CHAPTER 28

Muscle Tone

Muscle tone has been defined as the tension in the relaxed muscle or the resistance to passive movement when voluntary contraction is absent. Because of resting tone, normal muscles have slight resistance to passive movement even in the relaxed state. The inherent attributes of muscle tissue—such as viscosity, elasticity, and extensibility—contribute to resting tone. Even apparently relaxed muscle fibers have a constant slight fixed tension by which they hold their resting position, resist changes in length, prevent undue mobility at joints, and are in position to contract when necessary. Resting muscle tone is greatest in the antigravity muscles that maintain the body in an erect position.

The resting level of tone in a muscle is dependent on activity in the spinal cord segment that innervates it, primarily the gamma motor neuron. Efferent impulses from the gamma motor neuron set the level of contraction of the intrafusal fibers of the muscle spindles. Spindle afferents in turn convey impulses to the spinal cord segment to complete the gamma loop. Descending influences from higher motor centers regulate and modulate the activity at the local spinal cord segment. All of these factors interact to determine the level of resting tone. When a muscle with normal segmental innervation is passively stretched, reflex shortening may occur; this is the stretch reflex.

The background level of muscle tone maintains normal resting limb positions and attitudes. Active muscle contraction takes place on the background of the resting level of muscle tone, and normal background tone is important for proper coordination of movement. Activity mediated by the reticular formation, the otolith organs, the vestibular apparatus, and other higher centers is important in maintaining the steady contraction of the antigravity muscles that is necessary to the standing position, as well as to other postural and righting reflexes.

Tone may be affected by disease at different levels of the nervous system. Interruption of the local spinal reflex arc abolishes resting muscle tone. Most types of hypertonicity can be abolished by interrupting either the gamma efferent impulses to the intrafusal fibers or the afferent impulses from the muscle spindles. Denervated muscle is flaccid and behaves as noncontractile tissue. Loss of impulses from the supraspinal pathways that normally inhibit lower reflex centers usually causes an increase in tone. Loss of the normal balance between higher facilitatory and inhibitory centers may either decrease or increase tone.

Examination of Tone

Tone is difficult to assess. The determination of tone is subjective and prone to interexaminer variability. There are no methods that can measure tone quantitatively. The determination is based solely on the clinical judgment of the examiner; accurate assessment of tone requires clinical experience. It is difficult to separate slightly increased tone from poor relaxation in a tense or apprehensive patient. Tone is especially difficult to evaluate in infants, where there may be wide variations in apparent tone on different examinations, in either health or disease.

The examination of tone requires a relaxed and cooperative patient. Small talk may help the patient relax. Simple observation may reveal an abnormality of posture or resting position that indicates an underlying change in tone. Muscle palpation is sometimes useful, but well-muscled individuals may have firm muscles despite normal resting tone, whereas in other individuals, the muscles may feel flabby despite an underlying hypertonicity. Muscles may have a firm consistency to palpation because of edema, inflammation, spasm due to pain, or pseudohypertrophy.

The most important part of the examination of tone is determination of the resistance of relaxed muscles to passive manipulation as well as the extensibility, flexibility, and range of motion. Abnormalities of tone are more easily detected in extremity than in trunk muscles. The limb is moved passively, first slowly and through a complete range of motion and then at varying speeds. The examiner may shake the forearm to and fro and note the excursions of the patient’s hand, brace a limb and then suddenly remove the support, or note the range of movement of a part in response to a slight blow. Bilateral examination of homologous parts helps compare for differences in tone on the two sides of the body.

Tone should be assessed by both slow and rapid motion and through partial and full range of motion, documenting the distribution, type, and severity of any abnormality. Certain specific maneuvers may be helpful in evaluation of abnormal tone.

The Babinski Tonus Test

The arms are abducted at the shoulders, and the forearms are passively flexed at the elbows. With hypotonicity, there is increased flexibility and mobility, and the elbows can be bent to an angle more acute than normal. With hypertonicity, there is reduced flexibility, and passive flexion cannot be carried out beyond an obtuse angle.

The Head-Dropping Test

The patient lies supine without a pillow, completely relaxed, eyes closed, and attention diverted. The examiner places one hand under the patient’s occiput and with the other hand briskly raises the head and then allows it to drop. Normally, the head drops rapidly into the examiner’s protecting hand, but in patients with extrapyramidal rigidity, there is delayed, slow, gentle dropping of the head because of rigidity affecting the flexor muscles of the neck. When meningismus is present, there is resistance to and pain on flexion of the neck.

