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394 Cards in this Set
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Definie Delirium and list subcategories
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Delirium is marked by short-term confusion and changes in cognition. There are four subcategories based on several causes: (1) general medical condition (e.g., infection); (2) substance induced (e.g., cocaine, opioids, phencyclidine [PCP]); (3) multiple causes (e.g., head trauma and kidney disease); and (4) delirium not otherwise specified
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Describe dementia and list subcategories
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Dementia is marked by severe impairment in memory, judgment, orientation, and cognition. The six subcategories are (1) dementia of the Alzheimer's type, which usually occurs in persons over 65 years of age and is manifested by progressive intellectual disorientation and dementia, delusions, or depression; (2) vascular dementia, caused by vessel thrombosis or hemorrhage; (3) other medical conditions (e.g., human immunodeficiency virus [HIV] disease, head trauma, Pick's disease, Creutzfeldt-Jakob disease, which is caused by a slow-growing transmittable virus); (4) substance induced, caused by toxin or medication (e.g., gasoline fumes, atropine); (5) multiple etiologies; and (6) not otherwise specified (if cause is unknown).
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Describe Amnestic Disorder and subcategories
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Amnestic disorder is marked by memory impairment and forgetfulness. The three subcategories are (1) caused by medical condition (hypoxia); (2) caused by toxin or medication (e.g., marijuana, diazepam); and (3) not otherwise specified.
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What diagnosis would Mild Neurocognitive disorder fit under?
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Cognitive Disorder Not Otherwise Specified
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What would postconcussional disorder fit under?
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Cognitive Disorder Not Otherwise Specified
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What info in cognitive disorders do you want?
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Sx
Changes in daily routines premorbid fxn important pursuits goal: obtain baseline and impact of illness |
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What domains of cognition should be tested?
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Attention,
Memory Visuospatial and construction ability Reading, Writing, Math Abstraction |
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Give details of cognitive portion of MSE
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Cognition
Memory Spontaneous (as evidenced during interview) Tested (incidental, immediate repetition, delayed recall, cued recall, recognition; verbal, nonverbal; explicit, implicit) Visuospatial skills Constructional ability Mathematics Reading Writing Fine sensory function (stereognosis, graphesthesia, two-point discrimination) Finger gnosis Right-left orientation “Executive functions” Abstraction |
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Tests to order with cognitive disorder?
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Complete blood cell count
Electrolytes Blood urea nitrogen and serum creatinine Liver function tests Serum protein Erythrocyte sedimentation rate Glucose Serum calcium and phosphorus Thyroid function tests Levels of all drugs Urinalysis Pregnancy test for women of childbearing age Electrocardiography |
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What might be ancillary lab tests to consider in cognitive disorders by?
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Blood
Blood cultures Rapid plasma reagin test Human immunodeficiency virus (HIV) testing (enzyme-linked immunosorbent assay [ELISA] and Western blot) Serum heavy metals Serum copper Ceruloplasmin Serum B12, red blood cell (RBC) folate levels Urine Culture Toxicology Heavy metal screen Electrography Electroencephalography Evoked potentials Polysomnography Nocturnal penile tumescence Cerebrospinal fluid Glucose, protein Cell count Cultures (bacterial, viral, fungal) Cryptococcal antigen Venereal Disease Research Laboratory test Radiography Computed tomography Magnetic resonance imaging Positron emission tomography Single photon emission computed tomography |
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EEG ... high sensitivity or specificity?
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sensitivity
DDX to mild delirium = Space Occupying Lesion Complex Partial Seizures (conscious but impaired) Metabolic, Toxic States |
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Which patients need CT more than MRI?
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acuture cerebral hemorrhages
hematomas |
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What can MRI help clarify?
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white mater abnormalities with MS or HIV or older patients with HTN, Dementia, Dementia of Alzheimers type
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Delirium is defined by
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the acute onset of fluctuating cognitive impairment and a disturbance of consciousness.
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Approximately ? percent of medically ill patients who are hospitalized exhibit delirium.
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10 to 30%
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High risk groups for delirium?
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Severe Burns (20%)
Surgical ICU's (30%) Cardiac Units (30%) AIDS (30 to 40% Hip # (40 to 50%) Terminally ill (80%) |
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The highest rate of delirium is found in ? patients, more than ? percent in some studies.
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The highest rate of delirium is found in postcardiotomy patients, more than 90 percent in some studies.
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The causes of postoperative delirium include :
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the stress of surgery,
postoperative pain, insomnia, pain medication, electrolyte imbalances, infection, fever, and blood loss |
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Risk factor for delirium?
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advanced age
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Approximately ? percent of hospitalized patients older than age 65 have an episode of delirium, and another ? percent of elderly persons exhibit delirium on admission to the hospital.
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Approximately 30 to 40 percent of hospitalized patients older than age 65 have an episode of delirium, and another 10 to 15 percent of elderly persons exhibit delirium on admission to the hospital.
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Of nursing home residents over age 75, ? percent have repeated episodes of delirium
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60%
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Predisposing factors for the development of delirium are:
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predisposing factors for the development of delirium are preexisting brain damage (e.g., dementia, cerebrovascular disease, tumor), a history of delirium, alcohol dependence, diabetes, cancer, sensory impairment (e.g., blindness), and malnutrition
Male gender is an independent risk factor for delirium according to DSM-IV-TR. |
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The 3-month mortality rate of patients who have an episode of delirium is estimated to be ? percent
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23 to 33%
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The 1-year mortality rate for patients who have an episode of delirium may be as high as ? percent
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50%
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Elderly patients who experience delirium while hospitalized have a ? percent mortality rate during that hospitalization. After discharge, up to X percent of these persons die within a 1-month period, and ? percent die within 6 months.
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Elderly patients who experience delirium while hospitalized have a 20 to 75 percent mortality rate during that hospitalization. After discharge, up to 15 percent of these persons die within a 1-month period, and 25 percent die within 6 months.
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The major causes of delirium are
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central nervous system disease (e.g., epilepsy), systemic disease (e.g., cardiac failure), and either intoxication or withdrawal from pharmacological or toxic agents
Drugs Infections Metabolic (systemic, cardiac disease) Structural (head lesion, CNS ds) |
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Key factor to look into cause of delirium?
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any drug patient has taken
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Core features of delirium?
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he core features of delirium include altered consciousness, such as decreased level of consciousness; altered attention, which can include diminished ability to focus, sustain, or shift attention; impairment in other realms of cognitive function, which can manifest as disorientation (especially to time and space)
and decreased memory; relatively rapid onset (usually hours to days); brief duration (usually days to weeks); and often marked, unpredictable fluctuations in severity and other clinical manifestations during the course of the day, sometimes worse at night (sundowning), which may range from periods of lucidity to severe cognitive impairment and disorganization. |
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EEG patttern in delirium?
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The electroencephalogram (EEG) usually shows diffuse slowing of background activity,
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EEG pattern in delirium caused by etoh/sedative withdrawal?
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although patients with delirium caused by alcohol or sedative-hypnotic withdrawal have low-voltage fast activity.
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The major neurotransmitter hypothesized to be involved in delirium is ?, and the major neuroanatomical area is the ?.
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The major neurotransmitter hypothesized to be involved in delirium is acetylcholine, and the major neuroanatomical area is the reticular formation.
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The reticular formation of the brainstem is the principal area regulating attention and arousal; the major pathway implicated in delirium is the ?pathway, which projects from the ? to the ? and ?.
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The reticular formation of the brainstem is the principal area regulating attention and arousal; the major pathway implicated in delirium is the dorsal tegmental pathway, which projects from the mesencephalic reticular formation to the tectum and thalamus.
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Several studies have reported that a variety of delirium-inducing factors result in ? (increased or decreased) acetylcholine activity in the brain
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decreased
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One of the most common causes of delirium is toxicity from
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too many prescribed medications with anticholinergic activity.
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Mechanism of alcohol withdrawal delirium?
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In particular, the delirium associated with alcohol withdrawal has been associated with hyperactivity of the locus ceruleus and its noradrenergic neurons.
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Along with Acetylcholine, other NT's involved?
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Other neurotransmitters that have been implicated are serotonin and glutamate.
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Workup of delirious patient?
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Full physical
Bloowork: Standard + Vascular: EEG, Chest Xray Infectious: CBC/diff: Syphilis, HIV, Urine Neoplam: Head CT, LP Drugs: Pharmanet, Urine Tox Screen Idiopathic Cardio/Congenital Auto-immune: ESR Trauma: CT Endo: TSH, Ca, Mg, P04, Metabolic: B12, Folic Acid, Ferritin Cardiac: |
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In delirium, the EEG characteristically shows a ?and may be useful in differentiating delirium from depression or psychosis
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In delirium, the EEG characteristically shows a generalized slowing of activity and may be useful in differentiating delirium from depression or psychosis
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The EEG of a delirious patient sometimes shows focal areas of ?
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The EEG of a delirious patient sometimes shows focal areas of hyperactivity
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In rare cases, it may be difficult to differentiate delirium related to ? from delirium related to other causes.
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epilepsy
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The major differential points between dementia and delirium are the
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time to development of the condition and the fluctuation in level of attention in delirium compared with relatively consistent attention in dementia
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Compare delirium and dementia
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1. The time to development of symptoms is usually short in delirium and, except for vascular dementia caused by stroke, it is usually gradual and insidious in dementia.
2. Although both conditions include cognitive impairment, the changes in dementia are more stable over time and, for example, usually do not fluctuate over the course of a day 3. A patient with dementia is usually alert; a patient with delirium has episodes of decreased consciousness. |
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Delirium vs Dementia
1. Attention 2. Memory 3. Speech 4. Sleep-wake cycle 5. Thoughts 6. Awareness 7. Alertness |
Onset Slow Rapid
Duration Months to years Hours to weeks Attention Preserved Fluctuates Memory Impaired remote memory vs Impaired recent and immediate memory Speech Word-finding difficulty vs Incoherent (slow or rapid) Sleep–wake cycle Fragmented sleep vs Frequent disruption (e.g., day–night reversal) Thoughts Impoverished vs Disorganized Awareness Unchanged vs Reduced Alertness Usually normal vs Hypervigilant or reduced vigilance |
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Delirium vs Sz ... compare
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1. In general, however, the hallucinations and delusions of patients with schizophrenia are more constant and better organized than those of patients with delirium.
2. Patients with schizophrenia usually experience no change in their level of consciousness or in their orientation. |
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Delirium vs depression?
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Patients with hypoactive symptoms of delirium may appear somewhat similar to severely depressed patients, but they can be distinguished on the basis of an EEG.
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DDX of delirium
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Brief Psychotic Disorder
Schizophreniform Disorder Dissociative Disorder |
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Delirium prodrome? duration?
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lthough the onset of delirium is usually sudden, prodromal symptoms (e.g., restlessness and fearfulness) can occur in the days preceding the onset of florid symptoms. The symptoms of delirium usually persist as long as the causally relevant factors are present, although delirium generally lasts less than a week.
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How long after causative factors removed does it take for delirium symptoms to resolve?
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After identification and removal of the causative factors, the symptoms of delirium usually recede over a 3- to 7-day period, although some symptoms may take up to 2 weeks to resolve completely.
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Recall of delirium?
