Dynamics

•acute •monophasic•biphasic

•subacute•fluctuating

•chronic•intermittent•progressive

Localization

•meningitis•encephalitis•abscess•epidural empyema•sinus thrombophlebitis

Inflammations of the nervous system

Pathology

1. Meningeal infiltration2. Blood-brain barrier damage

• perivascular cellular infiltration• extracellular edema

3. Glial proliferation4. Damage of the nervous tissue(neuron, axon, oligodendroglia, myelin sheath)

The routes of infection

1. Hematogen (abscess)

2. Paranasal sinuses (meningitis)

3. Respiratory tract (nose, lung) (meningo-encephalitis)

4. Scull fracture (abscess, epidural empyema, meningitis)

5. Peripheral nerve (rabies, HSV, VZV)

MENINGITIS

Pathology

•Cellular infiltration of the meningxes•Brain parenchyma is intact, except edema and radicular/cranial nerve lesions

Clinical picture : ("Meningeal syndrome”)

• general symptoms (fever, weakness)• signs of meningeal irritation (nuchal rigidity, Kernig-, Brudzinsky signs, headache, hyperirritability)• changes in mental status (apathy, somnolence, delirium)• focal neurological signs are absent • "CSF syndrome" (increased cell&protein)

Acute aseptic meningitis

Pathogens : •virus

HERPES (HSV, HZV, EBV, CMV), ENTERO (echo, coxaci, polio, etc.), ARBO (tick-bite encephalitis virus), ADENO, LCMV, HIV, etc.

•spirochete (leptospira, borrelia, treponema)

Clinical pictureIncubation 7-10 day, "dromedary" course

CSF: •cell count 50-1000/ul, lymphocytes•protein level moderately elevated (0.4-lg/1)•sugar: normal•microbiol. culture: negative Dg: serology (repeated)

Others :EEG, neuroimaging: usually normal

Therapy : supportive

Subacute/chronic meningitis

Pathogens : •mycobacterium, mycoplasma •fungus (candida, cryptococcus, aspergillus)•spirochete (leptospira, borrelia)•virus (LCMV)•toxoplasma•non-infective (leukemia, SLE, tumour cells)

Clinical picture (weeks-months)intermittent febrile states slowly progressive mental changes, mild (or absent) meningeal signs, progressive cranial nerve palsies

CSF: •50-100/ul cells, lymphocytes•high protein level - 1-3 g/1 (severe BBB damage)•low sugar level (>2 mmol/l)

Dg: need special culture technique, serology

Therapy : for tbc: Isonicid, Rifampycin, Dexamethason. for fungus: Amphotericin B

Purulent meningitis

Pathogens : •adult: Pnemococcus, N. meningitidis, •child: Hemophylus, Enterobacteria

Clinical picture :primary extracranial manifestation (lung, paranasal)severe condition, high fever, prominent meningeal signs, confusion (high mortality !) residual signs (hydrocephalus, hypacusis, ment. retard., epileptic seizures)

CSF: green-like•1000 to several 10,000 cells/ul, granulocytes •high protein level (1-3 g/1)•low sugarDg: microbiol. cultureOther : eradication of the (respiratory) sourceEEG: generalized slowing CT/MRI: look for "pus-cap”, brain abscess, hydrocephalusTherapy : based on the culture. Before:Penicillin + Ampicillin + Ceftriaxon iv., in severe cases + Dexamethason (Steptokinaze)

„Covered syndrome”

(pretreated/masked form of purulent meningitis)

Clinical pictureheadache, intermittent febrile state, butno prominent meningeal signs antibiotic therapy in the recent history

CSF•no more than 1000 cells, granulocytes/mixed•protein elevated >1 g/l•sugar: decreased•negative culture result

Diagnosis based on CSF findings

Therapy should be the same as in acute purulent meningitis (combined antibiotics)

Brain abscess

Etiol. : direct or haematogenic spreading Clinical picture : focal signs, seizures, rised intracranial pressureDg: CT, MRITH: antibiotics, surgical

ENCEPHALITIS

Pathology :

Blood-brain barrier damage+Central nervous system damage

Clinically : "Encephalitis syndrome"

meningeal syndrome +neurological signs (focal signs of motor-, sensory, autonomic systems, sings of inreased intracranial pressure)seizuresaltered mental state

EEG, MRI, CSF alterations

Polio- leuko- panencephalitis

Polioencephalitis:

Herpes simplex encephalitis•Clinical: primary [subclinical] infection with HSV-1, endogenous reactivation,• flu-like phase followed by encephalitis located to temporal lobe (aphasia, paresis, seizures, psychoorganic syndrome). •Dg: CSF, EEG, MRI, biopsy (PCR), serology. •Treatment with Acyclovir 30mg/bwkg a day for weeks

Tick-born encephalitis•Clinical: tick bite, •flu-like illness followed by meningitis or encephalitis syndrome, predilection for cervical spinal cord motoneurons and temporal lobe•Dg: typical CSF findings, serology•TH: supportive

