Basal Subarachnoid Cisterns Research Articles

The Mini-Spheno-Supraorbital Craniotomy for Treatment of Ruptured Anterior Circulation Aneurysms.

Objective:Yasargil introduced the pterional approach mainly for clipping of anterior circulation (AC) aneurysms. We implemented the mini-spheno-supraorbital (MSS) craniotomy, changing the shape and reducing the size of the classical pterional craniotomy. The literature on clipping ruptured AC aneurysms through reduced-in-size craniotomies is sparse. This study aims to describe the technique and present our experience in clipping ruptured AC aneurysms through the MSS approach. Materials and methods: The MSS craniotomy was used in 114 cases of clipping ruptured AC aneurysms. A single burr hole was placed at the "keyhole" and an ellipsoid bone flap in the spheno-supraorbital region was raised. The tabula interna was thinned circumferentially, the roof of the orbit was flattened. Among aneurysm clipping, the lamina terminalis and the subarachnoid basal cisterns were opened. The imaging modality, the severity of the subarachnoid hemorrhage (SAH) according to Hunt & Hess (H&H), the size of the bone flap, the surgery duration and the aneurysm obliteration rate seen at the postoperative DSA were examined. Results:Out of all patients in the study, 71% had exclusively CT-angiogram as initial imaging and suffered low-grade (H&H I°) SAH (71%). The mean size of the bone flap was 1.6 x 4.5 cm (1.3 x 4.3 - 2 x 8.5 cm). The approach allowed adequate 360°-dissection, sufficient proximal and distal control, brain relaxation though laminoterminotomy and opening of the basal cisterns. The mean duration from skin incision to clip application was 130 minutes (64-236 mins). Total obliteration rate was 97.3%. Conclusion:The MSS craniotomy is feasible in terms of safety and speed for clipping of ruptured AC aneurysms especially in lower-grade SAH.

Post-Infective Hydrocephalus

Post-infective hydrocephalus (PIH) arises as a complication of any CNS infection, and can be either communicating or noncommunicating. The aim of this article is to study the various causes of PIH and its pathophysiology and treatment. The literature was searched for articles describing the causes of PIH. Common causes of PIH are CNS tuberculosis (TB), neurocysticercosis, and perinatal or neonatal infection. TBM is most likely to result in hydrocephalus out of all these manifestations of CNS TB, and hydrocephalus is more likely to occur early in the course, typically 4-6 weeks after the onset of TBM, and is more common among children as compared to adults. A trial of medical management (antitubercular therapy, steroids, and decongestants) can be given to patients with communicating hydrocephalus. Ventriculoperitoneal shunt is the most employed method of CSF diversion in these patients. Though traditionally considered contraindicated, many recent studies have found ETV to be a reasonable option in patients with PIH. HCP in patients with neurocysticercosis can be associated with intraventricular cysts and racemose cysts in the basal subarachnoid cisterns. Surgical intervention is required either for cyst removal or CSF diversion. Endoscopic approaches can be used to remove the intraventricular cysts, which takes care of the HCP. PIH in infants can result either from antenatal infections (TORCH infections) or postnatal infections such as meningitis. Management of PIH can be challenging. Management has to be individualized.

Active regulation of CSF flow with the subarachnoid basal cisterns as one of the key regulators: a novel concept and review of the literature

Active regulation of CSF flow with the subarachnoid basal cisterns as one of the key regulators: a novel concept and review of the literature

Subarachnoidal Neurocysticercosis non-responsive to cysticidal drugs: a case series

BackgroundNeurocysticercosis (NC) is one of the most frequent parasitic diseases of the central nervous system. Cysticidal drugs, albendazole and praziquantel, are generally effective when parasites localize in the parenchyma. In contrast, parasites lodged in the subarachnoid basal cisterns are less responsive to treatment.Case PresentationThe clinical and radiological pictures of six Mexican patients non-respondent to cysticidal treatment are presented.ConclusionsThe possible factors involved in the cysticidal non-response are discussed and hints are provided of potentially useful changes to therapeutic protocols.

