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January2011 Vol.48 Issue:      1 Table of Contents
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Epileptic Vertigo: Overview of Clinical Semiology

Mohamed Saad, Shereen Zakarya, Mohammad Abu-Hegazy

 

Department of Neurology, Mansoura University; Egypt

 



ABSTRACT

 Background: Epileptic vertigo is a rare form of partial seizures. It is often distinctive with sudden very brief episodes followed by rapid recovery without sequelae. Objective: Of this study was to establish the contribution of clinical semiology of epileptic vertigo in absence of convulsions and loss of consciousness. Patients and Methods: Thirty epileptic vertigo patients (19 males and 11 females) were included. Their ages ranged from 12 to 40 years and mean age at onset 26.7 years. All patients were subjected to neurological examination, interictal electroencephalogram (EEG), caloric otologic test, audiogram, nystagmography, carotid Doppler; brain stem evoked potential and brain MRI. Results: Family history of epilepsy was reported in 20%, no past history of febrile convulsion, tunnel voices aura was reported in 6.7%. Dizziness was report in 8 patients (26.7%), 14 patients with true vertigo (46.6%), nausea in 6 (20%) and tinnitus in 2 patients (6.7%). EEG abnormality was documented in all cases: Fifteen (50%) and 6 (20%) patients illustrated focal left and right temporal epileptiform discharges consecutively. In addition, there were bitemporal 2 (6.7%), 2 (6.7 %) frontotemporal and 5 cases (16.8%) temporal with secondary generalization discharges. MRI of brain was normal in 20 (66.6%), 4 cases with temporal lobe tumors, cerebral infarction was in one and small cyst. Frontal lobe lesions were detected in 4 patients. No mesial temporal sclerosis was detected. Conclusion: Epilepsy is an important cause of transient dizziness and vertigo, but misdiagnosis due to absence of convulsions and loss of consciousness, is common. [Egypt J Neurol Psychiat Neurosurg.  2011; 48(1): 31-36]

 

Key Words: Epilepsy, Epileptic vertigo, EEG in epileptic vertigo

 

Correspondence to Mohamed Saad. Department of Neurology, Mansoura University, 35516 EL-Jomhoria st. Mansoura, Egypt.

Email; prof_mohamedsaad@yahoo.com




INTRODUCTION

 

Epileptic vertigo is a rare form of partial seizures, due to epileptic activity in parts of the cortex that represent the vestibular system: the parietal, the temporal and frontal cortex. The episodes usually last no more than seconds to minutes; unconsciousness will follow only if the seizure becomes generalized.1

In epileptic vertigo, vertigo is not simply an aura, but constitutes a part of seizure, and may be its only manifestation. Vertigo here  is often characteristic, consisting of sudden very brief episodes followed by rapid recovery without sequelae, the person notes that the world makes a quick horizontal movement ,lasting one or two seconds at most, not followed by confusion (True vertigo, from the Latin, vertere, to turn, is a distinct, often severe form of dizziness that is movement hallucination).2,3

Epileptic vertigo is thought to be caused by stimulation of parts of the cortex that represent the vestibular system. Based  on brain imaging studies, researchers now feel that vestibular information is processed by several different coordinating areas within the brain, specific areas include the superior lip of intraparietal sulcus, the posterior superior temporal lobe and the temporal-parietal border regions.4,5

 

Epileptic vertigo is only a diagnostic problem when the person does not have a full seizure, in other wards does not have convulsions, psychomotor symptoms or twitching characteristic of classic partial or generalized seizures.6,7

Diagnostic tests that are particularly helpful include the electroencephalography (EEG), which detects abnormal electrical activity in the brain, and magnetic resonance imaging (MRI) scan of the head which can detect a mass or lesion in the brain.

The present study was designed to assess the semiology, characteristic EEG and Brain MRI of epileptic vertigo. Inspite of the fact vertigo is a common neurological problem; EEG is usually restricted to cases associated with loss of consciousness. So usually the diagnosis of epileptic vertigo is missed.

 

MATERIALS AND METHODS

 

A total of 30 patients with epileptic vertigo (19 males and 11 females) were selected from   outpatient clinic of neurology department at Mansoura University Hospital during the period from July, 2008 to Dec, 2008. Their ages ranged between 12 and 40 years.

 

 

Inclusion Criteria:

1.        Age above 12 years and below 40 years (above 12 to exclude benign paroxysmal vertigo of childhood, below 40 to exclude (vertebrobasilar insufficiency).

