Download Anatomy Lecture 6 Stretch reflex: The doctor started by emphasizing

Anatomy Lecture 6
Stretch reflex:
The doctor started by emphasizing that the stretch reflex is not a totally
local mechanism i.e. the stretch reflex is affected also by the higher centers.
The higher centers affect both alpha and gamma, however they affect
gamma more because gamma motor neurons have a lower threshold in
comparison to alpha motor neurons.
The descending pathways could be divided also into inhibitory and
excitatory pathways. The Pontine Reticulospinal Tract (originates from the
pontine reticular formation) is an excitatory tract to both extensors and flexors
but mainly extensors. This tract is also associated with the Lateral Vestibulospinal
Tract (originates from Dieter’s nucleus), which means that the latter is also
excitatory. The inhibitory pathways, on the other hand, originate from the
medullary reticular formation i.e. the Medullary Reticulospinal Tract.
NOTE:
- The Lateral Vestibulospinal Tract is inhibited by the cerebellum.
- The descending pathways (inhibitory and excitatory) are balanced, this
balance is the reason we have moderate amount of muscle tone; thus
the stretch reflex works normally.
- The following experiments are done on animals and it’s considered the
same thing as an extensive infarction in the human brain.
Decerebrate Rigidity:
If we cut the brain stem at the level of the midbrain, above the level of the
reticular formation, there will be a loss of connection between the higher centers
and the brain stem.
The Pontine Reticulospinal Tract is always under inhibition from higher
centers (area 4S, 6 and the Caudate Nucleus of the basal ganglia) and most of our
neurons are hyper-excitable. If we cut the connection, then the Pontine
Reticulospinal Tract would be released from inhibition and will start firing
excessive impulses to both alpha and gamma, but mainly gamma. This results in
the hyperactivity of gamma which leads to the hyper-excitability of the muscle
spindle.
This phenomenon is known as decerebrate rigidity which means that there
is an increase in the tone of the antigravity muscles of humans.
NOTE:
- The doctor said that we mainly focus on the Pontine Reticulospinal Tract
because it is the one that is continuously active and inhibited by higher
centers not like the Medullary Reticulospinal Tract that does not work
unless it’s activated by higher centers.
Gamma Rigidity:
Gamma motor neurons are the main neurons responsible for the
decerebrate rigidity. This point is proved by cutting some of dorsal root ganglia; if
some dorsal ganglia were cut this will abolish the decerebrate rigidity indicating
that the gamma motor neurons are the reason for this rigidity.
NOTE:
- The dorsal roots are the ones responsible for carrying the activity of the
muscle spindle to the alpha motor neurons causing the extrafusal
muscles to contract (rigidity). If cut there will be no rigidity due to an
decrease or disappearance of the activity of gamma and the excitability
of the muscle spindle.
- Keep in mind that the hyperactivity of the gamma motor neurons is due
to the release of the Pontine Reticulospinal Tract from inhibition.
Is it possible to increase the rigidity again after the gamma is inactive (dorsal
root is cut)?
This could happen if we activate a descending tract that would re-increase
the rigidity by acting on alpha motor neurons. This tract is the Lateral
Vestibulospinal Tract which is usually inhibited by the cerebellum, so removing
the cerebellum would increase this tract’s activity and rigidity is observed again.
How?
The released Lateral Vestibulospinal Tract would send impulses to both
alpha and gamma motor neurons and since gamma is useless (due to cutting of
the dorsal root) alpha’s activity is the one responsible for the reoccurrence of
rigidity.
Decorticate vs. Decerebrate Rigidity:
Decorticate rigidity
Decerebrate rigidity
Injury in the brainstem is
above the red nucleus
Injury site
Injury is in the brainstem
below the red nucleus
Is still active
Rubrospinal Tract
Is inactivated
There will be an increase in
the tone of the antigravity
muscles (extended lower
limbs and flex upper limbs)
Result (action of
muscles)
There will be an increase in
the tone of the upper and
lower limbs (both arms and
legs are extended)
Both patients are in coma
NOTE:
- The Rubrospinal Tract’s action is the same as the lateral corticospinal
tract; facilitatory to both proximal and distal flexors but mainly distal.
