Egyptian Journal of Neurosurgery

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Egyptian Journal of Neurosurgery Volume 29 / No. 3 / July - September 2014 25-28

Egyptian Journal of Neurosurgery


Original Article

Arachnoid Cyst is it a Risk Factor for Chronic Subdural Hematoma in Young Adults? (A Report of Four Cases and Review of Literature)

Mohammed Mustafa Adawi*

Department of Neurosurgery, Benha University, Egypt


Background: Chronic subdural hematomas (CSDH) tend to occur in elderly patients

with a history of mild head injury few weeks prior to the onset of symptoms. Arachnoid

cysts (AC) are relatively common congenital intracranial mass lesions that arise during

the development of the meninges. However, these two distinct clinical entities

sporadically occur together in relatively young patients. Objective: In light of a

literature review, a trial to explain the association between arachnoid cyst and subdural

hematoma is proposed. Patients & Methods: This is a report of four cases presented

with chronic subdural hematoma over the frontoparietal region, with an incidental

finding of an arachnoid cyst over the Sylvian fissure. Results: Three patients were males

and one female. Age ranged from ten years to forty one years. All patients had history of

minor head trauma. Their symptoms were due to intracranial hypertension, like those

with isolated CSDH. All patients’ symptoms regressed after evacuation of CSDH.

Conclusion: Arachnoid cyst is a possible risk factor for subdural hematoma in young

adults. A burr hole procedure with drainage of hematoma is an adequate treatment.


Chronic subdural hematoma (CSDH) is a common

type of intracranial hemorrhage and is predominantly

seen in the elderly. It typically consists of darkish red

liquefied blood breakdown products with an associated

neomembrane and located in the otherwise potential

space between the arachnoid and the dura13.

The space that the CSDH occupies is technically

the intradural space. It is a disruption of the dural border

cell layer from the deep pachymeninges5.

Blood in this space provokes an inflammatory

reaction, which results in an enveloping membrane

surrounding the blood. If this follows clearly dated

trauma, a CSDH may become symptomatic days to

weeks after the event. Most of the time, there is no clear

traumatic history that precedes the discovery of a

CSDH. In the cases in which there is no associated

trauma, other etiologies have to be considered13.

Arachnoid cysts (AC) are the most frequent

congenital cystic intracranial abnormality. They

represent extra cerebral, intra-arachnoidal cerebrospinal fluid collections comprising 1% of intracranial spaceoccupying

lesions4. Subdural hematomas are

infrequently an encountered complication of AC8.

This study was designed to describe four cases with

AC associated with CSDH and in light of a literature

review; we discuss arachnoid cysts as a possible risk

factor for subdural hematoma, especially in young



Four cases of CSDH related to AC underwent

surgery during the period between October 2011 and

January 2013 in the Department of Neurosurgery,

Benha University. Before coming to our attention, none

of the patients complained of neurological disorders or

received a diagnosis of AC. All patients had reported

minor head trauma from 30 to 45 days with a mean of

37 days before hospital admission. There were three

males and one female aged between 10 to 41 years with

a mean of 26.75 years (Table 1). All four patients

underwent cerebral CT scanning in the emergency

department, and assessment of their coagulation status

by screening with complete blood count, liver function

tests, prothrombin time (PT), international

normalization ratio (INR), and activated partial

prothrombin time (PTT).

Table 1: Summary of data in four patients with CSDH in association with ACs

Case No. Age (years), Sex Minor Head Injury Presenting symptom

1 10, Male Bicycle fall Headache

2 22, Male Soccer related Headache

3 41, Female Fall Headache

4 34, Male Aggression Headache, and Right Hemiparesis


It was obvious that these patients in whom a CSDH

was associated with an AC were young with mean age

of 26.75 years, and as in cases involving an isolated

CSDH, their CSDH manifested typically within few

weeks after a minor head injury with a mean duration of

37 days and their neurological symptoms were due to

intracranial hypertension.

Illustrative Cases

Case 1

A 10 years old boy presented with a 14 days history

of gradually worsening headache accompanied by one

attack of vomiting. His recent history was remarkable

for head injury caused by falling from his bicycle, one

month before. His level of consciousness was normal

without any visual disturbances and examination

revealed no neurologic deficit. Of note, the patient did

not receive any drug that could have implicated with

hemorrhagic phenomena, and laboratory assessment of

his coagulation status was within normal. CT Brain

demonstrated a left frontotemproparietal CSDH of

mixed hypo and isodenisty (Fig. 1 a&b).

Fig. 1 a&b: Preoperative CT brain showing left

frontotemporoparietal CSDH

The patient underwent emergency surgery to

evacuate the CSDH through a burr hole under general

anesthesia. During the postoperative course the patient

recovered smoothly and his headache disappeared.

Early postoperative CT brain revealed satisfactory

drainage of CSDH and demonstrated an arachnoid cyst

over the ipsilateral Sylvian fissure (Fig. 2). The patient

was completely free of neurological symptoms at

regular follow-up visits.

