S10: neurotrauma Flashcards by Aashi Rawat

Define stroke and TIA

Stroke = serious life-threatening condition that occurs when the blood supply to part of the brain is cut off
-symptoms & signs persist for more than 24 hours
Transient ischaemic attack = similar clinical features of a stroke but completely resolve within 24 hours

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Outline the types of stroke

Ischaemic – thromboembolic
Haemorrhagic – intracerebral & subarachnoid
Other – dissection, venous sinus thrombosis & hypoxic brain injury

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Describe the emergency management of stroke

Are they within the window for thrombolysis? (<4 hours)
Do a CT head to determine if it is a bleed (if bleed cannot proceed with thrombolysis)
CT: ischaemic area of brain not visible early on, a bleed will show up as a bright white area
MRI: sometimes performed, ischaemia shows up as a high signal area

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Describe symptoms of an anterior cerebral artery infarct

Contralateral motor & sensory weakness in lower limb
Urinary incontinence due to paracentral lobules being affected
Apraxia (inability to do familiar movements on command)
Dysarthria/aphasia
Split brain syndrome/alien hand syndrome (rare) -> involvement of the corpus callosum

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Describe symptoms of a proximal middle cerebral artery infarct

Contralateral full hemiparesis – internal capsule affected
Contralateral sensory loss
Visual field defects – contralateral homonymous hemianopia
Aphasia – global if dominant hemisphere affected
Contralateral neglect

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Describe symptoms of a lenticulostriate artery infarct

Cause destruction of small areas of internal capsule and basal ganglia
Different types:
1) Pure motor – face, arm & leg affected equally
2) Pure sensory – face, arm & leg affected equally
3) Sensorimotor – mixed, caused by infarct occurring somewhere at boundary between motor & sensory fibres

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Describe symptoms of a distal middle cerebral artery infarct

Superior division – contralateral face & arm weakness, expressive aphasia if left hemisphere affected
Inferior division – contralateral sensory change in face & arm, receptive aphasia, contralateral visual field defect without macular sparing (homonymous hemianopia)

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Describe symptoms of a posterior cerebral artery infarct

Contralateral homonymous hemianopia (with macular sparing due to collateral supply from MCA)
Contralateral sensory loss due to damage to thalamus

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Describe symptoms of cerebellar infarcts

Nausea, vomiting, headache, vertigo/dizziness
Ipsilateral cerebellar signs (DANISH)
Possible ipsilateral brainstem signs
Possible contralateral sensory deficit/ipsilateral Horner’s

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Describe symptoms of brainstem strokes

Contralateral limb weakness
Ipsilateral cranial nerve signs
-can be explained by damage to corticospinal tracts & damage to cranial nerve nuclei on same side

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Describe symptoms of distal basilar artery occlusion

Visual and oculomotor deficits
Behavioural abnormalities
Somnolence, hallucinations & dreamlike behaviour
Motor dysfunction often absent

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Describe symptoms of proximal basilar occlusion

Can cause locked in syndrome
Complete loss of movement of limbs, however preserved ocular movement -> eyes still move because midbrain getting supply from PCAs
Preserved consciousness

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List risk factors for subarachnoid haemorrhage

Hypertension 
Smoking
Excess alcohol consumption 
Family history
Trauma
Cocaine use

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Describe the pathophysiology of subarachnoid haemorrhage

Occur following rupture of an aneurysm in the circle of Willis
Most are berry aneurysms, common sites:
1) Anterior communicating artery: can compress nearby optic chiasm & may affect frontal lobe/pituitary
2) Posterior communicating artery: can compress the adjacent oculomotor nerve
3) Bifurcation of the middle cerebral artery as it splits into superior & inferior divisions

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Describe what bleeding into the subarachnoid space causes

1) Early brain injury – microthrombi, vasoconstriction, cerebral oedema & apoptosis of brain cells
2) Cellular changes – oxidative stress, release of inflammatory mediators, platelet activation
3) Systemic complications – sympathetic activation, myocardial necrosis, systemic inflammatory response

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Describe the clinical features of a subarachnoid haemorrhage

Thunderclap headache
Frequent loss of consciousness and confusion
Meningism – neck stiffness, photophobia & headache
May be focal neurology
May be history of sentinel bleed
May present as cardiac arrest

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Describe investigations for subarachnoid haemorrhage

CT head
CT angiogram if bleed confirmed
Lumbar puncture – xanthochromia (yellow colouring of CSF due to metabolism of Hb to bilirubin), high protein, high RBC

Describe treatment for subarachnoid haemorrhage

ABC approach
Neurological observations
Neurosurgery:
- Decompressive surgery
- Coiling: insertion of a platinum wire into the aneurysm sac, which causes thrombosis of blood within aneurysm itself (neuroradiologists)
- Clipping: placement of a spring clip around the neck of the aneurysm, causing it to lose blood supply (neurosurgeons)

