Arachnoid bands and venous compression as rare causes of hemifacial spasm: analysis of etiology in 353 patients.

BACKGROUND: Hemifacial spasm is usually caused by arterial compression at the root exit zone of the facial nerve. However, other etiologies have been reported. The aim of this study was to analyze the frequency of other causes of hemifacial spasm. METHODS: Our prospectively maintained hemifacial spasm database containing all patients who underwent microvascular decompression (MVD) for hemifacial spasm from 2002 to 2018 was reviewed. All offending structures were identified and recorded by the surgeon at the time of surgery. Additionally, the operative videos were analyzed retrospectively. RESULTS: MVD was performed in 353 patients. Arterial compression was the main cause of hemifacial spasm in 341 (96.9%) patients. Combined venous-arterial compression was seen in 7 (2.0%) patients. In one patient, the compression was from a large vein. In two patients, no compression was found. One patient who suffered from Bell's palsy many years previously had severe synkinesis and the other had facial tics. In two patients, the spasm was caused due to strangulation of the facial nerve by arachnoid bands. Long-term follow-up of more than 18 months was available in 249 patients with total resolution or near total resolution of spasms in 89.96% of patients. CONCLUSIONS: In most patients with hemifacial spasm, arterial vessels are involved in compressing the facial nerve. Purely venous compression is rarely encountered. We report for the very first time arachnoid bands strangulating the nerve as a cause for hemifacial spasm without involvement of any vessel.

The value of lateral spread response monitoring in predicting the clinical outcome after microvascular decompression in hemifacial spasm: a prospective study on 100 patients.

Microvascular decompression represents an effective treatment for hemifacial spasm. The use of lateral spread response (LSR) monitoring remains a useful intraoperative tool to ensure adequate decompression of the facial nerve. The aim of this study was to assess the value of LSRs intraoperative monitoring as a prognostic indicator for the outcome of microvascular decompression in hemifacial spasm. Our study included 100 patients prospectively. The patients were classified into four groups whether LSRs were totally, partially, not relieved, or not detected from the start. According to clinical outcome, the patients were classified into four groups depending on the clinical course after surgery and the residual symptoms if any. Then, correlations were made between LSR events and treatment outcome to detect its reliability as a prognostic indicator. LSRs were relieved totally in 56 % of the patients, partially relieved in 14 %, not relieved in 10 %, and were not detected in 20 % of the patients from the start. HFS was relieved directly after operation in 62 % with clinical improvement of 90-100 %. Thirty-one percent described 50-90 % improvement over the next 3 months after surgery. Almost all of these 31 % (28 out of 31 patients) reported further clinical improvement of 90-100 % within 1 year after surgery. Three percent suffered from a relapse after a HFS-free period, and 4 % reported minimal or no improvement describing 0-50 % of the preoperative state. The percentage of the satisfied patients with the clinical outcome who reported after 1 year a clinical improvement of 90-100 % was 90 %. Statistical analysis did not find a significant correlation between the relief of LSRs and clinical outcome. LSRs may only represent an intraoperative tool to guide for an adequate decompression but failed to represent a reliable prognostic indicator for treatment outcome.

Prevalence of hypopituitarism after intracranial operations not directly associated with the pituitary gland.

BACKGROUND: Over the last few years, awareness and detection rates of hypopituitarism following traumatic brain injury (TBI) and subarachnoid hemorrhage (SAH) has steadily increased. Moreover, recent studies have found that a clinically relevant number of patients develop pituitary insufficiency after intracranial operations and radiation treatment for non-pituitary tumors. But, in a substantial portion of more than 40%, the hypopituitarism already exists before surgery. We sought to determine the frequency, pattern, and severity of endocrine disturbances using basal and advanced dynamic pituitary testing following non-pituitary intracranial procedures. METHODS: 51 patients (29 women, 22 men) with a mean age of 55 years (range of 20 to 75 years) underwent prospective evaluation of basal parameters and pituitary function testing (combined growth hormone releasing hormone (GHRH)/arginine test, insulin tolerance test (ITT), low dose adrenocorticotropic hormone (ACTH) test), performed 5 to 168 months (median 47.2 months) after intracranial operation (4 patients had additional radiation and 2 patients received additional radiation combined with chemotherapy). RESULTS: We discovered an overall rate of hypopituitarism with distinct magnitude in 64.7% (solitary in 45.1%, multiple in 19.6%, complete in 0%). Adrenocorticotropic hormone insufficiency was found in 51.0% (partial in 41.2%, complete in 9.8%) and growth hormone deficiency (GHD) occurred in 31.4% (partial in 25.5%, severe in 5.9%). Thyrotropic hormone deficiency was not identified. The frequency of hypogonadism was 9.1% in men. Pituitary deficits were associated with operations both in close proximity to the sella turcica and more distant regions (p = 0.91). Age (p = 0.76) and gender (p = 0.24) did not significantly differ across patients with versus those without hormonal deficiencies. Groups did not significantly differ across pathology and operation type (p = 0.07). CONCLUSION: Hypopituitarism occurs more frequently than expected in patients who have undergone neurosurgical intracranial procedures for conditions other then pituitary tumors or may already exists in a neurosurgical population before surgery. Pituitary function testing and adequate substitution may be warranted for neurosurgical patients with intracranial pathologies at least if unexplained symptoms like fatigue, weakness, altered mental activity, and decreased exercise tolerance are present.

