1).B.I.

Sharapov– thefounderoftheMoldavian neurologicalschool

The Department of Neurology was founded in October 1945 by Professor Boris

Sharapov, eminent representative of Neurological Sciences in St. Petersburg, Russia.
He led the department until 1969. Professor Sharapov established the basis of
educational, clinical and scientific activity, and initiated research devoted to clinical
and pathological manifestations of brain and spinal trauma.

2 )Primary and secondary serous meningitis

The meningitis is classified into serous and purulent

Serous is devided into primary and secondary

The etiology of primary serous meningitis is most often of viral origin the clinic is
characterised only by meningeal syndrome (acute lymphocytic choriomeningitis,
mosquito and tick – borne encephalitis , meningeal form of poliomyelitis)

Secondary serous meningitis develop on the background of main disease usually of

viral etiology(enterovirus infection,respiratory viral infection,chicken pox , measles ,
rubella, mumps, HIV infection)

Less serous meningitis occurs by bacterial infections (typhoid,

tuberculosis,brucellosis,leptospirosis,) parasitic (malaria , toxoplasmosis,amebiasis) ,or
fungal infections (cryptococcosis, aspergiliosis)

ARENAVIRUS (Lymphocytic Choriomeningitis Virus) ASEPTIC MENINGITIS

Epidemiology and Risk Factors

The natural reservoir for the lymphocytic choriomeningitis virus (LCMV) is the common
house mouse. Hamsters and laboratory animals can also be infected with this virus.

Most human infections result from contact with house mice.

Pathogenesis and Pathophysiology

These animals shed the virus in saliva, nasal secretions, semen, milk, urine, and feces.

The route of transmission to humans remains unknown but is presumed to occur

through contamination of open cuts or aerosolized spread of virus.
 There is no evidence of person- to-person transmission of LCMV infection.

Local replication of LCMV is followed by dissemination to the reticuloendothelial

system with a subsequent viremia.

The CNS is infected during the course of the viremia.

Clinical Manifestations

there is often a history of a biphasic illness.

The first stage resembles an influenza-like illness.

This is then followed by a symptom-free period of time varying from a few days
to 3 weeks, which is followed in turn by the acute onset of high fever, headache,
vomiting, and signs of meningeal irritation.

Diagnosis

appearance of IgM antibodies in a serum sample or by a fourfold or greater rise in

antibody titer between the acute and convalescent serum samples.

CSF: : (1) a lymphocytic pleocytosis of 300 to 3000 cells/mm3 , and (2)

hypoglycorrhachia

Treatment ; . Intravenous immune globulin

ENTEROVIRAL (Echoviruses and Coxsackieviruses) ASEPTIC MENINGITIS

Epidemiology and Risk Factors

Enteroviral infections occur primarily in the summer and autumn months in temperate
climates; infants, young children, and immunocompromised patients are at greatest risk
of infection

Pathogenesis and Pathophysiology

Enteroviruses may enter the host through the mucosal surfaces of the gastrointestinal
or respiratory tract. Enteroviruses are acquired most commonly by fecal-oral
contamination and, less commonly, via aerosolized respiratory droplets
Most enteroviruses spread to the CNS via the bloodstream, but a small percentage may
reach the CNS by direct neural spread from nerves terminating in the intestinal tissue.
Virus traverses the blood-brain barrier either at the choroid plexus, where it may infect
endothelial cells and spread into the cerebrospinal fluid causing a meningitis, or at the
endothelium of the cerebral capillary cells in the brain parenchyma causing an
encephalitis

The clinical Presentation

The clinical presentation of aseptic meningitis includes fever (38° to 40° C), severe
headache, nausea and vomiting, photophobia, and nuchal rigidity.

Diagnosis

The opening pressure should be normal or slightly increased,

mild lymphocytic pleocytosis,

a normal or slightly increased protein concentration,

and a normal glucose concentration

. The white blood cell count typically is less than 1000 cells/mm3 .

MANAGEMENT : IMMUNOGLOBULINS

3.Classification of traumatic brain injuries.

Concussion:clinicalmanifestations,treatment.

Direct Brain Injury Categories

 Focal
o Cerebral Contusion
o Intracranial Hemorrhage
 Epidural hematoma
 Subdural hematoma
 Intracerebral Hemorrhage
 Subarachnoid Hemorrhage
 Impalement injury 
 Bullet wounds
  Diffuse
 Concussion
 Moderate Diffuse Axonal Injury
 Severe Diffuse Axonal Injury

Diffuse Brain Injury

 Due to stretching forces placed on axons

 Pathology distributed throughout brain
 Types
o Concussion
o Diffuse Axonal Injury

Concussion:clinicalmanifestations,treatment.

 Transient LOC < 30 min

 Nerve dysfunction without anatomic damage

 Usually complete recovery

 Mild form of diffuse injury

 Often presents with a brief period of confusion

 Patients often have normal findings on neurologic examination 

 The diagnosis is usually a retrospective one

 Patients may exhibit retrograde or posttraumatic amnesia

Treatment : physically and mentally rest to recover from a concussion. Relative

rest, which includes limiting activities that require thinking and mental
concentration, is recommended for the first two days after a concussion.