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Transcript of Sida snc i.o_oct_2010 corti
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COMPROMISO DEL SNC EN PACIENTES CON SIDA
Profesor Dr Marcelo CortiJefe División “B” HIV/sidaHospital de Enfermedades
InfecciosasFrancisco J. Muñiz
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COMPROMISO DEL SNC EN EL SIDA
Neurotropismo del Propio Retrovirus
ENCEFALOPATIA / DEMENCIA
Compromiso de la Inmunidad Celular
INFECCIONES OPORTUNISTAS
TUMORES
Síndromes Neurológicos de Reconstitución Inmune
LEMP, CRIPTOCOCOSIS, TBC
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COMPROMISO DEL SNC EN LA ENFERMEDAD DEBIDA AL HIV y SIDA
PREVALENCIA
30 a 70 % de los casos
60 a 75 % en autopsias
2da. causa de internación en pacientes con SIDA
1ra. causa de mortalidad
ELEVADA MORBIMORTALIDAD
Collazos J. Opportunistic infections of the CNS in patients with AIDS. CNS Drugs 2003; 17:869-887.
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0%
5%
10%
15%
20%
25%
30%
TBC NeumoníasBacterianas
PCP Criptococosis Toxoplasmosis
512 casos
313 casos
220 casos
145 casos 139 casos
ENFERMEDADES PREVALENTES AÑOS 1997 – 2004
(1809 internaciones)
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COMPROMISO DEL SNC EN LA ENFERMEDAD HIV/SIDA
• CON CD4 (+) < 200 cel/mm3
ToxoplasmosisCriptococosisEncefalopatía HIV-1
• CON CD4 (+) < 100 cel/mm3
LEMP Linfomas primarios del SNC (LPSNC)
• CON CD4 (+) < 50 cel/mm3
CMVEnfermedad de Chagas
• CON CUALQUIER NIVEL DE CD4 (+)
Neurosífilis
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COMPROMISO DEL SNC EN EL SIDAINFECCIONES OPORTUNISTAS
FrecuentesCRIPTOCOCOSIS (M/E)TOXOPLASMOSIS (abscesos)LEMP
Menos comunesENFERMEDAD DE CHAGAS (M/E,
abscesos)TBC (M/E; tuberculomas; abscesos)CMV / HSV / HVZ / HHV-6
Raras ASPERGILOSISNOCARDIOSISHISTOPLASMOSIS
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COMPROMISO DEL SNC EN EL SIDAINFECCIONES OPORTUNISTAS
COMPROMISO FOCAL
COMPROMISO DIFUSO
LESIONES DE MASA CEREBRAL OCUPANTE
MENINGOENCEFALITIS
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COMPROMISO DEL SNC EN EL SIDA
MENINGOENCEFALITIS
Cryptococcus neoformans
Mycobacterium tuberculosis
Trypanosoma cruzi
Citomegalovirus
Neurolúes
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CRIPTOCOCOSIS
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CRIPTOCOCOSIS y SIDA
4ta. I.O. grave en frecuencia (TBC, Neumonías bacterianas,
PCP)
Cryptococcus neoformans var neoformans serotipo A
Tasas de antigenemia y antigenorraquia 100 veces > que
en HIV (-)
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CRIPTOCOCOSIS y SIDA
• Enfermedad diseminada• Compromiso multiorgánico• Evolución aguda o subaguda• Frecuente compromiso de SNC• Pronóstico siempre grave• Escasa respuesta a
antifúngicos• Altas tasas de recaídas
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CRIPTOCOCOSIS y SIDA
LCR directo (+) > 80% de casos
LCR cultivo (+) 90% de casos
Hemocultivos (+) > 60% de casos
Antigenemia (+) > 95% de casos
Antigenorraquia (+) > 90% de casos (similar al cultivo)
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LCR – TINTA CHINA POSITIVA
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CRIPTOCOCOSIS - SEUDOQUISTES
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CRIPTOCOCOSIS / RM / ESPECTROSCOPIANAA Cho
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PSEUDOQUISTES + CRIPTOCOCOMA
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PSEUDOQUISTES GELATINOSOS
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PSEUDOQUISTES - CRIPTOCOCOMAS
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CRIPTOCOCOS EN LCR CRIPTOCOCOMAS
GROCOTT
PAS
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TBC DEL SNC EN EL SIDA
1)MENINGOENCEFALITIS
2)TUBERCULOMAS
3)ABSCESOS DE CEREBRO
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Tuberculous meningitis in HIV-infected and non-infected patients: a comparative study – IAS - 2005
Ambrosioni Czyrko J, Cecchini D, Brezzo C, Corti M, Rybko A, Ambroggi M.