Blunt craniocervical artery injury in cervical spine lesions: the value of CT angiography.

OBJECTIVE: The awareness of traumatic craniocervical artery injuries has increased over the last years, and the detection rate varies in published trauma series. These injuries are often associated with cervical spinal and cranial trauma. The purpose of this prospective study was to determine the frequency and injury characteristics of blunt traumatic cervical artery injuries in patients suffering from cervical spine injuries by using a standardized CT angiography (CTA) protocol of the craniocervical vessels. METHODS: Over a period of 32 months (February 2006 to September 2008), we prospectively evaluated 53 patients with osseous cervical spine injuries. Of these, 41 patients were screened for blunt craniocervical vessel injuries using CT angiography in 718 consecutive patients requiring a whole-body trauma CT due to the mechanism of their injury and injury patterns. All examinations were performed using a 16-row multi-slice computed tomography (Sensation 16, Siemens, Erlangen, Germany). Initially, a scan of the neurocranium angulated in orbito-meatal orientation was acquired. Then, a CT angiography of the craniocervical vessels with 40 ml of iodinated contrast agent (flow 4 ml/s; 40 ml saline flush, flow 4 ml/s) was performed starting at the level of Th2 up to the roof of the lateral ventricles. The scan was started using bolus tracking. Finally, a contrast-enhanced spiral thoraco-abdominal scan was performed with a delay of 20 s after administering a second contrast bolus of 60 ml. Besides, 11 patients with already detected isolated cervical spine injury, who were not initially involved in the whole-body trauma imaging protocol, underwent a secondary CT angiography with 60 ml of contrast agent (flow 4 ml/s; 40 ml saline flush, flow 4 ml/s), starting at the level of Th2 up to the roof of the lateral ventricles. The craniocervical vessels were analyzed in the source images, with the use of maximum-intensity projections and curved multi-planar reconstructions. Alternatively, a duplex ultrasound (DUS) was performed in one patient with respect to pregnancy. RESULTS: CTA was considered adequate for diagnosis in all but one case due to reduced CTA imaging quality. In one patient, DUS instead of CTA was performed with respect to pregnancy. We detected isolated osseous cervical spine injury in 53 consecutive patients. Of these patients, 18.9% suffered from vertebral artery injuries (VAI) (14 VAI in 10 patients). Carotid artery injuries were not detected in these patients. In five (50%) patients, we observed cerebral infarction due to VAI. CONCLUSION: Craniocervical vessel injury is a life-threatening and underdiagnosed event in cases of cervical spine injury. CTA of the craniocervical vessels offers a fast, safe, and feasible method for detecting vascular injuries of the craniocervical region and allows prompt further treatment if necessary to reduce the risk of cerebral infarction. CTA of the craniocervical vessels is strongly indicated in cases of cervical spine trauma and in trauma mechanisms involving the cervical spine. Our data underscore the need for screening of blunt carotid and vertebral injury especially in injured cervical spine.

Nerve Compression Syndromes in the Posterior Cranial Fossa.

