EATING EPILEPSY
MONICA S. HADDAD — P. PUGLIA JR. — JESSIE M. NAVARRO — G. GRONICH
H. B. SCAPOLAN — F. S. ALOE — M. M. VILELA — F. G. M. NAYLOR
A. CUKIERT — R. MARIANO JR.
S U M M A R Y — E a t i n g e p i l e p s y is a r a r e t y p e of r e f l e x e p i l e p s y . A 24 y e a r s - o l d m a l e w i t h e a t i n g r e f l e x c o m p l e x p a r t i a l s e i z u r e s w a s s u b m i t t e d t o c l i n i c a l , n e u r o l o g i c a l , n e u r o r a d i o - ¬ l o g i c a l a n d E E G s t u d i e s . N e u r o l o g i c a n d C T e x a m i n a t i o n s w e r e n o r m a l . E E G r e c o r d i n g s i n -c l u d i n g v i d e o - E E G m o n o t o r i n g d u r i n g m e a l s d i s -c l o s e d f o -c a l a b n o r m a l i t i e s r e l a t e d t o b o t h t e m p o r a l l o b e s p r e v a i l i n g a t t h e l e f t s i d e a n d s e c o n d a r y b i l a t e r a l s y n c h r o n y m a i n l y i n m o r e a n t e r i o r r e g i o n s . I c t a l f i n d i n g s w e r e s i m i l a r t o the i n t e r i c t a l s e c o n d a r y b i l a t e r a l s y n c h r o n y e x c e p t f o r i t s l o n g e r d u r a t i o n . P B , V P A a n d D P H m o n o t h e r a p i e s w e r e i n e f f e c t i v e . H i g h d o s e C B Z m o n o t h e r a p y y i e l d e d g o o d b u t u n c o m p l e t e s e i z u r e c o n t r o l . S i n c e a b i g n u m b e r o f p r e c i p i t a n t s c o u l d b e i n v o l v e d , n o s p e c i f i c p h y s i o p a t h o l o g i c a l b a s i s c o u l d b e s t a b l i s h e d .
Epilepsia ao comer
R E S U M O — A e p i l e p s i a r e f l e x a a o c o m e r é f o r m a r a r a d e e p i l e p s i a r e f l e x a . U m p a c i e n t e d e 2 4 a n o s c o m c r i s e s p a r c i a i s c o m p l e x a s r e f l e x a s a o c o m e r f o i s u b m e t i d o a a v a l i a ç õ e s c l í nica, n e u r o l ó g i c a , n e u r o r r a d i o l ó g i c a e e l e t r e n c e f a l o g r á f i c a . O exame, n e u r o l ó g i c o e a t o m o g r a f i a d e c r â n i o f o r a m n o r m a i s . R e g i s t r o s d e E E G , i n c l u i n d o m o n i t o r i z a ç ã o v í d e o E E G d u -r a n t e a -r e f e i ç ã o , m o s t -r a -r a m p -r e s e n ç a d e a n o -r m a l i d a d e s f o c a i s -r e l a c i o n a d a s a a m b o s o s l o b o s t e m p o r a i s , p r e d o m i n a n d o à e s q u e r d a , e s i n c r o n i a b i l a t e r a l s e c u n d á r i a , p r e d o m i n a n d o e m r e g i õ e s a n t e r i o r e s . O s a c h a d o s i c t a i s s ã o s e m e l h a n t e s à s i n c r o n i a b i l a t e r a l s e c u n d á r i a i n t e -rictal e x c e t o p o r s u a m a i o r d u r a ç ã o . M o n o t e r a p i a s c o m P R , D P H e V P A n ã o s u r t i r a m e f e i t o . M o n o t e r a p i a c o m altas d o s e s d e C B Z t r o u x e b o n s r e s u l t a d o s p o r é m c o m c o n t r o l e i n c o m p l e t o d a s c r i s e s . C o m o g r a n d e n ú m e r o d e f a t o r e s p r e c i p i t a n t e s e s t a v a p o t e n c i a l m e n t e e n v o l v i d o , n ã o f o i p o s s í v e l d e t e r m i n a r c o m p r e c i s ã o a b a s e f i s i o p a t o l ó g i c a d a s c r i s e s r e f l e x a s n e s t e o a s o .
The reflex epilepsies include those epileptic syndromes consisting of seizures that are triggered by specific stimuli usually a clearly recognized somatosensitive or sensory one. Eating epilepsy is an uncommon form of t h e s e5. Several physiopatho-logical mechanisms involved in the genesis of these seizures have already been dis-cussed ! .2.4.6. W e present a case of eating epilepsy, its therapeutical evaluation and clinical follow-up.
