Search PubMed⌕ Search

Biomedical subjects

M B Stein

Publications and source records attributed to M B Stein.

At least 145 records · Page 8Linked to original sources
PubMed1989

Infrequent occurrence of EEG abnormalities in panic disorder.

EEG abnormalities have been frequently reported in patients with panic disorder, although controlled studies are lacking. The authors examined the EEGs of 35 consecutively evaluated, medication-free patients with panic disorder and found that only five (14%) had nonspecific abnormal EEGs and none displayed EEG evidence supportive of an ictal process. The presence or absence of EEG abnormalities was not significantly associated with the presence or absence of psychosensory symptoms. Although it is not likely that panic disorder is an epileptiform disorder, temporal lobe and limbic structures probably play a major role in the pathophysiology of panic.

Adult↗
PubMed1988

The E beta hot spot of recombination in wild-derived natural recombinant MHC haplotypes. Cross-over site mapping and the identification of a 1.0-kb E beta deletion in the p and w14 haplotypes.

Detailed molecular analysis of three wild-derived MHC haplotypes provided evidence for an important role of the E beta recombinational hot spot in the recent evolution of the mouse I region. Examination of RFLP and restriction maps of cloned DNA permitted the mapping of the natural cross-over events in the haplotypes carried by strains B10.GAA37 (w21) and B10.KPB128 (w19) to a fragment of DNA not exceeding 4.1 kb, which lies almost entirely within the intron separating the beta 1 and beta 2 exons of the E beta gene. In the w14 haplotype (strain B10.STC77), which appears to be a natural recombinant between a p-like parental haplotype and another wild-derived haplotype, the site of crossing over can be mapped to a segment between the beta 2 exon of the E beta gene (left border) and the E beta 2 gene (right border). This segment containing the cross-over site in the w14 haplotype includes the E beta hot spot. In addition, the w14 haplotype as well as the standard p haplotype contain a deletion of approximately 1.0 kb in the second intron of the E beta gene, which may represent the product of an unequal cross-over event in a E beta recombinational hot spot.

Animals↗
PubMed1988

Cortisol response to clonidine in panic disorder: comparison with depressed patients and normal controls.

Abnormalities in regulation of noradrenergic function have been proposed as part of the pathology of depressive and panic anxiety disorders. However, abnormalities in hypothalamic-pituitary-adrenal (HPA) axis function have largely been limited to patients with depressive disorders. Using the cortisol response to clonidine, an alpha 2-adrenergic receptor agonist, this study examined the relationship between the noradrenergic system and the HPA axis in 10 patients with major depression (4 unipolar, 6 bipolar), 10 patients with panic disorder, and 10 normal controls. Baseline cortisol was significantly elevated in depressed as compared with panic patients, but not with controls. Depressed patients also tended to exhibit a greater absolute fall in plasma cortisol (5.2 +/- 4.0 micrograms/dl) compared with panic patients (1.7 +/- 2.4 micrograms/dl) (p less than 0.06, t-test). When expressed as a percentage of baseline, however, the cortisol response to clonidine did not differ significantly between diagnostic groups (p greater than 0.10). Basal levels of cortisol were highly correlated with the degree of decrease in cortisol induced by clonidine in the group of 30 subjects (r = -0.81, p less than 0.0001). These findings are discussed in the context of the utility of clonidine as a probe of the functional relatedness of the noradrenergic system and the HPA axis in these disorders.

Adult↗
PubMed1988

Thyroid indices in panic disorder.

The authors compared indices of thyroid function in 26 patients with panic disorder and 26 closely matched control subjects. No significant differences in T3, T4, free T4, thyrotropin, or thyroxine-binding globulin were found between the two groups. Clinical and theoretical implications are discussed.

Adult↗
PubMed1988

Lack of efficacy of carbamazepine in the treatment of panic disorder.

The authors conducted a controlled study of carbamazepine in the treatment of 14 patients with panic disorder. Although there was a statistically significant reduction in symptoms of anxiety on several measures, only one of the patients was judged to have a marked and sustained clinical improvement while taking carbamazepine. Forty percent of the patients had a decrease in frequency of panic attacks during carbamazepine treatment, 50% had an increase, and 10% showed no change. The presence of either EEG abnormalities or prominent psychosensory symptoms did not predict response to carbamazepine. These findings are discussed within the context of an epileptiform model for panic disorder.

Adult↗
PubMed1988

Panic disorder and major depression. A tale of two syndromes.

Considerable research has been conducted to clarify relationships between panic disorder and major depression. From a number of perspectives, it now appears that panic disorder and major depression are not identical illnesses. While many patients with panic disorder are likely to experience an episode of major depression at some point during their lives, the timing of this occurrence is highly variable. While depression may be an expected and understandable result of having to live with chronic anxiety and phobic avoidance, the available evidence suggests that such a hypothesis is not particularly tenable. Depression can occur in individuals with or without severe agoraphobia and in individuals ill with panic for greater or lesser periods of time. Comorbidity in panic, particularly for social phobic or obsessive-compulsive symptomatology, does serve as a risk factor for the lifetime occurrence of depression and may denote a more severe illness. Biologic markers (Table 4), while of limited diagnostic utility in clinical practice, may reveal important pathophysiologic similarities and differences between panic disorder and major depression. Current evidence points to many areas of biologic overlap, with some important areas of independence (Fig. 7A). Although not extensively discussed in this chapter, several clinical parameters paint an analogous picture (Fig. 7B). There is a need for future studies of biologic markers in individuals over time, in various phases of illness. Furthermore, the study of multiple biologic markers in the same individuals would be a worthwhile pursuit, perhaps leading toward the delineation of underlying pathophysiologic mechanisms. In summary, then, we favor a conceptualization of panic disorder and major depression as nonidentical disorders with many shared characteristics. Future studies as suggested above, particularly when coupled with the power of genetic studies not described in this chapter, may eventually lead to a clearer demarcation of the boundaries between these two intriguing psychiatric syndromes.

Anxiety Disorders↗
PubMed1986

Depression associated with ranitidine.

The authors report three cases of depression associated with ranitidine. These illustrate that ranitidine, like cimetidine, may produce an organic affective disorder. The authors discuss clinical implications for the treatment of depression in patients with peptic ulcer disease.

Adult↗
PubMed1986

Acute paranoid disorder and Klinefelter's syndrome.

A twenty-five-year old man presented with an acute paranoid disorder, and was subsequently diagnosed as having Klinefelter's Syndrome. Our review of previous reports suggests that the literature pointing out a particular association between Klinefelter's and schizophrenia may be misleading. In fact, Klinefelter's patients are liable to suffer from schizophrenia, paranoid disorders, or possibly other disorders.

Acute Disease↗
PubMedDate not supplied

Dot-probe evaluation of cognitive processing biases in patients with panic disorder: a failure to replicate and extend.

A number of cognitive psychology paradigms have been used to demonstrate that panic disorder patients selectively process stimuli that are related to themes of physical threat and catastrophe. The present investigation was an attempt to replicate and extend initial findings obtained with the dot-probe paradigm, a visual attention paradigm which allows for the assessment of allocation of visual attention to stimuli of varied emotional valence via the measurement of detection latencies for visual probes that follow their presentation. Twenty-two panic disorder patients and 20 healthy control subjects were tested using neutral, social threat, and panic symptom/fear cues. No between-group differences were observed in detection latencies for visual probes that followed neutral, social threat, or panic symptom/fear cues. These results represent a failure to replicate previous reports of selective processing in panic disorder and suggest that panic disorder patients may not selectively process cues related to bodily sensation and panic-related fears. Implications of this finding are discussed.

Adult↗