1. VIRAL ENCEPHALITIS
A range of viruses can cause encephalitis but only a minority of patients with viral encephalitis have a history of recent viral infection. In Europe, the most serious cause of viral encephalitis is herpes simplex type-1, which probably reaches the brain via the olfactory nerves. Herpes simplex type-2 usually cause v. meningitis.

2. Viruses that cause CNS infections:
Enteroviruses (echo, coxsackie, polio)
Mumps
Influenza
Herpes simplex type 1
Varicella zoster
Epstein-Barr
HIV
Lymphocytic choriomeningitis
HSV type 2 (Mollaret's meningitis)

3. Pathology
Inflammation can occur in the cortex, white matter, basal ganglia and brain stem, and the distribution of lesions varies with the type of virus. In herpes simplex encephalitis, the temporal lobes are usually primarily affected. Inclusion bodies may be present in the neurons and glial cells and there is an infiltration of polymorphonuclear cells in the perivascular space. There is neuronal degeneration and diffuse glial proliferation, often associated with cerebral oedema.

4. Clinical features
Viral encephalitis presents with acute onset of headache, fever, focal neurological signs (aphasia and/or hemiplegia) and seizures. Disturbance of consciousness ranging from drowsiness to deep coma supervenes early and may advance dramatically as in herpes simplex encephalitis. Signs of meningial irritation occurs in many patients but less than meningitis.

5. Investigations
1) CT of the head, which should precede lumbar puncture, may show low- density lesions in the temporal lobes in case of herpes simplex encephalitis.
2) MRI of brain is more sensitive in detecting early abnormalities.
3) The CSF usually contains excess lymphocytes. The protein content either normal or mildly elevated (<100mg/dl) but the glucose is normal. Opening pressure also either normal or mildly elevated. Occasionally , CSF is totally normal in 5 % of cases. Virological investigations of the CSF, including PCR for viral DNA, may reveal the causative organism but the initiation of treatment should not await this. Sensitivity & specifity of PCR vary according to the causative agent.
4) The EEG is usually abnormal in the early stages, especially in herpes simplex encephalitis, with characteristic periodic triphasic slow-wave activity at regular intervals of 2-3 sec. over one of or both temporal lobes.

6. MRI in herpes simples encephalitis show hypo intense area take enhancement on T1 (right fig.) within left temporal lobe , appear hyper intense in T2 (left fig.)

7. Example on triphasic rhythm (This figure for non-viral encephalitic case)

8. Management
Anticonvulsant treatment not given if no fit. But it is necessary if fit occur (usual story) & in this case usually should continue life long because we have permanent brain damage.
Raised intracranial pressure is treated with I.V dexamethasone mg/kg/day ÷ 4 for 4 days.
Herpes simplex encephalitis responds to Acyclovir (Zovirax)® 10 mg/kg i.v. 8-hrly each dose over 1 hr (each 7 mg of drug diluted in 1cc of fluid) for 2-3 weeks. This should be given early to all patients suspected of suffering from viral encephalitis.
Even with optimum treatment, mortality is 10-30% and significant proportions of survivors have residual epilepsy or cognitive impairment.

9. Polio Virus Infection
• It is caused by an RNA virus of the picornavirus group.
• The usual route of infection is fecal-oral
• incubation period varies between 5 and 35 days.

10. Clinical features:
• Neurologic involvement occur in small number of cases & here it follows a prodromal phase of fever, myalgia, malaise, and upper respiratory or gastrointestinal symptoms.
• The neurological involvement in the majority of cases may consist merely of aseptic meningitis but in some instances leads to weakness or paralysis.
• Weakness develops over the course of one or a few days, sometimes in association with recrudescence of fever, and is accompanied by myalgia and signs of meningeal irritation.
• The weakness is asymmetric in distribution and can be focal or unilateral.
• The bulbar and respiratory muscles may be affected either alone or in association with limb muscles.
• There are 4 forms of the disease: bulbar, pseudo bulbar, lateral amyotrophic, spinal muscular atrophy (anterior horn cell disease).
• Tone is reduced in the affected muscles, and tendon reflexes may be lost.
• There is no sensory deficit.

11. Diagnosis may be confirmed by virus isolation from the stool or nasopharyngeal secretions—and less commonly from the CSF.
L.P: C.S.F picture is that of viral encephalitis.

12. Management: Symptomatic; in the early stages, bed rest is imperative because exercise appears to worsen the paralysis or precipitate it. At the onset of respiratory difficulties, a tracheostomy and ventilation are required. Subsequent treatment is by physiotherapy and orthopaedic measures.

13. The postpolio syndrome is characterized by the occurrence some years after the original illness of increasing weakness in previously involved or seemingly uninvolved muscles. Muscle pain and ease of fatigue are common. Slow progression occurs and may lead to increasing restriction of daily activities. It probably relates to loss of anterior horn cells with aging from a pool that was already depleted by the original infection. There is no specific treatment.

