Temporal Lobe Epilepsy Caused by Unruptured Middle Cerebral Artery Aneurysms ROBERT P. KAMRIN, MD, PHILADELPHIA THE SURGICAL therapy of temporal lobe epilepsy has achieved increasing importance as large series of good results have been reported.1-3 Preoperative study of candidates for surgery has included pneumoen- cephalography (PEG) as the radiographic contrast examination of choice. Arteriography has been added only when thought specifically indicated. The pathological en- tities most often encountered in the resected temporal lobe have been mesial incisural sclerosis in approximately 50% of patients, cryptic tumors and vascular malformations in 20%, scars and infarcts in 15% and no definite pathology in 15%.4 In the last four years four patients with aneurysms of the middle cerebral artery had symptoms of temporal lobe epilepsy prior to rupture of the aneurysms. All were treated at the Neurological Institute of New York. These patients could not clinically be distinguished from other patients with idiopathic temporal lobe seizures. Diagnosis was established only by arteriographic study either before or after rupture of their aneurysms. The clinical picture of these pa¬ tients is presented so that diagnosis may be achieved prior to aneurysm rupture with its attendant morbidity. Materials and Methods From January 1961 to December 1964, 168 pa¬ tients with intracranial aneurysms were treated consecutively at the Neurological Institute of New York by direct clipping of their aneurysmal sac. Submitted for publication Aug 16, 1965; accepted Dec 14. From the Department of Neurological Surgery, College of Physicians and Surgeons, Columbia University, and the Neurological Institute, Presbyterian Hospital, New York. Reprint requests to 1930 Chestnut St, Philadelphia 19103. Of these patients 30, or 18%, had aneurysms of the middle cerebral artery. This percentage of middle cerebral artery aneurysms agrees well with the 17% figure given by Housepian and Pool6 and falls between the figures reported elsewhere.""8 Four of these patients, or 13% of patients with middle cerebral artery aneurysms, presented with an initial history of temporal lobe seizures. Three of the patients never bled from their aneurysm, and one bled only after 11 years of seizures (Table). Report of Cases Case 1.—This 33-year-old, right-handed, white male physician had a severe right-sided throbbing headache for one year before hospitalization. The headache was episodic and would be constant for two or three weeks, then remit for a similar period of time. An electroencephalogram (EEG) taken during this time showed a right temporal slow wave focus. Two months before admission both visual and olfactory illusions were experienced coincident with the headaches. The visual illusions consisted of seeing a man sitting in a chair. The patient could not identify the man but was certain that he knew him. This illusion would last 15 to 30 seconds and was always in the left visual field. Immediately following the visual illusion, the patient would experience an olfactory aura of a burning pleasant odor, like incense. A trial of diphenylhydantoin (Dilantin) was found to stop the visual illusions completely but did not affect the olfactory ones. Examination of the patient on hospitalization in April 1964 revealed a normal general physical and neurological state. Skull x-rays and lumbar puncture were normal. Bilateral carotid arteriography demonstrated an aneurysm of the right mid¬ dle cerebral artery 1.0 X 2.5 cm, located 1.0 cm distal to the carotid bifurcation. There was eleva¬ tion of the middle cerebral artery suggesting a temporal lobe hematoma (Fig 1). At craniotomy under moderate hypothermia, a 4.0 X 5.0 cm partially thrombosed aneurysm was found arising from the first major branch of the Downloaded From: http://archneur.jamanetwork.com/ by a Penn State Milton S Hershey Med Ctr User on 05/22/2015 Middle Cerebral Artery Aneurysms Causing Temporal Lobe Seizures Rupture Before EEG Seizure Aneurysm Sex Side Seizures Focus Type Calcified Arteriogram PEG Size Thrombosis 33 M Right No Yes Uncinate No Aneurysm Not done 4X5 cm Yes Normal >1 cm Yes Not done >1 cm No Normal 2X1 No Age and Reference Case 1 Visual Case 2 45 M Right No Yes seen Déjà vu Psychomotor Yes Grand mal Case 3 48 F Right No Yes Aneurysm not seen No Uncinate Auditory Déjà vu Aneurysm seen Grand mal Focal 53 F Right No Yes Yes Uncinate Auditory Hook and 11 F ? No Yes Viscereal Uncinate ? Norlen (1958) 24 F Left No No 34 F Left Yes Visual ? Aneurysm Not done 1 cm No Normal >1 cm No Not done 1 cm No Possible 4 cm No seen ? Aneurysm seen 46 M Frankel and 49 F Right Yes ? Visual No Aneurysm seen Alpers (1955) Right No No Uncinate Grand mal Focal Allégre and Vogouroux (1957) No ? immediately subpial in the Sylvian fissure and was covered on its lateral surface by only a thin layer of the superior temporal gyrus. One arterial branch entered the aneurysm and two left it. These three branches were sacrificed. There was no evidence of new or old hemorrhage in the brain adjacent to Following operation, the Yes Aneurysm seen temporal tumor Uncinate middle cerebral artery. The aneurysm presented patient exhibited agitation and paranoid ideation against the nurses but this resolved within four days. The patient was discharged to home, neurologically in¬ tact, two weeks postoperatively. The patient has been followed for lyí years since operation and has had no seizures during this time. Fig 1.—Right carotid arteriogram showing patient in case 1 arising from the first bifurcation of the middle cerebral artery. This aneurysm was partially thrombosed and aneurysm of two times greater than the size demon¬ strated by the arteriogram. was No Visceral Speech arrest Hook and Norlen (1958) the aneurysm. ? Aneurysm seen Norlen (1958) Hook and 1 X 1 seen Norlen (1958) Hook and Aneurysm Case 2.—This 45-year-old, right-handed white male was first admitted to the hospital in June 1960 because of two grand mal seizures, one 6 weeks and one 2 weeks before hospitalization. Hy¬ pertension had been present for four years and examination demonstrated a blood pressure of 160/114. The results of neurological examination were normal. Skull x-rays revealed a rounded calcification in the right middle fossa (Fig 2 and 3). Electroencephalogram showed a right temporal slow wave focus. Lumbar puncture revealed no cells and a protein of 29 mg/100 cc. On right carotid arteriography the middle fossa calcification was seen to lie immediately below the trifurcation of the right middle cerebral artery. No abnormal vascularity or aneurysm was seen, but slight bowing Fig 2.—Skull x-ray of patient in case 2 demonstrating a ring of calcification seen through the orbit. This ring lays in the an¬ terior part of the middle fossa. Downloaded From: http://archneur.jamanetwork.com/ by a Penn State Milton S Hershey Med Ctr User on 05/22/2015 Fig 3.—Skull x-ray of patient in case 2 demonstrating the position of the calcification in the middle fossa anteriorly. of the supraclinoid portion of the right internal carotid artery was present. Pneumoencephalography was normal except for slight dilatation of the right lateral ventricle (Fig 4). No temporal horn dis¬ tortion was present. Following discharge from the hospital, psychomotor seizures started consisting of automatisms with amnesia for two to three minutes. By 1962 these attacks occurred from five to six times a month. Rehospitalization in July 1962 revealed mild left-sided weakness and left hyperreflexia on neurological examination but no other changes. The EEG focus was unchanged, and right carotid arteriography again was normal. Lumbar puncture now demonstrated a protein of 97 mg/100 cc and no cells. Following these studies the patient was again discharged. In February 1963 the patient was again hos¬ pitalized and examination showed increased leftsided weakness, mainly in the upper extremity. Seizure activity had increased in frequency. Lumbar puncture now revealed a protein of 116 mg/100 cc. Right carotid arteriography was again normal. A right temporal lobectomy was then elected with a presumptive diagnosis of infiltrative glioma. During resection a large calcine mass with a base 1.0 cm wide was seen arising from the right middle cerebral artery trifurcation. This mass was incised and found to be an aneurysm with laminar thrombosis. After much of the thrombus was removed, the sac was closed over a muscle stamp. There was no evidence of old or Fig 4.