REVIEW OF SOME SURGICAL CONCEPTS IN
THE TREATMENT OF PERIPHERAL NERVE LESIONS
G.Penkert; W. Bini* and M. Samii
Neurosurgical Dept., Nordstadt Hospital / Hannover - Germany; * Neurochirurgia, Ospedale Civico / Lugano - Switzerland.
Neurocirugía, Vol.7 N.4, pp. 255-262; Diciembre, 1996
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SUMMARY
The treatment of peripheral nerve lesions still represents a challenge in spite of today´s diagnostic and surgical sophistication. Clear anatomo-clinical and surgical notions must guide the treatment planning in this field which has been somewhat "neglected" by clinical neurosurgery. The results can be spectacular, nevertheless the decisive information will often be adquired only after surgical exposure that is in situ. The basic prerequisite of principle is to be able to create optimal conditions for axonal regrowth.
Key words: Peripheral nerves. Surgery of peripheral nerves lesions.
El tratamiento de lesiones de los nervios periféricos sigue representando un desafío a pesar de los avances diagnósticos y la sofisticación quirúrgica. Claros conceptos anatomo-clínicos y quirúrgicos deben guiarnos a la hora de planear un tratamiento en este campo el cual ha sido en parte "olvidado" por la neurocirugía clínica. Si bien los resultados pueden ser espectaculares, con mucha frecuencia tendremos la información decisiva sólo después de haber expuesto el campo quirúrgico, es decir, "in situ". El principio básico es obtener o crear condiciones óptimas para la regeneración axonal.
Palabras clave: Nervios periféricos. Cirugía de las lesiones de los nervios periféricos.
As in other areas of neurosurgical practice in peripheral nerve surgery treatment planning must begin with accurate anatomical and neurological orientation in order to judge which nerve or combination of nerves have been injured (1,4,5). For this prerequisite we have fond it helpful to compare the nerve ramifications of the upper and lower extremity. Each nerve of the arm will correspond to a special nerve of the leg and important distintions do not exist with exception of the level of ramification ( see scheme 1 ).
Scheme 1: Compariton of ramification of upper and ower extremity nerves.
The smallest anatomical unit of a nerve is the axon. Around the axon membrane we find the myelin sheath and its schwann cells. These components together form the so-called nerve fiber. Each nerve fiber is enclosed in two or more layers; One with latticed and the other with longitudinal collagen and elastic elements ( the endoneurium ). If we transect a nerve, its stumps will allways retract due to these elastic elements. A bundle of nerve fibers together with their endoneurium is again surrounded by connective tissue and this is refered to as a fascicle. This truely represents the surgical unit.
The numerous fascicles of each nerve are arranged into groups of fascicles, changing their arrangement of distribution from central levels to the periphery. Nerve roots consist of fewer but ciquer fascicles which can be divided into some sectors whereas more in the periphery the nerve has its typical group arrangement with 3-5 groups of fascicles. Between these groups only loose conective tissue with longitudinal oriented vessels is present. At the peripheral end these groups further subdivide into many small fascicles so that the nerve structure adquires a multifascicular nature. In summary, the nerve begins mono or oligofascicular containing a typical group arrangement and at the end this is lost in favor of multiple small no longer distinguishable fascicle groups. The surgeon has to be aware of this changing arrangement. An interfascicular microsurgical neurolysis is only possible in the segment with group arrangement, whereas at the root level a disection of fascicles would damage their continuity.
Following nerve trasection all elements constituting the nerve fiber degenerate from the level of the lesion until the periphery. Only the schwann cells remain viable and are able to build up a new myelin sheath when new axons find their way to sprout. Our surgical efforts presently aim at establishing as optimal conditions as possible for the axon sprouting over the level of the lesion to achieve its distal target (2).
Depending on the amount compressing and injuring forces, Seddon, in 1943 established the wellknown idea of neurapraxia, functional block of the electrical conductivity due to myeling degeneration; axonotmesis, interruption of continuity of the axons and neurotmesis, complete interruption of nerve continuity (6). In comparison, Sunderland distinguished five degrees of lesion in 1951. We consider this latter clasification to be much more useful in understanding the different disterbing events which occur within the nerves and is still valid today:
Nevertheless, each axon remains enclosed by its basal membrane and endoneurium so that during axon sprouting it will reach its former muscle end-plate. This process will last some months but the end result is nearby a restitution ad integrum.
The quality of regeneration, the number of axon sprouts, the amount of miss-sprouting and the functional results at the end of regeneration depend on the degree of fibrosis and on the possible disintegration of the group arrangement of all the fascicles. Therefore the idea of axonotmesis contains a wide field of different types of nerve lesion and we are now able to explain the possible unexpected poor results after neurolysis.
The time span between nerve lesion and possible regeneration will often last several months.
During this period we can test the behaviour of the axon sprouts only by eliciting the "Tinelsign". The palpation of the nerve and where sprouting occurs triggers and electric pain which is experienced in the sensitive area previously belonging to the injured nerve. If the trigger point moves downwards ( distally ) during the period of several months, outgrowth of axons is taking place. This is a positive prognostic factor.
In a very simplified way we have used to distinguish between nerve lesions with and without continuity. In reality we often enough find a nerve which seems to be in continuity but by means of microsurgical dissection we discover a complete distraction of the nerve structure.
On the other hand we can find a markly thickened nerve segment similar to a large neuroma but the dissection shows only scar tissue between the fascicle groups ( pseudoneuroma ). Thus the microsurgical findings often influence the therapeutical actions.
