Clopidogrel resistance has been used as one of the terms employed in the literature to describe different degrees of ex vivo low platelet inhibition after clopidogrel administration. In addition to the diverse nomenclature, the characterisation of clopidogrel resistance has also been problematic because different authors have given different definitions. The mechanisms responsible for this decreased platelet response are not yet clearly defined, some hypotheses have been put forward but not yet demonstrated. Although there have been no large prospective studies demonstrating that the degree of platelet inhibition is directly related to clinical outcomes, several recent studies and reports have shown an association between less platelet inhibition and more adverse events after percutaneous coronary interventions with clopidogrel therapy suggesting that clopidogrel resistance may be a marker for increased risk of recurrent cardiovascular events. Larger scale investigations are needed to support these findings.
SUMMARY Myo-inositol was given orally to nine multiple sclerosis patients and nine healthy control subjects. Pattern reversal evoked potential testing was used to assess its effect. The principal positive wave increased in amplitude, duration and area in a dose-dependent manner in the multiple sclerosis group compared with controls. Cerebrospinal fluid concentrations of myo-inositol in multiple sclerosis and controls were similar. The significance of these observations is discussed in relation to recent discoveries in inositol phospholipid function. Myo-inositol and inositol phospholipids are components of plasma membrane and myelin.' They have achieved recent recognition for roles in metabolic regulation of nervous tissue2 and in receptor physiology.3In a preliminary report Holm'0 showed that 27% of patients with multiple sclerosis appeared to metabolise myo-inositol abnormally: when myo-inositol was added to their sera a large change in redox potential occurred compared with controls. Altered myo-inositol metabolism in diabetes mellitus has also been proposed as a cause of altered nerve conduction." We decided to pursue a possible role of myo-inositol in multiple sclerosis by: (I) examining the electrophysiological effects of orallyadministered myo-inositol in multiple sclerosis patients and control subjects and (2) measuring myoinositol in the cerebrospinal fluid (CSF) in multiple sclerosis and control patients. MethodsThe experiment was divided into two parts: (A) measurement of the effects of myo-inositol on pattern reversal evoked potentials in multiple sclerosis patients and controls and (B) determination of myo-inositol concentrations in the CSF in multiple sclerosis patients and controls.(A) Myo-inositol and pattern reversal evoked potentials Nine patients with clinically definite multiple sclerosis (using Schumacher criteria'2) were matched within 3 years for age and for sex with nine healthy volunteers. Patients ranged in age from 22-44 years. Six were female and three were male. better. We tested all subjects in an identical manner with the same ambient lighting and at approximately the same time of day for each subject using a Nicolet CA 1000 Clinical Averager System. The reversing black and white checker board pattern was one metre from the subject's eye, with each square subtending 27 minutes of arc. Luminance was 700 cd/M2 for white and 0 7 cd/M2 for dark squares. The pattern reversed at 1-88 times/second. Each eye was tested separately twice at each testing session, with 100 repetitions per determination. Bandpass filter settings were 5-100Hz.Scalp disk electrodes were used with O.-C. derivation; impedances were 2-4 k ohms. Printout was on an X-Y plotter.The major positive wave was clearly identified in each case. N,, P2 and N2 peaks were identified (fig 1). Latency was from the time from the stimulus trigger to the peak of the P2 wave. Amplitude was defined as the voltage difference between the N, and P2 peaks. Duration was the N2-N, peak to peak time difference. When values differed slightly i...
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