—Pneumoencephalography of patient in 2 showing filling of the right temporal horn and its relation to the calcified aneurysm. The dis¬ tance separating the aneurysm from the tip of the temporal horn should be noted. case uary 1960. Left hemiparesis immediately followed the seizure. The patient lapsed into stupor four hours later and did not regain full consciousness for three days. Hospitalization during this time revealed a right temporal slow wave focus on EEG. Lumbar puncture was not performed. The patient's blood pressure was 180/100, though no previous history of hypertension was known. Dis¬ charge diagnosis in March 1960 was cerebrovascular accident. The patient was well, except for very mild residual left hemiparesis, until July 1960 when a second seizure occurred, this time a left focal seizure which became generalized. Following this seizure, olfactory and auditory illusions and déjà vu phenomenon were experienced frequently. The olfactory illusion was of an unpleasant metallic medicinal odor. Auditory illusions were varied and consisted of bells, music, or children scream¬ ing. The déjà vu took the form of the patient feeling that she anticipated what people were going or to say. A third grand mal seizure occurred in Decem¬ ber 1960. The patient was briefly hospitalized and lumbar puncture performed which was normal. Fig 5.—Right carotid arteriogram of patient in case 3 showing large aneurysm arising from the middle cerebral artery trifurcation. hemorrhage in the brain parenchyma sur¬ rounding the aneurysm. Recovery from operation was rapid, and the patient was discharged in ten days. The patient was able to return to work postoperatively for the first time in several years. No further seizures were experienced except for new two minor motor seizures five months after opera¬ tion. In October 1963 ten months after operation, the patient died suddenly of a myocardial infarc¬ tion. Case 3.—This 48-year-old, right-handed white woman experienced a grand mal seizure in Jan- Downloaded From: http://archneur.jamanetwork.com/ by a Penn State Milton S Hershey Med Ctr User on 05/22/2015 results of examination were again normal, as were lumbar puncture and skull x-rays. The patient was Fig 6.—Right carotid arteriogram of patient in case 4 showing large aneurysm of the middle cerebral artery trifurcation. Although only one aneurysm is were demonstrated, two large aneurysms found at operation. Hospitalization reoccurred in March 1961 follow¬ ing a fourth grand mal seizure. Blood pressure was 200/100, and neurological examination re¬ vealed a mild left-sided hyperreflexia and Babinski sign. Electroencephalogram again showed a prominent right temporal slow wave focus. Lum¬ normal. Bilateral carotid arteriography demonstrated a 3 cm-long aneurysm of the trifurcation of the right middle cerebral artery, with slight elevation of the middle cerebral artery suggesting hematoma (Fig 5). Craniotomy was performed under moderate hypothermia and the aneurysm clipped. No evidence of old or new hemorrhage was present in the brain surrounding the aneurysm. The patient was discharged two weeks after operation with continued mild hemi¬ bar puncture was paresis. In the four years since operation, both grand mal seizures and olfactory illusions have been ex¬ perienced occasionally. Their frequency, how¬ ever, has been markedly reduced. Case 4.—This 53-year-old, right-handed Negro woman, also reported by Pool and Potts,27 was hospitalized elsewhere in 1952 with a diagnosis of meningitis. She was treated with penicillin and discharged without residua. In February 1953 left focal seizures started. The results of studies elsewhere, including skull x-ray, EEG, and lum¬ bar puncture, were normal. The onset of various aurae, either preceding her focal seizures or in¬ dependent of them, led to hospitalization at the Neurological Institute of New York in 1955. The aurae were either visceral, usually a feeling of nausea or chest tightness ; olfactory, described as an unpleasant odor like acetone; or auditory, dis¬ tortions of spoken sounds. The results of neurological examination were normal. Electro¬ encephalogram revealed a right temporal slow focus. Lumbar puncture showed normal re¬ sults. Pneumoencephalography demonstrated pos¬ sible cerebral atrophy on the right. Increasing frequency of seizure activity led to a second hospitalization in December 1960. The wave discharged following study. In May 1963 the patient sustained a subarach¬ noid hemorrhage resulting in a left hemiparesis, the arm being affected more than the leg. Skull x-rays now demonstrated a 1.2 cm rim of calci¬ fication, 2.5 cm medial to the right inner table of the skull. Bilateral carotid arteriography re¬ vealed a large middle cerebral artery aneurysm on the right (Fig 6). At craniotomy under moderate hypothermia, two aneurysms within 1 cm of each other were found on the major middle cerebral artery trunk. One