Sistemas Motores

Question 1

Tractos aferentes del cerebelo

Answer 1

Question 2

Tracto espinocereberal

Answer 2

Question 3

Tractos cerebelares eferentes

Answer 3

Question 4

Circuitos cerebelares

Answer 4

Question 5

Circuito de control del movimiento (cerebro-cerebelar)

Answer 5

Question 6

Proyección de las areas somatosensoriales en la corteza cerebelar

Answer 6

Question 7

Estructura del cerebelo

Answer 7

Question 8

Organización del cerebelo según el tipo de movimiento coordinado

Answer 8

The vestibulocerebellum.

• flocculonodular cerebellar lobes + adjacent portions of the vermis.
• It provides neural circuits for most of the body’s equilibrium movements.

The spinocerebellum.

• vermis of the posterior and anterior cerebellum + adjacent intermediate zones on both sides of the vermis.
• It coordinates mainly movements of the distal portions of the limbs, especially the hands and fingers.

The cerebrocerebellum.

• This consists of the large lateral zones of the cerebellar hemispheres, lateral to the intermediate zones.
• It receives virtually all its input from the cerebral motor cortex and adjacent premotor and somatosensory cortices of the cerebrum.
• It transmits its output information in the upward direction back to the brain, functioning in a feedback manner with the cerebral cortical sensorimotor system to plan sequential voluntary body and limb movements, planning these as much as tenths of a second in advance of the actual movements.
• This is called development of “motor imagery” of movements to be performed.

Question 9

Características de los tractos corticoespinales

Answer 9

This tract originates in the precentral gyrus > internal capsule > divides in:

1. Lateral division > decussation of the pyramids > lateral white matter of the spinal cord > spinal motor neuron (monosynaptic connection) > distal muscle
2. Ventral division> spinal cord (uncrossed) > spinal interneuron (crosses) > motor neuron> proximal muscle

Question 10

Efectos del daño en las motoneuronas inferiores

Answer 10

Lower motor neurons are those whose axons terminate on skeletal muscles.

Damage to these neurons is associated with

• flaccid paralysis
• muscular atrophy
• fasciculations
• hypotonia
• **hyporeflexia or areflexia. **

Question 11

Características de la Esclerosis Amiotrófica Lateral

Answer 11

• An example of a disease that leads to lower motor neuron damage is amyotrophic lateral sclerosis (ALS).
• “Amyotrophic” means “no muscle nourishment” and describes the atrophy that muscles undergo because of disuse.
• “Sclerosis” refers to the hardness felt when a pathologist examines the spinal cord on autopsy; the hardness is due to proliferation of astrocytes and scarring of the lateral columns of the spinal cord.
• ALS is a selective, progressive degeneration of -motor neurons.
• This fatal disease is also known as Lou Gehrig disease because Gehrig, a famous American baseball player, died of it.
• The worldwide annual incidence of ALS has been estimated to be 0.5–3 cases per 100,000 people.
• Most cases are sporadic, but 5–10% of the cases are familial.
• Forty percent of the familial cases have a mutation in the gene for Cu/Zn superoxide dismutase (SOD-1) on chromosome 21.
• SOD is a free radical scavenger that reduces oxidative stress.
• A defective SOD-1 gene permits free radicals to accumulate and kill neurons.
• The disease has no racial, socioeconomic, or ethnic boundaries.
• The life expectancy of ALS patients is usually 3–5 years after diagnosis.
• ALS is most commonly diagnosed in middle age and affects men more often than women.
• The worldwide incidence of ALS is 2 per 100,000 of total population.
• The causes of ALS are unclear, but possibilities include viruses, neurotoxins, heavy metals, DNA defects (especially in familial ALS), immune system abnormalities, and enzyme abnormalities.

Question 12

Efectos del daño en las motoneuronas superiores

Answer 12

Upper motor neurons typically refer to corticospinal tract neurons that innervate spinal motor neurons, but they can also include brain stem neurons that control spinal motor neurons.

Damage to these neurons initially causes muscles to become weak and flaccid but eventually leads to

• spasticity (forma de hipertonía muscular con aumento de la resistencia al estiramiento).
• hypertonia (increased resistance to passive movement),
• hyperactive stretch reflexes,
• and abnormal plantar extensor reflex (Babinski sign).

