Beruflich Dokumente
Kultur Dokumente
Abstract This consensus prepared by the Scientific Department of Cognitive Neurology and Aging of the
Brazilian Academy of Neurology is aimed at recommending new criteria for the diagnosis of dementia and
Alzheimers disease (AD) in Brazil. A revision was performed of the proposals of clinical and of research criteria
suggested by other institutions and international consensuses. The new proposal for the diagnosis of dementia
does not necessarily require memory impairment if the cognitive or behavioral compromise affects at least two of
the following domains: memory, executive function, speech, visual-spatial ability and change in personality. For
the purpose of diagnosis, AD is divided into three phases: dementia, mild cognitive impairment and pre-clinical
phase, where the latter only applies to clinical research. In the dementia picture, other initial forms were accepted
which do not involve amnesia and require a neuroimaging examination. Cerebrospinal fluid biomarkers are
recommended for study, but can be utilized as optional instruments, when deemed appropriate by the clinician.
Key words: dementia, Alzheimers disease, mild cognitive impairment, diagnosis, consensus guidelines, Brazil.
1
Medicine Course, University of Fortaleza (Unifor). Neurology Service of Fortaleza General Hospital (HGF), Fortaleza CE, Brazil; 2Cognitive Neurology
and Behavior Group, Hospital das Clnicas, School of Medicine, University of So Paulo (FMUSP). Referral Center for Cognitive Disorders (CEREDIC)
of the FMUSP, So Paulo SP, Brazil; 3Department of Neurology, State University of Campinas (FCM-UNICAMP), Campinas PS, Brazil; 4Neurosciences
Laboratory-LIM 27, Department and Institute of Psychiatry, School of Medicine, FMUSP; 5Neurologist, Hospital de Base, Federal District, Braslia DF,
Brazil; 6UNINEURO, Recife PE, Brazil; 7Department of Internal Medicine, School of Medicine of Catanduva, Catanduva SP, Brazil; 8Geriatrics Service,
Hospital das Clnicas, FMUSP and Referral Center for Cognitive Disorders, Hospital das Clnicas, FMUSP, So Paulo SP, Brazil.
Norberto Anzio Ferreira Frota Rua Repblica do Lbano, 992 / Apto 801 - 60160-140 Fortaleza CE - Brazil.
Disclosure: The authors report no conflicts of interest.
Received March 17, 2010. Accepted in final form June 17, 2011.
2. Cognitive compromise is detected and diagnosed ba- 3B. Non-amnesic presentation (should have another affec-
sed on a combination of: ted domain):
2A. Anamnesis with patient and close family members/ Speech (remembering words).
friends who have knowledge of the patients history; and Visual-spatial (spatial cognition, agnosia of objects or
2B. Objective cognitive evaluation through a brief cognitive faces, simultaneous agnosia and alexia).
examination of mental state or a neuropsychological Executive functions (alteration in reasoning, judgment
assessment. Neuropsychological assessment should be and resolution of problems).
done when anamnesis and the brief cognitive examina- 4. Tomography or preferentially, magnetic resonance, of
tion carried out by a clinician are insufficient to reach the head should be done to exclude other diagnostic
a reliable diagnosis. possibilities or comorbidities, particularly cerebral vas-
3. Cognitive or behavioral compromise affects at least cular disease.
two of the following domains: 5. The diagnosis of dementia of probable AD should not
3A. Memory, characterized by compromise of the capacity be applied when there is:
to acquire or recall recent information, with symptoms 5A. Evidence of significant cerebrovascular disease de-
that include: repetition of the same questions or sub- fined by history of cerebral vascular accident (CVA)
jects, forgetting of events, agreements or place where temporally related to the onset or worsening of cogni-
belongings are kept. tive compromise, or presence of multiple or extensive
3B. Executive functions, characterized by compromise infarcts, or marked lesions in white matter evidenced
in reasoning, carrying out complex tasks and judg- by neuroimaging examinations; or
ment, with symptoms such as: poor comprehension of 5B. Central characteristics of dementia with Lewy bodies
risk situations and reduced ability to take care of fi- (visual hallucinations, parkinsonism and cognitive fluc-
nances, make decisions and plan complex or sequential tuation); or
activities. 5C. Prominent characteristics of the behavioral variant of
3C. Visual-spatial abilities, with symptoms that include: frontotemporal dementia (hyperorality, hypersexuality,
inability to recognize faces or common objects and find perseverance); or
objects in the visual field, difficulty handling utensils 5D. Prominent characteristics of primary progressive apha-
and dressing oneself for reasons other than visual or sia manifesting as the semantic variant (also called se-
motor deficiency. mantic dementia, with fluent discourse, anomia and
3D. Speech (expression, comprehension, reading and wri- difficulties with semantic memory) or as the non-fluent
ting), with symptoms that include: difficulty in finding variant, with substantial agrammatism; or
and/or understanding words, errors in speaking and 5E. Evidence of another concomitant and active disease,
writing, and exchange of words or phonemes, not ex- neurological or non-neurological, or of the use of me-
plicable by a sensory or motor deficit. dication that can have a substantial effect on cognition.
