Paralysis, paresis

A pressure sore is also called a decubitus ulcer and bed sore. A classification system for pressure sores is presented in Table 47-5. Many factors are thought to predispose patients to the formation of pressure ulcers paralysis, paresis, immobilization, malnutrition, anemia, infection, and advanced age. Four factors thought to be most critical to their formation are pressure, shearing forces, friction, and moisture however, there is still debate as to the exact pathophysiology of pressure sore formation. The areas of highest pressure are generated over the bony prominences. 

A number of OPC are capable of rendering a delayed neurotoxic effect (DNE). This effect becomes apparent gradually, after a certain latent period (usually 14 to 21 days, sometimes 1 to 5 years after the acute poisoning survived) and is characterized clinically by the development of ataxia, muscular weakness, paresis and paralysis of the extremities. Morphologically, it is characterized by fiber demyelinization of spinal pathways and peripheral nerves. Till present time, near 40,000 cases have been described, when paresis and paralysis developed in human beings as a result of their exposure to OPC (TOCP, mipaphox, chloropyrophos, trichlorfon, etc.) [1],... 

The usage of specific therapeutic means (quaternary ChE reactivators, cholinolytics) with this purpose prevents only the development of cholinergic symptoms of intoxication, but does not exert influence on the development of paresis and paralysis in the remote period. 

Similar signs of toxicity were observed in male rats exposed to 4.2 mg/kg/day triethyltin bromide for 3 weeks (Richman and Bierkamper 1984). The rats developed hindlimb weakness in week 1 followed by paresis and paralysis by week 3. There was apparent recovery at the end of week 3. The primary histopathological findings were demyelination in the spinal cord, degeneration of axons of the sciatic nerve, and atrophy of fibers of the soleus muscle. This study demonstrated that both nerve and muscular components are involved in producing peripheral motor dysfunction. 

Most dithiocarbamates have neurotoxic effects, including maneb. Rats exposed orally to maneb twice a week for 4 months at doses of 350 and 1750 mg kg produced high mortality and paresis in the hind limb progressing to complete paralysis. Exposure to maneb in combination with some... 

The symptoms of decompression sickness include bends (local pain), skin rashes, itching, neurological disturbances (scotomata, hemianopsia, diplopia, paresis, paralysis, abnormal reflexes, dysesthesia, aphasia, vertigo), respiratory distress ( chokes )> nausea, and shock (neurocirculatory... 

One of early manifestations of neuropathy consists in a sharp (by 35 to 40%) reduction in conduction velocity of stimulation along peripheral nerves and a decrease in action potential amplitude of nerve, which are noted prior to the development of other clinical signs (ataxia, paresis, paralysis). The changes observed indicate the loss of excitability firstly by the A-6 thick fast-conducting nerve fibers [34, 36], In the pathogenesis of DNE induced by OPC, there take place an immunopathological component (the development of autoimmune process) [38,39], intensification in lipid peroxidation in neural tissue, labilization of lysosomal membranes, and activation of acid hydrolases [40, 41],... 

Neurological Ataxia, coma, convulsions, papilledema, headache, peripheral neuritis, wristdrop or footdrop, weakness, paralysis, mild facial or ocular motor nerve paresis, aphonia, laryngeal paralysis, fasciculations, encephalopathy, death... 

Facial paresis (ask patient to show teeth or raise eyebrows and close eyes tightly) SCORE 0 Normal symmetrical movement 1 Minor paralysis (flattened nasolabial fold, asymmetry on smiling) 2 Partial paralysis (total or near total paralysis of lower face) 3 Complete paralysis of one or both sides (absence of facial movement in the upper and lower face)... 

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