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Year : 2001  |  Volume : 49  |  Issue : 1  |  Page : 71--4

Intramedullary cysticercosis : MRI diagnosis.

SN Mathuriya, VK Khosla, RK Vasishta, MK Tewari, A Pathak, S Prabhakar 
 Department of Neurosurgery, Postgraduate Institute of Medical Education and Research, Chandigarh - 160012, India., India

Correspondence Address:
S N Mathuriya
Department of Neurosurgery, Postgraduate Institute of Medical Education and Research, Chandigarh - 160012, India.


Three cases of dorsal intramedullary cysticercosis presenting as spastic paraparesis or paraplegia are reported. A definite preoperative diagnosis, using MRI, was made in two cases while in the third it was strongly suspected. One paraplegic patient regained full function whereas in the other two the deficit persisted even after successful cyst excision. The pathogenesis and recovery are discussed in the light of the MRI findings.

How to cite this article:
Mathuriya S N, Khosla V K, Vasishta R K, Tewari M K, Pathak A, Prabhakar S. Intramedullary cysticercosis : MRI diagnosis. Neurol India 2001;49:71-4

How to cite this URL:
Mathuriya S N, Khosla V K, Vasishta R K, Tewari M K, Pathak A, Prabhakar S. Intramedullary cysticercosis : MRI diagnosis. Neurol India [serial online] 2001 [cited 2023 Jun 9 ];49:71-4
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  ::   IntroductionTop

Cysticercosis (CS) is the commonest infestation of central nervous system (CNS).[1] CNS involvement occurs in 60-90% of CS patients.[2] The incidence of spinal CS is around 5.85%.[3] Sotelo et al reported an incidence of 0.77% in an isolated analysis of 753 cases.[4] The cysts are commonly located in spinal subarachnoid space (SAS).[5] Cysticercus cysts in spinal SAS are eight times frequent than intramedullary (IM) location.[3] Only 42 cases of intramedullary cysticercosis (IMC) have been reported in literature.[1],[3],[5],[6],[7],[8],[9],[10],[11],[12],[13],[14],[15] IMC was first diagnosed on MRI by Zee in 1986.[16] Diagnosis of IMC was based on MRI in only four patients.[6],[15],[16] Antihelminthic therapy is routinely used in treating parenchymal cerebral cysticercosis (CCS). Their use in managing IMC is advocated and a clinico radiological cure was attained in one patient of IMC.[15] This was based on the fact that IMC is a form of parenchymal CS.[17] Surgery does not provide an unequivocal cure without morbidity in all cases of IMC. Antihelminthic drugs have proven so in one case. Hence, it demands an imagining tool which can not only make a correct diagnosis, but can also predict the prognosis. This can be fulfilled by present generation MRI.

  ::   Case reportTop

Case 1 : A 28 years male presented with severe localised upper dorsal pain of 10 weeks duration, followed by progressive heaviness, tingling, numbness and weakness of both lower limbs. At admission, the patient was bed-ridden with spastic paraplegia (grade 0/5) and urinary retention. He had minimal sensory preservation below D2 level. There was no evidence of systemic or cerebral CS. Plain Xrays of dorsal spine were normal. CT myelography demonstrated localised IM lesion at D1. MRI showed a low intensity lesion with a slightly hyperintense nodule suggestive of protoscolex on T1WI and a high intensity lesion on T2WI with widened cord [Figure]. A diagnosis of an IMC was made. The CSF sugar was 30 mg% and protein was 80 mg%. There were 40 cells with equally distributed polymorphs and lymphocytes. At surgery, the cord was widened at D1

2. A one cm diameter cyst with thin opalescent wall was delivered intact at myelotomy. Histopathological examination (HPE) proved the lesion to be a cysticercus cyst with scolex. There were no surrounding adhesions or inflammation. The patient resumed his work 6 months after surgery. At follow up, a year later he had regained almost full sensory, motor and bladder functions.

Case 2 : A 55 years male, diagnosed case of cerebral CS on CT, was admitted with pain and numbness in both the lower extremities, progressive paraparesis and urinary retention of seven months duration. Subcutaneous nodules were palpable over the left forearm. Neurological examination revealed spastic paraplegia (grade 0/5), marked sensory loss distal to D1 and upper motor neuron bladder. Myelography and CT indicated an IM lesion at D2. MRI delineated a swollen cord at D1-2 with a low intensity lesion on T1WI. There was bright signal intensity around the lesion on T1WI [Figure 2]. Laminectomy at D1-2 revealed an enlarged cord. A cyst was delivered after myelotomy. The cyst wall was adherent to the surrounding cord tissue by flimsy adhesions. Histology confirmed a cysticercus cyst with acute and chronic inflammatory cell infiltration around the cyst wall. Patient did not show improvement on follow up after one year.

Case 3 : A 50 years male attended neurology clinic with burning pain over both the lower extremities for the last two years. A year later, he experienced paraparesis, hypoaesthesia and dysuria. Neurological examination revealed that both lower limbs were hypotonic with grade IV power in all the muscle groups. There was graded sensory loss of all modalities below L1 including the perianal region. Plain X-rays, lower dorsal spine, blood and serum analysis did not suggest any abnormality. A small IM lesion was visualised on MRI, which was hypointense on T1WI and hyperintense on T2WI, which was located at D11. There was a perilesional hyperintensity [Figure 3a] and [Figure 3b]. A diagnosis of an IM lesion was made with IMC being a strong possibility.

