curs neuroinfectii

NEUROINFECII

Bogdan O. Popescu, MD, PhDClinica de Neurologie S.U.U.B

U.M.F. Carol Davila Bucureti

SINDROAME

Localizare

spaii LCR + leptomeninge (meningita) sistemul ventricular (ventriculita) substana cenuie i alb a encefalului (encefalita) maduva spinrii (mielita) infecia focal bacterian

la nivel cerebral = abces cerebral (faza encefalitica / faza de colectare) ntre dura mater i arahnoida = abces (empiem) subdural n afara durei mater = abces (empiem) epidural

http://www.umm.edu/neurosciences/neuro_infect.html

Evoluie manifestri clinice acute (meninigite purulente, listerioza SNC, encefalita

herpetica, etc.)

manifestri clinice subacute (abces cerebral, encefalita focal, neuroborelioza, neurosifilisul, meningita tuberculoas, neurobruceloza,

actinomicoza, etc.)

manifestri clinice cronice (meningita tuberculoas, neurosifilisul, neuroborelioza, boala Creutzfeldt-Jakob, etc.)

Epidemiologie sporadice

endemice

epidemice

Manifestri clinice

meningita i encefalita apar rar n forma pur examenul LCR stabileste diagnosticul

manifestri specifice grupelor de pacieni: nou-nscuii: agitaie, abandonarea suptului, febr sau hipotermie, agitaie,

tulburare de ritm respirator, crize epileptice, bombare de fontanel

btrnii: febr, tulburri de comportament, sindrom confuzional, crize eplieptice, astenie, alterarea strii de constien pn la com

imunodeprimaii: febr, cefalee, redoare de ceaf, somnolen + semnele afeciunii de baz

Sindromul meningeal

febr sever cefalee intratabil / durere radicular fotofobie / fonofobie grea / vrsturi alterarea strii de constien redoare de ceaf / durere la flexia capului (iritarea

leptomeningelui) postura in hiperextensie / opistotonus semn Kernig: rezistena la ridicarea membrului inferior cu

genunchiul in extensie semn Brudzinski: flexia involuntara a membrelor inferioare

produsa de flectarea capului

Sindromul encefalitic

cefalee febr crize epileptice (adesea focale) semne focale neurologice (deficite n sfera nn.

cranieni III, IV, VI, VII, afazie, hemiparez, piramidalitate, hemianopsie, ataxie, coreoatetoz)

tulburri de comportament alterarea strii de constien (agitaie, iritabilitate,

confuzie, somnolen, letargie, com) semnele neurologice pot fi precedate de:

mialgii/artralgii, subfebr, stare de prostraie

Encefalita - forme speciale cerebelita acut (infecii virale: varicella-zoster, EB,

rubeolos, gripal, CMV, echo, coxsakie, HSV mai ales la copii) ataxie, astazo-abazie

encefalita de trunchi cerebral oftamoplegie, parez facial, dizartrie, disfagie, ataxie, hipoacuzie

rar: encefalite bacteriene (Legionella, TBC, Listeria, Brucella)

Sindromul mielitic

durere local sever paraparez (tetraparez) parestezii tulburri sfincteriene (retenie acut / incontinena

prin preaplin) nivel de sensibilitate instalare a deficitelor n ore (acut) sau zile (subacut)

diferite sindroame n funcie de localizarea leziunii

Mielita transvers exemplu RMN

www.uiowa.edu

CLASIFICAREA MIELITELOR MIELITE VIRALE

enterovirusuri v. varicelo-zosterian HIV v. EB, CMV, HSV v. rabic v. gripal japonez HTLV-1

MIELITE INFLAMATORII NON-INFECIOASE

mielita postinfecioas i postvaccinal SM mielita necrozant subacut mielopatia LES i din alte vasculite mielopatia i poliomielita

paraneoplazic

MIELITE SECUNDARE BOLILOR BACTERIENE, FUNGICE, PARAZITARE SI GRANULOMATOASE

Mycoplasma pneumoniae B. Lyme mielite piogenice

abcesul epidural acut si granulomul epidural

abcesul spinal mielita TBC

morbul Pott meningomielita TBC tuberculomul medular

infecii parazitare i fungice mielita sifilitic

meningoradiculita cronic (tabes dorsalis)

meningomielita cronic sifilisul meningo-vascular meningita gomatoas pahimeningita spinal cronic mielita sarcoidotic

