In my presentation, I will be addressing an old topic, but I will try to turn the old topic around and look at it in a new way, so you could say this is also a kind of oscillation.
In my presentation, I would like to discuss two oscillations.
1) Ankle clonus, which is usually accompanied by spasticity and upper motor lesions,
2) patellar pendulum, which is triggered by the patella T reflex
Clonus does not only occur in pathological conditions. After long walks, ankle clonus could be observed in healthy/normal subjects.
As we see in this video, clonus was observed following quick ankle dorsal flexion and when the foot was held in this position. Clonus can vary from 1-2 beats 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 pendulum oscillations can be observed under both normal and pathological conditions.

Rhythmic Oscillations are a prominent feature of all biological systems,
They can be summarized in three parts;

1) mechanical oscillations.
2) reflex oscillations; the most typical example of this is clonus and some of the tremor is also considered in this context.
3) Central oscillations; observed in Parkinson's disease.
In general, for all oscillations, describing function is "y (t) = A ept sin (2 π ft + φ)" .
The important constants in this equation are:
A: A constant that defines the amplitude.
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,

In any system, there are only three classes of oscillations;
1) Growing oscillations,
2) Decaying oscillations,
3) Maintained oscillations.
Factors which 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.
Different methods can be used for the recording and examination of oscillations.
A significant part of our work, which I will present here, is examined by image and motion analysis.

Sustained ankle clonus recordings contain important information. As you can see, in an independent recording, very stable oscillation can be obtained.
During Achilles clonus. Here we can see two of the fundamental ankle joint movements, plantar flexion and dorsal flexion of the foot.
The tibialis anterior muscle is the effector muscle for dorsal flexion and the gastrocnemius-soleus muscles are the effector muscles for plantar flexion. These two antagonistic muscles have a spinal level relationship and are quite straightforward.
The phase diagrams of the ankle clonus show that the dorsal flexion and plantar flexion parts of the movement each have different characteristics.
This is quite an interesting case:
The patient had right hemiplegia and spasticity due to a cerebral vascular accident and, sadly, he/she also had total axonal degeneration of the right peroneal 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 and afferents and efferents of the clonus are related to the tibial nerve.

In this part of my presentation I will try to convey what we know on the factors that determine the frequency of ankle clonus reflex oscillations. Different clonus oscillations can be observed in the human body.
If you review these frequencies
We can clearly understand from this record that the ankle clonus frequency is 5-6 Hz.
Surface EMG recordings from the soleus and tibialis anterior muscle activity and acceleration of the ankle during sustained clonus. With three different epochs of these records frequency are in the 5-6 Hz range.
Using two different recording techniques we recorded 31 and 18 different époque of ankle clonus. The frequency of the clonus is quite stable in a range of frequencies.
In addition, as observed clearly in these records, the load affects the frequency of clonus.
Another type of clonus is patellar clonus. By rapid 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.

A similar frequency characteristic was detected by goniometric recordings in patients with advanced spasticy. The continuous activity in the biceps femoris muscle is particularly interesting.
When alternating discharges are observed in agonists and antagonist muscles, the frequency drops to 8.
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 actively participating in the oscillations.
One rare type of clonus is jaw clonus. It has been observed in spastic patients, reaching frequencies of 12 Hz.. In this case, jaw clonus is triggered by the jaw T reflex.
If we consider all of the above cases, we can see how frequencies 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 and efferent pathway.
So, the frequency of the reflex oscillation correlates with the length of the path.

While there is no uncertainty about the efferent path of the reflex, 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 comes up increases and a relaxation period follows the response. A vicious circle is induced by stretching again.
Furthermore, during this period, two different moving components, such as the DF and PF are observed. We can predict that the DF and PF would be the same with half of this period.