Intraventricular and subarachnoid basal cisterns neurocysticercosis: a comparative study between traditional treatment versus neuroendoscopic surgery

The purpose of this study was to evaluate the efficacy of traditional treatment and minimal invasive flexible endoscopy surgery (MIFNES) in the treatment of intraventricular and subarachnoid basal cisterns neurocysticercosis (NCC). This was an observational comparative study of two independent series with a total of 140 patients with extremely severe forms of NCC from two different institutions. All 83 patients submitted for traditional treatment series received albendazole, and some of them received additionally praziquantel. Each cycle of both regimens lasted 4 weeks. The majority of these patients had at least one ventriculoperitoneal (VP) shunt. The rest 57 patients were submitted to the MIFNES treatment. The follow-up period was at least 6 months. In all patients of both series cysticercal cysts disappeared, became calcified, or were removed. Symptoms of 136 patients improved. Four patients died. The average in the quality of life measured using the Karnofsky scale improved from a mean of 52.22 and 52.44 at the beginning to 85.48 and 90.37 at 6 months (p < 0.003), in the traditional treatment and MIFNES series, respectively. From traditional treatment, almost all patients remained with at least one VP shunt, and from the MIFNES series only 12 patients. The authors postulate that MIFNES is a good alternative for the management of intraventricular and subarachnoid basal cisterns NCC because it allows removal of most of the parasites, rapid recovery of the patients, and removal and placement of shunt under direct vision when necessary. Traditional treatment is a second option where the MIFNES procedure is not available.

Bruns syndrome caused by intraventricular neurocysticercosis treated using flexible endoscopy

Neurocysticercosis is the most frequent cause of hydrocephalus in adults in regions where the disease is endemic, including Latin America. The prognosis for intraventricular neurocysticercosis is worse than that for the intraparenchymal form of the disease, making treatment especially important. Although active and viable intraventricular cysts produce no reaction in the host, they can cause noncommunicating hydrocephalus, whose onset is frequently abrupt. Sometimes the increasing intracranial pressure due to obstruction of the cerebral aqueduct (ball-valve mechanism) is intermittent, producing relapsing/remitting symptoms; this life-threatening phenomenon is called "Bruns syndrome." Between 1996 and 2004, among a group of 285 patients with neurocysticercosis and Bruns syndrome caused by cysticercal cysts of the third ventricle was diagnosed in seven patients by using magnetic resonance imaging. An endoscopic procedure with a flexible cerebral endoscope was performed, intact parasitic cysts were removed, and a complete exploration was undertaken to look for more cysticercal cysts in the whole ventricular system and the subarachnoid basal cisterns. There were no deaths or complications. All seven patients were asymptomatic during a follow-up period ranging from 1 to 5 years. Flexible cerebral endoscopy allows one, in a minimally invasive manner, to approach the ventricular system and subarachnoid basal cisterns and to remove intraventricular neurocysticercal cysts. Flexible endoscopy is an alternative treatment for Bruns syndrome caused by neurocysticercosis of the third ventricle.

The possible role of CSF hydrodynamic parameters following in management of SAH patients.

It is suggested that reduced intracranial compliance may be present even when measured ICP is normal and may precede clinical deterioration. Our findings reflect a decompensation of hydrodynamic parameters more pronounced 4-7 postictal days, when compliance is reduced not only in patients with poor clinical condition, but also in patients with Hunt-Hess grade I-III. Increased CSF outflow resistance in the first few days is not surprising; it is thought to be due to the blockage of flow of CSF through the basal subarachnoid cisterns and clogging of the arachnoid villi with erythrocytes and fibrin. Enlargement of ventricles seen on CT scan at the same time suggests the development of acute hydrocephalus. During the first days after SAH, our data reflects evidence of ventricular enlargement in patients presenting with both poor and better clinical condition. We conclude that the monitoring of ICP and dynamic measuring of CSF hydrodynamic parameters is important for longer than the generally accepted few days for selected cases after SAH.

Heme-oxygenase-1 induction in glia throughout rat brain following experimental subarachnoid hemorrhage

