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HIV ENCHEPHALITIS
Dr . PUJI PINTA O. SINURAT, SpSDepartemen Neurologi FK USU/
RSUP Haji Adam Malik2016
Spektrum NeuroAIDS
• Primary complication • (non-opportunistic disease)
– HIV-Dementia– HIV-Sensory neuropathy
• Secondary complication (opportunistic disease)
– Cerebral Toxoplasmosis – TB Meningitis / tuberculoma– Cryptococcal meningitis– Other opportunistic diseases....
HIV Neuropathogenesis Chronic CNS infection begins during
primary systemic infection and continues in nearly all untreated seropositive individuals
progress to HIV-1 encephalitis (HIVE) manifests as a clinical syndrome of
cognitive, motor, and behavioral dysfunction known as the HIV-dementia
Blood BBB CNS Infections
Neuronal damage
CognitiveMotor weaknessEncephalopathy
Blood
Brain parechyma Scarano et al Nature Vol 5 Jan 2005
HIV Entry into CNS
Komplikasi neurologi HIV Brain Predominantly nonfocal AIDS dementia complex Acute HIV-related encephalitis Cytomegalovirus encephalitis Varicella-zoster virus encephalitis Herpes simplex virus encephalitis Metabolic encephalopathies
Brain Predominantly focal Cerebral toxoplasmosis Primary CNS lymphoma Progressive multifocal leukoencephalopathy Cryptococcoma Brain abcess / tuberculoma Neurosyphilis (meningovascular) Vascular disorders
Spinal cord Vacuolar myelopathy Herpes simplex or zoster myelitis Meninges Aseptic meningitis (HIV) Cryptococcal meningitis Tuberculous meningitis Syphilitic meningitis Metastatic lymphomatous meningitis
Peripheral nerve and root Cytomegalovirus lumbar polyradiculopathy
Virus or immune-related acute and chronic inflammatory HIV polyneuritis mononeuritis multiplex sensorimotor demyelinating polyneuropathy distal painful sensory polyneuritis Muscle polymyositis and other myopathies
Perjalanan penyakit infeksi HIV Infeksi virus (2-3 minggu) sindroma retro-
viral akut (2-3 minggu) gejala menghilang + serokonversi infeksi kronis HIV asimptomatik (rata2 8 thn) infeksi HIV / AIDS simptomatik (rata2 1,3 thn) kematian.
Window period masa dimana pemeriksaan test serologis utk antibodi HIV masih negatif, tapi virus sdh ada dlm darah (sudah mampu menularkan kpd orang lain)
HIV dementia (AIDS Dementia Complex) This progressive dementia occurs in AIDS,
owing to a direct primary HIV infection of neurons or an indirect neurotoxicity induced by presence of the virus in the brain
Pathology: the virus may be transported into the brain by infected peripheral monocytes (Trojan horse theory).
Manifestasi klinis demensia HIV:Cognititive disorders
Gangguan kognitif, kesulitan konsentrasi, forgetfullness, cognitive slowing. Kadang2 agitasi, mania. Pd std awal sulit membedakan dgn keluhan psikiatri.
Motor abnormalities: ataksia, hiperrefleks. Babinski refleks srg muncul. Pada std lanjut : paraparese dgn inkontinansia urin et alvii
Behavioural dysfunction : Apathy, altered personality, disorientasi. Std akhir Mutism
APNAC STUDYNeurologic disorders are prevalent in HIV-positive outpatients in the Asia-Pacific region Neurology Vol 71(1), 1 July 2008, pp 50-56
Beijing Hongkong Bangkok KLumpur JakartaNeurocognitive
impairment2/49(4%)
14/61(23%)
13/73(18%)
2/39(5%)
7/61
(11%)Neuropathy 13/50
(30%)9/62
(14%)20/68(30%)
8/40(20%)
10/60(17%)
Wright EJ, Brew B, Imran D, Kamarulzaman A, McArthur J The Asia Pacific NeuroAIDS Consortium ( APNAC )
Anti Retroviral ARV reduce the opportunistic infection
ARV can arrest HIV-dementia and reverse its neurological disability.(Price J Infect Dis. 2008 May 15 )
Neurologist should have a competency in prescribing ARV
Anti Retroviral Treatment HAART (highly active antiretroviral treatment )
Combination of three ARV ARV indication
AIDS defining illnessCD4 < 350 cell/uLViral load > 50.000 copy/ml
When to start ? (first : treat opportunistic infection, than start ARV)
Lamivudine
Zidovudine Stavudine
Nevirapine Efavirenz
First Line ARV(HAART : 3 drugs combination)
HAART : highly active antiretroviral therapy
ARV Lini Satu
First Line ARV (1)
Stavudine 2 X 1 . Neuropati, pankreatitis, atrofi ototLamivudin 2 X1Efavirens 600 1 X 1, vivid dream, ngantuk, imbalance, wanita hamil
First Line ARV (2)
Stavudine sdaLamivudin sdaNevirapin 1 X 1 2 minggu pertama, selanjutnya 2 X 1Alergi, fungsi hati
First Line ARV (3)
Duviral : 2 X 1 (Zidovudin dan lamivudin)Anemia, sakit kepala Nevirapin sda
First Line ARV (4)
Second line ARV
ARV brain penetration Low
○ Tenofovir ○ Didanosine○ Ritonavir
Medium○ Stavudine○ Lamivudine○ Efavirenz○ Emtricitabine
High○ Zidovudine○ Nevirapine
Initiation of ARV Therapy Indication
AIDS defining illnessCD4 < 350 cell/uLViral load > 50.000 copy/ml
Patients preparation before starting ARVLonglive treatmentRule-out and treat opportunistic infection firstARV adverse effect
○ Side effect
Focal Brain Lesion (FBL)
Lesi fokal otak pd imaging ?
