Preserved arachnoid membrane acts as a predictor of postoperative visual improvement in clinoidal meningioma.

OBJECTIVES: Improvement of patient visual outcome is very important in the treatment of clinoidal meningioma (CLM). The purpose of this study is to determine the association between arachnoid preservation and visual outcome. PATIENTS: Fifteen patients with CLMs that caused visual impairment underwent surgery in our hospital. The patients included 4 men and 11 women, and the mean age was 53.3 years. METHODS: The clinical findings of these patients were retrospectively reviewed. We divided the patients into two groups based on the presence or absence of the arachnoid membrane. Group 1 comprised cases in which arachnoid preservation was intraoperatively confirmed. Group 2 comprised cases in which the arachnoid membrane was not preserved. The Landolt C chart was used to evaluate visual acuity, and dynamic visual field tests using Goldmann perimetry were used to evaluate the visual field. Results were compared before and after surgery. RESULTS: The visual acuity of the ipsilateral eye was significantly improved in Group 1 (p = 0.038). There were no other significant differences between the two groups in terms of tumor volume, patient age, and symptom duration. CONCLUSIONS: Patients in which arachnoid preservation could be intraoperatively confirmed had good improvement in visual acuity. Further research with an increased number of cases is needed to confirm these findings.

The Role of Arachnoid Veils in Chiari Malformation Associated with Syringomyelia.

Chiari malformation type I (CM-I), or hindbrain herniation syndrome, has traditionally been defined as a dislocation of the cerebellar tonsils 5 mm or more below the foramen magnum on sagittal magnetic resonance imaging (MRI) [1, 2]. An association of this anomaly with syringomyelia is observed in 45-68% of patients [3, 4].

Protection of cortex by overlying meninges tissue during dynamic indentation of the adolescent brain.

Traumatic brain injury (TBI) has become a recent focus of biomedical research with a growing international effort targeting material characterization of brain tissue and simulations of trauma using computer models of the head and brain to try to elucidate the mechanisms and pathogenesis of TBI. The meninges, a collagenous protective tri-layer, which encloses the entire brain and spinal cord has been largely overlooked in these material characterization studies. This has resulted in a lack of accurate constitutive data for the cranial meninges, particularly under dynamic conditions such as those experienced during head impacts. The work presented here addresses this lack of data by providing for the first time, in situ large deformation material properties of the porcine dura-arachnoid mater composite under dynamic indentation. It is demonstrated that this tissue is substantially stiffer (shear modulus, µ=19.10±8.55kPa) and relaxes at a slower rate (τ1=0.034±0.008s, τ2=0.336±0.077s) than the underlying brain tissue (µ=6.97±2.26kPa, τ1=0.021±0.007s, τ2=0.199±0.036s), reducing the magnitudes of stress by 250% and 65% for strains that arise during indentation-type deformations in adolescent brains. STATEMENT OF SIGNIFICANCE: We present the first mechanical analysis of the protective capacity of the cranial meninges using in situ micro-indentation techniques. Force-relaxation tests are performed on in situ meninges and cortex tissue, under large strain dynamic micro-indentation. A quasi-linear viscoelastic model is used subsequently, providing time-dependent mechanical properties of these neural tissues under loading conditions comparable to what is experienced in TBI. The reported data highlights the large differences in mechanical properties between these two tissues. Finite element simulations of the indentation experiments are also performed to investigate the protective capacity of the meninges. These simulations show that the meninges protect the underlying brain tissue by reducing the overall magnitude of stress by 250% and up to 65% for strains.

Dorsal spinal arachnoid web diagnosed with the quantitative measurement of cerebrospinal fluid flow on magnetic resonance imaging.

