Robert J. Jackson

Expectancy theory posits that anxiety sensitivity may serve as a premorbid risk factor for the development of anxiety pathology (S. Reiss, 1991). The principal aim of the present study was to determine whether anxiety sensitivity acts as a specific vulnerability factor in the pathogenesis of anxiety pathology. A large, nonclinical sample of young adults (N = 1,401) was prospectively followed over a 5-week highly stressful period of time (i.e., military basic training). Anxiety sensitivity was found to predict the development of spontaneous panic attacks after controlling for a history of panic attacks and trait anxiety. Approximately 20% of those scoring in the upper decile on the Anxiety Sensitivity Index (R. A. Peterson & S. Reiss, 1987) experienced a panic attack during the 5-week follow-up period compared with only 6% for the remainder of the sample. Anxiety sensitivity also predicted anxiety symptomatology, functional impairment created by anxiety, and disability. These data provide strong evidence for anxiety sensitivity as a risk factor in the development of panic attacks and other anxiety symptoms.

Stereotactic biopsy is often performed for diagnostic purposes before treating patients whose imaging studies highly suggest glioma. Indications cited for biopsy include diagnosis and/or the "inoperability" of the tumor. This study questions the routine use of stereotactic biopsy in the initial management of gliomas. At The University of Texas M. D. Anderson Cancer Center, we retrospectively reviewed a consecutive series of 81 patients whose imaging studies suggested glioma and who underwent stereotactic biopsy followed by craniotomy/resection (within 60 days) between 1993 and 1998. All relevant clinical and imaging information was reviewed, including computerized volumetric analysis of the tumors based on pre- and postoperative MRI. Stereotactic biopsy was performed at institutions other than M. D. Anderson in 78 (96%) of 81 patients. The majority of tumors were located either in eloquent brain (36 of 81 = 44%) or near-eloquent brain (41 of 81 = 51%), and this frequently was the rationale cited for performing stereotactic biopsy. Gross total resection (>95%) was achieved in 46 (57%) of 81 patients, with a median extent of resection of 96% for this series. Diagnoses based on biopsy or resection in the same patient differed in 40 (49%) of 82 cases. This discrepancy was reduced to 30 (38%) of 80 cases when the biopsy slides were reviewed preoperatively by each of three neuropathologists at M. D. Anderson. Major neurologic complications occurred in 10 (12.3%) of 81 surgical patients and 3 (3.7%) of 81 patients undergoing biopsy. Surgical morbidity was probably higher in our series than it would be for glioma patients in general because our patients represent a highly selected subset of glioma patients whose tumors present a technical challenge to remove. Stereotactic biopsy is frequently inaccurate in providing a correct diagnosis and is associated with additional risk and cost. If stereotactic biopsy is performed, expert neuropathology consultation should be sought.

Increasing evidence suggests that anxiety sensitivity (AS) may be a premorbid risk factor for the development of anxiety pathology. The principal aim of this study was to replicate and extend a previous longitudinal study evaluating whether AS acts as a vulnerability factor in the pathogenesis of panic (N. Schmidt, D. Lerew, & R. Jackson, 1997). A large nonclinical sample of young adults (N = 1,296) was prospectively followed over a 5-week, highly stressful period of time (i.e., military basic training). Consistent with the authors' initial study, AS predicted the development of spontaneous panic attacks after controlling for a history of panic attacks and trait anxiety, and AS was found to possess symptom specificity with respect to anxiety versus depression symptoms. AS 1st-order factors differentially predicted panic attacks, with the Mental Concerns factor being the best predictor of panic in this sample.

Blaschko's lines are the pattern assumed by many different naevoid and acquired skin diseases on the human skin and mucosae. They were described and drawn by Blaschko 75 years ago. These lines are to be distinguished from other linear patterns such as Voight's lines, Langer's lines, and the lines of innervation of the spinal nerves. They do not follow any known nervous, vascular or lymphatic structures in the skin. The epidermis and its appendageal structures, the melanocytes, the vascular system, and the fatty hypoderm, all, separately or in combination, may be involved in the morphological manifestations which follow Blaschko's lines. Many of the naevoid skin conditions are lifelong (e.g. linear sebaceous naevus, unilateral naevoid telangiectasia); many of the acquired skin diseases (e.g. lichen striatus, linear psoriasis) are of relatively short duration (e.g. 1-2 years). The cause of the distribution pattern is unknown. It is possibly a form of human 'mosaicism' where certain specific cells or groups of cells react differently from other cells due to chromosomal abnormalities. The embryological explanation of Blaschko's lines is not at all clear. Other markers in addition to the skin findings are needed to determine the time and the nature of the change responsible for these lines. The main purpose of this article is to introduce the concept of Blaschko's lines into the medical, paramedical, and general biological fields of science. In this way, it is hoped that some inter-reaction can occur between those who regularly see Blaschko's lines and those who regularly see and study other chromosomal and embryological abnormalities.