NCC KRISHNA CLINICAL MEET interesting cases.pptx

Clinical meet

1. Neurocysticercosis DR PADMAVATHI 1 ST YR POSTGRADUATE DEPT OF PEDIATRICS GOVT CUDDALORE HEADQUATERS HOSPITAL

2. CHIEF COMPLAINTS A 7yr old / MCH ,informant was his mother whose reliability was good came with c/o headache for 2 days C/O vacant stare & abnormal movements of rt UL &LL and deviation of angle of mouth to rt side . HISTORY OF PRESENTING ILLNESS The child was apparently normal before 2 days after which he developed Headache for 2 days ,insidious onset ,progressive in nature not associated with nausea,projectile vomiting,photophobia ,blurring of vision, trauma ,no aggrevating factor ,relieved by medication. H/0 vacant stare and abnormal movements of rt upper and lower limb with deviation of angle of mouth to rt side sustained for 1 min resolved spontaneously.post ictal event including headache was present .not associated with aura , automatisms,abnormal movement of bowel and bladder during the event.

3. Hopi…. h/o increased outside food intake No h/0 recent trauma No h/o fever No h/o any drug intake No h/o accidental ingestion of any toxins No h/o neck stiffness /altered sensorium No h/o loss of weight or loss of appetite No h/o nausea , vomiting,loose stools No h/o visual disturbances No h/o chronic cough

4. PAST H/O No h/o similar complaints in the past Not a k/c/o diabetes ,bronchial asthma , tuberculosis,hypertension,congenital heart disease No h/o previous hospitalisation

5. Antenatal history Booked and immunized Iron and folic acid taken 2 doses of td given All three trimesters were uneventful BIRTH H/O 1 ST born, full term , NVD,cried immediately after birth ,no nicu admission , b.wt : 2.7 kgs .

6. …. DEVELOPMENTAL HISTORY Attained normal developmental milestones for age ,good scholistic performance. IMMUNIZATION H/O Immunised as per NIS, last immunization at 5 years of age. Diet H/O Takes both vegetarian and non vegetarian foods predominantly non vegetarian h/o beef intake before Normal bowel and bladder habit present

7. Family h/o No h/o seizure disorder / mental retardation in family members Non consanguineous marriage CONTACT H/O No significant h/o contact with tb cases SOCIO ECONOMIC H/O According to modified kuppuswamy scale ,family belongs lower middle class family TREATMENT H/O No h/o intake of AED ,ATT or any other drugs .

8. General examination At time of admission , child alert ,oriented to place ,sensorium normal , gcs 15/15 No pallor,no icterus ,cyanosis, clubbing, pedal edema ,generalised lymphadenopathy. Head to toe examination – normal No congenital malformation ,neurocutaneous markers ,dysmorphic features . VITALS HR – 104 /Min RR -26 /min Spo2 -97% under RA TEMP – 98.6 ‘F Bp – 100/ 64 mm hg CRT < 2 SEC +++/++

9. SYSTEMIC EXAMINATION CNS higher functions : alert, right handedness,speech normal,oriented to place , memory and intelligence normal CRANIAL NERVES olfactory –able to smell objects optic – b/l perl + , n visual acuity oculomotor , trochlear,abducent – EOM full trigerminal – N sensation of face ,able to chew facial – no deviation of angle of mouth

10. Contdd … Vestibulo cochlear – rinnes ,weber test normal Glossopharyngeal – N sensation on posterior part of tongue Vagus – gag reflex + Spinal accessory – able to move neck side to side Hypoglossal – no deviation of tongue muscle . MOTOR SYSTEM bulk – no muscle wasting in all 4 limbs Tone - grade 1 in rt ul and ll ,normal in left ul and ll Power - > 3/5 in all 4 limbs Coordination –normal No abnormal movements

11. Contdd … Superficial reflexes conjunctival ,corneal, abdominal,cremastic - ++ plantar – flexor in both ll Deep reflexes biceps , triceps,supinator,jaw jerk,knee , ankle - ++ Cerebellar /extra pyramidal system –normal Sensory system- normal senastions present Autonomic system- no abnormal bowel ,bladder movements, sweating,postural hypotension Spine and cranium – normal Meningeal signs – no signs of meningeal irritation Signs of raised intracranial pressure – nil Musculoskeletal system – no fasiculations Gait - normal