Efek desak ruang ?
HIV positif
Simptom intrakranial
YA
tidak
CEREBRAL TOXOPLASMOSIS Reactivation of latent infection Toxo seroprevalence 12-46% IgG indicates past infection (FN <3-6%)
CD4 > 200 virtually excludes Toxo Over 80% have CD4 < 100
Typically multiple ring enhancing lesions on CT/MRI 27-43% have single lesions Up to 10% may have diffuse encephalitis without any
visible focal lesions
The course of HIV/AIDS
Notes:
MRI
CT Scan
Atrofi Meningeal enhancement
hidrosefalus SOL
Evaluasi LCS Shunt(kalau perlu)
Positif Negatif
Terapi sesuai etiologi
Observasi
Lesi massa(-) Lesi massa (+)
Skema 2
Keluhan intrakranial
Skema-1. Algoritme Penatalaksanaan Keluhan Intraserebral bagi Penderita HIV-AIDS
normal
Terapi toksoplasmosisSeumur hidup
Terapi sesuaietiologi
Dekompresi dan biopsi terbuka
Lesi massa intrakranial
Alert-lethargic stabil
Steroid ? Stupor-komaPerburukan cepat, massa
besarDengan resiko herniasi
Lesi multipel Lesi tunggal
Serologi toksoplasma
NegatifPositif
Obat antitoksoplasmosis
Perbaikan
Ya Tidak Biopsi stereotaktik
Ancaman herniasi
Skema-2. Algoritme Penatalaksanaan Lesi massa Intrakranial pada penderita HIV-AIDS
Toxoplasmosis – Clinical Features Usually subacute over weeks Headache 50% Fever 45% Behaviour changes 40% Confusion 15-52% Focal signs Seizures 24-29%
TREATMENT Acute treatment : 3-6 weeks.
Induction : pyrimethamine 200 mg First line :
○ Pyrimethamin 75-100 mg/day + sulfadiazine + folinic acid or
○ Pyrimethamin + clindamycin + folinic acid.Second line :
○ Azithromycin, clarithromycin, or atovaquone can substitute for sulfadiazine.
Glucocorticoid life threatening condition.
TREATMENT Maintenance :
Until the immune system has sufficiently reconstituted.
Pyrimethamine and sulfadiazine orPyrimethamine and clindamycin.
Stop :Asymptomatik.CD4+ > 200/cmm until 6 months.
CT - Multiple ring enhancing lesions
Toxo more likely
Tuberculomas still possible
Differential DiagnosisToxoplasmosis P CNS L
Location Basal ganglia.Gray-white junction
Periventricular
Number of lesion Multiple Solitary>multiple
Enhancement pattern Ring Heterogeneous or homogeneous.
Edema Moderate to marked Variable
T2-weighted image (lesion relative to white matter)
Hyperintense Isointense to hyperintense.
Diffusion-weighted image
Usually hypointense Often hyperintense (positive)
Differential DiagnosisToxoplasmosis P CNS L
MR perfusion Decreased Increased
MR spectroscopy Markedly elevated lactate.
Markedly elevated choline
SPECT thallium (lesion relative to white matter)
“Cold”-no thallium uptake
“Hot”-increased thallium uptake.
Other Toxoplasma IgG Ab (+) (90% of patients)
EBV DNA amplified by PCR in CSF (most patients)
Cytomegalovirus infections
Central or peripheral nervous system In adults occur in immunocompromised individual Etiology: CMV (DNA Virus) of the herpetic group Clinical features: -Encephalitis complication of organ
transplantation and AIDS. CD 4 < 50 cell/ mm3 - Symptoms enceph: headache, fever and seizure Treatment: antiviral agent (ganciclovir or foscarnet)