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Recall of what transpired during a delirium, once it is over, is characteristically spotty; a patient may refer to the episode as a bad dream or a nightmare only vaguely remembered.
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Treatment of delirium?
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1. Tx underlying cause
2. Tx anticholinergic toxicity with physostigmine 3. Environmental Support - don't deprive but not overly stimulate - regular sitter |
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Delirium risk with eye patch?
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Delirium can sometimes occur in older patients wearing eye patches after cataract surgery (“black-patch delirium”). Such patients can be helped by placing pinholes in the patches to let in some stimuli or by occasionally removing one patch at a time during recovery.
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Which two major sx of delirium require treatment usually?
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Psychosis and Insomnia
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Treatment of delirium related psychosis?
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Typical or atypical (usually haldol in books); locally use loxapine or po risperidone
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Dosing regime for antipsychotics in delrium?
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Two daily doses:
2/3's of dose at bedtime 1/3 earlier |
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What agent to use with delirious patient with parkinsonian sx?
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clozapine or quetiapine
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how treat delirium related insomnia?
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lorazepam 1 to 2mg at bedtime
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when is rare situation when you would use longer half life benzo?
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alcohol withdrawal
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Delirium caused by severe pain?
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opioid
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Delirium with parkinson's ... how to best manage?
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If the antiparkinsonian agents cannot be further reduced, or if the delirium persists after attenuation of the antiparkinsonian agents, clozapine is recommended
quetiapine other agent to consider |
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Dementia is defined as a
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progressive impairment of cognitive functions occurring in clear consciousness (i.e., in the absence of delirium)
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Essential features of dementia?
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Global impairment of intellect is the essential feature, manifested as difficulty with memory, attention, thinking, and comprehension
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Approximately ? percent of people with dementia have reversible illnesses if treatment is initiated before irreversible damage takes place.
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15%
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The prevalence of moderate to severe dementia in different population groups is approximately ?percent in the general population older than 65 years of age, ? percent in the general population older than 85 years of age, ? percent in outpatient general medical practices, and ? percent in chronic care facilities.
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The prevalence of moderate to severe dementia in different population groups is approximately 5 percent in the general population older than 65 years of age, 20 to 40 percent in the general population older than 85 years of age, 15 to 20 percent in outpatient general medical practices, and 50 percent in chronic care facilities.
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Of all patients with dementia, ?percent have the most common type of dementia, dementia of the ?
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Of all patients with dementia, 50 to 60 percent have the most common type of dementia, dementia of the Alzheimer's type (Alzheimer's disease)
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For persons aged 65 years, men have a prevalence rate of ? percent and women of ? percent. At age 90, rates are ? percent
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For persons aged 65 years, men have a prevalence rate of 0.6 percent and women of 0.8 percent. At age 90, rates are 21 percent
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over 65, who has more dementia men or women?
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The rates of prevalence (males to females) are 11 and 14 percent at age 85, 21 and 25 percent at age 90, and 36 and 41 percent at age 95.
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The second most common type of dementia is ?
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vascular dementia, which is causally related to cerebrovascular diseases.
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What predisposes a person to dementia?
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HTN
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Approximately ?percent of patients have coexisting vascular dementia and dementia of the Alzheimer's type.
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Approximately 10 to 15 percent of patients have coexisting vascular dementia and dementia of the Alzheimer's type.
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The most common causes of dementia in individuals older than 65 years of age are ?
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(1) Alzheimer's disease; (2) vascular dementia and, (3) mixed vascular and Alzheimer's dementia.
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List common reversible dementias?
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Many types of dementias evaluated in clinical settings can be attributable to reversible causes, such as metabolic abnormalities (e.g., hypothyroidism), nutritional deficiencies (e.g., vitamin B12 or folate deficiencies), or dementia syndrome caused by depression.
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Some studies have indicated that as many as ? percent of patients have a family history of dementia of the Alzheimer's type
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40%
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Factors supporting genetic factor in Alzheimers?
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concordance rate for monozygotic twins, which is higher than the rate for dizygotic twins (43 percent vs. 8 percent, respectively). In several well-documented cases, the disorder has been transmitted in families through an autosomal dominant gene, although such transmission is rare. Alzheimer's type dementia has shown linkage to chromosomes 1, 14, and 21.
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What protein associated with Alz?
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amyloid protein
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Gene associated with Alz? give factor rate for gene and risk of alz? is genetic testing recommended?
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E4 ..
eople with one copy of the gene have Alzheimer's disease three times more frequently than do those with no E4 gene, and people with two E4 genes have the disease eight times more frequently than do those with no E4 gene Diagnostic testing for this gene is not currently recommended because it is found in persons without dementia and not found in all cases of dementia. |
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The classic gross neuroanatomical observation of a brain from a patient with Alzheimer's disease is
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diffuse atrophy with flattened cortical sulci and enlarged cerebral ventricles.
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The classic and pathognomonic microscopic findings are
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senile plaques, neurofibrillary tangles, neuronal loss (particularly in the cortex and the hippocampus), synaptic loss (perhaps as much as 50 percent in the cortex), and granulovascular degeneration of the neurons.
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Neurofibrillary tangles are not unique to Alzheimer's disease; they also occur in
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Down syndrome, dementia pugilistica (punch-drunk syndrome), Parkinson-dementia complex of Guam, Hallervorden-Spatz disease, and the brains of normal people as they age.
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Neurofibrillary tangles are commonly found in what brain regions?
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cortex,
the hippocampus, the substantia nigra, and the locus ceruleus. |
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Describe senile plaques and relation to alz
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Senile plaques, also referred to as amyloid plaques, more strongly indicate Alzheimer's disease, although they are also seen in Down syndrome and, to some extent, in normal aging. Senile plaques are composed of a particular protein, β/A4, and astrocytes, dystrophic neuronal processes, and microglia. The number and the density of senile plaques present in postmortem brains have been correlated with the severity of the disease that affected the persons.
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The neurotransmitters that are most often implicated in the pathophysiological condition of Alzheimer's disease are ? and ?, both of which are hypothesized to be (hyper/hypo)active in Alzheimer's disease
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The neurotransmitters that are most often implicated in the pathophysiological condition of Alzheimer's disease are acetylcholine and norepinephrine, both of which are hypothesized to be hypoactive in Alzheimer's disease
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Several studies have reported data consistent with the hypothesis that specific degeneration of ? neurons is present in the ? in persons with Alzheimer's disease
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Several studies have reported data consistent with the hypothesis that specific degeneration of cholinergic neurons is present in the nucleus basalis of Meynert in persons with Alzheimer's disease
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What evidence is there supporting a cholinergic deficit in Alz?
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Alzheimer's disease demonstrate decreased acetylcholine and choline acetyltransferase concentrations in the brain.Choline acetyltransferase is the key enzyme for the synthesis of acetylcholine, and a reduction in choline acetyltransferase concentration suggests a decrease in the number of cholinergic neurons present.
Additional support for the cholinergic deficit hypothesis comes from the observation that cholinergic antagonists, such as scopolamine and atropine, impair cognitive abilities, whereas cholinergic agonists, such as physostigmine and arecoline, enhance cognitive abilities. |
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Evidence linking NE and Alz?
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Decreased norepinephrine activity in Alzheimer's disease is suggested by the decrease in norepinephrine-containing neurons in the locus ceruleus found in some pathological examinations of brains from persons with Alzheimer's disease.
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Other NT's linked to Alz?
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Two other neurotransmitters implicated in the pathophysiological condition of Alzheimer's disease are the neuroactive peptides somatostatin and corticotropin; decreased concentrations of both have been reported in persons with Alzheimer's disease.
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Other theories of Alz disease?
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rigid membrane
aluminum toxicity (not really ) exitotoxicity & glutamate |
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A recently discovered type of dementia,? shares some brain abnormalities found in people with Alzheimer's disease. The gene that causes the disorder is thought to be carried on chromosome ?
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A recently discovered type of dementia, familial multiple system taupathy, shares some brain abnormalities found in people with Alzheimer's disease. The gene that causes the disorder is thought to be carried on chromosome 17.
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Familial Multiple System Taupathy with Presenile Dementia:
The symptoms of the disorder include short-term memory problems and ?. The onset of disease occurs in the ? and persons with the disease live an average of ? years after the onset of symptoms. |
The symptoms of the disorder include short-term memory problems and difficulty maintaining balance and walking. The onset of disease occurs in the 40s and 50s, and persons with the disease live an average of 11 years after the onset of symptoms.
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Familial Multiple System Taupathy with Presenile Dementia:
As in patients with Alzheimer's disease, ? protein builds up in neurons and glial cells of persons with familial multiple system taupathy. Eventually, the protein buildup kills brain cells. The disorder (is or is not) associated with the senile plaques seen with Alzheimer's disease. |
As in patients with Alzheimer's disease, tau protein builds up in neurons and glial cells of persons with familial multiple system taupathy. Eventually, the protein buildup kills brain cells. The disorder is not associated with the senile plaques seen with Alzheimer's disease.
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Mechanism of Vascular Dementia?
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The disorder affects primarily small- and medium-sized cerebral vessels, which undergo infarction and produce multiple parenchymal lesions spread over wide areas of the brain.
The causes of the infarctions can include occlusion of the vessels by arteriosclerotic plaques or thromboemboli from distant origins (e.g., heart valves). |
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Vascular Dementia physical findings
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An examination of a patient may reveal carotid bruits, fundoscopic abnormalities, or enlarged cardiac chamber
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Binswanger's disease, also known as subcortical arteriosclerotic encephalopathy, is characterized by
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the presence of many small infarctions of the subcortical white matter that spare the cortical region
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In contrast to the ? distribution of pathological findings in Alzheimer's disease, Pick's disease is characterized by a preponderance of atrophy in the ? regions.
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In contrast to the parietal-temporal distribution of pathological findings in Alzheimer's disease, Pick's disease is characterized by a preponderance of atrophy in the frontotemporal regions.
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Pick's ds microscopic findings?
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These regions also have neuronal loss, gliosis, and neuronal Pick's bodies, which are masses of cytoskeletal elements. Pick's bodies are seen in some postmortem specimens but are not necessary for the diagnosis.
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The cause of Pick's disease is ?
The disease constitutes approximately ?percent of all irreversible dementias. |
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Pick's disease most common in?
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It is most common in men, especially those who have a first-degree relative with the condition
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Compare Pick's Disease with Alzheimer's disease
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Pick's disease is difficult to distinguish from dementia of the Alzheimer's type, although the early stages of Pick's disease are more often characterized by personality and behavioral changes, with relative preservation of other cognitive functions, and it typically begins before 75 years of age.
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Pick's disease and genetics?
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Familial cases may have an earlier onset, and some studies have shown that approximately one half of the cases of Pick's disease are familial
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When see the following?
hypersexuality, placidity, and hyperorality |
Features of Klüver-Bucy syndrome (e.g., hypersexuality, placidity, and hyperorality) are much more common in Pick's disease than in Alzheimer's disease.
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Lew Body Disease features, biology?
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Lewy body disease is a dementia clinically similar to Alzheimer's disease and often characterized by hallucinations, parkinsonian features, and extrapyramidal signs (Table 10.3-2). Lewy inclusion bodies are found in the cerebral cortex (Fig. 10.3-6). The exact incidence is unknown. These patients show marked adverse effects when given antipsychotic medications.
