ISSN 0972-978X 

  About COAA








Neuropathic Joint Following Spinal Anaesthesia – A Case Report

Gopakumar T S *,  Rajanish R**,  Kavitha E***  Rejith Valsalan****

* Associate Professor in Orthopaedics, Dept. of Orthopaedics
** DNB Trainee, Dept. of Orthopaedics
*** Post Graduate Trainee Dept. of Anaesthesia
****  Post Graduate Trainee Dept. of Orthopaedics, Medical College, Calicut 673008.

Address for Correspondence:  

Dr. Rajanish R
“Sreerangam”, Kizhuthally, Kannur – 670018
Phone: +91 9846239349



Adverse neurological sequelae following spinal anaesthesia although not common, have been documented in a number of cases.
We present a case of neuropathic knee joint in a 32 years old female who now presents with dissociative sensory loss and areflexia on right lower limb, as a result of spinal anaesthesia complication, leading to the development of syrinx from T12 to conus.

J.Orthopaedics 2008;5(3)e2

Spinal anaesthesia, neuropathic joint, syrinx.

Neurological complications following spinal anaesthesia are rare1.  They range from anterior spinal artery syndrome transverse myelitis cauda equina syndrome, chronic arachnoiditis to complete flaccid paralysis2.

Postulated theories regarding causes of such complications are direct trauma, chemical irritation and sepsis3.

We report a case of Charcot’s joint right knee, following spinal anaesthesia due to the development of secondary syrinx.

Case Report :

32 years old second gravida with a history of previous uneventful LSCS, underwent elective LSCS for the second time under spinal anaesthesia 8 years ago in 1998.  Patient was apparently normal before the procedure. At the time of giving spinal anaesthesia, she experienced local discomfort and brief shooting pain through both lower limbs. But adequate analgesia was attained and surgery was carried out uneventfully. In the post operative period, the patient failed to regain motor and sensory perception below the level of umbilicus.  Bowel and bladder functions were preserved.  Motor power in both lower limbs gradually recovered to normal over a period of two years.  Sensory perception over the left lower limb recovered completely over a period of six months.  However on the right side, pain and temperature sensations did not recover below the T12 level.  Two years ago the patient developed painless, progressive effusion and deformity of the right knee joint.  She also developed a trophic ulcer on the right foot.

 On examination she was found to have unstable right knee joint with gross effusion and synovial thickening.  Neurological examination of right lower limb revealed near normal motor power, bilaterally comparable bulk of muscles, hypotonia with areflexia and dissociative sensory loss ( pain and temperature) below T12  level. Vibration and proprioception senses were preserved.  Plantar reflex was found to be equivocal on right side.


On investigating the patient haemogram, serum electrolytes, blood sugar estimations and renal function tests revealed normal values. Immunological marker for syphilis was found to be negative. Cerebrospinal fluid study by lumbar puncture was normal.

Radiological assessment of right knee joint showed changes of osteoarthritis with joint space narrowing, subchondral bone sclerosis, large osteophytes and joint effusion.   There was marked destructive and hypertrophic changes also.

Magnetic resonance imaging of the dorsolumbar spine showed that the spinal cord ends at the middle of the L2 vertebrae in this patient; longitudinal hyperintense signals were noted eccentrically in the cord parenchyma on the right side from T12 till the conus in T2 sequences, which are hypointense in T1 sequences - suggestive of syringomyelia.  There was no evidence of tumour or any other abnormality.

Diagnostic arthroscopy of right knee joint revealed gross synovial thickening and erosion of articular cartilage.

Discussion :

Neurological complications, though rare, have been documented following spinal anaesthesia.  Serious neurological events like anterior spinal artery syndrome, transverse myelitis, cauda equine syndrome, complete flaccid paralysis have occurred.

In the above case scenario, we propose the mechanism for neurological complications to be direct penetration4 and consequent injury of the spinal cord leading to the production of post traumatic synrix5,6,7.  Post traumatic syrinx after spinal anaesthesia can occur due to arachnoid scarring8.

Neuropathic arthropathy (Charcot Joint)9,10 develops mostly in weight bearing joints.  The predominant cause is diabetes mellitus, but also associated with neuropathic arthropathy are tabes dorsalis, leprosy, yaws, meningomylocele, synringomyelia, spina bifida, spinal cord injury, congenital insensitivity to pain,  aerodystrophic neuropathy, amyloid neuropathy, peripheral neuropathy, secondary to alcoholism and avitaminosis, peripheral nerve injury, post renal transplant arthropathy and intraarticular steroid injections.

Although the exact underlying mechanism in the pathogenesis of neuropathic arthropathy remains unclear it is generally believed to be related to the destruction of afferent proprioceptive fibres and or subsequent unrecognized trauma to the joint due to dissociative sensory loss.   The loss of sensation to the joint is followed by severe degenerative changes, osteophyte formation, articular and subchondral fractures and often calcification in the surrounding soft tissues.  The progression of neuropathic arthropathy is extremely variable.

Patient is presently treated with orthosis, and repeated aspirations are being done when joint effusions become tense.  We further plan for complete debridement of all hypertrophic synovium and arthrodesis if necessary.


Reference :

  1. Seigne TD. Aseptic meningitis following spinal analgesia Anaesthesia 1970; 25: 402-407.

  2. Ravindran RS, Bond VK, Tasch MD, Gupta CD, Luerssen TG. Prolonged neural blockage following regional analgesia with 2- Chloroprocaine.  Anaes. Analg. 1980; 59: 447-451.

  3. Usubiaga J.  Neurological complications following epidural anaesthesia. Int. Anaesthesiol Clin. 1975; 3: 69-75.

  4. Kane RE.  Neurological deficits following epidural or spinal anaesthesia. Anesth Analg. 1981; 60: 150-161.

  5. Umbachi, Heilporn A, Post spinal cord injury syringomyelia paraplegia 1991; 29: 219- 221.

  6. Schurch B, Wichmann W, Rossier AB.  Post traumatic syringomyelia (cystic myelopathy) A prospective study of 449 patients with spinal cord injury.  J Neurol Neurosurg Psychiatry 1996; 60: 61.

  7. Shannon N, Simon L, Logue V.  Clinical features investigation and treatment of post traumatic syringomyelia J. Neurol Neurosurg Psychiatry 1981; 44; 35.

  8. Youman’s Neurological surgery 4th edn. Vol 2. pg 1090-1092.

  9. Campbell’s Operative Orthopaedics 10th edn. Vol 1 Pg 957 – 958.

  10. Harrison’s Principles of Internal Medicine


This is a peer reviewed paper 

Please cite as : Gopakumar T S : Neuropathic Joint Following Spinal Anaesthesia – A Case Report

J.Orthopaedics 2008;5(3)e2





Arthrocon 2011

Refresher Course in Hip Arthroplasty

13th March,  2011

At Malabar Palace,
Calicut, Kerala, India

Download Registration Form

For Details
Dr Anwar Marthya,
Ph:+91 9961303044



Powered by



© Copyright of articles belongs to the respective authors unless otherwise specified.Verbatim copying, redistribution and storage of this article permitted provided no restrictions are imposed on the access and a hyperlink to the original article in Journal of Orthopaedics maintained. All opinion stated are exclusively that of the author(s).
Journal of Orthopaedics upholds the policy of Open Access to Scientific literature.