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  1. 1. NEUROCYSTICERCOSIS By Dr. Sheelendra Shakya Dept. of Paediatrics, KMCTH
  2. 2. INTRODUCTION <ul><li>A major cause of adult-onset epilepsy in the developing world. </li></ul><ul><li>Cysticercosis is a disease caused by the presence of cysticercus cellulosae and cysticercus racemose, the larval forms of T. solium </li></ul>
  3. 3. TYPES OF CYSTS <ul><li>Cysticercus cellulosae </li></ul><ul><li>Less virulent form </li></ul><ul><li>Small (<2cm), round, thin walled </li></ul><ul><li>Lodges in the parenchyma or the subarachnoid space </li></ul><ul><li>Provokes only a minor inflammation </li></ul><ul><li>Often remain silent </li></ul>
  4. 4. TYPES OF CYSTS <ul><li>Cysticercus racemose </li></ul><ul><li>Large lobulated cysts with predilection for basal cisterns </li></ul><ul><li>Causes cysticercotic arachnoiditis and presents as meningitis </li></ul><ul><li>Causes obstruction of 4 th ventricle and resultant raised ICP and hydrocephalus </li></ul><ul><li>Can cause occlusion of vessels and vasculits resulting in stroke </li></ul><ul><li>Causes intense inflammatory reaction and seizures </li></ul>
  6. 6. MODE OF INFECTION <ul><li>Humans are both intermediate and definitive hosts. </li></ul><ul><li>Cysticercosis develops when humans become intermediate hosts by ingesting the embryonated eggs of the tapeworm, which release oncospheres that penetrate the intestinal wall, enter the bloodstream, and disseminate into the tissue. </li></ul>
  7. 7. MODE OF INFECTION <ul><li>HETEROINOCULATION </li></ul><ul><ul><li>eggs may come from the environment </li></ul></ul><ul><li>INTERNAL AUTOINOCULATION </li></ul><ul><ul><li>regurgitated from proglottids into the stomach </li></ul></ul><ul><li>EXTERNAL AUTOINOCULATION </li></ul><ul><ul><li>from the fingers of an infected person </li></ul></ul>
  8. 8. TARGET TISSUES <ul><li>Predilection for migration to eyes, CNS and striated muscles, probably due to high glycogen and glucose content of these tissues. </li></ul><ul><li>CNS and Eye involvement is termed as Neurocysticercosis. </li></ul>
  9. 9. PRESENTATION <ul><li>The manifold and diverse clinical presentation of NC is determined by </li></ul><ul><li>Location of cysts </li></ul><ul><li>Size of cysts </li></ul><ul><li>Cyst load (number of cysts) </li></ul><ul><li>Host’s immune response </li></ul>
  10. 10. CLASSIFICATIONS <ul><li>Anatomical classification </li></ul><ul><li>Sotelo et al classification </li></ul><ul><li>Carpio et al classification </li></ul><ul><li>Chorobski Classification </li></ul>
  11. 11. Anatomical Classification <ul><li>Parenchymal NC </li></ul><ul><li>Intraventricular NC </li></ul><ul><li>Meningeal NC </li></ul><ul><li>Spinal NC </li></ul><ul><li>Ocular NC </li></ul>Nelson
  12. 12. CLINICAL PRESENTATION <ul><li>Parenchymal NC </li></ul><ul><ul><li>Seizures (87%) </li></ul></ul><ul><ul><ul><li>Simple partial with secondary generalization, generalized, complex partial or complex partial with secondary generalization </li></ul></ul></ul><ul><ul><li>Headache, nausea and vomiting </li></ul></ul><ul><ul><li>Stroke </li></ul></ul><ul><ul><ul><li>Hemiparesis </li></ul></ul></ul><ul><ul><ul><li>Focal neurologic deficits </li></ul></ul></ul><ul><ul><li>Frontal lobe involvement </li></ul></ul><ul><ul><ul><li>Psychosis, dementia, parkinsonism, intellectual impairment </li></ul></ul></ul><ul><ul><li>Cerebellar Ataxia </li></ul></ul><ul><ul><li>Fulminant encephalitis in massive initial infection </li></ul></ul>
  13. 13. CLINICAL PRESENTATION <ul><li>Intraventricular NC </li></ul><ul><ul><li>5- 10% of all cases </li></ul></ul><ul><ul><li>4 th ventricle most common site for obstruction </li></ul></ul><ul><ul><li>Cysts in lateral ventricles less likely to cause obstruction </li></ul></ul><ul><ul><li>Hydrocephalus and acute, subacute or intermittent signs of raised ICP without localizing signs </li></ul></ul>
