Refractory Lesional Parietal Lobe Epilepsy: Clinical, Electroencephalographic and Neurodiagnostic Findings.
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.
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.
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.
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 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).
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).
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).
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.
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.
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.
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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
Correspondence Address: Hulya Karatas, Hacettepe Universitesi, Norolojik Bilimler ve Psikiyatri Enstitusu, Ankara, Turkiye E-mail: firstname.lastname@example.org
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|
|Date:||Sep 1, 2016|
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