Radiation Induced Health Hazards
Hiroshima Bombing: 6 August 1945
THE ATOMIC BOMBING OF HIROSHIMA
Hiroshima (August 6, 1945)
In the early morning hours of August 6, 1945, a B-29 bomber named Enola Gay took off from the island of Tinian and headed north by northwest toward Japan. The bomber's primary target was the city of Hiroshima, located on the deltas of southwestern Honshu Island facing the Inland Sea. Hiroshima had a civilian population of almost 300,000 and was an important military center, containing about 43,000 soldiers.
The bomber, piloted by the commander of the 509th Composite Group, Colonel Paul Tibbets, flew at low altitude on automatic pilot before climbing to 31,000 feet as it neared the target area. At approximately 8:15 a.m. Hiroshima time the Enola Gay released "Little Boy," its 9,700-pound uranium bomb, over the city. Tibbets immediately dove away to avoid the anticipated shock wave. Forty-three seconds later, a huge explosion lit the morning sky as Little Boy detonated 1,900 feet above the city, directly over a parade field where soldiers of the Japanese Second Army were doing calisthenics. Though already eleven and a half miles away, the Enola Gay was rocked by the blast. At first, Tibbets thought he was taking
flak. After a second shock wave (reflected from the ground) hit the plane, the crew looked back at Hiroshima. "The city was hidden by that awful cloud . . . boiling up, mushrooming, terrible and incredibly tall," Tibbets recalled. The yield of the explosion was later estimated at 15 kilotons (the equivalent of 15,000 tons of TNT).
On the ground moments before the blast it was a calm and sunny Monday morning. An air raid alert from earlier that morning had been called off after only a solitary aircraft was seen (the weather plane), and by 8:15 the city was alive with activity -- soldiers doing their morning calisthenics, commuters on foot or on bicycles, groups of women and children working outside to clear firebreaks. Those closest to the explosion died instantly, their bodies turned to black char. Nearby birds burst into flames in mid-air, and dry, combustible materials such as paper instantly ignited as far away as 6,400 feet from ground zero. The white light acted as a giant flashbulb, burning the dark patterns of clothing onto skin (right) and the shadows of bodies onto walls. Survivors outdoors close to the blast generally describe a literally blinding light combined with a sudden and overwhelming wave of heat. (The effects of radiation are usually not immediately apparent.) The blast wave followed almost instantly for those close-in, often knocking them from their feet. Those that were indoors were usually spared the flash burns, but flying glass from broken windows filled most rooms, and all but the very strongest structures collapsed. One boy was blown through the windows of his house and across the street as the house collapsed behind him. Within minutes 9 out of 10 people half a mile or less from ground zero were dead.
People farther from the point of detonation experienced first the flash and heat, followed seconds later by a deafening boom and the blast wave. Nearly every structure within one mile of ground zero was destroyed, and almost every building within three miles was damaged. Less than 10 percent of the buildings in the city survived without any damage, and the blast wave shattered glass in suburbs twelve miles away. The most common first reaction of those that were indoors even miles from ground zero was that their building had just suffered a direct hit by a bomb. Small ad hoc rescue parties soon began to operate, but roughly half of the city's population was dead or injured. In those areas most seriously affected virtually no one escaped serious injury. The numerous small fires that erupted simultaneously all around the city soon merged into one large firestorm, creating extremely strong winds that blew towards the center of the fire. The firestorm eventually engulfed 4.4 square miles of the city, killing anyone who had not escaped in the first minutes after the attack. One postwar study of the victims of Hiroshima found that less than 4.5 percent of survivors suffered leg fractures. Such injuries were not uncommon; it was just that most who could not walk were engulfed by the firestorm.
Even after the flames had subsided, relief from the outside was slow in coming. For hours after the attack the Japanese government did not even know for sure what had happened. Radio and telegraph communications with Hiroshima had suddenly ended at 8:16 a.m., and vague reports of some sort of large explosion had begun to filter in, but the Japanese high command knew that no large-scale air raid had taken place over the city and that there were no large stores of explosives there. Eventually a Japanese staff officer was dispatched by plane to survey the city from overhead, and while he was still nearly 100 miles away from the city he began to report on a huge cloud of smoke that hung over it. The first confirmation of exactly what had happened came only sixteen hours later with the announcement of the bombing by the United States. Relief workers from outside the city eventually began to arrive and the situation stabilized somewhat. Power in undamaged areas of the city was even restored on August 7th, with limited rail service resuming the following day. Several days after the blast, however, medical staff began to recognize the first symptoms of radiation sickness among the survivors. Soon the death rate actually began to climb again as patients who had appeared to be recovering began suffering from this strange new illness. Deaths from radiation sickness did not peak until three to four weeks after the attacks and did not taper off until seven to eight weeks after the attack. Long-range health dangers associated with radiation exposure, such as an increased danger of cancer, would linger for the rest of the victims' lives, as would the psychological effects of the attack.
