Chapter 3.

organic--symptomatic ,mental disorder

delirium ( 复 deliria) 谵 妄 , 发 狂 , 妄 想 a. 精 神 错 乱 ， 谵 妄 ； 极 度 兴 奋 ； 发 狂 ;

lapse into ~ 陷 入 谵 妄 状 态 ， 说 起 胡 话 来 .a ~ of joy 欣 喜 若 狂 .In his ~ the man talked nonsense. 他 精 神 错 乱 时 说 胡 话

A disorder characterized by CONFUSION; inattentiveness; disorientation; ILLUSIONS; HALLUCINATIONS; agitation; and in some instances

autonomic nervous system overactivity. It may result from toxic/metabolic conditions or structural brain lesions.

illusion 错觉,幻觉

inattentiveness注意迟钝
disorientation 定向力障碍,定向消失

causation 因果,引起,原因作用,因果关系

Amnestic syndrome遗忘综合征

neurosyphilis神经梅毒

abrupt a.突然的, 唐突的

ubiquitous随遇的,普遍存在的

organic catatonic disorder器质性紧张性(畸张症性)障碍

Persecutory Delusions, sometimes called Querulant delusions, are when a person believes
(wrongly) that they are being picked on, or threatened by ...
Schneiderian first rank symptoms
PARANOID schizophrenia类偏狂型精神分裂症,妄想型精神分裂症
情感不稳（脆弱）障碍，器质性—organic emotionally labile-asthenic disorder F06.6 因脑器质
性疾病导致的情感失禁、不稳定、易疲乏和各种躯体不适。 ..
. The presentations of substance-induced dissociative states may resemble those of
functional dissociative disorders, or organic and psychogenic dissociative
分离性障碍主要特点是记忆丧失，通常是重要的近期事件，

Transient amnesias, fugues, twilight states, automatisms, depersonalization, and

furors or explosive disorders can occur in association with, or be caused by,
various medications or substance-induced organic brain states. Agents capable
of precipitating dissociative-like states include alcohol, barbiturates and similarly
acting hypnotics, benzodiazepines, scopolamine, clioquinol, beta-adrenergic
blockers, marijuana and certain psychedelic drugs, general anesthetics, and
others. The presentations of substance-induced dissociative states may
resemble those of functional dissociative disorders, or organic and psychogenic
dissociative factors may coexist and be intertwined or indistinguishable. Organic
dissociative states are distinct from intoxication, amnestic disorder, frank
delirium, or other organic mental disorders as specified in DSM-III and DSM-III-
R, yet these diagnostic manuals have no inclusive category or coherent
nosological approach to dissociative states not strictly psychogenic in etiology.
Substance-induced and other organic dissociative disorders can have clinical,
medicolegal, and neuropsychological significance. They provide a unique
 opportunity for the study of mind-brain relationships and should be included in
psychiatric nosology.

Creutzfeldt Jakob disease克罗伊茨费尔特-雅各布病,痉挛性假性硬化

The main symptoms of Parkinson's disease are usually stiffness,
shaking (tremor), and slowness of movement. Other symptoms (listed
below) may also develop. Symptoms typically become gradually worse
over time. Treatment often provides good relief of symptoms for
several years.

Parkinson's disease (PD) is a chronic (persistent) disorder of part

of the brain. It is named after the doctor who first described it. It
mainly affects the way the brain co-ordinates the movements of the
muscles in various parts of the body.

Steele-Richardson-Olszewski syndrome斯-里-奥三氏综合征:核上性麻痹综合征Progressive
supranuclear palsy is a term used to describe a neurodegenerative disease 神经变性疾病 that
was first described in 1964.1 It affects cognition, eye movements, and posture. Characteristics
include supranuclear, primarily vertical, gaze dysfunction accompanied by extrapyramidal
symptoms and cognitive dysfunction. The cause is unknown.
Dementia
Huntington's disease

Huntington's disease (also known as Huntington disease,

Huntington's chorea , chorea major , or HD ) is a genetic
neurological disorder[1] characterized after onset by uncoordinated,
jerky body movements and a decline in some mental abilities. These
characteristics vary per individual, physical ones less so, but the
differing decline in mental abilities can lead to a number of
potential behavioral problems. The disorder itself is not fatal, but
as symptoms progress, complications reducing life expectancy
increase.[2] Research of HD has increased greatly in the last few
decades, but its exact mechanism is unknown, so symptoms are managed
individually.[3] Globally, up to 7 people in 100,000 have the
disorder, although there are localized regions with a higher
incidence.[4] Onset of physical symptoms occurs gradually and can
begin at any age, although the mean age at onset is 35 to 44 years.[5]
If onset is before the age of twenty, the condition is classified as
juvenile HD .[6]
The disorder is named after George Huntington, an American physician
who published a remarkably accurate description in 1872.[7] In 1983 a
marker for the altered DNA causing the disease was found,[8] followed
a decade later by discovery of a single, causal, gene.[9] As it is
caused by a single gene, an accurate genetic test for HD was
developed; this was one of the first inherited genetic disorders for
which such a test was possible. Due to the availability of this test,
and similar characteristics with other neurological disorders, the
amount of HD research has increased greatly in recent years.[10]

Dementia (from Latin de- "apart, away" + mens (genitive mentis)

"mind") is the progressive decline in cognitive function due to
damage or disease in the body beyond what might be expected from
normal aging. Although dementia is far more common in the geriatric
population, it may occur in any stage of adulthood. This age cutoff
is defining, as similar sets of symptoms due to organic brain
dysfunction are given different names in populations younger than
adulthood (see, for instance, developmental disorders).

