Convulsive syndrome ICD 10. Get treatment in Korea, Israel, Germany, USA. Symptoms in children and adults

Class VI. Diseases of the nervous system (G00-G47)

This class contains the following blocks:
G00-G09 Inflammatory diseases of the central nervous system
G10-G13 Systemic atrophies affecting primarily the central nervous system
G20-G26 Extrapyramidal and other movement disorders
G30-G32 Other degenerative diseases of the central nervous system
G35-G37 Demyelinating diseases of the central nervous system
G40-G47 Episodic and paroxysmal disorders

INFLAMMATORY DISEASES OF THE CENTRAL NERVOUS SYSTEM (G00-G09)

G00 Bacterial meningitis, not elsewhere classified

Included: arachnoiditis)
leptomeningitis)
meningitis) bacterial
pachymeningitis)
Excluded: bacterial:
meningoencephalitis ( G04.2)
meningomyelitis ( G04.2)

G00.0 Influenza meningitis. Meningitis caused by Haemophilus influenzae
G00.1 Pneumococcal meningitis
G00.2 Streptococcal meningitis
G00.3 Staphylococcal meningitis
G00.8 Meningitis caused by other bacteria
Meningitis caused by:
Friedlander wand
Escherichia coli
Klebsiella
G00.9 Bacterial meningitis, unspecified
Meningitis:
purulent NOS
pyogenic NOS
pyogenic NOS

G01* Meningitis in bacterial diseases classified elsewhere

Meningitis (with):
anthrax ( A22.8+)
gonococcal ( A54.8+)
leptospirosis ( A27. -+)
listeriosis ( A32.1+)
Lyme disease ( A69.2+)
meningococcal ( A39.0+)
neurosyphilis ( A52.1+)
salmonellosis ( A02.2+)
syphilis:
congenital ( A50.4+)
secondary ( A51.4+)
tuberculosis ( A17.0+)
typhoid fever ( A01.0+)
Excluded: meningoencephalitis and meningomyelitis due to bacterial
diseases classified elsewhere ( G05.0*)

G02.0* Meningitis in viral diseases classified elsewhere
Meningitis (caused by a virus):
adenoviral ( A87.1+)
enteroviral ( A87.0+)
herpes simplex ( B00.3+)
infectious mononucleosis ( B27. -+)
measles ( B05.1+)
mumps ( B26.1+)
rubella ( B06.0+)
chickenpox ( B01.0+)
herpes zoster ( B02.1+)
G02.1* Meningitis due to mycoses
Meningitis (with):
candida ( B37.5+)
coccidioidomycosis ( B38.4+)
cryptococcal ( B45.1+)
G02.8* Meningitis in other specified infectious and parasitic diseases classified elsewhere
Meningitis caused by:
African trypanosomiasis ( B56. -+)
Chagas disease ( B57.4+)

G03 Meningitis due to other and unspecified causes

Included: arachnoiditis)
leptomeningitis) due to other and unspecified
meningitis) causes
pachymeningitis)
Excluded: meningoencephalitis ( G04. -)
meningomyelitis ( G04. -)

G03.0 Non-pyogenic meningitis. Nonbacterial meningitis
G03.1 Chronic meningitis
G03.2 Benign recurrent meningitis [Mollaret]
G03.8 Meningitis caused by other specified pathogens
G03.9 Meningitis, unspecified. Arachnoiditis (spinal) NOS

G04 Encephalitis, myelitis and encephalomyelitis

Includes: acute ascending myelitis
meningoencephalitis
meningomyelitis
Excluded: benign myalgic encephalitis ( G93.3)
encephalopathy:
NOS ( G93.4)
alcoholic origin ( G31.2)
toxic ( G92)
multiple sclerosis ( G35)
myelitis:
acute transverse ( G37.3)
subacute necrotizing ( G37.4)

G04.0 Acute disseminated encephalitis
Encephalitis)
Encephalomyelitis) post-immunization
If necessary, identify the vaccine
G04.1 Tropical spastic paraplegia
G04.2 Bacterial meningoencephalitis and meningomyelitis, not elsewhere classified
G04.8 Other encephalitis, myelitis and encephalomyelitis. Postinfectious encephalitis and encephalomyelitis NOS
G04.9 Encephalitis, myelitis or encephalomyelitis, unspecified. Ventriculitis (cerebral) NOS

G05* Encephalitis, myelitis and encephalomyelitis in diseases classified elsewhere

Includes: meningoencephalitis and meningomyelitis in diseases
classified elsewhere

If it is necessary to identify the infectious agent, use an additional code ( B95-B97).

G06.0 Intracranial abscess and granuloma
Abscess (embolic):
brain [any part]
cerebellar
cerebral
otogenic
Intracranial abscess or granuloma:
epidural
extradural
subdural
G06.1 Intravertebral abscess and granuloma. Abscess (embolic) of the spinal cord [any part]
Intravertebral abscess or granuloma:
epidural
extradural
subdural
G06.2 Extradural and subdural abscess, unspecified

G07* Intracranial and intravertebral abscess and granuloma in diseases classified elsewhere

Brain abscess:
amoebic ( A06.6+)
gonococcal ( A54.8+)
tuberculous ( A17.8+)
Granuloma of the brain in schistosomiasis ( B65. -+)
Tuberculoma:
brain ( A17.8+)
meninges ( A17.1+)

G08 Intracranial and intravertebral phlebitis and thrombophlebitis

Septic(s):
embolism)
endoflibit)
phlebitis) intracranial or intravertebral
thrombophlebitis) venous sinuses and veins
thrombosis)
Excluded: intracranial phlebitis and thrombophlebitis:
complicating:
abortion, ectopic or molar pregnancy ( O00 -O07 , O08.7 )
pregnancy, childbirth or the postpartum period ( O22.5, O87.3)
non-purulent origin ( I67.6); non-purulent intravertebral phlebitis and thrombophlebitis ( G95.1)

G09 Consequences of inflammatory diseases of the central nervous system

NoteThis category should be used to indicate
conditions primarily classified under headings

G00-G08(excluding those marked with *) as the cause of consequences that are themselves attributed to
Other headings The concept of “consequences” includes conditions specified as such or as late manifestations or consequences that exist for a year or more after the onset of the condition that caused them. When using this rubric, it is necessary to be guided by the appropriate recommendations and rules for coding morbidity and mortality, given in volume 2.

