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Cognitive Disorders Flashcards

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1
Q

Specific Disorders

A

Resulted from focal damage to the brain
— injuries caused by bullets, strokes

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2
Q

Generalized Disorders

A

More distributed effects on brain tissue, breakdown is not restricted to one domain, multiple cognitive abilities are affected simultaneously
— closed head injuries, dementias, demyelinating diseases

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3
Q

Closed Head Injury

A
  • Brain sustains damage when the head forcefully comes into contact with another object (but object does not penetrate the brain)
    — leading cause of TBI (traumatic brain injury)
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4
Q

Acceleration-Deceleration Injury

A

Primary mechanism of damage in closed head injury
Damage from rapid acceleration of the head followed by sudden deceleration
Focal damage due to the impact of the brain on the skull
Diffuse damage due to twisting and shearing of neurons
Neurons most vulnerable to twisting are those in white-matter tracts, which have long axons and connect distant brain regions

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5
Q

Consequences of Acceleration-Deceleration Injury

A

Secondary biochemical effects include glutamate excitotoxicity which can cause cell death

Disease state lasts beyond initial incident. 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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6
Q

Focal Injuries: Coup and Contrecoup

A

Focal damage at site of impact: coup injury
Focal damage opposite of site of impact: contrecoup injury

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7
Q

Glasglow Coma Scale

A

— Prominent clinical sign of a closed head injury is a significant alteration in consciousness
— The coma scale:
——- Provides a method for classifying the severity of damage in the brain
——- Evalulates: visual responsiveness, motor capabilities, verbal responsiveness
(check slides for chart and recovery prediction)

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8
Q

Head Injury Consequences

A

– All types can impact mental functioning
—- mild traumatic Brain Injury (mTBI) = concussion
– Attention and executive functioning often affected by closed head injury
-Posttraumatic Amnesia
— Varies from an inability to learn new info to an inability to report basic info

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9
Q

Long Term Consequences of a brain injury

A

Sustaining a closed head injury:
— Raises risk for sustaining another injury
— raises the risk for additional neurological consquences in the future
— associated with posttraumatic epilepsy, which may begin over a year after the head injury
— May put the individual at the risk of dementias

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10
Q

Interventions for Closed Head Injury

A

Preventions and Interventions
- Prevention: safety protections, violence prevention
- Pharmacological treatments to lessen biochemical cascade effects like excitotoxicity and inflammation
- Interventions can specifically target the cognitive level

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11
Q

Dementia

A

Syndrome involving loss of cognitive functions, sometimes accompanies by personality changes, that interferes with work or social activities

Progresses in stages (mild, moderate, severe) that lead to death

3 varieties
— Cortical Dementia
— Subcortical Dementia
— Mixed-Variety Dementia

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12
Q

Cortical Dementias

A
  • one of three varieties (cortical, subcortical, mixed-variety)
  • Manifest as the co-occurence of specific cognitive deficits such as aphasia, apraxia, agnosia, spatial/ calculation deficits, memory problems

___
Alzheimer’s disease
Frontotemporal Dementia

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13
Q

Subcortical Dementias

A
  • one of three varieties (cortical, subcortical, mixed-variety)
  • Result in general cognitive deficits (rather than specific)
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14
Q

Mixed-variety Dementias

A
  • one of three varieties (cortical, subcortical, mixed-variety)
  • include aspects of both cortical and subcortical dementias, midway between cortical and subcortical
  • specific deficits + general deficits
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15
Q

Cortical Dementia: Alzheimer’s Disease

A

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 judgment.

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

Two subtypes:
— 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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16
Q

AD diagnosis

A

Alzheimer’s

Based on behaviour and cognition
—– The defining biological characteristics 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 behavioral pattern is consistent with the disease

Research has focused on potential biomarkers to serve as additional indicators of disease presence

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17
Q

AD Symptoms

A

Alzheimer’s patients have an inability to acquire new information as a result of severe, global anterograde amnesia
— People with AD remain in familiar areas, 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

___
AD patients can also experience difficulty/decline in:
—- Language: verbal fluency, semantic aspects of language
—- Visuospatial processing
—- Conceptual aspects of motor behavior
—– Executive functioning
—- Changes in emotional functioning and personality

Varies from person to person, as the disease becomes more global, becomes more impaired

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18
Q

Neurobiological characteristics of AD

A

Seen in greater levels in AD brains:

Neurofibrillary tangles- thought to interfere in with neurons/ cognition, twisted pairs of helical filaments found within the neuron.