PATOGENEZA

Germenii patogeni pot ajunge la nivelul SNC

extensie local de la un focar infecios apropiat cale venoas (sinuzita, mastoidita cel mai frecvent infectii otice)

traumatism local prin nsmnare hematogen de la un focar la distan abilitatea de a disemina hematogen depinde de

virulena germenilor Imunocompetena gazdei

diferite ci de a depi BHE

centripet de-a lungul nervilor cranieni sau periferici (ex. HSV, v. varicelo-zosterian, v. rabic)

endocitoz (Neisseria meningitiditis) transport intracelular (P. falciparum via hematii, T.

gondii via macrofage) invazie intracelular (H. influenzae) pot ajunge n spaiul subarahnoidian pe la nivelul

plexului coroid, sinusurilor venoase sau plcii cribriforme

la nivelul spaiilor subarahonidiene - rspuns inflamator (eliberare de factori ai complementului, citokine, influx de leucocite si macrofage, activarea microgliilor si astrocitelor) componenta encefalitic a sindromului meningeal

alterarea integrittii BHE influx de lichide si proteine de-a lungul endoteliului vascular i n interiorul SNC, declannd edemul cerebral vasogen HIC

leziuni cerebrale ischemice, metabolice, hipoxice necroza focal, infarct cerebral

INFECTII BACTERIENE

MECANISME PATOGENICE N MENINGITELE BACTERIENE

1. INFLAMATIA MENINGEAL ACUT arahnoidita pura encefalopatia subpiala afectarea inflamatorie / vasculara a rr. nn. cranieni tromboza vv. meningeale epidurita, plexita coroidal hernie de esut cerebral

1. MENINGITE SUBACUTE SI CRONICE hidrocefalie hipertensiv infiltrare subdural (sd. HIC + tablou infecios) infarcte extensive arteriale si venoase

1. SECHELE fibroza meningeala (arahnoidita opto-chiasmatica, meningo-mielita) meningo-encefalita cronica cu hidrocefalie hidrocefalia persistenta a copilului

ETIOLOGIA MENINGITELOR BACTERIENE

Germen patogen Pneumococ (S. pneumoniae)

Meningococ (N. meningitidis)

H. influenzae

Listeria

Stafilococul auriu

M. tuberculosis

Poarta de intrare mucoasa nazala/faringeala, TCC,

neurochirurgie, drenaj LCR

nazofaringe

nazofaringe

tract gastrointestinal

endocardita, TCC, drenaj LCR, punctie lombara, tract urinar

TBC extracerebral

Examenul LCR n meningitele bacteriene

esenial pentru diagnostic pleiocitoz 1.000-10.000 neutrofile 90%, cu timpul

creste procentul de mononucleare presiune LCR crescuta LCR turbulent, purulent hipeproteinorahie (100-500 mg/dl) glicorahie scazut (sub 40 mg/dl) coloratii Gram din sedimentul LCR culturi din LCR, antibiograma ELISA, RIA, contraimunoelectroforeza, PCR

TRATAMENTUL MENINGITELOR BACTERIENE

penicilina G, ampicilina, cefalosporinele nu trec BHE indemna dar trec BHE cu inflamaie

vancomicina

cloramfenicol trece BHE pericol de aplazie medular - de rezerva

Meningita purulent

ABCESUL CEREBRAL (I)

debuteaz ca o cerebrit (faza encefalitic) apoi stadiul de abcedare (regiune ncapsulat de necroz purulent cu edem perifocal)

diseminare a germenilor patogeni local (mastoidit, otit medie, sinuzit, osteomielit)

localizare temporal cel mai frecvent nsamnare la distan (endocardit, pneumonie, infecie

dentar, diverticulit, pacieni cu malformaii cardiace severe tetralogie Fallot, fistule AV pulmonare) eventual embolii multiple tablou clinic de encefalit la pacient cu endocardit

inoculare direct (traum, intervenie neurochirurgical)

