Эпилептические приступы
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Бағалау критерийлері-ойлау дағдысы , Микроорганизмдерді тасымалдау (копия)
- Бұл бет үшін навигация:
- Clonic phase of GTCSs
- Recovery phase of GTCSs
| Tonic phase of GTCSs The tonic phase is a 10–20 s sustained contraction of all skeletal muscles, producing a succession of characteristic body postures. The tonic extension phase is heralded by forced closure of the previously widely open mouth, which often causes tongue biting. The ‘epileptic cry’, a high, pinched, loud scream occurring at this stage, is caused by the tonic contraction of thoracic abdominal muscles, which forcibly emit air across the tightly closed vocal cords.
Clonic phase of GTCSs This is characterised by continuously repetitive, mas sive, symmetrical and synchronous flexor clonic convulsions of the facial, trunk and limb musculature. They last for 30 s to 1–2 min with progressively decreasing force, amplitude and frequency They may finally restrict only in the facial muscles or end with a massive clonic convulsion. The tongue is often bitten repeatedly during this clonic phase and each convulsion may produce an epilep tic cry. Towards the end of the clonic phase, the clonic convul sions may become asynchronous and asym met ri cal, and side-to-side head and eye movements may also occur. Contraction of the bladder sphincter blocks urinary incontinence until the end of the clonic phase. Recovery phase of GTCSs Immediate post-ictal phase of GTCSs (comatose or stertorous phase): Recovery starts with the cessation of clonic convulsions, although the patient remains in a coma, is unresponsive and markedly hypotonic. Respiration is restored with a deep inspiration, followed by usually noisy deep breathing associated with the secretion of frothy and bloodstained saliva. Urinary incontinence occurs only at this stage (Figure 2.4). Faecal incontinence or ejaculation is rare. Skin resistance and blood pressure return pro gres sively to pre-seizure levels; the patient becomes pale Autonomic abnormalities include mydriasis, tachycardia, sometimes with marked cardiac arrhythmia, and intense tachypnoea. This state is associated with hypometabolism predominating in cortical structures.46 It is of variable duration, from seconds to 3 or 4 min, or it may not occur. The patient remains unconscious throughout this post-ictal state. Pupillary and cutaneous reflexes are absent, deep tendon reflexes are often exaggerated and the Babinski sign is elicited in half the patients. Unilateral pyramidal signs indicate SGTCSs of contralateral cortical onset. Late post-ictal phase of GTCSs: This period of recovery is characterised by a gradual return to normality. Autonomic nervous system function normalises and pupillary, cutaneous and tendon reflexes reappear, but muscle atonia persists. Reactivity to pain stimuli returns. Cognitive functions also return to normal, but confusion and automatisms may initially be marked (post-ictal epileptic automatisms). The patient is extremely tired and drowsy and goes into a deep and lengthy sleep if left undisturbed. On awakening the patient feels exhausted, usually complaining of severe throbbing headache and withcomplete retrograde amnesia. The usual duration of the late post-ictal phase (not including the sleep period) is 2–10 min. Upon full recovery, the patients are totally amnesic of what happened during the GTCS and most of the postictal state. However, they are aware that something happened to them mainly because of the memory gap, aching muscles and traumas. Tonic phase: The ictal EEG onset of the GTCSs is marked by a brief (1–3 s) period of flattening or with low-voltage fast rhythmic activity at about 20 Hz or fast spiking. This gradually becomes more synchronised, increases in amplitude and slows in frequency to a sustained 10 Hz rhythm (‘epileptic recruiting rhythm’ is the preferred term of Gastaut). Intermediate phase and clonic phase: Slow waves of increasing amplitude and decreasing frequency super impose and gradually rhythmically interrupt the 10 Hz fast rhythms of the tonic phase. Finally, the EEG assumes a pattern of repetitive, high-amplitude polyspike–slow-wave complexes that increase in amplitude and slow down to 1 Hz. The clonic convulsions correspond to the polyspikes, whereas the periodic muscle atonia corresponds to the slow waves. The post-ictal period is characterised by diffuse background suppression (flat or isoelectric EEG) or a burst-suppression or triphasic wave pattern of several seconds to 2 or 3 min (longer in children). This is followed by diffuse slow waves that gradually increase in frequency and amplitude. The periods of coma and confusion and the return to normality correlate fairly well with dominant delta activity, theta activity and the return of a normal alpha rhythm after several minutes. жүктеу/скачать 272,31 Kb. Достарыңызбен бөлісу:
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