H&n B6: Motor Output From The Brain And Brainstem Lecture 15

Front 1

What is the motor system divided into? Do they interact? Why is this division useful?

Back 1

Pyramidal and extrapyramidal. They do interact. Division is useful because lesions in each produce contrasting disorders of movement.

Front 2

1) Why is the pyramidal system named the pyramidal system? Where do its primary neurons originate? Where do their fibers travel to?

2) What are the two general pyramidal motor tracts?

Back 2

Primary neurons are shaped like pyramids. Originate in precentral gyrus and premotor cortex in the cerebral cortex. Fibers from primary neurons descend through internal capsule and cerebral peduncles to reach the brainstem or spinal cord.

2 general pyramidal motor tracts:

1) Corticobulbar - synapse in brainstem

2) Corticospinal - synapse on ventral horn cells

Front 3

What is the extra-pyramidal system composed of? Where do neurons of the extra-pyramidal system synapse?

Back 3

Basal ganglia, cerebellum, some areas of the brainstem. Neurons synapse within the brain and spinal cord, exert different effects from those of the pyramidal system.

Front 4

Where do motor fibers involved in the control of speech originate? Which motor system is this a part of?

Back 4

Broca's area, or the inferior frontal gyrus. This is part of the pyramidal system.

Front 5

1) When do common lesions of the pyramidal tracts usually affect the fibers?

2) Lesions of these tracts produce what syndrome?

3) What are symptoms of an upper motor lesion?

4) What are symptoms of a lower motor lesion?

Back 5

1) After they have left the motor cortex (internal capsule, brainstem, spinal cord).

2) Pyramidal syndrome

3) Upper motor lesion - spastic paralysis, positive Babinski sign, hyper-reflexia, hypertonia, mild atrophy

4) Lower motor lesion - flaccid paralysis, fasciculations, hypo-reflexia, hypotonia, severe atrophy

Front 6

1) Map the pathway of the pyramidal tract.

2) What are the notable exceptions of this pathway?

3) Describe the pathway of the lateral corticospinal tract. What does this control?

4) Describe the pathway of the anterior corticospinal tract. What does this control?

Back 6

1) Axons from the precentral gyrus/premotor cortex -> corona radiata -> anterior limb of internal capsule -> genu of internal capsule -> posterior limb of internal capsule -> nuclei in brainstem (corticobulbar) or cerebral peduncles of brainstem (corticospinal)

2) Fibers that travel in the oculomotor and trochlear nuclei do not go through genu and posterior limb of internal capsule; they exit the anterior limb to go to their nuclei.

3) From pathway listed above -> cerebral peduncles (mesencephalon) -> pons -> inferior to medulla, where 90% decussate, travel caudally to form LATERAL CORTICOSPINAL TRACT. This control of muscles involved with fine motor movements.

4) Pathway from #1 -> cerebral peduncles in mesencephalon -> pons -> medulla -> ONLY cross at the level of the spinal segment where they will synapse. Do not decussate at the medulla. Controls axial musculature (trunk, proximal limbs), maintains posture and gross positioning of limbs.

Front 7

1) Describe the pathway of the corticobulbar tract.

2) What else synapses on motor nuclei in the brainstem?

3) What does the motor nucleus of V do?

Back 7

Primary neurons in precentral gyrus/premotor cortex -> corona radiata -> internal capsule's anterior limb -> genu -> posterior limb -> synapse on motor nuclei in the brainstem.

2) Frontal eye centers in the frontal lobe

3) Innervate muscles of mastication, tensor tympani, tensor veli palatini, mylohyoid, anterior belly of the digastric.

Front 8

For the vast majority of the motor nuclei in the brainstem, how many are there on each side? What is an exception to this rule?

Back 8

1 on each side. Exception - facial nerve. Has two motor nuclei on each side of the brainstem, one upper and one lower. Upper motor nucleus bilaterally innervated by fibers from cerebral cortex. Lower motor nuclei only contralaterally innervated.

Front 9

Facial motor nucleus:

1) What does the upper motor nucleus supply? Will a unilateral stroke affect it? Why?

2) What does the lower motor nucleus supply? Will a unilateral stroke affect it?

Back 9

1) Muscles of facial expression above the zygomatic arch. Unilateral stroke will not affect it because it's bilaterally innervated by fibers from the cerebral cortex.

2) Muscles of facial expression beneath the zygomatic arch. Unilateral stroke will result in total dysfunction of these muscles on the contralateral side.

Front 10

Hypoglossal nuclei:

1) How is it innervated? (Ipsilaterally, contralaterally, bilaterally?)

