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The article discusses studies that shows an increased risk for polypharmacy and early development of autonomic dysfunction in patients with Parkinson's disease (PD). Topics include clinical outcome of polypharmacy for people with PD; and evaluating among patients with PD the association between the number of medications and incident hospitalizations.

With interest we read the article by Patodia I et al i . about a I post mortem i study by 9.4T MRI and autopsy (Cavalieri method for medulla volume estimation, immune-histochemistry for myelin basic protein (MBP), microtubule-associated protein-2 (MAP2) and synaptophysin) of brainstem specimens from patients with sudden unexplained death in epilepsy (SUDEP) ( I n i = 18), patients with epilepsy and non-SUDEP death (epilepsy controls (EPC), I n i = 11), and non-epilepsy controls (NEC, I n i = 18) [1]. Cortical and subcortical atrophy in epilepsy patients is not only dependent on the genetic background but also on seizure types, seizure frequency (seizure control) [3], seizure intensity [4], extension of epileptogenic area [5] and epilepsy duration [3,6]. [Extracted from the article]

Abstract: Neonatal handling in rats persistently alters behavioral parameters and responses to stress. Such animals eat more sweet food in adult life, without alterations in lab chow ingestion. Here, we show that neonatally handled rats display greater incentive salience to a sweet reward in a runway test; however they are less prone to conditioned place preference and show less positive hedonic reactions to sweet food. When injected with methylphenidate (a dopamine mimetic agent), non-handled rats increase their sweet food ingestion in the fasted state, while neonatally handled rats do not respond. We did not observe any differences regarding baseline general ambulatory activity between the groups. A lower dopamine metabolism in the nucleus accumbens was observed in handled animals, without differences in norepinephrine content. We suggest that early handling leads to a particular response to positive reinforcers such as palatable food, in a very peculiar fashion of higher ingestion but lower hedonic impact, as well as higher incentive salience, but diminished dopaminergic metabolism in the nucleus accumbens. [Copyright &y& Elsevier]

The mechanism underlying the serotoninergic neurotoxicity of some amphetamine derivatives, such as p-chloroamphetamine (pCA) and 3,4-methylenedioxymethamphetamine (MDMA), is still debated. Their main acute effect, serotonin (5-HT) release from nerve endings, involves their interaction with 5-HT transporters (SERTs), as substrates. Although this interaction is required for the neurotoxic effects, 5-HT release alone may not be sufficient to induce long-term 5-HT deficits. Some non-neurotoxic compounds, including p-methylthioamphetamine (MTA) and 1-(m-chlorophenyl)piperazine (mCPP), have 5-HT releasing properties in viva and in brain slices comparable to that of neurotoxic amphetamine derivatives. We measured 5-HT release in superfused rat brain synaptosomes preloaded with [³H]5-HT, a model that distinguishes a releasing effect from reuptake inhibition. MTA and mCPP induced much lower release than pCA and MDMA. The striking difference between our findings in synaptosomes and those obtained in viva or in brain slices is probably related to a different compartmentalisation of 5-HT in the different experimental models. Studies in synaptosomes, where the vesicular storage of 5-HT is predominant, could therefore bring to light differences between neurotoxic and non-neurotoxic 5-HT releasing agents which cannot be appreciated in other experimental models and might be useful to identify the mechanisms responsible for the neurotoxicity induced by amphetamine derivatives. [ABSTRACT FROM AUTHOR]