Laminectomy at D10-12 revealed an IM cystic lesion, which was stuck to the adjacent cord tissue. The cyst was carefully dissected and excised. Histology revealed a thick collagenous wall with connective tissue and inflammatory cells (lymphocytes, plasma cells and macrophages), the findings suggested cysticercosis. The patient deteriorated in the immediate postoperative period and improved gradually to the preoperative status only. Cranial CT carried out in the post operative period depicted an infarct in the left caudate nucleus and cerebral paraenchymal CS.

  ::   DiscussionTop

Intramedullary cysticercosis is an extremely uncommon entity. 42 cases have been reported in literature till date.[1],[3],[5],[6],[7],[8],[9],[10],[11],[12],[13],[14],[15] 32 patients were diagnosed at surgery, and nine at necropsy.[3],[8] The lesion was diagnosed on MRI and was treated with albendazole therapy in one patient.[15] We have operated 54 patients of neurocysticercosis (NCC) and only four were located in lM location (7.4%). One patient was before MRI era and has been reported earlier.[12]

90% of reported cases of lMC due to NCC ranged between 20-45 years of age. The duration of symptomatology varied from a week to 10 years.[7],[12] Majority of patients presented within 6 to 8 months. Two of our three patients were in the fifth decade and all the three had significantly progressive course of 2 to 7 months duration.[3],[13] In 64% of patients, the cysts were located in the dorsal cord which is in accordance with the regional blood flow to the spinal cord.[3],[12] The cysts in all the three patients under study were also located in the dorsal cord. The mode of spread of IMC is either haematogenous or ventriculoependymal. There are strong pointers to favour haematogenous genesis of lMC.[4]

Some of the patients with IMC are known to harbour cerebral cysticerci.[3],[13] Presumptive preoperative diagnosis of spinal cysticercosis is easy when there is associated CCS,[15] which was the case in two of our patients. There is an adequately correct MRI correlation of various pathological stages of NCC. High quality resolution, multiplanar, multi sequential imaging and variability of contrast take up in different phases helps in excellent diagnostic imaging on MRI.[20] Treatment modality (drug therapy and surgery, drug therapy followed by surgery) can be planned as per the pathological stage imaged on MRI.

The pathological finding depend upon the stage of the cyst.[4] In vesicular stage, larva is around 5mm diameter with marginal projecting nodule (scolex) surrounded by clear cyst fluid within thin capsule (live cyst). The colloidal vesicular stage suggests commencement of degeneration and mineralization. The cyst fluid becomes turbid jelly like and capsule thickens.[6] In granular nodular phase, there is cyst retraction due to mineralised and granular contents. Capsule thickness collagenises and hyalinises in degenerating ageing cyst. Adjacent neural tissue shows inflammatory changes in the form of increased vascularity, capillary endothelial proliferation, infiltration by lymphocytes, plasma cells, eosinophils, histiocytes and multinucleated giant cells, alongwith oedema and gliosis.[22] These are conspicuously absent in live cyst. Finally these changes reduce and vanish when cyst is totally mineralized as calcific nodule.[20],[21]

On MRI, live parasite i.e. vesicular stage appears as a clearly marginated hypointense cyst with hyperintense scolex within on T1WI, and just the reverse on T2WI.[23],[24] In colloidal vesicular stage, the thickened cyst capsule is visualized as slightly bright signal on T1WI and hypointense on T2WI. Cyst contents appear comparatively hyperintense on T1WI and hence scolex is not seen. The changes in neural tissue around as described above impart a hyperintense signal on T1WI which enhances on contrast.[16],[20],[25] These findings are prominent in ageing, degenerating cyst (colloidal and granular stage) and becomes minimal in mineralised cyst. Cysts with hyalinisation

or collagenisation show lower intensity signal on T2WI and brighter signal on T1WI.[20] Calcified cyst is seen as low intensity both on T1w1 and T2W1. These are observations in parenchymal CCS and IMC. This is a form of parenchymal NCC, hence, IMC is likely to have the same images.[18]

Mural nodule could be nicely perceived in case 1 in this study on MRI. Case 2 and 3 exhibited pericystic hyperintense signal on T1WI which lacked in case 1. Similarly, scolex was not seen in case 2 and 3. These findings correlated well with histopathological examination i.e. scolex in case 1, pericystic inflammation in case 2 and 3, and associated collagenisation in case 3. Hence, there was a proper correlation between MRI and pathological features.

The culminant factors for neurological damage in IMC include (i) mechanical compression by cyst, (ii) inflammatory changes, and cord oedema, secondary to metabolic products/degenerative larval remains, and (iii) gliosis due to vasculopathy.[8] Surgery can eliminate only compressive element and this should be performed before the cord changes take place.[8] Intermittent long term albendazole therapy of 75 days along with steroids led to a clinical as well as MRI disappearance of lesion in one patient.[15] Long term therapy related probably to variant life history of parasite in lM location, poor drug penetrance due less vascularity of the cord and may be an intact neural barrier.

Postoperative recovery was observed in 60% of the published cases in literature.[18] Only one patient with live cyst under study with no pericystic inflammation, oedemia, gliosis, adhesions and capsule collagenization showed total post operative recovery from parapligia and bladder involvement. These changes are responsible for interminable disability inspite of safe cyst excision at surgery in the other two patients. These changes detected on MRI can foretell the probable prognosis, hence, MRI is not only diagnostic but can even be decisive for likely ultimate recovery in IMC.


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