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At least 559 records · Page 31Linked to original sources

PubMed2003

Atrophy of the abdominal wall muscles after extraperitoneal approach to the aorta.

OBJECTIVE: We retrospectively assessed computed tomography (CT) scans to determine degree of anterolateral abdominal muscle atrophy in patients who underwent infrarenal aortic repair with 2 kinds of incisions for the extraperitoneal approach. METHODS: CT scans obtained before surgery and final scans obtained 2 to 100 months after surgery were assessed in 12 patients with paramedian incision (PM group) and 27 patients with flank incision (F group) who could be followed up at our hospital. We considered muscle thickness before surgery on the incision side to be 100% thickness (baseline value), and we calculated, by measuring the incision side after surgery, the corrected percent thickness (CPT%), which represents percentage of remaining muscle thickness that has escaped incision-induced atrophy. CT scans obtained at the level of the third (L3) and fifth (L5) lumbar vertebrae and the center of the sacrum (S) were selected for CPT% measurement. RESULTS: Duration from surgery to final CT scan was 2 to 65 months (mean +/- SD, 34.33 +/- 21.38 months) in PM group and 3 to 96 months (27.85 +/- 20.74 months) in F group. In PM group, mean CPT% values of the rectus abdominis muscle were 55.83 +/- 21.65% at L3, 35.50 +/- 10.79% at L5, and 31.92 +/- 11.00% at S; these values were statistically much smaller than baseline (P <.01). Mean CPT% values of the lateral abdominal muscles were not statistically different from baseline. In F group, mean CPT% values of the rectus abdominis muscle were 82.19 +/- 23.15% at L5 and 64.41 +/- 31.34% at S; these values were statistically smaller than baseline (P <.01). Mean CPT% values of the lateral abdominal muscles were 87.59 +/- 22.30% at L3 and 84.59 +/- 26.90% at L5; these values were statistically smaller than baseline (P <.05). CONCLUSIONS: Paramedian incision induced severe rectus abdominis muscle atrophy. Although flank incision induced various degrees of atrophy in both muscles, some patients had no muscle atrophy. These data indicate that further anatomic investigation into the relation between flank incision and abdominal wall innervation may contribute to prevention of muscle atrophy after flank incision.

Abdominal Muscles↗

PubMed1999

Masticatory muscle function in patients with spinal muscular atrophy.

The purpose of this study was to determine whether spinal muscular atrophy affects masticatory muscle strength and mandibular range of motion. A sample of 15 subjects with spinal muscular atrophy was compared to a sample of age-matched and sex-matched controls. Maximum bite force, masticatory muscle electromyography activity, mandibular ranges of motion and masticatory muscle endurance were evaluated. Results showed that maximum bite forces were one-half as great for the sample with spinal muscular atrophy than for the controls, even though their EMG activity was not significantly different. Slopes of the relationship between electromyography activity and bite force were two to four times steeper for patients with spinal muscular atrophy than controls. Maximum opening and protrusion were reduced to approximately one-half control values. Fatigue times of patients with spinal muscular atrophy were reduced by 30% (17.9 seconds versus 11.1 seconds). We conclude that the masticatory muscles of patients with spinal muscular atrophy are weakened, that their muscles are less efficient, and that they fatigue more quickly than controls. In addition, mandibular movements of these patients take place over a more limited range than unaffected controls.

Adolescent↗

PubMed2002

Autosomal dominant distal spinal muscular atrophy: an Italian family not linked to 12q24 and 7p14.