3E. Personality or behavior, with symptoms that include The following items, when present, increase the degree
changes in mood (instability, uncharacteristic fluctua- of reliability of the clinical diagnosis of dementia of pro-
tions), agitation, apathy, disinterest, social isolation, loss bable AD:
of empathy, disinhibition, and obsessive, compulsive or a) Evidence of progressive cognitive decline, found on
socially unacceptable behavior. successive assessments.
b) Proof of the presence of causative genetic mutation
II. DEMENTIA OF ALZHEIMERS DISEASE: CENTRAL (genes of APP and presenilins 1 and 2).
CLINICAL CRITERIA c) Positivity of biomarkers that reflect the pathogenic pro-
1. Dementia of probable Alzheimers disease (modified cess of AD (molecular markers by PET or spinal fluid,
from McKhann et al., 2011) or structural and functional neuroimaging).
Meets criteria for dementia and has the following addi- The occurrence of item (a) confirms the existence of a
tional characteristics: degenerative mechanism, despite not being specific for AD.
1. Insidious onset (months or years).
2. Clear history or observation of cognitive decline. 2. Dementia of possible Alzheimers disease
3. Initial and more prominent cognitive deficits in one of The diagnosis of dementia of possible AD should be
the following categories: designated when the patient meets the clinical diagnostic
3A. Amnesic presentation (should have another affected criteria for dementia of AD by presenting some of the signs
domain). and symptoms below:
1. Atypical course: abrupt onset and/or pattern of evo- used because they are more sensitive. There is no norm for
lution distinct from that usually observed i.e. slowly cut-off values, but suggestions have been made of between
progressive. 1 and 1.5 standard deviations below expected levels. Cog-
2. Mixed presentation: there is evidence of other etiolo- nitive screening tests, such as the capacity to write down
gies as described in item 5 of the criteria of dementia and recall an address, or remember objects shown at office
of probable AD (concomitant cerebrovascular disease, visits and then hidden, can be used in clinical practice, des-
characteristics of dementia with Lewy bodies, other pite being less sensitive.9
neurological disease or a non-neurological comorbidity
or use of medication that can have a substantial effect 1.2. ETIOLOGY CONSISTENT WITH AD
on cognition) Discard other systemic or neurological diseases that
3. Insufficient details of history of the establishment and could be responsible for cognitive decline.
development of the disease. Evidence of longitudinal decline of cognition consistent
with natural development of AD, when possible.
3. Dementia of definite Alzheimers disease History consistent with family AD.
Meets the clinical and cognitive criteria for dementia Other neurological diseases that can lead to cogni-
of AD. Neuropathological examination demonstrates the tive decline (trauma, vascular, medications) should be
presence of AD pathology according to the criteria of the ruled out. Parkinsonian symptoms, important cardio-
NIA and Reagan Institute Working Group.16 vascular risk factors and significant vascular alterations
on neuroimaging examinations, besides prominent
III. DIAGNOSIS OF MILD COGNITIVE IMPAIR- signs of frontotemporal lobe degeneration should be
MENT (MCI) DUE TO AD (MODIFIED FROM ALBERT considered, as suggested in the diagnosis of dementia of
ET AL., 2011) probable AD.9
There are two combinations of criteria that can be uti- The presence of dominant autosomal genetic altera-
lized for the diagnosis of MCI due to AD. tions of AD in family members of the patient make it more
1. Central clinical criteria: for use in clinical practice, wi- likely that MCI is the cause of the disease.
thout the need for tests or highly specialized procedures.