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Describe Huntingont's Disease
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The dementia seen in this disease is the subcortical type of dementia, characterized by more motor abnormalities and fewer language abnormalities than in the cortical type of dementia (Table 10.3-3). The dementia of Huntington's disease exhibits psychomotor slowing and difficulty with complex tasks, but memory, language, and insight remain relatively intact in the early and middle stages of the illness
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Hungtington's early vs late?
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The dementia of Huntington's disease exhibits psychomotor slowing and difficulty with complex tasks, but memory, language, and insight remain relatively intact in the early and middle stages of the illness. As the disease progresses, however, the dementia becomes complete; the features distinguishing it from dementia of the Alzheimer's type are the high incidence of depression and psychosis, in addition to the classic choreoathetoid movement disorder.
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Core features of Lewy Body Disease?
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Fluctuating levels of attention and alertness
Recurrent visual hallucinations Parkinsonian features (cogwheeling, bradykinesia, and resting tremor) |
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Supporting Features of lewy Body Disease?
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Repeated falls
Syncope Sensitivity to neuroleptics Systematized delusions Hallucinations in other modalities (e.g. auditory, tactile) |
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As with ? disease, parkinsonism is a disease of the ?, commonly associated with dementia and ?
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As with Huntington's disease, parkinsonism is a disease of the basal ganglia, commonly associated with dementia and depression
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An estimated ? percent of patients with Parkinson's disease have dementia, and an additional ? percent have measurable impairment in cognitive abilities.
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An estimated 20 to 30 percent of patients with Parkinson's disease have dementia, and an additional 30 to 40 percent have measurable impairment in cognitive abilities.
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Key motor features of parkinson's?
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The slow movements of persons with Parkinson's disease are paralleled in the slow thinking of some affected patients, a feature that clinicians may refer to as bradyphrenia
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Compare Subcortical and Cortical Dementia:
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The slow movements of persons with Parkinson's disease are paralleled in the slow thinking of some affected patients, a feature that clinicians may refer to as bradyphrenia
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SC vs C Dementia
Language |
SC: No aphasia (anomia, if severe)
C: Aphasia early Test: FAS test Boston Naming test WAIS-R vocabulary test |
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SC vs C Dementia:
Memory |
SC: Impaired recall (retrieval) > recognition (encoding)
C: Recall and recognition impaired T:Wechsler memory scale; Symbol Digit Paired Associate Learning (Brandt) |
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SC vs C Dementia:Attention and immediate recall
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Impaired in both
WAIS-R digit span |
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SC vs C Dementia:Visuospatial skills
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SC: Impaired
C: IMpaired Picture arrangement, object assembly and block design; WAIS subtests |
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SC vs C Dementia: Calculation
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SC: Preserved until late
C: Involved early Mini-Mental State |
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SC vs C Dementia: Frontal system abilities (executive function)
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Disproportionately affected
c: Degree of impairment consistent with other involvement T: Wisconsin Card Sorting Test; Odd Man Out test; Picture Absurdities |
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SC vs C Dementia: Speed of cognitive processing
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SC: Slowed early
C: Normal until late in disease Test: Trail making A and B: Paced Auditory Serial Addition Test (PASAT) |
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SC vs C Dementia: Personality
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SC: Apathetic, inert
C: Unconcerned MMPI |
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SC vs C Dementia: Mood
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SC: Depressed
C: Euthymic T: Beck and Hamilton depression scales |
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SC vs C Dementia:Speech
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SC: Dysarthric
C: Articulate until late T:Verbal fluency (Rosen, 1980) |
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Posture
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SC: Bowed or extended
C: Upright |
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Coordination
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SC: Impaired
C: Normal until late |
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Motor Speed and Control
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SC: Slowed
C: Normal Finger-tap; grooved pegboard |
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Adventitious Movements
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SC: Chorea, tremor tics, dystonia
C: Absent (Alzheimer's dementia—some myoclonus) |
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Abstraction
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SC: Impaired
C: Impaired Category test (Halstead Battery) |
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Patients infected with HIV experience dementia at an annual rate of approximately ? percent
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14%
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The development of dementia in people infected with HIV is often paralleled by the appearance of ? in MRI scans
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The development of dementia in people infected with HIV is often paralleled by the appearance of parenchymal abnormalities in MRI scans
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Other than HIV infectious dementias are caused by
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Cryptococcus or Treponema pallidum
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The AIDS Task Force criteria for AIDS dementia complex require:
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laboratory evidence for systemic HIV, at least two cognitive deficits, and the presence of motor abnormalities or personality changes. Personality changes may be manifested by apathy, emotional lability, or behavioral disinhibition.
s with the DSM-IV-TR, the AIDS Task Force criteria also require the absence of clouding of consciousness or evidence of another etiology that could produce the cognitive impairment. |
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The so-called punch-drunk syndrome (dementia pugilistica) occurs in boxers after repeated head trauma over many years. It is characterized by
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emotional lability, dysarthria, and impulsivity.
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How make dx of Dementia?
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The diagnosis of dementia is based on the clinical examination, including a mental status examination, and on information from the patient's family, friends, and employers. Complaints of a personality change in a patient older than age 40 suggest that a diagnosis of dementia should be carefully considered.
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Describe memory fxn in dementia's over time?
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Memory impairment is typically an early and prominent feature in dementia, especially in dementias involving the cortex, such as dementia of the Alzheimer's type. Early in the course of dementia, memory impairment is mild and usually most marked for recent events; people forget telephone numbers, conversations, and events of the day. As the course of dementia progresses, memory impairment becomes severe, and only the earliest learned information (e.g., a person's place of birth) is retained.
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Personality type features that might suggest dementia?
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Lability of emotions, sloppy grooming, uninhibited remarks, silly jokes, or a dull, apathetic, or vacuous facial expression and manner suggest the presence of dementia, especially when coupled with memory impairment.
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Describe language features of dementia?
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Dementing processes that affect the cortex, primarily dementia of the Alzheimer's type and vascular dementia, can affect patients' language abilities. DSM-IV-TR includes aphasia as one of the diagnostic criteria. The language difficulty may be characterized by a vague, stereotyped, imprecise, or circumstantial locution, and patients may also have difficulty naming objects.
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Describe psychiatric and neuro changes associated with dementia
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Personality Change
Hallucinations and Delusions Mood Cognitive Changes Catastrophic REaction Sundownder Syndrome |
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Describe Dementia personalit change?
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Preexisting personality traits may be accentuated during the development of a dementia. Patients with dementia may also become introverted and seem to be less concerned than they previously were about the effects of their behavior on others. Persons with dementia who have paranoid delusions are generally hostile to family members and caretakers.
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Patients with?region? involvement are likely to have marked personality changes and may be irritable and explosive
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Patients with frontal and temporal involvement are likely to have marked personality changes and may be irritable and explosive
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An estimated? percent of patients with dementia (primarily patients with dementia of the ? type) have hallucinations, and ? percent have delusions, primarily of a ? nature,
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An estimated 20 to 30 percent of patients with dementia (primarily patients with dementia of the Alzheimer's type) have hallucinations, and 30 to 40 percent have delusions, primarily of a paranoid or persecutory and unsystematized nature, although complex, sustained, and well-systematized delusions are also reported by these patients.
Physical aggression and other forms of violence are common in demented patients who also have psychotic symptoms. |
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In addition to psychosis and personality changes, depression and anxiety are major symptoms in an estimated ? percent of patients with dementia,
the full syndrome of depressive disorder may be present in ? percent. |
In addition to psychosis and personality changes, depression and anxiety are major symptoms in an estimated 40 to 50 percent of patients with dementia, although the full syndrome of depressive disorder may be present in only 10 to 20 percent.
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Patients with dementia also may exhibit ? laughter or crying—that is, extremes of emotions—with no apparent provocation.
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Patients with dementia also may exhibit pathological laughter or crying—that is, extremes of emotions—with no apparent provocation.
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Cog neuro changes in dementia?
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In addition to the aphasias in patients with dementia, apraxias and agnosias are common, and they are included as potential diagnostic criteria in DSM-IV-TR.
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neurological signs that can be associated with dementia are seizures, seen in approximately 10 percent of patients with dementia of the ? and in 20 percent of patients with ? dementia, and atypical neurological presentations, such as nondominant parietal lobe syndromes
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neurological signs that can be associated with dementia are seizures, seen in approximately 10 percent of patients with dementia of the Alzheimer's type and in 20 percent of patients with vascular dementia, and atypical neurological presentations, such as nondominant parietal lobe syndromes
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Primitive reflexes, such as the ? may be present on neurological examination, and myoclonic jerks are present in? percent of patients
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Primitive reflexes, such as the grasp, snout, suck, tonic-foot, and palmomental reflexes, may be present on neurological examination, and myoclonic jerks are present in 5 to 10 percent of patients.
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Pseudobulbar palsy, dysarthria, and dysphagia are also more common in ? dementia than in other dementing conditions.
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vascular
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Patients with vascular dementia may have additional neurological symptoms, such as
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headaches, dizziness, faintness, weakness, focal neurological signs, and sleep disturbances, possibly attributable to the location of the cerebrovascular disease
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Dementia and generalizing?
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Patients have difficulty generalizing from a single instance, forming concepts, and grasping similarities and differences among concepts
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Dementia and Judgement?
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Furthermore, the ability to solve problems, to reason logically, and to make sound judgments is compromised
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What is a catastropic reaction?
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Goldstein also described a catastrophic reaction marked by agitation secondary to the subjective awareness of intellectual deficits under stressful circumstances
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Persons usually attempt to compensate for defects by ?
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using strategies to avoid demonstrating failures in intellectual performance; they may change the subject, make jokes, or otherwise divert the interviewer
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Lack of judgment and poor impulse control appear commonly, particularly in dementias that primarily affect the ? lobes.
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frontal
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Describe sundowner syndrome
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Sundowner syndrome is characterized by drowsiness, confusion, ataxia, and accidental falls. It occurs in older people who are overly sedated and in patients with dementia who react adversely to even a small dose of a psychoactive drug. The syndrome also occurs in demented patients when external stimuli, such as light and interpersonal orienting cues, are diminished.
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The DSM-IV-TR diagnostic criteria for dementia of the Alzheimer's type emphasize the presence of
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memory impairment and the associated presence of at least one other symptom of cognitive decline (aphasia, apraxia, agnosia, or abnormal executive functioning)
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Vascular dementia criteria?
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The general symptoms of vascular dementia are the same as those for dementia of the Alzheimer's type, but the diagnosis of vascular dementia requires either clinical or laboratory evidence in support of a vascular cause of the dementia
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Vasc vs Alz dementia?
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Vascular dementia is more likely to show a decremental, stepwise deterioration than is Alzheimer's disease.
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What diagnosis to compare alcohol-induced persisting dementia with? describe
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To make the diagnosis of alcohol-induced persisting dementia, the criteria for dementia must be met. Because amnesia can also occur in the context Korsakoff's psychosis, it is important to distinguish between memory impairment accompanied by other cognitive deficits (i.e., dementia) and amnesia caused by thiamine deficiency. To complicate matters, however, evidence also suggests that other cognitive functions, such as attention and concentration, may also be impaired in Wernicke-Korsakoff syndrome. In addition, alcohol abuse is frequently associated with mood changes, so poor concentration and other cognitive symptoms often observed in the context of a major depression must also be ruled out. Prevalence rates differ considerably according to the population studied and the diagnostic criteria used, although alcohol-related dementia has been estimated to account for approximately 4 percent of dementias.
