Infections of the central nervous system. General provisions An infectious lesion of the central nervous system is always the result of the interaction “guest - host. Presentation section on the topic of infectious diseases Diseases of the central nervous system presentation

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Infectious diseases with contact mech...

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Hyperhomocysteinemia Migraine Sleep Apnea Syndrome infectious diseases An increased risk of developing dyscirculatory encephalopathy with ... NINDS-AIREN) Presence of dementia Presence of manifestations of cerebrovascular diseases(anamnestic, clinical, neuroimaging data) The presence of a causal ...

Migrating, they open the gates to pathogenic microflora, contributing to the emergence of various infectious diseases. Immunity has not been studied. Disease symptoms ... changes consistent with allergic and toxic manifestations diseases. Pathological and anatomical changes At autopsy, they note ...

Signs: Incarceration of the penis from the very beginning diseases expressed by the impossibility of self-retraction into the cavity of the prepuce ... inflammatory - diseases spinal cord and its membranes, sacral nerves, lumbago, hemoglobinemia and prepuce vein thrombosis; 5) infectious- influenza...

farms. Medical contraindications: diseases central nervous system, mental; diseases of cardio-vascular system; diseases musculoskeletal system; diseases bronchi, lungs; chronic diseases stomach and intestines; chronic...

"Treatment room" - Mode in the treatment room. Sanitary and anti-epidemic regime. Complex of anti-epidemic measures. Sanitary maintenance of premises. Asepsis. Sanitary and anti-epidemic regime of the treatment room. used syringes. Primary requirements. Amidopyrine test technology.

"History of Medicine" - General. I. General history of medicine. Ancient writing documents. Witch Doctors; Healers; healers; Folk hygiene; Connection with modernity. In primitive society, healing was a collective activity. Tasks of studying the history of medicine. Sections of the history of medicine. Methods of healing in primitive society.

"Medicine in Ancient Egypt" - Gynecological section. Physicians of Egypt. Medicine in Ancient Egypt. Dentistry. Medicine prescriptions. Hesi-ra. Anubis. A patient with a broken leg. Large medical papyrus. Military doctors. Papyrus E. Smith. God of wisdom Thoth. clinical picture. The body of the deceased. Imhotep. Egypt. Book of preparation of medicines for all parts of the body.

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"Medicine of Russia of the 18th century" - Peter II. The staff of the medical college in 1799. Paul I (1754-1801), Russian emperor since 1796. In the first half of the 18th century. There were 5 medical schools in Russia. Transformations of archiater Rieger. About the position of the operator. State in the Medical Office. Anna Ivanovna. At the end of 1803, the Medical College was liquidated.

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Meningitis, encephalitis

Meningitis

Meningitis (meningitis, singular; Greek meninx, meningos
meninges + -itis) - inflammation of the membranes of the brain
and/or spinal cord.
leptomeningitis (inflammation of the soft and arachnoid membranes)
arachnoiditis (isolated inflammation of the arachnoid
rare)
pachymeningitis (inflammation of the dura mater).
Inflammatory changes are observed not only in soft and
arachnoid membranes of the brain and spinal cord, but also in ependyma and
choroid plexuses of the ventricles of the brain, which is accompanied by
overproduction of cerebrospinal fluid. In inflammatory
the process may involve intrathecal structures of the brain
(meningoencephalitis).

Classification of meningitis

Depending on the nature of the inflammatory
process and from the pathogen:
Purulent (bacterial
Serous (viral)
Depending on location:
- Cerebral (convexital,
basal and posterior cranial fossa)
- spinal

by pathogenesis: by the flow:

Primary (from purulent -
meningococcal; from serous
- choreomeningitis and
enteroviral meningitis)
Secondary (from purulent -
pneumococcal, streptococcal, staphylococcal;
from serous - with influenza, TVS,
syphilis, brucellosis,
mumps, etc.)
Spicy
subacute
chronic

Pathogenesis

The pathogenesis is based on dissemination
pathogen in the body (on the first
stage), then a breakthrough through
blood-brain barrier and implantation
into shells, where it develops rapidly
inflammation and swelling involved
choroid plexuses and vessels,
increased production of CSF, impaired
resorption, increased ICP)

Sources of infection - sick and healthy carriers of people (cerebrospinal and enteroviral meningitis)

or animals (with choreomeningitis - mice).
Transmission routes:
1) airborne way
(cerebrospinal), with dust particles
(choreomeningitis)
2) fecal-oral route (enteroviral
meningitis)

