels on pre-synaptic membrane
