Motor disturbancies of nerve system

Prof. P. Angelova, MD
Motor disturbancies

Spinal α-motoneurons are controlled by several motoneurons are controlled by several
supraspinal neuronal tracts:

– the pyramidal tract from the motor

cortex;

– the rubrospinal tract from the red nucleus

– the medial reticulospinal tract from the pontine
reticular formation

– the lateral reticulospinal tract from the medullar
reticular formation and

– the vestibulospinal tract

The medial reticulospinal and the vestibulospinal
tracts predominantly promote the activity of the
so-motoneurons are controlled by several called antigravity muscles, i.e., the muscles
that flex the arms and stretch the legs.



The pyramidal, rubrospinal, and lateral
reticulospinal tracts, on the other hand,
predominantly promote the activity of the flexors of
the leg and extensors of the arms.
Regulation of the posture
Pyramidal tract
 Paralysis Due to Upper Motor
Neuron-
(UMN) Lesions - Spastic paralysis

The vestibulospinal and medial reticulospinal

tracts are less affected, because they are
under stronger noncortical influence, for
example,from the cerebellum. An interruption
of transmission in the area of the internal
capsule thus ultimately results in an excessive
activity of the extensors in the legs and the
flexors in arms
If the motor cortex or the internal capsule is
damaged (e.g., by bleeding or ischemia in the
area supplied by the middle cerebral artery)
impulse transmission in the immediately adjacent
descending cortical tracts is interrupted.

These make up the pyramidal tract and other

connections of the motor cortex, such as those to
the red nucleus and to the medullary reticular
formation. The result is a reduced activity not
only of the pyramidal tract but also of the
rubrospinal and medial reticulospinal tracts.
Impairment of fine motor function.
Voluntary movement of paretic limbs requires greater
effort than normal and causes greater muscular
fatigue. Moreover, rapid alternating movements are
slowed by hypertonia in the opposing agonist and
antagonist muscles of paretic limbs.There may be
synkinesia (involuntary movement of paretic limbs
associated with other, e. g., yawning), undifferentiated
accessory movements (mass movements), or spinal
automatisms (involuntary movements triggered by
somatosensory stimuli)
 Paralysis
Paralysis of UMN type affects multiple (but not all) muscle groups
on one side of the body. Bilaterally innervated movements (e. g., of
eyes, jaw, pharynx, neck) may be only mildly paretic, or not at all.
Paralysis that is initially total usually improves with time, but
recovery may be accompanied by other motor disturbances such as
tremor, hemiataxia, hemichorea, and hemiballism.

●
Fine motor control is usually more severely impaired than strength.

Neurogenic muscular atrophy does not occur in paralysis of UMN

type.
Another consequence is spasticity.
After loss of function of the
descending tracts, the activity of the
α-motoneurons are controlled by several motoneurons comes under the
increasing influence of the muscle
spindles and Golgi tendon organs.
 Spasticity
The defining feature of spasticity is a velocity-
dependent increase of muscle tone in response to
passive stretch. Spasticity is usually, but not
always, accompanied by hypertonia.
●

●
The “clasp-knife phenomenon” (sudden slackening
of muscle tone on rapid passive extension) is rare.
●
Spasticity mainly affects the antigravity muscles
(arm flexors and leg extensors).
 Reflex abnormalities.
●
The intrinsic muscle reflexes are enhanced
(enlargement of reflex zones, clonus) and the
extrinsic reflexes are diminished or absent.
●
Pathological reflexes such as the Babinski
reflex can be elicited.
Babinski reflex
The predominance of the extensor muscles leads to
extension of the big toe on stroking the sole of the foot,
instead of its normal plantar flexion. This is called
Babinski’s sign or the Babinski reflex. It is taken as
evidence for a lesion in the pyramidal tract. In fact the
Babinski reflex is the result of a lesion of several
descending cortical tracts, including the pyramidal tract.

