الفهرس يوجد فقط 14 صفحة متاحة للعرض العام
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المستخلص
Acute CNS infections are one of the commonest neurological emergencies. They have variable non specific presentations and wide differential diagnosis. For the many CNS infections that are treatable, prompt diagnosis and aggressive management afford the best chance of recovery without sequelae.
Acute viral CNS infections can present as acute viral meningitis (aseptic meningitis) that must be differentiated from non infectious causes of aseptic meningitis syndrome such as immune mediated diseases (e.g., Systemic Lupus Erythematosis), immunomodulating drug therapy, antibiotics (particularly sulpha containing compounds) and Mollaret meningitis. They also can present as acute viral encephalitis and acute viral myelitis.
CSF examination, neuroimaging and EEG often give non specific clues for the diagnosis of acute viral CNS infections. Specific diagnosis usually rests on PCR (not available and expensive), serology (in EBV and Arboviruses) and in many cases tissue biopsy and culture are needed. This causes that the treatment should be started empirically.
The common causative viruses include Enteroviruses (Polioviruses, Coxsakieviruses A and B and echoviruses) that commonly affect children and the severity of illness is related to immune status of the child. It causes commonly aseptic meningitis and less commonly encephalitis and encephalomyelitis. The only expected treatment is by Pleconaril and it shortens the duration of illness by 1-2 days.
Herpes simplex virus is the most common cause of sporadic fatal encephalitis. It affects all ages and specially affects the temporal lobes. It has to be differentiated from brain abscess, tuberculosis, cryptococcal infection and other viral infections such as Mumps virus and EBV. Spike and slow wave activity in the EEG has 84% sensitivity for diagnosis, however, PCR remains the diagnostic method of choice. The treatment of choice is Acyclovir for 14-21 days.
Varicella and Herpes zoster infections can be complicated by CNS involvement. Varicella occurs in children with the most common neurologic complication is cerebellar ataxia before, after or simultaneously with the rash. It is usually self limiting in 1 to 3 weeks with no treatment. Acyclovir is given in cases of encephalitis and aseptic meningitis.
Herpes zoster neurologic complications occur more often in immunocompomised patients with acute rash, before or even weeks to months later in the form of encephalitis or myelitis. The treatment is by Acyclovir.
CMV prevalence increased with HIV, It usually presents with subacute encephalitis that is difficult to be differentiated from HIV dementia. Treatment is by gancyclovir, foscarnet and cidofovir.
Neurologic complications of EBV are rare, occurring in less than 0.5% of cases. CNS symptoms may occur before, during or after infectious mononucleosis. The presentations include aseptic meningitis, acute hemiplegia, metamorphopsia and SIADH. The diagnosis depends on presence of heterophil antibodies at titer of more than 40 and atypical lymphocytes in serum and in CSF; also the presence of IgM to VCA indicates acute infection. The treatment is symptomatic.
Arboviruses affecting humans mostly presents with fever (may be saddleback), arthralgia and rash. They include St. Louis encephalitis virus which presents as aseptic meningitis especially in age more than 60 years in which it is more fatal and West Nile virus which presents with encephalitis more commonly than meningitis. Most of them present with psychiatric manifestations commonly misdiagnosed with acute psychiatric conditions. MRI picture of bilateral affection of basal ganglia and thalami suggests infection with Flaviviruses (SLE, JE, MVE, and WNV). This group of viruses is diagnosed by serology and responds to IFN- alpha, ribavirin and IV immunoglobulin.
Neurologic complications of mumps virus affect young male child between 4 and 7 years of age. Mumps meningitis presents with fever, vomiting and headache associated with parotiditis in 50% of patients. The main treatment is by supportive measures.
Rabies virus is transmitted by bite of infected animals or corneal transplantation, it presents after variable incubation period that can extend to up to years followed by non specific prodrome of constitutional symptoms followed by the more common furious form in which patient is markedly agitated and excited with hyDROPhobia. There is another less common form of ascending paralysis. Once diagnosed, there is no treatment, the condition is usually fatal. The most important step in the management of rabies is prevention which may be before exposure in high risk individuals with the vaccine or after exposure with rabies immunoglobulin in the wound simultaneously with rabies vaccine in the deltoid at 0 3 7 14 and 28 days of exposure. Recently there are trials to use monoclonal antibodies.
