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ORIGINAL ARTICLE
Year : 2014  |  Volume : 1  |  Issue : 1  |  Page : 26-31

Videonystagmography findings in epileptic children


1 Audiology Unit, ENT Department, Al-Azhar University (Girls), Cairo, Egypt
2 Neurology Department, ENT Department, Zagazig University, Egypt
3 Audiology Unit, ENT Department, Zagazig University, Egypt

Date of Web Publication28-Jul-2014

Correspondence Address:
Ebtessam Nada
Mit Ghamr, Dkahleia, 65 Sadek Street N. 65 post
Egypt
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/2314-8667.137561

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  Abstract 

This study included 60 epileptic children (6-18 years) and 20 neurologically free age-matched children. It was conducted to identify vestibular system abnormalities associated with or caused by epilepsy in patients either complaining of dizziness or not. Otoneurological testing was performed including videonystagmographic testing. More than one type of epilepsy was encountered. Dizziness was reported as a complaint in most patients diagnosed with partial epilepsy. Variable videonystagmographic findings were found. Among patients with dizziness, the most prominent abnormality was abnormal oculomotor test results (23 of the 37 patients). Only two patients showed abnormal Dix-Hallpike testing. Positive vestibular findings were found among patients without dizziness, in only three of the 23 patients who had unilateral caloric weakness during caloric testing.

Keywords: video-nystagmgraphy, epilepsy, Dizziness


How to cite this article:
El-Gohary M, Elmously M, Esmail N, Abdel Gawwad EA, Mekki S, Nada E. Videonystagmography findings in epileptic children. Adv Arab Acad Audio-Vestibul J 2014;1:26-31

How to cite this URL:
El-Gohary M, Elmously M, Esmail N, Abdel Gawwad EA, Mekki S, Nada E. Videonystagmography findings in epileptic children. Adv Arab Acad Audio-Vestibul J [serial online] 2014 [cited 2017 Dec 11];1:26-31. Available from: http://www.aaj.eg.net/text.asp?2014/1/1/26/137561


  Introduction Top


Dizziness is a symptom, not a disease. It may be defined as a subjective sensation of unsteadiness, imbalance, or disorientation with respect to one's surroundings. It is a matter of fact that episodic vertigo and/or dizziness in children are not frequent and vertiginous attacks are not dramatic.

However, epilepsy is characterized by repeated seizures that may occur as often as several times a day or as frequent as once every few months. Nearly one-third of people newly diagnosed each year with epilepsy are children. Electronystagmography (ENG)/videonystagmography (VNG) abnormalities in epileptic patients were reported [1]. The character of pathology suggested central origin. Moreover, drugs used in the treatment of epilepsy, such as levetiracetam, were found to cause dizziness as a side effect [2].

On the way of vestibular diagnosis, ENG is the most readily available test for assessing the vestibular system. Eye movements are recorded by means of corneoretinal potential by surface electrode, and the results are printed on a strip-chart recording paper or analyzed by computer [3].

However, VNG visualizes nystagmus on a television monitor and records it on video tape for later study, records, and for reproduction. It has the following advantages over ENG: visualization of torsional and oblique nystagmus, no interference of visual stimuli being working in complete darkness, mechanical and electrical stability, speed, and low cost [4].

Using VNG technology, demographic representation of the possible vestibular findings in epilepsy was performed.


  Materials and methods Top


The control group consisted of 20 normal children (13 boys and seven girls). Their age ranged between 6 and 18 years. They were chosen from the Audiology Unit, ENT Department, Zagazig University Hospitals.

The children were chosen with normal hearing and normal middle ears. There was no complaint suggestive of vestibular disorder, including dizziness, vertigo, motion sickness, or headache. Furthermore, there was no history of seizures.

Both groups were matched in age and sex.

The study group consisted of 60 epileptic children (36 boys and 24 girls). Their age ranged from 6 to 18 years. They were chosen from the Brain Topography Unit, Neurology Department, Zagazig University Hospitals.

The children were diagnosed as having epilepsy mainly on the basis of typical history of epileptic fit and clinical picture with or without electroencephalographic (EEG) findings [5].

