Peripheral Nervous System Damage in Experimental Chronic Chagas' Disease

1987 ◽  
Vol 36 (1) ◽  
pp. 41-45 ◽  
Author(s):  
Cappa S. M. González ◽  
O. P. Sanz ◽  
L. A. Muller ◽  
H. A. Molina ◽  
J. Fernández ◽  
...  
1996 ◽  
Vol 54 (2) ◽  
pp. 190-196 ◽  
Author(s):  
Osvaldo Genovese ◽  
Carlos Ballario ◽  
Ruben Storino ◽  
Elsa Segura ◽  
Roberto E. R. Sica

We conducted a clinical and electromyographical study in patients with Chagas' disease in the indeterminate or chronic stages of the illness. Altogether 841 patients were examined. Only 511 were admitted within the protocol; the remainder patients were rejected because they showed other causes able to damage the nervous system. Fifty two (10.17%) out of the 511 patients showed signs and symptoms of peripheral nervous system involvement in the form of sensory impairment and diminished tendon jerks suggesting the presence of neuropathy. Forty five of them were submitted to a conventional electromyographical examination. Fifteen of mem showed normal results, while the remainder 30 disclosed a reduced interference pattern, being most of the remaining motor unit potentials fragmented or poliphasic, reduced sensory and motor conduction velocities and diminished amplitude of the sensory action potential. The findings suggest that some chagasic patients in the indeterminate or chronic stages of the disease may develop a clinical mild sensory-motor peripheral neuropathy.


1978 ◽  
Vol 36 (4) ◽  
pp. 316-318 ◽  
Author(s):  
M. A. Pagano ◽  
G. G. Aristimuño ◽  
Susana Basso ◽  
A. Colombi ◽  
R. E. P. Sica

An electromyographical investigation of 80 patients with chronic Chagas' disease was made. It was found that 79% of the studied patients had EMG manifestations of old and chronic denervation of the upper and lower limbs without clinical features of nervous system involvement.


1989 ◽  
Vol 41 (5) ◽  
pp. 539-547 ◽  
Author(s):  
A. Losavio ◽  
R. E. P. Sica ◽  
M. C. Jones ◽  
O. P. Sanz ◽  
G. Mirkin ◽  
...  

Author(s):  
S.S. Spicer ◽  
B.A. Schulte

Generation of monoclonal antibodies (MAbs) against tissue antigens has yielded several (VC1.1, HNK- 1, L2, 4F4 and anti-leu 7) which recognize the unique sugar epitope, glucuronyl 3-sulfate (Glc A3- SO4). In the central nervous system, these MAbs have demonstrated Glc A3-SO4 at the surface of neurons in the cerebral cortex, the cerebellum, the retina and other widespread regions of the brain.Here we describe the distribution of Glc A3-SO4 in the peripheral nervous system as determined by immunostaining with a MAb (VC 1.1) developed against antigen in the cat visual cortex. Outside the central nervous system, immunoreactivity was observed only in peripheral terminals of selected sensory nerves conducting transduction signals for touch, hearing, balance and taste. On the glassy membrane of the sinus hair in murine nasal skin, just deep to the ringwurt, VC 1.1 delineated an intensely stained, plaque-like area (Fig. 1). This previously unrecognized structure of the nasal vibrissae presumably serves as a tactile end organ and to our knowledge is not demonstrable by means other than its selective immunopositivity with VC1.1 and its appearance as a densely fibrillar area in H&E stained sections.


2000 ◽  
Vol 5 (2) ◽  
pp. 3-3
Author(s):  
Christopher R. Brigham ◽  
James B. Talmage

Abstract Lesions of the peripheral nervous system (PNS), whether due to injury or illness, commonly result in residual symptoms and signs and, hence, permanent impairment. The AMA Guides to the Evaluation of Permanent Impairment (AMA Guides) describes procedures for rating upper extremity neural deficits in Chapter 3, The Musculoskeletal System, section 3.1k; Chapter 4, The Nervous System, section 4.4 provides additional information and an example. The AMA Guides also divides PNS deficits into sensory and motor and includes pain within the former. The impairment estimates take into account typical manifestations such as limited motion, atrophy, and reflex, trophic, and vasomotor deficits. Lesions of the peripheral nervous system may result in diminished sensation (anesthesia or hypesthesia), abnormal sensation (dysesthesia or paresthesia), or increased sensation (hyperesthesia). Lesions of motor nerves can result in weakness or paralysis of the muscles innervated. Spinal nerve deficits are identified by sensory loss or pain in the dermatome or weakness in the myotome supplied. The steps in estimating brachial plexus impairment are similar to those for spinal and peripheral nerves. Evaluators should take care not to rate the same impairment twice, eg, rating weakness resulting from a peripheral nerve injury and the joss of joint motion due to that weakness.


2004 ◽  
Author(s):  
G. Galietta ◽  
A. Capasso ◽  
A. Fortuna ◽  
F. Fabi ◽  
P. Del Basso ◽  
...  

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