SYSTEMIC ATROPHY AFFECTING PRIMARILY THE CENTRAL NERVOUS SYSTEM (G10-G13)

G10 Huntington's disease

Huntington's chorea

G11 Hereditary ataxia

Excluded: hereditary and idiopathic neuropathy ( G60. -)
cerebral palsy ( G80. -)
metabolic disorders ( E70-E90)

G11.0 Congenital non-progressive ataxia
G11.1 Early cerebellar ataxia
Note: Usually begins in people under 20 years of age
Early cerebellar ataxia with:
essential tremor
myoclonus [Hunt's ataxia]
with preserved tendon reflexes
Friedreich's ataxia (autosomal recessive)
X-linked recessive spinocerebellar ataxia
G11.2 Tardive cerebellar ataxia
Note: Usually begins in people over 20 years of age
G11.3 Cerebellar ataxia with impaired DNA repair. Telangiectatic ataxia [Louis-Bar syndrome]
Excludes: Cockayne syndrome ( Q87.1)
xeroderma pigmentosa ( Q82.1)
G11.4 Hereditary spastic paraplegia
G11.8 Other hereditary ataxia
G11.9 Hereditary ataxia, unspecified
Hereditary cerebellar:
ataxia NOS
degeneration
disease
syndrome

G12 Spinal muscular atrophy and related syndromes

G12.0 Pediatric spinal muscular atrophy, type I [Werdnig-Hoffmann]
G12.1 Other hereditary spinal muscular atrophies. Progressive bulbar palsy in children [Fazio-Londe]
Spinal muscular atrophy:
adult uniform
child form, type II
distal
juvenile form, type III [Kugelberg-Welander]
scapuloperoneal form
G12.2 Motor neuron disease. Familial motor neuron disease
Lateral sclerosis:
amyotrophic
primary
Progressive:
bulbar palsy
spinal muscular atrophy
G12.8 Other spinal muscular atrophies and related syndromes
G12.9 Spinal muscular atrophy, unspecified

G13* Systemic atrophies affecting primarily the central nervous system in diseases classified elsewhere

G13.0* Paraneoplastic neuromyopathy and neuropathy
Carcinomatous neuromyopathy ( C00-S97+)
Neuropathy of the sensory organs in the tumor process [Denia-Brown] ( C00-D48+)
G13.1* Other systemic atrophies, affecting primarily the central nervous system, in tumor diseases. Paraneoplastic limbic encephalopathy ( C00-D48+)
G13.2* Systemic atrophy due to myxedema, affecting primarily the central nervous system ( E00.1+, E03. -+)
G13.8* Systemic atrophy, affecting primarily the central nervous system, in other diseases classified elsewhere

EXTRAPYRAMIDAL AND OTHER MOTOR DISORDERS (G20-G26)

G20 Parkinson's disease

Hemiparkinsonism
Shaking paralysis
Parkinsonism, or Parkinson's disease:
NOS
idiopathic
primary

G21 Secondary parkinsonism

G21.0 Neuroleptic malignant syndrome. If necessary, identify the drug
use an additional code for external causes (class XX).
G21.1 Other forms of drug-induced secondary parkinsonism.
G21.2 Secondary parkinsonism caused by other external factors
If it is necessary to identify an external factor, use an additional code of external causes (class XX).
G21.3 Postencephalitic parkinsonism
G21.8 Other forms of secondary parkinsonism
G21.9 Secondary parkinsonism, unspecified

G22* Parkinsonism in diseases classified elsewhere

Syphilitic parkinsonism ( A52.1+)

G23 Other degenerative diseases of the basal ganglia

Excludes: multisystem degeneration ( G90.3)

G23.0 Hallervorden-Spatz disease. Pigmented pallidal degeneration
G23.1 Progressive supranuclear ophthalmoplegia [Steele-Richardson-Olszewski]
G23.2 Striatonigral degeneration
G23.8 Other specified degenerative diseases of the basal ganglia. Calcification of the basal ganglia
G23.9 Degenerative basal ganglia disease, unspecified

G24 Dystonia

Included: dyskinesia
Excludes: athetoid cerebral palsy ( G80.3)

G24.0 Drug-induced dystonia. If necessary, identify the drug
use an additional code for external causes (class XX).
G24.1 Idiopathic familial dystonia. Idiopathic dystonia NOS
G24.2 Idiopathic nonfamilial dystonia
G24.3 Spasmodic torticollis
Excludes: torticollis NOS ( M43.6)
G24.4 Idiopathic orofacial dystonia. Orofacial dyskinesia
G24.5 Blepharospasm
G24.8 Other dystonias
G24.9 Dystonia, unspecified. Dyskinesia NOS

G25 Other extrapyramidal and movement disorders

G25.0 Essential tremor. Familial tremor
Excludes: tremor NOS ( R25.1)
G25.1 Drug-induced tremor
If it is necessary to identify the drug, use an additional code for external causes (class XX).
G25.2 Other specified forms of tremor. Intention tremor
G25.3 Myoclonus. Drug-induced myoclonus. If it is necessary to identify the drug, use an additional code for external causes (class XX).
Excluded: facial myokymia ( G51.4)
myoclonic epilepsy ( G40. -)
G25.4 Drug-induced chorea
If it is necessary to identify the drug, use an additional code for external causes (class XX).
G25.5 Other types of chorea. Chorea NOS
Excludes: chorea NOS with cardiac involvement ( I02.0)
Huntington's chorea ( G10)
rheumatic chorea ( I02. -)
Sydenchen's chorea ( I02. -)
G25.6 Drug-induced and other organic tics
If it is necessary to identify the drug, use an additional code for external causes (class XX).
Excludes: de la Tourette syndrome ( F95.2)
tick NOS ( F95.9)
G25.8 Other specified extrapyramidal and movement disorders
Restless legs syndrome. Shackled person syndrome
G25.9 Extrapyramidal and movement disorder, unspecified

G26* Extrapyramidal and movement disorders in diseases classified elsewhere

OTHER DEGENERATIVE DISEASES OF THE NERVOUS SYSTEM (G30-G32)

G30 Alzheimer's disease

Includes: senile and presenile forms
Excluded: senile:
brain degeneration NEC ( G31.1)
dementia NOS ( F03)
senility NOS ( R54)

G30.0 Early Alzheimer's disease
Note The onset of the disease usually occurs in people under 65 years of age
G30.1 Late Alzheimer's disease
Note The onset of the disease usually occurs in people over 65 years of age
G30.8 Other forms of Alzheimer's disease
G30.9 Alzheimer's disease, unspecified

G31 Other degenerative diseases of the nervous system, not elsewhere classified

Excluded: Reye's syndrome ( G93.7)

G31.0 Limited brain atrophy. Pick's disease. Progressive isolated aphasia
G31.1 Senile degeneration of the brain, not elsewhere classified
Excludes: Alzheimer's disease ( G30. -)
senility NOS ( R54)
G31.2 Nervous system degeneration caused by alcohol
Alcoholic:
cerebellar:
ataxia
degeneration
cerebral degeneration
encephalopathy
Alcohol-induced autonomic nervous system disorder
G31.8 Other specified degenerative diseases of the nervous system. Gray matter degeneration [Alpers disease]
Subacute necrotizing encephalopathy [Leigh's disease]
G31.9 Degenerative disease of the nervous system, unspecified

G32* Other degenerative disorders of the nervous system in diseases classified elsewhere

G32.0* Subacute combined degeneration of the spinal cord in diseases classified elsewhere
Subacute combined degeneration of the spinal cord due to vitamin deficiency AT 12 (E53.8+)
G32.8* Other specified degenerative disorders of the nervous system in diseases classified elsewhere

DEMYELINATING DISEASES OF THE CENTRAL NERVOUS SYSTEM (G35-G37)

G35 Multiple sclerosis

Multiple sclerosis:
NOS
brain stem
spinal cord
disseminated
generalized

G36 Other form of acute disseminated demyelination

Excluded: post-infectious encephalitis and encephalomyelitis NOS ( G04.8)

G36.0 Neuromyelitis optica [Devic's disease]. Demyelination in optic neuritis
Excluded: optic neuritis NOS ( H46)
G36.1 Acute and subacute hemorrhagic leukoencephalitis [Harst disease]
G36.8 Another specified form of acute disseminated demyelination
G36.9 Acute disseminated demyelination, unspecified

