WEEK 2
Chapter 13: Vascular Cognitive Impairment (VCI)
Overview: VCI encompasses a spectrum of cognitive impairments caused by
cerebrovascular conditions, including strokes, cerebral infarcts, hemorrhages, and
small vessel disease.
Stroke: Acute loss of functioning, difficulty speaking, sensory disorders, loss of
coordination or control of movements; consequences: range from mild cog. decline
and fatigue to severe impairment and lasting sensorimotor deficits
Vascular Cognitive Impairment
-Mild (consequences of vascular risk factors; lacunar infarctions) to Major (Dementia:
post-stroke, subcortical ischemic vascular, multi-infarct; mixed)
-while dementia is generally thought to be progressive, after stroke that is not always
the case
-mean age in hemorrhages lower than in infarcts
Cerebral Infarcts (80% of strokes):
• Cause: Blood clots or artery blockages deprive regions of oxygen.
• Acute symptoms: One-sided facial droop, speech difficulty, and loss of motor
coordination.
• Risk factors: Hypertension, diabetes, obesity, atrial fibrillation, smoking, and
unhealthy lifestyles.
• Brain imaging: CT scan without contrast, after that: CT with contrast to
determine location and presence -> if present, drugs to dissolve the clot or
removed mechanically sometimes
• Neurological and Cognitive Impacts:
o Middle cerebral artery (MCA): Affects frontal, temporal, and parietal
regions; deficits in memory, language (aphasia), and hemispatial neglect.
-memory; acute phase: anterograde amnesia; retention is relatively good
-infarct in left hemisphere can lead to language impairment; difficulty writing or reading:
impairment at semantic, phonological, or syntactic level; (ideomotor) apraxia in
addition to aphasia
o Anterior cerebral artery (ACA): Affects the dorsal and medial parts of the
frontal and parietal lobes, leading to deficits in EF, language (word-finding
issues), social cognition (e.g., emotion recognition), cognitive flexibility,
, and inhibition. Damage in the right hemisphere leads to more severe
behavioral and emotional changes.
o Posterior cerebral artery (PCA): Causes visual field defects, visual
agnosias, and cortical blindness known as Anton’s Syndrome, where
patients are unaware of their blindness.
o Subcortical infarcts: Lead to impairments in EF, basal ganglia:
visuospatial processing, brainstem and thalamus: attention, and
cerebellar cognitive affective syndrome (mood and motor effects).
• Transient Ischemic Attacks (TIAs): Temporary blockages with symptoms
resolving in 24 hours. Diffusion-weighted imaging shows acute infarction in 1/3
of patients. Can cause long-term fatigue and cognitive complaints (30–70% of
cases). 25% are lacunar infarcts: small penetrating arteries supplying deeper
structures. Associated with damage to small blood vessels -> risk factor for
dementia!!
Cerebral Hemorrhage (20% of strokes):
• Cause: Burst blood vessels, often with intracranial pressure or edema.
• Subarachnoid hemorrhage (SAH): Severe subtype; presents with intense
headache, light sensitivity, and neck stiffness.
• Treatment: Includes managing blood pressure and surgical intervention (coiling,
clipping).
• Cognitive effects: Generally diffuse, with impairments in memory, EF,
processing speed, and visuospatial abilities.
Acute and chronic effects
-acute: impairment can be diffuse and severe
-long-term: impairment in 40% to ¾ of patients
-hemorrhage: depends on severity and size; infarct: depends on location
Neuropsychological consequences
1. Vascular risk factors: Cerebral Small Vessel Disease (CSVD): increase risk of
cognitive decline and dementia
• Pathology: Damage to white matter tracts causes leukoaraiosis, leading to
slower processing, EF deficits, memory issues, and motor difficulties.
• Long-term impact: Major risk factor for vascular dementia.
,-cognitive functioning lower in diabetes, hypertension patients
-30% of dementia diagnoses attributed to high blood pressure
-association between vascular risk factors and cognitive decline probably caused by
pathology of small blood vessel
Mild Stroke or TIA:
• Up to 70% show mild cognitive impairment, affecting memory, EF, and attention.
• Persistent complaints may reduce work productivity and social engagement.
Major Stroke:
• Impacts all cognitive areas depending on location.
• Common deficits: Attention, processing speed, EF, memory (anterograde
amnesia), and aphasia.
Vascular Dementia:
• Progression depends on lesion location and severity.
• Symptoms: Slowed cognition, impaired attention, and memory deficits, with EF
typically affected most.
