Intracranial metastases surgery

Intracranial metastases surgery

see Intracranial metastases surgery indications.

Intracranial Metastases Surgical Technique.


Automated classification of brain metastases and healthy brain tissue is feasible using optical coherence tomography imaging, extracted texture features, and machine learning with principal component analysis (PCA) and support-vector machines (SVM). The established approach can prospectively provide the surgeon with additional information about the tissue, thus optimizing the extent of tumor resection and minimizing the risk of local recurrences 1).

Wolpert et al. defined risk profiles for the development of BM-related epilepsy and derived a score which might help to estimate the risk of post-operative seizures and identify individuals at risk who might benefit from primary prophylactic antiepileptic drug therapy 2).


1)

Möller J, Bartsch A, Lenz M, Tischoff I, Krug R, Welp H, Hofmann MR, Schmieder K, Miller D. Applying machine learning to optical coherence tomography images for automated tissue classification in brain metastases. Int J Comput Assist Radiol Surg. 2021 May 30. doi: 10.1007/s11548-021-02412-2. Epub ahead of print. PMID: 34053010.
2)

Wolpert F, Lareida A, Terziev R, Grossenbacher B, Neidert MC, Roth P, Poryazova R, Imbach L, Le Rhun E, Weller M. Risk factors for the development of epilepsy in patients with brain metastasis. Neuro Oncol. 2019 Sep 10. pii: noz172. doi: 10.1093/neuonc/noz172. [Epub ahead of print] PubMed PMID: 31498867.

Noninvasive intracranial pressure monitoring

Noninvasive intracranial pressure monitoring

Intracranial pressure monitoring is necessary in many neurological and neurosurgical diseases.

There is no established method of noninvasive intracranial pressure (NI-ICP) monitoring that can serve as an alternative to the gold standards of invasive monitoring with external ventricular drainage or intraparenchymal monitoring.

To avoid lumbar puncture or intracranial ICP probes, non-invasive ICP techniques are becoming popular.

In a study a new method of NI-ICP monitoring performed using algorithms to determine ICP based on acoustic properties of the brain was applied in patients undergoing invasive ICP (I-ICP) monitoring, and the results were analyzed.

In patients with traumatic brain injury and subarachnoid hemorrhage who were undergoing treatment in a neurocritical intensive care unit, the authors recorded ICP using the gold standard method of invasive external ventricular drainage or intraparenchymal monitoring. In addition, the authors simultaneously measured the ICP noninvasively with a device (the HS-1000) that uses advanced signal analysis algorithms for acoustic signals propagating through the cranium. To assess the accuracy of the NI-ICP method, data obtained using both I-ICP and NI-ICP monitoring methods were analyzed with MATLAB to determine the statistical significance of the differences between the ICP measurements obtained using NI-ICP and I-ICP monitoring. RESULTS Data were collected in 14 patients, yielding 2543 data points of continuous parallel ICP values in recordings obtained from I-ICP and NI-ICP. Each of the 2 methods yielded the same number of data points. For measurements at the ≥ 17-mm Hg cutoff, which was arbitrarily chosen for this preliminary analysis, the sensitivity and specificity for the NI-ICP monitoring were found to be 0.7541 and 0.8887, respectively. Linear regression analysis indicated that there was a strong positive relationship between the measurements. Differential pressure between NI-ICP and I-ICP was within ± 3 mm Hg in 63% of data-paired readings and within ± 5 mm Hg in 85% of data-paired readings. The receiver operating characteristic-area under the curve analysis revealed that the area under the curve was 0.895, corresponding to the overall performance of NI-ICP monitoring in comparison with I-ICP monitoring.

This study provides the first clinical data on the accuracy of the HS-1000 NI-ICP monitor, which uses advanced signal analysis algorithms to evaluate properties of acoustic signals traveling through the brain in patients undergoing I-ICP monitoring. The findings of this study highlight the capability of this NI-ICP device to accurately measure ICP noninvasively. Further studies should focus on clinical validation for elevated ICP values 1).