Distal spinal muscular atrophy is genetically heterogeneous, as sporadic cases and both autosomal dominant and recessive inheritance have been described. An autosomal dominant distal spinal muscular atrophy with upper limb predominance has been mapped to chromosome 7p, and more recently, an autosomal dominant distal spinal muscular atrophy with lower limb predominance has been linked to chromosome 12q24. We describe a four generation Italian family with autosomal dominant distal spinal muscular atrophy starting between 8 and 30 years with weakness and atrophy of distal leg muscles. The older patients also presented sensorineural deafness. We performed genetic linkage analysis with microsatellite markers D12S366, D12S349, D12S86, D12S321, D12S1612, D12S1349, D12S342, PLA2A on chromosome 12q24 and D7S516, D7S2496, D7S632, D7S2252 on chromosome 7p14. No support for linkage to chromosome 12q24 and 7p14 was found in our family, confirming a genetic heterogeneity within autosomal dominant distal spinal muscular atrophy.

Adolescent↗

PubMed2006

The measurement and clinical relevance of brain atrophy in multiple sclerosis.

Brain atrophy has emerged as a clinically relevant component of disease progression in multiple sclerosis. Progressive loss of brain tissue bulk can be detected in vivo in a sensitive and reproducible manner by MRI. Clinical studies have shown that brain atrophy begins early in the disease course. The increasing amount of data linking brain atrophy to clinical impairments suggest that irreversible tissue destruction is an important determinant of disease progression to a greater extent than can be explained by conventional lesion assessments. In this review, we will summarise the proposed mechanisms contributing to brain atrophy in patients with multiple sclerosis. We will critically discuss the wide range of MRI-based methods used to quantify regional and whole-brain-volume loss. Based on a review of current information, we will summarise the rate of atrophy among phenotypes for multiple sclerosis, the clinical relevance of brain atrophy, and the effect of disease-modifying treatments on its progression.

Atrophy↗

PubMed2004

The detection and management of vaginal atrophy.

OBJECTIVE: To support the practitioner in the diagnosis of vaginal atrophy and in the management of the related symptoms. OPTIONS: The modalities of evaluation range from basic pelvic examination, examination of the vulva, and laboratory tests. OUTCOMES: A comprehensive approach to the detection of vaginal atrophy and a discussion of available therapeutic and nontherapeutic options. EVIDENCE: Published opinions of experts, supplemented by evidence from clinical trials, where appropriate. VALUES: The quality of the evidence is rated using the criteria described by the Canadian Task Force on the Periodic Health Examination. BENEFITS, HARMS, AND COSTS: Diagnosis of vaginal atrophy is often a challenge because women are unwilling to report symptoms, which have the potential to significantly decrease their quality of life. Increased clinical suspicion is the first step in the diagnosis of vaginal atrophy, which will prompt the initiation of safe therapies with proven efficacy. RECOMMENDATIONS: 1. Health-care providers should routinely assess postmenopausal women for the symptoms and signs of vaginal atrophy, a common condition that exerts significant negative effects on quality of life. (III-C) 2. Regular sexual activity should be encouraged to maintain vaginal health. (II-2B)3. Women experiencing recurrent urinary tract infections should be instructed that consumption of pure cranberry-lingonberry juice, rather than cranberry drink, will decrease their risk of urinary tract infections. (I-A) 4. Vaginal moisturizers applied on a regular basis have an efficacy equivalent to local hormone replacement for the treatment of local urogenital symptoms such as vaginal itching, irritation, and dyspareunia, and should be offered to women wishing to avoid use of hormone replacement therapy. (I-A) 5. Women experiencing vaginal atrophy can be offered any of the following effective vaginal estrogen replacement therapies: conjugated equine estrogen cream (I-A), a sustained-release intravaginal estradiol ring (I-A), or a low-dose estradiol tablet (I-A). 6. Although systemic absorption of estrogen can occur with local preparations, there is insufficient data to recommend annual endometrial surveillance in asymptomatic women using local estrogens. (III-C) 7. For menopausal women experiencing recurrent urinary tract infections and who have no contraindication to local hormone replacement, vaginal estrogen therapy should be offered. (I-A).

Administration, Intravaginal↗

PubMed2000

Callosal atrophy correlates with temporal lobe volume and mental status in Alzheimer's disease.