No one will ever know for certain how many died as a result of the attack on Hiroshima. Some 70,000 people probably died as a result of initial blast, heat, and radiation effects. This included about twenty American airmen being held as prisoners in the city. By the end of 1945, because of the lingering effects of radioactive fallout and other after effects, the Hiroshima death toll was probably over 100,000. The five-year death total may have reached or even exceeded 200,000, as cancer and other long-term effects took hold.
At 11:00 a.m., August 6 (Washington D.C. time), radio stations began playing a prepared statement from President Truman (right) informing the American public that the United States had dropped an entirely new type of bomb on the Japanese city of Hiroshima -- an "atomic bomb." Truman warned that if Japan still refused to surrender unconditionally, as demanded by the Potsdam Declaration of July 26, the United States would attack additional targets with equally devastating results. Two days later, on August 8, the Soviet Union declared war on Japan and attacked Japanese forces in Manchuria, ending American hopes that the war would end before Russian entry into the Pacific theater. By August 9th, American aircraft were showering leaflets all over Japan informing its people that "We are in possession of the most destructive explosive ever devised by man. A single one of our newly developed atomic bombs is actually the equivalent in explosive power to what 2,000 of our giant B-29s can carry on a single mission. This awful fact is one for you to ponder and we solemnly assure you it is grimly accurate. We have just begun to to use this weapon against your homeland. If you still have any doubt, make inquiry as to what happened to Hiroshima when just one atomic bomb fell on that city." Meanwhile, Tibbets's bomber group was simply waiting for the weather to clear in order to drop its next bomb, the plutonium weapon nicknamed "Fat Man" (right) that was destined for the city of Nagasaki.
Hiroshima (August 6, 1945)
In the early morning hours of August 6, 1945, a B-29 bomber named Enola Gay took off from the island of Tinian and headed north by northwest toward Japan. The bomber's primary target was the city of Hiroshima, located on the deltas of southwestern Honshu Island facing the Inland Sea. Hiroshima had a civilian population of almost 300,000 and was an important military center, containing about 43,000 soldiers.
The bomber, piloted by the commander of the 509th Composite Group, Colonel Paul Tibbets, flew at low altitude on automatic pilot before climbing to 31,000 feet as it neared the target area. At approximately 8:15 a.m. Hiroshima time the Enola Gay released "Little Boy," its 9,700-pound uranium bomb, over the city. Tibbets immediately dove away to avoid the anticipated shock wave. Forty-three seconds later, a huge explosion lit the morning sky as Little Boy detonated 1,900 feet above the city, directly over a parade field where soldiers of the Japanese Second Army were doing calisthenics. Though already eleven and a half miles away, the Enola Gay was rocked by the blast. At first, Tibbets thought he was taking
flak. After a second shock wave (reflected from the ground) hit the plane, the crew looked back at Hiroshima. "The city was hidden by that awful cloud . . . boiling up, mushrooming, terrible and incredibly tall," Tibbets recalled. The yield of the explosion was later estimated at 15 kilotons (the equivalent of 15,000 tons of TNT).On the ground moments before the blast it was a calm and sunny Monday morning. An air raid alert from earlier that morning had been called off after only a solitary aircraft was seen (the weather plane), and by 8:15 the city was alive with activity -- soldiers doing their morning calisthenics, commuters on foot or on bicycles, groups of women and children working outside to clear firebreaks. Those closest to the explosion died instantly, their bodies turned to black char. Nearby birds burst into flames in mid-air, and dry, combustible materials such as paper instantly ignited as far away as 6,400 feet from ground zero. The white light acted as a giant flashbulb, burning the dark patterns of clothing onto skin (right) and the shadows of bodies onto walls. Survivors outdoors close to the blast generally describe a literally blinding light combined with a sudden and overwhelming wave of heat. (The effects of radiation are usually not immediately apparent.) The blast wave followed almost instantly for those close-in, often knocking them from their feet. Those that were indoors were usually spared the flash burns, but flying glass from broken windows filled most rooms, and all but the very strongest structures collapsed. One boy was blown through the windows of his house and across the street as the house collapsed behind him. Within minutes 9 out of 10 people half a mile or less from ground zero were dead.
