Brain And Cognition 2 PDF

Ch. 13 i Vascular 1. Introduction A Crebrovascular Diseases includes : small vesselLisease (SVD( - -...

Ch. 13 i Vascular 1. Introduction A Crebrovascular Diseases includes : small vesselLisease (SVD( - - cerebral infarcts -Cerebral haemorrhage (stroke) B) Stroke-acute loss of function + diff in arm/leg on our side of body - speaking = loss strength of = 2nd leading cause of diate = women prevalance 2-Vascular Cognitive Impairment = Subcortical Dementia ar = Multi-intact Dementit · umbrella term for cognitive cousey due to vascular diseases Spectrum mild to disorders major · :. 3 Epidemiology age 65y · = · 40, 000 NL 4. Aetiology · Grebral stroke-part of the braim is deprived of because of disturbed blood flow oxygen Al Grebral Interet = Ischemic ↳ the location is leading for the Cognitive Stroke Characteristics · blockage - impairment > blooddot lembolisml closes an artery - in the brain or bloodstream => reduced supply of oxygen which leads to (permanent) damage > - Acute symptoms - dropping of function of face of the - loss body diff Speaking -. usually 1 side of body - or · Staying Consciouss o FRY · Types Embolic lout) > - - clofted mat From. somewhere else ice the body > - Arthro. (froml - clotted mat from. the brain artery  b) Transient Ischaemic Attack (mini) Characteristics temporary reduction · - in flood flow to small part of the brain - 24h. sympt. resolve after IA having - A second stroke is likely ( SVD C) Lunar Infact - 25 % of - Ischemic Strokes Characteristics · infarct the small that - in arties supply brain's deeper structures, after which a small cavity (luccar) forms - small ; between 3-20mm smallflood vessels may damage - not location D) Cerebral haemorrhage-cognitive disorder are mainly related to severity/size of hemorrhage Characteristics-bleeding(pozziane) · - blood vessel ruptures - 20 Y. - lose consciousness · Types (mainly > - Intracerebral within the brain - (SAH) > subarachnoid ↳ severe - outside the bein results in death - in caused by subtype - most cases ruphied intracranial , aneurysm  of SAH headache, - symptoms : severe stiffness to light , house neck , hypesers. -treatment for SAH X aneurysm closing neurosurgical clipping using endovascular treat. a the ancurism is Y closed by metal clip ex · coilsinserted into flood vessel · Treating Acute Symptoms ↓ blood ressure - · Risk factors - hypertension - accord consumpt - smoking - diabetes fall I shock heratoma causing -. 5 Acute and chronic effects Al Acute - cognitive impairments may be diffuse and severe/conscious car be deceased - in first 3 weeks B) drance - decreased daily function. reduced of life and quality  6. Neurological consequences a) Risk factors Lisbetes 2 -type increases - hypertension with 15 % - obesity cholesterol high - ↑ the risk significally it If they are co-occuring of decline. For each cognitive factor the risk of dimentia with 1. 5 times · Association between Vascular riskEactors and cognitive decline is caused by smallest flood vessels disease (CSDV) = white matter lesions luncar infarcts Very in over Joy. = common pp - = microgleeds > - Damaged domains - memory - attention - executive b) TIA and luncar infarct Transient Ischemic Attack - 1/3 of potients have in 24h symptoms resolve Cognitive deficit -. results in wild - cognitive dependi - ou ar - impairment locati - emot. recognition impaired - SVD  2) Major Stroke · 2/3 of patients have impaired cognit with significant predictor of reduced quality life i n all · cognitive domains sustained > - Attention dissiatly susser watching from movies > memory-majority - - nuterograde amnesia int. is impaired learning new > - executive - around 40 % -difficulty planning activities switching between tasks - > - aphasia · Talanic infarct - symptones don't stroke immediately indicate - has unusual cognitive impairments ex speech /motor sensory symplays contribulations acute memory impairment thalamus switching station crucial connection role = , between Liff. brain regions 7. Type and Severity of cognitive impair. relates the to specific blood supply weas in area Cerebral > ACA-Anterior Artery - MCA-middle cerebral > - > PCA Posterior Grebral artery arteig - - Language auct-middle areaartery · % of the 80 strokes occur there Common · impaired cognitive domains > memory - entergrade &newintlearna > - amnesit dominant (left) leads > - Language to language impairment ex. Broca's aphasia - speech Wernicke's aphasia - comprehension => apraxit - inability to do meaningful movements and gestures in assence of primary motor. impairment sensory or > - benispatial neglect-damade to 52 % paretotemporal frain regions Attention Lisorder. in which patients fail to attention to pay stimuli contraraletal to the losion. Patience are unware of that Perception 3A9 o HPCA = posterior crebral ertig visi ↳ supplies to : occipital temporal · Visual problems - Hemianopia-impaired half > Quadronopia-impaired - quarter > - Visual agnosia/Colour agnosia un objects/people not recognised not ex of recognising a hot up soup to > Prosopagnosit-inability recognise - faces =text reading sil a Executive Behav - ) ↳ ACA-anterior supplies O omupes to : cerebral frontal artey parietal Connection · disturbances between : Brock Wernicke caution process written ex - language or communicate verbally but can repeat words/sentences · Executive issues -Planning  > - cognitive flexibility-switching betwee tasks · Behav. insuff behav. inhibiting > -. > - ecot. ex · apathy lempathy facial ex , recognising expressions more severe in ight herei stroke 8. Subcortical Rufarcts ! Higher cognitive functions, such as reasoning, problem-solving, planning, and decision- making, are primarily associated with cortical areas of the brain, particularly in the prefrontal cortex, which is part of the frontal lobe. The cortex is responsible for complex thought processes and higher-level cognitive tasks. Subcortical structures, such as the thalamus, basal ganglia, and limbic system, play supportive roles in regulating emotions, processing memory, and coordinating movement, but they are not the main sites for higher cognitive functions. However, they do interact with cortical areas to influence cognitive processes. In summary, higher cognitive functions mainly occur in the cortex, especially in the prefrontal cortex. 1. Cortical Stroke Location: Occurs in the outer layer of the brain (the cortex), which includes areas responsible for higher cognitive functions, sensory processing, and voluntary movement. Common causes: Most often caused by blockages in larger arteries that supply blood to the cerebral cortex, such as the middle cerebral artery. Symptoms: ◦ Motor and sensory deficits: Weakness or paralysis on one side of the body (hemiparesis), depending on which hemisphere is affected. ◦ Cognitive and language impairments: Aphasia (difficulty with language) if the stroke affects the dominant hemisphere, especially the left side for most people. ◦ Visual-spatial issues: Neglect of one side of the body or difficulty perceiving space if the stroke is in the non- dominant hemisphere. ◦ Seizures: More common with cortical strokes. ◦ Higher cognitive dysfunction: Deficits in executive functions, attention, memory, and reasoning can occur if areas like the prefrontal cortex are affected. 2. Subcortical Stroke Location: Occurs in the deeper, subcortical regions of the brain such as the basal ganglia, thalamus, and internal capsule. These areas are crucial for motor control, sensory relay, and coordination between different brain regions. Common causes: Often caused by small vessel disease, where tiny arteries deep within the brain become blocked (also known as lacunar strokes). Symptoms: ◦ Pure motor or sensory deficits: Weakness or loss of sensation on one side of the body, but without the more complex deficits seen in cortical strokes. ◦ Lacunar syndromes: These include isolated motor strokes (e.g., hemiparesis without cognitive dysfunction) or isolated sensory strokes (numbness or tingling). ◦ Movement disorders: Subcortical strokes affecting areas like the basal ganglia can lead to issues with movement coordination (e.g., tremors, dystonia). ◦ Less frequent cognitive deficits: Since subcortical areas are less involved in higher cognitive functions, cognitive impairments are often less severe than in cortical strokes. However, subcortical strokes can still disrupt motor learning and executive function when there is extensive