Posterior Reversible Encephalopathy Syndrome Developing after Aggressive Posterior Fossa Tumor Surgery.

Posterior reversible encephalopathy syndrome (PRES) is a rare neurologic disorder, having such common radiological findings as vasogenic edema and white matter changes in watershed areas. The clinic and radiological outcome may not be reversible in 10 to 20% of patients, like in the case of our patient. Here, we discuss the pathogenetic factors that are essential in developing PRES after posterior fossa surgery. A 4-year-old female was admitted to our clinic with a recurrent/residual mass in the posterior fossa. She previously underwent posterior fossa surgery three times (for what was diagnosed as anaplastic astrocytoma through pathohistology) in another center. She was operated thrice in 5 days, and the tumor radically removed. Two days later, after the last surgery, while waking up, our patient developed seizures and altered consciousness. Her neurological condition was severe. Magnetic resonance imaging findings were compatible with those of PRES. Our patient had multiple risk factors for PRES that were as follows: multiple posterior fossa surgeries, anamnesis of chemotherapy and radiotherapy, high-dose steroid use, intracranial pressure changes, and hypertensive attacks due to surgical manipulation. In preventing the development of PRES, we should beware of sudden changes in blood pressure during surgery and meticulously manipulate the brain stem to avoid any disturbance of the central nervous system homeostasis. PRES may transform into real encephalopathy. If the patient has some of these risk factors, PRES would probably develop after surgery.

Measurement of the length of vertebrobasilar arteries: A three-dimensional approach.

Under the assumption that neurovascular compression can be caused by elongation or kinking of the artery, we measured the length of each section of the vertebrobasilar artery, compared the lengths between various age groups, and evaluated the involvement of the arterial sections in brain stem compression in 1000 cases. The lengths of the posterior inferior cerebellar artery (PICA)-union of both vertebral arteries (union), union-anterior inferior cerebellar artery (AICA), AICA-superior cerebellar artery (SCA), and union- superior cerebellar artery were measured using an arterial length measuring tool applied to three-dimensional images. The presence of arterial compression of the brain stem was also evaluated. The mean age of the participants was 66.8 ± 12.9 years, and 44.8% were men. Intraclass correlation coefficients for both inter-rater reliability and intra-rater reliability were high in all sections. The vessel lengths of left AICA-SCA (P < 0.001), left union-SCA (P < 0.0001), left PICA-union (P = 0.03), right AICA-SCA (P = 0.002), right union-SCA (P < 0.0001), and right PICA-union (P = 0.04) increased with age, but each R2 was less than 0.05. Brain stem compression by PICA or vertebral artery was identified in 13.8% of cases. The proportion of the presence of brain stem compression was significantly higher in the cases with arterial elongation than in those without (P = 0.01). Vessel length increased with age, but age had a relatively small impact on the elongation of vertebrobasilar arteries. Brain stem compression might be caused by kinking of the artery rather than arterial elongation.

[Malignant cerebellar infarction: clinical course and surgical treatment]. / Zlokachestvennyi infarkt mozzhechka: klinicheskoe techenie i khirurgicheskoe lechenie.

AIM: To clarify the indications for surgical treatment of malignant cerebellar infarction (CI). MATERIAL AND METHODS: Eighty patients with CI were studied. The malignancy of CI was understood as the development of mass effect in the posterior cranial fossa, accompanied by the decrease in consciousness due to compression of the brain stem and/or the development of occlusive hydrocephalus. The patients were divided into 2 groups. The group of malignant CI included 55 patients (68.75%) (group I), the group of benign CI included 25 patients (31.25%) (group II). Patients of group I were divided into subgroups, one of them underwent surgical treatment (surgical subgroup), and another only conservative (conservative subgroup) treatment. Surgery efficacy criteria were: restoration of consciousness to 15 points according to GCS and/or restoration of the fourth ventricle and the quadrigeminal cistern configurations. Results of treatment were assessed according to the Glasgow outcome scale. RESULTS: Malignant CI occurred more frequently in patients with the volume of ischemia exceeding 20 cm3 (p<0.05) in the first day of the disease. The threshold value of mass effect, which can cause further a malignant CI, was 3 points according to the M. Jauss scale. In the group of patients with malignant CI, surgical treatment reduced the mortality rate from occlusion and dislocation syndrome by 35.8%. The most effective type of intervention was a combination of decompressive trepanation of the posterior cranial fossa and external ventricular drainage. CONCLUSION: In patients with CI with the volume more than 20 cm3 and signs of mass effect in the posterior cranial fossa on the scale of M. Jauss 3 points or more, the malignant course of the disease develops in 67% of cases. These patients require careful monitoring, and, in case of development of malignant CI, surgical treatment is necessary.

