Brain Tissue Swelling and Seizure Activity in Inactive Cysticercosis
Status: | Completed |
---|---|
Conditions: | Neurology |
Therapuetic Areas: | Neurology |
Healthy: | No |
Age Range: | 18 - Any |
Updated: | 4/21/2016 |
Start Date: | August 1999 |
End Date: | April 2012 |
Analysis of the Occurrence of Perilesional Edema and Seizures in Patients With Inactive Cysticercosis
This study will examine what causes seizures in patients with cysticercosis (pork tapeworm
infection). A better understanding of this could lead to improved methods of controlling or
preventing seizures.
In humans, the pork tapeworm (Taenia solium) lives in the small intestine. The parasite's
microscopic eggs travel around the body-including to the brain-where they develop into
cysts. Usually, the cysts don't cause symptoms until they die. Then, they provoke an
inflammatory reaction that irritates the brain, causing seizures and other symptoms. The
inflammation eventually goes away, but the dead cysts remain. Calcium deposits often form
where the cysts are. Some of the calcified cysts develop swelling around them that seem to
be associated with the development of seizures.
This study will explore how and why these dead, calcified cysts continue to cause seizures.
In so doing, it will try to determine: 1) the best diagnostic imaging method for detecting
swelling around the cysts; 2) how often swelling occurs; and 3) what makes some cysts prone
to swelling and related seizure activity, while others are not.
Patients with cysticercosis who have had seizures or who have known or possible swelling
around calcified cysts will be studied with various tests, including magnetic resonance
imaging (MRI), computed tomography (CT) scans, electroencephalography (EEG), blood tests,
and possibly lumbar puncture. Patients will be studied for two cycles of seizures (during
active and quiet periods) or a maximum 4 years.
infection). A better understanding of this could lead to improved methods of controlling or
preventing seizures.
In humans, the pork tapeworm (Taenia solium) lives in the small intestine. The parasite's
microscopic eggs travel around the body-including to the brain-where they develop into
cysts. Usually, the cysts don't cause symptoms until they die. Then, they provoke an
inflammatory reaction that irritates the brain, causing seizures and other symptoms. The
inflammation eventually goes away, but the dead cysts remain. Calcium deposits often form
where the cysts are. Some of the calcified cysts develop swelling around them that seem to
be associated with the development of seizures.
This study will explore how and why these dead, calcified cysts continue to cause seizures.
In so doing, it will try to determine: 1) the best diagnostic imaging method for detecting
swelling around the cysts; 2) how often swelling occurs; and 3) what makes some cysts prone
to swelling and related seizure activity, while others are not.
Patients with cysticercosis who have had seizures or who have known or possible swelling
around calcified cysts will be studied with various tests, including magnetic resonance
imaging (MRI), computed tomography (CT) scans, electroencephalography (EEG), blood tests,
and possibly lumbar puncture. Patients will be studied for two cycles of seizures (during
active and quiet periods) or a maximum 4 years.
Seizures are the most common clinical manifestation of cerebral cysticercosis and occur in
the presence of viable, dying, and calcified or non-calcified dead cysts. How calcified
cysts provoke seizures is not known but recent observations demonstrated edema around some
calcified lesions at the time of seizure activity and disappearance during periods when
seizures were not occurring. Edema associated with foci in idiopathic epilepsy is highly
unusual so that this observation suggests that the mechanism(s) associated with calcified
cysts is unique. Documenting and understanding this phenomenon is important for a number of
reasons. First, although by definition these lesions are inactive, e.g., not living larvae
and do not require anti-parasitic treatment, they are frequently mistaken for active lesions
and patients undergo unnecessary treatment. Second, a likely reason for perilesional edema
is intermittent antigen release and subsequent host immune response resulting in
inflammation and edema. If proved, then the treatment for this would not only involve
suppression of seizure activity with anti-seizure medication but also the use of
anti-inflammatory medications such as corticosteroids. The present protocol will
systematically assess the presence of edema associated with calcified lesions at the time of
seizure activity and attempt to determine why some calcified lesions in the same patient are
foci of seizures while others are clinically silent. There are three related but separate
questions. 1) What is the most sensitive MRI technique that can detect edema around
calcified or inactive lesions? It is essential to determine the most sensitive methods
initially because the use of insensitive techniques will lead to inaccurate assessments of
which lesions are prone to lead to seizure activity and how many patients are affected. 2)
How common is perilesional edema around calcified or inactive lesions associated with
seizure activity? 3) What factors determine which lesions are prone to cause seizure
activity? 4) Can perilesional edema be effectively treated or prevented? 5) Can perilesional
edema be treated? We have reported from long term longitudinal studies in a handful of
patients that only some of many lesions seem to be associated with seizure activity and
edema.
the presence of viable, dying, and calcified or non-calcified dead cysts. How calcified
cysts provoke seizures is not known but recent observations demonstrated edema around some
calcified lesions at the time of seizure activity and disappearance during periods when
seizures were not occurring. Edema associated with foci in idiopathic epilepsy is highly
unusual so that this observation suggests that the mechanism(s) associated with calcified
cysts is unique. Documenting and understanding this phenomenon is important for a number of
reasons. First, although by definition these lesions are inactive, e.g., not living larvae
and do not require anti-parasitic treatment, they are frequently mistaken for active lesions
and patients undergo unnecessary treatment. Second, a likely reason for perilesional edema
is intermittent antigen release and subsequent host immune response resulting in
inflammation and edema. If proved, then the treatment for this would not only involve
suppression of seizure activity with anti-seizure medication but also the use of
anti-inflammatory medications such as corticosteroids. The present protocol will
systematically assess the presence of edema associated with calcified lesions at the time of
seizure activity and attempt to determine why some calcified lesions in the same patient are
foci of seizures while others are clinically silent. There are three related but separate
questions. 1) What is the most sensitive MRI technique that can detect edema around
calcified or inactive lesions? It is essential to determine the most sensitive methods
initially because the use of insensitive techniques will lead to inaccurate assessments of
which lesions are prone to lead to seizure activity and how many patients are affected. 2)
How common is perilesional edema around calcified or inactive lesions associated with
seizure activity? 3) What factors determine which lesions are prone to cause seizure
activity? 4) Can perilesional edema be effectively treated or prevented? 5) Can perilesional
edema be treated? We have reported from long term longitudinal studies in a handful of
patients that only some of many lesions seem to be associated with seizure activity and
edema.
- INCLUSION CRITERIA:
18 years of age or older. If children are evaluated they can be seen under the
general protocol and they may be entered into the present protocol under an
exception.
Likely diagnosis of inactive cysticercosis and present or past seizure activity. Requires
"a" and "b" plus any one of the remaining criteria:
1. History of seizures or present seizure activity;
2. Previously treated or has inactive disease and declines treatment;
3. Single calcified lesions and positive serology;
4. Multiple calcified lesions;
5. Multiple small enhancing nodular lesions;
6. History of cystic lesions responding to specific chemotherapy.
If female, not pregnant and using effective birth control methods.
EXCLUSION CRITERIA:
Less than 18 years of age.
Pregnant or unwilling to use effective birth control measures.
Refuse blood tests.
Unwilling or unable to undergo testing according to the schedule.
Unable to undergo MRI or CT examinations.
Patients who require anesthesia to undergo imaging studies.
We found this trial at
2
sites
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9000 Rockville Pike
Bethesda, Maryland 20892
Bethesda, Maryland 20892
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