Isolated damage of the pyramidal tract (extremely rare)

results in neither spasticity nor the Babinski reflex, but
only minor disturbance of fine movement.
 Cerebral lesions
Monoparesis
Isolated lesions of the primary motor cortex (area 4)
cause flaccid weakness of the contralateral face, hand,
or leg.
●
Lesions affecting adjacent precentral or postcentral
areas, or areas deep to the cortex, cause spasticity and
possibly an associated sensory deficit.
●

●
It may be difficult to determine by examination alone
whether monoparesis is of upper or lower motor neuron
type
 Cortex injury
●
If there is aphasia, corical
sensory disturbancies, cognitive
impairment, visual-motoneurons are controlled by several spatial
sensitivity, apraxia, seizures
●
 Contralateral hemiparesis
●
Lesions of the internal capsule cause spastic hemiparesis.
Involvement of corticopontine fibers causes (central) facial
paresis, and impairment of corticobulbar fibers causes
dysphonia and dysphagia.
●

●
Sensory disturbances are also usually present.
●

●
Unilateral lesions in the rostral brain stem cause
contralateral spastic hemiparesis and ipsilateral nuclear
oculomotor nerve palsy (crossed paralysis).
 Ipsilateral paresis.
●
Lesions of the lower medulla below the
pyramidal decussation cause ipsilateral
paralysis and spasticity (as do lesions
●
of the lateral corticospinal tract)
 Quadriparesis.
●
Decortication syndrome is caused by extensive bilateral
lesions involving both the cerebral cortex and the underlying
white matter, possibly extending into the diencephalon;
●

●
midbrain involvement produces the decerebration syndrome.
●

●
Involvement of the pons or medulla causes an initial
quadriplegia , in the later course of illness, spinal
automatisms may be seen in response to noxious stimuli.
Central paresis
 UMN lesions

Distal muscle are predominantly affected



Axial muscles are not affected



In corticobulbar lesions are affected
predominantly lower part of the face and the
tongue


If the pyramidal tract is affected
above the pons, arm muscles are
affected



Bilateral movements are poorly
affected – eyes, jaws, larynx.
Pyramidal
syndrome
Common Stroke Symptoms
 Weakness or paralysis
 Numbness, tingling,
decreased sensation
 Vision changes
 Speech problems
 Swallowing difficulties or
drooling
 Loss of memory
 Vertigo (spinning sensation)
 Loss of balance and
coordination
 Personality changes
 Mood changes (depression,
apathy)
 Drowsiness, lethargy, or loss
of consciousness
 Uncontrollable eye
movements or eyelid
drooping
 Pseudobulbar paralysis
In bilateral corticobulbar damage
Dysarthria
Dysphagia
dysphonia
Emotional instability
Face weakness bilateral
Overactive stretch reflex

Symptoms of frontal desinhibition


Pharyngeal
paresis
 Spinal shock
At first, however, spinal shock will set in due to cessation of supraspinal
innervation of α-motoneurons are controlled by several motoneurons. In spinal shock the muscles are
flaccid and no reflexes are elicited (areflexia).

However, partial “denervation” of the α-motoneurons are controlled by several and γ-motoneurons are controlled by several motoneurons as well
as of interneurons leads to a gradual increase in sensitivity of
these neurons.
In addition, the endings of supraspinal neurons that are out of
action are replaced by synapses with the spinal cord neurons . As
a consequence, the reflexes gradually gain a stronger influence on
the activity of the α-motoneurons are controlled by several motoneurons, and hyperreflexia occurs.
Lower motoneuron paresis -motoneurons are controlled by several LMN
Paralysis of peripheral origin can be caused by
lesions of the anterior horn (lower motor
neuron, LMN), nerve root, peripheral nerve, or
motor end plate and must be distinguished from
weakness due to disease of the muscle itself
(myopathy).
 Paralysis
Paralysis is accompanied by diminution of
muscle tone (flaccidity). The extent of
weakness depends on the type, severity, and
distribution of LMN or myopathic involvement.
 Reflex abnormalities
●
The intrinsic muscle reflexes are diminished or
absent to a degree that may be disproportionate
to the degree of weakness: in LMN-type
paralysis, loss of reflexes is independent from the
loss of strength;
●

