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Year : 2012  |  Volume : 56  |  Issue : 6  |  Page : 596-597  

Complex regional pain syndrome - I following eye injury

Department of Anaesthesia and Intensive Care, Government Medical College and Hospital, Sector 32, Chandigarh, India

Date of Web Publication14-Dec-2012

Correspondence Address:
Vanita Ahuja
Department of Anaesthesia and Intensive Care, Government Medical College and Hospital, Sector 32, Chandigarh
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0019-5049.104596

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How to cite this article:
Thapa D, Ahuja V. Complex regional pain syndrome - I following eye injury. Indian J Anaesth 2012;56:596-7

How to cite this URL:
Thapa D, Ahuja V. Complex regional pain syndrome - I following eye injury. Indian J Anaesth [serial online] 2012 [cited 2020 Oct 25];56:596-7. Available from: https://www.ijaweb.org/text.asp?2012/56/6/596/104596


Complex regional pain syndrome (CRPS) commonly affects limbs with sensory and motor disturbances. [1] CRPS in the orofacial region has not been clearly defined. The signs and symptoms of CRPS in the face occur after significant traumatic event, e.g., a penetrating lesion on facial skin, tooth extraction, or surgical trauma to the craniofacial region and never as trivial injury. [2]

A 25-year-old male was referred to pain clinic with complaints of deep seated pain with cutaneous swelling and discomfort over left eye. Past history included a trivial swipe injury in the same eye with the tail of a cow. The initial symptoms of redness and lacrimation subsided with local eye drops and there was complete resolution of initial injury. After two months, patient started having deep seated orbital pain associated with swelling off and on around the eye with mild burning sensation. Patient was taking Tab Diclofenac 100 mg twice daily for one week. On examination, the patient had persistent pain, moist skin over left eye lid and minimal resolving oedema over left eye lids. Rest of the examinations in the patient was inconclusive. A diagnosis of CRPS I was suspected and he was prescribed Aceclophenac 100 mg BD, along with incremental doses of Gabapentin reaching 300 mg thrice a day for four weeks as an initial management. His pain and edema improved in one week and was pain free in three weeks.

Incidence of CRPS I is more common than CRPS II and comprises 90% of all cases of CRPS with a varied annual incidence of 5.5 to 26.2 new cases of CRPS I per 100,000. [3] The pathophysiologic mechanism of CRPS is multi-factorial and poorly understood. It includes peripheral and central sensitization along with inflammatory changes, altered sympathetic function, changes in the somatosensory cortex, genetic and psycho physiologic interactions. [1] Intermittent or persistent pain is a dominant feature with patients typically describing pain as a burning sensation which occurs spontaneously or spreads beyond the site of injury. [4] Clinical features supporting the diagnosis of CRPS I in our patient are the following: history of trivial injury, persistent peribulbar pain with occasional burning character and cutaneous hyperalgesia even after healing of primary pathology, recurrent oedema of eye lids, non-detection of obvious cause for the pain, increased moisture of skin during episode of oedema, and finally a favorable response to gabapentin.

An inflammatory injury in trigeminal nerve area had been shown to sensitize afferent nociception pathway and also microglia in spinal nucleus caudalis (Sp5C) nucleus and astrocytes at the borders of spinal nucleus interpolaris (Sp5I) and Sp5C nuclei of trigeminal nerve. [5] Photophobia and reflexive blinking after eye injury could induce sensitization of corneal afferent nociceptive pathways in eye. Cornea also has mechanical and polymodal nociceptors that are stimulated by lid movements over dry eye. Nociceptive afferent in iris may also become another source of nociception in response to pupillary dilation. [6] Abnormal sympathetic nerve response has also been seen in CRPS at different stages of its progression. [7] Post ganglionic sympathetic fibers following the carotid plexus have been seen entering the orbit along with ophthalmic artery and first and second divisions of trigeminal nerve. While travelling anteriorly, these sympathetic nerves supply eyelid muscles, skin of forehead and by following ophthalmic artery also regulate blood flow to ocular and orbital regions. [8] The abnormal proliferation of afferent sympathetic nerves around spinal dorsal root ganglion is responsible for maintaining pain in chronic pain conditions in other regions of body. [9] Such proliferations, however, have not been seen in trigeminal ganglia. [5]

A reduction of sympathetic flow has been held responsible for oedema and warmth in early stages of CRPS in addition to other local factors. [7] Early intervention is essential in CRPS to prevent up regulation and expression of adrenergic receptors on nociceptive fibers. [7]

The primary aim of the therapy is to relieve pain, improve function and provide psychological support to the patients. Nonsteroidal anti-inflammatory drugs have been partially helpful in our patient, as it controlled the peripheral component of the pain due to inflammation. However, the persistent neuropathic pain of CRPS I markedly improved after Gabapentin and ruled out the necessity of further investigations and treatment modalities described for CRPS.

Early aggressive management of CRPS has been described to produce excellent results [10] and this was evident in our patient too. Delaying can be debilitating and disabling. A mechanism-based approach and better understanding of its pathophysiology may eventually lead the pathway to successful management. [11]

   References Top

1.Borsook D, Rosenthal P. Chronic (neuropathic) corneal pain and blepharospasm: Five case reports. Pain 2011;152:2427-31.  Back to cited text no. 1
2.Gregg JM. Studies of traumatic neuralgias in the maxillofacial region: Surgical pathology and neural mechanisms. J Oral Maxillofac Surg 1990;48:228-37, discussion 238-9.  Back to cited text no. 2
3.de Mos M, de Bruijn AG, Huygen FJ, Dieleman JP, Stricker BH, Sturkenboom MC.The incidence of complex regional pain syndrome: a population-basedstudy. Pain. 2007;129:12-20.  Back to cited text no. 3
4.McCabe CS, Haigh RC, Halligan PW, Blake DR. Referred sensations in patients with complex regional pain syndrome type 1. Rheumatology (Oxford) 2003;42:1067-73.  Back to cited text no. 4
5.Davies AJ, Kim YH, Oh SB. Painful neuron-microglia interactions in the trigeminal sensory system. Open Pain J 2010;3:14-28.  Back to cited text no. 5
6.Moulton EA, Becerra L, Borsook D. An fMRI case report of photophobia: Activation of the trigeminal nociceptive Pathway. Pain 2009;145:358-63.  Back to cited text no. 6
7.Bruehl S. An update on the pathophysiology of complex regional pain syndrome. Anesthesiology 2010;113:713-25.  Back to cited text no. 7
8.Thakker MM, Huang J, Possin DE, Ahmadi AJ, Mudumbai R, Orcutt JC, et al. Human orbital sympathetic nerve pathways. OphthalSurg 2008;24:360-6.  Back to cited text no. 8
9.Attala N, Cruccua G, Haanpää M, Hanssona P, Jensena TS, Nurmikko T, et al. EFNS Task Force/CME article EFNS guidelines on pharmacological treatment of neuropathic pain. Eur J Neurol 2006;13:1153-69.  Back to cited text no. 9
10.Lee J, Nandi P. Early aggressive treatment improves prognosis in complex regional pain syndrome. Practitioner 2011;255:23-6, 3.  Back to cited text no. 10
11.Fechir M, Geber C, Birklein F. Evolving understandings about complex regional pain syndrome and its treatment. Curr Pain Headache Rep 2008;12:186-91.  Back to cited text no. 11


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