Chapter 13, Neurocognitive Disorders, Last Exam
Genetic Factors in AD
-40% of AD patients have family history for the disease -some families exhibit pattern of inheritence that suggests possible autosomal-dominant gene transmission -some studies indicate early-onset cases are more likely than late-onset to be familial -may be link between AD and gene mutations found on chromosomes 21, 14, and 1 -mutations on chromosome 21 cause abnormal formation of APP -mutations on 14 cause abnormal presenilin 1 to be made -mutations on chromosome 1 leads to the formation of abnormal presenilin 2 -each mutation results in increased amount of the amyloid protein -individuals with down syndrome (carry an extra copy of chromosome 21) have been found to be unusually susceptible to AD -molecular and cellular pathways that may be involved include: glial cell activation, inflammation, glucose transport systems, and abnormal neuronal circuit activity -keytone bodies have a protective effect on neurons, so some researchers believe keytones will help with memory, learning, and reduce toxic proteins associated with the development of AD
Substance Witdrawal Delirium
-Withdrawal from substances can precipitate symptoms of delirium that are sufficiently severe and warrant clinical attention -alcohol -opioids -sedative-hypnotics -anxiolytics -others
NCD Impairments Incude
-abstract thinking -judgment -impulse controle -conventional rules of social conduct are often disregarded -uninhibited and inappropriate behavior -neglect of personal appearance/hygiene
NMDA Receptor Antagonist for AD
-act by blocking NMDA receptors from excessive glutamate, preventing continuous influx of calcium into the cells, and ultimately slowing down neuronal degradation. -MEMANTINE (NAMENDA) -POSSIBLE SIDE EFFECTS ARE DIZZINESS, HEADACHE, AND CONSTIPATION.
MEMANTINE (NAMENDA) KNOW THIS MED!!!
-act by blocking NMDA receptors from excessive glutamate, preventing continuous influx of calcium into the cells, and ultimately slowing down neuronal degradation. -NMDA receptor agaonist -treatment of cognitive impairment -daily dosage range is 5-20 mg -dizziness, headache, constipation are side effects
Cholinesterase Inhibitors for AD
-act by inhibiting acetylcholinesterase, which slows the degradation of acetylcholine, therby increasing concentrations of the neurotransmitter in the brain. -DONEPEZIL (ARICEPT) -RIVASTIGMINE (EXELON) -GALANTAMINE (RAZADYNE) -MOST COMMON SIDE EFFECTS ARE DIZZINESS, GI UPSET, FATIGUE, AND HEADACHE.
DONEPEZIL (ARICEPT) KNOW THIS MED, LOOK OVER ARICEPT HANDOUT!!!
-act by inhibiting acetylcholinesterase, which slows the degradation of acetylcholine, therby increasing concentrations of the neurotransmitter in the brain. -cholinesterase inhibitor -treats cognitive impairment -daily dosage range is 5-10 mg -side effects include: insomnia, gi upset, dizziness, and headache -A RICE PT
Delirium Symptom Resolution
-age of patient and duration of delirium influence rate of symptom resolution -once underlying cause is eliminated, symptoms usually diminish in 3-7 days, but could take up to 2 weeks
Mild NCD
-also known as mild cognitive impairment -critical because can be a focus of early intervention to prevent or slow progression of the disorder.
