ELEKTROTHERAPI ON SHOULDER PAIN

Shoulder pain syndrome that is very complex in terms of cause and specifications of common network when the network structure of the body (musculoskeletal) lesions, almost always followed by tissue damage. Damage to a network will result in the stimulation of pain receptor (nociceptor) as a "defense mechanism" that goes into the process of inflammation. But the condition / specific inflammatory lesions very disturbing functional activity even at physiological inflammation inflammatory process followed the healing process (repair).

In certain circumstances may be pathological inflammation or chronic so it needs proper handling. So on the condition of sports injuries will always appear some symptoms such as:

painful

swelling

tissue damage collagen and soft tissue

disruption due to damage to the structure of joint stability stabilizer

even disruption due to decreased function of the reaction coordinate arthrokinetik

disfunction

Here are some factors that need to be identified as the cause of pain in the musculoskeletal system according to the "physiological Mechanisms"

Nociceptor mechanism

Nerve root compression or (neuropathic)

Trauma (deafferentation pain)

Inappropriate function in the control of muscle contraction

Psychosomatis mechanism

Often we see, the causes and symptoms of clinical pain in the muscles and bones are mixed and some of these factors are due to nociceptor and pain in the joints of the spine. Also neuropathic pain from diskuis hernatus and pain due to hipertonus reflex reaction of the spinal muscles. In this case there is also the possibility psychosomatis factor.

Muscle Spasms and Pain

Classification of Pain Mechanisms According to pathogenetic

Nociceptor pain: Specialized sensory nerve endings excited by pathophysiological processes eg inflamed joint

Neuropathic pain: Become Afferent nerve fibers directly responsive to stimuli after damage by compression or biomechanical disorders eg herniated disk diabetic polyneuropathy

Deafferentation pain: Neurons in the central nervous system after hyperexcitable Become loss of output, eg root avulsion, nerve transection.

Reactive pain: nociceptor excitation by dysfunctional or motorcycle or symphatetic efferent reflex Mechanisms, eg hypertonus sympathetic dystrophy algodystrophy

Psychosomatis pain: Psychic and psychosocial problems or aggravate existing pain are Expressed in the language of pain

Physiological mechanisms of pain in the musculo-skeletal system

Nociceptor

Sensory elements which can send signals to the CNS will be the things that are potentially harmful. Very much present in our body afferent fibers it consists of:

A delta fibers, the nerve fibers with thin myelin

C fibers, nerve fibers without myelin sheath

Not all fibers are nociceptors sebagal function, there is also that reacts to heat stimuli or mechanical stimulation. Instead nociceptor large sensory fibers, such as A Alpha, Beta A or Group I, II. Large sensory fibers is working on "proprioception" and "motor control".

Nociceptor very sensitive to chemical stimuli (chemical stimuli). At our bodies are "algesic chemical substance" as Bradykinine, Potassium ions, Serotonin, Prostaglandins and others.

Substance P, a Neuropeptide released from peripheral nerve endings nociceptive C-type, resulting in increased local microcirculation, plasma extravasation. This phenomenon is called sebagal "neurogenic inflammation" that the state generate noxious advanced / chemical stimuli, thus causing pain.

Motor system dysregulation that causes pain. We know hipertonus muscles can cause pain. In general, the muscles involved are eg rotaor shoulder cuff brachial biceps muscle stabilizers, elevator scapula, thermocleido mastoid.

Nociceptive stimulus received by the afferent fibers to the spinal cord, resulting in muscle contraction due to a "spinal reflexes motors". Nociceptive stimuli can be found in several places such as the skin, visceral organs, even the muscles themselves. Reflex itself is actually beneficial for our body, such as "withdrawal reflex" is a survival mechanism of the organism.

Besides these functions we also realize that the contraction of the muscles can improve pain earlier, through nociceptor stimulation on the muscles and tendons. The more frequent and stronger the nociceptor stimulated, the stronger reflex activity to the muscles. This will increase the pain, giving rise to a state of "vicious circle" in condition will be exacerbated by the presence of local ischemia, as a result of strong muscle contractions and continuous or inadequate microcirculation as, a result of dysregulation of the sympathetic system.

In this situation, the modulation of pain is at the receptor level characterized by symptoms of severe pain, inflammation, with high or low activity. Pain based on the region surrounding the glenohumeral joint lesions such as anterior part. In the following situations if the pain can be spread sympatis uncontrolled activation function called neurovegetative disbalance as contained in the image.

Physiological mechanisma of pain in the musculo-skeletal system

Look at the picture input from the afferent fibers of the visceral organs, skin, joints, tendons, muscles or impulse from the brain down to the spinal stimulation can affect (excitability) of Alpha and Gamma motor neurons result in muscle contraction (muscle stiffnes) eg increasing input nociceptive of intratorakal will increase the muscle tone of the muscle that gets somatic innervation thorakal example: intercostalis, and serratus anterior muscles that cross the structure of the C5 and C6 segments.

