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Stroke: "Brain Attack" (Stroke Recovery (regaining QoL?) (Other…
Stroke: "Brain Attack"
What is it?
occurs when blood flow to an area of the brain is cut off (if for longer than 10 minutes, all cells die)
abilities controlled by that area are lost eg. memory, muscle control --> symptoms depend on location
brain cells are deprived of oxygen & die
up to 80% of strokes can be prevented
often produces an infarct: area of dead or dying tissue
can result from many vascular disorders
Types
Other
Angiomas
collection of abnormal vessels that divert the normal blood flow
Aneurysms
vascular dilations due to defects in vessels' dilations (balloon-like expansions of vessels)
Migraine stroke
due to constriction of vessels, reduced blood flow (posterior cerebral artery)
TIA Transient ischemic attack
can mimic stroke-like symptoms
symptoms last less than 24h
don't cause permanent brain damage but are a warning sign that a stroke may happen in the future
Ischemic
vessel blockage
when a blood vessel carrying blood in the brain is blocked by a blood clot
embolic: blood clot forms somewhere in the body (usually the heart) and travels to the brain --> clot brought through the blood of a larger vessel is forced into a smaller one --> no circulation
middle cerebral artery of the left side
thrombotic: blood clot that forms inside one of the arteries supplying blood to the brain (in place)
cerebral anteriosclerosis: thickening & hardening of arteries
Hemorrhagic
less common (15%) but responsible for ca. 40% of all stroke deaths
rupture
either a brain aneurysm or a weakened blood vessel leak
blood spills into or around the brain and creates swelling and pressure --> damaging cells & brain tissue
intracerebral: blood vessel inside the brain bursts and leaks out into surrounding brain tissue
Causes: high blood pressure, aging blood vessels, hypertension, blood disorders eg. leukemia, toxic chemicals
subarachanoid: bleeding in the area between the brain & the tissue covering the brain (subarachnoid space)
usually occurs when a person is awake
Basic Division: Cerebral Vascular Accident
TIA --> no tissue damage
stroke --> tissue damage
Stroke & TBI?
stroke as a longterm complication of TBI
more likely to die following stroke if also a history of TBI
more severe TBI associated with greater risk of stroke & post stroke mortality
Risk factors
we can control them
high blood pressure, smoking, diabetes, high cholesterol, physical inactivity, obesity, artery disease, TIAs, heart disease, high red blood cell count, excessive alcohol intake, drug use eg. cocaine, ecstasy, sleep apnea (sleep disordered breathing)
we can't control them
increasing age, heredity, gender (women have greater risk), prior stroke, African Americans have greater risk
Stroke Recovery (regaining QoL?)
variance between people (intelligence, age, handedness, personality, treatment)
functional restitution: slow, often revealing a gradual reemergence of functions that resembles the developmental stages in infants
Physiology: LTP, kindling, new neurons produced in the injured cortex, exposure to stress (--> bad effect on cell survival & cell proliferation)
Overall, recovery for brain damage seems likely to be the best if the patient is young, intelligent, optimistic, left-handed female
Therapeutic approaches
electrical stimulation to increase brain or nerve activity
stem cell treatments: transplantation of stem cells to replace lost neurons
pharmacological treatments designed to stimulate brain plasticity & to reduce inflammation
diet
rehabilitation emphasizing the repeated use of affected limbs or cognitive processes
functional improvement after stroke corresponds to a change in functional organization of the remaining brain (reorganization is bilateral)
capacity for reorganization declines with increasing size of stroke & increasing age
if the primary sensorimotor cortex survives after stroke, some functional improvement is likely with time
Other treatment?