The Babinski sign is dorsiflexion of the great toe and fanning of the other toes when the lateral aspect of the sole of the foot is scratched.

In adults, the normal response to this stimulation is plantar flexion in all the toes.

The Babinski sign is believed to be a flexor withdrawal reflex that is normally held in check by the lateral corticospinal system.

It is of value in the localization of disease processes, but its physiologic significance is unknown.

However, in infants whose corticospinal tracts are not well developed, dorsiflexion of the great toe and fanning of the other toes is the natural response to stimuli applied to the sole of the foot.

Question 13

Características del área motora suplementaria

Answer 13

For the most part, the supplementary motor area projects to the motor cortex. This region also contains a map of the body, but it is less precise than in M1. It appears to be involved primarily in organizing or planning motor sequences, while M1 executes the movements. Lesions of this area in monkeys produce awkwardness in performing complex activities and difficulty with bimanual coordination.

When human subjects count to themselves without speaking, the motor cortex is quiescent, but when they speak the numbers aloud as they count, blood flow increases in M1 and the supplementary motor area. Thus, the supplementary motor area as well as M1 is involved in voluntary movement when the movements being performed are complex and involve planning. Blood flow increases whether or not a planned movement is carried out. The increase occurs whether the movement is performed by the contralateral or the ipsilateral hand.

Question 14

Función de la corteza premotora

Answer 14

The premotor cortex, which also contains a somatotopic map, receives input from sensory regions of the parietal cortex and projects to M1, the spinal cord, and the brain stem reticular formation.

Its function is still incompletely understood, but it may be concerned with setting posture at the start of a planned movement and with getting the individual prepared to move. It is most involved in control of proximal limb muscles needed to orient the body for movement.

Question 15

Características de la corteza parietal posterior

Answer 15

In addition to providing fibers that run in the corticospinal and corticobulbar tracts, the somatic sensory area and related portions of the posterior parietal lobe project to the premotor area.

Lesions of the somatic sensory area cause defects in motor performance that are characterized by inability to execute learned sequences of movements such as eating with a knife and fork.

Some of the neurons in area 5 are concerned with aiming the hands toward an object and manipulating it, whereas some of the neurons in area 7 are concerned with hand–eye coordination.

Question 16

Función de los tractos corticoespinal y corticobulcar.

Answer 16

The corticospinal and corticobulbar system is the primary pathway for the initiation of skilled voluntary movement. This does not mean that movement—even skilled movement—is impossible without it. Only in primates are relatively marked deficits produced.

Section of the pyramids >destruction of the lateral corticospinal tract>loss of control of the distal musculature of the limbs (fine-skilled movements).

lesions of the ventral corticospinal tract > axial muscle deficits > difficulty with balance, walking, and climbing.

Question 17

Características del tracto corticobulbar

Answer 17

1. The corticobulbar tract is composed of the fibers that pass from the motor cortex to
2. motor neurons in the trigeminal, facial, and hypoglossal nuclei.
3. Corticobulbar neurons end either directly on the cranial nerve nuclei or on their antecedent interneurons within the brain stem.
4. Their axons traverse through the genu of the internal capsule,
5. the cerebral peduncle (medial to corticospinal tract neurons),
6. to descend with corticospinal tract fibers in the pons and medulla.

Question 18

Características de los tractos vestibuloespinales

Answer 18

The medial tract

• originates in the medial and inferior vestibular nuclei
• projects bilaterally to cervical spinal motor neurons that control neck musculature.

The lateral tract

• originates in the lateral vestibular nuclei and projects ipsilaterally to neurons at all spinal levels.
• It activates motor neurons to antigravity muscles (eg, proximal limb extensors) to control posture and balance.

Question 19

Características de los tractos reticuloespinales

Answer 19

• The pontine and medullary reticulospinal tracts project to all spinal levels.
• They are involved in the maintenance of posture and in modulating muscle tone, especially via an input to gamma-motor neurons.
• Pontine reticulospinal neurons are primarily excitatory
• medullary reticulospinal neurons are primarily inhibitory.

