Compression Of Cranial Nerves Research Articles

Clinical Features and Management of Skull Base Fractures in the Pediatric Population: A Systematic Review.

Pediatric basilar skull fractures (BSFs) are a rare type of traumatic head injury that can cause debilitating complications without prompt treatment. Here, we sought to review the literature and characterize the clinical features, management, and outcomes of pediatric BSFs. We identified 21 relevant studies, excluding reviews, meta-analyses, and non-English articles. The incidence of pediatric BSFs ranged from 0.0001% to 7.3%, with falls from multi-level heights and traffic accidents being the primary causes (9/21). The median presentation age ranged from 3.2 to 12.8 years, and the mean age of patients across all studies was 8.68 years. Up to 55% of pediatric BSFs presented with intracranial hematoma/hemorrhage, along with pneumocephalus and edema. Cranial nerve palsies were a common complication (9/21), with the facial nerve injured most frequently (7/21). While delayed cranial nerve palsy was reported in a few studies (4/21), most resolved within three months post-admission. Other complications included CSF leaks (10/21) and meningitis (4/21). Management included IV fluids, antiemetics, and surgery (8/21) to treat the fracture directly, address a CSF leak, or achieve cranial nerve compression. Despite their rarity, pediatric skull base fractures are associated with clinical complications, including CSF leaks and cranial nerve palsies. Given that some of these complications may be delayed, patient education is critical.

A case of vertebrobasilar dolichoectasia manifesting as sudden sensorineural hearing loss with vertigo

Vertebrobasilar dolichoectasia (VBD) is a rare vascular condition characterized by the elongation, widening, and tortuosity of the vertebrobasilar artery. It can lead to various symptoms due to compression of cranial nerves and brainstem structures. We report a rare case of VBD presenting as sudden sensorineural hearing loss (SSNHL) with vertigo and spontaneous downbeat nystagmus in a 65-year-old woman with a history of hypertension. Magnetic resonance imaging revealed a tortuous and dilated right vertebrobasilar artery compressing the brainstem and left 8th cranial nerve root entry zone, without signs of acute cerebellar stroke. The compression of the anterior inferior cerebellar artery and cervicomedullary junction was also noted, suggesting a vascular cause for her symptoms. Following high-dose steroid treatment, the patient showed significant hearing improvement. This case underscores the importance of considering VBD in patients with unexplained SSNHL and vertigo, highlighting the role of detailed vascular imaging in the diagnosis and management of such cases.

A Comprehensive Guide to Paget’s Disease of Bone

PDB is a long-standing pathological stateillustrated by aberrant bone remodeling and metabolism arising in structural anomalies of the bone tissue. While this disease may remain asymptomatic, mild symptoms such as joint and bone discomfort may be present. However, an early warning sign is intense nocturnal bone pain. Moreover, PDB may result in complications such as deafness, fractures, compression of cranial nerves or the spinal cord, and hydrocephalus. This disease is more frequently observed in individuals above the age of 50, affecting individuals of all races and ethnicities, with a slightly higher prevalence in males. Diagnosis of PDB involves comprehensive clinical assessment, patient history, and specialized tests. Pharmacological treatments such as bisphosphonates, calcitonin, and surgical intervention may be employed to manage the disease. Supplementation is essential to prevent hypocalcemia. PDB may lead to rare complications, including sarcomatous conversion of the pagetic lesion and high-output congestive heart failure which concerns healthcare professionals.

Neurovascular Compression-Induced Intracranial Allodynia May Be the True Nature of Migraine Headache: an Interpretative Review.