Describe typical organisms causing meningitis

Neonates – E. coli, group B strep, listeria monocytogenes
Children – haemophilus influenzae type B, Neisseria meningitidis
Elderly – strep pneumonia, listeria monocytogenes

List risk factors for meningitis

CSF defects
Spina procedures 
Endocarditis
Diabetes
Alcoholism
Splenectomy
Crowded housing

Describe clinical presentation of meningitis

Triad of meningism with fever
Flu-like symptoms, joint pains and stiffness
Meningococcal rash
Babies: inconsolable crying, rigidity, bulging fontanelle

Describe pathophysiology of meningitis

Bacteria in nasopharynx enter circulation, cause damage to vessel walls in the brain & meninges, allowing pathogen to enter the subarachnoid space
Once in subarachnoid space, pathogens multiply rapidly -> purulent CSF & severe meningeal inflammation
Vasospasm of cerebral vessels = cerebral infarction
Oedema of brain parenchyma = raised ICP

Describe investigations for meningitis

Bloods
Chest x-ray or mid-stream urine if suspect a particular septic focus
Lumbar puncture

Compare lumbar puncture findings for bacterial vs viral causes of meningitis

Bacterial meningitis – cloudy CSF, high protein, high WBCs (neutrophils), low glucose
Viral meningitis – maybe clear but can be cloudy, protein normal or high, high WBCs (lymphocytes), normal glucose

Describe treatment for meningitis

Supportive – analgesia, antipyretics, fluids Medical – IV ceftriaxone, dexamethasone (prevent hearing loss) If viral: aciclovir for herpes, ganciclovir for CMV

List complications of meningitis

``` Septic shock DIC Raised ICP Coma Cerebral oedema Death ```

What is the normal ICP?

``` Determined by volume of blood, brain & CSF Adults: 5-15mmHg Children: 5-7mmHg Term infants: 1.5-6mmHg Raised ICP: >20mmHg ```

Explain the Monro-Kellie doctrine

Any increase in the volume of one of the intracranial constituents must be compensated by a decrease in the volume of one of the others In a mass, first components to be pushed out of the intracranial space are CSF & venous blood -at the lowest pressure

State the equation for cerebral perfusion pressure

CPP = MAP – ICP

Describe cerebral autoregulation in response to increased ICP

If ICP increases then CPP decreases, triggering cerebral autoregulation to maintain cerebral blood flow (CBF) If CPP < 50mmHg, CBF cannot be maintained as cerebral arterioles maximally dilated ICP can be maintained at a constant level as an intracranial mass expands up until a certain point beyond which ICP will increase exponentially Damage to brain can impair/abolish cerebral autoregulation

Describe Cushing’s triad

Rise in ICP -> hypertension (body increases MAP to maintain CPP) Increase in MAP is detected by baroreceptors -> bradycardia via increased vagal activity (cause stomach ulcers as a dangerous side effect) Continuing compression of the brainstem leads to damage to respiratory centres, causing irregular breathing

List ‘too much blood’ causes of raised ICP

Too much blood within cerebral vessels – raised arterial pressure, raised venous pressure Too much blood outside of cerebral vessels – extradural, subdural, subarachnoid, haemorrhagic stroke, intraventricular haemorrhage

Describe congenital hydrocephalus

Obstructive – neural tube defects, aqueduct stenosis; communicating – increased CSF production, decreased CSF absorption Clinical signs – bulging head with head circumference increasing faster than expected, sunsetting eyes

Describe management of congenital hydrocephalus

Tapping fontanelle with a needle Medium term drainage can be achieved by external ventricular drain – allows continuous pressure monitoring, can be at risk of infection Long term drainage by ventricular shunts – V-P shunts most common

List causes of acquired hydrocephalus

Meningitis Trauma Haemorrhage Tumours

List ‘too much brain’ causes of raised ICP

Cerebral oedema: 1) Vasogenic 2) Cytotoxic 3) Osmotic 4) Interstitial

Describe idiopathic intracranial hypertension

May present with headache & visual disturbance Usually obese middle aged females Diagnosis confirmed by raised opening pressure on an LP Treat with weight loss & blood pressure control

Describe the clinical features of raised ICP

``` Headache – constant, worse in the morning, worse on bending/straining Nausea, vomiting Difficulty concentrating or drowsiness Confusion Double vision Focal neurological signs Seizures ```

Outline the different types of brain herniation

Tonsillar herniation (coning) – cerebellar tonsils herniate through foramen magnum, compressing medulla Subfalcine herniation – cingulate gyrus pushed under free edge of falx cerebri, can compress ACA Uncal herniation – uncus of temporal lobe herniates through tentorial notch compressing adjacent midbrain, can cause CN III palsy Central downward herniation – midline structures pushed down through tentorial notch External herniation through skull fracture/therapeutic craniectomy

Describe management of raised ICP

``` ABC Sedation, analgesia & paralysis Head up tilt Temperature Anticonvulsants Nutrition & PPIs Other treatments: mannitol, ventricular drainage, decompressive craniectomy as last resort ```