The painful hand

Mechanism of injury

An appreciation of the physical mechanism of trauma is essential to understand the pathology in post-­traumatic neuropathic pain. These mechanisms are often mixed but can be considered as mainly penetrating or blunt.

Subjective descriptors

Pain description can be considered under the mnemonic SOCRATES. This allows a structured history to be taken of the patient’s experience of the pain. It is also often helpful to ask the patient what they think caused the pain, as this can provide the clinician with an insight into the concerns that the patient has about their symptoms.

The complex nature of trauma and nerve injuries and their effects on the musculoskeletal system can often generate secondary soft-tissue dysfunctions (e.g., edema, joint stiffness, and scar tissue). These give rise to pain which can be nociceptive and/­or neuropathic in nature. Location and distribution of pain symptoms can be mapped and monitored via the use of body charts.

Patient-­reported measures

Pain intensity is commonly assessed using visual (VAS) and numerical (NRS) rating scales. However, the experience of pain goes well beyond this. Neuropathic pain is well known to manifest as sharp, sudden, shooting, electric, and burning in nature. These descriptors of pain can be identified, assessed, and recorded with patient-­reported measures such as the Leeds Assessment of Neuropathic Symptoms and Signs pain scale (LANSS), McGill Pain Questionnaire, PainDetect tool, and the Brief Pain Inventory.

Neuropathic pain is known to affect outcomes and increase disability. There is strong evidence that people with neuropathic pain have worse health-­related quality of life than those with other long-­term conditions and those with non-­neuropathic pain. For example, the presence of neuropathic pain in diabetic neuropathy further diminishes quality of life. Therefore, the inclusion of health-­related quality of life (HRQoL) measures should be considered as part of a holistic assessment.

Clinical examination

Expert clinical assessment must seek out the subtle clinical signs of nerve dysfunction. This requires sound knowledge and application of human nervous system anatomy. However, it is important to remember that diagnostic testing can yield inconclusive or even inconsistent data when investigating neuropathic pain. In such instances, clinical judgment is required to reduce the totality of findings in a patient into one putative diagnosis (or concise group of diagnoses).

The presence of altered distal nerve function will direct the clinician towards possible diagnosis. The assessment of nerve function is multidimensional and involves the fundamentals of any clinical assessment. Specifically in relation to nerve injury, it is important to note the appearance of the affected region. Trophic changes and sympathetic function (such as: skin quality, colour, hair/­nail growth, and sweating) will be altered with degenerative nerve injuries ( Video 31.1 ). In addition, muscle wasting and the holding of the limb in a dystonic posture may also be evident. Assessment of sensory function should include a record of the ability to feel light touch and deep muscle tenderness upon squeezing a muscle. The presence of allodynia, dysthesia, and hyperalgesia should also be noted. Motor function (power, pain inhibition, coordination, co-­contraction and tone) are also important factors which will assist in building the clinical picture. Anatomical knowledge and assessment of nerve pathways give information with regards to the function of each nerve. The Hoffman–­Tinel test should be carried out along the course of the nerve (from distal to proximal). A positive sign can assist in localizing the point of a pain-generating pathology ( Video 31.2 ).

Neuritis

Nerve tissue, like any other, experiences dysfunction when inflamed. In a nerve, this is due to chemical stimulation by inflammatory cytokines, hormones, and small molecules. Additionally, the effect of swelling can cause pressure externally (through deformation and tension altering the course of the nerve) and internally (diminished venous outflow can lead to low pressure compression, causing an effect which is similar to compartment syndrome within the epi/­perineurium). This effect can be seen at all timeframes of recovery. Hyper-­acutely, it is demonstrated in percussive neuritis (where a physical force or impact creates a neuropathic pain). Acutely and sub-­acutely, it can manifest from the inflammation following direct nerve injury and in particular due to local tissue inflammatory reactions to trauma. Chronically, it can occur as a consequence of contracted scar tissue commonly seen secondary to chemical, thermal, or radiation burns.

Neurostenalgia

The neuropathic reaction that nerves (which are in continuity) demonstrate when encased in scar tissue is similar to, and can follow on from, that created by the processes of neuritis. Neurostenalgia is the pathologic effect of scar upon nerve function, where neuropathic pain is created in the distribution of the affected nerve. A nerve that is surrounded by scar will be tethered, and this will act as a focal point of strain. This area of constriction has a lesser ability to withstand the effects of strain and elongation, so it exhibits a higher peak strain. The nerve’s reaction to this increased strain can be physical and chemical, giving rise to pain. In addition to the tethering effects of adhesions, many regions of scar tissue undergo contraction which can compress and strangle the nerve, creating local hypoxia, ischemia, and release of inflammatory cytokines. This pain state can often be associated with motor and sensory dysfunction of the nerve (often via a conduction block pathology). Over time, this can often progress to degenerative axonal loss. The cardinal sign of a neurostenalgic lesion is allodynia. Clinically, the presence of allodynia denotes that the nerve is in continuity; if a sensory experience can be detected (even if misperceived), it is evidence that the nerve is not divided.

