Flashcards in NS 9: Strokes, CNS Imaging and Head trauma Deck (60):
3 areas involved in producing clinical signs with raised intracranial pressure causing damage to these and adjacent compression?
arteries comprising the anterior circulation of the brain?
arteries comprising posterior circulation of brain?
branches of ICA?
how does the middle cerebral artery from the ICA supply the basal ganglia?
gives rise to the lateral striate arteries
which artery supplies most of brainstem?
basilar artery from united vertebral arteries at causal border of pons
structures supplied by the posterior cerebral arteries which go around the midbrain?
temporal and occipital lobes
Aetiology and clinical presentation of a total anterior circulation stroke (20% of strokes)?
Proximal occlusion (ICA or proximal MCA)
Large volume infarct
Superficial and deep territories
Presentation= contralateral hemiparesis (weakness) +/- contralateral hemianaesthesia
Higher cerebral dysfunction e.g. dysphasia, dyspraxia- inability to carry out skilled, purposeful movements= cortical signs
What is dysphasia?
Disorder of language
2 types: Receptive dysphasia= often have language that is fluent with a normal rhythm and articulation but it is meaningless as they fail to comprehend what they are saying.
Expressive dysphasia are not fluent and have difficulty forming words and sentences. There are grammatical errors and difficulty finding the right word. In severe cases they do not speak spontaneously but they usually understand what is said to them. Know the word they want to say but can't say it. Aphasia= can't think of the word.
Aetiology and clinical presentation of a partial anterior circulation stroke (35% of strokes)?
Occlusion of MCA branch
2 of 3 found in total anterior OR
Restricted motor deficit
(face OR arm OR leg only)
OR isolated cortical signs
High early recurrence rate
Aetiology and clinical presentation of a lacunar stroke (20% of strokes)?
Single perforating artery
Pure motor, pure sensory, sensorimotor, ataxic
clinical presentation of a posterior circulation stroke (25% of strokes)?
Brainstem, cerebellar or occipital involvement, cranial nerve signs
complex presentation, thrombosis
2 secondary complications of a SA haemorrhage?
communicating hydrocephalus- could treat with a ventriculo-peritoneal shunt
cerebral ischaemia- to prevent give nimodipine (Ca2+ antagonist- *link to amlodipine- used in hypertension)- prevent vascular spasm and so cerebal ischaemia.
appearance of an extradural haematoma on a CT scan and why?
lentiform (lens shape)= convex appearance, as ED haematoma occurs with arterial disruption e.g. pterion fracture= depressed skull fracture highlighted as bone discontinuity on CT, which tears the A division of the middle meningeal artery from maxillary from ECA, so high pressure arterial blood forces periosteal layer of dura mater away from calvaria (not normally a space here.)
Lens shaped white appearance as blood and bone appear white on CT
what colour does CSF appear on CT?
*water also appears black, so an arachnoid cyst would appear black.
appearance of a subdural haematoma on CT scan and why?
white concavity, blood follows brain contours as torn cerebral veins, so low pressure venous blood following brain surface.
which members of the population is a subdural haematoma common in?
elderly- as brain shrinks as you get older, so cerebral veins are put under tension, weakened and prone to rupture with minute head trauma e.g. a fall.
appearance of a SA haemorrhage on CT and why?
white appearance around brain, follows sulci, blood fills gravity dependent spaces.
Commonly result of aneurysm withing arterial circle of Willis.
Can cause a communicating hydrocephalus as blood remains, in space, and rbc block the arachnoid granulations, blocking CSF from moving from the SA space into the dural venous sinuses. This would raise intracranial pressure.
Signs of raised IC pressure?*
headache-worse on a morning
nausea-worse on a morning and vomiting
what is a stroke?
abrupt onset of a focal neurological defecit, lasts >24hrs
why MUST and ECG be carried out in suspected stroke?
Look for AF= absent P waves, irregularly irregular
additonal emboli may occur producing repeat ischaemic strokes.
managment of a SA haemorrhage?
nimodipine= Ca2+ antagonist- prevents vasospasm and cerebral ischaemia
phenytoin- prevent spread of seizure activity, *CYP450 inducer
may give a vasodilator to treat hypertension that could result in further haemorrhage
referral to specialist unit, usually neurosurgical, within 24 hrs
symptoms of SA haemorrhage?
