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ORGANIC MENTAL DISORDER LBM_4

STEP 7

1. Mengapa ditemukan leukosit menurun dan widal positif ?


LEUKOSIT MENURUN

WIDAL (+)
 Aglutinin serum meningkat tajam selama minggu kedua dan ketiga pada
infeksi salmoonela. Sedikitnya 2 spesimen serum, yang diambil dengan selang
waktu 7-10 hari, dibutuhkan untuk membuktikan adanya kenaikan titer
antibodi. Pengenceran serial (2 x lipat) dari serum yang tidak diketahui diuji
terhadap antigen salmonela. Interpretasi hasilnya adalah sebagai berikut :
Titer O yang tinggi atau meningkat ( ≥ 1:160 ) menandakan adanya
infeksi aktif.
Titer H yang tinggi ( ≥ 1:160 ) menunjukkan riwayat imunisasi atau
infeksi di masa lampau.
Titer antibodi yang tinggi terhadap antigen Vi timbul pada beberapa
carrier.

Hasil pemeriksaan serologi pada infeksi salmonela harus diinterpretasikan


dengan hati-hati. Kemungkinan adanya antibodi yang bersilang, membatasi
penggunaan serologi dalam diagnosis infeksi salmonela.

Jawetz

2. Macam macam GMO ?

Organic mental disorders

Classification and external resources

ICD-10 F06.9
ORGANIC MENTAL DISORDER LBM_4

ICD-9 310.9

DiseasesDB 9266

MedlinePlus 001401

eMedicine emerg/345

MeSH D019965

3. Apa hunbungannya demam tinggi (typhoid) dengan keluhan ?


Bakteriemia dengan lesi fokal
 Keadaan ini umumnya disebabkan oleh S choleraesuis, tetapi juga disebabkan
oleh serotipe salmonela apapun. Setelah infeksi melalui mulut, terjadi invasi dini
ke aliran darah (dengan kemungkinan lesi fokal di paru, tulang, meninges, dan
lain-lain), tetapi manifestasi di usus sering tidak ada. Biakan darah (+).

Pathophysiology

Altered mental status can be divided into 2 major subgroups: acute (delirium or acute
confusional state) and chronic (dementia). A third entity, encephalopathy (subacute
organic brain syndrome), denotes a gray zone between delirium and dementia; its early
course may fluctuate, but it is often persistent and progressive.

The final common pathway of all forms of organically based mental status change is an
alteration in cortical brain function, at times in concert with abnormalities of deep brain
structures. These conditions result from (1) an exogenous insult or an intrinsic process
that affects cerebral neurochemical functioning and/or (2) physical or structural damage
to the cortex, subcortex, or to deeper structures involved with memory. Some of the
etiologies include trauma, mass lesions, hydrocephalus, strokes (ie, multi-infarct
dementia), atrophy, infection, toxins, or dementing processes.

The end result of these disruptions of function or structure is impairment of cognition that
affects some or all of the following: alertness, orientation, emotion, behavior, memory,
perception, language, praxis, problem solving, judgment, and psychomotor activity.
Knowledge of which areas of this spectrum are affected or spared guides both the workup
and the diagnosis.

4. Perbedaan demensia dengan psikotik ?


DEMENSIA
ORGANIC MENTAL DISORDER LBM_4
ORGANIC MENTAL DISORDER LBM_4
ORGANIC MENTAL DISORDER LBM_4
ORGANIC MENTAL DISORDER LBM_4
ORGANIC MENTAL DISORDER LBM_4
ORGANIC MENTAL DISORDER LBM_4

(Syamsir Bs, Psikiater,Departemen Psikiatri,FK-USU)

ORGANIC PSYCHOSIS

Organic psychosis, formerly known as organic brain syndrome, refers to a wide group of
psychological and behavioral abnormalities thought to be secondary to a disturbance in brain
structure or function, although the specific cause is unknown. These abnormalities in brain
function may be temporary or permanent. An organic cause is suspected when there is no
indication of a clearly defined psychiatric or "inorganic" cause such as a mood disorder.
However, as more is understood about derangement in the brain chemistry underlying
psychiatric disorders, the distinction between organic and inorganic processes has become
increasingly unclear.

Now the DSM-IV-TR (Diagnostic and Statistical Manual of Mental Disorders, 4th Edition,
Text Revision) has broken up the diagnoses that once fell under the diagnostic
category organic mental disorder into three categories: delirium, dementia, andamnestic and
other cognitive disorders; mental disorders due to a general medical condition; and substance-
related disorders. This change was made because the descriptive word organic gives the false
impression that conditions that are not organic have no biological explanation. An example of
a mental disorder due to a general medical condition is major depression caused
byhypothyroidism. An example of substance-related disorder is psychosis secondary to drug
abuse.
Incidence and Prevalence: Delirium has a prevalence of 0.4% in those aged 18 and
above; at age 55 and older, the prevalence increases to 1.1% (DSM-IV-TR 138).

Causation and Known Risk Factors

Men are more at risk for delirium. Children are more susceptible, as well as the
elderly

Diagnosis
ORGANIC MENTAL DISORDER LBM_4

History: The individual may have a history of major disturbances in thinking, emotions,
behavior, and/or level of consciousness. Observation of the individual's orientation, dress,
mannerisms, behavior, and content of speech provides essential clues for diagnosing this
illness.

Physical exam: The exam may reveal decreased levels of consciousness, stupor, agitation,
restlessness, response to hallucinations, or neurological abnormalities such as tremors or
other abnormal movement patterns.

Tests: To rule out more specific causes of these findings, the following tests may be
done: blood chemistries and cell count, drug and alcohol screen, brain computed tomography
(CT) or magnetic resonance imaging (MRI), toxicological
screen, electroencephalogram (EEG), and spinal tap (lumbar puncture), if indicated. These
tests are negative or nondiagnostic in unspecified organic psychosis. Experimental studies
looking at brain function, such as positron emission tomography (PET) or single photon
emission computed tomography (SPECT), are considered more of a research tool than a true
help in diagnosing this syndrome.

Treatment

Once specific, treatable causes are ruled out, treatment is directed at maintaining
safety for the individual and for others. It can involve antipsychotic, anti-anxiety, or
antidepressant medication, and confinement. Observation and testing, if indicated, should
continue in hopes of clarifying the diagnosis and lead to more specific treatment. When
dementia (disturbances in thinking and memory) is prominent, cholinergic agonists should be
considered. In central nervous system disease, aggressiveness and rage states can be reduced
with lipophilic beta-blockers.

Visiting nurses, homemakers, and adult protective services may be helpful in keeping the
individual at home. Counseling may help the family cope with problems involved in keeping
the individual at home as long as possible. When family is no longer able to care for the
individual, substitute home care, board and care, or convalescent home care may be helpful.
The setting should include familiar people and objects, light at night, and a simple schedule.

Prognosis

The course and outcome are extremely variable. There can be lucid intervals between
disturbances. If the cause is transient, such as unsuspected drug overdose or withdrawal, the
disorder will totally clear within a few days. If it is caused by a progressive condition such
as Alzheimer's disease, the individual never recovers. Efforts to clarify the diagnosis should
be ongoing, because a specific diagnosis will help predict the outcome and may even lead to
treatment that could improve or reverse the condition.

Complications
ORGANIC MENTAL DISORDER LBM_4

The individual may become injured falling out of bed, wander, get lost, or may be
unable to take care of basic nutritional and hygienic needs. Other possible complications
include susceptibility to infections, severe depression, suicide, or injury to others.

Ability to Work (Return to Work Considerations)

It is unlikely that the individual with organic brain syndrome is able to maintain
competitive employment.

Failure to Recover

If an individual fails to recover within the expected maximum duration period, the reader
may wish to consider the following questions to better understand the specifics of an
individual's medical case.

Regarding diagnosis:

 Has diagnosis of organic psychosis been confirmed?


 Did evaluation include a comprehensive physical examination (including a search for
neurologic abnormalities, infection, or hypoxia), laboratory tests (including a
toxicologic screen), and a lumbar puncture for cerebrospinal fluid analysis?
 Did diagnostic tests include electroencephalography, CT, MRI, PET, and SPECT?
 Has organic psychosis, which is caused by structural brain changes, been
differentiated from functional psychiatric illness?

Regarding treatment:

 Has a primary brain disease or underlying medical disorder been identified?


 Is individual receiving appropriate treatment to resolve or control underlying
condition(s)?
 Has physician explored the option of using drugs to increase cholinergic activity?
 If condition is due to a central nervous system disease, would individual benefit from
the use of lipophilic beta-blockers to reduce aggressiveness and rage?
 Is individual receiving proper care in an appropriate setting?
 Has family received the counseling and support necessary to cope with problems
involved in keeping individual at home for as long as possible?
 As family becomes unable to care for individual, have appropriate arrangements been
made for substitute home care, board and care, or convalescent home care?