Fig. 2 a&b: a. Early postoperative CT brain

demonstrating Galassi type 2 arachnoid cyst over the

left Sylvian fissure, and b. adequate drainge of the

hematoma with drain in place

Case 2

A 22 years old healthy man presented with severe

headache accompanied by blurring of vision. His recent

history was remarkable only for insignificant head

trauma five weeks ago, during a football game. CT

brain demonstrated right frontotemporoparietal isodense

CSDH with intracerebral edema and midline shift. The

aforementioned findings were inconsistent with a mild

head trauma. Therefore, a contrast enhanced CT brain

was ordered, and no other space-occupying lesions were

identified (Fig. 3 a&b). CSDH was evacuated through a

burr hole. The postoperative course of the patient was

uneventful, postoperative CT brain revealed right

Sylvian AC (Fig. 4 a) and satisfactory drainage of the

hematoma with insignificant residual (Fig. 4 b).

Fig. 3 a&b: CT brain with contrast showing isodense

CSDH hematoma with midline shift.

Fig. 4 a&b: a. Post-operative CT brain showing

ipsilateral Galassi type I AC (blue arrow) and b.

satisfactory evacuation of CSDH with improvement of

midline shift.


In all these four cases, as in reported cases3,11 the

CSDH was ipsilateral to the AC and the AC caused no

symptoms until the CSDH manifested neurologically.

True arachnoid cysts are congenital. The lesion

could arise from a minor developmental aberration of

the subarachnoid space, owing to changes in

mesenchymal condensation or CSF flow into the piaarachnoid

space. Ultrastructural studies that involved

transmission electron microscopy have specified that the

cyst lining consists of single or multiple layers of cells

and that ACs are wholly situated within the arachnoid


They can develop anywhere within the

subarachnoid space, intimately related to the cisterns. In

the general population, nearly half of cysts occur within

the Sylvian fissure. Arachnoid cysts show a slight

predilection for the male sex. A majority of the

arachnoid cysts are recognized during the first two

decades of life9.

The coexistence of an intracranial AC with

subdural haematoma is quite rare, and the first

description of such case was described in 193814.

Current histological knowledge also leaves the

pathogenesis of CSDH unclear. In an electronic

microscopic study, researchers described the dural

border cells that extend from the dura and adhere tightly

to the arachnoid membrane, delimiting a “potential

space”—namely ،the “subdural compartment"5. This

space remains virtual until it is created and opened by a

traumatic event. In an earlier study of patients with posttraumatic

acute SDH investigators found that

neuroimaging studies showed the hematoma in the

“intradural” compartment. From anatomical findings

and studies involving transmission electron microscopy

it seems that the membrane separating an AC from a

CSDH forms when the membranous structures of the

AC and CSDH overlap and adhere tightly to each other.

The presence of a congenital arachnoid malformation

such as an AC weakens the subdural compartment at the

level of the junction of the dural border cells and favors

subsequent bleeding; causing a minimal and asymptomatic acute SDH that ultimately evolves into a

symptomatic CSDH2.

Some investigators found small bridging vessels

between the dura and outer membrane of the AC, and

suggested that these small vessels are the source of

initial bleeding leading to CSDH in AC. Moreover, the

fragile supporting stroma also predisposes to rupture

even after a minor injury. In some occasions,

subsequent re-bleed or osmotic influx of fluid could

explain the gradual increase in the subdural fluid


Preoperative CT brain, obtained in all patients

demonstrated the AC and CSDH in 2 cases (case 3 &

case 4), while in case 1 & case 2 AC was completely

concealed by the ipsilateral CSDH. CSDHs differed

from the brain parenchyma in density, appearing

hypodense, isodense, or slightly hyperdense according

to whether bleeding was longlasting or recent13.

In all our four patients the AC appeared similar to

cerebrospinal fluid in signal density. After the CSDH

was removed the AC reexpanded in case 3 & case 4,

and became apparent in case 1 & 2. AC in case 1&3

was type II according to Galassi classification, while the

remaining cases demonstrated AC of type I according to

the same classification.

The satisfactory results obtained by performing

burr hole irrigation of the CSDH and by leaving the AC

for follow-up, agree with some previous reports10,12.

All patients’ neurological symptoms regressed

within days of surgery, and at long-term follow-up (3–

18 months) none of them had recurrent lesions. The

patients’ postoperative clinical course resembled that of

patients with the more usual CSDH uncomplicated by

an AC.

Other investigators have evacuated the CSDH and

inserted a cysto-peritoneal shunt1. Some have proposed

using craniectomy or craniotomy with evacuation of the

CSDH and fenestration of the AC12. Endoscopic

membrane excision has also been used6.

There are only a few published cases in which

authors described a CSDH associated with an AC that

were treated conservatively. Most of these patients

harboring these lesions had only mild neurological

symptoms and the CSDH resolved spontaneously12.


As also reflected in a literature review, patients

with AC, especially when located in Sylvian fissure,

appear to harbour a life-long risk of contracting

subdural hematoma. Data suggest that when a CSDH

and AC are diagnosed in the same patient, the

neurological symptoms arise exclusively from the mass

effect of the CSDH, and can be successfully treated by

undergoing CSDH drainage alone while the AC is left

intact for follow-up. Neurosurgeon should consider the

possibility of CSDH in young patients with prior history

of minor head injury, as AC is not uncommon.


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Arachnoid cysts of the middle cranial fossa:

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