G37 Other demyelinating diseases of the central nervous system

G37.0 Diffuse sclerosis. Periaxial encephalitis, Schilder's disease
Excluded: adrenoleukodystrophy [Addison-Schilder] ( E71.3)
G37.1 Central demyelination of the corpus callosum
G37.2 Central pontine myelinolysis
G37.3 Acute transverse myelitis in demyelinating disease of the central nervous system
Acute transverse myelitis NOS
Excluded: multiple sclerosis ( G35)
Neuromyelitis optica [Devic's disease] ( G36.0)
G37.4 Subacute necrotizing myelitis
G37.5 Concentric sclerosis [Balo]
G37.8 Other specified demyelinating diseases of the central nervous system
G37.9 Demyelinating disease of the central nervous system, unspecified

EPISODICA AND PAROXYSMAL DISORDERS (G40-G47)

G40 Epilepsy

Excluded: Landau-Kleffner syndrome ( F80.3)
seizure NOS ( R56.8)
status epilepticus ( G41. -)
Todd's paralysis ( G83.8)

G40.0 Localized (focal) (partial) idiopathic epilepsy and epileptic syndromes with seizures with focal onset. Benign childhood epilepsy with EEG peaks in the central temporal region
Childhood epilepsy with paroxysmal activity and EEG in the occipital region
G40.1 Localized (focal) (partial) symptomatic epilepsy and epileptic syndromes with simple partial seizures. Seizures without changes in consciousness. Simple partial seizures, developing into secondary
generalized seizures
G40.2 Localized (focal) (partial) symptomatic epilepsy and epileptic syndromes with complex partial seizures. Seizures with changes in consciousness, often with epileptic automatism
Complex partial seizures progressing to secondary generalized seizures
G40.3 Generalized idiopathic epilepsy and epileptic syndromes
Benign(s):
myoclonic epilepsy of early childhood
neonatal seizures (familial)
Childhood epileptic absence seizures [pycnolepsy]. Epilepsy with grand mal seizures on awakening
Juvenile:
absence epilepsy
myoclonic epilepsy [impulsive petit mal]
Nonspecific epileptic seizures:
atonic
clonic
myoclonic
tonic
tonic-clonic
G40.4 Other types of generalized epilepsy and epileptic syndromes
Epilepsy with:
myoclonic absence seizures
myoclonic-astatic seizures

Baby spasms. Lennox-Gastaut syndrome. Salaam's tick. Symptomatic early myoclonic encephalopathy
West syndrome
G40.5 Special epileptic syndromes. Epilepsy partial continuous [Kozhevnikova]
Epileptic seizures associated with:
drinking alcohol
use of medicines
hormonal changes
sleep deprivation
exposure to stress factors
If it is necessary to identify the drug, use an additional code for external causes (class XX).
G40.6 Grand mal seizures, unspecified (with or without minor seizures)
G40.7 Minor seizures, unspecified, without grand mal seizures
G40.8 Other specified forms of epilepsy. Epilepsy and epileptic syndromes not defined as focal or generalized
G40.9 Epilepsy, unspecified
Epileptic:
convulsions NOS
seizures NOS
seizures NOS

G41 Status epilepticus

G41.0 Status epilepticus grand mal (convulsive seizures). Tonic-clonic status epilepticus
Excluded: partial continuous epilepsy [Kozhevnikova] ( G40.5)
G41.1 Zpileptic status petit mal (minor seizures). Status epilepticus absence seizures
G41.2 Complex partial status epilepticus
G41.8 Other specified status epilepticus
G41.9 Status epilepticus, unspecified

G43 Migraine

Excludes: headache NOS ( R51)

G43.0 Migraine without aura [simple migraine]
G43.1 Migraine with aura [classical migraine]
Migraine:
headache-free aura
basilar
equivalents
familial hemiplegic
hemiplegic
With:
aura in acute onset
long lasting aura
typical aura
G43.2 Migrainous status
G43.3 Complicated migraine
G43.8 Another migraine. Ophthalmoplegic migraine. Retinal migraine
G43.9 Migraine, unspecified

G44 Other headache syndromes

Excluded: atypical facial pain ( G50.1)
headache NOS ( R51)
trigeminal neuralgia ( G50.0)

G44.0 Histamine headache syndrome. Chronic paroxysmal hemicrania.

Histamine headache:
chronic
episodic
G44.1 Vascular headache, not elsewhere classified. Vascular headache NOS
G44.2 Tension type headache. Chronic tension headache
Episodic tension headache. Tension headache NOS
G44.3 Chronic post-traumatic headache
G44.4 Drug-induced headache, not elsewhere classified
If it is necessary to identify the drug, use an additional code for external causes (class XX).
G44.8 Other specified headache syndrome

G45 Transient transient cerebral ischemic attacks [attacks] and related syndromes

Excludes: neonatal cerebral ischemia ( P91.0)

G45.0 Vertebrobasilar arterial system syndrome
G45.1 Carotid artery syndrome (hemispheric)
G45.2 Multiple and bilateral cerebral artery syndromes
G45.3 Transient blindness
G45.4 Transient global amnesia
Excludes: amnesia NOS ( R41.3)
G45.8 Other transient cerebral ischemic attacks and associated syndromes
G45.9 Transient cerebral ischemic attack, unspecified. Cerebral artery spasm
Transient cerebral ischemia NOS

G46* Vascular brain syndromes in cerebrovascular diseases ( I60-I67+)

G46.0* Middle cerebral artery syndrome ( I66.0+)
G46.1* Anterior cerebral artery syndrome ( I66.1+)
G46.2* Posterior cerebral artery syndrome ( I66.2+)
G46.3* Brainstem stroke syndrome ( I60-I67+)
Syndrome:
Benedicta
Claude
Fauville
Millard-Jublay
Wallenberg
Weber
G46.4* Cerebellar stroke syndrome ( I60-I67+)
G46.5* Pure motor lacunar syndrome ( I60-I67+)
G46.6* Pure sensory lacunar syndrome ( I60-I67+)
G46.7* Other lacunar syndromes ( I60-I67+)
G46.8* Other vascular syndromes of the brain in cerebrovascular diseases ( I60-I67+)

G47 Sleep disorders

Excluded: nightmares ( F51.5)
sleep disorders of non-organic etiology ( F51. -)
night terrors ( F51.4)
sleepwalking ( F51.3)

G47.0 Disturbances in falling asleep and maintaining sleep [insomnia]
G47.1 Disturbances in the form of increased sleepiness [hypersomnia]
G47.2 Disturbances in sleep-wake cycles. Delayed sleep phase syndrome. Disturbance of the sleep-wake cycle
G47.3 Sleep apnea
Sleep apnea:
central
obstructive
Excludes: Pickwickian syndrome ( E66.2)
sleep apnea in newborns ( P28.3)
G47.4 Narcolepsy and cataplexy
G47.8 Other sleep disorders. Kleine-Levin syndrome
G47.9 Sleep disorder, unspecified

Febrile seizures occur in children under 3 years of age when body temperature rises above 38 °C in the presence of a genetic predisposition (121210, Â). Frequency- 2-5% of children. The predominant gender is male.

