Neurocysticercosis
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Neurocysticercosis
Dr Bhupendra Shah(Assistant Professor)B.P.koirala institute of health Sciences
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Case scenario:
24 year old gentle man from Dharan presented with
Jerky movement of all limbs:4 hours
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Provisional diagnosis
Seizure Disorder Metabolic disorder Neurocystecercosis Alcohol withdrawl Metastatic malignancy
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Final Diagnosis
Generalised Tonic Clonic Seizure Secondary to Neurocysticercosis
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Neurocysticercosis
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Outline
Introduction Epidemiology . Life cycle Transmission Clinical features Diagnostic modalities of
neurocysticercosis Treatment of neurocysticercosis Follow up Prevention
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Clinical features
Taenia solium has a predilection for skeletal muscles, eyes, and the nervous system
Two distinct types of infection Intestinal Taeniasis Cysticercosis
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PARENCHYMAL Seizures – may be generalized, focal Pyramidal tract signs
Sensory deficit
Involuntary movement
Brainstem dysfunction
Intellectual deterioration
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SUBARACHNOID Headache Vomiting Vertigo Cranial Nerve dysfunction Gait disturbances Mental deterioration
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INTRAVENTRICULAR Subacute or intermittent intracranial
hypertension Sudden death with acute hydrocephalus BRUNS SYNDROME – Transient LOC
due to sudden interruption of CSF flow related to movement of head
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STAGING OF NCC
CLINICAL (SOTELO & CARPIO) Active Transitional Inactive PATHOLOGICAL (ESCOBAR) Vesicular Colloidal vesicular Granular nodular Nodular calcified Case report: the value of MRI in diagnosis of
neurocysticercosis, Singapore medical journal 2000; Vol 41 (3): 132 – 134
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Vesicular stage minimal inflammatory responseParasites look healthy clear vesicular fluid with a visible
scolex
Colloidal stageinflammation, mononuclear cellsvesicular fluid becomes turbidscolex shows early signs of
degeneration
Granular nodular stage gradual replacement by fibrotic
tissuecollapse of cell wall
Calcific stage replacement of the wall with
calcium
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Diagnosis and Diagnostic modalities of neurocysticercosis
Neuroimaging – mainstay of diagnosis
Lesions suggestive of NCC on CT, with compatible clinical picture in endemic areas are usually diagnosed as NCC
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D/D of ring enhancing lesions on neuroimaging
NeurocysticercosisTuberculomaBrain abscess – fungal as well as
pyogenicFungal granulomaToxoplasmosisInfectious vasculitisPrimary malignancy in brainSecondary metastasis to brain
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NCC vs. Tuberculoma *
Cysticerci usually round in shape 20 mm or less in size with ring enhancement or visible scolex Cerebral edema severe enough to produce midline shift No Focal neurological deficit
Tuberculomas usually irregular Solid and greater than 20 mm in size Severe perifocal edema Focal neurological deficit
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Treatement
Depend on – -Site - Stage of
neurocystecercosis - Number of lesion - Location - Presentation
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Treatment cont…. Medical:
a) Cysticidal Albendazole, Praziquantel
b) Steroid Dexamethasone, Prednisolone
c) Anti-epeleptics - Phenytoin, Carbamazepine
Surigicala) Endoscopic removalb) Shunting surgeryc) Local excision
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Cysticidal Agents
Albendazole Imidazole group acts by inhibiting the uptake of glucose by parasitic
membranes thus causing energy depletion 15 mg/kg/day in 2 divided doses
Praziquantel Isoquinolone group spastic paralysis of the parasite musculature and destroys the
scolex 50- 100 mg/kg /day in 3 divided dose
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Role of steroids Corticosteroids are an adjunct to cysticidal
therapy
High dose corticosteroids are the primary therapy for cysticercotic encephalitis
In case of subarachnoid cyst, chronic meningitic form or in case of multiple viable cysts steroids should be given along with cysticidal drugs
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Anti epileptic drugs
The antiepileptic drugs are no different in NCC than in other seizure disorder
Single first line antiepileptic drugs like phenytoin, carbamazepine result in adequate control of seizures
The optimal length of antiepileptic drug
therapy in patients with NCC has been a subject of debate
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Follow Up
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THANK YOU