The animal nature of the hydatid disease was not suspected until the 17th century (Redi 1684, Hartmannus 1685, Tyssen 1691). Pallas in 1766 was the first to mention the similarity of the hydatid cysts in humans and other animals, and Goerze in 1782 was the first to study the scolices of the larva of Echinococcus. Cullerier in 1806 described the first case of hydatid cyst of the bone, and Chaussier in 1807 reported a case of spinal hydatid disease. 1,2,3 The term Echinococcus was coined by Rudolphi in 1808. 4 The first patient treated surgically for hydatid disease of the nervous system was reported by Reydellet in 1819; the patient had a hydatid cyst of the lumbar spine. 5 Montansey in 1827 described the brain of an idiot-epileptic woman containing a large number of cerebellar and cerebral hydatid cysts. Surgeons from New Zealand, Australia, and South America led the way in clarifying the pathology and advising the correct treatment for cranial hydatid cyst. Maunsell in 1889 operated successfully on a case of probable subtentorial hydatid cyst in an 18-year-old boy in New Zealand. 6 Graham and Clubb in 1890 first reported the successful removal of an undoubted hydatid cyst of the brain. 1 Barnett in 1896 (from New Zealand. and Morquio in 1901 (from Uruguay. were others reporting their success in treatment of hydatid cyst of the brain. 7–12 The Australian surgeon Dew in 1928 published the first classic book on hydatid disease. 2
Nearly half of the human race harbors some kinds of worms, usually in the intestinal tract. Of these worms, the Cestodes (tapeworms. have a predilection for the nervous system. Hydatid cyst is caused by the larval stage of Echinococcus granulosus, a cestode. The other cestodes, such as Echinococcus multilocularis, Cysticercus cellulosae, and Coenurus cerebralis, occasionally affect the human nervous system. The adult worm is found in the duodenum of the dog, fox, and other carnivores. It measures 3 to 6 mm in length and has four segments: a scolex carrying four suckers and a double row of hooklets (about 36) (Fig. 1), the immature proglottid, and the terminal gravid segment or the ovary, which carries 500 to 800 eggs in various stages of development. This segment detaches when it is fully developed and the eggs contaminate the fields used by sheep and cattle. The eggs are resistant to certain degrees of heat and cold and desiccation. At temperatures of −16 to −18°C, viable eggs were still found after 35 days. About 10% to 30% of the eggs placed for 1 hour in 95% alcohol, 10% Lysol, or 20% formalin were still viable. When ingested, the ova hatch in the intestine of sheep, migrate through the intestinal wall, enter the hepatic circulation, and lodge in the liver and lung, where hydatid cysts develop. 4,13,14
Humans are infected, usually in childhood, by ingesting the ova from the muzzle and coat of a farm dog or by eating uncooked contaminated green vegetables. 15 Mature worms do not develop in the human intestine. In the human digestive tract, the ingested ova are detached from their membrane, freeing hexacanth embryos measuring 0.025 mm in diameter. These embryos pass through the intestinal wall into the portal system. On reaching the liver, the hepatic capillaries act as the first filter, holding 75% of the embryos. Twenty-five percent pass through the right side of the heart and reach the lungs, where another 15% are held by pulmonary capillaries, acting as the second filter. The remainder (10%. reach the left side of the heart and are disseminated throughout the body by the arterial system. A few of these ova lodge in the brain or vertebrae. Brain hydatids account for 2% of all hydatid lesions that are treated; the vertebrae account for 1% of these lesions. The hexacanth embryos of Taenia solium, which travel the same pathway, are not held in the liver or lung but lodge in the muscular and cerebral tissues. 16 On reaching the final host, the hydatid embryo produces a cyst. The rate of growth of the cyst varies in different structures—faster in soft tissues such as brain and liver and slower in hard tissues, notably in the bones. Experimentally, it has been demonstrated that it takes 5 to 16 months for the cyst to grow 1 cm in diameter. 17
The hydatid cyst has a wall composed of two layers: an inner layer of germinal epithelium (endocyst. and an outer layer of laminated hyaline membrane (ectocyst) (Fig. 2). The ectocyst is striated and nonnucleated, and the endocyst is granular, nucleated, and friable. In most parts of the body, the host reacts to the presence of this alien organism by enveloping it in a fibroblastic capsule (adventitial membrane), but in the brain this membrane hardly develops. 18–24 The fluid in the cyst is colorless and has a low specific gravity (1005–1015). The albumin content is 2 to 2.5 g/L, the glucose content is 0.30 to 0.50 g/L, and the chloride content is 6.49 g/L. Some lymphocytes, scolices, and hooks are also present in each milliliter of the fluid. 4,16,25