BACKGROUND: Nerve compression syndromes in the posterior cranial fossa can severely impair patients' quality of life. There is often uncertainty about the best treatment. In this article, we provide an overview of these conditions and the corresponding treatment strategies. METHODS: This review is based on pertinent publications retrieved by a selective search in PubMed and on a scientific analysis of the authors' patient collective. RESULTS: These syndromes are caused by compression of a cranial nerve by an artery or vein at the zone of the nerve's entry to or exit from the brainstem. The best-known neurovascular compression syndrome is trigeminal neuralgia, followed by hemifacial spasm. Less well known are glossopharyngeal neuralgia, nervus intermedius neuralgia, and vestibular paroxysmia. The initial treatment of trigeminal neuralgia is medical: the first line of treatment is with sodium-blocking anticon- vulsants, such as carbamazepine. For patients with hemifacial spasm, botulinum toxin injection is the recommended initial treatment and often leads to a satisfactory regression of the spasms. If these treatments fail, a microvascular decompression operation is indicated. The aim of the procedure is to separate the irritating vessel from the nerve and to keep these structures apart permanently. There is hardly any available evidence on these treatment strategies from randomized controlled trials. CONCLUSION: Nerve compression syndromes in the posterior cranial fossa can generally be treated nonsurgically at first. Over the course of the condition, however, treatment failure or intolerable side effects may arise. In such cases, a microvascu- lar decompression operation is indicated. This is a causally directed form of treat- ment that generally yields very good results.

Endoscope-Assisted Microvascular Decompression for the Management of Hemifacial Spasm Caused by Vertebrobasilar Dolichoectasia.

OBJECTIVE: Vertebrobasilar dolichoectasia (VBD) is a rare cause of hemifacial spasm. The ectatic vessel hinders microscopic visualization of the root exit zone. The aim of this study was to evaluate the benefit of endoscopic visualization during microvascular decompression (MVD) in managing this type of neurovascular compression. METHODS: Retrospective evaluation of patients with VBD treated by endoscope-assisted MVD for hemifacial spasm between 2007 and 2016 was performed. A prospectively maintained database of all patients treated by MVD for hemifacial spasm was screened for vascular compression. Magnetic resonance imaging was evaluated to detect patients who had VBD according to defined criteria. The value of endoscopic inspection to detect offending vessels was analyzed, and clinical outcome was evaluated. RESULTS: VBD was detected in 11 of 290 patients (incidence 3.8%). In these patients, 12 MVD procedures were performed. The endoscope was useful in identifying the offending vessels and adjacent perforators without any brain retraction in all patients. At last clinical follow-up, all patients had almost complete to complete resolution of clinical symptoms. The interposing technique alone was effective with excellent results in 8 patients. Three patients required an additional transposition-fixation technique to achieve sufficient decompression. CONCLUSIONS: VBD is a rare cause of hemifacial spasm. Because of the large diameter of the offending vessel, MVD is technically more demanding. Endoscopic inspection with a 45° endoscope enables accurate visualization of the root exit zone, offending vessels, and perforating arteries. Furthermore, accurate placement of the Teflon pledgets can be confirmed leading to a favorable outcome.

Voriconazole as mono-therapy in orbitofrontal erosive aspergillosis without gross total resection: A case report and review of literature.

In this case report we present an immunocompetent 64-year-old patient presenting with an orbitofrontal invasive aspergillosis treated successfully with voriconazole monotherapy following biopsy and orbital decompression.

Microvascular Decompression for Patients With Hemifacial Spasm Associated With Common Trunk Anomaly of the Cerebellar Arteries-Case Study and Review of Literature.

BACKGROUND: Few previous studies have described the origin of both anterior and posterior inferior cerebellar arteries from one vessel as a common trunk anomaly. No previous studies have clearly described the aforementioned anomaly depending on intraoperative endoscopic visualization. OBJECTIVE: To evaluate the association of a common trunk anomaly with hemifacial spasm, which makes microvascular decompression more challenging. METHODS: All patients with common trunk anomaly associated with hemifacial spasm who received surgical treatment between 2006 and 2015 in our institution were identified in our prospectively collected database. Detection of the common trunk anomaly was performed using the intraoperative high-definition endoscopic inspection and confirmed by a retrospective review of the obtained operative videos. RESULTS: Out of 248 cases of hemifacial spasm, 21 cases with a common trunk anomaly were detected, with an incidence rate of 8.5%. In 6 cases, the spasm was caused by more than 1 offending vessel "complex compression." In 19 cases, total recovery occurred on follow-up, while in 1 case, 90% recovery occurred. One patient was spasm-free immediately after surgery, but died 3 wk after operation from herpes encephalitis. CONCLUSION: Common trunk anomaly in hemifacial spasm is rare. The surgical technique is mostly identical to decompression with normally arising vessels. However, in case of a bifurcation situated close to the compression site where the offending vessel cannot be transposed freely, an extensive cushioning along the trunk and the offending vessels with teflon pledgets should be performed. The presence of a common trunk anomaly does not affect the surgical results.

Cerivastatin reduces cytokine-induced surface expression of ICAM-1 via increased shedding in human endothelial cells.

