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Biomedical subjects

G Perna

Publications and source records attributed to G Perna.

At least 37 records · Page 2Linked to original sources

Hypersensitivity to inhalation of carbon dioxide and panic attacks.

Thirteen healthy subjects with infrequent panic attacks and without agoraphobia who did not meet DSM-III-R criteria for panic disorder, 43 patients with panic disorder, and 43 healthy control subjects who never experienced panic attacks underwent one vital capacity inhalation of 35% CO2. Healthy subjects with infrequent panic attacks reacted similarly to patients with panic disorder and more strongly than healthy subjects who never experienced panic attacks. The results suggest that (a) subjects with sporadic unexpected panic attacks and patients with panic disorder belong to the same spectrum of vulnerability and (b) CO2 hypersensitivity might be a trait marker of panic attacks rather than of a clinical diagnosis of panic disorder.

Administration, Inhalation

Menstrual cycle-related sensitivity to 35% CO2 in panic patients.

In a double blind, random, cross-over design, 10 patients and seven controls inhaled one vital capacity of 35% CO2-65% O2 during their early-follicular and midluteal phases. Anxiety after CO2 intake was significantly stronger in the early-follicular phase than in the midluteal phase for patients. Controls had no anxiety reactions.

Administration, Inhalation

35% CO2 challenge in panic and mood disorders.

20 patients with Panic Disorder (PD), 19 patients with Mood Disorder (MD) and 20 healthy controls inhaled one vital capacity of 35% CO2-65% O2 gas mixture and of compressed air in a double-blind, random, cross-over design. Only PD patients showed a strong reaction to 35% CO2 while MD patients and controls did not react significantly. These results support the specificity of the 35% CO2 challenge in PD patients and suggest that PD and MD are separate disorders.

Adult

Alpha 2-adrenergic receptor sensitivity in panic disorder: I. GH response to GHRH and clonidine stimulation in panic disorder.

Baseline levels of GH and somatomedin C (SmC) and GH responses to GHRH (1 microgram/kg b.w.) and to clonidine (150 micrograms) were measured in 10 outpatients with panic disorder before and after 30 days of 2-2.5 mg of alprazolam therapy, and in 10 psychophysically healthy controls. Basal levels of GH were normal in the patients and those of SmC significantly elevated, both before and after therapy. Basal GH responses to GHRH stimulation were normal and did not change change after alprazolam treatment. Basal GH responses to clonidine stimulation were blunted in the patients and improved after therapy, in parallel with an amelioration of the psychopathology. Our data suggest that adrenoceptor sensitivity, investigated by the clonidine test, is reduced in panic disorder.

Adult

Alpha 2-adrenergic receptor sensitivity in panic disorder: II. Cortisol response to clonidine stimulation in panic disorder.

The cortisol responses to acute administration of saline and of clonidine (Clon), 150 micrograms IV, were examined in 12 patients with panic disorder and agoraphobia, before and after 32 days of alprazolam therapy (2.5 mg/day), and in 12 normal controls. The responses in the Clon test corrected for the responses to saline differed in the two groups, and in patients were not changed by the therapy even though significant symptomatological improvement was achieved. The results suggest that presynaptic alpha 2- or postsynaptic alpha 1-beta-adrenoceptor sensitivity is impaired in panic disorder.

Adult

Laboratory response of patients with panic and obsessive-compulsive disorders to 35% CO2 challenges.

OBJECTIVE: The DSM-III-R anxiety disorders section includes both panic disorder and obsessive-compulsive disorder. To evaluate the relationship between these two disorders, subject responses to inhalation of a 35% CO2 and 65% O2 mixture were assessed. METHODS: Twenty-three patients with panic disorder, 23 with obsessive-compulsive disorder, 12 with both obsessive-compulsive and panic disorder, and 23 healthy comparison subjects were given a single vital capacity inhalation of 35% CO2 and 65% O2 or a placebo mixture of compressed air. A double-blind, random, crossover design was used. RESULTS: Patients with panic disorder and patients with both panic disorder and obsessive-compulsive disorder showed similar strong anxiogenic reactions to 35% CO2; while patients with obsessive-compulsive disorder alone did not differ from comparison subjects. CONCLUSIONS: These results confirm that obsessive-compulsive disorder and panic disorder are two distinct syndromes and that patients with these disorders have different sensitivity to CO2 inhalation.