Surgical deactivation of migraine trigger sites by extracranial neurovascular decompression has produced encouraging results and challenged previous understanding of primary headaches. However, there is a lack of in-depth discussions on the pathophysiological basis of migraine surgery. This narrative review provides interpretation of relevant literature from the perspective of compressive neuropathic etiology, pathogenesis, and pathophysiology of migraine. Vasodilation, which can be asymptomatic in healthy subjects, may produce compression of cranial nerves in migraineurs at both extracranial and intracranial entrapment-prone sites. This may be predetermined by inherited and acquired anatomical factors and may include double crush-type lesions. Neurovascular compression can lead to sensitization of the trigeminal pathways and resultant cephalic hypersensitivity. While descending (central) trigeminal activation is possible, symptomatic intracranial sensitization can probably only occur in subjects who develop neurovascular entrapment of cranial nerves, which can explain why migraine does not invariably afflict everyone. Nerve compression-induced focal neuroinflammation and sensitization of any cranial nerve may neurogenically spread to other cranial nerves, which can explain the clinical complexity of migraine. Trigger dose-dependent alternating intensity of sensitization and its synchrony with cyclic central neural activities, including asymmetric nasal vasomotor oscillations, may explain the laterality and phasic nature of migraine pain. Intracranial allodynia, i.e., pain sensation upon non-painful stimulation, may better explain migraine pain than merely nociceptive mechanisms, because migraine cannot be associated with considerable intracranial structural changes and consequent painful stimuli. Understandingmigraine as an intracranial allodynia could stimulate research aimed at elucidating the possible neuropathic compressive etiology of migraine and other primary headaches.

Endovascular treatment of large posttraumatic false aneurysm of the S2 segment of the subclavian artery: clinical case and literature review

Introduction. Pseudoaneurysms of the subclavian artery are a rare pathology and most frequently occur due to trauma. According to the current literature, subclavian artery aneurysms account for 1 % of all peripheral artery aneurysms. This pathology, although rare, may be accompanied by the risk of rupture, thrombosis, or distal embolism of the arterial lumen. Objective. To demonstrate a clinical case of a patient with successful treatment of subclavian artery pseudoaneurysm by means of modern minimally invasive endovascular technique. Material and methods. The article presents our clinical case with the use of endovascular technique for the treatment of large posttraumatic pseudoaneurysm of the S2 segment of the left subclavian artery using the Bard LifeStream balloon stent graft.Discussion. Currently, direct surgery is considered to be the gold standard of treatment in extracranial aneurysms. Meanwhile, availability of minimally invasive methods allows minimizing the risk by performing endovascular treatment and thus reducing the risk of foreign bodies and infectious complications associated with a large volume of surgical intervention in direct surgery, reducing damage to the brachial plexus, decreasing the number of beddays, and contributing to early rehabilitation measures. The strategy of choice in favor of endovascular treatment should be individual for each patient taking into account such factors as localization, aneurysm size, compression of nearby cranial nerves, and concomitant pathology with high risk of open surgical treatment. Conclusions. Careful selection of patients for endovascular technique will ensure good long-term outcome using all advantages of this technique. At present, it is still relevant and crucial to minimize complications and iatrogenic postoperative lesions in patients with this disease. For this reason, endovascular surgeries should be performed at the stage of specialized medical care by an experienced surgeon.Key words: subclavian artery, false aneurysm, posttraumatic aneurysm, stent graft, endovascular treatment, open surgery, minimally invasive surgery.

Abstract PO-099: Short-term outcomes of an extended endoscopic endonasal resection of a clival giant cell tumor with adjuvant RANK-L inhibitor therapy: Case report

