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Biomedical subjects

J Zandbergen

Publications and source records attributed to J Zandbergen.

At least 19 recordsLinked to original sources
PubMed1999

[Severe withdrawal symptoms with fever during paroxetine tapering off].

A 30-year-old man with depression who was treated with paroxetine (Seroxat) developed severe withdrawal symptoms when the medication was gradually diminished and stopped: agitation, irritability, vertigo, lightheadedness and fever up to 40 degrees C. The symptoms disappeared after the medication was reintroduced but recurred after rediscontinuation. When the dosage was diminished very gradually the symptoms were mild. The depression did not recur. Such withdrawal symptoms are most prevalent after discontinuation of paroxetine but can occur after use of all selective serotonin reuptake inhibitors. The withdrawal syndrome includes both physical and psychiatric symptoms and needs to be distinguished from a relapse of the psychiatric disorder. Good information and gradual discontinuation of the antidepressant after long-term use are adequate measures to prevent severe withdrawal symptoms.

Adult↗
PubMed1993

No chronic hyperventilation in panic disorder patients.

Arterial blood gases were measured and base excess calculated in 18 nonpanicking panic disorder (PD) patients, 12 subjects suffering from other anxiety disorders, and 18 normal control subjects. There was neither chronic nor clinically significant acute hyperventilation in either group.

Acid-Base Equilibrium↗
PubMed1991

Ventilatory response to CO2 in panic disorder.

The Read rebreathing technique was used to measure the ventilatory response to inhalation of carbon dioxide in 15 panic disorder patients, 15 obsessive-compulsive disorder patients, and 15 healthy control subjects. No significant differences in ventilatory response were found among the three groups. The tidal volume and frequency components of the ventilatory response also did not differ among the groups. The hypothetical pCO2 value corresponding with zero ventilation was significantly lower in the panic disorder patients than in normal control subjects.

Adult↗
PubMed1991

Attenuation of carbon dioxide-induced panic after clonazepam treatment.

Ten patients meeting the DSM-III-R criteria for panic disorder were treated with clonazepam. Prior to clonazepam treatment and after a 5-week treatment period, patients underwent a 35% carbon dioxide challenge procedure. Following clonazepam treatment, a significant reduction in carbon dioxide vulnerability was observed.

Adult↗
PubMed1991

Higher lifetime prevalence of respiratory diseases in panic disorder?

Current and past frequencies of respiratory diseases were assessed in 30 patients with panic disorder, 30 patients with obsessive-compulsive disorder, and 30 patients with eating disorders. Lifetime prevalence of respiratory disorders was significantly higher in patients with panic disorder (47%) than in patients with either obsessive-compulsive disorder (13%) or eating disorder (13%). Point prevalences showed no differences.

Adult↗
PubMed1991

Low doses of clonazepam in the treatment of panic disorder.

In order to assess the efficacy of a high-potency benzodiazepine in the treatment of panic disorder, an open trial was conducted with clonazepam. Clonazepam was administered in relatively low doses and, after four weeks, was shown to be effective in reducing the number of panic attacks and associated features of the disorder.

Adult↗
PubMed1990

Waning of panic sensations during prolonged hyperventilation.

Recent theories about panic emphasize that a hyperventilatory positive feedback loop is involved in panic: catastrophic misinterpretation of bodily sensations may trigger anxiety, anxiety may stimulate hyperventilation, hyperventilation may promote the salience of feared sensations etc. Such models leave unexplained how and when panics come to an end. It was hypothesised that panic with hyperventilation may end because pronounced hyperventilation becomes, in the course of time, less powerful in generating perceivable bodily sensations. Twenty healthy subjects hyperventilated forcefully and experienced clear panic symptoms as defined by DSM IIIR. When pCO2 was kept 55% below base line for 90 min, panic symptoms waned. The mean intensity of the symptoms declined as did the number of symptoms occurring. No panic symptoms were observed in the control group (n = 20) who ventilated normally. In so far as hyperventilation is involved in the positive feedback loops that characterize panic, panic attacks may be time-limited because sensations induced by hyperventilation become less salient even if massive hyperventilation continues. As to the explanation of the reported phenomenon, it is suggested that, apart from habituation, local physiological changes due to prolonged hyperventilation may produce a decrease in interoceptive input.

Adult↗
PubMed1990

Hypercarbia versus hypocarbia in panic disorder.

In order to compare the panicogenic effects of hypercarbia and hypocarbia in panic disorder (PD), 12 PD patients and 11 healthy controls underwent a 35% CO2 challenge as well as a hyperventilation provocation test in a random cross-over design. Both anxiety and anxiety symptoms proved to be significantly higher during the 35% CO2 challenge in PD patients as compared to the response during 35% CO2 in normals and during hyperventilation in both patients and normals. The results suggest that PD patients are specifically hypersensitive to an increase in pCO2.

Adolescent↗
PubMed1990

Specific sensitivity of patients with panic attacks to carbon dioxide inhalation.

