Neurocognitive Disorders Flashcards
Delirium
- disturbance in attention and awareness that develops over a short period of time (few hours to a few days)
- represents a change from baseline attention and awareness
- tends to fluctuate in severity over the course of a day
- at least one additional disturbance in cognition (memory or language impairment)
- symptoms aren’t better explained by a pre-existing revolving or a cognitive disorder and do not occur in context of reduced level of arousal (coma)
- evidence that symptoms are a direct physiological consequence of a medical condition, substance toxication, withdrawal, or exposure to toxin
Causes of delirium
- high fever
- nutritional deficiency
- electrolyte imbalance
- renal or hepatic failure
- head injury
- certain drugs and medications (alcohol, lithium, sedatives, and anticholinergic drugs)
Treatment of delirium
- addressing causal and contributing medical problems
- reducing disorientation through environmental manipulation
-haloperidol or other antipsychotic drugs may help reduce agitation and psychotic symptoms
Environmental manipulation
- providing sufficient lighting
- reducing noise
- minimizing number of visitors
Major neurocognitive disorder
- cognitive dysfunction that is acquired
- sufficient decline from a previous level of functioning in one or more cognitive domains (executive functioning, learning and memory, social cognition)
-does not occur only in the context of delirium
-interferes with the person’s independence in every day activities
Mild neurocognitive disorder
- cognitive dysfunction that has acquired
- modest decline from previous level of functioning in one or more cognitive domains that does not occur only in the context of delirium and does not interfere with the person’s independence in everyday activities but may require greater efforts or the use of compensatory strategies
Neurocognitive disorder due to Alzheimer’s disease
- 60 to 80% of all cases of NCD
- person meets the criteria for major or mild NCD
- insidious onset and gradual progression of impairment in 1+ cognitive domains for mild and does not interfere with daily activities
- two or more cognitive domains that interfere with daily activities for major
- meet the criteria for probable or possible forms of Alzheimer’s
Major NCD due to Alzheimer’s
- the diagnosis of Alzheimer’s requires evidence of causative genetic mutation from genetic testing or family history
- and or evidence of decline in memory and learning in at least one other cognitive domain, steady progressive and gradual decline in cognition and no evidence of mixed etiology
Mild NCD due to Alzheimer’s
- evidence of causative genetic mutation from genetic testing or family history
- diagnosis a possible Alzheimer’s disease is given when there’s no evidence of a positive genetic mutation, but evidence in a decline of memory and learning, steady, progressive and gradual decline and cognition, and no evidence of mixed etiology
Overall Prevalence rates of Alzheimer’s disease
-higher for women
- maybe due to women living longer
- One considered age. Not clear that women have higher rates for men the same age
Alzheimer’s and race
- blacks have highest prevalence rate in incident rates
- followed by Hispanics and whites
Age and Alzheimer’s disease
- onset usually 70 to 89 years old
- early on set 49 to 59(chromosome on mutations)
Younger individuals and Alzheimer’s
- more likely to survive full course of disease
Older individuals and Alzheimer’s
- more likely to have medical comorbidities that affect the course and management of illness
Diagnosis of Alzheimer’s
- definitively confirmed only with the brain biopsy or autopsy
Brain biopsy and Alzheimer’s disease
- really done because of discomfort and risks
In vivo clinical diagnosis of Alzheimer’s
- requires the presence of characteristic symptoms as well as elimination of other explanations for symptoms
-
Eliminating alternative explanations in Alzheimer’s
- obtain information from a variety of sources including family history, physical and neurological exams, lab test, CT scans or MRIs, mental status evaluation, and neuropsychological testing
Pseudodementia
- depression that has prominent cognitive symptoms
- people usually respond well to treatment
- abrupt onset of symptoms
- exaggerate cognitive problems.
