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ISSN: 2155-9562
Journal of Neurology & Neurophysiology

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Lateralizing and Localizing Findings in Focal Epilepsies: A Concise Review

Ali A. Asadi-Pooya1,2*

1Department of Neurology, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran

2Jefferson Comprehensive Epilepsy Center, Department of Neurology, Thomas Jefferson University, Philadelphia, USA

Corresponding Author:
Ali A. Asadi-Pooya
Department of Neurology
Shiraz University of Medical Sciences
Shiraz, Iran
Tel: +98-9352274990
E-mail: [email protected]

Received date: October 24, 2011; Accepted date: April 20, 2012; Published date: April 26, 2012

Citation: Asadi-Pooya AA (2012) Lateralizing and Localizing Findings in Focal Epilepsies: A Concise Review. J Neurol Neurophysiol S2. doi:10.4172/2155-9562.S2-003

Copyright: © 2011 Asadi-Pooya AA. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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Abstract

Knowledge of lateralizing and localizing value of seizure semiology and other clinical findings is necessary in the management process of patients with focal epilepsy, particularly with widespread use of surgery in the management of patients with refractory focal epilepsy. The advent of video-EEG monitoring has permitted careful analysis of semiologic features of seizures and their correlation with simultaneous EEG activities. The availability of new imaging and functional studies could be considered as a revolution in localization of the epileptogenic zone. In the current concise review, a list of well-documented lateralizing and localizing findings in focal epilepsies is prepared. This paper is designed as a practical tool for physicians, aiming to serve as a practical, problem-oriented reference.
While I include the correlated symptomatogenic zone and the possible mechanism in generating the finding in the context of a focal seizure, this paper emphasizes how to localize the epileptogenic zone according to any given specific finding. I hope that this paper leads to improved patient care.

Keywords

EEG; Focal epilepsy; Lateralization; MRI; Semiology

Introduction

Knowledge of lateralizing and localizing value of seizure semiology (symptoms and signs) and other clinical findings is not only helpful, but also necessary in the management process of patients with focal epilepsy. The importance of these findings has specifically increased during the past three decades and with widespread use of surgery in the management of patients with refractory focal epilepsy. The advent of video-EEG monitoring has permitted careful analysis of semiologic features of seizures and their correlation with simultaneous EEG activities. The availability of new imaging and functional studies could be considered as a revolution in localization of the epileptogenic zone in patients with focal epilepsy [1].

One should consider that seizure semiology has several limitations in localizing and even lateralizing the seizure onset. Although, many semiologic features have high positive predictive values, none is perfect in determining the seizure onset or epileptogenic zones. Seizure semiology is sometimes dictated by the pathway of electrical seizure propagation [2] and can reflect only the symptomatogenic zone [3]. Therefore, video recordings of multiple seizures should be reviewed carefully to find as many useful semiologic features as possible. A seizure that is representative of the rest of the recorded seizures should be reviewed with the patient’s relatives to verify that habitual seizures have been captured and analyzed. It is noteworthy to mention that age and brain maturation has some effects on seizure semiology and ictal features are less conclusive in children with focal epilepsy [4]. Concordance between seizure semiology and EEG activity increases the value of localization process and judgment [2,5]. Furthermore, concordance of the above-mentioned findings with imaging, functional studies, and neuropsychological studies increase the reliability of the localization and / or lateralization of the seizure onset zone or epileptogenic zone significantly [6-10].

In the current concise review, a list of presumably well-documented lateralizing and localizing findings in focal epilepsies is prepared (Table 1-6). The purpose is to provide a complete and easy to use list of clinical findings, which are helpful in lateralization and localization of the epileptogenic zone in patients with focal epilepsy. This paper is designed as a practical tool for physicians, aiming to serve as a practical, problem-oriented reference. While, I include the correlated symptomatogenic zone and the possible mechanism in generating the finding in the context of a focal seizure, this paper emphasizes how to localize the epileptogenic zone according to any given specific finding. These findings are organized in a series of tables (Table 1-6). These tables are organized in a way, so that the reader can easily review the relevant information. I hope that this concise paper leads to improved patient care.