ABCESUL CEREBRAL (II)

Manifestari clinice: cefalee great, vrsturi febr alterarea strii de contien crize epileptice focale / generalizate redoare de ceaf semne neurologice focale

Diagnostic: RMN/CT cerebral confirmare prin culturi din LCR

Tratament: antibiotic chirurgical de luat in considerare la cele unice si superficiale

ABCES CEREBRAL -CT

ABCESE CEREBRALE IRM

www.ispub.com/journal

T1 cu contrast

Stafilococ auriu BK

ALTE TIPURI DE ABCESE

subdural (glicorahia scazut) peridural (LCR poate fi normal) complicaii ale meningitelor purulente sau post

TCC

abces medular: paraparez la un pacient cu focar infecios

Neuroborelioza (boala Lyme)

Patogeneza:

B. burgdorferi transmis prin capue (Ixodex ricinus) probabilitatea infeciei e mic (1-2% din oamenii mucai se infecteaz) incubaie 3-30 de zile afeciunea are 3 stadii

Manifestari clinice:

stadiul I (infecia localizat): 90% din pts dezvoltmacul sau papul eritematoas nedureroas - treptat se deplaseaz de la locul iniial form inelar erythema chronicum migrans

+ diseminare patogen (febr, astenie, artralgii, mialgii, alte sindroame algice + mai rar adenopatii regionale sau generalizate;

toate aceste semne dispar spontan

Manifestri clinice: stadiul II (infecia diseminat): 10-15% dezvolt simptome

generale (astenie, anorexie, artralgii, mialgii, cefalee, subfebr, discret opoziie a cefei)

+ manifestri cardiace (miocardita, pericardita, bloc AV)

+ manifestari neurologice ( pareze de nn. cranieni, poliradiculitdureroas, meningit limfocitar, dureri radiculare importante, deficite neurologice variate motorii, senzitive, atrofie muscular)

+ meningita Lyme (cefalee moderata, durere cervicala), LCR cu pleiocitoza mononucleara, hiperproteinorahie, glicorahie normala

+ rar encefalita (deficite neurologice focale, tulburare de concentrare, modificari de personalitate, depresie), RMN leziuni de substan alb)

stadiul III (infecia persistent) - rar - latena 1-17 ani(neuroborelioza cronic, encefalomielita Lyme)

deficite neurologice ataxie, pareze de nn cranieni, para/tetraparez, incontinen urinar, encefalopatie (tulburri de concentrare si memorie, insomnie, astenie, depresie) + miozit + vasculit cerebral + acrodermatita cronic atrofic

Boala Lyme Diagnostic

lipsa anamnezei muscaturii de capu (?!) eritemul cronic migrator e un semn clinic relativ constant confirmarea infeciei prin ELISA sau culturi, PCR examenul LCR: meningita limfocitar

Tratament Ceftriaxona sau cefotaxim (Rocephine) pt 2-3 sptmni

Mycoplasma pneumoniae determin o meningoencefalit sever sindrom cerebral, cerebelos, de trunchi cerebral sau

spinal n timpul sau dup pneumonie/traheobronit cu

mycoplasma coreoatetoz, convulsii, delir, hemipareza, edem

cerebral encefalomielit postinfecioas sau leucoencefalit

hemoragic (mecanism direct sau mediat imun) LCR clar, pleiocitoza limfocitar moderat,

proteinorahie moderat crescut, glicorahie normala sau moderat scazut

tratament: eritromicina sau tetraciclina

Neuroinfecia tuberculoas forme: meningita (meningita bazala tipica),

meningoencefalita, tuberculom cerebral (semn de focar), mielita, mieloradiculita, arahnoidita opto-chiasmatica

factori de risc: istoric de TBC, alcoolism, terapie cortizonica, HIV, imunodepresie, arie endemica

nsmnare n parenchimul cerebral prin microtuberculi i n LCR, la nivelul arahnoidei

proteinorahie foarte crescut, fibrina foarte crecuta in LCR (semnul vlului!)

