Week 2

1. Epidemiology of human cysticercosis especially in developing countries

Frequency
United States
Approximately 2,000 patients are hospitalized for neurocysticercosis each year in the
United States. [2] Most occur among Latin American immigrants in locations such as
California, Arizona, and Texas. Less frequently, cysticercosis is observed in immigrants
from other areas, including India, Asia, and Africa. A small number of cases of cysticercosis
develop in people born in the United States who have traveled to areas in which the
infection is endemic. These travelers are often the children of immigrants. Locally acquired
infection is rare and is associated with contact with a tapeworm carrier. All tapeworm
carriers acquire infection from areas of endemic disease.
In a mortality study using data from the National Center for Health Statistics from 1990 to
2002; 62% of patients with cysticercosis had emigrated from Mexico.  [3]
International
An estimated 50-100 million people are infected with cysticercosis worldwide. This is
probably an underestimate since many infections go undiagnosed. The World Health
Organization (WHO) estimates suggest 2.56-8.30 million cases of neurocysticercosis
globally. [2] Neurocysticercosis is one of the leading causes of adult-onset seizures
worldwide. CT scanning and MRI of the brain have greatly improved the diagnosis of
neurocysticercosis.
Areas of endemic disease include Central and South America, India, China, Southeast
Asia, and sub-Saharan Africa. [4] Studies in Latin America and India have noted adult-onset
seizures in approximately 2% of the population, with as many as half due to
neurocysticercosis. In Latin America, the seroprevalence rate ranges from 4.9-24%. In
India, the estimated prevalence is similar. Rural China and Korea have lower infection
rates. The seroprevalence in certain rural South American communities is as high as 10-
25%. [5] The estimated true prevalence of human taeniasis and cysticercosis in rural Vietnam
is as high as 13% for each.  [6] There is also an indication that cysticercosis and taeniasis are
present across eastern European countries.  [7]

Mortality/Morbidity
Neurocysticercosis is the most frequent preventable cause of epilepsy worldwide and is
estimated to cause 30% of all epilepsy cases in endemic countries. In 2015, the WHO’s
Foodborne Disease Burden Epidemiology Reference Group identified T solium as a leading
cause of death from foodborne diseases, resulting in a considerable total of 2.8 million
disability-adjusted life-years. Neurocysticercosis was found to be responsible for 10% of
newly onset seizures in one Los Angeles, California, emergency department.  [8] Overall,
among patients who presented to emergency departments with newly onset seizure,
neurocysticercosis was found to be responsible for 2.1-5.7% of cases.  [9]
A total of 221 deaths were attributed to cysticercosis in the United States from 1990-2002.  [3]
Although some patients die of status epilepticus in areas with poor access to medical care,
mortality due to parenchymal disease is rare. With modern medical and surgical care,
mortality due to extraparenchymal disease is also unusual. However, without aggressive
surgical management, hydrocephalus is potentially life-threatening. Even with shunting
procedures, subarachnoid cysticercosis is associated with a high 10-year fatality rate.

Race
Immigrants from countries where T solium is endemic are more likely to be infected. While
most of these immigrants are Hispanic and some are Asian, prevalence rates appear to be
related more to exposure than to genetic predisposition.
Nearly 75% of all hospitalized patients in the United States with neurocysticercosis were
Hispanic. [10]

Sex
Cysticercal encephalitis, a severe form of cysticercosis, is more common in children and
young females. The cause is unknown.
US hospitalizations were more common among males.  [10]
No other sex predisposition has been noted.

Age
Patients with cysticercosis are typically aged 10-40 years. However, cases have been
described in every age group.
People aged 20-44 years were at an increased risk for hospitalizations in the United
States. [10]

2. Clinical Manifestations made on the basis of combination of clinical presentation,

radiographic studies, serologic tests and exposure history

Cysticercosis is an infection caused by the larvae of the parasite Taenia solium.  This

infection occurs after a person swallows tapeworm eggs. The larvae get into tissues such
as muscle and brain, and form cysts there (these are called cysticerci). When cysts are
found in the brain, the condition is called neurocysticercosis.
Symptoms can occur months to years after infection, usually when the cysts start dying.
When cysts die, the brain or other tissue around the cyst may swell. The pressure of the
swelling is what usually causes the symptoms of the infection.  Sometimes symptoms are
caused by the pressure of cyst in a small space. Signs and symptoms will depend on the
location and number of cysts in your body.

History
Postmortem studies in endemic areas suggest that 80% of neurocysticercal infections are
asymptomatic. [11] Consequently, many cases are never diagnosed or are found incidentally
during imaging procedures.
The peak severity of neurocysticercosis has been estimated to occur 3-5 years after initial
infection, but it can be delayed for more than 30 years. After a variable period of
degeneration, cysts can become calcified and may then become inactive. Once they are
calcified, they may cease to cause symptoms or may serve as a focus for epileptic activity.
The symptoms of neurocysticercosis depend on the stage, site, and number of cysticerci.
Cysts frequently develop in multiple locations, and a combination of active and inactive
cysts in the same patient is not uncommon.
Symptoms of cysticercosis may include seizures, elevated intracranial pressure (ICP),
meningoencephalitis, psychiatric disorder, stroke, and/or radiculopathy or myelopathy, if the
spinal cord is involved.
The symptoms are mainly due to mass effect, an inflammatory response, or obstruction of
the foramina and ventricular system of the brain. The most common symptoms include
seizures, focal neurologic signs, and intracranial hypertension.
Generally, the patient’s history includes exposure to an area where the parasite is endemic
and an adolescent- or adult-onset seizure disorder. Symptoms of hydrocephalus should
raise concerns about extraparenchymal disease. [12]
 Parenchymal CNS disease
o Seizures may be focal, focal with secondary generalization, or generalized.
o Headaches are common and may be migrainelike or tension-type.
o Neurocognitive deficits, while rare, may include learning
 [13] 
disabilities, depression, or even psychosis .
 Extraparenchymal disease
o Most patients present with headaches or symptoms of hydrocephalus.
o Symptoms of increased ICP may include headache, nausea or vomiting,
altered mental status, dizziness, and decreased visual acuity due to papilledema.
o Patients with numerous cysticerci in the basilar cisterns may present with
communicating hydrocephalus, meningismus (without fever), symptoms of
lacunar infarcts due to small-vessel vasculitis, or symptoms of large-vessel
infarcts due to cysticercal erosion into major arteries or severe inflammation of
those arteries.
o Patients with spinal cysticerci typically present with radicular symptoms, but
rarely with motor or sensory deficits traceable to a spinal level.
o Patients with ocular cysticerci report visual changes.
 Spinal cord involvement
o Radiculopathy
o Myelopathy
 Other
o Meningoencephalitis
 o Stroke (in young adults)
o Subcutaneous nodules
o Ocular cysts
Physical
Meningoencephalitis may manifest as pyrexia, altered senses, seizures, increased ICP,
multiple cranial nerve involvement, or even brainstem or cerebellar involvement.
Both parenchymal and extraparenchymal disease can cause elevated ICP. Signs include
hyperreflexia, papilledema (a late sign), and the Cushing reflex (a preterminal event).
Parenchymal disease
Physical examination findings are usually normal.
Patients who have had seizures may have typical manifestations of the postictal state, with
somnolence, an altered level of consciousness, and poor memory.
Focal neurologic deficits are unusual and suggest alternative diagnoses, such as
tuberculoma, tumor, or, rarely, extraparenchymal neurocysticercosis.
Extraparenchymal disease
Ocular cysticerci are visible upon ophthalmologic examination.
Rare spinal cysticerci manifest as sensory or motor deficits or back tenderness.
Patients with neurocysticercosis of the cisterns may present with lacunar infarcts or large-
vessel infarction with associated upper motor neuron signs.
Approximately half of all cysticercosis cases have cutaneous manifestations, which can
present as subcutaneous swellings. [14]
Subcutaneous cysts may be palpable as fluid-filled nodules that resemble sebaceous cysts.