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The detection of ? for example, should alert the clinician to the probable presence of AIDS and the associated possibility of AIDS dementia complex.
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The detection of Kaposi's sarcoma, for example, should alert the clinician to the probable presence of AIDS and the associated possibility of AIDS dementia complex.
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Focal neurological findings, such as asymmetrical hyperreflexia or weakness, are seen more often in ? than in ?
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Focal neurological findings, such as asymmetrical hyperreflexia or weakness, are seen more often in vascular than in degenerative disease
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Clinicians should distinguish TIA episodes involving the vertebrobasilar system from those involving the carotid arterial system.
Describe differences |
In general, symptoms of vertebrobasilar disease reflect a transient functional disturbance in either the brainstem or the occipital lobe
carotid distribution symptoms reflect unilateral retinal or hemispheric abnormality |
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Three key differences in depression vs dementia?
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Patients with depression-related cognitive dysfunction generally have prominent depressive symptoms, more insight into their symptoms than do demented patients, and often a history of depressive episodes.
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normal aging versus dementia?
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Aging is not necessarily associated with any significant cognitive decline, but minor memory problems can occur as a normal part of aging. These normal occurrences are sometimes referred to as benign senescent forgetfulness or age-associated memory impairment. They are distinguished from dementia by their minor severity and because they do not interfere significantly with a person's social or occupational behavior.
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Dep or dementia?
Family always aware of dysfunction and its severity Onset can be dated with some precision Symptoms of short duration before medical help is sought Rapid progression of symptoms after onset History of previous psychiatric dysfunction common |
Depression
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Depression or Dementia?
Family often unaware of dysfunction and its severity Onset can be dated only within broad limits Symptoms usually of long duration before medical help is sought Slow progression of symptoms throughout course History of previous psychiatric dysfunction unusual |
Dementia
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Patients usually complain little of cognitive loss
Patients' complaints of cognitive dysfunction usually vague Patients conceal disability Patients delight in accomplishments, however trivial Patients struggle to perform tasks Patients rely on notes, calendars, etc., to keep up |
Dementia
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Patients usually complain much of cognitive loss
Patients' complaints of cognitive dysfunction usually detailed Patients emphasize disability Patients highlight failures Patients make little effort to perform even simple tasks |
Depression
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Patients usually communicate strong sense of distress
Affective change often pervasive Loss of social skills often early and prominent Behavior often incongruent with severity of cognitive dysfunction Nocturnal accentuation of dysfunction uncommon |
Depression
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Patients often appear unconcerned
Affect labile and shallow Social skills often retained Behavior usually compatible with severity of cognitive dysfunction Nocturnal accentuation of dysfunction common |
Dementia
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Attention and concentration often well preserved
“Don't know” answers typical On tests of orientation, patients often give “don't know” answers Memory loss for recent and remote events usually severe Memory gaps for specific periods or events common Marked variability in performance on tasks of similar difficulty |
Depression
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Attention and concentration usually faulty
Near-miss answers frequent On tests of orientation, patients often mistake unusual for usual Memory loss for recent events usually more severe than for remote events Memory gaps for specific periods unusuala Consistently poor performance on tasks of similar difficulty |
Dementia
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Difference between amnestic disorder and dementia?
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mnestic disorder is characterized by circumscribed loss of memory and no deterioration
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The average survival expectation for patients with dementia of the Alzheimer's type is approximately ? years, with a range of ? years.
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The average survival expectation for patients with dementia of the Alzheimer's type is approximately 8 years, with a range of 1 to 20 years.
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Data suggest that in persons with ?e is likely to have a rapid course.
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Data suggest that in persons with an early onset of dementia or with a family history of dementia the disease is likely to have a rapid course.
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A gradual onset of symptoms is most commonly associated with dementia s:
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of the Alzheimer's type, vascular dementia, endocrinopathies, brain tumors, and metabolic disorders
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Sudden onset demementia?
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Conversely, the onset of dementia resulting from head trauma, cardiac arrest with cerebral hypoxia, or encephalitis can be sudden
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The course of the dementia varies from a steady progression (commonly seen with ?) to an incrementally worsening dementia (commonly seen with ? dementia) to a stable dementia (as may be seen in ?).
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The course of the dementia varies from a steady progression (commonly seen with dementia of the Alzheimer's type) to an incrementally worsening dementia (commonly seen with vascular dementia) to a stable dementia (as may be seen in dementia related to head trauma).
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The severity and course of dementia can be affected by psychosocial factors.
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The greater a person's premorbid intelligence and education, the better the ability to compensate for intellectual deficits.
People who have a rapid onset of dementia use fewer defenses than do those who experience an insidious onset. Anxiety and depression can intensify and aggravate the symptoms. Pseudodementia occurs in depressed people who complain of impaired memory but, in fact, are suffering from a depressive disorder. When the depression is treated, the cognitive defects disappear. |
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Tx of Vasc Dementia?
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Such measures might include changes in diet, exercise, and control of diabetes and hypertension. Pharmacological agents might include antihypertensive, anticoagulant, or antiplatelet agents. Blood pressure control should aim for the higher end of the normal range, because that has been demonstrated to improve cognitive function in patients with vascular dementia. Blood pressure below the normal range has been demonstrated to further impair cognitive function in the patient with dementia.
Surgical removal of carotid plaques may prevent subsequent vascular events in carefully selected patients. |
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Choice of AntiHTN in dementia?
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The choice of antihypertensive agent can be significant in that β-adrenergic receptor antagonists have been associated with exaggeration of cognitive impairment. Angiotensin-converting enzyme (ACE) inhibitors and diuretics have not been linked to exaggeration of cognitive impairment and are thought to lower blood pressure without affecting cerebral blood flow, which is presumed to be correlated with cognitive function.
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General treatment approach to Dementia?
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The general treatment approach to patients with dementia is to provide supportive medical care, emotional support for the patients and their families, and pharmacological treatment for specific symptoms, including disruptive behavior.
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? memory is lost before ? memory in most cases of dementia, and many patients are highly distressed by clearly recalling how they used to function while observing their obvious deterioration.
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Recent memory is lost before remote memory in most cases of dementia, and many patients are highly distressed by clearly recalling how they used to function while observing their obvious deterioration.
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Emotional reactions ranging from depression to severe anxiety to catastrophic terror can stem from t
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he realization that the sense of self is disappearing
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Psycho tx of dementia?
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Patients often benefit from a supportive and educational psychotherapy in which the nature and course of their illness are clearly explained. They may also benefit from assistance in grieving and accepting the extent of their disability and from attention to self-esteem issues. Any areas of intact functioning should be maximized by helping patients identify activities in which successful functioning is possible. A psychodynamic assessment of defective ego functions and cognitive limitations can also be useful. Clinicians can help patients find ways to deal with the defective ego functions, such as keeping calendars for
P.341 P.342 P.343 orientation problems, making schedules to help s |
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Donepezil (Aricept), rivastigmine (Exelon), galantamine (Remiryl), and tacrine (Cognex) are ? inhibitors used to treat severity ? cognitive impairment in Alzheimer's disease. They reduce the ? of the neurotransmitter acetylcholine and, thus, ? the cholinergic neurotransmitter, which in turn produces a modest improvement in ? and?. These drugs are most useful for persons with ? memory loss who have sufficient preservation of their basal forebrain cholinergic neurons to benefit from augmentation of cholinergic neurotransmission
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Donepezil (Aricept), rivastigmine (Exelon), galantamine (Remiryl), and tacrine (Cognex) are cholinesterase inhibitors used to treat mild to moderate cognitive impairment in Alzheimer's disease. They reduce the inactivation of the neurotransmitter acetylcholine and, thus, potentiate the cholinergic neurotransmitter, which in turn produces a modest improvement in memory and goal-directed thought. These drugs are most useful for persons with mild to moderate memory loss
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Which ACHEI is most used in dementia?
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Donepezil is well tolerated and widely used. Tacrine is rarely used, because of its potential for hepatotoxicity. Fewer clinical data are available for rivastigmine and galantamine, which appear more likely to cause gastrointestinal (GI) and neuropsychiatric adverse effects than does donepezil.
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Rx? protects neurons from excessive amounts of glutamate, which may be neurotoxic.
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Memantine
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Vitamin E role in dementia?
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Vitamin E has not been shown to be of value in preventing the disease.
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The amnestic disorders are a broad category that includes a variety of diseases and conditions that present with an amnestic syndrome. The syndrome is defined primarily by
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impairment in the ability to create new memories
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Three variations of the amnestic disorder diagnosis, differing in etiology, are offered:
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amnestic disorder caused by a
general medical condition (e.g., head trauma), substance-induced persisting amnestic disorder (e.g., caused by carbon monoxide poisoning or chronic alcohol consumption), and amnestic disorder not otherwise specified for cases in which the etiology is unclear. |
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Amenestic disorder modifiers?
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The two modifiers are (1) transient, for duration less than 1 month, and (2) chronic, for conditions extending beyond 1 month.
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In general practice and hospital settings, the frequency of amnesia related to chronic alcohol abuse has ?, and the frequency of amnesia related to head trauma has ?.
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In general practice and hospital settings, the frequency of amnesia related to chronic alcohol abuse has decreased, and the frequency of amnesia related to head trauma has increased.
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|
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he major neuroanatomical structures involved in memory and in the development of an amnestic disorder are particular diencephalic structures such as the
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dorsomedial and midline nuclei of the thalamus and midtemporal lobe structures such as the hippocampus, the mamillary bodies, and the amygdala
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Amnesia result of unilateral of bilateral damage usually?
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Although amnesia is usually the result of bilateral damage to these structures, some cases of unilateral damage result in an amnestic disorder,
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evidence indicates that the ? hemisphere may be more critical than the ? hemisphere in the development of memory disorders.
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evidence indicates that the left hemisphere may be more critical than the right hemisphere in the development of memory disorders.
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? lobe involvement can result in such symptoms as confabulation and apathy, which can be seen in patients with amnestic disorders.
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Frontal
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Thiamine deficiency, hypoglycemia, hypoxia (including carbon monoxide poisoning), and herpes simplex encephalitis all have a predilection to damage the ? lobes, particularly the ?, and thus can be associated with the development of amnestic disorders.
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Thiamine deficiency, hypoglycemia, hypoxia (including carbon monoxide poisoning), and herpes simplex encephalitis all have a predilection to damage the temporal lobes, particularly the hippocampi, and thus can be associated with the development of amnestic disorders.
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Similarly, when tumors, cerebrovascular diseases, surgical procedures, or multiple sclerosis plaques involve the ? regions of the brain, the symptoms of an amnestic disorder may develop
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Similarly, when tumors, cerebrovascular diseases, surgical procedures, or multiple sclerosis plaques involve the diencephalic or temporal regions of the brain, the symptoms of an amnestic disorder may develop
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Transient global amnesia is presumed to be a (type of disorder)?
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cerebrovascular disorder involving transient impairment in blood flow through the vertebrobasilar arteries.