Abstract Background Clival giant cell tumors (GiCT) are rare neoplasms that commonly target the epiphysis. Recently, skull base GiCTs have been reported, predominantly in the sphenoid and temporal bones. Although typically benign, GiCTs of the skull-base can cause neurologic deficits due to compression of cranial nerves or intracranial contents. The efficacy of adjuvant chemotherapy in treating GiCTs is not known. One potential treatment option neoplastic mononuclear stromal cells in GiCTs express NF-κB ligands (RANK-L), which can be therapeutically targeted with Denosumab, a monoclonal antibody against RANK-L. Here, we describe the case of a GiCT invasive to the clivus, an extended endoscopic endonasal resection of the tumor, and management of the lesion with Denosumab. Methods A retrospective chart review was performed on the patient of interest. Magnetic resonance imaging (MRI) and computed tomography (CT) scans were used to assess disease growth and response to surgical and therapeutic intervention. Case presentation A previously healthy seventeen-year-old female presented with headaches and numbness of the left V2 and V3. A diagnosis of a clival giant cell tumor was confirmed with strict pathologic, radiographic, and clinical correlation. She was found to have a clival mass extending into the sphenoid sinus. Surgical excision was performed by both the otolaryngology and neurosurgery departments at a single institution. She underwent an extended endoscopic endonasal resection of the clival mass. Following surgery, the numbness on the left V2 and V3 distribution improved. She occasionally reported bilateral V3 distribution symptoms without definite anatomic correlates for right sided complaints. Due to the presence of residual tumor, we recommended adjunctive medical therapy. We performed adjunctive medical therapy with Denosumab, a RANKL inhibitor. Discussion When complete surgical excision with negative margins is not feasible in lesions of the skull base, adjuvant treatment is commonly required to achieve local disease control. Our case demonstrates the efficacy of a combined approach where surgery is used to achieve a histologic diagnosis, decompression and evaluate for respectability. Adjuvant medical therapy using RANKL inhibitors is a promising approach that may be effective to achieve lifelong disease control but requires continued maintenance on therapy. Citation Format: Myra A. Zaheer, Abhisri Ramesh, Aadit P. Mehta, Adriana S. Fonseca, Daniel A. Donoho. Short-term outcomes of an extended endoscopic endonasal resection of a clival giant cell tumor with adjuvant RANK-L inhibitor therapy: Case report [abstract]. In: Proceedings of the AACR-AHNS Head and Neck Cancer Conference: Innovating through Basic, Clinical, and Translational Research; 2023 Jul 7-8; Montreal, QC, Canada. Philadelphia (PA): AACR; Clin Cancer Res 2023;29(18_Suppl):Abstract nr PO-099.

Exposure to the aryl hydrocarbon receptor agonist dioxin disrupts formation of the muscle, nerves, and vasculature in the developing jaw

Human exposure to environmental pollutants can disrupt embryonic development and impact juvenile and adult health outcomes by adversely affecting cell and organ function. Notwithstanding, environmental contamination continues to increase due to industrial development, insufficient regulations, and the mobilization of pollutants as a result of extreme weather events. Dioxins are a class of structurally related persistent organic pollutants that are highly toxic, carcinogenic, and teratogenic. 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is the most potent dioxin compound and has been shown to induce toxic effects in developing organisms by activating the aryl hydrocarbon receptor (AHR), a ligand activated transcription factor targeted by multiple persistent organic pollutants. Contaminant-induced AHR activation results in malformations of the craniofacial cartilages and neurocranium; however, the mechanisms mediating these phenotypes are not well understood. In this study, we utilized the optically transparent zebrafish model to elucidate novel cellular targets and potential transcriptional targets underlying TCDD-induced craniofacial malformations. To this end, we exposed zebrafish embryos at 4 h post fertilization to TCDD and employed a mixed-methods approach utilizing immunohistochemistry staining, transgenic reporter lines, fixed and in vivo confocal imaging, and timelapse microscopy to determine the targets mediating TCDD-induced craniofacial phenotypes. Our data indicate that embryonic TCDD exposure reduced jaw and pharyngeal arch Sox10+ chondrocytes and Tcf21+ pharyngeal mesoderm progenitors. Exposure to TCDD correspondingly led to a reduction in collagen type II deposition in Sox10+ domains. Embryonic TCDD exposure impaired development of tissues derived from or guided by Tcf21+ progenitors, namely: nerves, muscle, and vasculature. Specifically, TCDD exposure disrupted development of the hyoid and mandibular arch muscles, decreased neural innervation of the jaw, resulted in compression of cranial nerves V and VII, and led to jaw vasculature malformations. Collectively, these findings reveal novel structural targets and potential transcriptional targets of TCDD-induced toxicity, showcasing how contaminant exposures lead to congenital craniofacial malformations.

