Mood disorders sleep disturbances

Adverse effects of ACE inhibitors include hypotension, dizziness, headache, fatigue, GI disturbances, bad taste in the mouth, persistent dry cough, skin rashes, renal impairment, hypokalemia, and blood disorders. ACE inhibitors also can cause chest pain, palpitation, tachycardia, abdominal pain, cholestatic jaundice, alopecia, mood and sleep disturbances, and impotence. 

Neurological adverse effects of ciclosporin have been reported in up to 39% of all transplant patients. Most are mild. The most frequent is a fine tremor, the mechanism of which is not known. From many case reports or studies in transplant patients, the pattern of ciclosporin neurotoxicity ranges from common and mild to moderate symptoms, such as headaches, tremors, paresthesia, restlessness, mood changes, sleep disturbances, confusion, agitation, and visual hallucinations, to rare but severe or hfe-threatening disorders, including acute psychotic episodes, cerebellar disorders, cortical blindness (permanent in one report), spasticity or paralysis of the limbs, catatonia, speech disorders or mutism, chorea, seizures, leukoencephalopathy, and coma (SED-13,1124) (SEDA-16, 516) (SEDA-17, 520) (SEDA-20, 343) (SEDA-21, 383) (17-19). 

Depression is one of the most common psychiatric disorders. It is characterized by feeling of intense sadness, helplessness, worthlessness, and impaired functioning. Those experiencing a major depressive episode exhibit physical and psychological symptoms, such as appetite disturbances, sleep disturbances, and loss of interest in job, family, and other activities usually enjoyed. A major depressive episode is a depressed or dysphoric (extreme or exaggerated sadness, anxiety, or unhappiness) mood that interferes with daily functioning and includes five or more of the symptoms listed in Display 31-1. 

Disturbances of sleep are typical of mood disorders, and belong to the core symptoms of major depression. More than 90% of depressed patients complain of impaired sleep quality [60], Typically, patients suffer from difficulties in falling asleep, frequent nocturnal awakenings, and early morning awakening. Not only is insomnia a typical symptom of depression but, studies suggest, conversely, insomnia may be an independent risk factor for depression. In bipolar disorders sleep loss may also be a risk factor for the development of mania. Hypersomnia is less typical for depression [61] and, in contrast to insomnia, may be related to certain subtypes of depression, such as seasonal affective disorder (SAD). 

Compared to controls, 41 MEK workers with an average of 14 years exposure exhibited significantly lower motor nerve conduction velocities in the median, ulnar, and peroneal nerves irritation of the eyes and upper respiratory tract and a neurotoxic syndrome characterized by mood disorders, irritability, memory difficulties, sleep disturbances, headache, and numbness were also more prevalent in the exposed workers/... 

Bipolar affective (manic-depressive) disorder occurs in 1-3% of the adult population. It may begin in childhood, but most cases are first diagnosed in the third and fourth decades of life. The key symptoms of bipolar disorder in the manic phase are excitement, hyperactivity, impulsivity, disinhibition, aggression, diminished need for sleep, psychotic symptoms in some (but not all) patients, and cognitive impairment. Depression in bipolar patients is phenomenologically similar to that of major depression, with the key features being depressed mood, diurnal variation, sleep disturbance, anxiety, and sometimes, psychotic symptoms. Mixed manic and depressive symptoms are also seen. Patients with bipolar disorder are at high risk for suicide. 

Mental disorders, also called affective disorders, are multi-level, multi-scale and multiple-system diseases (Fig. 7.1). Mental disturbances generally go along with disturbances of autonomous functions. These essentially are (1) sleep disturbances, both sleep duration and sleep pattern, and (2) disturbances of the hypothalamic-pituitary-adrenal (HPA) axis, the so-called stress axis with elevated cortisol levels. It can be expected that disturbances of autonomous control systems as well as mood are caused by neuronal malfunctioning which may concern practically all neuronal levels systemic interactions, neuronal network connections, single neuron dynamics, synaptic transmitters and/or receptors, ion channels, second messengers, and gene expression (Fig. 7.1a). Nevertheless, despite a manifold of data, there are only vague ideas so far about the differences in neuronal dynamics in the brain of a chronically depressed person compared with a person with a sensitive but balanced mood. 