A. Lesions without loss of continuity.
These are lesions which can be overcome by axon sprouting without any surgical reconstruction. Typical entrapment syndromes in anatomicaly narrowed regions ie. carpal tunnel, supinator canal, median nerve under the pronator teres, interosseous anterior nerve entrapment, meralgia paresthesica and the thoracic outlet syndrome are examples of this type of lesion. Furthermore numerous chronic nerve lesions due to repited traction forces such as the ulnar tunnel syndrome exist.
The best condition for optimal regeneration is when only a fibrosis of the epineurium is present. In more severe cases also the epineurium between the fascicle groups ( epifascicular perineurium ) can be fibrotic perhaps even the epifascicular endoneurium.
In treatment the first step is to open the outer epineurium in a longitudinal direction for proximal and distal towards the level of the lesion. If we observe a persisting compression we will have to peel and remove the surrounding epineurium. In cases of an interfascicular fibrosis we will have to dissect between the fascicle groups ( Fig. 1-2 ).
Fig. 1.- Sever acute traumatic median nerve compression at the wrist.
Fig. 2.- Interfascicular dissection (multifascicular arrangement ).
If the fascicles themselves remain fibrotic due to scarred endoneurium rather easily palpable between two finger tips one must decide if resection of the neuromatous segment and nerve grafting should be performed.
Our goal is always to achieve a sufficient decompression in order to enable the axon sprouts to overcome the lesion and reach again their target. In cases of pseudoneuroma, microsurgical neurolysis will be the treatment of choice, but in case of a real neuroma, perhaps affecting only one fascicle group, resection and grafting for this group has to be carried out ( see scheme 2 ).
Intraoperative nerve stimulation is fundamental to confirm fascicles which are still anatomofunctionaly intact.
B. Lesions with loss of continuity.
These lesions which cannot be bridged by axon sprouts, that is completely interrupted nerves but also cases with real neuromas, have a lots of functional continuity. As mentioned previously it can happen that in cases of a grade IV lesion the post-traumatic tissue fibrosis compresses the axons to such a point that their outgrowth is parcially or even totally hindered.
Without surgical intervation, regeneration will fail.
Primary causes are: gun shot wounds, sharp injuries and severe traction trauma due to fractures or joint distortion. Specially after distortion injuries we must expect to have to bridge defects of 20-30 cm. The nerve stumps retract due to their elastic elements.
Additionally, we always have to resect long fibrotic and neuromatous segments to find viable stumps. In relation to nourishment and revascularization there doesn´t exist any argument against the use of long free nerve grafts.
The treatment of choice is to restore the nerve continuity. If we would try and end-to-end suture, we would be faced with two disadvantages. On one hand we would have to overcome strong tension forces which tend to pull all the nerve stumps due to the elastic nerve fibers and secondly, after resection of fibrotic segments the nerve defect increases. Alternatively, since the last 30 years free autologous nerve grafts are used to interposition between the nerve stumps. In case of nerve segment with the typical, previously mentioned group arrangement each fascicle group can be coactated to one nerve graft ( Fig. 3-7 ).
Fig. 3.- Transected mediam nerve with a neuroma at the proximal stump.
Fig. 4.- Separation of the fascicle groups.
Fig. 5.- Site after neuroma resection.
Fig. 6.- Coaptation of the sural graft ( proximal suture line ).
Fig. 7.- Median nerve reconstructed with five grafts.
This method ensures control on the individual coaptation and avoids any disturbing tension which induces tissue fibrosis in the area of the junction. One suture through the epineurium of the sural nerve graft and through the epineurium of each fascicle group is sufficient to avoid foreign body granulomas. If the nerve is unifascicular or multifascicular the grafts have to be coaptated over the whole cross section of the nerve stump. Fibring glue does hinder a timely revascularization in the suture area for some days. The question of increased scar tissue formation by glueing or stitching is often discussed controversialy but not completely answered till now. The introduction of laser tecniques to seal the coaptation should always consider the excess cost of this method. Important to remember is that the patient´s own fibring will mantain the coaptation naturaly after 10-20 min. Post-operative immobilization of the site is adviceble for some days.
If we tent to judge and treat peripheral nerve lesions we must have a clear idea of the anatomical ramification of the nerve of the upper and lower extremities completed by an assessment of the degree of the nerve lesion. Our surgical goal should be to create conditions for regrowth of axon sprouts. We have to decide between several microsurgical tecniques and this often remains an intraoperative decision making. All options must be dicussed with the patients preoperatively.
References.
1.- Goodrich, J.T. : Acute Repair of Penetrating Nerve Trauma. En : C.M. Loftus ed. Neurosurgical Emergencies Vol. II Park Ridge ( Illinois ), AANS Publications committee, 1994; 299-312.
2.- Millesi, H. : Microsurgery of peripheral nerves. En: B. McKibbin ed. Recent Advances in Orthopaedics. Edinburg, Churchill Livingstone, 1983; 1-22.
3.-Penkert, G. ,Bini, W. , Samii, M. : Revascularization of Nerve Grafts: an experimental study. J. Reconstr. Microsurg. 1988; 4: 319-325.
4.- Robertson, S. C., Traynelis, V. : Acute management of Compressive Peripheral Nerve Injuries. En : C. M. Loftus ed. Neurosurgical Emergencies. Vol. II. Park Ridgie ( Illinois ), AANS Publications Committe, 1994; 313-326.
5.- Samii, M. : Fascicular Peripheral Nerve Repair. Modern Techniques in Surgery. Neurosurg 1980; 17: 1-21.
6.- Seddon, H.-J. : Three types of nerve injury. Brain 1943; 66: 237-288.
7.- Sunderland, S. : A classification of peripheral nerve injuries producing loss of function. Brain 1951; 74: 491-516.
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