Muscle weakness intermediate syndrome

A delayed syndrome of muscle weakness (the so-called intermediate syndrome ) that occurs within days of recovery from severe acute effects and is typically reversible. 

Neurological Headache, coma, loss of reflexes, Cheyne-Stokes respiration, seizures, electroencephalogram abnormalities Organophosphate-induced delayed polyneuropathy manifested by flaccidity or paralysis of extremities, paresthesias, footdrop, gait ataxia, spasticity develops 1-2 weeks after exposure Intermediate syndrome 1-4 days after exposure manifested by weakness of proximal limb and respirator muscles, loss of knee reflexes, cranial nerve palsy, death... 

After acute effects subside, OPs produce a condition called the intermediate syndrome mediated through the enzyme neurotoxic esterase (Annau 1992). Symptoms consist of muscle weakness developing days after initial symptoms. Organophosphate-induced delayed neurotoxicity, a second delayed OP effect, develops weeks after exposure (Davis and Richardson 1980 Ecobichon 1996 Willems et al. 1984). Another condition described as wasting away results from toxic by-products generated during synthesis of OP insecticides, especially malathion (Chambers 1992). 

Delayed symptoms appearing after 1 days and marked by persistent low blood ChE and severe muscle weakness are termed the intermediate syndrome. A delayed neurotoxicity also may be evident after severe intoxication ("see below). 

D. Intermediate syndrome. Patients may develop proximal muscle weakness over a few days even after resolution of the acute cholinergic crisis. This is often first not as neck weakness, progressing to proximal limb weakness and cranial nerve palsies. Respiratory muscle weakness and respiratory arrest may occur abmptly. The intennediate syndrome is probably caused by prolonged overstimulation of the neuromuscular junction, and may be associated with inadequate oxime therapy. Atropine is not effective. 

D. Inadequate dosing of 2-PAM may be linked to the intermediate syndrome, which is characterized by prolonged muscle weakness. 

Subsequent to the acute cholinergic manifestations of OP toxicity in humans, and approximately 24-96 hours after exposure, the onset of an "intermediate syndrome" which includes ocular effects has been recognised more recently for some OPs (Senanayake and Karalliedde, 1987 Karademir et aL, 1990). The associated clinical signs, which are characteristically different from those seen in OP-induced delayed pol)meuropathy, are paralysis and weakness of proximal limbs, respiratory, neck and cranial muscles, including those innervated by the oculomotor nerve. The occurrence of myopathy in rats exposed to diisopropylfluorophosphate, paraoxon or soman (Wecker et aL, 1978 Vanneste and Lison, 1993) resembled the features of the "intermediate syndrome". The severity and duration of the myopathy in rats appeared directly related to the degree of inhibition of AChE. 

The term intermediate syndrome refers to a delayed onset of muscle weakness that occurs shortly after recovery from severe acute effects of OP exposure and... 

---