Rochen-Duvigneaud syndrome with nasopharyngeal carcinoma

Nasopharyngeal carcinoma is an uncommon head and neck malignancy which can rarely present with cranial nerve palsies. Here we report a case of nasopharyngeal mass which presented initially with ophthalmic complaints due to compression of cranial nerves in superior orbital fissure resulting in Rochen-Duvigneaud syndrome. It was histologically proven as non keratinising differentiated type of Nasopharyngeal carcinoma

Association Between Serum Homocysteine Concentration, Aneurysm Wall Inflammation, and Aneurysm Symptoms in Intracranial Fusiform Aneurysm

The pathophysiology of fusiform intracranial aneurysm (FIA) involves inflammatory processes, and homocysteine plays a role in the inflammatory processes in the vessel wall. Moreover, aneurysm wall enhancement (AWE) has emerged as a new imaging biomarker of aneurysm wall inflammatory pathologies. To investigate the pathophysiological mechanisms of aneurysm wall inflammation and FIA instability, we aimed to determine the associations between the homocysteine concentration, AWE, and FIAs' related symptoms. We retrospectively reviewed the data of 53 patients with FIA who underwent both high-resolution magnetic resonance imaging and serum homocysteine concentration measurement. FIAs' related symptoms were defined as ischemic stroke or transient ischemic attack, cranial nerve compression, brainstem compression, and acute headache. The contrast ratio of the signal intensity of the aneurysm wall to the pituitary stalk (CRstalk) was used to indicate AWE. Multivariate logistic regression and receiver operating characteristic (ROC) curve analyses were performed to determine how well the independent factors could predict FIAs' related symptoms. Predictors of CRstalk were also investigated. Spearman's correlation coefficient was used to identify the potential associations between these predictors. Fifty-three patients were included, of whom 23 (43.4%) presented with FIAs' related symptoms. After adjusting for baseline differences in the multivariate logistic regression analysis, the CRstalk (odds ratio [OR]=3.207, P=.023) and homocysteine concentration (OR=1.344, P=.015) independently predicted FIAs' related symptoms. The CRstalk was able to differentiate between FIAs with and without symptoms (area under the ROC curve [AUC]=0.805), with an optimal cutoff value of 0.76. The homocysteine concentration could also differentiate between FIAs with and without symptoms (AUC=0.788), with an optimal cutoff value of 13.13. The combination of the CRstalk and homocysteine concentration had a better ability to identify symptomatic FIAs (AUC=0.857). Male sex (OR=0.536, P=.018), FIAs' related symptoms (OR=1.292, P=.038), and homocysteine concentration (OR=1.254, P=.045) independently predicted the CRstalk. A higher serum homocysteine concentration and greater AWE indicate FIA instability. Serum homocysteine concentration may be a useful biomarker of FIA instability; however, this needs to be verified in future studies.

Menière's Syndrome Associated With Fibrous Dysplasia of the Temporal Bone.

Menière's Syndrome Associated With Fibrous Dysplasia of the Temporal Bone.

