Acute paraplegia in the early postoperative period is a challenging and potentially devastating anesthetic complication, which can occur when neuraxial techniques are used. Several clinical differential diagnoses are possible. Emergent MRI in this patient excluded cord compression by lesions such as herniated intervertebral discs, dislocated vertebral body or bony material, tumor, epidural abscess or epidural hematoma. According to the topographical distribution of neurological deficits, a thoracic intramedullary hyperintensity lesion (between T10 and T12) on the T2 weighted MRI scan and elevated protein in the CSF analysis, the diagnosis of thoracic ATM was established [4].

 ATM is a rare clinical syndrome with an incidence of one to four patients per million, per year [5]. It is characterized by acute inflammation affecting the white and gray matter in multiple spinal cord segments, and causes rapid development of neurological deficits in motor, sensory, and autonomic functions. Motor weakness typically occurs initially in the lower legs and ascends to the waist rapidly, although bilateral arms may be involved occasionally. Loss of sensation in all modalities below a fixed level usually can be documented. Autonomic dysfunction varies, however, including increased urinary urgency, bowel or bladder incontinence, difficulty or inability to void, incomplete evacuation, or bowel constipation.⁶ Mostly, these neurological deficits progress to their nadir within hours or days [4]. The most common level in adults is the mid-thoracic region, whereas children have a higher frequency of involvement of cervical levels [7]. Based on expert opinion of the Transverse Myelitis Consortium Working Group, causes of ATM can be classified as either idiopathic or disease-associated ATM. The latter is usually a part of manifestations of systemic autoimmune disease, such as systemic lupus erythematous, multiple sclerosis, Sjogren syndrome, or neurosarcoidosis [8]. The remaining idiopathic ATM is difficult to find the definite causes but is generally thought as a parainfectious or autoimmune-based neuroinflammatory process [4]. Nearly half of the patients diagnosed with idiopathic ATM have a preceding febrile event such as respiratory, gastrointestinal, or systemic illness [9,10].

 In the majority of cases of acute transverse myelitis the aetiology is unknown; preceding infections, mainly viral account for 27-37% of cases [11,12]. Syphilitic endarteritis was probably a common cause of acute transverse myelitis at the beginning of the century [13]. At present, vascular causes resulting mainly from atherosclerosis and collagen diseases are probably more common than syphilis [14,15].

Berman et al [12] developed a criterion for the diagnosis of Acute transverse myelitis which included:

1. Acutely developing paraparesis affecting motor and sensory system as well as sphincters.
2. Spinal segmental level of sensory disturbance (patients with patchy sensory deficit or Brown

Sequard syndrome were excluded).

1. Stable, non progressive clinical course.
2. No clinical or laboratory evidence of spinal cord compression and
3. Absence of other known neurological disease, including malignant disease with metastasis, severe

back trauma and encephalitis. Patients with irradiation of the spine were also excluded.

In a study conducted by Berman et al [12], 3 patients gave history of unusual physical strain before the onset of acute transverse myelitis and 1 occurred after obstetric delivery. 8 patients had malaise without fever 3 days to 3 weeks before the onset of acute transverse myelitis.

The temporal relationship and proximity of an spinal needle for TEA to the affected regions of spinal cord easily raises the concern that spinal anesthesia or local anesthetic neurotoxicity may be the cause of the neurological deficits [16]. Although sporadic cases of ATM have been described following spinal [17] or epidural [18,19] anesthesia and even general anesthesia without neuraxial invasion, [20] none of them suggested a direct causal relationship after cautiously ruling out vascular and compressive etiologies of cord injury. Direct cord trauma either by needle was hardly possible in our patient since the needle was inserted while she was fully conscious. Once the cord was inadvertently penetrated or injected with local anesthetic, she should be aware of the injury and reported his suffering at the first moment. Importantly, the patient was doing well after surgery with freely movable extremities until acute deterioration of spinal cord function on POD 1. Excessive sensory and motor blockade from epidural local anesthetics was excluded since the sensory and motor deficits were not reversed after removal of spinal needle. Therefore, the progression of sensory, motor, and autonomic deficits, along with development of characteristic inflammatory spinal cord lesion determined by an MRI scan, strongly support the diagnosis of ATM. [4,17,18,19,20].

The causes of ATM in this patient in the early post- operative period may be secondary to an occult infection or by an immune-mediated neuroinflammatory mechanism. Since the autoimmune profile was normal, negative bacterial cultures may be explained by the aggressive use of postoperative antibiotics. Although high dose intravenous corticosteroid treatment to this situation is usually anecdotal, it was reasonable in this patient who yielded partial improvement in motor function⁸. In spite of failure of identification of an infectious source, the cord lesion was evidently neuroinflammatory in etiology, which explained the effect of high-dose steroid therapy.

Lack of information regarding temporal sequence of needle trauma, injection of lignocaine and paresthesias limits the ability to ascertain the etiology of such profound neurological deficit. The severe pain and the electric shock-like sensation passing symmetrically through both lower limbs immediately after insertion of needle, during the procedure were highly suggestive of direct cord injury by the needle. Paresthesias associated with spinal cord injury can occur at the time of needle placement but has also been reported at the time of injection or secondary to irritation, edema or hematoma [21, 22].

The assessment of the lumbar intervertebral space by palpation of anatomical landmarks for lumbar puncture can be grossly wrong, which explains the rather rostral lesion in our patient. Surveys have shown that the correct position was often not clearly identified and errors can range from one to several spaces above the presumed level of puncture site [23]. Similar discordance has been observed between actual level of puncture site and those recorded in operative notes [23,24]. Some such accidents occur when this is tried under sedation and the patient is unable to react to the initial pain on touching the nerve root of the spinal cord but cases have also been reported where paraplegia occurred during injection in an awake patient as evident in our case [24,25]. Pain is more common and severe in extra-axial lesions affecting the nerve roots or blood vessels that are innervated by sensory neurons mediating pain. Surprisingly, some patients do not experience any pain during the puncture of spinal cord and pass unnoticed even if the procedure is done under fluoroscopy [23,24].

 In addition to direct needle trauma, neurotoxicity of the anesthetic agent or arterial occlusion or hypoperfusion could have contributed to paraplegia in this patient, since cytotoxicity of local and regional anesthesia is well established [26] This patient had paresthesias immediately after needle had traumatized the spinal cord and the injection of anesthetic agent most likely worsened the damage resulting in such a dense paraplegia.

The possible value of high-dose steroid treatment in this setting is unknown but given the poor prognosis, treatment by MPS should be considered. If used within eight hours, it has been shown to improve the outcome in other forms of injury [22].

Investigations to date strongly support that acute transverse myelitis is an autoimmune disease, lending support to studies which suggests that immunosuppressive therapy is beneficial [27]. In our case, acute transverse myelitis developed on the first postoperative day after a complete and normal recovery from the effect of spinal anesthesia. Also, the patient gave a history of malaise without fever 2 weeks prior to surgery.

Neurological complications following general anesthesia are not unknown [28,29]. Earlier studies and case reports have shown that transverse myelitis may follow even after an uncomplicated general anaesthesia [21]. Therefore, it appears that it is not always true to assume a close temporal relationship between regional anesthesia and transverse myelitis, since the aetiology remains unknown in majority of the cases.