Question 20

Características de las vías mediales del tronco cerebral

Answer 20

Controls axial and proximal muscles

The medial brain stem pathways, which work in concert with the ventral corticospinal tract, are

1. the pontine and medullary reticulospinal,
2. vestibulospinal,
3. and tectospinal tracts.

• These pathways descend in the ipsilateral ventral columns of the spinal cord.
• terminate predominantly on interneurons and long propriospinal neurons in the ventromedial part of the ventral horn .
• A few medial pathway neurons synapse directly on motor neurons controlling axial muscles.

Question 21

Características de los tractos tectoespinales

Answer 21

The tectospinal tract

• originates in the superior colliculus of the midbrain.
• It projects to the contralateral cervical spinal cord
• controls head and eye movements.

Question 22

Lateral Brain Stem Pathway (Rubrospinal)

Answer 22

• Help the corticospinal tract (most important) to control distal muscles.
• Pathway: Midbrain Red Nucleus > dorsolateral part of the spinal ventral horn (interneuron) > limbs distal muscles.
• This rubrospinal tract excites flexor motor neurons and inhibits extensor motor neurons.
• This pathway is not very prominent in humans, but it may play a role in the posture typical of decorticate rigidity.

Question 23

Características de la descerebración

Answer 23

Midcollicular decerebration:A complete transection of the brain stem between the superior and inferior colliculi permits the brain stem pathways to function independent of their input from higher brain structures.

This lesion interrupts all input from the cortex (corticospinal and corticobulbar tracts) and red nucleus (rubrospinal tract), primarily to distal muscles of the extremities.

The excitatory and inhibitory reticulospinal pathways (primarily to postural extensor muscles) remain intact.

The dominance of drive from ascending sensory pathways to the excitatory reticulospinal pathway leads to hyperactivity in extensor muscles in all four extremities which is called decerebrate rigidity.

This resembles what ensues after supratentorial lesions in humans cause uncal herniation.

Uncal herniation can occur in patients with large tumors or a hemorrhage in the cerebral hemisphere.

In midcollicular decerebrate cats, section of dorsal roots to a limb immediately eliminates the hyperactivity of extensor muscles. This suggests that decerebrate rigidity is spasticity due to facilitation of the myotatic stretch reflex. That is, the excitatory input from the reticulospinal pathway activates gamma-motor neurons which indirectly activate alpha-motor neurons (via Ia spindle afferent activity). This is called the gamma loop.

The exact site of origin within the cerebral cortex of the fibers that inhibit stretch reflexes is unknown. Under certain conditions, stimulation of the anterior edge of the precentral gyrus can cause inhibition of stretch reflexes and cortically evoked movements. This region, which also projects to the basal ganglia, has been named area 4s, or the suppressor strip.

There is also evidence that decerebrate rigidity leads to direct activation of alpha-motor neurons.

If the anterior lobe of the cerebellum is removed in a decerebrate animal, extensor muscle hyperactivity is exaggerated (decerebellate rigidity). This cut eliminates cortical inhibition of the cerebellar fastigial nucleus and secondarily increases excitation to vestibular nuclei. Subsequent dorsal root section does not reverse the rigidity, thus it was due to activation of alpha-motor neurons independent of the gamma loop.

Question 24

Características de la decorticación

Answer 24

Removal of the cerebral cortex produces decorticate rigidity which is characterized by

1. flexion of the upper extremities at the elbow. Can be explained by rubrospinal excitation of flexor muscles in the upper extremities
2. extensor hyperactivity in the lower extremities. The hyperextension of lower extremities is due to the same changes that occur after midcollicular decerebration.

Decorticate rigidity is seen on the hemiplegic side in humans after hemorrhages or thromboses in the internal capsule. Probably because of their anatomy, the small arteries in the internal capsule are especially prone to rupture or thrombotic obstruction, so this type of decorticate rigidity is fairly common. Sixty percent of intracerebral hemorrhages occur in the internal capsule, as opposed to 10% in the cerebral cortex, 10% in the pons, 10% in the thalamus, and 10% in the cerebellum.

Question 25

Shock Espinal

Answer 25

In all vertebrates, transection of the spinal cord is followed by a period of spinal shock during which all spinal reflex responses are profoundly depressed. Subsequently, reflex responses return and become hyperactive.