Activation of endothelial cells is an incipient process in atherogenesis and leads to induction of the cellular adhesion molecules ICAM-1 and VCAM-1. Their expression can be induced by cytokines as well as other inflammatory mediators. The effects of HMG-CoA reductase inhibitors (statins) include mediation of anti-inflammatory properties. The aim of this study was the comparison of cerivastatin and simvastatin-mediated effects on inflammation-induced ICAM-1 and VCAM-1 expression in human umbilical venous endothelial cells (HUVEC). In HUVEC, TNF-alpha induced ICAM-1 and VCAM-1 mRNA and surface expression. Co-incubation with cerivastatin, but not simvastatin reduced TNF-alpha-induced up-regulation of ICAM-1 surface expression whereas both statins reduced VCAM-1 surface expression; all reductions in surface expression correlated with an increase in the soluble forms of ICAM-1 and VCAM-1 in cell culture supernatants. Mevalonate and nonsteroidal isoprenoids significantly reversed protein expression and shedding. Both statins caused an aggravation of TNF-alpha-induced ICAM-1 and VCAM-1 mRNA expression which was dependent on RNA synthesis. The statin-mediated increase in ICAM-1 and VCAM-1 mRNA expression correlated with the degradation of IkappaBa. Nuclear translocation of p65 was not significantly affected by statin-treatment of cytokine-treated cells. We conclude that cerivastatin and simvastatin reduce TNF-alpha-induced up-regulation of ICAM-1 and VCAM-1 surface expression via increased protein shedding mediated by HMG-CoA reductase inhibition and subsequent isoprenoid depletion.

A New Score to Predict the Risk of Hearing Impairment After Microvascular Decompression for Hemifacial Spasm.

BACKGROUND: Intraoperative monitoring of brainstem auditory evoked potentials (BAEPs) has been implemented to reduce the risk of hearing impairment during microvascular decompression for hemifacial spasm. OBJECTIVE: To evaluate intraoperative monitoring of BAEPs during microvascular decompression in patients with hemifacial spasm for predicting the risk of hearing impairment after surgery. METHODS: This prospective study included 100 patients. BAEPs were recorded for all patients. We established a scoring system for the changes in wave I amplitude, I-III interpeak latency, and wave V amplitude and latency. For each change, total points were calculated, and a score out of 6 was assigned to every patient. We classified the patients based on the points scored into 3 risk groups: low-risk (0-3), medium-risk (4-5), and high-risk (6). Further, the correlation between the score and the hearing outcome was evaluated to detect the incidence and degree of hearing impairment. RESULTS: Eighty-seven patients scored 0 to 3, 10 scored 4 to 5, and 3 scored 6. The degree of hearing impairment was proportionate to the score recorded at the end of surgery, and patients in the low-risk group showed no impairment; medium-risk group, deterioration of maximum 2 grades according to World Health Organization classification of hearing impairment; and high-risk group, deterioration of 3 to 4 grades. CONCLUSION: Intraoperative monitoring of BAEPs evaluated through our scoring system was valuable in predicting hearing impairment after surgery.

3-Tesla Kinematic MRI of the Cervical Spine for Evaluation of Adjacent Level Disease After Monosegmental Anterior Cervical Discectomy and Arthroplasty: Results of 2-Year Follow-Up.

STUDY DESIGN: We prospectively evaluated adjacent disc levels after anterior cervical discectomy and arthroplasty (ACDA) using kinematic magnetic resonance imaging (MRI) and plain functional radiographs. OBJECTIVE: ACDA is an established treatment for degenerative cervical disc disease. The objective of this study was to evaluate the use of kinematic MRI for assessing the range of motion (ROM) before and after ACDA compared with plain functional radiographs and to evaluate adjacent degenerative disc disease (aDDD) at mid-term follow-up. SUMMARY OF BACKGROUND DATA: Twenty patients (12 females, 8 males; median age 45.6 ±â€Š6.9 yrs) treated by ACDA (BryanDisc; Medtronic, MN) underwent plain functional radiography and kinematic MRI of the cervical spine at 3 T before and 6 and 24 months after surgery. METHODS: A sagittal T2-weighted (T2w) 2D turbo spin echo (TSE) sequence and a 3D T2w dataset with secondary axial reconstruction were acquired. Signal intensity of all nonoperated discs was measured in regions of interest (ROI). Disc heights adjacent to the operated segment were measured. ROM was evaluated and compared with plain functional radiographs. Clinical outcome was evaluated using the visual analog scale (VAS) for head, neck and radicular pain, and the neck disability index (NDI). RESULTS: Mean ROM of the cervical spine on functional plain radiographs was 21.25 ±â€Š8.19°, 22.29 ±â€Š4.82°, and 26.0 ±â€Š6.9° preoperatively and at 6-month and 24-month follow-up, respectively. Mean ROM at MRI was 27.1 ±â€Š6.78°, 29.45 ±â€Š9.51°, and 31.95 ±â€Š9.58°, respectively. There was a good correlation between both techniques. Follow-up examinations demonstrated no signs of progressive degenerative disc disease of adjacent levels. All patients had clinical improvement up to 24 months after surgery. CONCLUSION: After ACDA, kinematic MRI allows evaluation of the ROM with excellent correlation to plain functional radiographs. Mid-term follow-up after ACDA is without evidence of progressive DDD of adjacent segments. LEVEL OF EVIDENCE: 3.