Neuroinfecia tuberculoas

simptome: febr, sindrom confuzional, cefalee, redoare de ceaf, debut insidios, pe parcursul a 2 sptmni

histopatologic: exudat n spaiul subarahnoidian, bazal, cu meningoencefalit bazal, neuropatii de nervi cranieni, arterite, posibil tromboze, obstrucia cisternelor bazale, posibil hidrocefalie

prognostic: 10-33% (!) din pts mor in ciuda tratamentului

tratament 3-4 tuberculostatice (hidrazida, rifampicina, pirazinamida, etambutol) nu streptomicina (nu trece BHE)

http://www.granuloma.homestead.com/TB_extrapulmonary_gross.html

Sag. T1 & T2 WI: florid lumbosacral tuberculosis (Pott's disease) with epidural and sacral abscesses

Neurosifilisul Patogeneza: Treponema pallidum trei stadii

Perioada asimptomatica (luni - ani = sifilis latent), apoi apar manifestari clinice, cum ar fi goma (tegument, oase, rinichi, ficat) leziuni cardiovasculare (anevrism de aorta)

Manifestri clinice: TP poate invada SN n orice stadiu al bolii, fr s genereze

neaprat simptome Meningita precoce rar - deficite n sfera nervilor cranieni

(n.VIII surditate brusc instalat, n.VII pareza faciala, n. II AV) LCR pleiocitoz limfocitar (100-400 celule/microlitru) i hiperproteinorahie

Meningita asimptomatic de obicei - modificari LCR fr sindrom meningeal

Sifilisul meningo-vascular cefalee, tulburri de AV, vertij 5-12 ani de la infecia initial vasculita duce la AVC multiple ischemice, mai ales n teritoriul ACM i a vaselor mici perforante + afectare de nn cranieni (VIII, VII, V) + hidrocefalie + modificri de personalitate, crize epileptice, semne de suferin medular (paraparez, sindrom medular anterior, incontinen urinar) VDRL pozitiv n LCR

Paralizia progresiv meningoencefalita cronic cu paralizie progresiva la 10-25 de ani de la infectare demen, tulburri mnestice, de personalitate, dizartrie, disfazie, tremor, apraxie, tulburri de mers, incontinen urinar, RFM abolit (pupile Argyll-Robertson)

Tabes dorsalis complicaie meningo-vascular tardiv 25-30 de ani de la infecie manifestri oculare (strabism, modificari pupilare, atrofie papilara), sindrom hiperalgic (dureri lancinante n membrele inferioare, tulburri de mers (deficit de propriocepie), disfuncie autonom (impoten, incontinen urinar), deformri articulare

Tratament: penicilin

Cerebral atrophy, most prominent in frontal lobes seen in general paresis (a form of neurosyphilis).

medic.med.uth.tmc.edu/ edprog/Path/InfDis.htm

Cross section of spinal cord showing Wallerian degeneration of the dorsal or posterior columns that is seen in Tabes dorsalis (a form of

neurosyphilis)

medic.med.uth.tmc.edu/ edprog/Path/InfDis.htm

INFECII VIRALE

TIPURI DE NEUROINFECII VIRALE

MENINGITE (LCR clar !) ENCEFALITE

MIELITE MIELORADICULITE ENCEFALOMIELITE

primare (cale direct tropism pentru SN) secundare (focar la distan, mediate imun)

Tipuri de virusuri: -arbo, -entero, varicelo-zosterian, HSV, EB, gripale, v. rabic)

Examenul LCR n meningita viral pleiocitoz (mononucleare) (zeci-sute) discret proteinorahie (50-100 mg/dl) glicorahie normal LCR- ap de stnc

Alte cauze de meningite aseptice: meningita tuberculoasa (glicorahie scazut, proteinorahie

crescuta) meningita carcinomatoas meningita Lyme meningita din vasculite i boli granulomatoase

ENCEFALITA HERPETIC

Patogeneza

HSV1 n copilarie leziuni ale mucoasei orale gg. trigeminal acces centripet SNC dormant reactivare

