Anamnestic notes concerning exogenous causes of GE (cf. above): patients mainly report pain at the inner side of the elbow joint as main symptom, developing or deteriorating in motion of the elbow joint, especially against resistance, for example, in carrying a bag. In maximum extension of the elbow joint, for example, in playing golf and in carrying and lifting heavy weights, pain is reported as well. These pain radiations are also demonstrated by some patients (Fig. 2.15). Additionally minor pain radiation distally and proximally is reported as well as minor disturbance of sensibility and some impairment of crude strength and delicate motion.

The anterior pain area apart from a periosteal fibre of the forearm medial cutaneous nerve posterior branch is mainly innervated by final fibres of median nerve muscular branches destined for the humeral origins of the pronator teres muscle and the superficial finger flexor muscle (Fig. 2.1 right). These structures can be confirmed by a corresponding nerve blockade, at the same time localising the pain area.

As early as 1963, “neuro-irritation impulses” have been discussed as cause of anterior pain radiation, transferred by the median nerve, the causes remaining obscure, however. Systemic clinical and intraoperative examinations of the median nerve and its proximal myokinetic branches have shown a predominant localisation for irritations in the proximal area of the cubital fossa. This was confirmed in 7 out of 12 surgically treated GE of this series, supporting that also in GE there are pain radiations caused by further proximal nerve irritation. In the remaining five patients, the cause was finally supposed to be in the area mentioned above.

A median nerve and myokinetic branches pressure damage of minor degree (irritation!) at the humeral trochlea, caused by direct pressure of the bicipital aponeurosis in 5 out of 12 patients is responsible for the anterior pain radiation (Figs. 2.16 and 2.17). In these cases after resection of the bicipital aponeurosis, a protruding and broadened median nerve with parallel fascicles and missing subepineural blood flow at the humeral trochlea is found in extension of the elbow joint, so also a disturbance of the intraneural flow can be concluded in both remaining cases, clinically initially also presenting as a compression syndrome of the bicipital aponeurosis. The main cause was a pressure damage by a fascia bridge of several cm, lying deep and being tense, connecting the pronator teres muscle and the brachial muscle, as well as disturbing the median nerve in its side movement (Figs. 2.18, 2.19, and 2.20). After resection of this fascia, there is a severe disturbance of blood flow and a slight broadening of the nerve diameter and in one case even a circumscribed loosening of the epineurium, as well as a stronger notch. In extension of the elbow joint, the results of this compressing fascial plate are evident (Figs. 2.18, 2.19 and 2.20).

As the bicipital aponeurosis spreads into the forearm fascia, in contraction of the biceps muscle, a certain functional tension band wiring effect develops, pushing a contracted pronator teres muscle stronger against the humeral trochlea and the brachial muscle above. As a result, also the median nerve and its motoric branches suffer from additional pressure, as shown in two patients. This finding supports the technique of always resecting the bicipital aponeurosis in decompression of the median nerve. A neural irritation by a supracondylar process or by a Struther ligament was not seen in this series.

The posterior pain area, including the origin of the flexor carpi ulnaris humeral head and the medial collateral ligament in contrast to the anterior area, is exclusively innervated by fibres of the three articular branches of the ulnar nerve (Rüdinger 1857) (Fig. 2.1 left) and can be extinguished, as well as identified by blocking this nerve 2 cm proximal to the epicondyle peak. On demand, the subcutaneous posterior branch of the cutaneous medial nerve of the forearm can be blocked from here as well. Routine blocks like this are not necessary in GE and TE contrary to wrist denervation.

In pathogenetic aspect of pain radiation to the posterior part, the following endogenous causes are found as predisposing factors: in a normal grooved sulcus of the ulnar nerve (Fig. 2.3), the nerve is found dorsal of the elbow joint axis, thus permanently experiencing traction and pressure stress in articular flexion, caused and at the same time caught by the epicondyle mass. Hereby in changing pressure and extension of the joint, the nerve experiences a continuous change of its diameter, resulting in repeated shifting of individual fascicles, change of nerve pressure and traction stress as well as a recurrent medial shift of the nerve. This can even be supported by the effect of the short triceps muscle head. These irritations lead to disturbances of nervous blood flow and axonal flow, basically responsible for pain radiation and the change in surface sensitivity. In a normal epicondyle, there can still be a tendency towards luxation if the ulnar nerve in increasing flexion finds its hypomochlion in the distal area of the epicondyle circumference, at this point moving into a more or less obtuse angle into the trochlea (Güney et al. 1977).

Main causes of GE in endogenous aspect are dysplasia of medial epicondyle and quality of roof above the ulnar nerve sulcus. Whether there is subluxation or luxation of the ulnar nerve depends on the ulnar nerve sulcus roof stability. This is accomplished either by the atavistic epitrochleoanconaeus muscle, first described by Gruber (1866), bridging the sulcus in diagonal direction, innervated by a branch of the ulnar nerve, or by its ligamentary rudiment, being the epitrochleoanconaeus ligament. The rudimentary character of this ligament is supported by the fact that it can contain transverse muscle fibres, corresponding to the fibre flow of the epitrochleoanconaeus muscle. According to anatomic research, this muscle is found in 17.9–28.7 %, according to clinical findings in 9–17.3 % (Table 2.1). Intraoperatively the muscle was found in 9.0–17.3 % (Table 2.2). The epitrochleoanconaeus muscle and its ligamentary rudiment come from the medial epicondyle mass and connect to the opposite olecranon circumference between articular capsule and final tendon fibres of the triceps muscle medial head (Figs. 2.3 and 2.5). The epitrochleoanconaeus muscle and the ligament develop a rhombic shape in articular extension, whereas in increase of flexion a trapezoid shape develops, due to change of distance and transposition of the points of origin and insertion. At the same time a significant extension of these structures up to one third is accomplished, as seen in Fig. 2.4, leading to a very strong tension of the proximal muscular and ligamentary rim, whereas only a slight lengthening is seen at the distal rim (Fig. 2.6). The epitrochleoanconaeus muscle is innervated by a branch coming from the ulnar nerve together with the upper articular branch (Fig. 2.2) (Wachsmuth and Wilhelm 1968). Mummenthaler (1961) described the tension of the epitrochleoanconaeus ligament, possibly “leading to a compression of the nerve in the sulcus itself”; in this context, the author also elaborates that “the nerve is more or less compressed between the descending triceps and the ulnar epicondyle”.