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C.Muscle reflexes (Table 2.8)

1.  Stretch (myotatic) reflex—knee jerk (Figure 2.9)

■is monosynaptic.

a.  Muscle is stretched, and the stretching stimulates group Ia afferent fibers.

b.  Group Ia afferents synapse directly on a-motoneurons in the spinal cord. The pool of α-motoneurons that is activated innervates the homonymous muscle.

c.  Stimulation of α-motoneurons causes contraction in the muscle that was stretched. As the muscle contracts, it shortens, decreasing the stretch on the muscle spindle and returning it to its original length.

d.  At the same time, synergistic muscles are activated and antagonistic muscles are inhibited.

e.  Example of the knee-jerk reflex. Tapping on the patellar tendon causes the quadriceps to stretch. Stretch of the quadriceps stimulates group Ia afferent fibers, which activate α-motoneurons that make the quadriceps contract. Contraction of the quadriceps forces the lower leg to extend.

■Increases in g-motoneuron activity increase the sensitivity of the muscle spindle and therefore exaggerate the knee-jerk reflex.

2.  Golgi tendon reflex (inverse myotatic)

■is disynaptic.

■is the opposite, or inverse, of the stretch reflex.

Ia afferent

Figure 2.9 The stretch reflex.

a.  Active muscle contraction stimulates the Golgi tendon organs and group lb afferent fibers.

b.  The group Ib afferents stimulate inhibitory interneurons in the spinal cord. These interneurons inhibit a-motoneurons and cause relaxation of the muscle that was originally

contracted.

c.  At the same time, antagonistic muscles are excited.

d.  Clasp-knife reflex, an exaggerated form of the Golgi tendon reflex, can occur with disease of the corticospinal tracts (hypertonicity or spasticity).

■For example, if the arm is hypertonic, the increased sensitivity of the muscle spindles in the extensor muscles (triceps) causes resistance to flexion of the arm. Eventually, tension in the triceps increases to the point at which it activates the Golgi tendon reflex, causing the triceps to relax and the arm to flex closed like a jackknife.

3.  Flexor withdrawal reflex

■is polysynaptic.

■results in flexion on the ipsilateral side and extension on the contralateral side.

Somatosensory and pain afferent fibers elicit withdrawal of the stimulated body part from the noxious stimulus.

a.  Pain (e.g., touching a hot stove) stimulates the flexor reflex afferents of groups II, III, and IV.

b.  The afferent fibers synapse polysynaptically (via interneurons) onto motoneurons in the spinal cord.

c.  On the ipsilateral side of the pain stimulus, flexors are stimulated (they contract) and

extensors are inhibited (they relax), and the arm is jerked away from the stove. On the contralateral side, flexors are inhibited and extensors are stimulated (crossed extension reflex) to maintain balance.

d.  As a result of persistent neural activity in the polysynaptic circuits, an afterdischarge occurs. The afterdischarge prevents the muscle from relaxing for some time.

D.Spinal organization of motor systems

1.  Convergence

■occurs when a single α-motoneuron receives its input from many muscle spindle group Ia afferents in the homonymous muscle.

■produces spatial summation because although a single input would not bring the muscle to threshold, multiple inputs will.

■also can produce temporal summation when inputs arrive in rapid succession.

2.  Divergence

■occurs when the muscle spindle group Ia afferent fibers project to all of the α-motoneurons that innervate the homonymous muscle.

3.  Recurrent inhibition (Renshaw cells)

■Renshaw cells are inhibitory cells in the ventral horn of the spinal cord.

■They receive input from collateral axons of motoneurons and, when stimulated, negatively feedback (inhibit) on the motoneuron.

E.Brain stem control of posture

1.  Motor centers and pathways

■Pyramidal tracts (corticospinal and corticobulbar) pass through the medullary pyramids.

■All others are extrapyramidal tracts and originate primarily in the following structures of the brain stem:

a.  Rubrospinal tract

■originates in the red nucleus and projects to interneurons in the lateral spinal cord.

■Stimulation of the red nucleus produces stimulation of flexors and inhibition of extensors.

b.  Pontine reticulospinal tract

■originates in the nuclei in the pons and projects to the ventromedial spinal cord.

■Stimulation has a general stimulatory effect on both extensors and flexors, with the predominant effect on extensors.

c.  Medullary reticulospinal tract

■originates in the medullary reticular formation and projects to spinal cord interneurons in the intermediate gray area.

■Stimulation has a general inhibitory effect on both extensors and flexors, with the ­predominant effect on extensors.

d.  Lateral vestibulospinal tract

■originates in Deiters nucleus and projects to ipsilateral motoneurons and interneurons.

■Stimulation causes a powerful stimulation of extensors and inhibition of flexors.

e.  Tectospinal tract

■originates in the superior colliculus and projects to the cervical spinal cord.

■is involved in the control of neck muscles.

2.  Effects of transections of the spinal cord a.  Paraplegia

■is the loss of voluntary movements below the level of the lesion.

■results from interruption of the descending pathways from the motor centers in the brain stem and higher centers.

b.  Loss of conscious sensation below the level of the lesion c.  Initial loss of reflexes—spinal shock

■Immediately after transection, there is loss of the excitatory influence from α- and

γ-motoneurons. Limbs become flaccid, and reflexes are absent. With time, partial recovery and return of reflexes (or even hyperreflexia) will occur.

(1)  If the lesion is at C7, there will be loss of sympathetic tone to the heart. As a result,

heart rate and arterial pressure will decrease.

(2)  If the lesion is at C3, breathing will stop because the respiratory muscles have been

disconnected from control centers in the brain stem.

(3)  If the lesion is at C1 (e.g., as a result of hanging), death occurs.