(imunodepresie, afectiuni febrile, UV) herpes labial, keratoconjunctivit, encefalit (NC I i V) nu exista

asociere intre herpes labial si encefalit

HSV2 gg. lombosacrai prin transport axonal de la nivelul infeciei uro-genitale (posibil asimptomatic)

la adult meningit aseptic, poliradiculit, mielit la nou nascut encefalit

encefalita HSV1 extrem de rar la nou-nascuti, encefalita HSV2 exterm de rar la aduli

Semiologie

inflamaia prilor mediale i caudale ale lobilor temporali i frontali

prodrom: febr, cefalee, grea, anorexie, letargie cteva zile simptome focale: halucinaii olfactive / gustative, afazie,

tulburri de comportament (confuzie/psihoz), crize epileptice focale sau partiale complexe cu generalizare secundara, HIC (cu alterarea contienei pn la coma), redoare de ceaf, sindrom piramidal

ex LCR: pleiocitoz limfomonocitar, hiperproteinorahie moderat, glicorahie normal, uneori xantocromie sau eritrocite numeroase (encefalita necrozant hemoragic), PCR

EEG: unde ascutite, hipervoltate periodice si complexe de unde lente cu frecventa de 2-3 Hz, focal sau difuz, mai ales la nivel temporal

CT normal sau hipodensitate discreta temporo-bazala fara captare de contrast

RMN T2 hiperintensitate precoce

Tratament aciclovir injectabil 10 mg/kgc x 3/zi 2-3 sptmni esenial administrarea ct mai precoce anticonvulsivante

ENCEFALITA HERPETICA

INFECIA CU HIV

nu exist pacient n stadiul de SIDA care s nu aib afectare neurologic

afectare neurologic: generat de HIV generat de infectii cu agenti patogeni oportuniti de la encefalita la poliradiculonevrit poate mima orice

afectiune neurologic encefalopatia HIV mecanismul patogenic nu este

direct HIV modific sinteza proteic apare sinteza unei

peptide la nivelul esutului cerebral care se comport ca un agonist de receptor NMDA apare neuroexcitotoxicitate prin fals neurotransmitor

COMPLICAII NEUROLOGICE IN INFECTIA CU HIV-1 (I)

1. CEREBRALE

Predominant non-focale

complexul SIDA-demen

encefalita acuta HIV encefalita cu CMV encefalita cu v. varicelo-

zosterian encefalopatii metabolice

Predominant focale toxoplasmoza cerebral limfomul primar SNC leucoencefalita multifocala

progresiva (LEMP) criptococoza abces / tuberculom

cerebral neurosifilisul tulburri vasculare

endocardita nonbacterian si hemoragia cerebral asociate cu trombocitopenia

COMPLICAII NEUROLOGICE N INFECIA CU HIV-1 (II)

2. MEDULARE

mielopatia vacuolar mielita cu HSV sau zosterian

3. MENINGEALE

meningita aseptic (HIV) meningita criptococozic meningita TBC meningita sifilitic meningita limfomatoasa metastatic

COMPLICATII NEUROLOGICE IN INFECTIA CU HIV-1 (III)

4. RDCINI SI NERVI PERIFERICI

sunt infecioase (HIV, v. varicelo-zosterian, CMV) forme:

polineuropatia acut i cronic HIV poliradiculopatia lombar cu CMV mononevrita multiplex polineuropatie demielinizant senzitivo-motorie polineuropatia senzitiv dureroas distal

5. MUSCULARE

polimiozit i alte miopatii (induse inclusiv de medicamente)

Figure 1. HIV encephalitis in a 35 year-old man. Hyperintense lesions are noted on this conventional spin-echo T2WI, located in the periventricular white matter and centrum semiovale, with relative sparing of the subcortical (arcuate) U-fibers. The lesions are "fluffy" or "cotton-like" and poorly circumscribed, showing confluence and a diffuse appearance. Cortical atrophy is apparent as indicated by enlargement of the subarachnoid spaces (cortical sulci) and lateral ventricles. The central atrophy is especially prominent. The white matter lesions were poorly appreciated on T1WI (not shown) and non-enhancing (not shown). There is no associated mass effect.

