cognitive disorders

Question 1

specific disorders

Answer 1

result from focal damage to the brain

ie/ injuries caused strokes, bullet wounds

Question 2

generalized disorders

Answer 2

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

Question 3

closed head injuries

Answer 3

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)

Question 4

TBI

Answer 4

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

Question 5

causes of closed head injury

Answer 5

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

Question 6

focal damage

Answer 6

due to the impact of the brain on the skull

Question 7

diffuse damage

Answer 7

due to twisting and shearing of neurons

Question 8

acceleration-deceleration injury

Answer 8

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)

Question 9

consequences of acceleration-deacceleration injury

Answer 9

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

Question 10

what areas are most likely to sustain a head injury

Answer 10

orbitalfrontal and temporal regions

bones at these points are rough and potrude through cavity

Question 11

coup injury

Answer 11

focal damage at the site of impact

Question 12

contrecoup injury

Answer 12

focal damage opposite the site of impact

Question 13

glasgow coma scale

Answer 13

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

Question 14

concussion

Answer 14

mild traumatic brain inries

Question 15

head injury consequences

Answer 15

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

Question 16

post traumatic amnesia

Answer 16

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

Question 17

long term consequences of sustaining a closed head injury

Answer 17

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

Question 18

interventions for closed head injury

Answer 18

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

Question 19

cortical dementia: alzheimer’s disease (AD)

Answer 19

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

Question 20

what are the two types subtypes of cortical dementia: AD

Answer 20

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

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

Question 21

how is alzheimer’s disease diagnosed?

Answer 21

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

Question 22

alzheimer’s disease symtoms

Answer 22

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

Question 23

neurofibrillary tangles

Answer 23

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

Question 24

amyloid plaques

Answer 24

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

Question 25

amyloid plaques and AD

Answer 25

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

Question 26

Advanced AD and neuron loss

Answer 26

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

Question 27

Genetic bases and risk factors

Answer 27

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)

Question 28

APP mutation

Answer 28

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

Question 29

presenilin 1 or presenilin 2 mutation

Answer 29

affects the presenilin protein and results in accumulation or amyloid plaques

Question 30

Apolipoprotein E

Answer 30

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

Question 31

increased risk factors for AD

Answer 31

smoking cardiovascular disease diabetes head injury

Question 32

decreased risk factors for AD

Answer 32

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

Question 33

AD treatment

Answer 33

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

Question 34

Two main subtypes of FTD

Answer 34

behavioural-varient FTD primary progressive aphasia (semantic aphasia)

Question 35

cortical dementia: frontotemporal dementia (FTD)

Answer 35

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

Question 36

behavioural-variant FTD subtype

Answer 36

characterized by anterior temporal as well as orbitofrontal damage

Question 37

behavioural-variant FTD subtype symptoms

Answer 37

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)

Question 38

primary progressive aphasia FTD subtype

Answer 38

progressive decline in language (breakdown in vocab knowledge) involves more specific left-sided anterior temporal deterioration

Question 39

primary progressive aphasia FTD subtype symptoms

Answer 39

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

Question 40

frontotemporal dementia vs. alzheimer's disease

Answer 40

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

Question 41

neurological characteristics of FTD

Answer 41

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

Question 42

risk factors and treatment for FTD

Answer 42

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

Question 43

subcortical dementia: Parkinson's disease (PD)

Answer 43

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

Question 44

parkinson's disease: cognitive symptoms

Answer 44

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

Question 45

parkinson's disease and dopamine

Answer 45

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

Question 46

cognitive decline in PD patients

Answer 46

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

Question 47

PD and dopamine treatments

Answer 47

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)

Question 48

PD and other treatments

Answer 48

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

Question 49

subcortical dementia: Huntington's disease

Answer 49

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

Question 50

neurological degeneration in HD

Answer 50

smaller caudate enlarge ventricles because of lost tissue in basal ganglia

Question 51

chorea

Answer 51

jerky movements

Question 52

HD cognitive symptoms

Answer 52

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

Question 53

HD changes in emotional functioning

Answer 53

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

Question 54

HD diagnosis

Answer 54

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

Question 55

mixed variety dementias

Answer 55

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

Question 56

HD treatment

Answer 56

no cure aim is to address motor and psychiatric symptoms

Question 57

vascular dementia

Answer 57

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

Question 58

the brain and vascular dementia

Answer 58

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

Question 59

evidence for vascular dementia

Answer 59

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

Question 60

vascular dementia vs AD

Answer 60

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

Question 61

multiple sclerosis (MS)

Answer 61

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

Question 62

MS symptoms

Answer 62

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

Question 63

MS functional connectivity

Answer 63

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

Question 64

MS treatment

Answer 64

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

Question 65

interferons

Answer 65

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

Question 66

classes of epilepsy

Answer 66

1. generalized onset seizure 2. focal onset seizure

Question 67

epilepsy

Answer 67

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.

Question 68

generalized onset seizure

Answer 68

abnormal activation in large networks on both sides of the brain

Question 69

focal onset seizure

Answer 69

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

Question 70

tonic-clonic seizures

Answer 70

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

Question 71

absence seizures

Answer 71

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

Question 72

symptomatic

Answer 72

when the cause of the seizure is known

Question 73

idiopathic

Answer 73

seizure disorders with no known cause

Question 74

seizure causes

Answer 74

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.

Question 75

epilepsy: cognitive symptoms

Answer 75

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)

Question 76

Epilepsy treatment options

Answer 76

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