2) Damage in the cerebrum will result in what kind of symptoms?

Back 10

1) Contralaterally
2) Contralaterally loss of motor to extrinsic and intrinsic muscles of the tongue.

Front 11

What are the four major motor pathways that originate from the brainstem and what are their functions?

Back 11

1) Tectospinal - cell bodies are in tectum (in superior colliculus) coordinates eye movements with movements of head, neck, upper torso. Axons travel contralaterally, terminate on ventral horn cells in spinal levels C1 - T2.

2) Rubrospinal - axons from the red nucleus in the midbrain. Nucleus receives axons from cerebral cortex and cerebellum. Axons travel contralaterally, cross in decussation of pyramidal tract, synapse on ventral horn cells throughout spinal cord. The red nucleus coordinates inputs and MODULATES motion of large muscles groups.

3) Reticulospinal - reticular nuclei (scattered throughout the brainstem) influence our ANS, cause awareness, wakefulness. Travel bilaterally to synapse on ventral horn cells and motor cells in the intermediate horn. General modulation of muscle groups, modulates heartbeart, perspiration, shivering, sphincters in the GI and urinary system.

4) Vestibulospinal - involved with balance. Axons originate in vestibular nuclei in medulla, terminate on ventral horn cells. Medial vestibulospinal tract travels bilaterally, axons of lateral vestibulospinal tract travel ipsilaterally.

Front 12

1) Where are the basal ganglia found?

2) Specific examples of basal ganglia?

Back 12

1) Deep in the telencephalon.

2) Caudate nucleus, globus pallidus, putamen, amygdala.

Front 13

What is the function of the amygdala?

Back 13

Visceral/emotional responses mediated by limbic system (telencephalic structures). Short-term, anterograde memory.

Front 14

What are the caudate nucleus, putamen, and globus pallidus connected to? What is the function of these basal ganglia?

What can dysfunction of the basal ganglia input affect?

Back 14

Subthalamic nucleus of the diencephalon, substantia nigra.

Essential for functioning of motor systems, control descending corticobulbar and corticospinal systems.

Can affect all descending motor pathways.

Front 15

What is the:

1) Striatum
2) Lenticular nucleus
3) Pallidum

Back 15

1) Striatum = caudate nucleus + putamen

2) Lenticular nucleus = putamen + globus pallidus

3) Pallidum = globus pallidus.

Front 16

What is the inhibitory neurotransmitter that travels between the motor and premotor cortices? Excitatory?

Back 16

Inhibitory = GABA

Excitatory = glutamate

Dopamine can be either, travels from substantia nigra.

Front 17

Describe the mechanism by which the cerebral cortex is DIRECTLY excited, starting with excitatory impulses from the cerebral cortex being sent to the putamen.

How does the substantia nigra factor into all this?

Back 17

Areas of cerebral cortex (motor, premotor, somatosensory cortexes) -> excite putamen -> inhibit globus pallidus interna -> inhibit thalamus -> excite cerebral cortex (final result)

Substantia nigra can send dopamine to putamen which further stimulates and causes further excitement of cerebral cortex.

Front 18

Describe the indirect mechanism that affects the cerebral cortex, starting with excitatory impulses from the cerebral cortex being sent to the putamen.

How does the substantia nigra factor into all of this?

Back 18

Cerebral cortex + putamen - GPE - subthalamic nucleus + globus pallidus interna - thalamus + cerebral cortex

Dopaminergic fibers from the substantia nigra synpase in putamen, are INHIBITORY. Causes increase in activity of the thalamus, stimulates motor cells of cortex. (THIS CHANGES THE WHOLE PATHWAY, MAKES IT EXCITATORY FOR THE CEREBRAL CORTEX)

Front 19

Besides sending impulses back to the cerebral cortex, how else can the basal ganglia directly influence motion?

Back 19

Globus pallidus synapses on red nucleus, fibers from red nucleus travel down ventral horn cells of the spinal cord in the rubrospinal tract.

Fibers from the globus pallidus can also travel to the reticular nuclei and influence the reticular system and the reticulospinal tract.

Front 20

Define the following:

1) Dyskinesia
2) Bradykinesia
3) Chorea
4) Athetosis
5) Hemiballismus
6) Dystonia

Back 20

1) Impairment of the power of voluntary movement
2) Abnormal slowness of movement
3) Can be extreme/violent series of almost continuous rapid movements of the face, tongue, or limbs.
4) Slow, writhing movements, most evident in hands/fingers. Cannot keep affected limb in fixed position.
5) Wild flailing movement of one arm or leg. Can result from stroke, burst posterior cerebral artery
6) Muscle tone increased in some muscles so body is in bent/abnormal fixed posture

Front 21

Parkinson's disease:

1) Symptoms?
2) What is Parkinson's characterized by?
3) Why is treatment with dopamine ineffective? Why is L-dopa effective?
4) What kind of disease?

