Infectious of Nervous system in children

2. According to the structure of neurological diseases wAccording to the structure of neurological diseases wee
distinguishdistinguish three groups of lesions of the nervousthree groups of lesions of the nervous
system in children:system in children:
1) inherited diseases1) inherited diseases (chromosomal syndromes,(chromosomal syndromes,
metabolic diseases with the lesion of the nervousmetabolic diseases with the lesion of the nervous
system and so on),system and so on),
2)2) pre-and perinatal lesionspre-and perinatal lesions (malformations, obstetric(malformations, obstetric
trauma, asphyxia, congenital infections and the like),trauma, asphyxia, congenital infections and the like),
andand
3)3) postnatal lesionspostnatal lesions (infectious diseases of the nervous(infectious diseases of the nervous
system, trauma, tumors, etc.). The part of the first twosystem, trauma, tumors, etc.). The part of the first two
groups is 55% of diseases, 45% are postnatal lesions,groups is 55% of diseases, 45% are postnatal lesions,
among them the first place is occupied by infectiousamong them the first place is occupied by infectious
diseases. Most often they occur in children 3-6 years ofdiseases. Most often they occur in children 3-6 years of
life.

3. The possibility of the nervous system damage at
infectious diseases is predetermined by neurotropism
of infectious-toxic factors. Besides neurons lesions
because of the toxic effects, circulatory and
liquorodynamic disturbances , changes in the vessels of
the brain and its membranes, edema and swelling of
the brain, brain tissue hypoxia and the like takes place.
Manifestations of such changes are often nonspecific
and determine the leading clinical manifestations in
the acute period of illness.

4. Neurotoxic syndrome (encephalitic reaction) - the
general reaction to the infectious agent which leads to
violation of the basic functions of internal organs and
systems, particularly the CNS, and metabolic changes.
Pathological picture: vascular stasis , punctate
hemorrhages, edema, focal necrosis, dystrophic changes.
Clinical manifestations: fever, considerable excitement,
tremor, twitching, hyperreflexia. Then there are
convulsions. Pale skin, rapid breathing, tachycardia,
blood pressure rises. Oliguria. This is the first phase of
clinical manifestation of encephalitic reaction. Further
the second phase develops. There is a growing
oppression, weakness, confusion, reflexes are depressed,
skin is gray, there is severe deficiency of peripheral
circulation. Heart tones are deaf, pulse is weak, blood
pressure falls, pulmonary edema occurs. Anuria. In
young children often convulsive form is registered, in
elder – delirious form.

5. Medical Lecture Notes – All Subjects
USMLE Exam (America) – Practice

6. Edema and swelling of the brain - one of the most
dangerous manifestations of nervous system lesions of
infectious origin. The degree of cerebral edema is the
decisive prognostic factor. Clinically, cerebral edema is
characterized by symptoms of growing intracranial
hypertension - an intense headache, vomiting like a
fountain, short-lasting blurred vision in the form of a mist
or veil feelings in front of the eyes (a result of mechanical
compression of the optic nerve and blood vessels). Face skin
is of purple blue color, there is pupillary constriction. Often
there are convulsions, agitation or depression, there is
unexplained hiccups. The character of respiration changes,
tachypnea appears with auxiliary respiratory muscles,
severe dyspnoe, respiratory disorders of Cheyne-Stokes
type. The appearence of resistant tachycardia, especially
after bradycardia, reduction in respiratory rate indicate a
serious threatening condition of the patient. Cerebral
edema usually develops during the 1st day of the disease, in
older patients it may occur later - on the 5-7th day.

7. Purulent meningitis – acute infectious diseases
that are characterized by intoxication, meningeal and
other symptoms of nervous system lesion, the
presence of a primary site of infection or
pyosepticemic process is possible . Purulent
meningitis in 90% of cases are associated with
meningococcus, pneumococcus, Haemophilus
influenzae, sometimes streptococcus, staphylococcus,
salmonellas and so on. Primary meningitis occur in
clinically healthy children, secondary result from the
development of pus focus in the body (pneumonia,
otitis media, sepsis, and so on).

8. Meningococcal disease. Meningococcal
disease - acute infectious disease that is caused by
meningococcus (Neisseria meningitis), is transmitted by
droplet way and is characterized by nasopharyngitis,
meningococcemia, purulent meningitis, which run
across separately, sequentially or simultaneously.
Infection often leads to the meningococcus bacteria
carrying. Meningococcal disease (MD) is common
throughout the world. According to WHO, it is registered
in 200 countries. The causative agent Neisseria
meningitidis, 9 different serotypes (A, B, C, and the like)
of meningococcus exist. This gram-negative diplococcus,
is shaped like the coffee bean, in typical cases is placed
in pairs inside the neutrophils. The pathogen is not
stable to environmental factors, dies quickly after
cooling, that’s why the material for research must be
delivered in a water bath at 37 ° C.

