Compared to impedance of resting brain tissues (see section 1.2.1.3.), impedance changes
during brain activity are more complicated because various pathophysiological or physiological processing are involved during brain activity. All of these processes may cause changes in brain impedance.
Physiological basis of functional brain activity: Physiologically, neuronal activity is based on
action potentials, which are generated in a nerve either by sensory receptors or by activation from other neurones. Brain activity can be classified as spontaneous or evoked. Spontaneous brain activity is the result of rhythms generated by neural networks. This spontaneous activity of
the brain is generally divided into four-frequency band of delta (up to 4 Hz), theta (4 - 8 Hz), alpha ( 8 - 1 4 Hz) and beta (above 14 Hz). Evoked brain activity or response is the activity
evoked by peripheral sensory stimulation projecting to the cortex along neuronal pathways.
These responses are commonly classified as visual, auditory and somatosensory evoked responses according to the type of sensors being stimulated. Compared with spontaneous brain activity, evoked responses have a clearly defined location and are usually smaller in amplitude. They may be monitored by recording the evoked potentials using an ‘averaging technique’, as to
they are time-locked to the specific stimuli. Furthermore, spontaneous and evoked brain activity could be recorded using both depth and surface electrodes (Binnie and Prior, 1994).
Changes in cerebral impedance during physioiogicaiiy evoked activity: Klivington and
Galambos (1968) using surface electrodes, detected impedance changes of approximately 0.05% over tens of milliseconds during physiologically evoked activity in the visual and auditory cortices of anaesthetised cats. Adey e t a l(1962) using chronically implanted deep electrodes in the limbic system, measured small impedance decreases of about 2%, when cats were exposed to milk or when a female cat was exposed to a male cat. These changes occurred over a period of seconds and were probably related to changes in blood volume, blood flow or cortical
temperature (see section 1.2.1.5.). The probable explanation is that during evoked brain activity, neuronal activity in the cortex increases following arrival of the conducted peripheral sensory input. Consequently, increases in local tissue metabolism and rOBF occur to maintain ionic
gradients across the neuronal membrane required for generating action potentials. In addition, metabolites such as 0 0 2 reduce the tension of the smooth muscle in cerebral vessels to allow increase in rCBF following evoked brain activity, and induce decreases in cerebral impedance (Freygang and Landsu, 1955).
Changes in cerebral impedance during sleep: Impedance of the brain during sleep was
1966). The local cerebral impedance varied during different stages of sleep. An increase in impedance of 2.2% and a decrease in capacitance of 2.7% were measured from wakefulness to
sleep in cats and humans (Adey etal., 1962; Porter etal., 1964). Similar results were also found by controlling the level of anaesthesia. An increase in impedance occurred when anaesthesia became deeper (Adey etal., 1962). They suggested that the possible reasons for the changes in cerebral impedance were due to changes in CBF and metabolism following the changes in neural excitation during different stages of sleep and different depths of anaesthesia.
Changes in cerebral impedance during cerebral ischaemia; Approximately 20 - 100%
increases in cerebral impedance over tens of minutes were experimentally detected using 2 or 4 cortical electrodes during experimental ischaemia in animals (Gamache et al., 1975). Such increases in cerebral impedance were frequency (Hossmann, 1971) and temperature dependent (Barone etal., 1997).
Changes in cerebral impedance following changes in size of ceiis; Van Harreveld et al
(1961) found that an increase of 36% in cerebral impedance could be measured 30 minutes after intravenous injection of 50% glucose. They concluded that the increase in impedance was due to shrinkage of the extracellular space. In contrast, Veen et al (1973) measured changes in impedance at 10 kHz during cooling-induced oedema in cat brains. They found a decrease in
cerebral impedance about 30% from 1395 ± 467 O (Mean ± SD, n = 14) in normal cortex to 840
± 159 i l in a region of cooling-induced oedema. They concluded that the decrease in cerebral
impedance was significantly correlated with the increase in tissue water content and with the enlargement of the extracellular space.
Changes in cerebral impedance during hyperventilation: Porter et al (1964) found that increases in cerebral resistance of 1.2 - 2.2% occurred during hyperventilation. The increases were probably due to decreases in rCBF caused by decreases in pC02 via the blood flow autoregulation mechanism (see section 1.2.1.5.).
Changes in cerebral Impedance during cortical spreading depression (OSD): Adrian (1936)
first recorded a spreading depression of electrical activity using two electrodes from the cerebral
cortex in Urethane, Chloroform or Ether anaesthetised rabbits. Leao at a! published a series of papers about OSD in anaesthetised rabbits and cats (Leao, 1944, 1947; Leao and Morison, 1944). They found that OSD could be induced by direct electrical stimulation on the cortex in
cats and in rabbits. The depression spread slowly (approximately 2.2 mm/minute) in all directions and lasted for 4 - 5 minutes. Ranck (1964) performed a similar detailed study on OSD
in Urethane anaesthetised rabbits. Impedance was measured by two cortical surface electrodes at 5, 50, 500, and 5,000 and 50,000 Hz. The peak impedance increases were 73, 73, 77, 64 and
43%, respectively. Hoffman et al (1973) measured cortical impedance during OSD with an implanted microelectrode with a 20 pM in diameter tip from rat cerebral cortex at frequencies of
0.4 and 3.2 kHz. The cerebral impedance varied according to the depth of recording sites within