Pendulousness of the Legs

The patient sits on the edge of a table, relaxed with legs hanging freely. The examiner either extends both legs to the same horizontal level and then releases them (Wartenberg pendulum test, see Video Link 28.1) or gives both legs a brisk, equal backward push. If the patient is completely relaxed and cooperative, there will normally be a swinging of the legs that progressively diminishes in range and usually disappears after six or seven oscillations. In extrapyramidal rigidity, there is a decrease in swing time but usually no qualitative change in the response. In spasticity, there may be little or no decrease in swing time, but the movements are jerky and irregular, the forward movement may be greater and more brisk than the backward, and the movement may assume a zigzag pattern. In hypotonia, the response is increased in range and prolonged beyond the normal. In all of these maneuvers, a unilateral abnormality will be more apparent.

The Shoulder-Shaking Test

The examiner places her hands on the patient’s shoulders and shakes them briskly back and forth, observing the reciprocal motion of the arms. With extrapyramidal disease, there will be a decreased range of arm swing on the affected side. With hypotonia, especially that associated with cerebellar disease, the excursions of the arm swing will be greater than normal.

The Arm-Dropping Test

The patient’s arms are briskly raised to shoulder level and then dropped. In spasticity, there is a delay in the downward movement of the affected arm, causing it to hang up briefly on the affected side (Bechterew’s or Bekhterew’s sign); with hypotonicity, the dropping is more abrupt than normal. A similar maneuver may be carried out by lifting and then dropping the extended legs of the recumbent patient.

Hand Position

Hypotonicity, especially that associated with cerebellar disease or Sydenham’s chorea, may cause the hands to assume a characteristic posture. With the arms and hands outstretched, there is flexion at the wrists and hyperextension of the fingers (“spooning”) accompanied by moderate overpronation. With the arms raised overhead, the overpronation is exaggerated with the palms turned outward. This overpronation phenomenon differs from the pronator drift sign, in which the overpronation is due to weakness of corticospinal innervated muscles or increased tone in the pronator muscles.

Myotatic Irritability, Myoedema, and Tenderness

In addition to the inspection, palpation, and resistance to passive motion used in the assessment of tone, it is sometimes useful to observe the reaction to direct percussion of the muscle belly. The idiomuscular contraction is the brief and feeble contraction of a muscle belly after it is tapped with a percussion hammer, causing a slight depression even when the deep tendon reflex (DTR) is absent. Myotactic irritability has been defined as both the response to direct percussion as well as the ability of a muscle to contract in response to sudden stretch.

The response to direct muscle percussion in normal muscle is very slight and, in most muscles, is seen or felt with difficulty. The reaction may be more pronounced in wasting diseases, such as cachexia and emaciation, and in some diseases of the lower motor neuron. Hyperexcitability to such stimulation occurs in tetanus, tetany, and certain electrolyte disturbances. Occasionally, after a muscle is percussed with a reflex hammer, a wave of contraction radiates along the muscle away from the point of percussion. A small ridge or temporary swelling may persist for several seconds at the point of stimulation. This stationary muscle mounding is known as myoedema. There is no accompanying electrical muscle activity. The idiomuscular contraction causes a slight depression, myoedema a rounding up. The mechanism of myoedema is poorly understood, but it is probably a normal physiologic phenomenon. Its presence alone does not indicate a neuromuscular disorder, but the response may be exaggerated in some circumstances, most notably hypothyroid myopathy and cachexia. Myoedema is electrically silent on electromyography. Hypothyroidism may also cause an electrically active muscle mounding and spreading contraction, manifest by a burst of normal motor unit action potentials upon percussion (for video, see Loomis et al.). Myotonia is a persisting contraction following mechanical stimulation of muscle that is quite different from myoedema (see below). In rippling muscle disease, there are wave-like muscle contractions evoked by muscle stretch that move laterally along the muscle over 5 to 20 seconds. The phenomenon is especially prominent in large proximal muscles (see Video Link 28.2).

During muscle palpation, muscle tenderness may sometimes be elicited. Muscle tenderness on squeezing the muscle belly, or even with very slight pressure, may cause exquisite pain. Widespread muscle tenderness to palpation may occur with inflammatory myopathy, especially polymyositis and dermatomyositis, in some neuropathies, and in acute poliomyelitis. Focal muscle tenderness occurs with trauma or overexertion of muscles.

