Agecace 2] atwoduneloy mints Mosk Meordrognitivts disdrded develop mich later in IY, whereas (9 ard SLD_ove_betiored +o be. Prtdent fim birth - > Mithough hearty having) Ortans Carpet, awrokgnbive ditorded arti incoded im DAN becauty it offtm indder prfornd Danses 19. portent behavior 9 peesoralitys . Aa maT, hove or day ang itnategel @) Pein ~ choractengyed by impaired consuousness and cognitvon during the v2vers of See ON hoor Or dongs, = Hey appear Wopuced, disowentd, ord out of touch a there wna = cansst Poy oral exitein Hic attention wea ea Fhe simplest tashs impairment in__memory 4 laoquage, ~ PeADIent Ory older odulls, people undergoing medical proudiets 4 Canc patients, od peop | gans- = it gobside_ relatively quiddy » = DSN= S seeoymi ya sereral subtypes depending on ie comes TABLE 15.1 Di A iagnostic Criteria for Delirium A disturbance inattention (ie, reduced ability to direct, focus, sustain, and shift attention) andawareness (reduced orientation to the environment). The disturbance develops over a short period of time (usually hoursito.a few days), represents a change from baseline attention and awareness, nd tends to fluctuate: severity during the course of a day. An additional disturbance in cognition (eg. memory deficit disorientation, language, visuospatial ability, or perception), The disturbances in Criteria A and C are not better explained disorder and do not occur in the context of a severely reduced level of arousal, such as coma There is evidence from the history, physical examination, or laboratory findings that the disturbance isa'direct physiological ‘consequence of another medical condition, substance intoxica: tion oF withdrawal (ie. due to a drug of abuse or to a medica tion), oF exposure to a toxin, or is due to multiple etiologies. Leo. substance -imtvced ddinion 7 OEE od ols Ore meets suscep- Kible: 40 devetoping dlirem os A result of mild infechtn or edicorion chonar cal hep daprivection, immobilite), and cxersive great can ako COdkl dadiicivm - = Antoxicetion by derma foWsons withdrawal s, infech'On, head inyory cor als? cnages &-yreamenr First whey + address the sederaying Caused, [Pt He tense, feuntnaan by withdraval ~ halopesdot of otter ankipryd0he medi Cedvong infections, brain jiquy, ta — NECeSKOY G APRFOPHOLe intervention ~ Petommunded fist Hine of treatekat ! psychosocial intervention. G geal. recassore te individvorl 19 help him or hor deal vel the asytehon, anichy, ard boll udretens SF delim - @ Mase 4 WILO NeUROCOGAITIVE Disoepers r previous, dementia TABLE 15.2 Diagnostic Criteria for Major Neurocognitive Disorder A. tderce of srvbeancognve deine om aprevous eve! of performance in ane oF more cognitive domains (complex _attention, executive function. learning and memory, language. documented by standardized newopsychologcal test {ng oxi its absence, another quantified clinical assessment. 8. The ctv (1. ata minimum requiTngasstance with complex instrumental activites of daily Ining such as paying bls or managing medications). The copnte des do nor occur excisey in the context of | adeirium: ° The cognitive deft are not better explained by another ‘mental sore (eg, major depressive disorder, schizophrenia). ther due to ey TABLE 15.3 Diagnostic Criteria for Mild Neurocognitive Disorder |A. Evidence of modes cognitive decline from a previous level of performance in one or more cognitive domains (complex attention executive function leaming and memory language. 1m xs absence, another quantified cnc assessment The cognitive deficits do not nurse wth capaciy for (2, complex instrumental activites of daly ving such as paying bls or managing medica tons are preserved. but greater effort, compensatory satepes accommodation may be requ). iH mental disorder (eg. major depressve disorder schaophvensa) ‘Specify whether de co Atzhewmer’s disease Fromotemporal lobar degeneration Lewy body disease Vascular dea TRaumatic rain ny ‘Substance/medcauon use “HAV infection ‘Pron disease - Paknsons ease ‘Huntingtons disease Anciber medical condition ‘Muivpie evoioges “Unspecthed GQ aay ute A cynite dedtice,; modest impairments in @gnitive abilisealong i0yt, Ord otter oddnnced cPg nite bot con conimes +9 functvon ede - Processed... Peadentty — Cowes of nero mgnitve diserden indude sertral medical cnditions and tHe obs of Andy oF aliohol - = be tte oihiol uteayd ,memany impairment j¢ 4220 ta on inability te cepue— Ac Onegin events Coan cemterber the post but net what