This record clearly shows the relationship between the foot position changes and the response in the soleus muscle.
We recently described a reflex response induced by stretching the soleus muscle. Stimulation of the peroneal nerve brings about a medium latency response. We defined it as the soleus MLR that is triggered by a sudden dorsal flexion of the foot.
If the tibial nerve is stimulated from the popliteal fossa, the soleus H reflex is recorded. However, when the common peroneal nerve is stimulated supramaximally from the fibular head, there is a late response in the soleus muscle which is longer than the soleus H reflex.
The response latency was measured using an accelerometer. The latency from the beginning of stretching the soleus muscle by foot dorsal flexion is about 55 ms.
If the peroneal nerve is stimulated at the fibular head and the foot is kept at a position of 90 degrees extension, soleus MLR is obtained and, subsequently, clonus beats are observed in a spastic patient. I want to draw your attention to the similarity of responses to MLR and clonus.
When the foot is in the dorsal flexion position, the soleus MLR corresponds directly with the clonus beats. However, during plantar flexion, the soleus MLR and clonus beats are lost.
In this study we examined the similarities between clonus beats and the soleus MLR in terms of latency and amplitude. We emphasized the relationship between these two responses.
The similarities between stretch induced ankle clonus and peroneal nerve stimulation induced soleus MLR give a chance for speculation about the afferents of the responses.
Even if previous publications considered mainly Group I afferents as clonus afferents, we propose Group II afferents to be evaluated in the formation of clonus because of findings about soleus MLR afferents.
FCR MLR is an example of a response in the upper extremity. Stimulation of an antagonist muscle nerve results in a medium latency response by the agonist muscle. Radial nerve stimulation causes the EDC muscle to contract and MLR is achieved by latency much later than the FCR H reflex.
Clonus can be obtained through radial nerve stimulation during wrist extension, as with lower extremities ankle clonus.
Latency of the response obtained from the FCR is about 42-43 ms. However, FCR -H or T reflex latency does not exceed 20 ms.
In the lower extremities, Patellar clonus could establish correlation with MLR, such as ankle clonus. In this case, clonus can be obtained by femoral nerve stimulation.
The medium latency response is about 50 ms at the antagonist Biceps femoris muscle during the patellar T reflex.
However, latency of the H-reflex obtained by femoral nerve stimulation is about 15-20 ms. Clearly it is much shorter than the MLR latency.
And bringing together all of these values​, an interesting comparison can be made with clonus latencies. We have already mentioned the values ​​of clonus frequencies.
H / T reflex latencies and clonus periods were compared to MLR latency. The Group II afferents constitute a more convenient time for the clonus period as opposed to Group Ia afferents.
When the measured clonus frequencies are compared to the calculated frequencies that are formed by Group Ia and Group II afferents, we can say that Group II afferents contribute to the clonus.
We examined the effects of the afferent paths on the frequency of clonus. Returning to the formula for oscillation again; we can ask what the factors that determine p are. So, which factors determine dumping or building oscillation?
Factors which 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.
Sustained clonus has to have p=0 value because it is a maintained oscillation.
It seems the Pendulum has less than 0 p value.
We can calculate the damping ratio by dividing the amplitude of the first and second beats. In Ash 1 spasticity which mildly increase gain of the reflexes.
In Ash 2 spasticity, the damping ratio is increased. The gain of the reflex is much higher than in Ash 1 spasticity.
But even if the gain of the reflex is increased, the damping ratio is decreased in Ash 3 spasticity.
The damping ratio decreases in Ash 3 spasticity.
And in Ashworth 4, even if there is maximum increase gain, the damping ratio is not high because the damping ratio could not be calculated due to the second beats cancellation.
When all the data is put together, what we see is quite interesting. The damping ratio is 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 the reflex but the reverse occurs in Ash 3 and 4.
We can conclude that as the reflex gain increases, decaying of the oscillation is lowered.
Similarly, if you look at the pendulum counts, they increase with high reflex gain but reverse in Ash 3.
We can summarize by saying that; p ; Related to the gain of the stretch reflex and f ; Related to the delay of the stretch reflex afferents (paths).
So, in response to the question Why do we have reflex oscillations? we could say, Because our reflexes have reflex gain and a delay in the reflex afferent path.
I would like to come back to the old story.
Stein and Oguztöreli's model can explain the oscillation phenomenon by gain and delay of the reflexes.
With a very nice prediction in this model they showed that 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 different delays and different reflex gains, afferents lead up to stabilize the oscillation.
Stein and Oguztöreli put forward the theory that sharing the rates of p and f between different paths can have stabilizing effects. As is graphed in this figure, each individual path is prone to oscillation with its own reflex gain, the cumulative effects of the different paths suppress oscillation and the system becomes more stable.
Perhaps "Why do we have reflex oscillations?" is not the right question. It might be better to ask: "Why don't we have reflex oscillations in normal conditions?" The answer is multiple delays and divided gain in multiple paths. This phenomenon may be referred to as "stabilizing factors".