- Any painful stimulus has its course which passes normally through the
brainstem. During its path, it will stimulate the reticular formation
causing an increase in the action of the Reticulospinal and Rubrospinal
(if present) Tracts.
If we apply a painful stimulus to the comatosed patient:
a- In a decorticate state: the lower limb will extend and the
upper limb will flex.
b- In a decerebrate state: both upper and lower limbs will
extend.
A decerebrate patient after a couple of days may become a decorticate patient.
Is this a good sign (prognosis)?
The prognosis is good because although the injury seems to have shifted
upwards (lesion increases to include the red nucleus), at the same time this lesion
is shifting away from the vital centers in the Pons and medulla. The brain damage
seems to increase which sounds bad, however, if the lesion reaches the vital
centers it will definitely kill the patient by respiratory failure.
Flexor reflex (withdrawal reflex):
If you step on a painful (noxious) stimulus you will raise your foot up away
from the stimulus (flex the leg) and the other leg would become fully extended to
support your body wait. Explanation:
Stepping on this noxious stimulus will alert the afferent fibers I, III and IV
exiting from the sensory receptors, present in the skin, muscles and joints. The
resulting action would be inhibiting the extensors and exciting the flexors of the
withdrawn leg and also exciting the extensors while inhibiting the flexors of the
other leg (the one that supports the body).
Depending on the intensity of the stimuli, we can divide the responses into
strong responses and simple muscle twitches (weak responses).
1- If the stimulus was extremely noxious, the person could move both his legs
or even move all the limbs together (hands and legs together).
2- If the stimulus was innocuous (a gentle stroke) you will notice that the
muscles underlying the skin will twitch.
NOTE:
- A noxious stimulus is any stimulus that is about to produce tissue
damage.
- How could the person move all limbs together?
This could happen with the help of the Propriospinal Tract which
connects and coordinates the movement between the upper and lower
limbs.
- If you gently stroke the belly, the underlying abdominal muscles will
twitch. This is known as abdominal reflex (this is a type if flexor reflex, in
addition to the cremastric reflex).
- Stretch reflex vs. flexor reflex:
The stretch reflex is monosynaptic which makes is very fast to
maintain many important body functions such as muscle tone and
posture. On the other hand, the flexor reflex is a protective reflex that is
di-or polysynaptic.
Both stretch and flexor reflexes are also known as reciprocal
inhibition: this is because the body excites some muscles (agonists) and
inhibits others (antagonist) in order to obtain a certain reflex.
Do NOT mix between recurrent (Renshaw Cells) and reciprocal
inhibitions.
- The flexor reflex is also known as flexion crossed-extension reflex:
which means that at the same time the impulses are causing flexion to
one leg some fibers have passed (crossed) to the other side causing the
exact opposite action (extend the other leg).
- The afferent (sensory) fibers I, III and IV are collectively called flexor
reflex afferents (FRA).
Mechanism (during voluntary knee flexion): (follow the numbers in the figure page 33)
1- Descending impulses through the pyramidal tract would first activate the Ia
inhibitory interneurons. These interneurons will inhibit the alpha motor
neurons of the antagonist (extensors).
2- These descending impulses will also directly activate the alpha and gamma
motor neurons of the agonist (flexors).
3- The activated alpha motor neurons will excite the extrafusal muscles while
the gamma motor neurons will activate the muscle spindle causing flexion.
4- Feedback impulses from the muscle spindle will go back through afferent
fibers (Ia) to increase the activity of the agonist muscles further more
(increase alpha motor neuron excitation) and also inhibit the antagonist
muscles by acting through the Ia inhibitory interneurons.
5- Due to the extension of the antagonists, their muscle spindles will become
activated and new impulses are sent to their alpha motor neurons.