• 65-75 years
• progressive course not necessary
• post-stroke dementia requires temporal relationship stroke – cognitive decline;
shouldn’t be diagnosed within first 6 months
Non-cognitive consequences
Depression and Anxiety:
• Risk factors: Premorbid conditions, stroke severity, social isolation.
• Anxiety often linked to recurrence fears or PTSD-like symptoms.
Fatigue and Sensory Sensitivity:
• Characterized by exhaustion, irritability, and sensory hypersensitivity.
• Likely linked to inflammation or neuroendocrine dysregulation.
, Chapter 19 Alzheimer’s Disease
Overview: AD is a progressive neurodegenerative disorder causing dementia, initially
affecting episodic memory and later global cognition. Atypical variants can affect
language, visuospatial abilities, or EF.
Diagnostic Criteria for Alzheimer’s Disease (AD):
• Distinction: Differentiate between clinical dementia (significant cognitive
decline interfering with independence) and its underlying etiology.
• Diagnosis Steps:
1. Establish dementia (objective decline ≥ 2 SDs in cognitive domains like
memory, EF, language, or visuospatial abilities, reported by
patient/informant).
2. Assess likelihood of AD as the cause. Probable AD: insidious onset,
gradual progression, impairment in at least two cognitive domains, and
exclusion of other conditions.
3. Certainty increased by progressive symptoms and supporting evidence
(e.g., neuroimaging, CSF biomarkers, or genetic mutations).
Mild Cognitive Impairment (MCI):
• Preceding dementia, patients experience episodic memory impairment and
slowed task execution while remaining relatively independent.
• Progression: MCI may lead to dementia, often AD (50% chance within 5–10
years) or stabilize/improve. Biomarkers can aid prediction.
Epidemiology:
• Higher risk in women, influenced by longer life expectancy, hormonal factors,
and socio-economic disparities.
• Declining incidence, likely due to improved cardiovascular health management.
Etiology and Neuropathology:
1. Amyloid Cascade Hypothesis:
o Accumulation of amyloid-beta plaques initiates tau pathology, synapse
loss, neuronal death, and eventual cognitive decline.
o Presence of plaques alone does not always indicate AD; efficacy of anti-
amyloid drugs is unclear.
2. Vascular Hypothesis:
Chapter 13: Vascular Cognitive Impairment (VCI)
Overview: VCI encompasses a spectrum of cognitive impairments caused by
cerebrovascular conditions, including strokes, cerebral infarcts, hemorrhages, and
small vessel disease.
Stroke: Acute loss of functioning, difficulty speaking, sensory disorders, loss of
coordination or control of movements; consequences: range from mild cog. decline
and fatigue to severe impairment and lasting sensorimotor deficits
Vascular Cognitive Impairment
-Mild (consequences of vascular risk factors; lacunar infarctions) to Major (Dementia:
post-stroke, subcortical ischemic vascular, multi-infarct; mixed)
-while dementia is generally thought to be progressive, after stroke that is not always
the case
-mean age in hemorrhages lower than in infarcts
Cerebral Infarcts (80% of strokes):
• Cause: Blood clots or artery blockages deprive regions of oxygen.
• Acute symptoms: One-sided facial droop, speech difficulty, and loss of motor
coordination.
• Risk factors: Hypertension, diabetes, obesity, atrial fibrillation, smoking, and
unhealthy lifestyles.
• Brain imaging: CT scan without contrast, after that: CT with contrast to
determine location and presence -> if present, drugs to dissolve the clot or
removed mechanically sometimes
• Neurological and Cognitive Impacts:
o Middle cerebral artery (MCA): Affects frontal, temporal, and parietal
regions; deficits in memory, language (aphasia), and hemispatial neglect.
-memory; acute phase: anterograde amnesia; retention is relatively good
-infarct in left hemisphere can lead to language impairment; difficulty writing or reading:
impairment at semantic, phonological, or syntactic level; (ideomotor) apraxia in
addition to aphasia
o Anterior cerebral artery (ACA): Affects the dorsal and medial parts of the
frontal and parietal lobes, leading to deficits in EF, language (word-finding
issues), social cognition (e.g., emotion recognition), cognitive flexibility,
, and inhibition. Damage in the right hemisphere leads to more severe
behavioral and emotional changes.
o Posterior cerebral artery (PCA): Causes visual field defects, visual
agnosias, and cortical blindness known as Anton’s Syndrome, where
patients are unaware of their blindness.
o Subcortical infarcts: Lead to impairments in EF, basal ganglia:
visuospatial processing, brainstem and thalamus: attention, and
cerebellar cognitive affective syndrome (mood and motor effects).
