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
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
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
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.
ipsilateral Galassi type I AC (blue arrow) and b.
satisfactory evacuation of CSDH with improvement of
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
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
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
Other investigators have evacuated the CSDH and
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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