Physiology - An Illustrated Review

6. Motor Systems

6.1 Organization of the Motor System

The system for control of movement is hierarchically organized. At the lowest level, the spinal cord contains motoneurons and elemental reflex circuits. Superimposed on these basic circuits are descending tracts arising from the brainstem, which control basic postural functions, and from the motor cortex, which control more skillful movements.

The cerebellum is responsible for coordinating motor activity, and the basal ganglia are responsible for initiating motor programs.

The Motoneuron and the Motor Unit

– Skeletal muscle fibers, termed extrafusal fibers, form the bulk of muscle and generate its force and contraction.

– Skeletal muscle is innervated by α motoneurons, whose cell bodies are situated in the ventral horn of the spinal cord gray matter and in cranial nerve motor nuclei in the brainstem.

– The motor unit is the functional unit of motor control. It is composed of a single α motoneuron and the skeletal muscle fibers it innervates.

– The number of muscle fibers innervated by an α motoneuron ranges from about three in the ocular muscles to several hundred in some postural muscles.

– Small motor units are employed where fine movements are necessary. The cell bodies of motoneurons of small motor units are smaller in diameter than those of large motor units.

The Size Principle

The force of muscle contraction is graded primarily by the number of motor units activated. The size principle states that small diameter motoneurons are more excitable than large motoneurons. Therefore, as the excitatory input to a pool of motoneurons increases, the smaller motor units generating less tension are recruited first. Later the larger motor units, generating greater muscle tension, are brought into play.

Muscle Sensory Receptors

Muscle Spindles

Muscle spindles, termed intrafusal fibers, are stretch receptors embedded within muscles to monitor muscle length and its rate of change. They consist of about a dozen modified skeletal muscle fibers surrounded by a capsule (Fig. 6.1) innervated by afferent nerve fibers.

– Intrafusal fibers do not contain actin and myosin except near the polar ends of the spindle.

– Contraction of intrafusal fibers does not contribute to the force exerted by the mass of the muscle.

Types of intrafusal muscle fibers. There are two types of intrafusal muscle fibers: nuclear bag fibers and nuclear chain fibers. Nuclear bag fibers bulge in the middle due to a cluster of cellular nuclei in the central part of the fiber. Nuclear chain fibers have nuclei linearly arranged in the central region.

Muscle spindle afferent output. Intrafusal fibers are innervated by two types of afferent nerve fibers: group Ia and group II.

– Group Ia fibers (annulospiral endings) innervate both nuclear bag and nuclear chain fibers. They are dynamic, rapidly adapting sensory afferents and as such are sensitive to the rate of change in length of the muscle.

– Group II endings innervate nuclear chain fibers. They are slowly adapting sensory afferents that signal muscle length rather than the rate of change of length.

Fig. 6.1 image Muscle spindles and Golgi tendon organs.

Muscle spindles are sensors that function to regulate muscle length. Group Ia afferent neurons coil around the nuclear chain and nuclear bag fibers (intrafusal fibers), whereas group II coil around nuclear chain fibers only. These annulospiral endings detect longitudinal stretching of intrafusal fibers and transmit information about their length (II) and rate of change in length (Ia) to the spinal cord. Efferent γ motoneurons innervate both types of intrafusal fibers, allowing variation of their length and stretch sensitivity.

Golgi tendon organs are sensors found in tendons that function to regulate muscle tension. Group Ib a fferent fibers that originate in Golgi tendon organs transmit information regarding muscle tension to inhibitory interneurons in the spinal cord. These interneurons inhibit α motoneurons of the muscle from which the type Ib afferent impulse originated. They also activate antagonistic muscles via excitatory mechanisms. These factors combine to adjust muscle tension.
From Thieme Atlas of Anatomy, Head and Neuroanatomy, © Thieme 2007, Illustration by Markus Voll.


Muscle spindle efferent input. Gamma (γ) motoneurons are also present in the ventral horn and innervate only the polar ends of the spindle fibers, which can contract and thereby stretch the central regions of the intrafusal fibers.

