Effect of alkyl chain length on inhibition of N-nitrosomethylbenzylamine-induced esophageal tumorigenesis and DNA methylation by isothiocyanates.

This study was undertaken to evaluate the inhibitory effects of benzyl isothiocyanate (BITC), phenethyl isothiocyanate (PEITC), 3-phenylpropyl isothiocyanate (PPITC) or 4-phenylbutyl isothiocyanate (PBITC) on N-nitrosomethyl-benzylamine (NMBA)-induced esophageal tumorigenesis in male Fischer 344 rats. Groups of 15 male rats were fed modified AIN-76A diet or diet containing the four isothiocyanates at concentrations of 2.5, 1.0 and 0.4 mumol/g diet for 25 weeks. After two weeks, rats were administered 0.5 mg/kg NMBA s.c. once weekly for 15 weeks. Additional controls received modified AIN-76A diet only or diet containing the high concentration of isothiocyanates (2.5 mumol/g) only. No tumors were found in any of the groups that were not administered NMBA. Rats treated with NMBA only developed 6.7 +/- 0.8 tumors/animal. Tumor incidences in rats treated with 2.5 and 1.0 mumol PEITC/g diet, and with all three dietary concentrations of PPITC were inhibited by 60-100% compared to controls. Tumor multiplicities were inhibited by 83-100% by PEITC or PPITC at all dietary concentrations tested. PPITC clearly had a stronger inhibitory effect on NMBA tumorigenesis than did PEITC. Compared to PEITC and PPITC, BITC and PBITC had little inhibitory effect on tumor multiplicity and no effect on NMBA tumor incidence. In general, the occurrence of preneoplastic lesions (acanthoses, hyperkeratoses, leukoplakias and leukokeratoses) was inhibited in a similar manner as tumor incidence and multiplicity, except that no experimental diet resulted in a significant reduction of the incidence of acanthoses and hyperkeratoses.(ABSTRACT TRUNCATED AT 250 WORDS)

Combined third and sixth nerve paresis following optic nerve sheath fenestration.

The authors report a case of transient third and sixth nerve paresis as a complication of optic nerve sheath fenestration in a patient with pseudotumor cerebri. The motility and pupillary abnormalities that are commonly associated with this procedure are reviewed briefly.

Blink reflex in patients with hemispheric cerebrovascular accident (CVA). Blink reflex in CVA.

A blink reflex consists of an early unilateral component, R1, and a late bilateral component, R2. During an acute phase of hemispheric cerebrovascular accident, R1 and R2 were abnormal in 30 and 50 of 66 patients, respectively. Paired stimuli usually corrected R1 but not R2, which was profoundly suppressed. The discrepancy between polysynaptic R2 and oligosynaptic R1 indicates a greater disfacilitation at the level of interneurons than at the motoneuron, which serves as the final common path. Abnormality of R2 occurred bilaterally with stimulation on the affected side of face and contralaterally after stimulation on the normal side in 31 patients. This finding suggests a diffuse loss of internuncial excitability, contralateral to the hemispheric lesion. Changes of R2 implicated the brainstem pathways forming the afferent and efferent arc of the reflex in 7 and 8 patients, respectively. The remaining 4 comatose patients had no R2 irrespective of stimulus sites. Clinical localization of the hemispheric lesion showed no consistent correlation with the type of blink reflex abnormalities. The CT scans revealed widely scattered changes in 29 patients with abnormal blink reflex but with a tendency to overlap in the inferior Rolandic area. This contrasted with conspicuous sparing of the inferior post-central region in 10 patients with normal blink reflex. These findings suggest the presence of crossed facilitation to this reflex from wide areas of the cortex but most prominently from the sensory representation of the face.

Short- and long-latency median somatosensory evoked potentials. Findings in patients with localized neurological lesions.

Short- and long-latency somatosensory evoked potentials (SEPs) were elicited by stimulation of the median nerve in 43 patients with neurological disorders. Abnormalities of short-latency peaks, P9, N13, and P14, were seen in patients with lesions of the peripheral nerve, cervical spinal cord, and brain stem, respectively. Subsequent component, N18, was affected in patients with thalamic or hemispheric disease. In some patients with parietal lobe lesions, however, abnormalities were limited to later components, N32 or N63. Analysis of SEPs is helpful in localizing a lesion along the somatosensory pathway, although differentiation between thalamic and other subcortical or cortical involvement may not be possible with the present SEP technique. Both short- and long-latency SEPs should be studied for maximal clinical information. The latter can be most reliably evaluated by simultaneous bilateral stimulation.

Short- and long-latency somatosensory evoked potentials in multiple sclerosis.

Thirty-nine of 52 patients, with definite (29) or probable (23) multiple sclerosis (MS) had unequivocal alterations of somatosensory evoked potentials (SEPs). In 28 patients both short- (up to N18) and long-latency (after N18) components were affected, whereas the abnormality was limited to the long-latency SEPs in the remaining 11 patients. These findings indicate that a substantial number of SEP abnormalities may be overlooked if the test is determined solely on the basis of short-latency components. Furthermore, a questionable change of short-latency SEPs could often be decidedly abnormal by finding extreme asymmetry of long-latency components. The long-latency SEPs are therefore a useful adjunct in evaluating cases of MS, especially if bilateral stimulation is used.

Convulsions after carotid endarterectomy.

Convulsions have not been emphasized as a possible complication of carotid endarterectomy. We describe here three patients in whom seizures with a focal component developed postoperatively. We suspect that the convulsions were secondary to a cerebral embolus arising from the operative site. An unstable preoperative neurological status is not a prerequisite for this complication.