damage. Key Differences Cortical strokes typically result in more complex neurological and cognitive impairments, including language, visual processing, and higher executive functions. Subcortical strokes tend to produce more localized motor and sensory deficits but can be severe if they affect the pathways connecting the cortex and other brain areas. · damage to cerebellum/Grebellar Cognitive - motor problems Affective Syndrome S. Grebral - haemorrhage ↓ consciousness Cognation - confusion - Lisorientation · Cognitive impairment - severe  al Prevalence - rare ligh mortality rate - b)Sevent to extend and size of the haemorrage than location Subarachnoid c) LSAH) ~ extensive impact relatively young (55y) - case profile 5by (female) - headache while Symptoms - acute severe bedroom - cleaning vouits + losses consciousnesi Examination SAH wite - meyrism in posterior artery Problems - headaches - concentration anxiety -  1. Vascular Dementia Al Risk factors - cardiac arrhythmias logh slook pressive - - Liabetes of BI Age Liagnosis- 65-75 2) Criteria - interference with daily life is progressiveness not necessary - to dementia used diagnose E in at least - cognitive impairment official 1 domain - significant interference with life S criteria caut which explained by be motor sensory problems or T o -mpairments in slowness thinking/speaking - - diff to concentrate. diff multitasking -. ⑪ Non-cognitive consequences al auxiety/depression in - 113 patients · Predictors - premorbid depression - symptoms of anxiety > - Depressive symptoms could be due to the stroke kousey ) will factors ↑ the risk of depression. such as large lesion : undetected intorets > - Anxiety symptoms (fear of reacurance are common after stroke. > - PTSD-10/31 % most potients have symptoms' but not enough to cover DSM-5 criteria b) Sensory Activity Fatigue and overwhelming feeling sensory hypersensitivity I - - of exhaustion - diff to stimuli. process during mental activities as int is not filtered ex · sensitivedo light fatigue - is more melte thom physical ex - irritability when concentrating 12. Conclusion A) Risk factors age - - hypertension - alcol -Liabetes obesity - Isolation smoking - - Penumbra-brain area around damaged area 1. What is vascular cognitive impairment? COGNITIVE DISORDERS WITH A CEREBROVASCULAR AETIOLOGY continuity Vascular Cognitive Impairment (VCI) All forms of cognitive disorder associated with cerebrovascular disease Aetiology Large vessel disease Small vessel disease VCI covers the entire spectrum from mild cognitive disorders to vascular dementia No impairments Mild cognitive Vascular disorders dementia Severity 2. Normal and abnormal blood supply of the brain From artery to vein Arteries: Carry oxygenated blood from the heart Veins: Carry deoxygenated blood to the heart Small vessels Large vessels 2. Normal and abnormal blood supply of the brain The blood vessels in our brain: https://www.youtube.com/watch?v=uMMMqkVZAhk successes in subcortical ↑ 2. Normal and abnormal blood supply of the brain Large versus small vessel disease subcortical 2. Normal and abnormal blood supply of the brain Large versus small vessel disease Rao et al. Cureus 2018 2. Normal and abnormal blood supply of the brain fluidliuap b E Large versus small vessel disease Cerebral White matter 1 microbleeds hyperintensities signs ter Telgte et all., 2018, Wardlaw et al., 2013 - Lacunes 3. Vascular risk factors and SVD: Aging Causes: prevalence of vascular risk factors LaPlume et al. Alzheimers Dement 2022 3. Vascular risk factors and SVD: Aging Vascular risk relates to accelerated cognitive decline witen ege is normal but will the risk factor increases tee risk of developing dimensio LaPlume et al. Alzheimers Dement 2022 3. Vascular risk factors and SVD: Aging Causes: vascular risk factors and dementia > - lifestyle Kloppenborg et al. Eur J Pharmacol 2008 3. Vascular risk factors and SVD: Aging Global increases in unhealthy lifestyles Obesity Sedentary behavior Agha et al., 2017; López-Valenciano et al. (2020) risk factors considering A 78-year-old man with history of lifestyle are modifiable hypertension and type 2 diabetes awoke with inability to move his right side. On examination, his blood pressure was 