Patients were classified according to the presence or absence of dizziness into two groups: those complaining of dizziness and those who did not report dizziness in their complaint.

Exclusion criteria

We excluded children with abnormalities regarding middle ear, for example, otitis media with effusion or Eustachian tube dysfunction, to omit middle ear pathology as an etiology for vestibular defect if present.

Similarly, patients with personal history or family history of headache were excluded to exclude migraine. Finally, we excluded patients with a history of motion sickness or similar condition in the family.

The control group was subjected to the following:

(1) Complete history taking.

(a) Prenatal history : TORCH syndrome.

(b) Neonatal history : jaundice, cyanosis, neonatal sepsis, and neonatal convulsions.

(c) Postnatal history : fever, convulsions, and trauma.

(d) History of the seizure attack, including detailed description of the attack, onset of first complaint, duration of the attack, and medications if present.

(e) Antiepileptic drug intake, including type of the drug, and dosage duration of drug intake.

(f) Family history of consanguinity and other affected members of the family.

(g) History of dizziness, including description, duration, relationship with epileptic attack, and response to treatment if present.

(h) Past history of ototoxic drug intake or head trauma.

(i) Past history of any medications.

(2) Basic audiological evaluation : It included pure tone audiometry, speech tests, and tympanometry testing.

(3) Bedside vestibular testing : It included spontaneous nystagmus, oculomotor tests (saccade and pursuit), gaze test, and Dix-Hallpike test.

(4) VNG test battery.

The study group was subjected to the following:

(1) Complete history taking.

(2) General examination : gait and posture.

(3) Otoscopic examination to exclude the presence of wax and tympanic membrane abnormalities.

(4) EEG was performed at the Neurology Department, Zagazig University Hospitals. Electrodes were arranged according to the international 10-20 system of surface electrode placement using monopolar and bipolar montages.

All EEGs were carried out under normal standard conditions. The EEG tracing was analyzed carefully with respect to frequency, amplitude, and symmetry of the background activity as well as the presence of any abnormality. The EEG findings were described as normal or abnormal. The abnormal epileptogenic activity was described as generalized, focal, and focal with secondary generalization.

It took 7 min of standard recording, at different montages (monopolar and bipolar), 3 min of hyperventilation, and 1 min of postventilation.

(5) Computed tomography (CT) scan examination was performed in Radiology Department, Faculty of Medicine, Zagazig University Hospitals to reach the etiology of epilepsy.

(6) Basic audiological evaluation : It included pure tone audiometry, speech tests, and immitancemetry testing.

(7) Bedside vestibular testing : It included spontaneous nystagmus, oculomotor tests (saccade and pursuit), gaze test, and Dix-Hallpike test.

(8) VNG test battery : The system used was Computerized Videonystagmography Ulmer version 0.1. The patient was seated on a test chair 1.05 m from the center of the TV monitor. We had to make sure that the patient can see the two edges of the sighting frame and he is keeping his head still. A VNS Goggles (SYNAPSYS, France), which is an infrared high-resolution CCD camera mounted on a mask, is applied with complete blocking of visible light and biocompatible infrared (IR) lightening.

A noisy trace is easily detected by observing that the cross fails to follow the center of the pupil. Without calibration, the software uses a default value, which allows measuring the ocular movements with errors of less than 20% in 95% of patients.


  Results Top


The control group showed normal EEG traces [Table 1], [Table 2], [Table 3].
Table 1 Results of saccadic test in the control group

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Table 2 Pursuit test results in the control group

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Table 3 Optokinetic test results in the control group

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CT scan was performed routinely for all epileptic patients presented to neurology clinic to assess the possible etiology of epilepsy if present. Patients with abnormal CT that could affect VNG findings were excluded.

Reviewing neurological findings, we found that 53.33% (n = 32) had generalized epilepsy, whereas 46.67% (n = 28) had partial type of epilepsy. On further classification, generalized epilepsy that was encountered in the study group was classified into: generalized tonic-clonic convulsions (50%, n = 16), generalized myoclonic convulsions (31.25%, n = 10), generalized atonic convulsions (9.38%, n = 3), and Petit mal epilepsy (9.37%, n = 3).