Infectious Diseases Hospital F. J. Muñiz, Buenos Aires, Argentina.
Table 1. Demographic characteristics
HIV (-) HIV (+)
n 40 101
age (median) 32 33
male 53% 69%
Table 2. CSF findings
HIV (-) HIV (+) p
CSF cell count (cell/ml)* 167 47 <0.05
CSF pleocytosis (>5 cells/ml) 98% 80% <0.05
CSF proteins (g/l)* 1.15 0.77 <0.05* median
0%
20%
40%
60%
80%
HIV (+) HIV (-)
Figure 2. Global mortality
0%
10%
20%
30%
40%
50%
HIV (+) HIV (-)
Figure 1. Multirresistant strains
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TUBERCULOMAS DEL SNC
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ABSCESO TBC DE CEREBRO / SIDA
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ABSCESO TBC DE CEREBRO
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ABSCESO TBC DE CEREBRO - POSOPERATORIO
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ABSCESO TBC COMO SIRICorti M y col. IJTLD 2006
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COMPROMISO DEL SNC EN EL SIDA
MENINGOENCEFALITIS POR HERPESVIRUS
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LESIONES CEREBRALES EN SIDA
DIAGNÓSTICO
ESTUDIO DEL LCR
NEUROVIRUS
• SÍNTESIS INTRATECAL DE ANTICUERPOS (HSV-HVZ-CMV-HHV-6-VEB)
• PCR (HSV-HVZ-CMV-HHV-6-VEB)
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METODOLOGÍA DIAGNÓSTICA PARAEL ESTUDIO DEL COMPROMISO DEL SNC POR HERPES VIRUS EN PACIENTES CON
HIV/SIDA
UNIDAD 10, DIVISIÓN “B” y LABORATORIO DE VIROLOGÍA, HOSPITAL F. J. MUÑIZ, BUENOS AIRES
VIII CONGRESO ARGENTINO DE VIROLOGÍA (Abstract 10707)
• 272 pacientes
• Meningitis, encefalitis, poliradiculitis, mielitis, retinitis
• 245 PCR-Multiplex Herpes virus
• 180 Síntesis intratecal de atcs (muestras pareadas de suero)
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PCR en LCR para HERPES VIRUS
245 muestras 30 (+): 12,2% 70%
16,7%13,3%
6,7%3,3% 3,3%
0
10
20
30
40
50
60
70
CMV VZV EBV coinfecciones HSV-2 HHV-6
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COMPROMISO DEL SNC POR CITOMEGALOVIRUS
1) MENINGOENCEFALITIS
2) MIELITIS AGUDA NECROTIZANTE
3) POLIRRADICULITIS ASCENDENTE
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MENINGOENCEFALITIS POR CMV
DIAGNÓSTICO LCR: Hiperproteinorraquia,
Hipoglucorraquia, Pleocitosis con 50% PMN
Síntesis intratecal de atcs antiCMV
PCR en LCR
RMN: leucoencefalopatía con periventriculitis y ventriculitis. Refuerzo
del contraste en epéndimo y región subependimaria.
