Conjugate eye deviation: a disorder of the frontal eye fields?

C.C. Tijssen (Tilburg), J.A.M. van Gisbergen and B.P.M. Schulte (Nijmegen)

Conjugate eye deviation (CED) is a well-known sign occurring rather frequently in patients with a he- mispheral stroke. Generally, the eyes were deviated towards the side of the affected cerebral hemisphere. Based upon experimental studies it is supposed that CED is caused by a lesion of the frontal eye fields (FEF), leading to a contralateral saccadic paresis. However, this theory is not quite supported by the findings of few clinical studies.

Therefore we performed a prospective study of 82 patients with CED in order to establish the location of the responsible lesion and to see whether the eye movement disturbances were indicative for an FEF lesion. This was investigated by computerized tomo- graphy and eye movement recordings.

The results indicate that: 1. CED occurs more fre-

quently after right hemispheral lesions with a ratio of 2:l compared to the left; 2. the lesions of the right hemisphere are predominantly located in the sub- cortical fronto-parietal region and in the ventral and dorsal limb of the internal capsule; 3. on the left the entire fronto-temporo-parietal cortical and subcorti- cal area is usually involved; 4. the eye movement disorders are not in accordance with direct damage to the FEF region.

In conclusion, one exclusive location of the lesion responsible for CED seems less plausible. Probably an interruption at different sites within the circuit formed bij the inferior parietal lobule, FEF, superior colliculus and paramedian pontine reticular forma- tion can lead to the occurrence of this sign.

Long term effects of tolrestat, an aldose reductase inhibitor, on symptomatic diabetic sensnory polyneuropathy

J.M. A. van Gerven, H.H.P. J. Lemkes, and J.G. van Dij k (Leiden)

The effects of the aldose reductase inhibitor tolrestat on chronic symptomatic diabetic polyneuropathy were examined by double blind tolrestat (20 patients) or placebo (17 patients) treatment for 6 months, fol- lowed by 6 months tolrestat treatment of all patients, without breaking the double blind code. Both groups were clinically comparable.

Motor nerve conduction velocity (MNCV, median of 4 nerves) deteriorated during placebo (-1.4 m/s, midspread: -3.JO.9 m/s; p=O.O58) and improved dur- ing tolrestat (0.6 m/s, midspread: -0.7/3.2 m/s; p=O.O89). This difference was significant (p<O.O5). Sensory nerve conduction velocity (median of 2 nerv- es) worsened during placebo (-3.6 m/s, midspread: -20.7/0.7 m/s; p=O.O36), but not during tolrestat (0.0 m/s, midspread: -12.412.9 m/s; p=O.95). The differ- ence was nearly significant (p=O.O81). Metatarsal vi- bration threshold (measured with a biothesiometer) deteriorated during placebo (0.06+0.07 log Volts; p=O.O08), but not during tolrestat (-O.Ol+O.lO log Volts; p=O.60). The contrast was significant (p=O.O35).

During tolrestat treatment of the placebo group, the initially deteriorated MNCV improved signifi- cantly (2.4k3.6 m/s; p=O.O09). Metatarsal vibration threshold decreased nonsignificantly (-0.02f0.10 logvolt). The difference with the initial increase was significant (p=O.O45). Changes during masked and unmasked tolrestat treatment were similar.

During one year tolrestat, MNCV improved 2.7 m/s (95% confidence interval: 0.315.1 m/s). Meta- carpal vibration threshold decreased 9.1% (95% con- fidence interval: 2.3/15.9%). Hypersensitivity, as- sessed by standardized neurological examination, in- creased significantly. Neuropathic symptoms remained unchanged.

One year tolrestat treatment has gradually im- proved MNCV in diabetic polyneuropathy, with some sensory recuperation in the end. The relevance of these changes remains uncertain. Longer treat- ment of earlier neuropathy may be necessary for clin- ically satisfactory effects. However, the polyol path- way is involved in clinical diabetic polyneuropathy.

185