9. Nasopharynx is a place of primary localization and
multiplication of meningococci. In most cases, the
presence of the agent on the nasal mucosa is not
accompanied by significant changes and ends with
healthy carriering or nasopharyngitis. If the
meningococcus spreads in the organism (the main way is
hematogenous) generalized forms of the disease
develop. Bacteremia is accompanied by a massive
collapse of the meningococcus - toxemia, which leads to
the damage of the vascular endothelium. At
meningococcemia choroid and synovial joints
membrane are also affected, damage of the adrenal
glands, kidneys, endocardium is also possible. With the
penetration of the pathogen through the blood brain
barrier stimulation of the receptors of the pia mater and
cerebrospinal fluid forming systems by toxic factors
occurs which leads to the development of inflammation
and increased secretion of cerebrospinal fluid, edema,
swelling of

10. the brain with excessive irritation of meninges, roots of
cranial and spinal nerves. In the pathogenesis of severe
meningococcemia forms the leading role the infectious-
toxic shock plays, which turns out to be as acute circulatory
collapse on the background of severe intoxication. Toxemia
leads to hemodynamic disorders, disturbance of
microcirculation in tissues and organs, disseminative
intravascular coagulation (DIC-syndrome), an expressed
violation of the metabolic processes and fluid and
electrolyte balance, endocrine function. Progressive
infectious toxic shock can cause severe damage of the
adrenal glands, kidneys (shock kidney) with the following
development of acute failure. There are also vascular and
degenerative changes in parenchymal organs – septic
spleen, glomerulonephritis, endocarditis, signs of the brain
and spinal cord and their membranes injury can be absent.

11. The clinical manifestation. The incubation period is 1-
10 days, usually 5-7. According to the accepted
classification of Pokrovsky we distinguish:
1) localized forms (meningococcal carriage and acute
nasopharyngitis),
2) generalized forms (meningitis, meningococcemia
typical and fulminant, meningoencephalitis, mixed
form),
3) rare forms (arthritis, endocarditis, pneumonia,
iridocyclitis, and the like).
Meningococcal carriage is not accompanied by
clinical signs and is identified during the investigation
of contacted persons.

12. Acute nasopharyngitis – is the most spread form. It is
characterized by headache, nasal congestion, sore throat,
mucous or purulent mucus discharge from the nose,
subfebrile temperature, bright erythema and edema of the
posterior pharyngeal wall. Inflammatory changes are
observed for 5-7 days. In 30-50% of patients nasopharyngitis
precedes generalized form of the disease.
Meningitis can develop after nasopharyngitis, or the first
symptoms appear suddenly, among the overall health. The
clinical manifestation is characterized by a triad of primary
pathognomonic symptoms : fever, headache, vomiting. If any
doctor observes this symptoms it is always necessary to check
the meningeal symptoms. Body temperature rises suddenly,
can reach 40-41° C for several hours. Headache is without
known localization, strong, increases in bright light, sharp
sounds. Vomiting occurs suddenly, without nausea, like a
fountain. Often there is a general hyperesthesia.

13. There may be tonic, clonic, or mixed seizures in infants,
the appearance of seizures may be the first sign of meningitis.
During the physical examination meningeal symptoms are
positive, which appear during first twenty four hours and
disease progress quickly. The most constant is the stiff neck,
Kernig's and Brudzinsky’s symptoms (upper, middle, lower).
In infants, there is fontanelle triad: bulging, tension, the
absence of its normal pulsation. The typical patient’s position
- lying on side with head thrown back and legs toned down to
the stomach (posture of erected trigger or setter dog).
Severity of meningeal syndrome can not correlate with the
severity of the disease. Sometimes, especially in young
children, there is a dissociated meningeal syndrome when
some of the leading symptoms are absent.

14. In case of the meninges inflammation local symptoms
may be present, caused by distribution of the
inflammatory process to the roots of the cranial and
spinal nerves, the brain substance. Some patients may
have abnormal Babinski, Oppenheim, Rossolimo and the
like symptoms positive, reduction or disappearance of
spinal reflexes, strabismus, ptosis, paresis of facial
muscles, paresis and paralysis of the limbs and the like.
Often the autonomic nervous system is affected
(persistent red dermographism). There may be disorders
of consciousness: sopor that goes into a deep coma from
the first hours of the disease (unfavorable prognostic
sign.) Herpes simplex is activated, a characteristic rash on
the wings of the nose, mucous membrane of the lips
appear. In the blood test- neutrophilic leukocytosis,
increased erythrocyte sedimentation rate.

15. Meningococcemia is characterized by a rapid
start. The temperature rises to 39-41°C and
maintains at a high level for 2-3 days. Along with
fever headache, severe weakness, pallor or
cyanosis of the face and extremities is observed.
Blood pressure rises at the beginning, at shock it
may decrease sharply (to collapse). Permanent
feature of meningococcemia is rash. Skin rash
appears after 5-15 hours, sometimes on the 2nd day
of illness. The typical rash - haemorrhagic,
irregular shape, with a clear outline, stellate. The
elements vary in size - from the point of petechiae
in significant bleeding. As a result of new elements
appearence you can see different colors,
brightness, often with typical, barely visible gray
(steel) shade necrotizing deep and large
hemorrhages, the formation of defects that do not
heal for a long time, with further scarring.