Lorazepam (Ativan)
-antianxiety/benzodiazepine -for anxiety -1-2mg daily dosage range -side effects include drowsiness, dizziness, GI upset, hypotension, tolerance, and dependence
Haloperidol (Haldol)
-antipsychotic -used for aggitation, aggression, hallucinations, thought disturbances, and wandering -daily dosage range is 1-4mg, increase dosage cautiously -side effects include dry mouth, blurred vision, orthostatic hypotension, EPS, and sedation
NCD Progression
-apraxia may develop -may be irritable, moody, or exibit sudden outbursts over trivial issues -ability to work/care for individual needs will no longer be possible -cannot be left alone because they can't comprehend thier limitations, leaving them AT RISK FOR INJURY -wandering becomes a problem (might look for bathroom and think the door to outside is the door for the bathroom)
Delirium Symptom Onset
-begin abrubtly (head injury or seizure) -may be preceded by several hours/days of prodromal symptoms (restlessness, difficulty thinking cleary, insomnia or hypersomnolence, and nightmares) -slower onset of symptoms more common if underlying cause is systemic illness or metabolic imbalance
NCD Stage 2: Forgetfulness
-begins to lose things and forgets names -losses in short-term memory are common -individual aware of intellectual decline and may feel ashamed, become anxious or depressed, and in turn worsen symptom -maintaining and organizing with lists and a atructured routine provide some compensation -SYMPTOMS OFTEN NOT OBSERBED BY OTHERS
Vascular Neurocognitive Disorder Etiology
-blood flow to brain is impaired, progressive intellectual deterioration occurs -impairment may occur in large vessels or microvascular networks, so symptoms may vary due to type, extent, and locaton of vascular lesion -hypertension leads to the lining of blood vessels being damaged -can rupture with subsequent hemorrhage or an accumulation of fibrin in the vessels with intravascular clotting and inhibitied blood flow -particulate matter traveling through the bloodstream gets to the brain and causes infarcts -can be clots, cellular debris, air, nitrogen, and fat from soft tissue trauma or fracture of long bones (so clots can be solid, gaseous, or liquid) -CLIENTS CAN HAVE BOTH VASCULAR NCD AND AD AT THE SAME TIME, REFERRED TO AS MIXED DISORDER.
Neurocognitive Disorder Due to HIV Infection
-called HIV-1 associated cognitive/motor complex, less severe form known as HIV-1 associated minor cognitive/motor disorder -severity of symptoms is related to brain pathology -immune dysfunction from HIV can lead to brain infections -HIV-1 causes NCD directly -neuropsychiatric symptoms of early stages manifest as: barely perceptible changes in person's normal psychological presentation -later stages include: severe cognitive changes, PARTICULARLY CONFUSION, behavior changes, and possible psychoses -HAART, or highly active antiretroviral therapies, have caused declines in the incidence rates of NCD due to HIV infection
Neurocognitive Disorder (NCD)
-can be mild or major -distinction made by severity of symptoms
Psychomotor Activity in Delirium
-can fluctuate between agitation, purposeless movements (restlessness, hyperactivity, striking out at nonexistent objects), and vegetative state that resembles catatonic stupor -various forms of tremors are frequently present
Substance or Medication Induced Neurocognitive Disorder
-can occur from substance reaction, overuse, or abuse -symptoms consistent with major or mild neurocognitive disorder and persist beyond usual duration of intoxication and acute withdrawal -associated substances include: alcohol, sedatives, hypnotics, anxiolytics, and inhalants -drugs that cause anticholinergic side effects and toxins like lead or mercury have also been implicated
NCD Due to AD
-characterized by mild/major NCD and 7 stages -symptom onset is slow and insidious -course is generally progressive and deteriorating -MEMORY IMPAIRMENT IS AN EARLY AND PROMINENT FEATURE
Vascular Neurocognitive Disorder
-cognitive symptoms due to cerebrovascular disease -2ND MOST COMMON FORM, FIRST IS AD -different than AD because it has more abrubt onset and runs a highly variable course -progression occurs in steps rather than gradual deterioration, so SYMPTOMS MAY SEEM TO CLEAR UP AT TIMES AND INDIVIDUAL MAY EXHIBIT FAIRLY LUCID THINKING -MEMORY MAY SEEM BETTER AT THESE TIMES AND CLIENT MAY THINK THEY ARE IMPROVING UNTIL FURTHER DECLINE STARTS -causes intense anxiety for client with this disorder -may suffer from small strokes, destroying many areas of the brain, so parts of the brain affected will be displayed by symptoms -COMMON FOCAL NEUROLOGICAL SIGNS SEEN ARE WEAKNESS OF THE LIMBS, SMALL-STEPPED GAIT, DIFFICULTY WITH SPEECH, AND MORE COMMON IN MEN.