The heme released following subarachnoid hemorrhage is metabolized by heme-oxygenase (HO) to biliverdin and carbon monoxide (CO) with the release of iron. The HO reaction is important since heme may contribute to vasospasm and increase oxidative stress in cells. HO is comprised of at least two isozymes, HO-2 and HO-1. HO-1, also known as heat shock protein HSP32, is inducible by many factors including heme and heat shock. HO-2 does not respond to these stresses. To begin to examine HO activity following subarachnoid hemorrhage (SAH), the expression of HO-1 and HO-2 was investigated after experimental SAH in adult rats. Immunocytochemistry for HO-1, HO-2 and HSP70 proteins was performed at 1, 2, 3 and 4 days after injections of lysed blood, whole blood, oxyhemoglobin and saline into the cisterna magna. A large increase in HO-1 immunoreactivity was seen in cells throughout brain following injections of lysed blood, whole blood, and oxyhemoglobin but not saline. Lysed blood, whole blood and oxyhemoglobin induced HO-1 in all of the cortex, hippocampus, striatum, thalamus, forebrain white matter and in cerebellar cortex. HO-1 immunoreactivity was greatest in those regions adjacent to the basal subarachnoid cisterns where blood and oxyhemoglobin concentrations were likely highest. Double immunofluorescence studies showed the HO-1 positive cells to be predominately microglia, though HO-1 was induced in some astrocytes. HO-1 expression resolved by 48 h. HO-2 immunoreactivity was abundant but did not change following injections of blood. A generalized induction of HSP70 heat shock protein was not observed following injections of lysed blood, whole blood, oxyhemoglobin, or saline. These results suggest that HO-1 is induced in microglia throughout rat brain as a general, parenchymal response to the presence of oxyhemoglobin in the subarachnoid space and not as a stress response. This microglial HO-1 response could be protective against the lipid peroxidation and vasospasm induced by hemoglobin, by increasing heme clearance and iron sequestration, and enhancing the production of the antioxidant bilirubin.

New surgical treatment of middle fossa arachnoid cyst

BACKGROUND A new surgical treatment of middle fossa arachnoid cyst is reported. The benefit of our surgical procedure is to maintain the physiologic pathway of the cerebrospinal fluid (CSF) without a shunting procedure. METHODS Following a small frontotemporal craniotomy, a linear incision in the outer wall of the cyst is made. The basal subarachnoid cisterns and distal sylvian cisterns are widely opened microsurgically. The outer wall of the cyst is then closed to prevent CSF leakage (arachnoidplasty). RESULTS We have experienced six patients who underwent this new surgical treatment. All their cysts showed no or delayed influx of the contrast medium on preoperative computed tomography cisternogram. A favorable outcome was attained in the long-term follow-up without any complications. CONCLUSIONS The present technique was designed to secure physiologic CSF circulation and to avoid the use of a shunting system. A total of six patients treated with our new technique have been followed-up 6 years, and a good clinical outcome has been observed in all of them without complications.

A Randomized Trial of Intraoperative, Intracisternal Tissue Plasminogen Activator for the Prevention of Vasospasm

A multicenter, randomized, blinded, placebo-controlled trial was conducted to study the possible role of intracisternally administered fibrinolytic agent recombinant tissue plasminogen activator (rt-PA) in preventing delayed onset cerebral vasospasm following aneurysmal subarachnoid hemorrhage (SAH). The target population was patients with ruptured saccular aneurysms causing severe SAH, placing them at high risk for vasospasm. Treatment consisted of a single 10 ml intraoperative injection of either vehicle buffer solution or rt-PA (1 mg/ml) into the opened basal subarachnoid cisterns immediately following aneurysm clipping. The major efficacy endpoint in this trial was angiographic vasospasm, and the major safety concern was intracranial hemorrhage. One hundred patients were randomized, 49 to placebo and 51 to rt-PA treatment. Baseline population characteristics were similar between the two groups. Severity of intracranial hemorrhage on computed tomographic scans was also similar between groups: 87.2% of both placebo and rt-PA treated patients had thick subarachnoid clots, and the rates for intracerebral and intraventricular hemorrhage were, respectively, 16.3% and 22.5% for placebo and 23.5% and 21.6% for rt-PA. Nine randomized patients did not receive treatment in the operating room, and in 8 this was due to conditions felt unsafe for the administration of a fibrinolytic agent. The overall incidence of angiographic vasospasm measured between the seventh and eleventh day following SAH was similar between the two groups, with arterial narrowing detected in 74.4% of dosed placebo patients and 64.6% of rt-PA treated patients. However, there was a trend toward lesser degrees of vasospasm in the rt-PA treated group. The rates for no or mild, moderate, and severe vasospasm were 69%, 16% and 15% in the rt-PA treated group, versus 42%, 35% and 23% in the placebo group (P = 0.07). When only those patients with thick subarachnoid clots were considered at the treating centers, there was a 56% relative risk reduction of severe vasospasm in the rt-PA treated group, which was significant (P = 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)

