Summary Clinical Neuropsychology
Ch. 13. Vascular cognitive impairment
Introduction
Cerebral vascular disease includes several clinical syndromes and disorders, including small
vessel disease, cerebral infarcts and cerebral heamorrhages. In most cases, stroke is
manifested as an acute loss of function in an arm or a leg on one side of the body and/or
difficulty speaking. Loss of strength, sensory disorders or loss of coordination or control of
movements may be involved.
Vascular cognitive impairment
Vascular cognitive impairment (CVI) is an umbrella term used to cover the cognitive
consequences of vascular disease, from mild cognitive impairment to dementia.
In clinical practice (severe) cognitive impairment due to stroke I often referred to without
using the term dementia. This is partly because dementia is traditionally thought of as
progressive; this is not always the case with cognitive impairment after stroke.
Aetiology of cerebral infarct and haemorrhage
in cerebral stroke, part of the brain is deprived of oxygen because of disturbed flow to the
brain. Patients experience acute neurological symptoms, such as the inability to speak or to
use an arm/leg unilateraly.
Cerebral infarct
A blood clot (embolism) accludes an artery or the bloodstream becomes obstructed by local
stenosis of a blood vessel. This causes reduced oxygen to certain brain areas. Most common
acute symptoms: sudden drooping of the face, loss of function of the body and difficulty
speaking. The neurological symptoms usually occur on one side of the body. Less common
signs: ndecreased vision, balance, impaired coordination, severe headache or fainting.
In the acute phase, a ct scan is usually done in the hospital since it is reliable and quick to
perform. The presence and location of the stroke can be determined.
Within a few hours intravenous thrombolytic therapy (drug) can be administered to dissolve
the clot. Some patients are eligible for endovascular treatment, in which microcatheters are
inserted into the brain to remove the blood clot mechanically.
Risk factors: hypertension, hypercholesterolemia, type 2 diabetes, obesity, arteriosclerosis,
and arterial fibrillation. Behavioral risk factors: smoking, inactive lifestyle and unhealthy
eating.
,Transient ischaemic attack and lacunar infarct
In transient ischaemic attack (TIA), a temporal reduction in blood flow to a small part of the
brain occurs, and neurological symptoms disappear within 24 hours. After a TIA the risk of
having a second stroke increases. No abnormalities are found on brain imaging. Many
patients report persistent cognitive complaints after a TIA.
About 25% of ischaemic strokes are referred as lacunar infarct. This is an infarct in the small
penetrating arteries that supply the brain’s deeper structures, after which a small cavity
(lacuna) forms. Specific locations the infarct could lead to motor impairments, loss of
sensation or dysarthria in the acute phase. Usually the symptoms disappear in week/months
following the infarct, but some patients report persistent cognitive complaints, fatigue, and
difficulty resuming work. Lacunar infarcts are associated with damage in the small blood
vessels, which is a risk factor for dementia.
Cerebral heamorrhage
Ruptured blood vessel that causes bleeding in brain. Reduces consciousness, confusion, and
disorientation are common in the early phase after cerebral haemorrhage. Loss of
consciousness is often caused by increased intracranial pressure, by mass effect of the
haemorrhage, and oedema (fluid in the brain tissue surrounding the haemorrhage).
In most cases, the bleeding is into the brain tissue (intracerebral). Treatment in acute phase:
lowering blood pressure, reducing the pressure in the brain to stop the bleeding. In case of a
subarachnoid heamorrhage (SAH) the bleeding accurs in the space between the meninges
surrounding the brain. It is a severe subtype of a stroke, which results in death in half of the
patients. 85% is caused by ruptured intracranial aneurysm, called aneurysmal sah (ASAH). In
15%, no cause can be found. Most common symptom is severe headache. In addition:
nausea, neck stiffness, hypersensitivity to light, and loss of consciousness. Aneurysm: two
treatment options. First is can be closed using endovascular treatment (coiling and/or stent
placement). Other option is neurosurgical intervention (clipping), where the aneurysm is
closed with a mental clip. Common complications: increased intracranial pressure
(hydrocephalus), vasospasm, cerebral ischaemia, and rebleeding. Major risk is hypertension.
