Nonepileptic paroxysmal events are episodes that mimic seizures but do not result from abnormal cortical electrical activity. The most common types are syncope (fainting) and psychogenic seizures. Syncope can be neurally-mediated (e.g. vasovagal) where there are vegetative prodromal symptoms before loss of consciousness, or due to orthostatic hypotension on standing. Transient ischemic attacks from cerebrovascular issues can also mimic seizures. A detailed history of the episodes is important to differentiate epileptic from nonepileptic events.

1. NON EPILEPTIFORM PAROXYSMAL EVENTS
Anurag kumar singh

2. 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

3. 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.

4. 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

5. 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.

6. 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).

7. 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.

8. 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.

9. 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

10. 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

11. 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.

12. 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.

13. 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

14.  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

15. 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.

16. 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.

17. 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.

18. 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.

19. 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."

20. 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

21. 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.

22.  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.

23. THANKS