aneurysm was 2.2 X 1.1 cm and the other 1.3 X 0.9 cm. The proximal aneurysm ruptured during dissection, and excision of both aneurysms and the arterial trunk was performed. Despite this sacrifice of a major branch, the patient was discharged three weeks postoperatively with only slight left hemiparesis. During the one year the patient was followed after operation, only one seizure, psychomotor in nature, occurred. Additional Cases From the Literature The extensive literature on temporal lobe epilepsy contains no specific reports of an¬ eurysms causing temporal lobe seizures. Gastaut et al,9 in a discussion of nine au- topsied cases of temporal lobe epilepsy, described two cases, 4 and 5, with orbital and inferior frontal intracortical hema¬ tomas, presumably secondary to anterior cerebral artery aneurysms. In neither case was an aneurysm identified. Review of articles on the surgical treat¬ ment of middle cerebral artery aneurysms, however, yields six patients having temporal lobe seizures. In four patients the seizures started prior to aneurysm rupture and in two patients after rupture (Table). Hook and Norlen 10 reviewed 80 cases of middle cerebral artery aneurysm. One pa¬ tient, an 11-year-old girl, had uncinate sei¬ zures for six months before rupture of her aneurysm. Another patient with an unruptured aneurysm presented with temporal lobe seizures of speech arrest and visceral aura and had ligation of a pea-sized middle cerebral artery aneurysm. Two further pa¬ tients had formed visual illusions of persons and objects but only after rupture of their aneurysms. One aneurysm was on the right and described as pea-sized, the other on the left and of coffee bean size. Thus, 6% of Downloaded From: http://archneur.jamanetwork.com/ by a Penn State Milton S Hershey Med Ctr User on 05/22/2015 their cases and 25% of their unruptured aneurysms had temporal lobe seizures (Ta¬ ble). Frankel and Alpers,11 despite their state¬ "In our series, the only symptom of significance before the acute onset (of sub¬ arachnoid hemorrhage) was headache ," described one patient in their series of 12 as having temporal lobe seizures. Case 10, a 49-year-old man, had a li/^-inch right middle cerebral artery trifurcation aneurysm which ment: . . . surgically ligated prior to rupture. This patient had three years of uncinate seizures consisting of unpleasant odors and tastes as well as focal seizures on the left (Table). An additional case, case 12, with a ruptured was 0.8 cm left middle cerebral artery aneurysm, had a vague history of psychomotor sei¬ zures prior to aneurysm rupture. Allégre and Vigouroux12 described one patient, in their series of five unruptured middle cerebral artery aneurysms, who pre¬ sented with uncinate seizures (Table). An¬ other patient, described by Walton,13 had uncinate seizures for three months prior to subarachnoid hemorrhage. No study is mentioned for delineation of the site of hemorrhage. Comment Despite the large numbers of temporal lobectomies now being performed and re¬ ported, the literature on this surgery fails to reveal any patients having intracranial aneurysms as the cause of their seizure activity. Vascular malformations of the temporal lobe, usually small and often calci¬ fied, are frequently reported and are found in about 10% of resected temporal lobes.14 These are most often not diagnosed by pre¬ operative contrast study but are discovered during the course of lobectomy or during examination of the resected specimen. The accidental discovery of a middle cerebral artery aneurysm during the performance of a temporal lobectomy would not be as be¬ nign and courts probable operative difficulty. The usual preoperative study of patients with temporal lobe seizures includes PEG. Arteriography is used only rarely. It is thought easier to detect subtle changes in the air shadow of the temporal horn than to appreciate distortions of the vascular pattern of the middle cerebral vessels. Notwith¬ standing any validity of this rationale, the temporal tip, that 4 to 5 cm segment of the temporal lobe between the anterior end of the middle fossa and the tip of the temporal horn, is a blind area on PEG. If a rapidly expanding mass lesion, such as a tumor, is present in this area and shifts normal struc¬ tures, distortion of the air-filled temporal horn will reveal its presence. If a slowly expanding mass lesion, such as an aneurysm, is present, however, it may cause local de¬ struction and atrophy of