Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030567 (Parkinson's disease)
 63,064 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a 39-year-old man with Parkinson's disease and a history of anxiety disorders, anxiety-provoking situations such as group psychotherapy precipitated panic attacks and caused pronounced worsening of the parkinsonian symptoms. Extra doses of carbidopa-levodopa failed to control the intensified symptoms. During a 1-month hospitalization period, the anxiety disorders diminished when a combination of psychotherapy, behavioral therapy, and desipramine was used; however, the relationship between increased anxiety and worsened parkinsonian symptoms persisted. In patients with refractory Parkinson's disease, clinicians should consider the possibility of the presence of an anxiety disorder that may be affecting the neurologic condition.
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PMID:Parkinson's disease complicated by anxiety. 360 42

Monoamine oxidase is an iron containing enzyme that exists as 2 isozymes, A and B, that have different affinities for various amines as substrates. The activity of monoamine oxidase helps to maintain neuron firing rates throughout the body within homeostatic limits. It does this by metabolizing in the liver bioactive amines absorbed into the bloodstream from food, by metabolizing in the endothelial cells of cerebral vascular microvessels, as part of the blood brain barrier, bioactive amines in the bloodstream, and by metabolizing in the cytoplasm of neurons, molecules of biogenic amine neurotransmitters that are not enclosed in vesicles. Part of the biochemical activity of monoamine oxidase generates hydroxyl radicals, very toxic members of the oxygen free radical group, that may be involved in neurodegenerative disorders such as Parkinson's disease. Inhibiting monoamine oxidase with selegiline (1-deprenyl) seems to have neuroprotective actions but this may be due to inducing the release of neuronal growth factors rather than by preventing the formation of free radicals. Other drugs that inhibit monoamine oxidase are used to treat patients with atypical depression, panic attacks or post traumatic stress syndrome. It is hypothesized that the emotions act as positive or negative reinforcers of behavior patterns that increase the probability of survival of the organism. The original releasing stimuli for the emotions are related to the basic survival reflexes of the hypothalamus but the emotional response can be easily conditioned to formerly neutral stimuli by association. In the absence of the original releasing stimuli, these learned emotions increase the frequency of survival oriented behavior and decrease the frequency of behavior that jeopardizes survival. The emotional disorders are conditions in which the brain's reinforcement system is inoperative, the person loses contact with reality and the person's behavior bears no relationship to survival. Aversive stimulation evokes a negative emotional response that motivates the organism to escape from the aversive stimulation, and to avoid it, and any conditioned stimuli associated it, in the future. When the aversive stimulation and to avoid it, and any conditioned stimuli When the aversive stimulation is inescapable or unavoidable, the organism experiences stress. When the stressful aversive situation is not lethal, survival does not depend on escape but rather on conservation of energy. With repeated exposure, the negative emotional response to the aversive stimulation extinguishes, the organism adapts to the situation and takes on a passive, energy saving behavior pattern.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:On the functions of monoamine oxidase, the emotions, and adaptation to stress. 808 27

A series of 31 Parkinson's disease (PD) patients suffering from panic attacks (PA), late in the evolution of their disease, was analyzed from a group of 131 levodopa-treated PD patients. We found that many of motor, sensory, and vegetative symptoms, previously described as complicating phenomena in PD, constituted some of the symptoms of panic disorders. Comparing PA series with the series of PD patients who did not complain of PA, we discovered a clear-cut relationship of PA with the presence of standing/gait troubles (p < 0.001), depression (p < 0.001), and dyskinesias/fluctuations (p < 0.001). The patients of the PA series also presented a more precocious age of PD onset, were put on levodopa therapy earlier, and needed to be treated with higher doses of levodopa than the patients without PA. Finally, we hypothesize that PA could be considered to be a sort of abstinence syndrome from levodopa, because they appears mostly (90.3%) in the OFF phase of fluctuations, and are relieved administering new doses of levodopa or dopaminergic agonists. Nevertheless, we suggest PA are not directly related to the pharmacological properties of levodopa, but to alterations of the noradrenergic systems in the CNS.
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PMID:"Panic attacks" in Parkinson's disease. A long-term complication of levodopa therapy. 842 7

