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Painful sensory neuropathy can be attributed to several causes.3 Our patient's neuropathy was accompanied by abnormal nerve conduction, with electromyography results showing significant abnormalities, but laboratory findings were unremarkable. In addition, decreased position and vibratory sensation were found during the clinical examination. This makes the presence of pure smallfiber disease unlikely. According to several studies, 3-5 the diagnosis of small-fiber painful sensory neuropathy represents the most common type of painful sensory neuropathy in patients older than 50 years. Our patient's peripheral neuropathy could be related to the presence of diabetes mellitus. Patients with diabetes mellitus often experience painful sensory changes associated with reduced tendon reflexes and reduced distal sensation. Results of nerve conduction and electromyographic studies are usually abnormal, revealing axonal neuropathy rather than a demyelinating process. However, because most lesions in polyneuropathy consist of a mixture of myelin involvement and axonal loss, one usually sees a combination of changes. Results of the electromyographic and nerve conduction studies in our patient disclosed evidence of a mixed injury, with predominating demyelinating findings. However, features associated with mild axonal loss were also observed. These were secondary to the main process or could be attributed to another entity, such as the presence of diabetes mellitus. On the other hand, diabetic neuropathy can occasionally mimic the presentation and findings of the small-fiber painful sensory neuropathy subtype.6 In the case under discussion, diabetes mellitus was well controlled during the entire course of the patient's illness, as evidenced. Of these drugs in the basal ganglia confound the study of spontaneous dyskinesia. In a recent retrospective study, 15% of preneuroleptic era schizophrenic patients showed oral-facial dyskinesia, and 23% had some dyskinetic-like movements 7 ; . In another study, never-medicated schizophrenic patients had significantly greater motor force instability strongly associated with dyskinesia ; , and 14% had dyskinesia 8 ; . A recent study of never-medicated schizophrenic patients in Morocco reported that 14% exhibited spontaneous dyskinesia, and 36% experienced some dyskinetic-like movements 9 ; . However, earlier reports from Morocco found only two of 70 never-medicated schizophrenic patients who displayed spontaneous dyskinesia 10 ; . No cases of spontaneous dyskinesia were found among 12 never-medicated Nigerian patients with schizophrenia 11 ; . Among 89 never-medicated, first-episode schizophrenic patients, only one experienced dyskinesia, while 15 displayed parkinsonism 12 ; . Never-medicated schizophrenic patients are difficult to find for observation. However, subjects with milder manifestations of schizophrenic-like symptoms may be. The mevalonate pathway Figure 2 ; is important not only for cholesterol synthesis but also for cell-signaling processes. Statins, as inhibitors of the rate-limiting enzyme 3-hydroxy-3methylglutaryl CoA HMG CoA ; reductase, have become one of the most successful pharmacologic interventions of the past decade for primary and secondary prevention of cardiovascular disease CVD ; . The evidence that these drugs are effective and valuable is overwhelming reviewed in detail in reference 19 ; , leading to their almost universal use among cardiologists. Not only are the benefits of statins related to their cholesterol-lowering function, but also secondary effects 20 ; on cell signaling, antiinflammation 21, 22 ; , cell proliferation, plaque stabilization 23 ; , and improvement of endothelial function 24 ; all are thought to occur by inhibition of the mevalonate pathway.

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