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Progressive supranuclear palsy (Steele et al.) has a characteristic pattern of dementia: (1) forgetfulness, (2) slowing of thought processes, (3) emotional or personality changes (apathy or depression with occasional outbursts of irritability), and (4) impaired ability to manipulate acquired knowledge. In many neurological disease states associated with subcortical pathology a similar pattern of dementia exists. The neurobehavioural changes of progressive supranuclear palsy thus typify a clinical pattern which may be referred to as subcortical dementia. The subcortical dementias have a striking clinical resemblance to the dementia which occurs after bifrontal lobe disease. However, the subcortical dementias can be clearly distinguished clinically from cortical dementias, other than frontal dementias. We propose as a tentative hypothesis that there may be common pathophysiological mechanisms underlying the subcortical dementias-in particular, disturbances of timing and activation. There are immediate practical implications of this hypothesis: drugs which have an effect on subcortical timing and activating mechanisms may be useful in the treatment of subcortical dementias.

The stimulation, in the encéphale isolé cat, of the basal preoptic hypnogenic area be brief electrical pulses evokes bilaterally an extracellular positive (P) field potential of 20 to 60 msec duration in the brain stem and thalamic activating ascending reticular system. The properties of this P wave have led to consider it as the extracellular and abbreviated counterpart of an hyperpolarizing postsynaptic inhibitory process which, by the functional depression it exerts on the arousal system, would be instrumental in the induction and maintenance of synchronized sleep. The positive field potential response of the reticular system shows the same recruiting build-up and amplitude modulation, and the same sensibility to amphetamine and to barbiturates, as the cortical potential of diffuse distribution which is evoked simultaneously. It is strychnine--and picrotoxin--resistant. Preoptic stimulation exerts, within a 100 msec interval, a strong suppressive effect on the excitatory response evoked in the n. centromedian by a mesencephalic reticular testing shock. On the other hand, the application of the latter as a conditioning stimulus results in a marked increase of the amplitude of the P wave response of the CM to a testing preoptic shock. A negative feedback interpretation of this interaction is suggested. No clear evidence of a tonic functioning of the preoptic hypnogenic structure could be found in experiments involving the production of small bilateral lesions in the basal preoptic area in the encéphale isolé cat. Reasons limiting the interpretation of this negative result are given. The functional significance, on the basis of experimental data, of the diffuse cortical synchronization produced by the low frequency stimulation of the basal preoptic area and of other hypnogenic structures is discussed.