PSYC 301 midt 2

Circle of Willis: ACA? AComA? MCA? PComA? PCA? ICA? BA?

MCA

• feeds basal ganglia

• MCA Superior division: parietal frontal

• MCA Inferior division: temporal lobe

ACA

• medial frontal

• sweeps back into parietal

What areas of cortex do ACA, MCA, PCA apply to?

• MCA: lateral, prefrontal, parietal, temporal

• ACA: medial, prefrontal, parietal

• PCA: occipital

Types of stroke: Ischemic? Hemorrhagic?

I. Ischemic: a clot of plaque buildup that floats and blocks blood flow to an area of the brain, and then artery narrows

II. Hemorrhagic: rupture/bleed that weakens vessel

• hematoma, on the outside

Aneurysm

a kind of bleed:

• the ballooning out and weakening of blood vessels (small and not likely to rupture)

• runs in the family

• most common to take place in orbitofrontal

  • confabulation, personality changes

• can clip or coil the balloon

Epidemiology for Stroke

• major cause of disability and death

• likelihood increases w age

• people who have risk factors (hypertension, diabetes, smoking, sodium intake) can modify these things

• (hemorrhage) anticoagulant meds—that help for clots

• (ischemic) atrial fibrillation—heart

Pathophysiology of Ischemic Stroke; Penumbra? Ischemic Core?

• Ischemic core: brain tissue that’s dead

• Penumbra: brain tissue at risk of dying

Pathophysiology of Hemorrhagic Stroke; Midline Shift? Herniation?

• increased intracranial pressure

• brain tissue getting pushed elsewhere

• Midline Shift: brain matter swells and decentres middle structure of the brain

• Herniation: brain matter shifts into places it shouldn’t

Clinical Presentation: Acute Stroke

• focal, unilateral deficits

• (hemorrhagic): bad headaches, vomiting, severe hypertension, coma

Prognosis for Acute Stroke

prog is better for ischemic (hemorrhagic more likely for death)

• most recovery happens in first 3 months

• predicted by age, stroke size, severity of initial deficits

Treatment for Acute Stroke? For ischemic, hematoma?

• ischemic: thrombolytics—tPA, thrombectomy

• hematomas: anticoag reversal, IV antihypertensive drugs, surgical evac—open up skull

• secondary prevention (meds and lifestyle management of risk factors for second stroke)

• early mobalization after 24 hours

• multirehab (PT, OT, SLP)

What Consists of Brain Aging? (4) How Does the Brain Adapt with Age?

• volume shrinks 5% per decade after 40, then accelerates after 70

• declined serotonin and dopamine levels

• decreased cerebral blood flow and white matter lesions

• mild Alzheimer’s pathology (not disease)

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adaptive

1. ongoing neuroplasticity

2. downregulates neural metabolism; doing the least it could do

3. increases clearance of cellular debris and protein buildup

Least vs. Greatest Cognitive Functions Declining with Age?

decline: episodic memory, learning speed, exec function

increased: wisdom/verbal knowledge

Mild Cognitive Impairment

mild cog difficulties (more than expected) but no dysfunction

Dementia

impairment of multiple cog functions + dysfunction

• slow and lowk decline

• onset in middle-to-late adulthood

List the Strongest Modifiable Risk Factors for Dementia

• hearing loss

• depression

• TBI

• less education

• hypertension

• obesity

• smoking

• social isolation

Diagnosis of Dementia? Blood Biomarkers?

• history of progressive devline

• interview people around them to survey activities of daily living

• blood biomarkers

  • what allele of APOE gene; apoE4/4 has 3-4x risk for AD

  • only available for Alzheimer’s pathology (no other dementia)

  • high positive rate in people without cognitive impairment and then don’t develop dementia

  • confounding med conditions

  • confirmed to work on white people (probably diet/genes)

Dementia vs. Delirium vs. Depression

Clinical Presentation for Alzheimer’s? (Early, Middle, Late)

Alzheimer’s Pathophysiology? What Happens in the Brain?

• ventricles get larger, brain tissue around them breaking

• healthy aging but exaggerated

• accumulation of amyloid-b (or plaque) between neurons

Treatment for Alzheimers? (NOT Reversible)

• acetylcholinesterase inhibitors

• glutaminergic antagonists (slows the rate of decline memory func)

• anti-amyloid antibody (lecanemab)

Frontotemporal Dementia (FTD)? Behavioural Variant (bvFTD)?

• most common to have early onset, 50s

behavioural

• inhibition

• apathy

• social inappropriateness

• exec dysfunction

• anosognosia (unaware of own deficit)

language

• pnon-fluent aphasia ; brocas

• semantic dementia (losing concepts, can’t name object knowledge) ; ant temporal

Neuropathology FTD?

Treatment for FTD?

• symptom management only—for behaviours

• diff pharmacological agents needed for each underlying pathology

Clinical Presentation for Lewy Body Dementia?

• fluctuations in attention and alertness

• visuospatial difficulties; can’t copy or interpret objects

• hallucinations

• parkinsonism

• REM sleep behaviour disorder (they act out their dreams since that inhibitor is lost)

Neuropathology for Lewy Body Dementia?

protein clumping

• aggregation of a-synuclein

Treatment for Lewy Body Dementia? Why Not Antipsychotics?