People farther from the point of detonation experienced first the flash and heat, followed seconds later by a deafening boom and the blast wave. Nearly every structure within one mile of ground zero was destroyed, and almost every building within three miles was damaged. Less than 10 percent of the buildings in the city survived without any damage, and the blast wave shattered glass in suburbs twelve miles away. The most common first reaction of those that were indoors even miles from ground zero was that their building had just suffered a direct hit by a bomb. Small ad hoc rescue parties soon began to operate, but roughly half of the city's population was dead or injured. In those areas most seriously affected virtually no one escaped serious injury. The numerous small fires that erupted simultaneously all around the city soon merged into one large firestorm, creating extremely strong winds that blew towards the center of the fire. The firestorm eventually engulfed 4.4 square miles of the city, killing anyone who had not escaped in the first minutes after the attack. One postwar study of the victims of Hiroshima found that less than 4.5 percent of survivors suffered leg fractures. Such injuries were not uncommon; it was just that most who could not walk were engulfed by the firestorm.
Even after the flames had subsided, relief from the outside was slow in coming. For hours after the attack the Japanese government did not even know for sure what had happened. Radio and telegraph communications with Hiroshima had suddenly ended at 8:16 a.m., and vague reports of some sort of large explosion had begun to filter in, but the Japanese high command knew that no large-scale air raid had taken place over the city and that there were no large stores of explosives there. Eventually a Japanese staff officer was dispatched by plane to survey the city from overhead, and while he was still nearly 100 miles away from the city he began to report on a huge cloud of smoke that hung over it. The first confirmation of exactly what had happened came only sixteen hours later with the announcement of the bombing by the United States. Relief workers from outside the city eventually began to arrive and the situation stabilized somewhat. Power in undamaged areas of the city was even restored on August 7th, with limited rail service resuming the following day. Several days after the blast, however, medical staff began to recognize the first symptoms of radiation sickness among the survivors. Soon the death rate actually began to climb again as patients who had appeared to be recovering began suffering from this strange new illness. Deaths from radiation sickness did not peak until three to four weeks after the attacks and did not taper off until seven to eight weeks after the attack. Long-range health dangers associated with radiation exposure, such as an increased danger of cancer, would linger for the rest of the victims' lives, as would the psychological effects of the attack.
No one will ever know for certain how many died as a result of the attack on Hiroshima. Some 70,000 people probably died as a result of initial blast, heat, and radiation effects. This included about twenty American airmen being held as prisoners in the city. By the end of 1945, because of the lingering effects of radioactive fallout and other after effects, the Hiroshima death toll was probably over 100,000. The five-year death total may have reached or even exceeded 200,000, as cancer and other long-term effects took hold.
At 11:00 a.m., August 6 (Washington D.C. time), radio stations began playing a prepared statement from President Truman (right) informing the American public that the United States had dropped an entirely new type of bomb on the Japanese city of Hiroshima -- an "atomic bomb." Truman warned that if Japan still refused to surrender unconditionally, as demanded by the Potsdam Declaration of July 26, the United States would attack additional targets with equally devastating results. Two days later, on August 8, the Soviet Union declared war on Japan and attacked Japanese forces in Manchuria, ending American hopes that the war would end before Russian entry into the Pacific theater. By August 9th, American aircraft were showering leaflets all over Japan informing its people that "We are in possession of the most destructive explosive ever devised by man. A single one of our newly developed atomic bombs is actually the equivalent in explosive power to what 2,000 of our giant B-29s can carry on a single mission. This awful fact is one for you to ponder and we solemnly assure you it is grimly accurate. We have just begun to to use this weapon against your homeland. If you still have any doubt, make inquiry as to what happened to Hiroshima when just one atomic bomb fell on that city." Meanwhile, Tibbets's bomber group was simply waiting for the weather to clear in order to drop its next bomb, the plutonium weapon nicknamed "Fat Man" (right) that was destined for the city of Nagasaki.
Neurocysticercosis: Tanea Solium
Tanea Solium: Devastaiting effect.
Medical Care
Treatment of neurocysticercosis depends upon the viability of the cyst and its complications. Management includes symptomatic treatment as well as treatment directed against the parasite.