Similarly, patients with partial seizures were classified into: temporal lobe epilepsy (46.43%, n = 13), frontal lobe epilepsy (28.57%, n = 8), secondary generalized epilepsy (7.14%, n = 2), and parietal, occipitoparietal, and frontoparietal epilepsy that were collected in one category, named others (17.86%, n = 5).

Regarding VNG findings in the group of patients with vertigo, spontaneous nystagmus was detected in five patients; three of them showed no nystagmus on visual fixation suggesting peripheral vestibular lesion, whereas two of them showed no fixation suppression [Figure 1] and [Figure 2].
Figure 1: Types of generalized epilepsy.

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Figure 2: Types of focal epilepsy.

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Similarly, regarding VNG findings in the group of patients with vertigo, oculomotor test results showed abnormal saccade in 37.83% (n = 14) of patients [Figure 3]. Abnormal pursuit was noticed in 40.54% (n = 15) of patients and abnormal optokinetic in 37.83% (n = 14) of patients [Figure 4].
Figure 3: Oculomotor test results in group of patients with dizziness.

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Figure 4: Vestibular diagnosis associated with epilepsy in the study group.

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Positioning tests were normal with no nystagmus in any position. Dix-Hallpike maneuver revealed two patients with benign paroxysmal positional vertigo.

Regarding caloric test results, there were only three patients with unilateral weakness and directional preponderance, suggesting peripheral lesion. In contrast, two patients had unilateral weakness with no directional preponderance and absent fixation suppression, suggesting central vestibular disorder.

VNG findings in the group of noncomplainers revealed normal oculomotor tests, no nystagmus on Dix-Hallpike or positional tests. However, there were three patients with caloric weakness with no directional preponderance and preserved fixation suppression. A compensated peripheral vestibular lesion was discovered in these patients, which is more likely due to previous vestibular insult.

Studying saccadic test parameters between the study and control groups, it was found that there was a statistically significant difference between the two groups regarding velocity. However, there was an insignificant difference between them regarding latency or accuracy.

From other point of view, comparing the EEG findings with VNG findings, the highest incidence of central vestibular affection was met with focal EEG abnormality; the highest incidence of peripheral vestibular affection was met with generalized EEG abnormality; and the highest incidence of normal VNG was met with normal EEG. This difference was statistically significant.

Similarly, relationship between clinical diagnosis (type of epilepsy) and vestibular findings revealed that 62.07% (n = 18) of patients with partial epilepsy had central vestibular affection compared with 6.06% (n = 2) of patients with generalized epilepsy. However, 3.45% (n = 1) of patients with partial epilepsy had peripheral vestibular lesion compared with 30.3% (n = 10) in patients with generalized epilepsy. This difference was statistically significant.

Returning to our study, when comparing the incidence of vestibular affection with subtypes of epilepsy, there was statistically insignificant difference between different types of either generalized or focal epilepsy with respect to different patterns of vestibular affection.

[Table 4] shows that there was a statistically significant difference between focal and generalized epilepsy with respect to time of occurrence of dizziness.
Table 4 Relation between timing of dizziness and type of epilepsy present

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  Discussion Top


Classification of epilepsy was made mainly according to clinical picture (typical epileptic fit with or without EEG findings) [6-8]. Generalized seizures were found to predominate in this young age group [9].

Similar findings of VNG testing were reported, where central vestibular lesion in the form of abnormal eye tracking and optokinetic test were reported among their study group of epileptic children [1].

However, vestibular disorder of irritative nature and disturbances of optokinetic nystagmus were reported in majority of patients in their study group diagnosed as having temporal lobe epilepsy [10]. Furthermore, abnormal vestibular responses among epileptic patients were attributed to the presence of a common cerebral lesion responsible for both focal seizures and vestibular abnormality [11].

These findings may be explored by reviewing higher-level control of saccades in intact patients [12]; more 'reflective' saccades are probably triggered through direct projections from the parietal lobes [from the lateral intraparietal area and area (7a) to the superior colliculus]. However, more 'voluntary' saccades are probably generated from the frontal structures (the frontal eye field, the supplementary eye fields, and other prefrontal areas) either directly or through the basal ganglia to the superior colliculus. Hence, a lesion in the frontal lobe is associated with impaired saccadic initiation.

