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Diencephalic seizures Responsiveness to bromocriptine and morphine.

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Diencephalic Seizures:
Responsiveness
to Bromocriptine
and Morphine
Dennis E. Bullard, MD
T w o patients with posttraumatic diencephalic seizures,
characterized by autonomic dysfunction and extensor
posturing, had partial responses to bromocriptine and
complete responses to morphine. Probable synergism
between the two agents was noted. These 2 cases suggest
the potential effectiveness of this regimen for the treatment of diencephalic seizures, raise questions regarding
the role of the dopaminergic and opioid systems in this
disease entity, and support the hypothesis that diencephalic seizures represent a release phenomenon in the
brain.
Bullard DE: Diencephalic seizures:
responsiveness to bromocriptine and morphine.
Ann Neurol 21:609-611, 1987
In 1929, Penfield described a patient with periodic
headaches and acute episodes of vasodilation of the
skin, sudden rise in blood pressure, lacrimation, diaphoresis, pupillary change, hypertension, slowing of
respiratory rate, transient shivering, and eventually,
Cheyne-Stokes respiration [lo]. He termed this con~~
~
From the Division of Neurosurgery, Box 3128, Duke University
Medical Center, Durham, NC 27710.
Received July 1, 1986, and in revised form Aug 25, Sept 24, and
Oct 10. Accepted for publication Oct 10, 1986.
stellation of symptoms and signs diencephalic autonomic
seizure5 (DS). At autopsy, his patient was found to have
an encapsulated tumor at the level of the foramen of
Monro. Penfield initially suggested that the autonomic
dysfunction was d u e to pressure exerted directly o n
the thalamic nuclei. Subsequently, he accumulated a
series of cases that varied from the initial clinical syndrome, and proposed that these episodes were due to
true epileptic discharges rather than to a release phenomenon [lo]. Researchers have since reported similar individual cases of paroxysmal autonomic dysfunction and have suggested alternative hypotheses for
these episodes, including epilepsy, hydrocephalus, and
various release mechanisms [2, 4, 9, 13, 141. I n this
study, I describe 2 patients with DS following head
trauma who showed a partial response to bromocriptine and complete response to morphine. DS occurred
in both patients when they had decerebrate posturing
and evidence of cortical dysfunction. These observations suggest a role for the dopaminergic and opioid
pathways in this disease.
Case Reports
Patient 1
A 24-year-old man was involved in a motorcycle accident,
sustaining a closed head injury and subsequent cardiorespiratory arrest. His score on the Glascow Coma Scale was l/
411. While in the emergency room, he experienced transient
episodes of increased temperature (to 39.6”C), pulse (to 165
bpm), respirations (to 52 breaths per minute), and blood
pressure (to l60/100 mm Hg), as well as generalized increased extensor tone. A computed tomographic (CT) scan
of the head demonstrated a slight swelling in the right frontal
lobe, without midline shift.
On the third day after trauma, an acute decline in the
patient’s condition occurred; his intracranial pressure (ICP)
level increased, but treatment with mannitol and cerebrospinal fluid (CSF) drainage lowered it quickly. A repeat CT scan
showed obliteration of the basilar cisterns.
On the sixth day after trauma, severe episodes of autonomic dysfunction developed with sudden dilation of both
pupils, intense flushing and diaphoresis over the face and
upper torso, tachycardia (100 to 150 bpm), hypertension
(190/120 mm Hg), hyperthermia (38 to 40°C rectally), hyperventilation (60 to 148 breaths per minute), and a marked
increase in decerebrate posturing. Following onset of these
episodes, ICP increased to 30 cm HzO. As the episodes
subsided, ICP would spontaneously decline. Treatment with
mannitol or CSF venting did not reduce autonomic dysfunction, and autonomic dysfunction consistently preceded the
rise in ICP. In virtually all episodes, a rise in temperature
preceded the other events. During this time, control of ICP
could be rapidly achieved with intravenously administered
morphine, but not with methadone, phenytoin, clonazepam,
phenobarbital, or propranolol. Four electroencephalograms
(EEGs) were performed and demonstrated only severe dowing and low voltage in the background. A CT scan performed 3 weeks after trauma showed an apparent bilateral
infarct in the caudate and putamen, together with bilateral
609
infarct of the occipital and posterior parietotemporal cortex,
which were consistent with a severe hypoxic insult at the
time of accident (Figure).