•If the parasite is dead, the treatment is directed primarily against the symptoms (eg, anticonvulsants for management of seizures). Monotherapy is usually sufficient. Duration of the treatment remains undefined, and depends neither on the type of seizure at presentation nor on other risk factors for recurrence, such as age at onset and number of seizures before diagnosis. Calcification remains an epileptogenic focus. Treating patients with viable cysts with a course of anticysticercal drugs in order to achieve better control of seizures is common practice.
•If the parasite is viable or active and the patient has vasculitis, arachnoiditis, or encephalitis, a course of steroids or immunosuppressants is recommended before the use of anticysticercal drugs. Antiparasitic treatment8 with albendazole is also useful in cysticercosis of the racemose type. If only parenchymal, subarachnoid, or spinal cysts are present without the complications mentioned, anticysticercal treatment can be considered, with the concomitant use of steroids, even in patients with massive brain infection. Reports indicate that multiple trials with anticysticercal treatment may be required for giant subarachnoid cysts.
•A recent double-blind, placebo-controlled study has shown that in patients with seizures due to viable parenchymal cysts, antiparasitic therapy decreases the burden of parasites and is safe and effective, at least in reducing the number of seizures with generalization.
Surgical Care
•In the presence of hydrocephalus due to intraventricular cyst, placement of a ventricular shunt is recommended, followed by surgical extirpation of the cyst and subsequent medical treatment.
•In cases of multiple cysts in the subarachnoid space (ie, the racemose form), surgical extirpation, on an urgent basis, is recommended.
•If the obstruction is due to arachnoiditis, placement of a ventricular shunt should be followed by administration of steroids and subsequent medical therapy.
•Because of frequent shunt dysfunctions due to entry of inflammatory tissue as well as parasitic debris inside the ventricular cavities, Sotelo designed a device that functions at a constant flow without the valvular mechanism of Pudenz-type shunts.
•Neuroendoscopy is a new tool with great potential for use in the management of ventricular cysticercosis.
•Surgical treatment in the particular case of medically refractory epilepsy due to a single lesion has been reported. Evaluation in an epilepsy center is indicated.
Introduction
Neurocysticercosis (NCC) is the most common parasitic disease of the nervous system and is the main cause of acquired epilepsy in developing countries. Lately, it has also been a problem in industrialized countries because of immigration of tapeworm carriers from areas of endemic disease. Tanae Solium.
Clinical Features:
History
NCC is a pleomorphic disease, although it sometimes produces no clinical manifestation. This pleomorphism is due to variations in the locations of the lesions, the number of parasites, and the host's immune response.
•Many patients are asymptomatic; others report vague symptoms such as headache or dizziness.
•The onset of symptoms is usually subacute to chronic, with the exception of seizures, which present in an acute fashion. Patients may present with the following:
◦Epilepsy
■Epilepsy is the most common presentation (70%)
■Seizures secondary to NCC may be generalized or partial.
◦Headache
■Chronic headaches associated with nausea and vomiting (simulating migraines)
■Headaches associated with intracranial hypertension and indicative of hydrocephalus
■Headaches due to meningitis
◦Intracranial hypertension
■Most often, intracranial hypertension is due to obstruction of cerebrospinal fluid (CSF) circulation caused by basal or ventricular cysticercosis. It may also result from large cysts displacing midline structures, granular ependymitis, arachnoiditis, or the so-called cysticercotic encephalitis caused by the inflammatory response to a massive infestation of cerebral parenchyma with cysticerci.
■These patients may have seizures and deterioration of their mental status, mainly due to the host's inflammatory reaction as an exaggerated response to the massive infestation.
◦Strokes5
■Ischemic cerebrovascular complications of NCC include lacunar infarcts6 and large cerebral infarcts due to occlusion or vascular damage.
■Hemorrhage also can occur, and has been reported as a result of rupture of mycotic aneurysms of the basilar artery.
■Strokes may be responsible for the following signs and symptoms: paresis or plegias, involuntary movements, gait disturbances, or paresthesias.
◦Neuropsychiatric disturbances
■These range from poor performance on neuropsychological tests to severe dementia.
■These symptoms appear to be related more to the presence of intracranial hypertension than to the number or location of parasites in the brain.
◦Diplopia: This is a result of intracranial hypertension or arachnoiditis producing entrapment or compression of cranial nerves III, IV, or VI.
◦Hydrocephalus
■Ten to thirty percent of patients with NCC develop communicating hydrocephalus due to inflammation and fibrosis of the arachnoid villi or inflammatory reaction to the meninges and subsequent occlusion of the foramina of Luschka and Magendie.
■Noncommunicating hydrocephalus may be a consequence of intraventricular cysts.
