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Folstein Mini M ental S tatus Examination



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Folstein Mini M ental S tatus Examination

Task Instructions Scoring

Date


Orientation "Tell m e the date?"

One point each for

year, season, date, day

of week, and m onth

5

Place


Orientation "Where are you?"

One point each for

state, county, town,

building, and floor o r

room

5

Register 3



Objects

Name three objects slowly and clearly.

Ask the patient to repeat them.

One point for each item

correctly repeated 3

Serial


Sevens

Ask the patient to count backwards

from 100 by 7. Stop after five answers.

(Or ask them to spell "world"

backwards.)

One point for each

correct answer (or

letter)


5

Recall 3


Objects

Ask the patient to recall the objects

mentioned above.

One point for each item

correctly remembered 3

Naming Point to your w atch and ask the patient

"what is this?" Repeat w ith a pencil.

One point for each

correct answer 2

Repeating a

Phrase

Ask the patient to say "no ifs, ands, or



buts."

One point if successful

on first try 1

Verbal


Commands

Give the patient a p lain piece of paper

and say "Take this paper in your right

hand, fold it in half, and put it on the

floor."

One point for each



correct action 3

Written


Commands

Show the patient a piece of paper w ith

"CLOSE YOUR EYES" printed on it.

One point if the

patient's eyes close 1

Writing Ask the patient to w rite a sentence.

One point if sentence

has a subject, a verb,

and m akes sense

1

Drawing



Ask the patient to

copy a pair of

intersecting

pentagons onto a

piece of paper.

One point if the figure

has ten corners and two

intersecting lines

1

Scoring A score of 24 or above is considered normal. 30

Biological assessment of psychiatric PT’s:

Ie.. significance of CT scan, GCS (glascow scale) what are the scoring system:

Then aging death and bereavement:

Cobler Ross:

Stages of death and dying:

-she intervied many PT what the response wherei ie.. denial, anger, bargaining,
Stages of dying and death…..Elizabeth Kubler Ross…………DABDA


  • Denial – Patient refuses to believe he is dying….eg laboratory made an error…

  • Anger – Patient blames physician and hospital staff for his dying….Patient says its their fault.

  • Bargaining – The patient tries to strike a bargain with God….eg he will give half of his wealth to charity if God can remove the disease.

  • Depression – The patient becomes emotionally detached as they are preoccupied with death.

  • Acceptance – patient is calm and accepts his/her fate

On Death and Dying

Grieving One’s Own Impending

Death

Elisabeth Kubler-Ross, MD



• Swiss Born Psychiatrist

• Attacked by colleagues for interviewing

dying patients (considered taboo)

• Prior to her contributions, American and

Western doctors never directly told

patients that they were dying


Five Stages of Grief

• Kubler-Ross described five stages of grief

in her 1969 bestseller, Death and Dying

• Stages do not strictly follow one another,

but can ebb and flow depending on the

type of personality or situation

• In the elderly, the grief process may be

associated with the “loss of youth” or

function
Hospice Movement ‘N Kubler-

Ross


• Kubler-Ross was a pioneer of the hospice

movement of the early 70’s, which pushed

patient palliative care to the forefront

• Her work on death removed the taboo and

allowed patients, doctors, and families to

talk about death

• Patients were given autonomy and dignity

with death


Five Stages of Grief: DABDA

Denial

Anger

Bargaining

Depression

Acceptance



KUBLER ROSS: STAGES OF

DYING (5):

• Dying person may

experience several intense

emotions.


DENIAL:

• "No, not me!"

• patient rejects the news

• initial positive defense

mechanism but can become

a problem if reinforced by

family and friends, leading to

poor coping.

13

Stage One: Denial (D) and



Shock

• Patients may appear dazed, or confused about

the diagnosis or deny that anything is wrong

• Resistance to accepting the diagnosis is usually

an unconscious phenomenon

• Physician’s tasks:

– Respect patient’s denial while still communicating

information clearly about the diagnosis, prognosis,

and options for treatment

– Decrease patient’s fears of abandonment by clarifying

that they will continue to care for them

Stage One: Denial (D)

• Can be adaptive or maladaptive

• This stage usually resolves within hours or

days, but…

• Some patients never pass beyond this

stage

ANGER

ANGER:

• "Why me?"

• resentment and rage

over impending

death;

• may be directed



outwards at loved

ones.


Stage Two: Anger (A)

• Anger, irritability, frustration

• “Why me!”

• Anger can be directed at God, family, even self

• Anger may be displaced onto hospital staff or

physicians

• May reflect frustration at lack of control over

situation

• Physician’s task:

– Maintain a non-defensive, empathic manner

14

BARGAINING

acknowacknowledgement

but……...

try to bargain with

GOD

in this stage e.g

Exchange recovery

promise to be a better

person

Stage Three: Bargaining (B)

• Bargain or barter with doctors, family, or

God


• Bargaining may involve keeping pledges-

– i.e. giving to charity, attending church, or

becoming a non-questioning, compliant

patient


• Physicians task:

– Encourage patients to be partners in their

care

– Be honest and straightforward with their



symptoms and care

DEPRESSION:

gradual realization of



consequences

difficult time - persons



needs to be watched and

supported

a period of grieving



must be allowed to work

through this stage

trying to cheer up isn’t an



asset now!

Stage Four: Depression (D)

• Patients may show clinical signs of

depression such as apathy,

withdrawal/social isolation, sleeplessness,

hopelessness, suicidal ideation

• Signs of sadness over impending death

are normal…but,

Major depressive symptoms and

suicidal thoughts are NOT Normal and

may warrant treatment with medications,

etc.
ACCEPTANCE

• “I’m m scared but,



I'm ready."

These stages may



overlap and

repeat.

Stage Five: Acceptance (A)

• Patients come to accept the inevitability

and universality of death

• Able to use/enjoy remaining time

• Moods may range from neutral to euphoric

• Resolution of discomfort with thoughts of

death


• Patients may gain comfort talking about

death


• Belief in an afterlife is comforting to many

For most, transition thru the 5

stages takes time...but not for

everyone…

Kubler-Ross: “Dying with

Dignity”

• Kubler-Ross died in August, 2004

• “What does it mean to die with dignity?“

– "To die with dignity to me means to die within

your character. That means there are people

who have used denial all their life long; they

will most likely die in a stage of denial. There

are people who have been fighters and rebels

all their life long, and by golly they want to die

that way. And to those patients we have to

help them, to say it's OK."