-a sudden headache, may last a few s or even a fraction of a second. The patient may even look round and accuse someone of hitting them on the back of the head.
-SAH should be considered in any patient presenting with sudden-onset, severe and unusual headache with or without any associated alteration in consciousness.
-The headache is often diffuse.
-The dominant feature is the severity, rather than the suddenness, of the headache, often being described as the most severe ever experienced.
-It usually lasts a week or two. Occipital headache.
-Vomiting may occur
-Seizures, which occur in only about 7% but,when they do, are highly suggestive of a haemorrhage
why might a patient have white blobs within their ventricles on a CT scan, commonly in older patients?
presence of a glomus= calcified bits of choroid plexus within the ventricles. This is normal in older patients.
Tment of a subdural haematoma (between the dura mater and arachnoid mater)?
decompress intracranium, STOP bleeding, evacuate blood clots
Tment of an extradural haematoma e.g. resulting from a fracture of the pterion?
evacuate blood clots that could lead to cerebral ischaemia
what compound needs to be present in tissues being imaged with MRI?
what is the basis of T1 and T2 weighting on MRI scans?
It is the computer driven pulsing and relaxation of magnetisation of H+ ions. The pulse sequences of magnetisation can be varied, producing different signals from the protons, hence different images.
why is MRI not good for imaging a skull fracture?
not as effective as CT for imaging bone or hard tissues, better at imaging soft tissues e.g. brain tissue
why is a CT scan used to image a potential fracture rather than an X-ray?
A CT allows you to see the brain tissue aswell as the skull bones which may be fractured, which is important as a fracture may have associated intracranial bleeding, or oedema and inflammtion, which could cause raised intracranial pressure and may need emergency decompression of the intracranium and stopping of the bleeding to ensure adequate perfusion of brain tissues.
colour of H20/CSF on a T1 weighted MRI?
colour of H20/CSF on a T2 weighted MRI?
colour of blood on a CT scan?
bone also white
CSF, water= black
name given to condition in which brain ventricles dilated?
what are the 3 different patterns in which the facial bones can fracture depending upon the severity of the trauma?
Le Fort's fractures:
Le Fort 1 (horizontal maxillary fracture)= fracture of maxilla just above teeth which remain in the detached portion of the bone.
2- body of maxilla separated from facial skeleton with a horizontal fracture through nose and vertical fractures from floor of orbit.
3-horizontal fracture through top of nose, sphenoid, and fronto-zygomatic sutures and zygomatic arches. Maxilla and other facial bones entirely separated from cranium.
what is the likely pathology in an young individual who falls and bangs his head, is briefly knocked out but quickly recovers, but then later becomes unconscious?
fracture of pterion resulting in an extradural haematoma- IC arterial bleeding causes deterioration of patient.
within what time period should alteplase be given if being used to treat an acute ischaemic stroke?
within 4.5 hrs of symptom onset
what is lateral medullary syndrome?
this occurs with occlusion of the posterior inferior cerebellar artery.
symtoms/signs: ipsilateral sensory loss on face (trigeminal nerve)
ipsilateral ataxia (cerbellar peduncle and cerebellum)
vertigo/nausea/vomiting (vestibulocochlear nerve)
ipsilateral Horner's syndrome- partial ptosis, miosis, hemifacial anhydrosis, descending sympathetic tract
dysphagia, dysarthria (glossopharyngeal and vagus nerves)
what does the posterior inferior cerebellar artery supply?
posterior and inferior surfaces of cerebellum
differential diagnoses for stroke?
Hypoglycaemia & other metabolic disturbance
SOL (secondary vs primary tumour, others)
▪ Retinal Bleeds, or infarcts (same pathology, but not defined under stroke)
▪ Peripheral neuropathy
▪ Hyperventilation (usually transient)
▪ Functional or Psychological
investigations in stroke?
Haematological: FBC, INR
Biochemical: U&E, LFT, TFT, glucose, lipid
ECG (no excuses for no ECG!)