Regarding prognosis:

 Has individual responded to treatment of underlying medical condition?


 If underlying condition was reversible, to what extent has mental functioning been
recovered?
 Because medication (particularly sedatives) may further impair thinking abilities and
contribute to overall problems, could unnecessary medications be discontinued?
ORGANIC MENTAL DISORDER LBM_4

 Have impulsive behavior, poor judgment, and deterioration in the total behavior of
individual made major rearrangement of lifestyle necessary?
 What input has the physician given individual and family in this regard?
 Does individual exhibit both the organic effects due to brain damage and
psychological reactions to the deficits?

Do impulsive behavior, depression, and suicide attempts pose a threat to individual's


safety? Would individual benefit from closer observation, monitoring, or confinement?

References

Cited

Frances, Allen, ed. Diagnostic and Statistical Manual of Mental Disorders (DSM-IV-
TR). 4th ed. Washington, DC: American Psychiatric Association, 2000.

http://www.mdguidelines.com/organic-psychosis

5. Gejala gejala GMO ?

Physical

Any patient who presents with altered mental status (AMS) needs a complete physical
examination, with particular attention to general appearance, vital signs, hydration status,
evidence of physical trauma, and neurologic signs. The delirious or obtunded patient
should be evaluated for pupillary, funduscopic, and extraocular abnormalities; nuchal
rigidity; thyroid enlargement; and heart murmurs or rhythm disturbances. Other clues
include a pulmonary examination that reveals wheezing, rales, or absent breath sounds; an
abdominal examination that reveals hepatic or splenic enlargement; or a cutaneous
examination that shows rashes, icterus, petechiae, ecchymoses, track marks, or cellulitis.
Cellulitis in elderly persons often is hidden under clothing, particularly pants and socks.
Checking these areas in patients with diabetes is critical. Any serious infection can lead to
acute mental status changes.

General appearance (eg, unkempt and/or malnourished) may suggest the possibility of
drug or alcohol abuse.

Look for track marks.

Smell for alcohol, the musty odor of fetor hepaticus, or the fruity smell of ketoacidosis.

Icterus and asterixis point to liver failure with an elevation of the serum ammonia level.

Agitation and tremulousness suggest sedative drug or alcohol withdrawal.


ORGANIC MENTAL DISORDER LBM_4

Close attention to vital signs is essential and easy to overlook in the setting of extreme
behavioral difficulties in a delirious patient. It is unusual for a patient with acute delirium
to present to the ED with normal vital signs.

Fever may point to infection, heat illness, thyroid storm, aspirin toxicity, or the extreme
adrenergic overflow of certain drug overdoses and withdrawal syndromes (in particular,
delirium tremens). Extreme hyperthermia (with pinpoint pupils) may be seen in pontine
strokes. In patients with a rapid respiratory rate, consider diabetic ketoacidosis (ie,
Kussmaul respiration), sepsis, stimulant drug intoxication, and aspirin overdose. In
patients with a slow respiratory rate, consider narcotic overdose, CNS insult, or various
sedative intoxications.

A rapid pulse rate is seen in patients with fever, sepsis, dehydration, thyroid storm, and
various cardiac dysrhythmias and in overdoses of stimulants, anticholinergics, quinidine,
theophylline, tricyclic antidepressants, or aspirin. Patients with a slow pulse rate may
have elevated intracranial pressure, asphyxia, or complete heart block. Calcium channel
blockers, digoxin, and beta-blockers also may produce altered mental status and
bradycardia.

Blood pressure elevation is common in delirium because of resulting adrenergic overload.

In patients with acute altered mental status and severely elevated blood pressure, check
the ocular fundi for arteriolar spasm, disc pallor, papilledema, flame hemorrhages, and
exudates. These are all signs of malignant hypertension. Even with these changes, the
patient may be alert and minimally symptomatic.

In pregnant patients with a diastolic pressure greater than 75 mm Hg in the second


trimester or greater than 85 mm Hg in the third trimester, consider preeclampsia (ie,
hyperreflexia, edema, proteinuria).

In patients with hypertension and bradycardia, consider an elevated intracranial pressure


(Cushing reflex).

With delirium and hypotension, the differential diagnosis includes dehydration, diabetic
coma, hemorrhage due to trauma, aneurysmal rupture, or GI bleeding. Also, consider
adrenergic depletion secondary to cocaine; amphetamine; or tricyclic overdose, which
usually responds only to norepinephrine, not dopamine. Addisonian crisis, particularly in
those who are steroid dependent, should be considered.

Pupillary dilation is seen in anticholinergic overdose (diphenhydramine), stimulant use,


and hallucinogen use. A common feature of diphenhydramine and other antihistamine
overdoses is picking at imaginary objects in the air.

Pupillary constriction is seen in narcotic intoxication.


ORGANIC MENTAL DISORDER LBM_4

Serious head trauma is usually obvious. However, occult trauma may be discovered by
findings of basilar skull fracture, such as hemotympanum, Battle sign (ie, mastoid area
ecchymoses), raccoon eyes, or otorhinorrhea. The latter condition may be tested for by
placing a drop of the draining blood on filter paper and then looking for a clear ring of
cerebrospinal fluid (CSF). A funduscopic examination may show loss of venous
pulsations in cases of early intracranial pressure (ICP) elevation or papilledema in severe
ICP elevation. Pupillary inequality may be a late sign of uncal herniation.

At times, it may be difficult to distinguish between acute delirium, psychiatric crisis, or a


chronic process with exacerbation such as dementia. It is safest to presume delirium until
an alternative process can be proven through testing and/or clinical observation.

A brief bedside neurologic examination, including mental status testing, is an essential


part of the workup of organic brain syndrome and altered mental status when a rapidly
treatable cause, such as hypoglycemia or narcotic overdose, is not immediately apparent.

6. Cara mendiagnosis GMO ?

 Pemeriksaan laboratorium

Umumnya dilakukan pemeriksaan darah berikut hitung darah tepi, elektrolit serum
(terma kalsium), glukosa, ureum-creatinine, fungsi hepar, fungsi tiroid, kadar
vitamin B12 diserum, serologi terhádap sifilis.Tes lain, atas indikasi, dapat
mencakup laju endap darati, foto ronsen toraks, analisis urin, pungsi lumbal ( lihat
tabei4).

 CT-scan atau MRI

Pemeriksaan pencitraan, misalnya dengan CT atau MRI banyak membantu


menentukan etiologi demensia. Neoplasma, besar atau kecil, tunggal atau multipel,
primer.. atau metastatik, hematoma subdural, hidrosefalus, infark di otak, tunggal
atau multipel, letaknya kortikal atau subkortikal dengan mudah dapat diketahui
melalui pemeriksaan.CT atau MRI.

 Imejing otak dan demensia.

Beberapa hasH penelitian berikut perlu disimak, yaitu : diagnosis demensia


ditegakkan atas dasar kriteria behavioral, dan tidak dapat ditegakkan atas dasar
imejing otak, termasuk CTsken otak, MRI, PET, SPECT atau metoda laboratorium
lainnya. Pemeriksaan imejing otak lebih ditujukan pada penentuan penyebab
demensia, rnisalnya lesi-desak-ruang,hidrosefalus dan lain sebagainya. linejing otak
dapat membantu membedakan AD (penyakit Alzheiiner) dan MID
(multiinfarctdethentia), penyebab demensia yang paling sering

 EEG
ORGANIC MENTAL DISORDER LBM_4

EEG merupakan pemeriksaan yang jauh lebih murah daripada pemeriksaan


MRI,CT.Dalam menentukan etiologi demencia kemampuannya Sangay
terbatas.Bila gambaran EEG teratur dan normal,maka kemungkinan gangguan
kortikal lebih sedikit.Pada gangguan ginjal dengan kadar ureum yang tinggi yang
mengakibatkan gangguan fungís luhur,umumnya didapatkan gangguan EEG berupa
perlambatan.

(NEUROGERIATRI,FKUI,Prof.Dr.dr.S.M.Lumbantobing,SpS(K),SpKJ)
7. Penyebab ( etiologi ) dari GMO ?

