Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0040822 (tremor)
 18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Panic attacks occur more often in females than males with onset usually in the late 20s. A 27-year old woman who experienced a panic attach (heart palpitations, fatigue, bodily shaking, labored breathing, and feelings of terror and being out of control) after she stopped taking a combined oral contraceptive (COC) (.5 norgestrel and .05 mg ethinyl estradiol) was admitted to Osaka Medical College in Takatsuki, Japan. She experienced depression at 18 and took limited amounts of antidepressants for only 1 year. When she started taking the COC at 27, she experienced feelings of unreality and fear, hyperventilation, and heart palpitations. Laboratory results showed lower than normal levels of plasma luteinizing hormone (LH) and follicle stimulating hormone (FSH) and a low estradiol level. Yet the plasma cortisol level was much high than normal (22.5 mcg/d1 vs. 3-15.2 mcg/d1). Administration of 200 mg sulpiride/day and 1.2 mg alprazolam/day alleviated almost all symptoms. She did experience mild phobic avoidance and anxiety, however. After successful treatment in the hospital, she discharged herself. Because she was concerned that the panic attacks would recur, she was provided with information on her disorder. She agreed to continue the medication. 1 possible explanation for this case is rapid endocrinological change induced by the ingestion and stopping of the COC which in turn induced a sympatho-adrenal response (her high cortisol levels) to several simple physiological stimuli. Another possible explanation is the COC induced rapid endocrinological changes that may have brought on an anxiotropic effect in someone who had earlier experienced depression.
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PMID:A case of panic disorder induced by oral contraceptive. 131 8

Thirty-seven patients presented with paroxysmal neurological manifestations attributed to anxiety attacks. The manifestations included loss of consciousness, focal sensorimotor deficits, diffuse dysesthaesiae, visual disorders and tremor. They lasted 10 to 45 minutes and occurred once per day to once per week. Organic pathology was dismissed on the basis of normal examinations and atypical course. In all patients questioning revealed symptoms that were those of acute anxiety. The fact that these attacks took place in suggestive (circumstances e.g. in crowds and car driving), and that they could be induced by challenge tests hyperpnoea, infusion of lactate) suggested that these disorders were consecutive to panic attacks.
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PMID:[Paroxysmal neurological manifestations disclosing panic attacks]. 136 98

For phenomenological elucidation of panic attacks, 26 patients with panic attacks were requested to name the panic symptoms in order of their occurrence and specify the patterns of their abatement. Panic symptoms were found to be classifiable into three categories: early symptoms consisting of dizziness or faintness, palpitations, and sweating; intermediate symptoms dyspnea, nausea or abdominal distress, flush or chills, chest pain or discomfort, shaking, and choking; late symptoms paresthesias, fear of dying, and fear of going crazy. Panic symptoms disappeared in 61.6% irrespective of the sequence of their occurrence. Twenty-one patients were interviewed about the experience of nocturnal panic attacks, and 23.8% experienced them. These findings suggest that fear is caused by sudden physical abnormality triggered by some biological factors.
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PMID:The sequence of panic symptoms. 148 43

A review of the clinical efficacy of four structurally distinct antidepressant drugs is presented. Their antidepressant activity can be rationalised within current pharmacological hypotheses of drug action, despite markedly different effects on "in vitro" testing. Fluoxetine, a specific serotonin re-uptake inhibitor, has proven safe, effective treatment for depressive illness and may have a role to play in the treatment of obsessive-compulsive disorder and panic attacks. While it has few of the anticholinergic side effects of the tricyclic antidepressants, nausea, tremor, headache, weight loss, nervousness and sweating are side effects most frequently reported. Minaprine, a compound with weak MAO inhibiting properties and effects on serotonergic receptors, has clinical efficacy in the treatment of depression based on several comparative studies. It is claimed that minaprine lacks anticholinergic and sedative properties. Moclobemide, a specific, reversible inhibitor of MAO-A, has been extensively evaluated in depressive illness. The major advantage of this agent over other irreversible, non-specific MAO inhibitors, is the significant attenuation of the so-called "cheese effect" with doses of tyramine likely to be encountered in foodstuffs. Rolipram, a phosphodiesterase inhibitor, represents a new approach to antidepressant treatment. Limited clinical data suggest that the drug may be an effective antidepressant with few side effects. The place of these agents in therapy is yet to be established.
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PMID:New pharmacological approaches to the management of depression: from theory to clinical practice. 158 Aug 88

