Brachial plexus paresis

Anatomy
The brachial plexus (C4–Th1) is formed by the connection of the anterior branches of C5–C8, to which the connector from C4 arrives on the cranial side, and most of the fibers from Th1 connect to them caudally. Connections from C4 to Th1 are individually individuálně variable. The ventral branches of C5–Th1 join into three primary bundles (truncus superior, medius, and inferior).

These bundles pass through the fissure between the scalenus anterior and medius muscles (fissura scalenorum) together with the subclavian artery and are placed above the artery. The primary bundles plaitably descend further caudally and laterally behind the clavicle into the axilla. The clavicle divides the entire plexus into pars supraclavicularis and pars infraclavicularis. From the pars supraclavicularis depart the motor nerves supplying mainly the girdle muscles.

Below the clavicle, the three primary bundles (trunks) of the brachial plexus are further divided, each primary bundle is divided into an anterior and a posterior branch, the joining of these branches creates secondary bundles - fasciculi plexus brachialis. These gradually bypass the trunk of the axillaris artery, and their own peripheral nerves only emerge from them.

Brachial plexus paresis
Brachial plexus paresis is a peripheral paresis,that most often arises due to ischemic-compressive or traumatic etiology. Considering that the brachial plexus conducts both motor and sensitive and autonomic innervation, we find not only motor but also sensitive and autonomic symptoms. We distinguish between complete and incomplete paresis of the brachial plexus.

Complete brachial plexus paresis
With a complete lesion of the entire plexus, weak plegia of the entire upper limb (plexus, arm and hand) occurs. All that remains is the shoulder elevation ability. Hearing is impaired except for the inside and back. It can beHorner's syndrome from disturbed sympathetic innervation. There is a C5-8 areflexia, in a chronic stage of severe atrophy. The stated condition often has traumatic causes, such as the result of tearing out the roots from the spinal cord.

Incomplete paresis of the brachial plexus
We distinguish upper and lower type paresis.


 * Upper type palsy – Duchenne-Erb's palsy

In paresis of the plexus of the upper type (C5–6), there is a motor lesion in the area of ​​the shoulder and partially of the arm. Motor innervation of the own hand is normal. We characterize the disorder as "a good hand on a paralyzed shoulder and arm." The position of the limb is referred to as the so-called "waiter tip position", the shoulder is in adduction, internally rotated, the elbow is extended in pronation and the wrist is in flexion. In newborns, this palsy can be manifested by an asymmetric Moro reflex. In newborns, the most common cause is incorrect passage through the birth canal.There is C5–6 areflexia (bicipital and brachioradial).

We characterize paresis of the lower type (C8–Th1) as a “paralyzed hand on the good shoulder and arm”. C8 areflexion (r. finger flexors). Contemporary Horner's syndrome is common. Příčinou je silné táhnutí paže vzhůru nad horizontálu).
 * Paralysis of the lower type - Klumpkova-Dejerin's palsy

Causes of emergence
Damage to the plexus occurs for a variety of reasons. Traumatic causes, especially motorcycle traffic accidents, are among the most common. The most common injury is the traction mechanism. It occurs after violent stretching, e.g. after motorcycle accidents. The prognosis is very poor.
 * Traumatic causes

In case of traumatic paresis, it is important to distinguish between a traumatic lesion of the plexus and the pulling out of the roots from the spinal cord. A supraganglionic lesion has a minimal chance of repair. A neurosurgical solution is possible for infraganglionic lesions Postpartum paresis of the brachial plexus is caused by a traction mechanism during difficult births. The most common are the upper type.

These syndromes are determined by the anatomical conditions in the area of ​​the upper thoracic aperture, where there is often pressure damage to the nerve-vascular structures passing through here. It is not always possible to prove exactly the pathogenic mechanism
 *  Upper thoracic outlet syndromes (TOS = thoracic outlet syndrome)

These syndromes include:
 * cervical rib syndrome,
 * scalene syndrome,
 * costoclavicular syndrome,
 * hyperabduction (Wright) syndrome,
 * paresis of the brachial plexus from oppression by the tumor.

It should be borne in mind that this may be a combined disorder. Upper thoracic aperture syndrome itself is a combination of several functional disorders. A key role is played by muscle imbalance in the area of ​​the shoulder girdle, causing tension in the upper fixators of the scapula, and the upper type of breathing, during which the scalene muscle is overloaded. This increased tension is transferred to the muscles of the arm and forearm, where it manifests itself most in the form of epicondylalgia. Soon there will also be limited mobility of the movement segments of the spine and the joints of the upper limb and this increases the muscle spasm again. Pain radiating from the neck to the shoulder precedes pain in the elbow region and in the styloid process radii, then follows the carpal tunnel syndrome and associated dysesthesias caused by the blockade of the first rib, which again causes spasm of the scalenes and the upper part of the trapezius muscle.
 * Malfunction

Related Articles

 * brachial plexus
 * Horner's syndrome