– Gamma motoneurons increase the sensitivity of the spindle to overall muscle stretch.

– Gamma motoneurons also maintain the sensory function of the spindle when the muscle shortens during contraction. Shortening would collapse the spindle, terminate firing on the spindle afferents, and deprive the central nervous system (CNS) of information concerning muscle length. Therefore, there must be coactivation of α and γ motoneurons during voluntary movement.

Golgi Tendon Organs

Golgi tendon organs are sensory receptors located in muscle tendons that are activated by muscle tension (Fig. 6.1).

Golgi tendon organs are oriented in series with skeletal extrafusal muscle fibers while muscle spindles are in parallel. This means that although muscle lengthening will activate both receptors, muscle shortening will suppress spindle receptor activity but activate tendon organ receptors.

Interneurons in the Ventral Horn

The neuronal assemblies in the ventral horn contain, in addition to motoneurons, small interneurons that are either excitatory or inhibitory to motoneurons.

Renshaw Cells

Renshaw cells are inhibitory interneurons that receive input from collateral axons of α motoneurons. They synapse both with the motoneurons that activate them and with adjacent α motoneurons.

– Renshaw cells are activated by acetylcholine, the neurotransmitter synthesized by α motoneurons. They release glycine, an inhibitory transmitter. Strychnine, a rodenticide, blocks the receptors for glycine.

– By inhibiting motoneurons, Renshaw cells dampen firing and provide stability to motoneuron output.

6.2 Spinal Reflexes

Myotatic (Stretch) Reflex

The myotatic (stretch) reflex is a monosynaptic reflex (Fig. 6.2).


Stretching a muscle (and the spindles within it) induces firing of spindle afferents, which synapse directly on the α motoneurons that innervate the same (homonymous) muscle. Excitation of α motoneurons results in contraction (shortening) of the muscle.


The stretch reflex is a negative feedback system to maintain the constancy of muscle length. It automatically and rapidly resists perturbations of muscle position that might be produced by momentary fatigue or other disturbances. It is particularly important in postural and other muscles that maintain preset positions.

The stretch reflex is also responsible for generating muscle tone (basal level of contraction). It is activated by the slight stretching of the muscle by the force of gravity.

Clinically important monosynaptic reflexes

Some clinically important deep tendon reflexes include the biceps reflex, triceps reflex, patellar reflex, and Achilles reflex. In each case, tapping the tendon with a reflex hammer causes the attached muscle to contract, if the reflex arc is intact. Even though the test involves a single muscle, the muscle may be innervated by motoneurons in more than one spinal cord segment. The biceps reflex corresponds to the spinal cord segment of C5−C6; the triceps reflex corresponds to C6−C7; the patellar reflex corresponds to L3−L4; and the Achilles reflex corresponds to S1−S2. It is clinically necessary to routinely test the reflexes on both the right and the left sides to allow for comparison.


Fig. 6.2 image Myotatic (stretch) reflex.

The example given here is the patellar reflex. Tapping the patellar tendon by a reflex hammer causes stretching of the muscle spindles within the quadriceps muscle. This initiates group Ia afferent impulses, which enter the spinal cord via the posterior (dorsal) root and terminate in the anterior (ventral) horn on the α motoneuron of the same muscle. Activation of the α motoneuron causes the muscle to contract.


Inverse Myotatic Reflex

The inverse myotatic reflex (Golgi tendon organ reflex) is a disynaptic reflex.


Contraction of a muscle activates group Ib afferent fibers from Golgi tendon organs. The group Ib afferent fibers synapse on inhibitory interneurons, which inhibit α motoneurons to the homonymous muscle. Inhibition of the α motoneuron reduces the tension being produced by the muscle.


The reflex acts to dampen the force of muscle contraction and thereby participates in ongoing regulation of muscle force.