Causes
Extraneural cysticercosis: Extraneural infection with T solium typically involves the eye,
muscle, or subcutaneous tissue. It is not known whether oncospheres actively migrate to
those organs or passively enter tissues during high blood flow.
Neurocysticercosis: Infection of the CNS with T solium cysticercus and associated host
inflammation.

 Cysts in the muscles:

o Cysts in the muscles generally do not cause symptoms. However, you may be
able to feel lumps under your skin. The lumps sometimes become tender.
 Cysts in the eyes:
o Although rare, cysts may float in the eye and cause blurry or disturbed vision.
Infection in the eyes may cause swelling or detachment of the retina.
 Neurocysticercosis (cysts in the brain, spinal cord):
o Symptoms of neurocysticercosis depend upon where and how many cysts are
found in the brain. Seizures and headaches are the most common symptoms.
However, confusion, lack of attention to people and surroundings, difficulty
with balance, excess fluid around the brain (called hydrocephalus) may also
occur. The disease can result in death.

3. To know diagnostic criteria for human cysticercosis included absolute, major,

minor and epidemiologic criteria
Approach Considerations
The diagnosis of cysticercosis is often based on clinical presentation, abnormal findings on
neuroimaging, and serology. Occasionally, more invasive procedures (eg, brain biopsy) are
required. [15]
Del Brutto et al have previously defined and modified the diagnostic criteria for definitive
and probable neurocysticercosis in 2001 and 2012, respectively. These criteria were
revised in 2017. [16]
Absolute criteria
Absolute criteria include the following:
 Histological demonstration of the parasite on biopsy from the brain or spinal cord
lesion
 Visualization of subretinal cysticercus
 Conclusive demonstration of a scolex within a cystic lesion on neuroimaging studies
Neuroimaging criteria
Major neuroimaging criteria include the following:
 Cystic lesions without a discernable scolex
 Enhancing lesions
Confirmative neuroimaging criteria include the following:
 Resolution of cystic lesions after cysticidal drug therapy
 Spontaneous resolution of single small enhancing lesions
 Migration of ventricular cysts documented on sequential neuroimaging studies
Minor neuroimaging criteria: Obstructive hydrocephalus (symmetric or asymmetric) or
abnormal enhancement of basal leptomeninges
Clinical/exposure criteria
Major clinical/exposure criteria include the following:
 Detection of specific anticysticercal antibodies or cysticercal antigens via well-
standardized immunodiagnostic tests
 Cysticercosis outside the CNS
 Evidence of household contact with T solium infection
Minor clinical/exposure criteria include the following:
 Clinical manifestations suggestive of neurocysticercosis
 The patient came from or lives in an area where cysticercosis is endemic
Degrees of diagnostic certainty
Definitive diagnosis requires one of the following:
 One absolute criterion
 Two major neuroimaging criteria plus any clinical/exposure criterion
 One major and one confirmative neuroimaging criteria plus any clinical/exposure
criterion
 One major neuroimaging criterion plus two clinical/exposure criteria (including at
least one major clinical/exposure criterion), together with the exclusion of other
pathologies that produce similar findings
Probable diagnosis is supported by one of the following:
 One major neuroimaging criteria plus any two clinical/ exposure criteria.
 One minor neuroimaging criteria plus at least one major clinical/ exposure criteria.

4. To know the laboratory findings, complication, prevention and treatment of

cysticercosis

Diagnosis
Stool tests commonly include microbiology testing – the microscopic examination of stools
after concentration aims to determine the amount of eggs. Specificity is extremely high for
someone with training but sensitivity is quite low because the high number of eggs in small
amounts of sample.[12]
Stool tapeworm antigen detection: Using ELISA increases the sensitivity of the
diagnosis. The downside of this tool is it has high costs, an ELISA reader and reagents are
required and trained operators are needed.[12]
Stool PCR: This method can provide a species-specific diagnosis when proglottid material
is taken from the stool. This method requires specific facilities, equipment and trained
individuals to run the tests. This method has not yet been tested in controlled field trials. [12]
Serum antibody tests: using immunoblot and ELISA, tape-worm specific circulating
antibodies have been detected. The assays for these tests have both a high sensitivity and
specificity.[12]

Laboratory Studies
Findings from laboratory studies such as routine CBC counts and liver function tests are not
specific. The WBC count is usually within the reference range, and most patients do not
have eosinophilia unless a cyst is leaking, in which case the eosinophilia may be
pronounced.
Serologic studies can be helpful in the diagnosis of cysticercosis but are limited in their
usefulness in a community setting by general lack of availability, as follows:
 An enzyme-linked immunoblot transfer blot (EITB) assay can demonstrate serum or
CSF anticysticercal antibodies. The findings in the serum are more sensitive than
those in the CSF. The assay is highly specific for exposure to T solium. The sensitivity
is high (94%) in patients with multiple lesions or extraparenchymal infection but may
be as low as 28% in patients with a single parenchymal lesion. EITB assay findings
may revert to negative after the cysticercus dies and are often negative in patients with
only calcified lesions.
 ELISAs that use unfractionated antigen are fraught with problems regarding
sensitivity and specificity, and they are reliably diagnostic only when performed on
CSF.
 The observed cross-reactivity of infected sera with antigens of other parasites has
limited the accuracy of serologic techniques such as ELISA. The western blot kit
(QualiCode) offers qualitative detection of immunoglobulin G (IgG) antibodies to T
solium with a sensitivity of 95% and a specificity of 100%. It yields rapid results (< 90
min).
 The sensitivity of ELISA using CSF is approximately 80%. False positive results may
occur in patients with hydatid cysts, filariasis, tuberculous meningitis, or viral
encephalitis. An active inflammatory response is likely to cause high titers;
intraventricular cysts cause a low titer.
 An assay using monoclonal antibody HP10 to detect parasite secretory/excretory
antigens performed well in CSF samples, with results similar to those from the EITB
assay. [17]
 A 2017 meta-analysis found that ELISA for antibodies and EITB yield a similar
diagnostic value. [18]
 No polymerase chain reaction (PCR) tests are available.
Carriage of tapeworms in humans can be diagnosed via detection of proglottids or eggs in
feces, Taenia antigens in stool, or specific antibodies in serum. [19]
Stool examination for ova and parasites can occasionally be used to diagnose intestinal
infection with T solium. However, most people diagnosed with cysticercosis do not have
viable T solium tapeworm in their intestine, so eggs are not typically found.
 Because eggs are shed intermittently, most cases of taeniasis cannot be detected
with a single stool test.
 Furthermore, egg morphology is the same for T solium and Taenia saginata.
 Antigen detection tests for stool and serologic tests for tapeworms are being studied;
none is available for use in clinical practice.
 Identifying tapeworm carriers does not usually help in diagnosing neurocysticercosis,
but it may be useful in detecting the source of infection in cases among US residents
who have not traveled.

Imaging Studies
Neuroimaging with contrast-
enhanced CT scanning or MRI is the
mainstay of diagnosis.
MRI is better for detecting
intraventricular types and
extraparenchymal disease and
visualizing the scolex within the
cysticercus (as high intensity inside a
cyst). Fluid attenuation inversion
recovery (FLAIR) sequences are
particularly helpful for identifying
associated edema and the scolex. [20]
CT scanning is better for detecting
intracerebral calcifications.
Both modalities can reveal
hydrocephalus and active
intraparenchymal lesions.
The ventricles may be narrowed with
extensive low attenuated areas in
the parenchyma, sparing the cortex.
A ring enhancing active lesion with
surrounding edema is the second-
most-common finding.
A homogenously enhancing lesion
represents a dying larva.
Calcified lesions are also common
on CT scans.