Activators at secondary M. get into
meninges in various ways:
one). Hematogenous way
- generalized (in the presence of bacteremia or viremia)
- regional-vascular (if the primary focus
infection is located in the head and blood vessels,
supplying it are connected with the vessels of the meninges).
2). Lymphogenic route of pathogen introduction.
3). Contact route (infection occurs
in the presence of an inflammatory focus,
in contact with the meninges
(purulent otitis media, mastoiditis, frontal sinusitis, brain abscess,
thrombosis of the cerebral sinuses), with an open craniocerebral injury, vertebral and spinal
trauma (especially accompanied by liquorrhea)

Clinic of meningitis

General infectious syndrome (fever,
malaise, facial flushing, myalgia, tachycardia,
inflammatory changes in the blood
Cerebral syndrome (headache, vomiting,
confusion, seizures)
Meningeal syndrome (rigidity
neck muscles, opisthotonus, s-m Kernig,
s-m Brudzinsky upper and lower, total
hyperesthesia (photophobia, phonophobia)

Difdiagnostics

subarachnoid hemorrhage
intracranial hypertension
Volumetric processes
Carcinomatosis of the meninges
intoxication
TBI

Diagnostics

Lumbar puncture (contraindications: signs
intrusions - depression of consciousness, anisocoria, violation of the rhythm of breathing,
decortication rigidity)
Study of the cellular composition of CSF, protein content,
Immunological study of CSF, bacteriological,
bacterioscopic and virological examination of CSF,
bacteriological examination of urine, blood, stool and nasopharyngeal lavage
, serological tests for syphilis and HIV infection
PCR, which detects the DNA of the pathogen in the CSF, in the blood.
UAC expanded, OAM, biochemical analyzes
Chest x-ray
Ocular fundus
CT or MRI (in the absence of the effect of treatment)

Liquor syndromes

Diagnosis
Davlet
nie
mm.
water.st.
Color
Prozra Cytosis
neutrality
filly
in mm
cube
Norm
100180
b/color
transparency
chic
Pus above
ny M norm
Yellowgreen.
Turbid
Serozn higher
th M
norms
b/color
SAK
Above
norms
Tumor- Above
whether the central nervous system is normal
Cytosis Protein
lymph %
quotes in
mm.
cube.
Sugar
mg%
Syndrome
0,160,33
40-60
-
-
1-5
a lot of
thousand
-
3,0-6,0
Below
norms
Kletb.dis.
Opales Prime
circ.
camping
Dec. and
hundreds
Norm
norm
Cell-b.
dissociation
Red
cloudy
th
erythro
quotes
Above
norms
norm
-
b \ color
transparency
chic
1-5
Above
norms
norm
Protein cell
erythro
quotes
-

Meningococcal meningitis (features)

caused by meningococcus, more common
during cold months, sporadically, less often
epidemic, predominantly in children.
Forms of meningococcal infection:
carriage, nasopharyngitis, arthritis, pneumonia,
meningococcemia, purulent meningitis,
meningoencephalitis.
Meningococcemia is characterized by
hemorrhagic petechial rash, severe
lightning current.
In KLA - leukocytosis, elevated ESR

Tuberculous meningitis (features)

Develops more gradually over time
the clinic is characterized by the defeat of ch.m.s.
(3,6,7,8, 2 pairs)
in CSF - first neutrophils, then lymphocytosis, decrease in sugar, increase in protein,
when standing, CSF falls out for 12 hours
characteristic film, mycobacterium TBS in
CSF, sputum, urine.

Acute serous meningitis

Pathogens: enteroviruses, virus
choreomeningitis, mumps, mumps
encephalitis, herps, etc.
A characteristically benign course
spontaneous recovery
Lymphocytran pleocytosis, moderate
increased protein, normal sugar levels

Treatment:

Etiotropic
– Empiric antibiotic therapy
– Antiviral drugs
– Elimination of the primary focus
Pathogenetic therapy
diuretics, hormonal drugs, IVL,
detoxifiers, analgesics,
sedatives, plasmapheresis,
anticonvulsants, etc.