Dementia is a non-specific illness syndrome (set of signs and

symptoms) in which affected areas of cognition may be memory,
attention, language, and problem solving. Higher mental functions are
affected first in the process. Especially in the later stages of the
condition, affected persons may be disoriented in time (not knowing
what day of the week, day of the month, or even what year it is), in
place (not knowing where they are), and in person (not knowing who
they are or others around them).

Symptoms of dementia can be classified as either reversible or

irreversible, depending upon the etiology of the disease. Less than
10 percent of cases of dementia are due to causes which may presently
be reversed with treatment. Causes include many different specific
disease processes, in the same way that symptoms of organ dysfunction
such as shortness of breath, jaundice, or pain are attributable to
many etiologies. Without careful assessment of history, the short-
term syndrome of delirium can easily be confused with dementia,
because they have many symptoms in common. Some mental illnesses,
including depression and psychosis, may also produce symptoms which
must be differentiated from both delirium and dementia.[1]

Contents

[hide]

• 1 Diagnosis

o 1.1 Mini-mental state examination

o 1.2 Modified Mini-Mental State examination (3MS)

o 1.3 Abbreviated mental test score

o 1.4 Other examinations

o 1.5 Laboratory tests

o 1.6 Imaging

• 2 Types

o 2.1 Cortical dementias

o 2.2 Subcortical dementias

• 3 Treatment

o 3.1 Medications
 3.1.1 Off label
o 3.2 Contraindicated

• 4 Prevention

• 5 Risk to self and others

• 6 Services
 • 7 See also

• 8 References

o 8.1 Notes

o 8.2 External links

Diagnosis

Proper differential diagnosis between the types of dementia (cortical

and subcortical - see below) will require, at the least, referral to
a specialist, e.g. a geriatric internist, geriatric psychiatrist,
neurologist, neuropsychologist or geropsychologist.[citation needed]
However, there exist some brief tests (5-15 minutes) that have
reasonable reliability and can be used in the office or other setting
to screen cognitive status for deficits which are considered
pathological. Examples of such tests include the abbreviated mental
test score (AMTS), the mini mental state examination (MMSE), Modified
Mini-Mental State Examination (3MS),[2] the Cognitive Abilities
Screening Instrument (CASI),[3] and the clock drawing test.[4] An AMTS
score of less than six (out of a possible score of ten) and an MMSE
score under 24 (out of a possible score of 30) suggests a need for
further evaluation. Scores must be interpreted in the context of the
person's educational and other background, and the particular
circumstances; for example, a person highly depressed or in great
pain will not be expected to do well on many tests of mental ability.

[edi t] Min i-me ntal sta te e xami nati on

Main article: Mini-mental state examination

The U.S. Preventive Services Task Force (USPSTF) reviewed tests for
cognitive impairment and concluded:[5]

• MMSE

sensitivity 71% to 92%

specificity 56% to 96%
[edi t] Mod ifie d Mi ni-M enta l St ate e xam inat ion ( 3MS )

A copy of the 3MS is online.[6] A meta-analysis concluded that the

Modified Mini-Mental State (3MS) examination has:[7]

sensitivity 83% to 93.5%

specificity 85% to 90%

[edi t] Abb revi ated men tal t est sco re

Main article: abbreviated mental test score

A meta-analysis concluded:[7]

sensitivity 73% to 100%

specificity 71% to 100%

[edi t] Oth er e xami nati ons

Many other tests have been studied[8][9][10] including the clock-drawing

test (example form). Although some may emerge as better alternatives
to the MMSE, presently the MMSE is the best studied. However, access
to the MMSE is now limited by enforcement of its copyright.[citation needed]

Another approach to screening for dementia is to ask an informant

(relative or other supporter) to fill out a questionnaire about the
person's everyday cognitive functioning. Informant questionnaires
provide complementary information to brief cognitive tests. Probably
the best known questionnaire of this sort is the Informant
Questionnaire on Cognitive Decline in the Elderly (IQCODE).[11]

Further evaluation includes retesting at another date, and

administration of other (and sometimes more complex) tests of mental
function, such as formal neuropsychological testing.

[edi t] Lab orat ory t est s

Routine blood tests are also usually performed to rule out treatable
causes. These tests include vitamin B12, folic acid, thyroid-
stimulating hormone (TSH), C-reactive protein, full blood count,
electrolytes, calcium, renal function, and liver enzymes.
Abnormalities may suggest vitamin deficiency, infection or other
problems that commonly cause confusion or disorientation in the
elderly. The problem is complicated by the fact that these cause
confusion more often in persons who have early dementia, so that
"reversal" of such problems may ultimately only be temporary.

Chronic use of substances such as alcohol can also predispose the

patient to cognitive changes suggestive of dementia.

[edi t] Ima ging

A CT scan or magnetic resonance imaging (MRI scan) is commonly

performed, although these modalities (as is noted below) do not have
optimal sensitivity for the diffuse metabolic changes associated with
dementia in a patient who shows no gross neurological problems (such
as paralysis or weakness) on neurological exam. CT or MRI may suggest
normal pressure hydrocephalus, a potentially reversible cause of
dementia, and can yield information relevant to other types of
dementia, such as infarction (stroke) that would point at a vascular
type of dementia. However, the functional neuroimaging modalities of
SPECT and PET have shown similar ability to diagnose dementia as
clinical exam.[12] The ability of SPECT to differentiate the vascular
cause from the Alzheimer disease cause of dementias, appears to be
superior to differentiation by clinical exam.[13]

[edit ] Types
This article is in a list format that may be better presented using prose. You can help by
converting this section to prose, if appropriate. Editing help is available. (January 2009)

[edi t] Cor tica l de ment ias

Cortical dementias arise from a disorder affecting the cerebral

cortex, the outer layers of the brain that play a critical role in
cognitive processes such as memory and language.