180/98, his pulse was regular, and he had no carotid bruits. He had a dense right hemiparesis with no other associated neurological deficits. Initial CT of scan of the head did not reveal any acute intracranial abnormalities. Brain MRI (Figure 7-2) showed an acute small subcortical stroke in the posterior limb of the left internal capsule. Carotid ultrasound and cardiac workup were unremarkable. The patient was discharged on antiplatelet therapy, antihypertensives, an adjusted regimen for his diabetes, and a statin. He evolved favorably over the subsequent few months. https://radiologykey.com/small-vessel-disease/ 3. Vascular risk factors and SVD: Aging Modifiable risk factors of dementia Cardiovascular risk factors make aging- W less socialis. related changes more pronounced less sensory Stim E.g. hypertension, alcohol usage, obesity,. smoking, physical inactivity, diabetes Modifying these might prevent or delay up to nearly half of all dementia cases And generally improve healthy aging Livingstone et al. Lancet 2024 3. Vascular risk factors and SVD: Aging Aging, cerebral blood flow and grey matter loss Chen et al. Neuroimage 2011 Thompson et al.. J Neurosci 2003 3. Vascular risk factors and SVD: Aging Prevelance of SVD in aging white matter damage Mu et al. Neuropsychiatr Dis Treat 2022 3. Vascular risk factors and SVD: Aging Cognitive profile of aging affected Executive functioning and (psycho)motor speed are most prominently affected by SVD Levitt et al., Exp Aging Res 2006;32:263-295.  too fine to vascular longfinished so risk factors the had person 3. Vascular risk factors and SVD: Aging Time to start moving! 3. Vascular risk factors and SVD: Aging Cerebral perfusion more physical activity light a ↓ /I Physical t c hin on perfision lower less activity ↳ Carl-Johan Boraxbekk et al. NeuroImage, Volume 131, 2016, 133–141  3. Vascular risk factors and SVD: Aging they followed people for gy. The effect of physical activity 9 years later the who had better brains ones stayed physical 299 participants Average age: 78 years Minnesota Leisure-Time Activities Questionnaire (duration & frequency physical activity) (4 groups, based on quartiles) MRI-9 years later (grey matter volume) at old even age with consistent physical activity flue is improvem , Erickson et al. Neurology 2010;75:1415-1422  3. Vascular risk factors and SVD: Aging Exercise as an intervention short intervention 16 older adults (age 72.1) 4 weeks exercise, minimum of 2 to 3x a week, + additional activities at home 16 older control adults (no exercise, age 73.6) Cognitive functioning before and after intervention Executive functioning Psychomotor speed Yweeks of exercise already show ⑪ effects But the mom. You decline starts Stop no exercise Anderson-Hanley et al. JCEN 2010  risk factor 4. Cerebrovascular accident (CVA) Age is leading Stroke CVA = stroke 40 000 people per year 15% between 18 and 50 yrs Types higher mortality rate ±80% ±20% stops Hood flow sleeding/rephie  4. Cerebrovascular accident (CVA) Ischemic stroke = infarct – Penumbra: area located around the ischaemic core ⑪ & – Embolic stroke: clotted material that breaks off from elsewhere in the body (eg lungs) – Atherothrombosis: formation of blood clot (thrombotic stroke) in brain artery  4. Cerebrovascular accident (CVA) Haemorrhagic stroke Intracerebral haemorrhage (within brain) – Lobar: located in one of the cerebral lobes – Non-lobar: located in basal ganglia, thalamus, cerebellum or brain stem rar Subarachnoid haemorrhage (not within brain) – Bleeding in the subarachnoid space it's not in tissue tee Where insuallycaused by : > yanger age - > - severe headache  4. Cerebrovascular accident (CVA) Perfusion areas of the major arteries giti – Supratentorial: in the cerebrum – Infratentorial: in the brainstem or cerebellum 4. Cerebrovascular accident (CVA) Type of motor or cognitive dysfunction depends on location of stroke: anupes Supply area of anterior cerebral artery Frontal lose Supplies blood to the dorsal and medial parts of the frontal and parietal lobes. Impairments are found in: Neurological Language symptoms Executive function Behavioural Emotional Social cognition disorders disorders Behaviour and emotions Personality … changes Cognitive