S/S of Delirium
-difficulty sustaining and shifting attention -extremely distractable -needs constant reminders to focus attention -disorganized thinking that is reflected by rambling, irrelevant, pressured, or incoherent speech that switches from subject to subject -impaired reasoning and goal-directed behavior -disoriented to time and place (common) -recent memory impairment -misperception of enviroment like illusions (THINK IV IS A SNAKE) and hallucinations -distubances in sleep
Delirium Due to Another Medical Conditon/Mutiple Etiologies
-evidence from history/physical examination or laboratory findings may suggest symptoms of delirium are associated with another condition or attributed to more than 1 cause -DELIRIUM IS USUALLY RESULT OF MANY FACTORS, RATHER THAN ONE
Etiology of AD
-exact cause is unkown -may be genetic mutations -believed that there are multiple factors instead of 1 cause that influence the development of AD (neurotransmitter alterations, plaques and tangles, head trauma, and genetic factors)
Emotional Instability Manifestations in Delirium
-fear, anxiety, depression, irritability, anger, euphoria, or apathy -emotions may be eveidenced by crying, calls for help, cursing, muttering, moaning, self-destructive acts, fearful attempts to flee, and attacking others that are thought to be threatening
Treatment of Delirium
-first step is determining and correcting underlying causes. -additional attention to fluid and electrolyte status, hypoxia, anoxia, and diabetic problems -STAFF SHOULD REMAIN WITH CLIENTS AT ALL TIMES TO MONITOR BEHAVIOR AND PROVIDE REORIENTATION AND ASSURANCE -room should maintain low level of stimuli
Nuerocognitive Disorder Due to Huntington's Disease
-huntington's is transmitted as mendelian dominant gene -damage seen in areas of basal ganglia and cerebral cortex -onset of symptoms occur between age 30-50 and include: involuntary twitching of limbs/facial muscles, mild cognitive changes, depression, and apathy -client usually declines into profound state of cognitive impairment and ataxia -average durationis based on age at onset -one study concluded that juvenile and late onset have the shortest duration, median was 21.4 years
Neurocognitive Disorder Due to Another Medical Condition
-hypothyroidism -hyperparathyroidism -pituitary insufficiency -uremia -encephalitis -brain tumor -pernicious anemia -thiamine deficiency -pellagra -uncontrolled epilepsy -cardiopulmonary insufficiency -fluid and electrolyte imbalance -CNS and systemic infections -SLE -MS
Neurocognitive Disorder Due to Prion Disease
-identified by insidious onset, rapid progression, and manifestations of motor features of prion disease such as MYOCLONUS, ATAXIA, AND BIOMARKER EVIDENCE -small percent have genetic component -clinical presentation is typical of the syndrome of mild or major NCD, along with involuntary movements, muscle rigidity, and ataxia -symptoms may develop at any age in adults, but typically between 40-60 -course is extrememly rapid and prgression from diagnosis to dealth occurs in less than 2 years -most common form of prion disease in humans is Creutzfeldt-Jakob disease
Nuerocognitive Disorder Due to Traumatic Brain Injury
-impact/movement/displacement of brain in skull with one or more of the following: loss of consciousness, posttraumatic amnesia, disorientation and confusion, or neurological signs -AMNESIA IS MOST COMMON NEUROBEHAVIORAL SYMPTOM FOLLOWING HEAD TRAUMA. -other symptoms: confusion of changes in speech, vision, or personality. -symptoms may subside or become permanent -repeated head trauma (boxing) can result in dementia pugilistica
Head Trauma and AD
-individual's with history of head trauma are at risk for AD -some individuals that experienced head trauma subsequently (after years) developed AD -increased risk to develop AD in individuals with genetic predisposition and head trauma injury
Predisposing Factors for Delirium
-individuals with serious medical, surgical, or neurological conditions fall into the group that is most predisposed -individuals over 65 considered high-risk group
NCD Stage 3: Mild Cognitive Decline
-interference with work performance, which BECOMES NOTICEABLE by coworkers -may get lost while driving -concentration may be interrupted -difficulty recalling names or words, which BECOMES NOTICEABLE to family and close associates -decline occurs in ability to plan and organize
NCD Stage 5: Moderate Cognitive Decline
