Traumatic neuroma is a non-neoplastic proliferative overgrowth of axons, Schwann cells, and fibroblasts at the proximal end of a transected nerve (1). Complex regional pain syndrome (CRPS) is defined as a regional, posttraumatic, and neuropathic pain that most often affects one or more limbs (2). CRPS includes symptomatology caused by peripheral nerve entrapment and irritative lesions, as well as neuroma (3).
We report a patient with a traumatic neuroma as an unusual complication of a finger stick by a lancet. There was a referred pain with minimal localizing signs. The results of electrophysiologic and radiological investigations were normal. Thus, she was diagnosed as CRPS type I, and different pain management modalities were used without success before the diagnosis of neuroma.
A 36-yr-old woman was referred to our pain clinic with a 7-yr history of continuous pain on the left hand and arm. She described the pain as aching, burning, and knife-like. She also noted that her left hand sometimes felt cold. She denied any initiating event or any emotional stress at the time of onset of her pain. The patient had been followed for years in different hospitals. Physical therapy in conjunction with nonsteroidal antiinflammatory drugs (NSAIDs) failed to improve her symptoms. Four years after the onset of pain she had been diagnosed with CRPS. Radiological and electromyographic examinations did not reveal abnormalities. She had been started on carbamazepine, amitriptyline, and NSAIDs, which provided partial improvement in symptoms until 2–3 mo before admission to our hospital. The pain had become progressively worse over the previous few months. When she was admitted to our hospital her medications included amitriptyline 75 mg/day, carbamazepine 600 mg/day, and naproxen sodium 1000 mg/day. She was disabled in performing normal activities of daily living and diagnosed as having moderate somatic anxiety at her initial psychological evaluation in our clinic.
Her physical examination was normal except for hyperesthesia, hyperalgesia, and allodynia involving the volar side of her third, fourth, and fifth fingers, the palm, volar side of the wrist, medial and lateral forearm, and her elbow. There was no neuromuscular dysfunction or sensory deficit. She rated her pain as 8–9 on a visual analog scale of 0–10. Magnetic resonance imaging (MRI) and electromyography studies of her left arm were normal.
A diagnostic stellate ganglion block with 15 mg of 0.5% bupivacaine abolished all pain and symptoms except the pain at the tip of the fourth finger. Eventually, she recalled that her pain started after a finger stick by lancet to her fourth finger and became constant in time and that the intensity increased gradually. The review of the MRI of her left hand revealed a 5 mm nodular lesion, which was hypointense on T1-weighted images, and hyperintense on T2-STIR weighted images, at the palmar side of the distal phalanx of fourth finger (Fig. 1).
Surgery was performed under IV regional anesthesia (IVRA) with 1% lidocaine. The complete excision of the mass abolished the hand pain immediately and decreased the pain at the forearm and elbow. Histological diagnosis revealed neuroma. Over the next 3 weeks she graded the pain at the forearm and elbow as 4 on a 10-point scale. She therefore underwent two additional sessions of stellate ganglion block. After these procedures, a complete resolution of symptoms was achieved. Three months after the surgery she was pain-free with no medicine and 2 yr after the surgery her physical, social, and emotional states were completely normal with no pain.
Development of a traumatic neuroma after a finger stick by a lancet is a rare complication. In fact it has not been reported in the literature. Peripheral nerve lesions such as neuroma may cause symptoms that are attributed to CRPS type I or II. These lesions often project pain outside the territories of these peripheral nerves by the well-described phenomenon of pain referral. Referred pain secondary to peripheral nerve injury can create diagnostic difficulties if objective clinical and electrophysiologic data are lacking. In our case electrophysiologic studies that were performed twice were normal and the MRI was misdiagnosed as normal by both the radiologist and the clinicians during follow-up examinations.
Thimineur and Saberski (3) have reported three cases of peripheral nerve lesions with referred pain, autonomic changes, and minimal localizing signs. In this report, all three patients were diagnosed and treated as reflex sympathetic dystrophy. The authors concluded that injection of local anesthetic at sympathetic ganglia might obscure the diagnosis. In our case, however, abolishment of the sympathetic component of the patient’s symptoms, but not the pain of neuroma itself, by stellate ganglion block led us to the diagnosis of peripheral nerve lesion.
Proposed techniques and patient selection for surgical treatment of painful neuromas have met with poor results and controversy (4–7). In our case, surgical excision of the distal neuroma with IVRA provided complete abolishment of the pain at her hand but not the sympathetic component of the pain. Because the patient benefited from an initial sympathetic block, we decided to repeat sympathetic blocks to treat the residual pain at her forearm and elbow. These procedures resulted in a complete resolution of her symptoms.
In conclusion, this case study shows that even minor trauma can cause nerve lesions with severe pain. Our results emphasize the importance of careful clinical examinations in diagnosis of painful nerve lesions, which may be with or without CRPS, and in achieving palliation by surgical means.
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