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cognitive disorders Flashcards

1
Q

specific disorders

A

result from focal damage to the brain

ie/ injuries caused strokes, bullet wounds

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2
Q

generalized disorders

A

more distributed effects on brain tissue

breakdown is not restricted to one cognitive domain, but multiple cognitive abilities are effected simultaneously

ie/ closed head injuries, demetias and demyelinating diseases

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3
Q

closed head injuries

A

brain sustains damage when the head forcefully comes into contact with another object (but object does not actually penetrate brain

lead cause of traumatic brain injury (TBI)

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4
Q

TBI

A

traumatic brain injury

general term for referring to a sudden external trauma interfering with brain functioning

significant source of neuropsychological dysfunction
- more than 69 million cases each year worldwide

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5
Q

causes of closed head injury

A

adolescents and young adults = vehicle bicycle and other similar accidents

young children and older adults = falling causing injury

sports-related and combat related

alcohol is involved in about 1/2 of TBI

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6
Q

focal damage

A

due to the impact of the brain on the skull

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7
Q

diffuse damage

A

due to twisting and shearing of neurons

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8
Q

acceleration-deceleration injury

A

primary mechanism of damage in closed head injury

energy imparted to brain causes it to move within the skull

damage from rapid acceleration of the head followed by sudden deceleration

could be focal or diffuse damage

neurons most vulnerable to twisting are those in white-matter tracts, which have long axons and connect distinct brain regions

closed head injury results in neuronal loss in white matter, especially the corpus callosum

can be detected by edema (swelling)

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9
Q

consequences of acceleration-deacceleration injury

A

secondary biochemical effects include glutamate excitotoxicity (overproduction of glutamate) which can cause cell death

disease state lasts beyond initial accident. can appear as: enlargement of the ventricles, loss of volume in large myelinated tracts

longitudinal studies indicate white-matter deterioration continues for several years following TBI

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10
Q

what areas are most likely to sustain a head injury

A

orbitalfrontal and temporal regions

bones at these points are rough and potrude through cavity

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11
Q

coup injury

A

focal damage at the site of impact

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12
Q

contrecoup injury

A

focal damage opposite the site of impact

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13
Q

glasgow coma scale

A

one prominent sign of closed head injury is a significant alteration in consciousness

basic aspects of wakefulness and consciousness are controlled by the brainstem

assesses the level of consciousness - used in ER rooms around the world

provides a method for classifying the severity of damage in someone who has sustained head injury

evaluates three realms of functioning
1. visual responsiveness
2. motor capabilities
3. verbal responsiveness

3-8 severe head injury
9-12 moderate injury
13 or greater mild head injury

score has prognostic value for survival rates and fture level of functioning

not a perfect predictor of outcomes

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14
Q

concussion

A

mild traumatic brain inries

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15
Q

head injury consequences

A

vary in severity, but all can impact mental functioning

attention and executive functioning (memory) often affected by head injury

difficulty in selected and divided attention, response inhibition and cognitive flexibilty

lack of motivation (due to emotions)

lack of understanding deficits

poor behavioural control

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16
Q

post traumatic amnesia

A

varies from inability to learn new info to an inability to report basic information

initial presentation of these memory problems tend to predict the severity of injury

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17
Q

long term consequences of sustaining a closed head injury

A

raises risk for sustaining another injury (by 4-6 times) could be due to poor attention and judgement

risk factor for longer-term neurological problems

associated with post traumatic epilepsy, which may begin more than a year after the head injury

may put an individual at higher risk for dementias

if occurs in early adulthood, significant increase in drepression

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18
Q

interventions for closed head injury

A

preventions: safety protections, violence prevention (seat belts, helmets)

pharmacological treatments to lessen effects of biochemical cascades including excitotoxicity and inflammation

interventions can be specifically targeted at the cognitive level

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19
Q

cortical dementia: alzheimer’s disease (AD)

A

brain damage is diffuse

defined by a decline in memory and other aspects of cognitive functioning, including at least one of the following: language , visuospatial skills, abstract thinking, motor performance, and judgement
- at first subtle and then became profound

also see emotional dysfunction and personality changes, which tend to worsen over time

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20
Q

what are the two types subtypes of cortical dementia: AD

A

early-onset AD: onset occurs before the age of 65; progresses rapidly

late-onset AD: onset after the age of 65; slower cognitive decline

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21
Q

how is alzheimer’s disease diagnosed?