Flexor Reflex, Antagonist Inhibition, and Crossed Extensor Reflex

The flexor (withdrawal) reflex is multisynaptic and is accompanied by antagonist inhibition and the crossed extensor reflex (Fig. 6.3).


In this protective reflex, activation of nociceptors causes firing in group II, III, and IV afferent fibers. These afferents make multiple synapses via interneurons with α motoneurons, resulting in withdrawal of the limb from the painful stimulus (usually by flexion) and inhibition of motoneurons that project to antagonist muscles (antagonist inhibition). Thus, limb movement is facilitated and not impeded by the action of an opposing muscle. At the same time, the crossed extensor reflex extends the contralateral limb to support the body following flexor withdrawal.

Fig. 6.3 image Withdrawal reflex.

A painful stimulus in the sole of the right foot leads to flexion of all joints of that leg (flexor reflex). Action potentials from nociceptive afferents are conducted via stimulatory interneurons (1) in the spinal cord to motoneurons of ipsilateral flexors leading to their contraction and via inhibitory interneurons (2) to motoneurons of ipsilateral extensors (3), leading to their relaxation (antagonist inhibition). The crossed extensor reflex consists of contraction of the extensor muscles (5) and relaxation of the flexor muscles in the contralateral leg (4, 6). Action potentials from nociceptive afferents are also conducted to other segments of the spinal cord (7, 8) because different flexors and extensors are innervated by different segments.


6.3 Cortical Motor Control

Primary Motor Cortex

The primary motor cortex is located directly anterior to the central sulcus on the precentral gyrus (Fig. 6.4). It is somatotopically organized so that a map of the muscles of the body can be plotted on the surface of the precentral gyrus (Fig. 6.5). A disproportionately large area of the primary motor cortex is dedicated to the fingers and thumb and the muscles used in speech.

Afferent Input to the Primary Motor Cortex

The neurons of the motor cortex are influenced by inputs from several sources:

– The premotor cortex, located anterior to the primary motor area, is thought to play a role in planning movements.

Fig. 6.4 image Motor cortex.

Lateral view of the left hemisphere. The primary motor cortex (M1; area 4) is located in the precentral gyrus and is involved in the execution of voluntary movement. The premotor cortex is located a nterolaterally adjacent to the primary motor cortex and is involved in the planning and initiation of movement. The supplementary motor cortex is located on the medial surface of the precentral gyrus and is involved in controlling axial and girdle muscles on both sides of the body. The motor cortex is functionally related to the somatosensory cortex on the postcentral gyrus, as sensory information is required for the cortical representation of space, which allows for precision of movement. This is the reason these cortical areas are referred to as the sensorimotor system.
From Thieme Atlas of Anatomy, Head and Neuroanatomy, © Thieme 2007, Illustration by Markus Voll.


– The supplementary motor area, located on the medial surface of the premotor cortex, controls larger muscle groups than the primary motor area and is also involved in preparation for complex movements.

– The ventral anterior (VA) and ventral lateral (VL) nuclei of the thalamus are essential relays for excitatory input to the motor cortex.

Pyramidal Tracts

The pyramidal tracts, comprising mainly the corticospinal but also the corticonuclear and corticoreticular tracts, originate in the motor cortex. The corticonuclear and corticoreticular tracts innervate motor cranial nerve nuclei and the reticular formation in the brainstem, respectively. The corticospinal tracts pass through the pyramids of the medulla (Fig. 6.6). Most of the corticospinal fibers cross at the decussation of the pyramids. Because of the pyramidal decussation, the motor cortex of one hemisphere controls movement on the contralateral side of the body.

– The corticospinal fibers terminate directly on α or γ motoneurons and on interneurons that then synapse with α or γ motoneurons.

– The main function of these corticospinal tracts is control of the fine, skilled movements performed by the distal musculature of the limbs.

Fig. 6.5 image Somatotopic organization of the primary motor cortex.

The primary motor cortex exhibits somatotopic organization with respect to the target muscles it controls. Muscles that are involved in fine or complex tasks have more area of the primary motor cortex dedicated to them.