16. Possible cases of necrosis of the ears, nose tip, the
end phalanges. The most common rash localization -
buttocks, posterior thighs, ages, sclera, ears.
Hemorrhagic rash is often combined with roseolous,
papular, petechial. Histologically, a leukocyte-
ekzantema fibrinous thromboembolism (blood clots
or emboli contain meningococcus). Skin rash in
meningococcemia - is metastatic foci of infection.
Second place for the localization of metastases
occupied the joints (arthritis and polyarthritis),
choroid (iritis, iridocyclitis, uveitis). This sometimes
leads to the development of the characteristic triad -
hemorrhagic rash, arthritis, iritis. At a blood exhibit
moderate or severe neutrophilic leukocytosis with a
shift to the left to leukocyte young and myelocytes,
increased erythrocyte sedimentation rate,
thrombocytopenia often.

17. Fulminant meningococcemia (hyperacute
meningococcal sepsis, fulminant meningococcemia) -
prognostically unfavorable form of meningococcal disease,
it is infectious-toxic shock, that is characterized by acute
sudden onset and rapid progress. The body temperature is
40-41°C, in the first hours there is massive hemorrhagic
rash with a tendency to become extensive hemorrhage,
which soon becomes necrotic. On the skin purple cyanotic
spots are formed. The skin is pale with a total cyanosis,
cold, covered with sweat, facial features are sharpened.
Patients are excited, there are often tonic-clonic
convulsions, repeated vomiting. Prostration increases, lost
of consciousness occurs. Pulse is of weak filling, blood
pressure continuously decreases to zero, anuria is possible
as a manifestation of shock kidney. There are various
disorders of homeostasis: metabolic acidosis,
coagulopathy, fibrinolytic activity of blood is reduced.
Without adequate treatment, patients die of the disease in
the early days because of acute circulatory failure.

18. Clinical diagnosis of meningococcal meningitis is
based on acute onset, fever, headache, vomiting, presence
of meningeal syndrome (total hypertension, neck
stiffness, Brudzinsky’s, Kernig's symptoms and so on), in
infants – sunken fontanelle, neutrophilic pleocytosis in
the cerebrospinal fluid . At meningococcemia - rapid start,
fever, typical hemorrhagic-necrotic star-like rash,
sometimes - the damage of the joints and choroid.
Laboratory diagnosis of meningococcal infection - is
the identification of the meningococcus in the
cerebrospinal fluid, mucus from the nasopharynx and in
the blood. Smear method for detecting meningococci in
the sediment of cerebrospinal fluid and a thick drop of
blood is of auxiliary importance. General clinical tests of
cerebrospinal fluid (pressure, transparency, cell
structure), smear and bacteriological methods,
biochemical (protein, sugar, chlorides).

19. At meningococcal meningitis cerebrospinal fluid
pressure is raised, it is turbid and purulent. At 1 mm,
there are thousands of cells, of which 70-80% -
neutrophilic granulocytes. The amount of protein is
from 1 to 7 g/l, Pandi globulin reaction is positive.
Meningeal syndrome may occur at other viral and
bacterial meningitis etiology.

20. Treatment.
Therapeutic tactics depend on the clinical form, the
severity and presence of complications.
Patients with meningococcal nasopharyngitis are
prescribed antibiotics in normal doses according to age.
At generalized forms etiotropic treatment plays major
role. Cephalosporin intramuscularly or intravenously at
severe forms are prescribed. At fulminant form of
meningococcemia in the first day chloramphenicol
succinate is used 80-100 mg / kg per day every 6 hours
intramuscularly. Duration of antibiotic therapy is to 10
days. The indications for the antibiotictherapy stoping is
the normalization of temperature, negative meningeal
symptoms, and normal cerebrospinal fluid test (cell
number does not exceed 50 to 1 ml with a predominance
of lymphocytes). Cancel of the antibiotic is carried out
simultaneously.


21. Pathogenetic treatment is important: desintoxication,.
Reopoliglukin, reogluman, albumin, concentrated plasma, 5%
glucose solution with the parenteral use of diuretics for
dehydration. Glucocorticosteroids dose is individual and
depends on the dynamics of the main symptoms.
Hydrocortisone is assigned - 3-7 mg / kg per day and
prednisolone 1-3 mg / kg per day. With the development of
ITSH daily dose of glucocorticosteroids increases from 5-10
mg / kg to 15-20 mg / kg of prednisolone. Keep in mind that
some pathogenic agents alter the concentration of
antibiotics. Osmotic diuretics ( mannitol) and hypertonic
glucose solutions increase the excretion of penicillin in the
urine and reduce its concentration in blood and
cerebrospinal fluid, which requires reducing the interval
between the introduction of benzilpenitsilina to 2 hours. The
use of Lasix (furasemid) does not require this correction.
Important in treatment are also antihistamines,
antipsychotics excitation (sodium hydroxybutyrate,
droperidol, Relanium, seduksen), vitamins, nootropics
(Pantogram, nootropics) Angioprotectors (Parmidin,
tribenozid).

