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Epilepsy: Insights into Higher Brain Functions in Humans

Robert C. Collins

10.1002/cphy.cp010520

Source: Supplement 5: Handbook of Physiology, The Nervous System, Higher Functions of the Brain

Originally published: 1987

Published online: January 2011

Full Article on Wiley Online Library



Abstract

The sections in this article are:

1 Focal Neocortical Seizures
1.1 Basic Mechanisms of Seizure Discharges
1.2 Functional Organization of Interictal Focus
1.3 Functional Anatomy of Focal Motor Seizures
1.4 Focal Sensory Seizures
2 Summary: Neocortical Seizures
3 Limbic System Seizures
3.1 Basic Aspects
3.2 Ictal Phenomena
3.3 Interictal Behavior
4 Summary: Limbic System Seizures
5 Conclusions
Figure 1. Figure 1.

A: dog brain stimulation experiments of Fritsch and Hitzig 91 were first to show localization by direct cortical stimulation. Points indicate movement of contralateral parts as well as different movements in same part: Δ, neck; +, extension‐abduction of anterior leg; +• flexion‐rotation of anterior leg; #, posterior leg; and , face. These authors noted effects of repeated stimulation: facilitation, exhaustion, and occasional aftermovements and were first to produce experimental seizures. B and C: Ferrier 82,83 used weak faradic stimulation to produce first motor maps of primate brain. Note especially point 15 in C over periamygdaloid cortex of uncus, an area that produced ipsilateral movements of upper lip and ala of nose.

A from Fritsch and Hitzig 91; B and C from Ferrier 82,83
Figure 2. Figure 2.

Pathophysiology of epileptic discharges. Interictal electroencephalogram (EEG) spike is 1 hallmark of focal epilepsy. Physiological experiments in variety of models show that large neurons undergo paroxysmal depolarizing shift followed by prolonged afterhyperpolarization that coincides in time with surface spike. Many currents responsible for this abnormal event are related to increased Ca2+ influx in dendrites. Three hypotheses relate to changes in local circuits that might potentiate abnormal Ca2+ currents: 1) abnormal dendrites, 2) hypersynchronous excitatory input, and 3) loss of inhibition.
Figure 3. Figure 3.

Organization of seizure focus. Large populations of neurons must be temporally synchronized into burst firing to cause an epileptic spike on EEG (pyramidal neurons A and B). This change occurs predominantly through action of local excitatory interneurons, although failure of inhibitory interneurons and other factors probably also play a role. Most cells inside the focus show depolarizing shifts in membrane potential coincident with surface spikes. Inhibitory surround is characterized by predominance of cells that are hyperpolarized during surface spikes (pyramidal neuron C). Farther laterally, cortex remains normal. Inhibitory surround is created by axon terminals of inhibitory neurons driven within the focus and recurrent collaterals of pyramidal cells ending on inhibitory neurons outside the focus. Transition zone between excitation and inhibition is temporally and spatially dynamic, and the focus greatly expands when interictal spikes change to produce prolonged seizures.

Data from Prince and Wilder 260
Figure 4. Figure 4.

2‐Deoxyglucose autoradiography of intense focal occipital seizures induced by injecting 80 units of penicillin into cortex. A: metabolic focus occupies most of visual areas 17, 18, and 18a (pallor represents trauma surrounding needle track). There is drop‐off of activity in layer IV, and a metabolic depression surrounds the focus and extends laterally into temporal cortex. In contralateral homotopic cortex, glucose utilization is also depressed in area 17 medial to vertical band of activation on border of areas 17 and 18a. Temporal cortex lateral to this is normal. Bands of activation in subcortical sites are seen ipsilaterally in dorsal lateral geniculate nucleus (LGN) and lateralis posterior nucleus and are seen contralaterally in dorsal LGN. This particular locus of activation in contralateral LGN represents central portion of visual field, indicating activity in projections descending from border of areas 17 and 18a in visual cortex above it. B: increased activity can be seen in fiber tracts descending ipsilaterally to dorsal LGN and to tail of caudate (arrows, right), and in optic radiation to contralateral dorsal LGN (arrow, left). C: in addition to activation of cortical columns posterior to the focus, there is evidence for mild accentuation of activity ipsilaterally in postsubiculum (arrow). D: activation of columns posteriorly and laterally in temporal cortex. E: functional anatomy of focal seizures in visual cortex. Topical cortical maps and occipital lobe EEGs. Corticocortical spread of seizure activity into columns and strips is reflection of intensity, size, and location of cortical focus.

From Collins and Caston 42
Figure 5. Figure 5.

Body parts in motor cortex may be organized into “nested rings” 172,214,354. A: more distal parts (F, fingers) lie internal to proximal parts (W, wrist; E, elbow; S, shoulder). B: each ring is composed of vertical aggregates contained within horizontal clusters. C: in this scheme, Jacksonian march would begin in center of rings and spread centrifugally.

