1. MOTOR SYSTEMS REVIEW
Dr. G. R. Leichnetz

2. Pyramidal System

3. A representation of the body’s musculature is somatotopically-organized on the precentral gyrus and paracentral lobule, known as the motor homunculus.
The corticospinal tract originates from the dorsolateral precentral gyrus (arm/hand region) and paracentral lobule (leg).
The corticobulbar tract originates from the ventrolateral precentral gyrus (head).
Lower extremity
Upper extremity
Precentral Gyrus
Origin of Corticospinal Tract (body)
Paracentral lobule
Head
Origin of Corticobulbar Tract (head)
Motor Homunculus

4. Motor cortex, layer V
The corticospinal (pyramidal) tract axons (upper motor neurons) originate in lamina V of the motor cortex and descend thru the internal capsule and brainstem (crus cerebri, basilar pons, medullary pyramid) to the caudal medulla where 90% or more cross in the pyramidal decussation to the opposite side of the spinal cord (then called the lateral corticospinal tract).
A few corticospinals remain on the same side (ant. corticospinal tract) but cross at the level of termination.
Crus cerebri, midbrain
Basilar pons
Medullary pyramid
Pyramidal decussation
Lateral corticospinal tract
Anterior corticospinal tract

5. The lateral corticospinal tract is somatotopically-organized and is the largest tract in the dorsolateral quadrant of the lateral funiculus, with sacral most lateral and cervical most medial.
Lateral corticospinal tract C
Kahn et al, Correlative Neurosurgery

6. Head Region, VL Precentral gyrus
The corticobulbar tract originates from lamina V large pyramidal neurons in the head region of the motor cortex (ventrolateral precentral gyrus), and descends into the brainstem, projecting bilaterally to all cranial nerve motor nuclei.
Corticobulbar Tract (genu)
III IV
Cranial nerve motor nuclei
Most corticobulbars terminate on interneurons in the reticular formation near cranial nerve motor nuclei, but some go directly to lower motor neurons within the motor nuclei. VI V NA
VII
XII

7. Lesion of Corticobulbar Tract
Corticobulbar tract lesion
Corticobulbars to facial nucleus are unique. Lower half of the FN only receives crossed innervation.

8. Corticobulbar innervation of the hypoglossal nucleus is primarily crossed.
Corticobulbar tract lesion (UMN lesion) leads to contralateral paralysis of tongue; tongue deviated contralaterally.
Hypoglossal nucleus or XIIth nerve lesion (LMN lesion) leads to ipsilateral paralysis of tongue; tongue deviated ipsilaterally.
Corticobulbar tract lesion
Hypoglossal nerve lesion
Tongue deviates toward the paralyzed side

9. Pyramidal Lesions

10. Cortical vascular infarct involving the precentral gyrus (arm & head regions) and Broca’s speech area (middle cerebral artery).

11. Capsular hemiplegia- involving genu (corticobulbars) and post
Capsular hemiplegia- involving genu (corticobulbars) and post. limb (corticospinals) of the internal capsule (middle cerebral artery).

12. Weber’s Syndrome (Alternating Oculomotor Hemiplegia) involving crus cerebri of the midbrain (corticospinals and corticobulbars) and oculomotor nerve (branches of post. cerebral artery)
Ipsilateral exotropia, ptosis, mydriasis (pupillary dilatation) with contralateral spastic hemiplegia (positive Babinski).

13. Alternating abducent hemiplegia involving the basilar pons (corticospinals) and abducens nerve (br.’s of basilar artery)
Ipsilateral esotropia with contralateral spastic hemiplegia.

14. Medial Medullary Syndrome- Alternating hypoglossal hemiplegia involving the medullary pyramid (corticospinals) and hypoglossal nerve (anterior spinal artery). Medial lemniscus also involved.
Ipsilateral tongue paralysis (tongue deviates to side of lesion) with contralateral hemiplegia. Contralateral loss of conscious proprioception, vibratory sense.

15. Brown-Sequard Syndrome (Spinal Cord Hemisection)
Produces ipsilateral spastic paralysis (lateral corticospinal tract lesion) with ipsilateral loss of conscious proprioception (dorsal column lesion), and
contralateral loss of pain and temp. (lateral spinothalamic tract lesion) FG
CST
LSTT

16. Amyotrophic Lateral Sclerosis (ALS) (Lou Gehrig’s Disease)
Affects both upper and lower motor neurons
Demyelinization (sclerosis) of the lateral corticospinal tract. Twitches (fasciculations), uncontrolled small discharges, and atrophy occur in muscle groups as motor neurons in the brainstem and spinal cord degenerate. Slurred speech, difficulty swallowing.
No sensory impairment.
No cognitive or memory impairment.

