neuro mod 2 Flashcards
what is a stroke
interruption in blood flow to CNS
stroke rank among leading COD in US
3rd
common symptoms of stroke
- sudden numbness of face, arm or leg (one sided)
- sudden confusion, trouble speaking
- sudden trouble seeing in one or both eyes
- sudden trouble walking, dizziness, loss of balance
- sudden severe H/A with unknown cause
which stroke is more common - hemorrhagic or ischemic?
ischemic is more common
pathology of hemorrhagic stroke
- bleeding into brain parenchyma
- primary destruction of neurons from hemorrhage
- secondary destruction from potential rise in ICP
mechanism of injury of hemorrhagic stroke
- small vessel bleeding from HTN
- anticoagulation therapy
- cocaine use
cause of ischemic stroke
embolism/thrombus
what causes extra cranial embolism in ischemic stroke
most arise from heart
-valve, MI, afib, dilated myopathy, CHF
what causes intracranial thrombus in ischemic stroke
cerebral branches of circle of willis, internal carotid artery, small vessels of posterior circulation
intervention for ischemic stroke
thrombolytic intervention ASAP
what is the window of time for thrombolytic intervention of ischemic stroke
initial :
pathology of ischemic stroke - primary site
primary site of irreversible damage to neuron
- neuron becomes depolarized causing influx of Ca/ion channel dysfunction
- calcium influx leads to release of degradative enzymes
- neuron cell membrane destroyed releasing more substances to perpetuate inflammation/cell necrosis in the immediate area
- within hours/days - cytokines and other factors are released which promote additional inflammation/cell destruction
pathology of ischemic stroke - secondary site
Secondary site of reversible damage
Within hours the secondary site can be attacked by cascade of events in primary site
what is penumbra and what is it related to
“penumbra” = shadow
ischemic stroke - secondary site of reversible damage
which sites are reversible vs irreversible in the pathology of ischemic stroke
- primary site is irreversible damage to neuron
2. secondary site is reversible damage
what is the general pathology of ischemic stroke and how long does it take
cascade of inflammatory events occur within seconds to minutes
goal of tx for ischemic stroke
preserve neurons in the secondary site by
- restoring blood flow as soon as possible
- meds to block cascade of inflammation
risk factors for ischemic stroke
- family hx
- age >55
- HTN >140/90
- elevated chol/hyperlipidemia >200 total
- smoking
- diabetes
- obestiy BMI >30
- co-existing CV dz
- previous TIA
- high levels of homocysteine
- use of BC or hormone therapy
- heavy or binge drinking
- illicit drugs - cocaine
what is a TIA
transient ischemic attacks
-transient loss of blood flow
cause of TIA
numerous
atherosclerosis, emboli, arterial dissection, arteritis, cocaine, and other drug use
neurological symptoms usually last how long in TIA
TIA increases risk for what?
stroke
circle of willis receives blood from
ICA and VA (vertebral arteries/basilar artery)
function of circle of willis
- origin of major blood vessels of the brain
- anastomosis pathyways
- small perforating arteries
small perforating arteries off the circle of willis contribute to what
blood supply to the subcortical regions of the brain
what areas do the small perforating arteries of circle of willis supply
- diencephalon
- internal capsule
- limbic structures
- pons
what is included in the diencephalon
- thalamus
- hypothalamus
- subthalamus
what is the internal capsule
- pathway of myelinated axons leaving and entering the cerebral cortex
- located between thalamus and basal ganglia
what are limbic structures
amygdale, hippocampus, etc
what is the ACA
anterior cerebral artery
what does the ACA supply
- medial (saggital) regions of each hemisphere:
- motor and sensory areas - lower body (distribution can be observed in homunculus diaphragm)
- prefrontal lobe
what do the small perforating arteries of the ACA supply
portions of subcortical structures (internal capsule and basal ganglia)
motor function with infarction of ACA
- LE contralateral hemiparesis (motor loss)
- urinary incontinence
- possible motor disorders associated with basal ganglia (Parkinson’s)
sensory function with infarction of ACA
LE contralateral hemiparesthesia or hemianesthesia (loss of sensation)
behavioral/personality changes with infarction of ACA
- apathy, poor motivation
- perseverance
- social inappropriateness
what is akinetic mutism
bilateral damage to frontal lobe
Akinetic: lack of movement
Mutism: lack of speech
what functions are lost with akinetic mutism in ACA infarction
- conscious alert pt who retains ability to move/speak but fails to do so
- damaged pathways inhibit motivation/increase apathy cause passiveness to interact or respond
what is the MCA
middle cerebral artery
what does the MCA supply
lateral aspect of each hemisphere:
- motor and sensory areas (face, UEs, trunk)
- association areas
- prefrontal lobe
- portion of optic tract
infarction of MCA will have what effects
depends on location
major trunk occlusion of MCA
everything of MCA stroke??
