recent guidelines for management of neurocystcercosis
TRANSCRIPT
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Dr. Parag MoonSenior Resident, Neurology
GMC, Kota.
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Taenia saginata-beef
T. s. asiatica -pig organs
T. solium primarily in pork
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Cysticercosis and Taeniosis -foodbornezoonotic infections with larval or metacestodeand adult tapeworms, respectively
Larvae meat-borne (pork)
Adult stage-small intestine of the human host (obligate).
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Risk factors
Poor sanitation
Intimate contact between humans and their livestock
Use of untreated or partially treated wastewater in agriculture
Uncooked or partially cooked meat
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50 million people have cysticercosisworldwide.
Underestimate since many infections are not diagnosed.
Cestodes are cosmopolitan in distribution
Highly endemic in Latin America, Africa and Asia
NCC -most common cause of adult-onset seizures in developing countries
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Adult form-flat, opaque white or yellowish, long segmented parasites, measuring 1 to 12 m.
Head or scolex -attachment organ
Has four suckers and a rostellum that may be armed with hooks(T. solium), or unarmed and sunken (T. saginata), or with rudimentary hooklets (Taenia saginata asiatica)
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Scolex -size of a pin-head
Followed by a short and undivided region, the neck
Long chain of proglottids or segments (termed the strobila) proliferate
Strobila has the appearance of a ribbon and may consist of more than a thousand proglottids.
Posterior end of the tapeworm has the broadest, longest and oldest proglottids
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Eggs are spherical
Size -20 to 50 μm
Radial appearance on light microscopy
Eggs of all taeniids are morphologically indistinguishable by light and electron microscopy.
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Humans as the sole definitive host
Pigs are intermediate host.
Humans acquire taeniosis by eating undercooked or raw pork infected with cysticerci.
Acquire cystecercosis by ingesting eggs (exogenous or endogenous autoinfection)
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Cellulose -small, spherical or oval, white or yellow vesicle, 0.5 and 1.5 cm
Translucent bladder wall, through which scolexcan be seen as a small solid eccentric granule.
Generally separated from host tissue by a thin collagenous capsule, within which it remains alive
Racemose -large, round or lobulated bladder circumscribed by a delicate wall
Resembles a cluster of grapes,10 to 20 cm
More common in immmunosupressed
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1)Vesicular stage-cyst with a translucent vesicular wall, transparent fluid, and a viable invaginated scolex.
Little host inflammatory reaction.
2)Colloidal stage-thick vesicular wall, fluid turbid, scolex degenerates
Varying degrees of acute and chronic inflammation.
Radiography- cystic lesions with edema and enhancement and seizures are common.
3)Granular stage- thick vesicular wall, degenerated scolex, gliosis, little inflammatory host response.;
4)Calcific stage
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Asymptomatic to life threatening
Can affect parenchyma, subarachnoid space, or intraventricular system,ocular,spinal
Dependant on the location, number, and stage of the cysts at presentation
Leading cause of adult-onset epilepsy in endemic areas(Latin America, Asia, Africa)
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Commonly generalized tonic-clonic or simple partial
More frequent in patients with parenchymaldisease,
Can occur in patients with cysts in the cortical sulci
Usually occur when dying cyst incites an inflammatory reaction
Has been reported in cystic stage 50%–70% of patients experience recurrent
seizures
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Also occur secondary to vasculitis and infarction in setting of subarachnoid disease
Calcified NCC -development and maintenance of seizures and epilepsy
Positive correlation between endemic populations with increased proportions of calcification and seizure activity.
Calcified granulomas have increased risk of ongoing seizure
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Perilesional edema related to calcification occurs episodically associated with seizures
Accompanied by enhancement around the calcified focus
Appx. 23%–35%
Out of 110 patients, those with recurrent seizures, perilesional edema was noted on MRI in 50% as opposed to 9% of asymptomatic matched controls
The Lancet Neurology, vol. 7, no. 12, pp. 1099–1105, 2008
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Focal neurologic signs
Related to the number, size, and location of the parasites in individuals parenchymaldisease.