Code according to the international classification of diseases ICD-10:

• R56.0

Options. Simple febrile convulsions (85% of cases) - one attack of convulsions (usually generalized) during the day lasting from a few seconds, but not more than 15 minutes. Complex (15%) - several episodes during the day (usually local convulsions), lasting more than 15 minutes.

Symptoms (signs)

Clinical picture. Fever. Tonic-clonic seizures. Vomit. General excitement.

Diagnostics

Laboratory research. First episode: determination of the level of calcium, glucose, magnesium, other serum electrolytes, urine analysis, blood culture, residual nitrogen, creatinine. In severe cases - toxicological analysis. Lumbar puncture - if meningitis is suspected or the first episode of seizures in a child over 1 year old.

Special studies. EEG and CT scan of the brain 2-4 weeks after the attack (performed for repeated attacks, neurological diseases, afebrile seizures in the family history or in the case of the first manifestation after 3 years).

Differential diagnosis. Febrile delirium. Afebrile seizures. Meningitis. Head injury. Epilepsy in women combined with mental retardation (*300088, À): febrile seizures may be the first sign of the disease. Sudden cessation of anticonvulsant medications. Intracranial hemorrhages. Thrombosis of the coronary sinus. Asphyxia. Hypoglycemia. Acute glomerulonephritis.

Treatment

TREATMENT

Lead tactics. Physical cooling methods. The patient's position is to lie on his side to ensure adequate oxygenation. Oxygen therapy. If necessary, intubation.

Drug therapy. The drugs of choice are paracetamol 10-15 mg/kg rectally or orally, ibuprofen 10 mg/kg for fever. Alternative drugs.. Phenobarbital 10-15 mg/kg IV slowly (respiratory depression and hypotension are possible).. Phenytoin 10-15 mg/kg IV (cardiac arrhythmia and hypotension are possible).

Prevention. Paracetamol 10 mg/kg (orally or rectally) or ibuprofen 10 mg/kg orally (at body temperature above 38 °C - rectally). Diazepam - 5 mg up to 3 years of age, 7.5 mg - from 3 to 6 years, or 0.5 mg/kg (up to 15 mg) rectally every 12 hours up to 4 doses - at body temperature above 38.5 ° C. Phenobarbital 3-5 mg/kg/day - for long-term prophylaxis in children at risk with a complicated medical history, multiple repeated attacks, and neurological diseases.

Course and prognosis. A febrile attack does not cause physical or mental retardation or death. The risk of a second attack is 33%.

ICD-10. R56.0 Convulsions during fever

Convulsive syndrome in adults is an emergency condition that can develop for a variety of reasons, although this condition is more typical for children.

Muscle contractions during an attack can be localized or generalized. Localized ones appear in certain muscles, and generalized ones cover the entire body. In addition, they can be divided into:

1. Clonic.
2. Tonic.
3. Clonic-tonic.

The exact type of seizure a person has can be determined by a doctor based on the symptoms that appear during the attack.

Why does this happen

The causes of convulsive syndrome can be a variety of pathological conditions and diseases. For example, under the age of 25, it occurs against the background of brain tumors, head injuries, toxoplasmosis, and angioma.

In older people, this phenomenon often occurs due to the consumption of alcoholic beverages, metastases of various tumors in the brain, and inflammatory processes in its membranes.

If such attacks occur in people over 60 years of age, then there will be slightly different causes and predisposing factors. These are Alzheimer's disease, drug overdose, kidney failure, cerebrovascular disease.

Therefore, after providing emergency care, a person who suffers from seizures should definitely visit a doctor in order to find out what is causing this condition and begin treatment, because this is one of the symptoms of many diseases.

Symptoms

One of the most common types is alcoholic convulsive syndrome. Moreover, it develops not while drinking alcoholic beverages, but some time after binge drinking. Seizures can be of varying severity and duration - from short-term to long-term clonic-tonic, which later develop into status epilepticus.

The second most common cause is brain tumors. Most often these are myoclonic spasms of the facial muscles or other parts of the body. But tonic-clonic ones can also develop, with loss of consciousness and interruptions in breathing for 30 seconds or more.

After an attack, a person notes weakness, drowsiness, headache, confusion, pain and numbness in the muscles.

Almost all such syndromes occur in the same way, be it alcoholic, epileptic, developed against the background of a head injury or tumors, as well as those that occur due to brain pathologies associated with disruption of its blood supply.

How to help

First aid for the syndrome is provided on the spot. The patient lies on a hard surface, put a pillow or blanket under his head, and be sure to turn it on his side. During an attack, you cannot restrain a person, since this way he can get fractures - you just need to monitor your breathing and pulse. It is also necessary to call an ambulance and be sure to hospitalize this person.

In the hospital, if the attack recurs, it is stopped with the help of medications. This is basically a 0.5% solution of seduxen or relanium, which is administered intravenously in an amount of 2 ml. If everything happens again, then these drugs are reintroduced. If the status persists after the third administration, then a 1% sodium thiopental solution is administered.

Treatment of convulsive syndrome in adults is carried out after the seizure has been eliminated. It is important to understand what caused the seizures and to treat the cause itself.

So, for example, if it is a tumor, then surgery is performed to remove it. If it is epilepsy, then you should regularly take appropriate medications that help prevent the development of seizures. If this is alcohol intake, then treatment in specialized clinics is necessary. If these are head injuries, then you should be under constant supervision of a neurologist.

To find out exactly why this condition occurs, it is necessary to undergo a thorough investigation, which will include blood and urine tests, brain examination, MRI or CT scan. Special diagnostic measures may also be recommended, which are carried out if a particular disease is suspected.

It also happens that such a condition occurs only once in a lifetime, for example, against the background of high fever, infectious disease, poisoning, or metabolic disorder. In this case, no special treatment is required and after eliminating the main cause, this no longer happens.

But with epilepsy, seizures are very common. This means that a person must constantly be under medical supervision and be sure to follow all the doctor’s prescriptions, since intractable status epilepticus may develop, which can be very, very difficult to cope with.

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The cause of back pain can be myalgia, the symptoms of which can be varied. Back pain occurs quite often in every adult. They are often intense and painful. The pain may occur suddenly or gradually increase over hours or even days. Any gardener is familiar with the situation when, a few hours after working on the plot, muscle pain appears in the arm, back or neck area.

This pain is well known to athletes. In addition to physical activity, inflammation or emotional stress can cause muscle pain. But pain syndromes do not always arise due to myalgia. There are many reasons for back pain. How does myalgia manifest and how to get rid of it?

Myalgia is muscle pain. ICD-10 code (International Classification of Diseases, 10th revision) M79.1. The pain can vary in intensity and nature: sharp, shooting and tearing or dull and aching.

Muscle pain can be localized in the neck, chest, lumbar region or limbs, but can affect the entire body. The most common ailment is neck myalgia.

If muscle pain occurs as a result of hypothermia, painful compactions may be found in the muscle tissue - gelotic plaques (geloses). They usually appear in the back of the head, chest and legs. Geloses can reflect pain syndromes occurring in the internal organs. For this reason, an erroneous diagnosis of myalgia is possible. Geloses can spread to the tissues of joints, ligaments and tendons. These changes cause a person severe pain.

If the disease is not treated, it will provoke serious pathologies. Over time, osteoarthritis, osteochondrosis or intervertebral hernia may develop.