BACKGROUND: Recent studies have reported significant atrophy of the corpus callosum (CC) in Alzheimer's Disease (AD). However, it is currently unknown whether CC atrophy is associated with specific cortical volume changes in AD. Moreover, possible atrophy in extra-callosal commissures has not been examined to date. The purpose of the present study was to quantify atrophy in two cerebral commissures [the CC and the anterior commissure (AC)], to correlate this measure with cognitive status, and to relate commissural size to independent measures of temporal lobe volume in AD patients. METHODS: A sample of AD patients and of age- and education-matched normal control subjects (NCs) underwent MRI and a cognitive test battery including the Dementia Rating Scale and Mini Mental State examination. Mid-sagittal regional areas within CC and AC were measured along with superior, middle and inferior temporal lobes volumes. RESULTS: Alzheimer's Disease patients had significantly smaller callosa than did NCs. The callosal regions most affected in AD included the midbody, isthmus and genu. The isthmus and midbody areas of the CC were positively correlated with cognitive performance and with superior temporal lobe volume in AD patients. The mid-sagittal area of the AC and the superior temporal volumes did not differ between AD patients and NCs. CONCLUSIONS: The study demonstrated that the regional morphology of the CC correlates with current cognitive status and temporal lobe atrophy in AD. As well, the lack of difference for the AC suggests that commissural atrophy in AD is regionally specific.

Aged↗

PubMed1997

Age of onset and brain atrophy in Alzheimer's disease.

Using magnetic resonance imaging-based planimetry, we measured cortical and cerebral (cortical and ventricular) atrophy in 26 patients with Alzheimer's disease (AD) (age, 72.2 +/- 7.0) according to NINCDS-ADRDA criteria and 22 control subjects (age, 71.5 +/- 5.4). AD patients exhibited greater cerebral atrophy (p < .05) than control subjects. Cerebral atrophy was significantly correlated with age (r = .72, p < .0005) in healthy volunteers but not in AD patients. In AD patients, age of onset was negatively correlated with the estimated rate of disease-attributed cerebral degeneration ([observed atrophy--atrophy in normal aging calculated from the regression equation derived from the control group]/[duration of illness]) (r = -.54, p < .005). Multiple regression with interaction analysis demonstrated that age, age of onset, and their interaction successfully explained cerebral (R2 = .51, p < .05) and cortical (R2 = .64, p < .05) atrophy in patients with probable AD. Age of onset may be a strong predictor of the rate of cerebral degeneration in AD, and our results suggest that controlling age and the age of onset is essential in the quantitative study of AD.

Age of Onset↗

PubMed2004

Seronegative celiac disease: increased prevalence with lesser degrees of villous atrophy.

Our aim was to assess differences in the sensitivities of serologic tests used for the diagnosis of celiac disease among patients with varying degrees of villous atrophy. Among 115 adults with biopsy-proven celiac disease who fulfilled strict criteria, including serologic testing at the time of diagnosis and response to a gluten-free diet, 71% had total villous atrophy and 29% partial villous atrophy. Endomysial antibody was positive in 77% of those with total villous atrophy, compared to 33% with partial villous atrophy (P < 0.001). There was no difference in sensitivity when the type of presentation (classical vs. silent) was compared. Endomysial antibody-positive and negative patients did not differ with respect to age at diagnosis, duration of symptoms, mode of presentation, or family history of celiac disease. All anti-tissue transglutaminase-positive patients had TVA on biopsy. Seronegative celiac disease occurs. Endomysial antibody positivity correlates with more severe villous atrophy and not mode of presentation of celiac disease. Serologic tests, in clinical practice, lack the sensitivity reported in the literature.

Adult↗

PubMed2003

Indocyanine green angiography in pigmented paravenous retinochoroidal atrophy.

