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Dive into the research topics where Thomas W. McNeill is active.

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Featured researches published by Thomas W. McNeill.


Spine | 1983

Trunk muscle myoelectric activities in idiopathic scoliosis.

Mark Reuber; Albert B. Schultz; Thomas W. McNeill; David L. Spencer

Twenty adolescent girls with mild-to-moderate cases of idiopathic scoliosis and twelve adolescent girls with structurally normal spines performed 15 exercises isometrically while standing. The exercises included resisting flexion, extension, and lateral bending moments imposed on the trunk. Myoelectric activities in 12 trunk muscle groups were measured during these performances, using surface electrodes. For one set of comparisons, the patients were divided into those whose clinical records documented curve progression and those with no documented progression. No significant differences were noted in mean myoelectric activities between these two patient groups. For a second set of comparisons, the subjects were divided into patients with curves of more than 25 degrees, patients with curves of 25 or fewer degrees and normals. No significant differences in mean myoelectric activities were noted between the patients with the smaller curves, while the patients with the larger curves had significantly larger convex side myoelectric activities in their anterior, lateral and posterior muscles at lumbar levels compared to the normal girls. The findings of this study, along with biomechanical model analyses, suggest that the asymmetries in muscle actions evidenced by myoelectric measurements result from scoliosis. Scoliosis progression seems not to be caused by asymmetry in muscle contractions; rather it may be caused by a lack of adequate asymmetry.


Spine | 1982

Organic status, psychological disturbance, and pain report characteristics in low-back-pain patients on compensation.

Frank Leavitt; David C. Garron; Thomas W. McNeill; Walter W. Whisler

The relationship between compensation and three variables—psychologic disturbance, organic status, and pain report characteristics— was assessed. Patients on compensation were clinically similar to patients not on compensation in the relative frequency of cases of psychologic disturbance and nonorganic findings in each group. Patients on compensation differed only when objective evidence of organic disease and psychologic stability was present. Under these circumstances, the compensation group used 43% more words to describe their pain and endorsed more pain qualities on five independent dimensions of pain. These results indicate that compensation primarily affects the description of low-back pain in cases where objective evidence of injury is present and leads to an intensification of sensory discomfort. Little justification was found for the atmosphere of suspicion that surrounds patients on compensation who have no evidence of organic disease.


Pain | 1979

Low back pain in patients with and without demonstrable organic disease.

Frank Leavitt; David C. Garron; Charles M. D'Angelo; Thomas W. McNeill

&NA; Pain descriptors of patients with low back pain were analyzed to determine their usefulness in identifying patients without demonstrable organic disease. Using a standardized back pain questionnaire which scales qualities of pain along 7 independent factors, it was possible to make clear distinctions between the subjective reports of patients with and without demonstrable organic disease of the lower back. Pain described by patients with demonstrable organic disease tends to be consistent and specific; whereas pain described by patients without demonstrable organic disease tends to be more variable and diffuse. Pain reported by the latter group was also more intense. Factors which may underlie these findings were discussed.


Spine | 1994

The dose-related effect of intradiscal chymopapain on rabbit intervertebral discs

Douglass P. Kiester; James M. Williams; Gunnar B. J. Andersson; Eugene J.-M.A. Thonar; Thomas W. McNeill

Study Design This study analyzed the histological and biochemical respoonses of intervertebral disc tissue to intradiscal injection of varying amounts of chymopapain. Objective To determine the appropriate amount of chymopapain needed to accomplish effective degradation of proteoglycans (PG) in the nucleus pulposus of intervertebral discs. Summary of Background Data Chymopapain is an accepted treatment alternative for patients with disc herniations. The recommended clinical dose of 2,000–4,000 pkats per injection is derived from early animal studies and empirical results in man. A lower effective dose could reduce the complication rate while providding similar clinical results. Methods Twenty to 4,000 pkat of chymopapain was injected into rabbit discs, and the level of keratan sulfate (KS) epitope in serum was measured at different times after the injection. The animals were killed after 6 days and the injected and two neighboring discs were examined histologically. Results The serum KS level did not change appreciably after injection of 20 pkat, rose moderately at 100 and 200 pkat, and rose strongly at 500 pkat. Doses greater than 500 pkat did not result in further increase in the KS level. Conclusion Degradation of the disc proteoglycans is dose dependent and reaches a maximum at 500 pkat. Higher doses appear not to cause further loss of aggrecan molecules, and injection of more than, 1,000 pkat produces significant annual destruction.


Archive | 1989

The patient with spinal infection

Gunnar B. J. Andersson; Thomas W. McNeill

The key problem in spinal infection is the failure of the medical community to appreciate that these problems continue to exist and are actually relatively common and increasing in frequency. The increase in frequency is due to several factors: (1) Our elderly population is increasing, and even without concurrent illnesses this group has a less than normal competent immune system. (2) An increasing number of patients with immune deficiencies, either of the infectious acquired type or secondary to treatment of malignant or autoimmune disease. (3) Large migrations of populations from TB endemic regions.