• Alzheimer's disease
• Vascular dementia (also known as multi-infarct dementia), including Binswanger's
disease
• Dementia with Lewy bodies (DLB)
 • Alcohol-Induced Persisting Dementia
o Korsakoff's syndrome
o Wernicke's encephalopathy
• Frontotemporal lobar degenerations (FTLD), including Pick's disease
o Frontotemporal dementia (or frontal variant FTLD)
o Semantic dementia (or temporal variant FTLD)
o Progressive non-fluent aphasia
• Creutzfeldt-Jakob disease
• Dementia pugilistica
• Moyamoya disease
• Thebestia (Often mistaken for a cancer)
• Posterior cortical atrophy or Benson's syndrome.

[edi t] Sub cort ical dem enti as

result from dysfunction in the parts of the brain that are beneath
the cortex. Usually, the memory loss and language difficulties that
are characteristic of cortical dementias are not present. Rather,
people with subcortical dementias, such as Huntington's disease,
Parkinson's Disease, and AIDS dementia complex, tend to show changes
in their personality and attention span, and their thinking slows
down.

• Dementia due to Huntington's disease

• Dementia due to Hypothyroidism
• Dementia due to Parkinson's disease
• Dementia due to Vitamin B1 deficiency
• Dementia due to Vitamin B12 deficiency
• Dementia due to Folate deficiency
• Dementia due to Syphilis
• Dementia due to Subdural hematoma
• Dementia due to Hypercalcaemia
• Dementia due to Hypoglycemia
• AIDS dementia complex
• Pseudodementia (a major depressive episode with prominent cognitive symptoms)
• Substance-induced persisting dementia (related to psychoactive use and formerly
Absinthism)
• Dementia due to multiple etiologies
• Dementia due to other general medical conditions (i.e. end stage renal failure,
cardiovascular disease etc.)
• Dementia not otherwise specified (used in cases where no specific criteria is met)
Dementia and early onset dementia have been associated with
neurovisceral porphyrias. Porphyria is listed in textbooks in the
differential diagnosis of dementia. Because acute intermittent
porphyria, hereditary coproporphyria and variegate porphyria are
aggravated by environmental toxins and drugs the disorders should be
ruled out when these etiologies are raised.

[edit ] Treatment
This section does not cite any references or sources. Please help improve this article by
adding citations to reliable sources. Unverifiable material may be challenged and removed.
(January 2009)

Except for the treatable types listed above, there is no cure to this
illness, although scientists are progressing in making a type of
medication that will slow down the process.[citation needed] Cholinesterase
inhibitors are often used early in the disease course. Cognitive and
behavioral interventions may also be appropriate. Educating and
providing emotional support to the caregiver (or carer) is of
importance as well (see also elderly care).

A Canadian study found that a lifetime of bilingualism has a marked

influence on delaying the onset of dementia by an average of four
years when compared to monolingual patients. The researchers
determined that the onset of dementia symptoms in the monolingual
group occurred at the mean age of 71.4, while the bilingual group was
75.5 years. The difference remained even after considering the
possible effect of cultural differences, immigration, formal
education, employment and even gender as influences in the
results.[14]

Some studies world-wide have found that Music therapy may be useful
in helping patients with dementia.[15][16][17][18][19]

[edi t] Med icat ions

• Acetylcholinesterase inhibitors

Tacrine (Cognex), donepezil (Aricept), galantamine (Razadyne), and

rivastigmine (Exelon) are approved by the United States Food and Drug
Administration (FDA) for treatment of dementia induced by Alzheimer
disease. They may be useful for other similar diseases causing
dementia such as Parkinsons or vascular dementia.[20]

• N-methyl-D-aspartate Blockers. Memantine (Namenda) is a drug representative of this

class. It can be used in combination with acetylcholinesterase inhibitors.[citation needed]

[edit] Off label

• Amyloid deposit inhibitors

Minocycline and Clioquinoline, antibiotics, may help reduce amyloid

deposits in the brains of persons with Alzheimer disease.[21]

• Antidepressant drugs

Depression is frequently associated with dementia and generally

worsens the degree of cognitive and behavioral impairment.
Antidepressants may be helpful in alleviating cognitive and behavior
symptoms by reuptaking neurotransmitter regulation through reuptake
of serotonin, noradrenaline and dopamine.[citation needed]

• Anxiolytic drugs

Many patients with dementia experience anxiety symptoms. Although

benzodiazepines like diazepam (Valium) have been used for treating
anxiety in other situations, they are often avoided because they may
increase agitation in persons with dementia and are likely to worsen
cognitive problems or are too sedating. Buspirone (Buspar) is often
initially tried for mild-to-moderate anxiety.[citation needed]

Selegiline, a drug used primarily in the treatment of Parkinson's

disease, appears to slow the development of dementia. Selegiline is
thought to act as an antioxidant, preventing free radical damage.
However, it also acts as a stimulant, making it difficult to
determine whether the delay in onset of dementia symptoms is due to
protection from free radicals or to the general elevation of brain
activity from the stimulant effect.[citation needed]