Semiology Lateralizing value (PPV) Symptomatogenic zone Mechanism
Homonymous hemifield visual aura or defect 100% Brodmann areas 17-19 Activation
Unilateral ictal paresis or immobile limb 100% Negative motor areas Activation
Forced head version less than 10 second before secondary generalization > 90% Brodmann areas 6 & 8 (frontal eye and motor areas) Activation
Unilateral ictal dystonia > 90% Spread from seizure onset zone to ipsilateral basal ganglia Activation
Postictal (Todd’s) palsy > 90% Brodmann areas 4 & 6 (primary motor area) Exhaustion/ Inhibition
Fencing posture 90% SMA  Activation
Figure-of-4 sign (Asymmetric tonic limb posturing) ~ 90% SMA/ Prefrontal area Activation
Unilateral tonic activity ~ 90% SMA/Brodmann area 6 Activation
Unilateral sensory or painful aura ~ 90% Brodmann areas 1, 2, 3 (primary SSA) Activation
Unilateral clonic activity > 80% Brodmann areas 4 & 6 (primary motor area) Activation
Emotional facial asymmetry > 80% Unknown Unknown
Epileptic nystagmus N/A Posterior head regions Unknown

Table 1: Localizing semiologic findings pointing to the contralateral location (for the epileptogenic zone).

Semiology Lateralizing value (PPV) Symptomatogenic zone Mechanism
Unilateral automatisms with contralateral dystonic posturing* > 95% N/A Release phenomenon / Activation
Postictal nose wiping > 90%* Unknown Unknown
Unilateral ictal eye blinking > 80% Unknown Unknown
Ictal piloerection (goose bumps)* > 80% Unknown Unknown
Last clonic jerk > 80% Brodmann areas 4 & 6 (primary motor area)  ? Exhaustion of the hemisphere of onset

Table 2: Localizing semiologic findings pointing to the ipsilateral location (for the epileptogenic zone).

Semiology Lateralizing value (PPV) Symptomatogenic zone Mechanism
Preserved consciousness and automatisms* 100% Unknown Unknown
Ictal speech preservation* > 80% N/A Impairment of non-language areas
Ictal vomiting* > 80% Temporal lobe and Papez circuit Activation
Ictal spitting* 75% Unknown Unknown
Ictal urinary urge N/A Mesial frontal region/ Medial temporal gyrus Activation
Orgasmic auras N/A Mesiotemporal / frontal / amygdala Activation
Peri-ictal water drinking* N/A Lateral hypothalamus Activation

Table 3: Lateralizing semiologic findings pointing to the non-dominant hemisphere.

Semiology Lateralizing value (PPV) Symptomatogenic zone Mechanism
Ictal speech arrest* 67% language areas  Impairment of language areas
Postictal dysphasia > 80% language areas  Impairment of language areas

Table 4: Lateralizing semiologic findings pointing to the dominant hemisphere.

Semiology Symptomatogenic zone Mechanism
Auditory auras Superior temporal gyrus Activation
Ictal vocalization Broca’s area Activation
Postictal Cough N/A N/A
Gelastic Seizure Hypothalamus N/A
Olfactory and Gustatory auras Temporal lobe structures Activation

Table 5: Non-lateralizing semiologic findings in focal epilepsies.

Finding Lateralizing value (PPV) Mechanism
Interictal EEG in TLE 75% Activation 
Ictal EEG in TLE 80-92% Activation 
Ictal EEG + Semiology in TLE 95% _________
Interictal EEG in ETE 50-66% Activation 
Ictal EEG in ETE Variable  Activation 
CT scan abnormality Variable  Lesion
MRI abnormality 86-100%  Lesion
Interictal PET abnormality ~ 90% Hypometabolism
Ictal SPECT abnormality > 95%  Hyperperfusion
Interictal SPECT abnormality  > 80% Hypoperfusion
Wada test in TLE** 85% Memory asymmetry

Table 6: Lateralizing and localizing paraclinical findings in focal epilepsies.

References

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