2.        Intact neurological and otologic examination.

3.        Normal caloric test, Audiometry, Nystagmography, BAEP and carotid Doppler. 

4.        Abnormal EEG.

5.        Good response to carbamazepine (therapeutic dose for at least 3 months).

 

Exclusion Criteria:

1.        Patients above 40 years or below 12 years.

2.        Any neurological or otologic deficit.

3.        Patients with risk factors as diabetes mellitus, hypertension or cardiac disease.

4.        Abnormal caloric test, audiometry, nystagmography, BAEP or carotid Doppler.

5.        All patients with psychiatric problems.

6.        Patients with migraine.

7.        Vertigo associated with loss of consciousness.

 

All Patients Underwent:

1.        History taking (past, present and family).

2.        Full neurological examination.

3.        Otologic assessment with caloric test, Audiogram and nystagmography.

4.        Brainstem Auditory Evoked Potential (BAEP).

5.             Conventional interictal electroencephalography (EEG): An interictal EEG was done for all patients using the Nihon Kohden 16-channel EEG machine, electrodes were placed according to 10 - 20 international system of electrode placement using mono- and bipolar montages. All EEGs were carried out under normal standard conditions, with the patient awake, lying supine, completely relaxed in a quiet room. Hyperventilation for 3 minutes and intermittent photic stimulation were done for all patients to provoke any existing abnormality. The EEG tracings were analyzed as regards frequency, Amplitude and symmetry of the background activity, as well as the presence of any abnormalities.

6.        Magnetic Resonance Imaging (MRI): Enhanced and non enhanced MRI of the brain was performed for all patients included in this study in the MRI unit of Radiology Department using 1.5 Tesla General Electric Medical System.

 

Statistical Analysis:

The demographic, clinical, and technical data were collected. P-value less than 0.05 was considered statistically significant. All data were expressed as mean or patient’s number (n) and percentage (%) as appropriate.

 

RESULTS

 

Thirty patients were included in our study, their ages ranged from 12 to 40 years. Mean age at onset    was 26.7. As regard sex, 19 patients (63.3%) were males while 11(36.7) were females Family history of epilepsy was recorded in 6 patients (20 %). Past history of febrile convulsion was not reported in any one of our patients. Past history of head trauma was reported in 2 (6.7%) patients. Aura of epileptic vertigo was described in 2 (6.7%) patients in the form of voices in a tunnel. Semiology of epileptic vertigo was dizziness in 8 (26.7%) patients, true vertigo in 14 (46.6), vertigo with nausea in 6(20%), vertigo with tinnitus in 2 (6.7%) (Table1).

EEG was abnormal in all cases, It showed high voltage or slow waves or both in left temporal region in 15 (50%), right temporal in 6 (20%), bitemporal in 2 (6.6%), temporal with secondary generalization in 3 (10.20%), frontotemporal in 2(6.6%) and generalized epileptogenic dysfunction in 2 (6.6%) (Table 2 and Figures 1-4).

MRI of the brain was normal in 20 (66.6) patients. Temporal lobe lesions were detected in 6 patients (20%), 4 of them were tumors, one was cerebral infarction and the other one was a small cyst. Mesial temporal sclerosis was not reported in any of our patients. Frontal lobe lesions were detected in 4 patients (13.4), 3 of them were tumors and one was cerebral infarction (Table 3 and Figures 5 and 6).


 

Table 1. Semiology of epileptic vertigo.

 

Patients

n

%

Sex

Male: 19

Female: 11

63.3%

36.7%

Mean age at onset

26 .7 years

 

Family  History of Epilepsy

6

20%

Past History of Febrile convulsion

0

0

Past History of Trauma

2

6.7%

Aura

    Voices in tunnel

 

2

 

6.7%

Semiology

    Dizziness

    True Vertigo       

    Vertigo with nausea

    Vertigo with tinnitus

 

8

14

6

2

 

26.6%

46.7%

20.0%

6.7%

Table 2. EEG abnormalities in epileptic vertigo.

 

EEG Abnormalities

n

%

Left   temporal epileptic pattern

15

50.00%

RT temporal epileptic pattern

6

20.00%

Bitemporal epileptic pattern

2

6.60%

Temporal with secondary generalization

3

10.20%

Generalized epileptogenic dysfunction

2

6,7%

Frontotemporal epileptic pattern

2

6.7%

 

Table 3. MRI findings in epileptic vertigo.

 

MRI Findings

n

%

 Normal  MRI

 Temporal lobe lesions    

      Tumors

      Infarction

      Cyst  

 Frontal lobe lesions

     Tumors

     Infarction                          

20

6

4

1

1

4

3

1

66.6%

20%

 

 

 

13.4%

 

 

 

 

Figure 1. EEG showing left temporal spike and

slow wave complex epileptic activity.

Figure 2. EEG showing bitemporal high voltage

slow wave and spike epileptic activity.

 

 

 

Figure 3. EEG showing right temporal high voltage slow wave epileptic activity with tendency to be generalized.

Figure 4. EEG showing generalized

epileptogenic dysfunction.

 

 

Figure 5. MRI brain showing small patch of high signal intensity at left frontal subcortical area (cerebral infarction).

