Short Notes in Plastic Surgery

September 7, 2017

65. Compressive neuropathy of the peripheral nerves in the upper limb General information

Filed under: Chapter 65,Uncategorized — ravinthatte @ 6:26 am

Compressive neuropathy of the peripheral nerves in the upper limb: General information

The speciality of the surgery of the hand (also called hand surgery) is now over 50 years old in India but older in the western part of the world. Over the years both orthopaedic as well as plastic surgeons have first migrated towards this speciality and then taken it up as a full-time occupation. A general surgeon taking up this speciality is more an exception than a rule. This chapter has therefore been vetted by Mukund Thatte a plastic surgeon and a leading practitioner of surgery on the brachial plexus and peripheral nerves as well as two orthopaedic surgeons Sudhir Warrier and Pankaj Ahire both of who restrict their practice entirely to surgery of the hand. All three have their practice in Mumbai India.

This chapter focuses only on peripheral neuropathies in the arm and does not include conditions which involve the brachial plexus or conditions such as the thoracic outlet syndrome.

  1. All activity within living tissues can be described as electro chemical in nature and this in recent times has been collectively called physics. Slide1 Erwin Schrödinger’s work on the genetic makeup of living beings in his seminal work published as “What is Life” has shown that all living activity can be reduced and explained as principles of physics. Nowhere else in the body is this electro-chemical activity more evident than in the functioning of the nervous system. The nervous system is not only aware of the conditions that prevail within the body and is able to react to the changes that occur with appropriate responses but is also aware of the organism’s environment and allows suitable actions to be taken to safeguard the interests of the organism.
  2. The agents for the perception and execution of these actions are the nerves made up of axons the longer of the two cytoplasmic projections from the neuron or the nerve cell. The shorter of the two projections the dendrites, in a vast majority, serve as connections between adjacent neurons.
  3. The peripheral nerves in the limbs are the longest nerves in the body which traverse long distances through anatomical compartments and tunnels and are therefore prone to pressure and or compression at various sites. Because the hand as an organ is far more skilful than the foot and is vital to a myriad of daily activities, compressions of the nerves in the arm leading to clinical problems appear to be more frequent than those in the lower leg. As noted in the preamble to this chapter this statement excludes the conditions which arise because of problems related to the vertebral column in the inferior extremity.
  4. The basic unit of the nerve is the axon a long protoplasmic extension from the neuron and is called axoplasma. A few axons make a fascicle and several fascicles make a nerve. The axons are covered by a connective tissue layer called endoneurium, fascicles are sheathed by connective tissue called the perineurium and the nerve in turn by the epineurium which is quite thick sometimes up to forty percent of the cross section of the nerve. The epineurium has a mesentery called the meso-neurium through which blood vessels enter or leave to fulfil the nerve’s metabolic requirements.
  5. The axons can be large in diameter or small. They can also be myelinated or non-myelinated. The non-myelinated axons are fewer in numbers. Myelination is an attempt by nature through evolution to ensure faster conduction of the electrical impulse without spillage. The myelin coating of the axon is laid down by the Schwann cells. Because the distance that the electrical impulse must travel is long the axons have nodes first described by Ranvier (nodes of Ranvier). These nodes act as substations like in man-made electrical grids where conduction is optimised by a saltatory process. (Saltatory as in leaping). These nodes in fact are relay stations. The myelin sheath is interrupted at each node. As can be seen the non-myelinated fibres are inferior in their conducting efficiency. Though they are surrounded by Schwann cells they do not provide them with a myelin sheath.


  1. The axon is enclosed within a layer of endoneurium a layer not previously mentioned in the paragraph above. The endoneurim itself is extremely thin and is made of connective tissue of mesodermal origin and encloses a network of capillaries more profuse than in the sub-perineurial layer and the capillaries are broader in diameter than the capillaries elsewhere in the nerve probably on account of being the terminal vessels actually nourishing the nerve tissue. What is more the nerve mimics the brain by creating a blood nerve barrier here in which together with the subperineural blood vessels, a privileged environment is created which resists deleterious effects of metabolic changes that occur on the outside. When this limit is crossed by an external force as happens in a compressive neuropathy an ‘internal compartment syndrome’ results. Because the nerve itself has no lymphatic drainage the resultant oedema leads to accumulation of proteins and the loss of privilege incites an inflammatory response to antigens from which the axon had been protected earlier. Lymphocytes and macrophages follow into this zone of inflammation. The myelin sheath gets destroyed first in patches then over a length followed by formation of scar. The conductivity of the nerve suffers and if the condition is not treated till the effects of the compression are reversible the area of supply of a given nerve suffers consequences such as anaesthesia or loss of function of muscles. The following figures are schematic and do not purport to be real cross sections of a nerve but are drawn to understand how the structure of a nerve is organised. For example, the myelin sheath is pearly white in colour but shown here in black because it is very difficult to show a white pearly appearance in a diagram. The same applies to all the sheaths.