Fig. 6.6 image Course of the pyramidal tracts.

The pyramidal tracts originate in the motor cortex. The fibers of the main part, the corticospinal tract, travel through the pyramids of the medulla, where 80% cross and descend in the spinal cord as the lateral corticospinal tract. The remaining 20% descend without crossing, forming the anterior corticospinal tract. Most fibers of the anterior corticospinal tract ultimately cross at the segmental level. The axons of the corticospinal tract terminate either directly or via interneurons on α and γ motoneurons. The fibers of the corticonuclear tract innervate motor cranial nerve (CN) nuclei in the brainstem (CN III–VII and IX–XII). The corticoreticular tract fibers pass to the reticular formation in the brainstem (not shown).
From Thieme Atlas of Anatomy, Head and Neuroanatomy, © Thieme 2007, Illustration by Markus Voll.


6.4 Brainstem Motor Control

Descending Brainstem Motor Tracts

– These tracts, called the extrapyramidal tracts, originate from nuclei in the brainstem and do not pass through the medullary pyramids (Fig. 6.7). Their projections are concentrated on the neurons that control proximal and axial muscles — for postural control — rather than distal limb muscles.

– Their primary function is to control posture and positioning of the body and limbs.

Fig. 6.7 image Course of the extrapyramidal tracts.

The extrapyramidal tracts originate in various regions of the brainstem and terminate on interneurons that synapse with α and γ motoneurons, which they control. They also receive input (blue) from the cortex and the cerebellum.
From Thieme Atlas of Anatomy, Head and Neuroanatomy, © Thieme 2007, Illustration by Markus Voll.


Lateral and Medial Reticulospinal Tracts

– The lateral and medial reticulospinal tracts originate from the medullary and pontine reticular formation and have a strong influence on γ motoneurons.

– They are involved mainly in the control of axial and girdle muscles.

Lateral and Medial Vestibulospinal Tracts

– The lateral and medial vestibulospinal tracts originate from the vestibular nuclei.

– The lateral vestibulospinal tract projects to ipsilateral spinal cord neurons and is involved in the activation of extensor muscles in the maintenance of balance.

– The medial vestibulospinal tract innervates motoneurons of neck muscles and is involved in the control of head movements.

Tectospinal Tract

– The tectospinal tract originates in the superior colliculus and innervates motoneurons of neck muscles.

– It is involved in the control of head movements in response to moving visual stimuli.

Rubrospinal Tract

– The rubrospinal tract originates in the red nucleus of the midbrain.

– It is involved in activating flexor and inhibiting extensor motoneurons. It collaborates with the corticospinal tract in the control of motoneurons.

Decerebrate rigidity

Transection between the inferior and superior colliculi in the midbrain produces increased tone in extensor muscles. Normally, the rubrospinal and corticospinal tracts facilitate lateral reticulospinal activity, and this reticulospinal activity inhibits extensors. Damage to the midbrain removes this inhibition onto segmental levels. Extensor tone increases because there is still vestibulospinal excitement of extensors via γ motoneurons. This rigidity is removed if the sensory roots are cut. This indicates the importance of the spindle loop in maintaining the rigidity. Destruction of the lateral vestibular nuclei prevents decerebrate rigidity. Thus, the lateral vestibulospinal tract mediates the rigidity.


6.5 Upper and Lower Motoneurons

Upper and Lower Motoneuron Pathways

The projections that control muscle movement are broadly divided into lower and upper motoneuron pathways.

– Lower motoneurons are the α motoneurons that directly synapse with muscle at the neuromuscular junction.

– Upper motoneurons refer to descending motor pathways, principally the pyramidal tract, the most important of the motor control pathways.

Motoneuron Lesions

Lesions of both lower and upper motoneurons result in paralysis (lack of voluntary movement), but the physiological characteristics of the paralysis differ noticeably.

Lower Motoneuron Lesions

Lower motoneuron lesions sever the connection between the muscle and the CNS. Denervation induces accelerated atrophy of the muscle, possibly by removal of signaling molecules from the nervous system that maintain and nourish muscle cells. Denervation also provokes increased synthesis of acetylcholine receptor molecules by muscle cells. These receptor proteins are inserted all along the plasma membranes of the denervated muscle and are not confined to the neuromuscular junction as in normal muscle. As a result, the muscle membrane becomes supersensitive to acetylcholine and exhibits fasciculation (spontaneous rippling contraction of groups of muscle fibers).

The loss of lower motoneuron input also means that reflex circuits are interrupted, and the muscle shows no reflex responses and no tone. Thus, lower motoneuron lesions result in flaccid paralysis.

Upper Motoneuron Lesions

With upper motoneuron lesions, there is no denervation supersensitivity, much less muscle atrophy, and no loss of segmental reflexes. In fact, lesions of the motor cortex cause hypersensitivity of the stretch reflexes, resulting in elevated muscle tone. This type of paralysis is termed spastic paralysis.

Table 6.1 summarizes the signs of lower and upper motoneuron lesions.


The Babinski Sign

The Babinski sign is elicited by firmly stroking the outer border of the sole of the foot with a blunt obejct. This normally causes the toes to curl downward. If the great toe goes upward and the outer toes spread laterally, that is a sign of an upper motoneuron lesion.


6.6 Basal Ganglia


The basal ganglia, a group of nuclei situated deep to the cortex, receive and/or provide input to a number of brain areas. The main components of the basal ganglia are the following:

– the striatum, composed of the caudate and the putamen

– the globus pallidus, composed of the lateral globus pallidus and the medial globus pallidus

– the substantia nigra, composed of the substantia nigra pars reticulata and the substantia nigra pars compacta

– the subthalamic nucleus


The basal ganglia play a key role in voluntary motor control, by stimulating some motor circuits while inhibiting others. They do this as part of a circuit with three main participants, the cortex, the basal ganglia, and the thalamus.


Cortical neurons involved in movement planning project to the striatum of the basal ganglia releasing excitatory glutamate. Once excited, the cells of the striatum project to two pathways, the direct and the indirect (Fig. 6.8).

– In the direct pathway, the neurons of the striatum project inhibitory GABAergic neurons onto the cells of the substantia nigra reticulata-medial globus pallidus complex, which unless inhibited, acts to inhibit the thalamus from releasing excitatory glutaminergic input to the cortex. So the overall result of this pathway is that the striatum inhibits the inhibitory SNr-GPm complex freeing the thalamus from inhibition. The thalamus stimulates the cortex via glutaminergic input resulting in muscle action.

Fig. 6.8 image The pathways within the basal ganglia.

The excitatory glutaminergic pathways are green, the inhibitory GABAergic pathways are red, and the modulatory dopaminergic pathways are black. The GPi-SNr complex when stimulated is inhibitory to the thalamus. For the thalamus to excite the cortex to action, the GPi-SNr complex must be inhibited so that is cannot inhibit the thalamus. (GPm, medial globus pallidus; GPl, lateral globus pallidus; SNr, substantia nigra pars reticulata; SNc, substantia nigra pars compacta; STN, subthalamic nucleus)


– In the indirect pathway, the neurons of the striatum project inhibitory GABAergic neurons to the lateral globus pallidus, which then project inhibitory GABAergic neurons to the subthalamic nucleus. This inhibition of inhibitory outputs (disinhibition) of the lateral globus pallidus, results in the subthalamic nucleus projecting excitatory input to the SNr-GPm (which then inhibits the thalamus). The net result is a reduction in thalamic stimulation of the cortex, resulting in inhibition of muscle action.

– The antagonistic functions of the two pathways are modulated by the substantia nigra pars compacta that produces dopamine and which stimulates either D1 or D2 receptors in the striatum, which favor activation of the direct or indirect pathway, respectively.

Via these pathways the body maintains a balance of excitation and inhibition of motion.

GABA synthesis and degradation

Gamma-aminobutyric acid (GABA) is the principal inhibitory neurotransmitter in the CNS. It is released by interneurons in the cerebral cortex and cerebellum, by neurons of the basal ganglia, and by neurons in the spinal cord that control muscle tone. GABA is mainly synthesized from glucose via the GABA “shunt” of the Krebs cycle. This “shunt” converts ketoglutarate to glutamic acid, which is then converted to GABA. Thus, glutamate, the principal excitatory CNS neurotransmitter, is converted to GABA. Termination of the action of GABA is by reuptake into neurons and glial cells.


Basal Ganglia Disorders


Parkinsonism, a hypokinetic disorder, results from a loss of dopaminergic input to the striatum from the substantia nigra. Dopamine normally activates the direct pathway. Withdrawal of this activation gives free rein to the indirect pathway, resulting in excessive inhibition of the thalamus and a slowing of movement.

Symptoms of parkinsonism usually start between 60 and 70 years of age and include a “pill-rolling” tremor, “lead pipe” rigidity (limbs stay where they are placed when they are passively moved), and bradykinesia (slow execution of movement and speech), resulting in a masklike face and shuffling gait.

Treatment is with the dopamine precursor levodopa (l-dopa) and anticholinergic drugs, which are given as an adjunct for the tremor.

Dopamine: release, degradation, and uses

Dopamine is released from dopaminergic neurons following an action potential. It then binds to two major types of G-protein coupled receptors: D1 and D2. D1 receptors increase cyclic adenosine monophosphate (cAMP), whereas D2 receptors decrease cAMP, so the differing effects of dopamine binding depend on signal transduction. Dopamine’s action is terminated by reuptake into neurons, where it is stored in vesicles for reuse, or it is degraded by catechol O- methyltransferase (COMT) or monoamine oxidase (MAO). D2 agonists are used to treat Parkinson disease and to inhibit prolactin, whereas D2 antagonists are used as antiemetics and in the treatment of schizophrenia.


Lewy body dementia

Lewy body dementia (LBD) is the second most common form of dementia after Alzheimer disease. It occurs as a result of abnormal proteins (Lewy body proteins) being deposited throughout the cortex of the brain. If this deposition occurs in the substantia nigra, dopamine stores become depleted, causing parkinsonian symptoms. LBD manifests with cognitive impairment and increasing difficulty performing tasks, as well as memory problems and visual hallucinations. There is no cure for this disease, so treatment aims to reduce symptoms by using cholinesterase inhibitors, l-dopa, and neuroleptics.



Ballismus and hemiballismus are hyperkinetic disorders caused by damage, usually vascular, to the subthalamic nucleus, which interrupts the indirect pathway. The thalamus is thus freed from inhibition generating excessive activity of the motor cortex.

Ballismus is characterized by irregular, flinging movements of the limbs.

Treatment, when necessary, involves the use of dopamine-blocking agents (e.g., pimozide, haloperidol, and chlorpromazine), despite the fact that dopamine has not been definitively linked to the disorder.

Huntington Chorea

Huntington chorea is a genetic (autosomal dominant) hyperkinetic disorder associated with degeneration of striatal neurons that project via the indirect pathway.

Symptoms start insidiously in middle age with chorea (involuntary, continuous jerky movements) that involve the face and extremities and make the patient seem fidgety or jumpy. Neuronal degeneration progresses to involve the frontal cortex, resulting in dementia.

There is no cure nor any treatment to prevent progression of this disease.

Other Basal Ganglia Disorders

Dystonia (abnormal twisting movements), Tourette syndrome, and tics are also believed to involve abnormal activity in basal ganglia circuits.

6.7 Cerebellum


The cerebellum provides a mechanism for rapid feedback control of movement. It receives a copy of motor commands from the cerebral cortex, as well as ongoing information about the progress of movements from the periphery. After comparing the command and feedback information for errors, it issues correction signals to the motor cortex (via the thalamus) and other motor centers. It is also involved in planning, initiating, and learning movement sequences.