Monitoring mood symptoms of a patient experiencing a sleep disturbance after a significant loss or during a difficult time is important to prevent a long-term problem with insomnia and to provide appropriate therapy if a mood disorder occurs. 

Melatonin has been used to regulate the sleep-wake cycle and is used often to treat insomnia. It is not recommended during pregnancy and breast-feeding becanse of a lack of information abont its safety. Lower doses of melatonin (e.g., 0.1-1 mg at bedtime) are effective in initiating sleep higher doses may not improve the hypnotic effect. The rednction in daytime snnUght, which increases melatonin secretion, may exacerbate PMS in the winter this type of seasonal mood disorder may respond to phototherapy. Early sleep deprivation also may help to correct circadian rhythm disturbances in PMDD. ... 

Psychological disorders related to working conditions include sleep disturbances, mood disturbances, reduced motivation to work or recreate, somatic and psychosomatic compleiints, neuroses, psychoses, and dysfunctional coping behavior. The effects of stress on an individual are influenced by the nature of the exposures and the individual s physical and psychological characteristics and coping behaviors that may accentuate or mitigate the exposure. 

Depression Common mood disorder that involves severe and persistent sadness, lack of interest in pleasurable activities, suicidal thoughts, and physical symptoms, such as sleep disturbance, loss of appetite, and reduced sexual desire. 

Another approach considers the effects of various ligands on their receptors located in the diencephalic and mesiotemporal areas. Cell clusters in the hypothalamus coordinate the normal regulation of the vegetative functions of sleep, appetite, and sexual drive, which are typically disrupted in severe depression. In addition, the limbic area modulates many aspects of behavior and mood that are characteristically disturbed in affective disorders. 

The diagnosis of depression still rests primarily on the clinical interview. Major depressive disorder (MDD) is characterized by depressed mood most of the time for at least 2 weeks and/or loss of interest or pleasure in most activities. In addition, depression is characterized by disturbances in sleep and appetite as well as deficits in cognition and energy. Thoughts of guilt, worthlessness, and suicide are common. Coronary artery disease, diabetes, and stroke appear to be more common in depressed patients, and depression may considerably worsen the prognosis for patients with a variety of comorbid medical conditions. 

One unexpected observation, which I will discuss in chapter 10, is that some SSRI drugs that potentiate the serotonin system in favor of enhanced mood in depression cause disturbingly long-lasting alterations in REM sleep physiology, and these alterations sometimes cross the border into the REM sleep behavior disorder. 

For further progress towards mechanisms based models, such phenomenological descriptions shall also be examined in context with disease-related disturbances of autonomous functions. This mainly concerns disturbances of sleep-wake cycles and cortisol release which are the most reliable biological markers of mental diseases, especially major depression, and can provide objective and quantifiable parameters (e.g. EEG frequency components, cortisol blood level) for the estimation of an otherwise mainly subjective and only behaviorally manifested illness. Moreover, there is a manifold of data which interlink the alterations of the autonomous system parameters (sleep states, cortisol release) with alterations of neural dynamics. Therefore, the most promising approach also to understand the interrelations between neural dynamics and affective disorders probably goes via the analysis of mood related disturbances of autonomous functions. 

The significant meshing of the neuronal control areas for sleep and hormone release and their connections to mood relevant brain areas suggest that functional interdependencies also exist and that these also become evident in the system disturbances. The block diagram in Fig. 7.5 mainly emphasizes on the parts which are of particular relevance for those autonomous parameters which are the most clearly accessible markers of mental disorders the increased blood cortisol level and changes of the sleep EEG pattern. 

In mental disorders, in contrast to other neural diseases like epilepsy or Parkinson s disease, not much is known about the relevant alteration of neural dynamics. It can be just assumed from the pa lien I s inappropriate environmental responsiveness that neuronal adaptability and flexibility are disturbed, accompanied by a changed neuronal sensitivity on external stimuli. Fortunately, there is more information with regard to the neural control of sleep-wake cycles and cortisol release, which are very reliable biological markers of mental disorders and therefore may provide a link for a better understanding also of the neuronal dynamics which control mood. 

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