Administration, Inhalation

Sensitivity to 35% CO2 in healthy first-degree relatives of patients with panic disorder.

OBJECTIVE: The authors tested the hypothesis that hyperreactivity to CO2 in healthy subjects represents an underlying familial vulnerability to panic disorder. METHOD: One vital-capacity inhalation of 35% CO2 and 65% O2 was administered to each of 84 patients with panic disorder, 23 healthy first-degree relatives of probands with panic disorder, and 44 healthy subjects with no family history of panic disorder. RESULTS: The first-degree relatives of the probands with panic disorder reacted significantly more than the healthy subjects and significantly less than the probands. CONCLUSIONS: These findings suggest an association between family history of panic disorder and hyperreactivity to 35% CO2 in healthy subjects.

Administration, Inhalation

Age at onset of panic disorder: influence of familial liability to the disease and of childhood separation anxiety disorder.

OBJECTIVE: The authors investigated the relation of age at onset of panic disorder to liability to panic disorder and agoraphobia. METHOD: Two hundred thirty-one outpatients with panic disorder were compared with 131 surgical outpatients on demographic variables and familial risk of psychiatric disorders. The distribution of patients' ages at onset of panic disorder and several covariates were entered in a stepwise survival analysis. RESULTS: The patients with panic disorder had a significantly higher rate of childhood separation anxiety disorder and higher familial risks of panic disorder/panic disorder with agoraphobia and alcoholism. A family history of panic disorder with agoraphobia and the presence of childhood separation anxiety disorder influenced age at onset of panic disorder. CONCLUSIONS: Age at onset of panic disorder may reflect genetic penetrance, and separation anxiety disorder may be an individual predictor of earlier onset of panic disorder.

Adult

[Corono-radicular amputation of mandibular molars: indication, technic and prosthetic utilization. Apropos of a clinical case].

Lesions to the radicular bifurcation generally entail the removal of the tooth in question. This leads to the need to create a prosthetic bridge to compensate for the absence of the extracted tooth. This solution is not readily accepted by the patient who wishes to avoid involving other teeth. In these cases rhizectomy and the execution of an inlay on an adjacent tooth may satisfy the patient and resolve the clinical symptoms. The authors report a case of rhizectomy and prosthetic reconstruction of a tooth using inlay.

Dental Prosthesis

Subclinical impairment of lung airways in patients with panic disorder.

Lung function was assessed in 17 panic patients and 20 healthy controls. Panic patients had abnormal values for some dynamic lung volumes, namely Peak Expiratory Flow Rate (PEFR), Expiratory Flow at 75% of Vital Capacity (FEF75) and Maximum Mid-Expiratory Flow Rate (MMEF). Such functional abnormalities might indicate subclinical obstruction of lung airways, possibly relevant to the mechanisms related to panic disorder (PD).

Adult

Plasma interleukin-1 beta concentrations in panic disorder.

Plasma interleukin-1 beta (IL-1 beta) concentrations were measured in 10 outpatients with panic disorder before and on days 30 and 32 of treatment with alprazolam (2-2.5 mg/day). IL-1 beta concentrations were found to be significantly higher in patients than in control subjects both before and during therapy. Thus, IL-1 beta levels may be a marker of panic disorder that is not related to the current level of symptomatology.

Adult

Carbon dioxide/oxygen challenge test in panic disorder.

The effects of a single inhalation of a 35% CO2/65% O2 gas mixture were examined in 71 patients with panic disorder with or without agoraphobia and 44 normal control subjects. Compared with the placebo condition, inhalation of air, the CO2/O2 mixture elicited a clear anxiety reaction only in panic disorder patients, who experienced a sudden rise of subjective anxiety as well as of several panic symptoms. Respiratory symptoms and the fear of dying best distinguished the patients from the control subjects. Baseline anxiety was not the key factor in explaining this differential reaction. The clinical features of panic disorder (namely, frequency of panic attacks, agoraphobia, anticipatory anxiety, and duration of illness) were not significantly related to the response to the challenge test, suggesting that CO2 reactivity might be a trait marker of panic disorder.

