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15 décembre 2001
Archivio di psicologia neurologia e psichiatria
Yawning and epilepsy
Yawning as a paroxysmal sign of diencephalic seizures
S Flechter, F Cohen, F Borenstein, I Regev, J Vardi
Medical center Ichilov, Sackler Medical School, Tel Aviv Israel
Voir une autre observation reçue sur le site :
Excessive yawning and sleepy attacks
Muchnik, Finkielman, et al Yawning and temporal lobe epilepsy
The influence of the diencephalon and hypophysis upon general autonomic function W Penfield 1934


Yawning and seizures
Introduction : Diencephalic epilepsy displays itself as an automatic and autonomic seizure accompanied or not by headaches. Among the causes for this disorder one has to exclude tumors or vascular malformation. It is not always possible to differenciate this disorder from basilar migraine that can also be accompanied by seizures automatism and EEG-abnormalities. However in basilar migraine sometimes a specific vertebro-basilar spasticity demonstrated in angiogram can serve as an indication for proper diagnosis.
Often no pathological structure can be found in the so called diencephalic epilepsy. This kind of epilepsy and the basilar migraine benefit of common antiepileptic drugs. A new light was shed on the subcortical origin of epileptic activity by the finding thar 5-endorphin neurons and receptors localized in the thalamo-hypothalamic regions may be involved in the generation of epileptic-activiry. Based on these data we tried to treat a patient who suffered from diencephalic epilepsy with carbamezapine, and Naloxon HCL.
Case report : S.S. a 35 years old fernale, was admitted for a neurological check-up, because of attacks of yawning that were accompaniedby severe occipital headaches, and because those attacks became very frequent. This disease started 8 years ago, and it was characterized by attacks of yawning that had not fit her state, or without external cause, the attack was characterized by a series of yawnings with a frequency of 4-7 yawnings per minute, each attack lasted from 10 to 30 minutes. The attacks appeared suddendly («Out of the blue sky»), without any external or internal stimulation and without any aura. The attacks were accompanied very often by severe occipital headaches with extension of the head; the pains were characterized by a feeling of pressure in the sub-occipital region thar lasted as long as tlic yawning (10-12 seconds). Another characteristic of these attacks was their irregular appearance. The patient suffered very often of several attacks a day, sometirnes of one attack a day, and some times the intervals between the attacks lasted weeks or even months.
The attack was not accompanied by alteration or loss of conscious, or any other movement, but at the end of it the patient remained very tired physically and mentally, and she complained of difficulties in concentration and reduces capacity of comprehension; on the other hand she did not complain of distortion in the perception and in the interpretation of the reality, or any change in her self perception.During these 8 years no other signs appeared, and no change was observed in the attacks. Her ananmestic inquiry negated a head injury, or a cranio-cerebral disease congenital or acquired. The neurological and physical examnation were normal; the laboratory examination were normal and included: blood gas during the attack and in the intervals between the attacks; electrolites; T3/T,4, serological tests, coagulation factors and functions, including thrombocytes aggregation, and urine levels of serotonine, skull and cervical x-rays, computarized tomography (CT) of the brain, 4 vessels angiography of the brain.
The standard EEG examination was normal between the attacks and during the attack it registered a slight posterior irregularity without irritative tendency and without a focus. Registration with sphenoidal electrodes brings about general outburst in the intervals between the attacks and a disrhytmic state with general paroxysmal patterns during an attack. A psychodiagnostic examination demonstrated an organic pattern that was characterized by disturbed perception and space organization .
A therapeutic trial with carbamezapine (Tegretol) 20 x 4 ameliorated her clinical state. The frequency of the yawnings per attack was reduced to 1-2 per minute and the total number of attacks per day were reduced in comparison to that before the trial. Another observation was that the patient complained on less intense occipital headaches in spite of the improvement that was achieved with treatment with Tegretol, the patient continued to suffer from sporadic attacks. Therefore we decided on another therapeutic trial by injecting intravenously Naloxon HCI a pure opiate antagonist. (This trial was done after two weeks of washout from Tegretol). 0.8 mg of Naloxon was injected intravenously by a one a time shot, 1-2 minutes after the beginning of the attack; two minutes after the injection the yawning and the headaches stopped; paresthesia (burning) that the patient complained of in the frontal right orbital region disappeared as well. The drowsiness and weakness that normally appeared after an attack disappeared this time. Administration of a physiological solution as a placebo in the sanie conditions did not change the natural history of the attacks.