Kubler-Ross 1975


DEFINITION OF DEATH:

Spiritual death:

death of meaningful life

including responsiveness to others, with activity

of the brain and consciousness

ALSO: Unreceptive and unresponsive

to painful stimuli - CPR

No movement for an hour

No breathing for 3 minutes

No reflexes

Pupils fixed and dilated - flat EEG

LIFE SIGNS………………..

DEFINITION OF DEATH:

Traditional legal definition:

• failure of heart and lungs = functional

death.

Modern medicine:

• brain death = absence of electrical

impulse activity in the brain (EEG).

Cellular death:

• Cells die- e.g., heart, brain, muscle



CIRCUMSTANCES OF DEATH

Death at/or before 50 years of



age or younger emotional

trauma – unexpected

Religious belief = less fear

Pain and physical distress.

Immediately prior to death



there is often an increased in

vitality

People often "hold on" for a



specific life event or person

EUTHANASIA: Mercy killing.

INDIRECT INVOLUNTARY

(PASSIVE) -

remove life support

DIRECT VOLUNTARY

administer fatal drug as condition

worsens

DIRECT INVOLUNTARYdrug



once a patient is in a coma.

ILLEGAL / ETHICAL ISSUES


• Who will you disclose to someone that he

has terminal carcinoma pancreas.



how you would differnetiatewhether they are grieve or major depression and focus on the class i.e.major depression i.e. committing suicide and different between grieve and major depression.

Differentiate between major depression, grief or bereavement`


Normal grief is characterized by shock, denial and perhaps illusion.

It normally subsides after 1 to 2 years. There is usually minor weight loss, minor sleep disturbances and some guilty feelings, cries and expresses sadness….

Anything more than this is Abnormal grief (DEPRESSION).
In major depressive disorder, there is recurrent episodes of depression, each continuing for at least 2 weeks. The hallmark of this is that patient feels sadness, hopelessness, helplessness, low self esteem and excessive guilt.
Postnatal blue, bereavement, grieve:
Baby blue which starts a few days following post partum lasts up to 2 weeks after childbirth. This is as a result of stress of childbirth and change in hormonal level. Treatment includes emotional support from physician. Characterised by exaggerated emotions and good grooming.
Major depression and brief psychotic disorder which starts 4 weeks and 2 weeks (respectively) following postpartum onset are treated with antidepressant and antipsychotic medications. In major depression, mother develops poor self care, lacks pleasure or interest and feels hopeless.
In brief psychotic disorder, mother becomes psychotic and may harm infant.
The Grieving Process

Grief and Bereavement

• Grief and bereavement are finely

differentiated

• Essentially describe the process and

feelings following loss (death) of family,

friends, and others significant in the

individual’s life

• Can also grieve losses of function, status,

occupation, etc.

“Normal” Grief

• No “normal” way to grieve

• Grieving process may vary widely between

individuals AND within the same

individual:

– Same person may grieve different losses in

different ways

“Normal Grief”

• Grieving process varies widely between

cultures and individuals

• Not abnormal to experience shock,

disbelief, numbness initially

• Feelings of guilt are common, vary in

intensity (may become overwhelming in

pathological grief)

• May experience Survivor Guilt

“Normal” Grief

• Dreams about the deceased or actual

hallucinations-auditory or visual are not

uncommon


• These “mis-perceptions” are not

pathologic if the patient has insight that

they are not real

Grief versus Depression

• Many of the symptoms of grief are similar

to clinical depression

– Ex. Sadness, poor sleep, diminished

interests, feelings of weakness, decreased

appetite, weight loss, trouble concentrating

– Certain elements, including time-course/

duration help distinguish grief from clinical

depression



Fine Details:

Grief vs. Major Depression

GRIEF

– Bereaved rarely have

intense feelings of guilt

or worthlessness

– Active suicidal ideation

is uncommon; passive

thoughts are common

DEPRESSION:

– Guilt and feelings of

worthlessness are

common and often

excessive

– Suicidal ideation is

common in severe

depression

Grief vs. Major Depression

GRIEF

– Onset is usually within

the first two months of

the loss

– Acute symptoms of

grief usually resolve

within two months of

the loss. (upto 2 years)

DEPRESSION

– Onset at any time

– Depression is chronic,

intermittent or episodic

Grief vs. Major Depression

GRIEF

– Impairment in daily

living is mild and

transient

– There is no loss of

hope for return to

normal function

– Psychosis limited to

brief hallucinations

DEPRESSION

– Impairment in daily

living is significant

– A loss of hope for the

future is common

– More prominent

psychotic symptoms

possible
How you manage a person or person: loved one died in family: what support you can provide for those circumstances
MAKE IT IN SMALL packets: and we have ordered investigation nd they are suggesting and you are not hundred percent, porstate, if you think that it’s the last stage and they’re not going to live for more than 2 years: then first stage: you are diagnosed with: just tell him, he’s diagnosed with a cancer, don’t use medical jargon: then if PT asks: am I going to die: how much time and I going to live: am I going to die? If survie one month: investigation suggest that you’re cancer is not at the prime and ivnovled more organs: most people don’t live for more than 2 months: statis say this: A B and C. and I’ll be ale to reply to this: and so that they know what’s going on: and if they want to make a will or do some traveling: and they have some time to do what they want. Never GIVE THEM FALSE HOPE!!

If they’re suricidal don’t disclose the information


Inform family that they’re loved ones died and it’s difficult information has disclosed: first stament should not be: he’s dead:

It depends: after accident and he was bleeding and family member and mentally and made up their mind: so it’s not necessary very detailed: b/c they were the one that brought them, bu first of all: show sympathy that you feel sorry and you did everything but unforutnaly and unforutatnly they have died… don’t show smiling…

And if they’re cyring and denial again, it’s your duty to provide them and maybe they’re refered to to a pyschiatriast…

If someone died: 85 yeard old expiered, family members: and on the other hand: if they were 3 years of age, it would be difficult to accept this… and how close was the relationship and whether who was belonged is anelderly: and it’s bad and it’s acceptable…


Under supervision: and you screw up: they will never allow you to do this: chances of accident they’re not large: but it can happen: and there’s two answer:

-if you go to lawyer: they wil tell them something else:

but ethical aspect: you have to inform first of them and b/c of that mistake someone has died: most of the time: they won’t ask you: they’ll inform this through family member that the person has expired: depends on hospital will not disclose information: if you want to disclose: and you will also be scared and never disclose it…

screw up your career…



Gorss anatomy and biochemistr y and behaviour: focus on anaomtical difference based on gender: in CNS: if you do a CT scan: anatomically differences:

Anatomy & Biochemistry of Behavior

Chapter 4



NEUROANATOMY

  • THE HUMAN NERVOUS SYSTEM CONSISTS OF CENTRAL NERVOUS SYSTEM AND PERIPHERAL NERVOUS SYSTEM.