Back 21

1) Dyskinesia resulting in bradykinesia. Lost facial expression, mask like. Characteristic tremor at rest, most visible in peripheral extremities, can disappear during movement. "Pin rolling" motion. Head/shoulder depressed, gait changes, loss of swinging of arm. Depressed or trance.

2) Destruction of substantia nigra, decrease in amount of dopamine regulating the caudate nucleus, putamen, prefrontal cortex

3) Dopamine cannot cross blood brain barrier. L-dopa can pass through the barrier and be transformed into dopamine. However, effect wanes over long term, bad side effects.

4) Basal ganglia dysfunction

Front 22

Huntington's Disease:

1) Symptoms?
2) What is causing it?
3) What is the outcome of this disease?
4) How is this disease acquired?
5) Does this disease affect males or females?
6) What kind of disease is this?

Back 22

1) Athetosis, hemiballismus
2) Bilateral destruction of caudate nucleus, damage to the putamen and globus pallidus, some cerebral cortex.
3) Dementia
4) Genetically - faulty gene on chromosome 4, production of Huntingtin protein that damages nerve cells of BG and cerebral cortex. Autosomal dominant - only need to inherit one copy of the gene and you're screwed!
5) Both - the gene isn't a sex gene.
6) Basal ganglia dysfunction.

Front 23

1) What is the job of the cerebellum?
2) What symptoms are seen if the cerebellum is damaged?
3) Where is the gray matter/white matter located?
4) What is the most distinctive cell in the cerebellum? Where does the axon synapse?

Back 23

1) Prime coordinator of motor activity
2) No motor paralysis or specific motor responses lost, but rate, range, direction, accuracy is a little off.
3) Gray matter on outside, white matter on isnde, just like brain.
4) Purkinje cell - deeper cerebellar nuclei or vestibular nuclei.

Front 24

Cerebellum:

1) What connects the two lobes of the cerebellum?
2) What covers the of of the cerebellum?
3) What are the three basic regions of the inferior cerebellum? What is each part responsible for?
4) 4 important nuclei deep in the medulla of the cerebellum.
5) What are the 3 bundles of nerve fibers that pass from the cerebellum to the brainstem?
6) Where do the largest number of tracts enter and exit? Why is this prone to damage?
7) Where are the least number of tracts entering?

Back 24

1) Vermis
2) Tentorium cerebellum
3) Archicerebellum - oldest, central nodulus + paired flocculus that extends laterally from nodulus. Equilibrium.

Paleocerebellum - older, anterior lobe + part of vermis. Muscle tone.

Neocerebellum - newest. Posterior lobe + part of vermis. Coordination of muscle activity.

4) Dentate, emboliform, fastigial, globus.

5) Superior, middle, inferior cerebellar peduncles. Brachium conjunctivum, brachium pontis, restiform body.
6) Inferior cerebellar peduncle - largest number of tracts, prone to damage from blockage of posterior inferior cerebellar artery.

7) Only 1 group of axons in middle cerebellar peduncle, but largest b/c is major pathway for info from cerebrum entering cerebellum. Coordinates motor/premotor cortex w/ modulating info from cerebellum.

Front 25

Cerebellar dysfunction:

1) Which side is impaired?
2) Asynergia
3) Dysmetria
4) Adiadochokinesia
5) Intention tremor
6) Ataxia
7) Falling
8) Dysphonia
9) Nystagmus

Back 25

1) Ipsilateral
2) Loss of coordination
3) Can't judge distance and stop mvmt at a chosen spot
4) Can't perform rapidly alternating movements
5) During planned movement
6) Abnormal gait
7) From no balance
8) Slurred speech
9) Abnormal lateral/medial movements of eye
10) anddd hypo or hypertonia

Front 26

What are the 6 sources of input through the inferior cerebellar peduncle?

What does the inferior olive receive axonal impulses from?

Output of inferior cerebellar peduncle?

