A Case of Neurocysticercosis

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A Case of Neurocysticercosis

  1. 1. PROF DR K H NOOR UL AMEEN M6 UNIT DR.RAKESH PINNINTI CASE OF GIDDINESS
  2. 2. Chief complaints <ul><li>Mr. Elumalai aged 25yr a transport vehicle driver presented with complaints of </li></ul><ul><li>a) Giddiness 3 months </li></ul><ul><li>b) Headache 1 week </li></ul><ul><li>c) Fever 1day (1week ago) </li></ul>
  3. 3. Presentation <ul><li>Patient was apparently doing well 3 months back.... </li></ul><ul><li>On the day of onset of his symptoms patient experienced intense giddiness around 2pm while he was having a conversation with his friends, within minute or two he had a complete black out & later regained consciousness, was informed of fall & unconsious state that lasted for 4-5 min. </li></ul><ul><li>H/O nausea preceded the event. </li></ul>
  4. 4. Presentation <ul><li>Patient had similar episode 15-20days later but Patient wasn’t sure of the events that happened during the blackout period as those events always happened during his work as a driver in different towns , patient never had an accident from his symptoms, stopped driving after 3 rd episode, </li></ul><ul><li>After each episode patient felt fatigued & unable to concentrate for the rest of the day. </li></ul><ul><li>Now patient only complains of giddiness, not had LOC after the 3 rd episode. </li></ul>
  5. 5. Presentation <ul><li>Patient has Headache since 1 week, diffuse distribution of pain, intermittent throbbing quality initially, but patient having dull ache since 2 days </li></ul><ul><li>No specific time / diurnal variation with pain except that sometimes pain severe early morning </li></ul><ul><li>Pain adequately relieved on taking analgesics </li></ul>
  6. 6. Presentation <ul><li>No h/o chest pain; palpitations; dyspnea; </li></ul><ul><li>No h/o altered sensorium; nausea; vomiting. </li></ul><ul><li>No h/o memory disturbances, diplopia, dysphagia, weakness of limbs, loss of sensation, incordination, bowel;bladder disturbances. </li></ul><ul><li>No h/o reduced urine output/passage of stool ova/cyst; bleeding tendency/bleedingfrom any orifice. </li></ul>
  7. 7. HISTORY <ul><li>Past History: No relevant past history; not a K/C/O DMT2; SHT; RHD; Seizure disorder. </li></ul><ul><li>Family History: Nothing significant </li></ul><ul><li>Personal History: not a smoker or alcoholic </li></ul><ul><li>no bowel bladder disturbances </li></ul><ul><li>mixed diet </li></ul><ul><li>disturbed sleep since 3 months </li></ul>
  8. 8. Examination <ul><li>Patient an young adult male aged 23 yr moderately built & nourished. </li></ul><ul><li>conscious, oriented, responds & obeys commands, moves all 4 limbs. </li></ul><ul><li>His vitals were stable, </li></ul><ul><li>He is not anemic not jaundiced, no cyanosis, no clubbing ,no generalized lymphadenopathy. </li></ul><ul><li>System examination revealed no significant cardiovascular / respiratory abnormal findings. </li></ul>
  9. 9. CNS <ul><li>HIGHER MENTAL FUNCTIONS </li></ul><ul><li>Patient was conscious, </li></ul><ul><li>oriented in time, place & person, </li></ul><ul><li>MMSE >25 </li></ul><ul><li>no cognitive impairment (short orientation memory conc test) </li></ul><ul><li>normal speech & articulation </li></ul>
  10. 10. CNS <ul><li>CRANIAL NERVES </li></ul><ul><li>Pupils : Size R 4mm; L 3mm </li></ul><ul><li>B/L brisk reaction to light & accommodation </li></ul><ul><li>Fundus Normal </li></ul><ul><li>No other significant cranial nerve palsies observed. </li></ul>
  11. 11. MOTOR SYSTEM <ul><li>R L </li></ul><ul><li>TONE: NORMAL NORMAL </li></ul><ul><li>BULK: NORMAL NORMAL </li></ul><ul><li>POWER </li></ul><ul><li>UL 5/5 5/5 </li></ul><ul><li>LL 5/5 5/5 </li></ul><ul><li>REFLEXES </li></ul><ul><li>biceps N N </li></ul><ul><li>Triceps N N </li></ul><ul><li>Ankle BRISK BRISK </li></ul><ul><li>Knee BRISK BRISK </li></ul><ul><li>PLANTAR FLEXOR FLEXOR </li></ul><ul><li>` </li></ul>
  12. 12. <ul><li>SENSORY SYSTEM & CEREBELLAR SIGNS </li></ul><ul><li>NO SIGNIFICANT ABNORMALITY NOTED CLINICALLY </li></ul>
  13. 13. List of problems <ul><li>Black outs ?syncope;?seizures </li></ul><ul><li>Giddiness </li></ul><ul><li>Headache </li></ul><ul><li>Brisk reflexes on examination </li></ul>