22. Serous meningitis are the polyetiological group of
infectious lesions of the nervous system, which фку
characterized by acute development of hypertensive-
hydrocephalic and less expressed meningeal syndrome with a
favorable course. We distinguish primary serous meningitis
(etiology - Coxsackie viruses and ECHO, the virus of
Armstrong’s choriomeningitis) and secondary (associated
with mumps disease, herpes, measles, influenza,
poliomyelitis). There are serous meningitis caused by
bacteria (at tuberculosis, typhoid fever, brucellosis etc.).
The basis of the development of pathological changes at
serous meningitis is a serous inflammation of the pia mater
and vascular entanglements, which leads to the increase in
the number of liquor with violation of its outflow, acutely
developed hypertensive- hydrocephalic syndrome,
manifestations of which are headache and vomiting of central
origin.

23. Typical clinical signs: the beginning is acute, the
temperature rises to 38 ° C and above, there is
expressed headache, repeated vomiting. Meningeal
signs in the first day of illness are minor. Small
children may have seizures, unconsciousness,
delirium. In 30-40% of cases there are focal signs
(paresis of the facial nerve of the central type, hyper-
and anisoreflexia, ataxia). The acute period lasts 1-3
days with a gradual improvement, meningeal signs
disappear until 14-20 days.
The most important are enterovirus meningitis
and the lesion of the meninges with mumps disease.

24. Serous meningitis of enterovirus etiology is
characterized by inflammation of the meninges with
all the signs of hypertensive syndrome. The most
typical form of the disease begins acutely with fever to
39 ° C and above, patients complain of a sharp
headache, dizziness, nausea. Condition is
deteriorating rapidly, multiple vomiting which does
not give relief. Sometimes there are snags, delirium, a
considerable hyperesthesia. From the first days of
sickness meningeal symptoms are positive - stiff neck,
Brudzinsky’s, Kernig's symptoms and so on. During
the examination of the patient a slight face hiperemia
can be seen, possible small measleslike rash that
disappears quickly (ephemeral) is possible.

25. After 4-10 days of onset of illness the body
temperature returns to normal, but may be re-raising
with an interval of 3-5 days. Meningeal symptoms
disappear in 3 to 5 days, but normalization of
cerebrospinal fluid lags behind clinical recovery.
Relapses of serous meningitis are very rare. CSF is
transparent, colorless, it flows out with a stream or
frequent drops. There is pleocytosis from 15-30 to 1000-
1500 in 1 ml (an average is 100-300 in 1 ml), during first
days of sickness pleocytosis is mixed - lymphocytic-
neutrophilic. The amount of protein is slightly
increased, glucose and chloride content is not
changed. The prognosis is favorable. Diagnosis is
established after virus isolation from nasopharyngeal
smears, feces and cerebrospinal fluid.

26. Serological diagnosis is study of paired sera obtained
from patients at intervals of 2-3 weeks by CBR(complement
binding reaction) and IHAR (indirect hemagglutination
reaction).
The damage of the central nervous system at mumps
infection occurs in 50-80% of cases, and is in the form of
serous meningitis, meningoencephalitis, rare - cranial
nerve neuritis, polyradiculoneuritis. Mumps meningitis
begins on the 3-6 days after onset of symptoms of mumps,
rarely precedes them, or is accompanied by the swelling of
the salivary glands. Development of isolated meningitis
without indrawing in the process of the glands is possible.
The lesion of the meninges of the brain manifests by fever,
headache, multiple vomiting, meningeal symptoms.

27. Membranes of the brain are affected more
frequently than clinically diagnosed meningitis as the
inflammative changes in the cerebrospinal fluid are
possible in the absence of meningeal symptoms. CSF is
transparent, pleocytosis is 300-500, sometimes up to
2000 cells in 1 ml, lymphocytes dominate. The amount of
protein is in normal or slightly increased, the content of
glucose is normal. Mumps meningitis has benign
course. Meningoencephalitis belongs to severe nervous
system injuries, but it’s course is favorable. Diagnosis of
mumps meningitis in the presence of salivary gland
enlargement is quite simple.

28. Differential diagnosis of these forms is the most
important with tuberculous meningitis, which is
characterized by the gradual development with
increasing headache, infrequent vomiting, fever,
slow pulse, appearance of red dermographism.
Meningeal signs appear at the end of the first week,
and convulsions, impaired consciousness, paralysis -
on the second week of illness. In the cerebrospinal
fluid high protein, lymphocytic pleocytosis, reducing
the amount of glucose and chlorides cn be found,
while standing in the CSF falls soft fibrin film, which
can reveal tubercle bacilli. Small children may have
the rapid onset of the disease. The presence of
tuberculosis in the family is importance for the
diagnosis.

