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Behavioral Science Test #1
Mental Status Exam, Dementias, Personality Disorders
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MENTAL STATUS EXAMINATION:
- ALERT: Normal response to average level of stimulus.
- SOMNOLENT: Like when you wake up in the morning.
- STUPOR: No response to stimulus except brutal force, at which point only aversive behavior
is displayed.
- COMA: Absolutely no response to stimulus except autonomic responses and spinal reflexes.
Three components of behavior
- COGNITION: Learning and memory
- EMOTION: Also involves memory
- Aversive (avoidant) behavior
- Appetitive (desirous) behavior
- CONATION: Goal-seeking, directed, or planned motor behavior.
- FRONTAL LOBES are required for conation. Lesion of frontal lobes results in normal
cognition, but inability to execute planned (conative) motor tasks.
BROCA'S MOTOR SPEECH AREA 44: Inferior frontal gyrus, near temporal lobe, and near the
facial motor homunculus. Responsible for expressive speech.
WERNICKE'S RECEPTIVE SPEECH AREA 39: Superior temporal gyrus.
- Receptive Aphasia: Inability to interpret speech, results from damage to Wernicke's area.
MEMORY:
- IMMEDIATE (ATTENTIONAL) MEMORY: Ability to maintain conversation and focus
on immediate surroundings.
- Duration of seconds to minutes.
- ANATOMY:
- Neocortex must be intact to mediate attentional memory.
- Reticular Thalamic Nucleus exhibits inhibitory influence on cortices receiving
extraneous stimuli, to which you are not currently paying attention.
- DIGIT SPAN: 7 forward 5 backward, OK?
- SHORT-TERM MEMORY: Memory for a period of hours to about a day.
- ANATOMY: These two structures are responsible for putting attentional memory into
short-term memory
- Hippocampus:
- Dorsomedial Thalamic Nucleus:
- LONG-TERM (HISTORICAL) MEMORY:
- ANATOMY: Has a diffuse representation throughout the cortex. Around half of the cortex
must be gone before long-term memory is severely deficient.
- It is never lost, or is the very last thing to go in brain disease.
SPEECH ABNORMALITIES:
- Dysarthria: Abnormalities in motor production of speech, producing garbled sound.
- Aphasia: Inability to formulate meaningful speech, due to a language-based deficit -- not due
to motor deficit.
- Receptive Aphasia: WERNICKE'S APHASIA; inability to interpret speech.
- Expressive Aphasia: BROCA'S APHASIA; inability to generate speech
- COMMUNICATION APHASIA: Disconnection between Wernicke's and Broca's. Can
occur from multiple strokes in Carotid circulation.
- You can't hear yourself talk, which results in fluent language but in gibberish.
AMNESIAS:
- RETROGRADE AMNESIA: Loss of attentional memory immediately preceding a traumatic
event. The amnesia only goes back to the extent of short-term memory. It is an erasure of current
short-term memory, and long-term memory is unaffected.
- ANTEROGRADE AMNESIA: The inability to form new memories, at any time forward from
a traumatic event.
- LACUNAR MEMORY DEFICIT: A hole in memory surrounding a traumatic event; the sum
of retrograde plus anterograde amnesia.
| DELIRIUM |
DEMENTIA |
| Acute, often dramatic onset |
Gradual onset, often insidious |
| Global Amnesia: Complete loss of orientation,
attention, and short-term memory |
Selective Amnesia:
Short-term / Attentional loss is far more significant than long-term, if long-term loss is
present at all |
| Waxing and waning of severity |
Sundowning: It gets worse at night due to
loss of long-term-enabled orientation cues. |
| CAUSES: Infectious, metabolic, hemodynamic, respiratory, toxic, iatrogenic, traumatic |
CAUSES:
Idiopathic: Alzheimer's
Cumulative: Multi-Infarct Dementia
Residual: Untreated delirium leading to permanent neuronal damage |
| MISDIAGNOSIS: Confused with acute psychoses, agitated mania |
MISDIAGNOSIS: Pseudodementia in the
elderly. Elderly are often diagnosed with dementia when in fact they just have depression. |
| Frequently multifactorial etiology |
Frequently exacerbated by other conditions
which complicate it, such as depression or
alcoholism. |
| PROGNOSIS for recovery is good, reversible |
PROGNOSIS is poor. |
Acute Delirium:
- Wernicke's Encephalopathy
- DELIRIUM TREMENS: Sedative/hypnotic drug (alcohol) withdrawal.