  • THE CEREBRAL HEMISPHERES:

BOTH HEMISPHERE ARE CONNECTED BY CORPUS CALLOSUM, ANTERIOR COMMISURE, HIPPOCAMPAL COMMISURE AND HABENULAR COMMISURE.

  • THE FUNCTION OF HEMISPHERES ARE LATERALIZED.



  • LEFT DOMINANT HEMISPHERE:

  • ASSOCIATED WITH LANGUAGE

  • DOMINANT IN 97% OF PERSONS, 60-70% IN LEFT HANDED PERSONS

  • CALCULATION TYPE PROBLEM SOLVING

  • STROKE DAMAGE TO LT HEMISPHERE IS MORE LIKELY TO LEAD TO DEPRESSION

  • LARGER IN SIZE THAN RIGHT AND PROCESS INFORMATION FASTER

  • THE RIGHT NON DOMINANT HEMISPHERE:

  • ASSOCIATED WITH PERCEPTION, ARTISTIC AND VISUAL –SPATIAL ABILITIES

  • ACTIVATION FOR INUITION TYPE PROBLEMS SOLVING

  • STROKE DAMAGE TO TR SIDE LEADS TO APATHY AND INDIFFERENCE

  • PROSODY RESIDES HERE




  • SEX DIFFERENCES IN CEREBRAL LATERIZATION:

  • WOMEN HAVE A LARGER CORPUS CALLOSUM AND ANT. COMMISSURE AND APPEAR TO HAVE A BETTER INTERHEMISPHERIC COMMUNICATION THAN MEN.

MEN HAVE BETTER DEVELOPED RIGHT HEMISPHERE AND APPEARS TO BE BETTER AT SPATIAL TASKS THAN WOMEN.
Maybe few neurotransmitters that play an important rule in psychiatry

-role of neurotransmitter

NEUROTRANSMISSIONS

  • THREE MAIN TYPES OF NEUROTRANSMITTERS:

  • BIOGENIC AMINES

  • AMINOACIDS

  • PEPTIDES

BIOGENC AMINES

DOPAMINE


NOREPINEPHRINE

SEROTONIN



DOPAMINE

  • CATECHOLAMINE RESPONSIBLE FOR PATHOPHYSIOLOGY FOR SCHIZOPHRENIA, PARKINSON DISEASE, MOOD DISORDERS, CONDITIONED FEAR RESPONSE AND REWARDING NATURE OF DRUG OF ABUSE.

  • SYNTHESIS: FROM TYROSINE > DOPA > DOPAMINE > NE

  • HOMOVANILLIC ACID IS METABOLITE OF DOPAMINE USED AS SCREEN FOR DOPAMINE RELATED DYSFUNCTIONS.

Dopamine Pathways

4 Main Pathways:



  • Nigrostrital Pathway.

  • Mesolimbic /Mesocortical pathway.

  • Tuberoinfundibular Pathway.

  • Incertohypothalamic pathway

  • Chemoreceptor Trigger zone.

Nigrostriatal Pathway


  • INVOLVED IN REGULATION OF MUSCLE TONE AND MOVEMENT

  • CELL BODIES OF NEURONS IN S.NIGRA PROJECT TO STRIATUM, WHERE THEY RELEASE DOPAMINE. IN PARKINSON’S DISEASE LOSS OF DOPANERGIC NEURONS IN THIS PATHWAY LEADS TO EXCESSIVE ACTIVITY AND PYRAMIDAL DYSFUNCTION.

  • TREATMENT WITH ANTIPSYCHOTIC DRUGS, WHICH BLOCK POST SYNAPTIC DOPAMINE RECEPTORS RECEIVING INPUTS FROM NIGROSTRIATAL PATHWAY, CAN RESULT IN PARKINSON LIKE SYNDROME.

MESOLIMBIC MESOCORTICAL PATHWAY

  • DOPAMINE IN THIS PATHWAY LEADS TO PSYCHOMOTOR STIMULATION AND EXPRESSION OF MOOD DUE TO LINK TO LIMBIC SYSTEM

  • INCREASE DOPAMINE = EUPHORIA, PARANOIA, PSYCHOSIS, SCHIZOPHRENIA.

  • DECREASE DOPAMINE = DECREASE PSYCHOMOTOR ACTIVITY



  • TUBEROINFUNDIBULAR PATHWAY:

  • INHIBIT PROLACTIN SECRETION

  • PROLACTIN INHIBITORY FACTOR

  • USE OF ANTIPSYCHOTIC DRUGS BLOCK DOPAMINE RECEPTORS AND CAUSE GYNECOMASTIA IN MEN AND SECONDARY AMENORRHEA & GALACTORRHEA IN WOMEN DUE TO INCREASE PROLACTIN LEVELS

  • SIMILARY, USE OF DOPAMINE AGONISTS, BROMOCRIPTINE, CAUSE SUPRESSION OF PROLACTIN SECRETION IN PITUITARY ADENOMA SECRETING PROLACTIN (PROLACTINOMA)




  • INCERTOHYPOTHALAMIC PATHWAY:

  • CONTROL APPETITE (SURPRESSES) AND TEMPERATURE




  • CHEMORECEPTOR TRIGGER ZONE:

  • DOPAMINE STIMULATES EMESIS(VOMITING)

NOREPINEPHRINE (NE)

  • PLAYS MJOR ROLE IN MOOD, ANXIETY, AROUSAL, LEARNING AND MEMORY.

  • SYNTHESIES FROM TYROSINE.

  • MOST NE NEURONS ARE LOCATED IN LOCUS CERELUS IN PONS.