29. Encephalitis
is a brain lesion of inflammatory chracter with expressed signs of
focal damage of the CNS in the presence or absence of meningeal
and common infectious symptoms. Etiology: herpes, tick
encephalitis virus, enterovirus, influenza virus (primary
encephalitis), measles virus, rubella, chiсkenpox (secondary
encephalitis), encephalitis after vaccination, encephalitis of
unknown etiology.At primary viral encephalitis neurotropic virus
enters the central nervous system and affects glial cells, neurons.
At the tick-borne encephalitis the anterior horn of the spinal
cord and trunk are affected, at herpes encephalitis - the cerebral
cortex, at lethargic - subcortical structures, at the enterovirus -
the nuclei of cells of the brain stem and cerebellum. For the
development of secondary viral encephalitis
immunopathological delayed reactions are important, when
there are antibodies against brain tissue, which react with
myelin, microglia and destroy them. Also the effect of the virus,
which enters the central nervous system is possible.

30. For the disease incubation period, prodrome, the
acute phase with fever or without it is typical, then
comes the period of recovery lasting up to 2-3 years,
when focal neurological symptoms regress. Disease
finishes with the formation of residual changes or
complete recovery. The development of chronic
disease course is possible with convulsions, and
increased paresis, impaired psychological status.
The incubation period is from 7 to 12 days (can be
from 3 to 30 days, depending on the etiology). The
disease starts acutely with high fever, disturbance of
consciousness, convulsions (possible epistatus),
impaired breathing and pulse.

31. Sometimes there may be a gradual progression of the
disease with increased headache, lethargy, vomiting, and
drowsiness. From the earliest days of the disease there are
are focal symptoms: muscular hypotonia, impaired
language, expressed tremor, changes in coordination. If
the brain stem is damaged –there will be ptosis,
strabismus, dizziness, facial nerve lesions, bulbar
syndrome. If the hemispheres of the brain are damaged -
acute paralysis, aphasia, hyperkinesis develop. The
development of cerebral coma and bulbar lesions with
dysarthria, dysphagia, respiratory failure are the threat to
life. Meningeal signs throughout the disease are small,
may be absent. In the cerebrospinal fluid - lymphocytic
pleocytosis, elevated protein to 2.0 g / liter. The disease
course is severe, focal symptoms are enough stable. With
the development of chronical disease periods of remission
change periods of exacerbations process with the
formation of large residual defects.

32. The disease course is severe, focal symptoms
are enough stable. With the development of
chronical disease periods of remission change
periods of exacerbations process with the
formation of large residual defects. Main clinical
signs of disease are seizures, impaired
consciousness, focal symptoms of brain and spinal
cord up to 1 month or more on the background of
minor common infectious manifestations.
Laboratory diagnosis - detection of virus in the
blood (the first three days of illness), cerebrospinal
fluid (in the first week), from the smears of the
nasopharynx, of feces, paired sera with an interval
of 2-3 weeks for the detection of antibodies in
reactions CBR(complement binding reaction) and
IHAR (indirect hemagglutination reaction).

33. Differential diagnosis is made between different
nosological forms of encephalitis.
Epidemic lethargic encephalitis is characterized by
lethargic and hyperkinetic syndrome (leading to
parkinsonism). The lesion of cores 3 and 4 pairs of
cranial nerves with diplopia, paralysis of
accommodation, ptosis, a violation of convergence is
typical. The damage of the extrapyramidal system
causes hyperkinesis of all muscle groups and possible
attacks of convulsions. Transition to the chronic form
results in the development of parkinsonism with
violation of the psyche, memory, emotional and
associative activity. More favorable course of illness is
in small children without expressed signs of sleepiness
and oculomotor disorders.

34. Herpetic encephalitis is a severe disease with cerebral
and local brain lesions as a consequence of necrosis in the
parietal and temple lobes of the brain. The disease begins
acutely with fever, severe headache, impaired
consciousness. Herpetic skin rash occurs rarely. Meningeal
signs are not expressed. Repeated seizures are observed,
hemiparesis occurs early, hemiplegia, aphasia, join bulbar
disorders appear. The rapid development of cerebral coma
with a fatal consequence of the disease on the 1-2 weeks is
possible. In infants the disease is characterized by
dissemination of the process with visceral organs and
central nervous system damage, the first signs of disease
appear on the 3-14 days of life, death occurs within 6-7 days.
Herpes encephalitis causes severe residual effects:
dementia, episyndrome, mental changes.

