Há subdiagnóstico das demências tratáveis? Fluxograma de ...€¦ · ty at times ma y be...
Transcript of Há subdiagnóstico das demências tratáveis? Fluxograma de ...€¦ · ty at times ma y be...
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Há subdiagnóstico das demências tratáveis? Fluxograma de avaliação e
tratamentoNorberto A. F. Frota
Prof. Curso de Medicina da UNIFOR
Coordenador da Residência em Neurologia do HGF
Secretário de Neurologia da ABNPG
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Como Não deixar passar uma demência tratável
• Reversão total
• Reversão parcial
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Roteiro
• Caso 1
• Caso 2
• Investigação complementar
• HPN
• Fluxograma
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Caso 1
• Homem, 64 anos, médico
• QP: Alteração de marcha e comportamento
• Há dois anos mudança de comportamento:
Compras em excesso
Doando objetos
Agressividade
• Feito o diagnóstico de TAB
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Caso 1
• Iniciado tratamento, evoluiu com melhoracomportamental
• Nos últimos 6 meses apatia progressiva e lentificaçãode marcha com discreto tremor.
• Paciente negava os déficits
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Caso 1
• Med: Alipripazol (Suspenso 1 mês antes)+ Divalproatode sódio + Paroxetina + glicazida + indapamida + Candesartan
• AP: Etilismo importante + Hipernefroma operado + HAS + DM
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Caso 1
• EN: Parkinsonismo axial
Reflexo palmo-mentual bilateral
Hipoestesia em bota e luva
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Avaliação Cogntiva
• MEEM:
OT: 5 MI:3 ME: 2
OE: 4 A/C: 3
Ling: 9 = 26/30
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• P/N: 10/10
• M inc: 5
• M imed: 8
• M aprend: 8
• FA: 2
• M evoc: 6
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Avaliação Cognitiva
• BAF:9/18
Similaridades: 0
Fluência S: 1 ( Falou 4 palavras)
Programa motor: 3
Instruções Conflitantes: 3
Go-no-go: 0
Comportamento de preensão: 2
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Hipótese diagnóstica
A) Degeneração lobar fronto-temporal
B) Metástase do Hipernefroma
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Exames complementares
• RM cranio: discreta atrofia fronto-temporal
• SPECT:Hipoperfusão fronto-temporal
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Qual a prevalência de causas reversíveis de demência?
• 0 a 30%
• 8% (Takada et al 2003)
• Etiologias Diversas
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Drogas
• 5% dos casos em algumas séries
• Álcool – principal
• Medicações comumente mais relacionadas
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Sempre pesquisar a associação
Journal of Psychiat r ic Pract ice Vol. 21, No. 2154 March 2015
Chronic neurotoxicity caused by lithium salts can
be reversible or ir reversible and may appear after
years of treatment, even at serum levels consid-
ered within the usual therapeutic range. The
authors present the case of a patient with bipolar
disorder who developed dementia at the age of 54
after being treated with lithium carbonate at
therapeutic levels for 4 years. Nevertheless, lithi-
um treatment was continued. At age 56, the
patient presented with an acute encephalopathy
caused by toxic lithium levels, which resolved
only after lithium carbonate was discontinued.
Full recovery from the dementia, which had star t-
ed 2 years ear lier, occurred only after cessation of
lithium. The authors conclude that when patients
treated with lithium develop subacute cognitive
impairment, the possibility of lithium toxicity
should be considered, even if the serum levels are
considered within the therapeutic range. A long
duration of neurotoxicity associated with lithium
treatment does not necessar ily indicate an ir re-
versible prognosis. (Journal of Psychiatr ic Practice
2015;21:154–159)
KEY WORDS: l i thium, neurotoxici ty, reversible, bipo-
lar, dement ia
CASE PRESENTATION
The first case of neurotoxicity caused by l i thium
salts was descr ibed by Cleveland after a “self-intoxi-
cat ion” in 1931.1 Descr ipt ions of other dangerous
cases fol lowed, especial ly when l i thium was used as
a dietary subst i tute for sodium salt in the 1940s in
the United States,2 before the U.S. Food and Drug
Administ rat ion (FDA) approved l i thium as a t reat-
ment for mania in 1970 and as maintenance t reat-
ment for bipolar disorder in 1974. Common
neurological symptoms of acute l i thium intoxicat ion
are alterat ions in level of consciousness, seizures,
parkinsonian and choreiform movements, and cere-
bel lar signs (eg, dysar thr ia, ataxia, coordinat ion
impairment).3 Neurological problems in acute toxici-
ty at t imes may be ir reversible. A number of r isk fac-
tors (EEG abnormalit ies, cerebral impairment, and
epilepsy) can increase the r isk of l i thium toxicity.4
Therefore, fur ther research is needed to clar i fy the
biological causes involved.