An arachnoid web is an abnormal formation of the arachnoid membrane in the spinal subarachnoid space that blocks CSF flow and causes syringomyelia. Although the precise mechanism of syrinx formation is unknown, dissection of the arachnoid web shrinks the syrinx and improves symptoms. Precisely determining the location of the arachnoid web is difficult preoperatively, however, because the fine structure generally cannot be visualized in usual MRI sequences. In this report the authors describe 2 cases of arachnoid web in which the web was preoperatively identified using quantitative CSF flow analysis of MRI. By analyzing cardiac-gated phase-contrast cine-mode MRI in multiple axial planes, the authors precisely localized the obstruction of CSF flow on the dorsal side of the spinal cord in both patients. This technique also revealed a 1-way valve-like function of the arachnoid webs. Imaging led to the early diagnosis of myelopathy related to the derangement of CSF flow and allowed the authors to successfully excise the webs through limited surgical exposure.

Arachnoid cyst slit valves: the mechanism for arachnoid cyst enlargement.

Arachnoid cysts are common, accounting for approximately 1% of intracranial mass lesions. Most are congenital, clinically silent, and remain static in size. Occasionally, they increase in size and produce symptoms due to mass effect or obstruction. The mechanism of enlargement of arachnoid cysts is controversial. One-way slit valves are often hypothesized as the mechanism for enlargement. The authors present 4 cases of suprasellar prepontine arachnoid cysts in which a slit valve was identified. The patients presented with hydrocephalus due to enlargement of the cyst. The valve was located in the arachnoid wall of the cyst directly over the basilar artery. The authors believe this slit valve was responsible for the net influx of CSF into the cyst and for its enlargement. They also present 1 case of an arachnoid cyst in the middle cranial fossa that had a small circular opening but lacked a slit valve. This cyst did not enlarge but surgery was required because of rupture and the development of a subdural hygroma. One-way slit valves exist and are a possible mechanism of enlargement of suprasellar prepontine arachnoid cysts. The valve was located directly over the basilar artery in each of these cases. Caudad-to-cephalad CSF flow during the cardiac cycle increased the opening of the valve, whereas cephalad-to-caudad CSF flow during the remainder of the cardiac cycle pushed the slit opening against the basilar artery and decreased the size of the opening. Arachnoid cysts that communicate CSF via circular, nonslit valves are probably more likely to remain stable.

The relationship between localized subarachnoid inflammation and parenchymal pathophysiology after spinal cord injury.

Subarachnoid inflammation following spinal cord injury (SCI) can lead to the formation of localized subarachnoid scarring and the development of post-traumatic syringomyelia (PTS). While PTS is a devastating complication of SCI, its relative rarity (occurring symptomatically in about 5% of clinical cases), and lack of fundamental physiological insights, have led us to examine an animal model of traumatic SCI with induced arachnoiditis. We hypothesized that arachnoiditis associated with SCI would potentiate early parenchymal pathophysiology. To test this theory, we examined early spatial pathophysiology in four groups: (1) sham (non-injured controls), (2) arachnoiditis (intrathecal injection of kaolin), (3) SCI (35-g clip contusion/compression injury), and (4) PTS (intrathecal kaolin+SCI). Overall, there was greater parenchymal inflammation and scarring in the PTS group relative to the SCI group. This was demonstrated by significant increases in cytokine (IL-1α and IL-1ß) and chemokine (MCP-1, GRO/KC, and MIP-1α) production, MPO activity, blood-spinal cord barrier (BSCB) permeability, and MMP-9 activity. However, parenchymal inflammatory mediator production (acute IL-1α and IL-1ß, subacute chemokines), BSCB permeability, and fibrous scarring in the PTS group were larger than the sum of the SCI group and arachnoiditis group combined, suggesting that arachnoiditis does indeed potentiate parenchymal pathophysiology. Accordingly, these findings suggest that the development of arachnoiditis associated with SCI can lead to an exacerbation of the parenchymal injury, potentially impacting the outcome of this devastating condition.

Chronic subdural hematoma associated with arachnoid cyst. Two case histories with pathological observations.

