To understand the clinicopathology features of leptomeningeal dissemin
ation of malignant gliomas, a total of 157 consecutive patients treate
d between 1978 and 1989 were analysed. Twenty-two patients (14%) were
judged to have dissemination. In 20 patients, the dissemination was di
agnosed antemortem. Eleven patients had neurological deficits due to d
issemination, whereas the other 9 without these had CT or myelographic
evidence of dissemination. The peak incidence of dessemination was se
en in the first and second decades of life. The mean age of 22 patient
s with dissemination was 31 years, significantly lower than that (44.5
years) of patients without dissemination. Fifteen patients developed
dissemination within one year after diagnosis (early dissemination), 6
0% of them were less than 30 years of age. All patients with late diss
emination (more than one year after diagnosis) underwent a second cran
iotomy for tumour removal before dissemination, while none of the 15 p
atients with early dissemination did. Survival after diagnosis in pati
ents with dissemination was shorter, although statistically not signif
icant, than that of patients without dissemination. Survival after dis
semination was limited in all patients (mean 19 weeks, range 2-39 week
s). Immunohistochemical study revealed that the disseminated tumour ex
pressed less glial fibrillary acidic protein than the primary tumour.
Our results suggest that dissemination does not seem to result from ex
tended survival of the patients, but may occur at any time in malignan
t gliomas. Some malignant gliomas, especially in younger patients, hav
e a capability to acquire biological characteristics suitable for diss
emination in the earlier stage of the disease.