2. Clinical research criteria: which incorporate infor- 2. Criteria of clinical research for MCI due to AD
mation obtained from the use of biomarkers and are Once meeting the clinical criteria of MCI due to AD,
specifically intended for research purposes, specialized the information obtained by biomarkers can confer diffe-
centers and clinical trials. rent degrees of probability of the etiology of AD. This clas-
sification of probability needs to be tested in future studies
1. Central clinical criteria before being used in clinical practice.9
1.1. CLINICAL AND COGNITIVE CHARACTERISTICS High probability
Complaint of cognitive alteration reported by the pa- Biomarkers of A and neuronal lesion/damage are
tient, close relative/friend or health care professional. positive.
Evidence of compromise in one or more cognitive do- Intermediate probability
mains typically including memory, obtained through Only one of the modalities is positive and the other was
evaluation covering the following cognitive domains: not tested.
memory, executive function, speech and visual-spatial Low probability
abilities, or neuropsychological examination. Biomarkers of A and of neuronal lesion/damage are
Preservation of independence in daily life activities. negative.
Can have slight problems in performing complex pre- Inconclusive data:
viously habitual tasks, such as paying bills, preparing a Uncharacteristic or conflicting results (A biomarker
meal or shopping. The patient can take longer, be less positive and that of neuronal lesion/damage negative
efficient and make more mistakes in carrying out these or vice-versa).
activities. However, the patient is still able to maintain
independence with minimal assistance. The degree of certainty of high probability is also rela-
Does not meet the criteria for dementia. ted to the greater incidence and shorter development time
There is still no consensus on which batteries of tests for dementia. The absence of both types of biomarkers le-
should be utilized for the diagnosis of cognitive compro- ads to consideration of other etiologies (non-AD) for the
mise in MCI. Neuropsychological tests should preferably be picture of MCI.
IV. DIAGNOSIS OF PRE-CLINICAL ALZHEIMERS DI- and doctors on the best practice tends to vary over time,
SEASE FOR CLINICAL RESEARCH perhaps pointing to the need for periodic reevaluation of
For the purpose of clinical research, it is possible to the approach in a dynamic process which should be mo-
propose the diagnosis of AD before the appearance of clini- dified on account of the impact of new treatments. Indivi-
cal symptoms based on information obtained through the dualizing the approach on this issue appears to be the best
use of biomarkers, as proposed by Sperling and coworkers strategy given the current state of understanding.20
(2011). However, this proposal still requires experimental
validation through longitudinal studies. Conclusions
Stage 1: Asymptomatic cerebral amyloidosis These new recommendations for the diagnosis of AD
Elevated capture of A marker on PET. represent an advance in relation to those of 2005. Firstly,
Reduction of A-42 in spinal fluid. the condition designated as AD based on the criteria of
Stage 2: Amyloidosis + initial neurodegeneration 2005 is now called dementia of AD, while the general de-
Markers of -amyloid deposition positive. signation now encompasses the pre-clinical phase and MCI
Neuronal dysfunction on FDG-PET/fMRI. due to AD.
Increased tau/phosphor tau in spinal fluid. For the diagnosis of dementia, there is no longer the
Reduction of cortical thickness/hippocampal atrophy compulsory need of memory impairment, still required
by MR. by DSM IV,2 DSM-IIIR21 and CID -1022 and recommended
Stage 3: Positivity for amyloid + evidence of neurode- in 2005. This modification is very important since it allo-
generation + subtle cognitive decline (high cognitive ws the classification of cases of frontotemporal dementia,
demand tests) vascular dementia and other forms of dementia that have
Meeting requirements of stages 1 and 2. already been included under the designation of dementia,
Evidence of previous subtle alteration in cognitive level. although without consensus on recommendations and cri-
Low performance on more complex cognitive tests. teria followed.
Not meeting the criteria for MCI. Unlike previous criteria, the diagnosis of dementia or
AD only needs confirmation by means of neuropsycholo-
Revealing the diagnosis gical assessment in cases when anamnesis and cognitive
The question of disclosing the diagnosis warrants in- evaluation done by a clinician are insufficient for diagnosis.
clusion among the recommendations. In recent decades, The limitation in age of onset of between 40 and 90 years
there has been a major shift in diagnosis disclosure from a has also been dropped from the current criteria.