- moderate memory loss and symptoms of melancholia and anxiety
- often respond. I don’t know in response to assessment questions
Alzheimer’s versus pseudodimentia
- insidious onset
- minimize or deny cognitive problems
- severe memory impairment
- evolution and apathy
- respond to assessment questions with wrong answers
Etiology of Alzheimer’s disease
- chromosomal abnormalities
- neurotransmitter abnormalities
- brain abnormalities
Risk factors of Alzheimer’s disease
- ApoE4 variant on chromosome 19
Neurotransmitter abnormalities associated with Alzheimer’s
- reduced acetylcholine
- excessive glutamate
Both involved in learning and memory
Brain abnormalities and Alzheimer’s
- amyloid plaques
- neurofibularity tangles
- caused by buildup a proteins associated with aging but more pervasive in Alzheimer’s
-disrupt cell to cell communication
Extracellular amyloid plaques in Alzheimer’s
- clumps of beta amyloid protein which is caused by the breakdown of larger protein (amyloid precursor protein)
Interest cellular neurofibularities tangles
- abnormal accumulation of tau protein that forms threads that join to form tangles
Emily, plaques and neurofibular tangles
- first evident in medial temporal lobe structures (Entorhinial cortex, amygdala, and hippocampus)
- as disease progresses appear in frontal and parietal lobes and eventually throughout cortex
Locus coreleus and Alzheimer’s
- first area of the brain affected by Alzheimer’s disease
- shows abnormalities prior to symptoms
Neuronal loss in locus ceruleus
- linked to NCD with Larry bodies and NCD due to Parkinson’s disease
Rapper deterioration in sense of smell and Alzheimer’s
- during normal cognition predicts development of mild cognitive impairment or Alzheimer’s disease with greateral factory loss associated with greater cognitive impairment
- loss of smell is due to structural changes of the brain that are involved in olfactory processing and affected by Alzheimer’s disease
Factors associated with Alzheimer’s disease
- low education status
- obesity
- hearing loss
- down syndrome
Down syndrome and Alzheimer’s disease
- standard trisomy 21. Caused by an extra chromosome 21
- people with this disorder have an extra gene for the amyloid precursor protein gene
- amyloid accumulates in brains of people with Alzheimer’s disease in late teens to early 20s and increases the risk of early onset Alzheimer’s disease
Big 5 in Alzheimer’s disease
- high schoolers of neuroticism and low scores of conscientiousness had more deposits of amyloid in towel than people with low scores on neuroticism in high scores on conscientiousness
Average duration of Alzheimer’s disease from onset to death
- 8 to 10 years
- progression of symptoms varies
- three stages
Early stage of Alzheimer’s disease
- 2 to 4 years
- short-term memory loss (usually first symptom)
- personality changes (indifference in loss of spontaneity)
- anxiety or depression
- impaired attention and coordination
- poor judgment
- disorientation to time and space
Middle stage of Alzheimer’s
- last 2 to 10 years
- increasing short-term memory loss
- long-term memory loss
- labile mood
- irritability
- increasing disorientation
- delusions and hallucinations
- wandering and pacing
- perseveration( repetitive speech & actions)
- loss of impulse control
- impaired speech
- disruptive speech patterns
- problems with normal daily activities
- sundowning
Sundowning
- increased confusion, agitation, and restlessness in the late afternoon or evening
Late stage of Alzheimer’s
- 1 to 3 years
- severely deteriorated cognitive functioning
- severe disorientation
- apathy
- severely impaired communication
- agitation and aggression
- decreased appetite
- urinary and fecal incontinence
- loss of basic motor skills
- loss of most or all self-care skills
- abnormal reflexes
- seizures
- frequent infections
- seizures
Treatment of Alzheimer’s disease
- no cure
- treatments can temporarily reduce certain symptoms
cholinesterase inhibitors and treatment of Alzheimer’s disease
Used with memantine to reduce or stabilize memory loss, confusion, and other cognitive symptoms
Cholinesterase inhibitors
-donepezil & rivastigmine.