17. Poliomyelitis
(LMN lesion of the anterior horn motor neurons of the spinal cord)
produces an ipsilateral flaccid paralysis with hypotonia, hyporeflexia and atrophy.

18. Oculomotor System

19. Types of Eye Movements Conjugate Vestibulo-ocular (VOR)
Saccades- voluntary (FEF) and reflexive (SC)
Smooth Pursuit- tracking
Optokinetic- moving visual scene
Disconjugate
Convergence- “near response”

20. Vestibulo-ocular Reflex (VOR)
Vestibulo-ocular projections to the oculomotor, trochlear, and abducens nuclei coordinate reflexive eye movements that compensate for head movements (to maintain fixation).
Vestibulo-ocular Reflex (VOR)
III IV
Medial longitudinal fasciculus
Vestibular complex VI

21. Saccadic Eye Movements
Voluntary saccadic eye movements are initiated in the frontal eye field.
Reflexive saccadic eye movements are initiated in the superior colliculus. SC SC

22. The intermediate and deep (motor) layers of the SC are in registry with the visual map in the superficial layer.
There is a retinotopic map of the visual world on the surface of the SC S I
The intermediate layer is integrative; receives input from the FEF, cerebellum & basal ganglia, affecting motor output in deep layer.
The deep layer is “motor” and is in registry with the visual map in the superficial layer. D
When the SC initiates a reflexive saccade to look at an object, it can precisely target the location of the object in the visual world, so it can initiate an eye movement of appropriate amplitude and direction to bring the image onto the fovea of the retina.

23. The FEF and SC project to preoculomotor centers in the brainstem reticular formation. The preoculomotor centers for vertical saccades are located in the rostral midbrain reticular formation (riMLF, downward; INC, upward), and for horizontal saccades in the medial pontine reticular formation (PPRF).
Vertical Saccades IV
III VI
PPRF
Horizontal Saccades

24. Premotor centers for vertical saccades:
riMLF- downward (lesion results in downgaze paralysis)
INC- upward (lesion results in upgaze paralysis)
Subthalamic Nucleus
Substantia Nigra

25. Horizontal Gaze Center: PPRF
Abducens Nucleus
The center for horizontal saccades (PPRF) is located in the medial pontine reticular formation at the level of the abducens nucleus. It contains premotor neurons that project to lateral rectus motor neurons in the abducens nucleus, and also projects to the cervical spinal cord for “gaze” (eye movement + head movement). Thus a lesion in PPRF results in an ipsilateral paralysis of conjugate horizontal gaze.

26. Smooth Pursuit System
Smooth pursuit eye movements are slow eye movements used to follow a moving object across the visual field. To maintain fixation, the eyes must move at the same speed as the visual target (eye movement matches target velocity).
Therefore, the pursuit system involves seeing the object (visual cortex), analyzing its motion (pre-occipital cortex, area MT), and orchestrating eye movements (cerebellum) that are the same velocity as the target.

27. Smooth Pursuit Pathway
Visual Cortex to MT Visual Area (V5) to DLPN to “oculomotor part” of the posterior lobe vermis
Lesion of these structures can result in pursuit deficits
Visual Cortex
Oculomotor Vermis
Oculomotor vermis
DLPN
Dorsolateral pontine nucleus
Posterior lobe

28. Optokinetic System
When the visual scene is moving (eg. riding on a train) to maintain fixation on an object (eg. following telephone poles) produces oscillating eye movements which consist of a slow component that follows the object and then a fast component where eyes snap back to attach to the next pole.
Produces optokinetic eye movements, similar to nystagmus, called optokinetic nystagmus, OKN.
The neural network for these eye movements involves the pretectum (receives visual input from the retina), which projects to the reticulotegmental nucleus (NRTP) of the pons, which then relays the information to the cerebellum (flocculonodular lobe).

29. Optokinetic Pathway
Retina and/or visual cortex to pretectal area to nucleus reticularis tegmenti pontis (NRTP) to flocculonodular cortex
Lesion of these structures can produce OKN deficits.
Visual cortex
Retina
Flocculus
Flocculonodular lobe

30. Vergence Eye Movements
Vergence eye movements are the only disjunctive type of eye movement. In convergence, both medial rectus muscles contract.
The pathway subserving convergence is not well known. But what is known is that the neural pathway reaches the two medial rectus cell groups in the oculomotor nucleus w/o going through the MLF (convergence is preserved in an MLF lesion, ie. INO).
Convergence is part of the “near response,” ie. focussing on a near object, involves:
convergence accommodation (lens thickening) pupillary constriction

31. Oculomotor Lesions

32. Oculomotor (IIIrd) Nerve Palsy, left eye
Ptosis
right
left
Mydriasis
Exotropia
From: Fix, High-Yield Neuroanatomy
With lesion of the left oculomotor nerve (C.N. III), the left eye is abducted (due to unopposed action of the lateral rectus). There is ipsilateral ptosis (paralysis of levator palpebrae) and the ipsilateral pupil is dilated (mydriasis; disruption of parasymp. fibers to constrictor pupillae).