Abnormalities of Tone

Pathologic conditions may cause an increase or decrease in tone. In addition, there are different varieties of hypotonicity and hypertonicity. Hypotonicity may develop from disease of the motor unit, the proprioceptive pathways, cerebellar lesions and in the choreas. The muscle may be flaccid, flabby, and soft to palpation. The involved joints offer decreased resistance to passive movement. The excursion of the joint may be increased with an absence of the normal “checking” action on extreme passive motion. If the involved extremity is lifted and allowed to drop, it falls abruptly. A slight blow causes it to sway through an excessive excursion. The DTRs are usually decreased or absent when hypotonia is due to a lesion involving the motor unit or proprioceptive pathways.

Hypotonia

When hypotonia is due to disease of the motor unit, there is invariably some degree of accompanying weakness. The hypotonia that results from central processes (e.g., cerebellar disease) does not cause weakness; muscle power is preserved even though hypotonia is demonstrable on examination. Infantile hypotonia (floppy baby syndrome) is a common clinical condition in which there is a generalized decrease in muscle tone, typically affecting a neonate. There are numerous causes, both central and peripheral.

Tone may also be decreased when disease affects the muscle spindle afferent system. Tabes dorsalis affects proprioceptive fibers in the posterior root and may cause muscle hypotonia with joint hyperextensibility. Hypotonia may occur with some lesions of the parietal lobe, probably because of disturbances of sensation. Hypotonicity may occur with various types of cerebellar disease but is never as severe as that which occurs with diseases of the lower motor neuron. Cerebellar hypotonia is not associated with weakness and the reflexes are not lost, although they may be pendular; there are no pathologic reflexes. Muscle tone is, of course, decreased in deep sleep, coma, and other states of impaired consciousness.

Sudden attacks of impaired muscle tone in an awake patient occur in akinetic epilepsy and in cataplexy. With atonic (akinetic) seizures, the attacks of sudden loss of muscle tone occur spontaneously, and the patient may fall to the ground (drop attack or drop seizure). Less severe attacks may cause only a head drop. In cataplexy, there are attacks of decreased tone after strong emotion, such as laughter or anger. With severe attacks, the patient falls to the ground but without loss of consciousness. With incomplete attacks, there may be slackening of facial muscles, jaw drop, head drop, slumping of the shoulders, or knee buckling without a fall. Cataplexy is usually a component of narcolepsy. Sleep paralysis is a state common in narcolepsy, in which a patient has diffusely decreased tone and is unable to move immediately after awakening from sleep. The hemiparesis that is present acutely following hemispheric stroke may be associated with hypotonia (cerebral or neural “shock”), which gradually evolves into hypertonia with the passage of time. Some conditions may cause abnormal joint laxity, which may be confused with muscle hypotonia (e.g., Ehlers-Danlos syndrome).

Hypertonia

Hypertonia occurs under many circumstances. It is a routine feature of lesions that involve the corticospinal tract after the acute stage. It can occur with diffuse cerebral disorders, with disease involving the extrapyramidal system, with disease of spinal cord interneurons (e.g., stiff-person syndrome), and even with muscle disorders in continuous muscle fiber activity syndromes. The most common causes of hypertonia are spasticity and rigidity. For a discussion and demonstration of spasticity versus rigidity from the 2015 Stanford Medicine 25 Skills Symposium, see Video Link 28.3.

Extrapyramidal Rigidity

Extrapyramidal rigidity is a diffuse increase in muscle tone to passive movement that occurs primarily with lesions that involve the basal ganglia. There is a fairly constant level of increased tone that affects both agonist and antagonist and is equally present throughout the range of motion at a given joint. Both flexor and extensor muscles are involved, with resistance to passive movement in all directions. The increased tone is equally present from the beginning to the end of the movement and does not vary with the speed of the movement. This type of rigidity is referred to as “lead-pipe.” The involved muscles may be firm and tense to palpation. After being placed in a new position, the part may remain there, causing the limbs to assume awkward postures. Both neural-mediated excitation of shortening muscles (the shortening reaction) and inhibition of stretched muscles contribute to the rigidity; which mechanism predominates is associated with the direction of movement. An increase in spinal interneuron excitability mediated through specific descending motor pathways may underlie parkinsonian rigidity.