disorders 4. Cerebrovascular accident (CVA) Type of motor or cognitive dysfunction depends on location of stroke: Supply area of middle cerebral artery Temporal Visual neglect inrietal Supplies blood to the frontal, temporal and parietal lobes, and deep brain structures (eg thalamus). Accounts for approximately 80% of all stroke cases. Common consequences: incial to only or s a A Memory disorders Aphasia Apraxia is I Hemispatial neglect Extinction P left is neglected 4. Cerebrovascular accident (CVA) Type of motor or cognitive dysfunction depends on location of stroke: or zag Supply area of posterior cerebral artery Occipital Supplies blood to the occipital and temporal lobes. Common consequences: Hemianopsia or quandrantanopsia Visual agnosia (e.g., object agnosia, proposagnosia) ↳ can't the object recognise 4. Cerebrovascular accident (CVA) Transient Ischaemic Attack (TIA) Recovery < 24 hours. TIA: Brief ischaemic event temporary Focal symptoms: Problem is specific to a certain area of the brain Abnormalities often also appear on acute brain scan Increased risk of having a stroke 4. Cerebrovascular accident (CVA) Transient Ischaemic Attack (TIA) Many people still report cognitive problems three months after a TIA Impairments on neuropsychological assessment Van Rooij et al. Stroke 2014  Video: life after stroke the strike was under the circle where of vessels the majoring got dauged leading to paralysis 4. Cerebrovascular accident (CVA) Cognitive recovery 8 days post-stroke 6-10 months after first assessment Baseline Follow-up 35 30 25 Prevalence (%) 20 15 10 5 0 Perception/ Executive Reasoning Verbal Language Visual construction function memory memory 49% cognitive impairments in acute phase  31% at follow-up  4. Cerebrovascular accident (CVA) and severity of heamorrage - size the rupture Cognitive recovery Strokes-location  ‘Unimpaired’ patients still unimpaired after six months  Other group generally shows progress  Dynamic recovery and not ‘demented’  Dependent on affected domain  May be linked to location of recovery  Determinants  Schooling/age  ‘cognitive reserve’? (Stern et al., 2003; Robertson & Murre, 1999)  Lesion volume less important than location  small strategic infarcts sometimes accompanied by dementia (see Auchus et al., 2002)  4. Cerebrovascular accident (CVA) Mood disorders post-stroke Depressive symptoms occur in one third of stroke survivors 113 Frequency is highest within the first year after stroke event Associated with poor recovery and long-term outcomes Suggested underlying mechanisms: Biological hypothesis Reactive hypothesis Vascular depression hypothesis (Robinson et al.) (Gainotti et al.) (Alexopoulus et al.) Towfighi et al. Stroke 2017 Video: rehabilitation multisciplinary 5:10 e.v. 11:50 e.v. 14.15 e.v. systeem  5. Vascular dementia Dementia subtypes Dementia um daily life is impaired -whensig,, - co-occurance with Anheimer's 5. Vascular dementia Dementia Cortical v. subcortical profile No specific neuropsychological pattern Course often fluctuates Strategic infarct or multi-infarct may contribute Roman, J Am Geriatr Soc 2003 5. Vascular dementia Most important cognitive deficits Dementia Executive deficits (at the level of thought, behaviour, emotion) in Subcortical Additional deficits: Sortical Mental processing speed Memory Visuoconstruction Language neimer Roman, J Am Geriatr Soc 2003 5. Vascular dementia AD versus sVAD Dementia Strategic retrieval VanderPloeg et al., 2001 JINS LEARNING OBJECTIVES Knowledge of the circulatory system of the brain and the supply and perfusion area Knowledge of small and large vessel disease Knowledge of the neurocognitive profile of normal aging Knowledge of the importance of vascular risk factors and physical activity Knowing the differences between a brain infarct, a brain haemorrhage and TIA Insight in cognitive disorders after a stroke Insight in predictors of recovery after a stroke Being able to explain the relationship between localisation of the lesion and function loss Being able to explain what stroke is, along with its typical cognitive profile Knowing terms such as penumbra, diaschisis, embolism and thrombosis Knowing the criteria for vascular dementia and differences between subtypes