[edi t] Con trai ndic ated

• Antipsychotic drugs
Both typical antipsychotics (such as Haloperidol) and atypical
antipsychotics such as (risperidone) increases the risk of death in
dementia-associated psychosis.[22] Antipsychotics are therefore not
indicated for the treatment of dementia-related psychosis.[23]

[edit ] Prevention
Main article: Prevention of dementia

It appears that the regular moderate consumption of alcohol (beer,

wine, or distilled spirits) and a Mediterranean diet may reduce
risk.[24][25][26][27] A study has shown a link between high blood pressure
and developing dementia. The study, published in the Lancet Neurology
journal July 2008, found that blood pressure lowering medication
reduced dementia by 13%.[28][29]

[edit ] Risk to self and others

Driving with dementia could lead to severe injury or even death to

self and others. Doctors should advise appropriate testing on when to
quit driving.[30]

Florida's Baker Act allows law enforcement and the judiciary to force
mental evaluation for those suspected of suffering from dementia or
other mental incapacities.[citation needed]

[edit ] Services

Adult daycare centers as well as special care units in nursing homes

often provide specialized care for dementia patients. Adult daycare
centers offer supervision, recreation, meals, and limited health care
to participants, as well as providing respite for caregivers.

[edit ] See also

• Caregiving and dementia
• Montessori-Based Dementia Programming
• Alcohol dementia
• Sundowning (dementia)
• Wandering (dementia)
[edit ] References

[edi t] Not es

1. ^ American Family Physician, March 1, 2003 Delirium

2. ^ Teng E L, Chui H C. The Modified Mini-Mental State (3MS) examination. J Clin
Psychiatry 1987;48:314–18. PMID 3611032
3. ^ Teng E L, Hasegawa K, Homma A, et al. The Cognitive Abilities Screening Instrument
(CASI): a practical test for cross-cultural epidemiological studies of dementia. Int
Psychogeriatr 1994;6:45–58. PMID 8054493
4. ^ Royall, D.; Cordes J.; & Polk M. (1998). "CLOX: an executive clock drawing task". J
Neurol Neurosurg Psychiatry 64 (5): 588–94. doi:10.1136/jnnp.64.5.588. PMID 9598672.
http://jnnp.bmj.com/cgi/content/full/64/5/588.
5. ^ Boustani, M.; Peterson, B.; Hanson, L.; Harris, R.; & Lohr, K. (03 Jun 2003).
"Screening for dementia in primary care: a summary of the evidence for the U.S.
Preventive Services Task Force". Ann Intern Med 138 (11): 927–37. PMID 12779304.
http://www.annals.org/cgi/content/full/138/11/927.
6. ^ "Appendix: The Modified Mini-Mental State (3MS)".
http://www.cjns.org/27febtoc/predicting_appendix_.html. Retrieved on 2007-09-06.
7. ^ a b Cullen B, O'Neill B, Evans JJ, Coen RF, Lawlor BA. A review of screening tests for
cognitive impairment. J Neurol Neurosurg Psychiatry. 2007 Aug;78(8):790-9. Epub 2006
Dec 18. PMID 17178826
8. ^ Sager, M.; Hermann, B.; La Rue, A.; & Woodard, J. (2006). "Screening for dementia in
community-based memory clinics". WMJ 105 (7): 25–9. PMID 17163083.
9. ^ Fleisher, A.; Sowell B.; Taylor C.; Gamst A.; Petersen R.; & Thal L. (2007). "Clinical
predictors of progression to Alzheimer disease in amnestic mild cognitive impairment".
Neurology 68: 1588. doi:10.1212/01.wnl.0000258542.58725.4c. PMID 17287448.
10. ^ Karlawish, J. & Clark, C. (2003). "Diagnostic evaluation of elderly patients with mild
memory problems". Ann Intern Med 138 (5): 411–9. PMID 12614094.
http://www.annals.org/cgi/content/full/138/5/411.
11. ^ Jorm, A.F. (2004). The Informant Questionnaire on Cognitive Decline in the Elderly
(IQCODE): A review. International Psychogeriatrics, 16, 1-19.
12. ^ Bonte, FJ; Harris TS, Hynan LS, Bigio EH, White CL 3rd (July 2006). "Tc-99m
HMPAO SPECT in the differential diagnosis of the dementias with histopathologic
confirmation". Clinical Nuclear Medicine 31 (7): 376–8.
doi:10.1097/01.rlu.0000222736.81365.63. PMID 16785801.
13. ^ Dougall, NJ; Bruggink S, Ebmeier KP (Nov-December 2004). "Systematic review of
the diagnostic accuracy of 99mTc-HMPAO-SPECT in dementia". The American Journal
of Geriatric Psychiatry 12 (6): 554–70. doi:10.1176/appi.ajgp.12.6.554. PMID 15545324.
14. ^ "Bilingualism Has Protective Effect In Delaying Onset Of Dementia By Four Years,
Canadian Study Shows". Medical News Today. 2007-01-11.
 http://www.medicalnewstoday.com/medicalnews.php?newsid=60646. Retrieved on 2007-
01-16.
15. ^ Aldridge, David, Music Therapy in Dementia Care, London : Jessica Kingsley
Publishers, November 2000. ISBN 1853027766
16. ^ Tuet, R.W.K.; Lam, L.C.W. (September 2006) "A preliminary study of the effects of
music therapy on agitation in Chinese patients with dementia", Hong Kong Journal of
Psychiatry, Volume 16, Number 3
17. ^ Watanabe, Tomoyuki; et al., "Effects of music therapy for dementia: A systematic
review", (in Japanese) Aichi University of Education Research Reports, v.55, pp. 57-61,
March, 2005
18. ^ Koger, Susan M.; Chapin Kathyn; Brotons, Melissa, "Is Music Therapy an Effective
Intervention for Dementia? : A Meta-Analytic Review of Literature", Journal of Music
Therapy 36(1), February 1999, pp.2-15.
19. ^ Remington, Ruth, "Calming Music and Hand Massage With Agitated Elderly", Nursing
Research 51(5): 317-323, September/October 2002.
20. ^ Lleo A, Greenberg SM, Growdon JH. Current pharmacotherapy for Alzheimer's
disease. Annu Rev Med. 2006;57:513-33. Review. PMID 16409164
21. ^ Choi, Y., Kim, H.S., Shin, K.Y., Kim, E.M., Kim, M., Kim, H.S., Park, C.H., Jeong,
Y.H., Yoo, J., Lee, J.P., Chang K.A., Kim S., & Suh, Y.H. Related Minocycline Attenuates
Neuronal Cell Death and Improves Cognitive Impairment in Alzheimer's Disease Models.
Neuropsychopharmacology. 2007 Apr 4; PMID 17406652
22. ^ "FDA MedWatch - 2008 Safety Alerts for Human Medical Products". FDA.
http://www.fda.gov/medwatch/safety/2008/safety08.htm#Antipsychotics.
23. ^ "FDA MedWatch - 2008 Safety Alerts for Human Medical Products". FDA.
http://www.fda.gov/medwatch/safety/2008/safety08.htm#Antipsychotics.
24. ^ Mukamal KJ, Kuller LH, Fitzpatrick AL, Longstreth WT, Mittleman MA, Siscovick DS
(March 2003). "Prospective study of alcohol consumption and risk of dementia in older
adults". JAMA 289 (11): 1405–13. doi:10.1001/jama.289.11.1405. PMID 12636463.
25. ^ Ganguli M, Vander Bilt J, Saxton JA, Shen C, Dodge HH (October 2005). "Alcohol
consumption and cognitive function in late life: a longitudinal community study".
Neurology 65 (8): 1210–7. doi:10.1212/01.wnl.0000180520.35181.24. PMID 16247047.
26. ^ Huang W, Qiu C, Winblad B, Fratiglioni L (October 2002). "Alcohol consumption and
incidence of dementia in a community sample aged 75 years and older". J Clin Epidemiol
55 (10): 959–64. doi:10.1016/S0895-4356(02)00462-6. PMID 12464371.
27. ^ Sofi F, Cesari F, Abbate R, Gensini GF, Casini A (2008). "Adherence to Mediterranean
diet and health status: meta-analysis". BMJ 337: a1344. doi:10.1136/bmj.a1344. PMID
18786971.
28. ^ Fillit H, Nash DT, Rundek T, Zuckerman A (June 2008). "Cardiovascular risk factors
and dementia". Am J Geriatr Pharmacother 6 (2): 100–18.
doi:10.1016/j.amjopharm.2008.06.004. PMID 18675769.
29. ^ Peters R, Beckett N, Forette F, et al (August 2008). "Incident dementia and blood
pressure lowering in the Hypertension in the Very Elderly Trial cognitive function
assessment (HYVET-COG): a double-blind, placebo controlled trial". Lancet Neurol 7
(8): 683–9. doi:10.1016/S1474-4422(08)70143-1. PMID 18614402.
 30. ^ Drivers with dementia a growing problem, MDs warn, CBC News, Canada, September
19, 2007