  14. 14. CLINICAL PRESENTATION <ul><li>Meningeal NC </li></ul><ul><ul><li>Meningeal irritation resembling TBM </li></ul></ul><ul><ul><li>Raised ICP from oedema, inflammation and presence of cyst obstructing flow of CSF </li></ul></ul>
  15. 15. CLINICAL PRESENTATION <ul><li>Spinal NC </li></ul><ul><ul><li>Spinal cord compression </li></ul></ul><ul><ul><li>Nerve root pain </li></ul></ul><ul><ul><li>Transverse myelitis </li></ul></ul><ul><ul><li>Arachnoiditis </li></ul></ul><ul><li>Ocular NC </li></ul><ul><ul><li>Visual impairment (decreased visual acquity) </li></ul></ul><ul><ul><li>Scotoma, retinal detachment, iridocyclitis </li></ul></ul>
  16. 16. Sotelo et al classification <ul><li>Active forms of NC </li></ul><ul><li>(represents both viable, live and degenerating parenchymal cysts) </li></ul><ul><ul><li>Arachnoiditis </li></ul></ul><ul><ul><li>Hydrocephalus secondary to meningeal inflammation </li></ul></ul><ul><ul><li>Parenchymal cysts </li></ul></ul><ul><ul><li>Brain infraction secondary to vasculitis </li></ul></ul><ul><ul><li>Mass effect due to large cyst or cyst clumps </li></ul></ul><ul><ul><li>Intraventricular cysts </li></ul></ul><ul><ul><li>Spinal cysts </li></ul></ul><ul><li>Inactive forms of NC </li></ul><ul><ul><li>Parenchymal calcifications </li></ul></ul><ul><ul><li>Hydrocephalus secondary to meningeal fibrosis </li></ul></ul>
  17. 17. Carpio et al <ul><li>Active form </li></ul><ul><ul><li>Refers to live, viable parenchymal or extraparenchymal cysts, rarely produce symptoms apart from the rare instance of mass effect </li></ul></ul><ul><li>Transitional form </li></ul><ul><ul><li>Symptomatic seizures occur with this form. Degenerating subarachnoid cysts produce meningitis, arachnoiditis and hydrocephalus; ventricular cysts lead to acute hydrocephalus. </li></ul></ul><ul><li>Inactive form </li></ul><ul><ul><li>Single or multiple parenchymal calcification/s and /or hydrocephalus secondary to meningeal fibrosis </li></ul></ul>
  18. 18. Chorobski Classification CSF diversion procedure Basal meningeal or ventricular cysticercus giving rise to hydrocephalus and intracranial HTN, rarely focal signs and mental disturbances Group III Exeresis rarely useful but may be undertaken in life-threatening conditions Diffuse cerebral syndrome due to numerous cysticerci leading to cerebral oedema, intracranial HTN, organic brain syndrome Group II Exeresis often indicated Space occupying intracranial tumor like behaviour producing focal neurological manifestations and ultimately raised ICP Group I SURGICAL IMPLICATION CLINICAL FEATURES GROUP
  19. 19. INVESTIGATIONS <ul><li>Stool Routine and Microscopy </li></ul><ul><li>Fundoscopy </li></ul><ul><li>Biopsy and histopathology </li></ul><ul><li>CT with contrast </li></ul><ul><li>MRI </li></ul><ul><li>Serology </li></ul><ul><ul><li>EITB </li></ul></ul><ul><ul><ul><li>sensitivity of 98% specificity of 100% </li></ul></ul></ul><ul><ul><li>ELISA in CSF </li></ul></ul><ul><ul><ul><li>sensitivity of 87% specificity of 95% </li></ul></ul></ul>
  20. 20. RADIOLOGICAL STAGING (A) Viable cyst with scolex
  21. 21. (B) degenerating cyst
  22. 22. (C) calcified cyst (non-contrast CT)
  23. 23. STAGES OF NC <ul><li>Cystic or vesicular stage </li></ul><ul><ul><ul><li>Cyst wall & scolex do not enhance </li></ul></ul></ul><ul><ul><ul><li>Cyst is viable & has a well defined, fluid-filled membrane contains only one scolex. </li></ul></ul></ul><ul><li>Colloid stage </li></ul><ul><ul><ul><li>Enhancing walls with perilesional oedema </li></ul></ul></ul><ul><ul><ul><li>Earliest stage in the involution of the cyst. </li></ul></ul></ul><ul><ul><ul><li>the fluid contents of the cyst become more turbid and the scolex begins to degenerate. </li></ul></ul></ul><ul><li>Necrotic, granular stage </li></ul><ul><ul><ul><li>Characterized by parasite necrosis and surrounding inflammation </li></ul></ul></ul><ul><ul><ul><li>Gives an appearance of an eosinophilic structure in which the bladder and scolex are in various stages of disintegration </li></ul></ul></ul><ul><ul><ul><li>Oedema and/or necrosis of the surrounding neural tissue may be present in some cases </li></ul></ul></ul><ul><li>Fibro-calcified nodule </li></ul><ul><ul><ul><li>With time, fibrosis develops, progressively occupying the entire lesion </li></ul></ul></ul>D.Sharada et al