Complications of meningitis

early
ICP increase
epileptic seizures
Thrombosis, cerebral infarction
subdural effusion
subdural empyema
Hydrocephalus
Pneumonia, myocarditis
Cerebral edema with herniation
Endotoxic shock
DIC
late
Residual focal
neurological deficit
Epilepsy
dementia
Neurosensory
hearing loss

Acute encephalitis

At present, the classification is
according to which 2 groups of encephalitis are distinguished:
primary and secondary.
To the group of primary encephalitis caused by
direct effect of the virus on affected
cells include:
arbovirus (tick and mosquito) encephalitis,
encephalitis that does not have a delineated seasonality
(enteroviral, herpetic, adenovirus,
encephalitis in rabies)
epidemic encephalitis.

Tick-borne encephalitis

Distribution area: in the southern part
zones of forests and forest-steppe of the Eurasian
mainland from the Pacific to the Atlantic
ocean
The causative agent, arbovirus, enters
organism through a tick bite (transmissible
way) or after eating raw
milk (alimentary route)

Clinic

The most typical pattern of lesions of gray
brainstem and cervical spinal
brain. Against the background of acute general infectious
symptom complex, cerebral syndrome
bulbar disorders develop and sluggish
paralysis of the neck and upper limbs. Usually
meningeal symptoms are also observed. In heavy
cases, stunning, delirium, hallucinations are noted.
A two-wave course is characteristic (3-5 days - the first
wave, 6-12 days - apyrexia, 5-10 days - second wave
fever)

Clinical forms:

feverish
Meningeal
Meningoencephalitic
Polioencephalitic (Chmn)
Poliomyelitis ("hanging head")
Polioencephalomyelitis

Diagnostics

Clinical blood test
Lumbar puncture
serological examination: RSK, RN, RTGA
ELISA, PCR (polymerase chain reaction)
CT, MRI

Treatment of tick-borne encephalthia

Anti-encephalitis immunoglobulin (1:801:160) 0.1-0.15 ml/kg body per day IM for the first 34 days
RNase 2.5-3.0 mg/kg per day IM divided by 6
once a day
Detoxification, dehydration, IVL
Glucocorticoids are contraindicated!
With a progressive course,
vaccine therapy

Prevention

Vaccination - tissue inactivated
the vaccine is administered 1 ml s / c 3 times in the autumn
period, 1 time in the spring, followed by
annual revaccination
Persons who have been bitten by ticks
antiencephalitis is introduced
immunoglobulin (1:640-1:1280) once
0.1 ml/kg during the first 48 hours and
0.2 ml/kg from 48 to 96 hours.

epidemic encephalitis

(lethargic, Economo's encephalitis).
The causative agent is unknown, but it is transmitted by airborne droplets. In the acute stage
pathomorphological changes are pronounced
inflammatory in nature and localized mainly
in the gray matter around the aqueduct of the brain and nuclei
hypothalamus. Typical clinical manifestations are fever, drowsiness, and diplopia (the triad
Economo), the reverse symptom of Argyle-Robertson,
parkinsonism with chronic process.

Acute transverse myelitis

A condition in which one or
several parts of the spinal cord
complete blockage of nerve transmission
momentum both up and down.
Cause of acute transverse myelitis
is not exactly known, but in 30-40% of people it is
the disease develops after mild
viral infection.

Acute transverse myelitis

Usually begins with sudden pain in
lower back accompanied by numbness and
muscle weakness that begins in
feet and extends upwards. These phenomena
may progress over several
days. In severe cases, paralysis
and loss of sensation along with
involuntary urination and
disruption of the intestines.

Diagnostics

The listed severe neurological
symptoms can be caused by a variety of
diseases. To narrow the search range, doctor
appoints a lumbar puncture (research,
in which from the spinal canal they take
some liquid for research),
computed tomography (CT), magnetic resonance imaging (MRI), or
myelography, and blood tests.

treatment

Truly effective treatments
acute transverse myelitis was not found, but
high doses of corticosteroids, such as
prednisolone, can stop the process,
associated with an allergic reaction. At
most patients occur at least
least partial restoration of functions, although
some retain muscle weakness and
numbness of the lower half of the body (and sometimes
hands).

Secondary microbial and infectious-allergic encephalitis

Secondary microbial and infectious allergic encephalitis
The group of secondary encephalitis includes all
infectious-allergic encephalitis
(parainfectious, grafting, etc.), in
pathogenesis of which the leading role belongs to
various antigen-antibody complexes or
autoantibodies that form allergic
reaction in the central nervous system, as well as a group of demyelinating
diseases of the nervous system (acute disseminated
encephalomyelitis, Schilder's disease),
accompanied by various rashes on
skin and mucous membranes.