Back 26

Input through inferior cerebellar peduncle: Dudes Come Very ROTten

1) Spinal cord - lower limbs - dorsal spinocerebellar tract
2) External cuneate nucleus (spinal cord upper limbs) - cuneocerebellar tract
3) Vestibular nuclei - vestibulocerebellar tract
4) Reticular formation - reticulocerebellar fibers
5) Inferior olive - olivocerebellar fibers
6) Muscles of mastication and TMJ - trigeminocerebellar

Red nucleus, ocular nucleus, superior colliclus, spinal cord. (Red nucleus gets fibers from motor cortex)

1) Output - archie and neo to vestibular nuclei: cerebellovestibular tract

2) Cerebellar nuclei through reticular formation to pons and medulla.

Front 27

1) What is the input of the superior cerebellar peduncle?

2) Output?

Back 27

Scary Vipers Roam Mountains

1) Input - spinal cord - ventral spinocerebellar tract

2) Output -

1) from cerebellar nuclei -> cerebellorubral pathway -> red nucleus,

2) from cerebellar nuclei -> thalamus -> motor cortex

Front 28

What is the input to the middle cerebellar peduncle?

Output?

Back 28

Cerebral cortex through pontine nuclei -> pontocerebellar tract to neocerebellum and paleocerebellum.

No output.

Front 29

Where are the pyramidal cells found?

How does the pyramidal system contrast to the subcortical system?

Back 29

Motor cortex, premotor cortex, ventral horn cells.

Pyramidal system is typically all or none, subcortical is modulatory. Getting the pot over the flame = pyramidal, keep sleeve out of the fire = subcortical.

Front 30

Most motor fibers in the cerebrum travel ____ to reach their targets in the brainstem.

Back 30

Bilaterally.

Front 31

The reticulospinal tract travels in what direction?

Back 31

Bilaterally.

Front 32

1) Striatum =
2) Pallidum =
3) Lentiform nucleus =
4) Corpus striatum =
5) Archistriatum

What are all these?

Back 32

1) Caudate nucleus + putamen = neostriatium = striatum
2) Globus pallidus
3) Putamen + globus pallidus
4) Caudate nucleus + putamen + globus pallidus
5) Amygdala
6) Deep telencephalonic nuclei

Front 33

What are the basal ganglia in the:

1) Diencephalon
2) Mesencephalon

Back 33

1) Ventral anterior thalamic nucleus, ventral lateral thalamic nucleus, central median thalamic nucleus, subthalamic nucleus

2) Substantia nigra, red nucleus, reticular formation

Front 34

What are the functions of the basal ganglia?

How does it perform these functions?

Back 34

Modify output from motor cortex in conjunction with cerebellum

Control motor function by tempering extremes of on or off

Communicates with motor cortex, motor nuclei in brainstem, and motor cells spinal cord

Front 35

What are the 3 tracts from the globus pallidus and what do they do?

Back 35

1) GP -> red nucleus -> rubrospinal tract -> ventral horn cells

2) GP -> inferior olivary nucleus -> olivocerebellar tract -> ventral horn cells

3) GP -> reticular formation -> reticulospinal tract -> ventral horn cells

Directly effect motor function.

Front 36

1) What are the negative signs of basal ganglia dysfunction? Examples?

2) What are the positive signs of basal ganglia dysfunction?

Back 36

1) Patient wishes to perform actions, but can't. Akinesia, bradykinesia, dystonia (writer's cramp)

2) Patient does not wish to perform actions, but is unable to prevent it. Alterations in muscle tone. Dyskinesia (tremor, chorea, ballismus, tics)

Front 37

Hemiballismus:

1) What is it?
2) Caused by?

Back 37

1) Unilateral flailing of the extremities
2) Destruction of subthalamic nucleus - no modulation of GPI. Disrupted by unilateral stroke.

Front 38

What are other basal ganglia syndromes besides Huntington's and Parkinson's?

Back 38

Tourette's, motor tics

Front 39

What cognition skills are impaired in Parkinsons? What are spared?

Back 39

Impaired - in Parkinsons, FEDS Vanish

Fine motor skills, Executive function, Delayed recall, Sustainted attention, Visuospatial

Spared - general intelligence, language

Front 40

How do you surgically treat Parkinsons?

Back 40

1) Pallidotomy - surgical ablation of globus pallidus. Permanent, unilateral. Improves OFF, not ON. Don't change l-dopa dosage. Risk of hemiballismus.

2) Subthalamic stimulation - adjustable, reversible. Improves OFF, some ON. Less L-dopa dosage

Front 41

Why is it not a big deal if the superior cerebellar peduncle is injured?

Back 41

1) Ventral spinocerebellar tract only carries 10% of sensations from spinal cord

2) Red nucleus and thalamus also have backup - there are fibers going from the GP to both