Causes

Delirium or acute altered mental status may be caused by the following:

 Intoxication with a substance (eg, hallucinogens, alcohol, medications, toxins)


 Polypharmacy, most often with psychoactive medications
 Major surgery, orthopedic trauma, prolonged immobility, and “ICU psychosis”
 Occult infection (eg, UTI, meningitis, encephalitis, neurosyphilis, sepsis)
 Head trauma
 Seizure disorder
 Acute mania or other psychiatric etiology
 Endocrine crisis (eg, thyroid, adrenal, diabetic)
 High fever seen with infection or heat stroke
 Renal failure
 Liver failure
 Neoplasia
 Inflammation (eg, systemic lupus erythematosus)
 Cerebral vascular accident (CVA)
 Respiratory dysfunction (eg, hypoxia, hypercarbia)
 Shock
 Chronic neurological disorders such as dementia and Parkinson disease
 “Sundowning” (see below)

Penyebab Delirium:
Penyakit intrakranial:
1. Epilepsi atau keadaan pasca kejang
2. Trauma otak (terutama gegar otak)
3. Infeksi (meningitis.ensetalitis).
4. Neoplasma.
5. Gangguan vaskular
Penyebab ekstrakranial:
1. Obat-obatan (di telan atau putus),
ORGANIC MENTAL DISORDER LBM_4

Obat antikolinergik, Antikonvulsan, Obat antihipertensi, Obat antiparkinson. Obat


antipsikotik, Cimetidine, Klonidine. Disulfiram, Insulin, Opiat, Fensiklidine, Fenitoin,
Ranitidin, Sedatif(termasuk alkohol) dan hipnotik, Steroid.
2. Racun
Karbon monoksida, Logam berat dan racun industri lain.
3. Disfungsi endokrin (hipofungsi atau hiperfungsi)
Hipofisis, Pankreas, Adrenal, Paratiroid, tiroid
4. Penyakit organ nonendokrin.
Hati (ensefalopati hepatik), Ginjal dan saluran kemih (ensefalopati uremik), Paru-paru
(narkosis karbon dioksida, hipoksia), Sistem kardiovaskular (gagal jantung, aritmia,
hipotensi).
5. Penyakit defisiensi (defisiensi tiamin, asam nikotinik, B12 atau asam folat)
6. Infeksi sistemik dengan demam dan sepsis.
7. Ketidakseimbangan elektrolit dengan penyebab apapun
8. Keadaan pasca operatif
9. Trauma (kepala atau seluruh tubuh)
10. Karbohidrat: hipoglikemi.
Infeksi salmonella typhimenyebarsepsisperadangan otakggn mental organik.
Kaplan.H.I, Sadock. B.J, Sinopsis Psikiatri : Ilmu Pengetahuan Perilak Psikiatri
Klinis, Edisi ketujuh, Jilid satu. Binarupa Aksara, Jakarta 2010. hal 481-570.
Kapita Selekta Kedokteran, Edisi ketiga, Jilid 1. Penerbit Media
Aesculapsius Fakultas Kedokteran Universitas Indonesia, Jakarta 2008. hal
189-192
8. Faktor resiko GMO ?

Race

Delirium is seen more commonly in whites than in other races.

Sex

Delirium is seen more commonly in females than in males. Alzheimer disease is more
prevalent among women because of their longer life expectancy. Lifetime risk in women
is estimated to be 32%, whereas the lifetime risk in men is 18%. However, the age-
specific risk is equal in both sexes.

Age

Delirium due to physical illness is more frequent among the very young and those older
than 60 years. Delirium due to drug and alcohol intoxication or withdrawal is most
frequent in persons aged mid teens to the late 30s.

9. Bagaimana hubugan MPJ ( mekanisme pertahanan Jiwa ) dengan GMO ?



ORGANIC MENTAL DISORDER LBM_4

10. Bagaimana hubungan GMO dengan pemakaian zat tertentu , berserta gejalanya ?

11. DD dan penatalaksanannya ?

An organic mental disorder (OMD), also known as organic brain syndrome or chronic
organic brain syndrome, is a form of decreased mental function due to a medical or
physical disease, rather than a psychiatric illness. This differs from dementia.[1] While mental
or behavioral abnormalities related to the dysfunction can be permanent,[2] treating the
disease early may prevent permanent damage in addition to fully restoring mental functions.
An organic cause to brain dysfunction is suspected when there is no indication of a clearly
defined psychiatric or "inorganic" cause, such as a mood disorder.[3]
Now the DSM-IV-TR (Diagnostic and Statistical Manual of Mental Disorders, 4th Edition,
Text Revision) has broken up the diagnoses that once fell under the diagnostic category
organic mental disorder into three categories: delirium, dementia, and amnestic.[3]
Organic brain syndrome can be divided into 2 major subgroups: acute (delirium or acute
confusional state) and chronic (dementia). A third entity, encephalopathy (subacute organic
brain syndrome), denotes a gray zone between delirium and dementia; its early course may
fluctuate, but it is often persistent and progressive.[4] Damage to brain functioning could be
due not only to organic (physical) injury (a severe blow to the head, stroke, chemical and
toxic exposures, organic brain disease, substance abuse, etc.) and also to non-organic means
such as severe deprivation, abuse, neglect, and severe psychological trauma.[5]
Symptoms[edit]

Symptoms depend on the cause OMD. Confusion, memory impairment, delirium, dementia,
judgment, logical function and agitation are some common symptoms of OMD.
Associated conditions[edit]

 Brain injury caused by trauma


 Bleeding into the brain (intracerebral hemorrhage)
 Bleeding into the space around the brain (subarachnoid hemorrhage)
 Blood clot inside the skull causing pressure on brain (subdural hematoma)
 Concussion
 Breathing conditions
 Low oxygen in the body (hypoxia)
 High carbon dioxide levels in the body (hypercapnia)
 Cardiovascular disorders
 Abnormal heart rhythm (arrhythmias)
 Brain injury due to high blood pressure (hypertensive brain injury)
 Dementia due to many strokes (multi-infarct dementia)
 Heart infections (endocarditis, myocarditis)
 Stroke
 Transient ischemic attack (TIA)
ORGANIC MENTAL DISORDER LBM_4

 Degenerative disorders
 Alzheimer's disease (also called senile dementia, Alzheimer's type)
 Creutzfeldt-Jacob disease
 Diffuse Lewy Body disease
 Huntington's disease
 Multiple sclerosis
 Normal pressure hydrocephalus
 Parkinson's disease
 Pick's disease
 Dementia due to metabolic causes
 Drug and alcohol-related conditions
 Alcohol withdrawal state
 Intoxication from drug or alcohol use
 Wernicke-Korsakoff syndrome (a long-term effect of excessive alcohol consumption
or malnutrition)
 Withdrawal from drugs (especially sedative-hypnotics and corticosteroids)
 Infections
 Any sudden onset (acute) or long-term (chronic) infection
 Blood poisoning (septicemia)
 Brain infection (encephalitis)
 Meningitis (infection of the lining of the brain and spinal cord)
 Prion infections such as mad cow disease
 Late-stage syphilis
 Other medical disorders
 Cancer
 Kidney disease
 Liver disease
 Thyroid disease (high or low)
 Vitamin deficiency (B1, B12, or folate)[1]

 Lithium toxicity can cause permanent organic brain damage[6]


 Accumulation of heavy metals in the brains
 Aluminum
 Mercury poisoning (Dental amalgam)[7]
Treatment[edit]

Treatment depends on which disorder is involved in OMD.


Prognosis[edit]

Some disorders are short-term and treatable, but many are long-term or get worse over
time.[1]
ORGANIC MENTAL DISORDER LBM_4

Alternative names[edit]

 OBS
 Organic Brain Syndrome
 OMS
 Chronic organic brain syndrome
References[edit]

1. ^ a b c "Organic brain syndrome: MedlinePlus Medical Encyclopedia". Nlm.nih.gov.


Retrieved 2012-10-12.
2. ^ "Organic mental disorders". Depression-guide.com. Retrieved 2012-10-12.
3. ^ a b "Organic Psychosis - Medical Disability Guidelines". Mdguidelines.com.
Retrieved 2012-10-12.
4. ^ "Delirium, Dementia, and Amnesia in Emergency Medicine". Misc.medscape.com.
Retrieved 2012-10-12.
5. ^ "Differences between psychological and neuropsychological evaluation".
Webcache.googleusercontent.com. Retrieved 2012-10-12.
6. ^ "A Case of Lithium Poisoning?, Australian and New Zealand Journal of Psychiatry,
Informa Healthcare". Informahealthcare.com. 1970-01-01. Retrieved 2012-10-12.
7. ^ "Organic Brain Syndrome - Alzheimer's Disease Medical Information".
Webcache.googleusercontent.com. 2012-10-04. Retrieved 2012-10-12

Delirium, Dementia, and Amnesia in Emergency Medicine

http://misc.medscape.com/pi/android/medscapeapp/html/A793247-business.html

Background

Delirium, dementia, amnesia, and certain other alterations in cognition, judgment, and/or
memory are subsumed under more general terms such as mental status change, acute
confusional state, or altered mental status. While psychiatric conditions can at times mimic
some features of these conditions or complicate their presentation in the emergency
department, the primary etiology of such states is organic (ie, nonpsychiatric). Causes include
metabolic disruptions, endocrine dysfunction, drug toxicity, structural injury (eg, stroke,
dementing process), ischemia, severe physiologic stress, and infection.