35. Measles encephalitis usually develops on the 5-
8 days of illness, belongs to a group
paraencephalitis as the basis for its development is
a violation of the mechanisms of the immune
response. The beginning is acute with elevated
temperature, impaired consciousness, seizures.
The demage of the brain and spinal cord leads to
gemi- and tetraparesis, paresis of the lower
extremities, pelvic disorders. The course of
measles encephalitis is very severe. In the
cerebrospinal fluid - moderate lymphocytic
pleocytosis. Lethality is 10-15%, the third case, a
persistent residual symptoms are formed in 1/3 of
cases.

36. Varicella encephalitis develops on the 4-7 days of
illness (and possibly on the 10-15 days), the
temperature rises, the patient's status deteriorates,
there are cerebral symptoms. Ataxia syndrome is the
most typical for varicella encephalitis: a shaky walk,
dizziness, impaired coordination, skeletal muscle
hypotonia, tremor, dysarthria. Cerebrospinal fluid is
turbid, there is a slight increase of cytosis by
lymphocytes, the level of protein and glucose is
normal. Course of the disease is favorable, there
may be residual effects in the form of epileptic
seizures, mental retardation, behavioral
disturbance. Very rarely, encephalitis develops in
the early days of sickness on the background of rash.
In this case the disease is characterized by a severe
state, hyperthermia and rapid development of
cerebral and focal symptoms.

37.  Rubella encephalitis develops most often in children
of school age on the third day of the rash, sometimes
it can precede it. The expressed impairment of
consciousness - sopor, brain coma, convulsions or
epistatus on the background of hyperthermia,
vomiting, focal symptoms, meningeal syndrome are
typical. Lethality is 15-20%, recovery is without
residual effects.
 Reye syndrome: etiology has not been established,
most often it occurs during periods of increased
incidence of influenza B. It starts with symptoms of
ARVI, or the gastrointestinal tract lesion. The
patient’s state suddenly deteriorats, vomiting, fever,
disturbance of consciousness, excitement, delirium,
respiratory disorders. Cerebral coma develops
rapidly, focal neurological symptoms are not typical,
cerebrospinal fluid is normal. Hypoglycemia,
increased serum transaminases, hepatomegaly are
determined. Lethality is about 48-80%.

38. Treatment. Hospitalization of patients is obligatory.
The type of causal treatment is associated with the
etiology of encephalitis: human immunoglobulin
(encephalitis), acyclovir (Zovirax, viroleks) in herpetic
encephalitis, ribonuclease (tick-borne encephalitis and
measles), desoxyribonuclease (herpetic, varicella and
rubella encephalitis), leukocyte interferon. The main
treatment is the basic therapy aimed at reducing the
intracerebral hypertension, normalization of electrolyte
imbalance, cerebral hemodynamics. The symptomatic
therapy is important to: the struggle with hyperthermia,
the elimination of breathing disorders. Treatment is
conducted in the intensive care unit for 7-10 days.
Supervision of patients by medical personnel and the
child's mother is of great importance.

39. Рoliomyelitis
EPIDEMIOLOGY.
In 1952 there were more than 57,879 cases of polio in
the United States, including 21,269 cases of paralytic
polio that resulted in more than 3,000 deaths. The use
of poliovirus vaccine has eliminated, since 1979, wild
poliovirus in the United States. The last case of wild
poliovirus in the Americas occurred in Peru, in 1991. In
1994 the World Health Organization declared that
polio had been eradicated from the Western
hemisphere.

40. PATHOGENESIS.
The neuropathy of poliomyelitis and other paralytic
diseases caused by nonpolio enteroviruses is due to direct
cellular destruction. Secondary damage may be due to
immunologic mechanisms. In poliomyelitis, neuronal
lesions occur in the (1) spinal cord (chiefly in the anterior
horn cells and to a lesser degree in the intermediate and
dorsal horn and dorsal root ganglia); (2) medulla
(vestibular nuclei, cranial nerve nuclei, and the reticular
formation, which contains the vital centers controlling
respiration and circulation); (3) cerebellum (nuclei in the
roof and vermis only); (4) midbrain (chiefly the gray
matter but also the substantia nigra and occasionally the
red nucleus); (5) thalamus and hypothalamus; (6)
pallidum; and (7) cerebral cortex (motor cortex). Areas
that are spared include (1) the entire cerebral cortex except
the motor area; (2) the cerebellum except the vermis and
deep midline nuclei; and (3) the white matter of the spinal
cord.

41. Infants acquire immunity transplacentally from their
mothers. This immunity is usually complete during the
first 4-6mo of life and disappears at a variable rate.
Active immunity, after natural infection, probably lasts
for life. Neutralizing antibodies against polioviruses
develop within several days after exposure, often before
the onset of illness. The early production of
immunoglobulin (Ig) G antibodies is a result of
replication of the virus in the intestinal tract and deep
lymphatic tissues, which occurs before the central
nervous system is invaded. Local (mucosal) immunity,
conferred mainly by secretory IgA, is an important
defense against polioviral infection.