Figure 6. MRI brain showing small rounded abnormal high SI at right temporal lobe (para Hippocampal Cyst).

 

 

 


DISCUSSION

 

Although vertigo as a manifestation of epilepsy was recognized 100 years ago by, Hughlings Jackson8 and later by Gower9, the possibility of that brief episodes of vertigo may be due to epilepsy was not recognized. Today it is well known that epilepsy is an important cause of transient vertigo, 19% of temporal lobe epilepsy presents by vertigo only.10,11,12

Vertigo is a common symptom, but its diagnosis is not always easy. It may result from a dysfunction of the vestibular system at any point from the ear to the cerebral cortex. In these conditions the onset occurs later than in patients with epileptic vertigo, where the mean age, according to the study of Kogeorgos et al.6, is about 25 yeas which is nearly in concordance with our results (26.7 years).

A family history of epilepsy was elicited in 6 (20%) of our patients, although this suggests the possibility of a specific genetic element, the numbers are too small to allow firm conclusions to be drawn, this result matches those of Hughes and Drachman13.

Past history of febrile convulsions was not reported in any one of our patients this result copes with that of Williamson and Jobst in their study on epileptic vertigo that is why the origin of focus was not from mesial temporal lobe but mainly from superior and middle temporal areas3.

A head trauma can produce focal lesions that involve the temporal or parietal association cortex which receives vestibular projections. These lesions may occasionally form seizure foci which can lead to manifestations of episodic vertigo.  In our study past history of trauma was detected in 7% of patients. This did not correlates with the results obtained by  Friedman5 in his study on post traumatic epileptic vertigo, these differences may be due to variation of incidence of trauma between different countries.

      Vertigo alone may be an aura of epilepsy. Also, epileptic vertigo is sometimes preceded by aura as described by 2 patients (6.7%) as voices in a tunnel. Which is consistent with many studies1,10.  

      In all 30 patients vertigo occurred in brief episodes, each lasting no more than a few seconds. a feeling of only dizziness, not true vertigo was  described by 8 patients (26.7%), true vertigo was described by 14 patients (46.6%), vertigo associated with tinnitus was described by 2 patients (6.7%) and vertigo associated with nausea in 6 patients (20). Epileptic vertigo is a diagnostic problem because the person does not have a full seizure, these results coincides with other studies10,11,14-17. Cases of vertigo associated with tinnitus were not reported in Kahane13 study on epileptic vertigo which may be due to variations of underlying cause.

Hughes et al.10 in their study on EEG in epileptic vertigo reported that temporal lobe emphasis constitute more than 50 % of their cases. In our study EEG was abnormal in all cases, in the form of focal high voltage, or slow wave activity, reported mainly in left temporal region (50%), followed by right temporal in (20%), bitemporal in (6.7%), frontotemporal in (6.7%), temporal with secondary generalization in (6.7%), and generalized epileptogenic dysfunction in (10.20%).

         The underlying cause of epileptic vertigo  was uncertain in many cases18-21, MRI of the brain was normal in 20 of our patients (66.6%), temporal lobe lesions were detected in 6 patients only (20%), frontal lobe lesions were detected in 4 (13.4%)  and there was no evidence of temporal lobe sclerosis.

In our study temporal lobe lesions were the most common cause of epileptic vertigo, tumors were detected in 4 cases and cerebral infarction in only one, these results differ from that obtained by Williamson and Jobst3 in their study on causes of epileptic vertigo as cerebral infarction was the most common cause, this is explained by the exclusion of all cases above 40 years in our study to avoid misdiagnosis with vertebrobasilar insufficiency.

Frontal lobe lesions were the second most common cause of epileptic vertigo, 3 of the 4 cases had tumors which coincides with Kluge et al.2, who concluded that small frontal lobe tumors are one of the important causes of epileptic vertigo.

In conclusion epilepsy is an important cause of transient dizziness, with or without a rotatory component which occur without evident precipitating factors or sequelae, commonest age is around 25 years.

 

[Disclosure: Authors report no conflicts of interest]

 

REFERENCES

 

1.      Kluge M, Bayenburg S, Fernandez G, Elger CE. Epileptic vertigo: Evidence for vestibular representation in human frontal cortex. Neurology. 2000; 55(12): 1906-8.

2.      Miskov S, Hecimovic H. The Differential Diagnosis of Vertigo and Epilepsy. Epilepsia. 2007; 38 (4): 320-7

3.      Williamson PD, Jobst BC. Neocortical temporal lobe seizures. International league against epilepsy, 2004.

4.      O, Brain TJ, Kilpatrick C, Murrie V, Vogrin S, Morris K, Cook MJ. Temporal lobe epilepsy caused by mesial temporal lobe sclerosis and temporal neocortical lesions: A clinical and electroencephalographical study of 46 pathologically proven cases. Brain. 1996; 119: 2133-41.