Measles encephalitis

Measles is more common in children under 5 years of age. Source of infection
is sick, the route of transmission is airborne, contagious
period lasts 8-10 days. Typical development of measles
encephalitis occurs towards the end of the rash (3-5th day), when
temperature normalizes. Suddenly there's a new rise
temperature and the general condition of the child changes. Appear
drowsiness, weakness, sometimes psychomotor agitation,
then stupor or coma. At an early age, characteristic
convulsive seizures. Psychosensory disturbances are possible,
hallucinatory syndrome. Damage to the optic nerves
may reach amaurosis. In most cases, there are
inflammatory changes in the cerebrospinal fluid
moderate cellular-protein dissociation.

Chickenpox encephalitis

a rare but serious complication of chickenpox in children.
The causative agent is the varicella-zoster virus.
Chickenpox encephalitis usually develops on
background of generalized rash, high fever and
lymphadenitis. Cerebral
disorders - lethargy, weakness, headache,
dizziness, vomiting; rarely - generalized
convulsions, febrile delirium. Focal paresis
are of a transitory nature. Meningeal
symptoms develop in a third of patients.

rubella encephalitis

The source of infection is a patient with rubella, the route of transmission is airborne. Neurological manifestations in these cases may
occur on the 3rd-4th day of the rash, is rare, usually in
children of early age, is characterized by a severe course and
high lethality. In this case, the rubella virus cannot be isolated
succeeds. The onset is acute, with the onset of headache, high
fever; characterized by disorders of consciousness up to a deep
coma. In the clinic, convulsions, hyperkinesis of various
type, cerebellar and autonomic disorders. In the spinal
fluid moderate pleocytosis with a predominance of lymphocytes,
slight increase in protein. Separate forms:
meningeal, meningoencephalitic,
meningomyelitic and encephalomyelitis.

neurorheumatism

Rheumatism is a common infectious-allergic
disease with systemic damage to the connective tissue
tissues, predominant localization in the cardiovascular system, as well as involvement in the process
other internal organs and systems.
The disease can begin with a sore throat, then give
joint damage in the form of acute articular
rheumatism, brain damage in the form of a small chorea,
heart failure in the form of rheumatic heart disease without defects
valves or with recurrent rheumatic heart disease and defect
valves, myocardiosclerosis.

Damage to the nervous system in
rheumatism are diverse, but more often
most common cerebral rheumatic vasculitis,
chorea, cerebral embolism
mitral disease.
Role set in occurrence
neurorheumatism beta-hemolytic
group A streptococcus.

Clinic for chorea minor

The word "chorea" in Latin means
"dance, round dance". Disease
usually develops in school-age children
7-15 years, more often girls. A number of involuntary
uncoordinated (disproportionate) and
choppy movements with significant
decrease in muscle tone. Gordon reflex:
when eliciting a knee-jerk reflex
stays in the flexed position

Chorea minor treatment

bed rest due to the combination of chorea with rheumatic endocarditis;
sleep favorably affects the course of chorea, since violent
sleep movements stop;
salt and carbohydrate restricted diet
sufficient introduction of high-grade proteins and increased content
vitamins;
in case of severe hyperkinesis, it is recommended to combine sleep treatment with taking
chlorpromazine;
prescribe benzylpenicillin sodium salt, then drugs
prolonged (prolonged) action (bicillin-3, bicillin-5); at
intolerance to penicillins, they are replaced by cephalosporins;
glucocorticosteroids;
non-steroidal anti-inflammatory drugs (aspirin, indomethacin and
others);
aminoquinol preparations

Neurobrucellosis

caused by several types
Gram-negative bacteria Brucella. Main
patients are the source of infection
animals (large and small cattle).
Infection occurs by contact, alimentary,
airborne routes. Get sick in
mainly persons associated with animal husbandry, and
also when eating unpasteurized
milk or cheese. The disease occurs in the Urals,
in Siberia, in the North Caucasus, in Kazakhstan.

Anyone can be affected by brucellosis
parts of the nervous system (central,
peripheral and vegetative).
To typical neurological manifestations
brucellosis include neuralgia and neuritis
peripheral and cranial nerves,
radiculitis, plexitis (lumbosacral, shoulder), polyneuritis,
polyradiculoneuritis.