Other Tests
EEGs are frequently obtained in patients who have experienced seizures. The EEG is
abnormal in up to 50% of cases, demonstrating various findings (diffuse slowing, focal
paroxysmal activity, generalized spike waves) depending on lesion number, size, and
location.
No pattern is diagnostic for neurocysticercosis.
Focal abnormalities may be present in persons with active disease.
Seizures may also be caused by inactive disease (calcified nodules of the residual phase),
but, in these cases, the EEG does not usually reveal focal abnormalities.
In patients who will likely require prolonged corticosteroid therapy, screening for latent
tuberculosis and Strongyloides stercoralis infection is suggested before therapy is
initiated. [20]

Procedures
Lumbar puncture: Lumber puncture for a CSF study is usually unnecessary in the diagnosis
of neurocysticercosis. This procedure is also contraindicated upon suspicion of increased
ICP. If a lumber puncture is performed, examination of CSF shows a normal glucose
concentration and protein levels and WBC counts that are usually only mildly elevated. CSF
studies in individuals who have a leaking cyst that communicates with the CSF may reveal
prominent CSF eosinophilia.
Biopsy: Biopsy may be required in patients with suspected neurocysticercosis who have a
single brain lesion with no characteristic scolex and negative serology findings. Biopsy
specimens may be taken from subcutaneous nodules or a muscle lesion. Biopsy of CNS
lesions is rarely necessary.

Histologic Findings
Occasionally, CNS lesions are mistakenly identified as tumors and are diagnosed only at
surgery. Upon gross examination, the cysticerci appear as 5- to 10-mm semiopaque cysts
with a 1- to 2-mm mural nodule containing the scolex.
Histopathologic examination reveals a superficial tegument layer covered with microtriches,
a cellular layer below that containing the cell nuclei and musculature, and a loose reticular
layer characterized by canaliculi. When the parasites are viable, little surrounding
inflammation is observed. Degenerating parasites, on the other hand, are invaded with an
inflammatory infiltrate including lymphocytes, macrophages, plasma cells, neutrophils, and
eosinophils. Cavellani et al used autopsy protocols to study the influence of age and gender
on cardiac and encephalic inflammation caused by cysticercosis. They concluded that
inflammation decreases with age and depends on the stage of the disease; women have a
more intense response during senescence. [21]
Histologic studies have shown that viable cysticerci in humans and pigs have little or no
surrounding inflammation. [22]
Cysticerci can persist in the human host for long periods, often years, without eliciting a
surrounding inflammatory reaction.
In contrast, the immune-mediated inflammation around one or more degenerating cysts
may precipitate symptomatic disease.
When the parasite begins to involute, either naturally or after treatment with anticysticercal
drugs, granulomatous inflammation develops around the cysticerci. The predominant
components of this inflammatory response include plasma cells, lymphocytes, eosinophils,
and macrophages. The latter engulf parasite remnants, eventually leaving a gliotic scar with
calcifications.
Early granulomas in cysticercosis are predominantly associated with a Th1 response,
whereas later granulomas, in which parasite destruction is complete, have a mixture of Th1
and interleukin-4 (IL-4). The Th1 response appears to play an important role both in the
pathogenesis of disease and in the clearing of the parasites, with IL-4 involved in
downregulation of the initial response.
Complications:
Neurocysticercosis is classified as parenchymal or extraparenchymal based on the location
of the parasite and surrounding host tissue on neuroimaging.  [20]
Parenchymal form
 The viable parenchymal form is characterized by vesicular lesions, often with
evidence of associated contrast enhancement and/or surrounding edema. The
scolex is often visible on high-definition imaging. This represents parasites with an
intact cyst wall, vesicular fluid, and scolex, with variable degrees of inflammation
surrounding the parasite, sometimes invading the cyst wall.
 A single small enhancing cystic or nodular enhancing lesion smaller than 2 cm
represents parasites in the process of degeneration with surrounding inflammation
and variable cyst fluid.
 Nodular calcifications smaller than 20 mm in diameter with or without surrounding
edema and/or contrast enhancement are seen in nonviable form, representing
calcified granuloma with or without surrounding inflammation and/or gliosis.
Extraparenchymal  form
 Intraventricular cysticerci can be seen within the ventricles and may cause
obstructive hydrocephalus or loculated hydrocephalus with disproportionate dilation
of the ventricles on CT/MRI.
 Subarachnoid cysticerci are found in the sylvian fissure, basilar cisterns, or
interhemispheric spaces. These can present as stroke or meningitis without discrete
cysts. The cysticerci often appear in clusters with proliferating membranes
(racemose) and may lack a scolex.
 Spinal cysticerci are seen within the spinal subarachnoid space with or without
evidence of inflammation/diffuse spinal arachnoiditis. Intramedullary cysticerci can
also be within the spinal cord.
Parenchymal disease causes seizures but few long-term complications. However, studies
suggest that childhood infection may be associated with learning disabilities and cognitive
dysfunction.
Extraparenchymal disease may cause elevated ICP, resulting in herniation and death.
Vasculitis associated with cisternal neurocysticercosis may cause strokes, communicating
hydrocephalus, and death.

Medical Care
 Asymptomatic cysticercosis: As mentioned above, more than 80% of patients with
cysticercosis are asymptomatic. No evidence has shown that administering
antiparasitic therapy for asymptomatic nonviable cysticercal lesions found
incidentally in the brain is beneficial.
 Patients who are found to have cysticerci only in subcutaneous or intramuscular
sites generally do not require specific therapy.
 If a single extracranial lesion is found, excision can be considered after
neurocysticercosis is excluded with brain imaging.
 Patients with ocular cysticercosis who have extraocular muscle involvement may
present with diplopia and recurrent eye pain. Treatment with albendazole and
corticosteroids has proven to be beneficial. Some patients may require surgical
excision. For intraocular cysticerci, surgical removal is preferred over antiparasitic
drug therapy. [20]
  Patients with subcutaneous or intramuscular cysticercosis who develop symptoms
due to inflammation can be treated with cysticerci excision or anti-inflammatory
agents. Excision is the treatment of choice for a solitary symptomatic lesion.
Symptomatic therapy for neurocysticercosis should be the focus of initial and emergency
management, as follows:
 Antiepileptic drug therapy in patients presenting with seizures
 Anti-inflammatory drugs such as corticosteroids and methotrexate in patients with
cerebral edema or vasculitis
 Shunt surgery for hydrocephalus
Antiparasitic treatment is important but should never be considered emergently.
Antiparasitic drugs can worsen cerebral edema and should be avoided in patients with
increased intracranial pressure due to either diffuse cerebral edema or untreated
hydrocephalus. [23]

Parenchymal cystic neurocysticercosis has better outcomes if treated with antiparasitic

drugs along with corticosteroids. Treatment recommendations for parenchymal
neurocysticercosis depend on its form, as follows:  [20]
 In patients with untreated hydrocephalus or diffuse cerebral edema, management of
elevated intracranial pressure alone is recommended.
 For viable parenchymal cysticercosis, antiparasitic drugs should be administered
unless the intracranial pressure is increased. For 1-2 viable parenchymal cysts or a
single enhancing lesion, monotherapy with albendazole is recommended. The usual
dose is 15 mg/kg/day in 2 daily doses (up to 1200 mg/day) with food for 10-14 days.
 For more than two viable parenchymal cysts, a combination of albendazole (15
mg/kg/day in 2 daily doses up to 1200 mg/day) and praziquantel (15 mg/kg/day in 3
daily doses) for 10-14 days is recommended.
 Corticosteroids should be given whenever antiparasitic drugs are used.
 Antiepileptic drugs should be administered to all patients with seizures.
 Antiparasitic treatment is not recommended for calcified parenchymal
neurocysticercosis.