5.      Friedman JM. Post traumatic vertigo. Med Health RI, 2004, 87(10): 296-300.

6.      Kogeorgos J, Scott DF, Swash M. Epileptic dizziness. British Medical Journal, 1981; 282: 687-9

7.      Bladin PF. History of epileptic vertigo: its medical, social and forensic problems. Epilepsia, 1998; 39 (4): 442-7.

8.      Jackson H. Diagnosis of epilepsy .Medical Times and Gazette. 1879; 1:29. Cited in: Kogeorgos J, Scott DF, Swash M. Epileptic dizziness. BMJ, 1981, 282: 687-9.

9.      Gowers WR. The borderlands of epilepsy. London, Churchill; 1907, pp. 40-75.

10.    Hughes MR, Drachman DA. Dizziness, epilepsy and the EEG. J Neuro Ment Dis., 1977, 38: 341-5.

11.    Pedersen E, J Epson O. Epileptic-Vertigo. Acta Psychiatr Neurol Scand., 1956, 108: 301-10.

12.    Erbayat Altay E, Serdaroglu A, Gucuyener K, Bilir E, Karabacak NI, Thio LL. Rotational vestibular epilepsy from tempro-parieto-occipital junction. Neurology, 2005, 65(10): 1675-1676.

13.    Kahane P, Hoffmann D, Minotti L, Berthoz A. Reappraisal of the human vestibular cortex by cortical electrical stimulation study. Ann Neurol. 2003, 54(5): 615-24.

14.    Laff R, Mesad S, Devinsky O. Epileptic Kinetopsia: ictal illusory motion perception. Neurology, 2003, 61 (9): 1.

15.    Penfield W, Jasper H. Epilepsy and functional anatomy of the human brain. Boston: Little, Brown; 1954.

16.    Tussa RJ, Kaplan PW, Hain TC, Naidu S. Ipsiversive eye deviation and epileptic nystagmus. Neurology. 1990; 40(4): 662.

17.    Alexander MP. In the pursuit of proof of brain damage after whiplash injury. Neurology. 1998: 51: 336-40.

18.    Blanke O, Perrig S, Thut G, Landis T, Seeck M. Simple and complex vestibular responses induced by electrical cortical stimulation of the parietal cortex in humans. J Neurol Neurosurg Psychiatry., 2000, 69(4): 553-6.

19.    Fenoy AJ, Severson MA, Volkov IO, Brugge JF, Howard MA Hearing suppression induced by electrical stimulation of human auditory cortex. Brain Res., 2006,  1118(1): 75-83.

20.    Wiest G, Zimprich F, Prayer D, Czech T, Serles W, Baumgartner C. Vestibular processing in human paramedian precuneus as shown by electrical cortical stimulation. Neurology, 2004, 62(3): 473-5.

21.    Xue LY, Ritaccio AL. Reflex seizures and reflex epilepsy.” Am J Electroneurodiagnostic Technol., 2006, 46(1): 39-48.


 

 

 

 

 

 

 

 

 

 

الملخص العربى

 

رؤية عامة على سريرية الدوار الصرعي

 

يعتبر الدوار الصرعي أحد  أنواع الصرع الصدغي الجزئي وترجع صعوبة تشخيصيه إلي انه لا يصاحبه تشنج أو فقدان للوعي لذلك نحاول في هذا البحث توضيح سريرية الدوار الصرعي.

وقد أشتمل هذا البحث على ثلاثين مريضا تتراوح أعمارهم من 12 إلى 40 سنة بمتوسط عمري 26.7 سنة, 19 منهم كانوا ذكورا و11 كانو إناثا وقد خضع المرضى لفحص إكلينيكي شامل وتخطيط  كهربائي للمخ  وفحص بالرنين المغناطيسي للمخ.

وقد أوضحت النتائج ما يلي: 20% من الحالات لديهم أقارب يعانون من مرض الصرع. 7% من الحالات قد أصيبوا من قبل بإصابة بالرأس. وصف المرضى الدوار الصرعي على أنه دوخة  (26.7%)  أو دوار (46.6%) أو دوخة يصحبها شعور بالغثيان (20%)  أو دوخة يصحبها طنين في الأذن (6.7%).

وقد أظهر تخطيط المخ  وجود بؤرة صرعية في الفص الصدغي الأيسر في 50% من الحالات وفى الفص الصدغي الأيمن في 20% وفي الفصين الصدغيين 6.6% والفص الصدغي والجبهي معا في 6.6% والباقي (16.8%) بينما أظهر فى باقى الحالات تغيرات صرعية عامة.

كان الرنين المغناطيسي كان طبيعيا في 50% من الحالات بينما أظهرت  باقي الحالات  وجود أورام مخية أو أحتشاء مخي.



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