Polyactives: controlled and sustained bioactive release via hydrolytic degradation.

Significant and promising advances have been made in the polymer field for controlled and sustained bioactive delivery. Traditionally, small molecule bioactives have been physically incorporated into biodegradable polymers; however, chemical incorporation allows for higher drug loading, more controlled release, and enhanced processability. Moreover, the advent of bioactive-containing monomer polymerization and hydrolytic biodegradability allows for tunable bioactive loading without yielding a polymer residue. In this review, we highlight the chemical incorporation of different bioactive classes into novel biodegradable and biocompatible polymers. The polymer design, synthesis, and formulation are summarized in addition to the evaluation of bioactivity retention upon release via in vitro and in vivo studies.

Vertebral body infarction as a confirmatory sign of spinal cord ischemic stroke: report of three cases and review of the literature.

BACKGROUND: Acute spontaneous spinal cord syndromes often remain etiologically ambiguous despite extensive diagnostic efforts. In the previous literature five cases are described with acute spinal cord syndromes interpreted as spinal cord ischemic strokes because of association with vertebral body infarctions on MRI. CASE DESCRIPTIONS: Three cases are presented, and the literature is reviewed. In addition to an extensive diagnostic battery including an initial MRI without pathological signs, follow-up MRI at different time intervals from the onset of symptoms showed T2 hyperintense signals in vertebral bodies. Patient 1, who had plaques in the abdominal aorta, had suffered a thoracolumbar spinal infarction; this and a concomitant infarction of the left portion of T-12 could be demonstrated on follow-up MRI on day 12. Patient 2, who had incomplete transverse spinal artery syndrome below T-3, had an abnormal signal at the T-2 level of the spinal cord on follow-up MRI on day 5; this was one segment above infarction of the dorsal area of T-3, corresponding to the ascending course of the medullary artery. The spinal cord of patient 3, who had a posterior spinal artery syndrome below T-11, was unremarkable on follow-up MRI on day 14, but a T2 hyperintense signal was noted in the dorsal area of T-10. CONCLUSIONS: Vertebral body infarction represents the only confirmatory sign for the otherwise exclusionary diagnostic procedure for spinal cord ischemic stroke and must be searched for on follow-up MRI as a key to correct diagnosis.

Silent period evoked by transcranial magnetic stimulation in unilateral thalamic infarcts.

We studied 9 patients with isolated, unilateral thalamic infarcts of different location and size imaged by MRI and (in one case) by CCT. The cortical silent period (c-SP) of thenar muscles evoked by transcranial magnetic stimulation was evaluated on both sides with low (c-SP1) and high (c-SP2) stimulus intensity. Additionally, the motor-evoked thenar potentials by transcranial magnetic stimulation (MEP) and the central motor conduction time (CMT), the silent period of thenar muscles evoked by electrical median nerve stimulation (p-SP), electrically evoked short- (HR) and long-latency reflexes (LLR) of the thenar and somatosensory evoked potentials of the median nerve were investigated bilaterally. The c-SP1 was prolonged contralateral to the thalamic infarcts in 7 patients and c-SP2 in all 9 patients. Prolongation of c-SP did not correlate with location and size of the infarct, clinical symptoms or with the other parameters, which are based on pyramidal motor system (MEP, CMT), thalamocortical circuits (SEP, LLR), or spinal excitability level (p-SP, HR). These results suggest the central pathways of the c-SP to be independent from those of the remaining parameters and indicate the c-SP as a sensitive parameter reflecting thalamocortical modulation of cortical inhibition.

[Acute effect of metoclopramide on esophagus motility in diabetes mellitus]. / Akutwirkung von Metoclopramid auf die Osophagusmotilität bei Diabetes mellitus.

The acute effect of metoclopramide on oesophageal motility was investigated prospectively in 33 consecutive patients (20 men and 13 women; mean age 60.5 +/- 12.6 years) with type I (n = 8) or type II (n = 25) diabetes. 15 patients had a peripheral sensory-motor polyneuropathy only and three just an autonomic cardial neuropathy. Both lesions were present in ten, none in five. No patient had oesophago-gastroduodenal lesions. Sphincter pressure, relaxation time, contraction amplitude and propulsion velocity of bolus-induced oesophageal peristalsis were measured manometrically after intravenous administration of 10 mg metoclopramide. Resting pressure in the lower oesophageal sphincter rose significantly by 26.7%, contraction amplitude in the tubular portion of the oesophagus by more than 30%, and propulsion velocity by more than 20% (P for each < 0.05). At the same time the amount of segmental and aperistaltic oesophageal contractions regressed significantly. The effect of metoclopramide was demonstrated regardless of the type of diabetes, duration of diabetes and any manifestation of autonomic cardial or peripheral sensory-motor neuropathy.

Esophageal dysfunction in diabetes mellitus: is there a relation to clinical manifestation of neuropathy?

In a prospective study, we evaluated 33 diabetic patients [type I (n = 8) and type II (n = 25)]. Esophageal motor functions were examined by registering clinical symptoms and by performing esophageal manometry. We also investigated peripheral and autonomic neuropathy. In diabetics, the lower and upper esophageal sphincter pressure and amplitudes of peristaltic waves were reduced. Compared with controls (n = 30), in diabetics the esophageal peristaltic velocity was reduced significantly, and the duration of contractions were decreased as well. Multipeaked waves were uncommon in diabetics, while non-propulsive contractions were seen more often. No correlation was found between esophageal dysfunction and peripheral or autonomic neuropathy. Some 60% of diabetics reported esophageal symptoms; however, no relationship between these symptoms and the extent of dysfunction in esophageal motility was found.