Urinary tribulin output in patients with panic attacks.
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Biomedical subjects
Publications and source records attributed to F K Judd.
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Platelet serotonin uptake was measured in 59 patients with panic attacks and compared to 26 controls. Scatchard analysis of the data showed that the maximal rate of uptake (Vmax) of serotonin was significantly higher in patients than controls. The affinity constant (Km) was not different. In a sub-group of 24 patients, benzodiazepine treatment did not alter the kinetics of platelet serotonin uptake. These findings suggest an abnormality in serotonergic function in patients with panic attacks. Insofar as the platelet is a model of central neuronal function they support serotonergic hyperactivity as a biochemical basis of panic attacks.
The serotonergic hypothesis of depression has stimulated the development of a range of chemically diverse compounds that have an exclusive effect on this neurotransmitter for potential use as antidepressant drugs. The group of serotonin reuptake inhibitors are at various stages of clinical development. The authors review the efficacy, side effect profiles, and toxicity of zimelidine, fluvoxamine, and citalopram in detail and ifoxetine, fluoxetine, indalpine, paroxetine, and sertraline in brief. Evidence suggests that, compared with tricyclic antidepressants, these drugs may cause fewer anticholinergic effects and lower cardiotoxicity in the treatment of major depressive disorders. These advantages need to be weighed against an emerging pattern of gastrointestinal complaints, insomnia, and akathisia. The place of serotonin reuptake inhibitors in therapy can be fully evaluated only after further studies, particularly those involving long-term use. The adverse experience associated with zimelidine suggests that caution and vigilance should be exercised in future studies of agents in this class. These drugs will undoubtedly provide important insights into depressive illness and some anxiety disorders and may fulfill their initial promise.
Panic disorder, as defined by the DSM III diagnostic criteria, was diagnosed in 117 probands for whom age of onset ranged from 10 to 59 years, with a mean of 26.6 years. Diagnosis of parents and siblings was based on interviews with the probands, and only those with "definite" panic disorder by the FISC criteria were considered to be affected. The pattern of concordances for panic across different groups of relatives was estimated concurrently by a log-linear model for binary pedigree data, assuming different values for the cumulative risk. When an adjustment for age was made, based on the age of onset of probands, there was no significant difference between parent-offspring concordance and sibling concordance. There was a negative, but not significant, concordance between spouse pairs. Assuming the lifetime cumulative risk was 1.9% for males and 4.7% for females, values considered appropriate for this population, our model predicted that the presence of an affected parent or sibling incurs an approximately five times increase in the risk of developing panic disorder. Our model assumes in effect that this risk is multiplied for each further affected relative. Although the common concordance across relationship groups is consistent with a genetic hypothesis, it can also be explained by common family environmental factors. There is a need for further pedigree studies, using twins and relatives, for example, and reliable information on the cumulative risk.
Platelet alpha 2 binding was measured in 14 patients with panic attacks and 21 controls using the antagonist 3H-rauwolscine as radioligand. The mean (+/- SD) Bmax values of patients (116 +/- 45 fmoles/mg protein) and controls (106 +/- 32 fmoles/mg protein) was not significantly different (p greater than 0.05, Mann-Whitney U test). There was a nonsignificant trend for the Kd of patients (1.25 +/- 0.67 nM) to be higher than that of controls (0.96 +/- 0.32 nM). The results do not support an adrenergic abnormality in panic patients.
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The functions of a comprehensive Spinal Cord Unit do not cease with the discharge of the patient from in-patient treatment after rehabilitation; they extend to aftercare, both in medical follow-up and prevention and treatment of complications, and in ongoing support and education of the patient and his family. An effective aftercare service must offer a life-long commitment to patients, and the aftercare team must include members of the disciplines which were involved in the initial rehabilitation, and also often others. Although demanding of time, resources and money, good aftercare is cost-effective in terms of savings in the cost of out-patient treatment and of re-admissions to hospital for the treatment of complications, and in maintaining many patients in the community, often as contributing members of society.
The dexamethasone suppression test (DST) was performed in 35 patients with panic disorder and 21 normal control subjects. Non-suppression of plasma cortisol was determined as 4 micrograms/dl and using this figure 29% of panic patients and 9.5% of controls were non-suppressors. There was no significant difference in the number of suppressors and non-suppressors between patient and control groups (chi 2 = 1.81; P greater than 0.05). Both pre- and postdexamethasone cortisol concentrations were significantly different between the two groups possible indicating a cortisol hypersecretion in some panic patients.
Many studies have suggested that a genetic predisposition to the development of panic disorder exists. These studies are examined and their limitations discussed. It is suggested that only by the analysis of comprehensive family and twin data, coupled with other measures such as the search for possible single gene association or linkage and study of the children of panic disorder patients, will the mechanism for the 'familiarity' noted in panic disorder patients be elucidated. Delineation of the mode of transmission of panic disorder may allow preventative intervention with those at risk before they develop panic.
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In December 1984, the Victorian Government published its proposals for the reform of workers' compensation legislation. Many groups have expressed concern about the proposed changes. The literature contains studies of heterogeneous groups of patients from different countries with very different medical and legal systems. Assessment of the psychological outcome of patients with compensable injuries has not usually included the assessment of confounding variables such as other injuries, inter- and intrapersonal problems, and social circumstances. No firm conclusions can be reached about the relative benefits and disadvantages of lump sum and periodic payments from a psychological perspective.
Spinal cord injury may produce both immediate and long term stress and disability. The liaison psychiatrist may have an important role in dealing with the problems of the spinal cord injured patient, his family and the medical team. Problems occurring may cause or be exacerbated by psychological difficulties. Problems occurring during rehabilitation and long term adjustment have not been systematically studied. Many assumptions concerning the psychological responses to injury have been made. Such assumptions have important implications for both the short and long term treatment of patients. This paper examines some of these areas.
Panic disorder has recently been recognized as a distinct sub-type of anxiety which may occur with or without phobic avoidance. Controlled prospective trials have demonstrated the efficacy of the tricyclic antidepressants and monoamine oxidase inhibitors in the treatment of this disorder. The use of benzodiazepines and beta-blockers has been more controversial. Some preliminary studies assessing other pharmacological agents are available. Methodological problems limit the conclusions which may be drawn from available data.
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Panic disorder with or without phobic avoidance has recently been delineated as a distinct nosological entity. Several controlled studies have demonstrated the efficacy of various pharmacological agents in controlling panic attacks. Behaviour therapy, especially desensitisation, is of value in alleviating phobic avoidance but has not yet been shown to be effective in the alleviation of panic attacks. No systematic studies comparing pharmacological and psychological treatments in panic disorder are available.
The pineal hormone melatonin was measured in midnight plasma samples from 11 depressed patients and 18 control subjects. Plasma melatonin concentrations were significantly lower in the depressed patients. The implication of these findings for beta-adrenoceptor subsensitivity in depression is discussed.
There is an increasing concern about potential negligence actions being issued against psychiatrists. This has resulted from a greater interest by the community in the issues of informed consent and involuntary hospitalisation. This paper gives an overview of the present law relating to negligence relevant to the treating psychiatrist. Traditional views in the areas of contract and tort, with some comments on the current changes in that law, are described.