• acetylcholinesterase inhibitors

• L-Dopa (helps parkinsonism)

• sensitivity b/c personality problem

Vascular Dementia?

• ischemic vascular disease +- clinically symptomatic strokes

• subcortical dementia profile (cog slowing, exec dysfunc, language and visuospatial preserved)

Epidemiology for Parkinsons?

• onset between 45-70

• male>female

• white>black>asian

• familial risk

Clinical Presentation for Parkinsons? (5)

• Bradykinesia (slowness—in movement and thought)

• rigidity

• upper extremity resting tremor

• postural instability with shuffling gate (compensating for imbalanced torso)

• expressionless face

Neuropathology for Parkinsons?

• substantia nigra degeneration

• neuronal loss, and remaining cells have Lewy bodies

Treatment for Parkinsons?

• L-dopa (building block to make dopamine)

• dopamine agonists—to mimic dopamine

• deep brain stimulation (lead electrode trying to stimulate action potential)

Epidemiology for Huntington’s?

• hereditary (autosomal dominant)

  • child of a person who has it has 50% chance

Clinical Presentation for Huntington’s?

• chorea (dance-like fidgeting)

• dystonia (bursts of muscle tone, toes curling for ex)

• personality change from exec func

• subcortical dementia

Neuropathology for Huntingtons?

• increased number of trinucleotide CAG on chromosome = cell toxicity

• bilateral caudate degen

• frontal-subcortical circuits

Treatment for Huntington’s?

none

Functional Neurological Disorder (FND)? Voluntary or Involuntary?

sensory, motor, cognitive, or speech problems not fully explained by known neurological disease

What are the Clinical Phenotypes for FND?

• func weakness: face is not affected

• non-epileptic seizures: crying (ep are disoriented), stop/start (ep one and done)

• func cog disorder: vivid memory of forgetting

Pathophysiology for FND?

• ex: trauma/childabuse + injury/strain/new sensation

  

Diagnosis for FND?

• internal inconsistency: girl being able to walk into the office but can’t lift her leg while she’s on the table

• incompatibility: no lesion in the brain can output that

• distractibility: reduction/disappearance in the symptom when their mind gets pulled off it

• EEG for seizures

• EMG for tremor

Treatment for FND?

• educate

• therapy

• physiotherapy

Epidemiology for TBI?

• males get injured almost twice as much

1. adolescents and young adults by sports and rec

2. fall-related old people

Pathophysiology for TBI?

non-specific repolarization: extra firing

• hours to days

• ions imbalanced

• energy crisis where one pumps and cells work hard to release it; trying to reach homeostasis

Structural Neuropath in TBI? Prim-Acute? Secondary-Acute? Post?

1. Primary-Acute

• diffuse axonal injury (DAI)

• bleeds

• focal contusions (bruising)

2. Secondary-Acute, the killing one

• edema (swelling)

• ischemic-hypoxic injury (further damage from blood not flowing)

• seconds to weeks

3. Post-Acute

• risk factor for alzheimers

• neuroinflammation

• impaired clearance and cerebrovasc autoregulation

• months to years after

Diffuse Axonal Injury (DAI), Diffuse or Focal?

stretching and tearing of axons

• diffuse

• can have TBI but not DAI

Subdural Hematoma

too much blood where not supposed to be ; pressure and pushing of brain tissue

Contusions

bruising, brain bumping with skull

TBI; Why is it always Frontal-Temporal

1. Contracoup

2. Bony inner skull

What are the Causes for Anoxia

• blood not flowing

• suffocation

• carbon monoxide poisoning (blood still flows but blood is not oxygenated; cm binds to hemoglobin where oxygen would normally go)

• respiratory distress (ex, COVID)

• respiratory supression (ex, fent)

Pathophysiology for Anoxia? Brain Regions Most Sensitive to it?

lack of oxygen supply to brain

• insuff cerebral flow

• no oxygen saturated in blood

motor

• basal ganglia

• hippocampi

• cerebellum

• watershed areas of cortex

Clinical Presentation for Anoxia?

severe prolonged —> coma or brain death (beyond 15min)

if oxygen is resumed within 5-15min

• amnesia

• exec dysfunc

• ataxia (lack of vol coordination)

• proximal limb weakness (person-in-the-barrel)

• visual agnosia and cortical blindness

Prognosis for Anoxia?

• go to hopital, depth of coma? okay bet

• if outside hotpal, 10% survive, 5% make full neurorecov

• if inside hoptal, 50% survival

Primary vs. Metastatic Brain Tumour? Types of Primary?

metastatic is more common, that tumour originates in another part of the body (cancer) and those malfunctioning cells go to the brain

primary:

1. meningiomas: from meninges (outside of brain)

2. gliomas: from glial cells

3. pituitary tumours: pressure onto optic chiasm; hormonal changes and headaches, loss of peripheral vision

Benign vs. Malignant Brain Tumour

Benign: slow growing, clear borders

Malignant: fast growing, less surgically treatable and likely to come back

Clinical Presentation for Brain Tumour? (3)

• gradual onset, months -→ years

• depends on location

• non-pulsing headache

• seizures