In the germinal layer, budding occurs toward the cavity, producing scolices, daughter cysts, and even granddaughter cysts in various stages of development. The daughter cysts and scolices become detached from the wall and form a sediment inside the cyst, the hydatid sand. The hydatid cyst of the brain does not have a fully developed adventitial membrane and is invisible to the naked eye. Histologically, it is composed of a thin layer of collagen fibers. When there has been some infection or injury to the cyst, a thick adventitial membrane may develop. 26–28
Hydatid cysts occasionally degenerate and die; this is a slow process. The stages of this process include turbidity of the cyst fluid, appearance of linear calcifications, milky and caseous degeneration of the cyst fluid, and final shrinkage of the cyst. The hydatid cyst of the brain may become infected by organisms from the paranasal sinuses or of blood-borne origin, such as Salmonella. 26,27,29 All the degenerated and infected hydatid cysts are sterile.
There is ample evidence that different strains of E. granulosus exist; for instance, in the United Kingdom, both a sheep/dog strain and a horse/dog strain are recognized that have low or no infectivity to humans. 7,13,30
The disease has been known in Europe and the Middle East for centuries. 31,32 According to Costa, Scandinavian whalers in the eighth century introduced the disease into South America through their dogs. 2,10,11 The settlement of Australia and New Zealand by British immigrants with their sheep and dogs produced a fertile environment for the spread of the disease. The countries most affected by E. granulosus, in the order of estimated prevalence, are Uruguay, Australia, New Zealand, Tunisia, Syria, Lebanon, Iran, Greece, Argentina, Spain, Bulgaria, Romania, South Africa, Wales, Siberia, Mongolia, northern China, southern Japan, and the Philippines.
In all these countries, the incidence of infection in domestic animals far exceeds the number of human cases. In the southern part of Australia, 40% to 50% of the dogs were infected but the incidence was only 2% in humans. 9 In Lebanon, 32.9% of 237 dogs examined were infected. In western and southwestern Iran and neighboring Iraq, more than 40% of sheep, goats, and camels are infected. 31,32
The incidence of hydatid disease is changing in different countries. For example, in Iceland the disease is eradicated, and in several autopsy series from that area since 1953, there has been no sign of hydatidosis. 30 Control programs should be encouraged in rural areas that contain populations predisposed to infection.
Children represent most cases of brain hydatidosis. They are usually infected by ingestion of ova from a dog's muzzle or uncooked contaminated green vegetables. In the digestive system, the ingested ova lose their membrane and the hexacanth embryos pass through the intestinal wall into the portal circulation. The hepatic capillary filter can hold at least 75% of these embryos and the pulmonary filter can pick up another 15%; about 8% of the remaining embryos are disseminated into the viscera, and only 2% can reach the brain by means of the carotid arterial system. 4 When an embryo of E. granulosus is lodged in the brain, a solitary cyst develops, called the primary cyst. When a primary cyst is ruptured, multiple secondary cysts develop. Metastatic cysts are secondary cysts that develop in different parts of the brain after rupture of a number of embryos into the circulation from the left ventricle. Multiple primary hydatid cysts occur when more than one cyst is present in the same cavity. These occur in about 5% of the reported series. Past history of mild head trauma, dissemination of multiple larvae into a single location, and exogenous budding are the possible causes for this phenomenon. 5,6,20,29,32–35 As a rule, hydatid cysts of the brain are solitary, and so far no immunologic or pathologic theory has been advanced to explain this phenomenon. Daughter cysts that appear inside the mother cyst or outside the major cyst may be due to some environmental stress placed on the cyst or a threat to its existence, such as trauma, infection, chemical substances such as bile, or possible development of immunologic defense mechanisms.
