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Refractory Lesional Parietal Lobe Epilepsy: Clinical, Electroencephalographic and Neurodiagnostic Findings.

INTRODUCTION

Epilepsy centers, specialized in the management and surgical treatment of medically refractory epilepsy emphasize the importance of differentiating the varieties of localization related epilepsies (1). The traditional attempts to sub-classify these epilepsies have focused on their lobe of origin (2). The requirements for accurate localization include patients' medical history and neurological examination, EEG investigations, clinical seizure evaluation, neuropsychological studies and detailed neuroimaging (3). There has been considerable recent interest in temporal and frontal lobe epileptic syndromes and less attention has been paid to parietal and occipital lobe epilepsies (4). Knowledge about the clinical and electrical manifestations of parietal lobe seizures is based mainly on case studies and occasional larger series (2,3,5,6,7,8,9).

The incidence of parietal lobe seizures has been reported as almost 6% of all partial seizures (10). Epileptic seizures of parietal lobe origin are heterogeneous and mainly characterized by the presenting auras. Like all partial seizures, parietal lobe seizures consist of subjective and objective components. The most common subjective sensations or auras of parietal lobe seizures are paresthesia, usually numbness and tingling, but also a sensation of "pins and needles" and rarely crawling or itching (2).

When symptoms such as paresthesia or pain occur prominently and early in partial seizures, the origin of parietal lobe should be suspected. However, most patients with parietal lobe seizures have no symptoms or signs suggesting the parietal lobe. These patients can present with misleading findings because of the absence of detectable epileptogenic lesions. This results in erroneous localization, which can in turn lead to ineffective surgical intervention (2). Additionally parietal lobes are large, diffuse structures, so the potential for sampling error is high. Even when parietal lobe seizure origin is suspected in the absence of a structural lesion, documenting this with invasive EEG monitoring can be difficult (2).

The aim of this study was to identify the clinical, electrophysiological and neuroimaging characteristics of patients with medically refractory symptomatic parietal lobe epilepsy. These findings may help us to localize the seizure focus in some patients with cryptogenic partial epilepsy and warn clinicians when the parietal lobe should be sampled with more invasive techniques like intracranial electrodes prior to epilepsy surgery.

METHODS

We performed a retrospective, descriptive study of patients who underwent a comprehensive evaluation including clinical, electroencephalographic and neuroimaging procedure for intractable lesional parietal lobe epilepsy for 11 years at the Department of Neurology of our hospital. This study was conducted in accordance with Helsinki Declaration. All patients had parietal lesions and most of them were not candidate for epilepsy surgery for example tumor or arteriovenous malformation patients. That is why patients were not chosen from long-term video-EEG monitoring pool which is basically used for epilepsy surgery patients. Their detailed clinical history, neurological examination, routine surface EEG and neuroimaging features were noted. If patients' seizure semiology and brain lesions were indicative of parietal lobe epilepsy they were included in this study The parietal lobes have arbitrary anatomical borders. So we used the term "parietal lobe" to refer to the region behind the post central gyrus and in front of the occipital lobe according to the neuroimaging data (5). Patients were excluded if the lesion was large and extended beyond the parietal lobe and patients with dual pathology like an arachnoid's cyst or venous anomaly, which could be coincidentally found, were also excluded.

Patients' past medical history including febrile convulsions, family history of epilepsy and parental consanguinity were noted. All patients underwent a routine interictal scalp EEG, at least once, using the international 10-20 system. EEG recordings were interpreted by experienced epileptologists-neurophysiologists.

Nineteen patients had both brain computerized tomography (CT) and magnetic resonance imaging (MRI), 7 patients had only brain CT, the rest of them (23 patients) had only brain MRI scanning (including T1-weighted, T2-weighted, and fluid-attenuated inversion recovery [FLAIR] sequences).

Patients' follow up were performed by either routine control examinations or by phone call.

Statistical Analysis

SPSS 16.0 (Statistical Package for the Social Sciences Inc. released 2007. SPSS for Windows, version 16.0, Chicago, USA) was used for statistical analysis. Age data were presented as median and minimum-maximum levels. The patients' gender medical history types of aura, seizure types, ictal characteristics, presumed etiological factors and lesion side were shown as frequencies and percentages. Patients without aura and presumed etiological factors were compared by Kruskal-Wallis test. Mann-Whitney U test was used when appropriate. A value of p<0.05 was considered statistically significant.

RESULTS

Patients admitted to our clinic with medically refractory seizures and diagnosed as lesional parietal lobe epilepsy were included in this descriptive study. We combined their medical records and seizure semiology (aura and ictal characteristics) with EEG and neuroimaging results to obtain a clue guiding us to parietal foci.

At the time of data collection, there were 46 patients (21 female, 25 male) aged 14 to 71 years (median 24) who had lesional parietal lobe epilepsy. Their age at seizure onset ranged from 1 to 61 years (median 18). Their medical history, seizure semiology, surface EEG and neuroimaging characteristics are summarized in Table 1.

According to their past medical history, the rate of febrile convulsions was 21.7% (10/46), family history of epilepsy was 23.9% (M/46) and parental consanguinity was 8.7% (4/46) (Table 2.1).