 References

Pathophysiology

Altered mental status can be divided into 2 major subgroups: acute (delirium or acute
confusional state) and chronic (dementia). A third entity, encephalopathy (subacute organic
ORGANIC MENTAL DISORDER LBM_4

brain syndrome), denotes a gray zone between delirium and dementia; its early course may
fluctuate, but it is often persistent and progressive.

The final common pathway of all forms of organically based mental status change is an
alteration in cortical brain function, at times in concert with abnormalities of deep brain
structures. These conditions result from (1) an exogenous insult or an intrinsic process that
affects cerebral neurochemical functioning and/or (2) physical or structural damage to the
cortex, subcortex, or to deeper structures involved with memory. Some of the etiologies
include trauma, mass lesions, hydrocephalus, strokes (ie, multi-infarct dementia), atrophy,
infection, toxins, or dementing processes.

The end result of these disruptions of function or structure is impairment of cognition that
affects some or all of the following: alertness, orientation, emotion, behavior, memory,
perception, language, praxis, problem solving, judgment, and psychomotor activity.
Knowledge of which areas of this spectrum are affected or spared guides both the workup
and the diagnosis.

 References

Epidemiology

Frequency

United States

Delirium accounts for or develops during 10-15% of all admissions to acute-care hospitals
but is seen much more frequently in elderly persons (up to >50%, particularly following
major surgery or trauma).

The prevalence of dementia doubles every 5 years between ages 60 to about 90 years: 1% of
persons aged 60-64 years up to 30-50% of those older than 85 years. Approximately 60% of
nursing home beds are occupied by patients with dementia. In the ED, patients in nursing
homes are more likely to present with delirium than other patients, even after adjusting for
delirium risk factors.[1] Alzheimer disease (AD) accounts for most patients with dementia
who are older than 55 years (50-90% of all cases). It is estimated that over 4 million people in
the United States suffer from AD.

Although slowing of memory and word-finding are normal features of brain aging,
approximately 10-15% of patients with mild cognitive impairment, a transitional state
between normal functioning and dementia, progress to AD yearly.

International
ORGANIC MENTAL DISORDER LBM_4

Alzheimer disease is less common and has an older age of onset in Japan, China, and parts of
Scandinavia. In these countries, vascular causes of dementia may outnumber Alzheimer
disease.

Mortality/Morbidity

Some causes of delirium (eg, delirium tremens, severe hypoglycemia, CNS infection,
heatstroke, thyroid storm) may be fatal or result in severe morbidity if unrecognized and
untreated. With some exceptions (such as overdose of tricyclic antidepressants), drug
intoxications generally resolve fully with supportive care alone. Failure to provide thiamine
when administering glucose may rarely lead to acute Wernicke syndrome (ataxia, confusion,
oculomotor palsies in the setting of malnutrition). If unrecognized, Wernicke syndrome may
also result in chronic dementia.

Certain withdrawal syndromes that can present with delirium (eg, alcohol, benzodiazepines,
barbiturates) can be deadly if untreated.

Patients with primary dementia have a significantly reduced life expectancy, depending on
the cause of the dementia and its severity and rapidity of progression.[2]

Race

Delirium is seen more commonly in whites than in other races.

Sex

Delirium is seen more commonly in females than in males. Alzheimer disease is more
prevalent among women because of their longer life expectancy. Lifetime risk in women is
estimated to be 32%, whereas the lifetime risk in men is 18%. However, the age-specific risk
is equal in both sexes.

Age

Delirium due to physical illness is more frequent among the very young and those older than
60 years. Delirium due to drug and alcohol intoxication or withdrawal is most frequent in
persons aged mid teens to the late 30s.

Dementia, particularly Alzheimer disease, is seen predominantly in elderly persons; however,


certain types of dementia are seen in younger patients (eg, AIDS-related dementia, certain
familial forms of Alzheimer disease), and some cases of variant Creutzfeldt-Jakob disease (ie,
bovine spongiform encephalopathy or mad cow disease). AIDS-related dementia is the most
common nontraumatic dementia seen in younger persons.

 References
ORGANIC MENTAL DISORDER LBM_4

History

Mental status changes (MSCs) can evolve acutely with a rapidly fluctuating, usually transient
course (delirium) or insidiously and inexorably over months or years with a gradually
worsening or stuttering course (dementia).

Delirium presents with acute onset of impaired awareness, easy distraction, confusion, and
disturbances of perception (eg, illusions, misinterpretations, visual hallucinations). Recent
memory is usually deficient, and the patient is typically disoriented to time and place. The
patient may be agitated or obtunded, and the level of awareness may fluctuate over brief
periods. Speech may be incoherent, pressured, nonsensical, perseverating, or rambling, which
may make the taking of an accurate history from the patient impossible. Patients with
delirium have difficulty maintaining attention and/or changing the focus of their attention.

For patients with delirium, attempt to obtain a current and past history from other sources,
including prehospital workers, family or friends, and past medical records. Look specifically
for street drug, alcohol, and medication use; preexisting endocrine disorders; and recent
activities that may have resulted in exposure to toxins or environmental injury. Ask about
prior psychiatric illness and similar episodes of confusion in the past.

Dementia presents with a history of chronic, steady decline in short and, later, long-term
memory and is associated with difficulties in social relationships, work, and activities of daily
life. In contrast to delirium, the sensorium is usually clear. However, acute confusional states
can be superimposed on an underlying dementing process. The diagnosis is usually known
previously in a patient who presents to the ED with moderate-to-severe symptoms.

Earlier stages of dementia may present subtly, and patients may minimize or attempt to hide
their impairments. Patients at this stage often have an associated depression. Depression
alone can present as a dementia-like condition in elderly patients (see below). Dementia of
relatively recent onset has a higher likelihood of a potentially reversible etiology (5-47%).
Take a careful history, looking for past or present drug or alcohol abuse, current medications,
chronic or acute medical illnesses and psychiatric disorders to uncover a treatable or
modifiable cause for the cognitive impairment.

Elderly patients with depressed mood, hopelessness, and suicidality may be suffering from
"pseudodementia" (false dementia). When the depression is alleviated with treatment, the
dementia-like condition fully resolves.

A history of a stuttering course may point to multi-infarct dementia, which is caused by


repeated lacunar strokes. Treatment aimed at preventing future strokes may arrest further
progression of the dementia. However, small strokes in specific areas of the brain may trigger
the onset of Alzheimer-type dementia

 References
ORGANIC MENTAL DISORDER LBM_4

Physical

Any patient who presents with altered mental status (AMS) needs a complete physical
examination, with particular attention to general appearance, vital signs, hydration status,
evidence of physical trauma, and neurologic signs. The delirious or obtunded patient should
be evaluated for pupillary, funduscopic, and extraocular abnormalities; nuchal rigidity;
thyroid enlargement; and heart murmurs or rhythm disturbances. Other clues include a
pulmonary examination that reveals wheezing, rales, or absent breath sounds; an abdominal
examination that reveals hepatic or splenic enlargement; or a cutaneous examination that
shows rashes, icterus, petechiae, ecchymoses, track marks, or cellulitis. Cellulitis in elderly
persons often is hidden under clothing, particularly pants and socks. Checking these areas in
patients with diabetes is critical. Any serious infection can lead to acute mental status
changes.

General appearance (eg, unkempt and/or malnourished) may suggest the possibility of drug
or alcohol abuse.

Look for track marks.

Smell for alcohol, the musty odor of fetor hepaticus, or the fruity smell of ketoacidosis.

Icterus and asterixis point to liver failure with an elevation of the serum ammonia level.

Agitation and tremulousness suggest sedative drug or alcohol withdrawal.

Close attention to vital signs is essential and easy to overlook in the setting of extreme
behavioral difficulties in a delirious patient. It is unusual for a patient with acute delirium to
present to the ED with normal vital signs.

Fever may point to infection, heat illness, thyroid storm, aspirin toxicity, or the extreme
adrenergic overflow of certain drug overdoses and withdrawal syndromes (in particular,
delirium tremens). Extreme hyperthermia (with pinpoint pupils) may be seen in pontine
strokes. In patients with a rapid respiratory rate, consider diabetic ketoacidosis (ie, Kussmaul
respiration), sepsis, stimulant drug intoxication, and aspirin overdose. In patients with a slow
respiratory rate, consider narcotic overdose, CNS insult, or various sedative intoxications.

A rapid pulse rate is seen in patients with fever, sepsis, dehydration, thyroid storm, and
various cardiac dysrhythmias and in overdoses of stimulants, anticholinergics, quinidine,
theophylline, tricyclic antidepressants, or aspirin. Patients with a slow pulse rate may have
elevated intracranial pressure, asphyxia, or complete heart block. Calcium channel blockers,
digoxin, and beta-blockers also may produce altered mental status and bradycardia.