Other risk factors are coagulation disorders, alcohol consumption, smoking and diabetes
mellitus. Haemorrhages in deeper brain structures are often associated with cardiovascular
risk factors. Bleeding outside the brain tissue is strongly related to cerebral amyloid
angiopathy (CAA). Here protein amyloid b deposits in the brain damages the blood vessels.
Also a fall or shock of the head can cause a subdural haematoma (bruise withing the skull).
Acute and chronic effects
In cerebral haemorrhages, cognitive disorders are mainly related to the severity and size of
the haemorrhage, rather than it’s location. In contrast, cerebral infarcts are often linked to
the specific location in blood supply of the brain.
Neuropsychological consequences
Vascular risk factors: cerebral small vessel disease
Vascular risk factors like type 2 diabetes, hypertension, obesity and high cholesterol, are
highly prevalent in people over the age of 60. The risk factors often co-occur. It increases the
risk of cognitive decline and dementia. The association between vascular risk factors and
cognitive decline is probably (partly) caused by pathology of the smallest blood vessels in the
,brain (cerebral small vessel disease, csvd). Csvd is visible in the brain by damage to white
matter tracts (leukoraiosis). The extent and location will determine the extent of
impairments of cognitive functions. White matter abnormalities are associated with diffuse
cognitive impairments in memory, speed of information processing, attention and executive
functions, and perception/construction.
TIA and lacunar infarction
The prevalence of cognitive impairment after TIA depends on method of measurement,
timing of examination and the age of patients. NPA’s are most suitable (taking in account
factors like age and level of education). TIA’s namely result in deficits in information
processing speed, attention, working memory, and executive functions.
After lacunar infarcts one-third of the patients have cognitive deficits characterized by
decrease in mental capacity. Generally found in: attention, information processing speed
and executive functions. Also memory, language and visuospatial functions may also be
affected. Also disorders in social cognition, mainly in minor stroke or lacunar infarcts.
Major stroke
Because of interrelated areas, a diffuse profile of cognitive impairment is possible, which is
not specifically related to a certain location. Common disorders are seen in attention and
information processing speed. This can impact performance in other domains. Time pressure
seems to be a problem. Other deficitis are seen in sustained attention, memory impairment
(mostly anterograde amnesia in acute phase) and problems with learning new information.
Also problems are seen in executive functions. Also one third have aphasia in the acute
and/or chronic phase. Impairments in attention and executive functions are associated with
poorer long-term recovery from aphasia.
Thalamic infarct: special type which can be present with symptoms that are not immediately
indicative of stroke. This could be due to the thalamus which is the “switching station” of the
brain.
The brain is supplied by a number of major arteries: the anterior cerebral artery (ACA),
middle cerebral artery (MCA) and posterior cerebral artery (PCA).
Supply area of the middle cerebral artery (MCA)
Largest cerebral artery that supplies blood to the frontal, temporal and parietal areas of the
brain, as well as deep structures such as the thalamus. Memory disorders are often seen in
the acute phase (anterograde amnesia = learning new information) but also in the long term
encoding of information seems a problem. This may be the results of decreased speed of
information processing. Retention of stored information is generally relatively good.
MCA infarct can cause damage in various language areas, such as Broca’s areas and dorsal
and ventral networks. Damage in left posterior frontal gyrus: language productions (Broca’s
area). Damage of Wernicke’s area = impaired comprehension.
Also apraxia (inability to carry out meaningful movements and gestures) is seen often.
Mostly seeing ideomotor apraxia, where the individual is unable to make meaningful
movements, while understanding the task and recognizing the purpose of a certain tool.
Hemispatial neglect is seen in 82% of patients. Neglect is related to damage to the
parietotemporal brain regions, but also dorsolateral prefrontal cortex. Neglect is an
attention disorder in which patients fail to pay attention to stimuli contralateral to the lesion.
In the chronic phase, neglect recovers in many cases, but extinction may persist. In
, extinction patients are unable to perceive stimuli contralateral to the lesion, when two
stimuli are presented simultaneously (left and right). Impaired distinction between left and
right and in the mental representation of one’s own body may also occur.
Supply area of the posterior cerebral artery (PCA)
PCA supplies blood to the occipital and temporal lobes. Hemianospia and quadrantanopia
(impairments of half or a quarter of the visual field on the contralateral side) are common.