Neuropsychiatric symptoms frequently complicate the treatment of Parkinson's disease (PD). Approximately 27% of PD patients are demented, and approximately 19% are cognitively impaired without being demented. These 46% of patients are prone to development of delirium when they take antiparkinsonian drugs. Approximately 40% of PD patients are depressed. The depression may be endogenous or exogenous, apathetic or agitated. Approximately 40% of PD patients are anxious or have panic attacks. The attacks may or may not be associated with depression. This article reviews the diagnosis of these symptoms and discusses their management.
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PMID:Managing the neuropsychiatric symptoms of Parkinson's disease. 963 85

In this pilot study, we performed an oral yohimbine challenge in 6 patients with Parkinson's disease (PD) and anxiety or depression, 2 parkinsonian patients without psychiatric illness, and 2 healthy control subjects to determine whether patients with Parkinson's disease and anxiety respond to this adrenergic agent in the same way patients with idiopathic anxiety disorders respond. Given the atypical nature of depression in Parkinson's disease (characterized by prominent anxiety), we also wanted to see if patients with Parkinson's disease and depression (but no history of anxiety) are susceptible to yohimbine-induced panic. Parkinsonian patients with anxiety developed panic attacks at frequencies comparable to primary psychiatric patients with panic disorder. The one patient with PD and a history of major depression alone developed a panic attack. Regardless of their history of anxiety or depression, parkinsonian patients demonstrated a vulnerability to yohimbine-induced somatic symptoms.
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PMID:Parkinson's disease: a preliminary study of yohimbine challenge in patients with anxiety. 1036 82

During the last few decades, there has been a remarkable progress in our understanding of the biology of Parkinson's disease (PD), which has been translated into the development of numerous antiparkinsonian drugs. There are different therapeutic strategies for patients in an early stage versus patients in a late stage of the disease. The current therapeutic arsenal includes levodopa preparations, MAO-B inhibitors, dopamine agonists, COMT inhibitors and several other compounds that target non-dopaminergic systems. Much interest is focused on the potential neuroprotective effect of the already available drugs, as well as on new research approaches for the development of disease-modifying agents. These include mainly anti-glutamategic compounds, anti-apoptotic and antioxidative agents. Future therapy might include targeted delivery of trophic factors or genes involved in the pathogenesis of the disease. Apart from the classic levodopa-associated motor complications, such as dyskinesias and response fluctuations and psychosis, many other problems of advanced disease should be focused upon and solved including fatigue, freezing of gait, postural instability, depression, anxiety and panic attacks, sleep disturbances, autonomic dysfunction and sensory complaints.
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PMID:New drugs in the future treatment of Parkinson's disease. 1237 61

Apomorphine injectable has been used in Europe for more than a decade as a rescue therapy for intractable "off" periods in Parkinson's disease (PD). Some studies were performed as early as the 1970's. This article reviews double-blind and open studies with apomorphine for PD prior to the year 2000. Most were performed in Europe. Double-blind studies with injection doses of 1-5 mg have demonstrated that onset of clinical benefit typically occurs within 10 minutes, and lasts for up to two hours. The magnitude of benefit rivals that of levodopa. Long-term, open-label studies have demonstrated the persistent response to apomorphine injectable as a rescue therapy for as long as five years. Duration of benefit and dose of a single injection remains the same, but a need for increased number of doses per day is reported in keeping with disease progression. For many patients, the need for concomitant domperidone administration for antiemesis wanes over time. Apomorphine has also been shown in smaller studies to be effective for a variety of non-motor "off" phenomena, including pain, panic attacks, and a variety of gastrointestinal symptoms. Subutaneous intermittent bolus injects are also useful in patients post operatively who are unable to take oral medications.
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PMID:Literature review: intermittent subcutaneous apomorphine therapy in Parkinson's disease. 1503 66

