Central pontine myelinolysis (CPM) is a demyelinating disease of the pons often associated with demyelination of other areas of the central nervous system (CNS). The term ‘osmotic demyelinization syndrome’ is used for pontine and extrapontine myelinolysis. In this paper, we are concerned with CPM although the extrapontine one is based on the same pathogenesis. Both share the diagnostic methods, and their prevention and therapy are the same. The etiology and pathogenesis of this disorder are unclear and will be discussed. However, almost all cases of CPM are related to severe diseases. Chronic alcoholism is still the most common underlying condition of CPM patients. In the literature, 174 cases of CPM have been reported in alcoholics since 1986, which is equivalent to an incidence of 39.4%. Likewise, 95 cases of CPM following the correction of hyponatremia have been documented since 1986 (21.5%). The role of hyponatremia and its correction will be outlined in the discussion of the pathogenesis of CPM. The third largest group of CPM cases are liver transplant patients (17.4%), with the development of CPM being attributed to the immunosuppressive agent cyclosporine in particular. Depending on the involvement of other CNS structures, the clinical picture can vary considerably. The large-scale introduction of magnetic resonance imaging has increasingly facilitated the antemortem diagnosis of CPM, although the radiological findings lag behind and do not necessarily correlate with the clinical picture. As yet, there is no specific therapy of choice. A number of therapeutic approaches have been tested and although they have not been compared with regard to their rate of success, they have all led to a substantial improvement in the prognosis of CPM.

Background and Purpose-We performed a double-blind, placebo-controlled study to investigate the effectiveness of amitriptyline for the prophylactic treatment of patients with acute thalamic stroke in preventing central poststroke pain. Methods-Subject received, in a randomized sequence, either amitriptyline titrated from 10 to 75 mg in extended-release form or placebo over a therapy period of 365 days. We documented the time when pain developed; the intensity, type, site, and distribution of pain; and the presence/absence and type of allodynia. Results-Thirty-nine patients (23 women and 16 men; age range, 36 to 68 years) with central poststroke pain participated.The placebo group showed a pain rate of 21% within 1 year after the diagnosis of thalamic stroke compared with 17% in the group under prophylactic treatment with amitriptyline. Average (SE) time to pain was 318 (23) days for patients in the placebo group and 324 (24) days for patients in the amitriptyline group. Conclusions-With the achieved sample sizes of this study and a pain rate of approximately 21% in the placebo group, any near-perfect pain protection would have been detected. Near-perfect pain protection, in this context, refers to pain in Ͻ2.4% of the recruited patients treated with amitriptyline or in approximately 89% of placebo-treated patients. Larger studies are recommended to test the hypothesis that prophylactic amitriptyline reduces but does not completely prevent central poststroke pain. Key Words: amitriptyline Ⅲ antidepressive agents Ⅲ cerebrovascular accident Ⅲ pain Ⅲ thalamic diseases C entral poststroke pain (CPSP) was first described by Dejerine and Roussy 1 in 1906 as a spontaneous pain after a thalamic stroke. It has been known as "thalamic pain syndrome" for decades, and its management is still a challenge for treating physicians today. Since the discovery of the effects of carbamazepine and tricyclics, these substances have been used in the treatment of CPSP. In a carefully controlled trial performed in 15 patients with CPSP, the authors were unable to demonstrate a statistically significant effect of carbamazepine, whereas amitriptyline produced a statistically significant reduction of pain compared with placebo. 2 Thus far, no studies on CPSP have been published to answer the question of whether treatment at the beginning of stroke demonstrates a prophylactic effect in preventing central pain mechanism. The primary objective of this study was to evaluate, under controlled conditions, the efficacy of amitriptyline for preventing CPSP. We performed a placebocontrolled, double-blind study to determine whether amitriptyline at an increasing dose could significantly reduce CPSP in patients with thalamic stroke. Subjects and MethodsThe study was performed as a randomized, double-blind, placebocontrolled trial. Patients were randomized after they had provided informed consent to administration of amitriptyline or placebo within the first day after the onset of stroke was diagnosed. The study medication was slowly titrated from 10 t...

The effect of sumatriptan has not been previously described in the treatment of the headache of meningitis, although this headache has similarities to migraine. This study presents the clinical features of two patients who had fulminant bacterial meningitis with migraine-like headache and who experienced no improvement in headache intensity after administration of sumatriptan 6 mg s.c. On these grounds the lack of response of this type of headache to sumatriptan is discussed.

The effect of sumatriptan has not been previously described in the treatment of the headache of meningitis, although this headache has similarities to migraine. This study presents the clinical features of two patients who had fulminant bacterial meningitis with migraine-like headache and who experienced no improvement in headache intensity after administration of sumatriptan 6 mg s.c. On these grounds the lack of response of this type of headache to sumatriptan is discussed.

Austria is one of the countries, in which ergots are still the most commonly used acute anti-migraine drugs. Overuse and chronification is a clinical problem for ergots, but also for the recently developed triptans. In a retrospective study for the year 1999 we evaluated clinical data from all Austrian neurological hospitals including cost of withdrawal as well as the estimated cost for ergots and triptans on the pharmaceutical retail market. We identified a total of 96 patients that underwent withdrawal, all of whom because of ergot overuse, and some with considerable long-term side-effects. The cost of withdrawal (more than 1300 000) together with direct cost of medication amounted to more than 11 million. In contrast, cost of medication for triptans was 12.8 million for the same year, without any cost for withdrawal. If only cost aspects were to be considered in the prescription of acute anti-migraine drugs, our data would suggest to choose ergots rather than triptans. However, as scientific evidence is clearly in favour of triptans, decision making for the prescribing clinicians is more complex and will primarily focus on optimizing patient care, but also depend on the respective socio-economic situation.