•Other forms of neurocysticercosis
◦Ocular cysticercosis: This occurs most commonly in the subretinal space. Patients may present with decreased visual acuity, visual field defects, or monocular blindness.
◦Systemic cysticercosis: This is most common in the Asian continent. The parasites may be located in the subcutaneous tissue or muscle. Peripheral nerve involvement as well as involvement of liver or spleen have been reported.
Physical
Twenty percent or less of infected patients have abnormal neurological findings. Physical findings will depend on where the cyst is located in the nervous system and include the following:
•Cognitive decline
•Dysarthria
•Extraocular movement palsy or paresis
•Hemiparesis or hemiplegia, which may be related to stroke, or Todd paralysis
•Hemisensory loss
•Movement disorders
•Hyper/hyporeflexia
•Gait disturbances
•Meningeal signs
Causes
NCC can be acquired via fecal-oral contact with carriers of the adult tapeworm. This usually indicates the presence of a tapeworm carrier in the immediate environment (ie, household) or by accidental ingestion of contaminated food. Cases of autoingestion, in which persons with teniasis may ingest the eggs of T solium into their intestine, have been reported.
Laboratory Studies
•CSF analysis
◦Analysis of the CSF is indicated in every patient presenting with new-onset seizures or neurological deficit in whom neuroimaging shows a solitary lesion but does not offer a definitive diagnosis.
Eosinophilia in the CSF suggests neurocysticercosis (NCC); however, eosinophils also are elevated in neurosyphilis and tuberculosis of the CNS.
•Stool examination
◦Taeniasis and NCC coexist in 10-15% of patients with NCC. A recent study found that intestinal taeniasis is very common in patients with massive infestation with cysticerci but without cysticercotic encephalitis.
◦Tapeworm carriers may be identified by examining the stool of the relatives of a patient with cysticercosis encephalitis.
•Immunological tests
◦Enzyme-linked immunosorbent assay (ELISA) is the most widely used test of CSF; it has a sensitivity of 50% and a specificity of 65% for NCC.
Imaging Studies
•CT scan
•MRI
considering biopsy.
Neurocysticercosis (NCC) is the most common parasitic disease of the nervous system and is the main cause of acquired epilepsy in developing countries. Lately, it has also been a problem in industrialized countries because of immigration of tapeworm carriers from areas of endemic disease. Tanae Solium.
Clinical Features:
History
NCC is a pleomorphic disease, although it sometimes produces no clinical manifestation. This pleomorphism is due to variations in the locations of the lesions, the number of parasites, and the host's immune response.
•Many patients are asymptomatic; others report vague symptoms such as headache or dizziness.
•The onset of symptoms is usually subacute to chronic, with the exception of seizures, which present in an acute fashion. Patients may present with the following:
◦Epilepsy
■Epilepsy is the most common presentation (70%)
■Seizures secondary to NCC may be generalized or partial.
◦Headache
■Chronic headaches associated with nausea and vomiting (simulating migraines)
■Headaches associated with intracranial hypertension and indicative of hydrocephalus
■Headaches due to meningitis
◦Intracranial hypertension
■Most often, intracranial hypertension is due to obstruction of cerebrospinal fluid (CSF) circulation caused by basal or ventricular cysticercosis. It may also result from large cysts displacing midline structures, granular ependymitis, arachnoiditis, or the so-called cysticercotic encephalitis caused by the inflammatory response to a massive infestation of cerebral parenchyma with cysticerci.
■These patients may have seizures and deterioration of their mental status, mainly due to the host's inflammatory reaction as an exaggerated response to the massive infestation.
◦Strokes5
■Ischemic cerebrovascular complications of NCC include lacunar infarcts6 and large cerebral infarcts due to occlusion or vascular damage.
■Hemorrhage also can occur, and has been reported as a result of rupture of mycotic aneurysms of the basilar artery.
■Strokes may be responsible for the following signs and symptoms: paresis or plegias, involuntary movements, gait disturbances, or paresthesias.
◦Neuropsychiatric disturbances
■These range from poor performance on neuropsychological tests to severe dementia.
■These symptoms appear to be related more to the presence of intracranial hypertension than to the number or location of parasites in the brain.
◦Diplopia: This is a result of intracranial hypertension or arachnoiditis producing entrapment or compression of cranial nerves III, IV, or VI.
◦Hydrocephalus
■Ten to thirty percent of patients with NCC develop communicating hydrocephalus due to inflammation and fibrosis of the arachnoid villi or inflammatory reaction to the meninges and subsequent occlusion of the foramina of Luschka and Magendie.
