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Abnormalities of Motor Behavior After Cortical Lesions in Humans

Hans‐Joachim Freund

10.1002/cphy.cp010519

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 Frontal Lobe
1.1 Ablation of Prefrontal Cortex
1.2 Frontal Motor Fields
1.3 Disturbances of Movement Execution
1.4 Functional Considerations on Pyramidal Syndrome in Humans
1.5 Supplementary Motor Area
1.6 Lesions of Premotor Cortex
1.7 Functional Significance of Premotor Cortex for Proximal Musculature Control and Interlimb Coordination
1.8 Frontal Eye Fields
1.9 Output Organization of Frontal Agranular Motor Areas
2 Parietal Lobe
2.1 Sensory Deficits
2.2 Motor Dysfunction After Parietal Lesions
3 Temporal Lobe
4 Occipital Lobe
5 Motor Coordination After Commissurotomy
6 Observations in Patients After Hemispherectomy
7 Apraxias
7.1 Historical Aspects
7.2 Distribution of the Apraxias in Different Body Parts
7.3 Concept of Disconnection Syndromes
7.4 Apraxia and Left Hemisphere
8 Approach Toward a Functional Analysis of Movement Disorders
8.1 Effects of Sensory Disturbances Due to Cortical Lesions on Motor Function
8.2 Sensory‐Motor and Motor‐Sensory Interaction: Hand as a Sense Organ
8.3 Posterior Apraxias as Disorders of Sensory‐Motor Integration
8.4 Anatomical Considerations
9 Temporal Aspects of Motor Control
10 Summary and Conclusions
Figure 1. Figure 1.

Computerized tomography scan, horizontal plane. Left, hemorrhage in frontal lobe involving premotor area and primary motor cortex region and underlying white matter. Middle and right, large parietal lesion on horizontal and coronal planes of a nuclear magnetic resonance scan. Neither patient had clinically detectable neurological deficits. Right side of brain is seen on left side of scans.
Figure 2. Figure 2.

Surface view of left cerebral hemisphere of macaque monkey. Medial surface of hemisphere is shown, inverted, at top. MI, primary motor cortex; Mil, supplementary motor cortex; PM, premotor cortex (approximate locations). Each dotted line represents fundus of a sulcus. Open squares, rough estimation of rostral boundary of PM.

From Wise 325
Figure 3. Figure 3.

Motor fields of human brain according to Foerster. Numbers indicate cytoarchitectonic areas as designated by Vogt and Vogt 312.

From Foerster 74
Figure 4. Figure 4.

Arm‐hand movements and brain stem of patient with total destruction of arm‐finger field of left precentral region. Initially there was complete paralysis of right arm. After 2 yr of intense physiotherapy, patient was able to perform movements shown in the various pictures. Individual finger movements were not possible, but synergistic finger flexion and interaction between forefinger and thumb were possible. Bottom, section of medulla oblongata shows complete degeneration of left pyramid.

From Foerster 74
Figure 5. Figure 5.

Computerized tomography scan of right‐handed patient with small lesion involving hand area of left precentral gyrus. Left of brain is to reader's right. Arrow points to lesion.
Figure 6. Figure 6.

Percent of mean increase of regional cerebral blood flow during internal programming of motor‐sequence test performed by contralateral hand. Subjects had learned to perform quick sequence of opposing movements of fingers and thumb, in which thumb had to touch index finger twice, middle finger once, ring finger three times, and little finger twice. Thereafter, movements had to be performed in reverse order. Each run had to be accomplished within 10 s. Values corrected for diffuse increases of the blood flow. Left, left hemisphere, 3 subjects; right, right hemisphere, 5 subjects.

From Roland et al. 282
Figure 7. Figure 7.