The brain cysts are nearly always spherical. The wall of the cyst is white, smooth, soft to the touch, and elastic so that it can be removed through an opening smaller than its diameter. The wall consists of two layers: an outer layer of laminated hyaline membrane called exocyst, and an inner layer of germinative epithelium called endocyst. The cyst wall is thin and transparent in most parts but may be thicker and whitish as a result of budding of the fertile areas of the germinative epithelium, which may shed into the cyst cavity and appear as hydatid sand (Fig. 3). The wall of the brain hydatid cyst is made by the parasite and not by the host tissue, and the flimsy substance between the cyst wall and the brain is a thin layer of reactive collagen fibers. The fluid in the cyst is colorless and contains several scolices and hooks. Calcification of the wall and changes in the contents of the cyst are the earliest signs of spontaneous degeneration and death of the hydatid cyst; this appears in about 1% of the cysts.
The location of primary hydatid cysts of the brain is supratentorial in about 94% of cases. The hemispheres are equally affected, and about 75% of the cysts are located in the postrolandic parts of the hemispheres. 14,17,18,32,33,36–38
Our experience during the past 35 years with 69 cases of brain hydatid cysts in Tehran is been the basis for this manuscript. Anecdotal cases from other centers have also been included in this series because of their unusual or interesting characteristics. All the patients described have undergone surgery and been followed up for a long period. There was a slight preponderance for male patients. Fifty-two patients (77%. were younger than 20 years, with the youngest 3 years old. The oldest patient was 50. About 80% of our patients lived in rural areas. Of these 69 cases, 5 were posterior fossa cysts: cerebellar hemispheres in 2 cases, cerebellopontine angle in 1 case, fourth ventricle in 1 case, and body of the pons in 1 case. Of the supratentorial cysts, two were located in the ventricles.
The average duration of symptoms was 30 weeks in children and 50 weeks in adults. Epilepsy was often present for much longer. The presenting symptoms and signs were headache in 80%, nausea and vomiting in 70%, fits in 25%, hemiparesis in 60%, papilledema in 80% to 90% of children and almost 100% of the adults admitted for surgical treatment, tremor in 10%, cerebellar signs only in the patients with posterior fossa cysts, and corporal hemiatrophy in almost 10% of the patients. Other rare clinical manifestations of brain hydatidosis in our series were mental and endocrine disturbances, neck rigidity and signs of meningitis, and sudden herniation. We found hydatid cysts in other organs in 25% of our adult patients.
Of the standard biologic studies that we performed (eosinophil assessment in the blood and the Casoni and Weinberg reactions), none were of great help. We did not perform any of the new serologic tests in these patients, but they are expected to be of remarkable diagnostic value in brain hydatidosis.
Plain skull radiographs were of great value, showing signs of increased intracranial pressure in 100% of the children and 50% of the adults. Abnormal calcification was seen in 2% of the patients in skull x-rays. Pneumoencephalography was performed in one of our patients referred from another center who had a brain stem cyst. Angiography, performed in five of our patients, showed enormous displacement of normal-appearing vessels stretched around a completely avascular mass. Isotope brain scanning was used in 10 patients in this series and was of limited value, showing the focus of diminished activity.
Computed tomography (CT. has been used in our patients since 1976 and is the diagnostic method of choice in these patients. The typical features of CT, found in 90% of these patients, were a spherical and occasionally ovoid lesion with clearly defined borders, containing a low-attenuation fluid similar to cerebrospinal fluid in density and without perifocal edema or contrast enhancement (Fig. 4). In 2% of the patients, we found rim enhancement; in another 2%, calcification was seen in the cyst wall. Magnetic resonance imaging (MRI. was performed in only one patient and showed a well-defined lesion, hypointense on T1-weighted images and hyperintense on T2-weighted images (Fig. 5A,B).