  14. 14. <ul><li>A point score to identify cardiac syncope was developed in a multicenter cohort of 260 patients with syncope evaluated according to 2004 ESC guidelines </li></ul><ul><li>1) Palpitations preceding syncope - 4 points </li></ul><ul><li>2) Heart disease and/or abnormal electrocardiogram (sinus bradycardia, second or third degree atrioventricular block, bundle branch block, acute or old myocardial infarction, supraventricular or ventricular tachycardia, left or right ventricular hypertrophy, ventricular preexcitation, long QT, Brugada pattern) 3 points </li></ul><ul><li>3) Syncope during effort - 3 points </li></ul><ul><li>4) Syncope while supine - 2 points </li></ul><ul><li>5) Precipitating or predisposing factors (warm-crowded place, prolonged orthostasis, pain, emotion, fear) - minus 1 point </li></ul><ul><li>6) A prodrome of nausea or vomiting - minus 1 point </li></ul><ul><li>A score of ≥ 3 had 92 percent sensitivity and 69 percent specificity for cardiac syncope in the validation cohort. </li></ul>
  15. 16. Investigations
  16. 18. Imaging CT scan Brain
  17. 19. MRI
  18. 26. XRAYS <ul><li>Several X rays taken so to demonstrate active/ calcified lesions </li></ul><ul><li>But no findings suggestive of tissue cysticercosis were found. </li></ul>
  19. 28. INV further <ul><li>C.S.F CYSTICERCAL ANTIBODIES </li></ul><ul><li>EEG - NORMAL </li></ul><ul><li>ECHO - NORMAL </li></ul><ul><li>Muscle biopsy </li></ul><ul><li>Stool ova cyst larvae - NIL </li></ul><ul><li>B scan of Orbit </li></ul>
  20. 29. Diagnostic criteria The presence of two different lesions highly suggestive of neurocysticercosis on neuroimaging studies should be considered as two major diagnostic criteria..
  21. 30. MUSCLE BIOPSY <ul><li>Macroscopic: skeletal muscle tissue 1cm*.7cm with a cystic lesion observed. </li></ul><ul><li>Microscopy: skeletal muscle fibers noted with parts of cystic inflammatory lesion consistent with cross sectional scolex noted with peri-lesional inflamation with eosinophil infiltrate </li></ul><ul><li>Intra scolex features consistent with mouth parts with no evidence of hooklets </li></ul><ul><li>IMP : FEATURES CONSISTENT WITH CYSTECERCOSIS </li></ul>
  22. 31. DIAGNOSIS <ul><li>Parenchymal Neurocysticercosis (NCC) – </li></ul><ul><li>STAGE 1 vesicular cysts </li></ul><ul><li>Sub-cutaneous & Intra-muscular cysticercosis </li></ul>
  23. 32. TREATMENT <ul><li>The initial approach to patients with clinical manifestations of neurocysticercosis (NCC) should focus on management of symptoms such as seizure control with antiepileptics and treatment of increased intracranial pressure, if present. </li></ul><ul><li>Subsequently a determination should be made regarding the role of antiparasitic and anti-inflammatory therapy. </li></ul>
  24. 33. Antiepileptic therapy <ul><li>Antiepileptics should be administered to patients with NCC who present with seizures. </li></ul><ul><li>Most reports in the literature on management of seizure due to NCC describe use of phenytoin or carbamazepine. </li></ul><ul><li>Antiepileptic therapy may also be appropriate for patients who do not present with seizures but who are at high risk for seizures. The risk of seizures appears to be highest in the setting of multiple lesions. </li></ul><ul><li>Calcified, inactive lesions can also serve as foci for seizures but in an otherwise asymptomatic patient are not generally considered an indication for prophylactic antiepileptic drug therapy </li></ul><ul><li>The optimal duration of antiepileptic therapy is uncertain; most experts favor administering antiepileptic therapy for 6 to 12 months after radiographic resolution of active parasitic infection . </li></ul>
  25. 34. Antiparasitic therapy <ul><li>Consensus on the optimal role of antiparasitic therapy in the setting of cysticercosis is beginning to emerge. </li></ul><ul><li>The potential benefit of antiparasitic therapy for treatment of neurocysticercosis is hastened resolution of active cysts, decreased risk for seizures, and decreased recurrence of hydrocephalus. </li></ul><ul><li>The potential risk of treatment with antiparasitic therapy is exacerbation of neurologic symptoms due to increased inflammation around the degenerating cyst, particularly in patients with a large number of lesions. The inflammation can be so severe that it can lead to disability or death </li></ul>