In this repor t , we present a case of reversible
dement ia that developed in a pat ient who was t reat-
ed with l i thium carbonate for 4 years at therapeut ic
levels, with ful l recovery after the l i thium was dis-
cont inued 2 years later.
Case Descr iption
The pat ient , a 56-year-old man, had been diagnosed
with bipolar disorder type I based on DSM-IV-TR cr i-
ter ia. He had no history of physical i l lness, nor was
there any fami ly history of psychiat r ic i l lness.
Beginning at age 32, the pat ient had had 3 mild
depressive episodes for which he did not see a spe-
cial ist . At the age of 40, the pat ient was t reated with
a select ive serotonin reuptake inhibitor for major
depression. At the age of 50, after a first manic
episode, the pat ient was t reated with l i thium car-
bonate 1200 mg/day (with serum l i thium levels that
were always in the therapeut ic range, 0.84–0.91
mmol/L), combined with quet iapine 600 mg/day and
clonazepam 2 mg/day.
SORIANO-BARCELÓ, TAJES ALONSO, PORTELA TRABA, and
ARAÚXO VI L AR: Complexo Hospi talar io Univer si t ar io of
Sant iago de Compostela, Spain; KAHN: Columbia Universi ty
Col lege of Physicians and Surgeons, New York.
Copyr ight © 2015 Wolters K luwer Health, Inc. All r ights reserved.
Please send cor respondence to: Juan Sor iano-Barceló, MD,
Hospital Gil Casares, Travesía da Choupana s/n, 15706 Sant iago
de Compostela (A Coruña), Spain. jsor [email protected]
The authors declare no confl icts of interest .
DOI : 10.1097/01.pra.0000462608.02478.16
A Case With Reversible Neurotoxicity After
2 Years of Dementia Secondary to Maintenance
Lithium Treatment
Clinical Case Discussion
Case presentation:JUAN SORIANO-BARCELÓ, MD
MARÍA TAJES ALONSO, MDMARÍA BEGOÑA PORTELA TRABA, MD
ALBERTE ARAÚXO VILAR, MDCase discussion:
DAVID A. KAHN, MD
Copyright © Unauthorized reproduction of this article is prohibited.
Dautzenberg, 2015 Abbate, 2016
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• Trocado do Ac. Valpróico por Carbamazepina
• Melhora da marcha e da Cognição
• MEEM:30/30 FAB:15/18 e FAS:36
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Primeira Dica
• Rever:
• Todas as medicações utilizadas
• Exposição a fatores tóxicos
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Caso 2• Id: Mulher, 70 anos, dentista
• QP: ”Esquecimento”
• HDA: RVM 3 anos antes, com limitação para o trabalho.
• Apatia e dificuldade de memória/efeitos colaterias da medicação
• Há dois meses ficava sozinha e fazia suas atividades.
• Piora de apatia principalmente no ultimo mês, sem querer sair de casa, assim como mais repetitiva, trocando as medicações.
