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 24 year old gentle man from Dharan
presented with
 Jerky movement of all limbs:4 hours
 Seizure Disorder
 Metabolic disorder
 Neurocystecercosis
 Alcohol withdrawl
 Metastatic malignancy
Generalised Tonic Clonic Seizure Secondary
to Neurocysticercosis
 Introduction
 Epidemiology
. Life cycle
 Transmission
 Clinical features
 Diagnostic modalities of neurocysticercosis
 Treatment of neurocysticercosis
 Follow up
 Prevention
 Taenia solium has a predilection for skeletal
muscles, eyes, and the nervous system
 Two distinct types of infection
 IntestinalTaeniasis
 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
 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 response
Parasites look healthy
clear vesicular fluid with a visible scolex
Colloidal stage
inflammation, mononuclear cells
vesicular fluid becomes turbid
scolex shows early signs of degeneration
Granular nodular stage
gradual replacement by fibrotic tissue
collapse of cell wall
Calcific stage
replacement of the wall with calcium
 Neuroimaging – mainstay of diagnosis
 Lesions suggestive of NCC on CT, with
compatible clinical picture in endemic areas
are usually diagnosed as NCC
Neurocysticercosis
Tuberculoma
Brain abscess – fungal as well as pyogenic
Fungal granuloma
Toxoplasmosis
Infectious vasculitis
Primary malignancy in brain
Secondary metastasis to brain
 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
*
 Depend on –
-Site
- Stage of neurocystecercosis
- Number of lesion
- Location
- Presentation
 Medical:
a) Cysticidal
 Albendazole, Praziquantel
b) Steroid
 Dexamethasone, Prednisolone
c) Anti-epeleptics
- Phenytoin, Carbamazepine
 Surigical
a) Endoscopic removal
b) Shunting surgery
c) Local excision
 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
 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
 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
Neurocysticercosis
Neurocysticercosis

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Neurocysticercosis

  • 1. -
  • 2.  24 year old gentle man from Dharan presented with  Jerky movement of all limbs:4 hours
  • 3.  Seizure Disorder  Metabolic disorder  Neurocystecercosis  Alcohol withdrawl  Metastatic malignancy
  • 4.
  • 5.
  • 6.
  • 7. Generalised Tonic Clonic Seizure Secondary to Neurocysticercosis
  • 8.
  • 9.  Introduction  Epidemiology . Life cycle  Transmission  Clinical features  Diagnostic modalities of neurocysticercosis  Treatment of neurocysticercosis  Follow up  Prevention
  • 10.
  • 11.  Taenia solium has a predilection for skeletal muscles, eyes, and the nervous system  Two distinct types of infection  IntestinalTaeniasis  Cysticercosis
  • 12. PARENCHYMAL  Seizures – may be generalized, focal  Pyramidal tract signs  Sensory deficit  Involuntary movement  Brainstem dysfunction  Intellectual deterioration
  • 13. SUBARACHNOID  Headache  Vomiting  Vertigo  Cranial Nerve dysfunction  Gait disturbances  Mental deterioration
  • 14. 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
  • 15.  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
  • 16. Vesicular stage minimal inflammatory response Parasites look healthy clear vesicular fluid with a visible scolex Colloidal stage inflammation, mononuclear cells vesicular fluid becomes turbid scolex shows early signs of degeneration Granular nodular stage gradual replacement by fibrotic tissue collapse of cell wall Calcific stage replacement of the wall with calcium
  • 17.  Neuroimaging – mainstay of diagnosis  Lesions suggestive of NCC on CT, with compatible clinical picture in endemic areas are usually diagnosed as NCC
  • 18. Neurocysticercosis Tuberculoma Brain abscess – fungal as well as pyogenic Fungal granuloma Toxoplasmosis Infectious vasculitis Primary malignancy in brain Secondary metastasis to brain
  • 19.  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 *
  • 20.  Depend on – -Site - Stage of neurocystecercosis - Number of lesion - Location - Presentation
  • 21.  Medical: a) Cysticidal  Albendazole, Praziquantel b) Steroid  Dexamethasone, Prednisolone c) Anti-epeleptics - Phenytoin, Carbamazepine  Surigical a) Endoscopic removal b) Shunting surgery c) Local excision
  • 22.  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
  • 23.  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
  • 24.  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