Biopsia: necrosis + células de inclusión
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PERIVENTRICULITIS POR CMV - RM
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HHV-6: MANIFESTACIONES CLÍNICAS EN PACIENTES HIV +
MENINGOENCEFALITIS AGUDA MIELITIS AGUDA SÍNDROME FEBRIL CON CITOPENIAS NEUMONITIS RETINITIS LINFOMAS No HODGKIN COFACTOR EN LA PROGRESIÓN A SIDA
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MENINGOENCEFALITIS POR HHV-6
FIEBRE
CONVULSIONES (1/3 DE LOS CASOS)
SÍNDROME MENÍNGEO
LCR CON HIPERPROTEINORRAQUIA, PLEOCITOSIS MONONUCLEAR
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MENINGOENCEFALITIS POR HHV-6 / NEUROIMÁGENES
COMPROMISO DEL LÓBULO TEMPORAL
LESIONES COMPATIBLES CON VASCULITIS
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ENCEFALITIS POR HHV – 6
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ENCEFALITIS POR HHV – 6 / PCR + LCR
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MENINGOENCEFALITIS POR HHV-6 / DIAGNÓSTICO
PCR EN LCR
AMPLIFICACIÓN DEL DNA-HHV-6
Enferm Infecc Microbiol Clin 2004; 22: 150-5
AIDS Read 1999; 9: 198-221
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Patient 1 Patient 2 Patient 3 Patient 4 Patient 5
Gender Female Male Male Male Male
Age 55 30 42 43 37
Risk factor for HIV infection
IDU Homosexual Heterosexual Bisexual IDU
Opportunistic diseases
Meningeal cryptococcosis
Meningealtuberculosis
Meningealcryptococcosis
Disseminated tuberculosis
Disseminated tuberculosis
Neurological Symptoms
Meningeal syndrome Meningeal syndrome Meningeal syndrome Encephalitis Seizures
Fever + + + + +
CD4 cellCount
70 cell/µL 131 cell/µL ND 46 cell/µL 144 cell/µL
CSF ↑ proteins ↑ proteins ↑ proteins ↑ proteins ↑ proteins
PCR HHV-6 CSF + + + + +
Neuroimages MRI: cerebral and cerebellar atrophy
CT: cerebral atrophy.Hipodensities in
white matter
ND ND MRI: periventricular lesions compatible
with vasculitis
HAART in the onset of symptoms -- -- -- -- --
Treatment-- -- -- --
Ganciclovir/Foscarnet + HAART
Survival died died died died Good response to therapy
Patient 1Patient 1 Patient 2Patient 2 Patient 3Patient 3 Patient 4Patient 4 Patient 5Patient 5
GenderGender FemaleFemale MaleMale MaleMale MaleMale MaleMale
AgeAge 5555 3030 4242 4343 3737
Risk factor for HIV infection
Risk factor for HIV infection
IDUIDU HomosexualHomosexual HeterosexualHeterosexual BisexualBisexual IDUIDU
Opportunistic diseases
Opportunistic diseases
Meningeal cryptococcosis
Meningeal cryptococcosis
MeningealtuberculosisMeningeal
tuberculosisMeningeal
cryptococcosisMeningeal
cryptococcosisDisseminated tuberculosis
Disseminated tuberculosis
Disseminated tuberculosis
Disseminated tuberculosis
Neurological Symptoms
Neurological Symptoms
Meningeal syndromeMeningeal syndrome Meningeal syndromeMeningeal syndrome Meningeal syndrome Meningeal syndrome EncephalitisEncephalitis SeizuresSeizures
FeverFever ++ ++ ++ ++ ++
CD4 cellCount
CD4 cellCount
70 cell/µL70 cell/µL 131 cell/µL131 cell/µL NDND 46 cell/µL46 cell/µL 144 cell/µL144 cell/µL
CSFCSF ↑ proteins↑ proteins ↑ proteins↑ proteins ↑ proteins↑ proteins ↑ proteins↑ proteins ↑ proteins↑ proteins
PCR HHV-6 CSFPCR HHV-6 CSF ++ ++ ++ ++ ++
NeuroimagesNeuroimages MRI: cerebral and cerebellar atrophy MRI: cerebral and cerebellar atrophy
CT: cerebral atrophy.Hipodensities in
white matter
CT: cerebral atrophy.Hipodensities in
white matter
NDND NDND MRI: periventricular lesions compatible
with vasculitis
MRI: periventricular lesions compatible
with vasculitis
HAART in the onset of symptoms
HAART in the onset of symptoms ---- ---- ---- ---- ----
TreatmentTreatment---- ---- ---- ----
Ganciclovir/Foscarnet + HAART
