Cognitive Disorders and Special Topics Flashcards
Broca’s Aphasia
Lesions to the left front lobe, specifically to the motor strip area which controls the muscles that produce speech
Severe problems with articulation (dysarthria), speech slow and effortful
MOSTLY verbal comprehension
NO repeat phrases
NO fluency
aphasia
Language disorder
Results from damage (aka lesions) in the left hemisphere
Location of lesion determines nature of language disruption
Wernicke’s Aphasia
Lesions to left temporal lobe NO language comprehension NO execute verbal commands NO repeat phrases YES fluency, but say complete nonsense Unaware of problem, expect others to be able to understand them
Conduction Aphasia
Lesions in connections between expressive and receptive speech areas YES language comprehension YES execute verbal commands NO repeat phrases YES fluency, but don't make sense
Global Aphasia
Damage to most of cortex Most language functions impaired NO comprehension NO repeat verbal phrases NO fluency NO naming, reading, writing
One-sided neglect
When damage occurs to one side of brain, opposite side of body frequently affected\
Apraxia
Inability to carry out purposeful motor movements (e.g. waving), despite the absence of motor or sensory deficits
Can move limbs normally, but innervates wrong muscles, puts limbs in incorrect position, omits some element of action when asked to carry out specific motor command
Believed to be caused by left brain lesions, damage to left brain produces apraxia in both limbs
Agraphia
Impairment in ability to write acquired after person has learned to write
Can involve spelling, word selection, grammar, spatial arrangement
Left hemisphere damage in variety of areas - frontal lob, temporal, parietal regions, basal ganglia
Alexia
Acquired partial or complete inability to read Most commonly caused by stroke to dominant (left) hemisphere Pure alexia (without agraphia) - lesions that disconnect visual association cortex from temporoparietal cortices
Prosopagnosia
Most common of visual agnosias
Inability to recognize familiar face
Typically retrograde (can’t recognize faces of previously known individuals) AND anterograde (can’t learn new faces)
Despite normal or near normal visual perception, intact alertness, inattention, intelligence, langage
Injury to areas of visual association cortex
Anosagnosia
Lack of awareness of a disability or lack of awareness of nature of one’s illness
e.g. people with Wernicke’s typically don’t recognize they are speaking gibberish
Hydrocephalus
Accumulation of cerebrospinal fluid (CSF) in brain’s ventricles, causing increased intracranial pressure
Symptoms: dementia, urinary incontinence, unsteady gait
Can be treated with surgical procedure to increase drainage
Dementia
Impairment in memory PLUS: aphasia, apraxia, agnosia, or disturbance in executive functioning
Overall rate equal in men and women
Alzheimer’s Disease
-phases
Most common form of dementia, over half of all dementia cases
More prevalent in women
Progressive, rate of slope and decline varies
Early phase - impairments in recent memory, difficulty problem-solving, irritabilty, frustration, anger
Intermediate stage - further memory impairment, cognitive deficits (aphasia, apraxia, agnosia), confusion, socially undesirable behaviors
Late stage - gait and motor problems, may become mute or bedridden
Most rapid and relentless course occurs with early onset Alzheimer’s (before 65 years of age)
Genetic component of Alzheimer’s
First degree relatives of patients with AD carry six times greater risk of developing AD
Senile plaques, neurofibrillary tangles found throughout cortex and other brain structures (hippocampus - memory, amygdala)
Decreases in Acetylcholine, involved in memory and learning
Treatment of Alzheimer’s
Aricept (donepezil) - modest improvements in cognitive functioning (3-4 points in Folstein Mini Mental State)
Vascular Dementia
10-15% of all cases of dementia in older adults, sometimes coexists with Alzheimer’s
Twice as common in males
Why does Vascular Dementia occur
Numerous small CVAs (cerebrovascular accidents) or strokes believed to be caused by generalized cerebrovascular disease
Onset of Vascular Dementia
Typically abrupt
Course marked by rapid, step-wise changes - plateaus followed by further degeneration
Prognosis of Vascular Dementia, age of onset
Half die within two to three years of diagnosis
Age of onset usually much younger than AD
Prevention and treatment of Vascular Dementia
Primary and secondary prevention important
Lifestyle changes - reduction in smoking, weight loss, increased exercise effective in arresting progress of disease
No medications to reverse effects of stroke - but aspirin, anticoagulants, antihypertensives reduce likelihood of future stroke
Parkinson’s Disease - prevalence
Affects over a quarter of a million older adults in US
Slightly more men than women
What is Parkinson’s Disease
Movement disorder marked by tremor, rigidity, bradykinesia (slow initiation of movement) and shuffling gait
Neuropsychiatric symptoms - psychosis, dementia, depression
Parkinson’s dementia
30-50% of patients with PD have dementia
Sub-cortical dementia, affecting speed of processing and executive functions (planning, organizing, sequencing)
PD associated with…
Degeneration of neurons in the substantia nigra, section of basal ganglia
As a results, decrease in dopamine available in BG as a whole
BG involved in regulating voluntary movement
Treatment of PD
L-Dopa (Levodopa), precursor to dopamine
Does not alter progression of disease or decrease symptoms of dementia
Depression and PD
Occurs in 50-90% of patients with PD, may be direct effect of brain changes caused by disease
Antidepressants may improve emotional and cognitive functioning
Huntington’s Disease (Chorea)
Involves the BG
NTs Acetylcholine and GABA implicated
Does not become apparent until 35-45
Offspring have 50% change of being affected
Signs of Huntington’s Disease
Personality change first sign in 50% of cases
Progressively deteriorating dementia
Choreiform movements (frequent, discrete, brisk jerking movements of pelvis, trunk, limbs)
Athetosis (slow writhing movements)
Facial grimaces
Pick’s DiseaSE
Rare dementia that is clinically indistinguishable from AD
Affects women twice as often as men\Onset peaks between 50s and 60s
Affected neurons swell and have “Pick bodies” (irregularly shaped inclusions)
Lobes affected by Pick’s Disease
Frontal and temporal
Signs of Pick’s Disease
Decreases in initiative, episodes of tactless and inappropriate behavior, facetiousness and euphoria, explosive temper, disinhibition and poor impulse control, impaired insight –> all symptoms associated with frontal lobe dysfunction
Problems with memory and language also common (but less common than in AD)
Pick’s Disease vs. Alzheimer’s
PD: Unlike with AD, deterioration not wide-spead throughout brain, no senile plaques or neurofibrillary tangles
AID’s Dementia
AKA AIDS dementia complex (ADC)
10-15% of people with AIDS develop dementia
Cognitive, motor, and behavioral symptoms
Cognitive Symptoms of AIDs Dementia
memory problems (LT frequently remains intact), difficulty with attention and concentration, language difficulties
Motor Symptoms of AIDs Dementia
Weakness, lack of coordination, unsteady gait, jerky eye movements
Behavioral Symptoms of AIDs Dementia
Apathy, withdrawal, lack of motivation, personality changes, inappropriate affect, mood swings, and even hallucations
Dementia due to Head Trauma
Impaired memory most obvious and reliable complaint of head trauma
Closed-headed injuries
Skull not pierced or cracked
Frequently results in loss of consciousness
2 most common subtypes: concussions and contusions