12. Contdd … Cvs – s1s2 + , no murmur , normal apical impulse RS- BAE +,NO added sounds P/A- soft, non tender , no organomegaly . PROVISIONAL DIAGNOSIS UNPROVOKED SEIZURE / SOL FOR EVALUATION

13. …… After admission , child had no further episodes of seizures, c/o headache Proceeded with following investigations CBC RFT LFT SERUM ELECTROLYTES URINE ROUTINE CT BRAIN

14. Cbc,rft,lft Hb – 8.4 Na - 132 Tc -6100 k+- 3.6 Dc : 40 (p),47(l),13 (m) u.alb,glucose,bile salts,bile pigments –nil deposits -1-2 Pcv -30.3 pus cells Plt - 39.9 Rbc - 4.56 Mcv -65.8 Mch-18.4 Mchc -28 U-25 Cr-0.7 T.bil –0.9 D.bil -0.3

15. Ct brain Tiny cystic lesion with hyperdense central nodule with associated surrounding edema noted in left frontal cortex. Likely neurocysticercosis

16. …… In view of findings in ct brain,following further investigations done. chest xray montoux test cbnaat usg abdomen MRI /MR Spectroscopy

17. MRI BRAIN A Solitary well defined round lesion of size 5mm x 5mm seen in the left post central gyrus with thick wall which is hypointense in all sequences with eccentric dot sign which is t1 hyperintense There is rim enhancement on post contrast study MR spectroscopy- lactate,alanine peak seen Moderate perilesional edema seen Ventricle normal,posterior foss – normal Mild effacement of central sulcus,no e/o midline shift. Impression- p/o neurocysticercosis(colloidal vesicular stage ) solitary intraparenchymal in left post central gyrus

18. mri

19. Other inv USG ABDOMEN – NO E/O CYSTIC LESIONS IN LIVER. CHEST XRAY – NAD MONTOUX TEST – NON REACTIVE CBNAAT- MTB NOT DETECTED OPHTHAL OPINION OBTAINED no evidence of papilledema ,ocular cysticercosis fundus normal nil ophthal intervention needed

20. FINAL DIAGNOSIS : NEUROCYSTICERCOSIS NEUROLOGIST OPINION To start sodium valproate 200mg1-0-1 for 6months Follow up after 3weeks . TREATMENT GIVEN INJ dexamethasone (0.3 mg /kg /day ) iv bd started on day 1 ,2. Tab prednisolone from day 3 Tab albendazole ( 15mg/kg/day ) po bd started on day 3 along with tab. Prednisolone (1 mg/kg/day) Tab sodium valproate 200mg two divided doses.

21. neurocysticercosis It is a parasitic infection of human brain caused by encysted larvae – cysticercus of the pork tapeworm Taenia solium . LIFE CYCLE OF TAENIA SOLIUM Humans are the definitive host of adult T. solium . They acquire it by ingesting undercooked pork containing cysticerci . Once ingested, the cysts release larvae that attach to intestinal mucosa via their scolices and mature into adult worms. The adult female worm releases proglottids (segments) heavily laden with eggs that are passed in the stool of the carrier human. These eggs are later ingested by pigs grazing on soil contaminated by human Excreta . The eggs release larvae in the pig intestine to form larvae that traverse the intestinal mucosa and spread through the blood stream to the pigs’ muscles to form cysts; Rate of transmission is high in rural communities where open defecation is rampant.

22. Life cycle

23. Contd …. cysticercosis is caused by accidental human ingestion of T. solium eggs shed in stool of human tapeworm carriers. After entering the human gut, T. solium embryos (oncospheres) hatch in the small intestine and the larvae invade the bowel mucosa and disseminate hematogenously to brain, liver, striated muscle,subcutaneous tissue and eyes. They lodge at these sites and within 3 weeks to 2 months form tissue cysticerci which are fluid-filled membranous cysts with invaginated scolex. Cysticerci that reach the brain cause neurocysticercosis

24. TYPES OF ncc Intraparenchymal ncc (mc) Extraparenchymal ncc Intraventricular Neurocysticercosis Subarachnoid Neurocysticercosis Spinal Neurocysticercosis Ocular Cysticercosis

25. Types of ncc

26. Approach to diagnosis INVESTIGATIONS Neuroimaging Serology Cerebrospinal Fluid analysis

27. Contd … Screening of Contacts Routine screening of family members of children with NCC is not recommended. If at all screening is performed,fecal testing of the family for ova/cyst can be done Serological and Molecular Studies T. solium DNA has been detected by PCR or deep genomic sequencing using CSF of patients with subarachnoid NCC. The use of serological tests for diagnosis and clinical decision-making in children with NCC is not recommended.

