Motor System II: Brainstem and spinal cord LMN in CNS lesions

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Transcript Motor System II: Brainstem and spinal cord LMN in CNS lesions

Motor System II:
Brainstem and spinal cord
LMN in CNS lesions
Objectives
Motor System II: Brainstem and spinal cord
LMN in CNS lesions
I.
Functional Organization of Motor Neurons.
II.
Symptoms Following Lesions of Spinal
Lower Motor Neurons.
III.
The Oculomotor System.
IV.
The Trigeminal Motor Nucleus.
V.
The Facial Motor Nucleus.
VI.
The Nucleus Ambiguus.
VII.
The Spinal Accessory (XI) Nucleus.
VIII. The Hypoglossal Motor Nucleus
I. Functional Organization of Motor
Neurons
 Two types of motor neurons: a and g.
a are large, multipolar neurons with prominent Nissl
bodies and an axon innervating extrafusal motor fibers.
g are small, multipolar neurons with fine Nissl bodies
and axon innervating the polar regions of the muscle
spindle.
 Functionally there are two a subtypes: phasic (larger
cell, less easily excited, higher firing rate, faster
conducting axon) and tonic (smaller cell, more easily
excited, lower firing rate, slower conducting axon).
 Before a muscle contracts a “pool” of motor neurons is
temporally recruited as follow: g
tonic a
phasic a.
II. Symptoms Following Lesions of Spinal LMN
 Destruction of LMN from injury (e.g., trauma) or disease (e.g.,
poliomyelitis) causes the “LMN syndrome” characterized by:
1) Flaccid paralysis.
2) Hypotonia or atonia depending on severity of lesion.
3) Hyporeflexia (e.g., decreased DTRs) or areflexia (absence of
reflexes).
4) Muscle atrophy and reduction of muscle mass.
5) Fasciculations (random contractions of single motor units prior to
muscle degeneration).
4
III. The Oculomotor System (Figs 4 and 5)
 Includes motor III, IV and VI
 Motor III. Both nuclei make V-shaped structure next to midline
of rostral midbrain. Capping rostral pole is the EdingerWestphal nucleus. Axons course through midbrain tegmentum
and exit at interpeduncular fossa.
Unilateral III lesion: ipsilateral ptosis, lat strabismus (diplopia),
dilated pupil (myadrisis), loss of direct light reflex and
ipsilateral accomodation.
Unilateral III + PT at rostral midbrain: All of the above + PT
syndrome. This combo is called the superior alternating
hemiplegia (aka Weber’s syndrome).
III. The Oculomotor System (Continuation)

Motor IV (trochlear nucleus)
Small, round nucleus ventral to periaquaductal gray at level of caudal midbrain.
Axons course dorsally, cross the midline, exit at midbrain/pons transition and
ultimately innervate the sup oblique muscle which intorts the eye.
Unilateral 4th nerve lesion: causes ipsilateral extortion (eyeball slightly up and
out) and diplopia. Patient compensates by tilting head to the non paralyzed side
(which rotates the nonparalyzed eye).

