British Journal of Radiology (2004) 77, 681-684
© 2004 British Institute of Radiology
doi: 10.1259/bjr/90641678
MRI of spinal intradural arachnoid cyst formation following tuberculous meningitis
S Lolge, MD1,
A Chawla, MBBS1,
J Shah, MD2,
D Patkar, MD2 and
M Seth, DMRD, DNB2
1 Department of Radiology, King Edward VII Memorial Hospital, Parel, Mumbai-400012 and 2 Department of MRI/CT, Dr Balabhai Nanavati Hospital and Research Centre, Mumbai 400 057, India
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Abstract
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Secondary intradural arachnoid cyst involving the spine is uncommon. It is usually secondary to trauma, haemorrhage, surgery or inflammation. We present two cases of treated tuberculous meningitis, which presented with gradual onset of quadriplegia and paraplegia, respectively. MRI revealed intradural (cervical and thoracic) arachnoid cysts (ventral and dorsal to the spinal cord) with myelomalacic cord changes. Ventral location of such spinal arachnoid cysts, and being secondary to tuberculous arachnoiditis are distinctively uncommon features. The rarity of this condition and the relevance of MRI in the accurate diagnosis have been discussed here.
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Introduction
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Secondary intradural spinal arachnoid cyst formation is uncommon and is known to occur due to various causes such as trauma, surgery, lumbar puncture, intrathecal injections, arachnoiditis and inflammation. Tuberculous leptomeningitis causing radiculomyelopathy and leading to various neurological deficits is a common problem in developing countries. However, very few case reports of tuberculous arachnoiditis leading to secondary arachnoid cyst formation have been reported in the English literature [1]. We present two such uncommon cases.
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Case report
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Case 1
A 35-year-old woman presented with history of asymmetric gradually progressive weakness in all four limbs over a period of 2
years. This was associated with neck pain, tingling and numbness in all four extremities. She also complained of bladder involvement with increased frequency of micturition and passing small amounts of urine on straining. The patient had a prior history of pulmonary tuberculosis 6 years earlier. She was not taking medications regularly and re-presented after 3 years with tuberculosis of the spine involving D11-D12 and also with tuberculous meningitis and arachnoiditis. She again failed to take proper antitubercule treatment.
On general physical examination the patient was emaciated. Her neck movements were painful and restricted. Central nervous system examination revealed her higher mental functions and cranial nerves to be normal. On motor system examination, she had generalized wasting with increased tone and a power of 3/5 in all four limbs, with bilateral ankle clonus. Plantar reflexes were bilaterally extensor and superficial abdominal reflexes were absent. On sensory examination; touch, pain and temperature sense were decreased below C2 level. Position sense was impaired in all four limbs. The rest of the systemic examination was normal. Her laboratory investigations revealed a microcytic hypochromic anaemia with lymphocytosis and increased erythrocyte sedimentation rate (ESR) (54 mm at the end of 1 h). The other routine metabolic profiles were normal, and HIV status was negative. The chest radiograph showed scarring and fibrosis in both apices due to her previous chest tuberculosis. MRI was performed on a 0.5T (MR Max GE) MR scanner using a surface coil. Spin echo and modified gradient echo images of the dorsal spine were obtained in multiple planes. The images revealed an elliptical shaped cerebrospinal fluid intensity lesion, appearing hypointense on T1 weighted (Figure 1a
) and hyperintense on T2 weighted images posterior to the C1 to C3 vertebral bodies (Figure 1b), and compressing and displacing the cord dorsally (Figure 2a). The lower margin of the lesion was crescent shaped, suggesting that the lesion was intradural extramedullary in location. The spinal cord revealed extensive myelomalacic changes (Figures 1b and 2b), appearing hypointense on T1 weighted images, hyperintense on T2 and extending from C3 to D12 vertebral levels. The intrathecal space in the cervical canal revealed loss of cord–cerebrospinal fluid (CSF) interface on T1 weighted images (Figure 1a) and altered signal intensities on both T1 and T2 weighted images suggesting arachnoiditis. MRI of the thoracic spine showed bony ankylosis at D11-D12 vertebral levels with fatty marrow replacement, at the site of the previously noted spinal tuberculosis. The diagnosis of an intradural arachnoid cyst secondary to tuberculosis was considered. During surgery the cyst was found to be intradural and was decompressed. The cord was partially freed from adjacent adhesions. However there was no significant improvement in patient's neurological condition post-operatively.