[edi t] Ext erna l li nks

• Alzheimer's Disease Research

• Alzheimer's Research Trust - What is dementia? - Information produced by the
Alzheimer's Research Trust including statistics.
• Alzheimer's Society - About dementia - Information produced by the Alzheimer's Society
including factsheets and support.
• An Documentary About Dementia Produced by Knowledge Network
• [1] Bradford Dementia Group - provide education, training and research on dementia care
• Dementia Research News from ScienceDaily
• The Dementia Services Development Centre, University of Stirling
• Dementia tutorial for U.K. practitioners by the Alzheimer's Society
• Getting Started in Telecare for Patients with DementiaPDF (897 KiB)
• Understanding Dementia: a primer of diagnosis and management
• AlzOnline - AlzOnline provides education, information, and support to persons caring for
someone with Alzheimer's disease or a related memory problem.
• CSIP National Older Persons Mental Health Programme Includes an involvement toolkit
with tips on how people with dementia can get involved in the planning, development and
evaluation of services
• Dementia Advocacy and Support Network
• Dementia Care Mapping Bradford Dementia Group
• Dementia at GPnotebook
• Dementia at eMedicineHealth
• MedlinePlus Overview Dementia
• Merck Geriatrics 5-40a

神经 系统软体 征(soft neurological signs) 解释 :一组定义模糊的躯体所见，并可假设其反映了中枢神经系统的不成熟或亚临床

损伤。通常包括视觉精确度不良、说话不顺畅、明显的笨拙、舞蹈形式的运动或镜像运动、肌腱反射亢进及左右混淆。与神经系统硬

体征相对而言，软体征没有明确的临床意义或定位价值。见：注意缺陷障碍。

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Deliriu m
Classification and
 external resources

ICD-10 F05.

ICD-9 293.0

DiseasesDB 29284

eMedicine med/3006

MeSH D003693

This article is about the mental state and medical condition. For
other uses, see Delirium (disambiguation).

Delirium is an acute and relatively sudden (developing over hours

to days) decline in attention-focus, perception, and cognition. In
medical usage it is not synonymous with drowsiness, and may occur
without it. Delirium is not the same as dementia (the two entities
have different diagnostic criteria), though it commonly occurs in
demented patients.