brain parenchyma and thereby not increase the volume of tissue in the temporal tip. If no volume increase occurs, the temporal horn will not be dis¬ torted unless the lesion itself directly in¬ dents the wall of the horn. This is well illustrated by cases 2 and 4 in this series where PEG was normal despite the pres¬ ence of large trifurcation aneurysms. It must be noted that arteriography may also fail to delineate large aneurysms.15,le This is because large aneurysms tend to thrombose spontaneously, either partially or completely. Thirty percent to 40% of an¬ eurysms greater than 1.5 cm will exhibit thrombosis compared to 10% to 15% of smaller aneurysms. If thrombosis does oc¬ cur, calcification of the aneurysm wall will occur in 10% of the cases and yield a ring¬ like density on x-ray which will suggest that an aneurysm is present. If partial throm¬ bosis occurs, as in case 1 in this series, the arteriogram will demonstrate only the patent interior. The arteriographically demon¬ strated aneurysm size will then be much smaller than its actual size. Displacement of adjacent vessels, present in 50% of large aneurysms, should alert one to the proba¬ bility that the aneurysm is larger than its visualized size. All of the middle cerebral artery aneu¬ rysms causing uncinate seizures or déjà vu phenomena were on the right or minor hemisphere side. The literature on the sub¬ ject of déjà vu, well reviewed by Cole and Zangwill,17 suggests that déjà vu is usually elicited from the hemisphere that is minor for speech. The case reports presented here confirm this (Table). The eliciting of unci- Downloaded From: http://archneur.jamanetwork.com/ by a Penn State Milton S Hershey Med Ctr User on 05/22/2015 nate seizures from right-sided lesions only is also noted and suggests a minor hemisphere focus predominance for this phenomenon. It is of further interest that in one case, that of the 33-year-old physician, the uncinate seizures were always associated with a pleas¬ ant odor. Though this is unusual, no partic¬ ular significance can be attached to it. Patients with visceral seizures had aneu¬ rysms in either major or minor hemi¬ spheres.18 No age appeared immune to having mid¬ dle cerebral artery aneurysms as the causa¬ tive agent for their seizures. Patients reviewed ranged in age from 11 years to 53 years. The only limiting factor appeared to be the aneurysm size, for no unruptured aneurysms less than 1.0 cm elicited temporal lobe seizures. It is impossible to state whether the re¬ ported aneurysms caused seizures by their hemodynamic effects or solely through being an irritative mass lesion. Of the 30 cases of middle cerebral artery aneurysm re¬ viewed at the Neurological Institute of New York, all aneurysms ruptured except the cases reported here. Twelve patients had aneurysms 1.0 cm or greater in size. Dis¬ carding the four reported cases from this number leaves eight patients with large an¬ eurysms but without seizures. Three of these eight patients had severe ipsilateral headaches for four months or longer before rupture of their aneurysms. Thus, only five patients with aneurysms 1.0 cm or larger were completely asymptomatic prior to hem¬ orrhage. It is interesting to speculate whether more adequate and direct question¬ ing after hospitalization, if allowable by the patient's state of consciousness, would have brought to light further symptomatology. Patients with unruptured middle cerebral artery aneurysms could not be distinguished in any way from patients with temporal lobe epilepsy from any other cause. They often exhibited other seizure activity such as focal or grand mal epilepsy. Most had temporal lobe slow wave foci on EEG, a finding which has not been previously recog¬ nized (Table).19,20 In the present series three of the four patients were fortunate to have their aneurysms recognized before rupture, whereas one was operated upon only after hemorrhage despite 11 years of seizure activity. One additional case of interest should be mentioned. Dandy 21 described a patient with a 15-year history of petit mal seizures fol¬ lowing probably subarachnoid hemorrhage at age 37 years. Operation disclosed a 5.0 cm thrombosed middle cerbral artery tri¬ furcation aneurysm which replaced the brain parenchyma of the temporal lobe tip. Treatment The treatment of choice of all aneurysms is repair prior to rupture. The marked brain damage following hemorrhage from middle cerebral artery aneurysms has been well described