Auras

Auras were reported in 78.3% (36/46) of the patients. The most common one was somatosensory aura described by 72.2% (26/36) as tingling or numbness; they were contralateral to the lesion side in 73.0% (19/26) patients, and bilateral in 2 patients. Three patients described pain including left facial pain, leg pain, bilateral hand and gastric pain. Interestingly, the patient with gastric pain had gastric and gall bladder operations because of this symptom before the diagnosis of epilepsy. Two patients had a cold sensation contralateral to the lesion side. Other sensory auras were related to taste, such as sour-tasting or smell including anosmia or bad odor.

The second most common aura was headache reported by 36.1% (13/36) of the patients. The description of headache was like wearing a helmet or headache without a specific feature.

Nausea and vomiting were detected in 36.1% (13/36) of patients and again 36.1% (13/36) of the patients reported psychic symptoms including fear expression, feeling empty, annoyance, feeling dead, strange thoughts, panic, anxiety and de ja vu.

Visual symptoms were described by 16.6% (6/36) of the patients, as mottled flag, round shaped lights, black foals on visual field, blurred vision, flashing and macropsy. Vertigo was reported as an aura in 11.1% (4/36) of the patients. One patient mentioned dysarthria as an aura symptom (Table 2.2).

Case Presentations

Patient 1: A 14-year-old female patient was admitted to our neurology clinic for having seizures. Her past medical history revealed that she had head injury at 18 months of age and her first seizures started at the age 3.5. She had aura with vertigo, numbness in the left arm and feeling of her eye bigger than before. Her seizure characteristics were tonic posture of left arm and leg, vocalization without affecting consciousness lasting 15-20 seconds. EEG showed right parieto-occipital background abnormality and epileptiform abnormality. Her cranial CT was normal at that time. Her seizures were controlled with carbamazepine (CBZ) and diphenylhydantoin (DPH) for 6 years, then antiepileptic medication was discontinued. After that, seizures started with a frequency of 20 times a day. EEG revealed right parieto-occipital background abnormality and centro-temporal paroxysmal activity. Her cranial MRI was normal. Then she was put on CBZ and primidone (PRM) treatment. After 17 years of her seizure onset, her thin section cranial MRI revealed right parietal cortical dysplasia. She still has seizures starting with left arm numbness and weakness, then tonic posture once a month under antiepileptic treatment.

Patient 2: A 24-year-old, male patient was admitted to our clinic for headache and seizures. He had a history of cranial trauma at the age of 4, which caused unconsciousness. His seizures started when he was 14 years old. Seizure characteristics were gastric pain, epigastric raising, headache then secondary generalized tonic clonic seizures (GTCS). He also had seizures in sleep. During follow up he had gastric and gall bladder operations because of abdominal pain, which in fact was a seizure aura. His EEGs revealed right temporo-occipital epileptiform abnormality. Cranial CT showed right parietal infarct and there was right parietal cortical-sub-cortical infarct sequela in MRI. Carbamazepine and DPH treatment were given to the patient and his seizure frequency decreased to 2 times/year.

Objective Seizure Manifestations and Seizure Types

The most common ictal behavioral changes were paresthesia in 69.6% (32/46) and focal clonic activity was present in 39.1% (18/46) of the patients (Table 2.3). Tonic posture, various automatisms, head deviation, staring, sensation of pain and speech disturbances occurred to a lesser extent.

Simple partial seizures were the most common seizure type presenting in 69.6% (32/46) of the patients. Complex partial seizures occurred in 43.5% (20/46) and secondary GTCS were reported in 58.7% (27/46) of the patients (Table 2.4).

EEG Findings

Interictal EEG disclosed abnormal background activity in almost 1/3 of the patients (Table 2.5). Epileptiform abnormalities were found in 34.8% (16/46) and lateralized paroxysmal slow, sharp-slow waves were detected in 56.5% (26/46) of the patients. EEG findings were normal in 34.8% (16/46) of the patients. In none of the EEGs isolated parietal foci were detected.

Presumed Etiological Factors

Posttraumatic encephalomalacia 21.7% (10/46), stroke 21.7% (10/46), tumoral lesion 15.2% (7/46), malformation of cortical development 15.2% (7/46), arteriovenous malformation 15.2% (7/46) and atrophy 10.9% (5/46) were detected in decreasing order (Table 2.6). Lesion localizations were as follows: right hemisphere in 47%, left hemisphere in 44% and bilateral parietal atrophy in 9% of the patients.

Is the Presence of Aura Related to the Etiology?

In this study 10 patients (21.7%) did not present aura symptoms before seizure manifestation. Most of the patients without aura had tumoral lesions (5/10 patients). This finding was statistically significant (p=0.02). In the rest of them, two patients had stroke, one had malformation of cortical development, one had parietal atrophy and another had arteriovenous malformation. Age, seizure types, EEG characteristics, side of the lesion and antiepileptic treatment were not different between patients with or without aura (P>0.05).