Delirium may be of a hyperactive variety manifested by 'positive'

symptoms of agitation or combativeness, or it may be of a hypoactive
variety (often referred to as 'quiet' delirium) manifested by
'negative' symptoms such as inability to converse or focus attention
or follow commands. While the common non-medical view of a delirious
patient is one who is hallucinating, most people who are medically
delirious do not have either hallucinations or delusions. Delirium is
commonly associated with a disturbance of consciousness (e.g.,
reduced clarity of awareness of the environment). The change in
cognition (memory deficit, disorientation, language disturbance) or
the development of a perceptual disturbance, must be one that is not
better accounted for by a pre-existing, established, or evolving
dementia. Usually the rapidly fluctuating time course of delirium is
used to help in the latter distinction.[1]

Delirium itself is not a disease, but rather a clinical syndrome (a

set of symptoms), which result from an underlying disease or new
problem with mentation. Like its components (inability to focus
attention, confusion and various impairments in awareness and
temporal and spatial orientation), delirium is simply the common
symptomatic manifestation of early brain or mental dysfunction (for
any reason).

Without careful assessment, delirium can easily be confused with a

number of psychiatric disorders because many of the signs and
symptoms are conditions present in dementia, depression, and
psychosis.[2] Delirium is probably the single most common acute
disorder affecting adults in general hospitals. It affects 10-20% of
all hospitalized adults, and 30-40% of elderly hospitalized patients
and up to 80% of ICU patients.[3]

Treatment of delirium requires treatment of the underlying causes. In

some cases, temporary or palliative or symptomatic treatments are
used to comfort patients or to allow better patient management (for
example, a patient who, without understanding, is trying to pull out
a ventilation tube that is required for survival).

Educational information is available for medical and non-medical

persons with videos, management protocols, links to references,
lectures, recent evidence from studies, implementation packets for
hospitals, and even comments to families and loved ones for those
witnessing someone going through a delirious episode. [4] See the
Resources section

Contents

[hide]

• 1 Common versus medical usage

• 2 Diagnosis

• 3 Occurrence in hospitals

• 4 Commonly co-occurring mental symptoms, with a note on

severity
 o 4.1 Inability to focus attention, confusion and
disorientation
o 4.2 Memory formation disturbance

o 4.3 Abnormalities of awareness and affect

• 5 Duration

• 6 Causes

o 6.1 Critical illness

o 6.2 Substance withdrawal

o 6.3 Gross structural brain disorders

o 6.4 Neurological disorders

o 6.5 Circulatory

o 6.6 Lack of essential metabolic fuels, nutrients, etc.

o 6.7 Toxication

o 6.8 Mental illness per se is not a cause, as a matter of

definition
• 7 Treatment

• 8 Accounts of delirium

• 9 Resources

• 10 See also

• 11 References

• 12 Further reading

Common versus medical usage

In common usage, delirium is often used to refer to drowsiness,
disorientation, and hallucination. In broader medical terminology,
however, a number of other symptoms, including a sudden inability to
focus attention, and even (occasionally) sleeplessness and severe
agitation and irritability, also define "delirium," and
hallucination, drowsiness, and disorientation are not required.

There are several medical definitions of delirium (including those in

the DSM-IV and ICD-10). However, all include some core features.

The core features are:

• Disturbance of consciousness (that is, reduced clarity of

awareness of the environment, with reduced ability to focus,
sustain, or shift attention)
• Change in cognition (e.g., problem-solving impairment or memory
impairment) or a perceptual disturbance
• Onset of hours to days, and tendency to fluctuate.

Common features also tend to include:

• Intrusive abnormalities of awareness and affect, such as

hallucinations or inappropriate emotional states.

[edit ] Diagnosis

Differential points from other processes and syndromes that cause

cognitive dysfunction:

• Delirium may be distinguished from psychosis, in which

consciousness and cognition may not be impaired (however, there
may be overlap, as some acute psychosis, especially with mania,
is capable of producing delirium-like states).
 • Delirium is distinguished from dementia (chronic organic brain
syndrome) which describes an "acquired" (non-congenital) and
usually irreversible cognitive and psychosocial decline in
function. Dementia usually results from an identifiable
degenerative brain disease (for example Alzheimer disease or
Huntington's disease). Dementia is usually not associated with
a change in level of consciousness, and a diagnosis of dementia
requires a chronic impairment.
• Delirium is distinguished from depression.

• Delirium is distinguished by time-course from the confusion and

lack of attention which result from long term learning
disorders and varieties of congenital brain dysfunction.
Delirium has also been referred to as 'acute confusional state'
or 'acute brain syndrome'. The key word in both of these
descriptions is "acute" (meaning: of recent onset), since
delirium may share many of the clinical (i.e., symptomatic)
features of dementia, developmental disability, or attention-
deficit hyperactivity disorder, with the important exception of
symptom duration.
• Delirium is not the same as confusion, although the two
syndromes may overlap and be present at the same time. However,
a confused patient may not be delirious (an example would be a
stable, demented person who is disoriented to time and place),
and a delirious person may not be confused (for example. a
person in severe pain may not be able to focus attention, but
may be completely oriented and not at all confused).

It is a corollary of the above differential criteria that a diagnosis

of delirium cannot be made without a previous assessment or knowledge
of the affected person's baseline level of cognitive function.