-lose ability to perform some ADL's INDEPENDENTLY (hygiene, dressing, grooming) -may forget addresses, phone numbers, and names of close relatives -may become DISORIENTED TO PLACE AND TIME, but maintain knowledge about themselves -frustration, withdrawal, and self-absorption are common
Neurocognitive Disorder Due to Parkinson's Disease
-loss of nerve cells located in substantia nigra, and dopamine activity is decreased, resulting in involuntary muscle movements, slowness, and rigidity -TREMOR IN UPPER EXTREMETIES IS CHARACTERISTIC
Personality Changes in NCD
-manifested by either alteration or accentuation of premorbid characteristics -previously socially active may be apathetic and socially isolated -previously neat person may become untidy in their appearance -individual who had difficulty trusting others may become extremely fearful and paranoid as manifestations of the disorder
NCD Stage 6: Moderate to Severe Cognitive Decline
-may be unable to recall major recent life events or even name of spouse -disoriented to surroundings is common -may not be able to recall day, season, or year -UNABLE TO MANAGE ADL'S WITHOUT ASSISTANCE -INCONTINENCE IS COMMON -sleeping becomes a problem -start WANDERING -start showing obsessiveness, agitation, and aggression -sundowning occurs -loss of language skills makes COMMUNICATING HARDER -INSTITUTIONAL CARE USUALLY NEEDED AT THIS STAGE
NCD Stage 4: Mild to Moderate Cognitive Decline
-may forget major events in personal history (their own or thier child's birthday) -may experience declining ability to do tasks (shopping or managing personal finances) -may be unable to understand current news events -may deny problem exists by COVERING UP MEMORY LOSS WITH CONFABULATION -depression and social withdrawal are common
NCD Language Impairments
-may or may not be affected -may have difficulty naming objects -language may seem vague and imprecise -aphasia in severe forms of NCD -may know needs but unable to communicate them to caregiver
Delirium State of Awareness
-may range from hypervigilance to stupor or coma -sleep can fluctuate from hypersomnolence to insomnia -vivid dream and nightmares are common
Medication Induced Delirium
-medications have been known to precipitate delirium -anticholinergics -antihypertensives -corticosteroids -anticonvulsants -cardiac glycosides -analgesics -anesthetics -antineoplastic agents -antiparkinson drugs -h2 receptor antagonists (CIMETIDINE) -and others
NCD Predisposing Factors
-neurocognitive disorder due to alzheimer's disease -vascular neurocognitive disorder -frototemporal neurocognitive disorder -neurocognitive disorder due to traumatic brain injury -neurocognitive disorder due to lewy body dementia -neurocognitive disorder due to parkinson's disease -neurocognitive disorder due to HIV infection -substance-induced neurocognitive disorder -neurocognitive disorder due to huntington's disease -neurocognitive disorder due to prion disease -neurocognitive disorder due to another medical condition -neurocognitive disorder due to multiple etiologies -unspecified neurocognitive disorder
NCD Stage 1: No Apparent Symptoms
-no apparent decline in memory despite changes occuring in the brain
NCD Clinical Findings
-occuring because more people are surviving into high risk period for NCD, which is middle age and beyond -survival after diagnosis is usually 3-12 years with most time spent in severest stage -primary NCD is like AD, where NCD itself is the major sign of some organic brain disease not directly related to any other organic illnesses. -secondary NCD are caused by or related to another disease or condition such as HIV or cerebral trauma
Plaques and Tangles in AD
-overabundance found in brains of individuals with AD -plaques are made up of a protein called amyloid beta, which are fragments of a larger protein called amyloid precursor protein (APP) -plaques form whenfragments clump together and mix with molecules and other cellular matter -tangles are formed from a special kind of cellular protein, called tau protein, whose function is to provide stability to the neuron. In AD, the tau protein is chemically altered. -strands of the protein become tangled together, interfering with the neuronal transport system -not known if plaques and tangles cause AD or if they are a consequence of AD -thought that they contribute to destruction and death of neurons, leading to memory failure, personality changes, inability to carry out ADL's, and other features of AD -number and density of senile plaques (also called amyloid plaques) in postmortem studies is correlated with severity of AD.
