The crisis provoked refers to an epileptic seizure occurring at the time of acute cerebral aggression. It is distinguished from symptomatic epileptic seizures, without immediate precipitating factor, but related to a fixed or progressive brain injury.
To diagnose an epileptic seizure and differentiate it from another non-epileptic paroxysmal event, the clinician must first listen and ask the right questions. It is essential, in the event of a first crisis, to collect a reliable anamnesis thanks to all the available testimonials. The approach will have two axes: the diagnosis of the crisis and the search for an etiology to the latter.
DIAGNOSIS OF THE CRISIS:
Collection of antecedents:
Family history of epilepsy, head trauma, convulsions, metabolic diseases, cerebral, recent treatments.
Collection of information concerning the crisis:
C ONTEXT OF SURVIVAL:
Existence of factors that favored the crisis:
– alcohol: recent consumption, weaning; other toxic or drug withdrawal;
– sleep debt;
– alternating light: games on screen, disco.
TIME ORGANIZATION AND DURATION OF THE EVENT:
Existence of a partial phase
– To specify the existence of motor, self-propelled, sensory and vegetative symptoms and their neurological coherence.
– Evaluate the deterioration of vigilance (complex partial crisis).
Existence of a generalization
– Existence of a tonic phase in flexion, then in extension, then of a clonic phase during which the laryngeal clonies are audible. These clones, initially fast, slow down progressively in frequency and increase in amplitude.
– Look for a lateral tongue bite.
– The loss of urine has little discriminating value.
Duration of the crisis
Generally less than 2 minutes.
If multiple crises have occurred, evaluate their stereotyped character.
PHASE POSTCRITICAL:
A generalized tonicoclonic epileptic seizure will result in a hypotonic coma associated with a stertor, abundant salivation and usually a loss of urine. It is only gradually that the patient responds to stimulation and then presents a confusing state giving in a few tens of minutes. It will persist amnesia of the episode and, often, headaches and muscular pains.
After a partial seizure, the post-critical phase can also be marked by confusion, especially in seizures involving the temporal lobe. In addition, the existence of a transient neurological deficit will be investigated.
Clinic:
– Look for an acute medical condition, a persistent neurological deficit that may reveal a brain injury that causes seizures.
– Eliminate other etiologies of discomfort (cardiovascular …).
– Ensure the absence of complications of the crisis (inhalation, shoulder dislocation, wounds …).
Paraclinic:
BIOLOGICAL BILAN:
– Metabolic disorder: ionogram, blood glucose, calcemia.
– Standard + infectious balance: Blood count, platelets, CRP, hemostasis.
– Dosage of antiepileptics if treatment in progress.
– Alcoholemia, toxic if orientation.
– Arguments for a crisis:
• elevation of CPK, leukocytes, lactic acidosis, transient, unspecific;
• if there is diagnostic doubt, the elevation of prolactin measured within 60 minutes after the crisis has a good positive predictive value. It must be controlled at the same time the next day to overcome the pulsatile nature of secretion.
I CEREBRAL MAGAZINE:
If first crisis or change of the semiology of the attacks: MRI preferably (abnormal in 47% of cases after a first unprovoked crisis).
LUMBAR P ONCTION:
If febrile context, meningeal syndrome.
EEG:
Abnormal in 50 to 70% of cases if performed in the first 24 to 48 hours.
DIFFERENTIAL DIAGNOSTICS:
In a patient with transient loss of consciousness with or without abnormal movements the main differential diagnoses are cardiovascular syncope (Tables 11 and 12) and psychogenic non-epileptic seizures or somatoform seizures.
Parasomnias rarely pose diagnostic difficulties requiring registration EEG to clarify them.
AITs have a different presentation. They last more than 5 minutes. In the vertebrobasilar territory, there may be an alteration of the consciousness by attacking the ascending reticular but this then associates with other symptoms related to brainstem involvement such as: vertigo, diplopia, dysarthria, ataxia, hemiparesis. Syncope can have various etiologies that should be sought by clinical examination, and first-line ECG.
Somatoform crises are a sometimes difficult differential diagnosis with a seizure.
Table 13 illustrates some symptoms that should make them evoke.
THERAPEUTIC CONDUCT IN SOME POINTS:
In front of a first crisis:
– no systematic injection of benzodiazepine;
– if seizure caused, treatment of the acute responsible illness (fever, metabolic disorder, stroke, etc.). Most often, no antiepileptic treatment, or transient benzodiazepines;
– no introduction of antiepileptic treatment in the emergency. Plan a quick consultation in a specialized environment.
If it is a known epileptic, after verification of compliance (dosage), remotely refer to his neurologist. No hospitalization necessary in the absence of modification of the semiology of the crises or acute associated situation.
The decision of the setting up of antiepileptic treatment by the specialist will depend on:
– crises and their number;
– the EEG that contributes to the diagnosis and classification of epilepsy;
– etiology: symptomatic epilepsy with MRI lesion, idiopathic epilepsy;
– the existence of neurological disorders and learning;
– the expected benefit of reducing the risk of epileptic recurrence by taking into account the physical and psychosocial implications of setting up antiepileptic treatment.