Surgery

Seven of 46 patients had tumoral parietal lobe lesions and 6 of them underwent surgical procedures. Pathological examination showed that 4 of 6 patients had astrocytoma, one had low-grade glial tumor and one had meningioma. The seventh patient had nodular lesion with contrast enhancement. The pathological diagnosis of these 6 patients is shown in Table 1. After surgery 3 of them received chemotherapy with radiotherapy one was treated with radiotherapy only. They were also treated with two or three antiepileptic drugs for their seizures. The patient with meningioma became seizure free under antiepileptic medication (DPH+CBZ) followed by tumor resection. Postoperative follow-up duration was one year.

Seven of 46 patients had malformation of cortical development and lesionectomy was performed in two of them. Pathological investigation revealed focal cortical dysplasia. After surgery one of them had one seizure per month under multiple antiepileptic drug treatments. In the remaining 5 patients who did not have surgery, one was seizure free, one had a simple partial seizure (SPS) per month and one had a SPS per 6 months while taking one antiepileptic drug (AED).

One patient in the arteriovenous malformation group underwent embolization. Unfortunately her follow-up was not available. Totally 19.5% (9/46) of patients had surgical interventions because of their parietal lesions.

Prognosis

Twenty patients' follow-up records were obtained. Follow-up time ranged between 1-10 years. Five patients were seizure free under AED treatment. Thirteen patients were having seizures either simple partial or secondary GTCS while taking AED treatment. Two patients died because of cardiopulmonary arrest and respiratory failure during 10 years of follow-up. Detailed information is provided in Table 1.

DISCUSSION

Literature about parietal lobe seizures is limited to case reports or case series. Especially reports related to aura and seizure semiology with parietal localization are rare (3,5,8,11). Here we presented the clinical and laboratory findings of 46 lesional symptomatic parietal lobe epilepsy patients. In this retrospective study the main characteristic of parietal lobe seizures was the aura compatible with literature. The most common auras encountered were somatosensory; and 72.2% of patients experienced tingling or numbness of the extremities. Somatosensory auras have been assumed as the most common initial manifestations in patients with symptomatic parietal lobe epilepsy in the literature (4,5,12). Somatosensory aura was contralateral to the epileptogenic side in 73%, painful sensations were described in three patients and thermal sensations in two. Several authors have reported the lateralizing value of somatosensory aura in the literature (13). Painful sensations may also represent as an epileptic aura. In 1 of 3 patients the aura was contralateral to the epileptic side and in 2 of them painful sensations were bilateral. These signs may reflect the involvement of the secondary sensory areas. Although these sensory symptoms give an impression that the patient may have a parietal lesion, sometimes parietal lobe seizure manifestations are various and complex. The parietal lobe is the interface of all tracts coming from or going to other brain regions, especially to the frontal and temporal lobes (3,14). That is why parietal lobe seizures may have different kind of features like visual, gustatory motor psychic etc. It was the case also in our study Vestibular manifestations were reported in 11-23.5% of the series presented in the literature (5,8). They probably reflect the involvement of the vestibular cortex (15). Visual aura may show the spreading nature of seizures to the occipital lobe. In general, subjective manifestations of aura symptoms were present in 78.3% of the patients in our study The rate of subjective manifestations in parietal lobe epilepsy ranges between 57% to 94% in the literature (3,5,7,11), which is in agreement with our findings.

In this retrospective study the most common ictal behavioral changes were paresthesia and focal clonic activity. Tonic posture, various automatisms, head deviation, staring, sensation of pain and speech disturbances occurred to a lesser extent. These results again were in accordance with the literature (5,8,16).

Among localization related epilepsies, parietal lobe seizures have the highest percentage of non-localizing EEG findings, probably owing to the rich connectivity of the parietal lobe (3,9). In our study we also observed the same finding. None of our patients' EEGs revealed isolated parietal foci. This may explain the mislocalization of non-lesional parietal lobe epilepsy to other lobes in some cases.

According to our study, the most common presumed etiological factors were posttraumatic encephalomalacia and stroke making up nearly half of the patients. The rest of them were tumor, malformation of cortical development, atrophy, arteriovenous malformation. These results were compatible with previous studies (3,5,8). In this study we found that most patients without aura had tumoral lesions. This finding contradicts with the literature, where aura is reported in up to 90% of the patients with tumoral parietal lobe epilepsy. The reason for this discrepancy may be the low number of tumoral patients in our study

Roughly 30% of epilepsy patients have medically refractory seizures (17). For some treatment resistant focal epilepsy patients, surgical excision of the epileptic focus is an alternative choice to medical treatment (5). Although the parietal cortex comprises the second-largest cortical surface of the brain and despite the significant progress in video-EEG recording technology, imaging techniques, and invasive mapping methods with depth and/or subdural grid electrodes, resections in the parietal lobe are rare, constituting only 10.8% of the patients in large surgical series (5,18). In our study 19.5 % of patients had surgical intervention which is comparable to the literature.

