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M G Ciria

Publications and source records attributed to M G Ciria.

4 recordsLinked to original sources
PubMed1975

Assessment of severe damage to the brain by multiregional measurements of cerebral blood flow.

Regional cerebral blood flow (rCBF) was measured with a 32-detector device in patients with severe injury to the central nervous system. Most suffered head injiries in traffic accidents. Many patients were severely demented. Several were comatose or in a so-called persistent vegetative state. Flow was measured at rest and during various forms of stimulation. The resting values were on the whole markedly reduced. The flow patterns often showed distinct correlations with the original brain injury. In the best preserved patients, mental activation caused increases in flow with a normal or near-normal distribution. Cutaneous electric stimulation gave rise to increases in cortical flow even in highly reduced patients with severe brain damage. Patients with total or less than total loss of telencephalic structures with retained brainstem reflexes and respiration ('apallic' patients) did not show any changes in flow on sensory stimulation. We conclude that the technique for measuring rCBF enables us to assess severe damage to the central nervous system quantitatively and also to estimate whether higher functions are retained in severely reduced patients in coma, stupor and apallic state--patients who more or less completely lack behavioural responses.

Adolescent↗
PubMed1975

"In vivo" release of endogenous neurotransmitters in cat limbic regions: effect of chlorpromazine and of electrical stimulation.

The effect of chlorpromazine (10 mg/kg i.v.) on the spontaneous release of endogenous dopamine (DA), noradrenaline (NA) and acetylcholine (ACh) within limbic areas perfused by means of the push-pull cannula was investigated in the gallamine-immobilized cat. Chlorpromazine increased the liberation of DA and NA in the nucleus accumbens septi, indicating blockade of the amine receptors. However, the drug did not change the output of ACh from this nucleus nor from ventral and dorsal hippocampal formations which receive a cholinergic input from the septum as indicated by several published findings and by the increased liberation of ACh after electrical stimulation of the homolateral nucleus medialis septi. These results seem to exclude that cholinergic neurons of some limbic areas mediate the effect of the blockade of DA (and of NA) receptors which is possibly involved in the antipsychotic action of neuroleptic drugs.

Acetylcholine↗