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Clinical neuroscience > S10: neurotrauma > Flashcards

S10: neurotrauma Flashcards

1
Q

Define stroke and TIA

A

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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2
Q

Outline the types of stroke

A

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

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3
Q

Describe the emergency management of stroke

A

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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4
Q

Describe symptoms of an anterior cerebral artery infarct

A

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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5
Q

Describe symptoms of a proximal middle cerebral artery infarct

A

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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6
Q

Describe symptoms of a lenticulostriate artery infarct

A

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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7
Q

Describe symptoms of a distal middle cerebral artery infarct

A

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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8
Q

Describe symptoms of a posterior cerebral artery infarct

A

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

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9
Q

Describe symptoms of cerebellar infarcts

A

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

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10
Q

Describe symptoms of brainstem strokes

A

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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11
Q

Describe symptoms of distal basilar artery occlusion

A

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

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12
Q

Describe symptoms of proximal basilar occlusion

A

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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13
Q

List risk factors for subarachnoid haemorrhage

A 
Hypertension 
Smoking
Excess alcohol consumption 
Family history
Trauma
Cocaine use
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14
Q

Describe the pathophysiology of subarachnoid haemorrhage

A

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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15
Q

Describe what bleeding into the subarachnoid space causes

A

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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16
Q

Describe the clinical features of a subarachnoid haemorrhage

A

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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17
Q

Describe investigations for subarachnoid haemorrhage

A

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

18
Q

Describe treatment for subarachnoid haemorrhage

A

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)

19
Q

Describe typical organisms causing meningitis

A

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

20
Q

List risk factors for meningitis

A 
CSF defects
Spina procedures 
Endocarditis
Diabetes
Alcoholism
Splenectomy
Crowded housing
21
Q

Describe clinical presentation of meningitis

A

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

22
Q

Describe pathophysiology of meningitis

A

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

23
Q

Describe investigations for meningitis

A

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

24
Q

Compare lumbar puncture findings for bacterial vs viral causes of meningitis

A

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

25
Q

Describe treatment for meningitis

A

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

26
Q

List complications of meningitis

A 
Septic shock
DIC
Raised ICP
Coma
Cerebral oedema 
Death
27
Q

What is the normal ICP?

A 
Determined by volume of blood, brain & CSF 
Adults: 5-15mmHg
Children: 5-7mmHg
Term infants: 1.5-6mmHg
Raised ICP: >20mmHg
28
Q

Explain the Monro-Kellie doctrine

A

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

29
Q

State the equation for cerebral perfusion pressure

A

CPP = MAP – ICP

30
Q

Describe cerebral autoregulation in response to increased ICP

A

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

31
Q

Describe Cushing’s triad

A

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

32
Q

List ‘too much blood’ causes of raised ICP

A

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

33
Q

Describe congenital hydrocephalus

A

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

34
Q

Describe management of congenital hydrocephalus

A

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

35
Q

List causes of acquired hydrocephalus

A

Meningitis
Trauma
Haemorrhage
Tumours

36
Q

List ‘too much brain’ causes of raised ICP

A

Cerebral oedema:

1) Vasogenic
2) Cytotoxic
3) Osmotic
4) Interstitial

37
Q

Describe idiopathic intracranial hypertension

A

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

38
Q

Describe the clinical features of raised ICP

A 
Headache – constant, worse in the morning, worse on bending/straining 
Nausea, vomiting 
Difficulty concentrating or drowsiness 
Confusion 
Double vision
Focal neurological signs
Seizures
39
Q

Outline the different types of brain herniation

A

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

40
Q

Describe management of raised ICP

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

Clinical neuroscience (11 decks)

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