33. Abducens (Sixth) Nerve Palsy, right eye
left
Ipsilateral eye does not abduct
From: Fix, High-Yield Neuroanatomy
Lesion of the right abducens nerve (C.N. VI) results in paralysis of the right lateral rectus muscle. When looking to the right, the right eye will not abduct. Esotropia.

34. Abducens Nucleus Lesion
Cannot abduct the ipsilateral eye or adduct the contralateral eye
Right Left
Lesion of abducens nucleus produces ipsilateral paralysis of conjugate horizontal eye movements (cannot abduct ipsilateral eye due to lesion of lateral rectus motoneurons, and cannot adduct contralateral eye due to lesion of internuclear neurons that project to contralateral medial rectus motor neurons)

35. MLF Lesion: right MLF Ipsilateral eye will not adduct.
Right Left
Abducens internuclear neurons project thru MLF to contralateral medial rectus motor neurons
Lesion of MLF produces internuclear ophthalmoplegia, INO)
cannot adduct eye ipsilateral to MLF lesion due to interruption of internuclear axons, but medial rectus will contract with convergence)

36. MLF Lesion: Internuclear Ophthalmoplegia, right eye
Ipsilateral eye does not adduct
right
left
Fix
Lesion of the right MLF disrupts axons of internuclear neurons whose cell bodies are located in the abducens nucleus and which project to the right medial rectus cell group of the oculomotor nucleus.
On looking to the left, the ipsilateral eye (on the lesioned side) will not adduct on attempted conjugate horizontal eye movement to the opposite side..
But since the medial rectus cell group itself is intact, the ophthalmologist can get adduction in convergence.
Lesion of the MLF also produces nystagmus (disrupts VOR).

37. PPRF Lesion A lesion of the paramedian pontine reticular formation produces an ipsilateral paralysis of conjugate horizontal gaze.
Ipsilateral conjugate horizontal gaze paralysis

38. Frontal Eye Field Lesion on right
left
From: Fix, High-Yield Neuroanatomy
Lesion of the frontal eye field (area 8) on the right results in a paralysis of conjugate eye movements to the left. The eyes are deviated to the right (toward side of lesion).
The FEF lesion disrupts projections to contralateral PPRF, resulting in a contralateral paralysis of conjugate horizontal gaze

39. Cerebellum

40. Cerebellum: Three Lobes
Anterior Lobe- “paleocerebellum” proprioception
Posterior Lobe- “neocerebellum” cortical (receives input from cortex via basilar pons)
Flocculonodular Lobe- “archicerebellum” vestibular

41. Cerebellar Afferents:
Spinocerebellars Cuneocerebellars Pontocerebellars Vestibulocerebellars
Olivocerebellars
All of these inputs enter the cerebellum thru the inferior & middle cerebellar peduncles.
Anterior lobe
Basilar pontine nuclei
Posterior lobe
Vestibular complex
Flocculo-Nodular lobe
Accessory. (Lat.) Cuneate nucleus
Inferior olivary nucleus
Nucleus dorsalis

42. All inputs, except olivocerebellars, terminate as “mossy fibers” on granule cells.
Olivocerebellars terminate as “climbing fibers” directly on Purkinje cells.
Purkinge cells project to deep cerebellar nuclei

43. Purkinje cells of the cerebellar cortex project to deep cerebellar nuclei.G F D D E F G

44. Cerebellar efferents originate in the deep cerebellar nuclei.
The deep cerebellar nuclei (dentate, globose, emboliform nuclei) project thru the superior cerebellar peduncle to contralateral red nucleus and VL nucleus of the thalamus.
After the superior cerebellar peduncle decussates, there is a small contingent of cerebellar efferents that descend to “precerebellar nuclei” like the inferior olivary nucleus for feedback.
Cerebellar Efferents
To contralateral red nucleus and VL thalamus
Decussation of superior cerebellar peduncle
Deep cerebellar nuclei

45. Cerebellar Lesions: deficits expressed ipsilaterally
Ataxia- tendency to fall toward side of lesion
Intention Tremor (Action Tremor)
Dysdiadokinesia- inability to produce alternating antagonistic actions
Past-pointing
Nystagmus- flocculonodular lobe lesion

46. Basal Ganglia

47. The basal ganglia include: Caudate Putamen Globus pallidus
Caudate nucleus
The basal ganglia include:
Caudate Putamen
Globus pallidus
Subthalamic nucleus
Substantia nigra
Striatum
Subthalamic nucleus
Putamen
Globus pallidus
Substantia nigra