3.  Effects of transections above the spinal cord a.  Lesions above the lateral vestibular nucleus

■cause decerebrate rigidity because of the removal of inhibition from higher centers, resulting in excitation of α- and γ-motoneurons and rigid posture.

b.  Lesions above the pontine reticular formation but below the midbrain

■cause decerebrate rigidity because of the removal of central inhibition from the pontine reticular formation, resulting in excitation of α- and γ-motoneurons and rigid posture.

c.  Lesions above the red nucleus

■result in decorticate posturing and intact tonic neck reflexes.

F.Cerebellum—central control of movement

1.  Functions of the cerebellum

a.  Vestibulocerebellum—control of balance and eye movement b.  Pontocerebellum—planning and initiation of movement

c.  Spinocerebellum—synergy, which is control of rate, force, range, and direction of movement

2.  Layers of the cerebellar cortex a.  Granular layer

■is the innermost layer.

■contains granule cells, Golgi type II cells, and glomeruli.

■In the glomeruli, axons of mossy fibers form synaptic connections on dendrites of granular and Golgi type II cells.

b.  Purkinje cell layer

■is the middle layer.

■contains Purkinje cells.

■Output is always inhibitory. c.  Molecular layer

■is the outermost layer.

■contains stellate and basket cells, dendrites of Purkinje and Golgi type II cells, and parallel fibers (axons of granule cells).

■The parallel fibers synapse on dendrites of Purkinje cells, basket cells, stellate cells, and Golgi type II cells.

3.  Connections in the cerebellar cortex a.  Input to the cerebellar cortex

(1)  Climbing fibers

■originate from a single region of the medulla (inferior olive).

■make multiple synapses onto Purkinje cells, resulting in high-frequency bursts, or complex spikes.

■“condition” the Purkinje cells.

■play a role in cerebellar motor learning.

(2)  Mossy fibers

■originate from many centers in the brain stem and spinal cord.

■include vestibulocerebellar, spinocerebellar, and pontocerebellar afferents.

■make multiple synapses on Purkinje fibers via interneurons. Synapses on Purkinje cells result in simple spikes.

■synapse on granule cells in glomeruli.

■The axons of granule cells bifurcate and give rise to parallel cells. The parallel fibers excite multiple Purkinje cells as well as inhibitory interneurons (basket, stellate, Golgi type II).

b.  Output of the cerebellar cortex

■Purkinje cells are the only output of the cerebellar cortex.

■Output of the Purkinje cells is always inhibitory; the neurotransmitter is g-aminobutyric acid (GABA).

■The output projects to deep cerebellar nuclei and to the vestibular nucleus. This inhibitory output modulates the output of the cerebellum and regulates rate, range, and direction of movement (synergy).

c.  Clinical disorders of the cerebellum—ataxia

■result in lack of coordination, including delay in initiation of movement, poor execu-

tion of a sequence of movements, and inability to perform rapid alternating movements (dysdiadochokinesia).

(1)  Intention tremor occurs during attempts to perform voluntary movements.

(2)  Rebound phenomenon is the inability to stop a movement.

G.Basal ganglia—control of movement

■consists of the striatum, globus pallidus, subthalamic nuclei, and substantia nigra.

■modulates thalamic outflow to the motor cortex to plan and execute smooth movements.

■Many synaptic connections are inhibitory and use GABA as their neurotransmitter.

54Brs Physiology

■The striatum communicates with the thalamus and the cerebral cortex by two opposing pathways.

■Indirect pathway is, overall, inhibitory.

■Direct pathway is, overall, excitatory.

■Connections between the striatum and the substantia nigra use dopamine as their

neurotransmitter. Dopamine is inhibitory on the indirect pathway (D2 receptors) and excitatory on the direct pathway (D1 receptors). Thus, the action of dopamine is, overall, excitatory.

■Lesions of the basal ganglia include

1.Lesions of the globus pallidus

■result in inability to maintain postural support.

2.Lesions of the subthalamic nucleus

■are caused by the release of inhibition on the contralateral side.

■result in wild, flinging movements (e.g., hemiballismus).

3.Lesions of the striatum

■are caused by the release of inhibition.

■result in quick, continuous, and uncontrollable movements.

■occur in patients with Huntington disease.

4.Lesions of the substantia nigra

■are caused by destruction of dopaminergic neurons.

■occur in patients with Parkinson disease.

■Since dopamine inhibits the indirect (inhibitory) pathway and excites the direct (excitatory) pathway, destruction of dopaminergic neurons is, overall, inhibitory.

■Symptoms include lead-pipe rigidity, tremor, and reduced voluntary movement.

H.motor cortex

1.Premotor cortex and supplementary motor cortex (area 6)

■are responsible for generating a plan for movement, which is transferred to the primary motor cortex for execution.

■The supplementary motor cortex programs complex motor sequences and is active during “mental rehearsal” for a movement.

2.Primary motor cortex (area 4)

■is responsible for the execution of movement. Programmed patterns of motoneurons are activated in the motor cortex. Excitation of upper motoneurons in the motor cortex is transferred to the brain stem and spinal cord, where the lower motoneurons are activated and cause voluntary movement.

■is somatotopically organized (motor homunculus). Epileptic events in the primary motor cortex cause Jacksonian seizures, which illustrate the somatotopic organization.

Iv. HIgHer FunctIons oF tHe cereBrAL corteX

A.electroencephalographic (eeg) findings

■eeg waves consist of alternating excitatory and inhibitory synaptic potentials in the pyramidal cells of the cerebral cortex.

■A cortical evoked potential is an EEG change. It reflects synaptic potentials evoked in large numbers of neurons.

■In awake adults with eyes open, beta waves predominate.

■In awake adults with eyes closed, alpha waves predominate.

■During sleep, slow waves predominate, muscles relax, and heart rate and blood pressure decrease.