TREATMENT OF GENERALIZED SEIZURES BY CEREBRAL COMMISSUROTOMY

JOSEPH E. BOGEN, M.D., AND PHILIP J. VOGEL, M.D., F.A.C.S.

From the Department of Neurosurgery, White Memorial Hospital and Loma Linda University School of Medicine, Los Angeles, CA.

Reprint from Vol. XIV Surgical Forum, American College of Surgeons, 1963

  1. The anatomy of the corpus callosum (C.C.) and anterior commissure (A.C.) suggests an important role in the spread of seizure activity. Experimental results to 1956, reviewed by Bremer et al. (2), may be summarized as follows: spread of activity from a focus to the opposite side is often interrupted by section of C.C. whether the locus is established acutely by strychnine or electrical stimulation, or chronically by alumina cream lesions; however, generalized convulsions can occur in typical form after callosotomy and, indeed, the threshold may be lower than before operation. More recently, Seguin et al. (7) found that section of C.C. lowered the threshold and increased the severity of metrazol convulsions. On the other hand, Frost et al. (4), and Poblete et al. (6) found that spread from one temporal lobe to the other is interrupted by section of A.C. The data in human beings from Van Wagenen and Herren (8), with partial follow-up by Akelaitis (1), are quite heterogeneous with epilepsy of varying type, varying degree of C.C. section, and only one A.C. section. Improvement in some of these suggests that complete section of the forebrain commissures might be helpful in carefully selected cases. We present here a follow-up of a case reported in preliminary notes by Bogen and Vogel (3) and by Gazzaniga st al. (5).

  2. W. J. was 42 years old when first seen in 1956 because of "blackout spells" beginning several months after a parachute jump in 1944 which resulted in fractures of the left leg and unconsciousness of about 2 days. While in prison camp, he was rendered unconscious by a rifle-butt blow to the left parietal region. Following his return home he was plagued by "lost time"; he once drove away from home one morning and arrived 50 miles away that afternoon with no recollec- tion of the intervening events. In 1951, he had his first convulsion. The episodes increased in severity and frequency. They typically culminated in apnea, cyanosis, and severe clonism. Electroencephalograms showed a left temporoparietal focus as well as bitemporal abnormalities. A left carotid angiogram was normal, as was a pneumoencephalogram. In 1951 the patient was studied in another hospital; he was told that removal of the left convexity focus was inadvisable because of the risk of aphasia. On February 4, 1962, he was admitted for the twelfth time, for section of the forebrain commissures. During the first postoperative days, anticonvulsants were not given and there were frequent, brief (1 to 4 min.) episodes of right-sided clonism. As oral feedings were resumed, mysoline, zarontin, and barbiturates were resumed and have been continued.

  3. Whereas status epilepticus occurred every 2 to 3 months, requiring hospitalization or intravenous barbiturate in the emergency room, no such episode has occurred since operation. Whereas major seizures (with unconsciousness, apnea and severe clonism) occurred every week before, there have been only 2 episodes of complete loss of consciousness in the 16 months since operation; however, brief dreamy states, unnoticed before, have occurred many times. Muscular phenomena have been limited since surgery to mild shaking or stiffness lasting a minute or 2 at most, and only in 1 or the other limb on each occasion.

  4. The patient's improvement having persisted well over a year, it seems hardly ascribable to a placebo effect or the non-specific effect of a major operation. Moreover, the relative increase in minor episodes supports the view that section of C.C. and A.C. has served to prevent generalization. More interesting is the reduction in total number of spells, large and small. Bremer et al. suggested this might result from abolition of a reciprocal facilitation or, as we might say, a positive feedback favoring oscillation. Seguin st al. suggested that sensitization of denervation renders cortical neurons more susceptible to anti-convulsant drugs. This latter hypothesis might be tested by stopping medication, bur such a step does not appear to be in the patient's best interest at this time.

  5. REFERENCES

  6. 1. AKELAITIS, A. J. A study Of gnosis, praxis and language following section of the corpus callosum anti anterior commissure. J. Neurosurg., 1944, 1:91-102.

  7. 2. BREMER, F., BRIHAYE, J., and ANDRE-BALISAUX. Physiologie et pathologie du corps calleux. Schweiz. Arch. Neurol. Psychiat., 1956, 78:31-79.

  8. 3. Bogen J. E., and VOCEL, P. J. Cerebral commissurotomy in man: Preliminary case report. Bull. Los Angeles Neurol. Sec., 1962, 27:169-172.

  9. 4. FROST, L. I,., BALDWIN, M., and WOOD C. D. Investigation of the primate amygdala: Movements of the face and jaw. After-discharge and the anterior commissure. Neurology, 1938, 8:543-546.

  10. 5. GAZZANIGA, M., BOGEN, J. E., and SPERRY, R. W. Some functional effects of sectioning of the cerebral commissures in man. Prac. Nat. Acad. Sc. U. S., 1962, 48: l665-1769.

  11. 6. Poblete, R., RUBEN, R. J., and WAr.RrR, A. E. Propagation of after-discharge between temporal lobes. J. Neurophysiol., 1950, 22:538-553.

  12. 7. SEGUIN, J. J., I;RETZ, N. A., MANAX, S. J., and STAVRAKY, G. W. Corpus callosum and pentylenetetrazol convulsions. Arch. Neurol., 1961, 9:314-319.

  13. 8. VAN WAGENEN, WP, and HERREN, RY Surgical division of commissural pathways ill the corpus callosum Arch. Neurol. Psychiat., Chic., 1910, 44:740-759.