mise à jour du
15 septembre 2005
Appl Neurophysiol
Diencephalic Seizure
OJ Andy, M Jurko
Department of Neurosurgery, University Medical Center, Jackson, Miss., USA


Abstract. Intractable complex partial and diencephalic seizures in one patient are being treated effectively by intermittent daily electrical stimulation in the right thalamus in conjunction with phenytoin, 200 mg/day. Electrical stimulation in the right thalamus was found to suppress spike and sharp wave discharge activity temporarily in the right thalamus and in the left parietal and right scalp leads. It was postulated that beneficial effects from electrical stimulation were due to electrically "jamming a low-threshold discharge system".
A lesion placed in the thalamus for the treatment of intractable seizures was found beneficial for patients with minor and major motor seizures. The present case report presents preliminary observations in which minor motor and complex partial seizures are controlled by a combination of thalamic electrical stimulation and medication.
Case Report
A 46-year-old woman developed focal motor, major motor, diencephalis and complex partial seizures after a ruptured right middle cerebral aneurysm surgically clipped in 1971. Seizures consisted of circling to the left, focal jerking of the left hand and arm, suddenly falling to the floor and tonic clonic attacks with impaired consciousness. A right temporo-orbitofrontal cortical resection was performed on 3-3-81. The focal and major motor seizures were subsequently completely controlled, but not the complex partial and 'diencephalic' seizures. A recent complex partial seizure consisted of an episode of confused behavior, of which she had no memory the following day. The 'diencephalic' seizures consist of 'drop' spells and attacks described as a sensation of blood rushing upward in her body, beginning in her feet and rushing up her body to her head, immediately followed by a sensation of 'burning up'.
On examination, the patient was cooperative and well-oriented. She constantly moved the fingers and foot on the right side. The left hand and forearm revealed atrophy and spasticity with 75% reduction of hand grip. The seizures could not be adequately controlled unless anticonvulsants were taken to toxic levels (phenytoin levels of 25 mg% or above), with double vision and ataxia. Tegretol, Depakene and phenobarbital in various combinations did not control the seizures without producing side effects such as marked drowsiness, lethargy, mental dullness and depression.
In February 1981, a CT scan revealed a large area of infarcted brain in the right Sylvian and Rolandic areas. The EEG revealed a mixture of slow and sharp waves with interspersed spikes in the temporofrontal area, predominantly on the right side.
On 1-26-83 stereotactic right thalamic depth recordings were made with a bipolar electrode in preparation for the stimulation electrode implant under local anesthesia. The central electrode was 0.5 mm and the barrel I mm in diameter, with interelectrode distance less than 0.25 mm. The length of the central electrode is 1 mm and the barrel 3-5 mm. For 1 week subsequent to surgery, while the implant lead remained externalized for diagnostic purposes, unipolar recordings were made from the depth electrode refercentral inactive area of 2 mm. Note the low voltage background slow theta and delta activity, probably secondary to gliosis.
Electrical stimulation of the right thalamus at the site of the discharge suppressed the spontaneous thalamic discharge and the spike activity in the left scalp, but the spike discharge activity in the right scalp leads remained. Within 30 s after electrical stimulation, the discharge activity was absent throughout the right scalp leads in addition to the right thalamic and left parietal areas and a previously existing headache was reported better. Within 40 s after the second stimulation, the headache was reported to be gone. A slow thalamic theta wave was present in association with a slow sharp wave in the right temporal, occipital, and parietal area. Within 6 min after the second stimulation the electrical pattern was predominantly low voltage slow, and the patient stated she 'felt good'. There were no longer headache and back pain as experienced before stimulation. Spike discharge bursts only occurred at 2- and 4-min intervals following stimulation. These two spike paroxysms primarily involved the right thalamus and scalp leads. There was surprisingly minimal involvement in the left parietal area. Those were the only episodes of spike paroxysms during a 6-min poststimulation period, in contrast to more than five spike paroxysms having been recorded in the same time frame before stimulation.
Unipolar chronic electrical stimulation is conducted through a 3-mm electrode tip. Stereotactic coordinates for the electrode tip are AC-PC 4.5 mm, + 2.5 mm above ACPC, L 5 mm. The L proximal end of the 3-mm bare electrode is oriented anterodorsally at a 450 angle to horizontal zero. Stimulation parameters consist of 195 Hz, 200 /is, 14V for periods of 30 mm, 2-3 times during the day. She also uses the stimulator when visiting with others in order to prevent attacks of nervousness and spells from occurring. Phenytom, 100 mg b.i.d., has been continued in conjunction with the thalamic stimulation. There have been no recurrences of complex partial and diencephalic seizures over a 4month period. The patient states she feels better than in the past and is more relaxed.
The combined treatment of electrical stimulation in the thalamus and anticonvulsant medication has been sufficient to control this patient's otherwise intractable complex partial and diencephalic seizures, despite their obviously being multifocal in origin. Cortical discharges, especially in the right hemisphere, occurred independent of the right thalamic discharge, although at times they appeared to represent propagated activity from the thalamus. The left parietal discharge only appeared in concert with the thalamic, and thus most likely represented propagated activity, from the latter. Electrical stimulation invariably suppressed the left parietal discharge for a much longer time than the right hemispheric discharges and remained suppressed long after there was a return of the thalamic discharge. Behaviorally, in addition to keeping the seizures under control, the stimulation makes the patient feel relaxed and at times as if she has had an alcoholic drink. Her behavior, however, remains appropriate and not characterized by automatisms.
The neurophysiologic mechanism underlying the thalamic stimulation-induced seizure control remains unknown. For pragmatic purposes, however, it is conceptualized that the electric stimulation 'jams low-threshold discharge systems' and thus prevents the occurrence of clinical seizures. Both experimental and clinical observations support the thesis that electrical stimulation of the mesodiencephalon and cerebellum may suppress and even arrest ongoing seizures. It should be noted that stimulation of the mesencephalic reticular system appears to prevent the elicitation of cingulate discharges which have been evoked by fixed parameters of cingulate stimulation in the cat. A mixture of facilitatory and inhibitory effects upon the development of limbic seizures was observed in response to electrical stimulation of the mesencephalic, hypothalamic, and thalamic components of the mesencephalic reticular system. That mesodiencephalic stimulation tends to curtail forebrain seizure production is also supported by observation in which lesions of the mesodiencephalon were found to facilitate the prolongation of limbic seizures. Cerebellar stimulation was also found to inhibit cortically elicited seizures. Cerebellar stimulation in the human has been reported to stop some forms of telencephalic major motor and complex partial seizures dramatically.
Fig. 1. Simultaneous right thalamic and EEG scalp recordings in the awake patient. LE = Left ear; RE = right ear.
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