Other disturbance in perception, visual agnosia and colours agnosia, especially after damage
in the occipital lobe. Prosopagnosia (inability to recognize faces of acquaintances) may occur
due to bilateral PCA infarcts and damage to the occipiro-temporal areas. A rare effect is
Anton’s syndrome (cortical blindness) when patients are unaware of their blindness and
deny this. Lastly problems with writing and reading (agraphia and alexia) can occur.
Supply area of the anterior cerebral artery (ACA)
ACA supplies blood to the dorsal and medial parts of the frontal and parietal lobes. Various
impairments in language are found. Language disorders where the connections between the
broca’s area and wernicke’s area is disturbed is also possible. This can lead to no longer
processing written language or communicate verbally, but capable of repeating words and
sentences (transcortical aphasia). Bilateral infarcts could also cause complete inability to
communicate verbally (mutism).
Cognitive impairments in the more “frontally regulated” executive functions and social
cognition are expected. Executive function is more common after damage to the ACA area.
Also changes in behaviour and emotion, such as apathy, emotional lability and decreased
self-criticism is seen. These are often related to deficits in social cognition. More severe
impairments in social cognition are found in right hemispheric stroke.
Subcortical infarcts
Stroke in cortical regions increases the risk of cognitive impairment, but also in 50% of
patients in subcortical regions. Damage to the cerebellum is associated with motor
problems, but may also result in cognitive impairment. Cerebellar damage can even lead to
so-called cerebellar cognitive affective syndrome, characterized by cognitive impairment and
emotional changes. Damage in basal ganglia, the brainstem and thalamus could also lead to
cognitive impairment.
Cerebral haemorrhage
Early phase: decreased consciousness, confusion and disorientation. Cognitive impairment
can be severe and diffuse during this period, mainly caused by increased pressure and the
presence of a haematoma.
Cerebral haemorrhages do not have a very specific distinctive neuropsychological profile, but
disorders in memory, processing speed and executive functions are common. Disorders in
language and visuospatial functions are also found.
Cognitive impairment directly after could be due to the haemorrhage, but progressive
cognitive impairment could be due to diffuse vascular pathology. Long-term cognitive
impairment seems to be mainly related to the underlying pathology.
Vascular dementia
Ch. 13. Vascular cognitive impairment
Introduction
Cerebral vascular disease includes several clinical syndromes and disorders, including small
vessel disease, cerebral infarcts and cerebral heamorrhages. In most cases, stroke is
manifested as an acute loss of function in an arm or a leg on one side of the body and/or
difficulty speaking. Loss of strength, sensory disorders or loss of coordination or control of
movements may be involved.
Vascular cognitive impairment
Vascular cognitive impairment (CVI) is an umbrella term used to cover the cognitive
consequences of vascular disease, from mild cognitive impairment to dementia.
In clinical practice (severe) cognitive impairment due to stroke I often referred to without
using the term dementia. This is partly because dementia is traditionally thought of as
progressive; this is not always the case with cognitive impairment after stroke.
Aetiology of cerebral infarct and haemorrhage
in cerebral stroke, part of the brain is deprived of oxygen because of disturbed flow to the
brain. Patients experience acute neurological symptoms, such as the inability to speak or to
use an arm/leg unilateraly.
Cerebral infarct
A blood clot (embolism) accludes an artery or the bloodstream becomes obstructed by local
stenosis of a blood vessel. This causes reduced oxygen to certain brain areas. Most common
acute symptoms: sudden drooping of the face, loss of function of the body and difficulty
speaking. The neurological symptoms usually occur on one side of the body. Less common
signs: ndecreased vision, balance, impaired coordination, severe headache or fainting.
In the acute phase, a ct scan is usually done in the hospital since it is reliable and quick to
perform. The presence and location of the stroke can be determined.
Within a few hours intravenous thrombolytic therapy (drug) can be administered to dissolve
the clot. Some patients are eligible for endovascular treatment, in which microcatheters are
inserted into the brain to remove the blood clot mechanically.
Risk factors: hypertension, hypercholesterolemia, type 2 diabetes, obesity, arteriosclerosis,
and arterial fibrillation. Behavioral risk factors: smoking, inactive lifestyle and unhealthy
eating.
,Transient ischaemic attack and lacunar infarct
In transient ischaemic attack (TIA), a temporal reduction in blood flow to a small part of the
brain occurs, and neurological symptoms disappear within 24 hours. After a TIA the risk of
having a second stroke increases. No abnormalities are found on brain imaging. Many
patients report persistent cognitive complaints after a TIA.
About 25% of ischaemic strokes are referred as lacunar infarct. This is an infarct in the small
penetrating arteries that supply the brain’s deeper structures, after which a small cavity
(lacuna) forms. Specific locations the infarct could lead to motor impairments, loss of
sensation or dysarthria in the acute phase. Usually the symptoms disappear in week/months
following the infarct, but some patients report persistent cognitive complaints, fatigue, and
difficulty resuming work. Lacunar infarcts are associated with damage in the small blood
vessels, which is a risk factor for dementia.
Cerebral heamorrhage
Ruptured blood vessel that causes bleeding in brain. Reduces consciousness, confusion, and
disorientation are common in the early phase after cerebral haemorrhage. Loss of
consciousness is often caused by increased intracranial pressure, by mass effect of the
haemorrhage, and oedema (fluid in the brain tissue surrounding the haemorrhage).
In most cases, the bleeding is into the brain tissue (intracerebral). Treatment in acute phase:
lowering blood pressure, reducing the pressure in the brain to stop the bleeding. In case of a
subarachnoid heamorrhage (SAH) the bleeding accurs in the space between the meninges
surrounding the brain. It is a severe subtype of a stroke, which results in death in half of the
patients. 85% is caused by ruptured intracranial aneurysm, called aneurysmal sah (ASAH). In
15%, no cause can be found. Most common symptom is severe headache. In addition:
nausea, neck stiffness, hypersensitivity to light, and loss of consciousness. Aneurysm: two
treatment options. First is can be closed using endovascular treatment (coiling and/or stent
placement). Other option is neurosurgical intervention (clipping), where the aneurysm is
closed with a mental clip. Common complications: increased intracranial pressure
(hydrocephalus), vasospasm, cerebral ischaemia, and rebleeding. Major risk is hypertension.
Other risk factors are coagulation disorders, alcohol consumption, smoking and diabetes
mellitus. Haemorrhages in deeper brain structures are often associated with cardiovascular
risk factors. Bleeding outside the brain tissue is strongly related to cerebral amyloid
angiopathy (CAA). Here protein amyloid b deposits in the brain damages the blood vessels.
Also a fall or shock of the head can cause a subdural haematoma (bruise withing the skull).
Acute and chronic effects
In cerebral haemorrhages, cognitive disorders are mainly related to the severity and size of
the haemorrhage, rather than it’s location. In contrast, cerebral infarcts are often linked to
the specific location in blood supply of the brain.
Neuropsychological consequences
Vascular risk factors: cerebral small vessel disease
Vascular risk factors like type 2 diabetes, hypertension, obesity and high cholesterol, are
highly prevalent in people over the age of 60. The risk factors often co-occur. It increases the
risk of cognitive decline and dementia. The association between vascular risk factors and
cognitive decline is probably (partly) caused by pathology of the smallest blood vessels in the
,brain (cerebral small vessel disease, csvd). Csvd is visible in the brain by damage to white
matter tracts (leukoraiosis). The extent and location will determine the extent of
impairments of cognitive functions. White matter abnormalities are associated with diffuse
cognitive impairments in memory, speed of information processing, attention and executive
functions, and perception/construction.
TIA and lacunar infarction
The prevalence of cognitive impairment after TIA depends on method of measurement,
timing of examination and the age of patients. NPA’s are most suitable (taking in account
factors like age and level of education). TIA’s namely result in deficits in information
processing speed, attention, working memory, and executive functions.
After lacunar infarcts one-third of the patients have cognitive deficits characterized by
decrease in mental capacity. Generally found in: attention, information processing speed
and executive functions. Also memory, language and visuospatial functions may also be
affected. Also disorders in social cognition, mainly in minor stroke or lacunar infarcts.
Major stroke
Because of interrelated areas, a diffuse profile of cognitive impairment is possible, which is
not specifically related to a certain location. Common disorders are seen in attention and
information processing speed. This can impact performance in other domains. Time pressure
seems to be a problem. Other deficitis are seen in sustained attention, memory impairment
(mostly anterograde amnesia in acute phase) and problems with learning new information.
Also problems are seen in executive functions. Also one third have aphasia in the acute
and/or chronic phase. Impairments in attention and executive functions are associated with
poorer long-term recovery from aphasia.
Thalamic infarct: special type which can be present with symptoms that are not immediately
indicative of stroke. This could be due to the thalamus which is the “switching station” of the
brain.
The brain is supplied by a number of major arteries: the anterior cerebral artery (ACA),
middle cerebral artery (MCA) and posterior cerebral artery (PCA).
Supply area of the middle cerebral artery (MCA)
Largest cerebral artery that supplies blood to the frontal, temporal and parietal areas of the
brain, as well as deep structures such as the thalamus. Memory disorders are often seen in
the acute phase (anterograde amnesia = learning new information) but also in the long term
encoding of information seems a problem. This may be the results of decreased speed of
information processing. Retention of stored information is generally relatively good.
MCA infarct can cause damage in various language areas, such as Broca’s areas and dorsal
and ventral networks. Damage in left posterior frontal gyrus: language productions (Broca’s
area). Damage of Wernicke’s area = impaired comprehension.
Also apraxia (inability to carry out meaningful movements and gestures) is seen often.
Mostly seeing ideomotor apraxia, where the individual is unable to make meaningful
movements, while understanding the task and recognizing the purpose of a certain tool.
Hemispatial neglect is seen in 82% of patients. Neglect is related to damage to the
parietotemporal brain regions, but also dorsolateral prefrontal cortex. Neglect is an
attention disorder in which patients fail to pay attention to stimuli contralateral to the lesion.
In the chronic phase, neglect recovers in many cases, but extinction may persist. In
, extinction patients are unable to perceive stimuli contralateral to the lesion, when two
stimuli are presented simultaneously (left and right). Impaired distinction between left and
right and in the mental representation of one’s own body may also occur.
Supply area of the posterior cerebral artery (PCA)
PCA supplies blood to the occipital and temporal lobes. Hemianospia and quadrantanopia
(impairments of half or a quarter of the visual field on the contralateral side) are common.
Other disturbance in perception, visual agnosia and colours agnosia, especially after damage
in the occipital lobe. Prosopagnosia (inability to recognize faces of acquaintances) may occur
due to bilateral PCA infarcts and damage to the occipiro-temporal areas. A rare effect is
Anton’s syndrome (cortical blindness) when patients are unaware of their blindness and
deny this. Lastly problems with writing and reading (agraphia and alexia) can occur.
Supply area of the anterior cerebral artery (ACA)
ACA supplies blood to the dorsal and medial parts of the frontal and parietal lobes. Various
impairments in language are found. Language disorders where the connections between the
broca’s area and wernicke’s area is disturbed is also possible. This can lead to no longer
processing written language or communicate verbally, but capable of repeating words and
sentences (transcortical aphasia). Bilateral infarcts could also cause complete inability to
communicate verbally (mutism).
Cognitive impairments in the more “frontally regulated” executive functions and social
cognition are expected. Executive function is more common after damage to the ACA area.
Also changes in behaviour and emotion, such as apathy, emotional lability and decreased
self-criticism is seen. These are often related to deficits in social cognition. More severe
impairments in social cognition are found in right hemispheric stroke.
Subcortical infarcts
Stroke in cortical regions increases the risk of cognitive impairment, but also in 50% of
patients in subcortical regions. Damage to the cerebellum is associated with motor
problems, but may also result in cognitive impairment. Cerebellar damage can even lead to
so-called cerebellar cognitive affective syndrome, characterized by cognitive impairment and
emotional changes. Damage in basal ganglia, the brainstem and thalamus could also lead to
cognitive impairment.
Cerebral haemorrhage
Early phase: decreased consciousness, confusion and disorientation. Cognitive impairment
can be severe and diffuse during this period, mainly caused by increased pressure and the
presence of a haematoma.
Cerebral haemorrhages do not have a very specific distinctive neuropsychological profile, but
disorders in memory, processing speed and executive functions are common. Disorders in
language and visuospatial functions are also found.
Cognitive impairment directly after could be due to the haemorrhage, but progressive
cognitive impairment could be due to diffuse vascular pathology. Long-term cognitive
impairment seems to be mainly related to the underlying pathology.
Vascular dementia