To determine which symptoms characterized isoproterenol-induced panic attacks, we analyzed the presence of panic attacks in 54 panic disorder patients who panicked, 24 patients who did not panic, and 37 controls who did not panic during isoproterenol infusions. The increases over the baseline of the symptoms shortness of breath and fear of going crazy were highly associated with panicking patients when compared to nonpanicking patients and nonpanicking controls. The increases of the symptoms trembling and shaking, generally nervous, and fear of going crazy were highly associated with patients when compared to controls. The possibility of a cognitive theory of panic attacks is discussed.
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PMID:Somatic and psychological symptoms during isoproterenol-induced panic attacks. 219 75

beta-Adrenoceptor blocking drugs have been used for the treatment of acute stress reactions, adjustment disorders, generalised anxiety, panic disorder and agoraphobia. In general they are effective in these disorders if somatic or autonomic symptoms are prominent but not extreme in degree. Thus, they are of more value for the relatively mild tremor of the anxious violinist in public performance than in the severe shaking noticed during a panic attack. It is most likely that beta-blockers act primarily by blocking peripheral adrenergic beta-receptors; symptoms that are mediated through beta-stimulation, such as tremor and palpitations, are helped most. Improvement is noted within 1 to 2 hours and with relatively low doses (e.g. propranolol 40 mg/day). Some recent studies, however, have suggested that when longer treatment using higher doses (e.g. propranolol 160 mg/day) is given, improvement in other forms of anxiety is noted after several weeks of treatment. beta-blocking drugs are useful adjuncts to existing treatments for anxiety and are likely to enjoy wider use now that benzodiazepines are being avoided due to their dependence risks.
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PMID:Current status of beta-blocking drugs in the treatment of anxiety disorders. 290 81

Many aspects of panic attacks, eg, palpitations, tremor, sweating, and an emotional sense of "fear," have been theorized to arise from sympathetic nervous system activation. However, most studies have not demonstrated clearly increased levels of catecholamines during an attack, which is contrary to this hypothesis. To explore another possible cause for the physiological changes known to occur during a panic attack, we assessed parasympathetic nervous system activity by measuring vagal tone during treatments known to produce panic symptoms: sodium lactate administration and hyperventilation. Our findings showed a marked reduction in vagal tone during both procedures. We postulate that withdrawal of parasympathetic activity may explain some of the physiological changes occurring in panic attacks and be contributing to the origin of panic.
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PMID:Lactate and hyperventilation substantially attenuate vagal tone in normal volunteers. A possible mechanism of panic provocation? 291 73

Although much research has focused on the pathophysiology of panic attacks, little work has been done to describe the phenomenon itself. Twenty-one patients with panic attacks were asked to sequence the panic-related symptoms during an attack in an attempt to clarify the phenomenon. Overall, panic symptoms could be grouped into three categories: early symptoms--consisting of dyspnea, palpitations, chest discomfort, and hot flashes; intermediate symptoms--including shaking, choking, feelings of unreality, sweats, faintness, and dizziness; late symptoms-consisting of fear and paresthesias. Based on symptom clustering and temporal relationships, this study describes the panic phenomenon.
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PMID:The sequence of panic symptoms. 333 5

Thalamic structures involved in the unpleasant emotional or affective aspect of pain are poorly understood. We now describe studies of the region of the thalamic principal somatosensory nucleus (Vc) performed before thalamotomy for tremor in a patient who also had panic disorder. Microstimulation in the region posterior to Vc evoked chest pain, including a strong affective dimension, almost identical to that occurring during his panic attacks, as measured using a questionnaire. Results in our other patients indicate that stimulation-associated pain with a strong affective dimension occurred only in those patients who had previously experienced spontaneous pain with a strong affective component. These results are consistent with stimulation-evoked activation of limbic structures, which are connected through cortex with the region posterior to Vc and involved in the affective dimension of pain through conditioning by previous experience.
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PMID:Stimulation in the human somatosensory thalamus can reproduce both the affective and sensory dimensions of previously experienced pain. 758 11

Physiological dependence on benzodiazepines is accompanied by a withdrawal syndrome which is typically characterized by sleep disturbance, irritability, increased tension and anxiety, panic attacks, hand tremor, sweating, difficulty in concentration, dry wretching and nausea, some weight loss, palpitations, headache, muscular pain and stiffness and a host of perceptual changes. Instances are also reported within the high-dosage category of more serious developments such as seizures and psychotic reactions. Withdrawal from normal dosage benzodiazepine treatment can result in a number of symptomatic patterns. The most common is a short-lived "rebound" anxiety and insomnia, coming on within 1-4 days of discontinuation, depending on the half-life of the particular drug. The second pattern is the full-blown withdrawal syndrome, usually lasting 10-14 days; finally, a third pattern may represent the return of anxiety symptoms which then persist until some form of treatment is instituted. Physiological dependence on benzodiazepines can occur following prolonged treatment with therapeutic doses, but it is not clear what proportion of patients are likely to experience a withdrawal syndrome. It is also unknown to what extent the risk of physiological dependence is dependent upon a minimum duration of exposure or dosage of these drugs. Withdrawal phenomena appear to be more severe following withdrawal from high doses or short-acting benzodiazepines. Dependence on alcohol or other sedatives may increase the risk of benzodiazepine dependence, but it has proved difficult to demonstrate unequivocally differences in the relative abuse potential of individual benzodiazepines.
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PMID:The benzodiazepine withdrawal syndrome. 784 56


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