  • TWO METABOLITES ARE USED TO MONITOR ITS ACTIVITY:

  • VANILLYLMANDELIC ACID (VMA)

  • INCREASED IN PHEOCHROMOCYTOMA

  • 3-METHOXY4-HYDROXYPHENYLGLYCOL

  • DECREASED IN DEPRESSION AND ATTEMPTED SUICIDE

Symptoms of pheos

  • Headaches (severe)

  • Excess sweating (generalized)

  • Racing heart (tachycardia and palpitations)

  • Anxiety/nervousness (feelings of impending death)

  • Nervous shaking (tremors)

  • Pain in the lower chest or upper abdomen

  • Nausea (with or without nausea)

  • Weight loss

  • Heat intolerance

SEROTONIN (5-HT)

  • PLAYS A ROLE IN MOOD, SLEEP, SEXUALITY, AND INPULSE CONTROL

  • INCREASE SEROTONIN IS ASSCOCIATED WITH IMPROVED MOOD AND SLEEP BUT DECREASED IN SEXUAL FUNCTION

  • DECREASED SEROTONIN IS ASSOCIATED WITH POOR IMPULSE CONTROL, DEPRESSION AND POOR SLEEP.

  • SYNTESIZED FROM TRYPTOPHAN BY TRYPTOPHAN HYDROXYLASE

  • MOST OF SEROTONERGIC NEURONS ARE LOCATED IN DORSAL RAPHE NUCLEUS



  • ANTIDEPRESSENTS AND SEROTONIN:

  • ANTIDEPRESSENT INCREASES THE PRESENCE OF SEROTONIN AND NE IN SYNAPTIC CLEFT.

  • HETEROCYCLICS BLOCK REUPTAKE OF SEROTONIN AND NE

  • SSRI:SEROTONIN REUPTAKE INHIBITORS BLOCK REUPTAKE OF SEROTONIN ONLY

  • MAO INHIBITORS PREVENT THE DRGRADATION OF SEROTONIN AND NE BY MAO.

ACETYLCHOLINE

  • DEGENERATION OF CHOLIHERGIC NEURONS IS ASSOCIATED WITH DEMENTIA OF ALZHIEMERS TYPE, DOWN SYNDROME, AND MOVEMENT AND SLEEP DISORDERS.

  • IN THE SYNAPTIC CLEFT ACETYLCHOLINE IS BROKEN DOWN BY ACETYLCHOLINESTERASE (ACHE)

  • ACHE BLOCKERS SUCH AS TACRINE AND DONEPEZIL CAN DELAY PROGRESSION OF ALZHIEMER DEMENTIA .

  • BLOCKADE OF MUSCURANIC ACETYLCHOLINE RECEPTOR BY ANTDEPRESSENT AND ANTIPSYCHOTIC DRUGS RESULT IN CLASSICAL ANICHOLINERGIC OR ANTIMUCURANIC SIDE AFECTS SUCH AS DRY MOUTH, BLURRED VISION, URINARY HESITANCY AND CONSTIPATION.

AMINOACID NT’S

GABA


GLYCINE

GLUTAMATE




  • GABA:

  • GAMMA AMINOBUTYRIC ACID

  • PRINCIPLE INHIBITORY NT OF CNS

  • LIKED TO CL CHANNEL OPENING CAUSING INHIBITION OF NEURAL FIRING

  • BENZODIAZEPINES WORK BY INCREASE FREQUENCY OF CL CHANNEL OPENING BY STIMULATING GABA RECEPTORS

  • BARBITURATES INCREASE DURATION OF CL CAHNNEL OPENING.

  • Barbiturates and benzodiazepins are prescription drugs from the sedative-hypnotic group

  • GLYCINE:

  • INHIBITORY NT

  • WORK ON ITS OWN OR AS REGULATER OF GLUTAMATE ACTIVITY

  • GLUTAMATE:

  • EXCITAORY NT ASSOCIATED WITH EPILEPSY, SCHIZOPHRENIA, NEURODEGENERATIVE ILLNESS.


NEUROPEPTIDES

  • ENKEPHALINS AND ENDORPHINS ARE OPIODS PRODEUCED BY BRAINITSELF THAT DECREASE PAIN AND ANXIETY.

  • PLACEBO EFFECT:IS MEDIATED BY ENDOGENOUS OPIODS SYSTEM.PRIOR TREATMENT WITH OPOID ANTAGONIST SUCH AS NALAXONE CAN BLOCK PLACEBO AFFECT


brain lesion: depending on portion of scar and cerebral hemisphere: i.e. frontal lobe lesion, parietal, or occipital lesion, what are the findings.
lesions of CNS and psychiatric manifestations:


LOCATION OF LESION

EFFECTS OF LESION ON BEHAVIOR

Frontal lobe

Inability to speak properly (Broca’s aphasia), judgement and emotional difficulty, loss of concentration and personality changes

Temporal

Impaired memory, Inability to understand language (Wernicke’s aphasia), Changes in aggressive behavior

Parietal

Impaired processing….cannot copy simple diagram or count fingers.

Occipital

Visual hallucinations and blindness

Hippocampus

Poor new learning

Amygdala

Decreased aggression and conditioned fear response

Hypothalamus

Hunger leading to obesity, effect on sexual activity

Reticular system

Loss of consciousness (sleep wake mechanisms)

Basal ganglia

Movement disorders e.g. Alzheimers and Huntingtons



BRAIN LESIONS

FRONTAL CORTEX

  • KEY FUNCTIONS:

  • SPEECH

  • CRITICAL TO PERSONALITY

  • ABSTRACT THOUGHTS

  • MEMORY AND HIGHER ORDER MENTAL FUNCTIONS

  • CAPACITY TO INITIATE AND STOP TASKS

  • CONCENTRATION



  • LESION OF FRONTAL CORTEX

  • DEPRESSION & APATHY (ESP LT SIDED)

  • DECREASED DRIVE, INITIATIVE

  • POOR GROOMING

  • DECREASED ATTENTION & CONCENTRATION & BEHAVIOR

  • POOR ABILITY TO THINK ABSTRACTLY

  • INABILITY TO SPEAK FLUENTLY-BROCA APHASIA (DOMINANT HEMISPHERE)


TEMPORAL LOBE

  • FUNTIONS:

  • LANGUAGE

  • MEMORY

  • EMOTIONS

  • NEWLEARNING-MEDIAL TEMPORAL(ALSO HIPPOCAMPUS)

  • LESIONS FROM STROKE, TUMOR, TRAUMA, HERPES VIRUS CNS INFECTION OFTEN AFFECT TEMPORAL CORTEX

  • BILATERAL LESION CAN CAUSE DEMENTIA

  • LESIONS OF FRONTAL LEFT TEMPORAL LOBE CAN LEAD TO DEFICITS IN RECALL OR LEARNING OF PROPER NAMES


  • LESIONS OF DOMINANT TEMPORAL LOBE:

  • EUPHORIA

  • AUDITORY HALLUCINATION

  • DELUSIONS

  • THOUGHT PROCESS

  • POOR VERBAL COMPREHENSION (WERNICKES APHASIA)