anticoagulant therapy to remove or resolve a clot
dilators of vessels
neuroprotectant drugs that limit the changes leading to cell death
drugs to reduce blood pressure
neuroprotectant drugs that can block calcium channels or prevent ionic imbalance
most effective: PREVENTION
Examples of functional restitution
Recovery from Motor Cortex Damage
eg. if hemiplegia, the recovery looks like reaching & grasping development in infants
Recovery from Aphasia
posttrauma/head injury patients show the most rapid and almost complete recovery
recovery in stroke patients less pronounced and sometimes absent
initial deficits are least severe in anomic patients (unable to generate names for common objects) and most severe in global aphasics
most recovery in the first 3 months & additional recovery over the next 6 months (after that little/no recovery)
younger patients --> better recovery (also slight effects of intelligence, sex, occupation)
language components most resistant to brain damage: naming, oral imitation, comprehension of nouns, yes/no responses
Recovery from surgical lesions: no recovery
Neurobiology
we may be able to point to a specific event/immediate cause of stroke, but the damage is not the result of a single causative event --> cascade of cellular events compromises other regions too
Inflammation: brain tissues become inflamed and swollen, threatening cellular integrity
Also changes in metabolism & glucose utilization (eg. in stroke metabolic rate decreases by ca. 25%)
mRNA stimulated --> it alters the production of proteins in the neurons and proves to be toxic to the cells
Ionic changes: changes in ionic balance, changes in PH, changes in properties of cell membrane (pathological events: release of glutamate excess, prolonged opening of calcium channels)
Second messengers: The open calcium channels allow toxic levels of calcium to enter the cell --> direct tonic effects, provokes second messenger pathways that can be harmful to neurons
Language & its disorders (Aphasia: inability to comprehend or formulate language)
stroke in the middle cerebral artery could lead to aphasia
Fluent: fluent speech but difficulties either in auditory verbal comprehension or in repetition of words
Wernicke's/ Sensory Aphasia: word salad, inability to comprehend words or to arrange them into coherent speech but word production is intact
Transcortical/Isolation Syndrome: can repeat words & name objects but can't speak spontaneously or comprehend words (also words fail to arouse associations)
Conduction Aphasia: can speak easily, name objects, understand speech but can't repeat words
Amnesic/Anomic Aphasia: disruption of fibers between Broca & Wernicke areas, difficulty finding names of objects
Non-Fluent: difficulty in articulating but quite good verbal comprehension
Broca (expressive) severe: laborious articulation, speechlessness with recurring utterances, poor repetition
Broca (expressive) mild: slight but obvious articulatory disorders
Transcortical Motor Aphasia: repetition is good but no spontaneous speech
Global Aphasia: speech production & understanding is impaired (Broca + Wernicke areas = Para Sylvian Cortex)
Pure: selective impairments in reading, writing etc. in the absence of other language disorders
Wernicke-Lichtheim-Geschwind Model
Wernicke's area is crucial for language comprehension
arcuate fasciculus (major fibre bundle connecting language areas in temporal & frontal cortex): necessary information exchange between Broca & Wernicke areas eg. reading aloud
Broca's area is crucial for language production
language areas are bordering one of the major fissures: Sylvian fissure
Aphasias
Wernicke's aphasia: posterior temporal
conduction aphasia: arcuate fasciculus
Broca's aphasia: ventral PFC
transcortical motor aphasia: issue between broca's area & association cortex
transcortical sensory aphasia: issue between wernicke's area & association cortex
Cortical Language Components
Non-fluent Aphasia
apraxia of speech (difficulty producing sequences of speech sounds): core deficit comes from damage to insula
impairment in sentence comprehension: damage to dorsal part of superior temporal gyrus & middle temporal gyrus
recurring utterances: damage to arcuate fasciculus
impairment in articulation of sounds & Working memory for sentences: damage to ventral frontal cortex
Fluent Aphasia
lack of speech comprehension: damage to medial temporal lobe & underlying white matter --> stroke destroys local language regions & cuts off most of the occipital, temporal & parietal regions from the core language regions
deficits in holding sentences in memory until they can be repeated: damage to temporal cortex
Subcortical Language Components: thalamus as relay center activates/arouses the cortex
Right Hemisphere contributions
Left hemisphere in right-handed people is dominant & for left-handed is more bilateral
also has language abilities (studies with split brain patients)
little/no speech but good auditory comprehension of language
some reading ability but little writing ability
can recognize words (semantic processing) but little understanding of grammatical rules and sentence structures (syntactical)
Conclusion: language comprehension (right) & syntax e.g.. producing, timing, sequencing movements for speaking (left)
if left hemisphere is lost early in development, the right one can acquire language but still severe deficits in speech in adulthood
aphasia is rare after right-hemisphere lesions but there might be subtle linguistic impairments eg. vocabulary selection, repossess to complex statements, comprehending metaphors
right OFC lesions --> reduced verbal fluency
NP assessment of aphasia
Aphasia test batteries: subtests to explore language capabilities eg. tests of auditory & visual comprehension, oral & written expression, conversational speech BUT such tests are long and require special training to administer
Brief aphasia screening tests: conversational analysis eg. token test, aphasia screening test --> short & easy
Psychobiological approach: focus on individual differences (attempts to reconstruct brain's language-producing processes)
Brain Arteries
Middle Cerebral
to the cerebellum (lateral cerebral cortex), anterior temporal & insular cortices
if damage to the dominant hemisphere--> aphasia
sensory loss, paralysis, weakness of arm/face, neglect syndrome
Posterior Cerebral
to the occipital lobe
loss of pain & temperature sensations, visual field defects, visuospatial, prosopagnosia, naming colors/objects
Anterior Cerebral
supplies blood to most midline parts of frontal & superior medial parietal lobes, also to deeper structures eg. corpus callous, internal capsule, caudate, GP
Higher order processing, Motor, Sensory loss in feet, slowness, lack of spontaneity, Broca's aphasia
MRI Mechanisms Basics
T1 weighted
short TR & TE, CSF is dark, white matter is light, cortex is gray, inflammation is dark
T2 weighted
long TR & TE, CSF is bright, white matter is dark gray, cortex is light gray, inflammation is bright
Hyperintensity
areas of high intensity produced mostly by demyelination & axonal loss --> reflect lesions
observed on T2 MRI images within cerebral white matter (white matter lesions) or subcortical gray matter (gray matter hyperintensities)
in many neurological/psychiatric disorders eg. deep white matter hyper intensities are 3x more likely to occur in bipolar or depression
potential diagnostic measure
appear as bright signals/areas on MRI image