Olfaction and Mind

Compiled by Tim Jacob (jacob@cf.ac.uk)


  1. EEG and fMRI
  2. Freeman, brain waves and olfaction
  3. EEG - what is it?
  4. Measuring EEG during odour detection
  5. EEG and epilepsy
  6. References

 

EEG and fMRI

The are a number of ways of monitoring brain activity. EEG (electroencephalography) is very fast and shows the global activity of large numbers of cortical neurons (see below). It is very fast (in the millisecond range) but gives very little idea of which brain structures are involved. Functional magnetic resonance imaging (fMRI) is a powerful way of imaging brain activity and can localise which brain structures are involved very precisely. However, it is relatively slow (in the seconds timescale). Since the oscillations of cortical neurons at different frequencies is thought to be how brain regions co-ordinate and syunchronise (e.g. gamma-waves) and this can only be measured by EEG.

Freeman et al. A variety of methods have been used in an effort to understand olfaction. Some of the most revealing and exciting work has come from the work of Freeman ( "The physiology of perception" Scientific American 1991 (Feb) 34-41) and colleagues on the odor-related EEG. Early research with the EEG resulted in understanding the nature of CNS arousal mediated by the reticular activating system. Later studies identified drug effects on the CNS and the EEG has been used as an aid to understanding human cognition. Diagnosis of mental illness has been greatly supplemented by the use of EEG.

Recently a number of studies have examined the EEG changes associated with odors. Before looking at them let's consider the EEG.

 

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EEG waves

EEG waves reflect the mean excitation of pools of neurons. Excitatory inputs at synapses generate electric currents that flow in closed loops within the recipient neuron towards its axon, across the cell membrane into the extracellular space and, in that space, back to the synapse. Inhibitory inputs generate loops moving in the opposite direction. The cell body summates all the inputs and, if the threshold is reached, fires an action potential. Electrodes placed on the scalp record these currents after they leave the cell. The resulting EEGs indicate the excitation of whole groups of cells, not individuals, because the extracellular avenues from which the EEGs arise carry currents contributed by thousands of cells.

Why EEG waves oscillate

Alternating rises and falls in amplitude stem from negative-feedback circuits that are established by the interaction of pools of excitatory and inhibitory neurons. When the pools have been sensitized to input, even a small input can trigger a burst of high-amplitude oscillation.

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(Picture shamelessly stolen from Freeman's article in the Scientific American - I will ask permission)

Measurement of EEG during odor detection

The simplest (but least precise) use of EEG for understanding odor processing involves recording some segment of EEG data during sensory stimulation. Typically, the subject is seated quietly and asked to inhale an odorant. EEG data are gathered during this stimulation. In an early study (Moncrieff, J.W., The Chemical Senses, 1967, pp 108-112) it was found that rhythmic activity in an 8-13Hz band (alpha) decreased during presentation of a variety of odors. Decreases in alpha activity are common in EEG research and suggest increased cognitive activity or activity of the ascending reticular activating system. Lorig and colleagues (Lorig, T.S. (1989) Human EEG and odor response, Progress in Neurobiology 33, 387-398) have employed period analysis of the EEG during odor presentation. This particular form of analysis quantifies the number of waves which occur in various frequencies during an EEG sample. They found that a particular odor (spiced apple) increased the number of waves in the theta (4-7Hz) band when compared with a resting baseline or other odors. Increased activity in this band is associated with intensified self-reports of relaxation and is congruent with previous data indicating blood pressure reduction in the presence of this odor.

 

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Does odour alter physiological state?

This is the big question. There are many reports in the literature claiming to demonstrate psychological, emotional changes in response to odour exposure. For this to be the case, the brain must change state, and it should be possible to detect changes in brain activity. There are two ways to investigate this with EEG. Firstly, by event-related recording and, secondly, by continuous EEG recording. The former looks at the events triggered by a specific olfactory stimulus over the short term and the latter looks at global changes in brain wave activity in response to a longer term odour exposure.

 

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EEG and epilepsy

Epilepsy is a condition in which changes in transmitter and neuronal function disrupt the balance between excitatory and inhibitory forces in the brain producing characteristic synchronous firing of groups of neurones which has a conspicuous tendency to spread. There is good evidence that the ease with which seizure activity spreads to the rest of the brain is dependent on the level of arousal in the part of the brain which surrounds a discharging focus. There is, for most people with epilepsy, an optimum level of arousal where seizure spread is least likely to occur. Arousal can be modified and altered by life events, stress and by efforts of will or concentration.

Our sense of smell is extremely easily conditioned and such a conditioned "odor memory" is particularly resistant to deconditioning. Smell can be used as a countermeasure in people with epilepsy because it evokes activity in the same cortical system where epilepsy so often starts. Dr Tim Betts (Birmingham University) has conducted studies using aromatherapy essential oils with epileptic patients. Almost all patients were able to reduce the seizure frequency following odor conditioning (associating the odor with relaxation). The odor of choice (selected by 6/10 patients) was Ylang Ylang. One odor, rosemary (which is arousing) increased the frequency of seizures.

 

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References

  • Betts, T. (1992) Epilepsy and stress. Brit. Med. J. 305, 378-379.
  • Efron, R. (1957) The conditioned inhibition of uncinate fits. Brain 80, 251-261.
  • Freeman, W.J. (1991) The physiology of perception. Scientific American (Feb) 34-41.
  • Lorig, T.S. (1989) Human EEG and odor response, Progress in Neurobiology 33, 387-398
  • Moncrieff, J.W. (1967) The Chemical Senses, pp 108-112.

Please communicate your comments, ideas, discussion with me by e-mail [jacob@cf.ac.uk]

Return to Tim Jacob homepage. Last update 11/11/2003