This study emphasizes the importance of the symptomatology of the parietal lobe seizures. However it has some limitations. One drawback of the study is the presentation of only routine scalp EEG findings. Besides patients were not chosen from long-term video EEG monitoring or intracranial electrode implant pool, so that parietal foci were verified only with neuroimaging data. Also follow-up of all patients was not available. Despite these limitations, 46 patients of lesional parietal lobe epilepsy patients' information is valuable for the epilepsy literature.

In conclusion, clinical and laboratory findings of patients with parietal lobe epilepsy are scarce in the literature. This relatively large study results indicate that parietal lobe seizures may have different symptomatology owing to various patterns of seizure spread. Interictal scalp EEG recordings contain non-localizing epileptiform abnormalities in only 1/3 of the patients. Sensory aura is the most predictable sign of parietal lobe origin. Medically refractory cryptogenic partial epilepsy patients, who have various sensory symptoms like lateralized paresthesias or pain, should be investigated for parietal seizure foci.

Ethics Committee Approval: Authors declared that the research was conducted according to the principles of the World Medical Association Declaration of Helsinki "Ethical Principles for Medical Research Involving Human Subjects", (amended in October 2013).

Informed Consent: As this study was a retrospective one and medical file records were scanned, informed consent was not obtained.

Peer-review: Externally peer-reviewed.

Author Contributions: Concept--S.S., H.K.; Design--S.S., O.K., H.K.; Supervision--N.D., S.S.; Resources--S.S.; Materials--O.K.; Data Collection and/or Processing--O.K.; Analysis and/or Interpretation--O.K., H.K., N.D., S.S.; Literature Search--O.K., H.K.; Writing Manuscript--O.K., H.K., N.D.; Critical Review--H.K., S.S., N.D., O.K.; Other--O.K., H.K.

Conflict of Interest: No conflict of interest was declared by the authors.

Financial Disclosure: The authors declared that this study has received no financial support.

REFERENCES

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(2.) Siegel AM, Williamson PD. Parietal lobe epilepsy. Adv Neurol 2000; 84:189-199.

(3.) Williamson PD, Bonn PA, Thadani VM, Darcey TM, Spencer DD, Spencer SS, Novelly RA, Mattson RH. Parietal Lobe Epilepsy: Diagnostic Considerations and Result of Surgery. Ann Neurol 1992; 31:193-201. [CrossRef]

(4.) Sveinbjorsdttir S, Duncan JS. Parietal and occipital lobe epilepsy: a review. Epilepsia 1993; 34:493-521. [CrossRef]

(5.) Salanova V, Anderman F, Rasmussen T, Olivier A, Quesney LF. Parietal lobe epilepsy: Clinical manifestations and outcome in 82 patients treated surgically between 1929 and 1988. Brain 1995; 116:607-627. [CrossRef]

(6.) Cascino GD, Hulihan JF, Sharbrough FW, Kelly PJ. Parietal lobe lesional epilepsy. Epilepsia 1993; 34:522-527. [CrossRef]

(7.) Kim DW, Lee SK, Yun CH, Kim KK, Lee DS, Chung CK, Chang KH. Parietal lobe epilepsy: the semiology, yield of diagnostic workup, and surgical outcome. Epilepsia 2004; 45:641-649. [CrossRef]

(8.) Bartolomei F Gavaret M, Hewett R, Valton L, Aubert S, Regis J, Wendling F Chauvel P Neural networks underlying parietal lobe seizures: a quantified study from intracerebral recordings. Epilepsy Res 2011; 93:164-176. [CrossRef]

(9.) Ristic AJ, Alexopoulos AV, So N, Wong C, Najm IM. Parietal lobe epilepsy: the great imitator among focal epilepsies. Epileptic Disord 2012; 14:22-31.

(10.) Rasmussen T. Focal epilepsies of nontemporal and nonfrontal origin. In: Wieser HG, Elger CE, eds. Presurgical evaluation of epilepsies: basics, techniques, implications. Berlin: Springer-Verlag 1987:301-305.

(11.) Ho SS, Berkovic SF, Newton MR, Austin MC, McKay WJ, Bladin PF. Parietal lobe epilepsy: clinical features and seizure localization by ictal SPECT. Neurology 1994; 44:2277-2284. [CrossRef]

(12.) Fogarasi A, Boesebeck F Tuxhorn I. A detailed analysis of symptomatic posterior cortex seizure semiology in children younger than seven years. Epilepsia 2003; 44:89-96. [CrossRef]

(13.) Palmini A, Gloor P The localizing value of auras in partial seizures: a prospective and retrospective study. Neurology 1992; 42:801-808. [CrossRef]

(14.) Mauguiere F Courjon J. Somatosensory epilepsy. A review of 127 cases. Brain 1978; 101:307-332. [CrossRef]

(15.) Foldvary N, Klem G, Hammel J, Bingaman W, Najm I, Luders H. The localizing value of ictal EEG in focal epilepsy. Neurology 2001; 57:2022-2028. [CrossRef]

(16.) Kahane P Hoffmann D, Minotti L, Berthoz A. Reappraisal of the human vestibular cortex by cortical electrical stimulation study. Ann Neurol 2003; 54:615-624. [CrossRef]

(17.) Grefkes C, Fink GR. The functional organization of the intraparietal sulcus in humans and monkeys. J Anat 2005; 207:3-17. [CrossRef]

(18.) Kwan P Brodie MJ. Definition of refractory epilepsy: defining the indefinable? Lancet Neurol 2010; 9:27-29.