HSV

Acute anterior poliomyelitisClinical: gastrointestinal infection, viraemia followed by asymmetric flaccid paresis, predilection for large motoneurons in spinal cord and brainstem, Dg: typical CSF findings, Treatment : supportive, prevention with peroral immunization)

Lyssa, rabiesClinical: transmitted by bite of an rabid animal {small predators}, week to months of incubation period, Stages: 1. Prodrome (fever, fatigue) 2. Excitation (restlessness, hyperirritability, convulsions, 3. Paralytic phase (widespread paresis, death)Dg. Pathology (Negri-body in hippocampus), CSF, preventive immunization)

CMV

Negri

Leukoencephalitis

Pathology: immune demyelination Clinical picture: acute/subacute, monophasic disease with widespread white matter lesion, typical CSF (BBB damage +OB)

•parainfectious encephalomyelitis(measles, rubella, varicella, smallpox, mumps, infectious mononucleosis)

•postvaccination encephalomyelitis(vaccination against smallpox, measles, rabies, tetanus)

Panencephalitis

(„slow virus” diseases, progressive course)

•SSPE (subacute sclerotising panencephalitis)

•CJD (Kreutzfeld-Jakob disease)

•PML (progressive multifocal leuko-encephalopathy)

SSPE

Pathogenesis :

childhood infection with measles virusreactivation of "defective" virus (5-10y),

Clinical picture

no general signs, young patients, progressive dementia (impaired cognitive performance in school), ataxia, myoclonic jerks, decerebration, death

EEG: generalized slow waves (Rademecker complex) in every 3-10 sec.

CSF: OB, high anti-measles Ab's

Th: symptomatic

CJD

Etiology :

Prion (sporadic, iatrogenic, familial)

Clinical picture

Onset: 35-65 y, personality changes, progressive dementia within few months, extrapyramidal signs, ataxia, dysarthria, myoclonus, death within a years

EEG: triphasic slow complexes, 1-2 cps

CSF: unremarcable

Dg: clinical picture, (brain biopsy)

Th: symptomatic

GSS

(Gertsmann-Straussler-Scheinker disease)

AD inheritanceOnset: 40-50 y, duration 1-10 yClin.: spinocerebellar degen. + dementia

FFI

(Fatal familial insomnia)

Degen. of the medial nucleus of thalamus

Clin: lack of sleep + vegetative disturbances

Dg: clinical + EEG/polysomnography

PML

(progressive multifocal leukoencephalopathy)

Immunsuppression (HIV, cytostatics, leukemia, malignancies)

Mechanism : JC papova virus causes oligodendroglia degeneration

Clinical picture : subacute onset, changing in personality, pramidal signs, ataxia, dementia, death within a few months

CSF: unremarkable

MRI: demyelination (confluent, no enhancement)

Dg: brain biopsy

Th: stop immunsuppression, symptomatic

Neurosyphilis

Pathogen : treponema pallidum

Primer genital infection followed by hematogenous spreading

Forms :

1. Luetic meningitis (early)

2. Meningovascular syphilis (months)

3. Paralysis progressiva (dementia, psychosis, several years)

4. Tabes dorsalis (spinal ataxia)

Dg: CSF, serology, MRI

Th: penicillin

NEUROBORRELIOSIS

EtiologySpirochetal (Borrelia burgdorferi) infection by bite of a vector insect (tick borne)Symptoms and signsRelapsing-remitting course with multiple organ affection: skin- ECM, heart-carditis, joints- mono-, polyarthritis, and CNS/PNS -neuroborreliosis

Stages•(acute) flu-Iike symptoms (headache, myalgia, ECM)•(subacute) meningitis, meningoradiculitis, mono-, polyneuritis (+arthritis, and sometimes carditis)•(chronic) meningo-encephalo-myelitis

NEUROBORRELIOSIS

Characteristic neurological forms:

•Diplegia facialis-most common form of neuritis caused by BB. (1-3 weeks)

•Bannwarth-Sy. (meningo-polyradiculitis, 1-3 months)

•Encephalomyelitis (ataxia, memory disturbances, fatigue, progressive pyramidal signs, disturbances of bladder functions, neuritis retrobulbaris, peripheral neuritis, tetraparesis, dementia)

MRI: focal white matter lesions

CSF: OB

Dg: Based on clinical picture + serology

Th:Prolonged course with high doses of antibiotics (Doxycyclin, Penicillin,Rocephin )

NEUROLOGICAL COMPLICATIONS OF AIDS

1. DISEASES WITH DIRECT RELATIONS TO HIV-1•Meningitis (acute, or chronic form)•Encephalopatia (= AIDS-dementia complex)•Myelopathy•Neuropathy -symmetric polyneuropathy

-mononeuritis multiplex•Myopathy (direct or due to treatment)

2. SECONDARY COMPLICATIONS•Opportunistic infections (CMV; Toxopl., Cryptococcus, PML, HSV, TBC)•Neoplasms (lymphoma, metastases, etc)•Cerebrovascular diseases (vasculitis)•Metabolic disorders (Wernicke, vitamin deficyency)

HIV