Vestibulo-Cochlear Symptoms Revealing Vertebro-Basilar Dolicho-Ectasia

Introduction: Vertebrobasilar dolichoectasia (VBD) are uncommon arteriopathies defined by increased length and caliber of one or more intracranial arteries. The clinical picture is polymorphic. They are most often associated with ischemic or hemorrhagic stroke, but this pathology can also cause symptoms of cranial nerve compression. Objective: We report the case of a vertebro-basilar dolichoectasia collected in the radiology department of Ibn Tofail Hospital in Marrakech, revealed by vestibulo-cochlear symptoms and diagnosed by brain MRI. In the light of this observation, we review this uncommon pathology and the contribution of magnetic resonance imaging in its diagnosis. Case report: The patient was 68 years old and had a history of severe sleep apnea syndrome. He presented with rotatory vertigo, tinnitus and hypoacusis on the left side of the head for 3 months. The neurological examination was normal and the examination of the ENT sphere revealed bilateral sensorineural hearing loss and left hyporeflexia. A cerebral MRI was performed as part of the etiological workup, which revealed elongation and dilation of the vertebral arteries measuring 3.9 mm on the left and 5.2 mm on the right, with loops of which the left crossed the homolateral cochleovestibular nerve 7 mm from its emergence, responsible for a deviation of its path, and the glossopharyngeal nerve 4 mm from its emergence. It also showed an elongation and dilatation of the basilar trunk measuring 6.8 mm, presenting a loop lateralized to the left at the level of its origin (Smoker's Grade 2) with a bifurcation opposite the floor of the V3 (Smoker's Grade 2).Thus, the diagnosis of a DEVB responsible for a vascular-nervous conflict was retained. The indication for surgical management was given but was refused by the patient due to the deep location of the arteriopathy. Discussion and conclusion: DEVB is a rare and progressive condition with cranial nerve compression as a possible complication. Brain MRI is...

Acute psychosis as initial presentation for Neurofibromatosis Type 2 (P11-9.006)

<h3>Objective:</h3> To describe the clinical course of a pediatric patient presenting with acute auditory hallucinations with workup revealing a new diagnosis of NF2. <h3>Background:</h3> NF2 is an autosomal dominant neurocutaneous disorder characterized by vestibular schwannomas, meningiomas, neurofibromas, gliomas, cerebral calcifications, cataracts, and cognitive impairment. Acute onset psychosis is an uncommon sequela of NF2, and if present, is usually attributed to the known prior history of NF2. However, here we present a case of acute psychosis that precipitated the <i>initial</i> diagnosis of NF2. <h3>Design/Methods:</h3> NA <h3>Results:</h3> A 13-year-old Hispanic male with no known intracranial tumors or other neurocutaneous stigmata presented with acute-onset psychosis, agitation, delusions, and painless monocular vision loss. Upon further review, he was reported to have a remote history of morning headaches, right upper extremity weakness and paresthesias thought to be due to a trampoline accident, and multiple dermal lesions that were diagnosed as pilonidal cysts despite biopsy and sectioning. He presented with complaints of hearing a constant “airplane sound,” poor sleep, agitation, persecutory delusions and paranoia, pressured speech, and discontinuity of thought. On exam, he was agitated and not oriented to situation, responding rapidly to questions with the incorrect answer, hyperkinetic, and generally distressed and labile. MRI brain with and without contrast demonstrated bilateral enhancing vestibular schwannomas, a meningioma, and nerve sheath tumor, all radiographically diagnostic for NF2. Though he was initially treated empirically for encephalitis with steroids, he improved rapidly upon initiation of antipsychotics; all other workup for the psychosis was unremarkable and a pathogenic variant of NF2 was confirmed. <h3>Conclusions:</h3> It is important to look for stigmata of NF2 in patients with psychosis as bilateral vestibular schwannomas can cause auditory hallucinations secondary to continuous tinnitus. Early identification of NF2 will lead to targeted therapeutic/surgical intervention that may relieve cranial nerve compression and thus reduce the odds of developing psychosis. <b>Disclosure:</b> Dr. Domingue has nothing to disclose. Dr. Sandweiss has nothing to disclose. Dr. Salazar has nothing to disclose. Dr. Gill has received personal compensation in the range of $500-$4,999 for serving as an Expert Witness for Elite Medical Experts. The institution of Dr. Gill has received research support from NIH-NINDS.