Radiological: CXR where indicated
Carotid Ultrasound Scan
24 hour cardiac monitoring
investigations in younger/cryptogenic strokes?
Full coagulation profile
▪ Protein C/S, ATIII,
▪ anticardiolipin, lupus anticoagulant
Fasting plasma homocysteine
TFT, Syphilis serology, HIV serology
Tment of acute stroke?
IV thrombolysis (alteplase)- within 4.5 hrs of symtpom onset- reduces disability
Early Aspirin therapy (where not thrombolysed)
Management in an Acute Stroke Unit
Specialist rehabilitation therapists
Routine carer involvement
Education & training programs
Medical risk factor treatment
▪ Treat hypertension
▪ Treat hypercholesterolaemia
▪ Carotid surgery (if signif carotid stenosis)
▪ Treat diabetes
differentials for spinal artery disease symptoms?
▪ Tumour, Abscess, Granuloma, Haematoma, Herniated disc
Acute infl. Demyelinating polyneuropathy
▪ E.g. Guillain-Barré Syndrome
Demyelination, transverse myelitis
Sarcoid, TB, syphilis
management of spinal artery disease?
Early identification of reversible causes
Manage vascular risk factors (where indicated)
Prevention of complications
Prognosis variable (but poor)
initial assessment of someone coming in with a head injury?
airways, breathing, circulation, disability- AVPU and GCS and pupils
considerations in full evaluation of patient with head injury?
history= onset,[previous episodes, pattern of symptoms- initial LOC, then return to normal, then deteriorate- now a secondary brain injury that must be treated. Slow coming round following LOC- primary brain injury taking a while to recover from. what happened before, during and after.
examination= focal or generalised problem? loss of something?- initial weakness in stroke. Gain doesn't tend to happen in initial brain injury, does occur with epilepsy- e.g. aura with focal seziures.
investigations- CT when uncertainty, depend on differentials
symptoms of acute IC event?
Loss of function
Change in conscious level / collapse
things that can go wrong causing acute IC event?
lack of substrate- blood, glucose/O2- ischaemic stroke or haemorrhagic, raised ICP- block CSF circulation, SOL, brain swelling, hypotension, hypoglycaemia, CO poisoning.
abnormal activity- fitting, generalised or focal- focal signs worried about focal lesion e.g. tumour.
local damage e.g. injury or bleed. May be low BP in elderly person, causing brain hypoperfusion- could be due to chest infection, UTI- bacteroia- endotoxins- vasodilation?, GI bleed- systemic condition causing low BP. Head injury- damage reticular activating system- lose consciousness. May have amnesia.
symptoms of hypoglycaemia?
disorientated, slurring of speech, unsteady gait, dizziness, confusion
what is compensation when raised ICP?
blood and CSF squeezed out
decompensated= brain herniation- e.g. subfalcal, tentorial (uncus) and pressure coning- cerebellar tonsils and medulla.
what is the tentorial notch needed for?
passage of the brainstem*
clinical signs of raised ICP in clinical setting?
Change in behaviour – a cause of doctors being sued! Just not acting quite right.
Drop in level of consciousness - GCS
Neurological localising signs
Change in pupil reaction- dilate with oculomotor PNS fibres compression
Change in blood pressure, pulse and breathing, BP goes up= cushing's reflex
how can clinicians alter ventilation of a patient to cope with raised ICP?
can intubate them, so don't cough- as this would raise ICP< and control CO2 levels- don't want them increasing if not breathing very well as this will cause cerebral vasodilation, raising ICP further, and if low- constriction, so will cut off b.supply to already damaged areas of the brain.
causes of raised ICP?
- Head injury
- Infection - meningitis / encephalitis
- Impaired venous drainage
- Subarachnoid blood
- Trauma - extradural,subdural, intra-cerebral
- Haemorrhagic stroke
- Primary brain
what are secondary brain injuries?
blood clot causing raised ICP
what is the interval called following a brain injury where patient recovers, before rapidly deteriorating due to secondary brain injury e.g. with ED haematomas?
other than being elderly, what else can cause brain shrinkage increasing susceptibility to SD haematoma?