From Kwan et al. 172 and Murphy et al. 215
Figure 6. Figure 6.

Patterns of Jacksonian march within sensory system. Maximum spread of somatosensory symptoms beginning in hand are indicated for 45 patients. After arm is occupied there is much greater likelihood of spread to face than to lower extremity. There is no clear explanation for this pattern or for why seizures occasionally jump from hand to face (cheiro‐oral pattern).

From Mauguire and Courjon 197
Figure 7. Figure 7.

A: cortical connections of parahippocampal gyrus. Connections from neocortex to limbic system converge on cingulate and retrosplinial cortex (Rspl) from lateral prefrontal cortex, on entorhinal cortex from temporal and parietal cortex, and on periamygdaloid cortex from orbitofrontal cortex. B: cortical afferents to amygdala. Connections from neocortex directly to amygdala occur from frontal cortex (dark), temporal cortex (shaded), and insula (hatched).

A from Van Hoesen 326; B from Van Hoesen 325
Figure 8. Figure 8.

Multiple depth stereotaxic EEG recordings in select patients with partial complex seizures have been studied to localize site of onset and spread of discharges within limbic system. Common pattern in studies by Wieser 346 is the unilateral temporobasal limbic seizure type shown. Discharges originating in medial hippocampus spread anteriorly to amygdala and posteriorly to retrosplenial cortex and posterior part of cingulate gyrus. There is weaker spread to lateral neocortex and contralateral limbic system. Patients with this pattern of spread often have intellectual aura, fear, abdominal sensation, as well as simple facial, oral, and alimentary automatisms.

From Wieser 346
Figure 9. Figure 9.

Correlation of different symptoms with spread of limbic seizures is indicated for the 7 different functional types proposed by Wieser. Length of bar is proportional to correlation of symptoms. Symptoms with high correlation (observed at least 5 times) are accentuated.

From Wieser 346
Figure 10. Figure 10.

Depth‐electrode stimulation of patient with partial complex seizures. Anatomical site of response is indicated along 2 electrodes inserted from each lateral temporal neocortex into left (LT) and right (RT) amygdala. Height of vertical lines roughly indicates intensity of patient's response. AD, afterdischarge.

From Gloor et al. 113
Figure 11. Figure 11.

Neocortical‐limbic‐thalamic system proposed for visual learning and memory. Note dense neocortical projections from temporal cortex to hippocampus and amygdala (see Fig. 7A, B). Bilateral lesions located at arrows 1–5 produce deficits in visual recognition memory. Seizures within this visual → memory corridor can evoke complex hallucinations and visual memory flashbacks.

From Mishkin 208


Figure 1.

A: dog brain stimulation experiments of Fritsch and Hitzig 91 were first to show localization by direct cortical stimulation. Points indicate movement of contralateral parts as well as different movements in same part: Δ, neck; +, extension‐abduction of anterior leg; +• flexion‐rotation of anterior leg; #, posterior leg; and , face. These authors noted effects of repeated stimulation: facilitation, exhaustion, and occasional aftermovements and were first to produce experimental seizures. B and C: Ferrier 82,83 used weak faradic stimulation to produce first motor maps of primate brain. Note especially point 15 in C over periamygdaloid cortex of uncus, an area that produced ipsilateral movements of upper lip and ala of nose.

A from Fritsch and Hitzig 91; B and C from Ferrier 82,83


Figure 2.

Pathophysiology of epileptic discharges. Interictal electroencephalogram (EEG) spike is 1 hallmark of focal epilepsy. Physiological experiments in variety of models show that large neurons undergo paroxysmal depolarizing shift followed by prolonged afterhyperpolarization that coincides in time with surface spike. Many currents responsible for this abnormal event are related to increased Ca2+ influx in dendrites. Three hypotheses relate to changes in local circuits that might potentiate abnormal Ca2+ currents: 1) abnormal dendrites, 2) hypersynchronous excitatory input, and 3) loss of inhibition.



Figure 3.

Organization of seizure focus. Large populations of neurons must be temporally synchronized into burst firing to cause an epileptic spike on EEG (pyramidal neurons A and B). This change occurs predominantly through action of local excitatory interneurons, although failure of inhibitory interneurons and other factors probably also play a role. Most cells inside the focus show depolarizing shifts in membrane potential coincident with surface spikes. Inhibitory surround is characterized by predominance of cells that are hyperpolarized during surface spikes (pyramidal neuron C). Farther laterally, cortex remains normal. Inhibitory surround is created by axon terminals of inhibitory neurons driven within the focus and recurrent collaterals of pyramidal cells ending on inhibitory neurons outside the focus. Transition zone between excitation and inhibition is temporally and spatially dynamic, and the focus greatly expands when interictal spikes change to produce prolonged seizures.