Functional Subdivisions

Although there is considerable overlap of functions, the cerebellum can be divided into three general subdivisions: the vestibulocerebellum, the spinocerebellum, and the cerebrocerebellum (Table 6.2).


– The vestibulocerebellum (floculonodular lobe) functions to maintain balance and positioning of the body in space.

– It receives input from the vestibular organ and vestibular nuclei.

– Its output is directed at the vestibular nuclei, which project to spinal cord motoneurons innervating antigravity extensor muscles and to ocular motor centers responsible for positioning of the eyes.


– The spinocerebellum (anterior lobe and vermis) monitors and controls ongoing movements, ensuring their accuracy in direction and force level.

– It receives its principal input from the ascending spinocerebellar tracts that convey ongoing information from muscle and joint receptors.

– The outflow of the spinocerebellum is to the red nucleus and, most importantly, to the VA and VL nuclei of the thalamus. These thalamic nuclei are the major inputs to the motor cortex whose outflow, via the pyramidal tract, directly controls spinal motoneurons responsible for movement.


– The cerebrocerebellum (lateral hemispheres), the largest subdivision of the cerebellum in humans, has responsibilities in the planning and initiation of movements, particularly complex learned movements.

– It receives its major input from the cerebral cortex via the pontine nuclei.

– Its output is directed to the VA and VL nuclei of the thalamus.

Table 6.2 summarizes the afferent and efferent connections of the divisions of the cerebellum and the symptoms associated with damage to each section.


Neuronal Circuitry

The cerebellum of all three subdivisions consists of a cortex of gray matter and an underlying accumulation of white matter (Fig. 6.9). The deep cerebellar nuclei lie within this white matter. The only projection neurons from the cerebellar cortex, the Purkinje cells, project their axons to these nuclei (Fig. 6.10). It is the deep cerebellar nuclei that convey instructions from the cerebellum to the motor nuclei of the brainstem and thalamus.

Note: Purkinje cells are GABAergic and act solely by inhibitory modulation of the rapidly firing cells of the deep cerebellar nuclei.

Fig. 6.9 image Cerebellar cortex.

The inner granular layer of the cerebellar cortex mostly contains granule cells (blue) plus mossy fibers (green) and climbing fibers (orange). Golgi cells are also present (not shown). The Purkinje layer contains the cell bodies of Purkinje cells (purple). The molecular layer contains parallel fibers (axons of granule cells) that synapse with the dendrites of Purkinje cells. The molecular layer also contains axons from the inferior olive and its accessory nuclei (climbing fibers) and a small number of inhibitory interneurons (basket and stellate neurons). 
From Thieme Atlas of Anatomy, Head and Neuroanatomy, © Thieme 2007, Illustration by Markus Voll.


Fig. 6.10 image Synaptic circuitry of the cerebellum.

The afferent fibers to the cerebellum are mossy and climbing fibers (origins shown). Climbing fibers form multiple excitatory synapses on the cell bodies and dendrites of Purkinje cells. Mossy fibers form excitatory synapses with granule cells. Collateral axons of both mossy and climbing fibers excite inhibitory interneurons and neurons of cerebellar nuclei. The parallel fibers of granule cells form excitatory synapses with the dendrites of Purkinje cells, which, in turn, make inhibitory synapses with cerebellar and vestibular nuclei. Cerebellar efferent neurons arise from the cerebellar nuclei. This complex circuit provides a means for feedforward and feedback control of motor function. (Asp, aspartate; Glu, glutamate)
From Thieme Atlas of Anatomy, Head and Neuroanatomy, © Thieme 2007, Illustration by Markus Voll.


Cerebellar Disorders

Damage to the cerebellum from tumors or ischemia affects muscles on the ipsilateral side, resulting in the loss of coordination and balance. The underlying defect is the loss of feedback control and disturbed accuracy of motion.

Table 6.3 lists signs that may occur in cerebellar disorders.