  24. 24. DIAGNOSTIC CRITERIA <ul><li>Absolute criteria </li></ul><ul><ul><li>Demostration of cysticerci by histologic or microscopic examination of biopsy material </li></ul></ul><ul><ul><li>Visualization of the parasite in the eye by fundoscopy </li></ul></ul><ul><ul><li>Neuroradiologic demostration of cystic lesions containing a characteristic scolex </li></ul></ul><ul><li>Major criteria </li></ul><ul><ul><li>Neuroradiologic lesions suggestive of NC </li></ul></ul><ul><ul><li>Demostration of antibodies to cysticerci in serum by enzyme linked immunoelectrotransfer blot </li></ul></ul><ul><ul><li>Resolution of intracranial cystic lesions spontaneously or after therapy with albendazole or praziquantel alone </li></ul></ul><ul><li>Minor criteria </li></ul><ul><ul><li>Lesions compatible with NC detected by neuroimaging studies </li></ul></ul><ul><ul><li>Clinical manifestations suggestive of NC </li></ul></ul><ul><ul><li>Demonstration of antibodies to cysticerci or cysticercal antigen in CSF by ELISA </li></ul></ul><ul><ul><li>Evidence of cysticercosis outside the CNS (eg. Cigar shaped soft tissue calcification) </li></ul></ul><ul><li>Epidemiologic criteria </li></ul><ul><ul><li>Residence in a cysticercosis-endemic area </li></ul></ul><ul><ul><li>Frequent travel to a cysticercosis- endemic area </li></ul></ul><ul><ul><li>Household contact with an individual infected with T. solium </li></ul></ul>Del Brutto et al
  25. 25. DIAGNOSTIC CRITERIA <ul><li>Definitive </li></ul><ul><ul><li>1 absolute </li></ul></ul><ul><ul><li>2 major </li></ul></ul><ul><ul><li>1 major + 2 minor + 1 epidemiological </li></ul></ul><ul><li>Probable </li></ul><ul><ul><li>1 major + 2 minor </li></ul></ul><ul><ul><li>1 major + 1 minor + 1 epidemiological </li></ul></ul><ul><ul><li>3 minor + 1 epidemiological </li></ul></ul><ul><li>Possible </li></ul><ul><ul><li>1 major </li></ul></ul><ul><ul><li>2 minor </li></ul></ul><ul><ul><li>1 minor + 1 epidemiological </li></ul></ul>Del Brutto et al
  26. 26. SUGGESTED DIAGNOSTIC CRITERIA <ul><li>Absolute criteria </li></ul><ul><ul><ul><li>Histopathological demostration of the parasite in the tissues obtained from the biopsy of a brain or spinal cord lesion </li></ul></ul></ul><ul><ul><ul><li>Multiple cystic lesions with or without scolex on CT or MRI </li></ul></ul></ul><ul><li>Major Criteria </li></ul><ul><ul><ul><li>Lesion highly suggestive of NC in neuroimaging studies </li></ul></ul></ul><ul><ul><ul><li>Spontaneous resolution or eventual calcification </li></ul></ul></ul><ul><ul><ul><li>Positive serum EITB assay for the detection of antibodies against T. solium </li></ul></ul></ul><ul><li>Minor criteria </li></ul><ul><ul><ul><li>Presence of a characteristic clinical picture </li></ul></ul></ul><ul><ul><ul><li>Positive CSF ELISA </li></ul></ul></ul><ul><ul><ul><li>Cysticercosis outside the CNS </li></ul></ul></ul><ul><ul><ul><li>Aggravation of existing symptoms or appearance of a new symptom following anticysticercal therapy </li></ul></ul></ul><ul><li>Diagnosis with caution </li></ul><ul><ul><ul><li>Old age </li></ul></ul></ul><ul><ul><ul><li>Patients with pre existing systemic tuberculosis or malignancy </li></ul></ul></ul><ul><ul><ul><li>HIV infection </li></ul></ul></ul><ul><ul><ul><li>Grossly abnormal neurological examination </li></ul></ul></ul>Garg
