Psychomotor seizures

CASE REPORT psychomotor seizure; seizure, psychomotor; temporal lobe epilepsy

Psychomotor Seizures A 30-year-old woman presented to the emergency department after an episode of "dizziness" that caused her to lose control of her car. During the preceding 12-month period she had had recurrent "dizzy" spells and abdominal pains for which she was evaluated by several physicians in various emergency departments. Physical and general neurological examination on presentation was w~thm normal limits. Outpatient CT scan was normal, and an EEG revealed a right temporal lobe spike w~th slow wave pattern suggestive of temporal lobe focus. Since begun on therapeutic doses (300 mg per day of phenytoin), the patient has not experienced further spells or abdominal pains. This report emphasizes the need to be cognizant of an underlying seizure disorder as a possible etiologic agent responsible for a traumatic incident. [Soslow AR: Psychomotor seizures. Ann Emerg Med April 1984; 13:290-292.]

Arnold R Soslow, MD Worcester, Massachusetts From the Department of Emergency Services, The Memorial Hospital, Worcester, Massachusetts. Received for publication October 1, 1982. Revisions received January 13, March 15, June 20, and August 3, 1983. Accepted for publication November 8, 1983. Address for reprints: Arnold R Soslow, MD, The Memorial Hospital, 119 Belmont Street, Worcester, Massachusetts 01605.

INTRODUCTION A poorly understood and frequently misdiagnosed seizure state is psychomotor epilepsy. Difficulties in diagnosis occur because of the myriad of clinical manifestations associated with this seizure disorder. Although seen and described more commonly in children, l-7 psychomotor seizures with recurrent autonomic symptoms have been reported in adults. 8-Io Unless aware of these variable presentations, the emergency physician, frequently the physician of first contact, may misdiagnose this disorder and initiate inappropriate diagnostic or therapeutic strategies. Presented is a case report of a 30-year-old woman, eventually diagnosed as having psychomotor seizures, who had presented to many emergency departments and physicians during the preceding 12 months with complaints of recurrent abdominal pains and "dizzy" spells. CASE REPORT A 30-year-old woman presented to our emergency department after an "episode of dizziness" caused her to lose control of her car. She reported that she felt the episode "coming on" but was unable to pull over, and was amnesic other than remembering being moved to the ambulance from the scene. Police and ambulance attendants reported that she was able to walk from the scene but appeared to be dazed. Additional history revealed that the "dizzy" spells, which had begun approximately one year before, occurred many times during the day, lasted 10 to 15 seconds, and came completely "out of the blue" with no apparent precipitating cause. She reported that her head would feel "light" and that she feb she was "no longer inside her body." While she could hear people talking, she felt that she was away from them. There was no history of staring, abnormal movements, or automatisms. The current episode was the only one associated with an apparent period of unconsciousness. The patient also described recurrent bouts of abdominal pain and pressure for which she had visited many emergency departments and physicians during the preceding six to eight months. These attacks, described as a "pressure sensation" in her back radiating to her abdomen, did not coincide with the daily dizzy spells, lasted several hours, and were not associated with a headache. Barium enema, upper gastrointestinal series, urinalysis, cystoscopy, in13:4 April 1984

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PSYCHOMOTOR SEIZURES Soslow

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I!i Fig. EEG revealed a right temporal lobe spike and slow wave patterns suggestive of a right temporal lobe focus. travenous pyelogram, and exploratory laparoscopy were normal. The patient's mother and sister had "epilepsy." Eleven years prior to this incident, the patient had developed severe headaches subsequent to a head injury (fall) for which a right parietal subdural hematoma was eventually diagnosed and subsequently evacuated without difficulty. The patient denied use of any oral contraceptive or other medication at this time. Her blood pressure was 130/70 mail Hg; pulse, 72; respirations, 16; and physical and neurological examination at the time of this emergency department visit and at subsequent app o i n t m e n t s w i t h the neurological consultants were completely normal except for some minor facial and extremity contusions. Specifically abnormal parietal lobe findings were absent. The patient was discharged from the emergency department. An outpatient CT scan proved normal except for the right parietal craniotomy defect, and a lumbar puncture revealed an opening pressure of 20, no cells, protein of 32 mg%, and glucose of 62 rag%. An outpatient electroencephalogram (EEG) revealed a right temporal lobe spike and slow wave patterns strongly suggestive of a right temporal lobe focus (Figure). Since begun on therapeutic doses (300 rag/day) of phenytoin, the patient has not experienced further "spells" or abdominal pains. DISCUSSION