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The ? are the most commonly used prescription drugs associated with amnesia.
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benzo's
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Criteria A for Amenestic Ds Due to a GMC?
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The development of memory impairment as manifested by impairment in the ability to learn new information (antero) or the inability to recall (retro)previously learned information.
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Amenestic Ds: Short-term and recent memory (are or are not) usually impaired.
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Short-term and recent memory are usually impaired.
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Memory for ? information or events from the remote past, such as childhood experiences, is ? (poor or good);
memory for events from the less remote past (over the past decade) is (poor or good) |
Memory for overlearned information or events from the remote past, such as childhood experiences, is good; but memory for events from the less remote past (over the past decade) is impaired
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Digit span in amnestic disorder?
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Immediate memory (tested, for example, by asking a patient to repeat six numbers) remains intact
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Do people with amnestic ds have good insight into their condition?
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No
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Cerebrovascular diseases affecting the hippocampus involve the ?arteries and their branches
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Cerebrovascular diseases affecting the hippocampus involve the posterior cerebral and basilar arteries and their branches
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Infarctions are rarely limited to the hippocampus; they often involve the ?l lobes. Thus, common accompanying symptoms of cerebrovascular diseases in this region are focal neurological signs involving
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Infarctions are rarely limited to the hippocampus; they often involve the occipital or parietal lobes.
Thus, common accompanying symptoms of cerebrovascular diseases in this region are focal neurological signs involving vision or sensory modalities |
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Cerebrovascular diseases affecting the? are often associated with symptoms of amnestic disorders
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Cerebrovascular diseases affecting the bilateral medial thalamus, particularly the anterior portions, are often associated with symptoms of amnestic disorders
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A few case studies report amnestic disorders from rupture of an aneurysm of the ?, resulting in infarction of the ?
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A few case studies report amnestic disorders from rupture of an aneurysm of the anterior communicating artery, resulting in infarction of the basal forebrain region.
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The pathophysiological process of multiple sclerosis involves the seemingly random formation of plaques within the brain parenchyma. When the plaques occur in the ? symptoms of memory impairment can occur.
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temporal lobe and the diencephalic regions,
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The most common cognitive complaints in patients with multiple sclerosis involve
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impaired memory, which occurs in 40 to 60 percent of patients
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In MS:
Characteristically, digit span memory is ? normal or impaired? immediate recall and delayed recall of information are ?normal or impaired? |
MS Characteristically, digit span memory is normal, but immediate recall and delayed recall of information are impaired.
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Korsakoff's syndrome is an amnestic syndrome caused by ? deficiency, most commonly associated with the poor nutritional habits of people with chronic ? abuse
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Korsakoff's syndrome is an amnestic syndrome caused by thiamine deficiency, most commonly associated with the poor nutritional habits of people with chronic alcohol abuse
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Other causes of poor nutrition ? can also result in thiamine deficiency.
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Other causes of poor nutrition (e.g., starvation), gastric carcinoma, hemodialysis, hyperemesis gravidarum, prolonged intravenous hyperalimentation, and gastric plication can also result in thiamine deficiency.
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Wernicke's encephalopathy, which is the associated syndrome of ?
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confusion, ataxia, and ophthalmoplegia.
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In patients with these thiamine deficiency-related symptoms, the neuropathological findings include:
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hyperplasia of the small blood vessels with occasional hemorrhages, hypertrophy of astrocytes, and subtle changes in neuronal axons
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Along with memory changes, what other changes occur in Korsakoff's?
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Patients with Korsakoff's syndrome typically demonstrate a change in personality as well, such that they display a lack of initiative, diminished spontaneity, and a lack of interest or concern. These changes appear frontal lobe-like, similar to the personality change ascribed to patients with frontal lobe lesions or degeneration. Indeed, such patients often demonstrate executive function deficits on neuropsychological tasks involving attention, planning, set shifting, and inferential reasoning consistent with frontal pattern injuries.
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Korsakoff's onset: quick or gradual
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gradual
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Korsakoff's: what is affected more: recent or remote memory?
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recent
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With treatment, patients may remain amnestic for up to ? months and then gradually improve over the ensuing year.
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3
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Thiamine tx of Korsakoff's syndrome: what % recover?
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Administration of thiamine may prevent the development of additional amnestic symptoms, but the treatment seldom reverses severe amnestic symptoms once they are present. Approximately one third to one fourth of all patients recover completely, and approximately one fourth of all patients have no improvement of their symptoms.
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ECT and memory problems?
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Electroconvulsive therapy (ECT) treatments are usually associated with retrograde amnesia for a period of several minutes before the treatment and anterograde amnesia after the treatment. The anterograde amnesia usually resolves within 5 hours. Mild memory deficits may remain for 1 to 2 months after a course of ECT treatments, but the symptoms are completely resolved 6 to 9 months after treatment.
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Electroconvulsive therapy (ECT) treatments are usually associated with ? amnesia for a period of several minutes before the treatment and ?grade amnesia after the treatment. The anterograde amnesia usually resolves within ? hours. Mild memory deficits may remain for ? months after a course of ECT treatments, but the symptoms are completely resolved ? 9 months after treatment.
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Electroconvulsive therapy (ECT) treatments are usually associated with retrograde amnesia for a period of several minutes before the treatment and anterograde amnesia after the treatment. The anterograde amnesia usually resolves within 5 hours. Mild memory deficits may remain for 1 to 2 months after a course of ECT treatments, but the symptoms are completely resolved 6 to 9 months after treatment.
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mnestic disorders caused by head injuries are commonly associated with a period of ?grade amnesia leading up to the traumatic incident and ? for the traumatic incident itself
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mnestic disorders caused by head injuries are commonly associated with a period of retrograde amnesia leading up to the traumatic incident and amnesia for the traumatic incident itself
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Best predictor of amnestic syndrome outcome after brain injury?
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The severity of the brain injury correlates somewhat with the duration and severity of the amnestic syndrome, but the best correlate of eventual improvement is the degree of clinical improvement in the amnesia during the first week after the patient regains consciousness.
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Transient global amnesia is characterized by the (gradual/abrupt?) loss of the ability to ?
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Transient global amnesia is characterized by the abrupt loss of the ability to recall recent events or to remember new information
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TGA syndrome is often characterized by ? and a lack of ?, a ?, and,?
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he syndrome is often characterized by mild confusion and a lack of insight into the problem, a clear sensorium, and, occasionally, the inability to perform some well-learned complex tasks
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TGA lasts?
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6 to 25 hours
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Transient Global Amnesia pathophysiology?
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The pathophysiology is unknown, but it likely involves ischemia of the temporal lobe and the diencephalic brain regions. Several studies of patients with single photon emission computed tomography (SPECT) have shown decreased blood flow in the temporal and parietotemporal regions, particularly in the left hemisphere
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How does TGA compare to TIA?
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atients with transient global amnesia have been differentiated from patients with transient ischemic attacks in that fewer patients have diabetes, hypercholesterolemia, and hypertriglyceridemia, but more have hypertension and migrainous episodes.
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Amenestic Ds finding on MRI?
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Damage of midtemporal lobe structures is common, however, and may be reflected in enlargement of third ventricle or temporal horns or in structural atrophy detected by MRI.
Note: No specific or diagnostic features are detectable on imaging studies such as magnetic resonance imagery (MRI) or computed tomography (CT). |
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Difference between amnestic ds and alz/dementia?
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Although Alzheimer's dementia progresses relentlessly, amnestic disorders tend to remain static or even improve once the offending cause has been removed.
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Compare memory deificits in Alz versus Amnestic Ds
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Alzheimer's disease has an impact on retrieval, in addition to encoding and consolidation. The deficits in Alzheimer's disease extend beyond memory to general knowledge (semantic memory), language, praxis, and general function.
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The dementias associated with Parkinson's disease, acquired immune deficiency syndrome (AIDS), and other subcortical disorders demonstrate disproportionate impairment ?, but relatively intact ? and ? and, thus, can be distinguished from amnestic disorders.
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The dementias associated with Parkinson's disease, acquired immune deficiency syndrome (AIDS), and other subcortical disorders demonstrate disproportionate impairment of retrieval, but relatively intact encoding and consolidation and, thus, can be distinguished from amnestic disorders
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Other differences in subcortical dementia vs amnestic disroder
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The subcortical pattern dementias are also likely to display motor symptoms, such as bradykinesia, chorea, or tremor, that are not components of the amnestic disorders.
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Semantic memory: impaired in?
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dementia not amnestic ds
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Retrograde memory?
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impaired in dementia, temporal gradient in amnestic ds
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Episodic memory:
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impaired in both
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Langauge: dementia vs amnestic ds?
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impaired in dementia, not in amnestic ds
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Function in Amnestic ds?
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impaired in Alzheimer's
intact in amnestic ds |
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Amnestic Ds vs Dementia Onset?
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amnestic can be abrupt alz de usually insidious
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Dissociative Ds vs Amnestic Ds ... difference?
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Patients with dissociative disorders, however, are more likely to have lost their orientation to self and may have more selective memory deficits than do patients with amnestic disorders.
For example, patients with dissociative disorders may not know their names or home addresses, but they are still able to learn new information and remember selected past memories |
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Generally, the amnestic disorder has a static course. Little improvement is seen over time, but also no progression of the disorder occurs. The exceptions are
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the acute amnesias, such as transient global amnesia, which resolves entirely over hours to days, and the amnestic disorder associated with head trauma, which improves steadily in the months subsequent to the trauma
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Psychotherapy for amnestic ds phases?
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The first phase of recovery, in which patients are incapable of processing what happened because the ego defenses are overwhelmed, requires clinicians to serve as a supportive auxiliary ego who explains to a patient what is happening and provides missing ego functions.
In the second phase of recovery, as the realization of the injury sets in, patients may become angry and feel victimized by the malevolent hand of fate. They may view others, including the clinician, as bad or destructive, and clinicians must contain these projections without becoming punitive or retaliatory. Clinicians can build a therapeutic alliance with patients by explaining slowly and clearly what happened and by offering an explanation for a patient's internal experience. The third phase of recovery is integrative. As a patient accepts what has happened, a clinician can help the patient form a new identity by connecting current experiences of the self with past experiences. Grieving over the lost faculties may be an important feature of the third phase. |
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Mood Ds Due to a GMC specifiers?
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manic, depressed, or mixed, and if criteria for a fully symptomatic major depressive or manic syndromic are fulfilled
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Mood disorder due to GMC: gender ratio vs MDD?
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equal M/F unlike MDD which is > in Femalese
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Which GMC's especially associated with MDE?
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Post-stroke and Pancreatic Cancer 50%
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Depressive disorders associated with ? conditions carry the greatest risk of suicide.
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Depressive disorders associated with terminal or painful conditions carry the greatest risk of suicide.
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many experienced clinicians report a high rate of euphoria in patients with ?
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MS
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DSM criteria for Mood Ds Due to GMC
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1. A prominent and persistent disturbance in mood predominates in the clinical picture and is characterized by either (or both) of the following:
1. Depressed mood or markedly diminished pleasure in all, or almost all, activities 2. Elevated, expansive, or irritable mood. 2. There is evidence from the history, physical examination, or laboratory findings that the disturbance is the direct physiological consequence of a general medical condition. 3. The disturbance is not better accounted for by another mental disorder (e.g., adjustment disorder with depressed mood in response to the stress of having a general medical condition). 4. The disturbance does not occur exclusively during the course of a delirium. 5. The symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of functioning. |
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DSM Mood Ds Due to GMC specifiers?
