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| Year : 2001 | Volume
: 49
| Issue : 3 | Page : 317-9 |
Lorazepam : an adjuvant therapy in patients with seizure and heliotaxis.
Oomman A, Madhusudanan M
Department of Neurology, Medical College, Kottayam, Kerala, India.
Correspondence Address:
Department of Neurology, Medical College, Kottayam, Kerala, India.
Photosensitive epilepsy is a type of reflex epilepsy. Five percent of epileptics are photosensitive, i.e. they show photoconvulsive response (PCR) during intermittent photic stimulation. Patients with photogenic or photosensitive epilepsy have seizures with flickering light. They also exhibit heliotaxis. Sodium valproate and ethosuximide are the common drugs used. Even though benzodiazepines are useful, the specific effect of lorazepam is not mentioned. We report 5 cases of photosensitive epilepsy with inadequate response to usual antiepileptic drugs who had complete or near complete remission with lorazepam.
How to cite this article:
Oomman A, Madhusudanan M. Lorazepam : an adjuvant therapy in patients with seizure and heliotaxis. Neurol India 2001;49:317 |
Reflex epilepsies, although less common, have always evoked special interest due to their peculiar clinical presentations. Photosensitive or photic epilepsy is one of the reflex epilepsies. 5% of epileptics on intermittent photic stimulation (IPS) show photo convulsive response (PCR).[1] Pure photosensitive epilepsy indicates seizures occurring with flickering light. Patients have heliotaxis i.e. urge to seek out sunlight and hand-waving spells. We report the response of lorazepam in 5 cases of photosensitive epilepsy, poorly responsive to valproate.
The term photosensitive epilepsy was used in patients whose seizures occurred in response to various kinds of photic stimuli in everyday life. The clinical features included urge to seek sunlight (heliotaxis), hand waving across the face with or without generalised seizures. Patients who had no seizures with naturally occurring photic stimuli, but who showed PCR on IPS, were not included. Five patients with photosensitive epilepsy resistant to treatment with high doses of sodium valproate were evaluated. Lorazepam, 1 mg/day, was started and subsequently increased to 2mg/day.
Case 1 : J, a 17 year old female on treatment for photosensitive epilepsy was reassessed. At the age of 8 years, she was noticed to be unduly attracted to the sun, followed by hand waving across the face. There was no precipitation with TV or artificial light. Later episodes were followed by generalised tonic clonic seizures. There was no history of febrile seizure or family history of seizures. Clinical examination was normal. EEG showed asymmetrical slowing in theta range over the left temporal region, associated with sharp discharges. There was no PCR on IPS. She was on sodium valproate, 1000 mg/day. There was no relief of symptoms as far as heliotaxis was concerned. Lorazepam was added (1 mg/day increased to 2 mg/day). She became symptom free and valproate could be reduced to 200 mg/day. She was asymptomatic for the next 18 months.
Case 2 : VCM, a 55 year old labourer was having heliotaxis and hand waving for 40 years. Handwaving spells were mostly in the mornings and lasted 5-10 minutes. There was no ictal pleasure. Spells did not culminate in generalised seizures till 2 years back when he developed generalised seizures. He was put on valproate (400 mg/day). Seeing no response, the dose was subsequently increased to 1200 mg/day. Heliotaxis persisted, though generalised seizures did not recur. Physical examination and EEG were within normal limits. Lorazepam, 2 mg/day was added. There was complete relief of heliotaxis. The last episode occurred 16 months back when he discontinued his medicines.
Case. 3 : A, a 12 year old girl was having about 100 episodes of heliotaxis and hand waving/day, followed by unconsciousness, which could not be controlled by valproate (800 mg/day) and phenobarbitone (600 mg/day) for 4 years. She was born of caesarian delivery and had delayed mile stones. She could not attend school regularly because of frequent seizures. Physical examination and EEG were within normal limits. The frequency of seizure decreased to about 2-3 episodes per week on adding lorazepam (2 mg/day) .
