Nimodipine was administered at the daily dose of 90 mg po, for 30 days, to ten chronic undifferentiated schizophrenics, eight men and two women, aged 31-35 years, maintained on previously longlasting neuroleptic treatments. In five patients, a placebo period of 15 days preceded the administration of the drug. Monitoring of psychiatric symptomatology by the Brief Psychiatric Rating Scale (BPRS) revealed significant nimodipine-induced improvement. However, the Andreasen Rating Scale for Positive Symptoms (SAPS) showed favourable effects only in the five patients who had not received placebo, while in the others both SAPS and the Andreasen Rating Scale for Negative Symptoms (SANS) showed no significant effect of therapy. The Tardive Dyskinesia Scale revealed no improvements of neurological symptoms after either placebo or drug treatment. Measurement of plasma MHPG concentrations revealed no significant changes induced by either placebo or nimodipine, while HVA plasma levels showed a trend toward decrease, and prolactin a trend toward increase, after nimodipine.

A thirty-eight year old woman, suffering from schizoaffective disorder for approximately 17 years, improved significantly with the association of clozapine (CPZ) and nimodipine.

ABSTRACT

There is evidence for an association between vascular disease and depression, and in particular between cerebrovascular disease and depression, especially that occurring later in life. Among the diverse psychiatric diseases, the one which is most widely studied concerning the relationship with the vascular system, is depression. The risk relationship between depression and vascular events is a two-way road: the presence of depression increases the cerebrovascular and cardiovascular event risk (worsening its evolution and prognosis, as well) and a patient evidencing cerebrovascular or heart disease, will also show an increase in the risk of suffering depression (Taragano et al., 2005). Depression is a common cause of disability in the elderly. It reduces quality of life and represents a serious public health problem (Beekman et al., 2001; Steffens et al., 2000). Its prevalence in late life is 2–3% for major depression and 12–15% for all depressive syndromes (Beekman et al., 1999).

Background: Cerebrovascular disease may cause “vascular depression” (VaD). Calcium-channel blockers are presumed treatments for cerebrovascular disease and might be expected to improve depression and prevent recurrence.

Objective: To examine the efficacy and tolerability of the use of nimodipine as an augmentation of fluoxetine in the treatment of VaD.

Design: A double-blind, randomized clinical trial in which 101 patients with VaD (Alexopoulos criteria) were treated with fluoxetine at standard doses. Patients were randomized to placebo (n=51) or nimodipine (n=50). Treatment outcomes were assessed using the Hamilton Depression Rating Scale (HDRS) regularly up to 8 months after treatment initiation.

Results: Depression was reduced in 63% of patients, but those whose treatment was enhanced with nimodipine had greater improvements overall by repeated measures analysis of covariance (ANCOVA) (F(1.80)=9.76, p=0.001). In addition, a greater proportion of patients treated with fluoxetine–nimodipine (54% vs. 27%) exhibited full remission (χ2(d.f. 1)=7.3, p=0.006), with the number needed to treat (NNT) equal to 4 (95% CI 2–12). Of those experiencing full remission in the first 61 days, fewer patients on fluoxetine–nimodipine (3.7%) developed recurrence of major depression as compared to those on fluoxetine alone (35.7%) (χ2(d.f. 1)=7.56, p=0.006), NNT 3 (95% CI 2–9). Side-effects were noted in 33.3% of patients in the control group and 48% of the experimental group (χ2(d.f. 1)=2.25, p=0.133).

Conclusions: In treating VaD, augmentation of fluoxetine with nimodipine led to better treatment results and lower rates of recurrence. These findings support the argument that augmentation of antidepressant therapy might be helpful in the treatment of cerebrovascular disease, which is involved in the pathogenesis of this type of depression.

Nimodipine, a calcium channel blocking drug, is used in the treatment of cerebral arterial spasm after subarachnoid haemorrhage due to bleeding from an intracranial aneurysm. The purpose of this study was to evaluate the effects of nimodipine on neuromuscular blockade after vecuronium had been given to facilitate tracheal intubation and maintenance of muscle paralysis in patients undergoing clipping of intracranial aneurysm. Twenty patients were divided into two groups: a control group (n = 10) who received no calcium channel blocking drug, and a nimodipine group (n = 10) consisting of patients treated with nimodipine at clinically used doses of 0.03 mg kg−1 h−1 pre- and perioperatively. Anaesthesia was induced with atropine 10 μg kg−1, dehydrobenzperidol 5 mg, fentanyl 5 μg kg−1, thiopental 5 mg kg−1 and maintained with a mixture of N2O and isoflurane (0.5–1% inspired concentration) in O2, and additional doses of fentanyl 2.5 μg kg−1. Neuromuscular responses were monitored by acceleromyograpy. The first twitch of the train-of-four response (T1) was considered as twitch height.After a stabilization period, an intubating dose of vecuronium 0.1 mg kg−1 was administered. The onset of action, the time of first appearance of T−1 and clinical duration of action were recorded. Then, maintenance doses of vecuronium 0.03 mg kg−1were administered twice more when T1 had recovered to 25% of control twitch height. The study ended when the recordings of the 3rd 25% T1 recovery had been obtained. There were no statistical differences in the onset time (120±44 s in the control group, 141±33 s in the nimodipine group), in the first appearance time of T1 (28±6 min in the control group, 30±8 min in the nimodipine group), and in the times for 25% recovery in T1 (41±11, 32±2, 40±13 min in the control group, respectively, and 44±16, 36±15, 38±15 min in nimodipine group, respectively) between the groups studied. The time between the injection of the intubating dose of vecuronium and the third recovery of T1–25% of control was not significantly different between the control group (113±34 min) and the nimodipine group (117±42 min). This study indicates that nimodipine does not have any significant effect on the time course of action of vecuronium including the onset time and its clinical duration of action after the initial and the two maintenance doses in these patients.