S10 Stroke

Question 1

What is a stroke ?

Answer 1

Killing of brain cells starved of oxygen as a result of the blood supply being cut off

Question 2

What is a TIA

Answer 2

Stroke that recovers within 24 hours from the onset of symptoms

Question 3

What is a stroke syndrome ?

Answer 3

Constellation of signs and symptoms produced due to occlusion or damage of an artery supplying part of the brain

Question 4

What do stroke syndromes depend on ?

Answer 4

What artery and what region of it is affected
What part of the brain it supplies
What this part of the brain does
How the patient presents

Question 5

Where can a clot causing a stroke come from

Answer 5

Carotid/vertebral arteries, brain, heart, aorta

Strokes are usually ischaemic or haemorrhagic

Question 6

What does the left anterior cerebral artery supply ?

Answer 6

Medial frontal and parietal lobe, anterior corpus callosum

This part of the brain is responsible for motor and sensation of lower limbs and genital (medial homunculus)

Question 7

What happens when the left anterior cerebral artery gets occluded during a stroke ?

Answer 7

Motor - contralateral flaccid paralysis followed by spasticity
Sensory - contralateral loss of sensory modalities in the lower limb
Loss of voluntary micturition
Corpus callosum damage causing split brain syndrome (cant describe object and alien hand syndrome ( cerebral hemispheres dont communicate so hands disagree )

Question 8

What does the left middle cerebral artery supply ?

Answer 8

Supplies majority of hemisphere and basal ganglia, internal capsule , macular cortex
Affects lateral homunculus ; upper limb and face

Question 9

What happens if the left middle cerebral artery is occluded during a stroke ?

Answer 9

Motor - contralateral flaccid paralysis followed by spasticity
Sensory - contralateral loss of sensory modalities in upper limb and face NB occlusion at proximal MCA shall also affect legs at the lenticulostriate arteries shall be affect which supply the internal capsule, distal shall only affect upper limb and face
Visual effects - proximal occlusion of MCA leads to contralateral homonymous hemianopia, distal lead to contralateral homonymous quadrantanopia (blind quarter)
Speech - if dominant hemisphere affected (usually left) - can get global aphasia (B and W affected) or broca’s/wernickes aphasia
If non dominant hemisphere affected (right) left hemispatial neglect, tactile and visual extinction (cant feel or see in left )

Question 10

What does the left posterior cerebral artery supply

Answer 10

Supplies inferior temporal and occipital

Areas responsible for vision

Question 11

How does left posterior cerebral artery present ?

Answer 11

Contralateral homonymous hemianopia with macular sparing

Question 12

What happens if cerebellar artery gets occluded during a stroke

Answer 12

Supplies whole cerebellum
Area responsible for coordination of movement
Presentation : DANISH
Ca supplies brainstem, proximal occlusion can cause brainstem and cerebellar signs, distal occlusion only cerebellar signs
Brainstem signs : CN nuclei reside in brainstem, can get crossed deficits (long tract damage on one side of the body which affects face on the other side of the body)
Damage to ascending/descending tracts in the cerebral peduncles of the midbrain affects contralateral side of the body
Damage to cranial nerves or their nuclei gives ipsilateral signs

Question 13

What happens if the basilar artery gets occluded during a stroke

Answer 13

Supplies cerebellum and brainstem
Area responsible for co-ordination
Presentation : distal occlusion can get bilateral occipital lobe infarction, bilateral thalamus infarction, bilateral midbrain infarction
Proximal occlusion can get locked in syndrome

Question 14

what happens when the left lenticulostriate arteries are occluded in a lacunar stroke syndrome ?

Answer 14

small branch of the MCA
supplies internal capsule
posterior limb of internal capsule carries descending motor fibres of leg, trunk, arm
presentation : contralateral flaccid paralysis followed by spasticity of face, upper and lower limb
no higher cortical dysfunction - sensory not involved only motor

Question 15

what happens when the left thalamoperforator artery gets occluded in a lacunar stroke syndrome ?

Answer 15

supplies part of the thalamus
this area relays sensory information to the left post - central gyrus (somatosensory cortex)
presenation : contralateral sensory loss of all modalities in face, upper and lower limb
no higher cortical dysfunction - motor not involved only sensory

Question 16

how are strokes classified according to the OCSP ?