happend po hours ag). T VuMOSPahal shils ore impaired Ly cyaccin = THE irobillhy to eagninn and came object FOU O500Si0 — inarbrakty te rv gniae OVEN fomiliar faud- s_impajymtat in memory, ploonins Ord obstenee kasonings = emma n s\da_eppects delusions, dep 12asion., agitation, ognresston, ard apathy - = Cagritiyy foreHoning Conbayes 49 detenoby until He pedon larires, almost etal Support 42 comy oot day-+to-dowy aehvities T Mayor AUD cha develop at almcss any Gap, although 1M mde bequet in_oldee_adoter > CAPSSES OF NOD BASED on ENOLOEY + © P maslerd Plaga, As DME MAKERS DISEACE = indyde mol gle Logritiie dealt that develop gridrally ¢ shendihy = predamicant - impoirmtat in memowy , ovientonon, wudiytmtat , § reasoning — Hed te fork important events and (0 objets - Hoy He Border proytsses , fay bUOMU onrinkd , vontsed, dishtsed , aspiD% OF extn combortivts« = Meng of Ate diffierthes keane moe proaoonted Inia in He day — sindowinee Syadeame + Olko display one OF mire Sf Heal? aphosia ( diftiolty vw] longs , ciproxianUnpocctd _aotor gonchioning) , ayacsin , of diftioatty #] planning, orgyniging, dequending or abs rok infyrmahon | eee | ee Gor) 4 the Cotes of AUD arte ford 49 be tte ceastt OF atyheimer disears = Cora in wortn. TABLE 15.4 Diagnostic Criteria for Major or Mild Neurocognitive Disorder due to Alzheimer’s Disease 'A. The cteia are met for majo or mild neurocognitive disorder. 8 domains must be impaired) C._ Cteria are met for ether probable or possible Alzheimer’s disease as follows. For major nerocogntve disorder: Probable Auhimers dieses dagrose eer ofthe following & presen cherws posible Auneime’s eas shoud be dagosed 1. dence ofa causave Althemers dsease genetic mutation from fay AStory oF genet esting 2, Allee ofthe folowing ate present (for major newocogritive disorder ew _e Noewidence of mixed evology (e.absence of other neuodegenerative or cerebrovascular sense. oF another neurological mental ot systemic disease or condition key contrbuting to cognne decline) For mid newocogivedaorder: Probable Alsheimer’s diseases diagnosed f there evidence ofa causative Alheimer’ disease genetic mutation fom either genes testing ot far history. ‘Possbe Alhemers dseate = agnoued theres no ewdence ofa causative Alters disease genetic mutation from echer genet esting oF fai history and are f the folowing ae presen 1. lear evdence of decine im memory and tearing 2. Steady progresove gradual deci n cogition without extended plateaus 3. NO eerie of ied EHGIRY (ie absence of her neurodegenerative or cerebrovascular disease, or another neurological or sjtemic seas oF condivion lily contrbuting to cognitive dene) t 1. The disturbances not beter explained by cerebrovascular seas, another newodepeneratve disease the elects ofa substance or another mena neurological or systemic sore 2 MADR OR WILD VACOULAL 00. Diagnostic Criteria for Major or Mild Vascular Neurocognitive Disorder A. The eteria ae met for major or mild neurocognitive disorder 8. The inca features ae consent witha vascular eology 2 suggested by ether of the folowing: 1. Onset ofthe cognitive deft temporal rated tone or mere cerebrovacul ever. 2. xidence for decine ts prominent in complex attention including processing speed) and froncal-executive function There evidence ofthe presence of cerebrovascular dete from sory, phycl examination and/or neuromaging considered sufcent ‘o acount forthe neurocognitive defi. . Thesymptoms are not beter explained by another bran disease or systemic disor Probable vascular neurocognitive sores iagnosed ‘fone ofthe followings present. otherwise, possible vascular neurocognitive disorder should be diagnosed 1. Clinical eer are supported by newreimaging evidence of sigrifcane parenchymal injury atwibuted to cerebrovacubr eae (ceuroimaging supported) 2. The newrocognene syndrome temporay related to one of more documented cerebrovascular evens 3. Both cnc and genetic (¢3.cerebral autosomal dominant artenopathy wth subcortical farts and leukoencephalopathy) endence of cerebrovascular seas present. Posse vacuar neurocogrtve disorders cagnosed the cnical criteria are met but neuroimaging not avaiable andthe temporal relationship of ‘the neurocognitive smcrome with one or more cerebrovacua events nok established. DSM - 5 isk criti for vageulor NU) cognikve disturbances: deeiincs io epeed of Mformahen Prceasing tonal excteubrue actioned) Ces woking comp tex deriaioes).T the dak for mer 1S slightly higher than amore