  1. An acute compression neuropathy can occur following an improper use of a tourniquet on the arm ironically when surgery is being performed for treating conditions in the hand. The incidence of this kind of ‘palsy’ is much lower now because of the introduction of pneumatic tourniquets (some of them with alarms indicating the duration of application). Mercifully most patients recover completely. The available texts have paid little attention to the exact nature of the pathology that follows in the nerve in cases of a tourniquet ‘palsy’ and if any degree of rapid demyelination occurs in the affected nerves.
  2. The blood supply of the nerves develops as the nerves grow in the limb buds and it is this neuro-ectodermal tissue that orchestrates the development of the capillary network in its vicinity which later develops into vessels. The rationale of a neuro cutaneous flap is this synchronous development. The median nerve in the forearm for example is supplied by the median artery which overlies it and also by the branches of the anterior interosseous artery in the same fashion that the radial artery supplies branches to the radial artery forearm flap. The ulnar nerve near the elbow is supplied specifically by the ulnar collateral arteries which draw their blood supply from the brachial artery and have been used for a free ulnar nerve transfer. The blood supply to the nerve as can be seen is either axial or segmental.



  1. It has to be borne in mind that the axons are open live conduits and their axoplasmic flow is bidirectional. This means that the products of abnormal metabolism have a free play in either direction. Therefore, a compression pathology in the proximal part of a nerve may have consequences in a distal part of the same nerve when it lies in a vulnerable compressible area. For example, a patient with a thoracic outlet syndrome may later develop a carpal tunnel syndrome. This is called somewhat harshly as a ‘double crush’. This can happen the other way around as well and is called the reverse double crush in which a distal lesion can precipitate a proximal pathology. Diabetes obesity, hypothyroidism, abuse of alcohol and tobacco the usual culprits in many diseases have also been statistically proved to have a role as predisposing factors in the development of compression neuropathy. A hereditary condition in which trivial trauma precipitates demyelination in nerves leading to symptoms both motor and sensory might sometimes be confused with a compression neuropathy. These cases show a rapid onset and total recovery they may be recurrent and occur at various sites. Clinicians must have this condition at the back of their minds before arriving at a diagnosis of compression neuropathy which has a steady progressive course.
  2. Most living tissues have an optimal ability to stretch and the nerve is no exception. The nerve in some measure resembles a woven rope as fascicles traverse distally and get straightened if stretched. The mesoneurium also has a certain play when it gets stretched. Nature therefore protects the nerve while the body pursues normal activities but is vulnerable when a certain limit is crossed particularly when the stretching action is performed repeatedly. Modern life creates many situations which put the body and particularly the upper arm through repetitive abnormal movements in certain occupations. The significance of this is not so much in the causation of the compression pathology but in the effects that this stretching produces when the nerve is already beginning to get compressed because the compressed nerve tends to lose its elasticity and therefore suffers repeated trauma. Ironically the practice of yog now popular all over the world to ward off the ill effects of modern living if practiced with excessive and unnecessary vigour can aggravate many an existing condition in the limbs as well as a compressive neuropathy. These facts are important when taking the history of a patient with compression neuropathy.
  3. The preceding paragraphs form a background with which a clinician must be familiar so as to be able to diagnose a case of compression neuropathy. What follows is taking down a detailed history which includes the additional information that the patient gives on his own, physical examination and electro diagnosis when there is a doubt about the diagnosis.
  4. The patient’s complaints more often than not are sensory in nature for example tingling and numbness. It might be revealed on direct questioning that the sensations that the hand generates are not quite what they should be (paresthesia). Aching pain and fatigue are caused by muscular weakness but the ache that the patient complains of might in fact be severe numbness. The tingling might be getting aggravated by activity and there are patients who are miserable enough with their symptoms to lose their confidence for doing their daily activities. Insomnia is not unknown. A patient might complain that a particular action is difficult to perform for example turning the key for opening a lock or that a particular area of the palm is dry and rough. It might also have been noticed that the affected hand has become weak. There might be symptoms of intolerance to cold or hot objects. Generally speaking the symptoms of a compressive neuropathy vary greatly and only the common ones have been narrated here.
  5. Notwithstanding the variety of tests that have been described to test for loss or altered sensations the results of these tests are not always reliable or conclusive on account of their subjective nature. If the condition is unilateral it helps a great deal to make a comparison and then arrive at a firmer conclusion. Light touch can be measured by moving cotton across the affected and the contralateral normal part and then measured in ten grades (one to ten) and compared. The capacity to feel a vibratory impulse can be tested either by a tuning fork or by a specially designed instrument with multiple frequencies because there is a theory that high frequencies are lost the earliest in compression neuropathies. Cutaneous pressure thresh holds can be tested by mono filaments of increasing diameters till they bend and two – point discrimination formerly tested with a paper clip is now measured by instruments which are more sophisticated. However, as things stand two-point discrimination is one of the last sensory modalities to be lost in compressive neuropathy and is a poor diagnostic tool to diagnose the condition early.