Blood pressure elevation is common in delirium because of resulting adrenergic overload.


ORGANIC MENTAL DISORDER LBM_4

In patients with acute altered mental status and severely elevated blood pressure, check the
ocular fundi for arteriolar spasm, disc pallor, papilledema, flame hemorrhages, and exudates.
These are all signs of malignant hypertension. Even with these changes, the patient may be
alert and minimally symptomatic.

In pregnant patients with a diastolic pressure greater than 75 mm Hg in the second trimester
or greater than 85 mm Hg in the third trimester, consider preeclampsia (ie, hyperreflexia,
edema, proteinuria).

In patients with hypertension and bradycardia, consider an elevated intracranial pressure


(Cushing reflex).

With delirium and hypotension, the differential diagnosis includes dehydration, diabetic
coma, hemorrhage due to trauma, aneurysmal rupture, or GI bleeding. Also, consider
adrenergic depletion secondary to cocaine; amphetamine; or tricyclic overdose, which usually
responds only to norepinephrine, not dopamine. Addisonian crisis, particularly in those who
are steroid dependent, should be considered.

Pupillary dilation is seen in anticholinergic overdose (diphenhydramine), stimulant use, and


hallucinogen use. A common feature of diphenhydramine and other antihistamine overdoses
is picking at imaginary objects in the air.

Pupillary constriction is seen in narcotic intoxication.

Serious head trauma is usually obvious. However, occult trauma may be discovered by
findings of basilar skull fracture, such as hemotympanum, Battle sign (ie, mastoid area
ecchymoses), raccoon eyes, or otorhinorrhea. The latter condition may be tested for by
placing a drop of the draining blood on filter paper and then looking for a clear ring of
cerebrospinal fluid (CSF). A funduscopic examination may show loss of venous pulsations in
cases of early intracranial pressure (ICP) elevation or papilledema in severe ICP elevation.
Pupillary inequality may be a late sign of uncal herniation.

At times, it may be difficult to distinguish between acute delirium, psychiatric crisis, or a


chronic process with exacerbation such as dementia. It is safest to presume delirium until an
alternative process can be proven through testing and/or clinical observation.

A brief bedside neurologic examination, including mental status testing, is an essential part of
the workup of organic brain syndrome and altered mental status when a rapidly treatable
cause, such as hypoglycemia or narcotic overdose, is not immediately apparent.

The Mini-Mental Status Examination (MMSE) is a formalized way of documenting the


severity and nature of mental status changes.[3] The MMSE, as modified from Folstein, is
outlined here. The maximum score per item is indicated in parentheses.

 Orientation (5): What are the year, season, date, day, and month?
ORGANIC MENTAL DISORDER LBM_4

 Orientation (5): Where are we (ie, state, county, town, hospital, and floor)?
 Registration (3): Name 3 objects (ask the patient to repeat these 3 objects).
 Attention and calculation (5): The serial 7 test awards 1 point for each correct answer.
Stop after 5 answers. Spelling "world" backwards is optional.
 Recall (3): Ask for the 3 objects (from Registration) to be repeated. One point is
scored for each correctly recalled object.
 Language (2): Name a pencil and a watch.
 Repetition (1): Repeat the following: "No ifs, ands, or buts."
 Complex commands (6): Follow a 3-stage command, such as "Take a paper in your
right hand, fold it in half, and put it on the floor" (3 points). Next, read and follow
these printed commands: "Close your eyes" (1 point); "Write a sentence" (1 point);
and "Copy design" (1 point)

Instructions for administering the MMSE are as follows:

 Orientation: Ask for the date. Specifically, ask for any omitted information. Give 1
point for each correct response.
 Registration: Ask permission to test memory. Name 3 unrelated objects clearly and
slowly about 1 second apart. After all 3 objects have been named, ask the patient to
repeat them. The first repetition determines the score. Keep repeating the items, as
many as 6 times, until the patient can repeat all 3 of them. (This step is also required
for the Recall test.)
 Attention and calculation: Ask the patient to begin with 100 and count backwards by
7s. Stop after 5 subtractions and score correct answers. If the patient cannot calculate,
ask him or her to spell "world" backwards. The score is the number of letters in
correct order.
 Recall: Ask the patient to recall the 3 objects previously asked to remember (from
Registration). Zero to 3 points may be scored.
 Language: To test skills in naming objects, show a wristwatch and a pencil to the
patient, and ask the patient to name each item. Zero to 2 points may be scored.
 Repetition: Ask the patient to repeat a sentence. Allow 1 trial. Zero to 1 point may be
scored.
 Complex 3-stage command: Give the patient a piece of paper and repeat the
command. Score 1 point for each portion of the command that is performed correctly.
 Reading: Print clearly on a piece of paper in large letters the command "Close your
eyes." Ask the patient to read and perform the command. Score 1 point if the eyes are
closed.
 Writing: Provide a blank piece of paper and ask the patient to write a sentence of
his/her own choosing. It must contain a subject and a verb to be scored 1 point.
Punctuation does not matter for the purpose of scoring.
 Copying: On a clean piece of paper, draw intersecting pentagons, each side measuring
1 inch, and ask the patient to copy the figures exactly. All 10 angles must be present,
and the 2 figures must intersect to score 1 point. Any rotation of the figures or tremor
is ignored.
ORGANIC MENTAL DISORDER LBM_4

A score of less than 24 suggests the presence of delirium, dementia, or another problem
affecting the patient's mental status and may indicate the need for further evaluation.

In addition, or as an alternative to the MMSE, correctly drawing the face of a clock (to
include the circle, numbers, and hands) is a sensitive test of cognitive function. To perform
this test, ask the patient to draw a clock with the hands at 8:20. Two or more errors
significantly correlate with dementia. No errors rule against dementia.

The "Sweet 16" cognitive assessment tool offers a faster, simpler, and reasonably accurate
alternative to the MMSE.[4] Advantages include the absence of a requirement for frail patients
to manipulate pen and paper, freedom from props, and better accuracy across varying
educational levels. The "Sweet 16" test is less selective (72% vs 89%) than the MMSE but is
more sensitive (99% vs 87%). Therefore, a negative test result is highly accurate in ruling out
dementia.

Other simple screening tests include asking the patient to spell "world" backwards or
performing "serial 7's," which involves starting at the number 100 and subtracting 7
repeatedly in series (ie, 100, 93, 86, 79).

 References

Causes

Delirium or acute altered mental status may be caused by the following:

 Intoxication with a substance (eg, hallucinogens, alcohol, medications, toxins)


 Polypharmacy, most often with psychoactive medications
 Major surgery, orthopedic trauma, prolonged immobility, and “ICU psychosis”
 Occult infection (eg, UTI, meningitis, encephalitis, neurosyphilis, sepsis)
 Head trauma
 Seizure disorder
 Acute mania or other psychiatric etiology
 Endocrine crisis (eg, thyroid, adrenal, diabetic)
 High fever seen with infection or heat stroke
 Renal failure
 Liver failure
 Neoplasia
 Inflammation (eg, systemic lupus erythematosus)
 Cerebral vascular accident (CVA)
 Respiratory dysfunction (eg, hypoxia, hypercarbia)
 Shock
 Chronic neurological disorders such as dementia and Parkinson disease
 “Sundowning” (see below)
ORGANIC MENTAL DISORDER LBM_4

In the elderly, the combined effects of visual and auditory impairments, dementia or other
chronic brain dysfunction, medication side effects (particularly polypharmacy), and/or
unfamiliar environment or nighttime darkness can lead to acute confusion or psychosis,
which is known as sundowning. As the name implies, this condition usually occurs in the
evening hours. Vitamin B-12 deficiency is a potential cause of sundowning and progressive,
reversible dementia.

Head trauma, Korsakoff syndrome, transient global amnesia, and various dementing
processes can cause amnesia. Head trauma can lead to transient amnesia with retrograde
(events prior to injury) and anterograde (events following injury) features.

Postconcussive syndrome is a constellation of mental dullness, poor memory, depressed


mood, and headaches that may follow head trauma, often lasting days to weeks, with full
resolution in most cases. This may involve confusional state, but frank delirium is rare.

Transient global amnesia (TGA) is seen in previously well, usually middle-aged patients who
present with a sudden onset of confusion, amnesia, and anxious perseveration.[5] TGA can
occur spontaneously or following minor trauma, exertion, or emotional stress. The amnesia
usually lasts a few hours, with full recovery and rare recurrence.