Archive | 1989

The patient with a spine tumor

Gunnar B. J. Andersson; Thomas W. McNeill

Tumors of the spine are comparatively uncommon, but the consequences can be disastrous. Therefore the possibility of a tumor in a patient presenting with low back pain should be kept in mind. Tumors producing lower back pain can be either benign or malignant; they can be either primary or metastatic; they can be in the bone, in the epidural space or inside the thecal sac. Primary tumors of the spine or its contents are rare, but metastatic tumors are not uncommon in older age groups. Metastatic lesions most often involve the bone, less often the epidural space, and rarely metastatic lesions may be intrathecal. On occasion, tumors involving the pelvis can mimic one of the lumbar spine syndromes, and tumors of the lower extremity can mimic sciatica (Boland et al., 1987; Mindell, 1981; Schajowicz, 1981; Sim et al., 1977; Simone and Lawner, 1982; Weinstein and McLain, 1987).


Archive | 1989

The patient with acute low back pain

Gunnar B. J. Andersson; Thomas W. McNeill

The twelve symptoms and signs in Table 1 constitute the most common significant clinical syndrome in the constellation of syndromes in which “acute low back pain” is the central unifying symptom. It is rare, however, that the actual patient’s symptoms and signs have a one-to-one correspondence with this list. One or several of the twelve can be missing. However, significant deviations from this list should warn the clinician that a different and possibly more serious pathological condition may be present. Conversely, absolute correspondence with this list does not guarantee that the pathologies described below are the cause of the patient’s symptoms. The physician must be diligent in observing the patient’s changing state so as to detect changes that will require a new analysis of the patient’s status and a new approach to diagnosis and treatment.


Archive | 1989

The patient with inflammatory spine disease

Gunnar B. J. Andersson; Thomas W. McNeill

The syndrome described in Table 1 is caused by a group of inflammatory diseases which are thought to result from a derangement of the immune mechanism of the body. These so-called sero-negative spondylarthropathies share a variety of clinical, radiographic and genetic features (Kohler and Vaughan, 1982; Moll, 1974; Brewerton et al. 1973; Jayson, 1986). Although, both inflammatory arthritis and spondylitis are major components of each of these diseases, they are not to be thought of as variations of rheumatoid arthritis. This clinical distinction is important since complications, response to therapy and progress are quite different. Inflammatory spinal disease, extra-articular foci, particularly eye disease, and a tendency for onset in young, mainly male, adults are uniting features linking this group of diseases together. Additionally, three of the five subgroups in this category have a very high incidence of the histocompatibility antigen HLA-B27 among those afflicted with the spinal component of the disease, and an even greater proportion are HLA-B27 positive if they manifest both the eye and spinal components (Table 2). The five sub-groups to be considered are: (1) ankylosing spondylitis; (2) “reactive arthritis”; (3) Reiter’s syndrome; (4) inflammatory bowel disease; and (5) psoriasis (Table 3). In the inflammatory bowel disease and psoriasis the HLA-B27 antigen is not a factor unless there is spinal involvement and then not nearly in as great a proportion as in the other three groups (Mills et al., 1975).


Archive | 1989

The patient with functional disease/malingering

Gunnar B. J. Andersson; Thomas W. McNeill

The problem of the perception of pain, the patient’s potential advantages in having others perceive him as being the “victim” of a painful condition, and the inability of the physician to validly measure pain cause most examining physicians to delay the proper diagnosis of “psychogenic pain” and/or “central pain” to the potential detriment of all concerned. The detriment comes from the repetitive and redundant search for a nonexistent somatic cause for the pain and the institution of different unsuccessful treatments. In order for the physician to clearly understand the problem of functional disease and/or malingering it is essential to understand some basic modern concepts of pain, it is transmission, perception, and clinical presentation. In general, this was discussed in Chap. 1, and should be reviewed before reading further into this chapter.


Archive | 1989

The patient with lower back pain, sciatica, and inability to void

Gunnar B. J. Andersson; Thomas W. McNeill

The constellation of signs and symptoms listed in Group D of Table 1 are known collectively as the “cauda equina syndrome”. The distinguishing feature of this syndrome is the involvement of the sacral roots below the S-1 level. These symptoms distinguish the cauda equina syndrome from acute benign lower back pain (Group A), acute lower back pain with radicular symptoms (Group C) and the lower back pain which is not primarily spinal in origin (Group B). In the early reports on disc operations this, most severe of the disc hernia syndromes, was represented by a disproportionate number of case. Seven of Mixter and Barr’s original cases had a variation of this syndrome. Large recent studies (Spangfort, 1972; Raaf, 1959) indicate that the actual incidence of cauda equina syndrome in patients with disc herniation is low; closer to two percent overall. It is important to recognize that disc herniation is not the only cause of cauda equina syndrome; but, it is by far the most common. Other causes of sacral root neural compression are tumors and infections.

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Frank Leavitt

Rush University Medical Center

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David C. Garron

Rush University Medical Center

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Eugene J.-M.A. Thonar

Rush University Medical Center

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Charles M. D'Angelo

Rush University Medical Center

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David L. Spencer

University of Illinois at Chicago

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Glenda Sinkora

University of Illinois at Chicago

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Gunnarb. J. Andersson

Rush University Medical Center

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James M. Williams

Rush University Medical Center

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