Arachnoid cysts are well known to induce chronic subdural hematoma (CSDH) after head injury. However, histological observations of the arachnoid cyst and hematoma membrane have only been rarely described. An 8-year-old boy and a 3-year-old boy presented with CSDH associated with arachnoid cyst. Surgical removal of the hematoma and biopsy of the hematoma membrane and cyst wall were performed. Clinical courses were good and without recurrence more than 1.5 years after surgery. Histological examination suggested that the cysts did not contribute to hematoma development. Pediatric hematoma membranes, similar to adult hematoma membranes, are key in the growth of CSDH. Therefore, simple hematoma evacuation is adequate as a first operation for CSDH associated with arachnoid cyst.

Tuberculous optochiasmatic arachnoiditis: a devastating form of tuberculous meningitis.

Tuberculous meningitis is primarily a disease of the meninges of brain and spinal cord along with adjacent brain parenchyma. The characteristic pathological changes are meningeal inflammation, basal exudates, vasculitis and hydrocephalus. Tuberculous meningitis has a strong predilection for basal parts of the brain. Exudates, if dominantly present in the interpeduncular, suprasellar and Sylvian cisterns, result in optochiasmatic arachnoiditis and tuberculoma. Optochiasmatic arachnoiditis and tuberculoma are devastating forms of tuberculous meningitis and often associated with profound vision loss. This clinical entity more frequently affects young adults. In a recent study, on the multivariate logistic regression analysis, female sex, younger age and raised cerebrospinal fluid protein content were identified as predictors for developing optochiasmatic arachnoiditis. Frequently, optochiasmatic tuberculoma and optochiasmatic arachnoiditis develop paradoxically while a patient is being treated with anti-TB drugs. MRI reveals confluent enhancing lesions that are present in the interpeduncular fossa, pontine cistern, and the perimesencephalic and suprasellar cisterns. Management of tuberculous optochiasmatic arachnoiditis and optochiasmatic arachnoiditis tuberculoma has been variable. Treatment of optochiasmatic arachnoiditis continues to be a challenge and the response is generally unsatisfactory. In isolated case reports and in small series, corticosteroids, methyl prednisolone, thalidomide and hyaluronidase have been used with variable success. The benefit from neurosurgery is controversial and deterioration may follow the initial temporary improvement. Management of paradoxical optochiasmatic arachnoiditis is also controversial. Some patients regain vision following treatment with anti-TB drugs and continued usage of corticosteroids. Neurosurgery may be considered in the patients with either treatment failure or when diagnosis is in doubt. In conclusion, presence of optochiasmatic arachnoiditis or tuberculoma has important therapeutic and prognostic implications for patients of tuberculous meningitis.

Blood-arachnoid barrier disruption in experimental rat meningitis detected using gadolinium-enhancement ratio imaging.

Disruption of the central nervous system (CNS) barriers is one of the major pathophysiological consequences of bacterial meningitis. The increase in the permeability of the CNS barriers caused by the disruption is thought to contribute to the development of adverse neurological outcomes. We have established a method by which the CNS barrier permeability can be demonstrated by the gadolinium-enhancement ratio (GER) calculated from the T1 weighted image (T1WI) which is based on gadolinium-enhanced magnetic resonance imaging (GdEMRI). The present study examined the disruption of CNS barriers such as blood-brain barrier (BBB), blood-cerebrospinal fluid barrier (BCSFB) and blood-arachnoid barrier (BAB) in rats with meningitis induced by lipopolysaccharide (LPS)- or interleukin (IL)-1ß. Four hours after intracisternal injection of LPS or IL-1ß, severe disruption of the BAB, but not the BBB or BCSFB, was observed. This suggests that the BAB, rather than the BBB or BCSFB, plays a key role in the influx of blood-borne cells and substances during meningitis. The BAB is therefore more vulnerable to disruption than the BBB or BCSFB during meningitis in rats. In addition, GdEMRI with GER imaging analysis appears to be useful in spatio-temporal studies on the function of the CNS barriers under various physiological and pathological conditions.

Surgical treatment of posttraumatic syringomyelia.