  27. 27. Tuberculoma Versus Cysticercus Granuloma <ul><li>Cysticercus Granuloma </li></ul><ul><li>Round in shape </li></ul><ul><li>Cystic </li></ul><ul><li>20mm or less with ring enhancement or visible scolex </li></ul><ul><li>Cerebral edema not enough to produce midline shift or focal neurological deficit </li></ul><ul><li>Tuberculoma </li></ul><ul><li>Irregular in shape </li></ul><ul><li>Solid </li></ul><ul><li>Greater than 20mm </li></ul><ul><li>Associated with severe perifocal edema and focal neurological deficit </li></ul>Rajshekhar et al Target lesions: Lesions with central nidus of calcification or a dot enhancement
  28. 28. Magnetic Resonance Spectroscopy <ul><li>Tuberculomas had a high peak of lipids, more choline, and less N-acetylaspartate and creatine. </li></ul><ul><li>The choline/creatine ratio was greater than 1 in all tuberculomas but in none of the cysticerci. </li></ul>Cysticercosis working group in Peru
  29. 30. TREATMENT VS NO TREATMENT Understanding a controversy
  30. 31. NATURAL COURSE <ul><li>Rate of spontaneous resolution of a solitary cysticercus granuloma in patients with seizures </li></ul><ul><li>210 patients presenting with seizures with a solitary cerebral cysticercus on CT </li></ul><ul><li>3 months - 18.8% </li></ul><ul><li>6 months - 36.4% </li></ul><ul><li>1 year - 62.5% </li></ul>Vedantam Rajshekhar
  31. 32. TREATMENT <ul><li>Efficacy of albendazole and short-course dexamethasone treatment in children with 1 or 2 ring-enhancing lesions of NC: </li></ul><ul><li>Dexamethasone 0.15 mg/kg per day for 5 days plus </li></ul><ul><li>Albendazole 15 mg/kg per day for 28 days, starting on the third day of dexamethasone </li></ul><ul><li>Anti-epileptic therapy was given to both the study groups </li></ul>AIIMS
  32. 33. RESULTS AIIMS 33% 13% SEIZURES at 6 mths 32% 10% SEIZURES at 3mths 57% 79% RESOLUTION OF LESION (Complete or partial) CONTROL TREATED PARAMETERS
  33. 34. STEROIDS <ul><li>Corticosteroids represent the primary form of therapy for cysticercal encephalitis and arachnoiditis causing hydrocephalus and progressive entrapment of cranial nerves. </li></ul><ul><li>High doses of iv Dexamethasone along with Mannitol at 2mg/kg/day can be followed by chronic oral therapy with Prednisolone 1mg/kg/day or Dexamethasone 0.1mg/kg/day administered 3 times a week. </li></ul>JULIO SOTELO, M.D., AND OSCAR H. DEL BRUTTO, M.D
  34. 35. NEW PROTOCOLS <ul><li>Praziquantel three doses of 25-30 mg/kg at 2-hour intervals on a single day equally effective to the 50mg/kg 8 hourly dose for 15 days. Corona T, Lugo R, Medina R, et al </li></ul><ul><li>Albendazole 15mg/kg/day in 2 divided doses for 1 week equally effective to the 15 mg/kg/day 12 hrly for a 1-month period. Cysticercosis working group in Peru </li></ul>
  35. 36. Surgery restricted to: <ul><li>Placement of ventriculo-peritoneal shunts for hydrocephalus </li></ul><ul><li>Excision of single big cysts causing mass effect </li></ul><ul><li>Endoscopical excision of intraventricular parasites. </li></ul><ul><ul><ul><li>Unfortunately shunts are frequently occluded by the high protein content and debris in the CSF of patients with extraparenchymal neurocysticercosis, requiring multiple revisions. </li></ul></ul></ul><ul><ul><ul><li>Deaths due to shunt dysfunction may occur in up to 50% of cases, mainly in the initial 1–2 years after placement. </li></ul></ul></ul>Garcia et al
  36. 37. <ul><li>Group A (150 patients) were treated with 15 mg/kg/day albendazole for 14 days, plus 2 mg dexamethasone orally at 8-h intervals for 14 days, plus antiepileptic drugs at appropriate doses. The dexamethasone was tapered off over time. </li></ul><ul><li>Group B (150 patients) were treated with antiepileptic drugs and placebo. </li></ul>Current Consensus Guidelines for Treatment of Neurocysticercosis Garcia et al