Answer 16

total anterior circulation syndrome (TACS)
Partial anterior circulation syndrome (PACS)
Posterior circulation syndrome (POCS)
Lacunar syndrome (LACS)

Question 17

what are the clinical features and vascular basis of TACS

Answer 17

hemiparesis and higher cortical dysfunction (dysphasia or visuospatial neglect) and homonymous hemianopia
usually proximal middle cerebral artery or ICA occlusion

Question 18

what are the clinical features and vascular basis of TACS

Answer 18

isolated higher cortical dysfunction or any too of hemiparesis, higher cortical dysfunction, hemianopia
usually branch of MCA occlusion

Question 19

what are the clinical features and vascular basis of POCS

Answer 19

isolated hemianopia (posterior cerebral artery (PCA) brainstem or cerebellar syndromes 
occlusion of vertebral, basilar, cerebellar or PCA vessels

Question 20

what are the clinical features and vascular basis of LACS

Answer 20

pure motor stroke or pure sensory stroke or sensorimotor stroke or ataxic hemiparesis or clumsy hand dysarthria
small penetrating artery occlusion, usually in lenticulostriate branches of MCA or supply to brainstem or deep white matter

Question 21

how is ICP maintained

Answer 21

autoregulation (vasoconstriction/dilation)
chemoregulation (vasodilation in response to high Ph)
a mass can push out CSF and blood
Normally ICP is 5-15mmhg

Question 22

what is the pathophysiology of brain injury

Answer 22

o2 needed for ATP, which is needed for na k atpase which causes high na in the cell causing water retention leading to cytotoxic cell oedema
leads to further swelling so compression of arteries reducing blood supply to brain cells

Question 23

what are the signs and symptoms of a raised ICP ?

Answer 23

headache : worse in morning , aggravated by coughing
vomiting
visual disturbances : blurring (optic nerve compression), papilloedema, CN 6 palsy
depression

Question 24

describe subfalcine herniation symptoms

Answer 24

symptoms include headache and contralateral leg weakness if anterior cerebral artery affected
midline shift on CT

Question 25

describe uncal herniation symptoms

Answer 25

the uncus (medial part of the temporal lobe) is displaced across the tentorial opening and can put pressure on the midbrain
ipsilateral oculomotor nerve - ipsilateral dilated pupil
compression of cerebral peduncle - contralateral leg weakness
decreased level of consciousness

Question 26

describe the symptoms of tonsillar herniation

Answer 26

the cerebelllar tonsils herniate through the foramen magnum
compression of medulla and upper SC
brainstem affected - cardiac and respiratory dysfunction
decreased level of consciousness

Question 27

what is the cushings reflex

Answer 27

occurs if raised ICP is not treated and continues to rise
is a triad of :
High BP
bradycardia: ischemia at medulla causes sympathetic activation and a rise in BP + tachycardia. Baroreceptors react leading to bradycardia
low respiratory rate : ischemia at pons/medulla at the respiratory centres

Question 28

what are the main causes of ICP

Answer 28

increased cerebral blood volume - venous outflow obstruction and venous sinus thrombosis
cerebral oedema - meningitis, encephalitis, diffuse head injury, infarctions
Increased CSF - impaired absorption ; hydrocephalus, benign intracranial hypertension
excessive secretion - choroid plexus papilloma
expanding mass ‘other’ (space occupying lesions) - abscess, tumour, haemorrhage/ haematoma

Question 29

what is the most common cause of raised ICP

Answer 29

trauma (e.g subdural haemorrhage)

some other causes include meningitis

Question 30

what is hydrocephalus

Answer 30

accumulation of csf due to an imbalance between production and absorption of CSF
can be : non - communicating or communicating

Question 31

what is non-communicating hydrocephalus

Answer 31

CSF is obstructed within the ventricles or between ventricles and subrachnoid space. Due to aqueduct block or tumours

Question 32

what is communicating hydrocephalus

Answer 32

there is communication between the ventricles and the subarachnoid space due to reduced absorption of the venous drainage system. can be caused by meningitis or subarachnoid haemorrhage

Question 33

what kind of tumours do children tend to get

Answer 33

astrocytomas or medullablastomas

tend to be midline or posterior region

Question 34

what kind of tumours do adults tend to get

Answer 34

gliomas, meningiomas (metastases from lung, breast and kidneys)

Question 35

what is idiopathic intracranial hypertension

Answer 35

Raised ICP evidence of hydrocephalus or mass lesion. Common in obese young women
treatment - weight loss , CSF drainage

Question 36

what is the management of raised ICP

Answer 36

for increased cerebral blood volume - anticoagulation
for cerebral oedema - mannitol
for increased CSF - tumour resection
for expanding mass : surgical resection

Question 37

what are head injuries classified into

Answer 37

primary (the damage caused by the force of the injury) and secondary ( a reaction to the primary damage, itself worsening the injury)

Question 38

how is primary injury caused and what can it be divided into ?