In these 69 cases, we had the opportunity to operate on 58 cases of brain hydatid cyst. Under deep general anesthesia and administration of a sufficient amount of osmotic diuretic agents, the exact size and location of the lesion was mapped on the surface of the scalp. The bone flap was always larger than the cross section of the cyst and was made with a hand drill and a Gigli saw, slowly and with great care. The dura was opened without using electrocoagulation or silver clips, and any adhesions between the dura and the underlying brain were separated with sharp dissection. If the cortex overlying the cyst had to be opened, it was done without using electrocautery. Any unnecessary heating of the area was prohibited because the heat might increase the intracystic pressure, leading to its rupture. The opening in the brain was made large enough for the safe delivery of the cyst. At this point, thin strips of cottonoid were inserted between the cyst wall and the surrounding brain, and the brain was gently separated from the cyst with spatula retractors and saline irrigation. At this stage, the head was lowered 45° from the original position until the cyst was extruded. After delivery of the cyst, the space was carefully examined to ensure that there were no daughter cysts; we found unexpected daughter cysts in 10% of our patients. The smooth and glistening surface of the cavity was observed after delivery of the cysts, and the whole cavity was filled with saline solution. Careful and watertight closure of the dura was performed at the end of the procedure.
Despite such due care and attention, we had two cyst ruptures in this series of brain hydatid cysts. One was due to faulty anesthesia and the other to a faulty osteoplastic flap.
A marked reduction in the volume of intracranial contents after evacuation of a large cyst allows the brain to fall away from the dura, leading in stretching of the cortical veins and possible tear of these thin-walled vessels. Achieving full hemostasis in all our patients prevented this troublesome complication, and we have not encountered a frank subdural hematoma.
Since the introduction of CT scanning, we encountered a large subdural effusion on the operated side in 50% of the patients (Fig. 6) and one bilateral subdural effusion; most of them resolved spontaneously and only one patient required drainage.
We had three cases of postoperative Escherichia coli infection; all of these patients died of purulent meningitis. The death rate in this series was 5.8%: three deaths were due to fulminant meningitis and the other to pontine hemorrhage after evacuation of a hydatid cyst of the pons. 39
Rapid recovery of neurologic deficits such as confusion, hemiparesis, and tremor occurred in all the patients, but recovery of preoperative visual deficits was not so remarkable. All the patients who took antiepileptic medication before surgery still needed it after surgery.
Although recurrence is the rule after rupture of cerebral hydatid cysts, 28 we found no recurrences in the two ruptured cysts in this series.
Hydatidosis is an important member of the group of diseases naturally transmitted between animals and humans (zoonoses. and is widespread throughout the world. The death rate of the disease may be as high as 16% (in New Zealand), 9,28 so it should be regarded as a potentially malignant condition. Because there is no definite medical treatment for the condition, prevention is the only course available to control and ultimately to eradicate this disease. It has been recommended that farmers should be forbidden by law to slaughter sheep on their farms, and slaughter should be allowed only in authorized facilities; all infected organs should be burnt or buried; all farms should be visited by experts; and dogs should be given a suitable vermifuge and washed regularly.
When an embryo of E. granulosus is lodged in the brain substance, a solitary cyst develops. What is the mechanism that allows only one hydatid embryo to grow in the brain, because it is unlikely that only one reaches the cerebral circulation? Why does the brain not react to the presence of a foreign body of animal origin? It appears that the hydatid cyst does not trigger the cerebral defense mechanism. There is evidence that a unique sort of defense actually exists that may account for the presence of solitary cysts. Several authors agree that the average growth rate of solitary hydatid cysts in the brain is about 1 cm in 12 months. 17 In about 1% of the cases, a hydatid cyst of the brain dies. Death of the hydatid cyst is a slow process and may take years to complete. The wall of the cyst becomes rigid and thick and calcified patches appear in the wall (Fig. 7). In the next phase the content of the cyst becomes milky; later it becomes caseous. This phenomenon is five times more common in adults than in children. Occasionally one encounters multiple cysts, 45 which are classified into two groups: multiple primary cysts (one or two small cysts adjacent to a large cyst) (Fig. 8) or multiple secondary cysts (which occur at the site of the original operation as a result of recurrence or after traumatic rupture of the cyst during head injury). The location of primary hydatid cyst of the brain is supratentorial in more than 90% of cases, and nearly all authorities agree on the preponderance of cysts in the posterior part of the cerebral hemispheres and rare occurrence in the posterior fossa. Other rare locations reported for hydatid cysts of the brain are intraventricular, 14 cerebellopontine angle, 17,41 meningeal, 5 intrasellar, 38 and skull bone.