Amyloid plaques

__
unsure if they cause AD, or if AD produces an increase in them

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19
Q

Amyloid Plaques

A
  • Deposits of aluminum silicates and amyloid peptide that create a conglomeration of proteins
  • typically surrounded by neurofibrillary tangles, believed to cause vascular damage and neuronal cell loss

PET methods have made it possible to assess the presence of amyloid plaque in a living person

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

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20
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 visible 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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21
Q

Genetic Bases of AD and risk factors

A

Early-onset is typically associated with one of three gene mutations
– APP mutation
»» located on chromosome 21, codes for amyloid precursor protein, results in amyloid deposits

– Presenilin 1
– Presenilin 2 mutation
»» Affects the presenilin protein and results in accumulation of amyloid plaques

– Apolipoprotein E (ApoE)
»» thought to play a role in clearing amyloid plaques

– The ApoE-4 allele associated with an increased risk of AD:
»» Present in 15% of general population but 40% in AD patients.
»» AD patients with the ApoE-4 allele show faster rates of hippocampal atrophy.
»» AD patients with the ApoE-4 allele have greater levels of amyloid plaque accumulation.

22
Q

Non-genetic risk factors for AD

A

Increased risk:
— Smoking
— Cardiovascular disease
— Diabetes
— Head Injury

Decreasing risk:
— Increased amount of education
— Mentally challenging activities
— Physical activity
— Diet

23
Q

Treating AD

A
  • No cure
  • Treatment focuses on slowing cognitive decline

Neurofibrillary tangles lead to cell death in the nucleus basalis of Meynert and starves the brain of acetylcholine

Drugs given to AD patients attempt to increase acetylcholine activity

24
Q

Cortical Dementia: Frontotemporal Dementia (FTD)

A

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

Average age of onset: 56-58 years
— accounts for 10% of dementia cases under age 65, only 3% over 65

2 main subtypes:
1. Behavioural-variant FTD
2. Primary Progressive Aphasia

25
Q

Behavioural-variant FTD

A

Anterior temporal lobe and orbitofrontal damage

lack of inhibitory control, esp for social-emotional functioning

Other symptoms:
- Impulsiveness
- Swearing at inappropriate times, outbursts of frustration, and inappropriate sexual behaviour
- Little awareness of the inappropriate behaviour
- Preoccupation with repetitive or routinized behaviour
- Mood changes (especially depression and anxiety)

26
Q

Primary Progressive Aphasia FTD

A
  • left-sided anterior temporal deterioration
  • difficulties in the domain of language
    — difficulty in verbal expression
    — speech eventually has less and less content, eventually patients become mute
    — difficulties in reading and writing
27
Q

Neurobiological characteristics of FTD

A
  • FTD also differs from AD in the abnormal cellular characteristics within damaged regions:
    — Abnormal protein deposits within neurons
    — Pale neurons swollen as if they had “ballooned”
    — Clumps of fibers in the cytoplasm known as Pick’s bodies
28
Q

Risk Factors and Treatment for FTD

A

The greatest risk factor for FTD is the presence of FTD in a closely related family member.

> > > Genes that are linked to FTD include a gene coding for the tau protein, and other genes coding for pathological proteins

> > > FTD has no cure; treatment is targeted at managing symptoms. Pharmacological approaches seem to have little benefit.

29
Q

Parkinson’s Disease (PD) Symptoms

A
  • Difficulties with executive function
  • Deficits in memory encoding and retrieval
  • Bradyphrenia
  • Emotional changes
  • Parkinsonian Mask (expressionless face)
30
Q

Subcortical Dementia/ Parkinson’s Disease

A
  • Specific cell loss in the substantia nigra
  • motor symptoms
  • dementia is evident in 30% of PD patients
  • mild cognitive impairment that may develop into dementia
31
Q

PD and Dementia ***

A
32
Q

Cognitive Decline in PD

A
  • may occur when dopamine deficits of Parkinson’s combine w/ pathology of Alzheimers (amyloid plaques and neurfibrillary tangles
  • others say the Lewy Bodies- clumps of abnormal proteins in cells- account for it

Could be a combination of both

33
Q

PD and Dopamine Treatments (and side effects)

A
  • L-dopa is a precursor to dopamine that can cross the blood-brain barrier
    —– unfortunately associated with dyskinesia, in 35%, and hallucinations
    —- loses efficacy over time

Can improve some aspects of executive function

can also impair other factors (inhibitory control impaired, causes impulsiveness)

34
Q

Other PD Treatments

A

More invasive treatments (later on)

– Deep-brain stimulation
– ablation of the thalamus
– ablation of the internal portion of the globus pallidus

35
Q

Subcortical Dementia: Huntington’s Disease (HD)