A

based on behaviour and cognition

the defining biological characteristic can only be determined by post-mortem examination of brain

a probable diagnosis is made when other causes of dementia are ruled out and the person’s behavioural pattern i consistent with the disease

research has focused on potential biomarkers o serve as additional indicators of disease presence

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22
Q

alzheimer’s disease symtoms

A

AD have an inability to acquire new info as a result of severe, global anterograde amnesia

people with this remain in familiar environments and routines, reducing the need to acquire new information

widespread amnesia impacts procedural knowledge and implicit learning as well as working memory

more aspects of memory are affected because more brain regions are affected, including cortical regions

struggle with:
language: verbal fluency, semantic aspects of language
visuospatial processing
conceptual aspect of motor behaviour
executive functioning
changes in emotional functioning and personality

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23
Q

neurofibrillary tangles

A

twisted pairs of helical filaments found within the neuron

found in normal functioning brain, but increases in AD

disrupt neurons functional matrix

not equally disributed throughout the brain

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24
Q

amyloid plaques

A

deposits consisting of aluminium silicate and amyloid peptides that create a conglomeration of proteins

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25
Q

amyloid plaques and AD

A

observed in normal brain too - just concentrates in the hippocampus and cortex with AD

typically surrounded by neurons containing neurofibrillary tangles, and believed to cause vascular damage and neuronal cell loss

PET methods (involving a ligand that binds to amyloid) have made it possible to assess the presence of amyloid plaque for a living person

progressive accumulation of amyloid plaques is correlated with cognitive decline in living AD patients

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26
Q

Advanced AD and neuron loss

A

accumulating tangles and amyloid plaques result in loss of synapses and cells

in later stages, cell loss is viable on anatomical brain images; cortex is atrophied, ventricles enlarged

distributed across frontal, anterior temporal, and parietal cortex

subcortical structures affected include hippocampus, amygdala, and olfactory system

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27
Q

Genetic bases and risk factors

A

typically associated with one of three gene mutations which all involve the increase of production of amylad beta protein

APP mutation
presenilin one or presenilin 2
Apolipoprotein E (ApoE)

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28
Q

APP mutation

A

located on chromosome 21, codes for amyloid precursor protein and results in amyloid deposits

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29
Q

presenilin 1 or presenilin 2 mutation

A

affects the presenilin protein and results in accumulation or amyloid plaques

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30
Q

Apolipoprotein E

A

most closely associated with alzheimers

thought to play a role in clearing amyloid plaques

ApoE-4 allele associated with an increased risk of AD

present in 15% of general population but 40% in AD patients

AD patients with ApoE-4 allele show faster rates of hippocampal atrophy

AD patients with ApoE-4 allele have greater levels of amyloid plaque accumulation

the alone will not cause alzheimers - also genetic and environmental factors

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31
Q

increased risk factors for AD

A

smoking
cardiovascular disease
diabetes
head injury

32
Q

decreased risk factors for AD

A

increase amount of education
mentally challenging activities
social engagement
physical activity
diet

33
Q

AD treatment

A

no cure: ; treatment focuses on slowing cognitive decline

treatments attempt to influence the cholinergic system (b/c acetylcholine levels are linked to severity of memory loss and dementia)

neurofibrillary tangles lead to cell death (starved acetylcholine) in the nucleus basalis of meynert and starves (located at the base of the brain route to hippocampus and cortex) the rest of the brain of acetylcholine

drugs given to AD patients attempt to increase availability of acetylcholine - slow AD, but do not stop int

34
Q

Two main subtypes of FTD

A

behavioural-varient FTD

primary progressive aphasia (semantic aphasia)

35
Q

cortical dementia: frontotemporal dementia (FTD)

A

differs from AD in age of onset, symptom profile, and the brain regions most affected

average age of onset approx 56-58
- FTD accounts for about 10% of dementia cases under the age of 65, but only about 3% over 65

36
Q

behavioural-variant FTD subtype

A

characterized by anterior temporal as well as orbitofrontal damage

37
Q

behavioural-variant FTD subtype symptoms

A

lack of inhibitatory control, especially social-emotional functioning

impulsiveness

swearing at inappropriate times, outbursts of frusteration and inappropriate sexual behaviour

preoccupation with repetitive or routinized behaviour. ie/ going to the same appointment over and over again

mood changes (especially depression and anxiety)

38
Q

primary progressive aphasia FTD subtype

A

progressive decline in language (breakdown in vocab knowledge)

involves more specific left-sided anterior temporal deterioration

39
Q

primary progressive aphasia FTD subtype symptoms

A

patients mainly exhibit difficulties in the domain of language

difficulty in verbal expression

over time, speech has less and less content, and eventually patients become practically mute

difficulties in reading and writing also develop

later may develop parkinson-like motor functioning

40
Q

frontotemporal dementia vs. alzheimer’s disease

A

patients with AD have thinning across all major cortical regions

patients with FTD have characteristics thinning in frontal and anterior temporal regions

patients with FTD have greater loss of white matter in the frontal lobes than do AD patients

