The reflexoscillations; How and Why?

Prof.Dr. Hilmi Uysal


DearChair, Ladies and Gentlemen,
In mypresentation, I will be addressing an old topic, but I will try to turn the oldtopic around and look at it in a new way, so you could say this is also a kindof oscillation.
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In mypresentation, I would like to discuss two oscillations.
1) Ankle clonus, which is usually accompanied by spasticity and upper motorlesions,
2) patellar pendulum, which is triggered by the patella T reflex
Clonus does not only occur in pathological conditions. After long walks, ankleclonus could be observed in healthy/normal subjects.
As we see in this video, clonus was observed following quick ankle dorsalflexion and when the foot was held in this position. Clonus can vary from 1-2beats to minutes. If it continues for several minutes it is called"sustained clonus".
The pendulum patellar reflex is triggered by the patella T reflex and pendulumoscillations can be observed under both normal and pathological conditions.

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RhythmicOscillations are a prominent feature of all biological systems,
They can be summarized in three parts;
1) mechanical oscillations; such as those caused by the cardiac pulse
2) reflex oscillations; the most typical example of this is clonus and some ofthe tremor is also considered in this context.
3) Central oscillations; observed in Parkinson's disease.

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Ingeneral, for all oscillations, describing function is "y (t) = Aept sin (2πft + φ)" .
The important constants in this equation are:
A: A constant that defines theamplitude.
p:The rate at which an oscillation builds up or decays exponentially
f: The frequency of the oscillation,
φ :The phase of the oscillation at the time t = 0,

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In anysystem, there are only three classes of oscillations;
1) Growing oscillations,
2) Decaying oscillations,
3) Maintained oscillations.
Factorswhich tend to produce oscillation will increase the value of the p,while factors which tend to stabilize the system will decrease the value of p.
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Differentmethods can be used for the recording and examination of oscillations.
A significant part of our work, which I will present here, is examined by imageand motion analysis.

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Sustainedankle clonus recordings contain important information. As you can see, in anindependent recording, very stable oscillation can be obtained.
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DuringAchilles clonus. Here we can see two of the fundamental ankle joint movements,plantar flexion and dorsal flexion of the foot.
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Thetibialis anterior muscle is the effector muscle for dorsal flexion and thegastrocnemius-soleus muscles are the effector muscles for plantar flexion.These two antagonistic muscles have a spinal level relationship and are quitestraightforward.
If we consider all of the above cases, we can see howfrequencies vary for different types of clonus.
Those with a long afferent and efferent pathway have a low clonus frequency,whereas the clonus frequency is high for those with the shortest afferent andefferent pathway.
So, the frequency of the reflex oscillation correlates with the length of thepath. 10. Slide
The phasediagrams of the ankle clonus show that the dorsal flexion and plantar flexionparts of the movement each have different characteristics.
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This isquite an interesting case:
The patient had right hemiplegia and spasticity due to a cerebral vascularaccident and, sadly, he/she also had total axonal degeneration of the rightperoneal nerve due to traumatic peripheral nerve lesion.
The tibialis anterior muscle of the patient was totally denervated.
In this case, ankle clonus has been available.
Therefore, the effector muscle of the ankle clonus is gastrocnemius-soleus andafferents and efferents of the clonus are related to the tibial nerve.

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In this partof my presentation I will try to convey what we know on the factors thatdetermine the frequency of ankle clonus reflex oscillations. Different clonus oscillations can be observedin the human body.
If youreview these frequencies
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We can clearlyunderstand from this record that the ankle clonus frequency is 5-6 Hz.
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SurfaceEMG recordings from the soleus and tibialis anterior muscle activity andacceleration of the ankle during sustained clonus. With three different epochsof these records frequency are in the 5-6 Hz range.
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Using twodifferent recording techniques we recorded 31 and 18 different époque of ankleclonus. The frequency of the clonus is quite stable in a range of frequencies.
In addition, as observed clearly in theserecords, the load affects the frequency of clonus.
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Anothertype of clonus is patellar clonus. Byrapid up and down movements of the patella in patients with spasticity,rhythmic muscle contractions of the rectus femoris can easily be observed.
The patella clonus frequency is around 9-10 Hz. It is faster than that of ankle clonus.

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A similarfrequency characteristic was detected by goniometric recordings in patientswith advanced spasticy. The continuous activity in the biceps femoris muscle isparticularly interesting.
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Whenalternating discharges are observed in agonists and antagonist muscles, thefrequency drops to 8.
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It is also possible to observe clonus in the upper extremities.One example is hand-wrist clonus.
Clonus is recorded in the Flexor carpi radialis muscle, which has 9 Hz.frequencies. The antagonist extensor digitorum muscle is not activelyparticipating in the oscillations.

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One rare type of clonus is “jaw clonus”. It has been observed in spastic patients,reaching frequencies of 12 Hz.. In thiscase, jaw clonus is triggered by the jaw T reflex.
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If we consider all of the above cases, we can see howfrequencies vary for different types of clonus.
Those with a long afferent and efferent pathway have a low clonus frequency,whereas the clonus frequency is high for those with the shortest afferent andefferent pathway.
So, the frequency of the reflex oscillation correlates with the length of thepath.

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While there is no uncertainty about the means source? of the efferent path of thereflex, there is debate about the afferents.
We can model the components of the clonus can be taken as an example.
The process starts with a stretch, and then the muscle action potential comesup increases and a relaxation period follows the response. A vicious circle isinduced by stretching again.
Furthermore, during this period, two different moving components, such as theDF and PF are observed. We can predictthat the DF and PF would be the same with half of this period.