Symptomatic post-­traumatic neuroma

Any nerve which suffers a loss in axonal continuity and a breach of the endoneurium will create a neuroma. Any nerve that is completely transected will form a post-­traumatic end neuroma. Neuroma formation is not a pathologic state. It is a standard reaction to injury, as axonal re-­growth is the normal response to axonal injury. Neuromata (plural of neuroma) are not by definition painfully symptomatic, but they can generate spontaneous (without external stimulation of the neuroma) and/­or evoked (produced by external mechanical stimulation of the neuroma) pain. In transected nerves, there will be no function (sensation, sympathetic and no evoked symptoms) within the distal cutaneous branch supplied by the nerve. However, pain may still be perceived as originating in this territory of skin, despite it being insensate. Here, the brain will “project” the experience of pain to that territory if signals are generated by stimulation of the neuroma (similar to the projection of paresthesia in a Tinel’s sign).

Symptomatic post-­traumatic neuromata (SPTN) generate spontaneous pain when they are stimulated by their physical and/­or chemical environment and/­or their internal structure. The most common causes are scarring within the neuroma, compression by external scar, and chemical excitation by factors such as nerve growth factor (NGF) from the skin. This creates a constant pathologic environment which is a persistent pain generator. Evoked symptoms are created when a neuroma (which is not spontaneously firing to create neuropathic pain) is stimulated physically or chemically. This means it is in a location where it is vulnerable to compression or stretch, or resides in a suboptimal chemical environment.

Spinal nerve root avulsion (deafferentation)

Spinal nerve root avulsion injuries are most frequently seen in severe supraclavicular brachial plexus lesions from high-­energy trauma, for example motorcycle incidents. In avulsion injuries, a traction force causes the sensory and motor nerves to be disconnected (pulled out) from the spinal cord. In this situation, the motor cell bodies, situated in the anterior horn of the spinal cord, lose continuity from the motor fibers of the peripheral nerve. However, the cell bodies of sensory fibers (situated in the dorsal root ganglia) remain intact (but disconnected from the dorsal horn of the spinal cord), creating a pattern of injury which demonstrates classic neurophysiologic data of de-­innervated muscle and intact sensory potentials in insensate territories. The gold standard for distinguishing between pre-­ and post-­ganglionic lesions is the direct exploration of the rootlets during surgery ( Video 31.3 ). Imaging studies such as computed tomography (CT) myelography and magnetic resonance imaging (MRI) have lower accuracy for making this distinction (85% and 52%, respectively). Whilst there are multiple patterns of injury, a frequent pattern is rupture of the upper trunk or spinal nerves C5–­6 (which are more anatomically resistant to avulsion), and avulsion of the lower roots C8 and T1. Narakas found that at least one nerve root avulsion occurred in 70% of all traction injuries of the brachial plexus that were explored and treated operatively.

Due to the nature of the injury, a spinal nerve root avulsion may also be considered as a “longitudinal spinal cord injury” ; whereby subsequent disintegration and disruption of the posterior horn cells, Lissauer tract, and substantia gelatinosa can give rise to additional central nervous system pain mechanisms. Pain severity seems to be related to the number of roots avulsed. The pain is consistently characterized as burning or hot. Patients often report a feeling that the hand is: “on fire” , “boiling water is being poured over it” , “is being squeezed in a tight vice” or “being electrocuted” . The nature of the extreme neuropathic pain which accompanies avulsion injury has been described in detail by Parry. In a series of 275 patients with brachial plexus injuries, none of the 167 patients with lesions distal to the dorsal root ganglion were noted to have pain as a feature. In contrast, 98 of the 108 patients with avulsion lesions, experienced significant pain. This deafferentation pain has an immediate onset; certainly, being present by 8 weeks from injury.

Causalgia

Causalgia occurs following high-­energy trauma and commonly involves a combined nerve and vascular injury. The underlying pathology is not well understood, but could be secondary to a constant exacerbation of the nerve injury (from scarring between the traumatized nerve causing transmission of vibration from turbulent blood flow within an injured vessel). The neuropathic pain(s) that individuals present with are described as severe and can often be expressed as a constant exacerbation of pain and sensitivity. Allodynia within the area can be elicited by innocuous stimulation from environmental stimuli such as the movement of the air around the limb or even a loud noise. Once diagnosed, this can be a very rewarding nerve injury to treat as there is often swift and considerable improvement in symptoms from surgical decompression of the damaged area.

Complex regional pain syndrome

Complex regional pain syndrome (CRPS) is commonly diagnosed in the presence of post-­traumatic neuropathic pain. In general, the condition is related to an injury to the limb. However, there is no correlation between the severity of the trauma and the development of CRPS and, in 9% of cases, there is no precipitating trauma. CRPS was originally conceived as a diagnosis of exclusion, if no other diagnosis can better explain the signs and symptoms. Diagnosis is currently based on meeting the Budapest Criteria and ensuring elimination of any other possible diagnosis. It is important that the aforementioned pain states are therefore considered and excluded prior to a diagnosis of CRPS being made. In our experience, it is common to encounter patients that have been diagnosed with CRPS despite a clear wound over a nerve and a positive Hoffman–­Tinel sign. These clinical findings would be highly suggestive of a SPTN or a localizble lesion of a nerve indicating a neurostenalgic lesion.