Rohit Bakshi Buffalo Neuroimaging

Analysis Center, University at Buffalo, State University of New York, Buffalo, NY

Figure 2. Toxoplasmosis in a 44-year-old man with AIDS and a CD4 count of 91 presenting with several days of generalized weakness, malaise, fever, headaches, and new onset seizures. Serial studies are shown before and after antibiotic therapy (adapted in part from reference 7). (A-C) Initial scans, pre-treatment. Edematous lesions appear centrally hypodense on CT (A) and centrally isointense to hypointense on T1WI (B) and hypointense to markedly hyperintense on T2WI (C), exerting moderate to severe mass effect. Severe surrounding edema is noted which is much larger than the size of the lesions. On T2WI (C), a central and concentric hypointense core gives a "target" appearance to the lesions. A third subtle lesion is apparent on T2WI in the thalamus (C). Note the relatively poor sensitivity of CT vs. MRI for the lesions in the left hemisphere. After contrast administration on both CT (A) and MRI (B), avid ringlike and nodular enhancement is noted. (D) T2WI shows marked improvement in each of the lesions 2 weeks after the completion of anti-toxoplasmosis medical therapy.

Figure 3. Primary CNS lymphoma in two patients with AIDS. Adapted from reference 7. A-B. 24 year-old man with AIDS and hemiparesis, headaches and visual symptoms. Postcontrast T1WI (A) FLAIR (B) and T2WI (Figure 4) show a solitary large ring-enhancing lesion with mild mass effect and moderate vasogenic edema. The hypointensity of the lesion on T2WI (Figure 4) is characteristic of lymphoma. Note that the mass effect and edema is less than expected given the size of the lesion, as is typical for primary brain lymphoma while much more edema and mass effect vs. lesion size is expected in toxoplasmosis (Figure 2). C-D. 30 year-old man with AIDS. Postcontrast T1WI (C) and T2WI (D) show left temporal lobe vasogenic edema, related to a temporal lobe mass lesion (not shown). There are also bilateral lesions in the caudate nuclei on T2WI (D), with periventricular and ependymal extension of enhancement on the right (C). The ependymal spread is characteristic of primary CNS lymphoma.

Figure 5. Progressive multifocal leukoencephalopathy (PML) in 3 patients illustrate typical findings, including lesions that are markedly hypodense on CT (A), and hyperintense on FLAIR (B) and T2WI (C). As is characteristic of PML, lesions were markedly hypointense on T1WI and non-enhancing (not shown). Lesions follow the gray-white interface and prominently involve the subcortical U-fibers, while sparing the cortical ribbon, causing a "scalloped" or "heart of the gyrus" appearance.

Figure 6. Aspergillus cerebritis: serial non-contrast CT in a fatal case. Bilateral intermixed hypodense and hyperdense lesions are seen in the bilateral frontal, parietal and occipital lobes. Hyperdense areas represent hemorrhage. Hypodense areas represent varying degrees of ischemia/infarction, cerebritis, and edema. The two scans are separated by three days. A. Original scan. Note that the repeat CT (B) shows the emergence of diffuse brain edema (note loss of sulcal and gray/white definition). Autopsy revealed systemic and multiorgan aspergillus infection with multiple brain abscesses, angioinvasion and hemorrhage.

Figure 7. Cryptococcal brain infection. T2WI of a 33 year-old woman with AIDS shows multiple tiny bilateral hyperintense lesions in the caudate and putamen. These lesions represent mucoid material secreted by the fungal organisms.

Figure 8. Tuberculosis of the brain with cerebritis and tuberculoma formation. MRI scans of a patient are shown including post-contrast T1WI (A) and T2WI (B). Heterogeneous lesions are seen in the frontal and parietal region, involving both cortical and subcortical areas. The intermixed hypointensities on T2WI most likely represent hypercellularity, free radicals, or both. Postcontrast axial T1WI shows parenchymal and leptomeningeal enhancement, representing both meningitis and sub-pial extension.