Damage to the autonomic nervous system
observed in almost all patients with brucellosis
and is characterized by hyperhidrosis, dryness
skin, edema and acrocyanosis, prolapse
hair, brittle nails, arterial
hypotension, osteoporosis, weight loss,
dysfunction of internal organs
due to damage to the celiac (solar) and
mesenteric autonomic plexus.

Anamnestic data are important for making a diagnosis.
(profession of the patient, epidemiological features
place of residence, contact with animals). matter
prior periods of undulating fever with
intense pain (muscle, joint,
radicular, neuralgic, neuritic),
enlarged lymph nodes, liver, spleen,
profuse sweat, pronounced asthenic syndrome.
The diagnosis of brucellosis is confirmed by positive
laboratory results: reactions
Wright agglutination (titers 1400 and above), accelerated
Huddleson's reaction, Burne's allergy test.

treatment of neurobrucellosis

In acute and subacute forms of neurobrucellosis,
antibiotics (rifampicin, chloramphenicol, ampicillin, colistin,
erythromycin, gentamicin, kanamycin, tetracycline preparations
row) in courses of 5–7 days (2–3 courses with a week break).
The most common is rifampicin (600 mg orally once a day).
day). In the acute stage and in the presence of severe meningitis and
encephalitis, parenteral antibiotics are recommended.
In chronic forms of brucellosis, anti-brucellosis is indicated.
polyvalent vaccine. Symptomatic therapy is carried out
(painkillers, sedatives, desensitizers,
fortifying agents). With peripheral
lesions of the nervous system, physiotherapy is effective (UHF,
paraffin and mud applications, electrophoresis of novocaine and
calcium).

Neurosyphilis

Pale nervous system damage
spirochete or its products
vital activity.
Syphilis of the brain manifests itself
syphilitic meningitis,
gum formation, changes
vessels with proliferation of internal
membranes and adventitia, leading to
vasoconstriction.

Conventionally, two phases are distinguished during
neurosyphilis: early and late
Early neurosyphilis. (up to 5 years from start
diseases). During these periods, they are affected
meninges and vessels of the brain
(mesenchymal neurosyphilis).
- Latent (asymptomatic) syphilitic
meningitis

Acute generalized syphilitic
meningitis
Early meningovascular syphilis.
Syphilitic neuritis and polyneuritis
Syphilitic meningomyelitis

In general, the diagnosis of neurosyphilis requires the presence of 3
criteria:
positive non-treponemal and/or treponemal
reactions in the study of blood serum;
neurological syndromes characteristic of
neurosyphilis;
cerebrospinal fluid changes
(positive Wassermann reaction, inflammatory
CSF changes with cytosis over 20 µl and
protein content over 0.6 g/l, positive RIF).

Dorsal tabes

Dorsal tabes (tabes dorsalis; synonyms:
tabes of the spinal cord, syphilitic tabes,
progressive locomotor ataxia
Duchenne) - a form of late progressive
syphilitic lesions of the nervous system
(neurosyphilis) Develops after 6-30 years
(usually 10-15 years) after infection with syphilis, in
mainly in patients receiving insufficient
and non-systematic treatment or no treatment at all
treated in the early period of syphilis.

Morphological changes are seen in
posterior cords and posterior roots
spinal cord, they are especially pronounced in
sacral and lumbar regions. In
many cases of degeneration
cranial nerves in their extracerebral,
extracranial segment. Especially often
the optic nerve is damaged.

tabic pain
Argyll Robertson syndrome, anisocoria,
miosis, mydriasis, violation of the correct
round pupils, they can become
oval, polygonal.
complete lack of deep
sensation, locomotor ataxia.

Treatment

The most effective intravenous administration of high
doses of penicillin (2-4 million units 6 times a day) for
10-14 days. Intramuscular administration of penicillin
does not allow reaching therapeutic concentrations in
liquor and is possible only in combination with the reception
inside probenecid (2 g per day), delaying
renal excretion of penicillin. Retarpen 2.4 million units
1 time per week three times.
For allergies to penicillins, use
ceftriaxone (rocephin) 2 g daily IV or IM
within 10-14 days.

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Slides captions:

SPb SBEE SPO "Medical College No. 2" Diseases of the peripheral nervous system Lecture Teacher Solovieva A.A. 2016

The peripheral nervous system consists of the cranial and spinal nerves, as well as the nerves and plexuses of the autonomic nervous system, connecting the central nervous system to the organs of the body.

