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Brain pH in head injury: An image‐guided 31 P magnetic resonance spectroscopy study
Author(s) -
Rango Mario,
Lenkinski Robert E.,
Alves Wayne M.,
Gennarelli Thomas A.
Publication year - 1990
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/ana.410280510
Subject(s) - intracellular ph , glasgow coma scale , ventilation (architecture) , acidosis , mechanical ventilation , anesthesia , head injury , medicine , magnetic resonance imaging , traumatic brain injury , nuclear medicine , intracellular , surgery , radiology , chemistry , biochemistry , psychiatry , mechanical engineering , engineering
It has been suggested that brain acidosis may follow head trauma, and therapies aimed at correcting acidosis have been proposed. Direct measurements of intracellular pH, however, have thus far not been possible in clinical situations. We have studied the intracellular brain pH in 22 patients after head injury (mean Glasgow Coma Score 6.1). Patients were investigated by a combined approach of phosphorus 31 magnetic resonance spectroscopy and magnetic resonance imaging (overall examination time 50–75 min) at a mean time of 11 days after injury (36 hours to 24 days). 31 P spectra were obtained in 11 patients on assisted ventilation and in 11 patients on spontaneous ventilation. These spectra were analyzed to yield the pH in the regions studied in all the patients. All pH values were in the normal or alkalotic range when compared with 6 age‐matched normal controls. No differences were found between patients on assisted ventilation and patients on spontaneous ventilation. When analyzed as a group, the brain pH in the focal lesions appeared to increase in the first days, to reach a peak in the alkalotic range in the second week, and to return toward normal within 3 weeks from acute injury. Our results suggest that there is no evidence of posttraumatic intracellular brain acidosis in recent human head injury, and therefore, therapies aimed at alkalinizing brain cells need to be reconsidered.