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Neurology India, Vol. 59, No. 2, March-April, 2011, pp. 299-301 Letter to Editor Charcot foot in post-tubercular spinal arachnoiditis may indicate emerging dorsal cord syringomyelia Vimal Kumar Paliwal, Achal Kumar, Sushil Kumar Rahi, Sunil Pradhan Department of Neurology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, India Correspondence Address: Vimal Kumar Paliwal, Department of Neurology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, India, dr_vimalkpaliwal@rediffmail.com Date of Submission: 01-Dec-2010 Code Number: ni11082 PMID: 21483141 DOI: 10.4103/0028-3886.79155 Sir, Charcot foot is a neuro-osteoarthropathy of foot joints caused by propriospinal and nociceptive sensory loss in the affected area because of underlying neurological disease. We present a patient with tubercular spinal adhesive arachnoiditis who developed Charcot feet and thereby diagnosed to have cervico-dorsal syrinx. A 45-year-old man suffered from painless swelling at right ankle that progressed to mid foot region over 1 month. There was no pre-existing joint disease. In the previous year, he was diagnosed with tubercular spinal meningitis when he developed acute sensory-motor paraplegia, urinary and fecal incontinence (T3 ASIA A injury), low-grade fever and radicular pain in lower limbs. Magnetic resonance imaging (MRI) of dorso-lumbar spine revealed clumping of lumbar roots, cerebrospinal fluid (CSF) pockets in lumbar spinal canal and contrast enhancement of spinal meninges. CSF examination revealed 500 cells/cu mm with 80% lymphocytes, 250 mg% protein, 30 mg% glucose, and positive CSF PCR and culture for Mycobacterium tuberculosis. He improved partially after 8 months of anti-tubercular drug therapy and resumed walking for household distances with the support of a walker. However, the sensory impairment in lower limbs and autonomic symptoms persisted. On examination at the time of presentation with foot swelling, patient had hypotonic areflexic paraparesis with grade 3/5 power and partial asymmetric wasting of gluteal, thigh, and leg muscles. There was complete pin-prick sensory loss below T3 spinal segment with partial sparing of light touch sensations from L5 to S3 segments. A warm nontender swelling in the right ankle region was noticed. [Figure - 1]a Dorsalis pedis, popliteal, and femoral arteries were normally palpable. X-ray of the right foot showed sclerosis of calcaneum, talus and navicular bones, loss of trabecular pattern, and periarticular sclerosis in lower end of tibia [Figure - 1]b. X-ray of the left foot showed periarticular sclerosis of lower end of tibia, talus, calcaneum and navicular bones [Figure - 1]c. Repeat MRI spine showed cervico-dorsal syrinx with spinal arachnoiditis [Figure - 2]. CSF examination showed 65 mg% protein, no cells, negative culture for Mycobacterium and negative CSF VDRL test. ELISA for HIV was also negative. Patient was immobilized and given elastic stockings for 2 weeks for subsidence of foot edema. After another 2 weeks of immobilization in below knee total contact cast, partial weight bearing was allowed. Intermittently, cast was changed to look for foot swelling, ulcer or gangrene. At 3 months, X-ray of both feet showed partial resolution of sclerosis of Calcaneum and navicular bones in both feet. Patient was allowed limited weight bearing without cast. Syrinx was not operated in view of severe adhesive arachnoiditis. Tubercular spinal arachnoiditis results in thick adhesions in the dorso-lumbar spinal canal that involve multiple spinal roots and cause paraplegia, sensory loss, deep tendon reflex loss and radicular pains. Unlike Charcot shoulder, Charcot foot is never reported in patients with tubercular arachnoiditis [Table - 1]. [1] Possibly, Charcot foot is either rare or overlooked in these patients. Tubercular spinal arachnoiditis may produce complications like syrnigomyelia which is well known to produce Charcot arthropathy. [8] In patients with spinal arachnoiditis, an emerging syrinx may not be recognized on clinical examination as the hallmark clinical signs associated with syrnigomyelia, such as dissociative and suspended sensory loss in the affected spinal segments are obscured by the pre-existing sensory impairment secondary to spinal arachnoiditis. We propose that the clinical and radiological signs of Charcot foot in a patient with spinal arachnoiditis may be an indicator of developing syringomyelia. Patients with tubercular arachnoiditis should be monitored by clinical and X-ray examination of both feet for timely diagnosis of Charcot arthropathy before the development of its complications, such as foot ulcers, osteomyelitis, fractures, and deformities. References
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