Oguzhan KURSUN (1), Hulya KARATAS (2), Nese DERICIOGLU (2,3), Serap SAYGI (3)

(1) Clinic of Neurology, Numune Training and Research Hospital, Ankara, Turkey

(2) Institute of Neurological Sciences and Psychiatry, Hacettepe University, Ankara, Turkey

(3) Department of Neurology, Hacettepe University School of Medicine, Ankara, Turkey

DOI: 10.5152/npa.2016.13790

Correspondence Address: Hulya Karatas, Hacettepe Universitesi, Norolojik Bilimler ve Psikiyatri Enstitusu, Ankara, Turkiye E-mail: hulyak@hacettepe.edu.tr

Received: 12.01.2016 Accepted: 20.01.2016 Available Online Date: 01.03.2016

[c]Copyright 2016 by Turkish Association of Neuropsychiatry--Available online at www.noropskiyatriarsivi.com
Table 1. Characteristics of 46 lesional symptomatic parietal lobe
epilepsy patients

    Sex/age
    on          Onset   Medical                       Seizure
No  admission  (years)  History                       type

 1  Fe, 35     35       A: right arm-leg numbness,    SGTCS
                        dysarthria, right hand
                        weakness
                        S: right peroral focal
                        onset, unconsciousness
 2  Fe, 60     60       A: -                          GTCS
                        GTCS

 3  Fe, 38     38       A: left facial pain,          CPS
                        light-headedness, headache,   SGTCS
                        left tinnitus, right arm
                        and leg pain.
                        S: right peroral focal
                        convulsion, unconsciousness
 4  Fe, 20     20       A: -                          SPS
                        L focal motor seizure         SGTCS
                        SGTCS during sleep