There are two clinical findings that should make the clinician suspect hydatid disease of the brain. First, the patient is a child or young adult from a rural region of an endemic country with signs of increased intracranial pressure but minimal focal deficits suggestive of a supratentorial lesion. Other signs such as focal fits, tremor, hydrocephalus, pseudocerebellar signs, asymmetry of the skull, and corporal hemiatrophy should strengthen the suspicion. Second, the patient is an adult raised in an endemic region who has a long history of general or focal seizures and evidence of increased intracranial pressure of recent onset and minimal signs suggestive of a supratentorial lesion. A past history of abdominal or thoracic surgery for hydatid disease and recent signs of a central nervous system affliction are highly suggestive of brain hydatidosis. 8,18,21,23,25,28,32,33,42,43
Two types of biologic tests may be valid for the diagnosis of brain hydatidosis. The old biologic tests are not of great help. New tests include immunoelectrophoresis, immunofluorescence, the indirect hemagglutination test, and the latex agglutination test. The indirect hemagglutination test is extensively used and has proved 83% to 93% positive worldwide. For postoperative follow-up, immunoelectrophoresis is the best. 1,30,44
Although plain skull x-rays are of great value, showing signs of increased intracranial pressure, skull asymmetry, and abnormal calcification (2% of cases), important CT features of brain hydatidosis are characteristic: a spherical, occasionally ovoid lesion with clearly defined borders and no perifocal edema. The content of the cyst has a low attenuation coefficient, similar to cerebrospinal fluid, and there is no enhancement after contrast injection. Occasionally, parts of the cyst wall enhance after contrast injection; this may be due to thickening of the adventitial membrane from head trauma or localized hyperactivity of the germinal layer (Fig. 9). This enhancing adventitial membrane usually develops as a result of hemorrhage between the cyst and the surrounding brain after mild head injury. 17,20,24,31,32,40,44,45 Other imaging modalities such as isotope scanning and cerebral angiography are of limited value. In exceptional cases of brain hydatid cysts, MRI has been performed, showing the cyst as a well-defined spherical lesion, hypointense on T1-weighted and hyperintense on T2-weighted images. 41,46
In children, the differential diagnosis of brain hydatidosis includes congenital hydrocephalus, arachnoid cysts, brain abscesses, and cystic tumors. In adults, the condition must be differentiated from brain neoplasms. Absence of rim enhancement and perifocal edema is a good finding on CT and MRI scans for differentiation between hydatid cyst and brain abscesses and tumors. Physicians working in endemic zones and facing such problems should have an increased index of suspicion for a child with a large asymmetric head and signs of increased intracranial pressure and an adult with a long history of epilepsy and the recent appearance of mild neurologic deficit. Performing an appropriate study, preferably a contrast-enhanced CT scan, is mandatory before any lumbar, ventricular, or lesion puncture. 31,32
The fundamental treatment of brain hydatid cyst is surgical removal of the intact and unruptured cyst. This essentially benign lesion can become malignant if proper care is not taken during its removal. A large hydatid cyst contains 3 to 6 mL of hydatid sand, and 1 mL of this sand contains 400,000 scolices. It is not surprising that minimal seepage of the cystic fluid, which occurs during aspiration of the cyst with even the smallest of needles, causes recurrence of the lesion. The recurrent lesion consists of 100 or more small cysts at the site of the original cyst. Half of the patients with recurrent cysts die within 2 years. Every care must be taken to avoid rupture of the cyst, and it should never be aspirated.