The somatic nervous system is responsible for coordinating body movements as well as receiving external stimuli. It is a system that regulates consciously controlled activity. The autonomic nervous system is a department of the nervous system that regulates the activity of internal organs and metabolism in all organs. The autonomic nervous system, in turn, is divided into the sympathetic nervous system, parasympathetic nervous system.

Nervous system Nervous system CNS CNS

Sympathicotonia is characterized by tachycardia, blanching of the skin, increased blood pressure, weakening of intestinal motility, mydriasis, chills, a feeling of fear and anxiety. With a sympathoadrenal crisis, a headache appears or intensifies, numbness and coldness of the extremities, pallor of the face occur, blood pressure rises to 150/90-180/110 mm Hg, the pulse quickens to 110-140 beats / min, there are pains in the area heart, there is excitement, restlessness, sometimes the body temperature rises to 38-39 ° C. Vagotonia is characterized by bradycardia, shortness of breath, reddening of the skin of the face, sweating, salivation, lowering blood pressure, and gastrointestinal dyskinesias. A vagoinsular crisis is manifested by a feeling of heat in the head and face, suffocation, heaviness in the head, nausea, weakness, sweating, dizziness, urge to defecate, increased intestinal motility, miosis is noted, a decrease in heart rate to 45-50 beats / mi, a decrease in blood pressure up to 80/50 mm Hg Art.

GENERAL TERMINOLOGY OF PNS DISEASES NEUROPATHY - damage to the peripheral nerve of a non-infectious nature. RADICULOPATHY - the root of the spinal cord is affected. 1. Focal neuropathy is a disease of one nerve. Causes: compression, ischemia, trauma, intoxication, metabolic disorders. 2. Multifocal neuropathy - damage to several peripheral nerves. Causes: diabetic microangiopathy, systemic connective tissue diseases, hypothyroidism. If the nerve is damaged, FLADDY PARESIS OR PARALYSIS develops.

NEURITIS - damage to the peripheral nerve NEURITIS - DAMAGE TO THE PERIPHERAL NERVE BY INFECTION

Neuralgia is a disease of the peripheral peripheral nerve, in which the main clinical symptom is PAIN

POLYNEUROPATHY - multiple lesions of peripheral nerves, manifested by peripheral flaccid paralysis, sensory disturbances, trophic and vegetovascular disorders, mainly in the distal extremities. . diabetic

nature of the course of polyneuropathy ACUTE - symptoms develop within a month SUBACUTE - symptoms develop no longer than two months CHRONIC - symptoms develop within 6 months

POLYRADICULONEUROPATHY Simultaneous damage to the spinal roots and peripheral nerves of a symmetrical nature. Often leads to peripheral tetraparesis or tetraplegia with impaired respiratory function, which necessitates intensive care, mechanical ventilation.

PLEXOPATHY - damage to the plexus formed by the spinal nerves. Allocate cervical, shoulder, lumbar, sacral plexopathy. Involvement of at least 2 peripheral nerves is typical. More often the process is unilateral, the clinic is dominated by pain, weakness, muscle atrophy, and sensory disorders.

TUNNEL NEUROPATHY - damage to the peripheral nerve in anatomical constrictions (bone-fibrous canals, aponeurotic fissures, holes in the ligaments. The reason is mechanical compression in the area of ​​\u200b\u200bthe anatomical narrowing and ischemia of the nerve. For example, tunnel neuropathy of the median nerve in the carpal tunnel).

MAIN DISEASES OF THE PERIPHERAL NERVOUS SYSTEM

NEURITIS OF THE FACIAL NERVE (VII pair of cranial nerves) SYMPTOMS OF THE DISEASE: - drooping corner of the mouth - wide open palpebral fissure that does not close when squinting - mild or absent pattern of skin folds of half of the face

The patient cannot wrinkle his forehead, close his eyes, puff out his cheek, speech becomes slurred. There is a leakage of liquid food through the lowered corner of the mouth, dryness of the eye. REASONS: herpes simplex, diphtheria, syphilis, probably - with fractures of the bones of the skull, tumors of the cerebellopontine angle, with chronic otitis media. It is observed as a manifestation of nervous diseases - Guillain-Barré polyradiculoneuropathy, multiple sclerosis. TREATMENT 1. Glucocorticosteroids (prednisolone, dexamethasone) 2. Antihistamines 3. Group B vitamins PTO, exercise therapy.