PURPOSE: To report long-term follow-up of patients with pigmented paravenous retinochoroidal atrophy (PPRCA) and to assess the involvement of the choroid and retinal pigment epithelium (RPE) in PPRCA. METHODS: Clinical features of PPRCA were studied retrospectively in four patients followed for 6-26 years. Retinal pigment epithelium and choroidal changes were analysed with fluorescein and indocyanine green (ICG) angiography. RESULTS: The two younger patients, aged 16 and 28 years and followed for 6 and 18 years, respectively, showed stationary RPE atrophy and pigmentation. Indocyanine green angiography visualized slight to modest atrophy of the choriocapillaris. The two older patients, aged 69 and 70 years and each followed for 26 years, showed slow progression of disease during follow-up. Indocyanine green angiography revealed choriocapillaris atrophy partly extending into the areas shown as hyperfluorescent in fluorescein angiography. CONCLUSION: Pigmented paravenous retinochoroidal atrophy is probably a slowly progressive disease, particularly in older patients. The choriocapillaris atrophy in this disease is more properly evaluated by ICG angiography and can be underestimated by fluorescein anigiography.

Adult↗

PubMed1988

Evolution of geographic atrophy of the retinal pigment epithelium.

The aim of this study was to trace the evolution of geographic atrophy (GA) by clinical documentation and by clinico-morphological correlation in representative eyes. Geographic atrophy commonly commenced within a parafoveal band of incipient atrophy of varying width, characterised by semisolid drusen and a microreticular pigment pattern. Progression of atrophy mostly skirted fixation and visual acuity was a poor guide to the functional impact, an estimate of the percentage of fovea involved proving a more useful clinical parameter. The rate of progression slowed once GA had involved all the retina affected by incipient atrophy and the risk of choroidal neovascularization appeared to decline. An earlier histological classification of the evolution of GA is revised according to the ultrastructural findings. Membranous debris was not previously recognised and its contribution to the findings in incipient atrophy and to dot-like drusen is described.

Aged↗

PubMedDate not supplied

Localisation of the gene for a dominant congenital spinal muscular atrophy predominantly affecting the lower limbs to chromosome 12q23-q24.

Spinal muscular atrophies are a heterogeneous group of disorders. They differ in time of onset, clinical presentation, progression, severity and mode of inheritance. In 1985 a Dutch family was described with a dominant, non-progressive spinal muscular atrophy presenting at birth with arthrogryposis (MIM 600175). Linkage analysis was performed in this family. After having excluded the loci for Werdnig-Hoffmann's disease and for dominant distal spinal muscular atrophy with upper limb predominance, we were able to localise the gene to a 10 cM interval between the markers D12S78 and D12S1646 on chromosome 12q23-q24. Recently, dominant scapuloperoneal spinal muscular atrophy has been localised to an overlapping interval. However, the clinical appearances of scapuloperoneal spinal muscular atrophy and the present disorder make allelism unlikely. In 1994, a second Dutch family with a disorder similar to the present one was described. We excluded linkage to markers of the 12q23-q24 region in this family and thereby proved genetic heterogeneity of this type of dominant, congenital and nonprogressive spinal muscular atrophy.

Chromosome Mapping↗

PubMed1998

Muscle atrophy is prevented in patients with acute spinal cord injury using functional electrical stimulation.

