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MEDICATION FOR NARCOLEPSY
This is a literature survey intended as a source of background information for members of the Narcolepsy Association (U.K.) (UKAN) and for family medical practitioners not familiar with the current research and treatment planning. Information in this publication is derived from the following sources: publications of the American Narcolepsy Association (ANA and of its counterpart in Germany, the Deutsche Narcolepsie Gesellschaft (NG); recent monographs by medical specialists; and a study of research literature. Details of the drugs in Appendix II have been checked with the British National Formulary (B N F).
READERS ARE REMINDED THAT RESPONSIBILITY FOR PRESCRIBING MEDICATION RESTS WITH THE PATIENT'S DOCTOR AND THOSE SPECIALISTS WHOSE GUIDANCE THE DOCTOR HAS SOUGHT.
THE NATURE OF NARCOLEPSY
Narcolepsy is a chronic neurological disorder which interferes with the patient's normal functioning during his/her daily activities through one or more of the characteristic symptoms of narcolepsy described in Appendix I, namely:-
It is rare for all the symptoms to appear at the same time. Both the frequency and severity of their manifestations change with time, and differ greatly from case to case. As far as is know, Narcolepsy is not curable. Efective management of the disorder, however, is now well established, whereby the patient's performance and behaviour is brought within the range of what is exhibited by normal people of phlegmatic disposition. In milder cases, this may be achieved without medication simply by a change of occupation and living habits. Even in the more severe cases where drug treatment is indispensable such changes should be made if at all possible.
CHANGES OF LIFESTYLE
There is ample clinical evidence that the disabling effects of narcolepsy are markedly reduced and drug treatment rendered more effective in the long run by adopting the following measures:-
GENERAL MEDICAL GUIDELINES
The aim of the prescribed drug treatment is to ensure uninterrupted wakefulness in daytime and sound sleep at night. Most drugs in use are effective against either EDS or CA, but all have side-effects that restrict prolonged use or higher dosage. Patients' responses to particular drugs vary greatly and a drug's effectiveness may change with time, either through habituation or because of fluctuations in the severity of the disorder.
One also needs to allow for interactions between these drugs and anything prescribed for other ailments the patient may be suffereing from. For all these reasons, treatment has to be tailored to individual needs, and the appropriate regime takes time to find. A willingness to try more than one drug, dose and schedule is required, and even when a suitable one is found, treatment still needs to be kept under review. Results depend critically on both understanding and good communication between patients and physician.
TREATMENT OF EDS
Fo a long time the amphetamine group of central nervous stimulants has provided the drugs at first choice - despite their well-known tendency to cause dependence and psychotic states, a readily developed tolerance and other troublesome side-effects. The only amphetamine currently available in the UK is Dexamphetamine Sulphate (*Dexadrine). Methylphenidate (*Ritalin) has been the first choice for replacement of amphetamines, having fewer adverse side-effects; but this is no longer available for new patients. Pemoline (*Volital), one of the milder stimulants, is prescribed in the USA and found effective in the less severe cases of EDS.
In the UK the drug currently preferred is Mazindol (*Teronac), an appetite suppressant. This acts like amphetamines on EDS but without the side-effects of habituation, mood changes or increase in blood pressure. The arousal action of all drugs lasts about six hours, so they should not be taken in the evening, otherwise insomnia ensues, rebounding on the following day's EDS.
Canadian and German investigators have reported on the effective long-term treatment with Propranolol Hydrochloride (*Inderal), well-known in the treatment of raised blood pressure. It's advantages over the stimulants lies in non-impairment of night-time sleep and the absence of habituation. Good results have also been reported with Selegiline (*Elderpryl), a drug used in the treatment of Parkinsonism.
TREATMENT OF CA
All the drugs in use belong to the (tri)-cyclic antidepressant group with Cloripramine Hydrochloride (*Anafranil) as the drug of first choice in the UK. Impramine (*Tofranil), Desipramine (*Pertafran) and Protriptyline (*Concordin) are alternatives with progressively less sedative side-effects. The sedative effect can be turned to advantage by some patients, for whom a single dose at night is adequate for the control of cataplexy, and this helps to suppress DNS as well. By contrast, Viloxazine (*Vivalan) is midly stimulating and suits better those patients whose cataplexy is controlled best by a morning and midday dose.
The side-effects of prolonged intake of all these drugs include constipation, difficulty with passing urine, interference with the male sexual function and, in high dosage, cardio-vascular effects, including tachycardia, arrythmicity, and postural hypotension. Periodic 'drug holidays' may be necessary to reverse these side-effects, but cessation must not be abrupt, otherwise there is a risk of provoking a prolonged bout of cataplexy which can extend over several days.
TREATMENT OF DNS
This presents difficulties because of the conflict with EDS. Inevitably, daytime catnapping and taking stimulant drugs can contribute to night-time sleeplessness. Likewise drugs to tackle insomnia tend to aggrivate EDS the following day. If fully effective EDS medication is paramount and DNS is so troublesome that it undermines the action of the EDS medication, one can resort to the intermittent use of Temazepam (*Normison), the preferred drug for insomnia, as it has the shortest action and causes least drowsiness the next day.
Recent Canadian research speaks well of a combination of Dexamphetamine in the morning and Gammahydroxybutyrate (1 gram) at bed time (repeated, if necessary, during the night). Reputedly, this has resulted in satisfactory management of both EDS and DNS, with suppression of both CA and HH. Some of the 48 patients treated have been on the regime continuously for nine years.
Detailed information on the afore-mentioned drugs, with recommended doses and cautions are set out in Appendix II.
REFERENCES
(1). Narcolepsy: A non-medical presentation. Published by ANA, PO Box 1187, San Carlos, CA 94070, USA.
(2). W.C. Dement & W.P. Baird - Narcolepsy: Care & Treatment. Publ. as (1).
(3). K. Meier-Ewert - Die Medikamentőse Narcolepsie-Therapie. 'Der Weker', No.7, May 1987, pp 7-15. Published by DNG, Tennenkruppenstr. 19, 3500 Kassel.
(4). J.D. Parkes - Sleep and its Disorders. Publ. by W.B. Saunders, 1985, London & Philliadelphia.
(5). British National Formulary No.14/1987. Publ. by BMA and Pharm. Soc. GB Please update as required.
(6). P. Parish - Medicines: A Guide for Everybody. Penguin Reference Books.
(7). J. Shindler et al. - BMJ Vol. 290 (1985) pp 1167-70.
(8). K. Meier-Ewert et al. - Sleep, Vol. 8, No.2, (1985) pp 95-104.
(9). C. Guilleminault et al. - Sleep, Vol. 9, No.1, (1986) pp 275-279.
(10). M. Mamelak et al. - Sleep, Vol. 9, No.1, (1986) pp 285-289.
(11). S. Ijema et al. - Sleep, Vol. 9, No.1, pp 265-268.
- SYMPTOMS OF NARCOLEPSY - APPENDIX I (Under Construction - No Link)
- Narcolepsy - A Laymans Guide
- Members & Readers share their experiences with us
- Kharm Shares personal experiences (Under Construction - No Link)
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