TRIPENDIC NETURALGIA (V PAIR OF CNs) Symptoms: pronounced pain paroxysms up to 2 minutes, the nature of the pain is acute, shooting, burning, always accompanied by a painful grimace.

TREATMENT 1. For relief of pain - anticonvulsants (carbamazepine). 2. Anti-inflammatory drugs (actovegin). 3. Vitamins of group B. 4. With herpetic lesions - acyclovir. 5. Antidepressants, neuroleptics, tranquilizers, psychotherapy. 6. FTL: UHF, UVR, diadynamic currents, novocaine electrophoresis, laser therapy.

DEMIELINIZING INFLAMMATORY POLYNEUROPATHY. GUILLEN-BARRE SYNDROME

THE MAIN CLINICAL MANIFESTATION IS FLEXIBLE PARALYSIS The development of paralysis begins with the lower extremities, then the upper extremities, then muscle weakness captures the respiratory and cranial muscles. Weakness of the intercostal respiratory muscles and diaphragm leads to respiratory failure, requiring mechanical ventilation. CCC dysfunction is manifested by cardiac arrhythmias, which can be the cause of sudden death of the patient. TREATMENT 1. Emergency hospitalization in intensive care.

Hourly monitoring of the patient's vital functions Control of the state of consciousness Monitoring of respiratory function Monitoring of hemodynamics Monitoring of the excretory function Correction of pathological muscle tone and prevention of the formation of motor stereotypes Providing adequate nutritional support Complex anti-decubitus therapy

DYSMETABOLIC POLYNEUROPATHY. DIABETIC POLYNEUROPATHY. SYMPTOMS: 1. Violation of sensitivity in the legs: pain, paresthesia, numbness. 2. Decreased pain and temperature sensitivity by the type of "socks" or "golf socks". 3. Muscle weakness in the legs ("slapping gait"). 4. Atrophic processes in the muscles. 5. Complications: painful trophic ulcers, gangrene.

TREATMENT Normalization of blood glucose levels. For pain relief - NSAIDs, analgesics, anticonvulsants, antidepressants, psychotherapy. To combat ischemia - pentoxifylline. Teaching the patient to prevent trophic disorders of the skin of the feet.

POLYNEUROPATHY IN EXOGENOUS INTOXICATIONS. ALCOHOLIC POLYNEUROPATHY.

ALCOHOLIC POLYNEUROPATHY - axonal polyneuropathy with severe sensory and motor disorders. INITIAL SYMPTOMS: - burning, excruciating pain in the distal parts of the lower extremities - spasms of the calf muscles at night - weakness in the legs SYMPTOMS OF THE ADVANCED STAGE OF THE DISEASE - flaccid lower paraparesis - "cock's gait" - difficulty climbing stairs - trophic changes in the skin - sensitivity disorders by type of "socks", "golf"

TREATMENT 1. NO ALCOHOL. 2. COMPLETE NUTRITION. 3. RECOVERY OF THIAMIN DEFICIENCY (5% solution of vitamin B1 intramuscularly). 4. NOOTROPS. 5. ANTI-INFLAMMATORY, ANTICONVULSANTS, ANTIDEPRESSANTS, DETOXIFICATION (rheopolyglucin, hemodez). 6.FTL, exercise therapy, FAMILY PSYCHOTHERAPY.

CARPAN TANAL SYNDROME (MEDIAN NERVE NEUROPATHY) CAUSE - multiple physical overloads of the wrist (programmers, musicians) SYMPTOMS - painful paresthesia and a feeling of numbness on the palmar surface of the wrist, hand and I, II, III fingers. - Symptoms are aggravated by movements in the wrist, raising the arm up. - atrophy of the tenor muscles - "monkey paw"

PLEXOPATHY OF THE BRACHERIC PLEXUS

SYMPTOMS - physical weakness and atrophy of the biceps, deltoid, scapular muscles. - the arm does not bend at the elbow, does not abduct and HANGS in the position of internal rotation. -movements in the brush saved. TREATMENT OF PLEXOPATHY NSAIDs (diclofenac) Glucocorticoids (blockade with hydrocortisone, dexamethasone). Muscle relaxants (baclofen, mydocalm, sirdalut). Vitamins gr B, analgesics, anticonvulsants. FTL, LFC.