Several valid and reliable rating scales now exist which can be used
to accurately diagnose delirium.[5][6] www.icudelirium.org

[edit ] Occurrence in hospitals

The highest prevalence of delirium (often 50% to 75% of patients) is
generally seen in critically ill patients in the intensive care unit
or ICU (which used to be referred to by the misnomer ICU Psychosis, a
term largely abandoned now for the more widely accepted and
scientifically supported term delirium). Since the advent of
validated and easy to implement delirium instruments for ICU patients
such as the Confusion Assessment Method for the ICU (CAM-ICU)[7] and
the Intensive Care Delirium Screening Checkllist (IC-DSC)[8]. Of the
hundreds of thousands of ICU patients develop delirium in ICUs every
year, it has been recognized that most of them being of the
hypoactive variety that is easily missed and invisible to the
managing teams unless actively monitored using such instruments. The
causes of delirium in such patients depend on the underlying
illnesses, new problems like sepsis and low oxygen levels, and the
sedative and pain medicines that are nearly universally given to all
ICU patients. Outside the ICU, on hospital wards and in nursing
homes, the problem of delirium is also a very important medical
problem, especially for older patients. The most recent area of the
hospital in which delirium is just beginning to be monitored
routinely in many centers is the Emergency Department. Also, one on
four geriatric patients suffer from an episode of delirium at least
once during their stay in the hospital.

[edit ] Commonly co-occurring mental

symptoms, with a note on severity

Since delirium may occur in very many grades of severity, all

symptoms may occur with varying degrees of intensity. A mild
disability to focus attention may result in only a disability in
solving the most complex problems. As an extreme example, a
mathematician with the flu may be unable to perform creative work,
but otherwise may have no difficulty with basic activities of daily
living. However, as delirium becomes more severe, it disrupts other
mental functions, and may be so severe that it borders on
unconsciousness or a vegetative state. In the latter state, a person
may be awake and immediately aware and responsive to many stimuli,
and capable of coordinated movements, but unable to perform any
meaningful mental processing task at all.
[edi t] Ina bili ty t o fo cus a tte ntio n, c onfu sion and

dis orie ntat ion

The delirium-sufferer loses the capacity for clear and coherent

thought. This may be apparent in disorganised or incoherent speech,
the inability to concentrate (focus attention), or in a lack of any
goal-directed thinking.

Disorientation (another symptom of confusion, and usually a more

severe one) describes the loss of awareness of the surroundings,
environment and context in which the person exists. It may also
appear with delirium, but it is not required, as noted.
Disorientation may occur in time (not knowing what time of day, day
of week, month, season or year it is), place (not knowing where one
is) or person (not knowing who one is).

Cognitive function may be impaired enough to make medical criteria

for delirium, even if orientation is preserved. Thus, a patient who
is fully aware of where they are and who they are, but cannot think
because they cannot concentrate, may be medically delirious. The
state of delirium most familiar to the average person is that which
occurs from extremes in pain, lack of sleep, or emotional shock.

Because most high level mental skills are required for problem
solving, including ability to focus attention, this ability also
suffers in delirium. However, this is a secondary phenomenon, since
problem-solving involves many sub-skills and basic mental abilities,
any of which may be impaired in a delirious patient.

[edi t] Mem ory f orm atio n di stur banc e

Impairments to cognition may include temporary reduction in the

ability to form short-term or long-term memory. Difficult short-term
memory tasks like ability to repeat a phone number may be
continuously disrupted during a delirium, but easier short-term
memory tasks like repeating single words, or remembering simple
questions long enough to give an answer, may not be impaired.
Reduction in formation of new long-term memory (which by definition
survive withdrawal of attention), is common in delirium, because
initial formation of (new) long-term memories generally requires an
even higher degree of attention, than do short-term memory tasks.
Since older memories are retained without need of concentration,
previously formed long-term memories (i.e., those formed before the
period of delirium) are usually preserved in all but the most severe
cases of delirium (and when destroyed, are destroyed by the
underlying brain pathology, not the delirious state per se).

[edi t] Abn orma liti es o f aw aren ess a nd a ffe ct

Hallucinations (perceived sensory experience with the lack of an

external source) or distortions of reality may occur in delirium, but
they are not essential for the diagnosis. Commonly these are visual
distortions, and can take the form of masses of small crawling
creatures (particularly common in delirium tremens, caused by severe
alcohol withdrawal) or distortions in size or intensity of the
surrounding environment.

Strange beliefs may also be held during a delirious state, but these
are not considered fixed delusions in the clinical sense as they are
considered too short-lived (i.e., they are temporary delusions - such
as thinking that a nurse is a person from his/her past trying to
cause injury). Interestingly, in some cases sufferers may be left
with false or delusional memories after delirium, basing their
memories on the confused thinking or sensory distortion which
occurred during the episode of delirium. Other instances would be
inability to distinguish reality from dreams.

Abnormalities of affect which may attend the state of delirium may

include many distortions to perceived or communicated emotional
states. Emotional states may also fluctuate, so that a delirious
person may rapidly change between, for example, terror, sadness and
jocularity.

[edit ] Duration

The duration of delirium is typically affected by the underlying

cause. If caused by a fever, the delirious state often subsides as
the severity of the fever subsides. However, it has long been
suspected that in some cases delirium persists for months and that it
may even be associated with permanent decrements in cognitive
function. Barrough said in 1583 that if delirium resolves, it may be
followed by a "loss of memory and reasoning power." Recent studies
bear this out, with cognitively normal patients who suffer an episode
of delirium carrying an increased risk of dementia in the years that
follow. In many such cases, however, delirium undoubtedly does not
have a causal nature, but merely functions as a temporary unmasking
with stress, of a previously unsuspected (but well-compensated) state
of minimal brain dysfunction (early dementia).

