Pathology
Echinococcosis is caused by the larval or hydatid stage of the dog tapeworm Taenia echinococcosis. Hepatic and pulmonary forms of the disease are the most common and account for almost 85 percent of the cases. Involvement of the central nervous system is seen in only 2 to 3 percent of patients and bone, including vertebrae about 5% percent.

Hydatid disease is transferred to human adults by ingestion of the scolex, or eggs, that are present in infected foodstuffs. Whereas in children infection commonly takes place via accidental contamination with faeces of dogs harbouring the adult worm; man may also serve as an intermediate host.

After several months, the cyst wall differentiates into an internal layer (endocyst), and an external cuticular laminated layer (ectocyst).

The host reacts by forming an adventitial capsule, and the cyst contains fluid with daughter cysts which contain 400.000 scolices per millilitre.

Age distribution
Cerebral echinococcosis is considered a childhood disease, and indeed, other workers' estimation showed that 50 to 75 percent of cases involving nervous system occur in the pediatric age group. Sixty-five percent occur in children between the ages of 5 and 10. Up to 5 percent of children contracting other forms of the disease will eventually demonstrate cerebral involvement. The average age is 12 years.

Sex distribution
There appears to be no sex differentiation but in our group about 55 percent male and 45% percent female with more females in the late age group was noticed.

Localization, size and Number
Cerebral Hydatid cysts are usually single and supratentorial, and tend to occur in the middle cerebral artery distribution. Only 3 percent are seen in the cerebellum. These cysts can attain a large size of 12-15 cms in diameter because they encounter relatively little resistance.

Multiple cysts occur either by embolization of multiple larvae, or by spontaneous or iatrogenic cyst rupture, as with any expanding mass lesion. The cyst predilection for white matter is undisputed, but the exact reason for this is unknown and we believe it is because of the arterial distribution.

Clinical manifestation
Symptoms and signs are related to increased intracranial pressure and expanding mass effect which produce dissection, stasis and necrosis. Because the lesion is slow growing there will be a long interval before the onset of clinical symptoms.

Headache and vomiting are prominent and occur in 91%

	Visual field changes, usually hemianopia are seen in 35% of the cases. Papilledema occurs in 74%.
	Optic atrophy occur in 24%.
	Evidence of pyramidal tract dysfunction was noted in 62% of patients.
	Mental changes are noted in 22%.
	Seizure activity occurs in approximately 20%.

We found the clinical progression of the disease in adults to be faster than in children because adult patients are less able to accomodate increased intracranial pressure.

DIAGNOSIS

1. Clinical
A detailed clinical history and examination should be the first diagnostic step.

2. Serological

	Casoni's intradermal skin test.
	Weinberg's complement fixation test.
	Eosinophilic pleocytosis and elevated sedimentation rate are supportive evidence but not specific.

We do propose the epidemiological investigation as follows:

The initial investigations include radial double diffusion or latex agglutination test.

Positive results in either of these could be confirmed by immunoelectrophoresis and immunoflourescence, while negative results may be confirmed by electrosyneresis.

3. Radiological:
Plain skull x-ray frequently shows evidence of increased intracranial pressure and mass effect.

	CT scan reveals an intraparenchymal lesion with a clearly defined, rarely enhancing margin, cerebral edema is conspicuous in its absence, and this fact is helpful in differentiating the lesion from brain abscess and cystic tumors. The cyst fluid has more or less the same density as cerebrospinal fluid
	MRI: Usually shows a typical cyst with thin regular margin and cyst fluid having the CSF density.

	Figure 1 — Lateral skull X-ray showing signs of raised ICP due to intracranial hydatid cyst.		Figure 2 — CT scan showing intracranial cystic lesion causing mass effect and hydrocephalus.

	Figure 3 — MRI showing intracranial cystic lesion.

Differential diagnosis
The cerebral hydatid cyst should be differentiated from:

	Cerebral cystic astrocytoma
	Cerebral abscess

Therapy
Medical treatment has virtually no place in the treatment of cerebral hydatid disease.

Surgical removal of the cyst is the only effective treatment and successful operative treatment depends upon complete removal of the unruptured cyst.

Hydrostatic expulsion, that is forcing warm saline beneath the cyst in order to detach and displace it outward through a smaller opening than its diameter is the surgical technique of choice.

Chemical therapy
There is no need for chemical therapy if the cyst is removed completely unruptured. If the cyst ruptures during surgery, local hypertonic saline and formalin should be used. This is followed by systemic chemotherapy (Mebendazol) 30-40 mg/kg body weight 20-30 days course to be repeated after three weeks.

The number of cases ruptured accidentally during surgery were nine out of 54. Retrospective study showed that the ruptured cases are common when the patients fall in older age groups and when the cysts are large i.e., more than 5 cm in in diameter.

Postoperative
CT scan and MRI reveal that immediate re expansion of the brain substance was limited. Extra-axial collections of fluid may persist for some time, but seldom behave as mass lesions. In few weeks a compensatory shift of midline structures to a more normal position takes place.

Prognosis
Hydatid cysts are benign and noninvasive and complete recovery is expected when the cyst is extracted completely unruptured.

When accidental rupture of the cyst occurs there will be recurrence. Complete recovery will not take place because of the behavior (the white cystic cancer).

DISCUSSION

Although there is no national registry to establish the true prevalence of cerebral echinococcosis in Syria, it is correct to assume its high incidence in northern Syria.

We suggest a national screening survey in at least the rural area amongst the vulnerable population. This survery will isolate population susceptible to contracting the disease and elimination of all infective sources i.e., dogs, sheep etc.

REFERENCES

1.	Abbassiour,K., Sahmat, H.,Ameli, N. O., and Tafazob, M.:Coputerized tomography in hydatid cysts of the brain. J. Neurosurg.,49:908411,1978.
2.	Arana-iniguez,R., and San Julian, J.:Hydatid cysts of the brain. J. Neurosug.,12:323-335,1955
3.	Arana-iniguez,R., and Surri, J.: Ecinococcosis of the nervous system. In Van Bogaret, L.,peryra Kafer, J., and Poch. G. F,eds.: Tropical Neurology,. Buenos Aires. Lopez, 1963, pp. 91-111; Rev. iJeurol. B. Aires, 20:155-175,1962.
4.	Ayres, C., Davey, L. M., and German, W J.: Cerebral hydatidosis: Clinical case report with a review of Pathogenesis . J. Neurosurg., 20:371377,1963
5.	Balasubramanium, V, Ramanujan, P B., and Ramamurthi , B.: Hydatid Disease of the nervous system Neurology India, 18auppl. 1 :9295,1970.
6.	Beard , T C.: Evidence that a hydatid cyst is seldom " as old the patient." Lncet> 2:30-32,1978.