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Figure 1. (a) T1 weighted sagittal image of cervical spine shows cerebrospinal fluid (CSF) intensity cystic lesion ventral to spinal cord extending from C1 to C3. There is loss CSF–cord interface. (b) T2 weighted sagittal image of cervical spine shows CSF intensity cystic lesion ventral to cord extending from C1 to C3. Hyperintense foci are seen within the cord.
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Figure 2. (a) T2 weighted axial images at C3 level show cerebrospinal fluid (CSF) intensity cystic lesion ventral to cervical spinal cord displacing it posteriorly. (b) T2 weighted axial image at C5 level show hyperintense foci within spinal cord suggestive of myelomalacic changes.
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Case 2
A 58-year-old man presented with a history of gradual onset paraparesis over a period of 4 months. There was associated back pain and heaviness of his lower limbs on walking. Occasionally he had tingling and numbness in the lower limbs. There were no bowel and bladder complaints. He had a past history of CSF proven tuberculous meningitis 2 years earlier for which he had received a complete course of antitubercule therapy. On general examination, the patient was well built. Neurological examination revealed power of 3/5 in lower limbs with hyper-reflexia and upgoing plantars. Position sense was impaired in both the lower limbs. Scrotal reflex and anterior abdominal wall reflexes were lost. Routine laboratory examination revealed a haemoglobin count of 9 mg %, a lymphocytosis and an elevated ESR of 60 mm h–1. HIV ELISA test was non-reactive. MRI was performed on a 0.5 T MR scanner, using a surface spine coil. Spin echo and modified gradient echo images of the dorsal spine were obtained in multiple planes. These revealed a CSF intensity cystic lesion, appearing hypointense on T1 weighted images and hyperintense on T2 weighted images, situated dorsal to the thoracic spinal cord from D4 to D7 vertebral levels (Figure 3a, b). The spinal cord was displaced anterolaterally by this cyst, as seen on axial scans (Figure 4a, b). In addition, the MR scan revealed features of arachnoiditis. These were in the form of loss of cord–CSF interface on T1 weighted images (Figure 3a) and altered signal intensities on T1 and T2 weighted images.
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Figure 3. (a) T1 weighted sagittal image of thoracic spine shows cerebrospinal fluid (CSF) intensity lesion dorsal to cord D4 to D7 displacing it anteriorly with loss of CSF–cord interface. (b) T2 weighted sagittal image of thoracic spine shows CSF intensity lesion dorsal to cord D4 to D7 displacing it anteriorly.
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Figure 4. (a) T1 weighted axial at T4 level shows cerebrospinal fluid (CSF) intensity lesion dorsal to cord displacing it anterolaterally. (b) T2 weighted axial at T4 level shows CSF intensity lesion dorsal to cord displacing it anterolaterally.
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The cyst was decompressed after a posterior laminectomy. The cystic lesion was confirmed to be an arachnoid cyst on histopathological examination, which showed the cyst wall to be composed of arachnoid cells enclosing CSF space within it with predominant lymphocyte infiltration. There was no significant neurological improvement, at 5 months post-surgical follow-up.
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Discussion
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Spinal arachnoid cysts are relatively uncommon lesions that may be intradural or extradural with the intradural variety being rare [2]. The majority of intradural spinal arachnoid cysts occur in the thoracic region with only 15% in the cervical region and 5% in the lumbar region [2]. Most are dorsal to the spinal cord (80%) [3] as seen in our second case. Intradural arachnoid cysts ventral to the cervical spinal cord are distinctly uncommon. Lee et al reviewed 11 such cases and reported a similar case in 2001 [2].