- Symptoms:
- Hyperreflexia, clonus reflexes
- Autonomic instability (tachycardia, hypertension)
- Cortical hyperactivity: vivid dreams, hallucinations, sensory illusions)
- ICU PSYCHOSIS: Multifactorial delirium, acute brain failure.
- CAUSE: Sleep deprivation, effect of multiple drugs, no sense of time and place,
hemodynamic, respiratory, and metabolic problems.
- TREATMENT: Cause is unknown. Treat the underlying physiological problems where
possible, and eliminate all unnecessary drugs.
- WERNICKE'S ENCEPHALOPATHY: Acute Thiamine deficiency, resulting in edema and
hemorrhaging due to disruption of basement membranes.
- Cardinal Symptoms:
- Abducens Palsy (Double Vision), from hemorrhaging Abducens nerve in
Periaqueductal Grey.
- Truncal Ataxia, from hemorrhaging cerebellar vermis.
- Global Amnesia: Hemorrhage of hippocampus, dorsomedial thalamic nuclei,
mamillary bodies.
- Pathophysiology: Hemorrhaging and edema
- Mamillary bodies and dorsomedial thalamic nuclei
- Hippocampus
- Cerebellar Vermis
- Tegmentum and Periaqueductal gray.
PARKINSON'S DISEASE: Dopamine deficiency in Substantia Nigra ------> loss of inhibition
to motor output in Thalamus ------> tremor
- Symptoms:
- Resting Tremor: Inability to initiate movements, and tremor while not moving.
- Loss of facial expression and gestures
- EXTRAPYRAMIDAL NUCLEI:
- They provide inhibitory input to the motor strip.
- Motor learning skills
Visual Deficits:
- Cortical Blindness
- Visual reflexes still remain intact (flinching from a light stimulus) as long as you are intact
as far back as the LGN.
- BALINT'S SYNDROME: Lesion to dorsal secondary visual cortex.
- Simultagnosia: Inability to treat the visual field as a whole; inability to interpret the entire
visual field in association with other cortices (such is the job of the secondary cortex)
- Optic Ataxia: Inability to correctly and accurate target their vision and visually focus.
- Ocular Apraxia: Inability to shift gaze.
- VENTRAL VISUAL LESIONS: The effects are different than Balint's
- Alexia: Inability to read and write. Occurs primarily with left, but with either side since
right side is concerned with spatial recognition of shapes (letters).
- Anomia: Inability to name objects you are looking at. Occurs with left-side lesion.
- Prosopagnosia: Results from a lesion to the right ventral secondary cortex. Inability to
recognize faces.
- TERTIARY LESIONS: Unilateral Visual Neglect, as in neglect syndrome.
- Consistent lack of attention to objects in left visual field.
- When asked to draw a clock, only draw the right half of the clock face.
DEMENTIAS:
- ALZHEIMER'S DISEASE: Generalized brain atrophy occurring with age.
- Official diagnosis is used made post-mortem based on histological studies, but the disease
isn't treatable anyway so it doesn't matter.
- SIGN: Ventricular enlargement with brain atrophy. Atrophied brain results in enlarged
spaces in ventricles.
- MULTI-INFARCT DEMENTIA:
- Symptoms similar to Alzheimer's.
- Sudden onset, with large stepwise decrements in function.
- Showers of microemboli spread diffusely throughout cortex.
- KORSAKOFF'S PSYCHOSIS: Permanent loss of Mamillary Bodies and Dorsomedial Thalamic
Nuclei, resulting in complete lack of short-term memory. This is the residual effects of prolonged
Wernicke's Encephalopathy and is irreversible.
- Attentional Memory remains intact: neocortex is probably just fine, except for any unrelated
effected of alcoholism.
- Long term memory remains intact, although it may be difficult to retrieve directed
information.
- Person lives in permanent state of current world.
- Normal Pressure Hydrocephalus: Disturbance in CSF circulation.
- CSF is no longer absorbed and refluxes into the ventricular system
- SIGN: Ventricular enlargement without corresponding brain atrophy.
