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Year : 2003  |  Volume : 51  |  Issue : 1  |  Page : 118--120

Cauda-conus syndrome resulting from neurocysticercosis

NN Singh, R Verma, BK Pankaj, S Misra 
 Department of Neurology, Institute of Medical Sciences, Banaras Hindu University, Varanasi-221005, India

Correspondence Address:
N N Singh
Department of Neurology, Institute of Medical Sciences, Banaras Hindu University, Varanasi-221005
India

Abstract

A 60-year-old male, presented with insidious onset, gradually progressive, burning paresthesia over the saddle area, sphincteric disturbance, impotence and paraparesis. Investigations revealed a ring-enhancing lesion in the conus medullaris suggestive of neurocysticercosis . This was supported by quantitative enzyme-linked immunosorbant assay from purified cell fraction of taenia solium cysticerci. On treatment with steroids he showed marked improvement.



How to cite this article:
Singh N N, Verma R, Pankaj B K, Misra S. Cauda-conus syndrome resulting from neurocysticercosis .Neurol India 2003;51:118-120


How to cite this URL:
Singh N N, Verma R, Pankaj B K, Misra S. Cauda-conus syndrome resulting from neurocysticercosis . Neurol India [serial online] 2003 [cited 2023 Mar 31 ];51:118-120
Available from: https://www.neurologyindia.com/text.asp?2003/51/1/118/1058


Full Text

Conus medullaris is the caudal tip of the spinal cord lying against the L1 vertebra and comprises the sacral and coccygeal segments. Cauda equina consists of the lumbosacral root lying below the L1 vertebra, named so because of its resemblance to a horsetail. Cauda equina is a well-recognized polyradiculopathy syndrome, which is sometimes associated with the involvement of the conus, while isolated conus lesion being uncommon (less than 5-10%). Various compressive and non-compressive causes have been described, of which disc prolapse is the commonest etiology.[3] We report here an unusual but interesting cause of the cauda-conus syndrome.



  

   Case History



A 60-year-old male presented with burning pain in the saddle distribution of six months duration. After four months of symptoms, he developed acute onset retention of urine with overflow incontinence along with constipation and loss of penile erection. By this time he also complained of dragging of the right foot. In the next two weeks, he gradually became bedridden. He did not give a history of root pain, low backache, trauma to back, prolonged fever or claudication pain, weight loss, anorexia, diabetes or tuberculosis.

On clinical examination, he had a symmetric lower motor neuron type paraplegia with sensory bladder and bowel involvement. Spinal tenderness and deformity were absent. Examination of upper limbs revealed two pea-sized non-tender subcutaneous nodules which were biopsied. The rest of the general and systemic examinations were non-contributory.

He had a normal hemogram and erythrocyte sedimentation rate. X-rays of the lumbosacral spine and chest were normal. Contrast magnetic resonance imaging (MRI lumbosacral spine) revealed a small ring-enhancing lesion 13 x 9 x 11 mm within the conus medullaris with an eccentric nidus appearing isointense to hypointense on T2 weighted axial section.

Biopsy from the subcutaneous nodule showed a cysticercus larva. A quantitative ELISA for immunodiagnosis of neurocysticercosis using cerebrospinal fluid (CSF) and purified fraction from taenial solium cysticerci (PCF-ELISA) showed a strongly positive result. CSF routine and microscopy revealed normal findings with normal lactate dehydrogenase (LDH) and microglobulin. CSF immunocytochemistry for lymphoma was negative. Tuberculin test was negative. When treated with prednisolone (1.5 mg/kg), he showed a remarkable improvement after two weeks. Pain disappeared first and he started walking unsupported and regained continence of bladder and bowel. At the end of a month of steroid treatment, he became normal with return of bladder/bowel sensations, normal reflex, normal sensations and normal with power. Follow-up MRI studies revealed complete resolution of lesion.



  

   Discussion





The cauda-conus syndrome is a well-defined clinical entity. The typical cauda equina syndrome presents as a triad of asymmetric lower motor neuron paraparesis, variable areflexia and bladder bowel symptoms along with root pains. On the other hand, a pure conus lesion presents as symmetric dissociated saddle anesthesia, minimal (knee flexor, plantar flexor and hip abductor) or no weakness, early and marked bladder/bowel dysfunction and impotence. History of root pain is absent.[1],[2]

Mixed cauda-conus syndrome has a combination of features of the cauda equina and conus medullaris syndromes. Symptoms starting with symmetrical paresthesia, bladder bowel involvement, impotence and later weakness in lower limbs, with absent knee and ankle jerks point to an initial conus lesion later involving the lumbosacral roots (conus-cauda lesion). The most common clinical diagnosis of such a condition is an intramedullary tumor of the conus, usually an ependymoma.[3]

In the present case, contrast MR revealed a ring-enhancing lesion in the conus medullaris, compressing the lumbosacral nerve roots. The diagnosis of neurocysticercosis was based on the characteristic MR appearance, biopsy from the subcutaneous nodule, positive PCF-ELISA in CSF (sensitivity 95%, specificity 100%).[4] Hematogenous spread of the cysticercus larva to the conus medullaris resulted in the clinical and radiological manifestations in one patient. Several causes of the conus-cauda lesion have been described such as disc prolapse, arachnoiditis, ankylosing spondilytis, fluorosis, trauma, infarction of conus, conus myelitis and non-hodgkins lymphoma (NHL).[5],[6],[7],[8],[9]

Cysticercosis is the most common parasitic disease involving the nervous system. Involvement of the spinal cord is rare (ranging from 0.7%-5.8%).[9] Forty-five cases of intramedullary cysticercosis have been reported in the literature, presenting as quadriplegia or paraplegia, but none have been reported in the conus medullaris region.[10],[11]

As granulomas and calcified stages represent dying and dead cyst respectively, anticysticercus treatment is not required in such cases.[12] There is insufficient evidence to assess whether cysticidal therapy is associated with beneficial effects.[13] Present recommendation advocates use of corticosteroid for controlling inflammation in single ring-enhancing lesions.[14] This is in contrast with previous case reports of intramedullary cysticercosis where an overenthusiastic approach called for surgical intervention.[8],[9]

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