NON EPILEPTIFORM PAROXYSMAL EVENTS

Anurag kumar singh

ABSTRACT

Nonepileptic paroxysmal events are behavioral, motor, or sensory episodes that do not result from abnormal cortical electrical activity. *

They can mimic any type of epileptic seizures including simple partial, complex partial, and generalized tonic-clonic seizures.

Nonepileptic paroxysmal events may be physiological or psychogenic in nature.

*Semin Neurol. 2008;28(3):297-304

In clinical practice, the most common imitators of

epileptic seizures are syncope and psychogenic

seizures, but transient ischemic attacks, migraine,

movement disorders, and metabolic disturbances must

be considered at times in the differential diagnosis.

In most cases, the clinical history is enough to make a

correct diagnosis.

The clinical features suggestive of various types of

nonepileptic paroxysmal events, together with useful

diagnostic tests, will be reviewed.

INTRODUCTION

The differential diagnosis of epileptic seizures is very broad, partly because the symptomatology of epileptic seizures is varied, depending on the eloquent cortical areas activated by the epileptic activity (symptomatogenic zone).

There is a great amount of diseases which can produce focal neurological symptoms and signs, occurring repeatedly in a paroxysmal way, not unlike epileptic seizures, and which can be mistaken for epilepsy.

Yet, to make a definite diagnosis of epilepsy, it is necessary to demonstrate the epileptiform activity associated with the recurrent attacks

Nonepileptic seizures are behavioral, sensory, and

motor events that are not associated with epileptiform

activity.

However, in the case of some physiologic nonepileptic

seizures, like syncope, abnormal electrical activity may

be identified at the time of the event.

Nonepileptic seizures can mimic any type of epileptic

seizures.

The limited duration, the presence of an aura, the

postictal confusion, and the stereotyped nature of

symptoms are some of the clinical features of epileptic

seizures that help to make a correct diagnosis.

A detailed description of the symptoms and signs

exhibited during the paroxysmal episode is essential to

reach a correct diagnosis and classify the epileptic

seizures.

Accordingly, it is necessary to obtain information from

the patient and witnesses, including:

Triggering factors for the episodes: sleep deprivation,

alcohol intake, drugs, activity at the time of the onset of

the event Prodromal symptoms (e.g., vegetative

symptoms, dizziness, stereotyped sensations, etc).

Vegetative symptoms often precede syncope; other

types of stereotyped sensations such as rising epigastric

sensation, altered taste or smell, prolonged sense of déjà

vu, and formed or unformed visual hallucinations are seen

in the context of focal epilepsies. In this case, patients

often report having had these sensations also in isolation,

without loss of awareness.

Loss of awareness, and its duration.

Abnormal movements associated with the loss of

awareness: head-turning and stereotyped proximal and

distal movements (automatisms) are often seen during

seizures. Generalized stiffening and clonic jerking may be

seen in both seizures and convulsive syncope.

Urinary incontinence, tongue-biting (biting the side of the

tongue is highly suggestive of epileptic seizure, biting the

tip may be seen in other conditions such as syncope).

Degree of confusion after the episode.

Myalgias the next day, suggestive of seizures.

Focal neurological signs after the episode.

Based on the history, clinicians are able to generate

an initial diagnostic impression, which determines the

type of studies that should be ordered to reach a final

diagnosis.

Reasons for misdiagnosis include incomplete clinical

history, excessive importance being given to certain

symptoms such as jerks or urinary incontinence (which,

in addition to epileptic seizures, may also be seen in

syncope and psychogenic seizures), and the incorrect

interpretation as "epileptiform" of normal variants or

nonspecific findings on the electroencephalogram

(EEG).*

*Benbadis SR, Tatum WO. Overinterpretation of EEGs and

misdiagnosis of epilepsy. J Clin Neurophysiol 2003; 20: 42-44

Nonepileptic seizures are classified as physiologic or

psychogenic in origin. The two conditions which are

most commonly mistaken for epileptic seizures in

clinical practice are syncope and psychogenic seizures.

Physiologic Nonepileptic Paroxysmal Seizures

Syncope

Syncope consists of a transitory, brief loss of

consciousness accompanied by loss of postural tone,

caused by a decrease in global cerebral perfusion.

Several types of syncope are identified. *

*Brignole M, Alboni P, Benditt DG. Guidelines on management

(diagnosis and treatment) of syncope—update 2004. Executive

summary. Eur Heart J 2004; 25: 2054-2072

Neurally Mediated Syncope

Vasovagal (neurocardiogenic) syncope is caused

by an exaggerated response of normal cardiovascular

reflexes.

It happens in healthy people, especially young adults

and children.

Typical precipitating factors are prolonged periods of

time in a standing position, sudden change of position

from lying down to a standing position, hot or crowded

places, pain, or intense emotion.

It is characteristic that the patient has vegetative

prodromal symptoms of variable duration (from 10

seconds up to 1 to 2 minutes), also known as a

presyncope, consisting of lightheadedness or a "faint"

feeling, cold sweating, decreased hearing and vision, and

pallor.

