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

Provisional diagnosis

Seizure Disorder Metabolic disorder Neurocystecercosis Alcohol withdrawl Metastatic malignancy

Final Diagnosis

Generalised Tonic Clonic Seizure Secondary to Neurocysticercosis

Neurocysticercosis

Outline

Introduction Epidemiology . Life cycle Transmission Clinical features Diagnostic modalities of

neurocysticercosis Treatment of neurocysticercosis Follow up Prevention

Clinical features

Taenia solium has a predilection for skeletal muscles, eyes, and the nervous system

Two distinct types of infection Intestinal Taeniasis Cysticercosis

PARENCHYMAL Seizures – may be generalized, focal Pyramidal tract signs

Sensory deficit

Involuntary movement

Brainstem dysfunction

Intellectual deterioration

SUBARACHNOID Headache Vomiting Vertigo Cranial Nerve dysfunction Gait disturbances Mental deterioration

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

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

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

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

D/D of ring enhancing lesions on neuroimaging

NeurocysticercosisTuberculomaBrain abscess – fungal as well as

pyogenicFungal granulomaToxoplasmosisInfectious vasculitisPrimary malignancy in brainSecondary metastasis to brain

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

*

Treatement

Depend on – -Site - Stage of

neurocystecercosis - Number of lesion - Location - Presentation

Treatment cont…. Medical:

a) Cysticidal Albendazole, Praziquantel

b) Steroid Dexamethasone, Prednisolone

c) Anti-epeleptics - Phenytoin, Carbamazepine

Surigicala) Endoscopic removalb) Shunting surgeryc) Local excision

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

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

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

Follow Up

THANK YOU