M E T H O D S
A 24 years-old man ( P H C ) presenting with atonic, tonic-clonic and complex partial seizures during meals was submitted to clinical, electroencephalographic ( E E G ) , computerized tomography ( C T ) and cerebrospinal fluid ( C S F ) examinations and blood biochemistry. E E G studies included routine 16-channel E E G , sphenoidal electrodes recordings and video-EEG
monitoring during meals.
D e p a r t m e n t o f N e u r o l o g y a n d D i v i s i o n o f F u n c t i o n a l N e u r o s u r g e r y . T h e U n i v e r s i t y o f S ã o P a u l o F a c u l t y o f M e d i c i n e , S ã o P a u l o , B r a z i l .
CASE REPORT
PHC, a 24 years-old white male, first presented with daily atonic seizures at the age of 15. Eight months later, primarily generalized tonic-clonic seizures appeared with a daily frequency, together with complex partial seizures with automatisms, 2-3 times a day. exclu-sively during meals. The patient considered these episodes as «absences». Observers descri-bed that while starting to eat he suddenly stared, became unresponsive for seconds and started talking ilogical words and performing manual automatisms. The post-ictal state in-cluded confusion and amnesia for the entire episode. His clinical background was unremar-kable except for a febrile convulsion at the age of 2 years. His mother and brother are epileptics, both with primarily generalized tonic-clonic seizures and are under good clinical control in respect to their seizures. When he first presented to us at the age of 19, he was taking carbamazepine (CBZ), phénobarbital (PB), phenytoin (DPH) and primidone (PRM) at non-therapeutic levels. Generalized seizures were controlled but complex partial seizures remained with the frequency of 3-4/day, always related to meals. Physical and neurological examination revealed no abnormalities. CSF analysis and the haematological survey were normal. CT scans were normal. Conventional EEG showed frequent spikes and sharp-waves often associated to slow-waves over the left fronto-temporal region spreading diffusely to ipsi- and contralateral areas. Independent spikes were registered over the right temporal region (Fig. 1). Ictal recordings during video EEG monitoring were similar to the interictal secondary bilateral synchrony except for its longer duration (14 seconds). PB, DPH, VPA monotherapies were ineffective. CBZ monotherapy yielded the best results, lowering the com-plex partial seizures (CPS) frequency to 2/month. Clobazan add-on therapy (20mg/day) was also ineffective.
COMMENTS
Eating epilepsies represent an heterogeneous group with variable clinic and E E G findings. However some common features emerge from the reported cases. This young adult male disclosed C P S always related to the onset of eating and unrelated clinically primarily generalized tonic-clonic and atonic seizures.
Reflex seizures precipitated by eating usually begin in the second decade of life. There seems to exist a higher incidence in males. Eating reflex seizures are usually complex partial ones. Associated non-reflex seizures are very often present
and frequently appear earlier than the reflex ones, with a lower f r e q u e n c y3
.1 2
. Focal
E E G findings are common in such cases10
.n
specially related to the temporal lobe,
but secondary bilateral synchrony appeared to be a landmark in many p a t i e n t s3
and might correlate to the type of C N S involvement in cases of eating epilepsy 3,7,io,n.
Non-reflex seizures are easily controlled with current anticonvulsant therapy.
On the other hand, reflex seizures are often clinically r e f r a c t o r y2
. T h o u g h the use
of clobazan is described as effective in eating e p i l e p s y1
, 1-5 benzodiazepine therapy
has shown tolerance and poor clinical control in some cases 1
>2
.
Reflex seizures occur at specific stages of the meal in each patient, but can vary from one case to the other. This suggests different pathways and
physiopatho-logical mechanisms. Boudouresques and G a s t a u t4
and V i z i o l i1 2
pointed to the im-portance of gastric distention and to the role of the passage of food along the gas-trointestinal tract as triggers of visceral afferents which might represent the phy-siopathological basis of reflex seizures. T h e s e previous mechanisms are particularly
important when seizures occur at the end of a meal or at the post-prandial state M A1 2
. In the case described here, seizures occurred just after starting the meal. T h e trigger mechanism probably involves other factors such as mastication and swallowing. T h e role of masticatory movements, together with smelling and tasting food and the role of the amygdala and other structures within the limbic system should be
empha-sized 2
A
Cirignotta et a l .6
called the attention to the possibility of activation of hy-pothalamic nuclei involved in the cephalic phase of digestion and a C N S mediated reflex. T h e data obtained on the role of chemical agents in food and its taste,
tex-ture and temperatex-ture are unconclusive and probably variable 1
»2
A9
. T h e motor acts
associated to the food intake have also to be considered 1 0
Despite the existence of a multiplicity of precipitant factors not only the me-chanisms described should be considered. Environmental factors such as the familial
atmosphere may play a r o l e2
.8
. Finally, there appears to be regional differences in the prevalence of eating epilepsy around the world, which is for instance especially
high in I n d i a3
. T h i s complex of possible genetic, environmental and pathological aspects should be more extensively studied.
REFERENCES
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