Averaged curves from typical experiment showing movement‐related potentials preceding unilateral right‐sided (A) and bilateral (B) movements. Electrode positions over C'3, left precentral; C'4′, right precentral; Cz, vertex; P3, left parietal; P4, right parietal; Pz, midline parietal. Averages of 256 right‐sided and 256 bilateral movements performed alternately in blocks of 128 within same experiment. With unilateral movements, a larger Bereitschaftspotential (readiness potential) can be seen over contralateral precentral region (C'3). With bilateral movements, readiness potential is larger over right, or minor, hemisphere of right‐handed subjects. This difference is pronounced in precentral leads and is almost missing in parietal leads. Vertex amplitudes tend to be larger with bilateral movements than with unilateral movements.

From Kristeva et al. 184
Figure 8. Figure 8.

Common region of overlap of frontal lesions involving premotor cortex of patients with proximal weakness and limb‐kinetic apraxia. Right hemisphere is shown on left. CS, central sulcus.

Prom Freund and Hummelsheim 89
Figure 9. Figure 9.

Computerized tomography (CT) scan on right shows patient with proximal weakness and lesion involving precentral gyrus in area of body representation for proximal muscles. For comparison, CT scan of patient with premotor lesion is shown on left. Right hemisphere is on left in both scans. CS, central sulcus.

From Freund and Hummelsheim 90
Figure 10. Figure 10.

Relative size of some descending tracts and nuclei in primates.

From Nathan and Smith 242
Figure 11. Figure 11.

Major motor cortical projections. Left, premotor‐reticulospinal pathway originating from premotor cortex; right, cortical spinal (pyramidal) tract from primary and supplementary motor areas.

From Freund 84
Figure 12. Figure 12.

Hand of patient with excision of parietal cortex. Left, patient trying to make fist; right, patient trying to write.

From Foerster 74
Figure 13. Figure 13.

Lesion sites in different forms of visuomotor ataxia. A: unilateral direct visuomotor ataxia, localized to one hand in homonymous field. B: unilateral crossed visuomotor ataxia, localized to one hand in visual field of opposite side. C: bilateral crossed visuomotor ataxia, affecting each hand in opposite visual fields.

From Rondot et al. 286
Figure 14. Figure 14.

Liepmann's original scheme showing suggested lesion sites for limb‐kinetic apraxia (1), ideo‐kinetic apraxia (2), and ideational apraxia (3).

From Liepmann 206
Figure 15. Figure 15.

Liepmann's scheme illustrating his concept about dyspraxia of left hand after damage of fibers originating from left precentral gyrus. Cortical lesion at site 1 (left hand area) and subcortical lesion at site 2 will not only damage descending but also callosal fibers, causing hemiparesis of right hand and dyspraxia of left hand. Damage at lesion site 3 will only cause dyspraxia of left hand and at lesion site 4 hemiparesis of right hand without left‐hand dyspraxia.

From Liepmann 206
Figure 16. Figure 16.

Moberg's picking‐up test. Objects shown are picked up and placed in a container. Patient is not asked to identify object.

From Moberg 224
Figure 17. Figure 17.

Moberg's illustration of “eyes of the fingers” (left) and of significance of hand sensation for motor function of the hand.

From Moberg 226
Figure 18. Figure 18.

Apparatus designed by Johansson and Westling for measuring grip force and load force during precision grip, a: Table; b: holes in table; c: exchangeable weight shielded from subject's view by table; d: exchangeable discs; e and f: vertical position transducer with ultrasonic receiver (e) and ultrasonic transmitter (f); g: accel‐erometer; h: strain‐gauge force transducers for measurement of grip force and load force (vertical lifting force); i: peg with hemispherical tip on which object rests while standing on table.

From Johansson and Westling 158
Figure 19. Figure 19.

Relationship between pure sensory, pure motor, and integrated sensory‐motor functions of brain and their disturbance patterns as seen in human motor disorders.

From Freund 86
Figure 20. Figure 20.