The nature of the origin of myalgia varies. Depending on the causes of the disease, its symptoms vary.

The causes of muscle pain can be different. Myalgia can occur after a sudden or awkward movement, after a long stay in an uncomfortable position, as a result of hypothermia or injury, due to intoxication, for example, due to excessive alcohol consumption.

Myalgia is often caused by systemic inflammatory diseases of connective tissue and metabolic diseases. For example, gout or diabetes.

The disease can be caused by medications. Myalgia may occur as a result of taking medications that normalize blood cholesterol levels.

Often the cause of myalgia is a sedentary lifestyle.

There are several types of myalgia.

There are different types of myalgia depending on whether damage to muscle tissue has occurred or not.

When muscle tissue is damaged, the enzyme creatine phosphokinase (CPK) leaves the cells and its level in the blood increases. Damage to muscle tissue occurs, as a rule, with inflammatory myositis, due to injury or due to intoxication.

It is important to correctly diagnose the disease.

Manifestations of the disease are similar to the symptoms of neuritis, neuralgia or radiculitis. After all, pain when pressing on muscle tissue can occur not only due to damage to the muscles, but also to peripheral nerves.

If symptoms of myalgia occur, you should visit a doctor. If the diagnosis of myalgia is confirmed, only a doctor should prescribe treatment. He will recommend the patient complete rest and bed rest. Warmth in any form is useful. The affected areas can be covered with warm bandages - a woolen scarf or belt. They will provide “dry heat”.

To alleviate the condition of severe and unbearable pain, it is recommended to take painkillers. Your doctor will help you choose them. He will also determine the medication regimen and course duration. In cases of particularly severe pain, the doctor may prescribe intravenous injections. Treatment with medications should be carried out under the supervision of a physician.

With the development of purulent myositis, the help of a surgeon is necessary. Treatment with medications of such myositis is carried out with the obligatory opening of the source of infection, removal of pus and application of a drainage bandage. Any delay in treating purulent myositis is dangerous to human health.

Physiotherapy is effective in treating myalgia. The doctor may recommend ultraviolet irradiation of the affected areas, electrophoresis with histamine or novocaine.

Massage will help get rid of gelotic plaques. When diagnosing purulent myositis, massage is strictly contraindicated. Any massages for myalgia should be entrusted to a professional. Improper rubbing of the affected areas can provoke an increase in the disease and cause damage to other tissues.

At home, you can use warming ointments and gels. Such drugs are Fastum gel, Finalgon or Menovazin. Before using them, you must carefully read the instructions and perform all actions strictly according to the manufacturer’s recommendations.

Folk remedies will help alleviate the patient's condition. For example, lard. Unsalted lard must be ground and crushed dried horsetail added to it. For 3 parts lard take 1 part horsetail. The mixture is thoroughly ground until smooth and gently rubbed into the affected area.

White cabbage has long been famous for its analgesic and anti-inflammatory properties. A leaf of white cabbage should be generously soaped with laundry soap and sprinkled with baking soda. After this, the sheet is applied to the affected area. A woolen scarf or bandage is tied over the warming compress.

Bay oil has an analgesic and relaxing effect on tense muscles. To prepare the solution, add 10 drops of oil to 1 liter of warm water. A cotton towel is immersed in the solution, wrung out, rolled into a tourniquet and applied to the sore spot.

At night you can make a compress of potatoes. Several potatoes are boiled in their skins, mashed and applied to the body. If the puree is too hot, you need to place a cloth between the potatoes and the body. The compress should not be scalding. A warm bandage is tied on top.

In summer, burdock leaves will help. Large fleshy leaves should be doused with boiling water and applied in layers to the sore spot. A flannel or wool bandage is applied on top.

Prevention of pain syndrome

Some people suffer from myalgia regularly. It can be enough to walk in windy weather without a scarf or sit in a draft, and literally the next day neck myalgia appears. Such people need to pay more attention to the prevention of this disease.

To do this, you need to dress according to the weather. Since temperature changes can provoke muscle pain, you should not run outside in cold weather or into a cold room after physical activity.

Also at risk are people who, due to their professional activities, remain in one position for a long time and repeat monotonous movements.

These are drivers, office workers, musicians. Such people need to take regular breaks from work, during which it is recommended to walk around and stretch their muscles. While sitting, you need to monitor your posture, since if the body is positioned incorrectly, the muscles are subjected to unnatural static loads.

People with diseases of the musculoskeletal system need to further treat their ailments. This will reduce the likelihood of myalgia.

You should exercise regularly. Moderate physical activity will strengthen muscles and reduce the influence of various negative factors on them. Swimming in open water in the summer or in a pool during the cold season is very useful. Swimming also has a hardening effect and helps strengthen the immune system of the whole body.

Additional sources

Myalgia in therapeutic practice - approaches to differential diagnosis, treatment N.A. Shostak, N.G. Pravdyuk, I.V. Novikov, E.S. Trofimov GBOU VPO RNIMU im. N.I. Pirogova Ministry of Health and Social Development of Russia, Moscow, journal Attending Physician issue No. 4 2012

Pain syndrome in patients with fibromyalgia G.R. Tabeev, MMA named after. I.M.Sechenova, Moscow, RMJ magazine Independent publication for practicing doctors, issue No. 10 2003

RCHR (Republican Center for Health Development of the Ministry of Health of the Republic of Kazakhstan)
Version: Archive - Clinical protocols of the Ministry of Health of the Republic of Kazakhstan - 2007 (Order No. 764)

Generalized idiopathic epilepsy and epileptic syndromes (G40.3)

general information

Short description

Generalized epilepsy(HE) is a chronic brain disease characterized by repeated attacks with impairment of motor, sensory, autonomic, mental or mental functions, resulting from excessive neural discharges in both hemispheres of the brain.
GE is a single disease, representing separate forms with electro-clinical features, approach to treatment and prognosis.

Protocol code: H-P-003 "Generalized epilepsy in children, acute period"
For pediatric hospitals

ICD-10 code(s):

G40.3 Generalized idiopathic epilepsy and epileptic syndromes

G40.4 Other types of generalized epilepsy and epileptic syndromes

G40.5 Specific epileptic syndromes

G40.6 Grand mal seizures, unspecified (with or without petit mal)

G40.7 Petit mal, unspecified, without grand mal seizures

G40.8 Other specified forms of epilepsy G40.9 Epilepsy, unspecified

Classification

According to the International Classification of 1989 (International League Against Epilepsy), generalized epilepsy is based on the generalization of epileptic activity.

Within GE, forms are distinguished: idiopathic, symptomatic and cryptogenic.

Generalized types of epilepsy and syndromes:

1. Idiopathic(with age-dependent onset). ICD-10: G40.3:
- benign familial neonatal seizures;
- benign idiopathic neonatal seizures;
- benign myoclonic epilepsy of early childhood;
- childhood absence epilepsy (ICD-10: G40.3);
- juvenile absence epilepsy;
- juvenile myoclonic epilepsy;
- epilepsy with seizures of awakening;
- other types of idiopathic generalized epilepsy (ICD-10: G40.4);
- epilepsy with seizures provoked by specific factors.

2. Cryptogenic and/or symptomatic(with age-dependent onset) - ICD-10: G40.5:
- West syndrome (infantile spasms);
- Lennox-Gastaut syndrome;
- epilepsy with myoclonic-astatic seizures;
- epilepsy with myoclonic absence seizures.

