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82 Cards in this Set
- Front
- Back
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Causes of syncope
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- neurally mediated (vasovagal) : reflex mediated vascular change
- orthostatic hypotension - psychiatric conditions - primary cardiac condtions - unknown 1/3 |
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Cerebrovascular disease collapse is longer in duration than syncope/seizure
T/F |
T
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ICA supplies temporal neocortex
T/F |
F - vertebral-basilar supply
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Which of the main branches off vertebral-basilar system does not supply cerebellum?
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PCA
(AICA, PICA, SCA, PCA all support BS) |
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What a. supplies 'middle wedge' of caudal medulla?
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ant. spinal a.
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blood flow to the brain is dependant on systematic flow.
T/F? |
F - independent
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over what pressure is there normal cerebral autoregulation?
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50-150mmHg
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LOC implies decrease of blood flow to which areas?
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- diffuse cerebral cortex
- BRF |
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what is the effect of hypercapnia on cerebral blood flow?
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vasodilation.
cerebral vessel sensitivity to CO2 underlies rapid localised blood flow changes. |
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what is the autonomic innervation of cerebral blood flow?
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SNS - superior cervical ganglion
PNS - CN VII |
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autonomic regulation of cerebral blood flow is tonically present.
T/F |
F - they are important under abnormal conditions
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why are HT meds not indicated as Rx for post stroke HT
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even though there is higher pressure, due to disruption of normal cerebral autoregulation lowering of pressure may compromise cerebral perfusion
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what is the autonomic innervation of cerebral blood flow?
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SNS - superior cervical ganglion
PNS - CN VII |
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cause of stroke
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- cessation of blood flow (obstruction, reduced flow from low pressure)
- haemorrhage |
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what is commonest cause and location of cerebral infarct?
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- atheroma and superimposed thrombus
- ICA at origin |
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what can cause lacunar infarcts in deep brain structures?
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- atheroma
- thrombus - hypertensive thickening |
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causes of haemorrhage
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- rupture berry aneurysm (SAH)
- rupture small penetrating a. (intracerebral haemorrhage, less with better HT control) |
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current common medications used in stroke prevention/recurrence
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- anticoagulants: heparin, warfarin
- antiplatelets: aspirin - thrombolytic: tPA |
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why does ischaemia cause increase in intracellular Na
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- ATP reduced :. N-K-ATPase activity slowed
- Na channels malfunction and stay open longer |
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what causes influx of Ca
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- excitotoxicty associated Ca influx
- L-channel Ca influx - reduced efflux by Ca-ATPase |
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reperfusion injury occurs as a result of ROS
T/F |
T
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what is aim of therapy with neuroprotective agents?
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salvage 'at risk' from progression to infarction
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why does the functional effect of aspirin last after cessation of treatment?
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aspirin binds proteins irreversibly for the lifespan of the platelet
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what is dipyridamole?
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anti-platelet drug
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what are the benefits of low dose aspirin?
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- reduction of GIT bleeding side effects
- inhibition of platelet COX with minimum inhibition of PGI2 |
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what could explain the selective inhibition of TXA2 of aspirin?
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GIT absorbed ASA in portal circulation acetlylates platelets in portal circulation which then spreads to systemic circulation. eventually ASA then is inactivated by liver metabolism so when in circulation does not effect systemic endothelium
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what level of prevention is aspirin in cerebrovascular disease?
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secondary
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the penumbra contains unsalvagable tissue
T/F |
F - perfusion reduced so tissue is functionally inactive, not reached point of energy/ion pump failure where it can no longer maintain integrity
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what is a potential side effect of using tPA following acute stroke?
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increased risk of intracerebral haemorrhage
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what is the probability of stroke in the week following a TIA?
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8-10%
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why is an increased perfusion pressure needed post stroke?
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vascular resistance increased post stroke :. high pressure to maintain cerebral perfusion
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anticoagulation has been demonstrated to improve outcome following stroke.
T/F |
F
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it is critical to est swallowing status and prevent aspiration.
T/F |
T
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hyperglycaemia is associated with a worse outcome following stroke
T/F |
T - as is fever
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what percentage of patients recover functionality at 3 months?
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95%
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why would a DW MRI be used in conjunction with a Perfusion MRI
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to determine ischaemic penumbra
DW - i.d. infarcted core perfusion - areas of hypoperfusion |
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what Ix should be done following stroke?
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- CT/MRI
- carotid, vertrebral a. duplex - echocardiogram - CXR, ECG, FBC, EUC, glucose, PT, PTT |
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what is a critical sign in febrile children?
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difficulty arousing child
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what increases the likelihood of primary intracranial disorder?
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focal neurological signs in combination with signs of raised ICP
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what are the septa formed by the dura?
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- falx cerebri
- falx cerebelli - tentorium cerebellu - diaphragma selli |
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why does a subdural infection spread so rapidly?