BOLILE PRIONICE

encefalopatii spongiforme transmisibile

se transmit la oameni prin esut infectat sau instrumente chirurgicale infectate particule proteinacee (prioni) mutaii la nivelul proteinei prionice (PrP) cazuri cu transmitere genetic

PrP normala (PrPc) dup sintez transportat la nivelul membranei celulare i apoi returnat intracelular prin endocitoz lizat de proteaze o alt fraciune napoi n mb celular funcie fiziologic nc necunoscut protein ubicuitar, abundent n neuroni

gena PrNP cr. 20 mutaii cazuri genetice (PrP)

PrPsc forma mutant encefalopatie spongiform infecioas induce conversia PrP la PrPsc

PrPsc ajunge n SNC pe cale axonal retrograd sau pe cale limfocitar

PrPsc i PrP nu pot fi lizate de ctre proteazele intracelulare i se acumuleaz intracelular modificri neuropatologice, moarte neuronal

CJD boala Gerstmann-Straussler-Scheinker insomnia fatal familial

CJD(Creutzfeldt Jakob)

incidena 1/ 10

6

aduli, 60 de ani 90% sporadice, 10% familiale, foarte rare iatrogenice progres rapid, 4-12 luni deces precoce: astenie, vertij, tulburare cognitiva, anxietate,

insomnie, halucinaii, apatie, depresie demen rapid progresiv, mioclonii, rigiditate, atrofie,

fasciculaii, ataxie cerebeloas, tulburri de AV tardiv: mutism akinetic, mioclonii severe, crize

epileptice, disfuncie autonom

EEG: complexe periodice bifazice sau trifazice de unde ascutite 1Hz

CT atrofie corticala RMN T2 hiperintensitate la nivelul gg bazali LCR: enolaza neuron-specific, S100, tau, 14-3-

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NEUROINFECIISINDROAMESlide 3Slide 4Slide 5Slide 6Slide 7Slide 8Encefalita - forme specialeSlide 10Mielita transvers exemplu RMNCLASIFICAREA MIELITELORPATOGENEZASlide 14Slide 15INFECTII BACTERIENEMECANISME PATOGENICE N MENINGITELE BACTERIENEETIOLOGIA MENINGITELOR BACTERIENEExamenul LCR n meningitele bacterieneSlide 20TRATAMENTUL MENINGITELOR BACTERIENESlide 22ABCESUL CEREBRAL (I)ABCESUL CEREBRAL (II)ABCES CEREBRAL -CTABCESE CEREBRALE IRMALTE TIPURI DE ABCESENeuroborelioza (boala Lyme)Manifestari clinice: Manifestri clinice:Slide 31Boala LymeMycoplasma pneumoniaeNeuroinfecia tuberculoasSlide 35http://www.granuloma.homestead.com/TB_extrapulmonary_gross.htmlSag. T1 & T2 WI: florid lumbosacral tuberculosis (Pott's disease) with epidural and sacral abscessesNeurosifilisulSlide 39Slide 40Cerebral atrophy, most prominent in frontal lobes seen in general paresis (a form of neurosyphilis).Cross section of spinal cord showing Wallerian degeneration of the dorsal or posterior columns that is seen in Tabes dorsalis (a form of neurosyphilis)INFECII VIRALETIPURI DE NEUROINFECII VIRALEExamenul LCR n meningita viralENCEFALITA HERPETICSlide 47Slide 48ENCEFALITA HERPETICAINFECIA CU HIVCOMPLICAII NEUROLOGICE IN INFECTIA CU HIV-1 (I)COMPLICAII NEUROLOGICE N INFECIA CU HIV-1 (II)COMPLICATII NEUROLOGICE IN INFECTIA CU HIV-1 (III)Figure 1. HIV encephalitis in a 35 year-old man. Hyperintense lesions are noted on this conventional spin-echo T2WI, located in the periventricular white matter and centrum semiovale, with relative sparing of the subcortical (arcuate) U-fibers. The lesions are "fluffy" or "cotton-like" and poorly circumscribed, showing confluence and a diffuse appearance. Cortical atrophy is apparent as indicated by enlargement of the subarachnoid spaces (cortical sulci) and lateral ventricles. The central atrophy is especially prominent. The white matter lesions were poorly appreciated on T1WI (not shown) and non-enhancing (not shown). There is no associated mass effect. Slide 55Slide 56Slide 57Slide 58Slide 59Slide 60BOLILE PRIONICESlide 62Slide 63CJD (Creutzfeldt Jakob)Slide 65

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