 5  M, 33      33       A: -                          SPS
                        Convulsion of right           SGTCS
                        arm and contraction of
                        right peroral region
 6  M, 41      41       A: -                          SGTCS
                        SGTCS
 7  M, 36      35       A: -                          SGTCS
                        SGTCS
 8  M, 19      14       Head injury,                  SPS
                        A: left arm, numbness         SGTCS
                        feeling crash
                        S: SGTCS
 9  Fe, 18     12       Head injury, 5 monthsold      SPS
                        Aura: Right arm dullness.     CPS
                        S: clonic convulsion at
                        right arm and face,
                        vocalisation
10  M, 19      15       18 months old head injury     SPS
                        A: epigastric raising,        CPS
                        thougths of being a scary     SGTCS
                        place S: tonic neck
                        convulsion on awake and
                        sleep.
11  M, 44      43       Head trauma at 43yo           CPS
                        A: Headache like wearing a
                        helmet.
                        S: lag, oral-hand
                        automatism left peroral
                        contraction, aphasia
12  M, 19      12       Dystosia, mental              SPS
                        retardation, head injury      SGTCS
                        at 18 months.
                        A: Numbness of left
                        arm-leg
                        S: Left facial twitching,
                        bilateral tonic convulsion
13  Fe, 34     34       Head injury and               SPS,
                        intracerebral hemorrhage      SGTCS
                        at 18 months old.
                        A: Tingling of left arm,
                        flashing
14  M, 21       3       Dystosia, perinatal injury    SPS
                        A: numbness of right hand,    CPS
                        nausea, oral automatism.      SGTCS
                        Right focal seizure at 3 yo,
                        3 status epilepticus, Shunt
                        operation at 16 yo
15  Fe, 18     10       Intracranial cyst operation   SPS
                        at 13 yo,                     SGTCS
                        A: Numbness of left arm.
                        S: Left arm convulsion
                        then SGTCS
16  Fe, 24     15       A: electrification on head,   SPS
                        numbness of left hand,        SGTCS
                        feeling of landslide,
                        walking on space, bilateral
                        hand pain.
17  Fe, 18     13       Encephalitis at 9             CPS
                        months-old, Mental-motor      SGTCS
                        retardation A: Yawing,
                        crying, fear expression
                        S: bilateral limb
                        convulsions
18  Fe, 21      7       head injury at 11             SGTCS
                        months-old
                        A: -
                        S: left focal onset
                        secondary generalised
                        seizures (vocalisation
                        during sleep than seizure)
19  Fe, 65     60       A: Right sided headache,      SPS
                        vertigo, anosmia, hypogeusia
20  M, 71               2 mo meningitis               SPS
                        A: R arm pain                 SGTCS
                        S: R arm clonic convulsion
21  M, 19       4       Menengitis at I yo            SPS
                        A: vertigo, fatigue           CPS
                        S: turning around
                        himself for 2-4 tours,
                        oral automatism, gulping,
                        forced deviation of head
                        to the left then falling
22  Fe, 48      4       A: -                          CPS
                        Fainting when face with       Reflex
                        blood, GTCS (eyes are open,   epilepsy
                        pallor, head deviation to
                        the back for 5-6 seconds)
23  Fe, 60     60       A: numbness of                SPS
                        peroral region and hand
24  M, 30      30       Head injury at 4 yo           CPS
                        A: Epigastric raising,        SGTCS
                        vertigo, faint, nause,
                        sour taste, falling
25  M, 24      14       4 yo head injury              SPS
                        A: epigastric sensation,      SGTCS
                        gastric pain, headache and
                        loss of consciousness
                        (gastric, gall bladder
                        operations because of pain)
26  M, 32      17       A: Feeling cold, confusion,   CPS
                        oral-hand automatism          SGTCS
                        GTCS on sleep
27  Fe, 67     61       A: fainting                   CPS
                        Left hemiparesis              GTCS
28  Fe, 14      3,5     Head injury at 6 mo           SPS
                        A: Vertigo, macropsy,         CPS
                        left arm numbness
                        S: Tonic posture of left
                        body, vocalisation
29  M, 49      44       A: Fatigue, blurred           SGTCS
                        vision, vomiting
                        S: Loss of consciousness
30  M, 17      17       A numbness of left arm,       SPS
                        S:SGTCS on sleep              SGTCS
31  M, 22       2       A: Febril                     SPS
                        convulsion                    GTCS
                        Clonic convulsion
                        on right legGTCS
                        on sleep, vocalisation
32  Fe,        18       Infantil spasm at 20
                        day-old                       SPS
                        A: psychic+vizuel             CPS
                        (fear, palpitation, black     SGTCS
                        foals on visual field)
                        S: Contraction on left
                        eyelid, left arm, falling,
                        seizures on sleep
33  M, 21      19       A: Epigastric sensation       CPS
                        S: automatism, SGTCS          SGTCS
34  M, 16      13       Cafe au lait on R leg         SPS
                        A: Tongue numbness,           CPS
                        bilateral hand numbness,
                        blinking
35  Fe, 17      5       A: Nause, headache            SPS
                        S: Black heterogenous flag    CPS
                        on vision field, vomiting,    SGTCS
                        falls at 15 yo, myoclonic
                        jerks on legs, shivering,
                        atonic seizures. Oral
                        automatism, myoclonic
                        jerks during sleep.
36  M, 30      25       Head injury at 2 yo           CPS
                        A: -                          SGTCS
                        S: Bilateral convulsions
                        on arms lasting 15 s
37  M, 21       7       A: confusion, feeling         SPS
                        empty, can not find his
                        way, blinking                 SGTCS
                        S: Left face, arm and leg
                        contraction on sleep
38  M, 18               Head injury at I mo           SPS
                        A: Numbness of left side,     CPS
                        round shape lights coming     SGTCS
                        from left vision field
                        S: Staring, tonic posture
                        of left hand than convulsion
39  M, 26      26       A: psychic symptoms           SPS
                        (annoyance, feeling dead,     CPS
                        strange thoughts, panic,
                        unable to breathe)
                        S: Bilateral clonic act of
                        legs
40  M, 38      36       A: Nausea, numbness of        SPS
                        left arm                      SGTCS
                        S: Clonic convulsion of
                        left arm. SGTCS on sleep.
41  Fe, 25     25       Menengitis at 13 yo           SPS
                        A: Severe headache,           SGTCS
                        numbness of left body side,
                        anxiety, vertigo
                        S: Right arm clonus,
                        unable to talk
42  Fe, 24     23       Febril convulsion at 3 yo     SPS
                        A: left face, arm numbness,   SGTCS
                        blurred vision
                        S: right arm numbness,
                        right leg clonic convulsion
                        SGTCS
43  M, 33      30        A: oral bad smell, feeling   SPS
                        neck compression then         SGTCS
                        GTCS
44  Fe, 24     24       A: nausea, right arm          SPS
                        numbness                      SGTCS
                        S: right arm tonic
                        convulsion on sleep then
                        SGTCS
45  Fe, 24     20       A: Feeling empty              CPS
                        S: Block of speech, staring,
                        loss of contact, oral-hand
                        automatism
46  M, 28      21       A: -                          GTCS
                        GTCS on sleep

    Surface                  CT and
No  EEG                      /or MRI                   Diagnosis

