Background-Experimental studies have suggested both atherogenic and thrombogenic properties of lipoprotein (a) [Lp(a)], depending on Lp(a) plasma concentrations and varying antifibrinolytic capacity of apolipoprotein(a) [apo(a)] isoforms. Epidemiological studies may contribute to assessment of the relevance of these findings in the general population. Methods and Results-This study prospectively investigated the association between Lp(a) plasma concentrations, apo (a) phenotypes, and the 5-year progression of carotid atherosclerosis assessed by high-resolution duplex ultrasound in a random sample population of 826 individuals. We differentiated early atherogenesis (incident nonstenotic atherosclerosis) from advanced (stenotic) stages in atherosclerosis that originate mainly from atherothrombotic mechanisms. Lp(a) plasma concentrations predicted the risk of early atherogenesis in a dose-dependent fashion, with this association being confined to subjects with LDL cholesterol levels above the population median (3.3 mmol/L). Apo(a) phenotypes were distributed similarly in subjects with and without early carotid atherosclerosis. In contrast, apo(a) phenotypes of low molecular weight emerged as one of the strongest risk predictors of advanced stenotic atherosclerosis, especially when associated with high Lp(a) plasma concentrations (odds ratio, 6.4; 95% CI, 2.8 to 14.9). Conclusions-Lp(a) is one of the few risk factors capable of promoting both early and advanced stages of atherogenesis.Lp(a) plasma concentrations predicted the risk of early atherogenesis synergistically with high LDL cholesterol. Low-molecular-weight apo(a) phenotypes with a putatively high antifibrinolytic capacity in turn emerged as one of the leading risk conditions of advanced stenotic stages of atherosclerosis.

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Our observation has an impact on the indication for, and assessment of efficacy of intervention. This potential artifact should be investigated in ongoing large trials in renal patients as well as in nonrenal African American subjects who have on average markedly higher Lp(a) levels. In nonrenal Caucasian subjects with much lower Lp(a) concentrations, this issue will be less relevant.

We report the clinical and EEG findings in three patients presenting with seizures associated with intrathecal baclofen application for treatment of spasticity. All patients had a history of traumatic brain injury, while one patient also suffered a spinal cord injury. Two patients experienced their first seizure following intrathecal baclofen test bolus injection. Another patient had convulsions on two occasions: following postoperative baclofen dose adjustment, and after sleep deprivation. Structural brain disease seems prerequisite for baclofen to exert epileptogenic activity, since seizures have not occurred in patients receiving intrathecal baclofen for spasticity of solely spinal origin. Antiepileptic medication permitted the continuation of intrathecal baclofen treatment in the three patients.

Rostral cord injury causes postsynaptic changes (hyperpolarization) in caudal motoneurons. This hyperpolarization is a major physiologic derangement in spinal shock. The rise in H-reflex amplitude despite evidence of persistent hyperpolarization is due to enhanced transmission at Ia fiber-motoneuron connections below the SCI. Finally, the observation that the stretch reflex is proportionally more depressed than the H-reflex is consistent with fusimotor drive also being depressed after SCI.