A Randomized Trial of Intraoperative, Intracisternal Tissue Plasminogen Activator for the Prevention of Vasospasm

A MULTICENTER, RANDOMIZED, blinded, placebo-controlled trial was conducted to study the possible role of intracisternally administered fibrinolytic agent recombinant tissue plasminogen activator (rt-PA) in preventing delayed onset cerebral vasospasm following aneurysmal subarachnoid hemorrhage (SAH). The target population was patients with ruptured saccular aneurysms causing severe SAH, placing them at high risk for vasospasm. Treatment consisted of a single 10 ml intraoperative injection of either vehicle buffer solution or rt-PA (1 mg/ml) into the opened basal subarachnoid cisterns immediately following aneurysm clipping. The major efficacy endpoint in this trial was angiographic vasospasm, and the major safety concern was intracranial hemorrhage. One hundred patients were randomized, 49 to placebo and 51 to rt-PA treatment. Baseline population characteristics were similar between the two groups. Severity of intracranial hemorrhage on computed tomographic scans was also similar between groups: 87.2% of both placebo and rt-PA treated patients had thick subarachnoid clots, and the rates for intracerebral and intraventricular hemorrhage were, respectively, 16.3% and 22.5% for placebo and 23.5% and 21.6% for rt-PA. Nine randomized patients did not receive treatment in the operating room, and in 8 this was due to conditions felt unsafe for the administration of a fibrinolytic agent. The overall incidence of angiographic vasospasm measured between the seventh and eleventh day following SAH was similar between the two groups, with arterial narrowing detected in 74.4% of dosed placebo patients and 64.6% of rt-PA treated patients. However, there was a trend toward lesser degrees of vasospasm in the rt-PA treated group. The rates for no or mild, moderate, and severe vasospasm were 69%, 16% and 15% in the rt-PA treated group, versus 42%, 35% and 23% in the placebo group (P = 0.07). When only those patients with thick subarachnoid clots were considered at the treating centers, there was a 56% relative risk reduction of severe vasospasm in the rt-PA treated group, which was significant (P = 0.02). Other trends in the rt-PA treated group (not reaching statistical significance) included less hypervolemic and hypertensive treatment, lower mean velocities on transcranial Doppler, reduced delayed neurological worsening, a lower 14 day mortality rate, and improved 3 month outcome rate. Considering just the dosed patients with thick clot, 56% made a good recovery and 12% died in the rt-PA group, versus 38% making a good recovery and 22% dying in the placebo group (P = 0.17). Overall bleeding complication rates did not differ between the two groups. Two treatment-related severe hemorrhages resulted from incompletely secured aneurysms that rebled shortly following treatment. Although the fibrinolytic treatment used in this study may reduce angiographic vasospasm, its efficacy in preventing clinical vasospasm and its ischemic consequences require reexamination in a larger randomized trial.

PATHOLOGY AND PATHOGENETIC MECHANISMS IN NEUROTUBERCULOSIS

The mechanisms and the changes described herein typically begin with a dense basal meningeal exudate often resulting from a "Rich focus" along the basal surface of the cerebrum or ventricular ependyma. In the interpeduncular fossa, when the exudate is copious, among other structures the proximal parts of the optic nerves and of the internal carotid arteries are seen surrounded and compressed by the exudate. This exudate is made up of small and large mononuclear cells, including epithelioid cells, which also act as macrophages and may fuse to form Langhans' giant cells. Further extension of this exudate along small proliferating blood vessels into the brain substance constitutes a border zone encephalitis with the development of focal and diffuse ischemic brain changes due to vasculitis. Entrapment and occasional arteritic occlusion of larger arteries, such as the middle cerebral in the Sylvian fissures, results in infarction. Blockage of the basal subarachnoid cisterns around the midbrain and pons by the dense basal exudate or narrowing of aqueduct and third ventricle by a small tuberculoma causes consequent hydrocephalus. Development of many or one large focal granuloma (i.e., tuberculoma) occurs in the cerebrum, cerebellum, and/or brain stem. Similar pathogenetic mechanisms produce tuberculous spinal meningitis myeloradiculopathy that may be secondary to or occur before cranial tuberculous meningitis. More extensive damage to the white matter may occur together with the infrequent onset of perivascular demyelination on the basis of a hypersensitivity reaction to tuberculoprotein (i.e., "allergic tuberculous encephalopathy"). Finally, there may be a part played by NO in the production of the vascular and perivascular inflammatory central nervous system changes and a role for the the potential beneficial action of corticosteroids, especially in cases of tuberculous encephalopathy.