Depression, dementia, and physiologic changes contribute to the high prevalence of sleep disturbances in patients with Parkinson's disease (PD). Antiparkinsonian drugs also play a role in insomnia by increasing daytime sleepiness and affecting motor symptoms and depression. Common types of sleep disturbances in PD patients include nocturnal sleep disruption and excessive daytime sleepiness, restless legs syndrome, rapid eye movement sleep behavior disorder, sleep apnea, sleep walking and sleep talking, nightmares, sleep terrors, and panic attacks. A thorough assessment should include complete medical and psychiatric histories, sleep history, and a 1- to 2-week sleep diary or Epworth Sleepiness Scale evaluation. Polysomnography or actigraphy may also be indicated. Treatment should address underlying factors such as depression or anxiety. Hypnotic therapy for sleep disturbances in PD patients should be approached with care because of the risks of falling, agitation, drowsiness, and hypotension. Behavioral interventions may also be useful.
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PMID:Sleep disorders in Parkinson's disease. 1525 35

Behavioral impairments in parkinsonian patients include agitation, hypersexuality, stereotypic movement, pathological gambling, abuse of antiparkinsonian drugs, REM sleep behavioral disorder, and restless legs syndrome. Dementia, psychoses, and emotional disorders, such as depression and anxiety/panic disorder, also impair behavior. Symptoms may be produced by dysfunction of the central nervous system, medication, and/or the psychosocial problems associated with Parkinson's disease. Treatment therefore should be based on the cause of the symptoms seen. In some cases, the reduction or change of antiparkinsonian drugs, or both, may be effective. Treatment of the motor symptoms of Parkinson's disease, including motor fluctuations, may reduce the risk of panic attacks being evoked in the 'off' period. Use of antidepressants, sedatives, and neuroleptics may often be effective. Physicians should identify the causes of the symptoms of behavioral impairment and select appropriate treatments.
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PMID:[Behavioral impairments in Parkinson's disease]. 1546 83

Nocturnal disturbances are common in Parkinson's disease (PD) patients, with almost 70% of these patients reporting nocturnal disturbances. The etiology of sleep disturbances in patients with PD is still controversial. They might be dependent on dopaminergic drugs, on disease progression, or on a combination of these two factors. Nocturnal disturbances can be categorized in four groups: 1) PD-related motor symptoms, including nocturnal akinesia, early-morning dystonia, painful cramps, tremor, and difficulty turning in bed; 2) treatment-related nocturnal disturbances; 3) psychiatric symptoms, including hallucinations, vivid dreams, depression, dementia, insomnia, psychosis, and panic attacks; 4) other sleep disorders, including insomnia, REM behavioral disorder (RBD), restless legs syndrome (RLS), periodic leg movements (PLMS), and excessive daytime sleepiness (EDS). Specific treatment options are supplied for every group. A global evaluation of nocturnal disturbances would provide clinicians with a valuable tool to establish an optimal regimen that could positively influence all nocturnal disturbance categories and thus improve PD management on. However, it is important to consider that management of some nocturnal disturbances in a group may worsen nocturnal symptoms of another group or may increase EDS. PD-related symptoms can be treated with long-acting DA agonists to obtain continuous DA receptor stimulation during the night. Both treatment-related nocturnal disturbances and psychiatric symptoms may be related to drug treatment, and therefore, in both cases, drug reduction or discontinuance should be considered. Some sleep disorders, such as RLS and PLMS, may be controlled by DA agents, and others, such as insomnia and EDS, may be improved by reducing dopaminergic stimulation.
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PMID:Treatment of nocturnal disturbances and excessive daytime sleepiness in Parkinson's disease. 1550 42


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