3. Symptomatic.

3.1 Nonspecific etiology:
- early myoclonic encephalopathy;
- early infantile epileptic encephalopathy with “flare-suppression” complexes on the EEG;
- other types of symptomatic generalized epilepsy.

3.2 Specific syndromes.

Diagnostics

Diagnostic criteria

Complaints and anamnesis
Particular emphasis when collecting anamnesis:

Heredity;

A history of neonatal seizures, convulsions when the temperature rises (are risk factors for the development of epilepsy);

Toxic, ischemic, hypoxic, traumatic and infectious lesions of the brain, including the prenatal period (may be the causes of this disease).

Physical examination:
- presence of seizures;
- the nature of the attacks;
- family predisposition;
- age of debut;
- duration of the attack.

Laboratory research
The number of leukocytes and platelets is determined to exclude folate deficiency anemia and associated secondary changes in the bone marrow, which is clinically manifested by a decrease in the level of leukocytes and platelets;

A decrease in the specific gravity of urine may indicate the onset of renal failure, which requires clarification of the dosage of drugs and treatment tactics.

Instrumental studies: EEG data.

Indications for consultation with specialists: depending on concomitant pathology.

Differential diagnosis: no.

List of main diagnostic measures:

1. Echoencephalography.

2. General blood test.

3. General urine analysis.

List of additional diagnostic measures:

1. Computed tomography of the brain.

2. Nuclear magnetic resonance imaging of the brain.

3. Consultation with a pediatric ophthalmologist.

4. Consultation with an infectious disease specialist.

5. Consultation with a neurosurgeon.

6. Analysis of cerebrospinal fluid.

7. Biochemical blood test.

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Treatment

The first doctor who detects an epileptic seizure should describe it in detail, including the signs that preceded the seizure and occurred after its end.
Patients should be referred for a complete neurological examination to confirm the diagnosis and determine the etiology.
Treatment of epilepsy begins only after an accurate diagnosis has been established. According to most experts, treatment for epilepsy should begin after a recurrent attack.

Reducing the frequency of attacks;

Achieving remission.

Non-drug treatment: A full night's sleep is necessary.

Drug treatment

Treatment of epilepsy should be carried out depending on the form of epilepsy, and then on the nature of the attacks - with the basic drug for this form of epilepsy. The starting dose is approximately 1/4 of the average therapeutic dose. If the drug is well tolerated, the dosage is increased to approximately 3/4 of the average therapeutic dose over 2-3 weeks.
If there is no or insufficient effect, the dose is increased to the average therapeutic dose.
If there is no effect from the therapeutic dose within 1 month, a further gradual increase in the dose is necessary until a pronounced positive effect is obtained or side effects appear.
In the absence of a therapeutic effect and signs of intoxication appear, the drug is gradually replaced with another.

If a pronounced therapeutic effect is obtained and side effects are present, it is necessary to assess the nature and severity of the latter, then decide whether to continue treatment or replace the drug.
Replacement of barbiturates and benzodiazepines should be done gradually over 2-4 weeks or more due to the presence of severe withdrawal syndrome. Replacement of other antiepileptic drugs (AEDs) can be carried out more quickly - in 1-2 weeks. The effectiveness of the drug can be assessed only no earlier than 1 month from the start of its use.

Antiepileptic drugs used for generalized seizuresseizures and gastrointestinal tract

List of essential medications:
1. *Valproic acid 150 mg, 300 mg, 500 mg tab.
2. Clobazam 500 mg, 1000 mg tablet.
3. Hexamidine 200 tablets.
4. Ethosuximide 150-300 mg tablet.
5. *Clonazepam 25 mg, 100 mg tablet.
6. Carbamazepines 50-150-300 mg tablet.
7. *Acetozolamide 50-100-200 mg tablet.
8. *Lamotrigine 25 mg, 50 mg tablet.

List of additional medications:
1. *Difenin 80 mg tablet.
2. *Phenobarbital 50 mg, 100 mg tablet.

Further management: clinical observation.

Indicators of treatment effectiveness:

Reduction of attacks;

Seizure control.

* - drugs included in the list of essential (vital) medicines

Hospitalization

Indications for hospitalization:

Increased frequency of attacks;

Resistance to treatment;

Status flow;

Clarification of the diagnosis and form of epilepsy.

Information

Sources and literature

1. Protocols for diagnosis and treatment of diseases of the Ministry of Health of the Republic of Kazakhstan (Order No. 764 of December 28, 2007)
   1. 1. Hopkins A., Appleton R. Epilepsy: Oxford University Press. 1996. 2. International Classification of Diseases 10th revision; 3. International League Against Epilepsy (ILAE).Epilepsia 1989 vol. 30-P.389-399. 4. K.Yu.Mukhin, A.S.Petrukhin “Idiopathic epilepsies: diagnosis, tactics, treatment”. M., 2000. 5. Diagnosis and treatment of epilepsy in children. Edited by P.A. Temin, M.Yu .Nikanorova, 1997 6. Modern ideas about childhood epileptic encephalopathy with diffuse slow peak waves (Lennox-Gastaut syndrome).K.Yu. Mukhin, A.S. Petrukhin, N.B. Kalashnikov. Educational method. Benefit. RGMU, Moscow, 2002. 7. Progress in Epileptic Disorders “Cognitive Dysfunction in Children with Temporal Lobe Epilepsy.” France, 2005. 8. Aicardi J. Epilepsy in children.-Lippincott-Raven, 1996.-P.44-66. 9. Marson AG, Williamson PR, Hutton JL, Clough HE, Chadwick DW, on behalf of the epilepsy monotherapy trialists. Carbamazepine versus valproate monotherapy for epilepsy. In: The Cochrane Library, Issue 3, 2000; 10. Tudur Smith C, Marson AG, Williamson PR. Phenotoin versus valproate monotherapy for partial onset seizures and generalized onset tonic-clonic seizures. In: The Cochrane Library, Issue 4, 2001; 11. Evidence-based medicine. Annual Directory. Part 2. Moscow, Media Sphere, 2003. pp. 833-836. 12. First Seizure Trial Group (FIRST Group). Randomized clinical trial on the efficacy of antiepileptic drugs in reducing the risk of relapse after a first unprovoked tonic clonic seizure. Neurology 1993;43:478-483; 13. Medical Research Council Antiepileptic Drug Withdrawal Study Group. Randomized study of antiepileptic drug withdrawal in patients in remission. Lancet 1991; 337: 1175-1180. 14. Clinical guidelines for practicing physicians, based on evidence-based medicine, 2nd edition. GEOTAR-MED, 2002, pp. 933-935. 15. Never rugs for epilepsy in children. National Institute for Clinical Excellence. Technology Appraisal 79. April 2004. http://www.clinicalevidence.com. 16. Brodie MJ. Lamotrigine monotherapy: an overview. In: Loiseau P (ed). Lamictal – a brighter future. Royal Society of Medicine Herss Ltd, London, 1996, pp 43-50. 17. O'Brien G et al. Lamotrigine in add-on therapy in treatment-resistant epilepsy in mentally handicapped patients: an interim analysis. Epilepsia 1996, in press. 18. Karseski S., Morrell M., Carpenter D. The Expert Consensus Guideline Series: Treatment of Epilepsy. Epilepsy Epilepsy Behav. 2001; 2:A1-A50. 19. Hosking G et al. Lamotrigine in children with severe developmental abnormalities in a pediatric population with refractory seizures. Epilepsy 1993; 34 (Suppl): 42 20. Mattson RH. Efficacy and adverse effects of established and new antiepileptic drugs. Epilepsy 1995; 36 (suppl 2): ​​513-526. 21. Kalinin V.V., Zheleznova E.V., Rogacheva T.A., Sokolova L.V., Polyansky D.A., Zemlyanaya A.A., Nazmetdinova D.M. Use of the drug Magne B6 for the treatment of anxiety and depressive conditions in patients with epilepsy. Journal of Neurology and Psychiatry 2004; 8: 51-55 22. Barry J., Lembke A., Huynh N. Affective disorders in epilepsy. In: Psychiatric issues in epilepsy. A practical guide to diagnosis and treatment. A. Ettinger, A. Kanner (Eds.). Philadelphia 2001; 45-71. 23. Blumer D., Montouris G., Hermann B. Psychiatric morbidity in seizure patients on a neurodiagnostic monitoring unit. J Neuropsychiat Clin Neurosci 1995; 7:445-446. 24. Edeh J., Toone B., Corney R. Epilepsy, psychiatric morbidity, and social dysfunction in general practice. Comparison between hospital clinic patients and clinic non-attenders. Neuropsychiat Neuropsychol Behav Neurol 1990; 3: 180-192. 25. Robertson M., Trimble M., Depressive illness in patients with epilepsy: a review. Epilepsy 1983; 24: Supple 2:109-116. 26. Schmitz B., Depressive disorders in epilepsy. In: Seizure, affective disorders and anticonvulsant drugs. M. Trimble, B. Schmitz (Eds.). UK 2002; 19-34.