 1  1. L TP                  L P 3 cm                  Tumor
    background               diameter                  Pathology
    abnormality              cystic mass               Low grade
    2. L TP slow             lesion                    glial tumor
    and spike wave
    activity and PLED
 2  1.R CTP slow wave        R P meningioma            Tumor
    2.R CT paroxysmal                                  Pathology
    anomaly                                            Meningioma
 3  Normal                   L P mass lesion           Tumor Grade 1
                                                       astrocytoma
 4  1.R posterior            R P low grade glial       Tumor Pathology
    background anomaly,      tumor
    paroxysmal activity                                Low grade
    2. R posterior                                     astrocytoma
 5  Paroxysmal anomaly       L P                       Tumor Pathology
    at vertex and T regions  astrocytoma               astrocytoma
 6  Bilateral T slowing      L parietal tumor          Tumor Pathology
    of background rhythms,                             astrocytoma
    left paroxysmal anomaly
 7  N                        L P noduler lesions       Nodular lesion
 8  N (4 times)              R P focal                 Post traumatic
                             gliotic lesion            encephalomalacia
                             encephalomalacia
 9  N                        L P encephalomalacia      Post traumatic
                                                       encephalomalacia
10  R FT epileptiform        R P                       Post traumatic
    anomaly with             posttraumatic             encephalomalacia
    nasopharyngeal           lesions at
    electrodes               vertex level
11  N                        R P cortical              Post traumatic
                             hyperintense              encephalomalacia
                             lesion
12  L>R bilateral            L P cystic                Post traumatic
    CT paroxysmal            atrophic                  encephalomalacia
    epileptiform             lesion
    anomaly
13  I.Bilateral slowing of   R Post P                  Post traumatic
    background rhythms,      encephalomalacia          encephalomalacia
    R T focal epileptiform
    anomaly 2.R T PLED
14  1,2, 4 Slowing of        Hydrocephaly,             Post traumatic
    background rhythyms,     L P                       encephalomalacia
    L CT, L PO               porencephalic
    epileptiform anomaly     cyst, atrophy
    3. L generalised
    epileptiform
    anomaly.
15  I.R CT paroxysmal        R P                       Sequelaence
    anomaly                  hyperintense              phalomalacia
    2.N                      lesions related
    3.R CT slowing of        to operation
    background rhythms
16  R TO paroxysmal          R posterior               Encephalomalacia
    discharges               P cystic lesion
17  I. Generalised           Sequela
    background anomaly       encephalitis
    2, 3. N, N 4.Bifrontal
    epileptiform anomaly
    Bilateral P
    hyperintensi-ties,
    encepha-litissequela
18  1,2 R P slowing of       R P cystic                Stroke
    background rhythms       Encephalomalacia
    3.T dysryhthmia
    during HPV 4,6. N
    5.Anterior paroxysmal
    discharges duringHPV
    7,8.CT paroxysmal
    9.CT epileptiform
    paroxysmal discharges
19  R T background           R Post P subacute         Stroke
    rhythm anomaly           infarct
20  L CT paroxysmal          L P chronic               Stroke
    anomaly at HPV           infarct
21  R FT epileptiform        R P infarct               Stroke
    abnormality
22  I.Paroxysmal             L P chronic               Stroke
    anomaly with HPV         infarct
    2.-4. N,N,N
    5. Paroxysmal
    anomaly at vertex and
    temporal regions
23  N                        P subcortical             Stroke
    (2 times)                cystic infarct
24  R T paroxysmal           P leptomeningeal          Stroke
    anomaly                  cyst,
                             Posterior P
                             chronic infarct
25  I.R T paroxysmal         R P cortical-subcortical  Stroke
    epileptiform anomaly     infarct
    2. R TO epileptiform
    anomaly
    3.R TO epileptiform
    anomaly 4-10. N
26  L TP paroxysmal          R P subdural gyrus        Stroke
    anomaly                  hyper-intensities
27  I.N, 2.T paroxysmal      L P chronic               Stroke
    anomaly                  ischemic lesions          (amiloidangio-
    3.L T slow waves,                                  pathy)
    background anomaly

28  I.R PO background        R P dysplasia             MCD
    anomaly, epileptiform
    anomaly
    2.R PO paroxysmal
    anomaly
29  N                        L posterior               MCD
                             P gyrus thickness
30  Posterior paroxysmal     R P closed                MCD
    anomaly                  schisencephaly
31  Background               L P closed                MCD
    abnormality, C and       schisencephaly,
    L paroxysmal anomaly     polymicrogyri
    2.L CT paroxysmal
    anomaly, 3,4. N
32  R C paroxysmal           R P                       MCD Pathology
    abnormality              polymicrogyri
    2. R FC epileptiform                               Cortical
    abnormality                                        dysplasia
    3. R CTP epileptiform
    abnormality

33  I. R CT epileptiform     R P cortical              MCD
    abnormality              dysplasia                 Pathology
    2. R T epileptiform                                Cortical
    abnormality                                        dysplasia
34  C, 2. L FT               N (1999)                  MCD
    epilep-tiform            2. L P fold
    abnormality              asymmetry
    3.L FC paroxysmal        (200')
    anomaly
35  Bilateral O              Biparietal                Atrophy
    epileptiform             atrophy
    abnormality
36  Bilateral F              Biparietal                Atrophy
    paroxysmal anomaly       atrophy (R> L)
37  R C epileptiform         R P focal                 Atrophy
    anomaly                  cortical atrophy
38  Bilateral background     R P atrophy               Atrophy
    abnormality
39  I.L T diffuse slow       Biparietal                Atrophy
    wave activity            Atrophy
    2. R>L FCT
    epileptiform activity
    on sleep deprivation
40  I.R T background         R P AVM                   AVM
    abnormality,             embolization MT
    epileptiform
    abnormality
41  1,2. L CTP background    L P AVM                   AVM
    anomaly, epileptiform
    abnormality with
    HPV 3.L TPO active
    focal epileptiform
    anomaly
42  1,4. L CT background     L Posterior               AVM
    abnormality 2,5. L O,    P AVM                     AVM
    L FCT epilepti-iform                               embolization
    abnormality 3.                                     performed
    Subcortical
    epileptiform
    abnormality
43  I N                      L P cavernoma             AVM
44  I N                      L P cavernous             AVM
                             angioma
45  L>R T paroxysmal         L P cavernous             AVM
    abnormality              angioma
46  N                        L P vascular              AVM
                             abnormality