Acquired intradural cysts may be anterior, posterior or lateral to the spinal cord. Such secondary arachnoid cysts are believed to arise from arachnoiditis. This is caused by trauma (due to iatrogenic procedures like surgery and lumbar puncture), chemical meningitis (due to subarachnoid haemorrhage, contrast media and spinal anaesthetic agents), inflammatory meningitis (due to viruses, spirochetes or bacteria) [4]. In tuberculous meningitis the exudates surrounds the spinal cord, in a non-uniform circumferential manner and is often found posteriorly due to gravitational forces, as seen in our second case. Later, cysts are formed in this organizing exudates and as their size increases, they lead to displacement and compression of the cord. This combination of organizing exudates, chronic inflammatory reaction and intradural arachnoid cysts cause vascular changes which lead to ischaemic myelopathy, cord atrophy, intramedullary cysts and infrequently total infarction of the cord. We believe that similar mechanisms would have resulted in arachnoid cyst formation in our patients leading to extensive ischaemic changes in the spinal cord, seen as altered signal intensities on MRI.
Chronic tuberculous arachnoiditis causing myelopathy is a well-known sequel after cerebral tuberculous meningitis, most often involving the dorsal cord. The myelopathy comprises either paraplegia or a combination of motor symptoms and signs of involvement of the posterior columns and spinothalamic tracts. However, often the clinical signs and symptoms of myelopathy may become manifest for the first time only years after the arrest of primary disease [5]. Our patients too, developed features of myelopathy after a period of 3 years and 2 years, respectively, post tuberculous meningitis and arachnoiditis. Chronic non-compliance to treatment caused worsening of the arachnoiditis leading to arachnoid cyst formation. As this cyst increased in size, it caused progressive cord compression, resulting in myelopathy.
MRI is the imaging modality of choice for spinal canal cysts [6]. In our cases of arachnoid cysts slightly higher signal intensity than CSF is seen on T1 weighted images is because of slightly higher protein content in these cysts by loculation of CSF or because of the relative dephasing of the protons in the pulsatile CSF [2, 7]. T2 weighted images may show heterogeneous signal attributable to the flow effect in cyst fluid. MRI is useful to assess the size, nature and extent of the cystic lesion as well as the mass effect on the cord and associated signs of meningeal inflammation. Moderate to severe arachnoiditis can be diagnosed with even non-enhanced MRI [8]. Increased CSF signal intensity on T1 weighted images leading to loss of CSF–cord interface is strongly suggestive of the arachnoiditis [9].
The differential diagnosis on imaging includes other intradural cystic lesions like dermoids, epidermoids, hydatidosis and cysticercosis. Dermoids can be differentiated as they are most commonly seen in the midline and reveal few fat signal intensity areas, however the cystic lesions seen in our patients revealed CSF intensity. Epidermoids are usually seen in children and are mostly located in the lumbar spine. They are lobulated lesions with minimally different signal intensity as compared with adjacent CSF [3]. In a rare case reported by Ciftci et al, multiple intradural cysticercosis were found in the basal cistern, cisterna magna, and cervical subarachnoid space which were isointense with cerebrospinal fluid both on T2 and T1 weighted images [10]. Intradural hydatid cysts have been reported very sporadically in the English literature. The case reported by Pushparaj et al of an intradural hydatid cyst, in the dorsal spine revealed a cystic lesion with signal intensity similar to CSF on MRI [11]. However, in our patients with a past history of tuberculous meningitis/arachnoiditis and the presence of a single CSF intensity cyst supported the diagnosis of a secondary arachnoid cysts, which were later confirmed on histopathology.
In conclusion, secondary intradural arachnoid cyst formation can be a rare cause of progressive myelopathy in patients with prior history of tuberculous meningitis. The cervical location ventral to the spinal cord as seen in one of our cases is uncommon. MRI with its excellent soft tissue resolution plays a pivotal role in the diagnosis of such pathology.
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Footnotes
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Address correspondence to Dr Ashish Chawla. 
Received for publication November 11, 2002.
Accepted for publication November 19, 2003.
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References
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Abstract
Introduction