Ganciclovir/Foscarnet + HAART
SurvivalSurvival dieddied dieddied dieddied dieddied Good response to therapy
Good response to therapy
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COMPROMISO DEL SNC POR HHV-6
TRATAMIENTO
GANCICLOVIR + FOSCARNET14 a 21 días
International Herpes Mangement Forum
Herpes 2004; 11: 105A-111A
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ENCEFALITIS POR HZV – PCR + LCR
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SÍFILIS DEL SNC
NEUROLÚES ASINTOMÁTICA
MENINGITIS SIFILÍTICA
SÍFILIS MENINGOVASCULAR
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LESIONES CEREBRALES FOCALES
EN SIDA
TOXOPLASMOSIS
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TOXOPLASMOSIS y SIDA
Lesiones cerebrales focales
Meningoencefalitis subaguda
Encefalitis aguda difusa (rara)
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TOXOPLASMOSIS y SIDA
• Incidencia: 3% a 40% en pacientes con SIDA
• Causa más frecuente de lesiones focales
• Recuento de linfocitos T CD4 (+) < 100 cél/uL
• Tratamiento empírico inicial con clínica y TAC
• Mejoría clínica en 1 a 2 semanas
• Resolución de las lesiones en 4 a 8 semanas
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TOXOPLASMOSIS
2 A 3 VECES MÁS FRECUENTE QUE LPSNC
70 % LESIONES MÚLTIPLES
UBICACIÓN:
• SUSTANCIA GRIS SUBCORTICAL
• UNIÓN CORTICO/MEDULAR
• TÁLAMO Y GANGLIOS BASALES
REFUERZO DEL CONTRASTE NODULAR O EN ANILLO, CON EDEMA Y EFECTO DE
MASA
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TOXOPLASMOSIS CEREBRAL-SIDAHALLAZGOS EN LAS NEUROIMÁGENES
1. Lesiones hipodensas con refuerzo en anillo y edema perilesional
2. Lesiones hipodensas sin captación del contraste con edema perilesional
3. Lesiones nodulares (toman el contraste en forma homogénea) y edema perilesional
4. Edema cerebral localizado sin lesiones focales visibles
5. TAC sin lesiones y RNM con lesiones focales
1 y 3: 80% a 90% de las lesiones
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TOXOPLASMOSIS FOSA POSTERIOR
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TOXOPLASMOSIS DE FOSA POSTERIOR
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TOXOPLASMOSIS –T AC LESIÓN ÚNICA
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TOXOPLASMOSIS – RNM LESIONES MÚLTIPLES
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TOXOPLASMOSIS LESIONES MÚLTIPLES EN RNM
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TOXOPLASMOSIS ABSCESO EN MESENCÉFALO
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TOXOPLASMOSIS – RM – ESPECTROSCOPIA Cho y NAA Lípidos
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ENFERMEDAD de
CHAGAS
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ENFERMEDAD DE CHAGAS y SIDA
Reactivación de infección latente por T. cruzi
El paciente puede estar fuera del área endémica
Puertas de entrada: hemoderivados y ADEV
Enfermedad HIV/SIDA avanzada (CD4 + < 50 cél/uL)
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ENFERMEDAD DE CHAGAS y SIDA
ABSCESOS CEREBRALES FOCALES
MENINGOENCEFALITIS DIFUSA
AMASTIGOTES EN BIOPSIA CEREBRAL
TRIPOMASTIGOTES EN LCR
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ENFERMEDAD DE CHAGAS y SIDA
DIAGNÓSTICO
SEROLOGÍA
PARASITEMIA
NEUROIMÁGENES
ESTUDIO DEL LCR
BIOPSIA ESTEREOTÁXICA
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ENFERMEDAD DE CHAGAS y SIDA
DIAGNÓSTICO
LESIONES DE MASA CEREBRAL OCUPANTE
PARASITEMIA SEROLOGÍA P/CHAGAS
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CHAGAS DISEASE NEUROLOGICAL INVOLVEMENT AND HIV INFECTION IN ARGENTINA (1992-2006) - IAS – 2007 Cordova E., Boschi A., Ambrosioni Czyrko J., Cudos C, Corti M.