  • LESIONS OF NON DOMINANT TEMPORAL LOBE:

  • DYSPHORIA

  • IRRITABILITY

  • DECREASED VISUAL & MUSICAL ABILITIES

  • PSYCHOMOTOR SIEZURES



PARIETAL CORTEX

  • KEY FUNCTIONS:

  • INTELLECTUAL PROSCESSING OF SENSORY INFORMATION

  • LEFT:VERBAL PROCESSING (DOMINANT)

  • RT:VISUAL-SPATIAL PROCESSING (NON DOMINANT)

  • LESION OF DOMINANT LOBE: GERSTMANN SYNDROME

  • AGRAPHIA

  • ACALCULIA

  • FINGER AGNOSIA

  • RT-LT DISORIENTATION



  • LESIONS OF NON DOMINANT LOBE:

  • DENIAL OF ILLNESS (ANOSOGNOSIA)

  • CONSTRUCTION APRAXIA (DIFFICULTY OUTLINING OBJECTS)

  • NEGLECT OF OPPOSITE SIDE-HEMINEGLECT (NOT WASHING OR DRESSING OPPOSITE SIDE OF THE BODY)


OCCIPITAL LOBE

  • KEY FUNCTIONS:

  • VISUAL INPUT

  • RECAL OF OBJECTS ,SCENES AND DISTANCES; PET SCAN ACTIVITY IN THIS AREA DURING RECAL OF VISUAL IMAGES

  • DESTRUCTION : CORTICAL BLINDNESS

  • BILATERAL OCCLUSION OF POSTERIOR CEREBRAL ARTERIES:ANTON SYNDROME

  • CORTICAL BLINDNESS.

  • CANNOT SEE CAMOUFLAGED OBJECTS

  • OCCIPITAL EPILEPTIC FOCI: VISUAL HALLUCINATIONS.


LIMBIC SYSTEM

  • CONSISTS OF HIPPOCAMPUS, HYPOTHALAMUS, ANT. THALAMUS, CINGULATE GYRUS AND AMYGDALA.

  • KEY FUNCTIONS:

  • MOTIVATION

  • MEMORY

  • EMOTIONS (MEDIATION BETWEEN CORTEX AND LOWER CENTERS)

  • REFLEX ARC OF CONDITIONED RESPONSES

  • VIOLENT BEHAVIOR

  • SOCIOSEXUAL BEHAVIOR



  • ASSOCIATED DYSFUNCTIONS

  • HIPPOCAMPUS LESIONS:

  • LONG TERMMEMORY PROBLEM AND LEARNING NEW

  • IMPLICATED IN DEMENTIA OF ALZHIEMERS TYPE




  • HYPOTHALAMUS:

  • IMPLICATED IN INVOLUNTARY INTERNAL RESPONSES THAT ACCOMPANY EMOTIONAL STRATEGY

  • REEGULATION OF PHYSIOLOGICAL RESPONCES

  • INCREASED HEART RATE AND RESPIRATION

  • REGULATION OF ENDOCRINE BA,ANCE

  • CONTROLOF EATING

  • REGULATION OF BODY TEMPERATURE

  • REGULATION OF SLEEP-WAKE CYCLE



  • HYPOTHALAMIC DYSFUNTION:

  • EFFECTS ON SEXUAL ACTIVITY AND BODY TEMPERATURE

  • DESTRUCTION OF VENTROMEDIAL HYPOTHALAMUS: HYPERPHAGIA AND OBESITY

  • DESTRUCTION OF LATERAL HYPOTHALAMUS: ANOREXIA AND STARVATION




  • RETICULAR ACTIVATING SYSTEM.

  • FUNCTIONS:

  • MOTIVATION

  • AROUSAL

  • WAKEFULNESS

  • Lesions:

  • CHANGES IN SLEEP-WAKE MECHANISM

  • LOSS OF CONSCIOUSNESS:



  • AMYGDALA:

  • DORSOMEDIAL PORTION OF TEMPORAL LOBE

  • DIRECT LINK BETWEEN LIMBIC AND MOTOR SYSTEM

  • CRITICAL ROLE IN EMOTIONAL MEMORY AND RUDIMENTARY LEARNING

  • KLUVER BUCY SYNDROME:

  • REMOVAL OR TRAUMA TO AMYGDALA

  • TAME

  • HYPERACTIVE SEXUALLY

  • HIGH RAGE THRUSHOLD

  • MAKE LOVE NOT WAR




  • THALAMUS:

  • CRITICAL FOR PAIN PERCEPTION

  • DYSFUNCTION LEADS TO IMPAIRED MEMORY AND AROUSAL

  • KORASAKOFF SYNDROME:

  • AMNESIA FROM CHRONIC THIAMINE DEFICIENCY

  • ASSOCIATED WITH ALCOHOLISM

  • NEUROLOGICAL DAMAGE TO THALAMUS


BASAL GANGLIA

  • FUNCTIONS:

  • INITIATION AND CONTROL OF MOVEMENTS

  • IMPLICATED IN DEPRESSION AND DEMENTIA

  • DYSFUNCTIONS:

  • PARKINSONS DISEASE

  • HUNTINGTON CHOREA

  • WILSON DISEASE

  • FAHR DISEASE:

  • RARE HEREDITARY DISORDER

  • CALCIFICATION OF BASAL GANGLIA

  • ONSET AT AGE 30

  • DEMENTIA BY AGE 50

  • RESEMBLES NEGATIVE SYMPTOMS OF SCHIZOPHRENIA



  • PONS:

  • START OF NE PATHWAY

  • IMPORTANT FOR REM SLEEP

  • ANOMOLIES LINKED TO AUTISM




  • CEREBELLUM:

  • KEY FOR BALANCE

  • SKILL BASED MEMORY

  • FACILITATES VERBAL RECAL

  • IMPLICATED IN SOME LEARNING DIABILITIES


APHASIA

  • BROCA’S APHASIA:

  • LESION OF FRONTAL LOBE( BRODMANN AREA 44)

  • COMPREHENSION UNIMPAIRED

  • SPEECH PRODUCTION IS TELEGRAPHIC AND UNGRAMMATICAL

  • OFTEN ACCOMPANIED BY DEPRESSIVE SYMPTOMS

  • ‘I MOVIES’ INSTEAD OF SAYING ‘I WENT TO MOVIES’