paternalistic stance to one of greater autonomy of patients. The main difference between our recommendations
Some medical institutions always advise revealing the diag- and the proposals by NIA and AA for the diagnosis of de-
nosis of demential pictures to patients whenever possible, mentia of AD was the inclusion of our recommendations
but cultural, individual and regional factors should be of the need for imaging examinations, tomography of the
taken into account.17 head or preferentially magnetic resonance of the head, to
The percentage of family members of patients with AD exclude other etiologies or comorbidities. In fact, we be-
who would like to have the diagnosis revealed to the pa- lieve that this necessity is implicit in the exclusion criteria
tient ranges from 17 to 76% depending on the country of adopted by the NIA and AA, which we also followed.
study.17 In Brazil, 58% of family members of patients were The inclusion of biomarkers in the diagnosis was re-
found to be in favor of revealing the diagnosis,18 which commended but only in clinical research settings. These
is routinely done by 44.7% of doctors.19 Family members new methods are discussed in detail in the section on sup-
and physicians not wishing to reveal the diagnosis more plementary examinations. There is a need for further stu-
frequently would like such a diagnosis revealed to them- dies to validate the criteria of MCI associated with bioma-
selves if they were the patient (90% and 76.8%, respective- rkers, as well as the criteria of the pre-symptomatic phase
ly).18,19 Family members with a higher level of education18 of AD. However, optional instruments can be employed
and doctors with longer periods of training19 appear to be when considered appropriate by the clinician.
more in favor of not revealing the diagnosis.
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Ana Cludia Ferraz [Servio de Neurologia do Hospital Santa Fernandez [Departamento de Cincias Bsicas da Sade, Fundao
Marcelina (SP)]; Analuiza Camozzato de Pdua [Universidade Universidade Federal de Cincias da Sade de Porto Alegre (RS)]; Mr-
Federal de Cincias da Sade de Porto Alegre (UFCSPA); Hospital de cia Lorena Fagundes Chaves [Servio de Neurologia do Hospital
Clnicas de Porto Alegre (UFRGS) (RS)]; Antonio Lcio Teixeira de Clnicas de Porto Alegre, Universidade Federal do Rio Grande do Sul
[Departamento de Clnica Mdica, Faculdade de Medicina da Universida- (RS)]; Mrcia Radanovic [Laboratrio de Neurocincias - LIM27,
de Federal de Minas Gerais, Belo Horizonte (MG)]; Ayrton Roberto Departamento e Instituto de Psiquiatria da Faculdade de Medicina da
Massaro [Instituto de Reabilitao Lucy Montoro (SP)]; Carla Toc- Universidade de So Paulo (FMUSP) (SP)]; Mrcio Luiz Figueredo
quer [Universidade Federal do Rio de Janeiro (RJ)]; Carlos Alberto Balthazar [Universidade Estadual de Campinas (UNICAMP), Facul-
Buchpiguel [Departamento de Radiologia, Faculdade de Medicina dade de Cincias Mdicas (FCM), Departamento de Neurologia (SP)];
da Universidade de So Paulo (SP)]; Cssio Machado C. Bottino Maria Teresa Carthery-Goulart [Grupo de Neurologia Cogniti-
[Programa Terceira Idade, Instituto de Psiquiatria do Hospital das Clnicas va e do Comportamento do Departamento de Neurologia da Faculdade
da Faculdade de Medicina da Universidade de So Paulo (FMUSP) (SP)]; de Medicina da USP; Centro de Matemtica, Computao e Cognio,
Charles Andr [Faculdade de Medicina - UFRJ; SINAPSE Reabilitao Universidade Federal do ABC (SP)]; Mnica S. Yassuda [Grupo de
e Neurofisiologia (RJ)]; Cludia C. Godinho [Servio de Neurologia Neurologia Cognitiva e do Comportamento do Departamento de Neu-
do Hospital de Clnicas de Porto Alegre, Universidade Federal do Rio rologia da Faculdade de Medicina da USP; Departamento de Gerontolo-