Major NCD
-previously known as dementia -the two diagnosis may be used to identify earlier and late stages of same disease
Advanced Dementia
-profound memory deficits -minimal verbal communication -loss of ambulatory ability -inability to perform ADL's -incontinent -MOST COMMON COMPLICATIONS ARE EATING PROBLEMS AND INFECTIONS
Neurocognitive Disorder Due to Lewy Body Dementia
-progresses more rapidly than AD -earlier appearance of visual hallucinations and parkinsonian features -delusions and depression are common symptoms -Robin Williams had this disorder -lewy bodies or eosinophilic inclusion bodies are seen in the cerebral cortex and brainstem
Neurotransmitter Alterations in AD
-research indicates the enzyme required to produce acetylcholine is dramatically reduced -reduction seems to be greates in nucleua basalis of inferior medial forebrain -decrease of acetylcholine reduces amount of neurotransmitter that is released to cells in the cortex and hippocampus, resulting in disruption of cognitive process -other neurotransmitters implicated in the pathology and clinical symptoms of AD include: norepinephrine, serotonin, dopamine, and the amino acid glutamate -excess glutamate leads to overstimulation of the NMDA receptor, which causesincreased intracellular calcium and neuronal degeneration and cell death -decreased levles of somatostatin and corticotropin have also been found in individuals with AD.
Medication Therapy in Delirium
-some physicians diagress to medications reasoning additional agents may only compound the syndrome of brain dysfunction -psychosis with aggitation and aggresion may require chemical and/or physical restraint for patient's safety -choice of therapy made from clinical condition and underlying cause of delirium -low dose antipsychotics most common -Haloperidol (Haldol) commonly used for psychotic features. MONITOR CARDIAC STATUS BECAUSE IT CAN PROLONG QT INTERVAL IN HEART AND CAUSE DEATH FROM METABOLIC/KIDNEY ISSUES (KNOW THIS BECAUSE LILA SAID AVOID USING ANTIPSYCHOTICS FOR THESE REASONS!!!). -benzodiazepine like Lorazepine (Ativan) for substance withdrawal
Substance Intoxiaction Delirium
-symptoms attributed to intoxication from certain substances -alcohol -ampphetamines -cannabis -cocaine -hallucinogens -inhalants -opioids -phencyclidine -sedative -hypnotic -anxiolytics -other or unknown substances
Frontotemporal NCD
-symptoms occur as a result of shrinking of the frontal and temporal anterior lobes of the brain -IDENTIFIED AS PICK'S DISEASE -cause is unknown, but genetic factors appear to be involved -symptoms fall into two clinical patterns -1. behavior and personality changes -common behavior changes: increasingly innapropriate actions, lack of judgment and inhibition, and repetitive compulsive behavior. -2. speech and language problems -loss of speech -increasing difficulty using and understanding written/spoken language -DISEASE PROGRESSES STEADILY AND OFTEN RAPIDLY, RANGING FROM 2-10 YEARS.
Conditions Precipitating Delirium
-systemic infections -febrile illness (KIDS) -metabolic disorder (electrolyte imbalance, hypercarbia, hypoglycemia) -hypoxia and COPD -hepatic/renal failure -head trauma -seizures -migraine headaches -brain abscess/neoplasm -stroke -nutritional deficiency -uncontrolled pain -burns -heat stroke -orthopedic/cardiac surgeries -social isolation
Autonomic Manifestations in Delirium
-tachycardia, sweating, flushed face, dilated pupils, elevated blood pressure (fight or flight)
NCD Stage 7: Severe Cognitive Decline
-unable to recognize family members -most commonly bedfast and aphasic -problems of immobility occur like cubiti and contractures -muscles are rigid -primitive reflexes may be present -may have very active hands, grunting, and other vocalizations -depressed immune system (PLUS DECREASED IMMOBILITY COULD LEAD TO PNEUMONIA, UTI, SEPSIS, AND PRESSURE ULCERS) -decreased appetite and present dysphagia (ASPIRATION) -weight loss generally occurs -most ADL's need DONE BY CAREGIVER -spend a lot of time dozing -appears socially withdrawn and more unaware of enviroment/surroundings -DEATH MAY BE CAUSED FROM INFECTIONS, SEPSIS, OR ASPIRATION.
Delirium Symptom Duration
-usually breif -1 week -rarley more than 1 month
Assessment-Client History
-what age symptoms began -what symtpoms they have 1.need to know type, frequency, and occurences of mood swings, personality and behavior changes, and catastrophic emotional reactions 2. cognitive changes, such as problems with attention span, thinking process, problem solving, and memory (recent and remote) 3. language difficulties 4. orientation to person, place, time, and situation 5.apprpriateness of social behavior -info on past and current meds -history of drug or alcohol use -possible exposures to toxins -family history of diseases
Outcome Criteria
1. has not experience physical injury. 2. Has not harmed self or others. 3. maintains reality orientation to the best of his or her capability. 4. Is able to communicate with cosistent caregiver. 5. Fullfills ADL's with assisstance or for client who is unable to ensure needs are met. 6. Discusses positive energy aspects about self and life.