  • TROUBLE REPEATING STATEMENTS

  • MUSCLE WEAKNESS ON RT SIDE




  • WERNICKE’S APHASIA:

  • LESIONS OF SUPERIOR TEMPORAL LOBE ( BRODMANN AREA 22)

  • COMPREHENSION IMPAIRED

  • SPEECH IS FLUENT BUT INCOHERENT

  • TROUBLE REPEATING STATEMENTS

  • VERBAL PARAPHASIAS (SUBSTITUTING ONE WORD FOR ANOTHER, OR MAKING UP WORDS)

  • NO MUSCLE WEAKNESS

  • RESEMBLES FORMAL THOUGHT PROCESS

  • MANIALIKE, RAPID SPEECH HYPERACTIVITY



  • CONDUCTION APHASIA:

  • LESION IN PARIETAL LOBE OR ARCUATE FASICULUS

  • CONNECTION BETWEEN BROCAS AND WERNICKE AREAS IS BROKEN

  • WORS ARE COMPREHENDED CORRECTLY BUT CANNOT BE PASSED ON FOR SPEECH OR WRITING

  • TROUBLE REPEATING STATEMENTS




  • GLOBAL APHASIA:

  • WIDE LESION DAMAGING BOTH BROCA’S & WERNICKE AREAS

  • TROUBLE REPEATING WORDS

LABORED TELEGRAPHIC SPEECH WITH POOR COMPREHENSION
Mini mental status examination:

Mental status examination:
What is the significance of a MMSE: why do we do it? And what is the significance if it’s impaired…!!!
How do you differentiate between dementia and pseudodementia

Pseudodementia disorder – When depression mimics depression e.g. 78 yr old woman who lost her daughter and now has difficulty sleeping, poor appetite and lost weight.

Causes of dementia:

  • Alzheimer’s – most common type

  • HIV disease

  • Parkinson’s disease

  • Huntington’s disease

  • Crutz- Jacob disease

  • Pick’s disease

  • Substance induced persisting dementia



Then sleep:

EEG is very important: asked what are the finding in different cases of sleep: REM, nonREM sleep what are the phases, what are the EEG finding?
What are th changes that do occur that correspond to the phases of the sleep: i.e. REM, PT may move eyelids: i.e. excitation of body, palpitations, bodily changes that occur

Chap 10:

Know the sleep patterns of an elderly person versus that of a young person
Elderly: Elderly often have poor sleep quality bcos aging is associated with reduced REM sleep, delta sleep (stage 3-4 or slow wave) and increased night time awakenings…..more than 3 per night.

Normal young adult: 25% REM, increased REM toward morning
Awake……..Alpha and Beta waves

Stage 1- lightest stage of sleep, decreased b.p, slow pulse….(Theta waves)

Stage 2- largest % of sleep time, tooth grinding. (Spindle)

Stage 3 and 4 – deepest, most relaxed stage of sleep, sleep disorders e.g. night terrors, sleep walking, bed wetting etc. (Delta waves)

REM- penile erection, dreaming, increased pulse and respiration, skeletal muscle movement. (alpha, beta, theta).
Know the sleep disorders: Table 10.3
Normal Sleep.

SLEEP


•Circadian

•Humans spend 1/3

of life sleeping

(well over 175,000 hrs)

•typically 8 hours/day…so - 3/day =

extra 21 hrs/week �� 10,952 hrs/decade!!!

Natural cycle

• Circadian rhythm

– the biological clock

– regular bodily rhythms that occur on a 24

hour cycle

– wakefulness

– body temperature

SLEEP


•Amount of sleep changes with

age – younger ages sleep more



Role of sleep

• Essential for survival.

• Total sleep deprivation fatal.

• Restorative function. R and R.

• Activation of cortex.

• Dreaming as a result of activity.

• Important that cycle be preserved.

• Sleeping pills and alcohol disrupt cycle.

Sleep Deprivation

• Effects of Sleep Loss

– fatigue

– impaired concentration

– immune suppression

– irritability

– slowed performance

• accidents

– planes


– autos and trucks

Do we need sleep? Repair & Rest

1965 – Randy Gardner

Science fair project…break world record of

No sleep (260 hrs) �� 264 hr 12 min = 11 days!!!

“mind over matter”

First night: 15 hrs

Next night: 9 hrs

too bad randy, Mrs. Maureen Weston (1977)

18 days!!!! Rocking chair marathon

Sleep deprivation (3 to 4 hrs)

Humans


1. Increase in sleepiness

2. Mood test

3. Perform poorly on test of vigilance (ex: tones)

2 to 3 days (continuous sleep deprivation)

“Microsleeps” (2 to 3 sec long)

1. Eye lids droop

2. Less responsive to stimuli

3. Still standing

Performance on complex cognitive tasks?????

Performance in motor tests???????

1929, a German psychiatrist: Hans Berger,

Found the it was possible to record the

feeble electric currents generated on the brain,

without opening the skull, and to depict them

graphically onto a strip of paper.

Berger named this new form of recording as

the electroencephalogram (EEG, for short)

First EEG recorded by Hans Berger, circa 1928.

EEG (electroencephalograph)

records electrical activity of

the brain via electrodes

attached to the scalp

•Gross measurement of neuronal activity

takes an average of the whole population

of cells in the area under the electrode

•Output of the electrodes are amplified

and recorded

��EEGs tell you whether a person is asleep,

awake or excited

EEG lingo: Measurement of Brain Waves

Amplitude: index of voltage = larger

the voltage the higher the amplitude

(Height)


Frequency: index of waves across time,

cycles per second (hertz, Hz)

(how often they occur)

2 Basic EEG Patterns:

1. Desynchronized: neurons in the brain

firing at many different times

�� produces EEG patterns of low

amplitude & high frequency

(wakefulness)

2 Basic EEG Patterns:

2. Synchronized: neurons are firing at

the same time – produces well defined

waves of low frequency high

amplitude (characteristic of deep

sleep)

EEG/EMG/EOG



EMG: Electromyogram

- Leg

EOG: Electroculogram



- Eye muscle

There are two divisions of sleep

1. non-rapid eye movement (NREM)

2. rapid eye movement (REM)



Non-Rapid Eye Movement Sleep

About 80% of adult sleep is NREM sleep. NREM sleep is

divided into four stages:

•Stage 1—the drowsy transition from waking to sleeping

•Stage 2—intermediate sleep, when arousal is more

difficult

•Stage 3—the beginning of "deep," or slow-wave, sleep

•Stage 4—the deepest sleep, when there is little contact

with external sensations

During NREM: breathing, heart rates, body temperature, blood pressure decrease.