14. RABIES caused by a rhabdo virus
conveyed by animals saliva through their bites or licks
Humans are most frequently infected from dogs
incubation period rang from 9 days to many months but is usually between 4 and 8 weeks. Severe bites, especially if on the head or neck, are associated with shorter incubation periods

15. Clinical features
At the onset there may be fever, and paraesthesia at the site of the bite.
patient is increasingly anxious
characteristic 'hydrophobia'
Although the patient is thirsty, attempts at drinking provoke violent contractions of the diaphragm and other inspiratory muscles
Delusions and hallucinations may develop, accompanied by spitting, biting and mania, with lucid intervals in which the patient is markedly anxious
Cranial nerve lesions
Death ensues, usually within a week of the onset of symptoms.

16. Investigations: Treatment:
During life, the diagnosis is usually clinical but rapid immunofluorescent techniques can detect viral antigen in corneal impression smears or skin biopsies. After death the diagnosis depend on identification of inclusion (Nigri) bodies in the brain of the victim using brain biopsy technique.
Post exposure trail with antirabies antibodies.
Other wise if the symptom start only symptomatic treatment:
- Intensive care facilities to control cardiac and respiratory failures.
- The patient should be heavily sedated with diazepam 10 mg 4-6-hourly, supplemented by chlorpromazine mg if necessary.
- Nutrition and fluids should be given intravenously or through a gastrostomy

17. Viral Meningitis
Viral infection is the most common cause of meningitis. It is a much less serious illness than bacterial meningitis unless there is associated viral encephalitis, which is rare. A number of viruses can cause meningitis, the most common being echoviruses and, where specific immunization is not employed, the mumps virus.

18. Clinical features:
The condition occurs mainly in children or young adults, with acute onset of headache and irritability and the rapid development of meningial irritation’s signs. In viral meningitis, the headache is usually the more severe feature. There may be a high pyrexia, but focal neurological signs rarely occur.

19. Investigations:
L.P: The CSF picture is the same of that for viral encephalitis. It is extremely important to verify that the patient has not received antibiotics (for whatever cause) prior to the lumbar puncture, as this picture can also be found in partially treated acute bacterial meningitis.

20. Management:
There is no specific treatment and the condition is usually benign and self- limiting. The patient should be treated symptomatically in a quiet environment. Recovery usually occurs within days

21. OTHER FORMS OF MENINGITIS
Fungal meningitis: (especially cryptococcosis) usually occurs in patients who are immunosuppressed and is a recognised complication of HIV infection. The CSF findings are similar to those of tuberculous meningitis, but the diagnosis can be confirmed by microscopy or specific serological tests.
In some areas, meningitis may be caused by spirochaetes (leptospirosis, Lyme disease and syphilis), rickettsiae (typhus fever) or protozoa (amoebiasis).
Non-infective meningitis: meningitis can also be due to non-infective pathologies. This is seen in recurrent aseptic meningitis due to SLE, Behçet's disease or sarcoidosis, as well as a condition of previously unknown origin known as Mollaret's syndrome in which the recurrent meningitis is associated with epithelioid cells in the spinal fluid ('Mollaret' cells). Recent evidence suggests that this condition may be due to human herpes virus type 2, and therefore infective after all.
Neoplastic meningitis: can also be seen due to direct invasion of the meninges by neoplasm ('malignant meningitis‘)

22. Mucor Mycosis: It is a fungal infection. Usual causative agents are:
Rhizopus, Rhizomucor, and Cunninghamella

23. EPIDEMIOLOGY AND PATHOLOGY:
Rhizopus and Rhizomucor species appearing on foods of high sugar content.
The disease is largely confined to patients with serious preexisting diseases.
Mucormycosis originating in the paranasal sinuses and nose predominantly affects patients with poorly controlled diabetes mellitus.

24. The infection is acquired from nature, with no person-to-person spread.

25. the foremost histologic findings are:
1.Vascular invasion by hyphae
2.Ischemic or hemorrhagic necrosis

26. CLINICAL MANIFESTATIONS:
of the nose and paranasal sinuses:
Low-grade fever,
dull sinus pain,
nasal congestion
a thin, bloody nasal discharge
double vision,
increasing fever,
obtundation.

27. Unilateral opthalmoplegia, chemosis, and proptosis (so should be differentiated from orbital cellulites).
Dusky red or necrotic nasal turbinates on involved side.
Sharply delineated necrosis, respecting the midline in the hard palate.
Inflamed cheek
Blindness (globe or ophthalmic art. involvement)
Coma (frontal lobe invasion)
Clouding of the sensorium (D.K.A)
Cavernous sinus thrombosis (IN ORBITAL INVASION)

31. DIAGNOSIS: C.T scan & M.R.I: Opacification of one or more sinuses
Carotid arteriography:
Show invasion or obstruction of the carotid siphon.
Biopsy for histological exam & culture:
Diagnose lesions of craniofacial structures.

32. TREATMENT: 1) Regulation of diabetes mellitus and
2) A decrease in the dose of immunosuppressive drugs facilitate the treatment of mucormycosis.
3) Extensive debridement of craniofacial lesions appears to be very important. Orbital inoculation may be required.
4) Intravenous amphotericin B:
Optimal dose of mg/kg/day for a total of 12 weeks.

33. Prognosis:
Appropriate management results in cure of about half of craniofacial infections i.e.: mortality rate with optimal management is 50%.
Without treatment patient die after a few days to a few weeks.