Intracisternal recombinant tissue plasminogen activator after aneurysmal subarachnoid hemorrhage

Fifteen patients undergoing surgery within 48 hours of aneurysm rupture were administered recombinant tissue plasminogen activator (rt-PA) directly into the basal subarachnoid cisterns after minimal surgical clot removal and aneurysm clipping. Preoperatively, 13 patients had diffuse or localized thick subarachnoid blood clots on computerized tomography (CT), and two had diffuse thin clots. The rt-PA was given as a single intraoperative injection of 7.5 mg (one patient), 10 mg (nine patients), or 15 mg (five patients). Postoperative cisternal drainage was employed in three patients. All patients except one demonstrated partial to complete cisternal clot clearance on CT scans within 24 hours after surgery. The patient who showed no clot reduction was the only patient in this series to develop symptomatic vasospasm and was the only fatality, dying 8 days after rupture. No vasospasm was seen on follow-up cerebral angiography in six of the 14 responding patients, and mild-to-moderate arterial narrowing was seen in at least one major cerebral artery in the remaining eight patients. Severe angiographic vasospasm was not seen, although the patient who died did not undergo repeat angiography. There was one major complication early in the series which seemed clearly related to treatment, and that was a large extradural hematoma occurring within several hours of craniotomy. Intrathecal fibrinolytic treatment appears effective in clearing subarachnoid clot and reducing vasospasm, and may be associated with acceptable risks if given to patients with large-volume subarachnoid hemorrhages at high risk for severe vasospasm.

Clinical Significance of Traumatic Subarachnoid Hemorrhage

The clinical significance of traumatic subarachnoid hemorrhage (TSAH) was studied in 20 head-injured patients. They were classified into mild (9) and severe (11) groups by their initial Glasgow Coma Scale (GCS) scores. TSAH detected by computed tomography was localized in the Sylvian fissure in four of the nine mild group patients, but was also found in other basal subarachnoid cisterns in the other five. Except for one patient who developed delayed vasospasm and communicating hydrocephalus, all had favorable outcomes in this group. Massive TSAH was noted in the basal subarachnoid cisterns in 10 severe group patients and only one had a good outcome. Delayed intracerebral hematoma in the frontal or temporal lobe in the vicinity of the Sylvian fissure was found in two mild and two severe group patients with TSAH in the Sylvian fissures. Traumatic parenchymal lesions in the brainstem were minimal in one of the two autopsied patients and no evidence of diffuse axonal injury was found in both cases. Thus, TSAH in the Sylvian fissure is suggestive of focal brain contusion around the fissures. Massive TSAH in the basal subarachnoid cisterns is not necessarily associated with severe parenchymal injury of the brainstem.

Intrathecal Fibrinolytic Therapy after Subarachnoid Hemorrhage: Dosage Study in a Primate Model and Review of the Literature

Because of the naturally low fibrinolytic activity of CSF many erythrocytes entrapped in subarachnoid blood clot undergo hemolysis in situ, releasing vasogenic oxyhemoglobin (OxyHb) in high concentrations around the basal cerebral arteries. In order to promote more rapid clearance of erythrocytes from the basal subarachnoid cisterns we are currently investigating intrathecal thrombolytic therapy with human, recombinant, tissue plasminogen activator (rt-PA) in a primate model of subarachnoid hemorrhage (SAH) and cerebral vasospasm (VSP). In the present study 16 monkeys were divided into 4 groups of 4, and each group received a different dose of sustained-release gel rt-PA at the time of experimental SAH. Cerebral angiography seven days later showed that whereas no VSP occurred in the groups receiving 0.5 or 0.75 mg of rt-PA, mild to moderate VSP occurred in the groups receiving 0.125 or 0.25 mg of rt-PA. Analysis of the combined 2 smaller dosage groups revealed significant (P less than 0.05) reduction of lumen caliber in the clot-side internal carotid (C3 and C4), proximal anterior cerebral (A1) and middle cerebral (MCA) arteries. Gross subarachnoid clot remained in all of the animals in the 0.125 and 0.25 mg dose groups, in 2 of the animals in the 0.5 mg dose group, and none of the animals in the 0.75 mg dose group. It was concluded that 0.75 mg of gel rt-PA is sufficient to completely lyse a 4.25 ml SAH and prevent VSP in our primate model. The literature on fibrinolysis and erythrocyte clearance in cerebrospinal fluid (CSF) is reviewed.