These are followed by loss of muscle tone and loss of

awareness, with the patient falling to the ground.

Sometimes the loss of awareness may be followed by

generalized stiffening and some myoclonic jerks

(convulsive syncope), which may be mistaken for the

clonic jerks of a generalized tonic-clonic seizure.

The prodromal symptoms and the presence of pallor

and sweating prior to the loss of awareness help to

make the diagnosis.

Patients recover quickly after syncope; they are

initially able to hear, and then they recover complete

cognitive function, without "postsyncopal" confusion, and

are able to remember the events preceding the loss of

awareness.

Carotid sinus syncope is defined as syncope, which

by history, seems to occur in close relationship with

accidental mechanical manipulation of the carotid

sinuses.

Carotid sinus hypersensitivity is a common cause of

unexplained falls in elderly people.

The key presyncopal sign is that of the neck turning

before the presyncopal symptoms and loss of

consciousness.

This type of syncope can be reproduced with carotid

sinus massage. Yet, given the small risk of stroke, this

maneuver is contraindicated in those with known

carotid artery stenosis and in patients with carotid

bruits or recent cerebrovascular events where carotid

stenosis has not been excluded.*

*McKeon A, Vaughan C, Delanty N. Seizure versus syncope.

Lancet Neurol 2006; 5: 171-180

Situational syncope refers to those forms of neurally

mediated syncope associated with specific scenarios

(e.g., micturition, coughing, defecating, etc.).

Urinary incontinence, lateral tongue-biting, and

other lesions are uncommon during neurally mediated

syncope.

A good history, preferably with a witness account, is

usually enough to make the diagnosis.

Syncope Due to Orthostatic Hypotension

Syncope due to orthostatic hypotension takes place

during a postural change due to inability of the

autonomic nervous system to compensate for the fall in

blood pressure with a vasoconstrictive response.

There are different causes of this type of syncope,

including the use of drugs causing hypotension (such

as antihypertensive agents, diuretics, tricyclic

antidepressants) and peripheral neuropathies due to

diabetes or alcoholism.

The syncope occurs from a few seconds to a few

minutes after standing. Unlike vasovagal syncope, cold

sweating and bradycardia are usually not seen.

Cardiogenic Syncope

This type of syncope results from alterations in the

cardiac rhythm or cardiac structural abnormalities.

It is important to make a proper diagnosis as this

type of syncope may be life-threatening.

The alterations of cardiac rhythm include both tachy-

and bradyarrhythmias (such as Wolf-Parkinson-White,

atrioventricular block, and others) which cause a

decrease in cardiac output irrespective of the

circulatory demands.

Cerebrovascular Accidents

Cerebrovascular accidents, which are most often

mistaken for epileptic seizures, are transient ischemic

attacks (TIA) which cause neurological signs and

symptoms of brief duration resembling epileptic seizures.

TIA in the territory of the carotid artery usually produce

negative symptoms, either motor or sensory, generally

without associated loss of consciousness.

TIA in the territory of the vertebrobasilar artery

may be accompanied by loss of consciousness and

must be distinguished from atonic seizures,

myoclonic seizures, and partial seizures causing

falls.

Severe carotid stenosis may produce "limb-

shaking," consisting of rhythmic or arrhythmic

clonic jerking in the contralateral hand, arm, and

leg (though less frequently).

The patient may describe these jerks as tremor,

inability to control the arm, or "lack of coordination."

The trigger of symptoms with maneuvers that

decrease cerebral perfusion can serve as a clue to the

diagnosis, such as standing up or hyperextension of

the neck, and there is a short latency between these

triggers and the onset of symptoms of a few seconds'

duration, in general.

The jerks last for seconds to minutes, and stop when

the patient sits or lies down. Other neurological signs

suggestive of vascular dysfunction may be found in the

same patient, such as dysphasia, transitory dysarthria,

paresthesias in the limb affected by the jerking or

ipsilateral hemiparesis.*

* Ali S, Khan MA, Khealani B. Limb-shaking transient ischemic

attacks: case report and review of literature. BMC Neurol 2006; 6:

5

Global Transitory Amnesia

Episodes of global transitory amnesia (GTA) have

a sudden onset and are characterized by marked

alteration of anterograde memory, temporal

disorientation, and occasionally disorientation in

space, but orientation to person and recognition of

others is always preserved.

The level of consciousness and language

functions are maintained throughout the episode but

the patient looks confused, has motor and ideatory

perseveration, and may get lost.

Immediate memory is preserved, as well as abstract

thinking. Patients may repeat series of words or numbers

and perform complex tasks such as driving, reading,

writing, or solving arithmetical problems, which is

uncommon during nonconvulsive status epilepticus (SE).

Around 10% of patients may have headache during the

episode. Amnesia usually lasts several hours (less than

24).

GTA must be differentiated mainly from nonconvulsive,

complex partial, and absence SE. Specific deficits,

temporal course, and absence of ictal EEG patterns

during the episode help to make the diagnosis.

THANKS