Case 4 : RA, a 17-year-old student, had heliotaxis and hand-waving for 4 years. There was no pleasurable sensation. There was one episode of secondary generalised seizures. His EEG including IPS was normal. Sodium valproate alone , in a dose of 1200 mg/day could not control the episodes. He became symptom free on addition of lorazepam (2 mg/day) and had no further attacks.
Case 5 : N, a 14 year old male had heliotaxis and hand-waving for 9 years and generalised tonic clonic seizures (GTCS) following hand-waving spells for 2 years. His EEG, including photic stimulation, was normal. Although valproate in a dose of 1000 mg /day controlled GTCS, heliotaxis and hand-waving continued. Nitrazepam 10 mg/day was added but there was no response. Symptoms were totally controlled by lorazepam (2 mg/day). Nitrazepam was subsequently withdrawn. He was seizure free on follow up.
Historically, Apuleus[2] is credited with the earliest reference to photosensitivity. Gowers[3] in 1885 gave the first report of photosensitive epilepsy. The terminology of photosensitivity, photosensitive epilepsy and epileptics with photosensitivity created confusion. Doose et al[4] used the term 'photogenic
epilepsy' only when the seizures occurred with flickering light while those who had seizures without any light stimulus but showed a PCR during IPS were termed 'photosensitive'. Radhakrishnan et al[5] reported the geographical variations in the prevalence of PCR among epilepsy patients in Indian population. He reported a prevalence rate of 3.5% in South Indian population, compared to the 0.6% reported for North Indian epilepsy patients.
Jeavons and Harding[6] classified photosensitive subjects into 3 types: i) those with pure photosensitive epilepsy, i.e. with visually induced seizures only (40%). ii) epileptic patients with photosensitivity and spontaneous seizures, with or without known visually induced seizures (the majority). iii) photosensitive people without epilepsy. The age of onset of symptoms was reported to be between 8 and 19 years in 76%.[5] Our patients had a similar age of onset (5-15 years). There is a female preponderance[5],[6] and a hormonal influence has been suggested. However, in our study, there were more males (3 of 5). The precipitating environmental stimuli include, sun seen through trees or reflected on moving water, discotheque lighting, arcade games and television. In western countries, television is the commonest precipitating factor. But none of our patients' episodes were precipitated by television. All our patients had the urge to seek out sunlight which was described as 'heliotropism' by Ames[7] and 'heliotaxis' by Iyer et al.[8] The person stares at the sun or the light source, waving one hand across the face rapidly. It is controversial whether hand-waving is a part of the ictus.[9],[10],[11],[12] Self induced photosensitive seizures with ictal pleasure have been reported although the pleasure was absent in our cases.The most common type of seizure induced by flickering light is tonic clonic seizures. However, absences or myoclonic seizures can occur.
Demonstration of photosensitivity in the EEG laboratory depends on adequate apparatus and technique. The stimulus intensity should be atleast 100 nits/flash.[1] The stroboscope light should be centrally fixated. Red light is reported to be more epileptogenic than other colours or white.[1] The flash rate most likely to elicit a PCR is 15-18/s. Curiously none of our patients had PCR in the EEG, even though the incidence of PCR in patients with photic epilepsy has been reported to be 75%.[13] It is possible that the seizurogenic potential of intermittent natural light is different from that of artificial light. It is interesting to note that none of our patients had seizures induced by watching TV.
Treatment of photosensitive epilepsy includes various measures. Avoidance of epileptogenic stimuli may be helpful. Blue sunglasses are reported to be useful.[14] Every patient should be taught to cover one eye as an emergency measure on suddenly entering a brightly lit environment. Sodium valproate and ethosuximide are the most widely used drugs. The generalised seizures may be controlled but heliotaxis and PCR usually persist. Benzodiazepines have been tried. Effect of lorazepam on the EEG paroxysmal activity in epileptics has been studied[15],[16] and rapid reduction in paroxysms has been shown. However the role of lorezapam in photosensitive epilepsy which is not a common reflex epilepsy in India,[17] has not been stressed so far. Levetiracetem, an experimental drug, has shown an antiepileptic effect in the photosensitivity model.[18] But lorazepam if found to be effective in large scale trials may provide a cheap alternative in patients with drug resistant photosensitive epilepsy.