  26. 35. Albendazole <ul><li>Albendazole (15 mg/kg per day [usually 800 mg/day in two divided doses; taken with food to increase bioavailability]) facilitates the destruction of parenchymal cysticerci. </li></ul><ul><li>The optimal duration of therapy depends on the form of disease. </li></ul><ul><li>a) Patients with a single enhancing lesion appear to benefit from a short course of therapy (3 to 7 days). </li></ul><ul><li>b) Patients with multiple viable parenchymal lesions should receive a longer course of treatment (10 to 14 days); </li></ul><ul><li>c) Patients with subarachnoid disease may benefit from prolonged therapy guided by the response on imaging studies (≥ 28 days) </li></ul><ul><li>Praziquantel (50 to 100 mg/kg per day in three divided doses) is an alternative to albendazole. </li></ul>
  27. 36. Anti-inflammatory therapy <ul><li>Corticosteroids should be administered to patients with parenchymal neurocysticercosis receiving treatment with antiparasitic therapy, to reduce inflammation associated with the dying organisms. </li></ul><ul><li>Doses used are typically 1 mg/kg/d of prednisone or prednisolone or 0.1 mg/kg/d of dexamethasone for 5 to 10 days followed by a rapid taper. </li></ul><ul><li>Prior to the initiation of therapy with antiparasitic medications or corticosteroids, screening for latent TB infection, strongyloidiasis and ocular cysticercosis should be pursued </li></ul>
  28. 37. Multiple cysts <ul><li>In the setting of multiple parenchymal cysts, active and inactive cysts may be present in the same patient simultaneously. </li></ul><ul><li>Administration of antiparasitic therapy may hasten degeneration of viable cysts, thereby increasing inflammation at the site of these lesions and potentially increasing risk for seizure. </li></ul><ul><li>Nonetheless, most favor treatment of multiple viable, parenchymal cysticerci with antiparasitic therapy (albendazole 15 mg/kg/d in two daily doses for 8 to 15 days) administered together with high-dose steroids </li></ul>
  29. 38. <ul><li>Cysticercal encephalitis  — Cysticercal encephalitis (diffuse cerebral edema associated with multiple inflamed cysticerci) is a contraindication for antiparasitic therapy, since enhanced parasite killing can exacerbate host inflammatory response and lead to diffuse cerebral edema and potential transtentorial herniation. Most cases of cysticercal encephalitis improve with corticosteroid therapy. </li></ul>
  30. 39. STAGES OF NCC <ul><li>The four stages of cysts within the parenchyma of the brain: vesicular, colloidal, nodular/granular, and calcified granulomas. </li></ul><ul><li>The viable larval cyst is known as a vesicular cyst and has minimal enhancement, which is due to little or no host immune response. At this stage, the scolex usually is identified as an eccentric nodule within the cyst. </li></ul><ul><li>As the cyst degenerates, fluid from the larval cyst leaks into the parenchyma, generating a strong immune response, characterized by enhancement on contrast computed tomography (CT) and magnetic resonance imaging (MRI). An enhancing cyst, without a well-defined scolex, is termed a colloidal cyst . </li></ul><ul><li>As the cyst further deteriorates, it forms a nodule , which continues to demonstrate contrast enhancement. </li></ul><ul><li>Finally the degenerating cyst forms a calcified granuloma , which is recognized as nonenhancing punctuate calcifications on CT </li></ul>
  31. 40. Evidence based Managment <ul><li>TI - A trial of antiparasitic treatment to reduce the rate of seizures due to cerebral cysticercosis. </li></ul><ul><li>SO - N Engl J Med 2004 Jan 15;350(3):249-58 </li></ul><ul><li>TI - Perilesional brain oedema and seizure activity in patients with calcified neurocysticercosis: a prospective cohort and nested case-control study. </li></ul><ul><li>SO - Lancet Neurol. 2008 Dec;7(12):1099-105. </li></ul><ul><li>TI - Treatment of neurocysticercosis: current status and future research needs. </li></ul><ul><li>SO - Neurology. 2006 Oct 10;67(7):1120-7. </li></ul><ul><li>TI - Current consensus guidelines for treatment of neurocysticercosis. </li></ul><ul><li>SO - Clin Microbiol Rev 2002 Oct;15(4):747-56 </li></ul><ul><li>TI - A trial of antiparasitic treatment to reduce the rate of seizures due to cerebral cysticercosis. </li></ul><ul><li>SO - N Engl J Med 2004 Jan 15;350(3):249-58. </li></ul><ul><li>TI - Short course of prednisolone in Indian patients with solitary cysticercus granuloma and new-onset seizures. </li></ul><ul><li>SO - Epilepsia. 2003 Nov;44(11):1397-401. </li></ul>
  32. 42. THANK YOU

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