Severe muscle atrophy occurs rapidly following traumatic spinal cord injury (SCI). Previous research shows that neuromuscular or 'functional' electrical stimulation (FES), particularly FES-cycle ergometry (FES-CE) can cause muscle hypertrophy in individuals with chronic SCI (> 1 year post-injury). However, the modest degree of hypertrophy in these already atrophied muscles has lessened earlier hopes that FES therapy would reduce secondary impairments of SCI. It is not known whether FES treatments are effective when used to prevent, rather than reverse, muscle atrophy in individuals with acute SCI. This study explored whether unloaded isometric FES contractions (FES-IC) or FES-CE decreased subsequent muscle atrophy in individual with acute SCI (< 3 months post-injury). Twenty-six subjects, 14-15 weeks post-traumatic SCI, were assigned to control, FES-IC, or FES-CE against progessively increasing resistance. Subjects were involved in the study for 3 or 6 months. Total body lean body mass (TB-LBM), lower limb lean body mass (LL-LBM), and gluteal lean body mass (G-LBM) were determined before the study, and at 3 and 6 months using dual energy X-ray absorptiometry (DEXA). Controls lost an average of 6.1%, 10.1%, 12.4%, after 3 months and 9.5%, 21.4%, 26.8% after 6 months in TB-LBM, LL-LBM and G-LBM respectively. Subjects in the FES-IC group consistently lost less lean body mass than controls, however, only 6 month G-LBM loss was significantly attenuated in this group relative to the controls. In the FES-CE group, LL-LBM and G-LBM loss were prevented at both 3 and 6 months, and TB-LBM loss was prevented at 6 months. In addition, FES-CE significantly increased G-LBM and LL-LBM after 6 months of training relative to pre-training levels. Within the control group, there was no significant relationship between LL-LBM loss (3 and 6 months) and the number of days between injury and baseline measurement. In summary, this study shows that FES-CE, but not FES-IC, training prevents muscle atrophy in acute SCI after 3 months of training, and causes significant hypertrophy after 6 months. The magnitude of differences in regionalized LBM between controls and FES-CE subject raises hopes that such treatment may indeed be beneficial in preventing secondary impairments of SCI if employed before extensive post-injury atrophy occurs.

Adult↗

PubMed1977

The effect of disuse muscular atrophy on the forces generated in dynamic exercise.

1. Six patients were studied after prolonged immobilization of an injured leg resulting in muscle atrophy. 2. The forces exerted by the atrophied and normal legs during continuous dynamic exercise (one- and two-leg cycling) were examined by a specially adapted ergometer. 3. In one-leg cycling the peak force exerted on the crank at a given work rate, the net work rate performed on the crank, and the proportion of work rate performed in leg extension and flexion phases of the cycle were the same whether the atrophied or normal limb was used. 4. Despite these similarities there was an unexplained reduction in efficiency when using the atrophied leg to perform one-leg cycling. 5. In two-leg cycling the peak force exerted at a given work rate by the atrophied leg was reduced by about 40% as compared with the normal leg, which reflected a similar reduction in the contribution of that leg to the total net work rate. Possible reasons and implications for this disproportionate sharing of work between the normal and atrophied leg are discussed.

Adult↗

PubMed2003

Cutaneous polyarteritis nodosa in patients presenting with atrophie blanche.

BACKGROUND: The term 'atrophie blanche' is used both as a descriptive term denoting ivory-white stellate scars on the lower limbs as well as a diagnostic label synonymous with livedoid vasculitis, an ill-defined entity. Medium-sized vasculitides, such as polyarteritis nodosa (PAN), occasionally present with ulceration resulting in ivory-white stellate scarring on the lower limbs and may potentially be misdiagnosed as livedoid vasculitis. OBJECTIVES: To assess the occurrence, clinical and immunopathological features of medium-sized vasculitis in patients presenting with atrophie blanche without clinical and/or compression duplex ultrasonographic evidence of venous insufficiency. METHODS: We retrospectively evaluated patients presenting with atrophie blanche at the Department of Dermatology of Johns Hopkins Medical Institutions, from April 1996 until April 2002, following the diagnostic guidelines for leg ulcers of the Division of Immunodermatology. Deep and multiple skin biopsies were performed for histology. Investigations for underlying vasculitis, thrombophilia, nerve conduction studies and compression duplex ultrasonography of the lower extremities were performed in all patients. RESULTS: Of 29 consecutive patients presenting with atrophie blanche, six had underlying medium-sized vasculitis consistent with PAN, three of whom had previously been diagnosed to have segmental hyalinizing vasculitis/vasculopathy (livedoid vasculitis/vasculopathy) on superficial biopsies. All six patients with cutaneous PAN were women with a median age of 36.5 years (range 34-46) and with a median duration of the disease prior to diagnosis of 18 years (range 3-30). Of the six cutaneous PAN patients, four had neurological involvement evidenced by clinical symptoms and nerve conduction studies. No evidence of any other extracutaneous involvement was found. Erythrocyte sedimentation rate and tests for vasculitis and thrombophilic were normal in all six patients. None had evidence of venous insufficiency. Immunosuppressive therapy was effective in controlling PAN-associated cutaneous and neurological disease. Of the remaining 23 patients, two had antiphospholipid syndrome and one had homocystineaemia; all three also had evidence of venous insufficiency. One patient had multiple myeloma-associated type I cryoglobulinaemia and 19 patients had venous insufficiency alone. None of the non-PAN patients had abnormalities in the nerve conduction studies. CONCLUSIONS: In patients presenting with atrophie blanche without evidence of venous insufficiency and thrombophilia, PAN should be excluded, particularly in the presence of mononeuritis multiplex. Repeated and deep biopsies are often necessary to reveal the accurate underlying pathology of necrotizing medium-sized vasculitis in the reticular dermis and the subcutis, especially in the setting of atrophie blanche lesions. Immunosuppressive therapy was effective in controlling the PAN-associated clinical manifestations.