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Caso 2
• HPP: IAM + TCE + Depressão
Med: Aradois, Carvedilol 25mg 2x/d, Syntroid 88mcg; Liptor20mg , AAS (usou tb venlafaxina e oxcarbamazepina)
Alergia: nega
Hábito: nega
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Caso 2 • ACE:67/100
Atenção: 12/18Memória: 15/26Fluência: (3+3=6/14)LIng: 20/26V-E=14/16
• MInc:ar,ba,=2M1-sa,ca,ba,pe,li,=5M2-sa,av,ca,pe,ba,=5FFrurtas: =9M5-ba,pe,li,=3Go-no-go alterado, não abstrai itens da FAB
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Caso 2
• RM: atrofia de hipocampo e gliose temporal (laudo)
• HD: Demência Rapidamente progressiva/ Episódio depressivo
• CD: investigação e iniciado mirtazapina
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Caso 2
• RM: gliose temporal E, sem atrofia de hipocampo
• SPECT: hipoperfusão temporal E
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Depressão/Pseudodemência
• Sempre pensar e tratar
• Comorbidade inicial e fator de risco
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Evolução
• ACE:88/100
Atenção: 18/18
Memória: 22/26
Fluência: 10/14
Ling:22/26
V-E:16/16
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Dica 2
• Se observamos sintomas depressivos, trate antes de qualquer medicação específica para demência
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Alterações Metabólicas
• Deficiência de B 12
• Hipotireoidismo
• Insuficiência Renal
• Insuficiência Hepática
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Dica 3
• Alterações metabólicas/Infecciosas devem ser sempre pesquisadas e tratadas quando presentes
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ALTERAÇÕES ESTRUTURAIS
• Hematoma Subdural
• Lesões tumorais
• Fístula dural (Enofe I, 2017; Randal A, 2015)
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Hidrocefalia de pressão normalHakim e Adams 1965
- Alteração de Marcha
- Declínio Cognitivo
- Incontinência Urinária
- Sinais de Hidrocefalia
- Pressão Intracraniana Normal
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DIAGNÓSTICO DIFERENCIALMarcha Urina Cognição Pesquisar
D. Corpos de Lewy Sim Sim Sim DisautonomiaSono/Alucinações
D. Parkinson Sim Sim Sim Melhora com facilitadores
Degenaração Cortico-basal Sim Sim Sim Sintomas assimétricos
Paralisia Supranuclearprogressiva
Sim Sim Sim Alteração ocular
Atrofia de multiplossistemas
Sim Sim Sim DisautonomiaAlt. Cerebelar
D. Vascular Sim Sim Sim Micro-sangramentos
Neurossifilis Sim Sim Sim Pupila, VDRL
Medicamentoso Sim Sim Sim Sempre investigar
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Marcha Urina Cognição Pesquisar
Deficiência de B12 Sim x Sim Nível sérico
Estenose Canalcervical/Mielopatia
Sim Sim x Alteração piramidal
Estenose Canal Lombar Sim Sim x Claudicação
Polineuropatia Sim Sim x Sensibilidade
DIAGNÓSTICO DIFERENCIAL
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2014 AJNR
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Radiology 2017
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Pacientes
• 142 pacientes operados
• 115 re-examinados em 1 ano
Testes
• Resistência
• TAP TEST
Limitações
• 84% melhoraram em um ano
• Somente uma avaliação de marcha
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Metodologia
•Prospectivo 1 ano
SINPHONI 2
•DLP
Resultados
• Acurácia 0,74 (sensib 56,5% e espic 91,7%)
•Tempo <24 meses=0,76; 12 meses=0,91; 6 meses=0,97
Conclusão
•Relação entre o tempo de início dos sintomas e a sensibilidade do teste
• Marcha o domínio que deve ser avaliado
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40 % desenvolveram demência no seguimento (risco 2,8)
45 % HPN provável
Somente 3/14 ficaram assintomáticos
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HPN - Dicas
• Pensar quando alteração motora
• Intervenção o mais breve possível
• Assintomáticos – seguir de perto
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Dica 5
• Pensar em causas imunomediadas nos casos de evoluções rápidas
• Alterações motoras
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Fluxograma das Conclusões 1
Quadro demencialnovo, piora dossintomas cognitivos, asvezes com sintomasparkinsonianos
Utilização demedicaçõesanticolinérgicas;antipsicóticos;litium, ác.Valproico etopiarmato
Retirar/Trocar a medicação ereavaliar em 2 a 3 meses
Checar se existeassociação deoutras medicaçõesutilizadas (revisãoliteratura)
Fazer os testes de rastreio da ABN
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Fluxograma das conclusões 2
Quadro demencia novo,pioara dos sintomascognitivos as vezes cominstalação mais rápida esintomas de humor
Utilizar Antidepressivo: escitalopram/mirtazapina/sertralina
Teste de rastrio da ABN
Casos graves -ECT
Revaliação
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Fluxograma das conclusões 3
Quadro demencialnovo, piora dossintomas cognitivos,
Testes de Rastreio ABN
Tratamento Específico
HemogramaCreatininaTSHAlbumina,TGO/TGPVit B12Ác. FólicoCaTVDRL/FTA-Abs
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Fluxograma das Conclusões 4
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Fluxograma de conclusões 5
Síndrome demencial rapidamente progressiva
RM
Exames laboratorias(Auto-anticorpos/marcadorespecificios)
Punção lombar
EEG
DCJ frequente
Forma atípica de doença degenerativa
Causa imunomediada –passíveis de tratamento
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Obrigado pela atençã[email protected]