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Epilepsy enters the differential diagnosis of paroxysmal disorders of central nervous system function. The first step is to differentiate seizures from other common paroxysmal disorders, which are considered in another section (see p ii9). When the diagnosis of recurrent seizures is confirmed the next step is to diagnose the epilepsy syndrome in order to estimate prognosis and optimise treatment. The following guiding principles are useful in considering attack disorders.
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- The paroxysmal nature of seizures creates significant limitations in diagnostic precision.
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- The great majority of seizures cause an ictal scalp electroencephalogram (EEG) abnormality (below) and the gold standard diagnosis is made by ictal electroclinical correlation. It is often said that epilepsy is a clinical diagnosis but that is only because seizures are usually too infrequent to obtain ictal electrophysiological corroboration. When the diagnosis is in doubt, the key is to record the ictus, ideally with video-EEG, but alternatively with ambulatory EEG monitoring and home video recording.
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- The adage “wait and see” is often good counsel. The diagnosis may become clearer and in the meantime a diagnosis of “don't know” may be better than an incorrect diagnosis of epilepsy with all its psychosocial consequences.
KEY CLINICAL QUESTIONS IN DIAGNOSING ATTACK DISORDERS
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- Are all attacks the same? Organic attacks tend to be more stereotyped than psychogenic attacks.
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- Is there any pattern to the circumstances under which they occur—for example, time of day (morning myoclonus), relation to particular activities (syncope) or acute emotional distress (psychogenic non-epileptic seizures)? Sleep deprivation, fever, and alcohol are common triggers of epileptic seizures in susceptible individuals.
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- Do attacks occur from waking, sleep or both? Attacks arising from sleep are organic (though not always epileptic) but it may take an EEG to prove that the patient is asleep at the onset.
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- Sometimes there is a history of mild and unexplained symptoms that the patient may consider irrelevant such as olfactory hallucinations or profound deja-vu. Myoclonus or falls on waking are under recognised symptoms that often have to be sought specifically.
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- Did a witness try and communicate with the patient during the attack and what was the response?
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- How long did recovery take and was there anything abnormal during the recovery period? A long recovery time is one of the best discriminators between epilepsy and syncope. Focal weakness or dysphasia point to focal epilepsy and may signify a significant structural lesion.
THE SO-CALLED “CLASSICAL” SYMPTOMS OF CONVULSIONS
Convulsive epileptic seizures are usually easy to recognise despite the provisos in diagnosis imposed by the episodic nature of the condition and lack of a diagnostic test. The evolution is illustrated in fig 1. Although several symptoms have the reputation of being “diagnostic” of epilepsy, the clinical picture of the blackout must be viewed as a whole: no single symptom is diagnostic but some are helpful.
The characteristic evolution of symptoms in a tonic-clonic seizure enables it to be differentiated from other forms of attack. A clear description or a home video may show the typical onset with fast, low amplitude jerks evolving to slower, higher amplitude jerks.
Incontinence of urine is common in convulsive epileptic seizures but is not specific and occurs in up to 50% of syncope or any other collapse with a full bladder. Cyanosis implies an organic cause of the attack but a witnessed description of facial colour may be misleading. If a patient strains performing a Valsalva manoeuvre before syncope or in a psychogenic pseudoseizure the purple discolouration of their face may mimic cyanosis.
A severely bitten tongue is strongly suggestive that the attack was a seizure and the mouth should be inspected. Occasionally the tip of the tongue may be bitten in psychogenic non-epileptic seizures or syncope. Injuries may occur in any type of blackout if the circumstances are appropriate—for example, if a major …