Surgical treatment of brain hydatid cysts has evolved during the past 50 years. Mills and McCormick (1904. were the first neurosurgeons to remove an intact brain hydatid cyst. Dowling (1924. realized the importance of removal of the intact cyst and suggested his technique of saline irrigation between the cyst and the surrounding brain and proper positioning of the head to deliver the intact cyst. In surgical evacuation of the brain hydatid cyst, an expert anesthesiologist is essential to keep the brain relaxed and the surgical field free of bleeding, to prevent accidental rupture of the cyst. The exact size and location of the cyst should be mapped on the surface of the scalp, and the bone flap should be larger than the cross section of the cyst. Surgical drapes and the anesthesia tubes should be arranged so that later in the operation, the table can be lowered 45° from the original position. Drilling should be done by hand, slowly and without vibration. Special attention should be made regarding the insertion of the Gigli guide and saw to prevent any small dural tear. Electrocoagulation should be avoided on the exposed dura. Great care should be taken in the opening of the dura because in large cysts, the dome is often just underneath and covered by a thin layer of leptomeningeal adhesions. Unnecessary heating of the area by the use of extra light (even photographic and television lamps. should be avoided because the heat may increase the intracystic pressure and lead to rupture. To uncover such a dome, the arachnoidal adhesions can be separated from the cyst wall by careful dissection without coagulation. Once the dome of the cyst is exposed, the surgeon can decide whether the opening in the brain is large enough for safe delivery of the cyst. This opening should be at least two-thirds the cross section of the cyst. Cyst delivery can be assisted by gentle irrigation and application of slight pressure on the surrounding brain.
After delivery of the cyst, the space should be carefully examined and all the saline and cerebrospinal fluid in the cavity should be emptied with an aspirator held on one piece of cottonoid. A full search should be done to ensure that no daughter cysts are retained, and if present, they are not ruptured by the aspirator.
Even with due care and attention, a cyst may still rupture. The contents of the cyst should be aspirated rapidly and the cyst wall removed, and the area should then be irrigated with parasiticidal fluids (1% formalin, 10% hypertonic saline, or 0.5% silver nitrate solution).
To remove cysts in unusual locations (cysts in the subarachnoid space, intraventricular, intrasellar, or suprasellar and posterior fossa hydatid cysts), special attempts should be made for removing them without rupture. Fortunately, they are rare. 3,28,32
The postoperative course may be complicated by fever, probably resulting from subarachnoid bleeding after shrinkage of the brain, even with full hemostasis; subdural effusion, which usually resolves spontaneously; extradural hematoma; and infection. 47 With modern techniques and facilities, the death rate should be less than 5%. Recurrence of the brain hydatid cyst is nearly always due to spillage of the contents at the time of removal of the original cyst. Another rare cause of recurrence is that one of the two smaller cysts in the original cyst bed was overlooked in the first operation. Clinical signs of recurrence usually appear in 4 to 12 months; no case of first recurrence has been reported after 48 months. In the recurrent cases, it becomes almost impossible to remove all the cysts without rupturing one or more of them, and further recurrence is the rule. 37 All the available information suggests that at least 50% of the patients with ruptured cysts die within 3 years of the original operation. Surgical treatment does not hold much hope of cure in recurrent brain hydatidosis. We await progress in the medical treatment of this condition.
Medical treatment of hydatidosis has been growing during the past decade. The antihelmintic benzimidazole compounds mebendazole and albendazole are used widely in patients with hepatic or other system hydatidosis, and encouraging results have been reported. 48,49 The poor results of treatment with mebendazole in many patients were thought to be due to its poor absorption. Albendazole, with its better absorption properties (10 mg/kg/d in two divided doses, administered for an indefinite period of time, at least 1 month), has been reported to be effective in brain cysts. 48–52 Albendazole is teratogenic and may produce headache, nausea, vomiting, and neutropenia. All of these are reversible, but the patient's hepatic, renal, and bone marrow function should be monitored. Until some other chemical treatment with higher potency is available, it is wise to use albendazole or mebendazole in the hope that it may prevent or at least delay recurrence.
Hydatid cyst of the brain is a surgical challenge, and every attempt should be made to deliver the cyst unruptured. Physicians working in endemic areas must be familiar with specific clinical, paraclinical, and imaging characteristics of hydatid cyst of the brain to preclude inappropriate intervention.
1. Arana Iniguez R. Echinococcus. In: Vinken PJ, Bruyn GW, eds. Handbook of Neurology. North Holland Publishing Co., Amsterdam, 1978:175–208.