One inhalation of 35% CO2 in oxygen was administered to 36 patients with anxiety disorders and 14 healthy controls. Eighteen patients had a diagnosis of panic disorder (PD) and 18 of obsessive-compulsive disorder (OCD). As a placebo control for CO2, compressed air was administered in a double-blind design. Immediately before and after the inhalation, levels of anxiety and DSM-III-R symptoms of panic were assessed. CO2 elicited high levels of subjective anxiety in the PD group. Patients with OCD were hardly affected by the inhalation, and did not differ from healthy controls. These results suggest that CO2 challenge should be considered as a specific probe for subjects with panic-anxiety. It is speculated that CO2 may trigger some as yet undefined mechanisms, possibly linked to ventilation control, which demarcate panic from other types of pathological anxiety.

Administration, Inhalation↗
PubMed1990

Response to 35% CO2 as a marker of panic in severe anxiety.

One inhalation of 35% CO2 was administered to each of 32 patients with high anxiety ratings. Only patients with panic disorder had increases in reported anxiety upon CO2 intake. CO2-triggered anxiety appears specific for panic disorder and independent of baseline anxiety.

Adult↗
PubMed1989

A case of bulimia successfully treated by cue exposure.

In the present case-study, a 22-year-old female patient with a 7-year history of bulimia nervosa was treated by cue-exposure. During cue-exposure sessions the relationship between CS (stimuli associated with binge-eating behaviour) and UCS (the sensations related to the intake of binge food) was broken. As predicted, the patients' craving for food declined within as well as between cue exposure sessions and a radical decrease in the frequency of binge-eating persisted for at least nine months. Although during the therapy no explicit attention was paid to the patient's low mood and irrational self-talk, mood was improved and beliefs were less irrational after cue-exposure and at the follow-ups. The data suggest that cue exposure may be an effective part of the treatment of bulimia nervosa.

Adult↗
PubMed1989

The role of life events in the onset of panic disorder.

Twenty-five panic disorder patients and fifteen obsessive-compulsive patients are compared with regard to a number of Life Events over the last 12 months prior to onset of the disorder and additionally over the total life course up until onset of the disorder. Panic Disorder patients do not differ from obsessive-compulsive disorder patients in terms of the number of life events, they experience during the last year prior to onset of their disorder. However, over the total life course, Panic Disorder patients do seem to be exposed to more Life Events than obsessive-compulsive disorder patients. The findings are discussed in light of the existing literature.

Adult↗
PubMed1989

Effect of hypercapnia and other disturbances in the acid-base-balance on panic disorder.

Naturally occurring panic attacks and various interventions which trigger anxiety in panic patients are accompanied by disturbances in the acid-base balance. Carbon dioxide appears to play an important role in many experimental panic provoking conditions. The influence of respiratory and metabolic pH disturbances on cerebral physiology is discussed and speculations are made about the possible mechanisms underlying CO2-induced anxiety in panic disorder.

Acid-Base Equilibrium↗
PubMed1985

Comparison of secretion and subcellular localization of von Willebrand protein with that of thrombospondin and fibronectin in cultured human vascular endothelial cells.

Cultured human vascular endothelial cells synthesize von Willebrand protein, thrombospondin and fibronectin. These proteins are secreted in the culture medium and incorporated into the extracellular matrix. We have compared the subcellular localization and the secretion of these proteins in response to stimulants in cultured human umbilical vein endothelial cells. Density gradient centrifugation using colloidal silica showed that the storage and secretion organelle with von Willebrand protein did not contain thrombospondin or fibronectin. Indirect immunofluorescence microscopy indicated that thrombospondin and fibronectin are not located in the rod-shaped organelles containing von Willebrand protein. Thrombin, ionophore A23187 and phorbol myristate acetate did not affect secretion of thrombospondin and fibronectin, while von Willebrand protein secretion was stimulated upon incubation of cells with these agents for 30 min. Prolonged incubation of cultured endothelial cells after a 1-h treatment with phorbol myristate acetate resulted in an increased secretion of von Willebrand protein into the conditioned medium; in contrast, accumulation of thrombospondin and fibronectin in endothelial cell-conditioned medium was decreased. These findings indicate that, unlike in platelets, these major endothelial proteins are not located in the same subcellular compartments. Von Willebrand protein is distinguished from thrombospondin and fibronectin both by its unique subcellular localization and its secretion rate in response to stimuli.

Blood Coagulation Factors↗
PubMed1985

Cell cycle-dependent inhibition of human vascular smooth muscle cell proliferation by prostaglandin E1.

We examined the influence of prostaglandins on the initiation of proliferation of growth-arrested human adult aortic and fetal smooth muscle cells. Prostaglandins of the E series (25 nM) exerted a significant (p less than or equal to 0.05) inhibitory effect on DNA synthesis. Inhibition was observed when PGE1 was added in the G1 phase of the cell cycle. PGE1 had no effect when added once DNA synthesis had started. Thus prostaglandins of the E series may inhibit the responsiveness of smooth muscle cells to the mitogenic action of critical growth factors, such as PGDF. This inhibitory response is cell-cycle dependent. Once smooth muscle cells have entered S phase, PGE1 is no longer effective. Our data also suggest that cAMP is involved in the PGE1-induced growth inhibition, since concomitant with PGE1 addition, cAMP levels rose rapidly; addition of the cAMP analogue db-cAMP resulted in a cell-cycle-dependent inhibition pattern comparable to that observed with PGE1.

Alprostadil↗