"It is assumed that bromide acts by replacing part of the chloride in the body (Blumberg and Nelp, 1966). In spite of the use of bromides for their antiepileptic action for more than a century, we know little about the action of bromide on the cellular level in the CNS other than that it may influence synaptic processes by its action on the transport systems (Kunze, 1976), or by substituting for chloride ions in actions of neurotransmitters. (Neurotransmitters classically communicate by producing membrane voltage changes through the movement of ions, including chloride, through specialized ion channels associated with neurotransmitter receptors on the signal-receiving cell. For instance GABA, or gamma amino butyric acid, the chief inhibitory neurotransmitter in the brain, functions through specialized chloride ion channels (Allen and Albuquerque, 1987).)
Regional cerebral blood flow, that is, blood flow to different parts of the brain, may also be altered with bromism. Regional cerebral blood flow was assessed in a case of bromide psychosis using radioactive xenon (133Xe) inhalation (Berglund, Nielsen, et al., 1977). On the first exam, when the serum bromide level was 45 mEq/L (extremely high, within the potentially lethal range), the cerebral blood flow was reduced to approximately one-third of normal, with abnormal regional flow characterized by low flow in regions of the cortex, including frontal and parieto-occipital regions. Dialysis led to improvement in the clinical condition, and restoration of regional cerebral blood flow (Berglund, Nielsen, et al., 1977). Changes in regional cerebral blood flow--reflecting or perhaps influencing altered regional neuronal activity in the brain--could relate to symptoms of bromism."
aDepartment of Surgery (Neurosurgery), The University of New Mexico School of Medicine, Albuquerque, New Mexico USA
bthe Veterans Administration Hospital, Albuquerque, New Mexico USA
Received 10 September 1966.
Available online 12 April 2004.
The steady-state distribution of bromide (Br−) in the nervous system of the rabbit was studied at various plasma concentration levels (0.5–20 mm). In addition, utilizing a ventriculo-cisternal perfusion system, the flux of Br− between CSF and blood was measured under various experimental conditions. It was observed that the steady-state distribution of Br− in brain and cerebrospinal fluid was concentration dependent and that brain served as a “sink” for the plasma and CSF. The results of the flux experiments revealed that the efflux of Br− from the perfusion fluid was some 30% greater than the influx of Br− from the blood. In addition, the movement of Br− out of the perfusate was attenuated with increasing concentrations of Br− and on death of the animal. The results suggest that, at low concentration levels, Br− is rapidly cleared from the CSF (by an active transport system) and the brain (by either an active transport system or oxidation of Br− to BrO3−), while at high concentration levels, the relative ineffectiveness of the proposed systems results in the accumulation of Br− and the establishment of a state of equilibrium between blood, brain and CSF.