Narrowing Of Aqueduct Research Articles

Cystic transformation of the pineal gland (radiation anatomy and epiphysis cerebri structural variants): a prospective study

INTRODUCTION: Pineal cysts are a common finding on brain MRI, but their which remains unclear. A theory has been put forward that non-occlusive cysts can compress the deep cerebral veins, leading to intracranial hypertension.OBJECTIVE: Тo study the variant MRI appearance of the pineal gland.MATERIALS AND METHODS: 48 volunteers underwent an MRI examination using a 1.5 T Toshiba Exelart Vantage device to assess the presence of MRI signs of central venous hypertension, taking into account the morphological variants of the pineal gland structure, and a category was assigned based on the calculated tectum-splenium-cyst ratio and thalamic coefficient. The mean age of men was 41.27±4.63, of women — 31.5±2.58 years. The study participants were divided into three groups: the 1st group — no pineal cyst, the 2nd group — pineal cyst less than 10 mm, the 3rd group —a cyst larger than 10 mm.RESULTS: Based on the obtained tectum-splenium-cyst ratios and the ADC coefficient, it was found that in the volunteer group with cysts larger than 10 mm, 8 out of 15 people were at increased risk of developing central venous hypertension (categories 3 and 4). Category 4 patients had the narrowest aqueduct (1.1–1.2 mm). In the 2nd group, in persons with a pineal cyst less than 10 mm, there were no signs of aqueductal stenosis or tectal plate compression. In the 3rd group, in persons without a pineal cyst, there were also no signs of aqueductal stenosis or tectal plate compression, however, category 3 was assigned to 8 volunteers, which may be due to other causes of venous outflow impairment.CONCLUSION: A large pineal cysts occur in younger patients, and in the presence of aqueductal narrowing and an increased risk of venous hypertension may cause clinical manifestations such as headaches, dizziness, and sleep disturbances. When patients present with relevant complaints, categorization based on DWI and SSFP is an additional criterion that reflects the degree of impact of the pineal cyst on adjacent structures.

Endodermal cyst in pineal region: Rare location.

Background:Pineal tumors are very uncommon intracranial lesions, and endodermal cysts in this location are extremely rare.Case Description:A 49-year-old right-handed female presented with 3 weeks history of progressive dizziness and imbalance. Imaging studies showed 1.8 cm × 1.7 cm × 1.8 cm pineal lesion with small enhancing mural component displacing ventrally the quadrigeminal plate and narrowing of aqueduct of Sylvius without hydrocephalus. In addition, she was found with small interhemispheric lipoma, and small posterior falx possible meningioma. Cerebrospinal fluid markers obtained by lumbar puncture were all negative. She underwent tumor resection, and final pathology reported endodermal cyst. No new deficits were encountered, and her gait imbalance improved significantly by 3 months follow-up.Conclusions:With evidence of enlargement or symptomatic pineal lesions, surgical consideration is necessary. Among pineal lesions, endodermal cysts are extremely uncommon and although benign pathology, long-term follow-up is advised due to unknown chronic behavior.

Relapsing Dorsal Midbrain Syndrome Following Interventions for Hydrocephalus in Aqueductal Stenosis

Dorsal midbrain syndrome (DMS) is a recognized clinical manifestation of increased intracranial pressure (ICP) associated with ventricular enlargement, especially in shunt malfunction, but the mechanism by which DMS occurs in this setting is unsettled. We report a patient with triventriculomegaly attributed to aqueductal narrowing by a tectal mass who went through 2 cycles of developing and resolving DMS promptly after undergoing interventions that altered the size of the posterior third ventricle and proximal aqueduct but probably did not markedly alter ICP. This case provides additional evidence that DMS in this setting is caused by deformation of the dorsal midbrain region produced by rapid expansion of the posterior third ventricle or proximal aqueduct.

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.

Adult aqueductal stenosis with von recklinghausen's neurofibromatosis

A 28-year-old man with von Recklinghausen's neurofibromatosis was first seen with a spastic-ataxic gait and epileptic seizures of recent onset. Computerized to. mographic scan established the diagnosis of aqueductal stenosis, rarely reported in patients with von Recklinghausen's disease. The value of computerized tomography in the etiological diagnosis of hydrocephalus in von Recklinghausen's disease is emphasized and the pathogenesis of aqueductal narrowing in neurofibromatosis is discussed.

Clinical manifestations of aqueductal stenosis in adults.

The authors review 17 cases of aqueductal stenosis in adults and describe five modes of clinical presentation. The average duration of symptoms was 6 years. Dementia was infrequent. Skull x-ray films frequently demonstrated some degree of cranial enlargement and signs of chronic increased intracranial pressure. Characteristic alterations of the sella included elongation of the anterior wall and flattening, erosion, and anterior displacement of the dorsum. Aqueductal configurations as defined by ventriculography and pneumoencephalography in all cases, and the angiographic findings in seven cases are described. Most of the patients improved substantially after shunt insertion. The clinical findings suggested that aqueductal narrowing and associated hydrocephalus had been present in most of these patients since early life.

Aqueductal stenosis and hydrocephalus after mumps encephalitis.

STENOSIS of the aqueduct of Sylvius is a common cause of human hydrocephalus, occurring most often in infancy but also in childhood and in adult life. In a small proportion of cases, aqueductal narrowing occurs in a genetically determined pattern1 or complicates purulent meningitis and neoplastic disease. In most cases, however, the etiology of the stenosis cannot be determined.Recently, in rodents experimentally infected with human myxoviruses aqueductal stenosis and hydrocephalus were found to develop as delayed sequelae of the acute viral infection.2 Furthermore, by the time these abnormalities became apparent, there was no longer any evidence of infection.3 The . . .

Aqueductal Narrowing, Congenital and Acquired

Introduction Hydrocephalus secondary to narrowing of the Sylvian aqueduct was first reported in 1900 by Bourneville and Noir 1 and Oppenheim. 2 Many authors have described additional cases since then, often speculating whether they were congenital—the result of a developmental anomaly—or acquired. In some cases the narrowing was clearly acquired, as in gummatous 3 or tuberculous 4 occlusions; in others, such as hereditary aqueductal stenosis, the clinical, histologic, and genetic features proved it to be congenital. 5 Aqueductal and forking are entities that are not easily classified, however. Although they have been defined many times, the criteria vary from author to author. How many glial cells and fibers constitute gliosis of the aqueduct is not certain; nor is it clear when division of the main channel is an inborn defect or due to glial partitioning. Different authors fail to agree on which changes are acquired, which congenital. We have