    Treatment
    (surgery, RT,
No  ChT, AED)            Prognosis

 1  Tumor resection      NA
    ChT+RT+PT

 2  Tumor                Seizure free
    resection+ PT        under AED

 3  Tumor                NA
    resection
    ChT+RT+PT

 4  Tumor                NA
    resection
    ChT+RT+PT

    paroxysmal activity
 5  Tumor                NA
    resection
    RT[+ or -]PT

 6  Tumor                NA
    resection
    RT[+ or -] PT

 7  Close                NA
    follow-up+MT
 8  MT                   SGTCS
                         <1/year

 9  PT                   SPS 4 /month

10  MT                   Aura
                         1-2/ month

11  MT                   Seizure free
                         with AED

12  PT                   Aura 1-2/month
                         SGTCS
                         1/3-4
                         years

13  MT                   Aura 4-5/month,
                         GTCS 1/year

14  MT                   NA

15  PT                   NA

16  MT                   Seizures 2/y
                         in 3 years of
                         follow-up

17  PT                   NA

18  MT                   Seizure free for
                         9 years

19  MT                   Exitus
                         cardiopulmonary arrest
20  PT                   NA

21  PT                   NA

22  MT                   Seizures continue
                         in 7 years of
                         follow-up

23  MT                   Seizure free(6 y)
24  MT                   NA

25  PT                   Seizures 1/year
                         under AED treatment

26  MT                   NA

27  MT                   Exitus 10 y after 1st
                         seizure (respiratory
                         arrest)
28  MT                   SPS '/month

29  MT                   Seizure free under
                         treatment
30  PT                   NA

31  PT                   NA

32  Lesionectomy         Seizures
    PT                   1/month

33  Lesionectomy         NA
    PT

34  MT                   SPS/6 months

35  MT                   NA

36  MT                   NA

37  PT                   NA

38  PT                   NA

39  MT                   NA

40  AVM                  SPS /4 month

41  PT                   NA

42  PT                   NA

43  MT                   NA

44  PT                   NA

45  PT                   NA

46  MT                   NA

Note: Patients without aura were colored in grey. A: aura; AED:
antiepileptic drug; AVM: arteriovenous malformation; C: central; ChT:
chemotherapy; CPS: complex partial seizure; CT: computerized
tomography; F: frontal; Fe: female; M: male; HPV: hyperventilation; L:
feft; MCD: Malformation of Cortical Development; MRI: magnetic
resonance imaging; MT: monotherapy; N: normal; NA: not available; O:
occipital; P: parietal; PLED: Periodic Lateralised Epileptiform
Discharges; PT: polytherapy; R: right; RT: radiotherapy; S: seizure;
SGTCS: secondary generalized tonic clonic seizure; SPS: simple partial
seizure; T: temporal; yo: years old

Table 2. Patient characteristics, aura features, ictal symptoms,
seizure types, interictal EEG findings and presumed etiological factors

1. Medical history of patients
Febrile Convulsions                                   21.7%
Family History of Epilepsy                            23.9%
Parental Consanguinity                                 8.7%
2. Aura
Sensory symptoms                                      72.2%
Headache                                              36.1%
Nausea vomiting                                       36.1%
Psychic symptoms                                      36.1%
Visual symptoms                                       16.6%
Vertigo                                               11.1%
Others (smell, taste, pain, thermal, dysarthria)      26%
3. Ictal behavioral changes
Paresthesia                                           69.6%
Focal clonic activity                                 39.1%
Tonic posture                                         17.3%
Automatisms                                           17.3%
Staring                                               11.1%
Speech disturbances                                    8.7%
Vocalisation                                           8.7%
Others (Head deviation, sensation of pain)            15%
4. Seizure types
Simple partial seizures                               69.6%
Secondary generalised tonic clonic seizures           58.7%
Complex partial seizures                              43.5%
5. Interictal EEG findings
Lateralised paroxysmal activity                       56.5%
Epileptiform abnormalities                            34.8%
Abnormal background activity                          33.3%
Normal EEG                                            34.8%
6. Presumed etiological factors
Posttraumatic encephalomalacia                        21.7%
Stroke                                                21.7%
Tumor                                                 15.2%
Malformation of cortical development                  15.2%
Arteriovenous malformation                            15.2%
Atrophy                                               10.9%
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Title Annotation:Research Article
Author:Kursun, Oguzhan; Karatas, Hulya; Dericioglu, Nese; Saygi, Serap
Publication:Archives of Neuropsychiatry
Article Type:Report
Date:Sep 1, 2016
Words:5705
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