Administration, Inhalation

Alpha-2-adrenoceptor sensitivity in heroin addicts with and without previous attention deficit disorder/hyperactivity and conduct disorder.

Growth hormone (GH) and beta-endorphin (beta-EP) responses to clonidine stimulation were examined in 18 male heroin addicts, 9 with and 9 without previous histories of attention deficit disorder with hyperactivity (ADD-H) and conduct disorder (CD). Ten psychophysically healthy volunteers were used as controls. ADD-H/CD addicts had blunted GH and beta-EP responses as compared to controls while those of non-ADD-H/CD addicts were normal. This suggests that postsynaptic adrenoceptor sensitivity is decreased and, possibly, that presynaptic noradrenaline secretion is increased in ADD-H/CD patients with heroin addiction.

Adolescent

[The prevention of nitrate tolerance in angina patients treated with transdermal nitroglycerin: a comparison of 2 therapeutic regimens (therapeutic outlook versus dosage reduction)].

We studied the long-term antianginal and anti-ischemic effects of two dosage regimens designed to prevent tolerance to transdermal nitroglycerin (TNTG): (1) 10 mg TNTG applied for 16 h with a 'nitrate-free' interval of 8 h; (2) 10 mg TNTG applied for 16 h followed by a 'nitrate-low' interval of 5 mg applied for 8 h. 129 patients completing a 3-month study period were evaluated by repeated exercise tests. Both regimens significantly increased maximum exercise duration at 3 months, from 699.1 +/- 23.4 to 833 +/- 21.9 s and from 686.1 +/- 20 to 789.6 +/- 22.6 s, respectively, reduced the number of patients with 1 mm S-T segment depression and increased the time duration to 1 mm S-T segment depression. Marked reductions in anginal attacks was observed in both groups: from 6.5 to 0.15 attacks per week and from 6.0 to 0.15 attacks per week, respectively. No statistically significant differences were found between the groups, and both regimens were well tolerated. In conclusion, our results demonstrate sustained antianginal efficacy, without tolerance, of either 'nitrate-free' of 'nitrate-low' interval therapy with transdermal nitroglycerin.

Administration, Cutaneous

Pharmacologic effect of toloxatone on reactivity to the 35% carbon dioxide challenge: a single-blind, random, placebo-controlled study.

The effect of a short treatment (7 days) with the reversible monoamine oxidase type A inhibitor toloxatone on the reactivity to the inhalation of 35% CO2 was evaluated in 18 panic patients who responded to 35% CO2 inhalation with panic before treatment. A single-blind, placebo-controlled design was applied. Panic patients were randomly assigned to the toloxatone (N = 10) or placebo (N = 8) groups and were given the 35% CO2 challenge on days 1 (before starting the treatment), 3, and 7. Patients on placebo did not report any significant changes in their reactivity to 35% CO2 during the three sessions, whereas patients on toloxatone reported a significant attenuation of the reactivity on day 7. These results indicate that (1) anxiety provoked by the inhalation of 35% CO2 is reproducible; (2) placebo has a negligible effect on 35% CO2 reactivity; and (3) reactivity to 35% CO2 is significantly attenuated by short treatment with toloxatone, possibly related to its antipanic activity.

Administration, Inhalation

Lymphocyte cholecystokinin concentrations in panic disorder.

Since cholecystokinin (CCK) is known to be anxiogenic in experimental animals and to induce panic attacks in humans, lymphocyte CCK-8 concentrations were measured in 15 patients with panic disorder and 15 age- and sex-matched healthy subjects. The patients' levels were measured again after a 30-day course of alprazolam therapy, 1.5 mg/day. The CCK-8 concentrations were significantly lower in the patients than in the control subjects and did not change after alprazolam therapy. There was no correlation between the peptide values and levels of anxiety or frequency and severity of panic attacks.

Adolescent