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".
Introduction
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.
Discussion
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.
Andy OJ, M
Jurko Diencephalic Seizure Appl Neurophysiol
1983; 46; 62-67