In cogwheel rigidity, there is a jerky quality to the hypertonicity. As the part is manipulated, it seems to give way in a series of small steps as if the limb were attached to a heavy cogwheel or ratchet. The jerky quality of the resistance may be due to tremor superimposed on lead-pipe rigidity. Cogwheel rigidity is most commonly encountered in Parkinson’s disease and other parkinsonian syndromes. It appears first in proximal muscles and then spreads distally. Any muscle may be affected, but there is predominant involvement of neck and trunk muscles and the flexor muscles of the extremities. The rigidity of extrapyramidal disease may be brought out by the head-dropping, shoulder-shaking, and similar tests. The rigidity on one side may be exaggerated by active movements of the contralateral limbs (see Chapter 30).

In extrapyramidal disease, there is usually associated hypokinesia and bradykinesia, but no real paralysis. With repeated active movements, there is a gradual decrease in speed and amplitude. This may be brought out by having the patient rapidly open and close the eyes or mouth, open and close the hand, or oppose finger and thumb. Patients may also show slowness of starting and limitation of the amplitude of movement, loss of pendulousness of the arms and legs, inability to carry out rapid repeated movements or to maintain two simultaneous voluntary movements, and impairment of associated movements, such as swinging of the arms when walking.

Paratonia is an alteration in tone to passive motion that is often a manifestation of diffuse frontal lobe disease. It has been divided into inhibitory paratonia and facilitatory paratonia. Gegenhalten (inhibitory paratonia, paratonic rigidity) is a form of rigidity in which the resistance to passive movement seems proportional to the vigor with which the movement is attempted. The resistance of the patient increases in proportion to the examiner’s efforts to move the part; the harder the examiner pushes, the harder the patient seems to push back. It seems as though the patient is actively fighting, but the response is involuntary. It is said that the severity of gegenhalten can be judged by the loudness of the examiner’s exhortations to relax.

In the limb placement test, the examiner passively lifts the patient’s arm, instructs the patient to relax, releases the arm, and notes whether or not it remains elevated. The arm remaining aloft, in the absence of parkinsonism or spasticity, indicates paratonia. In facilatory paratonia (mitgehen), the patient cooperates too much. The patient actively assists the examiner’s passive movements, and the limb may continue to move even after the examiner has released it. In the modified Kral procedure, the examiner instructs the seated patient to relax and then passively flexes and extends the elbow several times through a full range of motion, releasing the arm with the patient’s hand at the level of the thigh. Further movement is scored on a scale of 0 (no movement) to 4 (elbow flexes fully or cycles of flexion and extension continue).

Using a Delphi procedure, experts agreed on the following definition of paratonia: paratonia is a form of hypertonia with an involuntary variable resistance during passive movement; the nature of paratonia may vary from active assistance to active resistance; the degree of resistance depends on the speed of movement (e.g., slow → low resistance, fast → high resistance); the degree of paratonia is proportional to the amount of force applied; and the resistance to passive movement is in any direction and there is no clasp-knife phenomenon. The Paratonia Assessment Instrument is an assessment tool for paratonia. For a training video on paratonia from the Geriatric Medicine Research Unit at Dalhousie University, see Video Link 28.4.

Spasticity

Spasticity is due to lesions involving the corticospinal pathways. The hypertonicity to passive movements differs from that of rigidity because it is not uniform throughout the range of movement, and it varies with the speed of movement. In addition, rigidity tends to affect all muscles to about the same degree, whereas the hypertonia of spasticity varies greatly from muscle to muscle. In spasticity, if the passive movement is made slowly, there may be little resistance. But if the movement is made quickly, there will be a sudden increase in tone partway through the arc, causing a catch or a block as though the muscle had impacted a stop. The relationship of the hypertonus to the speed of movement is a key feature distinguishing spasticity from rigidity. In the upper extremity, it is useful to look for spasticity involving the pronator muscles. With the patient’s elbow flexed to about 90 degrees and the forearm fully pronated, the examiner slowly supinates the patient’s hand. Unless spasticity is severe, there will be little or no resistance to this slow movement. If, after several slow repetitions, the examiner supinates the patient’s hand very quickly, there will be sudden resistance at about the midrange of movement, referred to as a “pronator catch.” The catch will then relax, and the supination movement can be completed. When hypertonus is severe, this maneuver may elicit pronator clonus.