2. Dew HR. Hydatid Disease. Adelaide: Spiller; 1928.
3. Dowling E, Orlando R. Quist hidatico del lobulo frontal derecho. Rev Espec Assoc Med Argent 1929; 4:209–17.
4. Craig & Faust's Clinical Parasitology. 8th ed. Lea & Feibiger, Holland; 1970.
5. Ba'assiri A, Haddad FS. Primary extradural hydatid disease, CT appearance. AJNR Am J Neuroradiol 1984; 5:474–5.
6. Dew HR. Primary cerebral hydatid disease. Aust NZ J Surg 1955; 24:161–71.
7. Anderson M, Bickerstaff ER, Hamilton JG. Cerebral hydatid disease in Britain. J Neurol Neurosurg Psychiat 1975; 38:1104–8.
8. De Viliers, Hamman H, Joubert MJ. A review of hydatid disease of the brain. South Afr Med J 1975;31:1163–7.
9. Kune GA, Jones T, Sali A. Hydatid disease in Australia. Med J Aust 1983; 2:385–8.
10. MacPherson CN, Zeykle E, Romig T. An Echinococcus pilot control program for north-west Turkana, Kenya. Ann Trop Med Parasit 1984; 78:188–92.
11. Walters TMH. Hydatid control scheme in South Powys, Wales, U.K. Ann Trop Med Parasitol 1984; 78:183–7.
12. Webster GA, Cameron TWM. Epidemiology and diagnosis of echinococcus in Canada. Can Med Assoc J 1967; 96:600–7.
13. McManus DP, MacPherson CN. Strain characterization in the hydatid organism, Echinococcus granulosus; current status and new perspectives. Ann Trop Med Parasitol 1984; 78:193–8.
14. Rahimizadeh A, Haddadian K. Hydatid cyst of the fourth ventricle. Neurosurgery 1984; 14:787–8.
15. Pearl M, Kosilimbos DG, Lehrer HZ, et al. Cerebral echinococcosis, a pediatric disease. Report of two cases with one successful five-year survival. Pediatrics 1987; 61:915–20.
16. Pool JB, Marcial-Rojas RA. Echinococcosis. In:Pathology of Protozoal and Helminthic Diseases. Williams & Wilkins. 1971:635–7.
17. Vaquero J, Jimenez C, Martinez R. Growth of hydatid cysts evaluated by CT scanning after presumed cerebral hydatid embolism. Case report. J Neurosurg 1982; 75:837–8.
18. Arana Iniguez R, San Julian J. Hydatid cyst of the brain. J Neurosurg 1978; 12:323–35.
19. Arana Iniguez R, Rodriques Barrios R., San Julian J. Surgical treatment of hydatid cyst of the brain. Trans Am Neurol Assoc 1952;210–1.
20. Begg NC, Begg AC, Robinson RG. Primary hydatid disease of the brain. Its diagnosis, radiological investigation, treatment and prevention. NZ Med J 1957; 56:94–8.
21. Bonakdarpour A. Echinococcus disease. Report of 112 cases from Iran and a review of 611 cases from the United States. AJR Am J Radiol 1967; 99:660–7.
22. Carrea R, Dowling E, Guevara JA. Surgical treatment of hydatid cyst of the central nervous system in pediatric age (Dowling's technique). Child Brain 1975; 1:4–21.
23. Goinard P. Descuns P. Les kust hydatique du nervaxe. Rev Neurol 1952; 86:369–415.
24. Hamza R, Tonibi S, Jamoussi M, et al. Intracranial and orbital hydatid cysts. Neuroradiology 1982; 22:211–4.
25. Robinson RG. Hydatid disease affecting the nervous system. Ann R Coll Surg Eng 1960; 26:146–56.
26. Alvarez F, Blazquez MG, Oliver B, Marquis M. Calcified cerebral hydatid cyst. Surg Neurol 1982; 17:163–4.
27. Obrador S, Uriquiza P. Two cases of cerebral abscess of unusual nature. Tuberculous abscess and suppurative hydatid cyst. J Neurosurg 1948; 5:572–6.