HIV can cause CNS infection directly in the form of acute meningitis, meningoencephalitis and acute myelitis or indirectly through opportunistic infections (Toxoplama, CMV, Cryptococci, subdural abscess and osteomylitis) or tumors (lymphoma, glioma and metastatic lymphoma). The diagnosis is by identifying viral p24 antigen in the blood and in 50% by isolation of HIV from CSF. Management includes antiretroviral chemotherapy and treatment of the causative organisms.
To establish bacterial CNS infections, pathogens must gain access either to subarachnoid space (in the case of meningitis) or to the brain parenchyma (in the case of brain abscess).
Acute bacterial meningitis in neonates is mostly due to Pseudomonous and Listeria monocytogenous while Haemophilus influenzae and Neisseria meningitides are major pathogens among children, meningitis in adults is primary caused by Meningococci and Pneumococci.
Neonates with meningitis may be hypothermic with no nuchal rigidity, in children nuchal rigidity occurs in 50% and in adults it carries poor prognosis. History of trauma is important as head trauma is the commonest cause of recurrent meningitis.
Acute bacterial meningitis should be differentiated from acute brain abscess, subdural empyema, acute epidural abscess and viral meningitis.
In CSF examination, glucose is less than 40 mg/dl in 58% with polymorphonuclear pleocytosis. Treatment is by empirical antibiotics according to age group and underlying conditions till culture results appear. Treatment of complications like increased intracranial pressure, seizures and subdural effusion is essential.
Brain abscess commonly occurs in the frontal lobe with most of the manifestations are due to expanding intracranial mass rather than infection. Brain abscess should be differentiated from glioblastoma, metastatic malignancy, subdural empyema and epidural abscess by MRI (especially diffusion weighted MRI). Treatment is medical with or without surgical intervention. Medical treatment is in the form of high dose broad spectrum intravenous antibiotics for at least 6-8 weeks. It is started empirically then according to the culture results. 2-3 months are added of oral antibiotics to prevent relapse.
Intracranial epidural abscess primarily results from otitis media and sinusitis with insidious onset. Patients present with fever, headache and scalp tenderness. MRI is superior on CT in showing intracranial epidural abscess. It is treated by surgical drainage and medical therapy.
Spinal epidural abscess is both a medical and a surgical emergency, its incidence increased due to increased use of spinal procedures and increased rate of intravenous drug abuse. It occurs more in lumbar and thoracic regions with back pain and tenderness on examination followed by root pain. It is diagnosed by contrast enhanced MRI. Treatment consists of decompression and drainage of abscess with parenteral antibiotic therapy.
Intracranial subdural empyema is more common in males (80% of cases) with two thirds of patients are aged 10-40 years. 10% of cases are infratentorial. Patient presents with fever, headache, altered level of consciousness and Jacksonian seizures. MRI with contrast is the study of choice. Treatment is by immediate surgical drainage.
Spinal subdural empyema is a rare condition. It most commonly occurs in thoracolumbar spine with absence of tenderness on the back. Treatment is by empirical antibiotic therapy with laminectomy followed by specific antibiotic therapy according to culture.
Suppurative intracranial phlebitis may be 1ry or 2ry to other intracranial infections such as subdural empyema. It can cause thrombosis in cavernous, superior saggital or lateral sinuses. Manifestations are usually of increased ICT, fits and localizing features according to the sinus affected. MRV is the modality of choice for diagnosis. Treatment is with empirical therapy directed towards gram +ve, gram –ve and anaerobes with early anticoagulation.
Host defenses are normally very effective in excluding fungi in the CNS but certain conditions can lead to failure of these defenses (head injury, corticosteroids, chemotherapy, AIDS and DM). They can affect immunocompetent patients (Cryptococci which are the most common cause of fungal meningitis, Histoplasma and Blastomyces) or immunocompromised patients (Aspergillus and Candida).