OBJECTIVE: The present study evaluates the effectiveness of 2 surgical procedures, shunting and untethering, for posttraumatic syringomyelia. METHODS: We retrospectively reviewed the medical charts of all surgical patients with posttraumatic syringomyelia in our department. Shunting was performed before 1997; after 1997, we used arachnoidolysis and untethering. RESULTS: Shunting was performed in 15 patients, and 19 patients underwent arachnoidolysis. Statistical analysis found that the 2 groups did not differ in age or initial clinical or radiological presentation. All patients suffered from progressively worsening symptoms. Reconstruction of the subarachnoid space by arachnoidolysis and untethering the cord allowed us to improve or stabilize 94% of our patients. Shunting exposed the patients to a higher rate of clinical recurrence and reoperation. Comparisons between the 2 groups found a significant difference (better results) in favor of arachnoidolysis for the McCormick classification (P = .03), American Spinal Injury Association motor score of the lower extremities (P = .02), and subjective grading (P = .001). There was no significant difference in the evolution of pain or the Vaquero index between the 2 groups; however, a tendency appeared in favor of arachnoidolysis for cyst evolution in regard to the extent of the cyst and the Vaquero index (P = .05). CONCLUSION: Our results confirmed that arachnoidolysis is an effective and safe treatment for posttraumatic syringomyelia. Because the majority of patients were stabilized, we concluded that surgery should be performed as soon as possible in patients with clearly progressing clinical features.

Management of giant pseudomeningoceles after spinal surgery.

BACKGROUND: Pseudomeningoceles are a rare complication after spinal surgery, and studies on these complex formations are few. METHODS: Between October 2000 and March 2008, 11 patients who developed symptomatic pseudomeningoceles after spinal surgery were recruited. In this retrospective study, we reported our experiences in the management of these complex, symptomatic pseudomeningoceles after spinal surgery. A giant pseudomeningocele was defined as a pseudomeningocele >8 cm in length. We also evaluated the risk factors for the formation of giant pseudomeningoceles. RESULTS: All patients were treated successfully with a combined treatment protocol of open revision surgery for extirpation of the pseudomeningoceles, repair of dural tears, and implantation of a subarachnoid catheter for drainage. Surgery-related complications were not observed. Recurrence of pseudomeningocele was not observed for any patient at a mean follow-up of 16.5 months. This result was confirmed by magnetic resonance imaging. CONCLUSIONS: We conclude that a combined treatment protocol involving open revision surgery for extirpation of pseudomeningoceles, repair of dural tears, and implantation of a subarachnoid catheter for drainage is safe and effective to treat giant pseudomeningoceles.

Oligodendroglioma presenting with intradural spinal metastases: an unusual cause of cauda equina syndrome.

We report a 37-year-old man with a primary intracranial oligodendroglioma presenting later with symptomatic multiple cerebrospinal fluid (CSF) intradural drop spinal metastases. This patient initially presented in 2006 with complex partial seizures. Initial histology demonstrated World Health Organization (WHO) grade 2 oligodendroglioma. The patient had further generalised seizures 7 months after initial tumour resection. MRI at that time confirmed tumour recurrence. The patient underwent a repeat craniotomy. Histology showed anaplastic transformation to a WHO grade 3 oligodendroglioma. About 30 months after his initial presentation, the patient developed a focal neurological deficit in the left leg with associated retention of urine. MRI of the neuraxis demonstrated widespread leptomeningeal metastatic drop deposits within the spinal canal. We discuss the mechanisms involved in tumour dissemination throughout the CSF. We also review the relevant literature regarding this phenomenon.

Vision impairment in tuberculous meningitis: predictors and prognosis.