The patient was administered bromocriptine initially,
which resulted in a decrease in diaphoresis and a reduction in
the hyperthermia within 72 hours. Dantrolene was then administered, which resulted in a mild-to-moderate improvement in the extensor posturing. Lower dosages of morphine
than had been previously required (as low as 4 mg) stopped
the episodes within 15 to 20 minutes.
The patient was subsequently twice taken off bromocriptine and dantrolene for reasons not related to central nervous
system problems. Both times, typical DS recurred within 36
hours. When bromocriptine and dantrolene were restarted,
the prior pattern of response was seen. While off bromocriptine, the patient was given 4 mg of naloxone hydrochloride
(Narcan) for apnea, and within 30 seconds a typical DS occurred. H e was then given morphine sulfate (10 mg) and his
vital signs returned to baseline. For 6 months following
trauma, he remained free of DS while receiving bromocriptine (10 mg t.i.d.) and dantrolene (100 rng t.i.d.) and required no narcotics.
Patient 2
A 24-year-old man was thrown from a car and sustained a
closed head injury and blunt abdominal trauma. On arrival at
the hospital, he was found to be unresponsive to verbal
stimuli and exhibited spontaneous roving eye movements to
the left. The right pupil was 2 rnm and the left 3 mm in
diameter; both were briskly responsive to light. Spontaneous
generalized extensor posturing was observed. CT scan demonstrated no brain swelling and patent cisterns. Subsequently, a laparotomy was performed for repair of a liver
laceration. Postoperatively, the patient's neurological findings were unchanged.
On the first postoperative day, however, he began having
episodes of increased temperature, respiratory rate, pulse,
and blood pressure, with associated diaphoresis and spontaneous extensor posturing. His baseline neurological findings were unchanged; his rectal temperature was 37.5"C; his
pulse was 82 bpm, his respiratory rate was 8 to 12 breaths
per minute; and his blood pressure was 140/70 mrn Hg.
During the episodes, his temperature increased to a maximum of 39.6"C, his pulse increased to 103 bpm, his blood
pressure increased to 170/80 mm Hg, his respirations increased to 60 breaths per minute, and he had a marked
increase in extensor tone. Multiple blood, sputum, and urine
cultures disclosed no evidence of infection. By the fourth
day after trauma, the patient had established a pattern of two
to three episodes per day, each lasting from 2 to 4 hours.
Two EEGs showed a diffusely slow pattern.
Over the next week, the patient began having less frequent but more severe and longer-lasting episodes. In contrast to prior episodes, these, once established, persisted for
4 to 5 hours and could be terminated only by administration
of 10 to 14 mg of morphine. Bromocriptine (2.5 mg t.i.d.)
was begun; within 72 hours, the hyperthermia and diaphoresis were reduced. Over the next 2 weeks, the episodes
diminished in both frequency and severity. Bromocriptine
was then discontinued. Over the next 3 months, no further
episodes were noted. During this time, the patient's condi-
610 Annals of Neurology Vol 2 1 No 6 June 1987
A
B
A computed tomographic scan performed on Patient 1 three
week following head injury, showing apparent infarct in the
caud?te and putamen bilaterally (A)w i t h a questionable low
density in the mesencephalic r'egmentum (B).
-
tion improved to the extent that he could answer questions
and follow simple commands.