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With depressive features: if the predominant mood is depressed, but the full criteria are not met for a major depressive disorder
With major depressive-like episode: if all criteria for major depressive episode are met, except, clearly, for the criterion that the symptoms are not due to the physiological effects of a substance or a general medical condition With manic features: if the predominant mood is elevated, euphoric, or irritable With mixed features: if the symptoms of mania and depression are present, but neither predominates |
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Psychotic Ds due to GMC ... what must be ruled out?
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rule out cognitive impairment ... ie delirium, dementia
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As much as 40 percent of individuals with ? experience psychosis
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temporal lobe epilepsy
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Psychotic Ds due to GMC specifiers?
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Specify:
With delusions: if delusions are the predominant symptom With hallucinations: if hallucinations are the predominant symptom |
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Temporal Lobe is associated with what psychotic sx?
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First-rank symptoms
Thoughts spoken aloud Voices commenting Third-person voices arguing Made actions Made feelings Thought withdrawal Thought diffusion Delusional perception |
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Complex delusions associated with what brain region?
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subcortical or limbic
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Anton syndrome ... region?
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occipital lobe, optic tract
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Anosognosia ... region?
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parietal lobe
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Misidentification brain region?
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Parietal, Temporal, Front lobes
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delirium-related psychosis is ? and ?, commonly associated with disturbance in consciousness and cognitive defect
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delirium-related psychosis is acute and fluctuating, commonly associated with disturbance in consciousness and cognitive defect
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Most cases of nonauditory hallucinosis are due to ?, or both.
Auditory hallucinations can occur? |
medical conditions, substances.
Auditory hallucinations can occur in primary and induced psychoses |
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Temporal lobe epilepsy often is associated with ?
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olfactory hallucinations and religious delusions
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Right parietal lobe lesions can induce ?
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a contralateral neglect state of delusional nature in which individuals disown parts of their bodies
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Occipital lesions, whether caused by tumor or cerebrovascular accident, can produce ? hallucinations.
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visual
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Approximately ?% of patients with hypothyroidism and ?% of patients with hyperthyroidism may experience anxiety symptom
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1/3
2/3 |
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As much as ? percent of patients with Parkinson's disease have anxiety disorders
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40%
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Prevalence of most anxiety disorders is higher in ? than in ?.
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women than in men
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Anxiety GMCs?
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sympathomimetic agents,
withdrawal from sedatives endcrine ds: thyroid, pheo, parathyroid, metabol: low 02, hi Ca, low glucose |
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Much attention has been paid to the association of panic attacks and ?
|
mitral valve prolapse
The nature of that association is unknown, and therefore the diagnosis of panic attacks secondary to mitral valve prolapse currently is premature. |
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Anx Ds Due to GMC criteria? specifiers?
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With generalized anxiety: if excessive anxiety or worry about a number of events or activities predominates in the clinical presentation
With panic attacks: if panic attacks predominate in the clinical presentation With obsessive–compulsive symptoms: if obsessions or compulsions predominate in the clinical presentation |
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What points more to 2ndary causes of anxiety vs primary ds?
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acute onset,
lack of fam hx happens in context of medical illness |
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What GMC's associated with sleep sx?
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Parkinsonism: poor circadian
Dementia: sundownding Epilepsy: initial insomnia, freq awak, parasomnias Hungtington's: Freq awakenings Kleine-Levin Syndrome: Hypersomnia Uremia: Restlessness, nocturnal myoclonus |
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Most frequent women's sexual problem?
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prevalence rates for sexual complaints are highest for female hypoactive sexual desire and orgasm problems and for premature ejaculation in men.
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Cerebrovascular accident impairs sexual functioning, with the possibility that, in men, greater impairment follows ?-hemispheric cerebrovascular injury than ?-hemispheric injury
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Right > Left
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Among inpatients with catatonia, ? percent are related to mood disorders (e.g., major depressive episode, recurrent, with catatonic features), and approximately ? percent are associated with schizophrenia
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Among inpatients with catatonia, 25 to 50 percent are related to mood disorders (e.g., major depressive episode, recurrent, with catatonic features), and approximately 10 percent are associated with schizophrenia
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What is the dx of a disturbance caused by GMC but criteria not met for specific disorder
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Mental Disorder Not Otherwise Specified Due to a General Medical Condition
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When a true personality change occurs in adulthood, the clinician should always suspect
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brain injury.
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Diseases that preferentially affect the ? structures are more likely to manifest with prominent personality chang
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Diseases that preferentially affect the frontal lobes or subcortical structures are more likely to manifest with prominent personality chang
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Personality Change due to GMC ... common causes?
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Head trauma
Front lobe tumours Subcortical Dementias White matter irradiation |
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Personality Change due to GMC specifiers?
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pecify type:
Labile type: if the predominant feature is affective lability Disinhibited type: if the predominant feature is poor impulse control as evidenced by sexual indiscretions, etc. Aggressive type: if the predominant feature is aggressive behavior Apathetic type: if the predominant feature is marked apathy and indifference Paranoid type: if the predominant feature is suspiciousness or paranoid ideation Other type: if the presentation is not characterized by any of the above subtypes Combined type: if more than one feature predominates in the clinical picture Unspecified type |
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lability and impulsivity what meds used to tx pers change due to GMC?
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Li, Anticonvulsants
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Aggression or explosiveness can be treated with?
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Lithium, Anticonvulsants, and propranolol
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Apathy and inertia have occasionally improved with
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psychostimulant agents
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With regard to the first of these concerns, ? percent of all persons with epilepsy have psychiatric difficulties sometime during the course of their illness
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up to 50%
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The most common behavioral symptom of epilepsy is?
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The most common behavioral symptom of epilepsy is a change in personality
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Difference between partial and generalized seizures?
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partial has a focus while genearlized involves the entire brain
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Partial seizure types?
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A. Partial with elementary sx (no change in consciousness): motor, sensory, autonomic
B. Partial with complex sx (with change in consciousness): 1. with impairment in consiousness 2. with cognitive sx 3. with affective sx 4. with psychosensory sx 5. with automatisms C. Partial seizures sedarily genarlized |
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Generalized seizure types?
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Bilaterally symmetrical and without local onset
A. Absences (petit mal) B. Myoclonus C. Infantile spasms D. Clonic seizures E. Tonic seizures F. Tonic-Clonic Seizures (grand-mal) G. Atonic seizures H. Akinetic seizures |
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Generalized tonic-clonic seizures exhibit the classic symptoms of
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loss of consciousness, generalized tonic-clonic movements of the limbs, tongue biting, and incontinence
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Petit mal epilepsy usually begins in ? and ceases by ?
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Petit mal epilepsy usually begins in childhood between the ages of 5 and 7 years and ceases by puberty
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Brief disruptions of consciousness, during which the patient suddenly loses contact with the environment, are characteristic of ?type of epilepsy, but the patient has no true loss of consciousness and no convulsive movements during the episodes
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petit mal
or absence seizures (generalized category) |
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The electroencephalogram (EEG) produces a characteristic pattern of three-per-second spike-and-wave activity ... type of seizure?
|
petit mal
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rhythmic sharp waves and then spike and wave .. seizure type?
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generalized tonic-clonic seizures
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Partial seizures are classified as either
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simple (without alterations in consciousness) or complex (with an alteration in consciousness).
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About ? percent of patients with complex partial seizures have major mental illness such as ?
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About 30 percent of patients with complex partial seizures have major mental illness such as depression.
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left-temporal spike discharges and rare, indepen-dent right-temporal sharp-wave activity
seizure type? |
complex partial seizure
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What sx might you see pre-seizure or pre-icatally?
|
reictal events (auras) in complex partial epilepsy include autonomic sensations (e.g., fullness in the stomach, blushing, and changes in respiration),
cognitive sensations (e.g., déjà vu, jamais vu, forced thinking, dreamy states), affective states (e.g., fear, panic, depression, elation), and, classically, automatisms (e.g., lip smacking, rubbing, chewing). |
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What sx describe ictal event?
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Brief, disorganized, and uninhibited behavior characterizes the ictal event.
Although some defense attorneys may claim otherwise, rarely does a person exhibit organized, directed violent behavior during an epileptic episode. |
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The most frequent psychiatric abnormalities reported in patients with epilepsy are, especially in patients with?
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personality disorders, and they are especially likely to occur in patients with epilepsy of temporal lobe origin
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The most common features of personality change with epilepsy are:
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religiosity, a heightened experience of emotions—a quality usually called viscosity of personality—and changes in sexual behavior
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A striking religiosity may be manifested not only by increased participation in overtly religious activities but also by unusual concern for moral and ethical issues, preoccupation with right and wrong, and heightened interest in global and philosophical concerns. The hyperreligious features can sometimes seem like ? and can result in a diagnostic problem in an adolescent or a young adult.
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the prodromal symptoms of schizophrenia
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The symptom of viscosity in epilepsy of personality is usually most noticeable in
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a patient's conversation, which is likely to be slow, serious, ponderous, pedantic,
overly replete with nonessential details, and often circumstantial. The listener may grow bored but be unable to find a courteous and successful way to disengage from the conversation |
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The speech tendencies, often mirrored in the patient's writing, result in a symptom known as ?, which some clinicians consider virtually pathognomonic for complex partial epilepsy.
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HYPERGRAPHIA
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Most common sexual behaviour in people with epilepsy?
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hyposexuality, lack of interest in sexual matters and by reduced sexual arousal
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? psychotic states are more common than ? psychoses.
ictal, interictal |
Interictal psychotic states are more common than ictal psychoses.
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An estimated ? percent of all patients with complex partial epilepsy have psychotic symptoms
Risk factors for the symptoms include |
An estimated 10 percent of all patients with complex partial epilepsy have psychotic symptoms.
female gender, left-handedness, the onset of seizures during puberty, and a left-sided lesion |
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Epilepsy: compare psychosis to sz
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The most characteristic symptoms of the psychoses are hallucinations and paranoid delusions. Patients usually remain warm and appropriate in affect, in contrast to the abnormalities of affect commonly seen in patients with schizophrenia.
The thought disorder symptoms in patients with psychotic epilepsy are most commonly those involving conceptualization and circumstantiality, rather than the classic schizophrenic symptoms of blocking and looseness. |
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Episodic violence has been a problem in some patients with epilepsy, especially epilepsy of location origin
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temporal and frontal lobe origi
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Is violence usually do to seizure?
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Only in rare cases should violence in the patient with epilepsy be attributed to the seizure itself.
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Mood disorder symptoms, such as depression and mania, are seen (more, equally, less) often in epilepsy than are schizophrenia-like symptom
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less
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The mood disorder symptoms that do occur tend to be episodic and appear most often when the epileptic foci affect the temporal lobe of the (dominant, nondominant) cerebral hemisphere.
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nondominant
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Differentiate pseudoseizre from seizure
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body movements asynchronous and nonstereotyped
affected by suggestion No: nocturnal sz, aura, cynanosis, self-injury, incontinence, |
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4 key features suggesting epilepsy?