In humans it usually lasts for a minimum of 2 wk.

The first reflex response to appear as spinal shock wears off in humans is often a slight contraction of the leg flexors and adductors in response to a noxious stimulus. In some patients, the knee jerk reflex recovers first. The interval between cord transection and the return of reflex activity is about 2 weeks in the absence of any complications, but if complications are present it is much longer. It is not known why infection, malnutrition, and other complications of SCI inhibit spinal reflex activity. Once the spinal reflexes begin to reappear after spinal shock, their threshold steadily drops.

The cause of spinal shock is uncertain. Cessation of tonic bombardment of spinal neurons by excitatory impulses in descending pathways undoubtedly plays a role, but the subsequent return of reflexes and their eventual hyperactivity also have to be explained.

The recovery of reflex excitability may be

1. denervation hypersensitivity to the mediators released by the remaining spinal excitatory endings.
2. sprouting of collaterals from existing neurons, with the formation of additional excitatory endings on interneurons and motor neurons.

Question 26

Relación entre los ganglios basales

Answer 26

• Solid lines indicate excitatory pathways, dashed lines inhibitory pathways.
• The transmitters are indicated in the pathways, where they are known.
• Glu, glutamate;
• DA, dopamine.
• Acetylcholine is the transmitter produced by interneurons in the striatum.
• SNPR, substantia nigra, pars reticulata;
• SNPC, substantia nigra, pars compacta;
• ES, external segment;
• IS, internal segment;
• PPN,pedunculopontine nuclei.
• The subthalamic nucleus also projects to the pars compacta of the substantia nigra; this pathway has been omitted for clarity.

Question 27

Estructura anatómica de los núcleos (ganglios) basales

Answer 27

The term basal ganglia (or basal nuclei) is generally applied to five interactive structures on each side of the brain.

These are

1. the caudate nucleus
2. Putamen
3. Globus pallidus. Is divided into external and internal segments (GPe and GPi).
4. the subthalamic nucleus
5. substantia nigra. Is divided into a pars compacta and a pars reticulata.

• The caudate nucleus and putamen are commonly called the striatum
• the putamen and globus pallidus are sometimes called the lenticular nucleus.

Question 28

Función de los núcleos (ganglios) basales.

Answer 28

Neurons in the basal ganglia, like those in the lateral portions of the cerebellar hemispheres, discharge before movements begin.

This observation, plus careful analysis of the effects of diseases of the basal ganglion in humans and the effects of drugs that destroy dopaminergic neurons in animals, have led to the idea that the basal ganglia are involved in the planning and programming of movement or, more broadly, in the processes by which an abstract thought is converted into voluntary action.

They influence the motor cortex via the thalamus, and the corticospinal pathways provide the final common pathway to motor neurons. In addition, globus pallidus internal segment projects to nuclei in the brain stem, and from there to motor neurons in the brain stem and spinal cord.

The basal ganglia, particularly the caudate nuclei, also play a role in some cognitive processes. Possibly because of the interconnections of this nucleus with the frontal portions of the neocortex, lesions of the caudate nuclei disrupt performance on tests involving object reversal and delayed alternation. In addition, lesions of the head of the left but not the right caudate nucleus and nearby white matter in humans are associated with a dysarthric form of aphasia that resembles Wernicke aphasia.

Question 29

Enfermedades de los núcleos (ganglios) basales

Answer 29

Three distinct biochemical pathways in the basal ganglia normally operate in a balanced fashion:

1. the nigrostriatal dopaminergic system,
2. the intrastriatal cholinergic system, and
3. the GABAergic system, which projects from the striatum to the globus pallidus and substantia nigra.

When one or more of these pathways become dysfunctional, characteristic motor abnormalities occur. Diseases of the basal ganglia lead to two general types of disorders: hyperkinetic and hypokinetic.

• The hyperkinetic conditions are those in which movement is excessive and abnormal, including chorea, athetosis, and ballism.
• Hypokinetic abnormalities include akinesia and bradykinesia.

Chorea is characterized by rapid, involuntary “dancing” movements. Athetosis is characterized by continuous, slow writhing movements. Choreiform and athetotic movements have been likened to the start of voluntary movements occurring in an involuntary, disorganized way. In ballism, involuntary flailing, intense, and violent movements occur. Akinesia is difficulty in initiating movement and decreased spontaneous movement. Bradykinesia is slowness of movement.