Answer 38

it can be divided into focal damage (where there is bruising and laceration of the brain) and diffuse damage (direct tearing of axon as a result of the injury)

Question 39

what is cerebral contusion ?

Answer 39

bruising of brain where blood mixes with cortical tissue due to microhemorrhages(MH) and small blood vessel leaks
pathophysiology : trauma –> MH —–> contusion —-> oedema —> raised ICP —–> coma
can get coup (focal damage at site of impact) or contre-coup (damage on the opposite side of the brainn)

Question 40

what is a concussion ?

Answer 40

head injury with a temporary loss of brain function
path : trauma –> injury to axons —-> impaired neurotransmission, loss of ion regulation —> temporary brain dysfunction
can get post - concussion syndrome (slow thinking, emotional etc)

Question 41

what is diffuse axonal injury ?

Answer 41

shearing of interface between grey and white matter damaging the intra-cerebral axons and dendritic connections
Path : trauma —> shearing ——> axonal death —–> oedema ——> raised ICP ——> coma

Question 42

what is basilar skull fracture

Answer 42

fracture in the base of the skull
path: trauma causes meningeal tear and CSF leakage which can accumulate by eyes noes ear symptoms: racoon eyes, CSF rhinorrhoea, battle sign

Question 43

what is the urgent CT head criteria ?

Answer 43

GSC < 13 at any point or GCS < 14 two hours after injury
focal neurological deficit or seizure
suspected skull fracture

Question 44

how does an extradural haemorrhage present

Answer 44

collection of blood between the inner skull and periosteal dura meter
lemon ct , secondary to trauma
loss of consciousness then a headache during the lucid interval phase then the haematoma shall enlarge increasing ICP compressing the brain and rapidly reducing consciousness
CN palsies may occur
management : ABCDE, may need craniotomy, some complications include brain damage and coma

Question 45

how does a subdural haemorrhage present

Answer 45

collection of blood between meningeal dura mater and arachnoid mater
banana CT, midline shift of falx cerebri (blood doesnt cross)
bleeding occurs due to shearing forces on cortical bridging veins due to trauma but can be spontaneous
acute SDH often due to trauma, subacute/chronic root
haematoma becomes hypodense (darker, seen in chronic) with time
management : acute - neurosurgical intervention s/c- burr holes, prognosis poor compared to EDH

Question 46

what is subarachnoid haemorrhage

Answer 46

collection of blood between arachnoid mater and pia mater
occurs spontaneously secondary to ruptured berry aneurysm but may also be traumatic, affects circle of willis
berry aneurysm can compress nearby structures. If risk of rupture can do surgical clipping. Risk factors include family history and hypertension
aneurysm commonly forms at bifurcational junctions in the cerebral bloodflow , majority in anterior circulation
presentation : thunderclap headache, meningism , fever
management : lumbar puncture , stabilise patient, prevent re bleeding , treat vasospasm
complications : hydrocephalus, coma , seizures

Question 47

give a clinical summary of EDH

Answer 47

mechanism : nearly always due to trauma
presentation : LOC followed by lucid interval and rapid decline in consciousness
Age group affected : usually young
Vessels affected : middle meningeal artery
CT Appearance : lentiform shape bleed, usually limited by suture line, can cross midline as bleed is above falx cerebri
Risk factors : high impact trauma
Management :urgent craniotomy to relieve raised ICP, observe if small EDH

Question 48

give a clinical summary of SDH

Answer 48

mechanism : usually traumatic but may be spontaneous
presentation : Acute : reduce GCS, neurological signs , Chronic : insidious neurological deficit
Age group affected : Acute : any age , Chronic : usually elderly
Vessels affected : bridging veins
CT Appearance : crescent shaped bleed, not bounded by suture lines, unable to cross midline, chronic bleeds appear hypodense
Risk factors : Infant : NAI Adults : head trauma Elderly : repeat falls, anticoagulants
Management : Acute : surgery to relieve raised ICP, Chronic : consider neurosurgical intervention if symptomatic

Question 49

give a clinical summary of SAH

Answer 49

mechanism : majority due to spontaneous berry aneurysm rupture
presentation : sudden thunderclap headache, N + V, meningism, LOC
Age group affected : typically older middle aged < 60
Vessels affected : 90 % anterior circulation of circle of willis
CT Appearance : variable appearance , usually focal, may be mixed density due to presnece of CSF
Risk factors : FH, HTN, connective tissue problems, smoking, alcohol
Management : ITU, prevent rebleeding, manage short term and long term complications, high mortality