Table 1. Clinical manifestations in HIV positive patients with confirmed diagnosis of Chagas disease involving CNS
Headache 11/14 79%
Fever 9/14 64%
Focal neurological deficits 8/14 57%
Meningismus 6/14 43%
Seizures 6/14 43%
Altered mental status (a) 4/14 29%
Concomitant cardiac involvement (b) 3/10 33%
(a) Include confusion, delirium, or a declining level of consciousness ranging from lethargy to coma.(b) Include signs and symptoms of acute myocarditis evaluated with electrocardiogram and echocardiogram without a history of previous miocardiophaty. Not confirmed by isolation of parasites in heart tissue.
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CHAGAS DISEASE NEUROLOGICAL INVOLVEMENT AND HIV INFECTION IN ARGENTINA (1992-2006) – IAS - 2007
Cordova E., Boschi A., Ambrosioni Czyrko J., Cudos C, Corti M.
CSF findings (n=12)
Median (range) cell count (cell/mL): 5 (2-90)
Median (range) protein level (gr/L): 0.66 (0.1-1.84)
Median (range) glucose level (gr/L): 0.4 (0.13-0.73)
Trypanosoma cruzi detected by DME: 10/12 83%
Neuroimages findings
Nº Lessions White matter
Gray matter
Supratentorial
Infratentorial
Mass effect
Enhance with
contrast
Single: 7 (54%)
9 (82%)2
(18%)9 (82%) 2 (18%) 5 (45%) 8 (73%)
2-5: 2 (15.3%)
Multiple: 2 (15.3%)
Normal images: 2 (15.3%)
Supratentorial lesions include: brain lobes 09/11 (+++ frontal lobe), basal ganglia/thalamus 2/11, brain stern 1/11.
Infratentorial lesions include: cerebellum lobes 2/11.
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CHAGOMA - ESPECTROSCOPIA
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CHAGOMA CEREBRAL ESPECTROSCOPIA
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CHAGOMA CEREBRAL
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CHAGOMA CEREBRAL
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CHAGOMA DE CUERPO CALLOSO
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CHAGOMAS CEREBRALES
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ENCEFALITIS CHAGÁSICAHISTOPATOLOGÍA
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NOCARDIOSIS CEREBRAL
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NOCARDIOSIS CEREBRAL
ABSCESOS CEREBRALES
ENFERMEDAD DISEMINADA (40% de casos)
HUÉSPEDES INMUNOCOMPROMETIDOS
Nocardia asteroides 98% de los casos
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NOCARDIOSIS CEREBRAL
Abscesos primarios o secundarios
Únicos o múltiples, multilobulados
Supratentoriales o infratentoriales
Cefalea y signos neurológicos focales
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NOCARDIOSIS CEREBRAL
DIAGNÓSTICO
BIOPSIA ESTEREOTÁXICA CULTIVOS
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NOCARDIOSIS CEREBRAL
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NOCARDIOSIS CEREBRAL-KINYOUN POSITIVA
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NOCARDIOSIS CEREBRAL (pos-tto)
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LEUCOENCEFALOPATÍA MULTIFOCAL
PROGRESIVA (LEMP)
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COMPROMISO DEL SNC EN EL SIDA
LESIONES DE LA SUSTANCIA BLANCA
LEMP Lóbulos parietooccipitales de ambos
hemisferios
