scholarly journals Clinico-radiological review of peripheral entrapment neuropathies – Part 2 Lower limb

2021 ◽  
Vol 135 ◽  
pp. 109482
Author(s):  
Dinesh Manoharan ◽  
Dipin Sudhakaran ◽  
Ankur Goyal ◽  
Deep Narayan Srivastava ◽  
Mohd Tahir Ansari
2010 ◽  
Vol 14 (05) ◽  
pp. 501-511 ◽  
Author(s):  
Luis Beltran ◽  
Jenny Bencardino ◽  
Varand Ghazikhanian ◽  
Javier Beltran

JAMA ◽  
1966 ◽  
Vol 197 (11) ◽  
pp. 915-916
Author(s):  
I. J. Schatz
Keyword(s):  

2019 ◽  
Vol 24 (6) ◽  
pp. 12-15
Author(s):  
Jay Blaisdell ◽  
James B. Talmage

Abstract Like the diagnosis-based impairment (DBI) method and the range-of-motion (ROM) method for rating permanent impairment, the approach for rating compression or entrapment neuropathy in the upper extremity (eg, carpal tunnel syndrome [CTS]) is a separate and distinct methodology in the AMA Guides to the Evaluation of Permanent Impairment (AMA Guides), Sixth Edition. Rating entrapment neuropathies is similar to the DBI method because the evaluator uses three grade modifiers (ie, test findings, functional history, and physical evaluation findings), but the way these modifiers are applied is different from that in the DBI method. Notably, the evaluator must have valid nerve conduction test results and cannot diagnose or rate nerve entrapment or compression without them; postoperative nerve conduction studies are not necessary for impairment rating purposes. The AMA Guides, Sixth Edition, uses criteria that match those established by the Normative Data Task Force and endorsed by the American Association of Neuromuscular & Electrodiagnostic Medicine (AANEM); evaluators should be aware of updated definitions of normal from AANEM. It is possible that some patients may be diagnosed with carpal or cubital tunnel syndrome for treatment but will not qualify for that diagnosis for impairment rating; evaluating physicians must be familiar with electrodiagnostic test results to interpret them and determine if they confirm to the criteria for conduction delay, conduction block, or axon loss; if this is not the case, the evaluator may use the DBI method with the diagnosis of nonspecific pain.


VASA ◽  
2008 ◽  
Vol 37 (4) ◽  
pp. 327-332 ◽  
Author(s):  
Koutouzis ◽  
Sfyroeras ◽  
Moulakakis ◽  
Kontaras ◽  
Nikolaou ◽  
...  

Background: The aim of this study was to investigate the presence, etiology and clinical significance of elevated troponin I in patients with acute upper or lower limb ischemia. The high sensitivity and specificity of cardiac troponin for the diagnosis of myocardial cell damage suggested a significant role for troponin in the patients investigated for this condition. The initial enthusiasm for the diagnostic potential of troponin was limited by the discovery that elevated cardiac troponin levels are also observed in conditions other than acute myocardial infarction, even conditions without obvious cardiac involvement. Patients and Methods: 71 consecutive patients participated in this study. 31 (44%) of them were men and mean age was 75.4 ± 10.3 years (range 44–92 years). 60 (85%) patients had acute lower limb ischemia and the remaining (11; 15%) had acute upper limb ischemia. Serial creatine kinase (CK), isoenzyme MB (CK-MB) and troponin I measurements were performed in all patients. Results: 33 (46%) patients had elevated peak troponin I (> 0.2 ng/ml) levels, all from the lower limb ischemia group (33/60 vs. 0/11 from the acute upper limb ischemia group; p = 0.04). Patients with lower limb ischemia had higher peak troponin I values than patients with upper limb ischemia (0.97 ± 2.3 [range 0.01–12.1] ng/ml vs. 0.04 ± 0.04 [0.01–0.14] ng/ml respectively; p = 0.003), higher peak CK values (2504 ± 7409 [range 42–45 940] U/ml vs. 340 ± 775 [range 34–2403] U/ml, p = 0.002, respectively, in the two groups) and peak CK-MB values (59.4 ± 84.5 [range 12–480] U/ml vs. 21.2 ± 9.1 [range 12–39] U/ml, respectively, in the two groups; p = 0.04). Peak cardiac troponin I levels were correlated with peak CK and CK-MB values. Conclusions: Patients with lower limb ischemia often have elevated troponin I without a primary cardiac source; this was not observed in patients presenting with acute upper limb ischemia. It is very important for these critically ill patients to focus on the main problem of acute limb ischemia and to attempt to treat the patient rather than the troponin elevation per se. Cardiac troponin elevation should not prevent physicians from providing immediate treatment for limb ischaemia to these patients, espescially when signs, symptoms and electrocardiographic findings preclude acute cardiac involvement.


Sign in / Sign up

Export Citation Format

Share Document