Data from Prince and Wilder 260


Figure 4.

2‐Deoxyglucose autoradiography of intense focal occipital seizures induced by injecting 80 units of penicillin into cortex. A: metabolic focus occupies most of visual areas 17, 18, and 18a (pallor represents trauma surrounding needle track). There is drop‐off of activity in layer IV, and a metabolic depression surrounds the focus and extends laterally into temporal cortex. In contralateral homotopic cortex, glucose utilization is also depressed in area 17 medial to vertical band of activation on border of areas 17 and 18a. Temporal cortex lateral to this is normal. Bands of activation in subcortical sites are seen ipsilaterally in dorsal lateral geniculate nucleus (LGN) and lateralis posterior nucleus and are seen contralaterally in dorsal LGN. This particular locus of activation in contralateral LGN represents central portion of visual field, indicating activity in projections descending from border of areas 17 and 18a in visual cortex above it. B: increased activity can be seen in fiber tracts descending ipsilaterally to dorsal LGN and to tail of caudate (arrows, right), and in optic radiation to contralateral dorsal LGN (arrow, left). C: in addition to activation of cortical columns posterior to the focus, there is evidence for mild accentuation of activity ipsilaterally in postsubiculum (arrow). D: activation of columns posteriorly and laterally in temporal cortex. E: functional anatomy of focal seizures in visual cortex. Topical cortical maps and occipital lobe EEGs. Corticocortical spread of seizure activity into columns and strips is reflection of intensity, size, and location of cortical focus.

From Collins and Caston 42


Figure 5.

Body parts in motor cortex may be organized into “nested rings” 172,214,354. A: more distal parts (F, fingers) lie internal to proximal parts (W, wrist; E, elbow; S, shoulder). B: each ring is composed of vertical aggregates contained within horizontal clusters. C: in this scheme, Jacksonian march would begin in center of rings and spread centrifugally.

From Kwan et al. 172 and Murphy et al. 215


Figure 6.

Patterns of Jacksonian march within sensory system. Maximum spread of somatosensory symptoms beginning in hand are indicated for 45 patients. After arm is occupied there is much greater likelihood of spread to face than to lower extremity. There is no clear explanation for this pattern or for why seizures occasionally jump from hand to face (cheiro‐oral pattern).

From Mauguire and Courjon 197


Figure 7.

A: cortical connections of parahippocampal gyrus. Connections from neocortex to limbic system converge on cingulate and retrosplinial cortex (Rspl) from lateral prefrontal cortex, on entorhinal cortex from temporal and parietal cortex, and on periamygdaloid cortex from orbitofrontal cortex. B: cortical afferents to amygdala. Connections from neocortex directly to amygdala occur from frontal cortex (dark), temporal cortex (shaded), and insula (hatched).

A from Van Hoesen 326; B from Van Hoesen 325


Figure 8.

Multiple depth stereotaxic EEG recordings in select patients with partial complex seizures have been studied to localize site of onset and spread of discharges within limbic system. Common pattern in studies by Wieser 346 is the unilateral temporobasal limbic seizure type shown. Discharges originating in medial hippocampus spread anteriorly to amygdala and posteriorly to retrosplenial cortex and posterior part of cingulate gyrus. There is weaker spread to lateral neocortex and contralateral limbic system. Patients with this pattern of spread often have intellectual aura, fear, abdominal sensation, as well as simple facial, oral, and alimentary automatisms.

From Wieser 346


Figure 9.

Correlation of different symptoms with spread of limbic seizures is indicated for the 7 different functional types proposed by Wieser. Length of bar is proportional to correlation of symptoms. Symptoms with high correlation (observed at least 5 times) are accentuated.

From Wieser 346


Figure 10.

Depth‐electrode stimulation of patient with partial complex seizures. Anatomical site of response is indicated along 2 electrodes inserted from each lateral temporal neocortex into left (LT) and right (RT) amygdala. Height of vertical lines roughly indicates intensity of patient's response. AD, afterdischarge.

From Gloor et al. 113


Figure 11.

Neocortical‐limbic‐thalamic system proposed for visual learning and memory. Note dense neocortical projections from temporal cortex to hippocampus and amygdala (see Fig. 7A, B). Bilateral lesions located at arrows 1–5 produce deficits in visual recognition memory. Seizures within this visual → memory corridor can evoke complex hallucinations and visual memory flashbacks.

From Mishkin 208
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Article Title: Epilepsy: Insights into Higher Brain Functions in Humans
 

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Robert C. Collins. Epilepsy: Insights into Higher Brain Functions in Humans. Compr Physiol 2011, Supplement 5: Handbook of Physiology, The Nervous System, Higher Functions of the Brain: 811-841. First published in print 1987. doi: 10.1002/cphy.cp010520