Stage EEG Rate

(Frequency)

EEG Size

(Amplitude)

Awake 8-25 Hz Low

1 6-8 Hz Low

2

4-7 Hz



Occasional "sleep spindles"

Occasional "K" complexes

Medium

3 1-3 Hz High



4 Less than 2 Hz High

REM More than 10 Hz Low

Note that as sleep

progresses from awake to sleep, brain activity

becomes more synchronized (low frequency hi amplitude)

Resting quietly

Eyes closed Arousal & awake

Transition btw wakefulness & sleep

Short burst of waves

2 to 5 tx a min 1-4 (aging)

Only here – pre to delta

Sleeping soundly – but report

Not asleep at all!

REM sleep resembles stage 1

“Saw Tooth”

Dreaming


• Are external stimuli incorporated into

dreams?


– Water was sprayed on dreaming subjects; 14 of

33 dreamed of water.



90 minutes to our first bout of

REM – average of 5 cycles –

REM lasts 10- 20 min then we

fall back to stage 2 and so

on…


* somnambolism

REM SLEEP

PGO spiking : Pontine-Geniculate-Occipital

Triggers the onset of REM

1. Waves of neural activity first in the pons

2. Then in the lateral geniculate

3. Then in the occipital cortex

- Wave is synchronized with eye movement

- At this time Pons is also sending inhibitory

messages to the spinal cord �� motor neurons

Neurochemistry: Pons releases ACh stimulate LGN

(inject carbachol=Ach agonist=REM)




Locus Coeruleus: Noradrenergic neurons: destroy this area

you get NO REM but SWS (stage 3 & 4)

Raphe Nucleus: Serontonergic neurons: destroy this area

you get NO SLEEP = insomnia…agonist=increase in SWS
Narcolepsy (hypersomnia):

- sleeping disorder (1 of 2000)

characterized by periods of

irresistible sleepiness

- "sleep attacks" happen without

warning and can occur even after a

good night's rest

- normally last about 20 minutes

- after waking up, the person feels

refreshed, only to feel sleepy again

a few hours later

- There is no known cause of this

chronic sleep disorder

TX: Antidepressants

Antidepressants tend to

suppress REM sleep

So need more 5HT

Gene found in dogs

Apnea is a Greek word meaning "want of breath”

disorder characterized by periods of time

when the sleeper stops breathing (apnea) or experiences

a sharp reduction in breathing (hypopnea)

These periods normally last between 10 and 30 seconds,

but can last longer �� males, overweight & elderly (SIDs)

The person wakes up shortly and falls back asleep, usually not

knowing there had been any interruption in sleep at all. These

"apneic events" can occur as many as 20 or 30 times an hour.

Sleep apnea

(Muscle atonia)



Sleep Disorders

��Insomnia

��Excessive Daytime

Sleepiness

��Narcolepsy

��Sleep Apnea

��Nightmare/Night



terror

��Sleepwalking

��Restless leg
Pathology:

All the disorders discussed by DR. Gall: i.e. sleep disorders
obesity: in some of the common problems associated with obesity: i.e. obstructive sleep apnea (OSP). In OSP, respiratory effort occurs but an airway obstruction stops air from reaching the lungs. It is common in the obese and patients often snore.

Sleep disorders:

Classification:


  • DSV-IV-TR classifies sleep into two major categories

    • Dyssomnias

    • Parasomnias

Dyssomnias:



  • characterized by problems in the timing, quality, or amount of sleep.

  • They include insomnia, narcolepsy, and breathing-related sleep disorder (sleep apnea), as well as circadian rhythm sleep disorder, nocturnal myoclonus, restless leg syndrome and the primary hypersomnias (e.g. Kline-Levin syndrome and menstrual-associated syndrome)

Parasomnias:



  • characterized by abnormalities in physiology or in behavior associated with sleep

  • they include bruxism (teeth grinding) and sleepwalking as well as sleep terror disorder, REM sleep behavior and nightmare disorders.

Insomnia: Difficulty falling asleep or staying asleep.



  • Occurs 3 times per week for at least one month

  • Leads to sleepiness during the day

  • Causes problems fulfilling social or occupational obligations

  • Present in 30% of the population

Psychological causes of insomnia



  • include affective and anxiety disorders

  • major depressive disorder

  1. characteristics of the sleep pattern in depression:

    • normal sleep onset

    • repeated nighttime awakenings

    • waking too early in the morning (terminal insomnia) is the most common sleep characteristics of depressed patients

  2. characteristics of sleep stages in depression:

    • short REM latency: appearance of REM within 4t minutes of falling asleep (what is normal REM latency?)

    • increased REM early in the sleep cycle and decreased REM later in the sleep cycle may lead to waking too early in the morning

    • long first REM period and increased total REM

    • reduced delta sleep (which is the deepest, most relax stage of sleep)

Bipolar disorder:



  • manic or hypomanic Pt’s have trouble falling asleep or sleep fewer hours

Anxiety:


  • anxious PT’s often have trouble falling asleep

Physical Causes:



  • use of CNS stimulants is the most common cause of insomnia. i.e. caffeine

  • withdrawal of drugs with sedating action can result in wakefulness

    • ex. Alcohol, benzodiazepines, opiates

  • medical conditions causing pain can result in insomnia, as do endocrine and metabolic disorders

Sleep Apnea:



  • breathing related sleep disorder

  • PT’s with sleep apnea stop breathing for brief intervals

  • Low Oxygen or high CO2 levels in the blood awakens the Pt repeatedly during the night

  • Resulting in daytime sleepiness

    • central sleep apnea

    • more common in elderly

    • little or no respiratory effort occurs

    • resulting in less air reaching the lungs

    • obstructive sleep apnea

    • respiratory efforts occur, but airway obstruction prevents air from reaching the lungs

    • more common in people between 40-60 year of age

    • more common in men (8:1 male to female ratio)

    • occurs in obese people

    • (pickwinian syndrome is a related condition)

    • characteristic snore

  • the exact cause of OSA remains unclear

    • site of obstruction in most Pt’s is soft palate, that extends to region at base of tongue

    • no rigid structures present: i.e. cartilage or bone, in this area to hold airway open

    • during the day, muscles in the region keep the passage wide open. But as a person with OSA falls asleep, these muscles relax to a point where the airway collapses and becomes obstructed

    • when the airway closes, breathing stops, and the sleeper awakens to open the airway