- SYMPTOMS:
- Truncal ataxia
- Urinary incontinence
- Dementia
- POST-TRAUMATIC DEMENTIAS: Physical injury to brain (auto-accident) resulting in damage
to anterior fossa (where the skull is bumpy) ------> damage to hippocampal and thalamic
structures.
- SYMPTOMS: Irreversible loss of short-term memory and attention, with long-term memory
intact.
KLÜVER-BUCY SYNDROME: Bilateral amygdalectomy.
ANTERIOR HYPOTHALAMUS: Associated with male-pattern sexual arousal.
CNS DEVELOPMENT:
- CRITICAL DEVELOPMENT PERIODS: As you develop, you make more and neuronal
(synaptic) interconnections, utilizing fewer and fewer and neurons. That is, many neurons
undergo apoptosis after initial neonatal period.
- 2nd and 3rd trimesters
- 8 months - 2 yrs old.
- 6-7 years
- 8-9 years
- HARLOW'S MONKEYS: Experiments raising monkeys in different environments and
observing them as adults. Three conditions were set up:
- Raised in bare-wire cage, artifical nipple, wooden armature, and source of food:
- Raised in similar cage, but arm and nipple were covered by terry cloth, providing snugly
cutaneous touch:
- They survived to become antisocials but had no reproductive success.
- Raised as in (2) but they saw a picture of a simple face
- Grew up to be nerd monkeys and tried to interact with other monkeys but had very
little reproductive success. They had more success than the other groups though.
- CRECHE SYNDROME: Baby's denied love in neonatal period have higher mortality rate and
higher rate of illness. Baby's raised in a prison where they were allowed to interact with their
mother thrived even better than the babies raised by an orphanage without such interaction.
- Talking to baby's is crucial for language development.
- PARENTING:
- Child should be able to engage parent's attention but should not have total control over
parent's attention (for fear of manipulation)
- Child should have reasonable boundaries for undergoing exploratory behavior.
PERSONALITY DISORDERS: There is a strong contribution of genetics to personality and
personality disorders, even though many disorders are difficult to characterize.
- ADJUSTMENT DISORDER: Usually comes to psychiatrist's attention as an adjustment disorder.
Episodic and self-limited disturbances of mood.
- CLUSTER-A DISORDERS: SCHIZOID
- DESCRIPTION: Emotional constriction, aloofness, difficulty forming relationships with
others
- EXAMPLES: Schizoid Personality, Paranoid Personality, Avoidant Personality
- CLUSTER-B DISORDERS: NARCISSISTIC
- DESCRIPTION: Self-absorption, indifference to the needs of others, self-centeredness,
emotional instability
- EXAMPLES: Antisocial Personality, Borderline Personality, Histrionic Personality
- ANTISOCIAL PERSONALITY:
- Characteristics:
- Repeated problems with rules and authorities as a child.
- No response to punishment; unaffected by it.
- Frequently impulsive.
- Demographics:
- Far more prevalent in males than females.
- Behaviors reach peak in early adult years and decline with age.
- Strong evidence for genetic determinant, and one of the most clearly delineated
disorders.
- Genetic link to Somatization Disorder.
- Son of antisocial disorder is 20x more likely to exhibit same behaviors.
- In contrast, learning (adoptive studies; no genetic component) only
increases risk by 2x. Thus genetics play a much larger role than learning!
- Schizotypal Disorder is the other disorder that is well characterized and
documented, and may have a genetic link.
- BORDERLINE PERSONALITY:
- Characteristics:
- Intense need for attachment, affection, and support from others.
- Narcissistic: only see world in relation to one's own needs.
- Reduced ego strength
- Treatment: Difficult; anti-depressants or anti-anxiolytics
- CLUSTER-C DISORDERS: OBSESSIVE
- DESCRIPTION: Rigid coping, restrictive behavioral patterns, dysfunctional relationships.
- EXAMPLES: Obsessive-Compulsive Personality, Passive-Dependent Personality.
- OBSESSIVE-COMPULSIVE DISORDER: There is no evidence of a link between
the personality and the true syndrome (which has physiological basis). Those
exhibiting the personality are not at increased risk of acquiring syndrome.
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