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Cysticercotic encephalitis-Intracranial hypertension in patients with parenchymalNCC
Seen in children and young woman
Acute inflammatory response to massive cysticercal infection resulting in brain edema
Presents with clouding of consciousness, seizures, decreased visual acuity, headache, vomiting, and papilledema- subacute or acute in onset
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Treated with mannitol and corticosteroids
May require decompressive temporal craniotomy
Not candidate for antiparasitic agents
Other causes of intracranial hypertension-large cyst displacing midline structures or obstructs the flow of CSF at aqueduct
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Psychiatric manifestations-depression, psychosis
Study showed chronic inpatient psychiatric pts were more likely to have a positive serology for T. solium than healthy controls
Increased risk with pts with mental retardation
American Journal of TropicalMedicineand Hygiene, vol. 73, no. 3, pp. 504–509, 2005
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Subarachnoid NCC
Seen in Sylvian fissure or basilar cisterns
Normal evolution not occur in the intraventricular or subarachnoid form
Racemose type-aberrant proliferating cestodelarvae
Local mass effect
Arachnoiditis resulting in communicating hydrocephalus secondary to chronic inflammation or fibrosis of arachnoid villi
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Cysticercotic arachnoiditis can lead entrapment of cranial nerves in the inflammatory exudates.
Extraocular muscle paralysis, diplopia and papillary abnormalities
Decreased visual acuity,visual field defects
Acute aseptic meningitis-signs of meningealirritation rare
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Cerebral infarction, transient ischemic attacks, brain hemorrhage
Mechanism-Cerebral arteritis, particularly with subarachnoid cysticercosis
Middle-size vessel involvement common
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Vary according to size of parasites, their location inside ventricular system, and the coexistence of granular ependymitis
Lateral ventricles -syndrome of increased intracranial pressure, may be associated with focal neurological signs due to compression.
Third ventricle cysticerci -progressively worsening headaches and vomiting due to developing obstruction
May present with sudden loss of conscious from acute hydrocephalus
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Paroxysmal headache and vomiting secondary to intermittent obstruction at the level of the cerebral aqueduct
Fourth ventricle-subacute hydrocephalus that may be associated with signs of brainstem dysfunction secondary to compression of fourth ventricle
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Bruns’ syndrome -Fourth ventricle cyst Characterized by episodic headache,
papilledema, neck stiffness, sudden positional vertigo induced by rotatorymovements of the head, nausea and vomiting, drop attacks and loss of consciousness
Rapid recovery and long asymptomatic periods
Cysts in the third and fourth-cause of sudden death due acute obstructive hydrocephalus
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Granular ependymitis
Degenerating cyst in the ventricles can result in inflammatory reaction throughout the ventricular system
Cyst fixed to the ventricular wall with strong
adhesions and fibrosis leading to hydrocephalus
Tend to have a more chronic course
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1%–5% of all cases Extramedullary more common Intramedullary cysts are most common in
thoracic spine Extramedullary cysts or leptomeningeal NCC-
extension of subarachnoid disease,migratedfrom basilar cisterns
Single or may form clumps Combination of radicular pain and motor
deficits of subacute onset and progressive course
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Subretinal space -progressive decrease in visual acuity
Vitreous cysts-worsening vision with perception of something moving within the eye
Anterior chamber cyst-may induce a severe iridocyclitis
Retro-ocular intraorbital cyst-decreased visual acuity due to pressure on the optic nerve
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In the vesicular stagem cysticerci appear as cystic lesions within the brain parenchyma
CT and MRI –thin walled cyst well demarcated from parenchyma,lack perilesional edema and do not enhance after administration of contrast medium.
May be a bright nodule in their interior giving the lesion a “hole with dot” appearance that represents the scolex
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Colloidal stage so-called “acute encephalitic phase” of NCC has intense host reaction
Appear as ill-defined lesions surrounded by edema which enhance after contrast medium administration
MRI reveals a thick and hypointense wall with marked perilesional edema
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Granular cysticerci appear as nodular hyperdense lesions surrounded by edema or a rim of gliosis after contrast medium administration
Calcified (dead) cysticerci appear on CT as small hyperdense nodules without perilesional edema
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Cysticerci within the basilar cisterns missed by CT scan, require MRI
Subarachnoid cysts located in the Sylvianfissure may reach 50mm or more in size;havea mulitlobulated appearance, behave as mass occupying lesions.
Hydrocephalus is most common CT finding in subarachnoid NCc.
Leptomeningeal enhancement at the base of the brain observed on MRI
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Appear on CT images as cystic lesions.
Initially isodense with the CSF so not well visualized.