41
Q

neurological characteristics of FTD

A

FTD also differs from AD in the abnormal cellular characteristics within damaged regions

abnormal protein deposits within the neurons

pale neurons swollen as if they had “ballooned”

clumps of fibers in the cytoplasm known as Pick’s bodies

42
Q

risk factors and treatment for FTD

A

the greatest risk is the presence of FTD in a closely related family member - strong genetic component

genes linked to this include a gene coding for the tau protein, and other genes coding for pathological proteins

no cure, treatment is targeted at managing symptoms. Pharmacological approaches seem to have little benefit

43
Q

subcortical dementia: Parkinson’s disease (PD)

A

specific cell loss in the substantia nigra region of the basal ganglia (primary source of dopaminergic neurons)

along with the motor symptoms that accompany the disease, dementia is evident in approximately 30% of PD patients, and others exhibit mild cognitive impairment that may develop into dementia during the course of the disease

44
Q

parkinson’s disease: cognitive symptoms

A

difficulties with executive function

deficits in memory encoding and retrieval processes

bradyphrenia (general slowing of motor processes

emotional changes, including depression

parkinson mask - expressionless face

general slowing of motor and thought processes

45
Q

parkinson’s disease and dopamine

A

deficient dopamine in the dopaminergic path from the midbrain to subcortical and cortical regions of the frontal lobe

dopamine in the prefrontal cortex facilitates executive function

deficient dopamine may not explain all cognitive symptoms seen in PD

not everyone with parkinson’s disease develops dementiaa, even though they all have insufficient dopamine

dopamine agonist drugs do not appear to improve memory deficits seen in some PD patients

46
Q

cognitive decline in PD patients

A

some researchers argue that dementia occurs when the typical dopamine deficits of parkinson’s are combined with pathology typical of alzheimer’s disease, ie/ amyloid plaqyes and neurofibrillary tangles

others argue that the presense in the cortex of “Lewy bodies” - clumps of abnormal porteins inside cells - can account for cognitive decline

could be a combination of both

47
Q

PD and dopamine treatments

A

Ldopa is a precursor to dopamine can cross the blood brain barrier

unfortunately associated with dyskinesia in about 35% of patients with hallucinations in other patients

it loses drug efficacy over time

levadopa (ldopa) can improve some aspects of executive function, but also impair other functions (inhibitory cointrol of behaviour is impaired resulting in impulsiveness)

48
Q

PD and other treatments

A

over time, ldopa resistance builds so more invasive treatment options may be considered:

deep brain stimulation or ablation of the thalamus or the internal portion of the globus pallidus

49
Q

subcortical dementia: Huntington’s disease

A

causes by a genetic mutation, abnormal protein folding destroys GABAergic (and cholinergic) neurons in the striatum (caudate nucleus and putamen) and to some degree in the globus pallidus

this destruction produces a movement disorder characterized by jerky , rapid and uncontrollable movements

50
Q

neurological degeneration in HD

A

smaller caudate

enlarge ventricles because of lost tissue in basal ganglia

51
Q

chorea

A

jerky movements

52
Q

HD cognitive symptoms

A

specific difficulties in intiating behaviour, selecting a response, selecting a stimulus on the basis of particular attributes, and switching mental sets

difficulty planning and scheduling

reduced verbal fluency, perseverative tendencies and a loss of cognitive flexibility

deficits in memory recal

difficulty making the kind of self-guided search through memory that is required to recal info

53
Q

HD changes in emotional functioning

A

half of the patients have major depressive episodes , which precedes motor symptoms

common: irritable, apathetic, impulsive, aggressive and emotionally labile

might exhibit psychotic symptoms (delusions)

often act in socially inappropriate ways and have difficulting recognizing emotions in others

54
Q

HD diagnosis

A

possible to identify people that will develop this disorder

people who carry HD gene but are asymptomatic with regard to motor signs, exhibit poorer performance than noncarriers on tasks of memory and executive functioning

55
Q

mixed variety dementias

A

characterized by a substantial degree of both cortical and subcortical damage, which makes the clinical profile of these disorders an mixture of the cortical and subcortical dementias

56
Q

HD treatment

A

no cure

aim is to address motor and psychiatric symptoms

57
Q

vascular dementia

A

also known as multi-infarct dementia

common form of mixed-variety dementia; second most common type of dementia overall

results from the cumlative effects of many small strokes that tend to create both cortical and subcortical lesions

affects multiple areas over time as the consequence of multiple small strokes accumulate

58
Q

the brain and vascular dementia

A

various brain areas affected

some cases the vascular damage is cortical, more often in the frontal lobes than any other

other cases especially people in with arterial, lesions occur in small blood vessels supplying subcortical area