Compromiso de fibras subcorticales en “U”
1/3 de casos tienen compromiso de fosa posterior
En 5% a 10% el compromiso de fosa posterior es la única manifestación
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LEMP FOSA POSTERIOR RNM T1
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LEMP CEREBELO RNM T2
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Lesiones cerebrales focales en sida
LEMP
PCR para DNA JCV (42 a 85% de sensibilidad; 90 a 100 % de especificidad)
Carga viral para VJC en LCR
ESTUDIO DEL LCR
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DIAGNOSIS OF PML AMONG AIDS PATIENTS: CLINICAL SENSITIVITY OF A COMMERCIAL PCR
ASSAY FOR THE DETECTION OF JCV-DNA IN CEREBROSPINAL FLUID
• 25 SAMPLES OF CSF OF PATIENTS WITH CLINICAL AND RADIOLOGICAL FINDINGS
OF PML
• JCV-DNA + : 12/25 (all with neuroimaging criteria for PML)
• SENSITIVITY: 48%Mamanna, Corti M, Trione N, Metta H, Bouzas MB.
23rd Annual Clinical Virology Symposium and Annual Meeting of the Pan American Society for Clinical Virology. April 29 – May 02,
2007. Clearwater Beach, Florida, EE.UU.
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LEMP: Oligodendrocito con un cuerpo de inclusión intranuclear
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LEMP: OLIGODENDROCITOS CON CUERPOS DE INCLUSIÓN
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LEMP PSEUDOTUMORAL - SIRI
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LEMP PSEUDOTUMORAL - SIRI
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POSTTO – CORTICOIDES - TARGA
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UTILIDAD DE LA BIOPSIA UTILIDAD DE LA BIOPSIA ESTEREOTÁXICA EN EL ESTEREOTÁXICA EN EL DIAGNÓSTICO DE LAS DIAGNÓSTICO DE LAS
LESIONES CEREBRALES LESIONES CEREBRALES FOCALES EN PACIENTES FOCALES EN PACIENTES
CON SIDACON SIDA
Hospital de Enfermedades Infecciosas F. J. Muñiz Hospital de Enfermedades Infecciosas F. J. Muñiz GCABAGCABA
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MATERIALES y MÉTODOSMATERIALES y MÉTODOS 83 procedimientos;83 procedimientos;
Enero de 1999 a Mayo 2007;Enero de 1999 a Mayo 2007;
Pacientes con lesiones cerebrales Pacientes con lesiones cerebrales ocupantes por TC o RM; ocupantes por TC o RM;
Sin respuesta al tratamiento empírico Sin respuesta al tratamiento empírico para toxoplasmosis (2 a 4 semanas);para toxoplasmosis (2 a 4 semanas);
Con lesiones cuyas características en Con lesiones cuyas características en las neuroimágenes sugerían otro las neuroimágenes sugerían otro diagnóstico.diagnóstico.
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CIRUGÍA ESTEREOTÁCTICA CIRUGÍA ESTEREOTÁCTICA BIOPSIA CEREBRALBIOPSIA CEREBRAL
Procedimiento mínimamente Procedimiento mínimamente invasivoinvasivo
Máxima eficaciaMáxima eficacia
Mínima morbilidadMínima morbilidad
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BIOPSIA ESTEREOTÁCTICA BIOPSIA ESTEREOTÁCTICA CEREBRALCEREBRAL
• Primer paso:Primer paso: colocación del colocación del marco referencial.marco referencial.
• Segundo paso:Segundo paso: adquisición de adquisición de imágenes (TC, RMN).imágenes (TC, RMN).
