CEREBRAL COMMISSUROTOMY IN MAN

JOSEPH E. BOGEN, M.D., AND PHILIP J. VOGEL, M.D.
From the Department of Neurosurgery, School of Medicine, Loma Linda University. Los Angeles 33, California.

Reprinted from the BULLETIN OF THE L08 ANCtELE8 NEUROLOGICAL SOCIETY, Vol. 27, No. 4, December. 1962

  1. Recent animal experiments have aroused renewed interest in the functions of the corpus callosum (Bremer, et al., 1958; Sperry, 1962). In this connection, considerable interest is attached to the results of dividing the forebrain commissures in man. Only one such case, done in two stages, has been reported (Akelaitis, 1944).We are reporting a second case, in which complete sectioning of the anterior commissure and corpus callosum was done at one operation, Emphasis will be given to the surgical approach and postoperative care; detailed neurological and psychological studies are being done in conjunction with the Psychobiology Department of the California Institute of Technology, Pasadena, and will be published elsewhere.

    REPORT OF CASE

  2. Multiple head injuries at age SO followed by blackout spells and automatisms. Generalized convulsions beginning at age Sr, progressively worsening. Recurrent status epilepticus. Cerebral commissurotomy .at age 48. No major convulsions for first 6 months postopsratively.

  3. Preoperative History,W. J., aged 42, was first seen at the White Memorial Hospital in 1958 because of "blackout spells" for the preceding 12 years. His first episodes occurred several months after a parachute jump over Holland during a bombing raid in 1944. Incomplete opening of the parachute resulted in fractures of the left leg, unconsciousness of unknown duration (approximately 48 hours) and hematuria lasting several weeks. During subsequent internment in a prison camp, he was rendered unconscious by a rifle butt blow to the left parietal region. Following his retum home, he was employed as a payroll courier, but he was recurrently plagued by LLlost time". On one occasion he recalled driving away from home one morning and arriving 50 miles away that afternoon with no recollection of the intervening events. In 1951, after an emergency laparotomy for adhesions causing an intestinal obstruction (residual of an earlier appendectomy with peritonitis), he had his first frank convulsion. The episodes increased both in severity and in frequency In 1953 he had a.particularly severe series of convulsions lasting several days. Afterward he had a profound loss of sensation on the left side of the body. This condition improved rapidly, but incompletely.

  4. When he was first examined at the White Memorial Hospital in 1956, the convulsions were occurring at a minimum of two or three times per day. They were occasionally preceded by an aura of dizziness described as "a Ferris wheel revolving". They often included turning of the head to the left. They typically culminated in apnea, cyanosis, and severe clonics which were most frequent in the right arm and leg. On one occasion in 1956 when the patient was in status epilepticus almost continually for a week, he was thought to have had a mild myocardial infarction.

  5. Intensive medical management since 1957 has included one to three visits to the Clinic each month and many hospital admissions. Complete control of the seizures, however, has never been obtained. Seizure frequency at worst (when taking Dilantin, phenobarhital and Tridione) was 7 to 10 per day. At best (when taking Mysoline 250 mg. cl.i.d., phenobarbital 30 mg. q.i.d., Diamox 250 mg. q.i.d., Thorazine 25 mg. q.i.d., and Zarontin 250 mg. t.i.d.) they were as infrequent as one per week. The onset of the seizures was often related to emotional upsets and the bizarre pattern was sometimes considered as an hysterical element. Facial grimacing and occasional utterances, such as "Bail out, Jerry i", were noted, especially during one inter-ictal period. Falls from the seizures caused scalp and facial injuries, and on at least one occasion a fall into a fire caused burns. Incontinence and tongue biting were rare. Status epilepticus occurred about every three to four months. Often, ether anesthesia, and on one occasion 18 grains of phenobarbital given intravenously over a 10 minute period, were required to stop the severe convulsions.

  6. While in a prison camp the patient suffered from malnutrition, losing nearly 100 pounds. His subsequent paresthesias, dystrophic skin changes in both hands and widespread, moderate muscular atrophy were studied by electromyogram. This revealed a peripheral polyneuropathy, possibly secondary to severe avitaminosis. A bleeding peptic ulcer was controlled by nightly Donnatal. Nitroglycerin was given for occasional angina pectoris. A recurrent urinary infection was treated with long-term sulf:t. Diabetes insipidus, a diagnosis repeatedly confirmed in several hospitals, was controlled with aqueous Pitressin by nebulizer. The patient was allergic to peanut oil, morphine (but not codeine), and several radio-opaque iodine compounds. Although vertiginous sensations occurred with his convulsions, 50 mg. of Dramamine every four hours gave partial relief from the mild ataxia and severe vertigo considered to possibly be secondary to traumatic labyrinthitis.