Surgical Care
Ventricular neurocysticercosis of the third and lateral ventricles should be treated with
minimally invasive surgery, when possible. Adherent cysticerci should be managed with
CSF diversion along with antiparasitic drugs. Minimally invasive and open craniotomies are
options for fourth-ventricular disease. Antiparasitic drugs should be deferred until after
surgical therapy. Treatment recommendations for extraparenchymal neurocysticercosis are
as follows: [20]
 For intraventricular neurocysticercosis of the lateral and third ventricles, removal of
the cysticerci via minimally invasive neuroendoscopy, when possible, is recommended
over other surgical or medical approaches for cysticerci. Antiparasitic drugs should not
be used preoperatively, since such treatment could result in disruption of parasite
integrity, and an inflammatory response could prevent successful cyst removal.
 When surgical removal of fourth-ventricular cysticerci is possible, this is
recommended over medical therapy and/or shunt surgery.
 When surgical removal is technically difficult, shunt surgery for hydrocephalus is
suggested.
 For intraventricular neurocysticercosis, corticosteroid therapy is recommended to
decrease brain edema perioperatively. Antiparasitic drug therapy along with
 corticosteroid therapy is suggested following shunt insertion to decrease subsequent
shunt failure in patients in whom surgical removal of isolated intraventricular cysts is
not possible.
 For subarachnoid cysts, antiparasitic drug therapy is recommended until radiologic
resolution of viable cysticerci on MRI and resolution of other evidence of cysticerci.
 Methotrexate is suggested as a steroid-sparing agent in patients who require
prolonged anti-inflammatory therapy.
 Shunt surgery in addition to medical therapy is recommended in patients with
hydrocephalus due to subarachnoid neurocysticercosis. Some patients may benefit
from surgical debulking over shunt surgery alone.
 For spinal neurocysticercosis, corticosteroid treatment is recommended in patients
with evidence of spinal cord dysfunction, along with antiparasitic therapy.
 For intraocular cysticerci, surgical removal is preferred over antiparasitic drug
therapy.

Consultations
Consultation with a neurosurgeon is essential in patients with hydrocephalus, significant
mass effect, or extraparenchymal CNS disease.
Consultation with a neurologist is needed if protracted or refractory seizures occur.
Consultation with an infectious disease specialist is recommended if active disease is
suspected.
An ophthalmologist should be consulted for patients with ocular neurocysticercosis. At a
minimum, a funduscopic examination should be performed before the initiation of
antiparasitic drug therapy.

Diet
No specific diet restriction is recommended.
Patients should avoid reinfection and reingestion of ova from original sources by observing
the following guidelines:
 Inspection of pork for cysticerci, which are visible in raw meat ("measly meat")
 Freezing or adequately cooking meat to destroy cysticerci (Pickling and salting are
inadequate.)
 Administering antiparasitic agents to pigs
 Good personal hygiene and hand-washing prior to food preparation

Activity
No activities are restricted if the patient is otherwise asymptomatic.
All patients who present with seizures should take seizure precautions. Patients with a
history of seizures may have state-required restrictions on driving motor vehicles.
Physicians may be responsible for informing patients about these restrictions.
Patients with hydrocephalus may have ataxia and may be at risk for falls.

Long-Term Monitoring
The initial brain reimaging should be performed two months after therapy completion.
MRI should be repeated at least every 6 months until resolution of the cystic component.  [20]
Parasite antigen levels typically fall by 3 months after successful treatment.
If the cysts are growing in the absence of therapy, antiparasitic therapy should be
considered.
In patients with seizures due to neurocysticercosis without calcification, perform imaging
studies every 3-6 months. If calcification develops, lifelong anticonvulsant therapy is
indicated, and further imaging studies can be performed as needed.
Tapering and discontinuation of antiepileptic therapy can be considered in patients with few
seizures prior to antiparasitic therapy, resolution of cystic lesions on imaging studies, and
no seizures for 24 consecutive months. In patients with a single enhancing lesion and no
risk factors for recurrence, antiepileptic drugs can be discontinued after resolution of cystic
lesions. Risk factors for recurrent seizures include the following:  [20]
 Calcifications on follow-up CT scanning
 Breakthrough seizures
 More than two seizures during the disease course
Patients with calcified lesions and a seizure disorder should be maintained on
anticonvulsants indefinitely, and they should undergo imaging studies only as needed.
Monitor anticonvulsant serum levels to prevent toxicity.

Further Inpatient Care

ICU monitoring is necessary in patients with uncontrolled seizures, elevated ICP, or severe
extraparenchymal disease.
If antiparasitic therapy is provided, patients should be hospitalized and monitored during the
initial phase.
 As cysticerci die, neurologic symptoms may worsen because of an increased
inflammatory response.
 Most symptoms associated with antiparasitic therapy develop within 3-5 days of
beginning therapy.
 Antiparasitic therapy may then be completed in an outpatient setting.
Prior initiation of therapy with antiparasitic medications or corticosteroids, the following
steps should be taken:
 Apply a purified protein derivative (PPD) skin test. Patients in whom the PPD result
is positive should be treated with isoniazid along with pyridoxine (vitamin B6) for the
duration of their steroid treatment.
 Because many patients with cysticercosis also have risk factors for strongyloidiasis,
these patients should be treated with ivermectin (200 μg/kg administered in two single
doses two weeks apart before steroids are initiated.
 An ophthalmologist should perform an eye examination to exclude ocular
cysticercosis.

Inpatient & Outpatient Medications

Discharge medications may include steroids, anticonvulsants, antiparasitics, and
cimetidine.
The anticonvulsants carbamazepine and phenytoin are first-choice treatments.

Transfer
Patients with extraparenchymal neurocysticercosis should be treated at hospitals with
active neurosurgical and neurological services because emergency procedures such as
shunt placement or ventriculostomy may be required in patients with worsening
hydrocephalus.
Arrange transfer if the facility is unable to provide neurologic or neurosurgical care.
5. To describe the life cycle of taenia solium, pathogenesis of taenia infection in
human

Images: Left: Taenia egg at a high magnification of 400x. When consumed by

humans, Taenia solium eggs can lead to cysticercosis, including a serious condition known
as neurocysticercosis. Center: A radiographic image of the brain of a patient who has
neurocysticercosis; the small dark spots within the brain are larval cysts of T. solium. Right:
A cross-section through a T. solium cyst from a human brain tissue specimen, stained with
hematoxylin and eosin (H&E). (Credit (L to R): Westchester Medical Center, PHIL, DPDx.)

Causal Agents:
The cestodes (tapeworms) Taenia saginata (beef tapeworm) and T. solium (pork
tapeworm). Taenia solium eggs can also cause cysticercosis.
Life Cycle:

Taeniasis is the infection of humans with the adult tapeworm of Taenia saginata or Taenia
solium. Humans are the only definitive hosts for T. saginata and T. solium. Eggs or gravid
proglottids are passed with feces (1); the eggs can survive for days to months in the
environment. Cattle (T. saginata) and pigs (T. solium) become infected by ingesting
vegetation contaminated with eggs or gravid proglottids (2). In the animal’s intestine, the
oncospheres hatch (3), invade the intestinal wall, and migrate to the striated muscles,
where they develop into cysticerci. A cysticercus can survive for several years in the
animal. Humans become infected by ingesting raw or undercooked infected meat  (4). In
the human intestine, the cysticercus develops over 2 months into an adult tapeworm, which
can survive for years. The adult tapeworms attach to the small intestine by their
scolex (5) and reside in the small intestine (6).