However, the alpha motor neurons are still in refractory period, thus, there
will be no antagonist action.
6- During this refractory period, the impulses sent from the muscle spindle of
the antagonists will be sent to the higher centers instead to inform them
that the muscle is contracted (feedback).
NOTE:
- Alpha and gamma motor neurons in this case are recruited (stimulated)
together. This is known as alpha-gamma co-activation.
- Gamma motor neurons reinforce the alpha motor neurons through the
gamma loop. Also the descending impulses act on alpha and gamma
simultaneously (at the same time)
- Breaking the reciprocal inhibition (by the destruction of the pyramidal
tract) will cause reciprocal excitation in which both the agonist and
antagonist are activated; the leg is neutral (neither completely flexed
nor completely extended). Reciprocal excitation occurs due to the loss
of control over the Ia inhibitory interneurons due to destruction of the
pyramidal tract.
The pyramidal tracts descend from area 4 mainly and the extra-pyramidal
tracts descend from area 6, keeping in mind there is an overlap. This indicates
that you can hardly induce damage of the pyramidal tract (or area 4) without
damaging the extra-pyramidal tract.
NOTE:
- Motor deficit depends on the damage extent (which area was the
mostly affected) or which was firstly damaged.
 Suppose that pyramidal tract was damaged alone (above the decussation), the
result would be:
1- Contra-lateral hemiplegia or hemiparesis in both upper and lower limbs.
2- Hypotonia (flaccidity): the pyramidal tract has a facilitatory effect
(increases the tone) on distal muscles.
 A lesion that involves areas 4 (pyramidal) and 6 (extra-pyramidal):
1- Contra-lateral hemiplegia or hemiparesis
2- Spasticity: the reticular formation is inhibited by a tract that descends
down from area 6 (extra-pyramidal); damaging this area would release the
Pontine Reticulospinal Tract from this inhibition causing an increase in the
tone or spasticity.
 An Internal capsule lesion, aka capsular hemiplegia, due to a stroke in the
middle cerebral artery supplying the internal capsule, where both the
pyramidal and extra-pyramidal tracts are affected:
- First hours/day (shock stage):
1- Contra-lateral hemiplegia or hemiparesis due to the damage of
the lateral corticospinal tract.
2- Hyporeflexia or areflexia (no reflex at all)
3- Hypotonia or atonia (no tone at all)
- At the end of the first day:
1- The hypotonia shifts to hypertonia: elbow will become flexed and
the knee will become extended.
2- Spactisity: due to the increase in the tone of antigravity muscles.
3- Hyper-reflexia
4- Clonus
5- Positive Babinski sign
6- Absence of abdominal and cremasteric reflexes
NOTE:
- If the stroke’s damage was at the internal capsule, this damage is
considered as extensive meaning that both upper and lower limbs are
affected on one side of the body.
- If the stroke’s lesion affected areas 4 or 6, then the damage would be
limited; causing monoplegia (paralysis in either the hand or the leg on
one side of the body). Explanation:
The body in the cotex (areas 4 and 6) is represented upside-down,
precisely but disproportionately and if a small artery was blocked, only a
small part of either area will be affected (msh ma32ool kol el cortex
tindarib)
- The doctor used paresis or paralysis interchangeably, however, he later
on explained that in the majority of case, paresis is the one that usually
occurs while paralysis occurs in a very severe extensive lesion.
- The pyramidal tract damage symptoms occur always before the extrapyramidal symptoms for an unknown cause. However the spasticity of
the extra-pyramidal overshadows the flaccidity of the pyramidal.
- The shock stage might not happen and may even they go unnoticed.
- Spasticity and hyper-reflexia occur due to the release of the Pontine
Reticulospinal Tract from inhibition as said before.
- The tone in the antigravity muscles is diagnosed by resistance to passive
movement or what is known as clasp-knife rigidity: initial resistance
followed by a sudden release as a result of golgi tendon organ action.
Regards 
Jumana Abbadi