Motor VI (abducens motor nucleus)
Fairly large, round nucleus close to midline of caudal pons. Fibers of internal
genu of VII wrap around this nucleus. Axons from motor VI course ventrally in
the tegmentum and exit at the junction of pons and medulla (inf pontine sulcus).
Unilateral nerve VI lesion. Results in ipsilateral medial strabismus with diplopia.
Unilateral abducens motor nucleus lesion. Produces the “lateral gaze
syndrome”. In this syndrome neither eye can be turned towards the lesion side
and both eyes tend to be conjugately deviated to the side opposite the lesion.
Unilateral nerve VI + PT lesion. This can occur at the basilar portion of the
caudal pons. Signs and symptoms are those of unilateral VI lesion together with
the PT syndrome. Facial paralysis does not occur because corticobulbar fibers
to motor VII do not travel with PT at this level.
IV. The Trigeminal Motor Nucleus (Fig 4)
 Large, round nucleus located just medial to the chief sensory nuclus
of V at mid pontine levels. Axons from motor V leave the pons with
the Vth nerve and then its mandibular (V3) division. Innervate the
ipsilateral muscles of mastication, tensor tympani and tensor veli
palatini.
Unilateral nerve V lesion. Results in paralysis of ipsilateral muscles
of mastication with jaw deviating to paralyzed side upon protusion.
Hyperacusis may occur from paralysis of the tensor tympani.
Sensory loses to the ipsilateral face are prominent but discussed
elsewhere.
Unilateral nerve V + PT. This results in the above signs + PT
syndrome signs. It may occur from a single lesion occuring in the
basilar portion of the pons at mid pontine levels. No facial paralysis
occurs (see reason for VI + PT).
V. The Facial (VII) Motor Nucleus (Fig 4)
 Large nucleus in the caudal pontine tegmentum at the same level as the
abducens motor nucleus. Axons from motor VII first course dorsomedial,
then wrap around the abducens nucleus (internal genu), then course
ventrolaterally between the spinal nucleus of V and the facial motor nucleus,
finally axons exit the pons at the cerebellopontine angle, just medial to
nerve VIII.
 Motor VII can be divided into a dorsal ½ (neurons innervate upper face
muscles) and a ventral ½ (neurons innervate lower face muscles).
Stapedius muscle also innervated.
Unilateral nerve VII lesion. Results in Bell’s palsy with patient unable to
smile, show the teeth, close the eyelid or wrinkle the forehead on the
paralyzed (ipsilateral) side. Hyperacusis may result from paralysis of the
stapedius. Ipsilateral corneal reflex is also abolished.
Unilateral lesion of corticobulbar fibers innervating motor VII. Results in
contralateral lower facial paralysis (patient can wrinkle forehead on both
sides but cannot smile contralateral to lesion side).
Unilateral VI + VII + PT. Produces the Millard-Gubler syndrome
VI. The Nucleus Ambiguus (Fig 5)
 Long narrow column of cells in the reticular formation at rostral and mid
medulla levels. Although nucleus cannot be seen in Atlas images, at
any given cross sectional level, it is located approximately half way
between the spinal nucleus of V and the inf olivary complex. Axons from
the ambiguus join cranial nerves IX and X (XIth portion ends up joining
X outside of the CNS). They innervate the ipsilateral pharyngeal
constrictors (for swallowing) and laryngeal muscles (for vocalization).
Also innervate soft palate muscle.
Unilateral ambiguus (or nerve X) lesion. Results in isilateral paralysis of
above muscles with dysphagia (difficulties in swallowing), dysarthria
(difficulties in vocalizing) and deviation of uvula to nonparalyzed side
when patient vocalizes.
Bilateral ambiguus (or nerve X) lesions. Results in aspiration
pneumonia, asphyxia and eventual death. Note that this is similar
to“pseudobulbar palsy” as described earlier.
VII. The Hypoglossal (XII) Motor Nucleus (Fig 5)
 Column of cells next to the midline at mid and caudal medulla levels.
Axons from nucleus course ventrally, just lateral to med lemniscus
and then lat to pyramid, after which they exit medulla at the
preolivary sulcus.
Unilateral XII nerve (or nucleus) lesion. Results in ipsilateral
paralysis of intrinsic and extrinsic tongue muscles. When protruded
tongue deviates to paralyzed side. In time fasciculations and atrophy
of ½ the tongue occur.
Unilateral XII nerve and PT lesion. Basically at levels of the
medullary pyramid, results in the inf alternating hemiplegia with
signs of XII as above + PT syndrome. No facial paralysis
accompanies this syndrome.
VIII. The Spinal Accesory (XI) Motor Nucleus (Fig 5)
 This is another long, narrow column of cells found in the gray horn at
the transition between medulla and spinal cord and from C1-5 spinal
levels. Axons from the nucleus leave spinal cord half way between
the dorsal and ventral roots, then rootlets coalesce to form the nerve
which ascends and enters into the skull through the foramen
magnum only to leave the skull through the jugular foramen. Axons
eventually innervate the ipsilateral sternocleidomastoid and
trapezius muscles.
Unilateral XI nerve lesion. Causes ipsilateral paralysis of the above
muscles downward and outward rotation of ipsilateral scapula. The
patient has difficulties turning the head to the side opposite the
lesion and shrugging at the shoulder.