Psychomotor epilepsy or temporal lobe epilepsy (TLE), when the symp118/291

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TABLE 1. Etiologic factors in psychomotor seizures (N = 666)* Definite Factors (25%) Tumor Head injury and amnesia Gliosis Cerebrovascular disease Angioma Miscellaneous

9.5% 7.0% 2.0% 2.0% 2.0% 2.5%

Possible Factors (23%) Positive family history Abnormal birth Seizures in infancy

11.0% 7.0% 5.0%

Other Disorders (54%) Presumed cerebrovascular disease Multiple sclerosis • Unknown *From Currie et ak8

toms are associated with a definitive lesion in the temporal lobe, is a form of focal cortical seizure disorder characterized by a great variety of clinical phenomena. Etiology is multifactorial, with tumors (hemagioma, gliomas, and glioblastomas), presumably of congenital origin, found in 9.5% of the cases (Table 1). Trauma, infections, and vascular disease are other commonly observed or implicated etiologies. There appears to be an 11% incidence of familial epilepsy.S Emotional experiences may range from auras that are unpleasant (ie, fear, anger, or depression) to those of pleasure, ecstasy, and sexual concomitants.9 Sensations of deja vu, depersonalization and/or distortion of reality may be noticed, and 40% report a visceral component to the attack, frequently gastrointestinal (Table 2). The amount of movement in these A n n a l s of E m e r g e n c y M e d i c i n e

9.0% 1.0%

44.0%

attacks is quite variable, with periods of automatic activity usually lasting less than five minutes. Such automatisms as lip-smacking, chewing, swallowing, fiddling or fumbling with the hands, smoothing the hair to the side, or attempting .to get an object from the pocket frequently are observed. Rarely non-goal-directed aggressive behavior and violent attacks also have been reported, n-13 Migraine, espedally when associated with visceral symptoms, frequently is confused with psychomotor seizures.6A 4 Classically patients with migraine have a normal EEG, almost always have associated headaches, and have a markedly lower incidence of familial epilepsy (Table 3). Other disorders that can be confused with psychomotor epilepsy are transient global amnesia, narcolepsy, and attacks of psychogenic origin.9 13:4 Apri! 1984

TABLE 2. Components of attacks in psychomotor seizures (N

=

666)*

that these two s y m p t o m complexes were etiologically related.

REFERENCES Disorder Visceral (gastrointestinal) Thought disorder (including deja vu) Speech disorder Vertigo Special sensory Visual Auditory Olfactory Gustatory Motor phenomena Sensory Emotional disorders *From Currie et al.8

Cases (%) 40 27 22 19 18 16 12 3 14 2 19

TABLE 3. Comparison of childhood migraine and recurrent abdominal syndrome*

Sex Headache Seizures Paroxysmal EEG Family history Seizures Migraine *From Prensky.6

Migraine > 60% Male 100% 8% (5.4%- 12.3%) 10%

Abdominal Syndrome < 40% Male 43% (0-85%) 15.1% (0-39%) 23.2% (7%-76%)

2%-3% 72% (44%-87%)

10% (0-30%) 22.3% (0-66%)