• Transient Ischemic Attacks (TIAs): Temporary blockages with symptoms
resolving in 24 hours. Diffusion-weighted imaging shows acute infarction in 1/3
of patients. Can cause long-term fatigue and cognitive complaints (30–70% of
cases). 25% are lacunar infarcts: small penetrating arteries supplying deeper
structures. Associated with damage to small blood vessels -> risk factor for
dementia!!
Cerebral Hemorrhage (20% of strokes):
• Cause: Burst blood vessels, often with intracranial pressure or edema.
• Subarachnoid hemorrhage (SAH): Severe subtype; presents with intense
headache, light sensitivity, and neck stiffness.
• Treatment: Includes managing blood pressure and surgical intervention (coiling,
clipping).
• Cognitive effects: Generally diffuse, with impairments in memory, EF,
processing speed, and visuospatial abilities.
Acute and chronic effects
-acute: impairment can be diffuse and severe
-long-term: impairment in 40% to ¾ of patients
-hemorrhage: depends on severity and size; infarct: depends on location
Neuropsychological consequences
1. Vascular risk factors: Cerebral Small Vessel Disease (CSVD): increase risk of
cognitive decline and dementia
• Pathology: Damage to white matter tracts causes leukoaraiosis, leading to
slower processing, EF deficits, memory issues, and motor difficulties.
• Long-term impact: Major risk factor for vascular dementia.
,-cognitive functioning lower in diabetes, hypertension patients
-30% of dementia diagnoses attributed to high blood pressure
-association between vascular risk factors and cognitive decline probably caused by
pathology of small blood vessel
Mild Stroke or TIA:
• Up to 70% show mild cognitive impairment, affecting memory, EF, and attention.
• Persistent complaints may reduce work productivity and social engagement.
Major Stroke:
• Impacts all cognitive areas depending on location.
• Common deficits: Attention, processing speed, EF, memory (anterograde
amnesia), and aphasia.
Vascular Dementia:
• Progression depends on lesion location and severity.
• Symptoms: Slowed cognition, impaired attention, and memory deficits, with EF
typically affected most.
• 65-75 years
• progressive course not necessary
• post-stroke dementia requires temporal relationship stroke – cognitive decline;
shouldn’t be diagnosed within first 6 months
Non-cognitive consequences
Depression and Anxiety:
• Risk factors: Premorbid conditions, stroke severity, social isolation.
• Anxiety often linked to recurrence fears or PTSD-like symptoms.
Fatigue and Sensory Sensitivity:
• Characterized by exhaustion, irritability, and sensory hypersensitivity.
• Likely linked to inflammation or neuroendocrine dysregulation.
, Chapter 19 Alzheimer’s Disease
Overview: AD is a progressive neurodegenerative disorder causing dementia, initially
affecting episodic memory and later global cognition. Atypical variants can affect
language, visuospatial abilities, or EF.
Diagnostic Criteria for Alzheimer’s Disease (AD):
• Distinction: Differentiate between clinical dementia (significant cognitive
decline interfering with independence) and its underlying etiology.
• Diagnosis Steps:
1. Establish dementia (objective decline ≥ 2 SDs in cognitive domains like
memory, EF, language, or visuospatial abilities, reported by
patient/informant).
2. Assess likelihood of AD as the cause. Probable AD: insidious onset,
gradual progression, impairment in at least two cognitive domains, and
exclusion of other conditions.
3. Certainty increased by progressive symptoms and supporting evidence
(e.g., neuroimaging, CSF biomarkers, or genetic mutations).
Mild Cognitive Impairment (MCI):
• Preceding dementia, patients experience episodic memory impairment and
slowed task execution while remaining relatively independent.
• Progression: MCI may lead to dementia, often AD (50% chance within 5–10
years) or stabilize/improve. Biomarkers can aid prediction.
Epidemiology:
• Higher risk in women, influenced by longer life expectancy, hormonal factors,
and socio-economic disparities.
• Declining incidence, likely due to improved cardiovascular health management.
Etiology and Neuropathology:
1. Amyloid Cascade Hypothesis:
o Accumulation of amyloid-beta plaques initiates tau pathology, synapse
loss, neuronal death, and eventual cognitive decline.
o Presence of plaques alone does not always indicate AD; efficacy of anti-
amyloid drugs is unclear.
2. Vascular Hypothesis:
