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Clinical and Neuropsychology - 1 > NP ch14: Cerebrovascular diseases > Flashcards

NP ch14: Cerebrovascular diseases Flashcards

1
Q

What does FAST mean in reference to strokes.

A

F: Face drooping
A: Arm weakness
S: Speech difficulty
T: Time to call ambulance

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2
Q

What are some other sudden onset symptoms of a stroke?

A

Headache
Loss of mental abilities
Loss of strength or paralysis
Sensory disorders
Confusion, disorientation, consciousness

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3
Q

What is the optimal clinical care for someone with a stroke arriving at hospital?

A

Optimal clinical care involves patients being admitted to a stroke unit. They are treated according evidence-based protocols that are implemented by a multidisciplinary team.

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4
Q

How do doctors distinguish the type of stroke? Why do they need to do this?

A
  • A CT scan is required to make the distinction between haemorrhage and infarct
    • Blood shows up white on a normal CT
  • In the case of infarcts, the patient usually remains conscious, whereas decline in consciousness is more often seen after brain haemorrhage.

It is important to distinguish the type of stroke as one treatment for an infarct would be aspirin (blood thinner), but in a haemorrhage, thinning the blood would kill the patient faster.

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5
Q

What are the two main risk factors for stroke?

A

Age >65
Hypertension (High blood pressure)
(There are other risk factors, but we will get into those in specific stroke types)

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6
Q

How common are strokes?

A
  • Worldwide: stroke every 2 seconds, 17 million times a year
  • Strokes are second leading cause of death in people over 60 years of age
  • Incidence varies widely between countries, and is related to age and standard quality of life.
    • About 40,000 first strokes in the Netherlands every year
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7
Q

Is stroke incidence increasing?

A
  • Yes,
  • Total number of people living with the consequences of strokes is increasing
  • Prevalence of strokes is increasing over the years due to ageing population
    • However, young strokes (18-50 years) are also becoming more common
    • Between 2005 and 2025, absolute number of people who have a stroke will increase by 40%
      • However due to improved prevention and new treatments, the number of deaths via stroke between 1980 and 2005 has decreased by 40%
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8
Q

What are the two types of Cerebrovascular accidents? How common are they?

A
  • Ischaemic stroke / cerebral infarct (80%)
    • Obstruction blocks blood flow to part of the brain
    • Oxygen deprivation causes irreversible brain damage
  • Haemorrhagic stroke/cerebral haemorrhage (20%)
    • Weakened vessel wall ruptures, causing bleeding in the brain
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9
Q

What is an infarct?

A

Infarcts are localized tissue death caused by lack of blood supply

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10
Q

What causes an infarct?

A
  • Infarcts can be the result of an embolism (blood clot) causing a temporary obstruction of an artery.
    • Embolism consists of coagulated blood platelets (thrombi) or fragments of calcifications in the vascular wall
  • Infarct can be the result of local stenosis of a blood vessel.
    • Stenosis (Narrowing of blood vessel) commonly occurs in the smaller and deep perforating arterioles.
  • Infarcts can also be caused by inadequate blood flow (perfusion) to the brain
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11
Q

Where can infarcts occur? How common is an infarct in a location?

A
  • Middle cerebral artery (MCA)
    • Occurs 80% of the time
  • Posterior cerebral artery (PCA)
    • 5-10% of infarct cases occurs here
  • Anterior cerebral artery (ACA)
    • Prevalence of isolated infarcts is 0.6-3%

Show them figure 14.1 alex

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12
Q

What is a Transient Ischaemic attack (TIA)?

A

An ischaemic stroke in which the neurological symptoms disappear with 24 hours.
Most TIAs cause symptoms for a considerably shorter period of time, usually less than 30 minutes.

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13
Q

What are some side effects of TIAs?

A
  • Despite loss of function being by definition temporary, persistent (subtle) cognitive disorders are described among TIA patients.
  • Patients are also at increased risk of stroke
    • At least 30% of TIA patients will suffer from a stroke within the next 5 years
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14
Q

What are the risk factors of an infarct?

A
  • Age is the main risk factor
  • Atherosclerosis is a second important risk factor. It is the thickening/hardening of the arteries.
    • It’s caused by smoking, hypertension, diabetes, obesity, or hypercholesterolaemia (High cholesterol levels)
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15
Q

What are the relative risks of risk factors for infarcts? (dont memorise this, but understand it)

A

The book provided a table of the main risk factors for stroke and the relative risk of an infarct, meaning someone with this factor is x times more likely to suffer an infarct than someone without

  • Age >75 years vs 55-64 = 5
  • High blood pressure = 4-6
  • Atrial fibrillation (irregular heart beat) = 4
  • Diabetes = 2-6
  • Physical inactivity = 3
  • Smoking = 2
  • Obesity = 2
  • Ischemic cardiac disease = 2
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16
Q

What are some acute treatments?

A

Treatments have to be within 4 hours of onset, and after the CT scan

  • Thrombolysis: injecting drug to dissolve the clot
    • This increases the likelihood of a positive outcome, but the effects are possibly limited with regard to the cognitive effects.
  • Thrombectomy: removal of the brain clot with a catheter
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17
Q

What are the consequences of an infarct in the MCA?

A

MCA → frontal, temporal, and parietal areas of the brain

  • Memory issues are most common (When the medial temporal lobe is affected)
  • Apraxia: Inability to carry out meaningful movements and gestures
    • E.g. using a fork to eat soup
  • Aphasia: Language dominant hemisphere (left)
  • Neglect: Parietotemporal lobe (right) → not aware of the stimuli on the contralesional site

This is a summary she gave in the lecture, I’ll go over the consequences in more detail by effect later, but this list is a short goody

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18
Q

What are the consequences of an infarct in the PCA

A

PCA - Occipital and temporal lobes
Disturbances in perception

  • Hemianopsia
  • Visual agnosia
  • Prosopagnosia
  • (There are more, this a short list)
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19
Q

What are the consequences of an infarct in the ACA?

A

ACA → dorsal and medial parts of of the frontal and parietal lobes

  • Executive functions and social cognitions
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20
Q

What is the most common cause of brain haemorrhages?

A

50% of BHs are caused by long-term exposure to hypertension

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21
Q

What is the most common type of brain haemorrhage (BH)?

A

An intracerebral haemorrhage (ICH).
Many haemorrhages occur in areas of the basal nuclei, usually as a result of the rupturing of deeper arterioles

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22
Q

What are other causes of ICHs?

A
  • Arteriovenous malformation (Like what happened to the expert by experience)
  • Inflammation of the vascular wall
  • Coagulopathy
  • Brain tumour
  • Lobar bleeding is more superficial and may be caused by amyloid angiopathy (degenerative disorder found in the elderly)
  • Haemorrhagic infarct, which is primarily a blockage but also bleeding because of damage to the vascular wall
  • Trauma can cause a haematoma (TBI chapter)
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23
Q

What acute treatment is used for ICHs?

A

Acute treatment is often conservative, the objective is to prevent important brain areas from becoming compressed
Medication to reduce swelling
Surgery to relieve pressure on the brain is done in more severe cases
Treatment focus on prevention of re-bleeding

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24
Q

What is another type of BH that doesn’t occur in the brain?

A

Subarachnoid haemorrhage (SAH), in which the haemorrhage doesn’t occur in the brain but in the subarachnoid space.
SAH causes sudden and extremely severe headaches, followed by neck stiffness after a few hours

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25
Q

What is the prevalence of SAHs? Where do they most commonly occur?

A

About 5% of all strokes involve SAH
In 85% of cases the cause of SAH is rupture of an aneurysm at or near the Circle of Willis

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26
Q

What are the types of treatment are used?

A
  • Surgery is usually needed to deal with the aneurysm, which involves either
    • closing the aneurysm with a metal clip (“clipping”)
    • endovascular treatment (using a catheter) in which platinum coils are inserted in the aneurysm via a blood vessel to close it off (“coiling”)
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27
Q

What are the outcomes?

A

Only one-third of patients survive SAH without significant loss of function
The other two-thirds present diffuse cognitive dysfunction symptoms which cause limitations and fatigue in daily life

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28
Q

What is the etiology of the neuropsychological consequence of stroke caused by an infarct?

(What causes the bad)

A

Impairment of specific cognitive functions is primarily caused by the infarct itself
Damage to more remote areas of the brain (Diaschisis) can occur due to anatomical connection with the remote area is decreased, resulting in dysfunction.

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29
Q

What is the etiology of the neuropsychological consequence of stroke caused by a brain haemorrhage??

(What causes the bad)

A
  • Problems may be caused by direct damage due to increased intracranial pressure
    • This is due to either ischemic damage as a result of increased intracranial pressure
    • Secondary ischemia can then be caused (meaning the increased pressure caused another blood vessel to be limited)
      • Or as a result of vasoconstriction (different to secondary ischemia as the vessel itself is constricting, it isn’t being constricted)
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30
Q

What are the differences between infarct damage and BH damage in early stages?

A

Following a BH, consciousness is decreased, disorders may be severe and diffuse, and patient often feels confused and disoriented
This is due to intracranial pressure, thus if the pressure is removed, normal functioning may be restored
A greater degree of recovery takes place, and more rapidly, than in patients who have suffered an infarct

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31
Q

What are the differences between infarct damage and BH damage in cognitive disorders?

A

The severity of cognitive disorders in patients with BH is linked to the extent of the haemorrhage rather than its location
In contrast to infarcts, the damage caused is not restricted to arterial areas because in BH the haematoma may affect an extensive area

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32
Q

Neuropsychological effects

This flashcard contains information about how the upcoming cards are structured

A

Impairments can occur in almost any cognitive domain. Similarities between infarct and BH will be discussed jointly. The differences will be discussed separately
Location of the infarct and any differences in damage to the areas in the left and right hemisphere will be discussed.
Disorders are described as they present during the acute phase (first week after stroke), when little or no recovery has occurred.

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33
Q

Neuropsychological effects

Can disorders occur at later stages? What is recovery like?

A

Disorders do occur at later stages, but the extent of occurrence depends on the degree of spontaneous recovery, the compensation for the function, and the mutual effects of coexisting disorders.
Disorders of cognitive functioning remains stable at 3, 6, and 15 months after the stroke
A dynamic recovery process is assumed to occur during the first 3-6 months.

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34
Q

Neuropsychological effects: Memory

How common are memory impairments?

A

13-50% of patients during the first week
Still present in 11-31% of patients after 1 year

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35
Q

Neuropsychological effects: Memory

Which area results in loss of memory when damaged?

A

Loss of memory frequently occurs after an infarct of the MCA, but can also occur following an infarct in other areas.
Loss of memory is more apparent after damage to left hemisphere or following bilateral damage than after damage to the right hemisphere.

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36
Q

Neuropsychological effects: Memory

What aspects of the damage alter which memory process is damage?
Which memory processes are most commonly damaged?

A

Depending on the nature, extent, and location of the damage, various memory processes may be affected

  • Anterograde vs. retrograde amnesia
  • Verbal vs. non-verbal memory
  • Declarative vs. procedural memory
  • Encoding vs. retaining information
37
Q

Neuropsychological effects: Memory

What type of amnesa is most common during the acute phase (1 week) after an infarct?

A
  • Most suffer from anterograde amnesia
    • This may be the result of a decreased ability to acquire new information, but can also be caused by a failure to retrieve the information that has been acquired.
  • Retrograde amnesia is less common, but may occur after damage to the non-medial parts of the temporal lobe
38
Q

Neuropsychological effects: Memory

What type of problems in encoding information occur after damage to which hemisphere?

A

Problems with encoding verbal information occurs after damage to the left hemisphere, and may partly be the result of language impairment
Sometimes difficult to differentiate between language impairment and problems with verbal memory

39
Q

Neuropsychological effects: Memory

What location, when damaged, causes problems with non-verbal encoding/memory

A

Specific problems with non-verbal memory can occur after damage to the right medial temporal lobe, the thalamus, the mammillary body, or the basal frontal lobe.
During acute phase these problems can be easily missed because patients report them less often

40
Q

Neuropsychological effects: Memory

Is declarative or procedural memory affected by an infarct?

A

Declarative memory is mainly affected after an infarct, whereas procedural memory remains unaffected.
Procedural memory may also be affected after damage to the basal ganglia

41
Q

Neuropsychological effects: Attention/speed of information processing

What is the prevalence of attention impairment?
What distinction is made in attention processes?

A

40% of patients show impaired attention
Distinction is made between basic attention processes (arousal) and more complex attention processes, such as directing, dividing, and maintaining attention.
This is because attention is a broad cognitive function that involves various cortical and subcortical networks

42
Q

Neuropsychological effects: Attention/speed of information processing

Disorders in basic attention processes…

A

Are observed if the patient falls asleep when they aren’t stimulated, or if their attention wanders during a discussion
Originate in the subcortical structures

43
Q

Neuropsychological effects: Attention/speed of information processing

Disorders in the complex attention processes…

A

Are detected if the patient is only able to focus for a limited period of time, and is easily distracted
Patients have difficulty doing more than one thing at the same time (divided attention)
Involves networks in the parietal lobe, temporal lobe, and prefrontal cortex.

44
Q

Neuropsychological effects: Attention/speed of information processing

What is the outcome of slow information processing speed?

A

Slowness is a common complaint in stroke patients, and it mainly occurs after an infarct in the subcortical brain areas.
Impaired attention is particularly apparent under time pressure, because of deceleration of information processing speed.

45
Q

Neuropsychological effects: Language

How common are language impairments?

A
  • During the acute phase following a stroke, 21-38% of patients suffer from a form of aphasia.
    • These difficulties decrease considerably in the months following the infarct.
      • Language problems persist in a milder form in some patients
46
Q

Neuropsychological effects: Language

Language disorders are most caused by an infarct in which area?
What aphasia results from this? Is it one particular aphasia?

A

The area supplied by the MCA in the left hemisphere.
Different aphasia’s exist, but a stroke is followed by mixed aphasia that is a combination of Wernicke’s aphasia and Broca’s aphasia.
This is because the affected area isn’t an anatomical structure, but an area supplied by an artery

47
Q

Neuropsychological effects: Language

What are some effects of severe/extensive infarcts?

A

Global aphasia: Both forms of aphasia are present in a severe form during the initial period
In cases of extensive infarct in the left hemisphere, patients are often not fully aware of their language impairment, and sometimes may become frustrated.

48
Q

Neuropsychological effects: Language

What are other language disorders and what areas are they related to?

A
  • An infarct to the area of the angular gyrus results in pure agraphia (writing) and pure acalculia (Calculations)
  • An infarct of the PCA in left hemisphere may cause alexia (reading impairments).
  • An infarct in the ACA in left hemisphere may cause Trans-cortical aphasia (Discussed on next card)
  • A bilateral infarct in the ACA may cause a complete inability to communicate verbally (akinetic mutism)
    • In contrast to aphasia, in mutism the intention to communicate verbally is lacking.
49
Q

Neuropsychological effects: Language

What does trans-cortical aphasia result in?

A
  • Trans-cortical aphasia leaves Broca’s/Wernicke’s area intact but communication between these areas and the rest of the brain is prevented
    • This results in the inability to communicate verbally or process written language
    • This is called isolation of the language area and it usually occurs in addition to specific damage to the supplementary motor areas.
      • Patients are capable of repeating words and sentences
50
Q

Neuropsychological effects: Language

Are all the language problems severe?

A

Milder forms of language problems also occur
Many patients experience word-finding problems and subtle limitations in understanding language.

51
Q

Neuropsychological effects: Perception

What area causes visual field defects? Whats some of the most common disorders?

A

Many patients suffer from visual field defects after an infarct in the PCA

  • Hemianopsia: Impairment of half of the visual field on the contralateral side
    • Patients with homonymous hemianopsia experience hallucinations in the blind visual field during the initial weeks after stroke.
  • Quadrantanopsia: Same thing but a quarter
52
Q

Neuropsychological effects: Perception

What are other visual disorders and what areas are they related to?

A
  • After damage to the posterior area of the right hemisphere, visual agnosia and colour agnosia may occur in addition to hemianopsia
  • Prosopagnosia and apperceptive agnosia may occur as a result of bilateral infarcts in the PCA.
  • A rare effect of these lesions is cortical blindness (aka Anton’s syndrome), in which the patient isn’t aware of their blindness and covers it with confabulations
53
Q

Neuropsychological effects: Perception

What causes Neglect? What were some examples of neglect?

A

In 25% of cases a infarct in the MCA in the right hemisphere results in neglect.
The parietal lobe is crucially important in neglect
Patients can draw things, but all the features will be pushed to the right, with the clock drawing, all the numbers were on the right

54
Q

Neuropsychological effects: Perception

Is it easy to assess neglect?

A

Nahhh, the following can occur that can make it complex

  • Hemianopsia and unilateral motor and/or sensory loss vary during the day.
  • Anosodiaphoria: A lack of concern about the impairment
  • Anosognosia (The inability to recognise the medical problem) for symptoms on the left side
55
Q

Neuropsychological effects: Perception

What are causes problems with body perception? What are some disorders that are related?

A

Problems with body perception may occur with damage to the parietal lobe

  • Finger agnosia: Incapable of naming, indicating, or recognising the various fingers of their own hand
  • Specific disorders in the patient’s mental representation of their own body (body image) or of the position of parts of their body in relation to the environment (body schema) are also seen in patients with parietal damage
56
Q

Neuropsychological effects: Perception

What causes problems with time perception?

A

Patients may experience problems with time perception with damage to the parietal lobe, the cerebellum, and prefrontal parts of the brain (not all 3, but related)

57
Q

Neuropsychological effects: Executive functions

How many patients experience executive function impairment?
Which area is most related?

A

~50% of patients experience impairments of executive functions during the acute phase.
This is particularly the case after an infarct in the ACA that affects the frontal lobe
The cerebellum also plays an important role in executive functioning

58
Q

Neuropsychological effects: Executive functions

What is the result of executive dysfunction?

A

The exec. functioning largely determines the patients independence.
Exec. function disorders may limit rehabilitation because these patients have difficulty initiating independent behaviour, maintaining the order of more complex behaviours, or adequately assessing their own capabilities.

59
Q

Neuropsychological effects: Executive functions

What is Abulia

A
  • Abulia: An extreme and rare form of executive function disorder in which the ability to take initiative is almost entirely absent.
    • The behaviour of these patients is compulsory, they have a tendency that cannot be suppressed to use objects in the appropriate way but in an inappropriate situation.
    • When patients are set a task through a directive concrete assignment, they are capable of doing this.
60
Q

Neuropsychological effects: Executive functions

What is the issue of testing for executive dysfunction?

A
  • Following an infarct in the anterior circulation (ACA and anterior MCA), patients aren’t always clearly limited in executive functioning in neuropsychological tasks, but they are in everyday tasks.
    • This is due to limited ecological validity of the tests and also that the impairment lies in the area of behaviour rather than cognitive functions.
61
Q

Neuropsychological effects: Praxis and the motor system

What is Apraxia? What area is it related to?

A

Apraxia: a type of cognitive disorder that is characterised by the inability to carry out meaningful movements and gestures.
Damage in the region of the MCA in the left hemisphere often results in apraxia

62
Q

Neuropsychological effects: Praxis and the motor system

What is the most common type of apraxia?

A

The most common is ideomotor apraxia, in which an individual is unable to make certain meaningful movements while the concept is intact and without any motor or sensory limitations

63
Q

Neuropsychological effects: Praxis and the motor system

What is Buccofacial apraxia?

A

Patients with buccofacial apraxia are unable or only partly able to verbally communicate, due to the impairment of voluntary control of the tongue and mouth musculature, which is required for adequate speech
It is often confused with language impairments

64
Q

Neuropsychological effects: Praxis and the motor system

Why is the cerebellum important?

A

The cerebellum is massively involved in motor planning.
Additionally, because of the large number of connections between the cerebellum and the cortices, the cerebellum is considered to be a modulator of the higher cognitive functions.

Patients may experience behavioural problems and impairments of their executive functions if there is damage to the posterior lobe and the vermis of the cerebellum.

65
Q

Neuropsychological effects: Changes in social cognition

What kind of changes in social cognition does a stroke cause?

A

It causes changes such as problems with the recognition of emotions, as well as impairments in the understanding of social situations or the regulation of interpersonal behaviour.

66
Q

Neuropsychological effects: Changes in social cognition

Which hemisphere did we think affects emotional functioning? What do we know now?

A

It is thought that a stroke in the right hemisphere in particular has consequences for emotional functioning, but this isn’t always the case.
Both hemispheres contribute to emotional well-being to some extent.

  • The left hemisphere is more involved in the inhibition and control of emotions
  • The right hemisphere mainly plays a part in the origin of emotions
67
Q

Neuropsychological effects: Changes in social cognition

What are some other changes and which area are they related to?

A
  • Behavioural changes can also occur after damage to the frontal lobe
    • Patients exhibit disinhibited or socially maladjusted behaviour.
  • If there is damage to the cerebellum, the patient may exhibit blunted affect and disinhibited behaviour in addition to motor and cognitive problems.
    • Pathological crying and laughter may occur within the framework of a pseudobulbar (cerebellar) syndrome caused by a bilateral lesion of the corticobulbar tract
68
Q

Neuropsychological effects: Changes in social cognition

What is Anosognosia?

A

Anosognosia: When patients lack insight into the seriousness of the motor, sensory, or cognitive effects of the stroke
It’s commonly seen after a stroke in the right hemisphere

69
Q

Vascular Dementia (VD)

What is Vascular dementia?
What are its risk factors?

A

In some patients, cerebrovascular disorders such as stroke result in such severe limitations and cognitive dysfunction that they may be referred to as vascular dementia.
Risk factors: Smoking, hypertension, high cholesterol levels, and obesity.

70
Q

Vascular Dementia

How prevalent is it?

A
  • 3-12 months after a stroke about 25% of patients are diagnosed with dementia.
    • Prevalence is somewhat higher among elderly people
  • Vascular dementia is the most common type of dementia after Alzheimer’s disease (AD).
  • Estimated that 10% of dementias in the western world have a vascular cause.
71
Q

Vascular Dementia

What can cause it?

A
  • VD can be caused by a single infarct in a strategic location, such as the thalamus.
  • However, VD is commonly a result of various major or minor infarcts that occur simultaneously or shortly after one another.
    • This is in connection with slowly progressive damage to the deep white matter in the brain (leukoaraiosis)
      • Even if there are no clinical infarcts, progressive damage to the smallest cerebral blood vessels can result in VD
72
Q

Vascular Dementia

What cognitive disorders are seen in patients with VD?

A

The cognitive disorders vary

  • In many, motor slowness and executive dysfunction are prominent.
  • Loss of memory may also occur, but less than in AD
  • In some patients, cognitive functions deteriorate gradually, but slowly progressive deterioration is also seen in many cases.
73
Q

Vascular Dementia

Can we distinguish VD from AD?

A
  • Its difficult to distinguish VD with AD
    • Recent studies show that there is a greater overlap than previously assumed.
    • Risk factors for VD also play a role for AD
      • Recent post-mortem examinations show signs of mixed dementia
74
Q

Vascular Dementia

Have we always called it Vascular Dementia?

A

Not really
Until recently, various terms were used to denote dementia caused by vascular diseases (e.g. multi-infarct dementia)
The term vascular cognitive impairment (VCI) has been used as an umbrella term.

75
Q

Other effects: Disorientation, delirium, and confusion

How prevalent is disorientation?

A

Disorientation with regard to time, place, and person occurs in ~40% of patients during the acute phase.
If the patient is properly oriented, they often have a better prognosis for recovery of cognitive functioning.

76
Q

Other effects: Disorientation, delirium, and confusion

How prevalent is delirium and confusion?

A

Delirium and confusion may occur after every type of infarct, but aren’t always diagnosed properly
Despite that delirium may represent the onset of a progressive dementia process, in the majority of cases it is temporary and may disappear completely.

77
Q

Other effects: Disorientation, delirium, and confusion

How fast does delirium develop?
What are its risk factors?

A

Delirium often occurs suddenly and may involve disturbed consciousness, hallucinations, emotional instability, and lethargy.
These symptoms may vary during the day
Risk factors include advanced age, delirium in the anamnesis, premorbid dementia, and severe visual disorders

78
Q

Other effects: Disorientation, delirium, and confusion

What is Reduplicative paramnesia?

A

Reduplicative paramnesia: The phenomenon in which the patient doesn’t recognise their environment and maintains, even after clear indications to the opposite effect, that it is not their home.

This phenomenon is sometimes found with delirium and is observed more often after a stroke in the right hemisphere.

79
Q

Other effects: Fatigue

How prevalent is fatigue?

A

Fatigue occurs in more than 50% of patients after a stroke and can have a strong negative influence in the longer term

80
Q

Other effects: Fatigue

What do patients report?
Can we treat it?

A

Many patients report a lack of energy and feelings of exhaustion when performing mental tasks

Little is known about the causes and possible treatment, but there are indications that patients benefit from
A combination of psychoeducation, a change in their attitudes to fatigue through CBT, and a gradual increase in physical activities.

81
Q

Other effects: Depression

How prevalent is mood change?

A

Almost all stroke patients experience mood changes during the initial period after the loss of function.

Around 90% of patients still report a change in their emotional functioning after 3-9 months
About one-third of these patients suffer from depression, but it isn’t always recognised

82
Q

Other effects: Depression

Why is depression not always recognised in stroke patients?
Why is it important to try and recognise it?

A

A reason for this is a lack of insight of the patient, or the inability to express or describe depressive symptoms (e.g. language disorders)
Another is that criteria for depression with respect to ‘vital signs’ are often a direct consequence of stroke cause problems with the correct diagnosis

It is important to consider depression because of its negative effects on cognitive function and on the rehabilitation process in general.

83
Q

Other effects: Depression

What % of patients meet the DSM-5 criteria for a depressive disorder? What % for dysthymic disorder?
When does depression commonly start?

A
  • About 50% of patients who suffer from low mood after a stroke meet the DSM-5 criteria for a depressive disorder
    • The other 50% can be classified as have a dysthymic disorder
  • The depression commonly starts during the first 6 months, with a peak at around 3 months
    • Such depression is usually temporary, but in some cases it may persist
84
Q

Other effects: Depression

Does the stroke cause depression? Or is depression a response to the stroke?

A

There has been much debate as to whether depression after a stroke is caused by the stroke itself, or is a reaction to a life-threatening event (i.e. reactive depression)

85
Q

Other effects: Depression

What evidence is there for reactive depression?

A

One study showed that the risk of developing depression after an infarct is the same as after a heart attack.

This supports reactive depression which occurs after a stroke

86
Q

Other effects: Depression

What evidence is there for strokes causing depression?

A

The vascular depression hypothesis states that the depression is caused by disruption of specific networks in the brain resulting from vascular damage, such as deep white matter changes.

87
Q

Other effects: Depression

What is the most plausible explanation for post-stroke depression?

A

A combination of the location of a lesion, a reactive component, and vascular risk factors seems to be the most plausible explanation for post-stroke depression

88
Q

Other effects: Depression

What is a catastrophic reaction?

A

A catastrophic reaction may develop during first few days after stroke, often when the patient has had to face the reality of their limitations. It’s basically a severe mental breakdown.

It is probably caused by the patient’s inability to deal with the loss of cognitive and physical functions, after being confronted with their limitations.
It isn’t known if a catastrophic reaction is a precursor to depression, but is linked to a poor prognosis for recovery.

Clinical and Neuropsychology - 1 (21 decks)

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