Adult↗

PubMed2001

Imaging and clinical characteristics of focal atrophy of segments 2 and 3 in primary sclerosing cholangitis.

BACKGROUND AND AIMS: Focal atrophy in primary sclerosing cholangitis (PSC) is usually thought to result from severe biliary stricture and focal biliary cirrhosis. Atrophy of the left lateral segments (segments 2 and 3) are striking when observed grossly. This type of atrophy may be subtle on cross-sectional imaging and by endoscopic retrograde cholangiopancreatography (ERCP) because of the peripheral location and compensatory hypertrophy of other parts of the liver. We examined 44 consecutive PSC patients to determine the incidence and clinical characteristics of this abnormality, and to correlate imaging studies with the gross appearance. METHODS: We reviewed all cases of PSC encountered over a 3 year period ascertained from the liver disease registry. Magnetic resonance imaging or CT images were re-examined for evidence of segment 2 and 3 atrophy. RESULTS: Four of 44 patients had focal segment 2 and 3 atrophy. These four had been confirmed laparoscopically or by inspection of the liver explant. The remaining segments of the liver were relatively spared of injury in two of the patients, and three of the four patients had preserved synthetic function without evidence of portal hypertension. While the abnormality is clearly visible on cross-sectional imaging, its peripheral location caused it to be an unobtrusive. Likewise, ERCP did not clearly reveal the abnormality on initial inspection. CONCLUSIONS: We conclude that focal atrophy of segments 2 and 3 is a sometimes early and subtle finding in PSC that may be overlooked in cross-sectional imaging or ERCP unless specifically sought.

Adult↗

PubMed2000

The prevalence of varicocele and varicocele-related testicular atrophy in Turkish children and adolescents.

OBJECTIVE: To determine the prevalence and site of varicocele and varicocele-related testicular atrophy in children and adolescents. PATIENTS AND METHODS: The study included 4052 boys aged of 2-19 years, divided into four age groups; the findings of a physical examination, any testicular atrophy and testicular volume were recorded. RESULTS: Varicocele was detected in 293 (7.2%) of the 4052 boys; the prevalence was 0.79% in those aged 2-6 years, 0.96% at 7-10 years, 7.8% at 11-14 years and 14.1% at 15-19 years. The prevalence was 0.92% in 1232 children aged 2-10 years and 11.0% in 2531 adolescents aged 11-19 years (P < 0.001). The prevalence increased significantly at age 13 years (P < 0.005). The varicocele was unilateral in 263 of the 293 (89.7%) boys with varicocele; of these, one (0.38%) was on the right and the others on the left side. Varicoceles were bilateral in 30 of 279 boys (10.8%) aged 11-19 years but none were detected in those aged < 11 years. Varicocele-related testicular atrophy was not present in those aged < 11 years, but seven boys (7.3%) aged 11-14 years and 17 (9.3%) aged 15-19 years had testicular atrophy. The difference in prevalence between the last two age groups with atrophy was not significant. CONCLUSION: These findings support the view that varicocele is a progressive disease and that the prevalence of varicocele and testicular atrophy increases with the puberty.