People get cysticercosis when they swallow T. solium eggs that are passed in the feces of
a human with a tapeworm. Usually, humans get the tapeworm infection after eating raw or
undercooked pork contaminated with cysts of T. solium. Tapeworm eggs are spread
through food, water, or surfaces contaminated with feces.  Humans swallow the eggs when
they eat contaminated food or put contaminated fingers in their mouth.  When swallowed
the cysts pass through the stomach and attach to the lining of the small intestine. In the
small intestine the cysts develop into adult tapeworms over about two months. Importantly,
someone with a tapeworm can infect him-or herself with tapeworm eggs (this is called
autoinfection), and can infect others in the family. Eating pork cannot give you cysticercosis.
The life cycle of T. solium is indirect. It passes through pigs or other animals, as
intermediate hosts, into humans, as definitive hosts. In humans the infection can be
relatively short or long lasting, and in the latter case if reaching the brain can last for life.
From humans, the eggs are released in the environment where they await ingestion by
another host. In the secondary host, the eggs develop into oncospheres which bore through
the intestinal wall and migrate to other parts of the body where the cysticerci form. The
cysticerci can survive for several years in the animal. [7]
Definitive host[edit]
Humans are colonised by the larval stage, the cysticercus, from undercooked pork or other
meat. Each microscopic cysticercus is oval in shape, containing an inverted scolex
(specifically "protoscolex"), which everts once the organism is inside the small intestine.
This process of evagination is stimulated by bile juice and digestive enzymes (of the host).
Then, the T. Solium lodges in the host’s upper intestine by using its crowned hooks and 4
suckers to enter the intestinal mucosa. Then, the scolex is fixed into the intestine by having
the suckers attached to the villi and hooks extended. It grows in size using nutrients from
the surroundings. Its strobila lengthens as new proglottids are formed at the foot of the
neck. In 10–12 weeks after initial colonization, it is an adult worm. As a hermaphrodite, it
reproduces by self-fertilisation, or cross-fertilisation if gametes are exchanged between two
different proglottids. Spermatozoa fuse with the ova in the fertilisation duct, where
the zygotes are produced. The zygote undergoes holoblastic and
unequal cleavage resulting in three cell types, small, medium and large (micromeres,
mesomeres, megameres). Megameres develop into a syncytial layer, the outer embryonic
membrane; mesomeres into the radially striated inner embryonic membrane or
embryophore; micromeres become the morula. The morula transforms into a six-hooked
embryo known as an oncosphere, or hexacanth ("six hooked") larva. A gravid proglottid can
contain more than 50,000 embryonated eggs. Gravid proglottids often rupture in the
intestine, liberating the oncospheres in faeces. Intact gravid proglottids are shed off in
groups of four or five. The free eggs and detached proglottids are spread through the host's
defecation (peristalsis). Oncospheres can survive in the environment for up to two months.
[3][8]
 However, during a British military outbreak due to cysticercosis, an accurate
Epidemiological data after 2 to 5 years of exposure, concluded that most tapeworms would
live less than 5 years inside of a definitive host
Intermediate host[edit]
Pigs are the most common host who ingest such eggs in traces of human faeces, mainly
from vegetation contaminated with it such as from water bearing traces of it. The
embryonated eggs enter intestine where they hatch into motile oncospheres. The
embryonic and basement membranes are removed by the host's digestive enzymes
(particularly pepsin). Then the free oncospheres attach on the intestinal wall using their
hooks. With the help of digestive enzymes from the penetration glands, they penetrate
the intestinal mucosa to enter blood and lymphatic vessels. They move along the
general circulatory system to various organs, and large numbers are cleared in the liver.
The surviving oncospheres preferentially migrate to striated muscles, as well as the brain,
liver, and other tissues, where they settle to form cysts — cysticerci. A single cysticercus is
spherical, measuring 1–2 cm in diameter, and contains an invaginated protoscolex. The
central space is filled with fluid like a bladder, hence it is also called bladder worm.
Cysticerci are usually formed within 70 days and may continue to grow for a year. [9]
Humans are also accidental secondary hosts when they are colonised by embryonated
eggs, either by auto-colonisation or ingestion of contaminated food. As in pigs, the
oncospheres hatch and enter blood circulation. When they settle to form cysts, clinical
symptoms of cysticercosis appear. The cysticercus is often called the metacestode.

6. To understand how to prevent taenia infection in human

 Wash your hands with soap and warm water after using the toilet, changing diapers,
and before handling food
 Teach children the importance of washing hands to prevent infection
 Wash and peel all raw vegetables and fruits before eating
 Use good food and water safety practices while travelling in developing countries
such as:
o Drink only bottled or boiled (1 minute) water or carbonated (bubbly) drinks in
cans or bottles
o Filter unsafe water through an “absolute 1 micron or less” filter AND dissolve
iodine tablets in the filtered water; “absolute 1 micron” filters can be found in
camping and outdoor supply stores
Prevention
 Educate patients regarding routes of transmission of cysticerci ova.
 Meat inspection has been effective at preventing transmission of tapeworms in
developed countries but has been uniformly unsuccessful in developing countries.
Thorough cooking of meat is a primary prevention measure. Freezing at -5°C for 4
days, -15°C for 3 days, or -24°C for one day kills the cysticerci.  [24]
 In areas of endemic cysticercosis, avoid undercooked pork to reduce the risk of
intestinal infection.
 Be vigilant about avoiding potential fecal-oral transmission to reduce the risk of
neurocysticercosis while in endemic areas. Individuals traveling to such areas should
observe the following guidelines:
o Eat only fruits and vegetables that you have peeled yourself.
o Thoroughly wash (with water from a clean source) all food prior to ingestion.
o Maintain good personal hygiene and wash hands prior to food preparation.
 A combination of mass treatment for tapeworm carriage, mass treatment of pigs, and
vaccination of pigs shows potential for interrupting transmission of T solium infection
in endemic regions, as demonstrated in Peru. [25]
 Mass chemotherapy has been used to interrupt transmission in some areas of
endemic infection, but disease usually returns within a few years.
 Mass anthelminthic therapy yields only limited success and may cause adverse
neurologic events in individuals with undiagnosed neurocysticercosis who receive
these drugs.
 Consider identifying human carriers of tapeworms, possibly based on a history of
proglottid passage, and instituting targeted treatment.
 Serologic screening of the contacts of patients should also be considered in the
management of cysticercosis, particularly in nonendemic countries when
transmission may have occurred within a household (eg, via food prepared by a
household worker from an endemic country).
 Vaccines for prevention of cysticercosis have proven effective for
other Taenia species and are in development for T solium.
  Transmission of cysticercal infections to pigs can be prevented with the following
measures:
 Changing pig-raising practices in endemic areas by confining the animals and
preventing them from roaming freely to avoid contact with infectious ova excreted in
human feces
 Improving sanitary conditions and proper disposal of human stool
 Possibly vaccinating pigs (Preliminary studies suggest this may be feasible.)

Prevention & Control

One way to prevent taeniasis is to cook meat to safe temperatures. A food
thermometer should be used to measure the internal temperature of cooked meat. Do not
sample meat until it is cooked. USDA recommends the following for meat preparation.
For Whole Cuts of Meat (excluding poultry) 
Cook to at least 145° F (63° C) as measured with a food thermometer placed in the thickest
part of the meat, then allow the meat to rest* for three minutes before carving or
consuming. 
For Ground Meat (excluding poultry) 
Cook to at least 160° F (71° C); ground meats do not require a rest* time.
   *According to USDA, “A ‘rest time’ is the amount of time the product remains at the final
temperature, after it has been removed from a grill, oven, or other heat source. During the
three minutes after meat is removed from the heat source, its temperature remains constant
or continues to rise, which destroys pathogens.”