Lateral surface of rhesus monkey cerebral hemisphere showing three major divisions of association cortex: 1) parasensory association cortex (auditory association areas AAI and AAII); somatic sensory association areas SAI and SAII; (visual association areas VAI and VAII); 2) frontal association cortex (premotor and prefrontal areas); and 3) paralimbic association cortex (cingulate gyrus, parahippocampal gyrus, temporal pole, and orbitofrontal cortex).

From Pandya and Seltzer 254
Figure 21. Figure 21.

Lateral surface of rhesus monkey cerebral hemisphere showing location and pattern of cortical sensory convergence in intraparietal sulcus (IPS and POa), superior temporal sulcus (TPO and PGa), and frontal lobe (premotor and prefrontal areas). V, visual; A, auditory; S, somatosensory.

Adapted from Pandya and Seltzer 254


Figure 1.

Computerized tomography scan, horizontal plane. Left, hemorrhage in frontal lobe involving premotor area and primary motor cortex region and underlying white matter. Middle and right, large parietal lesion on horizontal and coronal planes of a nuclear magnetic resonance scan. Neither patient had clinically detectable neurological deficits. Right side of brain is seen on left side of scans.



Figure 2.

Surface view of left cerebral hemisphere of macaque monkey. Medial surface of hemisphere is shown, inverted, at top. MI, primary motor cortex; Mil, supplementary motor cortex; PM, premotor cortex (approximate locations). Each dotted line represents fundus of a sulcus. Open squares, rough estimation of rostral boundary of PM.

From Wise 325


Figure 3.

Motor fields of human brain according to Foerster. Numbers indicate cytoarchitectonic areas as designated by Vogt and Vogt 312.

From Foerster 74


Figure 4.

Arm‐hand movements and brain stem of patient with total destruction of arm‐finger field of left precentral region. Initially there was complete paralysis of right arm. After 2 yr of intense physiotherapy, patient was able to perform movements shown in the various pictures. Individual finger movements were not possible, but synergistic finger flexion and interaction between forefinger and thumb were possible. Bottom, section of medulla oblongata shows complete degeneration of left pyramid.

From Foerster 74


Figure 5.

Computerized tomography scan of right‐handed patient with small lesion involving hand area of left precentral gyrus. Left of brain is to reader's right. Arrow points to lesion.



Figure 6.

Percent of mean increase of regional cerebral blood flow during internal programming of motor‐sequence test performed by contralateral hand. Subjects had learned to perform quick sequence of opposing movements of fingers and thumb, in which thumb had to touch index finger twice, middle finger once, ring finger three times, and little finger twice. Thereafter, movements had to be performed in reverse order. Each run had to be accomplished within 10 s. Values corrected for diffuse increases of the blood flow. Left, left hemisphere, 3 subjects; right, right hemisphere, 5 subjects.

From Roland et al. 282


Figure 7.

Averaged curves from typical experiment showing movement‐related potentials preceding unilateral right‐sided (A) and bilateral (B) movements. Electrode positions over C'3, left precentral; C'4′, right precentral; Cz, vertex; P3, left parietal; P4, right parietal; Pz, midline parietal. Averages of 256 right‐sided and 256 bilateral movements performed alternately in blocks of 128 within same experiment. With unilateral movements, a larger Bereitschaftspotential (readiness potential) can be seen over contralateral precentral region (C'3). With bilateral movements, readiness potential is larger over right, or minor, hemisphere of right‐handed subjects. This difference is pronounced in precentral leads and is almost missing in parietal leads. Vertex amplitudes tend to be larger with bilateral movements than with unilateral movements.

From Kristeva et al. 184


Figure 8.

Common region of overlap of frontal lesions involving premotor cortex of patients with proximal weakness and limb‐kinetic apraxia. Right hemisphere is shown on left. CS, central sulcus.

Prom Freund and Hummelsheim 89


Figure 9.