59
Q

evidence for vascular dementia

A

long standing medical history of arterial hypertension

focal neurological signs that suggest a stroke

MRI scans revealing specific and multiple infarcts of the cortex in either the white or grey matter

60
Q

vascular dementia vs AD

A

similar neuropsychological profile

vascular dementia occurs with a relatively abrupt onset, is accompanied by a stepwise rather than gradual course, and is not restricted to onset in the later years

the pattern of impairment in vascular dementia can fluctuate, being worse initially and then improving

61
Q

multiple sclerosis (MS)

A

One of the most common neurological diseases of non-traumatic origin
- affects cognitive function of young and middle ages adults

Cause is unknown; evidence suggests environmental and genetic contributions

One in five MS patients has a family member with MS

MS affects women about twice as often as men

Characterized by multiple discrete areas of scarring (sclerosis), ranging in size, in which neurons have absent or damaged myelin

The destruction of myelin in MS is thought to result from an immunological disruption
- autoimmune disorder (body identifies a part of its own system for foreign matter)
- or death of ogliodendrocytes
- either way may interfere with neural transmission because of axonal degration

62
Q

MS symptoms

A

MS symptoms depend on location of myelin damage in the nervous system
- commonly starts as blurred/lost vision, vision, muscle weakness/tingling, coordination difficulty

Symptoms get progressively worse and can come and go (appear/dissapear)

Cognitive deficits occur in 40–60 percent of patients

Variable, but difficulties may involve slowed information processing and difficulty in memory (affecting recall more than recognition), conceptual reasoning, and visuospatial cognition

Usually accompanied by changes in mood and personality
General sparing of language and knowledge systems

63
Q

MS functional connectivity

A

MS affects myelination of axons, which impacts communication between brain regions

Especially the frontal lobes and connections with subcortical structures

Research has found both increased and decreased functional connectivity

Researchers speculate that the increase in connectivity between brain regions reflects a compensatory process of some sort in order to maintain functionality

64
Q

MS treatment

A

No cure exists; treatments attempt to curtail symptoms and delay relapses

Main treatment: The drug “interferon beta-1b”
- interferons

Future treatment: Promoting axonal regeneration and myelin repair
- Stem cells may prove to be especially beneficial in repairing myelin

65
Q

interferons

A

are proteins produced by the body that have antiviral characteristics and modulate the immune response.

66
Q

classes of epilepsy

A
  1. generalized onset seizure
  2. focal onset seizure
67
Q

epilepsy

A

diagnosis based on 2 or more seizure

A disease with recurrent but intermittent seizure activity

Epileptic seizures are episodes with extreme hyperpolarization of neurons that spreads over a large area in an atypical and abnormal manner.

68
Q

generalized onset seizure

A

abnormal activation in large networks on both sides of the brain

69
Q

focal onset seizure

A

abnormal activity starts on one side of the brain
- fairly localized, may then spread to other regions

70
Q

tonic-clonic seizures

A

convulsive behavior due to changes in muscle activity, such as stiffness (tonic) and jerkiness (clonic)

71
Q

absence seizures

A

brief periods of altered awareness or “blacking out”
Other seizures can involve changes in breathing, thinking, speech, emotions, or sensations
Seizure types identifiable by characteristic EEG abnormalities

72
Q

symptomatic

A

when the cause of the seizure is known

73
Q

idiopathic

A

seizure disorders with no known cause

74
Q

seizure causes

A

Typical causes: head trauma, metabolic disorders, infection, toxins, and tumors.

Seizure episodes can be triggered by a variety of stimuli, with the likely trigger varying from person to person.

75
Q

epilepsy: cognitive symptoms

A

Impaired cognitive and psychosocial functioning
- Disrupted sustained attention and executive function

Consciousness is disrupted during the seizure

Interictal (between-seizure) consequences occur as well:
- Connectivity between brain regions and networks is altered
- Cognitive disruption reflect dysfunction of the area where the seizure originates (focal onset seizures)

76
Q

Epilepsy treatment options

A

Treatment option #1 – drug therapy:
- Anticonvulsant medication – 3 major classes of drugs:
- Barbiturates mimic neurotransmitter GABA
- Hydantoins block the influx of sodium into the neuron
- More recent anti-epileptic drugs attenuate the release of glutamate

Drug treatment effective for about 70–80% of patients
epilepsy treatment options

Treatment option #2 – surgery:
Drug-resistant epilepsy is much more difficult to treat
If a focal origin can be identified, surgery might be an option
Removing the tissue source of the seizure activity helps preclude healthy areas from becoming compromised.

Researchers continue the search for new treatments as medication is not always effective and surgery is invasive

cognitive neuroscience (15 decks)

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