7. Seizure all about

Seizure disorders (Epilepsy)
Summary
A seizure is irregular electrical activity in the brain caused by the hyperexcitability
of neurons, especially in cortical areas. Hyperexcitability, in turn, is the result of altered
cellular electrochemical properties, which may be caused, for example, by electrolyte
imbalances. The etiology varies according to age. Seizures may be provoked by acute
conditions (e.g., stroke, traumatic brain injury, alcohol withdrawal) or unprovoked, in which
case they are indicative of epilepsy. The lifetime risk for experiencing at least
one seizure is approx. 3% in the general population. Individuals who experience a
single seizure do not necessarily have epilepsy. Seizures may be classified as generalized
or focal. Generalized seizures arise from discharges in both hemispheres, whereas focal
seizures begin with discharges in one hemisphere. Depending on the origin of the
epileptiform discharge and the type of the seizure, various temporary motor, sensory,
autonomic, or psychological symptoms may occur. However, the most frequent clinical
presentation involves rhythmic twitching and loss of consciousness (tonic-clonic seizure).
After a first seizure occurs, the likely cause must be determined based on medical history
(evaluation of provocative factors and seizure type), laboratory tests, and imaging (to detect
or rule out structural or metabolic causes). Electroencephalography (EEG) is used to
establish the diagnosis. Important antiepileptic drugs are lamotrigine (first-line treatment
in focal seizures), valproate (first-line treatment in generalized seizures)
and ethosuximide (first-line treatment in typical absence seizures). With appropriate
pharmacotherapy, the majority of patients remain seizure-free in the long term.
Epileptic seizures can evolve into ongoing seizure activity (status epilepticus), which is a
potentially life-threatening event and must be addressed as soon as possible
(pharmacologic interruption of seizures with a benzodiazepine).
Definition
 Seizure: abnormal, unregulated electrical activity of cortical neurons that results in
transient changes in behavior and/or EEG findings
 Epilepsy: a chronic neurologic disorder characterized by any of the following:
 Two or more unprovoked seizures separated by more than 24 hours
 One unprovoked seizure with an underlying predisposition
to seizures (recurrence risk over the next 10 years that is similar to the
recurrence risk after two unprovoked seizures)
 Diagnosis of an epilepsy syndrome
 Symptomatic epilepsy: epilepsy due to an identifiable condition (e.g., brain tumor,
structural abnormalities of the brain) that causes an increased predisposition
to seizures
 Cryptogenic epilepsy: epilepsy due to an unknown cause (genetic association
suspected)
 Nonepileptic seizure: seizures that are provoked by acute conditions (e.g.,
intoxication, metabolic disturbances). See provoked seizure for details.
 Epilepsy syndromes: epileptic disorders defined by a collection of characteristic
clinical manifestations and other features (e.g., age of onset, brain lesions)
Epidemiology
 Prevalence:
 Infants: ∼ 100/100,000
 Adults : ∼ 40/100,000
 The elderly : ∼ 140/100,000
 Risk of experiencing at least one seizure up to the age of 75 (in the general
population): ∼ 3%
Etiology
Epilepsy
 Unprovoked seizure (epileptic seizure): due to a general increase in neuronal
hyperexcitability
 Genetic: genetic mutations of ion channels or
transmitter receptors, chromosomal abnormalities 
 Cryptogenic (idiopathic)
 Structural/metabolic: preexisting, chronic cerebral lesion
of CNS abnormality (e.g., hypoxic-ischemic injury, PKU, tuberous sclerosis,
congenital cerebral malformations)
Although these seizures are referred to as unprovoked, they may be triggered by certain
provocative factors!
Provocative factors for epilepsy
Situational factors that can trigger epileptic seizures in epilepsy patients:
 Excessive physical exertion
 Sleep deprivation
 Strobe light flashing
 Loud music
Provoked seizures
Acute symptomatic seizures that are secondary to acute conditions:
 Metabolic and electrolyte
disturbances: hypoglycemia and hyperglycemia, hyponatremia and hypernatremi
a, hypocalcemia, uremia, thyroid storm, hyperthermia, water intoxication
 Mass: brain tumors and metastases, hippocampal sclerosis
  Withdrawal
 Alcohol withdrawal (most common trigger in adults)
 Noncompliance with anticonvulsant treatment
 Medication withdrawal 
 Intoxication
 Acute intoxication: cocaine, ecstasy, carbon monoxide poisoning, metal
poisoning
 Pharmacotherapy: amitriptyline, penicillin,
maprotiline, lithium, lidocaine, antipsychotics, theophylline
 Infections: encephalitis, brain abscess, meningitis, septic shock
 Ischemia: stroke, perinatal injuries 
 Trauma: traumatic brain injury
 Increased ICP and cerebral edema: eclampsia, hypertensive encephalopathy,
cerebrovascular malformation
 Fever in infants and children (see febrile seizures)
Withdrawal from ABBA (alcohol, benzodiazepines, barbiturates, antiseizure drugs) can
cause seizures!
Common causes according to age group
Neonates Infants and Adolescent Younger Older adults (> 35 years)
children s adults
Congenit Fever  Trau Alco Alcohol withdrawal
al (idiopathic; Idiopat matic brain hol Stroke or TIA
genetic hic (genetic injury withdrawal Traumatic brain injury
association) association Ence Trau Brain tumors
Perinatal suspected) phalitis matic brain Metabolic disorders
injury Infecti Gene injury Vascular encephalop
Perinatal ons tic disorders Illicit  athies and vascular
or postnatal Trauma Illicit  substance dementia (in the elderly)
infections tic brain injury substance abuse
(e.g., CNS infect Brain m abuse Brain
ions) alformations tumors
Metabolic Metabo
disorders lic disorders
Classification
1. Etiological classification (ILAE 2010) 
 Genetic: without a discernible structural or metabolic cause 
 Structural or metabolic: with a discernible structural or metabolic cause 
 Unknown: no tangible cause (the cause is inferred from the clinical
presentation and history) 
2. Classification according to anatomical origin and clinical features 
 Focal seizures 
 Focal seizures without dyscognitive features
 Focal seizures with dyscognitive features
 Primary generalized seizures 
 Classic tonic-clonic seizures (see grand mal seizure)
 Further generalized seizures
 Absence (see also generalized epilepsies in childhood)
 Myoclonic (see juvenile myoclonic epilepsy)
  Clonic seizures
 Tonic seizures
 Atonic seizures
Clinical features
 Ictal phase
 Sudden onset
 Rapid progression of symptoms
 Duration usually 1–3 minutes 
 Postictal phase
 Varying degree of confusion, impaired alertness
 Residual neurologic symptoms (e.g., Todd's paralysis)
 Duration usually minutes or hours
 Symptoms of, e.g., CNS infection, stroke, intoxication, hypoglycemia, electrolyte
disturbances → indicative of acute symptomatic seizure
Focal seizures
Focal seizures are more likely to be caused by focal structural abnormalities. Symptoms
depend on the anatomical location of the lesion or disturbance within the brain.
Focal seizures  Origin Ictal phase Post-ictal phase
Focal Focal  Prodromal sympt  Residual
seizure with intact cons cerebral oms: auras  neurologic deficits
ciousness regions Intact consciou depending on the
(simple partial seizures) (confined to sness affected cerebral
one Motor symptoms region 
hemisphere)  Clonic, in  Todd's
voluntary, paralysis: Postict
repetitive al weakness or
movements of paralysis of the
the contralateral li affected limb or
mbs or facial facial
muscles.  muscles (for
 Jacksonia minutes or up to
n march (“march of hours)
convulsions”): prog
ressive
involvement of
muscle groups 
Sensory and
psychiatric symptoms
 Visual (e.
g., hallucinations,
micropsia,
macropsia)
 Somatic (
e.g., paresthesias)
 Position (
e.g., vertigo)
 Hearing (
e.g., hearing
Focal seizures  Origin Ictal phase Post-ictal phase
complex sounds)
 Olfactory 
(e.g., unusual or
intense smells)
Autonomic
symptoms
(e.g. flushing, sweating)
Focal seizure Often  Auras: sensory  Confusion 
with impaired the tempora and psychic  Anterograde a
consciousness (comple l lobe (70– symptoms (e.g., de mnesia 
x partial seizures) 80%) ja vu,  Aphasia
Subse disorientation,  Fatigue,
quent fear, vertigo, and possibly short
bilateral visual, acoustic, phase of coma
spread olfactory,  Muscular
or gustatory hallucin flaccidity and
ations) muscle pain 
 Sudden  Headache
behavioral
arrest (e.g., staring
without moving)
 Impaired consci
ousness
 Automatisms (e.
g., fumbling, lip
smacking,
chewing,
swallowing)
Focal seizures may evolve to generalized convulsive seizure (formerly secondarily
generalized tonic-clonic)