- delay the breakdown of ACh
Memantine
- NMDA receptor antagonist
- regulate scooter made activity
Treatments used for Alzheimer’s
- cognitive and behavioral interventions to improve cognitive functioning. Reduced problematic behaviors
- antidepressants to alleviate depression and irritability
- anxiolytics to reduce anxiety and restlessness
- antipsychotics to reduce behaviors related to maniac, psychosis, or pose a danger to self-ever others
Support skills, training and another interventions for caregivers in treating Alzheimer’s
- important
- reduced the likelihood that caregivers will place family member in nursing home
- remaining at home is associated with better patient outcome
NCD with lewy bodies
- due to a buildup of bodies in certain areas of the brain
- meet criteria major or mild NCD
- insidious, onset and gradual progression
- fluctuating cognition with variations and attention and alertness
- recurrent visual hallucinations
- symptoms of parkinsonisms that develop after cognitive symptoms
- suggest a features: symptoms of eye movement, sleep behavior disorder, and severe neuroleptic sensitivity
- for probable: two core features or one core feature in one suggested feature
- for possible: one core feature or one or both suggested features
Difference between NCD with lewy bodies and NCD due to Alzheimer’s
- Alzheimer’s: early cognitive symptoms are deficits in learning and memory
-lewy bodies: Early cognitive deficits and complex attention visual spatial and executive functions
NCD with lewy bodies and NCD due to Parkinson’s disease
- motor symptoms proceed cognitive symptoms in NCD due to parkinson’s disease
- cognitive symptoms proceed or are concurrent with motor symptoms and NCD with LB
Vascular neurocognitive disorder
- meat criteria for major or mild NCD
- symptoms are consistent when vascular ideology and suggest a temporal relationship between onset of symptoms and stroke or other cerebral vascular event
-or by prominent decline and complex attention and executive functioning and there’s evidence of a cerebral vascular disease from history exam or neuro imaging
Prognosis and course of vascular neurocognitive disorder
- depend on cause
- may involve an acute onset with partial recovery
- stepwise decline
- progressive course with fluctuations and symptoms severity and plateaus that vary in duration
Risk and causative factors of vascular neuro cognitive disorder
- hypertension
- heart disease
- diabetes mellitus
- obesity
- high cholesterol
- heavy cigarette smoking
NCD do to HIV infection
- presence of symptoms of major or mild NCD
- evidence of infection with HIV
- something was characteristic of damage to subcortical areas of the brain:
- forgetfulness
- impaired attention and concentration
- cognitive slowing
- psychomotor retardation
- clumsiness
- tremors
- apathy
- social withdrawal
NCD due to prion disease
- insidious onset followed by very rapid progression of impairment
- symptoms include motor features associated prion disease or there’s a biomarker evidence of disease (lesions on MRI)
Most common type of prion disease
-Creutzfeldt-jakob disease
CJD
- rapid progression of symptoms that meet criteria for major NCD in 6 months
- confusion and disorientation
- impaired memory and judgment
- other neuro cognitive deficits
- ataxia
-myoclonus
-chorea
- other prominent motor symptoms
- psychiatric symptoms: apathy, anxiety, and or mood swings
Types of CJD
- several types
- sporadic CJD is most common and has an unknown ideology
- familial CJD is inherited
- acquired CJD due to consuming infected or transmission during blood transfusion or other medical procedure (iatrogenic CJD)
Frontal temporal NCD
- most common cause of early onset NCD (before 65 yo)
- insidious, onset and gradual progression
- do not include significant impact on memory and learning or perceptual motor functioning, especially in early stages
- meet criteria for behavioral or language variant
Behavioral variant fronto, temporal NCD
- most common
- prominent declines in social cognition and or executive abilities plus three or more behavioral or personality symptoms
- behavioral disinhibition
- apathy and inertia
- loss of sympathy or empathy
- perseverative, stereotype, or compulsive/ ritualistic behaviors
-hyperorality
- dietary changes. (Overeating, preference for sweets)
Language variant for frontal temporal NCD
- prominent decline in language that includes deficits and speech production, word finding, object naming, grammar, or word comprehension
- aka primary progressive aphasia
Three sub types of primary progressive aphasia
- semantic: impaired comprehension of written is spoken language
- agrammatic/ non-fluent: and crack grammar and effortful, hesitant speech
-logopenic: impaired repetition of phrases and sentences, difficulty finding the right word
NCD due to another medical condition
- evidence of symptoms that are pathophysiological consequence of a medical condition.
- the course progresses in a manner that is commencement with the progress of underlying medical condition
- maybe irreversible but when medical condition is treatable may improve or not progress
Potentially reversible NCDs due to another medical condition
- hypoxia
- infections
- endocrine disorders
- normal pressure hydrocephalus
- poisoning
- nutritional eficiency