Computerized tomography (CT) scan on right shows patient with proximal weakness and lesion involving precentral gyrus in area of body representation for proximal muscles. For comparison, CT scan of patient with premotor lesion is shown on left. Right hemisphere is on left in both scans. CS, central sulcus.

From Freund and Hummelsheim 90


Figure 10.

Relative size of some descending tracts and nuclei in primates.

From Nathan and Smith 242


Figure 11.

Major motor cortical projections. Left, premotor‐reticulospinal pathway originating from premotor cortex; right, cortical spinal (pyramidal) tract from primary and supplementary motor areas.

From Freund 84


Figure 12.

Hand of patient with excision of parietal cortex. Left, patient trying to make fist; right, patient trying to write.

From Foerster 74


Figure 13.

Lesion sites in different forms of visuomotor ataxia. A: unilateral direct visuomotor ataxia, localized to one hand in homonymous field. B: unilateral crossed visuomotor ataxia, localized to one hand in visual field of opposite side. C: bilateral crossed visuomotor ataxia, affecting each hand in opposite visual fields.

From Rondot et al. 286


Figure 14.

Liepmann's original scheme showing suggested lesion sites for limb‐kinetic apraxia (1), ideo‐kinetic apraxia (2), and ideational apraxia (3).

From Liepmann 206


Figure 15.

Liepmann's scheme illustrating his concept about dyspraxia of left hand after damage of fibers originating from left precentral gyrus. Cortical lesion at site 1 (left hand area) and subcortical lesion at site 2 will not only damage descending but also callosal fibers, causing hemiparesis of right hand and dyspraxia of left hand. Damage at lesion site 3 will only cause dyspraxia of left hand and at lesion site 4 hemiparesis of right hand without left‐hand dyspraxia.

From Liepmann 206


Figure 16.

Moberg's picking‐up test. Objects shown are picked up and placed in a container. Patient is not asked to identify object.

From Moberg 224


Figure 17.

Moberg's illustration of “eyes of the fingers” (left) and of significance of hand sensation for motor function of the hand.

From Moberg 226


Figure 18.

Apparatus designed by Johansson and Westling for measuring grip force and load force during precision grip, a: Table; b: holes in table; c: exchangeable weight shielded from subject's view by table; d: exchangeable discs; e and f: vertical position transducer with ultrasonic receiver (e) and ultrasonic transmitter (f); g: accel‐erometer; h: strain‐gauge force transducers for measurement of grip force and load force (vertical lifting force); i: peg with hemispherical tip on which object rests while standing on table.

From Johansson and Westling 158


Figure 19.

Relationship between pure sensory, pure motor, and integrated sensory‐motor functions of brain and their disturbance patterns as seen in human motor disorders.

From Freund 86


Figure 20.

Lateral surface of rhesus monkey cerebral hemisphere showing three major divisions of association cortex: 1) parasensory association cortex (auditory association areas AAI and AAII); somatic sensory association areas SAI and SAII; (visual association areas VAI and VAII); 2) frontal association cortex (premotor and prefrontal areas); and 3) paralimbic association cortex (cingulate gyrus, parahippocampal gyrus, temporal pole, and orbitofrontal cortex).

From Pandya and Seltzer 254


Figure 21.

Lateral surface of rhesus monkey cerebral hemisphere showing location and pattern of cortical sensory convergence in intraparietal sulcus (IPS and POa), superior temporal sulcus (TPO and PGa), and frontal lobe (premotor and prefrontal areas). V, visual; A, auditory; S, somatosensory.

Adapted from Pandya and Seltzer 254
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Article Title: Abnormalities of Motor Behavior After Cortical Lesions in Humans
 

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Hans‐Joachim Freund. Abnormalities of Motor Behavior After Cortical Lesions in Humans. Compr Physiol 2011, Supplement 5: Handbook of Physiology, The Nervous System, Higher Functions of the Brain: 763-810. First published in print 1987. doi: 10.1002/cphy.cp010519