Primarily generalized seizures

Symptoms are produced by bilateral cerebral cortex disturbances.
Ictal phase Post-ictal phase
Generalize Tonic-clonic  Prodromal symptoms may  Unresponsive
d seizure  occur hours ness 
motor seiz before seizure onset (e.g., sleep  Confusion
ure disturbances, lightheadedness,  Amnesia 
mood changes,  Aphasia
anxiety/irritability, impaired  Fatigue
concentration)  Muscular
 Loss of flaccidity and
consciousness (sudden, often muscle pain 
without any warning)   Headache
Motor symptoms:   Hypersalivati
 Ictal phase Post-ictal phase
1. Tonic phase: on with or
 Generalized without airway ob
muscle contractions: rotated struction
eyes, apnea, lateral tongue
biting, pooled oral
secretions, cyanosis and utteri
ng of an “ictal cry” 
 Increased sym
pathetic tone: dilated,
unresponsive pupils, ↑
HR and ↑ blood pressure
1. Clonic
phase (rhythmic muscle
twitching)
 Bladder or bowel
incontinence
 Tongue bite lacerations

Clonic seizure  Loss of consciousness None

 Rhythmic jerking motor
movements (of the entire
body or only a part)

Tonic seizure  Loss of None

consciousness (often occur
when the patient is drowsy,
asleep, or after waking)
 Muscle
contractions (extension
or flexion of the head, trunk,
and/or extremities)

Myoclonic  Brief loss of None

seizure (associ consciousness
ated with  Myoclonic: sudden jerky
epilepsy muscle twitching (of the
syndromes) entire body or only a part)

Atonic  Brief loss of None

seizure (also consciousness
known as drop  Sudden loss of muscle
attacks; tone: sudden head drop or
associated with collapse (lasts ∼ 2 seconds)
epilepsy
syndromes)

Non-motor  Brief loss of  None

(absence) seizure (common consciousness  Consciousne
 Ictal phase Post-ictal phase
type of generalized epilepsy  Interrupted motion or ss returns
in childhood.)  activity, blank rapidly, without
stare, unresponsiveness  any impairment
 Can occur several hundred  Patient often
times a day and usually unaware of
ceases after 5–20 seconds interruption
 Very
subtle automatisms (often go
unnoticed!): lip
smacking, eye fluttering, or
head nodding are common
Focal seizures may eventually involve both cerebral hemispheres, thereby evolving into a
generalized seizure (typically focal frontal lobe seizures!). Distinguishing between pure
focal, focal → generalized, and purely generalized seizures is crucial!
Diagnostics
Confirm a seizure
 Patient history (from patient or witnesses): e.g., evidence of an aura, observation of
typical symptoms (e.g., twitching), identification of provocative factors (e.g., sleep
deprivation or unreliable intake of antiseizure medication )
 EEG 
 During the seizure (ictal)
 Epileptiform discharges (e.g., spikes, sharp waves, spike waves,
and hypsarrhythmia) are usually detected.  
 If no epileptiform discharges are detected, diagnosis
of pseudoseizures should be considered.
 Between seizures (interictal)
 Often normal findings (even after provocation via sleep
deprivation, hyperventilation, or visual stimuli)
 Possibly showing epileptiform activity (bursts of abnormal discharges
featuring spikes and/or sharp waves)
Exclude an underlying condition
 ECG: In every patient with loss of consciousness during an ictal event, cardiogenic
causes (e.g., cardiac arrhythmias resulting in cerebral hypoxia) should be ruled out.
 CT/MRI (with and without contrast): structural lesions (e.g., brain tumors) should be
ruled out after a first seizure. 
 Laboratory tests
 Blood
 Glucose
 Electrolytes
 Prolactin 
 Antiepileptic drug levels 
 Toxicology screen
 CBC
 ESR
 Rapid plasma reagin 
 Creatine kinase 
 Renal and liver function tests
  Lumbar puncture: cerebrospinal fluid analysis (e.g., if CNS infection is suspected)
The first focal seizure or the first focal seizure evolving into a generalized seizure in adults
indicates a seizure of structural or metabolic origin and requires further evaluation!
Differential diagnoses
 Psychological disorders:
 Pseudoseizures: not true seizures; paroxysmal events that may clinically
resemble epileptic seizures but have a psychiatric origin 
 Panic attacks
 Psychogenic hyperventilation
 Syncope: 
 Vasovagal syncope 
 Stokes-Adams attack 
 Carotid sinus syndrome 
 Cardiac failure
 Orthostatic hypotension
 Stroke (including transient ischemic attack ) 
 Migraine 
 Sleep disorders
 REM sleep behavior disorder
 Narcolepsy
 Breath-holding spell (benign condition)
 Occurs in children (6 months–6 years )
 Strong association with iron deficiency anemia
 Clinical features
 Episodes of prolonged expiratory apnea
 Followed by loss of consciousness (syncope)
 Transient paroxysms of cyanosis or pallor
 Possibly generalized stiffness and jerky movements of the limbs
(anoxic seizure) 
 Triggers: distress, strong emotions (e.g., anger, frustration) due to tantrums or
injury
 Diagnosis: based on typical presentation of BHS (no confirmatory test exists)
 Further work-up is generally not necessary. Only if atypical
presentation of BHS:
 EEG to differentiate from epileptic seizures
 ECG to rule out cardiac causes of syncope
 Laboratory analysis: CBC, serum ferritin (rule out iron deficiency
anemia)
 Treatment: reassurance
Postictal disorientation is key to differentiating
between seizures and syncope. Syncope may be accompanied by twitches; however,
patients become completely reoriented after a few seconds!
Treatment
Acute management
 Cardiopulmonary resuscitation (ABCs) 
 Avoid hazards 
 Monitor vital signs (especially oxygenation via pulse oximetry)
First seizure
 Long-term medical therapy is usually not required, unless there are abnormalities
seen on EEG or MRI (or the patient is in status epilepticus). 
 Remove cause or provoking factors (e.g., stop illicit drug abuse, treat underlying
disorders).
Recurrent seizures
Medical therapy
 Principles of treatment
 In epilepsy, the seizure threshold is pathologically lowered → Antiepileptic
drugs work by raising this lowered threshold and thus protecting against
future seizures.
 Criteria for the choice of antiepileptic drugs
 Type of epilepsy (as per clinical evaluation or instrumental findings)
 Patient age
 Comorbidities and contraindications
 Indications
 Recurrent seizures (2 seizures/6 months) of unknown cause or with a cause
that can not be eliminated
 After the first seizure → only if neuroimaging or EEG show specific
findings (e.g., hippocampal sclerosis, characteristic spike-wave patterns)
 Treatment options
Focal seizures   First-line treatment: lamotrigine, levetiracetam, phenytoin , car
bamazepine, oxcarbazepine, phenobarbital (children)
 Second-line treatment: gabapentin, valproate, pregabalin, topira
mate
Primary generali  Tonic-clonic:
zed seizures  First-line treatment: lamotrigine, valproate , phenobarbit
al (children)
 Second-line treatment: carbamazepine, zonisamide 
 Typical absence:
 First-line treatment: ethosuximide , valproate
 Second-line treatment: lamotrigine, clonazepam
 Atypical absence, myoclonic, atonic:
 First-line treatment: valproate, lamotrigine, topiramate
 Second-line treatment: clonazepam, felbamate
 Combination therapy
 If possible, monotherapy should be maintained → increase dosage before
initiating combination therapy 
 If combination therapy is administered, drugs from different classes and/or
with different pharmacologic modes of action should be tried. 
 Termination of treatment
 To be evaluated on a case-by-case basis
 May be considered if the patient has < 2 seizures/year, an inconspicuous
provocation EEG, normal psychological findings, and no hereditary
predisposition
 Generally possible after 2–5 seizure-free years with normal EEG results
 Medications must be tapered cautiously.
Nonpharmacological therapy
  Indications: pharmacoresistance 
 Surgery
 Prerequisite: epilepsy that does not respond to medications → often
epilepsies with structural origin (most commonly temporal lobe epilepsy)
 Procedures
 Resection (surgical removal of pathological lesions)
 Resection of the anteromedial temporal lobe or of
the amygdala and the hippocampus → in patients with temporal lobe
epilepsy
 Resection of an entire hemisphere (hemispherectomy) → in
patients with severe intractable seizures due to structural cerebral
abnormalities confined to one hemisphere
 Disconnection (surgical breaking of neuronal circuits)
 Stimulation techniques: vagus nerve stimulation, deep brain stimulation
 Dietary measures: ketogenic diet 
It is necessary to distinguish between focal and primary generalized seizures in order to
decide on the appropriate therapy!
Complications
Status epilepticus
Criteria
 ≥ 5 min of continuous seizures
 OR ≥ 2 seizures with consciousness not being fully regained in the interictal period
Etiology
 Common causes are withdrawal from antiepileptic drugs, metabolic
disturbances (e.g., hyponatremia), drug toxicity (e.g., tricyclic antidepressants),
structural brain lesions/injury (e.g., tumors, trauma, stroke), and CNS infections.
Treatment