A
  • Caused by a genetic mutation, abnormal protein folfing destroys GABAergic (and cholinergic) neurons in the striatum (caudate nucleus and putamen), and to some degree in the globus pallidus
  • Causes a movement disorder characterized by jerky, rapid, and uncontrollable movements
36
Q

HD cognitive symptoms

A
  • Difficulties with:
    —- initiating behaviour
    —- selecting a response
    —- selecting a stimulus on the basis of particular attributes
    —- switching mental tasks
  • Reduced verbal fluency
  • Perservative tendencies
  • Loss of cognitive flexibility
  • Deficits in memory recall
37
Q

HD and emotional functioning

A
    • about half have major depressive episodes (which precede motor symptoms)
    • Irritable, apathetic, impulsive, aggressive, emotionally liable
    • might show psychotic symptoms (delusions)
    • often act in socially inappropriate ways, have difficulty recognizing emotion in others
38
Q

HD diagnosis and treatment

A

It is possible to identify people who will develop the disorder
People who carry the Huntington’s gene, but who are asymptomatic with regard to motor signs, exhibit poorer performance than noncarriers on tasks of memory and executive functioning.
There is no cure for Huntington’s disease
Aim of treatment is to address the motor and psychiatric symptoms.

39
Q

Mixed-Variety dementias

A

Both cortical and subcortical damage (substantial)

clinical profile is an amalgamation of cortical and subcortical types

40
Q

Mixed-Variety: Vascular Dementia

A
  • Multi-infarct dementia
      • common form of mixed-variety dementia, second most common type of dementia
  • cumulative effects of many small strokes that tend to create both cortical and subcortical lesions
  • Affects multiple areas over time as the consequences of multiple small strokes accumulate
41
Q

Brain areas and Vascular Dementia

A

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

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

42
Q

Evidence for VD

A

Evidence for a vascular contribution to dementia:
» 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 gray matter

43
Q

Vascular Dementia vs. Alzheimer’s Disease

A
  • Similar neuropsychological profile
  • VD occurs with a relatively abrupt onset, rather gradual course, not restricted to onset in later years
  • The pattern of impairment in VD can fluctuate (such as being worse initially and then improving)
44
Q

Multiple Sclerosis (MS)

A

> > One of the most common neurological diseases of non-traumatic origin

— 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

45
Q

MS symptoms

A
  • Depend on location of myelin damage in the nervous system
    —– symptoms get progressively worse, they come and go
  • Cognitive deficits occur in 40-60% of patients
    —– variable, difficulties may involve slowed information processing and difficulty in memory (recall is affected more than recognition), conceptual reasoning, and visuospatial cognition
  • Usually comes with changes in mood and personality
  • General sparing of language and knowledge skills
46
Q

MS Functional Connectivity

A
  • Affects myelination of axons, which affects comms btwn brain regions
    —– esp frontal lobes and connections with subcort. structures
  • Research found both increased and decreased functional connectivity
    —– speculate that the increase in connectivity btwn brain regions reflects a compensatory process of some sort in order to maintain functionality
47
Q

MS Treatment

A
  • No cure exists, treatments aim to curtail symptoms and delay relapses
    —- Main treatment: “interferon beta-1b”
    ——– Interferons are proteins made by the body that have antiviral characteristics

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

48
Q

Epilepsy

A
  • Recurrent but intermitten seizure activity
  • Epileptic seizures are episodes with extreme hyperpolarization in an atypical and abnormal manner:

2 types:
1. Generalized onset seizure
—– all over the brain, everything activating abnormally
2. Focal onset seizure
—– starts in one point of the brain, potenitally spreads out

49
Q

Additional types of seizures

A
  • further categorization based on level of awarenes during seizure and kinds of behaviour that are exhibited

— Tonic-clonis seizures: convulsive behaviour based on changes in muscle stiffness

— Absence seizures: brief periods of altered awareness of blacking out

— Other seizures can involve changes in breathing, thinking, speech, emotions, or sensation
————> seizures identifiable by characteristic EEG abnormalities

50
Q

Seizure causes

A
  • known cause = symptomatic
    —> Typical causes: head trauma, metabolic disorders, infection, toxins, and tumours
  • no known cause: idiopathic

Can be triggered by a variety of stimuli, with the likely trigger varying from person to person

51
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
    »> Connectivity between brain regions and networks is altered
    »> Cognitive disruption reflect dysfunction of the area where the seizure originates (focal onset seizures)
52
Q

Epilepsy treatment options (drug therapy)

A

Anticonvulsant medication: 3 major classes of drugs

Psych 382 (15 decks)

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