  37. 38. RESULTS <ul><li>During the first year of treatment the incidences of seizure, encephalopathy, and readmission were greater for group A than group B. </li></ul><ul><li>Two patients in group A died from intractable seizures and encephalopathy in the first 3 months of treatment. </li></ul>Garcia et al
  38. 39. <ul><li>The proportion of patients with complete resolution of lesions was greater in group B than in group A </li></ul><ul><li>The proportion of patients with calcification of lesions was greater in group A than in group B. Calcified lesions may be the focal pathology for seizure recurrence. </li></ul>randomised controlled study and follow-up of at least 5 years (the longest follow-up period yet for this type of study) for 300 neurocysticercosis patients with more than one lesion Garcia et al
  39. 40. Calcification Vs Natural Resolution <ul><li>There is increasing evidence that calcified neurocysticercosis is not clinically inactive , and that perilesional oedema may at times be present around the apparently calcified foci. </li></ul><ul><li>Therefore, it is better to wait for spontaneous resolution of lesions, while treating the patient with appropriate antiepileptic drugs for control of seizures. </li></ul>Garcia et al
  40. 41. RECOMMENDATIONS <ul><li>Individualize therapeutic decisions, including whether to use antiparasitic drugs, based on the number, location, and viability of the parasites within the nervous system; </li></ul><ul><li>Actively manage growing cysticerci either with antiparasitic drugs or surgical excision; </li></ul>Garcia et al
  41. 42. <ul><li>Prioritize the management of intracranial hypertension secondary to neurocysticercosis before considering any other form of therapy; and </li></ul><ul><li>Manage seizures as done for seizures due to other causes of secondary seizures (remote symptomatic seizures) because they are due to an organic focus that has been present for a long time. </li></ul>Garcia et al
  42. 43. CONCLUSION <ul><li>Treatment with albendazole plus antiepileptic drugs has no benefit over treatment with antiepileptic drugs alone. </li></ul><ul><li>Albendazole treatment may cause problems or have adverse effects with regard to increased seizure frequency, encephalopathy and hospital readmissions in the early part of the treatment. </li></ul><ul><li>Albendazole treatment may be disadvantageous from an economical perspective because of the direct and indirect treatment costs and the loss of working days. </li></ul>Garcia et al
  43. 44. REFERENCES <ul><li>Review of neurocysticercosis Julio Sotelo M.D., and Oscar H. Del Brutto, M.D </li></ul><ul><li>New Concepts in the diagnosis and management of neurocysticercosis (Taenia Solium) Hector H. Garcia, Oscar H. Del Brutto, Theodore E. Nash, A. Clinton White, Jr., Victor C. W. Tsang, and Robert H. Gilman </li></ul><ul><li>Neurocysticercosis: some of the essentials Hector H Garcia, Armando E Gonzalez, Victor C W Tsang, Robert H Gilman, for the Cysticerocosis Working Group in Peru </li></ul><ul><li>Diagnostic criteria for neurocysticercosis: Some modifications are needed for Indian patients Garg Ravindra Kumar </li></ul><ul><li>Medical Management of Neurocysticercosis Garg RK </li></ul><ul><li>Current Consensus Guidelines for Treatment of Neurocysticercosis. Garcia et al </li></ul><ul><li>Rate of spontaneous resolution of a solitary cysticercus granuloma in patients with seizures Vedantam Rajshekhar, MCh </li></ul><ul><li>Differential diagnosis between cerebral tuberculosis and neurocysticercosis by magnetic resonance spectroscopy.C ysticercosis working group in Peru </li></ul><ul><li>Harrison Textbook of Medicine 19 th Edition </li></ul><ul><li>Bailey and Love’s Short Practice of Surgery 21 st edition </li></ul><ul><li>Rudolph’s Pediatrics 21 st edition </li></ul><ul><li>Nelson’s Textbook of Pediatrics </li></ul><ul><li>Others: D. Sharada et al, Carpio et al, Sotelo et al, Chorobski et al </li></ul>