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Zolpidem is a new imidazopyridine hypnotic with a pharmacological profile substantially different from benzodiazepines. In this observational multicenter study the possibility of shifting to zolpidem (10 mg at N1, 15 or 20 after N1) insomniac patients previously taking (for at least 15 days and not longer than 3 months) standard posology of triazolam (0.125-0.25 mg), lorazepam (1 mg) or lormetazepam (1 mg) was assessed. For ethical reasons the patients were mandatorily to be insomniacs despite their taking hypnotics or not tolerating them. Patients enrolled were 299 of whom 276 evaluable (139 males and 136 females; mean age 48.67 +/- 14.64, range 18-83). Study duration was 7 nights with visits at N0 (baseline), N1 (after 1st night), N3 (after 3rd night) and N7 (final evaluation); on each visit the Saint Mary Hospital Sleep Questionnaire and the benzodiazepine withdrawal symptom's rating scale were administered; moreover, after N7, investigators were asked a judgement of feasibility of such a shift. In 229 (83.5%) out of 274 patients such a shift to zolpidem was considered successfully (no occurrence of symptoms and/or signs of previously taken hypnotic withdrawal); in the remaining 45 patients, just 17 (6.2%) seemed to be real unsuccessful cases (reactions mild and transient, anyhow). In conclusion abrupt shift to zolpidem appeared to be largely feasible in the patients studied.

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The Authors investigated the sensitivity of the ecg thoracic derivations of Condorelli in detecting non-Q myocardial infarction demonstrated by 2-D echocardiography and 201-TL scintigraphy. This technique showed a good reliability, allowing a useful diagnostic approach.

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Two multicentre studies are described here; the first compared moclobemide with mianserin and the second with maprotiline, both in elderly patients with a DSM-III diagnosis of major depressive episode. In the first study, 80 eligible patients were randomized to either moclobemide 300-500 mg or mianserin 75-125 mg per day for 4 weeks. Mean reduction in Hamilton Rating Scale for Depression (HRSD) score was 52% in both groups. The overall assessment of efficacy was good or very good for 60% of the patients, and tolerance was considered good or very good for 85% of the patients in both groups; no significant differences between the 2 treatments were seen. The second study comprised 39 hospitalized patients randomized to either moclobemide 150-300 mg daily or maprotiline 75-150 mg daily for 6 weeks. At the end of treatment, HRSD scores declined 85% in both groups compared with baseline. The overall assessment of efficacy was over 90% good or very good in both groups. Tolerance was rated good or very good for 80% of moclobemide and 75% of maprotiline patients; none of these results differed significantly between the groups, indicating that moclobemide is as effective in elderly patients as the 2 second-generation antidepressants. In view of the safety of moclobemide, it should be considered first-line therapy for depression in elderly people.

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The most important current problem in the treatment of Parkinson disease in the so-called L-dopa long-term-treatment syndrome. We present here the results of our experience with Madopar HBS in the treatment of two groups of patients suffering from L-dopa long-term treatment syndrome. In the first study we replaced the standard Madopar with Madopar HBS. In the second study, after identifying the most disabling "off" periods, we added Madopar HBS to the previous treatment in such a way as to control these "off" phases. Our study suggests that Madopar HBS is useful in reducing typical fluctuation phenomena in the majority of patients.

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Results obtained in 22 patients with Parkinson's disease in whom treatment with standard Madopar was replaced by Madopar HBS, a CR formulation of the same product, are presented. All the patients presented with dyskinesia and akinesia phenomena related in part to the L-dopa treatment and in part to the disease itself. In 20 patients replacement of the standard agent by HBS led to a distinct improvement in the clinical condition and a significant reduction of the 'on-off' phenomenon. However, with the new formulation the dosage had to be increased by 86% on average as compared with standard Madopar. In 6 of the 22 patients treatment with the HBS formulation has continued for over 6 months and is still giving very good results.

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A double-blind closed sequential scheme study was carried out in 82 patients with insomnia to compare the hypnotic effectiveness of 15 mg midazolam and 1 mg lorazepam. Pairs of randomized patients were treated on one and the same night with midazolam or lorazepam, respectively. Eight parameters were recorded for each member of the pair. The time taken to fall asleep, the duration of sleep and the overall assessment of response showed that midazolam was significantly superior to lorazepam: the number of awakenings and evaluation by the patient verged on statistical significance. Both drugs were equal for the quality of sleep, dreams and the patient's condition on awakening. No side-effects were observed in any of the patients.

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The Authors describe a case of aphasia acquired in childhood together with epilepsy (syndrome of Landau and Kleffner) and treated for seven years. The patient had simple and complex partial attacks, motor dysphasia, frequent and heavy headache, and electroencephalographic paroxysmal anomalies with multifocal distribution. While the disease evolved with regression of disphasia and epilepsy, the EEG alterations persisted. In view of similar cases reported in the literature and the present treatment the Authors feel that syndrome is an inflammatory disease, its evolution being slow. The results of neuroradiological investigations support such hypothesis. The prognosis is poor (anomalies of speech persisted in 2 out of 3) and further studies are essential. A systematic use of cerebral biopsy is suggested.

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The authors describe two cases of "reading epilepsy" followed for nine and seven years respectively. In the first case the seizures consisted in an alexic aura followed by secondary tonic clonic convulsion; in the second case the seizures consisted in jaw clenching followed by loss of consciousness. In both patients neuroradiological studies including C.T. were negative and in both the seizures were controlled by anti-epileptic treatment. Clinical and electro encephalographic features tended to differ in the two cases and the authors review the literature on the subject. These observations led to recognise three groups of reflex epilepsy as follows: the first group includes focal secondary generalised seizures with parieto-occipital spikes and spikes and waves in parieto-occipital lobes; the second group includes seizures starting with jaw clenching corresponding with bursts of posterior sharp-waves; the third group consists of endogenous cases which can not be included in the other two groups.

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