Both cerebellum and neocortex receive input from the somatosensory system. Interaction between these regions has been proposed to underpin the correct selection and execution of motor commands, but it is not clear how such interactions occur. In neocortex, inputs give rise to population rhythms, providing a spatiotemporal coding strategy for inputs and consequent outputs. Here, we show that similar patterns of rhythm generation occur in cerebellum during nicotinic receptor subtype activation. Both gamma oscillations (30-80 Hz) and very fast oscillations (VFOs, 80-160 Hz) were generated by intrinsic cerebellar cortical circuitry in the absence of functional glutamatergic connections. As in neocortex, gamma rhythms were dependent on GABA(A) receptor-mediated inhibition, whereas VFOs required only nonsynaptically connected intercellular networks. The ability of cerebellar cortex to generate population rhythms within the same frequency bands as neocortex suggests that they act as a common spatiotemporal code within which corticocerebellar dialog may occur.

Very fast oscillations (VFOs, >80 Hz) are important for physiological brain processes and, in excess, with certain epilepsies. Putative mechanisms for VFO include interneuron spiking and network activity in coupled pyramidal cell axons. It is not known whether either, or both, of these apply in pathophysiological conditions. Spontaneously occurring interictal discharges occur in human tissue in vitro, resected from neocortical epileptic foci. VFO associated with these discharges was manifest in both field potential and, with phase delay, in excitatory synaptic inputs to fast spiking interneurons. Recruitment of somatic pyramidal cell and interneuron spiking was low, with no correlation between VFO power and synaptic inputs to principal cells. Reducing synaptic inhibition failed to affect VFO occurrence, but they were abolished by reduced gap junction conductance. These data suggest a lack of a causal role for interneurons, and favor a nonsynaptic pyramidal cell network origin for VFO in epileptic human neocortex.epilepsy | fast ripple oscillation | ripple oscillation A dvances in electroencephalogram (EEG) techniques have revealed a much larger temporal window of oscillatory activity exists than has been previously thought (1-4). Of particular interest are very fast oscillations (VFOs), lying outside the traditional EEG frequency bands (5). These oscillations, at frequencies over c.80 Hz, are readily observable in animal models of epilepsy in vivo (6, 7), in vitro (8, 9), and clinically (10-14). In the epileptic human brain, VFOs are seen in structures involved in the pathology of temporal lobe epilepsy (TLE) (10,(15)(16)(17)(18).Although VFOs are seen in epileptic tissue, similar, transient expression of VFOs is also seen in normal cortex, albeit at lower power. As part of "physiological sharp waves," brief ripples of VFOs at c.200 Hz are seen and are suggested to be involved in the time-compressed replay of previous spike sequences in principal cells (19). A number of putative mechanisms of generation exist: Initial observations in vivo showed that principal cell unit activity was low during sharp waves, but that certain fast spiking (FS) interneurons were capable of spiking at VFO frequencies immediately before and sometimes during the event (20, 21). In vitro observations showed a predominantly inhibitory somatic input to principal cells during sharp waves (22). These observations suggest a role for rapid discharges from inhibitory interneurons as causal for the sharp wave and possibly the accompanying VFO. However, other studies have shown that brief VFO discharges in nonepileptic tissue survive synaptic blockade in low calcium ioncontaining media (23), with principal cell spikelets, rather than full spikes manifest as units, being generated at VFO frequency. Computational modeling predicted that VFO was generated as an emergent property of gap-junctionally coupled axons forming a plexus driven by ectopic action potential generation (24). This form of network is the only one to date shown to support frequen...

Experimental intracerebral hemorrhage has been shown to cause extensive cerebral ischemia. This study was performed to ascertain the time course of these changes and also to examine the type of brain damage that may occur under such circumstances. Halothane anesthesia was induced in rats, and 25 microliter autologous blood was injected into the caudate nucleus; the effects were studied with autoradiographic measurement of local cerebral blood flow and capillary permeability, and also by light microscopy and histochemical techniques. Blood flow returned to normal or to slightly increased levels within the first 3 hours, and ischemic levels of flow were found to persist only to a marginal degree beyond 10 minutes after the lesions were made. Capillary permeability was maximum during the first 30 minutes after the hemorrhage and diminished with time. Structural evidence of ischemic damage was localized to the cortex overlying the hemorrhage, but was not seen in the caudate nucleus. Nevertheless, histochemical investigation did reveal an area of disturbed enzyme function in the striatum. This finding of biochemical disturbance without structural evidence of ischemic damage reveals that there is an area around the hematoma that, although demonstrating disturbed function, does not show structural damage, and the milieu of this partially injured brain may be implicated in the delayed development of the ischemic brain damage that follows intracerebral hemorrhage in man.

Cranioplasty harbours significant morbidity, a risk that appears to be higher with a bifrontal defect. The complications experienced influence subsequent functional outcome. The timing of cranioplasty, early or late, after the initial operation does not impact on the ultimate outcome. These findings should be considered when making decisions relating to craniectomy and cranioplasty.

A model of experimental intracerebral hemorrhage is described in which carefully controlled volumes of autologous blood were injected at arterial pressure into the caudate nucleus of the rat. A comparison of intracranial pressure changes and local cerebral blood flow (CBF) was made between three groups of rats, each receiving different injection volumes, and sham-operated control rats by monitoring intraventricular pressure and by obtaining quantitative autoradiographic measurements of CBF within 1 minute of the experimental hemorrhage. Cerebral blood flow was reduced both around the hematoma and in the surrounding brain. This change was strongly volume-dependent and was not accompanied by significant alterations in cerebral perfusion pressure. This finding suggests that the degree of ischemia at the time of an intracerebral bleed depends on the size of the lesion, and implicates local squeezing of the microcirculation by the hematoma, rather than a generalized alteration in perfusion pressure, as the cause of ischemia.