Clinical Features of Pituitary or Parasellar Tumor Onset with Cranial Nerve Palsy: Surgical Intervention Considerations

This study aimed to clarify the symptoms of pituitary or parasellar tumor onset with cranial nerve palsy (CNP) and to improve our knowledge of this rare symptom and its most appropriate treatment. Among 1281 patients with pituitary or parasellar tumors surgically treated from 2003 to 2020, 30 cases (2.34%; 15 men and 15 women; mean age: 55.6years, range: 6-83years) first presenting with CNP were reviewed to evaluate the neurological symptoms, histological diagnosis, interval from onset to surgery, and time before complete CNP recovery. Pathological diagnoses comprised 17 pituitary adenomas, including 10 pituitary apoplexies and 4 adrenocorticotropic hormone-positive adenomas, and 13 other tumors, including 3 chordomas, 2 xanthogranulomas, 2 malignant lymphomas, 2 metastatic tumors, 1 Rathke cleft cyst, 1 plasmacytoma, 1 craniopharyngioma, and 1 neuroendocrine carcinoma. The mechanisms causing CNP were pituitary apoplexy (n= 10), cranial nerve compression or involvement (n= 17), and inflammatory changes (n= 9). As the first manifestation, 20 (66.7%) patients presented with oculomotor nerve palsy, 2 (6.7%) with trochlear nerve palsy, and 13 (43.3%) with abducens nerve palsy. Full recovery of CNP was obtained in 25 patients (83.3%) after surgery alone and in 2 patients (6.7%) after adjuvant therapy. Early surgery provided no significant difference in full recovery rates although it reduced the time to reach full recovery. It is critical to determine the mechanisms of CNP and intervene surgically to improve symptoms, shorten the duration of the disorder, prevent relapses, and obtain the correct pathological diagnosis to select the proper adjuvant therapy.

Carbonic anhydrase II deficiency.

Carbonic anhydrase II deficiency (OMIM # 259730), initially called "osteopetrosis with renal tubular acidosis and cerebral calcification syndrome", reveals an important role for the enzyme carbonic anhydrase II (CA II) in osteoclast and renal tubule function. Discovered in 1972 and subsequently given various names, CA II deficiency now describes >100 affected individuals encountered predominantly from the Middle East and Mediterranean region. In 1983, CA II deficiency emerged as the first osteopetrosis (OPT) understood metabolically, and in 1991 the first understood molecularly. CA II deficiency is the paradigm OPT featuring failure of osteoclasts to resorb bone due to inability to acidify their pericellular milieu. The disorder presents late in infancy or early in childhood with fracturing, developmental delay, weakness, short stature, and/or cranial nerve compression and palsy. Mental retardation is common. The skeletal findings may improve by adult life, and CA II deficiency can be associated with a normal life-span. Therefore, it has been considered an "intermediate" type of OPT. In CA II deficiency, OPT is uniquely accompanied by renal tubular acidosis (RTA) of proximal, distal, or combined type featuring hyperchloremic metabolic acidosis, rarely with hypokalemia and paralysis. Cerebral calcification uniquely appears in early childhood. The etiology is bi-allelic loss-of-function mutations of CA2 that encodes CA II. Prenatal diagnosis requires mutational analysis of CA2. Although this enzymopathy reveals how CA II is important for the skeleton and kidney tubule, the pathogenesis of the mental subnormality and cerebral calcification is less well understood. Several mouse models of CA II deficiency have shown growth hormone deficiency, yet currently there is no standard pharmacologic therapy for patients. Treatment of the systemic acidosis is often begun when growth is complete. Although CA II deficiency is an "osteoclast-rich" OPT, and therefore transplantation of healthy osteoclasts can improve the skeletal disease, the RTA and central nervous system difficulties persist.

Nerve blocks for occipital headaches: A systematic review and meta-analysis.