Various causes have been proposed for TGA: most recently, transient ischemia-like attacks or
perhaps ministrokes in the hippocampal or thalamic memory areas of the brain. Although the
incidence of cerebrovascular risk factors in TGA is low, those patients with such risk factors
(eg, hypertension, smoking, diabetes mellitus, hypercholesterolemia) should be considered
for antiplatelet therapy. Although TGA may involve a transient ischemia to brain areas
involved with memory (hippocampus, thalamus, mediobasilar temporal lobe), TGA typically
resolves more slowly than TIA. In addition, future risk of stroke and death are lower than as
seen in TIA. All patients with TGA should be admitted for monitoring and further workup.

Traveler’s amnesia is typically seen following a nap on an airplane after taking a short-acting
hypnotic, such as alprazolam, triazolam, or zolpidem.

Korsakoff syndrome is caused by neuronal damage that results from thiamine deficiency in
association with chronic alcohol abuse. It is usually preceded by an episode of Wernicke
encephalitis (eg, ataxia, confusion, oculomotor palsy), typically precipitated by
administration of glucose to a malnourished alcoholic without concomitant parenteral
thiamine. Confabulation is a hallmark finding of Korsakoff syndrome (also called Korsakoff
psychosis).

Dementia can occur primarily or can be secondary to cerebrovascular disease, chronic CNS
infection, CNS trauma, increased ICP (eg, neoplasia, mass effect, hydrocephalus), toxins,
avitaminosis, autoimmune disease, and psychiatric illness.

Primary causes include Alzheimer disease and frontotemporal dementia (FTD). AD accounts
for up to 90% of all primary dementias and more than 50% of all dementing illnesses.
ORGANIC MENTAL DISORDER LBM_4

FTD is highly familial, presents at a younger age than Alzheimer disease, and is associated
with profound personality changes, social incompetence, and stereotypical behaviors, yet
with preserved visuospatial skills. Pick disease is a subtype of FTD. The brain invariably
shows a severe and asymmetric atrophy of the frontal and temporal lobes with only rare
involvement of the parietal or occipital lobes associated with sparing of the posterior two
thirds of the superior temporal gyrus. A thin, knife-edge appearance of the gyri is often seen
secondary to the severe atrophy present in Pick disease. The typical pattern of atrophy is
often prominent enough to distinguish Pick disease from Alzheimer disease macroscopically.

Some forms of Alzheimer disease are thought to have a genetic or familial basis. This is
particularly true of Alzheimer disease that begins at a relatively young age and follows a
fulminant course.

Alzheimer-like dementia is seen in 40% of patients with Parkinson disease and in a very high
percentage of patients with Down syndrome who live long enough to develop Alzheimer
disease.

Cerebrovascular causes include lacunar stroke syndrome (multi-infarct dementia), thalamic


stroke, and vasculitides as seen in systemic lupus erythematosus and other rheumatologic
disorders.

Infectious causes of dementia include HIV, Creutzfeldt-Jakob disease, neurosyphilis, and the
end stages of some cases of meningitis and encephalitis.

Traumatic causes of chronic dementia include anoxia, diffuse axonal injury (following a
severe blow to the head), and dementia pugilistica ("punch drunk"), which results from
repeated concussive trauma. A chronic subdural hematoma may present with a dementia-like
syndrome. Toxins causing chronic organic brain syndrome include heavy metals (eg, lead in
solder, ceramic glazes), organic chemical exposures, severe carbon monoxide poisoning, and
chronic substance abuse.

Avitaminoses, including deficiencies of vitamin B-12 and folate, can cause organic brain
syndrome.

Autoimmune causes include systemic lupus erythematosus, giant cell arteritis, and
sarcoidosis. Dementia has followed a corticosteroid-treated episode of polymyalgia
rheumatica.

Psychiatric illnesses mimicking dementia include the pseudodementia of major depression in


elderly persons and chronic schizophrenia (originally termed "dementia praecox"). Mania and
hypomania as seen in bipolar disorder can be confused with delirium (in a severe form:
“excited delirium”—often exacerbated by physical restraining, which can lead to sudden
death).
ORGANIC MENTAL DISORDER LBM_4

Other causes to consider include chronic endocrinopathies, Wilson disease (copper storage
disease), and lipid storage diseases.

 References

 Differential Diagnoses
 Brain Abscess
 Conversion Disorder
 Delirium Tremens
 Depression and Suicide
 Diabetic Ketoacidosis
 Encephalitis
 Epidural and Subdural Infections
 Heat Exhaustion and Heatstroke
 Herpes Simplex
 Herpes Simplex Encephalitis
 HIV Infection and AIDS
 Hypercalcemia
 Hypernatremia
 Hyperosmolar Hyperglycemic Nonketotic Coma
 Hypertensive Emergencies
 Hypoglycemia
 Hypothyroidism and Myxedema Coma
 Neoplasms, Brain
 Neuroleptic Malignant Syndrome
 Panic Disorders
 Plant Poisoning, Alkaloids - Isoquinoline and Quinoline
 Plant Poisoning, Alkaloids - Tropane
 Plant Poisoning, Glycosides - Cardiac
 Schizophrenia
 Status Epilepticus
 Subarachnoid Hemorrhage
 Subdural Hematoma
 Tick-Borne Diseases, Lyme
 Toxicity, Amphetamine
 Toxicity, Anticholinergic
 Toxicity, Antidepressant
 Toxicity, Antihistamine
 Toxicity, Cocaine
 Toxicity, Cyclic Antidepressants
 Toxicity, Hallucinogen
 Toxicity, Lead
 Toxicity, Lithium
 Toxicity, Mushroom - Hallucinogens
ORGANIC MENTAL DISORDER LBM_4

 Toxicity, Nonsteroidal Anti-inflammatory Agents


 Toxicity, Thyroid Hormone
 Toxicity, Toluene
 Toxicity, Toluene
 Toxicity, Valproate
 Toxicity, Valproate
 Variant Creutzfeldt-Jakob Disease and Bovine Spongiform Encephalopathy
 Wernicke Encephalopathy
 Withdrawal Syndromes

Laboratory Studies

Laboratory studies may be helpful for ruling in or ruling out specific diagnoses that cause
delirium or a dementialike presentation. Many of these tests may not be immediately
available to the ED physician, such as vitamin B-12 levels, Venereal Disease Research
Laboratory (VDRL) test, and thyroid function studies.

Oxygen saturation and, in some cases, ABG with a carbon monoxide level are helpful. CBC
count, electrolytes level, blood glucose level, BUN level, and creatinine level should be
checked. In older patients, consider vitamin B-12 and folate levels. Consider calcium level,
magnesium level, and liver function tests (LFTs), including serum ammonia, prothrombin
time (PT), and activated partial thromboplastin time (aPTT). Consider VDRL and/or
fluorescent treponemal antibody absorption (FTA-ABS) test to help rule out neurosyphilis
(see cerebrospinal fluid [CSF] studies below). Urinalysis is also indicated.

When alcohol, drugs, and/or toxins are suspected, consider the following:

 Serum ethanol, salicylate, acetaminophen, carbon monoxide, and other specific drug
or toxin levels as indicated
 Comprehensive drug analyses of blood and urine
 Such toxic screens are generally not helpful in the acute setting unless turnaround
time is rapid.

In a suspected endocrine emergency, the following are required:

 A bedside fingerstick blood glucose determination followed by serum glucose and


serum acetone
 Thyroid-stimulation hormone (TSH), possibly thyroid panel
 Serum cortisol
 Serum calcium, phosphorus, and parathyroid levels

In suspected CNS infection, the following may be ordered:

 Lumbar puncture may be done for CSF studies, including cryptococcal antigen or
India ink prep, and VDRL.
ORGANIC MENTAL DISORDER LBM_4

 CT scan of head should be done before lumbar puncture to rule out toxoplasmosis or
abscess, especially in patients with HIV who present with headache.

 References

Imaging Studies

A head CT scan without intravenous (IV) contrast should be obtained if CNS infection,
trauma, or a cerebral vascular accident (CVA) is suspected. A CT scan is excellent for
detecting acute hematomas and most subarachnoid hemorrhages (SAH) but is most accurate
early in the course. Follow-up lumbar puncture may be needed to rule out SAH.

One study found a high prevalence (41%) of abnormal CT scan findings in patients with
acute MSC in the ED. Eight clinical predictors were significantly associated with an
abnormal scan, including diastolic blood pressure of more than 80 mm Hg, focal weakness, a
Glasgow Coma Score of less than 15, antiplatelet use, upgoing plantar response, headache,
anticoagulant use, and dilated pupils.[6]

Although not typically part of the workup in the ED, a brain MRI may be considered if
readily available and the need confirmed by neurologist and/or radiologist. MRI helps
distinguish between Alzheimer disease and vascular causes of dementia. The MRI may show
subtle signs of stroke missed on CT and is the imaging modality of choice for multiple
sclerosis. An example of MRI in a patient with moderate Alzheimer disease is shown in the
image below.