28. Contd.. NEUROIMAGING In presence of following ct findings mri is not needed. i ) The CT conclusively demonstrates the presence of a scolex within the cyst; or ii ) In the absence of demonstration of scolex: a ) If a solitary cystic/ring-enhancing lesion has all other typical sizes, shape, and location characteristics of NCC. b ) Multiple lesions in different stages are present, including some cystic or ring enhancing or calcified. as a modality that can be used as an absolute diagnostic criterion for NCC

29. Contd.. MRI should be considered after CT in the following situations: i ) Atypical imaging features (conglomerate lesions, subarachnoid or intraventricular lesions) along with the absence of scolex; ii ) CT features create suspicion of intraventricular, subarachnoid, or intraspinal NCC; or iii ) Atypical clinical features including features of meningitis, encephalopathy, vision loss, fleeting headaches, stroke like features and behavioral changes.

30. Ct and mri findings

31. Differential diagnosis

32. Iap STG for ncc

33. Management of Intraparenchymal NCC Albendazole (15 mg/kg/day) or praziquantel (50 mg/kg/day) for 10-14 days is recommended for more than two viable cyst. Treatment of persistent viable cysts There are two options to treat the persistent lesion. One is retreatment with the same dose and duration of albendazole and the second option is the concurrent administration of albendazole and praziquantel as for multiple lesion NCC. Management of NCC at Atypical Sites Pulse intravenous steroids should be used to reduce the acute symptomatic edema in children with cysticercal encephalitis. The steroids suggested are methylprednisolone (10-30 mg/kg for 3-5 days; maximum 1000 mg/ day) or dexamethasone (3-6 mg/kg/day for 3-5 days; maximum 16 mg/day).

34. Subarachnoid, ventricular and spinal NCC There is no role for routine use of steroids in cases of contrast-enhancing calcified NCC presenting with recurrence of seizures. Steroid use should be reserved for symptomatic cerebral edema . Steroids and Anti-Seizure Drug can be used. Epilepsy Surgery Residual perilesional gliosis surrounding calcified NCC is thought to be responsible for long-term epilepsy Epilepsy surgery workup should be considered in children with NCC who failed two appropriately chosen ASM tried in optimal doses.

35. Optimal Duration of Anti-Seizure Medications Anti-seizure medication may be withdrawn after 6 months if there is no calcific residue, there is resolution of cyst on neuroimaging, and the child has had less than three seizures in the past. Children with evidence of calcification, persistent cyst, or a history of more than two seizures in the past may require a longer duration of therapy.(2 years )

36. Diagnostic criteria

37. DEGREE OF CERTAINITY FOR DIAGNOSIS OF NCC

38. OUTCOME Parenchymal disease has a much better outcome compared to extraparenchymal forms . single lesion has a much better prognosis compared to multiple lesions. Single lesions usually disappear within 6 months in 60% cases. Radiological resolution must therefore be documented by repeat imaging within 3–6 months. Persisting lesions may require a repeat course of antihelminthic therapy. Seizure recurrence occurs in 10–20% cases with single NCC. Multiple NCC and calcified lesions are associated with frequent seizures and may require prolonged course of antiepileptics.

39. Contd … There is frequent misconception that infected pork causes cysticercosis. Ingesting cyst infected pork causes taeniasis,which can by itself source of contamination with taenia eggs and cause cysticercosis to others.most likely in the close environment . However ingestion of t.solium eggs excreted by a tapeworm carrier is sufficient and the only form of acquiring cysticercosis. Studies says there is only fecal oral mechanism of NCC infection.

40. single enhancing lesion in ct scan It is the commonest radiological abnormality in patients with new onset seizure . ETIOLOGY neurocysticercosis tuberculoma metastatic tumors CNS lymphomas abscess toxoplasmosis fungal granulomas rarely infarction