Presence of patients with benign paroxysmal positional vertigo (BPPV) may be because of vigorous repeated convulsions with repeated head injury associated with repeated falling. BPPV is considered rare in children because otoconia are tightly bound to the macular membrane [13].

Regarding caloric test findings, similar findings were reported. ENG abnormality was reported among patients with vertigo during aura of generalized epilepsy in the form of directional preponderance to bithermal caloric irrigation [14].

When saccadic slowing is observed, drug ingestion should be the first consideration. Anticonvulsants, sedatives, and sedating antidepressants are the most common culprits. Saccades can be slowed as much as 50% when patients become drowsy [15]. In our study group, most of the patients (n = 39) were regularly using antiepileptic drugs for long periods, whereas the rest of them used antiepileptic drugs for not less than four doses over 2 days period.

If the patient is wide awake and not taking a centrally acting medication, then slowing saccades are consistent with various central nervous system or ocular disorders, including oculomotor weakness, degenerative conditions, basal ganglia pathology, and cerebellar disorders (after exclusion of drowsiness or drug effects). In contrast, abnormally fast saccades, if not artifacts due to technical difficulties, are indicative of central nervous system pathology or ocular pathology (ocular flutter). Asymmetric velocities are indicative of lesion in the medial longitudinal fasciculus, causing internuclear ophthalmoplegia [16].

It was mentioned that it is not the functional loss but the focal discharges that cause central vertigo. Electrical stimulation of human thalamus during stereostatic neurosurgical procedures induced sensation of movement in space, most frequently described as horizontal or vertical rotation or sensation of falling or rising. These sensations were similar to those induced by stimulation of the vestibular cortex [17].

Furthermore, identifying the cortical areas with vestibular input in humans, electrical stimulation of 260 patients with partial epilepsy who had undergone stereotactic intracerebral EEG recordings before surgery was performed. Vestibular symptoms were electrically induced on 44 anatomical sites in 28 patients. The patients experienced illusions of rotation (yaw plane, pitch plane, and roll plane), translations, or indefinable feelings of body motion. Almost all vestibular sites were located in the cortex (41/44): in the temporal, parietal, frontal, occipital, and insular lobes. Among these sites, they identified a lateral cortical temporoparietal site called the temporo-peri-Sylvian vestibular cortex, from which vestibular symptoms, and above all rotatory sensations, were particularly easily elicited. This area extended above and below the Sylvian fissure, mainly inside the Brodmann areas 40, 21, and 22. It included the parietal operculum, which was particularly sensitive for eliciting pitch plane illusions, and the mid and posterior part of the first and second temporal gyri, which preferentially caused yaw plane illusions [17].

Returning to our study, when comparing the incidence of vestibular affection with subtypes of epilepsy, there was statistically insignificant difference between different types of either generalized or focal epilepsy with respect to different patterns of vestibular affection.

This may be also described by the concept of neural networks in epilepsy that has been recently proposed. These included the medial temporal/limbic network, which is the best recognized, and other networks that have been identified, including the medial occipital/lateral temporal network [11].

This is in agreement with the study by Brandt and Dietrich, (1993) [18], who described vestibular epilepsy as a cortical vertigo syndrome, which means central affection. They reported that, if vestibular seizures arise from different areas, the sensorimotor symptomatology may differ with respect to apparent rotation or tilt with or without associated eye, head, and body deviation or epileptic nystagmus. In these patients, if the description is exact, a rotatory seizures (volvular epilepsy) is reported in addition to vertigo and dizziness in the form of light headedness.


  Conclusion Top


Dizziness is a common complaint among children with epilepsy whether before, after, or in between the attacks. Absence of dizziness in an epileptic patient is indicative of free central vestibular system. However, presence of dizziness is not necessarily associated with central vestibular disorder. When vertigo occurs during the aura of partial epilepsy, central vestibular disorder may be present-a condition in which we may consider that dizziness is caused by epilepsy. In contrast, dizziness and epilepsy coexisting as independent events may occur. Epilepsy is associated with VNG abnormalities mostly of central type of affection. VNG, especially caloric testing, is applicable in children.