Coronal T1-weighted MRI scan in a patient with moderate Alzheimer


disease. Brain image reveals hippocampal atrophy, especially on the right
View Image side.

Plain abdominal radiographs may reveal swallowed bags that contain drugs of abuse ("body
packing") or radiodense substances such as iron tablets.

 References

Other Tests

An ECG may be performed to search for myocardial infarction or atrial fibrillation with rapid
ventricular response. Low voltages, as seen in hypothyroidism and pericardial effusion, may
give a clue to the etiology. Look for tachycardia, widened QRS, or prolonged QT interval,
which suggest tricyclic overdose.

A postmortem examination of the brain is currently the only way to positively diagnose the
various dementing illnesses.
ORGANIC MENTAL DISORDER LBM_4

A blood test for apolipoprotein E (ApoE) subtype e4 is still under study, but it promises to
greatly enhance diagnostic accuracy for AD.

Researchers at the Stanford University School of Medicine developed a blood test that may
someday be a step toward predicting AD 2-6 years in advance of onset. The test identifies
changes in certain blood proteins that cells use to convey messages to one another and has a
90% positive predictive value.[7] Lack of test specificity has been a stumbling block to this
potential diagnostic tool.

Testing vitamin B-12 levels and thyrotropin is useful as part of a dementia workup.

 References

Procedures

Lumbar puncture to obtain CSF for analysis should be considered in certain circumstances,
including the following:

 To rule out SAH not seen on CT scan


 To diagnose CNS infections such as encephalitis or meningitis

 References

Prehospital Care

Prehospital care workers involved in the transport of an acutely confused, combative, or


delirious patient must ensure the safety of the patient and staff.

Prior to transport, consider sedation with a benzodiazepine with or without an antipsychotic if


unable to control a dangerous patient. Keep in mind that excess sedation may obscure the
Mini-Mental Status Examination (MMSE) in the ED.

Use physical restraints if necessary for safe transport.

Provide supplemental oxygen.

Intubate when the airway is at risk or when the patient is comatose or has a poor gag reflex.
Protect the cervical spine in the setting of trauma.

 References

Emergency Department Care

ED physicians caring for the patient with agitation, confusion, delirium, combativeness, or
obtundation must ensure the safety of both the patient and the staff while attending to issues
ORGANIC MENTAL DISORDER LBM_4

of airway protection and immediate recognition and treatment of rapidly reversible problems
(eg, hypoxia, hypoglycemia, narcotic overdose).

Provide supplemental oxygen unless oxygen saturation is above 93% on room air.

When carbon monoxide poisoning is suspected, ignore the oxygen saturation, obtain a
carboxyhemoglobin level, and provide 100% oxygen.

In cases of airway compromise, coma, or poor gag reflex, the ED physician should have a
low threshold for intubation. Use rapid sequence intubation (RSI), particularly in the settings
of possible head trauma, elevated ICP, or a combative patient. RSI/intubation may be
necessary to facilitate imaging studies.

Treat suspected overdose-induced delirium based on ingestion history and/or toxidromes.


Such treatment may range from simple observation and supportive care, activated charcoal,
lavage (rarely performed), sedation, specific antidotes to intubation/life support.

Behavioral control of a patient with delirium who is agitated and combative should be
primarily medication-based with physical restraining kept at a minimum and for protection of
both the patient and staff (see Medication).

Conversely, inpatient prevention and management of delirium should strive to avoid or


minimize use of sedating medications. These medications increase confusion, reduce
attentiveness, and impair orientation, thereby exacerbating delirium. A prospective study of
ICU patients, for example, found that lorazepam sedation increased the risk of delirium by
20%.[8] Most cases of delirium are helped by reassuring, compassionate human contact—
particularly by those with whom the patient is familiar (especially family members).

 References

Consultations

Specific cases may require consultation with neurosurgery, neurology, or internal medicine
subspecialists (eg, infectious disease, endocrinology, nephrology, gastroenterology,
toxicology, psychiatry).

In the setting of trauma or neurosurgical emergency, notify surgeons early in the workup.
When available, a neurosurgeon should be consulted before using mannitol or high-dose
steroid therapy.

The patient's private physician and/or family members are often the best sources of
information regarding baseline functioning, prior medical history, and current medications.

Consult social services for home evaluation and placement issues for patients with dementia.
ORGANIC MENTAL DISORDER LBM_4

 References

 Medication
 Medication Summary
 Sedatives
 Neuroleptics
 Atypical antipsychotics
 Antidotes
 Glucose supplements

Medication Summary

Medications typically used in the ED treatment of delirium or acute mental status changes
include sedatives, neuroleptics, and antidotes. Other drugs may be useful in treating specific
etiologies uncovered in the workup. The medications outlined here are used for acute
behavioral changes.

 References

 Sedatives
 Class Summary
 Lorazepam (Ativan)

Lorazepam (Ativan)

 Dosing, Interactions, etc.

Clinical Context: Benzodiazepine of choice in ED. Safe for a wide variety of acute
behavioral disturbances. Can be given PO/SL (for rapid effect in panic attack)/IV/IM and can
be mixed in syringe with neuroleptic agent. Sedative hypnotic with short onset of effects and
relatively long duration of action. By increasing action of GABA, a major inhibitory
neurotransmitter in the brain, may depress all levels of CNS, including limbic and reticular
formation. When patient needs to be sedated for longer than 24-h period, this medication is
excellent. Has longer CNS effect than diazepam and is preferred for seizure control. Easily
titrated for acute withdrawal syndromes (eg, alcohol, benzodiazepines, barbiturates) and
status seizures when given IV (10 mg or more may be needed in status epilepticus). Two mg
of lorazepam approximately equivalent to 5 mg of diazepam. Preferred over neuroleptics for
treating toxic effects of hallucinogens, cocaine, stimulants, or PCP.

 References

Class Summary

These agents are used to calm acute agitation, to control the behavior of combative patients,
and to facilitate procedures.
ORGANIC MENTAL DISORDER LBM_4

 References

 Neuroleptics
 Class Summary
 Haloperidol (Haldol)
 Droperidol (Inapsine)

Haloperidol (Haldol)

 Dosing, Interactions, etc.

Clinical Context: DOC for severe agitation, acute psychosis, and severe delirium when no
contraindications exist. Parenteral dosage form may be admixed in same syringe with 2 mg
lorazepam for better anxiolytic effects.

 References

Droperidol (Inapsine)

 Dosing, Interactions, etc.

Clinical Context: Some clinicians believe droperidol is DOC for control of severely
disturbed and/or violent patient. Somewhat faster acting and more sedating than haloperidol,
but more likely to cause hypotension. May exert antipsychotic activity through dopaminergic
system. May alter dopamine action in CNS. Parenteral dosage form may be admixed in same
syringe with 2 mg lorazepam for better anxiolytic effects.

Now has black-box warning regarding life-threatening torsade de pointes (TdP) (a rhythmic
pattern of sinusoidal ventricular complexes that lead to ventricular fibrillation and cardiac
arrest), especially in the setting of prolonged QT syndrome. Assessing QT interval via ECG
or rhythm strip advised before administering droperidol.

 References

Class Summary

These agents have more robust calming effects than benzodiazepines in acutely agitated
patients. They act fast when given IV. They can be mixed in the same syringe with lorazepam
for rapid chemical restraint (IM/IV). They are easily titrated and long acting.

Haloperidol and droperidol are of the butyrophenone class, which is noted for high potency
and low potential for orthostasis. However, they have great potential for extrapyramidal
symptoms (EPS)/dystonia.
ORGANIC MENTAL DISORDER LBM_4

Caveat: Neuroleptics can mask the signs of withdrawal from alcohol, benzodiazepines, and
barbiturates while failing to treat adrenergic and GABA-nergic dysregulation. They do not
prevent seizures.

 References

 Atypical antipsychotics
 Class Summary
 Ziprasidone
 Risperidone (Risperdal)

Ziprasidone

 Dosing, Interactions, etc.

Clinical Context: Indicated for acute behavioral control in setting of acute psychosis,
delirium, and as "chemical restraint." Less likely to cause severe dystonic reactions in
younger patients than haloperidol and droperidol.

 References

Risperidone (Risperdal)

 Dosing, Interactions, etc.

Clinical Context: Often used for sundowning in elderly patients but can increase mortality
rate in dementia. Binds to dopamine D2 receptor with 20 times lower affinity than for
serotonin 5-HT2 receptor. Improves negative symptoms of psychoses and reduces incidence
of EPS. Also may have antidepressant effects, probably because of its serotonin activity.