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According to the International League Against Epilepsy criteria, a first seizure (attack) is one or more first-time seizures that can recur within 24 hours, with full recovery of consciousness between them.

reference Information:

Conceptual definition of seizure disorder and epilepsy(ILAE report, 2005) Epileptic seizure (seizure) transient clinical manifestation of pathological excessive or synchronous neural activity of the brain Epilepsy is a brain disorder characterized by a persistent predisposition to epileptic seizures, as well as the neurobiological, cognitive, psychological and social consequences of this condition. This definition of epilepsy requires the development of at least one epileptic seizure (note: a seizure associated with the influence of some transient factor on the normal brain that temporarily lowers the seizure threshold is not considered epilepsy).

Practical clinical definition of epilepsy. Epilepsy is a brain disease corresponding to any of the following conditions: [ 1 ] at least two unprovoked (or reflex) epileptic seizures > 24 hours apart; [ 2 ] one unprovoked (or reflex) epileptic seizure and a probability of recurrent seizures corresponding to the overall risk of relapse (> 60%) after two unprovoked epileptic seizures, over the next 10 years; [ 3 ] diagnosis of an epileptic syndrome (eg, benign epilepsy with centrotemporal spikes, Landau–Kleffner syndrome).

The first attack is distinguished:

[1 ] epileptic - the transient appearance of signs and/or symptoms as a result of pathological or increased activity of brain neurons;
[2 ] acute symptomatic- an attack that develops with severe brain damage or in a clear temporal relationship with documented acute brain damage;
[3 ] long-term symptomatic- an attack that develops without an obvious precipitating factor, but with the presence of a diagnosable serious brain injury preceding the attack, for example, severe trauma or concomitant illness;
[4 ] progressive symptomatic- a seizure occurring in the absence of a potentially responsible clinical condition or outside the time interval for which acute symptomatic seizures are possible, and caused by a progressive disorder (for example, a tumor or degenerative disease);
[5 ] psychogenic - transient behavioral disturbances without any cause of organic nature (in the DSM-IV classification such an attack is classified as a somatoform disorder, while according to the ICD-10 classification [WHO, 1992] a similar attack is classified as dissociative seizures and belongs to the group conversion disorders.

read also the article: Psychogenic nonepileptic seizures(to the website)

Acute symptomatic seizures are episodes that occur in close temporal association with acute CNS damage that may be metabolic, toxic, structural, infectious, or inflammatory in nature. The time period is usually defined as the first week after the acute pathological condition, but can be shorter or longer. These seizures are also called reactive, provoked, induced, or situational seizures. For epidemiological studies, a precise definition is necessary, so the International League Against Epilepsy recommends using the term acute symptomatic seizures ( note: an acute symptomatic seizure is a “provoked seizure”, therefore, even with a high risk of recurrence, the diagnosis of “Epilepsy” is not made [see. "Reference information" - Practical clinical definition of epilepsy]).

Epileptic, remote symptomatic, and progressive symptomatic seizures are “unprovoked seizures.” An unprovoked seizure is a seizure or series of seizures that develops within 24 hours in a patient over 1 month of age in the absence of precipitating factors. Unprovoked seizures may be sporadic or recurrent. Although all patients with single unprovoked seizures are likely to develop epilepsy, seizure recurrence occurs in only half of the cases. According to population studies, the risk of seizure recurrence within 1 year was 36 - 37%, within 2 years - 43 - 45%. After the 2nd unprovoked seizure, the risk of developing a 3rd one reaches 73%, and a 4th - 76% (Anne T. Berg, 2008).

Acute symptomatic seizures differ from epilepsy in a number of important ways. [ 1 ] First, unlike epilepsy, the immediate cause of these seizures is clearly defined. If there is a clear temporal relationship, there is a possibility that the seizure was caused by conditions such as uremia, head trauma, hypoxia, or stroke, which always precede or develop simultaneously with the seizure. A causal relationship is also confirmed in cases where acute disruption of brain integrity or metabolic homeostasis develops in connection with a stroke. In many cases, more severe trauma increases the likelihood of developing seizures. [ 2 ] Secondly, unlike epilepsy, acute symptomatic seizures do not necessarily recur when the conditions that caused them recur. [ 3 ] Third, although acute symptomatic seizures are a clear risk factor for the development of epilepsy, they cannot be included in the definition of epilepsy, which requires the presence of 2 or more unprovoked seizures.

When a seizure develops for the first time, the following examination is recommended::

[1 ] General physical examination. [ 2 ] Neurological examination. Of the variety of symptoms, reliable indicators of the epileptic nature of a seizure are cyanosis and, to a lesser extent, hypersalivation (associated symptoms), tongue biting and disorientation (symptoms that appear after the seizure). Eyes closed during the tonic-clonic phase of the seizure indicate a dissociative (psychogenic non-epileptic) seizure with a sensitivity of 96% and specificity of 98%. [ 3 ] Biochemical blood tests: complete blood count, glucose, urea, electrolytes (including calcium), creatinine, aspartate aminotransferase, alanine aminotransferase, creatine kinase/prolactin; urine toxicology tests (if necessary).

With the exception of children in the first 6 months of life who have hyponatremia (<125 ммоль/л) в 70% случаев сопутствует эпилептическим припадкам, метаболические нарушения (гипер- и гипогликемия, электролитные нарушения и др.) редко обнаруживаются у детей и взрослых при биохимическом/гематологическом скрининге после припадка.

To differentiate epileptic seizures from psychogenic non-epileptic seizures, it is useful to determine the serum prolactin level (two times the basal level or >36 ng/ml suggests either generalized tonic-clonic or complex partial seizures.