BACKGROUND: Vision impairment is a devastating complication of tuberculous meningitis. In the present study we evaluated the predictors and prognostic significance of vision impairment in tuberculous meningitis. METHODS: In this study, 101 adult patients with tuberculous meningitis were evaluated for vision status and physical disability and were followed up for 6 months. Contrast enhanced magnetic resonance imaging (MRI) was performed at baseline and 6 months. RESULT: Out of 101 patients, 74 patients had normal vision and 27 patients had low vision or blindness at enrollment. Thirteen patients died during the study period. Out of 88 patients who survived at 6 months, 68 patients had good vision, 11 patients had low vision and 9 patients had blindness. Predictors of vision deterioration were papilledema, cranial nerve palsies, raised cerebrospinal fluid protein (>1g/L), and presence of optochiasmatic arachnoiditis in MRI. Predictors of blindness, at 6 months, were found to be papilledema, vision acuity < or =6/18, cranial nerve palsies, tuberculous meningitis stage II or III, raised cerebrospinal fluid protein (>1g/L), optochiasmatic arachnoiditis, and optochiasmal tuberculoma. At 6 months, 27 patients had death or severe disability. Predictors of death or severe disability at 6 months were vision acuity < or =6/18, cranial nerve deficits, hemiparesis, clinical stage II or III, and presence of infarct in MRI. CONCLUSION: Vision impairment occurred in one-fourth of patients with tuberculous meningitis. Principal causes of vision loss were optochiasmatic arachnoiditis and optochiasmal tuberculoma. Impaired vision predicted death or severe disability.

Pulsatile wall movement of spinal arachnoid cyst deteriorates spinal cord symptoms: report of three cases.

INTRODUCTION: Symptomatic spinal arachnoid cyst is a rare disease and the pathophysiology causing spinal cord symptoms has not been well clarified. PATIENTS AND METHODS: The authors report three symptomatic cases of spinal arachnoid cyst at the thoracic level. These patients, aged from 70 to 73 years, showed progressive gait disturbance for a few months before admission. Phase-contrast cine magnetic resonance imaging demonstrated significant compression at the rostral side of the cyst during the diastolic phase of the cardiac cycle. Intraoperative ultrasonography demonstrated that the maximum expansion of the cyst and compression of the dorsal spinal cord occurred when the cerebrospinal fluid moved rostrally during diastole. All patients showed good improvement of their symptoms after surgical removal of the arachnoid cyst. CONCLUSION: This report proposes the pathophysiology that the pulsatile enlargement of the arachnoid cyst during diastolic cardiac phase can be an important factor for deterioration of spinal cord symptoms.

Postural tremor as a manifestation of spontaneous intracranial hypotension.

Spontaneous intracranial hypotension (SIH) is a syndrome caused by low cerebrospinal fluid (CSF) pressure due to leakage of CSF. Clinically, orthostatic headache, neck pain, nausea, emesis, interscapular pain, diplopia, dizziness, changes in hearing, visual blurring and radicular upper extremity symptoms are most frequently observed. We describe a 57-year-old man with SIH who presented with postural tremor. CSF leakage was revealed by cranial MRI. Lumbar puncture identified low CSF pressure and intrathecal gadolinium enhanced MR cisternography showed diffuse CSF leakage in the thoracolumbar region. The patient underwent epidural blood patching, which resulted in complete resolution of postural tremor within 2 months.

Multiple spinal dural arteriovenous fistulae and deterioration post lumbar puncture.

We report a 73-year-old man presenting with bilateral leg numbness and weakness. Three spinal dural arteriovenous fistulae (SDAVF) were found after clinical deterioration post lumbar puncture (LP). This patient highlights the difficulties in the diagnosis and management of SDAVF, and the risks of LP.

Multiple meningeal cysts affecting the whole craniospinal axis. Case report.

A 61-year-old female presented with multiple meningeal cysts arising along the whole craniospinal axis, manifesting as trigeminal neuralgia, truncal ataxia, and gradually aggravating headache persisting for 2 years. The patient had suspected Sjögren syndrome, but no other contributory medical history such as infection, subarachnoid hemorrhage, trauma, malignancies affecting the central nervous system, or habitual drug use. Cerebral magnetic resonance imaging revealed displaced trigeminal root and midbrain, distorted cerebellar hemisphere, and ventriculomegaly, which were relieved by microsurgical resection of the cyst wall. Histological examination confirmed the diagnosis of arachnoid cysts without concomitant meningeal inflammatory reactions. We thought that the multiple meningeal cysts might have originated from undetected meningitis or undetermined underlying mechanism associated with the autoimmune reactions occurring in the arachnoid membrane covering the central nervous system.