Attempts at prevention and treatment of delayed ischaemic dysfunction in patients with subarachnoid haemorrhage.

Rupture of an intracranial aneurysm is frequently followed by evidence of intracranial arterial narrowing, which often is accompanied by the delayed onset of a related neurological deficit. During the decades since these detrimental phenomena were first recognized, many attempts have been made to prevent or treat them. Current emphasis in prophylaxis and treatment is on: 1. early operation to eliminate the threat of rebleeding and to allow the gentle removal of as much blood as feasible from the basal subarachnoid cisterns, 2. maintenance or elevation of circulating blood volume, and 3. maintenance or elevation of systemic blood pressure. In recent years, there has also been increasing evidence that the administration of the calcium channel blocking agent nimodipine can reduce the incidence of delayed ischaemic neurological deficits in patients with a ruptured aneurysm.

Intrathecal nimodipine therapy in a primate model of chronic cerebral vasospasm.

The safety, prevention, and treatment of chronic vasospasm by repeated administration of intrathecally applied nimodipine was evaluated in a primate model of chronic cerebral vasospasm. Twenty-four female cynomolgous monkeys were randomized into three groups of 8: sham, clot, and clot + intrathecal nimodipine. All animals underwent a subarachnoid hemorrhage (SAH) induction operative procedure after base line angiography. Nimodipine was administered postoperatively by subcutaneous injection of 1 ml/0.2 mg tid for 6 days through an Ommaya reservoir with the catheter placed in the subarachnoid basal cisterns. Angiography was performed on Day 7 post-SAH induction. Intrathecally applied nimodipine was not effective in the prevention of angiographic vasospasm. It also did not seem to decrease the degree of pathological change when compared to controls. One animal in the nimodipine group died 2 hours after an intrathecal injection secondary to a respiratory arrest. Transient sedation and hypoventilation were common. No adverse pathological effects were noted. Intrathecal nimodipine did not produce a significant dilation of vessels in moderate or severe spasm when assessed by angiography 2 hours after intrathecal injection. Only 1 animal in 8 showed diffuse dilation of vasospastic cerebral vessels after an intrathecal nimodipine injection. Three other animals in this group developed dilation only of the basilar artery, which was in mild spasm.

Cerebral vasospasm after subarachnoid hemorrhage: an update.

Symptomatic vasospasm, or delayed cerebral ischemia associated with arteriographic evidence of arterial constriction, is currently the most important cause of morbidity after acute subarachnoid hemorrhage. The development of vasospasm is directly correlated with the presence of thick blood clots in the basal subarachnoid cisterns, which can be detected by an early computed tomographic scan. Symptomatic vasospasm usually develops between 4 and 12 days after subarachnoid hemorrhage. The onset is gradual, occurring over hours or days. There is typically a gradual deterioration of the level of consciousness, accompanied by focal neurological deficits that are determined by the arterial territories involved. Hyponatremia frequently occurs and may exacerbate the symptoms. The patients are usually volume depleted, and therefore many authorities now treat them with replenishment and expansion of their intravascular volume with colloid and blood. Volume expansion, together with elevation of the systemic blood pressure and reduction of the intracranial pressure when elevated, constitute the only currently available effective therapy for symptomatic vasospasm. The cause of vasospasm remains obscure. Mechanisms of smooth muscle cell contraction and relaxation and experimental efforts to elucidate the nature of vasospasm are reviewed.

Ophthalmologic applications of computed tomography in nonhuman primates.

The orbital contents of 28 baboons are defined by computed tomography (CT), which provides a simple, reliable, reproducible, and accurate technique for the experimental investigation of the orbit of the nonhuman primate. This method is applied to the diagnosis of exophthalmos. The suprasellar and other basal subarachnoid cisterns are precisely delineated using intrathecal enhancement prior to CT imaging (metrizamide CT cisternography).

A New Method of Pneumography of Subarachnoid Basal Cisterns

A New Method of Pneumography of Subarachnoid Basal Cisterns