Discussion : Yawning is an autonomic and automatic phenomenon, that can express a metabolic disturbance with a decreased consumption of oxygen in the brainstem. On the other hand, the yawning, as an automatic and autonomic phenomenon, can express a situation of a diencephalic epileptic stimulation. An electroencephalographic dysrhytmia was described also in basilar migraine, which may be accompanied by neurological deficit. The fact that only the sphenoidal EEG registration brought out an EEG with a paroxysmal pattern, during an attack, demonstrated that we are dealing with a phenoinenon that has epileptic features. On the other hand the severe occipital headaches could suggest as though we were dealing with an attack of basilar migraine. Absence of a spastic arteriography picture does not negate this diagnosis because the examination was done between the attacks. The blood gas during the attacks and in the intervals between the attacks (with normal levels of P02 and PC02) negate metabolic disturbance as a reason for the attacks. Since all the laboratory examinations negate a structural reason for the attacks (in the vascular system of the meninges and nerves), it means that we are dealing with a pure diencephalic epliepsy. The organicity of the attack is sustained by the psychodiagnostic test that brings out an organic pattern and not an hysterical one.
The analysis of the attack demonstrates that it consists of a combination of three major components: automatism, pain, and paroxysimal EEG. The therapeutic trial with antiepileptic drugs ameliorates her suite, which suggests that the attack was eplieptic. The treatment with Naloxon that shortened the attack and changed its course (pains and paresthesla disappeared) may shed new light on the epileptic and algic mechanism of the diencephalic epilepsy and bind it to the opiatic systems of the brain. It is well known that leucinenkephalin and methionin-enkephalin, and ß-endorphin, cause epileptic attacks in rats, when the origin for this epileptic activity is sub-cortical in the thalamus. It was also demonstrated that there is an anatomico-topographical difference in the seat of the opiate receptors that are bound to the epileptic activity and to analgetic activity, and that there is a difference in the dosage of Naloxon that is required in order to block their activity . In addition, there is a difference between the opiate receptors that are involved in epilepsy, and those which are involved in analgesia . The µ receptors are probably involved in the analgetic mechanism, and the K (kappa) receptors involved in the epileptic activity.
These receptors are localized in the diencephalon (and in the thalamus as part of it), and the ß-endorphin, methioninenkephalin, and leticinenkephalin are active there in. On the other hand it is possible that alpha-hydroxybutyrate, which is in high concentration in the human brain and which possesses neurophysiological and neuropharmacological characteristics that are similar to those of the enkeplialins and endorphins, can be blocked as well by Naloxon. It is possible that alpha-hydroxybutyrate acts on the opiate receptors directly or through the enkephalinic system. Endogenous endorphins are released in the brain by a pain-stimuli and they are involved in the analgesic mechanism. In patients who suffered from neurogenic pains were fourid low levels of endorphins, whereas, in patients who were less sensitive to pains high levels of endorphins were found.
In our case it is possible that there is a shifting of endorphins from receptors that are involved in formation of analgesia to those that are involved in formation of epileptic states. This shifting can explain simultaneously the epileptic state, and the relative decrease in opiate ligands in the opiate receptors that have an important role in analgesia process (and pain control as well); and the opposal shifting after the treatinent with Naloxon. This explanation raises the question about the differences in the affinity of the different opiate receptors (those which are involved in pain and those which are involved in epilepsy) toward opiate agonists and antagonists. Another possibility is that the gamma-hydroxybutyrate acts upon different opiate receptors, and that the Naloxon activity on the opiate receptors is mediated through the gamma-hydroxybutyrate.
The fact that treatment with carbamazepine ameliorates the clinical state does not disagree with the «opiate-proposal» which was described: because carbamazepine acts on the membranes, stabilizing the nerves membranes. In conclusion there is a possibility that diencephalic epilepsy is related to a disturbed diencephalic opiate activity or to gamma-hydroxybutyrate activity in this region.
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Yawning as a paroxysmal sign of diencephalic seizures Flechter S, Cohen F, Borenstein F, Regev I, Vardi J
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Epilepsy Behav 2011;22(3):602-605