[edit ] Causes

Delirium, like mental confusion, is a very general and nonspecific

symptom of organ dysfunction, where the organ in question is the
brain. In addition to many organic causes relating to a structural
defect or a metabolic problem in the brain (analogous to hardware
problems in a computer), there are also some psychiatric causes,
which may also include a component of mental or emotional stress,
mental disease, or other "programming" problems (analogous to
software problems in a computer).

Delirium may be caused by severe physical illness, or any process

which interferes with the normal metabolism or function of the
brain.[9] For example, fever, pain, poisons (including toxic drug
reactions), brain injury, surgery, traumatic shock, severe lack of
food or water or sleep, and even withdrawal symptoms of certain drug
and alcohol dependent states, are all known to cause delirium.

In addition, there is an interaction between acute and chronic

symptoms of brain dysfunction; delirious states are more easily
produced in people already suffering with underlying chronic brain
dysfunction.[10]

A very common cause of delirium in elderly people is a urinary tract

infection, which is easily treatable with antibiotics, reversing the
delirium.

Too many to list by specific pathology, major categories of the cause

of delirium include:

[edi t] C riti cal i lln ess

The most common behavioral manifestation of acute brain dysfunction
is delirium, which occurs in up to 60% to 80% of mechanically
ventilated medical and surgical ICU patients and 50% to 70% of non-
ventilated medical ICU patients.[11] During the ICU stay, acute
delirium is associated with complications of mechanical ventilation
including nosocomial pneumonia, self-extubation, and reintubation.[3]
ICU delirium predicts a 3- to 11-fold increased risk of death at 6
months even after controlling for relevant covariates such as
severity of illness.[3] Of late, delirium has been recognized by some
as a sixth vital sign, and it is recommended that delirium assessment
be a part of routine ICU management.[12] The elderly may be at
particular risk for this spectrum of delirium and dementia.[12] A firm
understanding of the pathophysiologic mechanisms of delirium remains
elusive despite improved diagnosis and potential treatments.
www.icudelirium.org

[edi t] S ubst ance wit hdra wal

Drug withdrawal is a common cause of delirium. The most notable are

alcohol withdrawal and benzodiazepine withdrawal but other drug
withdrawals both from licit and illicit drugs can sometimes cause
delirium.

[edi t] G ross str uctu ral b rai n di sord ers

• Head trauma (i.e., concussion, traumatic bleeding, penetrating

injury, etc.)
• Gross structural damage from brain disease (stroke, spontaneous
bleeding, tumor, etc.)

[edi t] N euro logi cal d iso rder s

• Various neurological disorders

• Lack of sleep

[edi t] C ircu lato ry

 • Intracranial Hypertension

[edi t] L ack o f e ssen tial met abol ic f uels , nu trie nts,

etc .

• Hypoxia,

• Hypoglycemia

• Electrolyte imbalance (dehydration, water intoxication)

[edi t] T oxic atio n

• Intoxication various drugs, alcohol, anesthetics

• Sudden withdrawal of chronic drug use ("de-tox") in a person

with certain types of drug addiction (e.g. alcohol, see
delirium tremens, and many other sedating drugs)
• Poisons (including carbon monoxide and metabolic blockade)

• Medications including psychotropic medications

[edi t] M enta l il lnes s pe r se is n ot a ca use, as a

mat ter o f d efin itio n

Some mental illnesses, such as mania, or some types of acute

psychosis, may cause a rapidly fluctuating impairment of cognitive
function and ability to focus. However, they are not technically
causes of delirium, since any fluctuating cognitive symptoms that
occur as a result of these mental disorders are considered by
definition to be due to the mental disorder itself, and to be a part
of it. Thus, physical disorders can be said to produce delirium as a
mental side-effect or symptom; however primary mental disorders which
produce the symptom cannot be put into this category, once
identified. However, such symptoms may be impossible to distinguish
clinically from delirium resulting from physical disorders, if a
diagnosis of an underlying mental disorder has yet to be made.

[edit ] Treatment

Delirium is not a disease, but a syndrome (i.e. collection of

symptoms) indicating dysfunction of the brain, in the same way
shortness of breath describes dysfunction of the respiratory system,
but does not identify the disorder. Treatment of delirium is achieved
by treating the underlying dysfunction cause, or in many cases, the
causes (plural), as delirium is often multi-factorial.

Palliative or symptomatic treatment of delirium is sometimes

necessary to make a patient comfortable. Distressing symptoms of
delirium are sometimes treated with antipsychotics, preferably those
with minimal anticholinergic activity, such as haloperidol or
risperidone, or else with benzodiazepines, which decrease the anxiety
felt by a person who may also be disoriented, and has difficulty
completing tasks. Conversely, recent research however suggests that
delirium may in fact be exacerbated by benzodiazepines.[13] Bearing
this in mind, any drug does not address the underlying cause of
delirium, and may mask changes in delirium which themselves may be
helpful in assessing the patient's underlying changes in health,
their use is difficult. Other evidence also suggests that non-
pharmacological measures may also be effective in decreasing the
incidence of delirium.[14] Because delirium is a mere symptom of
another problem which may be very subtle, the wisdom of treatment of
the delirious patient with drugs must overcome natural skepticism,
and requires a high degree of skill.

Benzodiazepines are usually used in the treatment of delirium

associated with alcohol withdrawal.

There have been reports that cholinesterase inhibitors might be

effective in treating delirium, but there is little evidence for
this.[15]