Chapter 3.

organic--symptomatic ,mental disorder

delirium lapse into

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

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-IIIR, 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.


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 shortterm 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]


1 Diagnosis
o o o o o o

1.1 Mini-mental state examination 1.2 Modified Mini-Mental State examination (3MS) 1.3 Abbreviated mental test score 1.4 Other examinations 1.5 Laboratory tests 1.6 Imaging

2 Types
o o

2.1 Cortical dementias 2.2 Subcortical dementias

3 Treatment

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 o

8.1 Notes 8.2 External links

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, thyroidstimulating 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. 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. 6. ^ "Appendix: The Modified Mini-Mental State (3MS)". 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. 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.

15. 16.



19. 20. 21.

22. 23. 24.





29. Retrieved on 200701-16. ^ Aldridge, David, Music Therapy in Dementia Care, London : Jessica Kingsley Publishers, November 2000. ISBN 1853027766 ^ 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 ^ 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 ^ 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. ^ Remington, Ruth, "Calming Music and Hand Massage With Agitated Elderly", Nursing Research 51(5): 317-323, September/October 2002. ^ Lleo A, Greenberg SM, Growdon JH. Current pharmacotherapy for Alzheimer's disease. Annu Rev Med. 2006;57:513-33. Review. PMID 16409164 ^ 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 ^ "FDA MedWatch - 2008 Safety Alerts for Human Medical Products". FDA. ^ "FDA MedWatch - 2008 Safety Alerts for Human Medical Products". FDA. ^ 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. ^ 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. ^ 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. ^ 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. ^ 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. ^ 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 ICD-9

F05. 293.0

DiseasesDB 29284 eMedicine MeSH med/3006 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

• • • •

1 Common versus medical usage 2 Diagnosis 3 Occurrence in hospitals 4 Commonly co-occurring mental symptoms, with a note on severity


4.1 Inability to focus attention, confusion and disorientation

o o • •

4.2 Memory formation disturbance 4.3 Abnormalities of awareness and affect

5 Duration 6 Causes
o o o o o o o o

6.1 Critical illness 6.2 Substance withdrawal 6.3 Gross structural brain disorders 6.4 Neurological disorders 6.5 Circulatory 6.6 Lack of essential metabolic fuels, nutrients, etc. 6.7 Toxication 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 attentiondeficit 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]

[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 nonventilated 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.

[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
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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 .
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Hypoxia, Hypoglycemia Electrolyte imbalance (dehydration, water intoxication)

[edi t] T oxic atio n
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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)

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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 nonpharmacological 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]

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