●
in myopathy, it parallels the weakness.
●

●
Extrinsic reflexes are unaffected unless the
effector muscle is atrophic.
●
Pathological reflexes are absent.
 Muscle atrophy
●
Muscle atrophy due to an LMN lesion may be
disproportionate to the degree of weakness
(either greater or less).
●
Progressive atrophy of paralyzed muscles
begins 3 weeks after a peripheral nerve injury.
●
The distribution and severity of muscle atrophy
in myopathy depends on the etiology.
 Spontaneous movements
●
Spontaneous movements are seen in affected
muscles.
●
Fasciculations are involuntary, nonrhythmic
contractions of motor units in a relaxed muscle
 Anterior horn.
●
Loss of motor neurons in the spinal cord paralyzes the
motor units to which they belong. The flaccid segmental
weakness may begin asymmetrically and is
accompanied by severe muscle atrophy.
●
There is no sensory deficit.
●
The intrinsic reflexes of the affected muscles are lost at
an early stage.
●
The weakness may be mainly proximal (tongue,
pharynx, trunk muscles) or distal (hands, calf muscles)
depending on the etiology of anterior horn disease.
 Radicular syndrome
●
A lesion of a single ventral nerve root (caused, for
example, by a herniated intervertebral disk) produces
weakness in the associated myotome. Muscles supplied
by multiple nerve roots are only slightly weakened, if at
●
all, but those supplied by a single root may be frankly
paralyzed and atrophic (segment-indicating muscles).
●

●
Involvement of the dorsal root produces pain and
paresthesia in the associated dermatome, which may be
triggered by straining (sneezing, coughing), movement
(walking), or local percussion.
●
Autonomic deficits are rare.
 Peripheral nerve.
●
Paralysis may be caused by plexus lesions
(plexopathy) or by lesions of one or more
peripheral nerves (mononeuropathy,
●
polyneuropathy).
●

●
Depending on the particular segment(s) of
nerve(s) affected, the deficit may be purely motor,
purely sensory, or mixed, with a variable degree
of autonomic dysfunction.
Damage of n. facialis
 Motor end plate.
●
Disorders of neuromuscular transmission are
typified by exercise-induced muscle fatigue and
weakness.
●
The degree of involvement of specific muscle
groups (eyes, pharyngeal muscles, trunk
muscles) depends on the type and severity of
the underlying disease.
●
There is no associated sensory deficit.
 Myopathy
●

●
and musculoskeletal lesions of the tendons,
ligaments, joints, and bones may cause real or
apparent weakness and thus enter into the
differential diagnosis of LMN lesions.
●
They cause no sensory deficit.

https://www.youtube.com/watch?
v=b5rIEx9SsCo



Peripheral paralysis
 Bulbar paresis
Billateral damage of motor nuclei (LMN ) of cranial
nerves -motoneurons are controlled by several IX, X, XII
Jaws, face, pharynx, larynx are affected

Atrophy of muscles of the tongue

Changed speaking
Gag reflex diminished or absent
Difficult articulation

Flabby face muscles

Diminished mandibular reflex



Atrophy and fasciculations

Danger of aspiration, malnutrition,
dehydration, speech

 Paresis
sign Upper Lower myopathy
motoneuron motoneuron

atrophy -motoneurons are controlled by several severe mild

fasciculations -motoneurons are controlled by several frequently -motoneurons are controlled by several

Muscle tone Spastic, Decreased, Normal/

rigidity flabby decreased

Distribution Pyramidalis Dystal proximal

of fatigue regional segmental

Tendon reflexes Hyperreactive, Decreased Normal

Clasp knife Absent decreased
phenomenon No clonus
clonus
Babinski yes -motoneurons are controlled by several -motoneurons are controlled by several
 Upper MN Lower MN

Muscle groups are affected Might be affected single muscles

In the beginning – fine Asymetrically, in the beginning

movements one limb, then may be
generalized

Usually dystal weakeness is
neuropathic, (LMN), symetrical
proximal weakeness is myopathic
more frequently



Fasciculations and atrophy are
neuropathic


Paralysis – severe weakeness ,
inability for contractiona (Plegia)



Paresis – mild to moderate
weakeness

Hemi-motoneurons are controlled by several

Para -motoneurons are controlled by several

Quadri -motoneurons are controlled by several