Adolescent↗

PubMed1996

Sonographic endometrial thickness: a useful test to predict atrophy in patients with postmenopausal bleeding. An Italian multicenter study.

Eighteen centers took part in this prospective study into which 930 eligible patients were recruited. The selection criteria for admission were atypical bleeding after at least 6 months of postmenopausal amenorrhea, and absence of hormonal therapies for at least 6 months. The sonographic measurement of the maximum bi-endometrial thickness was made in a longitudinal plane. Sonographic measurements were always performed within 3 days prior to histological evaluation. In these patients the mean number of years from menopause (25-75th centile) was 6 (range 2-16). The prevalence of endometrial carcinoma was 11.5% and the prevalence of atrophy was 49.2%. The area under the receiver operator characteristic curves generated by sonographic thickness measurements reached the level of 85%, both for cancer and atrophy. The likelihood ratio for cancer, yielded by an endometrial thickness of < or = 4.0 mm, was 0.05, and for atrophy it was 7.1. This cut-off of > 4.0 mm yielded a sensitivity for the detection of cancer of 98% and a negative predictive value of 99%. The overall sensitivity and positive predictive value for atrophy achieved by this cut-off were 57.2% and 87.3%, respectively. A multivariate logistic model showed that age and body mass index were independent variables associated with a significantly higher risk of endometrial cancer. The post-test probabilities for cancer and atrophy were recalculated on the basis of the integration of age, body mass index and endometrial thickness. The estimated reduction of invasive procedures on the basis of this integration was 31%. Transvaginal sonographic measurement of endometrial thickness, integrated with individual risk factors, can help in the management of postmenopausal patients with atypical bleeding, with regard to either the need for histological evaluation in high risk cases, or the choice of possible expectant management. We have shown that an endometrial thickness of < or = 4.0 mm safely predicts endometrial atrophy and justifies expectant management when the patient understands the need for proper follow up. This could be achieved with a reduction in the use of invasive procedures without unwanted delay in cancer diagnosis.

Aged↗

PubMed2006

["True neurologic thoracic outlet syndrome" -- anatomical features and electrophysiological long-term follow-up of lateral thenar atrophy].

Atrophies of the intrinsic muscles of the hand are considered to be a typical symptom of the "true neurologic" form of thoracic outlet syndrome (TOS). The classical form of this entity was described as early as 1970, consisting of a cervical rib or a prolonged transverse process of C7, complete with a fibrous band to the first thoracic rib, resulting in atrophy of the intrinsic muscles of the hand. All our TOS patients presenting with such atrophy displayed anatomical findings consistent with this definition. Based on this observation, the TOS classification currently in clinical use, which differentiates between "disputed" and "true neurologic" subgroups of the neurologic form, is reviewed. In all cases of "true neurologic TOS" with atrophy of the intrinsic muscles of the hand, the lateral thenar muscles are affected first. We present the electrophysiological long-term results of such thenar atrophies of seven patients with eight operated extremities after brachial plexus decompression. The amplitude of the neurographically measured potential over the opponens pollicis and the abductor pollicis brevis muscle, respectively, was defined as quantitative parameter for muscles atrophy. Neither distinct reinnervation nor progressive denervation was evident in any of the cases after a follow-up period, on average, of more than five years post surgery. These findings are in conflict with clinical observations reporting a major postoperative improvement of the motor deficits.

Adolescent↗