Besides nociceptive input from the joint capsule can improve the "reflex excitability" of some antagonist muscles concerned with the movement of the joints so that it can block the joint is also called neurogenic block. Greatest influence comes from the brain, stress and emotions can lead to "descending excitatory pathway", thereby stimulating the reflex increase of postural muscles Cervical region. At this situation is spinal nociceptor activation towards supraspinal pain referral that will show on the somatic system and peripheral sympatis.

In somatic neurophysiological shoulder joint gets somatic innervation of the cervical segments 5, 6 (C5 and C6). This segment also provides innervation to the distribution structure of muscles, joints and skin (see scheme preganglioner neuron segmental C5, C6 and segments Th4, Th5, Th6).

Neurofysiologis indicate that the C5 and C6 segments do not have the sympathetic system that innervate the blood vessels in the somatic structures disarafi. Vascular supply to meet the needs of all somatic innervation structure of C5 and C6 branches receive innervation from peripheral sympatis thorakal derived from segments 5, 6 (Th5, Th6).

Thorakal 5, 6 also have to be responsible for the somatic innervation of structures: muscles, skin, joints and nerves intratorakal and intra-abdominal organs are: heart, lung, gastric, and liver osophagus.

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it can simply be understood that nociceptor activation in the shoulder joint can refer to the system will result in somatic pain referral to the structure of muscles, joints, skin gets somatic innervation segments C5, C6, such as shoulder pain can cause great pain in the muscles and the muscles rotator rhomboideus cuff.

In this situation the muscle spasm can also spread to other regions both in the structure of muscles, joints and skin so that pain is diffused. (See image below). Intervention simply physiotherapist should provide the level of spinal modulation of pain by TENS.

In case of further referral of pain to achieve thorakal segment. Thorakal segment is responsible for the region of somatic somatic innervation thorakal itself and is responsible for symnpatis peripheral somatic innervation of the structure of the C5, C6 and original sympatis intrathorakal and intra-abdominal organs. With the other terms of the source of pain syndrome shoulder pain can originate from peripheral somatic segmentation, sympatis sympatis peripheral and original.

Of the clinical picture is often encountered shoulder pain (pain syndroma shoulder) is often found that there is no entrapment of segments C5 and C6 or entrapment in the fourth thoracic syndrome is often referred to as Th4. But do not rule out the possibility that the organ thorakal felt shoulder pain infare myocord eg acute or angina pectoralis. On the other hand chronic stomach pain (chronic gastritis) is also often gives pain to the scapula thoracic region is characterized by a very strong spasms.

Based on the brief description of the picture in neurofysiologi shoulder pain and clinically it can be understood in a simple theory of pain as follows:

Theory of Pain

There are three theories that attempt to explain how it arises and feels pain, namely:

Specific theory

Theory that suggests that the receptor is devoted to receive a specific stimulus, which then delivered through the fibers A delta and C fibers in the peripheral and spinothalamikus tract in the spinal cord leading to pain centers in the thalamus. Tori is not put forward a psychological component.

Theory of pattern (pattern)

This theory states that pain is a major element in the pattern of sensory information. Patterns of action potential arising from the presence of a stimulus arises at the level of the peripheral nerves and certain stimuli cause certain patterns of action potential. Patterns of action potential for pain is different from the pattern for the sense of touch.

Gate control theory (gate control)

1965 Melzak and Wall gate control theory suggests that many received a lot of experts. This theory is developed in terms of neurophysiological mechanisms related to the control of peripheral and central pain. The concept essentially combines specific theory and the theory of pattern coupled with the interaction between peripheral afferent and different modulation systems in the spinal cord (subtansia gelatinosa). It also suggests descending modulation system (from the center to the periphery).

According to this theory, consists of two groups of afferent fibers, namely the large-diameter (A-beta) and small-diameter fibers (A-delta and C). Both of these afferent groups interact with substantia gelatinosa serves as a modulator (gate control) against A-fallow, A-delta and C

If subsatansia gelatinosa (SG) is active, the gate will close. Conversely, when the SG decreased its activity, the gate opens. SG is active and least dependent on afferent group which aroused.

If the large-diameter fibers stimulated, SG becomes active and the gate closes. This means that the central excitatory towards transitting through cell (T-cell) stalled or declined. A-beta fibers are conductive non-nociceptive stimulation (not pain) such as touch, proprioceptive.

When groups of small diameter (A-delta, C) aroused, SG will decrease activity so gerabang open. A-delta and C fibers of the carrier is nociceptive stimuli, so that the fibers are stimulated, the gates will open and the pain stimuli will be forwarded to the center.

Pain modulation

Pain is a symptom that drives a person to seek help health services including physiotherapy. To that end, the physiotherapist needs to understand the mechanisms of how pain is eliminated or reduced, in other words how to modulate pain.

