Page 320 - Color Atlas Of Pathophysiology (S Silbernagl Et Al, Thieme 2000)
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Lesions of the Descending Motor Tracts
       Spinal α-motoneurons are controlled by sever-  praspinal neurons that are out of action are re-
       al supraspinal neuronal tracts (→ A1):  placed by synapses with the spinal cord neu-
       – the pyramidal tract (violet) from the motor  rons (→ A3b). As a consequence, the reflexes
         cortex;                       gradually gain a stronger influence on the ac-
       – the rubrospinal tract from the red nucleus  tivity of the α-motoneurons, and hyperreflexia
    Systems  – the medial reticulospinal tract from the pon-  occurs.
         (red);
                                        Another consequence is spasticity. After loss
         tine reticular formation (orange);
                                       of function of the descending tracts, the activ-
                                       ity of the α-motoneurons comes under the in-
       – the lateral reticulospinal tract from the med-
    Neuromuscular and Sensory  – the vestibulospinal tract (green).  Golgi tendon organs (→ A4). Stretching the
                                       creasing influence of the muscle spindles and
         ullar reticular formation (brown); and
                                       muscle spindles stimulates the α-motoneu-
       The medial reticulospinal and the vestibulo-
                                       rons of the same muscle via a monosynaptic
       spinal tracts predominantly promote the activ-
                                       reflex; the increased influence of the muscle
       ity of the so-called antigravity muscles, i.e., the
                                       spindles results in massive contraction on
       muscles that flex the arms and stretch the legs.
       The pyramidal, rubrospinal, and lateral reticu-
                                       stretching. Nevertheless, the response of the
                                       muscle spindles is mainly phasic, i.e., if they
       lospinal tracts, on the other hand, predomi-
       the leg and extensors of the arms.
                                       activity slowly decreases. As a result, the influ-
                                       ence of the Golgi tendon organs becomes
         If the motor cortex or the internal capsule is
    10  nantly promote the activity of the flexors of  are stretched slowly or continuously their
       damaged (e.g., by bleeding or ischemia in the
                                       dominant: when the muscle is stretched they
       area supplied by the middle cerebral artery),  inhibit muscle contraction via an inhibiting
       impulse transmission in the immediately adja-  interneuron. It is also under the influence of
       cent descending cortical tracts is interrupted.  the Golgi tendon organs that on slow or con-
       These make up the pyramidal tract and other  tinuous stretching the muscle will suddenly
       connections of the motor cortex, such as those  become flaccid after initial increase in tone
       to the red nucleus and to the medullary reticu-  (clasp-knife effect).
       lar formation. The result is a reduced activity  The predominance of the stretching mus-
       not only of the pyramidal tract but also of the  cles leads to extension of the big toe on strok-
       rubrospinal and medial reticulospinal tracts.  ing the sole of the foot (→ A5), instead of its
       The vestibulospinal and medial reticulospinal  normal plantar flexion. This is called Babinski’s
       tracts are less affected, because they are under  sign or the Babinski reflex. It is taken as evi-
       stronger noncortical influence, for example,  dence for a lesion in the pyramidal tract. In
       from the cerebellum. An interruption of trans-  fact the Babinski reflex is the result of a lesion
       mission in the area of the internal capsule thus  of several descending cortical tracts, including
       ultimately results in an excessive activity of  the pyramidal tract. Isolated damage of the
       the extensors in the legs and the flexors in  pyramidal tract (extremely rare) results in nei-
       arms (→ A2).                    ther spasticity nor the Babinski reflex, but only
         At first, however, spinal shock will set in due  minor disturbance of fine movement.
       to cessation of supraspinal innervation of α-  If the red nucleus has been destroyed (e.g.,
       motoneurons (→ A3a). The antigravity mus-  due to ischemia of the mid-brain or in Wilson’s
       cles are also affected, less so than the other  disease [→ p. 252]), coarse tremor will result.
       muscles though, by the reduced supraspinal  Neurons of the red nucleus are, among other
       activation of the α-motoneurons. In spinal  functions, important for the dampening of os-
       shock the muscles are flaccid and no reflexes  cillations that can occur as a result of a nega-
       are elicited (areflexia).       tive feedback in the control of α-motoneurons.
         However, partial “denervation” of the α-  In lesions of the vestibular nucleus abnormal-
       and γ-motoneurons as well as of interneurons  ities of balance with vertigo, nystagmus, and
  310  leads to a gradual increase in sensitivity of  nausea predominate (→ p. 330).
       these neurons. In addition, the endings of su-
       Silbernagl/Lang, Color Atlas of Pathophysiology © 2000 Thieme
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