  Acknowledgements Top


 
  References Top

1.Pawlak-Osinska K, Kazmierezak H, Kuczynska R, Osinsiki P, Kaspro E, Sboszewska K. Vestibular findings in children's epilepsy. Otolaryngol Pol 1999; 53 :479-483.  Back to cited text no. 1
    
2.Salas-Puig J, Serratosa M, Viteri C, Gil-Nagel-Rein A. Safety of levetiracetam as adjuvant therapy in epilepsy: the trial in Spain. Rev Neurol 2004; 38 :1117-1122.  Back to cited text no. 2
    
3.Yellin W. In Roeser R, Valente M, Hosford-Dunn H, editors. Assessment of vestibular function. Chapter 24. Audiology: diagnosis. New York: Thieme Medical Publisher Inc.; 2000. 571-592  Back to cited text no. 3
    
4.Murueta-Goyena F, Rodriguez F. Simplified video-nystagmoscopy. Acta Otorrinolaringol Esp 1998; 49 :253-255.  Back to cited text no. 4
    
5.K So N. In: Lüders, H, editor. Diagnosis and differential diagnosis of epilepsy. Epilepsy: comprehensive review and case discussion. Wearset, Boldon: Tyne and Wear; 2001. 1-11.  Back to cited text no. 5
    
6.Commission of Classification and Terminology of International League Against Epilepsy: proposal of revised clinical and EEG classification of epileptic seizures. Epilepsia 1981; 22 :489.  Back to cited text no. 6
    
7.Commission of Classification and Terminology of International League Against Epilepsy: proposal for classification of epilepsies and epileptic syndromes. Epilepsia 1985; 26 :268-278.  Back to cited text no. 7
    
8.Commission of Classification and Terminology of the International League Against Epilepsy: proposal for revised classification. Epilepsia 1989; 30 :389-399.  Back to cited text no. 8
    
9.Hauser A. Seizure disorders: the changes with age. Epilepsia 1992; Suppl. 4 :6-14.  Back to cited text no. 9
    
10.Blagoveshchenskaia S, Karlov A, Urumova T. Study of vestibular disorders in epilepsy by means of electronystagmography and functional visual ad vestibular loads [article in Russian]. Zh Nevropatol Psikhiatr Im S.S Korsakova 1985; 85 :846-851.  Back to cited text no. 10
    
11.Tartara A, Manni R, Mira E, Mevio E. Polygraphic study of vestibular stimulation in epileptic patients. Rev Electroencephalogr Neurophysiol Clin 1984; 14 :227-234.  Back to cited text no. 11
    
12.Minor L, Zee D. In: Cumming C, et al. editors. Evaluation the patient with dizziness. Chapter 136. Otolaryngology. Head and neck surgery 1998; 26 :23-2671.  Back to cited text no. 12
    
13.Choung H, Park K, Moon K, Kim H, Ryu J. Various causes and clinical characteristics of vertigo in children with normal eardrums. Int J Pediatr Otorhinolaryngol 2003; 67 :889-894.  Back to cited text no. 13
    
14.Eviatar L. Dizziness in children. Otolaryngol Clin North Am 1994; 27 : 557-567.  Back to cited text no. 14
    
15.Hain C. In: Jacobson and Newman editors. Oculomotor testing: interpretation. In handbook of balance function testing. Mosby; 2 nd edition 1992.  Back to cited text no. 15
    
16.Schoup A. Electronystagmogrophy. e. medicine.com Inc., 2003  Back to cited text no. 16
    
17.Hauser A, Hersdorffer C. Epilepsy: frequency, causes and consequences. New York: Demas Publisher; 1990.  Back to cited text no. 17
    
18.Brandt T, Dieterich M. Vestibular falls. J Vestib Res 1993; 3 :3-14.  Back to cited text no. 18
    


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4]
 
 
    Tables

  [Table 1], [Table 2], [Table 3], [Table 4]



 

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