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This record clearly shows the relationship between thefoot position changes and the response in the soleus muscle.
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We recently described a reflex response induced bystretching the soleus muscle. Stimulation of the peroneal nerve brings about amedium latency response. We defined it as the soleus MLR that is triggered by asudden dorsal flexion of the foot.
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If the tibial nerve is stimulated from the poplitealfossa, the soleus H reflex is recorded. However, when the common peroneal nerveis stimulated supramaximally from the fibular head, there is a late response inthe soleus muscle which is longer than the soleus H reflex.
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Theresponse latency was measured using an accelerometer. The latency from thebeginning of stretching the soleus muscle by foot dorsal flexion is about 55ms.
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If theperoneal nerve is stimulated at the fibular head and the foot is kept at aposition of 90 degrees extension, soleus MLR is obtained and, subsequently,clonus beats are observed in a spastic patient. I want to draw your attentionto the similarity of responses to MLR and clonus.
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When thefoot is in the dorsal flexion position, the soleus MLR corresponds directlywith the clonus beats. However, duringplantar flexion, the soleus MLR and clonus beats are lost.
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In thisstudy we examined the similarities between clonus beats and the soleus MLR interms of latency and amplitude. We emphasized the relationship between thesetwo responses.
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Thesimilarities between stretch induced ankle clonus and peroneal nervestimulation induced soleus MLR give a chance for speculation about theafferents of the responses.
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Even ifprevious publications considered mainly Group I afferents as clonus afferents,we propose Group II afferents to be evaluated in the formation of clonusbecause of findings about soleus MLR afferents.
FCR MLRis an example of a response in the upper extremity. Stimulation of anantagonist muscle nerve results in a medium latency response by the agonistmuscle. Radial nerve stimulation causesthe EDC muscle to contract and MLR is achieved by latency much later than theFCR H reflex.
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Clonus canbe obtained through radial nerve stimulation during wrist extension, as withlower extremities’ ankle clonus.
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Latencyof the response obtained from the FCR is about 42-43 ms. However, FCR -H or Treflex latency does not exceed 20 ms.
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In thelower extremities, Patellar clonus could establish correlation with MLR, suchas ankle clonus. In this case, clonus can be obtained by femoral nervestimulation.
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Themedium latency response is about 50 ms at the antagonist Biceps femoris muscleduring the patellar T reflex.
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However,latency of the H-reflex obtained by femoral nerve stimulation is about 15-20ms. Clearly it is much shorter than theMLR latency.
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Andbringing together all of these values​, an interesting comparison can be madewith clonus latencies. We have already mentioned the values ​​of clonusfrequencies.
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H / Treflex latencies and clonus periods were compared to MLR latency. The Group IIafferents constitute a more convenient time for the clonus period as opposed toGroup Ia afferents.
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When themeasured clonus frequencies are compared to the calculated frequencies that areformed by Group Ia and Group II afferents, we can say that Group II afferentscontribute to the clonus.
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Weexamined the effects of the afferent paths on the frequency of clonus.Returning to the formula for oscillation again; we can ask what the factorsthat determine p are. So, which factors determine dumping or buildingoscillation?
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Factors whichtend to produce oscillation will increase the value of the p, whilefactors which tend to stabilize the system will decrease the value of p.
Sustainedclonus has to have p=0 value because it is a maintained oscillation.
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It seemsthe Pendulum has <0 p value.
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We cancalculate the damping ratio by dividing the amplitude of the first and secondbeats. In Ash 1 spasticity which mildly increase gain of the reflexes.
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In Ash 2spasticity, the damping ratio is increased. The gain of the reflex is muchhigher than in Ash 1 spasticity.
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But evenif the gain of the reflex is increased, the damping ratio is decreased in Ash 3spasticity.
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Thedamping ratio decreases in Ash 3 spasticity.
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And inAshworth 4, even if there is maximum increase gain, the damping ratio is nothigh because the damping ratio could not be calculated due to the second beatscancellation.
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When allthe data is put together, what we see is quite interesting. The damping ratiois below normal in Ash 1 and 2, but it is up to the normal level in Ash 3. So,decaying of the oscillation is low in the situation increasing gain of thereflex but the reverse occurs in Ash 3 and 4.
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We can conclude that as the reflex gainincreases, decaying of the oscillation is lowered.
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Similarly,if you look at the pendulum counts, they increase with high reflex gainbut reverse in Ash 3.
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We cansummarize by saying that; p ; Related to the gain of the stretchreflex and f ; Related tothe delay of the stretch reflex afferents (paths).
So, inresponse to the question “Why do we have reflex oscillations?” we couldsay, “Because our reflexes have reflex gain and a delay in the reflex afferentpath.”
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I wouldlike to come back to the old story.
Stein andOguztöreli’s model can explain the oscillation phenomenon by gain and delay ofthe reflexes.
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With a very nice prediction in this model they showedthat the afferent path of the stretch reflex is not one-way. If there are three different afferent paths,they change the situation relating to the oscillation of the system. Through differentdelays and different reflex gains, afferents lead up to stabilize theoscillation.
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Stein andOguztöreli put forward the theory that sharing the rates of p and f betweendifferent paths can have stabilizing effects. As is graphed in this figure, each individual path is prone tooscillation with its own reflex gain, the cumulative effects of the differentpaths suppress oscillation and the system becomes more stable.
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Perhaps “Whydo we have reflex oscillations?” is not the right question. It might be better to ask: “Why don’t wehave reflex oscillations in normal conditions?” The answer is multiple delaysand divided gain in multiple paths. This phenomenon may be referred to as“stabilizing factors”.
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Thank youfor your attention, I hope I finished on time.