A similar slow then rapid motion technique can be used to detect lower-extremity spasticity. With hands behind the knee, the examiner slowly flexes and extends the knee of the supine and relaxed patient. With adequate relaxation, the foot remains on the bed. After several slow repetitions, from the position of full extension, the examiner abruptly and forcefully pulls the knee upward. When tone is normal, the foot will scoot back, remaining in contact with the bed. When there is spasticity, the foot flies upward in a kicking motion (spastic kick). In the heel- or foot-dropping test, the examiner holds the patient’s leg flexed at the knee and hip, one hand behind the knee and the other supporting the foot. The foot is suddenly released. Normally, its descent is smooth, but when there is spasticity in the quadriceps muscle, the foot may hang up and drop in a succession of choppy movements.

Spastic muscles may or may not feel firm and tense to palpation. The range of movement of spastic extremities, and the degree of hypertonicity, often varies between examinations. No devices for quantitating spasticity exist, and clinical evaluation remains the most useful tool. The Ashworth scale is commonly used to quantitate spasticity on a scale from 1 (no increase in muscle tone) to 5 (affected part rigid in flexion or extension). Its validity and reliability have been questioned. In the presence of spasticity, the DTRs are exaggerated, and pathologic reflexes such as the Babinski and Chaddock signs can often be elicited. Clonus is often present. There may be abnormal associated movements.

Upper motor neuron weakness is often accompanied by sustained contraction of specific groups of muscles. With hemiparesis or hemiplegia, spasticity is most marked in the flexor and pronator muscles of the upper and the extensor muscles of the lower extremity; this causes a posture of flexion of the arm and extension of the leg, the characteristic distribution in cerebral hemiplegia (Figure 25.6). The arm is adducted, flexed at the elbow, and the wrist and fingers are flexed; there may be forced grasping. The lower extremity is extended at the hip, knee, and ankle, with inversion and plantar flexion of the foot; there may be marked spasm of the hip adductors. There is more passive resistance to extension than to flexion in the upper extremities and to flexion than to extension in the lower extremities. With bilateral lesions, the increased tone of the hip adductors causes a scissors gait, in which one leg is pulled toward the other as each step is taken (see Chapter 44). Although spasticity in the lower extremities usually affects the extensors most severely, in some patients with severe myelopathy or extensive cerebral lesions, there is marked hypertonicity in the flexor muscles, drawing the legs into a position referred to as paraplegia in flexion.

Catatonic Rigidity

The abnormal muscle tone in catatonia is in many respects similar to extrapyramidal rigidity and may be physiologically related. There is a waxy or lead-pipe type of resistance to passive movement that may be accompanied by posturing, bizarre mannerisms, and evidence of psychosis. It may be possible to mold the extremities into any position, in which they remain indefinitely. Catatonia may be induced by neuroleptics and may progress to neuroleptic malignant syndrome.

Decerebrate and Decorticate Rigidity

Decerebrate rigidity is characterized by marked rigidity and sustained contraction of the extensor muscles of all four extremities; in decorticate rigidity, there is flexion of the elbows and wrists with extension of the legs and feet. These are discussed further in Chapter 41.

Similar generalized rigidity with neck extension can occur with severe meningismus (opisthotonos), as well as in the tonic phase of a generalized seizure. Cerebellar or posterior fossa fits are probably attacks of decerebrate rigidity due to brainstem dysfunction related to mass effect in the posterior fossa.

Voluntary Rigidity

Various muscle groups may be consciously tensed or braced to protect against injury or in response to pain. It is often difficult to differentiate between tension that is truly volitional and that which is unconscious or involuntary, especially when related to excitement, alarm, pain, or fatigue. Tense, apprehensive individuals may show increased muscular tension at all times and may have exaggerated tendon reflexes. The reflex exaggeration is one of range of response, and the latent period is not shortened. Conversely, the reflexes may be suppressed because the semivoluntary contraction prevents normal movement.

Involuntary Rigidity

Rigidity that is involuntary, reflex, or nonorganic may resemble voluntary rigidity. Rigidity of psychogenic origin may be bizarre and may simulate any type of hypertonicity. Hysterical rigidity may simulate decerebration or catatonia. It may be extreme, with neck retraction and opisthotonos, the body resting with only the head and heels upon the bed (arc de cercle, Chapter 52).