NEUROLOGICAL MANIFESTATIONS OF OSTEOCHONDROSIS OF THE SPINE OSTEOCHONDROSIS is a degenerative-dystrophic lesion of the INTERVERTEBRAL DISC, which is based on the primary lesion of the nucleus pulposus with subsequent involvement of the bodies of adjacent vertebrae, intervertebral joints and ligamentous apparatus

LUMBAGO (LUMBAGO) - Sharp pain in the lumbosacral region, aggravated by movement. Most often occurs IMMEDIATELY after an awkward movement, physical activity. An analgesic posture and a sharp tension of the back muscles are characteristic.

LUMBALGIA - subacute or chronic pain in the lumbosacral region. Occurs late after exercise or without cause. There is a limitation of movements and tension of the muscles of the back. LUMBOISCHALGIA - pain in the lumbosacral region, radiating to the leg. Characterized by an antalgic posture with tension in the muscles of the back, buttocks, back of the thigh. VERTEBROGENIC RADICULOPATHY OF THE LUMBOSACRAL SPINE Manifested by severe pain in the lower back radiating to the buttock, back of the leg to the V toe. Pronounced antalgic scoliosis and muscle tension. Paresthesia and numbness in this area are characteristic. When walking, the severity of symptoms increases.

CERVICAGO (NECK LUMBER) Acute pain in the cervical spine, aggravated by movement. The forced position of the head and the tension of the muscles of the neck are characteristic. CERVICALGIA - the pain is less intense, more often chronic. Tension of the paravertebral muscles is characteristic. CERVICOCRANIALGIA - pain in the cervical spine, radiating to the occipital region.

Diagnosis Reduced disc height Convergence of neighboring vertebrae Marginal osteophytes Narrowing of the intervertebral foramens Subchondral sclerosis of the vertebral bodies Spondylarthrosis (narrowing of the joint spaces of the intervertebral joints) Disc herniation.

METHODS FOR THE TREATMENT OF BACK PAIN Rest for 2-5 days, the patient should not be prescribed a long-term protective regime. Wearing a bandage or corset can cause weakening of the ligamentous apparatus and abdominal muscles, which will increase the instability of the spinal motion segment. Therefore, the corset is worn no more than 2 hours a day during the period of maximum loads.

METHODS FOR THE TREATMENT OF BACK PAIN a very large number of patients experience recurrence of pain after 2.5-3 years

NSAIDs - one of the most widely used pharmacological groups NSAIDs should be prescribed in the first two days of the disease in order to interrupt the formation of the prostaglandin and cytokine cascade at the synapse level and prevent the development of neurogenic aseptic inflammation, and, moreover, chronic inflammation

Treatment of the acute period The action of non-narcotic analgesics may be enhanced by the addition of - anticonvulsants (gabapentin, finlepsin) - antidepressants (amitriptyline, paroxetine)

Finalgel ® first aid Quickly relieve pain and stop the inflammatory process will help Finalgel ® Finalgel ® based on piroxicam quickly and safely relieve pain and treat inflammation. restores the usual range of motion in the joint reduces tissue swelling has a local antipyretic effect has an antiplatelet effect

FINALGON - COMPLEX DRUG Nonivamide synthetic derivative of capsaicin locally irritating substance isolated from pepper Nicoboxyl derivative of nicotinic acid strong vasodilator

Chronic pain syndromes Antidepressants (Amitriptyline, Paroxetine, Fluoxetine, etc.) Selective NSAIDs (Movalis) Analgesics (Katadalon, Zaldiar) Anticonvulsants (Neurontin) Neuroprotectors (Cortexin) Drugs for the treatment of osteoporosis (Fosavans)

Physiotherapy for osteochondrosis - its types and features This type of therapy does not cause exacerbation and allows you to reduce the dose of drugs. Due to fewer drugs, the risk of allergies and side effects is reduced. In the acute stage - UHF, SMT, hydrocortisone phonophoresis, quartz, laser therapy, IRT. In the stage of sub-remission and remission - thermal procedures (paraffin, ozocerite, pelloidotherapy)

Factors contributing to the development of exacerbation or deterioration of well-being 1. Sedentary lifestyle, low physical activity 2. Significant physical activity (at home, at work, in the garden, lifting weights). 3. Overweight (body mass index over 25 kg/m2). 4. Inadequate loads on the joints that contribute to injuries: frequent climbing stairs and frequent carrying of heavy loads during work; regular professional sports; prolonged squatting or kneeling or walking more than 3 km while working; 5. Weather change, drafts and hypothermia. 6. Depressed mood and depression. Many risk factors can be changed!

THANK YOU FOR YOUR ATTENTION


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