M a n a g e m e n t has i m p r o v e d m a r k e d l y d u r i n g t h e p a s t s e v e r a l years. While newer agents such as s o d i u m valporate and carbamazepine probably have s o m e role, 1619 the m a j o r i t y of patients can be managed w i t h phenytoin if close a t t e n t i o n is directed to c o m p l i a n c e a n d m a i n t e n a n c e of therapeutic anti-convulsant blood levels. Phenobarbital and primidone also h a v e a r o l e i n t r e a t m e n t . 19 T h e efficacy of surgery is less clear, b u t s o m e p a t i e n t s w i t h s e v e r e a n d resistant seizures w i t h an anatomically identified and localizable focus have improved after surgical ablation of the affected site w i t h m i n i m a l or acceptable neuroresiduae.2O, 21 This p a t i e n t ' s p r e s e n t a t i o n re-emphasizes the need for emergency physicians to be cognizant of this disorder and consider the possibility that a seizure is responsible for a traumatic ac13:4 April 1984

cident, w h e t h e r or not the patient has an a b n o r m a l n e u r o l o g i c a l e x a m i n a tion at the time. A complete and thorough h i s t o r y is crucial. A h i s t o r y of cyclic, episodic or paroxysmal sympt o m s or a m n e s i a a b o u t t h e a c u t e event should alert the physician to the possibility of C N S or cardiovascular etiology. This patient displayed m a n y of the characteristics and s y m p t o m s associated w i t h p s y c h o m o t o r epilepsy, but it is unclear w h e t h e r her recurrent abd o m i n a l pains were a visceral manifestation of the seizure state. She did not become drowsy or develop headache t e m p o r a l l y related to these abdominal pains; however, as described by Scott, 9 a headache or postictal phen o m e n o n is not always present in patients w i t h proven "abdominal epilepsy." T h e p a t i e n t ' s i m p r o v e m e n t on a n t i - c o n v u l s a n t m e d i c a t i o n suggests Annals of Emergency Medicine

1. Chao D, Sexton JA, Davis SD: Convulsive equivalent syndrome of childhood. J Pediatr 1964;64:499-508. 2. Millichap JG, Lombroso CT, Lennox WG: Cyclic vomiting as a form of epilepsy in children. Pediatrics 1955;15:705714. 3. Livingston S: Abdominal pain as a manifestation of epilepsy. J Pediatr 1951; 38:687-695. 4. Sheeby BN, Little SC: Abdominal epilepsy. J Pediatr 1960;56:355-363. 5. Swaiman KE Frank Y: Seizure headaches in children. Dev Med Child Neurol 1978;20:580-585. 6. Prensky AL: Migraine and migraine variants in pediatric patients. Pediatr Clin North Am 1976;23:461-471. 7. Walsh GO: Unusual presentations of epilepsy. Pediatrics 1974;53:548-551. 8. Currie S, Health KW, Henson RA, et al: Psycho seizures. Brain Journal 1971;94: 173-179. 9. Scott DF: Temporal lobe epilepsy. Br [ Hosp Med 1978;12:178-185. 10. Ounsted C, Lindsay J, Norman R: Biological factors in temporal lobe epilepsy. Clinics in Developmental Medicine, no. 22. London, Heinemann, 1966. 11. Nanda RN: Fatal accident during an epileptic automatism. N Z Med J 1979; 90:193-195. 12. Ashford JW, Schultz SC, Walsh GO: Violent automatism in a partial complex seizure. Arch Neurol 1980;37:120-122. 13. Brewer C: Homicide during a psychomotor seizure. Med JAust 1971;1:857-859. 14. Biekerstaff ER: Basilar artery migraine. Lancet 1961;1:15-17. 15. Bower B: Management of psychomotor seizures. Br f Hosp Med 1978;19:8-12. 16. Epstein M: Intractable seizures: Review and guide for clinical usage of valproic acid. J Kans Med Soc 1981;82:58-60. 17. Rowan AJ: Sodium valproate. Neurology 1979;29:1450-1459. 18. Kosteljanetz M: Carbamazepines vs" phenytoin: A controlled clinical trial in focal motor and generalized epilepsy. Arch Neurol 1979;36:22-24. 19. Schwartz J: Carbamazepine as a substitute treatment of single and compound seizures. Clin Electroencephalog 1978;9: 90-95. 20. Falconer MA: Surgical management of temporal lobe seizures. Lancet 1974; 2: 767-769. 21. Falconer MA, Serafetinides EA: Temporal seizures. J Neurol Neurosurg Psychiatry 1963;26:154-157. 292/119