 References

Class Summary

These are newer neuroleptics with a lowered risk of extrapyramidal syndrome (EPS) and
improved efficacy for the negative symptoms (eg, withdrawal, apathy) of psychosis because
of their enhanced serotonergic activity as compared to older-style neuroleptics. These
medications have largely supplanted older neuroleptics for sedation and treatment of
psychosis in elderly patients with dementia.

 References

 Antidotes
 Class Summary
 Physostigmine
ORGANIC MENTAL DISORDER LBM_4

 Naloxone (Narcan)

Physostigmine

 Dosing, Interactions, etc.

Clinical Context: In setting of suspected antihistaminic/anticholinergic overdose, increased


concentration of acetylcholine can improve patient's delirium dramatically; for reasons that
are not entirely clear, appears to have less effect if administered within 4 h postexposure.
May be useful diagnostically. Avoid in suspected TCA OD.

 References

Naloxone (Narcan)

 Dosing, Interactions, etc.

Clinical Context: Prevents or reverses opioid effects (hypotension, respiratory depression,


sedation), possibly by displacing opiates from their receptors.

 References

Class Summary

These agents are used when the toxic agent is known and has an antidote or as a coma
cocktail in patients who are stuporous or comatose. Includes oxygen, thiamine (100 mg
IV/IM), glucose (50 mL of D50W IV push), and naloxone (Narcan; 2-10 mg SC/IM/IV or via
ETT). The use of flumazenil (Romazicon) for suspected or known benzodiazepine overdose
is controversial. Flumazenil may precipitate refractory seizures in the setting of long-term use
or mixed overdose with seizure-inducing agents (eg, TCAs). It may be useful in diagnosis
and in avoiding the need for intubation.

 References

 Glucose supplements
 Class Summary
 Dextrose

Dextrose

 Dosing, Interactions, etc.

Clinical Context: Should be given to any obtunded patient in whom hypoglycemia cannot
be rapidly ruled out via bedside testing. Monosaccharide, absorbed from intestine and
distributed, stored, and used by tissues. Parenterally injected dextrose is used in patients
ORGANIC MENTAL DISORDER LBM_4

unable to obtain adequate PO intake; direct PO absorption results in rapid increase of blood
glucose concentrations.

Serves to restore blood glucose levels. Each 100 mL of 5% dextrose contains 5 g of dextrose
while each 100 mL of 10% dextrose contains 10 g of dextrose.

Effective in small doses; no evidence indicates that it may cause toxicity; concentrated
infusions provide higher amounts of glucose and increased caloric intake with minimum fluid
volume.

 References

Class Summary

Monosaccharides absorbed from intestine after PO absorption of dextrose results in rapid


increase of blood glucose concentrations.

 References

Further Inpatient Care

All patients with unresolved delirium require admission and often require telemetry or ICU
care.

 References

Further Outpatient Care

Workup for most cases of newly recognized dementia can be completed in an outpatient
setting. In some cases, admission is needed until an appropriate living situation or a nursing
home placement is arranged.

 References

Inpatient & Outpatient Medications

Outpatient medications for primary dementia are coordinated best by health care providers
who have continuing contact with the patient. Medications may include the following:

 Anticholinesterase inhibitors, such as donepezil (Aricept), galantamine (Razadyne),


and rivastigmine (Exelon): These medications are useful early in the disease course,
but they lose their effectiveness or may worsen mental status in advanced stages of
the disease.
 N -methyl D -aspartate (NMDA) receptor antagonists, including memantine
(Namenda)
ORGANIC MENTAL DISORDER LBM_4

 Antidepressants, especially the selective serotonin reuptake inhibitors or bupropion


(Wellbutrin): Avoid tricyclic antidepressants because of their anticholinergic
properties, which can worsen dementia.
 Benzodiazepines for sedation or sleep: These drugs may worsen cognitive deficits and
increase the risk of falls.
 Antipsychotics for psychotic ideation or aggressive behavior: High-potency agents are
preferred. Risperidone (Risperdal), a newer atypical antipsychotic, is well tolerated
and useful for sundowning. However, the atypical antipsychotics as a group have been
associated with a slightly higher death rate in patients with dementia (3.5% vs. 2.3%
for placebo). Despite a US Food and Drug Administration (FDA) black box warning,
experts warn against abandoning this class of medications in the treatment of
dementia-related psychosis and aggression.

 References

Deterrence/Prevention

Various substances to prevent or retard the onset of dementia have been proposed and/or
studied. Prevention mechanisms have included preservation of CNS supporting cells,
prevention of CNS inflammation, or free-radical inhibition. Unfortunately, no supplement or
medication has been conclusively shown to prevent or retard the progression of dementia.

 Nonsteroidal anti-inflammatory drugs (NSAIDs): The mechanism of action is thought


to involve prevention of CNS inflammation.[9] More recent studies suggest that heavy
NSAID intake is a risk factor for dementia; however, moderate intake may delay but
not prevent dementia onset.[10]
 Vitamin E: The suggested dose for prevention is 200-400 IU/d; much higher doses are
sometimes given for treatment. The mechanism of action may be antioxidant, free-
radical inhibition. Efficacy is controversial and vitamin E can increase mortality risk.
Therefore, should only be considered for patients with AD or at high risk for AD.
 Vitamin B-6, vitamin B-12, and folate: These reduce levels of homocysteine, a
potential brain neurotoxin. Efficacy is controversial and recent studies show no
benefit.
 Statin cholesterol-lowering medications: Reports suggest that these drugs
substantially protect against dementia via an effect not related directly to blood levels
of cholesterol. Mechanisms of action may be reduction of insulin levels in the brain
and/or C-reactive protein (CRP) levels in the blood (indicative of inflammation). A
study of more than 17,000 adults older than 60 years in Finland concluded that statins
appeared to reduce risk by 58%.[11] Other studies have found no benefit to statins in
delaying dementia progression in patients with AD.
 Estrogen replacement: This is being studied, but no evidence of benefit has been
found at present.
 Ginko biloba: This is a medicinal herb considered safe but of questionable efficacy.
Preparations are of uncertain purity and dose consistency.
ORGANIC MENTAL DISORDER LBM_4

 A high intake of dietary fats and calories is associated with an increased risk of
Alzheimer disease.

Undertreated depression, hypertension, diabetes mellitus, hypercholesterolemia, and obesity


have all been associated with higher risk of Alzheimer disease.

Excessive amounts of alcohol act as a neurotoxin and can increase Alzheimer disease risk. In
moderate doses, alcohol inhibits cerebrovascular disease although it may still enhance brain
atrophy. However, recent studies suggest that moderate drinking is protective against
dementia as compared with abstinence. Antioxidants in wine (bioflavonoids) may be
additionally beneficial (over spirits and beer). Red wines grown in more grape-stressful
climates (eg, upstate New York) contain the highest concentrations of these nutrients.

Sedentary lifestyle is a risk factor for dementia, whereas regular exercise is protective.

 References

Complications

Delirium is a true medical emergency. Failure to recognize and aggressively treat the
underlying cause can be catastrophic.

Delayed recognition of dementia can result in trauma secondary to cognitively impaired


driving and the use of other hazardous equipment, including cooking stoves.

Patients with dementia are at increased risk of victimization by predatory business practices,
Internet scams, and other fraudulent or criminal attacks.

 References

Prognosis

Delirium is fully reversible in most cases with proper recognition and treatment of the
etiology. However, some cases of delirium can last weeks or months and can become
chronic.

Dementia is usually insidious and relentlessly progressive. However, about 20-30% of cases
are due to reversible causes. On average, patients with Alzheimer disease die within 8 years
of onset, with a range of 2-15 years. Younger patients usually have a more fulminant course.
Pick disease has a similar course.

Subacute organic brain syndrome (OBS), or encephalopathy, may be reversible, persistent, or


progressive.

 References
ORGANIC MENTAL DISORDER LBM_4

Author

Paul S Gerstein, MD, Attending Physician, Emergency Department, Baystate Mary Lane
Hospital

Disclosure: Nothing to disclose.

Specialty Editors

Eric M Kardon, MD, FACEP, Attending Emergency Physician, Georgia Emergency


Medicine Specialists; Physician, Division of Emergency Medicine, Athens Regional Medical
Center

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska


Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

J Stephen Huff, MD, Associate Professor of Emergency Medicine and Neurology,


Department of Emergency Medicine, University of Virginia School of Medicine

Disclosure: Nothing to disclose.

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School,
Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare
System and Harvard Medical School; Attending Physician, Division of Emergency Medicine,
Beth Israel Deaconess Medical Center

Disclosure: Nothing to disclose.

Chief Editor

Pamela L Dyne, MD, Professor of Clinical Medicine/Emergency Medicine, University of


California, Los Angeles, David Geffen School of Medicine; Attending Physician, Department
of Emergency Medicine, Olive View-UCLA Medical Center

Disclosure: Nothing to disclose.

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