Macrovascular Decompression of the Brainstem and Cranial Nerves: Evolution of an Anteromedial Vertebrobasilar Artery Transposition Technique.

BACKGROUND: Tortuous and dolichoectatic vertebrobasilar arteries can impinge on the brainstem and cranial nerves to cause compression syndromes. Transposition techniques are often required to decompress the brainstem with dolichoectatic pathology. We describe our evolution of an anteromedial transposition technique and its efficacy in decompressing the brainstem and relieving symptoms. OBJECTIVE: To present the anteromedial vertebrobasilar artery transposition technique for macrovascular decompression of the brainstem and cranial nerves. METHODS: All patients who underwent vertebrobasilar artery transposition were identified from the prospectively maintained database of the Vascular Neurosurgery service, and their medical records were reviewed retrospectively. The extent of arterial displacement was measured pre- and postoperatively on imaging. RESULTS: Vertebrobasilar arterial transposition and macrovascular decompression was performed in 12 patients. Evolution in technique was characterized by gradual preference for the far-lateral approach, use of a sling technique with muslin wrap, and an anteromedial direction of pull on the vertebrobasilar artery with clip-assisted tethering to the clival dura. With this technique, mean lateral displacement decreased from 6.6 mm in the first half of the series to 3.8 mm in the last half of the series, and mean anterior displacement increased from 0.8 to 2.5 mm, with corresponding increases in satisfaction and relief of symptoms. CONCLUSION: Compressive dolichoectatic pathology directed laterally into cranial nerves and posteriorly into the brainstem can be corrected with anteromedial transposition towards the clivus. Our technique accomplishes this anteromedial transposition from an inferolateral surgical approach through the vagoaccessory triangle, with sling fixation to clival dura using aneurysm clips.

Important casual association of carotid body and glossopharyngeal nerve and lung following experimental subarachnoid hemorrhage in rabbits. First report.

OBJECT: The glossopharyngeal nerves (GPNs) and carotid bodies (CBs) have an important role in the continuation of the cerebral autoregulation and cardiorespiratory functions. The relationship between degenerative injury of CB and the GPN in subarachnoid hemorrhage (SAH) was studied. METHODS: Twenty rabbits were included in this study. Five of them (n=5) were used as control group. The remaining animals (n=15) were exposed to experimental SAH. In the six animals of the SAH group, severe signs of illness were observed, and these six animals were killed in the first week after SAH. Others animals (n=9) were followed for 20 days and then sacrificed. GPNs and CBs were examined and, the live and degenerated GPN axon number, and of CB neuron numbers were stereologically estimated. RESULTS: The mean number of live neurons in CBs was 4206.67±148.35 and live axons of GPNs were 1211.66±14.29 in the animals of the control group. The number of degenerated neurons of CBs was 2065±110.27 and the number of degenerated axons of GPNs was 530.83±43.48 in early killed animals with SAH. The number of degenerated neurons of CBs and the number of degenerated axons of GPNs were found as 1013.89±4184 and 2270.5±134.38 in the living animals with SAH, respectively. CONCLUSIONS: High number of degenerated axons of GPN and neurons of CBs of the early killed animals suggest that the mortality in early SAH might be due to GPNs injury secondary to compression of their axons or supplying vessels by the probably herniated brainstem, and secondary denervation injury of CBs, and lung.