Intermediate syndrome

The degree of recorded jitter in SFEMG is directly related to the release of ACh and the function of the ACh receptors in the NMJ. SFEMG therefore provides a window into the operation of the NMJ. Jitter is characteristically increased in conditions (both pre- and post-junctional) of the NMJ which reduce the safety margins of neuromuscular transmission. Thus, there is increased jitter in conditions such as myasthenia gravis and Lambert-Eaton syndrome. Jitter is also increased following the administration of small doses 

Clinically, IMS resembles the syndrome of incomplete reversal of neuromuscular paralysis by non-depolarising blocking agents sometimes seen following general anaesthesia. Patients will recover after a week or 10 days if intensive care facilities are available with intermediate positive pressure variation. Unfortunately, OP pesticide poisoning often occurs in countries that have the least available resources in terms of intensive care. 

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De Bleecker J, Van Den Neucker K, Colard5m F. 1993. Intermediate syndrome in organophosphorus poisoning A prospective study. Crit Care Med 21 1706-1711. 

De Bleecker J, Willems J, Van Den Neucker K, et al. 1992. Prolonged toxicity with intermediate syndrome after combined parathion and methyl parathion poisoning. Clin Toxicol 30 333-345. 

Senanayake N, Karalliedde E. 1992. Intermediate syndrome in anticholinesterase neurotoxicity. In Ballantyne B, Marrs TC, ed. Clinical and experimental toxicology of organophosphates and carbamates. Jordan Hill, Oxford, England Butterworth-Heinemann Etd., 57-62. 

Because the "intermediate syndrome" has not been described for animals or humans exposed to hydraulic fluids, this syndrome is not discussed further in this profile. 

About 1-A days after apparent recovery from the acute poisoning, an intermediate syndrome of muscle paralysis can occur, requiring prolonged ventilation before strength returns. A minority of organophosphorus compounds can cause a delayed, chronic, peripheral neuropathy (organophosphorus-induced delayed neuropathy - OPIDN), first manifest some weeks after acute poisoning. 

An intermediate syndrome has been described in cases of poisonings in Sri Lanka, where patients experienced paralysis of limb, neck, and respiratory muscles 24 to 96 hours after exposure.71 7"1 Delayed neurologic problems have been observed 2 to 4 weeks after large exposures. Workers indicate symptoms of needle-type pain in the feet, legs, and hands. It has been observed that workers with high blood pressure, gastrointestinal disorders, heart, liver, lung, or nervous system problems may be more sensitive to methamidophos.72-74... 

De Bleecker, J. (1992). The intermediate syndrome in organophosphate poisoning presentation of a case and review of the literature. Clin. Toxicol. 30 321-9. 

Karalliedde, L., Baker, D., Marrs, T.C. (2006). Organophosphate-induced intermediate syndrome aetiology and relationships with myopathy. Toxicol. Rev. 25 1-14. 

The organophosphate (OP) insecticide-induced intermediate syndrome (IMS) was reported for the first time in human patients in Sri Lanka in 1987 (Senanayake and Karalliede, 1987 Karalliede and Henry, 1993). Thereafter, this syndrome has been reported in South Africa (1989), Turkey (1990), Belgium (1992), India (2003), and many other countries. IMS is clearly a separate entity from acute... 

DeBleecker, J.L. (2006). Intermediate syndrome in organ-phosphate poisoning. In Toxicology of Organophosphate and Carbamate Compounds (R.C. Gupta, ed.), pp. 371-80. Academic Press, Amsterdam. 

Paul, N., Mannathukkaran, T.J. (2005). Intermediate syndrome following carbamate poisoning. Clin. Toxicol. 43 867-8. 

Senanayake, N., Karalliedde, L. (1987). Neurotoxic effects of organophosphoms insecticides an intermediate syndrome. N. Engl. J. Med. 316 761-3. 

Exposure to these agents can also lead to long-term neurological impairments, including (1) a delayed intermediate syndrome affecting muscles, which occurs 24-96 h post-exposure and (2) subtle, long-term neurological... 

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. 

Quite frequently, and typically 1-4 days after resolution of symptoms of acute exposure, the intermediate syndrome may develop, characterised by a proximal flaccid limb paralysis which may reflect muscle necrosis. Even later, after a gap of 2-4 weeks, some exposed persons exhibit the delayed polyneuropathy, with sensory and motor impairment usually of the lower limbs. Claims of chronic effects (subtle cognitive defects, peripheral neuropathy) following recurrent, low-dose exposure, as with organophosphate used as sheep dip, continues to be the subject of investigation but, as yet, no conclusive proof. 

See also Cholinesterase Inhibition Neurotoxicity Organophosphate Poisoning, Delayed Neurotoxicity Organophosphate Poisoning, Intermediate Syndrome Organophosphates. 

Acute exposure to diazinon may result in acetylcholinesterase inhibition in the central and peripheral nervous system. Severity of poisoning varies with different formulations. Typical signs of poisoning include weakness, headaches, tighmess in the chest, blurred vision, salivation, sweating, nausea, vomiting, diarrhea, and abdominal cramps. Diazinon has been associated with the intermediate syndrome. 

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