    • the arousal from sleep usually lasts only a few seconds, but brief arousals disrupt continuous sleep

    • once normal breathing is restored, the person falls asleep only to repeat the cycle throughout the night

    • typically, the frequency of waking episodes is somewhere between 10 and 60

      • a person with severe OSA may have more than 100 waking episodes in a single night

    • RISK FACTORS:

      • Excessive weight gain is primary risk factor

        • Accumulation of fat on sides of upper airway becomes narrow and is predisposed to closure when muscle relaxes

    • Pickwinian syndrome affects pt’s with extreme obesity

      • Symptoms include:

        • Excessive daytime sleepiness

        • Shortness of breath

          • Due to elevated CO2 pressure in blood

        • Disturbed sleep at night

        • Flushed face

        • Bluish tint on skin

        • High blood pressure

          • Enlarged liver

          • Abnormally high red blood cell count

Sleep apnea occurs in 1% - 10% of population



  • related to depression, headaches, and pulmonary hypertension

  • may result in sudden death during sleep in ELDERLY and INFANTS


Central Sleep Apnea:

  • rare: caused by lesions in brain stem or metabolic disorder

    • more common in elderly

  • cessation of air flow 2ndary to lack of respiratory effort

  • Rx: mechanical ventilation or nasal CPAP


Narcolepsy:

  • sudden and uncontrollable, (though often brief), attacks of deep sleep, sometimes accompanied by paralysis and hallucinations

  • despite having normal amount of sleep at night

    • e.g. may fall asleep suddenly while driving


Other characteristics of Narcolepsy:

  • hypnagogic and hypnopompic hallucinations

    • these are strange perceptual experiences which occur just as the patient falls asleep or wakes up, respectively

      • occurs in 20% - 40% of pt’s with narcolepsy

    • very short REM latency -< 10 min

  • cataplexy

    • this is sudden physical collapse caused by the loss of all muscle tone after a strong emotional stimulus

      • occurs in 70% of pt’s

  • sleep paralysis:

    • inability to move body for a few seconds after waking:

      • occurs in 30% - 50% of pt’s

Narcolepsy is uncommon:



  • occurs most frequently in adolescents and young adults

  • may be linked to genetic component

Other sleep disorders:



  • sleep terror disorder:

    • repetitive experiences of fright in which a person (usually a child) screams in fear during sleep

    • person cannot be awakened and has no memory of having a dream

    • occurs during delta sleep

    • onset in adolescence may indicate temporal lobe epilepsy

  • nightmare disorder:

    • repetitive, frightening dreams that cause nighttime awakenings

    • person can usually recall the nightmare

    • occurs during REM sleep

    • how is this different from night terrors?

  • Sleepwalking disorder:

    • Repetitive walking around during sleep

    • No memory of the episode

    • Begins in childhood (usually 4-8 years of age)

    • Occurs during delta sleep\

  • Enuresis:

    • Delta sleep disorder

    • Boys twice as likely as girls

    • Often history with same sex parent

    • Common after change or new sibling born

      • Rx:

        • Behavioral therapy

        • Imipramine

  • Circadian rhythm sleep disorder:

    • Inability to sleep at appropriate times

    • Delayed sleep phase type involves falling asleep and waking later than wanted

    • Jet lag type lasts 2-7 days after a change in time zones

    • Shift work type

    • For example: in physician training

    • Can result in physician error

  • Resident should not have more than 80 duty hours/week averaged over a 4 week period:

    • Residents should not have more than 24 hours of continuous duty hours (although 3 hours of “sign out” is allowed)

  • Residents must have at least

    • 8-10 hours off between assignments (8 per NYS or 10 per ACGME); residents must have at least one 24 hour duty free period per week

Nocturnal myoclonus:



  • repetitive, abrupt muscular contractions in the legs from toes to hips

  • causes nighttime awakenings

  • more common in elderly

Restless leg syndrome:



  • uncomfortable sensation in the legs necessitating frequent motion

  • repetitive limb jerking during sleep

  • cause difficulty falling asleep and causes nighttime awakenings

  • more common with agining, pregnancy, and kidney disease

Primary hypersomnias:



  • kleine-Levin syndrome and menstrual-associated syndrome

  • recurrent periods of excessive sleepiness occurring almost daily for at least 1 month

  • sleepiness is not relieved by daytime naps

  • often accompanied by hyperphagia (overeating)

  • kleine-levin syndrome is more common in adolescence males

Menstrual associated syndrome:



  • hypersomnia and hyperphagia occurring only in the premenstrual period

Sleep drunkenness:



  • difficultly awakening fully after adequate sleep

  • rare, must be differentiated from substance abuse or other sleep disorder

  • associated with genetic factors

REM sleep behavior disorder:



  • REM sleep without skeletal muscle paralysis

  • Pt’s can injure themselves or their sleeping partners

Treatment of Major Sleep Disorders:



  • insomnia:

    • avoid caffeine (especially before bedtime)

    • development of a series of behaviors associated with bedtime

      • e.g. sleep ritual or sleep hygiene

    • maintaining a fixed sleeping and waking schedule

    • daily exercise

    • relaxation techniques

    • psychoactive agents

    • for e.g.: limited use of sleep agents to establish an effective sleep pattern and antidepressants or antipsychotics if appropriate

  • Obstructive sleep apnea:

    • Weight loss

    • Continuous positive airway pressure (CPAP)

      • A device applied to the face at night to gently more air into the lungs

    • Surgery to enlarge the airway (uvulopalatoplasty)

    • Tracheostomy (as a last resort)

  • Narcolepsy

    • Stimulant drugs

      • E.g. methylphenidate (Ritalin)

        • If cataplexy is present, antidepressants may be added

    • Timed daytime naps

Question:

A Pt reports that he is sleepy all day despite having 8 hours of sleep each night.

His wife reports that his loud snoring keeps her awake

Of the following, the best Rx for this Pt is?


  1. continuous positive airway pressure: answer

  2. an antipsychotic agent

  3. a stimulant agent

  4. development of a “sleep ritual”


You can leave CFS and Neurostamia:
Chronic Fatigue Syndrome:

Also named:

CEBV: chronic Epstein-barr syndrome

Duncan syndrome: CFS resembles and mimics in the same way and may complain of weight lost and fatigue

CFIDS: Chornic fatigue immune dysfunction syndrome:

ME : myalgic encephalitis

Yuppie flux :


  • usually strikes middle aged people, but not exclusively

  • under diagnosed in younger people. (under 20 years of age)

  • comes and goes


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