Can be inferred from distortions of the ventricular system causing asymmetric or obstructive hydrocephalus
Well visualized by MRI particularly using FLAIR techniques
Ventricular migration sign move within ventricular cavities in response to movements of patients’ head a phenomenon best observed with MRI
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CT -symmetrical enlargement of the cord (intramedullary cysts)
Pseudoreticular formations within the spinal canal (leptomeningal cysts).
MRI -intramedullary cysticerci to be ring enhancing lesions that have eccentric hyperintense nodule representing the scolex.
Myelography in spinal leptomeningealcysticercosis shows multiple filling defects in column of contrast material corresponding to each cyst
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Electroimmunotransfer blot (ETIB) using partially purified antigenic extracts
Specificity 100% & sensitivity 94%–98% in two or more cystic or enhancing lesions
False negative results in patients with single intracranial cysticerci
Detection of circulating parasite antigen reflects presence of live parasites, ongoing viable infection, permit quantitative verification of successful treatment
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Monoclonal antibody-based ELISA to detect T. solium antigens in urine
Sensitivity of urine antigen detection for viable parasites was 92%, which decreased to 62.5% in patients with a single cyst.
Only calcified cysticercosis were urine antigen negative
Indirect haemagglutination tests
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Lymphocyte transformation test (LTT) has sensitivity of 93.7% and specificity of 96.2%
Single cyst infection sensitivity of test was 87.5%
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For Parenchymal Disease-Praziquantel and albendazole are antiparasitic agents
Efficacy 60%-85%
Greater cyst reduction with albendazoleadministration
Praziquantel dose-50 mg/kg/d for 2 weeks
Albendazole dose-15mg/kg for four weeks later reduced to 15 days then to one week
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Between second and fifth day of treatment-exacerbation of neurologic symptoms attributed to inflammation secondary to killing of cysticerci
Steroids used in conjunction to control resulting edema
Steroids decrease the plasma level of praziquantel,but not albendazole
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Oral prednisolone preferred
Started 2-3 days before cysticidal therapy and continued for 7-10 days along with cysticidal therapy
High dose corticosteroids in cysticercoticencephalitis
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Whether provoked or acute symptomatic seizures and unprovoked seizures
Acute symptomatic seizures patients may be treated only for duration of acute condition
No guideline regarding duration
Unprovoked seizures-2 years seizure free period
SSECTG-monitor cyst activity with neuroimaging(6months) and to continue AED until resolution of the acute lesion.
Resolved then AED may be tapered off over next 12 weeks
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1. Ventricular, subarchanoid cysts-neuroendoscopic removal
2. Giant cysticerci
3. Hydrocephalus
4. Cysticercoid enchephalitis with raised ICT may require temporal hemicraniotomy.
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Current consensus guidelines for treatment of neurocysticercosis. Clin Microbiol Rev 2002; 15: 747-756
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Cochrane Database review on drugs for treating NCC concludes that there is insufficient evidence to assess whether cysticidal therapy in NCC is associated with beneficial effects
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Depends on degree of infection and host response to parasite
85% with a SCCG have good seizure outcome following resolution of lesion
With more than two seizures, breakthrough seizures, whose follow-up CT scan shows a calcific granuloma have a higher risk of recurrence
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Eradication of swine cysticercosis through improved animal husbandry and meat inspection procedures
No vaccine developed
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Thanks
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Neurocysticercosis: Management Issues;Tarun Dua,S. AnejaIndian Pediatrics 227-236 Volume 43;march 17, 2006
Human Cysticercosis And Indian Scenario: A Review ;KASHI NATH PRASAD Et Al. J. Biosci. 33(4), November 2008, 571–582
Diagnostic criteria for neurocysticercosis: Some modifications are needed for Indian patients; Ravindra Kumar Garg: Neurology India June 2004 Vol 52 Issue 2
Neurocysticercosis – Indian Scenario; G. Singh, M. Sappal; Medicine Update 2012 Vol. 22
Neurocysticercosis: Revisited; K.Kulkantrakorn; J INFECT DIS ANTIMICROB AGENTS Jan.-Apr. 2005
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Diagnosis and Treatment of Neurocysticercosis;C. Coyle, H. Tanowitz; Interdisciplinary Perspectives on Infectious Diseases Volume 2009, 9 pages
WHO/FAO/OIE Guidelines for the surveillance, prevention and control of taeniosis/cysticercosis 2005