There is some level in the afferent where pain can be modulated.

a. The receptor

At this level, the target modulation in the peripheral receptors. Modulation obtained by:

Lowered excitability receptors (eg by cooling)

Eliminate the incentive factor receptors, eg by expediting the process of disposal through the bloodstream.

Lower levels of gamma-neuron activity, for example by heating

b. Spinal level

At this level, the target modulation in subtansia gelatinosa with the aim of providing the transmission of pain stimulus inhibition. By tori gate control by Melzak and Wall, then to be able to eliminate or reduce pain, SG must be enabled so that gerbagn closed. To be able to shut the gate, there needs to be stimulation of large-diameter fibers (A-beta) with non-reciceptive stimuli, for example by:

TENS

Gentle manipulation

c. Supraspinal level

At this level of pain control is done by fairies aquaductal gray matter (PAG) in the mid brain. PAG sends stimulus to the nucleus raphe magnus (NRM) is further to the spinal cord dorsal horn (PHC). NRM will inhibits afferent A-delta. Besides NRM also also spur the emergence of serotonin. PAG modulate pain through endorphin production in PHC through NRM. Through the locus ceruleus (LC) in the lateral and medial brachial nucleus. PAG also modulates pain with enkephalin in PHC. Mayer and Price found that high voltage Low-frequency TENS produce endorphins (endogenous morphine like substance, identical to opium). With the above description, the modulation of pain at supraspinal level there are 2 possible mechanisms involved, namely the path endorphine and serotonin pathways.

d. Central level

At the central level, cognitive and psychological components play a role in modulating pain. This is determined by one's attitude toward pain and emotions that control man army who are fighting not nerasakan severe pain despite suffering serious injuries. This suggests that pain involves two aspects: sensory and psychological. Thus the central nervous system also plays a role in modulating pain.

The concept of place "dumping pain" with electro therapy

Strategy, based on knowledge of the course of therapy pathogenesis of pain before, for example when the pain of inflammasi or trauma, the therapy with the goal of reducing and reducing pain inflammasi said to be very precise, for example degan TENS, SWD Interference and pulse.

But of course we will also reduce hipertonus muscles in that location. Treatment to decimate stimulation (excitation) in the interneuronal pool or on the motor neuron itself will decrease the activity of the motor neurons so that muscle tension (muscle tension) also loosened.

This method would be more appropriate therapy using electrical stimulation with electrical current menengan frequency or frequency. high, such as interference, SWD, and so on.

Way to reduce this stimulation can be obtained by:

Meghambat impulse afferent fibers carrying pain (nociceptive) or type III afferent fibers b / IV (A delta., And C) through afferent fibers of type II / III a. This method can be done, using current or diadinamik interference with local application engineering, regional, segmental or trigger point. (Spinal Modulation)

Activate the inhibitory neuron system (inhibitory neuronal system) down to supraspinal sensory cells (dorsal horn) spinal cord interneuronal pool in the spinal cord. This method is known as the theory of "Gate Control". (Spinal Modulation)

3. Enabling system neurovegetatif

This method can use electrical stimulation with low frequency currents flow eg 2-5 and intermediate frequency (current interfernsi)). In principle, it will stimulate the release of substance P on nociceptive useful as vasodilatator peripheral vascular system so that there will be improved vascularity. While to stimulate nociceptor can use mechanical energy or electrical energy generated by the U.S. or by pulse electric current progressive (2-5 flow, flow interference). Method of application can be done in combination with ultrasonic inference in order to find a point that is less sensitive to stimuli can be detected with the current low frequency or high frequency electrical currents alone. The sensitive spot stimulation can be found along the vertebrae known as the "trigger point". Quality can be a trigger point allodynia, hyperaesthesia and hyperalgesia. Neurovegetative activation application can be done with the method or methods of segmental segmental somasis sympatis. (Supra Spinal Modulation)

Improve the process of inflammation (Modulation Peripheral / Receptor)

Basically any inflammation will damage the collagen network, so as to improve the regeneration of collagen network needs to know the healing phase of injury / soft tissue lesions, which include:

a. Phase of tissue damage

b. Phase bleeding

c. Phase of inflammation

d. Phase regeneration

e. Phase prolferasi, production, remondelling? recover

The use of high frequency current (U.S., SWD) is helpful in every fasem-altermal thermal stimulation process locally, regionally and segmental

In addition to the use of U.S. and or SWD, we must always pay attention to current events and a condition.

On the application of electrotherapy, need to understand at least three (3) aspects:

i. Berliubungan technical aspects with the basic physics of the device used elektrbterapi.

ii. Aspects of the network specification to be treated, to determine the indications and contra-indications and therapeutic treatment dose.

iii. Aspects of the pathogenesis of a lesion or abnormality that aims to determine the therapeutic dose.