Photosensitivity persists in atleast two thirds of patients with photosensitive epilepsy.[12] EEG abnormalities to patterned IPS can be used to signify the persistence of photosensitive epilepsy, but abnormalities to diffuse IPS are more likely to indicate that the patient is poorly controlled and at risk of further seizures.[19]
| 1. | KasteleijnNolst Trenite DG : Photosensitivity in epilepsy. Electrophysiological and clinical correlates. Acta Neurol Scand Suppl 1989; 125 : 3-149.  |
| 2. | Apuleius (Quoted by Jeavons and Harding). |
| 3. | Gowers WR : (Quoted by Jeavons and Harding) Epilepsy and other chronic convulsive diseases. Their cause, symptoms and treatment. Wood and Co. NewYork. 1885. |
| 4. | Doose J, Giesier K, Volzke E : Observations in photosensitive children with or without epilepsy. Zeitschift fur kinderheilkunde, 1969; 107 : 26. |
| 5. | Radhakrishnan K, Nayak SD, Nandini VS et al : Prevalence of photoparoxysmal response among South Indian epilepsy patients. Seizure 1998;7 : 397-401. |
| 6. | Jeavons PM, Harding GFA : Photosensitive Epilepsy Clinics in developmental Medicine. No 56, Spastic International Medical Publication 1975; 3-105. |
| 7. | Ames FR : 'Self-Induction' in photosensitive epilepsy. Brain 1971; 94 : 781. |
| 8. | Iyer GV, Ram Manohar S, Manorama Devi TK : Photosensitive epilepsy. Neurol India 1979; 3 :110-122. |
| 9. | Livingston S, Torres IC : Photic epilepsy. Report of an unusual case and review of literature. Clin Paediat 1964; 3 : 304. |
| 10. | Harley RD, Baird HW, Freeman RD : Self-induced photogenic epilepsy -Report of four cases. Arch Ophthal 1967; 78 : 730. |
| 11. | Andermann K, Cook PM, Dickson J et al : Self induced epilepsy. Arch Neurol 1962; 6 : 49-65. |
| 12. | Faught E, Falgout J, Nidffer D et al : Self induced photosensitive absence seizures with ictal pleasure. Arch Neurol 1986; 43 : 408-410. |
| 13. | Benjamin G, Zifkin, Frederick Andermann : Epilepsy with reflex seizures In: The Treatment of epilepsy: Principles and practice, Wyllie E (Ed): Second edition. Williams and Wilkins. Baltimore 1997; 573-583. |
| 14. | Takahashi T, Tsukahara Y : Usefulness of Blue Sunglasses in Photosensitive Epilepsy. Epilepsia 1992; 33 : 517-521. |
| 15. | Harding GF, Edson A, Jeavons PM : Persistence of photosensitivity. Epilepsia1997; 38 : 663-669. |
| 16. | Scott D.F, Moffet A : Lorazepam : its effect on the EEG paroxysmal activity in patients with epilepsy. Acta Neurol Scand 1981; 64 : 353-360. |
| 17. | Saleem SM, Thomas M, Jain S et al : Incidence of photosensitive epilepsy in unselected Indian epileptic population. Acta Neurol Scand 1994; 89 : 5-8. |
| 18. | Kasteleijn - Nolst Trenite DG, Marescaux C, Stodieck S et al : Photosensitive epilepsy a model to study the effects of antiepileptic drugs. Evaluation of the Piracetam analogue, levetiracetem. Epilepsy Research 1996; 25 : 225-230. |
| 19. | Fylan F, Edson AS, Harding GF : Clinical significance of EEG abnormalities during photic stimulation in patients with photosensitive epilepsy. Epilepsia 1999; 40 : 370-372. |
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