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abrupt onset psychosis in psychollogically healthy (i.e., no prodrome) person
abrupt delirium hx of similar abrupt episodes hx unexplained falling or fainting spells |
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First-line drugs for generalized tonic-clonic seizures are
|
valproate and phenytoin (Dilantin).
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First-line drugs for partial seizures include
|
carbamazepine, oxcarbazepine (Trileptal), and phenytoin.
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first-line drugs for absence (petit mal) seizures ?
|
Ethosuximide (Zarontin) and valproate are
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|
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side fx of anticonvulsants?
|
mild cog impairment
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clonazepam used in what kind of seizure ds?
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absence, atypical myoclonic
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Lamotrigine use in sz ds?
|
Complex partial seizures, generalized (augmentation)
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|
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Phenytoin (Dilantin) indication?
|
Generalized tonic-clonic, partial, status epilepticus
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|
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Valproate usage in sz ds?
|
Absence, myoclonic generalized tonic-clonic akinetic, partial seizures
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Mental symptoms are experienced at some time during the course of illness in approximately ? percent of patients with brain tumors.
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50%
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|
|
In approximately 80 percent of these patients with mental symptoms, the tumors are located in ? brain regions rather than ?
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In approximately 80 percent of these patients with mental symptoms, the tumors are located in frontal or limbic brain regions rather than in parietal or temporal regions
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|
|
Meningioma or Glioma?
? are likely to cause focal symptoms by compressing a limited region of the cortex, whereas ? are likely to cause diffuse symptoms |
Meningiomas are likely to cause focal symptoms by compressing a limited region of the cortex, whereas gliomas are likely to cause diffuse symptoms
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Delirium is most often a ? tumors
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Delirium is most often a component of rapidly growing, large, or metastatic tumors
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|
|
If a patient's history and a physical examination reveal bowel or bladder incontinence, a? tumor should be suspected;
|
If a patient's history and a physical examination reveal bowel or bladder incontinence, a frontal lobe tumor should be suspected;
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|
|
if the history and examination reveal abnormalities in memory and speech, a ? tumor should be suspected.
|
temporal lobe
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|
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Impaired ? functioning often accompanies the presence of a brain tumor, regardless of its type or location.
|
Impaired intellectual functioning often accompanies the presence of a brain tumor, regardless of its type or location.
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|
|
Type of memory loss with brain tumours?
|
Loss of memory is a frequent symptom of brain tumors. Patients with brain tumors exhibit Korsakoff's syndrome and retain no memory of events that occurred since the illness began. Events of the immediate past, even painful ones, are lost. Patients, however, retain old memories and are unaware of their loss of recent memory.
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Alterations of consciousness are common late symptoms of ? caused by a brain tumor.
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Alterations of consciousness are common late symptoms of increased intracranial pressure caused by a brain tumor.
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Tumors arising in ? can produce a unique symptom called akinetic mutism, or vigilant coma.
How does pt appear? |
Tumors arising in the upper part of the brainstem can produce a unique symptom called akinetic mutism, or vigilant coma. The patient is immobile and mute, yet alert.
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|
|
Although they are not brain tumors, ? located in the ? ventricle can exert physical pressure on structures within the diencephalon and produce such mental symptoms as ? The classic associated neurological symptoms are ?
|
Although they are not brain tumors, colloid cysts located in the third ventricle can exert physical pressure on structures within the diencephalon and produce such mental symptoms as depression, emotional lability, psychotic symptoms, and personality changes. The classic associated neurological symptoms are position-dependent intermittent headaches.
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|
|
Head trauma can result in an array of mental symptoms and lead to a diagnosis of
|
dementia due to head trauma or to mental disorder not otherwise specified due to a general medical condition (e.g., postconcussional disorder
|
|
|
Head trauma
After a period of posttraumatic amnesia, there is usually a? -month period of recovery, after which the remaining symptoms are likely to be permanent |
6 to 12 month
|
|
|
Head trauma: The most common cognitive problems are
Behaviorally, the major symptoms involve |
decreased speed in information processing, decreased attention, increased distractibility, deficits in problem-solving and in the ability to sustain effort, and problems with memory and learning new information
depression, increased impulsivity, increased aggression, and changes in personality. |
|
|
Tx of head trauma disorders?
|
Basically same as primary but One difference is that patients with head trauma may be particularly susceptible to the side effects associated with psychotropic drugs
|
|
|
Drug dosing post trauma?
|
therefore, treatment with these agents should be initiated in lower dosages than usual, and they should be titrated upward more slowly than usua
|
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|
MS: The disease is (less or more) frequent in cold and temperate climates than in the tropics and subtropics and (less or more) common in women than in men; it is predominantly a disease of (old or young) adults. In most patients, the onset occurs between the ages of ?years.
|
The disease is much more frequent in cold and temperate climates than in the tropics and subtropics and more common in women than in men; it is predominantly a disease of young adults. In most patients, the onset occurs between the ages of 20 and 40 years.
|
|
|
The neuropsychiatric symptoms of MS can be divided into
|
cognitive and behavioral types.
|
|
|
Research reports have found that ? percent of patients with MS have mild cognitive impairment and that ? percent of them have serious cognitive impairments
|
Research reports have found that 30 to 50 percent of patients with MS have mild cognitive impairment and that 20 to 30 percent of them have serious cognitive impairments
|
|
|
MS: most commonly affected cognitive fxn?
|
Although evidence indicates that patients with MS experience a decline in their general intelligence, memory is the most commonly affected cognitive function
|
|
|
MS: The severity of the memory impairment (is highly, not) correlated with the severity of the neurological symptoms or the duration of the illness
|
The severity of the memory impairment does not seem to be correlated with the severity of the neurological symptoms or the duration of the illness
|
|
|
Behavioural ds in MS?
|
25% euphoria
up to 50% depression up to 40% personality change |
|
|
Risk factors for suicide in patients with MS are
|
male sex,
onset of MS before age 30, and a relatively recent diagnosis of the disorder |
|
|
? is a progressive, noninherited disease of asymmetrical muscle atrophy
associated psych ds? |
ALS
dementia |
|
|
Herpes simplex encephalitis, the most common type of ? encephalitis, most commonly affects the lobes
|
focal
frontal and temporal lobes |
|
|
HSV sx?
|
he symptoms often include anosmia, olfactory and gustatory hallucinations, and personality changes and can also involve bizarre or psychotic behaviors
Complex partial epilepsy |
|
|
The incubation period for ? ranges from 10 days to 1 year, after which symptoms of restlessness, overactivity, and agitation can develop
other unique symptom? |
rabies
Hydrophobia, present in up to 50 percent of patients, is characterized by an intense fear of drinking water. The fear develops from the severe laryngeal and diaphragmatic spasms that the patients experience when they drink water. Once rabies encephalitis develops, the disease is fatal within days or weeks. |
|
|
Neurosyphilis (also known as general paresis) appears ? years after the primary Treponema infection.
|
Neurosyphilis (also known as general paresis) appears 10 to 15 years after the primary Treponema infection.
|
|
|
Neurosyphilis generally affects the ? lobes and results in
|
personality changes, development of poor judgment, irritability, and decreased care for self
|
|
|
Delusions of ? develop in 10 to 20 percent of affected patients with neurosyphilis
|
Delusions of grandeur develop in 10 to 20 percent of affected patients.
|
|
|
Neurosyphilis progression?
|
The disease progresses with the development of dementia and tremor, until patients are paretic.
|
|
|
The neurological symptoms of neurosyphilis include
|
Argyll-Robertson pupils, which are small, irregular, and unequal and have light-near reflex dissociation, tremor, dysarthria, and hyperreflexia.
|
|
|
Cerebrospinal fluid (CSF) examination shows what in neurosyphilis
|
lymphocytosis, increased protein, and a positive result on a Venereal Disease Research Laboratory (VDRL) test.
|
|
|
? is a disease of childhood and early adolescence, with a 3-to-1 male-to-female ratio. The onset usually follows either an infection with measles or a vaccination for measles. The initial symptoms may be behavioral change, temper tantrums, sleepiness, and hallucinations, but the classic symptoms of myoclonus, ataxia, seizures, and intellectual deterioration eventually develop. The disease progresses relentlessly to coma and death in 1 to 2 years.
|
Subacute sclerosing panencephalitis
|
|
|
?Disease?
A characteristic bull's-eye rash (Fig. 10.5-6) is found at the site of the tick bite, followed shortly thereafter by flu-like symptoms. Impaired cognitive functioning and mood changes are associated with the illness and may be the presenting complaint. These include memory lapses, difficulty concentrating, irritability, and depression. |
Lyme disease
bite of deer tick |
|
|
Lyme ds tx?
|
Treatment consists of a 14- to 21-day course of doxycycline (Vibramycin), which results in a 90 percent cure rate
|
|
|
Prion disease is a group of related disorders caused by a transmissible infectious protein known as a prion. Included in this group are
|
Creutzfeldt-Jakob disease (CJD), Gerstmann-Straussler-Scheinker disorder (GSS), fatal familial insomnia (FFI), and kuru.
A variant of CJD (vCJD), also called “mad cow disease,” appeared in 1995 in the United Kingdom and is attributed to the transmission of bovine spongiform encephalopathy (BSE) from cattle to humans |
|
|
Collectively, these disorders are also known as subacute spongiform encephalopathy because of shared neuropathological changes that consist of
|
(1) spongiform vacuolization,
(2) neuronal loss, and (3) astrocyte proliferation in the cerebral cortex. Amyloid plaques may or may not be present. |
|
|
Disease?
It manifests initially with fatigue, flu-like symptoms, and cognitive impairment. As the disease progresses, focal neurological findings such as aphasia and apraxia occur. Psychiatric manifestations are protean and include emotional lability, anxiety, euphoria, depression, delusions, hallucinations, or marked personality changes. The disease progresses over months, leading to dementia, akinetic mutism, coma, and death. |
CJD
|
|
|
How dx CJD?
|
need brain pathology
Although not specific for CJD, EEG abnormalities are present in nearly all patients, consisting of a slow and irregular background rhythm with periodic complex discharges. Computed tomography (CT) and MRI studies may reveal cortical atrophy later in the course of disease. Single photon emission computed tomography (SPECT) and positron emission tomography (PET) reveal heterogeneously decreased uptake throughout the cortex. |
|
|
Clinicians must be alert to the diagnosis in young people with behavioral and psychiatric abnormalities in association with cerebellar signs such as ataxia or myoclonus
?Dx? |
variant CJD
|
|
|
? is an epidemic prion disease found in New Guinea that is caused by cannibalistic funeral rituals in which the brains of the deceased are eaten.
Women are more affected by the disorder than men, presumably because they participate in the ceremony to a greater extent. Death usually occurs within 2 years after symptoms develop. Neuropsychiatric signs and symptoms consist of ataxia, chorea, strabismus, delirium, and dementia. |
Kuru
|
|
|
First described in 1928, ? is a neurodegenerative syndrome characterized by ataxia, chorea, and cognitive decline leading to dementia.
|
Gerstmann-Straussler-Scheinker Disease
|
|
|
It is caused by a mutation in the PrP gene that is fully penetrant and autosomal dominant; thus the disease is inherited, and affected families have been identified over several generations.
