Immunological and Endocrine Profile of Two Patients with Severe Subarachnoid Neurocysticercosis, Resistant to the Cysticidal Treatment

Research Article

Austin J Clin Neurol 2014;1(3): 1013.

Immunological and Endocrine Profile of Two Patients with Severe Subarachnoid Neurocysticercosis, Resistant to the Cysticidal Treatment

Laura Adalid-Peralta1,2, Gladis Fragoso3, Edda Sciutto3, Marisela Hernández3, Agnès Fleury2,3, Helgi Jung1 s and Graciela Cárdenas1*

National Institute of Neurology and Neurosurgery, Mexico

Peripheral Unit of the Institute for Biomedical Research at the National Institute of Neurology and Neurosurgery, México

Institute of Biomedical Research, National Autonomous University of Mexico; Mexico

*Corresponding author: Graciela Cárdenas, National Institute of Neurology and Neurosurgery, D.F., 14269, Mexico City, Mexico

Received: February 21, 2014; Accepted: July 21, 2014; Published: Aug 04, 2014


Neurocysticercosis (NC) is a disease caused by the establishment of Taenia solium larvae in the central nervous system. NC may exhibit different clinical pictures depending on the location of the established cysticerci, their degenerating stage, and the intensity of the immune-inflammatory profile induced by the infection. Moreover, the response to cysticidal treatment is also heterogeneous. When cysticerci establish in the subarachnoid space of the base (SABNC) they are more frequently resistant to the treatment.

To further deepen our understanding of this resistant status, the central and peripheral inflammatory and endocrine profiles of two SABNC patients who failed to respond to four treatment cycles (albendazole plus corticosteroids) are herein reported.

Several immunological and endocrinological treats were found altered: decreased levels of testosterone, cortisol, and prolactin were observed, accompanied by increased levels of immunomodulatory cytokines (TGF-β and IL-10), as well as LH.

Altogether, these results establish the impact of SABNC on the immune-inflammatory and endocrine status of both patients. The possible relevance of these changes in the NC pathogenesis is discussed.

Keywords: Taenia solium; Neurocysticercosis; Treatment resistance; Taeniasolium


NC: Neurocysticercosis; SABNC: Subarachnoid of the base Neurocysticercosis; CSF: Cerebrospinal Fluid; INNN: Instituto Nacional de Neurología y Neurocirugía; ABZ: Albendazole; ABZ-SO: Albendazole Sulfoxide; HPLC: High-performance Liquid Chromatography; CT: Computed tomography; MRI: Magnetic resonance imaging; DXM: Dexamethasone; PZQ: Praziquantel; MTX: Methotrexate; PDN: Prednisone


Human cysticercosis is a parasitic infection caused by the establishment of Taenia solium larvae (cysticerci) in human tissues. In most cases, the parasite establishes in muscles and in the brain. The latter location leads to neurocysticercosis (NC), the most severe form of the disease [1]. The clinical presentation of NC varies from asymptomatic to mild to a severe neurological disease with intracranial hypertension. This heterogeneity mainly depends on the parasite location in the central nervous system [2]. NC patients lodging cysticerci in the parenchyma generally show an inflammatory response restricted to the area surrounding the cysts, exhibit a non-inflammatory cerebral spinal fluid (CSF) [2], and an effective response to the cysticidal treatment is usually observed [3]. In contrast, when cysticerci are located in the ventricles or in the subarachnoid space of the base (SABNC), most cases are accompanied by an increased CSF cellularity and may result in secondary intracranial hypertension. Several findings support the hypothesis that the parasite gained, thorough millions of years of co-evolution with the host, the ability to manipulate its environment, promoting a comfortable milieu that favor its survival [4,5]. This is seems to be a common strategy developed by some large parasites that may persist for years in the host tissues without apparent inflammatory response [6].

The endocrine system could also participate in this immunomodulation, as it has been reported in other host-parasite interactions, both under experimental and natural conditions [7]. Regarding human NC few information and the role of immunoendocrine system is available [8].

In this report, we present the inflammatory and endocrine profiles of two SABNC patients harboring multiple parasites and who did not respond to several cycles of conventional cysticidal treatment (non-responder patients).

Case Presentations

Case 1

A 29 year-old Mexican man living in the United States of America suffered from sudden generalized seizures. CT scan showed NC. The patient was administered ABZ plus steroids. Afterward, progressive motor dysphasia, right sided weakness, and intracranial hypertension signs appeared and the patient came back to Mexico. MRI showed extensive racemose cysticerci on left Sylvian fissure with displacement of anatomical structures off the medial line. ABZ at 30 mg/kg, plus dexamethasone (DXM) at 0.3 mg/kg were administered during 8 days. Motor weakness improved in the following months, and a control MRI showed a 95%-reduction of the giant racemose cysticercus, along with asymmetric dilation of the left ventricle secondary to encephalomalacia (the side where parasites were previously lodged), and also multiple new parasitic lesions in the cerebral media artery cisterns. Clinical improvement continued until 4 months later, when the patient developed suddenly intense headache associated to visual blurring and diplopia. The patient was hospitalized to receive an additional ABZ cycle with close medical supervision. In the clinical and radiological follow-up at 7, 9, 11, and 19 months, basal parasites located in the perimesencephalic region persisted and a new parasite in the third ventricle appeared. A total of 6 ABZ and DXM cycles and two combined ABZ and praziquantel (PZQ) cycles were administered, with neither clinical nor radiological evidence of parasite elimination (Table 1). (Some data from this patient were partially reported in BMC Neurol 2010:10:16.) [9].