28. Robinson RG. Complication neurologique de la maladie hydatique. World Neurol 1961; 2:426–34.
29. Abdulla K, Tapoo AK, Agha HS. Ruptured cerebral hydatid cyst. Case report. J Tropical Med Hyg 1988; 91:302–5.
30. Barbour AG, Everett JR, Anderson FL. Hydatid disease screening, Sanpete County, Utah, 1971–1976. Am J Trop Med Hyg 1978; 27:94–100.
31. Abbassioun K, Rahmat H, Ameli NO, Tafazoli M. Computerized tomography in hydatid cyst of the brain. J Neurosurgery 1978; 94:408–11.
32. Abbassioun K, Sabouri-Deylami M, Rahmat H. Diagnostic preoperatoire des kystes hydatiques intra cerebraux par la tomodensitometrie et son importance pronostique. Neurochirurgie 1982; 28:21–4.
33. Arseni C, Samitca DC. Cranial and cerebral hydatid disease. Acta Psychiat Neurol 1957; 32:389–98.
34. Banzo J, Diaz F, Pina JI, et al. Multiple hydatid cysts. Eur J Nucl Med 1984; 9:84–98.
35. Sharma A, Abraham J. Multiple giant hydatid cysts of brain. Case report. J Neurosurg 1982; 57:413–5.
36. Fabiassi A, Trebini F, Torta R. Brain hydatidosis. Report of two cases. J Neurol Neurosurg Psychiat 1980; 43:91–4.
37. Haddad FS. Hydatid disease of the brain. Some considerations of its recurrence. Arch Int Hydatid 1957; 16:445–7.
38. Ozgen T, Bertan V, Kanzu T, Akalin S. Intrasellar hydatid cyst. J Neurosurg 1984; 60:647–8.
39. Abbassioum K, Amirjamshidi A, Moinipoor MT. Hydatid cyst of the pons. Surg Neurol 1986; 26:297–300.
40. Rudwan MA, Khaffaji S. CT of cerebral hydatid disease. Neuroradiology 1988; 30:496–9.
41. Mascalchi M. Pontine hydatid cyst in association with an acoustic neurinoma. MR appearance in an unusual case. AJNR Am J Neuroradiol 1991; 12:78–9.
42. Ayres CM, Davy LM, German WJ. Cerebral hydatidosis. J Neurosurg 1963; 20:371–7.
43. Tiberin P, Heilborn YD, Hirsch M, Barmeir E. Giant cerebral echinococcus cyst with galactorrhea and amenorrhea. Surg Neurol 1984; 21:505–6.
44. King TT, Couch RSC. The diagnosis of cerebral hydatid disease. Clin Radiol 1961; 12:190–3.
45. McCorkell ST, Lerwall DB. Computed tomography of intracerebral Echinococcus cyst in children. J Comp Assist Tomog 1985; 9:514–8.
46. Coates R. MR imaging of intracerebral hydatid cyst. AJNR Am J Neuroradiol 1990; 11:1249–50.
47. Garcia-Uria J, Cabezudo J, Nombela L. Subdural hematoma as a complication in the surgical removal of intracranial hydatidosis. Acta Neurochir (Wien) 1980; 52:51–4.
48. Singounas PC, Leventis AS, Sakas DE, et al. Successful treatment of intracerebral hydatid cysts with albendazole. Case report and review of literature. Neurosurgery 1992; 31:571–4.
49. Tortov T, Vutova K, Pektov F, Balkanski G. Albendazole in treatment of multiple cerebral hydatid cysts. Case report. Trans R Soc Trop Med Hyg 1988; 82:150–2.
50. Bekhti A, Schaaps JP, Capron M, et al. Treatment of hepatic hydatid disease with mebendazole. Preliminary results in 4 cases. Br Med J 1977; 2:1047–51.
51. Morris DL, Dykes PW, Dickson B. Albendazole in hydatid disease. Br Med J 1983; 286:103–4.
52. Morris DL, Dykes PW, Marriner S, et al. Albendazole. Objective evidence of response in human hydatid disease. JAMA 1985; 263:2053–7.
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