• Tercer paso:Tercer paso: planificación. planificación. • Cuarto paso:Cuarto paso: transferencia de transferencia de
datos y biopsia.datos y biopsia.
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1er. Paso: Colocación del 1er. Paso: Colocación del MarcoMarco
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2do. Paso: Adquisición de 2do. Paso: Adquisición de ImágenesImágenes
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3er. Paso: Planificación3er. Paso: Planificación
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4to. Paso: Transferencia de Datos 4to. Paso: Transferencia de Datos y Biopsiay Biopsia
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TOMA DE MUESTRAS e IMPRONTA
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El área de mayor rendimiento diagnóstico El área de mayor rendimiento diagnóstico es la zona de mayor captación de es la zona de mayor captación de
contrastecontraste
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BIOPSIAS ESTEREOTÁXICASExperiencia Htal. Muñiz – División B –
1999/2007N° %
LEMP 24 28,90%
LPSNC 19 22,90%
Toxoplasmosis 13 15,70%
Incaracterísticos 8 9,60%
Neoplasias no marcadoras (*) 7 8,40%
TBC 4 4,80%
Nocardia 3 3,60%
Chagas 2 2,40%
Histoplasmosis 1 1,20%
VVZ 1 1,20%
CMV 1 1,20%
Total 83 100,00% (*) gliomas (6) y LH (1)
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CONCLUSIÓN ICONCLUSIÓN I
• Rédito diagnóstico:Rédito diagnóstico:
75 biopsias 75 biopsias (90,3%)(90,3%)
• Hallazgos incaracterísticos:Hallazgos incaracterísticos:
8 biopsias 8 biopsias (9,6%)(9,6%)
•
Morbiletalidad:Morbiletalidad:2 pacientes (2,4%)2 pacientes (2,4%)
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CONCLUSIÓN IICONCLUSIÓN II
La biopsia cerebral estereotáctica La biopsia cerebral estereotáctica efectuada precozmente resultó ser un efectuada precozmente resultó ser un
método que permitió alcanzar el método que permitió alcanzar el diagnóstico etiológico y adecuar el diagnóstico etiológico y adecuar el
enfoque terapéutico en la mayoría de enfoque terapéutico en la mayoría de los pacientes de esta serie. Constituye los pacientes de esta serie. Constituye
un método efectivo, seguro y un método efectivo, seguro y mínimamente invasivo para pacientes mínimamente invasivo para pacientes
con enfermedad HIV/sida avanzada con enfermedad HIV/sida avanzada con lesiones cerebrales focales.con lesiones cerebrales focales.
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EN PACIENTES CON SIDA RECORDAR SIEMPRE QUE
PUEDEN COEXISTIR MAS DE UN AGENTE ETIOLÓGICO
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TOXOPLASMOSIS - SIDA
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CHAGOMA CEREBRAL
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TRIPOMASTIGOTES EN LCR
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LESIONES CEREBRALES FOCALES EN SIDA
DIFICULTADES PARA EL DIAGNÓSTICO
¿POR QUÉ LAS NEUROIMÁGENES NO SIEMPRE SON SUFICIENTES ?
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TOXOPLASMOSIS
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TOXOPLASMOSIS CEREBRAL
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LPSNC - SIDA
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LPSNC - SIDA
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CHAGOMA CEREBRAL - SIDA
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ENCEFALITIS CHAGÁSICA - SIDA
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MENINGIOMA DE LA TIENDA DEL CEREBELO – HIV+
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MENINGIOMA DE LA TIENDA DEL CEREBELO – HIV +
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MENINGIOMA DE LA TIENDA DEL CEREBELO – HIV +
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GLIOSARCOMA – HIV +
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GLIOSARCOMA – HIV +
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GLIOSARCOMA - TUMOR FUSOCELULAR CON ATIPÍAS
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GLIOSARCOMA – VIMENTINA +
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ADENOMA DE HIPÓFISIS – HIV +
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ADENOMA DE HIPÓFISIS – HIV +
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GRACIAS!!!