by Crompton.22 The method of choice of treatment of middle cerebral artery aneurysms is now agreed to be direct intracranial clipping.2327 It is not thought that ligation of the extracranial carotid ar¬ tery has any merit in the therapy of this le¬ sion. Conclusions The purpose of this presentation is to indicate the merit and the necessity of angiography for the full evaluation of temporal lobe seizures. Study of the patient with temporal lobe seizures cannot be considered complete if the first 4 to 5 cm of the tem¬ poral lobe, the radiographically blind area on PEG and also the area of the temporal lobe most likely to contain pathology causing these seizures, are not fully visualized. Fur¬ ther appreciation of the venous anatomy of the temporal lobe, as described by Wolf et al28 and Wolf and Huang,29 may well di¬ minish many of the advantages of PEG. The number of patients harboring middle cerebral artery aneurysms as the cause of their temporal lobe seizures is probably much higher than one would expect from examination of the literature. Since most of the patients summarized here exhibited their seizure activity prior to rupture of their aneurysm and many never bled from their aneurysm, it must be suspected that some patients now being followed in seizure clinics with controlled temporal lobe sei¬ zures have aneurysms. A normal neurologi- Downloaded From: http://archneur.jamanetwork.com/ by a Penn State Milton S Hershey Med Ctr User on 05/22/2015 cal examination in these patients cannot give any security since many patients re¬ ported here were neurologically intact, though demonstrating a persistent EEG focus. The criteria to be used for deciding which patients with temporal lobe seizures should be studied by contrast examination cannot be deduced from study of the selected pa¬ tients presented here. It can be strongly suggested, however, that should any contrast examination be decided upon, arteriography should be included in the radiographie pro¬ cedures employed. Amelioration of seizure activity or com¬ plete cessation was noted in all patients after operation. Since both the aneurysm and ad¬ jacent injured brain were removed at oper¬ ation, it is impossible to state which was the direct cause of seizure activity. In treatment of this lesion, however, one may be optimis¬ tic about obtaining symptomatic relief. Summary Four patients exhibiting temporal lobe ßeizures prior to rupture of large middle cerebral artery aneurysms have been studied. An additional six cases have been col¬ lected from the literature. These patients are clinically indistinguishable from others having idiopathic temporal lobe seizures. Persistent slow wave EEG foci have been noted. Of the seizure activity observed, déjà vu and uncinate attacks have arisen predominately from the minor hemisphere for handedness. The aneurysms observed have been 1.0 cm in size or greater. Some have been partially or completely thrombosed or have had radiographically visible calcification of their walls or both. Pneu¬ moencephalography has not yielded any in¬ dication of the presence of even large aneurysms. Since PEG fails to define masses in the anterior 5 cm of the temporal lobe, unless the temporal horn is displaced, arteriogra¬ phy is recommended in the evaluation of all patients with temporal lobe seizures who are studied with contrast radiography. Of the four cases reported here, one pa¬ tient had no further seizures after opera¬ tion. The other three had a marked reduction in seizure activity. REFERENCES 1. Rasmussen, T., and Branch, C.: Temporal Lobe Epilepsy, Postgrad Med 31:9-14, 1962. 2. Falconer, M.A., and Serafetinides, E.A.: A Follow-Up Study of Surgery in Temporal Lobe Epilepsy, J Neurol Neurosurg Psychiat 26:154-165, 1963. 3. Green, J.R., and Scheetz, D.G.: Surgery of Epilepto- genic Lesions of the Temporal Lobe, Arch Neurol 10:135\x=req-\ 148, 1964. Falconer, M.A.; Serafetinides, E.A.; and Corsellis, Etiology and Pathogenesis of Temporal Lobe Epilepsy, Arch Neurol 10:233-248, 1964. 5. 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Wolf, B.S.; Huang, Y.P.; and Newman, C.M.: The Superficial Sylvian Venous Drainage System, Amer J Roentgen 89:398-410, 1963. 29. Wolf, B.S., and Huang, Y.P.: The Insula and Deep Middle Cerebral Venous Drainage System: Normal Anatomy and Angiography, Amer J Roentgen 90:472-489, 1963. Downloaded From: http://archneur.jamanetwork.com/ by a Penn State Milton S Hershey Med Ctr User on 05/22/2015