Assesment-Physical
1. signs of damage to the nervous system 2. evidence of diseases of other organs that could affect mental function.
Mild NCD Comparison
A. evidence of MODEST cognitive decline from previous level of performance in 1 or more cognnitive domains (complex attention, executive function, learning and memory, language, perceptual-motor, or social cognition) based on: -concern of individual, a knowledgeable informant, or clinician that there has been a mild decline in cognitive function -and, a modest impairment in cognitive performance, preferably documented by standardized neuropsychological testing, or, in its absence, another quantified clinical assessment. B. cognitive deficits DON NOT INTERFERE with capacity for independence in everyday activities (complex instrumental activities of daily living such as paying bills or managing medications are preserved, but greater effort, compensatory strategies, or accomodation may be required). C. cognitive deficits do not occur exclusively in the context of a delirium. D. cognitive deficits are not better explained by another mental disorder (MD or schizophrenia). Specify what diagnosis it is due to. Also, specify if it is with or without behavior disturbance. -without if the cognitive disturbance is not accompanied by any clinically significant behavior disturbance -with if it is and specify disturbance (pyschotic symptoms, mood disturbance, agitation, apathy, or other behavior symptoms)
Major NCD Comparison
A. evidence of SIGNIFICANT cognitive decline from previous level of performance in 1 or more cognnitive domains (complex attention, executive function, learning and memory, language, perceptual-motor, or social cognition) based on: -concern of individual, a knowledgeable informant, or clinician that there has been a mild decline in cognitive function -and, a modest impairment in cognitive performance, preferably documented by standardized neuropsychological testing, or, in its absence, another quantified clinical assessment. B. the cognitive deficits DO INTERFERE with independence of everyday activities (at a minimum, REQUIRING ASSISTANCE with complex instrumental activities of daily living such as paying bills and managing medications) C. cognitive deficits do not occur exclusively in the context of a delirium. D. cognitive deficits are not better explained by another mental disorder (MD or schizophrenia). Specify what diagnosis it is due to. Specify if it is with or without behavior disturbance. -without if the cognitive disturbance is not accompanied by any clinically significant behavior disturbance -with if it is and specify disturbance (pyschotic symptoms, mood disturbance, agitation, apathy, or other behavior symptoms) ALSO SPECIFY CURRENT SEVERITY -mild: difficulties with instrumental activities of daily living (housework or managing money) -moderate: difficulties with basic activities of daily living (feeding and dressing) -severe: fully dependent
Aphasia
Condition where person does not speak at all.
1. Delirium
Delirium is a mental state characterized by an acute disturbance of cognition, which is manifested by short-term confusion, excitement, disorientation, and a clouding of consciousness. Hallucinations and illusions are common.
ATaxia
Muscular incoordination. (T-taxi driver can still drive, but not very well)
Pseudodementia
Symptoms of depression that mimic those of neurocognitive disorder.
Neurocognitive
Term used to describe cognitive functions closely linked to particular areas of the brain that have to do with thinking, reasoning, memory, learning, and speaking.
APraxia
The inability to carry out motor activities despite intact motor funtion. (taxi driver has a car, but police didn't like driving so they took license)
Reversible/Temporary NCD
can occur as a result of -cerebral lesions -depression -side effects of certain medications -normal pressure hydrocephalus -vitamin or nutritional deficiencies (especially b12 of folate) -CNS infections -metabolic disorder -THIS OCCURS IN A SMALL PERCENT -MOST NCD CLIENTS WILL RUN A PROGRESSIVE AND IRREVERSABLE COURSE
Confabulation
creating imaginary events to fill in memory gaps
Hypersomnolence
excessive sleeping
Precipitating Factors of Delirium
geriatric patients with syndromes such as -dementia -depression -falls -elder abuse
Hypervigilance
heightened awareness to enviromental stimuli
Sundowning
symptoms worsen in late afternoon and evening
Dementia Pugilistica
syndrome characterized by emotional lability, dysarthria, ataxia, and impulsivity
Aphasic
unable to communicate by speech, writing, or signs