Discussion
These observations suggest that posttraumatic DS may
represent a release phenomenon at the level of the
upper brainstem and diencephalon secondary to loss of
cortical and subcortical control. In both our patients,
DS were most severe when the baseline neurological
response was that of decerebrate posturing. This
would suggest a functional level between the colliculi
and red nucleus and the vestibular nuclei and pontine
reticular formation [11). Other reports of cases of DS
have suggested that hypothalamic lesions are the cause.
Although clinical decerebrate posturing has been reported with diencephalic injury 11, 111, the absence of
baseline pituitary dysfunction, baseline temperature
disturbance, or diabetes incipidus in both of our patients makes this an unlikely explanation. Rather, the
correlation seen between the level of consciousness
and DS and prior descriptions of decerebrate posturing with cerebral hemispheric dysfunction 16, 71 argue
that DS occur with release from cortical and subcortical control.
Pharmacologically, the responses to bromocriptine
and morphine appear to indicate a role for both the
dopaminergic and opioid systems in DS. Anatomically
there is a wide overlap of opioid receptor areas with
the dopaminergic system, including the nigrostriatal
system, the mesolimbic system, and the tuberoinfundibular system 13, 5 , 8, 12). A single structural lesion
could therefore potentially affect both systems. Why
an apparent synergism between bromocriptine and
morphine was seen cannot be explained from the present data.
In reviewing the description of Penfield’s original
patient with DS, Carmel {a) astutely noted that the
syndrome remitted on two occasions following ventricular puncture. He hypothesized that increased ICP in
the presence of a hypothalamic lesion may be the cause
of DS. I am aware of 2 patients with acute hydrocephalus who had DS that remitted promptly after a shunt
procedure W . Talman, personal communication,
1986). The posttraumatic DS described here, however, appear to be different. In Patient l, the temporal
course clearly demonstrated that elevation in ICP occurred after and not before the clinical manifestations
of the DS, and the DS were not relieved by control of
ICP.
It is unlikely that most DS have an epileptic basis. In
both of our patients, in the single patient described by
Solomon 1141, and in a patient described by Fox and
colleagues 141 who had periodic hypothalamic dysfunction, no response was seen to a variety of anticonvulsant medications. In addition, epileptic discharges have
not been demonstrated in any patients at the time of
DS. This circumstantial evidence makes it unlikely that
epileptic activity is a common etiological factor.
Dr B d a r d is the recipient of Teacher-Investigator Development
Award 1 K07NS00800 from the NINCDS of the National Institutes of Health.
I wish to thank Mrs Rose Hagan for her assistance in the preparation
of this manuscript.
References
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2. Carmel P W Vegetative dysfunctions of the hypothalamus. Acta
Neurochir (Wien) 75:113-121, 1985
3. Emson PC: Chemical Neuroanatomy. New York, Raven, 1983
4. Fox RH, Wilkins DC, Bell JA, et al: Spontaneous periodic
hypothermia: diencephalic epilepsy. Br Med J 2:693-695, 1973
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syndrome: successful treatment with dantrolene and bromocriptine. Ann Neurol 14539-90, 1983
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function in severe human head trauma with multimodality
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Neurosurg 47:163-177, 1977
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methods, and analysis. J Neurosurg 47:150-162, 1977
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Neurology 31:132-137, 1981
9. McLean AJ: Autonomic epilepsy. Report of a case with observations at necropsy. Arch Neurol Psychiatry 32:1891-1897, 1934
10. Penfield W, Jasper H: Epilepsy and the Functional Anatomy of
the Human Brain. Boston, Little, Brown, 1954
11. Plum F, Posner JB: The Diagnosis of Stupor and Coma, ed 3.
Philadelphia, Davis, 1980
12. Reid J L Dopamine supersensitivity in the hypothalamus? Adv
Neurol9:73-80, 1975
13. Sherrington CS: Cataleptoid reflexes in the monkey. Proc R SOC
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14. Solomon GE: Diencephalic autonomic epilepsy caused by a
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Brief Communication: Bullard: Diencephalic Seizures 61 1
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