■Noncommunicating hydrocephalus may be a consequence of intraventricular cysts.
•Other forms of neurocysticercosis
◦Ocular cysticercosis: This occurs most commonly in the subretinal space. Patients may present with decreased visual acuity, visual field defects, or monocular blindness.
◦Systemic cysticercosis: This is most common in the Asian continent. The parasites may be located in the subcutaneous tissue or muscle. Peripheral nerve involvement as well as involvement of liver or spleen have been reported.
Physical
Twenty percent or less of infected patients have abnormal neurological findings. Physical findings will depend on where the cyst is located in the nervous system and include the following:
•Cognitive decline
•Dysarthria
•Extraocular movement palsy or paresis
•Hemiparesis or hemiplegia, which may be related to stroke, or Todd paralysis
•Hemisensory loss
•Movement disorders
•Hyper/hyporeflexia
•Gait disturbances
•Meningeal signs
Causes
NCC can be acquired via fecal-oral contact with carriers of the adult tapeworm. This usually indicates the presence of a tapeworm carrier in the immediate environment (ie, household) or by accidental ingestion of contaminated food. Cases of autoingestion, in which persons with teniasis may ingest the eggs of T solium into their intestine, have been reported.
Laboratory Studies
•CSF analysis
◦Analysis of the CSF is indicated in every patient presenting with new-onset seizures or neurological deficit in whom neuroimaging shows a solitary lesion but does not offer a definitive diagnosis.
Eosinophilia in the CSF suggests neurocysticercosis (NCC); however, eosinophils also are elevated in neurosyphilis and tuberculosis of the CNS.
•Stool examination
◦Taeniasis and NCC coexist in 10-15% of patients with NCC. A recent study found that intestinal taeniasis is very common in patients with massive infestation with cysticerci but without cysticercotic encephalitis.
◦Tapeworm carriers may be identified by examining the stool of the relatives of a patient with cysticercosis encephalitis.
•Immunological tests
◦Enzyme-linked immunosorbent assay (ELISA) is the most widely used test of CSF; it has a sensitivity of 50% and a specificity of 65% for NCC.
Imaging Studies
•CT scan
•MRI
considering biopsy.
Medical Care
Treatment of neurocysticercosis depends upon the viability of the cyst and its complications. Management includes symptomatic treatment as well as treatment directed against the parasite.
•If the parasite is dead, the treatment is directed primarily against the symptoms (eg, anticonvulsants for management of seizures). Monotherapy is usually sufficient. Duration of the treatment remains undefined, and depends neither on the type of seizure at presentation nor on other risk factors for recurrence, such as age at onset and number of seizures before diagnosis. Calcification remains an epileptogenic focus. Treating patients with viable cysts with a course of anticysticercal drugs in order to achieve better control of seizures is common practice.
•If the parasite is viable or active and the patient has vasculitis, arachnoiditis, or encephalitis, a course of steroids or immunosuppressants is recommended before the use of anticysticercal drugs. Antiparasitic treatment8 with albendazole is also useful in cysticercosis of the racemose type. If only parenchymal, subarachnoid, or spinal cysts are present without the complications mentioned, anticysticercal treatment can be considered, with the concomitant use of steroids, even in patients with massive brain infection. Reports indicate that multiple trials with anticysticercal treatment may be required for giant subarachnoid cysts.
•A recent double-blind, placebo-controlled study has shown that in patients with seizures due to viable parenchymal cysts, antiparasitic therapy decreases the burden of parasites and is safe and effective, at least in reducing the number of seizures with generalization.
Surgical Care
•In the presence of hydrocephalus due to intraventricular cyst, placement of a ventricular shunt is recommended, followed by surgical extirpation of the cyst and subsequent medical treatment.
•In cases of multiple cysts in the subarachnoid space (ie, the racemose form), surgical extirpation, on an urgent basis, is recommended.
•If the obstruction is due to arachnoiditis, placement of a ventricular shunt should be followed by administration of steroids and subsequent medical therapy.
•Because of frequent shunt dysfunctions due to entry of inflammatory tissue as well as parasitic debris inside the ventricular cavities, Sotelo designed a device that functions at a constant flow without the valvular mechanism of Pudenz-type shunts.
•Neuroendoscopy is a new tool with great potential for use in the management of ventricular cysticercosis.
•Surgical treatment in the particular case of medically refractory epilepsy due to a single lesion has been reported. Evaluation in an epilepsy center is indicated.
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