woren: THe oreek OF Aoscvlar dementin is typically voc sodden thon Hey onsek for He Aigheimert type. (ceete onset) 3-_TRONMTEMPORAL NEULoLOGMITNE. Disorder = On overerthi ney $eem Obed 10 Colegdrints o> Vovicly oF brein ditordes Hat da- mony the frontal @r tempol reno Sf Abu rein — Ovens thet speck _perto- = 2 Nosiontt + throw dedtine in behosioe Leyy Seuoily ineppropiaby oekont. Dpathy, making peor qudry mak) or largooqe Ley problems wf pees finding HH ght word, ameng, obyeak * Pick’ Disease - @ care nevlogical Ordition thot prodows sjppiomy simiior 40_ Hat of Ayheined_dsroser ~ wtvahy stuart relttively coy in lifes (W0s oF S06) — am examele Hh Corly onsek ntwroemyntins disorder - TABLE 15.6 Diagnostic Criteria for Major or Mild Frontotemporal Neurocognitive Disorder ‘A. The tera ae met for major or mild neurocognitive disorder, 8B. The dsturbance has insidhous ont and radl progression. 2. Language vara «2. Prominent decline in language ability in the form of speech production, word finding, object naming, grammar. or word comprehension o. The daurbance no beer explained by cerebrovascular dense, another nevrodegeneative deat, the elects ofa substance of another mental SuBStANCE | sca CAMen-lNDNLED__ UD, ~ Pidlerged ver can domoye He brain g lead 49 nevrerrynite disorder = He impairment Louis bey Orel the zeriod VWOved in istoricerion OF withdetadol for Ha aobstanus- = Blehol, inhoranls , od sHdotne, hyertht, + omilyt dens = teddies renory imped nent ond aHtaat ones 94 He fF togaitive disturbonus * aphouia, rosin, aprenion aro disborbons iq entedkirgs funthion ings athe = NOC mOL presires hydro eprotut hypo ty cordinsnn = bein Mmer = vitowin Bir degui repented plod in A sera = dhario heunetc: crm phetegatty | dementrer papitierien CAused > Binley con ~ previoily adated disecats > Psy chelecgieal 5 seried lativen ces, Diagnostic Criteria for Substance/ Medication-Induced Major or Mild Neurocognitive Disorder ‘A. The criteria are met for major or mild neurocognitive disorder. B. The neurocognitive impairments do not occur exclusively during the course of a delirium and persist beyond the usual duration of intoxication and acute withdrawal. (C._The involved substance or medication and duration and extent ‘of use are capable of producing the neurocognitive impairment. . The temporal course ofthe neurocognitive deficits consistent with the timing of substance or medication use and abstinence | (eg. the deficits remain stable or improve aftr a period of E._ The neurocognitive disorder is not atibutable to another ‘medical condition and is not better explained by another imental disorder. = Mithough 9 would daim that pSyhoconal lativencts dintaty enste the hype: of brain dehenoratson gin in praple. vil Red, they meg lhelp detormints —enecrnoud covae+ determine onset and course, For example, a person’ lifestyle ‘may involve contact with factors that can cause neurocognitive disorder. You saw, for instance, that substance to ne Chapter 11), whether a person abuses drugs is determined by a combination of biological and psychosocial factors. In the case of vascular neurocognitive disorder, a persons biological vulnerabil ity to vascular disease will influence the chances of strokes that can lead to this form of disorder. Lifestyle issues such as diet, exer- can lead ocognitive disorder and, as we di ssed previously (see + Wilivral factor’ ety alse ote thu press G ce: Pron con be persed on Thevgh oa ital form of comm’ — cise, and stress influence cardiovascular disease and therefore help ne who experiences vascular neurocognitive disorder (see Chapter 9), boliem practice in Papua Ned Guinea os a pact of crooning» + Dleepotiontl corfety Cheek iqyerrg) ord cononie conditions jnpiven tng dick allo Offuk fre prevuteney of ceriuin formy of HOD + Peydrosodal faders tele irfivente who dees dud wshe does not develop coquin Pan ef RED. ( get~ uwidnrent inferortion, diatheis shes) TREATME ah TW] Optentive bemin dowsye) 92 knodn trembront Cam _rbatorts tose abilities, Tatas of trentment : 1) trying > prolent etetoin Condition thot ney bring on ACD Coy. SAF tote) 2) Aiyigg to datoy the ongat ef dymptows 40 provide batter quality of ify 2) attempting to help tiene i cing deterioration tvid9ALS 9 their conegues cope a] the odvan— = Biological trenkments ave aimed of stepping the. terth «til deterioretien, + Prythosociol trebtmenlt ower timed ot helping patient 5 congives copt- | een Seles ste ortck of the eyngites