Abstract
Impairment of cognitive functions following neurotoxic exposure is collectively termed cognitive toxicity. This oration is based on a series of studies carried out over last 12 years on cognitive toxicity of two groups of substances, viz. organophosphate (OP) pesticides and sedative psychotropic drugs. OP pesticide poisoning is a major clinical and public health problem in South Asia. OPs act as cholinesterase inhibitors, and bring about acute neurological deficits following exposure. Using neurophysiological and neuropsychological techniques, we assess long-term neurocognitive deficits of OPs, a less known yet important adverse effect of OP exposure. The findings hitherto indicate both acute large-dose poisoning and subclinical occupational exposure are associated with long-term cognitive impairment. In the same way the pesticide use and misuse are common in agricultural communities, use and misuse of sedative psychotropic medications are common in urbanised societies. Sedative drugs, even in therapeutic doses impair driving and underlying cognitive functions, and increase the risk of traffic accidents. When taken in overdose, these drugs have cognitively impairing effects that last beyond clinical recovery from acute poisoning. These patients are more prone to traffic crashes at least up to 4 weeks following exposure, and the cognitive recovery over this period mirrors the crash risk at different post-overdose time points. The above findings raise a number of clinical and medico legal implications in post-discharge management of patients with sedative drug overdose. As the agricultural communities transform into urban industrialised societies in Sri Lanka, the pattern of poisoning changes from agrochemicals into pharmaceuticals, particularly psychotropic dugs. The two lines of research discussed above highlight how this changing social fabric poses new challenges for the neurophysiologists, neurologists and psychiatrists who study cognition and apply their findings in clinical settings. Our latest work in generating age-, sex- and education-adjusted norms for cognitive tests for Sri Lankans, would set the foundation in interpreting the cognitive test results of clinical populations.
Highlights
OP pesticide poisoning is a major clinical and public health problem in South Asia
In the same way the pesticide use and misuse are common in agricultural communities, use and misuse of sedative psychotropic medications are common in urbanised societies
Even in therapeutic doses impair driving and underlying cognitive functions, and increase the risk of traffic accidents. These drugs have cognitively impairing effects that last beyond clinical recovery from acute poisoning. These patients are more prone to traffic crashes at least up to 4 weeks following exposure, and the cognitive recovery over this period mirrors the crash risk at different post-overdose time points
Summary
We know that different toxins adversely affect the nervous system and its functions. The toxicity sometimes involves brain, and impairs so called 'higher functions' or cognitive functions, giving rise to the entity collectively termed cognitive toxicity. Cognitive toxicity sometimes leads to overt clinical manifestations such as impaired consciousness, disorientation, delirium or amnesia. These can be readily detected in the acute stage of intoxication. What is less encountered by the clinician, are the delayed effects of acute poisoning and the subclinical effects of long-term exposure to toxins. These effects may include subtle deficits in different cognitive functions including perception, memory, attention and executive functions. These subtle effects – as we see later - are none the less detrimental to the health and wellbeing of the patients
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