Grande do Sul (RS)]; Cludia Sellitto Porto [Grupo de Neurolo- gia, Escola de Artes, Cincias e Humanidades da USP (EACH/USP Leste)
gia Cognitiva e do Comportamento da Faculdade de Medicina da USP (SP)]; Nasser Allam [Universidade de Braslia (UnB), Laboratrio de
(SP)]; Delson Jos da Silva [Ncleo de Neurocincias do Hospital Neurocincias e Comportamento, Braslia (DF)]; Paulo Caramelli
das Clnicas da Universidade Federal de Gois (UFG); Instituto Integrado [Departamento de Clnica Mdica, Faculdade de Medicina da Universida-
de Neurocincias (IINEURO), Goinia (GO)]; Denise Madeira Mo- de Federal de Minas Gerais, Belo Horizonte (MG)]; Paulo Henrique
reira [Departamento de Radiologia Faculdade de Medicina - UFRJ; Setor Ferreira Bertolucci [Universidade Federal de So Paulo (UNIFESP),
de Radiologia - INDC - UFRJ (RJ)]; Eliasz Engelhardt [Setor de Setor de Neurologia do Comportamento - Escola Paulista de Medicina,
Neurologia Cognitiva e do Comportamento - INDC - CDA/IPUB - UFRJ So Paulo (SP)]; Renata Areza-Fegyveres [Grupo de Neurologia
(RJ)]; Francisco de Assis Carvalho do Vale [Universidade Fede- Cognitiva e do Comportamento do Hospital das Clnicas da Faculdade
ral de So Carlos (UFSCar), Departamento de Medicina (DMed) (SP)]; de Medicina da Universidade de So Paulo (FMUSP) (SP)]; Renato
Gabriel R. de Freitas [Instituto Dor de Pesquisa e Ensino; Universi- Anghinah [Grupo de Neurologia Cognitiva e do Comportamento do
dade Federal Fluminense (RJ)]; Hae Won Lee [Instituto de Radiologia, Hospital das Clnicas da Faculdade de Medicina da Universidade de So
Hospital das Clnicas da Faculdade de Medicina da Universidade de So Paulo (FMUSP); Centro de Referncia em Distrbios Cognitivos (CERE-
Paulo e Hospital Srio-Libans (SP)]; Ivan Hideyo Okamoto [De- DIC) da FMUSP (SP)]; Rodrigo Rizek Schultz [Setor de Neurologia
partamento de Neurologia e Neurocirurgia; Instituto da Memria - Uni- do Comportamento do Departamento de Neurologia e Neurocirurgia da
versidade Federal de So Paulo - UNIFESP (SP)]; Jerusa Smid [Grupo Universidade Federal de So Paulo, Ncleo de Envelhecimento Cerebral
de Neurologia Cognitiva e do Comportamento do Hospital das Clnicas (NUDEC) - Instituto da Memria (UNIFESP) (SP)]; Rogrio Beato
da Faculdade de Medicina da Universidade de So Paulo (FMUSP) (SP)]; [Grupo de Pesquisa em Neurologia Cognitiva e do Comportamento, De-
Joo Carlos Barbosa Machado [Aurus IEPE - Instituto de Ensino partamento de Medicina Interna, Faculdade de Medicina, UFMG (MG)];
e Pesquisa do Envelhecimento de Belo Horizonte; Faculdade de Cincias Sonia Maria Dozzi Brucki [Grupo de Neurologia Cognitiva e do
Mdicas de Minas Gerais (FCMMG), Servio de Medicina Geritrica do Comportamento da Faculdade de Medicina da Universidade de So Paulo;
Hospital Mater Dei (MG)]; Jos Antonio Livramento [Laboratrio Centro de Referncia em Distrbios Cognitivos (CEREDIC) da FMUSP;
de Investigao Mdica (LIM) 15, Faculdade de Medicina da Universidade Hospital Santa Marcelina (SP)]; Tnia Novaretti [Faculdade de Fi-
de So Paulo (SP)]; Jos Luiz de S Cavalcanti [Departamento de losofia e Cincias, Campus de Marlia, da Universidade Estadual Paulista
Neurologia - INDC - UFRJ; Setor de Neurologia Cognitiva e do Com- (UNESP) (SP)]; Valria Santoro Bahia [Grupo de Neurologia Cog-
portamento - INDC - UFRJ (RJ)]; Letcia Lessa Mansur [Grupo de nitiva e do Comportamento do Hospital das Clnicas da Faculdade de Me-
Neurologia Cognitiva e do Comportamento do Departamento de Neuro- dicina da Universidade de So Paulo (FMUSP) (SP)]; Ylmar Corra
logia da FMUSP; Departamento de Fisioterapia, Fonoaudiologia e Terapia Neto [Universidade Federal de Santa Catarina (UFSC), Departamento
Ocupacional da Faculdade de Medicina da USP (SP)]; Liana Lisboa de Clnica Mdica, Florianpolis (SC)].