42. CLINICAL MANIFESTATIONS.
Poliovirus infections may follow one of several
courses: inapparent infection, which occurs in 90-95%
of cases and causes no disease and no sequelae,
abortive poliomyelitis, nonparalytic poliomyelitis, or
paralytic poliomyelitis.
Abortive Poliomyelitis.
Abortive poliomyelitis is a brief febrile illness with
one or more symptoms of malaise, anorexia, nausea,
vomiting, headache, sore throat, constipation, and
diffuse abdominal pain. Coryza, cough, pharyngeal
exudate, diarrhea, and localized abdominal
tenderness and rigidity are uncommon. The fever
seldom exceeds 39.5°C (103°F), and the pharynx
appears normal despite the frequent complaint of
sore throat.

43. Nonparalytic Poliomyelitis.
The symptoms in this form of poliovirus infection
are the same as those enumerated for abortive
poliomyelitis except that headache, nausea, and
vomiting are more intense, and there is soreness and
stiffness of the posterior muscles of the neck, trunk,
and limbs. Fleeting paralysis of the bladder is not
uncommon, and constipation is frequent.
Approximately two thirds of these children have a short
symptom-free interlude between the first phase (minor
illness) and the second phase (central nervous system
disease or major illness). This two-phase course is less
common in adults, in whom the evolution of symptoms
is more insidious. Nuchal and spinal rigidity are the
basis for the diagnosis of nonparalytic poliomyelitis
during the second phase.

44. Paralytic Poliomyelitis.
The manifestations are those enumerated for
nonparalytic poliomyelitis plus weakness of one or
more muscle groups, either skeletal or cranial. These
symptoms may be followed by a symptom-free
interlude of several days and then a recurrence of
disease culminating in paralysis. Bladder paralysis
lasting 1-3 days occurs in approximately 20% of
patients, and bowel atony is common, occasionally to
the point of paralytic ileus. In some patients muscular
paralysis may be the initial presentation.

45. Flaccid paralysis is the most obvious clinical expression
of the neuronal injury. The ensuing muscular atrophy is
due to denervation plus the atrophy of disuse. The pain,
spasticity, nuchal and spinal rigidity, and hypertonia
early in the illness are probably due to lesions of the
brain stem, spinal ganglia, and posterior columns.
Respiratory and cardiac arrhythmias, blood pressure and
vasomotor changes, and the like reflect damage to the
vital centers in the medulla. On physical examination
the distribution of paralysis is characteristically spotty.
To detect mild muscular weakness, it is often necessary
to apply gentle resistance in opposition to the muscle
group being tested.

46. In the spinal form there is weakness of some of the
muscles of the neck, abdomen, trunk, diaphragm,
thorax, or extremities. In the bulbar form there is
weakness in the motor distribution of one or more
cranial nerves with or without dysfunction of the vital
centers controlling respiration and circulation.
Components of both the preceding forms occur
together in bulbospinal poliomyelitis. In the
encephalitic form irritability, disorientation,
drowsiness, and coarse tremors not explained by
inadequate ventilation are noted; peripheral or
cranial nerve paralysis coexists or ensues. Hypoxia
and hypercapnia caused by inadequate ventilation
due to respiratory insufficiency may produce
disorientation without true encephalitis.

47. DIAGNOSIS
Poliomyelitis should be considered in any
unimmunized or incompletely immunized child with
nonspecific febrile illness, aseptic meningitis, or
paralytic disease. The combination of fever, headache,
neck and back pain, asymmetric flaccid paralysis without
sensory loss, and pleocytosis is not regularly seen in any
other illness.
The cerebrospinal fluid, while often normal during
the minor illness, demonstrates a pleocytosis between
20-300 cells/mm3 with central nervous system
involvement; the cells may be polymorphonuclear early
in the disease but shift to mononuclear cells soon
afterward. By the second week of the major illness, the
total WBC count falls to near-normal values. In contrast,
the cerebrospinal fluid protein is normal or only slightly
elevated at the outset of central nervous system disease
but usually rises to between 50-100mg/dL by the second
week of illness.

48. Serologic testing demonstrates seroconversion or
a fourfold or greater increase in antibody titers.
Poliovirus is easily cultured from the stool and
nasopharynx and infrequently from the cerebrospinal
fluid. Isolates should be submitted to the Centers for
Disease Control and Prevention for DNA sequence
analysis, which can distinguish wild poliovirus from
the strains used in the oral poliovirus vaccine.

49. Differential Diagnosis.
Several other conditions of muscular weakness
should be considered. Guillain-Barre syndrome is the
most common disease and the most difficult to
distinguish from poliomyelitis. Paralysis is
characteristically symmetric, and sensory changes and
pyramidal tract signs are common in Guillain-Barre
syndrome absent in poliomyelitis. Fever, headache, and
meningeal signs are less notable, and there are few
cells but an elevated protein level in the cerebrospinal
fluid. Peripheral neuritis may be due to lead toxicity,
cranial nerve herpes zoster, or postdiphtheritic
neuropathy.