Reflex Rigidity

Muscles may develop reflex rigidity, or spasm, in response to afferent impulses, particularly pain. Muscle spasm is a state of sustained involuntary contraction accompanied by muscle shortening. The abnormal contraction is visible and palpable. Common examples of reflex muscle spasm are the board-like abdomen of acute abdominal disorders, rigidity of the neck and back in meningitis, and the localized spasm in the extremities following trauma. Reflex rigidity may follow other sensory stimuli, such as cold. Muscle contracture may follow prolonged spasm. In some metabolic myopathies (e.g., McArdle’s disease), painful muscle cramps and spasms are brought on by exercise; the muscle cramp is a physiologic form of contracture due to abnormal metabolism and is not accompanied by electrical activity.

Myotonia

Myotonia is a disorder of the muscle membrane that can occur in many different conditions. Tone is usually normal when the muscles are relaxed, but contraction produces a temporary involuntary tonic perseveration of muscle contraction with slow relaxation ( Video 28.1). Sudden movements may cause marked spasm and inability to relax. In grip myotonia, the patient has difficulty letting go of an object after gripping it strongly. The myotonia usually decreases with repetition of the movement. In rare instances, the myotonia increases with repetitive movement (paradoxical myotonia). Percussion myotonia is elicited by tapping on the muscle. Percussion over the thenar eminence produces a prolonged tonic abduction and opposition movement lasting several seconds, over which the patient has no control. Tapping over the extensor digitorum communis to the middle finger causes the finger to snap into extension, after which it slowly falls over a much longer period of time than normal. Percussion myotonia can also be elicited over other muscles. Oblique elimination with a penlight may help to make the slowly disappearing depression or dimple more visible. Percussion of a tongue blade placed transversely on edge across the tongue may produce a segmental myotonic contraction that constricts the tongue circumferentially (napkin-ring sign, Chapter 20).

Other Types of Rigidity

Muscular rigidity may also occur in epilepsy, tetany, and tetanus. In epilepsy, there may be generalized rigidity during the tonic phase of the fit. Occasionally, there are tonic seizures with no clonic phase (tonic fits). In tetany, there is generalized irritability of the peripheral and central nervous systems, with tonic muscle spasms leading to localized or generalized hypertonicity, hypersensitivity to stimuli, cramps, and muscle twitching (see Chapter 52).

In tetanus, there is usually generalized rigidity with increased muscle tone in the entire body. In most instances, it begins in the face and jaw muscles and then spreads to affect the abdominal muscles, extremities, and spinal muscles, causing abdominal rigidity, extensor rigidity, and opisthotonos. In cephalic tetanus, disease manifestations occur primarily in head and neck muscles (for video, see You et al.). Both agonist and antagonist muscles are simultaneously hypertonic. Spasm of the muscles of mastication causes trismus (lockjaw). Retraction of the angles of the mouth causes the facial dystonia referred to as risus sardonicus. Paroxysms of muscle spasm progressively increase in intensity and propagate to other muscles. Spasms may occur spontaneously, after voluntary contraction or after mechanical, tactile, auditory, visual, or other stimuli. Between spasms, there is usually some persisting muscular rigidity. The reflexes are grossly exaggerated, and a light tap on a tendon may throw the limb into violent spasms. The clinical manifestations of tetanus are due to the action of the exotoxin of Clostridium tetani on the inhibitory internuncial neurons of the brainstem and spinal cord. In the stiff-person (stiff-man) syndrome, there are painful tonic muscular spasms and progressive rigidity of the muscles of the trunk, neck, abdomen, back, and proximal parts of the extremities. Other disorders causing increased muscle tone are discussed in Chapter 30.

Video Links

Video Link 28.1. Wartenberg pendulum test. https://www.youtube.com/watch?v=yYtGjvCcA7o

Video Link 28.2. Rippling muscle disease. https://www.youtube.com/watch?v=bdiwylu3Oro

Video Link 28.3. Discussion and demonstration of spasticity versus rigidity from the 2015 Stanford Medicine 25 Skills Symposium. https://www.youtube.com/watch?v=gLZoYLxdXCQ&index=5&list=PL5o6KWShAMajcL3piv2wiiVm0BIDyE9rL

Video Link 28.4. Training video on paratonia. https://www.youtube.com/watch?v=Z-NjgIPbuEU&t=89s

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