occlusion of superior branches of MCA (lateral frontal/parietal lobes)
global/broca’s aphasia & most calssic MCA s/s
occlusion of inferior branches of MCA (lateral temporal and inferior parietal lobes)
Wernicke’s and visual hemianopsia
motor changes with MCA infarct
- contralateral hemiparesis or hemiplegia (area 4&6)
- conjugate gaze (horizontal)
- apraxia (inability to perform purposeful voluntary movement)
where is the contralateral hemiparesis or hemiplegia in MCA infarct
lower face/trunk and UE
LEs spared
where will the eyes deviate with conjugate gaze brought on by MCA stroke (vs normal)
eyes deviate toward side of lesion
Normal: area 8 provides conjugate game toward opposite side, CN6&3
apraxia with MCA infarct
- common in which hemisphere
- which areas affected
- MC with dominant but may see in non dominant infarction
2. pre-motor, motor or sensory association areas - UE apraxia, sensory apraxia (ideational apraxia, conceptual apraxia)
sensory changes with MCA infarct
- contralateral hemiparaesthesia or hemianesthesia
- contralateral astereoagnosis
- Visual & auditory or smell
where do the contralateral hemiparaesthesia or hemianesthesia occur in MCA infarct
Lower face/trunk and UE
LE spared
what is contralateral astereoagnosis in MCA infarct
tactile agnosis: inability to judge/interpret object by touch
visual losses with infarct in MCA
visual: hemianopia - half of visual field loss, MCA supplies portion of optic tract
potential behavioral/personality changes with MCA infarct
- apathy, poor motivation
- perseverance
- social inappropriateness
dominant hemisphere loss with MCA infarction
- apraxia
2. language/communication loss - aphasia
types of aphasia in dominant hemisphere loss with MCA infarction
- Broca’s aphasia (non fluent or motor aphasia) - comprehend but can’t speak - area 44,45
- Wernicke’s aphasia (fluent or sensory aphasia) - speak but can’t comprehend, word salad - area 22
- Global aphasia - sensory and motor language loss, combo of fluent (sensory) and non fluent (motor), global damage to dominant hemisphere (massive infarct) - involve both parietal/temporal and frontal lobes
non dominant hemisphere with MCA infarction
- anosognosia
- construct apraxia
- dressing apraxia
- dysprosodia
- confusion
- extinction
- unintentional fabrication of info
what is anosognosia in MCA infarction non dominant hemisphere loss
neglect, denial of injury, won’t turn head to contralateral side
what is construct apraxia in non dominant loss of MCA infarction
ex. can’t draw a clock
what is dressing apraxia in non dominant hemisphere loss of MCA infarction
not actual motor area but occurs b/c of inability to connect motor to purpose/meaning
what is dysprosodia
language/communication loss
motor dysprosodia in non dominant hemisphere loss of MCA infarction
difficulty of speech in producing the normal pitch, rhythm and variation of stress/tone in speech (musical aspects of speech)
what is sensory dysprosodia in non dominant hemisphere loss of MCA infarction
difficulty of speech in interpreting the normal pitch, rhythm and variation of stress/tone in speech (musical aspects of speech)
what is the PCA
posterior cerebral artery
what does the PCA supply
occipital lobe
inferior regions of temporal lobe
infarction of PCA
- hemianopia (loss of same side in each eye - area 17)
- contralateral to lesion - visual changes
- possible memory impairments (temporal lobe involvement)
visual association loss with infarction of PCA
- visual agnosia
- prosopagnosia
- alexia
what is visual agnosia that occurs with PCA infarction
inability to recognize an object by site
lesion in secondary visual cortex of occipital lobe (areas 18,19)
what is prosopagnosia with PCA infarction
difficulty recognizing familiar faces
occipital lobe secondary area, and association areas temporal/parietal lobes
what is alexia with PCA infarction
can’t read
small branches of PCA supply
some of thalamus and midbrain
potential loss in PCA infarction with small branches
potential for sensory or motor symptoms in addition to visual changes
-thalamic damage = chorea, hemiballismus