  7. The patient was chronically thin and normotensive. He had a quiet systolic apical murmur and persistent, bilateral, costovertebral tenderness. The liver, usually tender, was palpable 2 or 3 inches below the costal margin. Neurological examination repeatedly confirmed the left hemihypesthesia for pain, touch, temperature, two-point discrimination and vibration. There was also a mild symmetrical hyperreflexia, but no other neurological abnormrtlities. Although speech and motion were slow and deliberate, the patient's intelligence, affect and insight were good when he was seizure free for several days.

  8. Roentgenograms of the skull were normal. Electroencephalograms showed a left temporoparietal focus as well as consistent bitemporal abnormalities. Sphenoidal electrodes inserted by the method of Rovit, et al. (1961) confirmed this diagnosis. A left carotid angiogram was normal, as was a pneumoencephalogram. In 1961 the patient was studied for several weeks in another hospital, where previous diagnoses were confirmed. At that time he was told that removal of the left convexity focus was inadvisable because of the risk of aphasia. On Feb. 4, 1962, he was admitted to the White Memorial Hospital for the twelfth time, for section of the forebrain commissures.

  9. Operation (Feb. 6, LB6,").-Three incisions were made in continuity; the first in the midline extending from approximately 4 cm. above the glabella to a point 6 cm. above the inion; the second was perpendicular to the first, extending from the posterior end of the midline incision to a point just above the right mastoid process; the third was in the brow line extending from the anterior end of the sagittal incision almost to the right zygomatic arch. The skin flap was reflected laterally. Eight burrholes were made in order to remove two quadrangular bone plates. Between these two bone plates a strip of bone approximately 5 cm. wide was left overlying the Rolrtndic veins. After removal of the bone plates, the dura was incised in a U-shaped fashion in each of the openings and reflected medially. On reflection of the dura in the anterior exposure, it was necessary to cauterize a vein bridging the subarachnoid space some distance from the midline. It was not necessary to cauterize any sizable veins bridging the sagittal sulcus. The parietal cortex appeared on inspection and palpation to be normal. In contrast there was definite atrophy of the frontal cortex producing an expanded subarachnoid space. The cortex on palpation felt almost rubbery.

  10. First the splenium, and then the body and genu were exposed by blunt dissection, with a minimal amount of retraction. The anterior cerebral arteries were teased aside without interruption of their branches and without signficant bleeding. The splenium was completely divided by suction, exposing the tela choroidea throughout the length of the divided callosum. The crtllosal section was carried forward into the lamina rostralis and the latter was followed down to the anterior commissure, which was divided The lamina terminalis was not molested. At this point a search was made for the massa intermedia but none was found.

  11. Before closing the dura it was apparent that the blood supply to the cortex was normally brisk (with rapid filling after light pressure) in all distributions; there was no evidence of retractor impressions on the surface of the brain.

  12. The dura was closed with interrupted sutures of No. 4-0 black silk, the bone plates wired in place with No. 3-0 stainless steel and the galea closed with No. 3-0 black silk sutures. The skin was closed with a running suture of No. 4-0 dermalene.

  13. Postoperative Course: Following the operation there was a profound left hemiplegia but with markedly hyperactive reflexes on the right side. Toe signs were positive bilaterally and a tonic grasp reflex was present on the right. F,ven when the patient could cooperate with requests (for example, protrusion of his tongue) he remained mute, unable to feed himself and without spontaneous movement for nearly a week. Progressive recovery followed with the only neurologic symptoms one month later being a sensory deficit and persistent tonic grasp reflex on the left. Four months following operation the patient walked well and performed complicated bimanual tasks (for example, lighting a cigarette) without obvious impairment. He has been followed closely with specific tests to be reported in detail elsewhere (Gazzaniga, et al., 1962). The principal defects were a left symbolic hemianopia, eupraxic anemia and agraphia in the left hand. The left hand performs excellently for automatic function but poorly under voluntary control.

  14. The principal postoperative complication was combined water intoxication (at worst Na 124 mEg/liter, C1 95 mEq/liter, K 2.4 mEq/liter) and respiratory alkalosis (arterial HCOs 15.5 mEq/liter, COn 30.7 volume per cent, and pH 7.48), complicated by the previous use of Diamox, the inability to take oral fluids and a variable need for Pitressin. This problem was handled satisfactorily with intravenous hypertonic solutions and careful daily weighing. Inspiratory rales and postoperative fever (102"F.) responded well to tracheal suction. In view of the history of pyelonephritis, preoperative sulfa drugs were continued and condom drainage was utilised to avoid an indwelling catheter. Sntibiot;ics, transfusion, and corticosteroids were not needed.