1. Initial assessment and supportive treatment: 

 Place patient in recovery position to prevent injury.
 Quick neurological examination (to determine type and cause of status
epilepticus) and general medical evaluation (particularly airway, breathing, and
circulation)
 Establish secure IV access (two, if possible), collection of blood for routine
blood tests (particularly electrolytes and glucose levels), toxicology
screen, antiepileptic drug levels, and arterial blood gas (ABG) analysis 
 Supportive therapy as necessary (e.g., oxygen, glucose, thiamine  naloxone )
 Monitoring of vital signs: especially oxygen saturation (via pulse oximetry),
blood pressure, cardiac action, and breathing
 If patient does not regain consciousness after seizures stop or
nonconvulsive status epilepticus is suspected → continuous EEG monitoring
 If acute brain injury (e.g., intracerebral hemorrhage) is suspected → obtain
a cranial CT
 If CNS infection is suspected → conduct a lumbar puncture 
2. Pharmacological interruption of seizures: initial treatment 
 First line: IV lorazepam; second line: IV diazepam or midazolam → if IV
access is not possible or drugs are administered by someone who is not a medical
professional → select another application form (e.g., rectal diazepam, buccal or
intranasal lorazepam/midazolam)
 If the patient does not respond within 1 minute →
administer additional lorazepam (or a second-line benzodiazepine)
 If the patient does not respond within another 10–20
minutes → saturation with fosphenytoin via separate
access (alternatively: phenobarbital, levetiracetam, or valproate)
 If seizure activity does not stop despite application of
a benzodiazepine and a nonbenzodiazepine antiseizure drug → refractory status
epilepticus
 No later than 45–60 min after onset: continuous administration of anesthetics
with intubation and ICU monitoring; e.g., thiopental, propofol, or midazolam
3. Nonbenzodiazepine therapy (to prevent recurrence): fosphenytoin or valproate
Prognosis
 Mortality of ∼ 20% (in adults with first occurrence of GCSE)
Status epilepticus is a life-threatening event! If not interrupted, it can lead to cerebral
edema, a dangerous rise in body temperature, rhabdomyolysis, and cerebral cardiovascular
failure!
General complications of seizures and epilepsy
 Acute
 Hyperthermia, cardiorespiratory deficits, excitatory toxicity → potentially
irreversible tissue damage (particularly to the CNS, for example in the form
of cortical laminar necrosis), which in turn may also result in further seizures
 Postictal transient anion gap metabolic acidosis with increased lactic acid and
reduced serum bicarbonate → usually resolves spontaneously within 60–90
minutes after seizure activity stops
 Physical trauma (e.g., posterior dislocation of the glenohumeral joint)
 Long-term
 Associated psychiatric disorders (e.g., anxiety, depression and risk of suicide,
cognitive impairments)
 Psychosocial issues (e.g., problems at the workplace)
Prognosis
Risk of seizure recurrence
 Overall risk of recurrence
 After the first unprovoked seizure (within 2 years): ∼ 40%
 After the second unprovoked seizure (within 1 year): ∼ 60%
 After a single tonic-clonic seizure: ∼ 40%
 In genetic epilepsy: ∼ 25–30% (within 3 months)
 Patients with normal EEG results: ∼ 15% (within 1 year)
 Patients with abnormal EEG results: ∼ 40% (within 1 year)
Impact of medical therapy
 Immediate initiation of pharmacotherapy after a first unprovoked seizure lowers risk
of recurrence in the short term (within 2 years) but does not significantly
improve long-term risk.
 Approx. 80% of epilepsy patients who are treated with antiepileptic
drugs remain seizure-free for extended periods (3–5 years).

8. Difference between taenia saginata and taenia solium

Taeniasis is the parasitic infection of humans caused by adult tapeworm species;

i.e. Taenia saginata (beef tapeworm), Taenia solium  (pork tapeworm) or Taenia asiatica
(Asian tapeworm). T. solium and T. saginata have a worldwide distribution but incidence is
higher in developing countries where as  Taenia asiatica is limited to Asia.

The major differences between T. solium and T. saginata is summarized in this table: 

Properties Taenia solium Taenia saginata
 Common
Name    
 Definitive
host  Human  Human
 Intermediate
Host  Pig  Cow/Cattle
 Disease   Taeniasis and Cysticercosis  Taeniasis only
 Infection is common among  Human beings are infected
those eating raw or insufficiently through the eating of
cooked measly pork containing the undercooked beef containing
 Transmission cysticerci. the cysticerci (“measly” beef)
 Size of adult worm: 5 m or less
 Size  Size of adult worm: 2-7 m (sometime up to 25 m)

 The scolex head is globular in
outline and has four circular
suckers.
 The head is provided with the  
rostellum armed with double
row of alternating large and
small hooklets. The rostellar
hooklets are shaped like
daggers or Arbian poniards
 Scolex (armed scolex)
 The scolex (“head”) is
quadrate in outline and
has four circular suckers.
 Rostellum and hooklets
are absent (i.e. unarmed
scolex)
  
 The number of proglottids
varies from 1000- 2000.
   The gravid uterus
 The total number of proglottids consists of a central
(segments) is an average of longitudinal stem with 15-
1000. 30 lateral branches on
 The gravid uterus consists of a each side; these in turn
median longitudinal stem sub-branch leaving
with 5- 13 compound lateral practically no space in
branches on each side between.
 The gravid segments are  The gravid segments are
expelled passively , in chains of expelled singly
5-6 at a time, and not singly.  T. saginata may produce
 T. solium may produce 50,000 up to 100,000 eggs per
 Proglottids  eggs per proglottid. proglottid.
 Eggs  Eggs
of Taenia solium and Taenia sa
ginata are morphologically
indistinguishable.

 
 The eggs are about 30-35
micrometers in diameter  and
are bile stained.
 The internal oncosphere
contains six refractile hooks.
 The eggs are not floated in
the saturated solution of NaCl.
 Eggs
 of Taenia solium and Taenia sa
ginata are  morphologically
indistinguishable.
 Infectious to humans (Human who  Eggs of Taenia saginata are not
 Eggs ingested  food contaminated with egg infectious. Human who ingest T.
(Infectious of Taenia solium may develop saginata eggs do not develop
nature) cysticercosis) cysticercosis.

Length of adult worms is usually 5 m or less for T. saginata (however it may reach up to 25

m) and 2 to 7 m for T. solium. The adults produce proglottids which mature, become gravid,
detach from the tapeworm, and migrate to the anus or are passed in the stool
(approximately 6 per day). T. saginata adults usually have 1,000 to 2,000 proglottids,
while T. solium adults have an average of 1,000 proglottids. The eggs contained in the
gravid proglottids are released after the proglottids are passed with the feces. T.
saginata may produce up to 100,000 and T. solium may produce 50,000 eggs per proglottid
respectively.