In addition to Parkinson disease, which is described below, there are several other disorders known to involve a malfunction within the basal ganglia. Huntington disease is one of an increasing number of human genetic diseases affecting the nervous system that are characterized by trinucleotide repeat expansion. Most of these involve cytosine-adenine-guanine (CAG) repeats (Table 16–1), but one involves CGG repeats and another involves CTG repeats. All of these are in exons; however, a GAA repeat in an intron is associated with Friedreich’s ataxia. There is also preliminary evidence that increased numbers of a 12-nucleotide repeat are associated with a rare form of epilepsy.

Question 30

Enfermedad de Parkinson

Answer 30

Parkinson disease has both hypokinetic and hyperkinetic features. In the 1960s, Parkinson disease was shown to result from the degeneration of dopaminergic neurons in the substantia nigra pars compacta.

The fibers to the putamen are most severely affected. Parkinsonism now occurs in sporadic idiopathic form in many middle-aged and elderly individuals and is one of the most common neurodegenerative diseases. It is estimated to occur in 1–2% of individuals over age 65. Dopaminergic neurons and dopamine receptors are steadily lost with age in the basal ganglia in normal individuals, and an acceleration of these losses apparently precipitates parkinsonism. Symptoms appear when 60–80% of the nigrostriatal dopaminergic neurons degenerate.

Parkinsonism is also seen as a complication of treatment with the phenothiazine group of tranquilizer drugs and other drugs that block D2 receptors. It can be produced in rapid and dramatic form by injection of 1-methyl-4-phenyl-1,2,5,6-tetrahydropyridine (MPTP). This effect was discovered by chance when a drug dealer in northern California supplied some of his clients with a homemade preparation of synthetic heroin that contained MPTP. MPTP is a prodrug that is metabolized in astrocytes by the enzyme MOA-B to produce a potent oxidant, 1-methyl-4-phenylpyridinium (MPP+). In rodents, MPP+ is rapidly removed from the brain, but in primates it is removed more slowly and is taken up by the dopamine transporter into dopaminergic neurons in the substantia nigra, which it destroys without affecting other dopaminergic neurons to any appreciable degree. Consequently, MPTP can be used to produce parkinsonism in monkeys, and its availability has accelerated research on the function of the basal ganglia.

The hypokinetic features of Parkinson disease are akinesia and bradykinesia, and the hyperkinetic features are cogwheel rigidity and tremor at rest.

The absence of motor activity and the difficulty in initiating voluntary movements are striking. There is a decrease in the normal, unconscious movements such as swinging of the arms during walking,

the panorama of facial expressions related to the emotional content of thought and speech,

and the multiple “fidgety” actions and gestures that occur in all of us.

The rigidity is different from spasticity because motor neuron discharge increases to both the agonist and antagonist muscles.

Passive motion of an extremity meets with a plastic, dead-feeling resistance that has been likened to bending a lead pipe and is therefore called lead pipe rigidity.

Sometimes a series of “catches” takes place during passive motion (cogwheel rigidity), but the sudden loss of resistance seen in a spastic extremity is absent.

The tremor, which is present at rest and disappears with activity, is due to regular, alternating 8-Hz contractions of antagonistic muscles.

A current view of the pathogenesis of the movement disorders in Parkinson disease is shown in Figure 16–11. In normal individuals, basal ganglia output is inhibitory via GABAergic nerve fibers. The dopaminergic neurons that project from the substantia nigra to the putamen normally have two effects: they stimulate the D1 dopamine receptors, which inhibit GPi via direct GABAergic receptors, and they inhibit D2 receptors, which also inhibit the GPi. In addition, the inhibition reduces the excitatory discharge from the subthalamic nucleus to the GPi. This balance between inhibition and excitation somehow maintains normal motor function. In Parkinson disease, the dopaminergic input to the putamen is lost. This results in decreased inhibition and increased excitation from the STN to the GPi. The overall increase in inhibitory output to the thalamus and brain stem disorganizes movement.

Question 31

Lesiones del encéfalo y consecuencias en el sistema motor

Answer 31