Migraine surgeons have identified six "trigger sites" where cranial nerve compression may trigger a migraine. This study investigates the change in headache severity and frequency following nerve block of the occipital trigger site. This PRISMA-compliant systematic review of five databases searched from database inception through May 2020 is registered under the PROSPERO ID: CRD42020199369. Only randomized controlled trials utilizing injection treatments for headaches with pain or tenderness in the occipital scalp were included. Pain severity was scored from 0 to 10. Headache frequency was reported as days per week. Included were 12 RCTs treating 586 patients of mean ages ranging from 33.7 to 55.8 years. Meta-analyses of pain severity comparing nerve blocks to baseline showed statistically significant reductions of 2.88 points at 5 to 20 min, 3.74 points at 1 to 6 weeks, and 1.07 points at 12 to 24 weeks. Meta-analyses of pain severity of nerve blocks compared with treatment groups of neurolysis, pulsed radiofrequency, and botulinum toxin type A showed similar headache pain severity at 1 to 2 weeks, and inferior improvements compared with the treatment groups after 2 weeks. Meta-analyses of headache frequency showed statistically significant reductions at 1 to 6-week follow-ups as compared with baseline and at 1 to 6 weeks as compared with inactive control injections. The severity and frequency of occipital headaches are reduced following occipital nerve blocks. This improvement is used to predict the success of migraine surgery. Future research should investigate spinous process injections with longer follow-up.

Could recurrent painful ophthalmoplegic neuropathy be caused by a neurovascular conflict?: A case report

Objective: Describe and discuss a typical case with recurrent painful ophthalmoplegic neuropathy (RPON), and demonstrate a likely extrinsic compression of the sixth cranial nerve by a vascular loop. Background: RPON is a rare, but well-known entity, characterized by attacks of ophthalmoplegia associated with ipsilateral headache. The etiology is unknown, but a neurovascular conflict (NVC) has been suggested as a cause. Method: A 62-year-old woman presented in the emergency department with a horizontal diplopia that developed a few hours after the onset of a left temporal headache. In the past she had presented to the clinic with the same problem several times. She had been thoroughly examined, but no cause had been found. The symptoms had resolved by themselves. In addition to a classic finding in RPON, gadolinium enhancement and thickening of a cranial nerve, the new MRI scanning detected an NVC. Herein we discuss the relevance of this finding. Conclusion: A neurovascular conflict causing inflammatory demyelination of a single cranial nerve and relapsing remitting painful ophthalmoplegic neuropathy is an alluring idea. However, it is hard to conceive theoretically, and more reported cases with compelling data are needed to give credibility to such an idea.

Pituitary Neuroendocrine Tumor: Is It Benign or Malignant?

The World Health Organization (WHO) updated the classification of pituitary tumors in 2022. The new classification presents detailed histological subtyping of a pituitary neuroendocrine tumor (PitNET) based on the tumor cell lineage, cell type, and related characteristics. The immunohistochemistry for pituitary transcription factors (PIT1, TPIT, SF1, GATA3, and ERα) is routinely needed in this classification. The controversy regarding the change of behavior code of all PitNET/pituitary adenoma from "0" for benign tumors to "3" for primary malignant tumors is a topic of debate among experts, nowadays. Some authors represent that pituitary adenoma has a tendency for hemorrhage and necrosis and frequent invasion of the cavernous sinus. However, most small PitNET/pituitary adenoma do not need any treatment because of benign biologic behavior or less than 5% recurrence after gross total removal. Pituitary apoplexy is also benign nature but has a tendency of cranial nerve compression or panhypopituitarism. Most of cavernous invasion is compression of the cavernous sinus. Aggressive PitNET/pituitary adenoma with malignant biological behavior is less than 1%.