  15. During the first postoperative days, anticonvulsants were not given and there were frequent, brief (1 to 4 minute) episodes of right-sided clonics without involrernent of consciousness. As oral feedings were resumed, Mysoline 250 mg. four times a day and Zarontin 250 mg. three times a day were re-instituted and have been continued up to the present. During the first 6 months following the operation, there occurred loss of consciousness for 2 to 3 minutes on four occasions. There have been several 30 to 90 second episodes of "shaking" involving either the left or the right limbs without any alteration of consciousness; there has not yet been a generalized convulsion. The electroencephalogram no longer shows spiking, but remains grossly abnormal with generalized bursts of slow waves, more marked on the left side.

  16. Comment.--This patient's desperate situation caused us to consider every possible approach to his problem. That the forebrain commissures contribute to the spread of seizures was shown by Erickson in 1940. But about the same time, Van Wagenen, et al. (1940) tried callosotomy on approximately 24 patients without major success, and the operation was largely abandoned. However, recent review of Van Wagenen's cases as described by Akelaitis (1944) led us to the following conclusions: (1) At least four of the patients had definite improvement. (2) Most of the remaining had only incomplete sectioning and only one of the many operative procedures included the anterior commissure, clearly important in cases suspected of having temporal foci (Frost, et al., 1958). We felt, therefore, that commissurotomy offered a reasonable chance of some improvement in this case. After the operation was practiced at postmortem several times, it became clear that adeqaute visualization required both a posterior and an anterior approach. Excellent exposure was obtained by using two openings, leaving the bone in place over the Rolandic veins and the nearby Pacchionian granulations.

  17. The postoperative neurologic deficit raises a question of operative trauma. This seems most unlikely in view of the nature of the deficits, the appearance of the brain at operation, and the rapid lifting of neurologic signs as the chemical problem was corrected. It remains possible, however, that the transient akinesia was related to slight septal damage on either side of the anterior commissure.

  18. On the other hand, for the following reasons there seems to be little doubt that the patient came to surgery with a right-sided lesion: (1) the history of head trauma suggesting multiple lesions, (2) the history of apoplectic acquisition of the slight hemihypesthesia, (3) the right frontal cortical atrophy, and (4) the persistent left grasp reflex not reasonably explained as a pure callosal symptom. One must therefore consider that the patient's left hand and left visual field deficits may reflect a combination of commissurotomy with a pre-existing lesion, although there was no sign of such deficit immediately before the commissurotomy. In any case, the persistent symptoms are such as to be expected from commissurotomy on the basis of animal experimentation, as well as the clinical material antedating Akelaitis (reviewed in the article by Sweet, 1941).

  19. The success of the operation in suppressing seieures must be evaluated over a longer period; but even if the seizures eventually recur to their preoperative frequency and severity, the operation has proved a boon to the patient (he has gained 40 pounds) and to his family who sleep regularly at night for the first time in nearly 10 years.

  20. SUMMARY

    A case is presented of a war veteran whose head injury lead to intractable convulsions. Complete section of the corpus callosum and anterior commissure was done at one operation. No generaliaed convulsions occurred in the first 6 months following operation.

  21. REFERENCES

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  23. BREYER, F., BRIIIYE, J. AND ANDRE-BALISAUX: Physiologie et pathologie du corps calleux. Schw. Arch. Neurol. Psychist. 78:31-79 (Mar.) 1958.

  24. ERICKSON, T.: Spread of the epileptic discharge. An experimental study of the after-discharge induced by electrical stimulation of the cerebral cortex. Arch. Neurol. IJsychirtt. 43:429-452 (Mar.) 1940.

  25. FROST, L. L., BALDWIN, M., AND WOOD, C. D.: Investigation of the primate smygdrtla: Movements of the face and jaws. After-discharge and the anterior commissure. Neurology 8:543-546 (July) 1958.

  26. GAZZANIGA, M., BOGEN, J. E., AND SPERRY, R. W.: Some functional effects of sectioning of the cerebral commissures in man. Proc. Nat. Acad. Sci. 48:1765-1769 (Oct.) 1962.

  27. ROVIT, R. L., GLOOR, P., AND RASMUSSEN, T.: Sphenoidal electrodes in the electrographic study of patients with temporal lobe epilepsy. J. Neurosurg. 18:151-158 (Mar.) 1981.

  28. SPERRY, R. W.: Cerebral organization and behavior Sci. 133:1749-1757 (June 2) 1961.

  29. SWEET, W. H.: Seeping intracranial aneurysm simulating neoplasm. Syndrome of the corpus callosum. Arch. Neurol. Psychiat. 45:86-104 (Jan.) 1941.

  30. VAN WAGENEN, W. P. AND HERREN, R. Y.: Surgical division of commissural pathways in the corpus callosum. Arch. Neurol. Psychirtt. 44:740-759 (Oct.) 1940.