Fever, altered consciousness, autonomic dysfunction and muscle rigidity are the hallmarks of the neuroleptic malignant syndrome. The neuroleptic malignant syndrome (NMS) is associated with a case fatality rate of about 20%. If withdrawal of dopaminergic therapy is suspected as the cause of NMS, dopaminergic therapy should be restarted. If a neuroleptic agent is suspected as the cause, the neuroleptic agent should be immediately discontinued. For patients with NMS suspected to be due to neuroleptic therapy, consideration should be given to dantrolene (or bromocriptine) administration. Intensive monitoring and supportive care are indicated for all patients with NMS. [ Ref ]
Their effect on muscle fibers and the tendency to cause fatigue brings up the topic of exercise and whether statins make it more difficult to execute a work-out routine. There are anecdotes about patients who think statins harm their athletic performance, but formal establishment of an effect is not so clear . A recently published study showed that rats given statins were not able to run as far as rats without the drug. Analysis of the muscle showed animals on the medicine had less glycogen and there was evidence of mitochondrial damage. Mitochondria are the parts of the cells that burn fuel for energy. If statin use makes exercise more difficult and less fun, it could inadvertently lead patients to become more sedentary, which is the opposite of what is desired. Increasing concerns about muscle-related adverse events are leading to the idea that lower doses of statins should be prescribed than current practice.
Fish oil fatty acids interact with the peroxisome proliferator-activated receptor (PPAR) system, which are a class of receptors (PPARα, PPARβ/δ, and PPARγ) that seem to respond to dietary lipids and similarly structured molecules. They are highly involved in the treatment of diabetes and metabolic syndrome (via the drug classes of fibrates and thiazolidinediones), with varying effects on fat mass (PPARα increases beta-oxidation of fatty acids,  while PPARγ promotes fat storage but improves insulin tolerance;  PPARδ appears to be similar to PPARα in this regard  ).