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there are few attachments between arachnoid and dura
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what's the difference between meningitis and a focal collection?
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meningitis has even pressure spread and no displacement, whereas a focal collection causes early displacement
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what are common signs of displacement?
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- herniation of temporal lobe causing paresis of CNIII
- compression contralateral cerebral peduncle causing ipsilateral CST signs - coning causing coma - CN VI |
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where is the polio virus tropic?
where is HSV tropic? |
- polio in VH
- HSV in temporal lobes |
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what are the different bacterial pathogens dependant on age?
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- neonates: e.coli, l.monocytogenes, group B strep
- childhood: n.meningitidis, s.pneumoniae, h.influenzae - adult: n.meningitidis, s.pneumoniae |
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all immunocompromised patients will have be colonised with the same organisms
T/F |
F - dependant on part of immune system affected (e.g. cellular, humoral, complement, multifactorial)
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why do children need Hib immunisation?
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antibody needed to act in conjunction with complement to prevent encapsulated bacterial colonisation isn't produced until 2 yrs
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why are anti-inflammatory agents given?
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to dampen inflammatory response and subsequent cytokine induced damage
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what is the gold standard for diagnosis in bacterial meningitis?
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gram stain and culture of CSF
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what structure of the vestibular system detects what force?
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semi-circular canals - detect angular force (head rotation)
otoliths - linear force (head tilt) |
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what do the vestibular neural signals relay?
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- perception: head relative to gravity
- oculomotor response: fast neural pathways to eye motor nuclei. eyes to compensate head movement. - postural: corrective response of mm. of neck and trunk |
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why is vestibular function testing done in a dark room?
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to eliminate other inputs to eye movements
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what are components of semicircular canal?
what are components of otolith? |
- duct, ampulla, crista, receptors
- utricular, saccular, maculae, otoconia |
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what are the five main oculomotor systems?
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- pursuit
- saccades - vestibulo-occular reflex - optokinetic response - vergence |
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why might cerebellar dysfunction cause deranged pursuit?
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feedback control of prusuit mediated by cerebellar flocculus and basal ganglia
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what drugs can affect pursuit?
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- phenytoin
- carbamazepine - benzo - alcohol |
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what pathways are involved in production of saccades?
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- pontine paramedian reticular formation
- frontal eye fields |
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velocity of ADDuction is greater than velocity of ABDuction
T/F |
T
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what can slow saccades indicate?
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pontine lesion
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the indirect pathway of VOR is via MLF (from vest n. to oculomotor n.)
T/F |
F - MLF is direct pathway.
Indirect is via reticular activating system. |
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where would a lesion be in hyperactive VOR?
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hyper always caused by CENTRAL lesions. hypo can be peripheral or central.
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what are the inputs of the optokinetic response?
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- fovea ( to striate cortex)
- peripheral retina ( to vest n.) |
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what is the function of the fast phase in the optokinetic response?
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reflex, corrective, anticipatory
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what can cause convergence failure?
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INO
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vestibular nystagmus is accentuated in the dark
T/F |
T
gaze paretic nystagmus maximal in light |
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ab. treatment in meningitis should always be delayed for lumbar puncture
T/F |
F - only non-critical pts. may have delayed therapy, all others must commence immediately
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what are contraindications for LP?
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- infection in local area
- shock - coagulopathy - raised ICP signs - focal neuro signs |
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what rx can be given to reduce ICP?
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- reduce CO2 (intubation, hyperventilation)
- osmotic diuresis (mannitol) |
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what are recommend ab. therapies dependant on age?
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- < 3m: 3G-C, ampicillin(listeria)
- > 3m: 3G-C vancomycin(pneumococcal) in association with dex |
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what are the main factors contributing to neurological outcomes?
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- raised ICP
- reduced CPP |
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how common is seizure before presentation in meningitis?
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20%
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what may cause secondary fever?
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- nosocomial
- dexamethasone therpay - immune phenomena |
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what is the most common long-term complication following bacterial meningitis?
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sensori-neural hearing loss
dex. can reduce hearing loss |
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what percentage of children are hospitalised before school ?
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25%
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what age is associated with a poorer response to hospitalization?
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between 6m and 4y
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space occupying lesions(SOL) only cause negative symptoms
T/F |
F - can cause epileptical (positive) manifestations
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what are secondary effects of a space occupying lesions?
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- cerebral oedema
- hydrocephalus - raised ICP |
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which type of oedema is more common with SOL?
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vasogenic (BBB integrity compromised, lymphatics not adequate for drainage)
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which type of oedema causes intercellular fluid build up?
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vasogenic.
cytogenic has intracellular fluid gain. |
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where is the most common obstruction of SOL causing hydrocephalus?
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cerebral aqueduct
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why might age impact ICP?
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consequences of age (atrophy, presence of fontanelle) provide more room for expansion without increase in ICP
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which is cerebellar tonsillar herniation life-threatening?
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compression of vital structures in BS
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