They represent large nuclear masses located deep at the base of cerebrum and in midbrain.

The rules for understanding the concept of basal motor nuclei are:

they extend from the base of cerebrum through the diencephalon to the midbrain

they modulate the somatomotor activity by numerous feed-back circuits connecting them with:

each other (between them)

cerebellum

cerebral motor cortex

Lesions in these nuclei or their pathways result in motor clinical signs as:

muscular rigidity

involuntary movements

History and classificat 21121g621v ion

Before these nuclei were well known and understood, they were totally called basal ganglia and they were classified as it follows:

Today, all neuroanatomists include the amygdala into limbic system, but the function of claustrum remains unknown. The nuclear masses concerned with the control of the skeleta1 muscular activity were called basal motor nuclei and they include different cerebral, diencephalic and midbrain components as it follows:

Connections of basal motor nuclei

Myelinated axons around basal nuclei form the next formations:

field H of Forel is a bundle of axons which arise from the capsule of fibers around red nucleus and extend dorsomedial;

field H₁ of Forel (thalamic fasciculus) conveys 3 major pathways to the thalamus:

pallidothalamic tract

dentatothalamic tract

medial lemniscus

field H₂ of Forel (lenticular fasciculus) conveys fibres from globus pallidus to thalamus;

lenticular ansa - it also conveys fibers from globus pallidus to thalamus but it loops under the internal capsule instead to penetrate the internal capsule like lenticular fasciculus;

Connections of striatum (caudate-putamen)

afferents

cortico-striatal projections come from pre- and postcentral gyri principally but also from the other areas including the limbic cortex;

thalamo-striatal projections from IL, centrum medianum, and probably VA and VL nuclei;

nigro-striatal afferents arise from pars compacta and pass via internal capsule and field H of Forel;

raphe-striatal afferents.

efferents

striato-pallidal fibres

striato-nigral fibres project through internal capsule to pars reticulata of the substantia nigra;

Connections of globus pallidus

afferents

striato-pallidal fibres

subthalamo-pallidal fibres via subthalamic fasciculus;

efferents

lenticular ansa

lenticular fasciculus.

subthalamic fasciculus

pallido-tegmental fibres for the pedunculo-pontine nucleus of midbrain reticular formation

as a simplified conclusion we can say that:

pallidum acts as a final common pathway from the basal nuclei to the thalamus and

thalamus projects, in turn, these influences to motor cerebral cortex and from here they are projected down to the lower motor neurons (LMN); this is the most important circuit from clinical point of view

Connections of subthalamic nucleus

afferents

pallido-subthalamic fibres via subthalamic fasciculus,

cortico-subthalamic fibres from the cerebral motor cortex;

efferents:

subthalamo-pallidal fibres via subthalamic fasciculus

Connections of the red nucleus:

afferents

cortico-rubral fibres come from the ipsilateral precentral gyrus via the internal capsule;

dentato-rubral fibers come from the contralateral dentate nucleus of cerebellum via the contralateral sup. cerebellar peduncle; it decussates just caudal to the red nucleus;

efferents:

rubro-olivary tract descends ipsilaterally in the central tegmental tract;

rubro-spinal tract decussates in the ventral tegmental decussation and enters the lat. funiculus of the spinal cord just ventral to the lat. cortico-spinal tract;

Connections of substantia nigra:

afferents reach mostly the pars reticulata; they are:

striato-nigral fibers which project through the internal capsule

thalamo-nigral fibers are less numerous;

efferents arise mostly from pars compacta; they are:

nigro-striatal fibers traverse globus pallidus after they run superiorly over subthalamic nucleus

nigro-thalamic fibers have the same way like the nigro-striatal ones and project into VL and VA thalamic nuclei;

the concept of extra-pyramidal system includes all the motor pathways of the brain that influence the LMN but do not send their axons directly into the pyramidal tract; it includes:

the circuits of basal motor nuclei,

reticulospinal tract,

rubrospinal tract,

olivospinal tract,

vestibulospinal tract,

tectospinal tract

many authors have argued in favor of abolishing the pyramidal/extrapyramidal concept totally, but clinicians maintain this concept because there are distinctive pyramidal and extrapyramidal clinical syndromes and this concept serves to localise the lesions and to separate different disease entities;

Phylogeny of pyramidal/extrapyramidal system:

in submammals all the movements are extrapyramidal because these animals have no cerebral cortex and no pyramidal tract;

in lower mammals (such as marsupials) the cerebral cortex appears but the pyramidal tract is short and not very useful;

- in lower primates the cerebral cortex and pyramidal tract have an increased importance, but the extrapyramidal system can compensate considerably for the interruption of pyramidal tract

- in humans the movement depends principally on the cerebral cortex and pyramidal system; the next clinico-pathological correlations can be made:

complete unilateral interruption of pyramidal tract paralyses most contralateral voluntary movements, especially of the hand;

complete bilateral interruption of the pyramidal tract paralyses all the voluntary movements of the body caudal to the lesion; the involuntary movements that result from lesions of the basal motor nuclei are also paralysed;

*** as a conclusion we may say that the somatomotor activity is essentially pyramidal in humans; the regulation of this somatomotor activity is made by various afferent pathways that originate in reticular formation, cerebellum, basal motor nuclei and sensory systems and run through the thalamus to the cerebral motor cortex to regulate its activity; the motor cortex, in turn, sends efferences to many of these sources; the lesion of these afferent pathways results in dysmodulation of the cerebral motor cortex which becomes expressed through an intact pyramidal tract by chorea, ataxia and other clinical signs which appear usually on the contralateral side of the lesion;