[4 ] Conducting an EEG. If a standard EEG recorded during wakefulness is uninformative, it is recommended to record an EEG during sleep. EEG recorded within 24 hours after a seizure is more likely to detect epileptiform activity than recorded in subsequent days. In contrast, the slowing of basal EEG activity 24 to 48 hours after a seizure may be transient and should be interpreted with caution.

read also the article: Video-EEG monitoring(to the website)

[5 ] Carrying out computed tomography (CT) and magnetic resonance imaging (MRI) of the brain. Although pathological changes can be detected in almost half of adults and 1/3 of children, the contribution of neuroimaging methods is limited in patients with existing epileptogenic brain damage and/or partial seizures. There is no evidence that MRI is more informative than CT in emergency conditions, at least in children. The value of CT examination in the absence of pathological changes in neurological status was 5 - 10%. Although up to 1/3 of children have pathological changes that are detected using neuroimaging, most of these findings do not affect further treatment and management of patients, such as the need for hospitalization or the appointment of further examination.

[6 ] Indications for cerebrospinal fluid (CSF) examination. Because of its high sensitivity and specificity, CSF examination is usually performed in febrile seizures accompanied by meningeal symptoms to rule out brain infection. In children under 6 months of age with impaired and incomplete restoration of consciousness, pathological changes may be observed in the CSF even in the absence of symptoms of meningeal irritation. In contrast, the value of CSF testing in patients with a first nonfebrile seizure has not yet been determined.

Treatment. In the presence of a first acute symptomatic seizure (metabolic encephalopathy, acute CNS injury in patients with a treatable underlying condition), treatment of the underlying disease is recommended. Symptomatic (antiepileptic) therapy for the first unprovoked seizure is inappropriate unless the seizure is status epilepticus. The decision to initiate antiepileptic drug treatment after the first seizure depends largely on the risk of relapse (patients with acute symptomatic seizures and a high risk of relapse should not be treated with antiepileptic drugs (AEDs) on a long-term basis, although such treatment may be justified in the short term while the acute condition was not compensated; in the treatment of acute symptomatic attacks, it is advisable to use injection forms for intravenous administration of AEDs, such as Konvulex, Vimpat, Keppra). Although this risk may vary significantly between cases, it is highest in patients with abnormal EEG changes and documented brain injury. Such situations also include a single epileptic seizure at least one month after the stroke, or a single seizure in a child with a structural pathology, or a remote symptomatic seizure in the presence of epileptiform changes on the electroencephalogram (EEG). Another example is a specific epileptic syndrome with a persistent decrease in the seizure threshold, identified after a single seizure. In general, the risk of recurrence is highest during the first 12 months and decreases to almost 0 by 2 years after the seizure. Studies meeting levels of evidence A, C have shown that treatment of the first unprovoked seizure reduces the risk of recurrence in the next 2 years, but does not affect long-term outcomes in both children and adults.

Since acute symptomatic seizures partly reflect the severity of central nervous system damage, it is clear that their occurrence is associated with a poor prognosis of treatment. However, the direct impact of acute symptomatic seizures on prognosis has not yet been proven.

In order to assess the risk of relapse, make a differential diagnosis and decide on treatment, a consultation with a neurologist specializing in epilepsy is necessary. That is why all patients with a first-time seizure should be consulted in specialized centers or offices (by an epileptologist) within 1 to 2 weeks after the seizure.

Diagnosing epilepsy after a single unprovoked seizure, even with a high risk of relapse, does not always lead to treatment. The proposed practice definition of epilepsy (see above) supports initiating treatment in a patient at high risk of relapse after a single unprovoked seizure. However, the decision to initiate treatment should be made individually, taking into account the patient's wishes, risk-benefit ratio, and available treatment options. The doctor must weigh the possibility of preventing attacks against the risk of side effects of the drugs and the patient's costs of treatment.

It should be clarified once again that the diagnosis of epilepsy and the decision to treat are two related but different aspects of the problem. Many epileptologists treat for some time after an acute symptomatic attack (eg, herpetic encephalitis) that is not related to epilepsy. In contrast, patients with mild seizures, long intervals between seizures, or those who refuse treatment may not receive treatment even if there is a clear diagnosis of epilepsy.

read also the article “ First epileptic seizure: to treat or not?» based on materials from the educational course of the European Academy of Neurology, April 27-29, Odessa (medical newspaper “Health of Ukraine” No. 2 (41), June 2017 ) [read ]

Literature:

article “Organization of medical care for patients with a first-time convulsive seizure” Naumova G.I., Center for Paroxysmal States, Vitebsk Regional Diagnostic Center, Republic of Belarus (magazine “Neurology, neuropsychiatry, psychosomatics” No. 2, 2009) [read];

official report of the International League Against Epilepsy "A Practical Clinical Definition of Epilepsy" R.S. Fisher, C. Acevedo, A. Arzimanoglou et al. (magazine “NeuroNEWS: psychoneurology and neuropsychiatry”, collection of clinical recommendations for 2015) [read];

article “Acute symptomatic seizures” Vaichene-Magistris N., Department of Neurology, Lithuanian University of Medical Sciences, Kaunas (journal “Epilepsy and Paroxysmal Conditions” No. 4, 2011) [read];

article “Acute symptomatic attacks: current state of the problem” by B.P. Gladov, P.N. Vlasov, Department of Nervous Diseases, State Budgetary Educational Institution of Higher Professional Education, Moscow State Medical University named after. A.I. Evdokimov (materials of the scientific and practical conference “Current problems of practical neurology and evidence-based medicine”, Kursk, 2013, pp. 23 - 29) [read];

article “Acutely occurring symptomatic epileptic seizures and status epilepticus” by L.V. Lipatova, I.G. Rudakova, N.A. Sivakova, T.V. Kapustina; FSBI "St. Petersburg Research Psychoneurological Institute named after. V.M. Bekhterev", St. Petersburg; GBUZ MO "Moscow Regional Research Clinical Institute named after. M.F. Vladimirsky”, Moscow (Journal of Neurology and Psychiatry, No. 4, 2015) [read];

article “Epilepsy: clinical and pathogenetic features of onset in adulthood” Al-Holaidi Mahfud, Vitebsk State Medical University, Department of Psychiatry and Neurology (magazine “Bulletin of VSMU” No. 3, 2003) [read];

article “Conditions with epileptic seizures that do not require a diagnosis of epilepsy” S.R. Boldyreva, Children's Hospital No. 1, St. Petersburg, A.Yu. Ermakov, Ph.D., Moscow Research Institute of Pediatrics and Pediatric Surgery, Moscow (Medical Council magazine No. 1 - 2, 2008) [read];

article “Epileptic syndromes in endocrine diseases” by A.A. Dutov, Yu.L. Lukyanova, G.A. Goltvanitsa; Research Institute of Medical Ecology; Chita State Medical Academy; Regional Children's Consultative Clinic, Chita (Journal of Neurology and Psychiatry, No. 3, 2012) [read];

article (review) “Symptomatic epilepsy of vascular origin (review)” B.N. Bain, K.B. Yakushev; FSBEI HE "Kirov State Medical University"; Treatment and Diagnostic Center MIBS, Kirov (magazine “Medical Almanac” No. 5, 2017) [