50. Arthropod-borne viral encephalitis, rabies, and
tetanus have been confused with bulbar
poliomyelitis. Botulism may closely simulate bulbar
poliomyelitis, but nuchal-spinal rigidity and
pleocytosis are absent. Demyelinating types of
encephalomyelitis are associated with or follow the
exanthems and other infections or occur as an
untoward sequel of antirabies vaccination.
Neoplasms originating in and around the spinal cord
rarely have a fairly abrupt onset. Familial periodic
paralysis, myasthenia gravis, and acute porphyria are
uncommon causes of muscle weakness. Hysteria and
malingering are rare in children.

51. TREATMENT.
The broad principles of management are to allay fear,
to minimize ensuing skeletal deformities, to anticipate
and meet complications that may occur in addition to
the neuromusculoskeletal problems, and to prepare the
child and family for the prolonged treatment that may
be required and for permanent disability if this seems
likely. Patients with the nonparalytic and mildly
paralytic forms of poliomyelitis may be treated at home.
Abortive Poliomyelitis.
Supportive treatment with analgesics, sedatives, an
attractive diet, and bed rest until the child's temperature
is normal for several days is usually sufficient. Avoidance
of exertion for the ensuing 2wk is desirable, and there
should be a careful neuromusculoskeletal examination
2mo later to detect any minor involvement.

52. Nonparalytic Poliomyelitis.
Treatment for the nonparalytic form is similar to
that for the abortive form; in particular, relief is
indicated for the discomfort of muscle tightness and
spasm of the neck, trunk, and extremities. Analgesics
are more effective when they are combined with the
application of hot packs for 15-30min every 2-4hr. Hot
tub baths are sometimes useful. A firm bed is desirable
and can be improvised at home by placing table leaves
or a sheet of plywood beneath the mattress. A
footboard should be used to keep the feet at a right
angle to the legs. Because muscular discomfort and
spasm may continue for some weeks, even in the
nonparalytic form, hot packs and gentle physical
therapy may be necessary. Such patients should also be
carefully examined 2mo after apparent recovery to
detect minor residual effects that might cause postural

53. Paralytic Poliomyelitis.
Most patients with the paralytic form require
hospitalization. A calm atmosphere is desirable.
Suitable body alignment is necessary to avoid
excessive skeletal deformity. A neutral position with
the feet at a right angle to the legs, knees slightly
flexed, and hips and spine straight is achieved by use
of boards, sandbags, and, occasionally, light splint
shells. Active and passive motions are indicated as
soon as the pain has disappeared. Opiates and
sedatives are permissible only if no impairment of
ventilation is present or impending. Constipation is
common, and fecal impaction should be prevented.
When bladder paralysis occurs, a parasympathetic
stimulant such as bethanechol (5-10mg orally or 2.5-
5.0mg subcutaneously) may induce voiding in 15-
30min; some patients do not respond, and others
respond with nausea, vomiting, and palpitations.

54. COMPLICATIONS.
Paralytic poliomyelitis may be associated with
numerous complications. Melena severe enough to
require transfusion may result from single or
multiple superficial intestinal erosions;
perforation is rare. Acute gastric dilatation may
occur abruptly during the acute or convalescent
stage, causing further respiratory embarrassment;
immediate gastric aspiration and external
application of ice bags are indicated. Mild
hypertension of a few days or weeks duration is
common in the acute stage, probably related to
lesions of the vasoregulatory centers in the
medulla and especially to underventilation. In the
later stages, because of immobilization,

55. hypertension may occur along with hypercalcemia,
nephrocalcinosis, and vascular lesions. Dimness of
vision, headache, and a lightheaded feeling
associated with hypertension should be regarded
as premonitory of a frank convulsion. Cardiac
irregularities are uncommon, but
electrocardiographic abnormalities suggesting
myocarditis are not rare. Acute pulmonary edema
occurs occasionally, particularly in patients with
arterial hypertension. Pulmonary embolism is
uncommon despite the immobilization. Skeletal
decalcification begins soon after immobilization
and results in hypercalciuria, which in turn
predisposes the patient to urinary calculi,
especially when urinary stasis and infection are
present. A high fluid intake is the only effective
prophylactic measure. The patient should be
mobilized as much and as early as possible.

56. PROGNOSIS.
Mortality in poliomyelitis epidemics in the United
States prior to vaccine use was 5-7%. Most deaths occur
within the first 2wk after onset. Mortality and the
degree of disability are greater after the age of
puberty. In general, the more extensive the paralysis
in the first 10 days of illness, the more severe is the
ultimate disability. Unexpected improvement may
appear soon after defervescence and again about 6wk
after onset, a time that corresponds to functional
restoration of temporarily inactive neurons. The
degree of functional recovery also depends upon the
adequacy and promptness of supportive therapy:
proper body positioning, active motion, use of
assistive devices, and, of great importance, the
phsychologic motivation of the patient to return to as
full and normal a life as possible.

61. POLIOMYELITIS

62. POLIOMYELITIS