Disease? |
Gerstmann-Straussler-Scheinker Disease
|
|
|
? is an inherited prion disease that primarily affects the thalamus. A syndrome of insomnia and autonomic nervous system dysfunction consisting of fever, sweating, labile blood pressure, and tachycardia occurs that is debilitating. Onset is in middle adulthood, and death usually occurs in 1 year. No treatment currently exists.
|
Fatal Familial Insomnia
|
|
|
?is an autoimmune disease that involves inflammation of multiple organ systems
|
Systemic lupus erythematosus (SLE) is an autoimmune disease that involves inflammation of multiple organ systems
|
|
|
The major symptoms are depression, insomnia, emotional lability, nervousness, and confusion. Treatment with steroids commonly induces further psychiatric complications, including mania and psychosis.
Dx? |
Systemic lupus erythematosus (SLE)
|
|
|
hyperthyroidism sx?
|
Hyperthyroidism is characterized by confusion, anxiety, and an agitated, depressive syndrome. Patients may also complain of being easily fatigued and of feeling generally weak. Insomnia, weight loss despite increased appetite, tremulousness, palpitations, and increased perspiration are also common symptoms. Serious psychiatric symptoms include impairments in memory, orientation, and judgment; manic excitement; delusions; and hallucinations.
|
|
|
Describe sx of HYPOthydroism
|
In 1949, Irvin Asher named hypothyroidism “myxedema madness.” In its most severe form, hypothyroidism is characterized by paranoia, depression, hypomania, and hallucinations. Slowed thinking and delirium can also be symptoms. The physical symptoms include weight gain, a deep voice, thin and dry hair, loss of the lateral eyebrow, facial puffiness, cold intolerance, and impaired hearing. Approximately 10 percent of all patients have residual neuropsychiatric symptoms after hormone replacement therapy.
|
|
|
Describe hypercalcemia
|
Dysfunction of the parathyroid gland results in the abnormal regulation of calcium metabolism. Excessive secretion of parathyroid hormone causes hypercalcemia, which can result in delirium, personality changes, and apathy in 50 to 60 percent of patients and cognitive impairments in approximately 25 percent of patients. Neuromuscular excitability, which depends on proper calcium ion concentration, is reduced, and muscle weakness may appear.
|
|
|
Describe hypocalcemia
|
Hypocalcemia can occur with hypoparathyroid disorders and can result in neuropsychiatric symptoms of delirium and personality changes. If the calcium level decreases gradually, clinicians may see the psychiatric symptoms without the characteristic tetany of hypocalcemia. Other symptoms of hypocalcemia are cataract formation, seizures, extrapyramidal symptoms, and increased intracranial pressure.
|
|
|
Adrenal disorders disturb the normal secretion of hormones from the adrenal cortex and produce significant neurological and psychological changes. Patients with chronic adrenocortical insufficiency (Addison's disease), which is most frequently the result of adrenocortical atrophy or granulomatous invasion caused by tuberculous or fungal infection, exhibit ? mental symptoms, such as Occasionally, ? or ? reactions develop. ? or one of its synthetic derivatives is effective in correcting such abnormalities.
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Adrenal disorders disturb the normal secretion of hormones from the adrenal cortex and produce significant neurological and psychological changes. Patients with chronic adrenocortical insufficiency (Addison's disease), which is most frequently the result of adrenocortical atrophy or granulomatous invasion caused by tuberculous or fungal infection, exhibit mild mental symptoms, such as apathy, easy fatigability, irritability, and depression. Occasionally, confusion or psychotic reactions develop. Cortisone or one of its synthetic derivatives is effective in correcting such abnormalities.
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Excessive quantities of ? produced endogenously by an adrenocortical tumor or hyperplasia (Cushing's syndrome) lead to ?
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excessive cortisol
lead to a secondary mood disorder, a syndrome of agitated depression, and often suicide Decreased concentration and memory deficits may also be present. Psychotic reactions, with schizophrenia-like symptoms, are seen in a few patients. |
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The administration of high doses of exogenous corticosteroids typically leads to a ?. Disorder? can follow the termination of steroid therapy.
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The administration of high doses of exogenous corticosteroids typically leads to a secondary mood disorder similar to mania. Severe depression can follow the termination of steroid therapy.
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Patients with ? failure can exhibit psychiatric symptoms, particularly postpartum women who have hemorrhaged into the ?, a condition known as? syndrome. Patients have a combination of symptoms, especially of thyroid and adrenal disorders, and can show virtually any psychiatric symptom.
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Patients with total pituitary failure can exhibit psychiatric symptoms, particularly postpartum women who have hemorrhaged into the pituitary, a condition known as Sheehan's syndrome. Patients have a combination of symptoms, especially of thyroid and adrenal disorders, and can show virtually any psychiatric symptom.
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Severe hepatic failure can result in hepatic encephalopathy, characterized by
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asterixis, hyperventilation, EEG abnormalities, and alterations in consciousness
The alterations in consciousness can range from apathy to drowsiness to coma. Associated psychiatric symptoms are changes in memory, general intellectual skills, and personality. |
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Renal failure is associated with sx?
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memory, orientation, and consciousness.
Restlessness, crawling sensations on the limbs, muscle twitching, and persistent hiccups are associated symptoms |
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Hypoglycemic encephalopathy can be caused either by
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excessive endogenous production of insulin or by excessive exogenous insulin administration
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Describe progression of hypoglycemic encephalopathy
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The premonitory symptoms, which do not occur in every patient, include nausea, sweating, tachycardia, and feelings of hunger, apprehension, and restlessness. As the disorder progresses, disorientation, confusion, and hallucinations, as well as other neurological and medical symptoms, can develop. Stupor and coma can occur, and a residual and persistent dementia can sometimes be a serious neuropsychiatric sequela of the disorder.
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? begins with feelings of weakness, easy fatigability, and listlessness and increasing polyuria and polydipsia. Headache and sometimes nausea and vomiting appear.
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Diabetic ketoacidosis
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The triad of symptoms is acute, colicky abdominal pain, motor polyneuropathy, and psychosis.
Dx? |
Acute Intermittent Porphyria
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Acute intermittent porphyria is an (genetic type?) disorder that affects more gender? and has its onset between ages?
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Acute intermittent porphyria is an autosomal dominant disorder that affects more women than men and has its onset between ages 20 and 50.
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The psychiatric symptoms of Acute Intermittent porphyria include:
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anxiety, insomnia, lability of mood, depression, and psychosis
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Drug? precipitate or aggravate the attacks of acute porphyria
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Barbiturates precipitate or aggravate the attacks of acute porphyria
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The neuropsychiatric symptoms of ? include apathy, irritability, insomnia, depression, and delirium; the medical symptoms include dermatitis, peripheral neuropathies, and diarrhea.
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pellagra
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Pellagra is due to?
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Dietary insufficiency of niacin (nicotinic acid) and its precursor tryptophan is associated with pellagra, a globally occurring nutritional deficiency disease seen in association with alcohol abuse, vegetarian diets, and extreme poverty and starvation.
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The course of pellagra has traditionally been described as “five Ds”
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dermatitis, diarrhea, delirium, dementia, and death
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? deficiency leads to beriberi, characterized chiefly by cardiovascular and neurological changes, and to Wernicke-Korsakoff syndrome, which is most often associated with chronic alcohol abuse
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Thiamine (Vitamin B1)
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Describe sx of beriberi
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Beriberi occurs primarily in Asia and in areas of famine and poverty. The psychiatric symptoms include apathy, depression, irritability, nervousness, and poor concentration; severe memory disorders can develop with prolonged deficiencies.
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macrocytic megaloblastic anemia,
Mental changes, such as apathy, depression, irritability, and moodiness disorder? |
Deficiencies in cobalamin (vitamin B12) arise because of the failure of the gastric mucosal cells to secrete a specific substance, intrinsic factor, required for the normal absorption of vitamin B12 in the ileum. The deficiency state is characterized by the development of a chronic macrocytic megaloblastic anemia (pernicious anemia) and by neurological manifestations resulting from degenerative changes in the peripheral nerves, the spinal cord, and the brain. Neurological changes are seen in approximately 80 percent of all patients. These changes are commonly associated with megaloblastic anemia, but they occasionally precede the onset of hematological abnormalities.
Mental changes, such as apathy, depression, irritability, and moodiness, are common. In a few patients, encephalopathy and its associated delirium, delusions, hallucinations, dementia, and, sometimes, paranoid features are prominent and are sometimes called megaloblastic madness. The neurological manifestations of vitamin B12 deficiency can be rapidly and completely arrested by early and continued administration of parenteral vitamin therapy. |
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depression, irritability, and psychosis. Associated neurological symptoms are headache, tremor, and weakness.
Associated symptoms are sensory neuropathies, cerebellar ataxia, dysarthria, paresthesias, and visual field defects = what? |
Mercury poisoning can be caused by either inorganic or organic mercury. Inorganic mercury poisoning results in the “mad hatter” syndrome (previously seen in workers in the hat industry who softened felt by putting it in their mouths),
Organic mercury poisoning can be caused by contaminated fish or grain Mercury poisoning in pregnant women causes abnormal fetal development. No specific therapy is available, although chelation therapy with dimercaprol has been used in acute poisoning. |
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dizziness, clumsiness, ataxia, irritability, restlessness, headache, and insomnia = what disorder?
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lead level of 200 ml/L
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lead poisoning progression?
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Later, an excited delirium occurs, with associated vomiting and visual disturbances, and progresses to convulsions, lethargy, and coma
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How tx lead poisoning?
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Treatment of lead encephalopathy should be instituted as rapidly as possible, even without laboratory confirmation, because of the high mortality. The treatment of choice to facilitate lead excretion is intravenous administration of calcium disodium edetate (calcium disodium versenate) daily for 5 days.
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How does lead poisoning occur?
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Lead poisoning occurs when the amount of lead ingested exceeds the body's ability to eliminate it. It takes several months for toxic symptoms to appear.
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causes symptoms of headache, irritability, joint pains, and somnolence.
An eventual picture appears of emotional lability, pathological laughter, nightmares, hallucinations, and compulsive and impulsive acts associated with periods of confusion and aggressiveness. gait impairment, rigidity, monotonous or whispering speech, tremors of the extremities and tongue, masked facies (manganese mask), micrographia, dystonia, dysarthria, and loss of equilibrium |
Early manganese poisoning (sometimes called manganese madness)
Lesions involving the basal ganglia and pyramidal system result in gait impairment, rigidity, monotonous or whispering speech, tremors of the extremities and tongue, masked facies (manganese mask), micrographia, dystonia, dysarthria, and loss of equilibrium |
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Managense exposure occurs how?
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The disorder is found in persons working in refining ore, brick workers, and those making steel casings.
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Early signs of toxicity are skin pigmentation, gastrointestinal complaints, renal and hepatic dysfunction, hair loss, and a characteristic garlic odor to the breath. Encephalopathy eventually occurs, with generalized sensory and motor loss. Chelation therapy with dimercaprol has been used successfully to treat
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Chronic arsenic poisoning most commonly results from prolonged exposure to herbicides containing arsenic or from drinking water contaminated with arsenic. Arsenic is also used in the manufacture of silicon-based computer chips. Early signs of toxicity are skin pigmentation,
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