Value of postictal prolactine studies for differential diagnosis in epilepsy.

W. van Emde Boas and E. Endert (Heemstede, Amsterdam).

Postictal prolactine (PRL) elevation after epileptic seizures has repeatedly been reported and use of PRL for differential diagnosis bet- ween real and pseudo-seizures has been proposed. Published findings are inconsistent in some types of seizures and concerning maximum postictal PRL values. Physiological PRL fluc- tuations are consistently ignored, which may contribute to clinical misinterpretation.

Spontaneous and postictal PRL fluctuations during 24-28 hours were studied in 15 patients with various types of epilepsy under continuous EEG and video monitoring. Blood samples were collected at 60 min. intervals through an indwelling catheter; additional postictal samp-

les were collected in three patients. Eight patients showed one or more seizures

during monitoring; a pseudoseizure was recorded in one patient.

Results show that postictal PRL peaks can remain within physiological limits, even after generalized fits. After partial seizures PRL peaks are inconsistent and may not exceed 2-3x preictal values; comparable fluctuations can be found after pseudoseizures or emotional stress.

PRL peaks within physiological limits may have clinical or diagnostic significance in epileptology, but knowledge of a patient’s spontaneous PRL profile is necessary for reli- able interpretation. Routine use of PRL for differential diagnosis of seizures thus seems of limited value, especially in the case of partial seizures.

Locked-in syndrome with bilateral ptosis; combination of biiateral pontim hmimutal gaze paralysis and nuclear oculomotor nerve paralysis

I. Dehaene, R. Dom. M. Marchau and K. Geens (Brugge, Leuven)

A classical locked-in syndrome is reported. Eye movements were characterized, in a first phase, by a bilateral horizontal gaze palsy with preserved abduction elicited by oculovestibular reflex. Vertical optokinetic and caloric nys- tagmus were present. A bilateral lesion involv- ing the pontine paramedian reticular formation (P.P.R.F.) and the medial longitudinal fasciculi (M.L.F.), sparing the abducens nuclei, is hypothesizedl.

In a second phase a bilateral ptosis appeared. The ophthalmoplegia was now complete with the exception of downward movement of the right eye. This is explained by the association of a bilateral horizontal pontine gaze palsy and a unilateral nuclear oculomotor nerve palsy. A lesion of the superior rectus subnucleus is

responsible for the heterolateral elevation palsy. The homolateral elevation palsy is ex- plained by destruction of the crossing radicular fibers2. The nearly total ophthalmoplegia combined with a tetraplegia approximates the ‘total locked-in syndrome’ of Bauel3. Autopsy findings confirmed the pontine and mesencephalic destruction. Massive lesions ex- clude detailed correlations.

References

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laires colontaires. Rev Neural W82; 138: 5 17-32. PIERROT-DESEILLIGNY C, SCHAISON M, BOUSSER MC,

BRUNET P. Syndrome nucldaire du nerf oculomoteur

commun: a propos de deux observations cliniques. Rev

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BAUER G, GERSTENBRAND F, RUMPL E. VarieteS Of the

locked-in syndrome. J Neurol 1979; 22 1: 77-9 I.

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