There is no safe threshold for lead exposure: Α literature review.

Lead was one of the most dangerous environmental toxic substances for a long time in western countries, and this is still the case for many places on earth today. Its neurotoxic potential is highly significant but its secure blood level concentration remains unknown. The aim of this study was to approach the above issue from the perspective of social psychiatry. A systematic search was made of Dialog and Datastar interfaces for data regarding the neuropsychiatric complications of direct or chronic exposure to lead, and a review of the relevant literature was conducted using the databases Medline, Embase, CAB Global Health and Cochrane. Lead affects the cholinergic, dopaminergic and gloutamergic systems, thus intervening in the normal function of neurotransmion. The consequence of neurotoxicity in the central nervous system includes apoptosis and excitotoxicity. Direct as well as chronic exposure causes serious neurological symptoms and possibly constant cognitive impairment. Acute encephalopathy, the most serious expression of lead poisoning, occurs in blood level concentrations over 100 µg/dL in adults and 80-100 µg/dL in children. Early symptoms of lead neurotoxicity include irritability, headaches and difficulties in concentration in both children and adults. Continuous exposure in children produces neurobehavioral symptoms, such as decreased concentration, inability to follow instructions, difficulty to play games and low IQ, which are associated with concentrations of 10-35 µg/dL. However, some studies claim that cognitive decline and low IQ can occur in concentrations <10 µg/dL. The commonest symptom in adults is peripheral neuropathy with foot drop. Prenatal exposure to lead has been correlated with antisocial behavior and schizophrenia. Long-term lead exposure causing low and medium lead concentration in blood has been linked to depression as well as generalized anxiety disorder and other behavioral disorders. High blood level concentrations correlate with psychotic symptoms like delusions and hallucinations but more rarely with psychotic syndromes. Despite the fact that lead has been banned from gasoline, paint and water pipes, quite significant quantities of lead still exist, particularly in deprived areas of modern cities, in transition zones and city centers, and there are also great concentrations around lead mines and in developing countries, but even for the remaining areas there is no safe threshold. CONCLUSIONS: Lead was and still is an environmental factor that increases neurologic and psychiatric morbidity. It also causes developmental disorders, especially in deprived areas. Prevention should be the single most important way of dealing with lead poisoning.

[Post-stroke depression: recognition and treatment interventions].

Depression is the most common neuropsychiatric complication of a stroke (Post Stroke DepressionPSD) and has been shown to impede the recovery and rehabilitation of these patients. Prevalence rates of PSD vary between 6% and 79%. Direct comparison between studies is limited due to their different methodology. Etiology of PSD is determined by biological and psychosocial factors. Symptoms of PSD appear in three areas: affective, somatic and cognitive. Differential diagnosis includes post-stroke fatigue and pseudo-depressive manifestations of ischemic infarctions (apathy, aprosody, athymhormia, pseudobulbar palsy). Mortality in post-stroke patients is higher than in non-depressed stroke patients and suicide ideation is observed in 6.6-11.3% of stroke patients. Selective serotonin reuptake inhibitors (SSRI) are considered as the first choice treatment of PSD. Other therapeutic approaches include cognitive and functional rehabilitation. PSD is a potentially treatable condition, yet under-diagnosed, and has a negative effect on functional recovery and survival of stroke patients.