Extracranial Carotid Artery Aneurysms: 20-Year Experience of Surgical Management

Extracranial carotid artery aneurysm (ECAA) is a rare vascularpathology with reported incidence of 0.2-5.0% of all carotid artery surgical interventions. Most of ECAAs remain clinically asymptomatic, however, they can manifest in neurological symptoms as transient ischemic attack or stroke. The presence of a pulsating formation, swallowing disorders, signs of compression of cranial nerves may beindicative of the aneurysm growth, which is associated with higher risk of thromboembolic complications and less oftenwith rupture. Surgical treatment is a method of choice in symptomatic patients or in cases of the aneurysm growth and includes resection with arterial reconstruction, ligation of the artery or endovascular intervention.&#x0D; The aim. To improve the results of surgical treatment of ECAAs.&#x0D; Materials and methods. The results of clinical examination, laboratory, instrumental, intraoperative observations were analyzed in 39 patients (35 [89.7%] men and 4 [10.3%] women) with 44 ECAAs, who were admitted to the Vascular Surgery Department of Lviv Regional Clinical Hospital for the period from 2003 to 2022. To conϐirm the diagnosis of ECAA, preoperative instrumental examination included duplex ultrasonography and multispiral computed tomography angiography.&#x0D; Results. Etiological causes of ECAAs included: atherosclerosis (79.5%),ϐibromuscular dysplasia (7.7%), trauma (5.1%), previous operations in the neck region (5.1%) and infection (2.6%). The justiϐication of the choice of surgical tactics depended on the localization of aneurysm, concomitant carotid occlusive disease or pathological deviation of carotid arteries. Early results of surgical treatment were evaluated up to 30 days of the postoperative period. The postoperative complications included: transient ischemic attack in 1 (2.6%), ischemic stroke in 2 (5.1%), cranial nerve damages in 4 (10.3%), thrombosis of arterial reconstruction in 2 (5.1%), hematoma of postoperative wound in 4 (10.3%), infection of postoperative wound in 1 (2.6%) cases. Postoperative mortality was 2.6%.&#x0D; Conclusion. ECAA is a rare clinical disease that requires an active surgical approach to reduce the risk of ischemic stroke. Reconstructive surgery of ECAAs is a highly effective method of treatment that allows to achieve satisfactory results and prevent the development of severe complications.

Intracranial aneurysms in pediatric population treated with flow diverters: A single-center experience.

Pediatric intracranial aneurysms (PIAs) are uncommon. Flow diverters (FDs) have shown to be effective on treatment of selected aneurysms. We describe 10 cases of PIAs treated with FDs at one medical center in Mexico, from April 2015 to April 2020. Out of 230 patients treated with FDs, 10 (4.3%) were pediatric. Average age was 9.4 years old (R: 6-15). Two patients (20%) had subarachnoid hemorrhage, 3 had epilepsy (30%), 3 (30%) had clinical signs of cranial nerve compression, and 4 (40%) had only headache. Two patients were in 1a grade of Hunt and Kosnik scale. Out of the nonruptured aneurysms, 7 (70%) were in 15 points of Glasgow Coma Scale and 1 patient (10%) was in 13 points. Treatment was performed without complications; nevertheless, appropriate distal deployment was not achieved in one case. At discharge, nine patients had 5 points of Glasgow Outcome Scale. All patients underwent computed tomography angiography or digital subtraction angiography at 1, 3, 6, and 12 months, 2 patients (20%) had a 2-year follow-up, and 3 patients (30%) had a 3-year follow-up. According to Kamran grading scale, 9 patients (90%) were classified as Grade 4 and 1 patient (10%) as Grade 3. Even though it is a small series, as this is an uncommon disease, we may suggest that FDs are useful to treat properly selected PIAs. Our study has consecutive imaging assessment at least a year of follow-up in which aneurysm stable occlusion was observed in 90% of patients.

Spreading of Trigeminal Neuralgia and Hemifacial Spasm to Blepharospasm: What the Role for Neurovascular Compression of the Vth Cranial Nerve?

Blepharospasm (BB) in an involuntary movement disorder characterized by stereotyped, bilateral, and synchronous spasms of the orbicularis oculi (OO) muscles. Spasms may be either brief or sustained and give rise either to narrowing or spasmodic closure of eyelids thus leading to functional blindness [1]. Dystonia of the lower face is frequently associated with BB [2].