Is it safe to sacrifice the superior hypophyseal artery in aneurysm clipping? A report of two cases.

Clipping of paraclinoid internal carotid artery aneurysms related to the superior hypophyseal artery (SHA) carries risk of occlusion of this artery when originating distal to the neck of the aneurysm. Sometimes it is inevitable to sacrifice the artery to achieve total aneurysm occlusion. Otherwise a residual aneurysm would remain, which may lead to aneurysm regrowth and subsequent rupture. However, consequences of SHA sacrifice are rarely reported in the literature. In the two presented cases, the SHA was found originating distal to the neck and within the wall of the aneurysm, making the optimal clipping of the aneurysm at the neck unfeasible without trapping of the SHA. Intraoperative indocyanine green (ICG) angiography revealed a retrograde blood flow in the SHA distal to the clip in both patients, indicating some collateral circulation. No endocrinologic deficits were encountered after surgery. The vision was not affected in one patient. In the other patient, bilateral visual field defects occurred, which improved partially in the follow-up 2 months after surgery. The consequences of SHA occlusion are difficult to predict. A large variety of anatomical variations of the vascular anatomy exists. Intraoperative ICG angiography may help to estimate collateral blood flow but is not able to predict visual decline. Although final conclusions cannot be drawn from two patients, it seems that in case of multiplicity of superior hypophyseal complex, sacrifice of one even larger branch is safe. However, visual sequelae have to be taken into consideration when a single SHA has to be sacrificed for total aneurysm clipping.

Hemifacial spasm: conservative and surgical treatment options.

BACKGROUND: Hemifacial spasm is a neuromuscular movement disorder characterized by brief or persistent involuntary contractions of the muscles innervated by the facial nerve. Its prevalence has been estimated at 11 cases per 100 000 individuals. Among the patients who were operated on by our team, the mean interval from diagnosis to surgery was 8.2 years, and more than half of them learned of the possibility of surgical treatment only through a personal search for information on the condition. These facts motivated us to write this article to raise the awareness of hemifacial spasm and its neurosurgical treatment among physicians who will encounter it. METHODS: This review article is based on a selective literature search and on our own clinical experience. RESULTS: Hemifacial spasm is usually caused by an artery compressing the facial nerve at the root exit zone of the brainstem. 85-95% of patients obtain moderate or marked relief from local injections of botulinum toxin (BTX), which must be repeated every 3 to 4 months. Alternatively, microvascular decompression has a success rate of about 85%. CONCLUSION: Local botulinum-toxin injection is a safe and well-tolerated symptomatic treatment for hemifacial spasm. In the long term, however, lasting relief can only be achieved by microvascular decompression, a microsurgical intervention with a relatively low risk and a high success rate.

Sudden intraaqueductal dislocation of a third ventricle ependymoma causing acute decompensation of hydrocephalus.

The authors report an unusual sudden intraaqueductal dislocation of a third ventricle ependymoma causing acute loss of consciousness, and they detail its neuroendoscopic treatment. This case is unique and has never been described in the literature before. The patient suffered from headache and recurrent nausea. Admission MR images revealed a contrast-enhancing lesion within the posterior part of the third ventricle. During the course of the day of admission, the patient suddenly became comatose. Emergency MR imaging demonstrated a deeply intraaqueductal dislocation of the pedicled tumor, with complete obstruction of the aqueduct and ventricular dilation. Immediate surgical intervention with endoscopic third ventriculostomy and complete tumor removal was performed. After surgery, the patient made a rapid recovery. In this case, the authors presume a sudden intraaqueductal dislocation of the ependymoma caused by aspiration of the tumor as a result of the caudal CSF flow.