48. Striatum: Caudate and Putamen
The striatum is organized into subsectors, the striosomes and matrix, that have differential connections.
Caudate Nucleus
Striosomes
Matrix
Putamen
Haines, Fundamental Neuroscience
D1 Dopaminergic receptors predominate in the striosomes; D2 receptors in the matrix
From Parent, Carpenter’s Human Neuroanatomy

49. Corticostriates (glutamatergic, excitatory)
Striatal Afferents
Cortex
There are three principal sources of afferents to the striatum (green):
Corticostriates (glutamatergic, excitatory)
Thalamostriates (glutamatergic, excitatory)
Nigrostriates (dopaminergic)
CM/Pf
Intralaminar complex, thalamus
Substantia nigra
From Haines, Fundamental Neuroscience

50. Striatal Efferents
The principal efferents of the striatum (red) are:
Striatopallidals “striosomes” to internal segment of the globus pallidus (GPi) & “matrix” to external segment (GPe)
Striatonigrals “striosomes” to pars compacta (SNc) & “matrix” to pars reticulata (SNr) of substantia nigra
All of the efferents of the caudate and putamen are GABA-ergic (inhibitory).
From Haines, Fundamental Neuroscience

51. The direct pathway facilitates movement, while the indirect pathway inhibits movement.
D1 receptors predominate in striosomes (patches) and project directly to the GPi (direct pathway).
D2 receptors predominate in the matrix and project to the GPe (indirect pathway).

52. Huntington’s Chorea is an inherited disease with onset in middle age.
Atrophy of the striatum
Choreiform (dance-like) movements, rigidity
Post-mortem coronal section thrrough the brain of a patient with Huntington’s disease. Note atrophy of caudate and putamen and enlarged lateral ventricles.

53. Globus Pallidus
External segment
Internal segment

54. Pallidal Afferents and Efferents
The principal source of pallidal afferents is the striatum (striatopallidals; inhibitory). All efferents of the globus pallidus are GABA-ergic (inhibitory). The external segment projects to the subthalamic nucleus (“indirect loop”; in green) and the internal segment projects directly to the motor thalamus (primarily VA) and to intralaminar complex (CM/Pf). VA
Indirect Loop
Striatum Matrix to GPe
Striatum Striosomes to GPi
GPe
STN
GPi
Modified Burt, Textbook of Neuroanatomy

55. Modified from Kandel
The direct pathway facilitates movement, while the indirect pathway inhibits movement.
D1 receptors predominate in striosomes and project directly to the GPi (direct pathway).
D2 receptors predominate in the matrix and project to the GPe (indirect pathway).

56. A lesion of the subthalamic nucleus results in contralateral hemiballism.
Ballism- violent flinging movements caused by contractions of the proximal limb muscles as a result of lesion of the subthalamic nucleus.
Huntington’s disease and hemiballism are hyperkinetic disorders (excessive motor activity)

57. SN Substantia Nigra The substantia nigra has two parts:
pars compacta (DA) and the pars reticulata (GABA). SN
Pars reticulata
Pars compacta

58. Substantia Nigra Afferents
Substantia Nigra Afferents Striatonigrals: from caudate & putamen, GABA-ergic
Striosomes- to pars compacta, SN (SNc) Matrix- to pars reticulata, SN (SNr)
Caudate
Putamen
SNc
SNr
From Haines, Fundamental Neuroscience

59. Nigrostriatals (DA)- from SNc to caudate and putamen
Nigral Efferents:
Nigrostriatals (DA)- from SNc to caudate and putamen
Nigrothalamics- from SNr to motor thalamus (VA/VL) (GABA-ergic)
Nigrotectals- from SNr to superior colliculus (GABA-ergic)
Modified from Haines, Fundamental Neuroscience

60. The nigrostriatal projection from the pars compacta of the SN to the caudate and putamen is dopaminergic.
Loss of dopaminergic neurons in the SNpc is associated with Parkinson’s disease.
L-dopa therapy is recommended to replace depleted DA (crosses blood brain barrier)
Post-mortem section of the midbrain from a patient with Parkinson’s disease shows loss of neuromelanin in the SN

61. Festinating Gait- baby steps
Parkinson’s Disease
Resting tremor
Bradykinesia
Festinating Gait- baby steps
“Freezing”(inertia)- difficulty initiating movements
Rigidity
Masked face
Parkinson’s disease is a hypokinetic disorders (deficient motor activity)

62. The basal ganglia are involved in automated patterns of movement.
The outflow influences the SMA premotor cortex where movements are programmed.
Dysfunctions (functional deficits) are expressed contralaterally.

63. The basal ganglia are connected in a loop with the ipsilateral motor cortex
Therefore, if lesioned, the dysfunction affects the ipsilateral motor cortex, and deficits (thru the pyramidal system) are expressed on the contralateral side of the body.