Clinical manifestations are usually non specific with subacute to chronic course and only few cases are acute including fever, headache, stiff neck and vomiting. Diagnosis rests on clinical suspicion and subsequent specific investigations including CSF mononuclear pleocytosis except in Aspergillosis in which there is polymorphonuclear leucocytes predominance. However, CSF may be normal in severe immunocompromised patients. India ink is diagnostic to identify encapsulated yeast of Cryptococci in CSF. Diagnosis can be aided by serological testing and PCR, definitive diagnosis is reached by tissue culture and biopsy. Treatment of Cryptococci, Candida, Histoplasma, and Blastomyces is by Amphotericin B plus 5-flucytosin then fluconazole with premedication with diphenhydramine before Amphotericin B. Amphotericin B is followed by kidney function, CBC and serum K. Asperigillus treatment is by Voriconazole. Prognosis depends on early diagnosis and treatment and correction of immunosuppressive state.
Fungal infection can also present as space occupying lesion either single due to direct spread or multiple lesions in grey and white matter interface due to heamatogenous spread. Definitive diagnosis is reached by investigating systemic manifestations of the disease; specific diagnosis of CNS infection is reached by biopsy. Treatment is by antifungal therapy according to organism plus surgery if indicated.
Toxoplasma is a protozoan that can infect CNS in both immunocompetent and immunocompromised hosts where in immunocompetent host it gives non specific manifestations with encephalitis with or without other organ failure. While in immunocompromised hosts it is more severe causing necrotizing encephalitis and forming abscesses mainly in basal ganglia, corticomedullary interface and thalamus.
The initial symptoms and signs may be focal including extrapyramidal symptoms or nonfocal like general weakness, confusion and personality changes. Acute infection is diagnosed by double-sandwich IgM ELISA and monoclonal antibodies to purified P30 parasite protein. In AIDS patients, multiple MRI lesions mean toxoplasmosis while single lesion means lymphoma. Also, Thallium 201 brain SPECT can differentiate between both by uptake (increased uptake in lymphoma and decreased uptake in toxoplasmosis). Definitive diagnosis of toxoplasmic encephalitis is by brain biopsy. The main treatment of toxoplasmic encephalitis is combination of pyrimethamine loading 200mg then 75mg per day oral for 3-6 weeks plus sulphadiazine 4-6 gm per day in 4 divided doses orally then pyrimethamine 50mg plus sulphadiazine 4gm daily, by trimethoprim-sulfamethoxazole (TMP-SMX) or by clindamycin 1.2gm IV/6hrs + pyrimethamine 75mg/day orally.
Primary prophylaxis in high risk patients with CD4 less than 200cells/mm3 and seropositivity for antitoxoplasma gondii by oral TMP-SMX of one double strength tablet/day.
CNS infection with free living and parasitic amoeba is rare but life threatening. Naegleria fowleri causes fatal primary amoebic meningoencephalitis initially causing change in taste or smell and progress to coma and death without development of focal neurologic signs. CSF is purulent with amoebic trophozoites. PCR, CSF culture and monoclonal antibodies are used in the diagnosis. Mortality is more than 95% yet treatment is tried with amphotrecin B and rifampicin. Entamoeba Histolytica causes brain abscesses in combination with hepatic and/or lung abscess in young men. They are multiple in BG, frontal and occipital lobes. It is diagnosed by identification of entamoeba histolytica trophozoites by periodic acid-stain in periphery of abscess. Treatment is by aspiration and drainage with metronidazole.
Acute helminthic CNS infections are caused by 2 major groups of helmithes. The first is Nematodes (Angiosrongyliasis, Gnathostomiasis, Strongyloidiasis and Toxocariasis). Manifestations are caused by larval migration and local host reactions, causing meningitis, encepahalitis and transverse myelitis with non specific systemic and CNS manifestations. Diagnosis is mainly by identifying the worm in brain tissue and by serology. Treatment is by albendazole 15mg/kg/day oral for 5 days for Gnathostomiasis and Toxocarisis, thiabendazole 25mg/kg twice daily for Strongyloidiasis while Angiostrongyliasis is self limiting.
The second group is Trematods including Paragonimiasis with 1% of patients developing cerebral Paragonimiasis causing epilepsy in 80% and meningitis in 10%. The most characteristic imaging finding is Conglomerate of ring enhancing grape like cysts in one cerebral hemisphere in C-T or MRI. Definitive diagnosis is by identifying parasite or ova in brain biopsy and by serology. Treatment is by praziquantel 25mg/kg, 3times/day for 2-3 days.