Circadian (24-hour) rhythms are important to the practice of medicine. The phasing and amplitude of key physiologic and biochemical circadian rhythms contribute to predict in-time patterns in the manifestation and exacerbation of most medical conditions. Moreover, body rhythms can significantly affect responses of patients to diagnostic tests and medications. Rhythmicity in the pathophysiology of medical conditions is the rationale for chronotherapeutics—the purposeful variance of the concentration of medicines in synchrony with biological rhythm-determinants of disease activity—to optimize treatment outcomes. This article discusses the concept of biological time structure and its relevance to the practice of medicine, with a focus on neurologic issues.

Seasonal affective disorder (SAD) is a form of depression that starts in the fall and ends in the spring. This article reviews existing theories about the relationship between circadian rhythms and the disorder. Recent research indicates that as with pharmacologic antidepressants, at least 2–4 weeks are needed to demonstrate the effectiveness of bright-light therapy compared to placebo. The response to such treatment is strongest with precisely timed light exposure: treatment is optimal during the morning hours when the circadian systemt is susceptible to phase advance. Such clinical improvement is correlated with the magnitude of the phase shift induced. These observations suggest a model of circadian function in SAD and provide important guidelines for its treatment.

Biological aging is often associated with sleep problems and daytime napping. Complaints of difficulty in initiating and maintaining sleep, as well as daytime drowsiness, are more common in the elderly than in any other age group. This report reviews evidence that impaired melatonin secretion is associated with sleep disorders in old age. Circulating melatonin levels have been found to be significantly lower and onset and peak times have been delayed in elderly insomniacs as compared to age-matched control subjects. In view of these findings, we investigated the effects of melatonin treatment on melatonin-deficient insomnia in the elderly. From the results of our study, it seems likely that melatonin replacement therapy may be beneficial in the initiation and maintenance of sleep in this population.

Sleep problems, day somnolence, and fatigue as a result of psychotropic drugs are very common. Psychiatrists usually consider these effects a result of insomnia and treat them by prescribing sleeping pills or other benzodiazepine agents.

We describe here 10 cases of circadian rhythm sleep disorders (CRSD)—and not merely insomnia—as a possible side effect of fluvoxamine (FVA). Two other serotonin reuptake inhibitors, fluoxetine and clomipramine, did not induce CRSD in any of these 10 patients. We speculate that FVA-induced CRSD is caused by the effect of FVA on serotonin and melatonin levels in the central nervous system.

CRSD as a side effect of FVA can be treated by replacing the suspected FVA or adding melatonin to a beneficial FVA treatment. Thus, it is important to be aware of possible iatrogenic CRSD in order to treat appropriately. Prospective studies are needed to confirm our observation and to study the influence of other psychotropic drugs on sleep-wake schedule.

Studying brainstem auditory evoked potentials (BAEPs) and comparing the specific waves in smokers vs nonsmokers in both positive- and negative-symptom schizophrenia may elucidate the role of smoking in information processing. BAEPs were recorded in 40 patients with schizophrenia; 20 had predominantly positive symptoms (10 smokers and 10 nonsmokers) and 20 had predominantly negative symptoms (10 smokers and 10 nonsmokers). The severity of positive and negative symptoms was assessed by scale of assessment of positive symptoms and scale of assessment of negative symptoms (SANS). The BAEP results were compared with 15 healthy control individuals matched with the patients by age, sex, and cultural background. The smokers with negative symptoms showed a significant increase in the alogia, summary, and composite scores of SANS as compared to the nonsmokers. Although, most of the BAEP abnormalities were among patients with positive symptoms. The effect of smoking on the BAEPs was only in patients with negative symptoms.

We also studied the interaction between smoking factor (smokers vs nonsmokers) and group type (group with mostly positive symptoms vs group with mostly negative symptoms) on the BAEPs and found a significant difference only for the first-wave latency mainly on the right side (P=0.012). The absence of a significant effect of smoking on most of the parameters of the BAEPs on interaction with the group factor suggests that the effect of smoking on the BAEPs is more apparent when negative symptoms prevail. However, studies are warranted to substantiate this finding.