  1. The motor impairment in the palm is somewhat easier to diagnose though the exact amount of loss of power in the small muscles of the hand cannot be graded as is done in the larger muscles in other parts of the body. Wasting of muscles in the palm is also easier to diagnose particularly when compared to the opposite side but here too the clinician must take into account which of the two hands is dominant. Many a times the non-dominant hands have leaner palms. While the hand is being examined it is worthwhile to observe palmer sweating. Though there is very little that we know of the autonomic component of the nerves in the hand the region supplied by the affected nerve is more likely to be dry.
  2. Perhaps the more reliable methods to diagnose nerve entrapment are by the use of percussion or pressure on the known course of the nerve or to cause provocation by bending the joint to an extreme position for a minute across which the nerve passes in a canal. The manoeuvre causes reduction in the space of the canal in which the nerve lies and produces exaggeration of the symptoms that the patient is suffering from. In the case of the median nerve pressure can be applied over the middle of the pronator teres resulting in pain, percussion can be done proximal to the carpal tunnel leading to unpleasant tingling along the nerve and provocation can be induced by extending or flexing the wrist through its maximum range with the forearm in the supine position for a minute which causes the symptoms to increase several folds. These tests will be given in detail with figures in sections on individual nerves later in this blog.
  3. The nature of the impulse in the nerve being electrical and the result of that impulse on the muscle also being electrical the rational thing has been to subject cases of compressive or other neuropathies to electro diagnosis. This is a speciality in itself and only the bare minimum information is provided here. The electro diagnosis is divided in two parts, electro- myography and nerve conduction studies. In myography a sharp needle is inserted in a muscle and its electrical activity is noted on a graph. A muscle which has been denervated for a long time and is wasted and in which the muscle fibres are replaced with fibrous and collagenous tissue is silent and will not transmit any impulse across the needle. A muscle which has lost its nerve supply completely approximately for a period of more than two weeks will show fibrillations which denote an autonomous electrical activity in the muscle. A normal muscle upon insertion of the needle responds with a brief burst of electrical activity. When the patient is asked to contract the muscle with the needle in place a normal muscle recruits a large number of muscle fibres leading to what is known as interference pattern because of overlapping. In a muscle recovering after a successful repair of a nerve serial myographies will show a greater recruitment of muscle fibres over a certain duration.
  4. Nerve conduction studies are performed by placing two electrodes along a nerve one of which is the stimulating electrode and the other is the receiving electrode. The conduction can be studied in either direction. Unlike the motor axons which are bigger the sensory axons are smaller the amplitude of the waves generated in them is also smaller and the electrical activity is expressed in microvolts as compared to in the motor axons which are designated in milli-volts. It is customary to measure the speed with which the impulse passes in milliseconds. Because the quantities involved are very small the investigation can be marred by room temperature the temperature of the surface on which the electrodes are placed or by technical problems. Therefore, a comparison with values on the normal side is far more important in nerve conduction studies. A difference of about fifty percent between the two sides is considered diagnostic of a pathological entrapment of the nerve.





  1. It is a moot point as to if in clinical practice treatment should or can be undertaken without recourse to electro diagnostic methods in cases of compressive neuropathy or if these methods are used only when the diagnosis is doubtful and in those cases where the patient needs to be convinced of the diagnosis.




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