Flow velocity signals from transcranial Doppler (TCD) have been used to estimate ICP; however, the relative accuracy of these methods is unclear. This study aimed to compare four previously described TCD-based methods with directly measured ICP in a prospective cohort of traumatic brain-injured patients. Noninvasive ICP (nICP) was obtained using the following methods: 1) a mathematical “black-box” model based on interaction between TCD and arterial blood pressure (nICP_BB); 2) based on diastolic flow velocity (nICP_FVd); 3) based on critical closing pressure (nICP_CrCP); and 4) based on TCD-derived pulsatility index (nICP_PI). In time domain, for recordings including spontaneous changes in ICP greater than 7 mm Hg, nICP_PI showed the best correlation with measured ICP (R = 0.61). Considering every TCD recording as an independent event, nICP_BB generally showed to be the best estimator of measured ICP (R = 0.39; p < 0.05; 95% confidence interval [CI] = 9.94 mm Hg; area under the curve [AUC] = 0.66; p < 0.05). For nICP_FVd, although it presented similar correlation coefficient to nICP_BB and marginally better AUC (0.70; p < 0.05), it demonstrated a greater 95% CI for prediction of ICP (14.62 mm Hg). nICP_CrCP presented a moderate correlation coefficient (R = 0.35; p < 0.05) and similar 95% CI to nICP_BB (9.19 mm Hg), but failed to distinguish between normal and raised ICP (AUC = 0.64; p > 0.05). nICP_PI was not related to measured ICP using any of the above statistical indicators. We also introduced a new estimator (nICP_Av) based on the average of three methods (nICP_BB, nICP_FVd, and nICP_CrCP), which overall presented improved statistical indicators (R = 0.47; p < 0.05; 95% CI = 9.17 mm Hg; AUC = 0.73; p < 0.05). nICP_PI appeared to reflect changes in ICP in time most accurately. nICP_BB was the best estimator for ICP “as a number.” nICP_Av demonstrated to improve the accuracy of measured ICP estimation 2).


A technology uses Two Depth Transcranial Doppler to compare arterial pulsations in the intra- and extra-cranial segments of the ophthalmic artery for non-invasive estimation of ICP 3).

Numerous techniques have been described with several novel advances. While none of the currently available techniques appear independently accurate enough to quantify raised ICP, there is some promising work being undertaken 4).

see Optic nerve sheath diameter ultrasonography.

Flanders et al. compared non-invasive and invasive ICP measurements in infants with hydrocephalus. Infants born term and preterm were eligible for inclusion if clinically determined to require cerebrospinal fluid (CSF) diversion. The ventricular size was assessed preoperatively via ultrasound measurement of the fronto-occipital (FOR) and fronto-temporal (FTHR) horn ratios. Invasive ICP was obtained at the time of surgical intervention with a manometer. Intracranial hypertension was defined as invasive ICP ≥15 mmHg. Diffuse optical measurements of cerebral perfusionoxygen extraction, and non-invasive ICP were performed preoperatively, intraoperatively, and postoperatively. Optical and ultrasound measures were compared with invasive ICP measurements, and their change in values after CSF diversion was obtained.

They included 39 infants; 23 had intracranial hypertension. No group difference in ventricular size was found by FOR (p=0.93) or FTHR (p=0.76). Infants with intracranial hypertension had significantly higher non-invasive ICP (p=0.02) and oxygen extraction fraction (p=0.01) compared with infants without intracranial hypertension. Increased cerebral blood flow (p=0.005) and improved oxygen extraction fraction (P < .001) after CSF diversion were only observed in infants with intracranial hypertension.

Noninvasive diffuse optical measures (including a non-invasive ICP index) were associated with intracranial hypertension. The findings suggest impaired perfusion from intracranial hypertension was independent of ventricular size. Hemodynamic evidence of the benefits of cerebrospinal fluid diversion was seen in infants with intracranial hypertension. Non-invasive optical techniques hold promise for aiding the assessment of CSF diversion timing 5).


1)

Ganslandt O, Mourtzoukos S, Stadlbauer A, Sommer B, Rammensee R. Evaluation of a novel noninvasive ICP monitoring device in patients undergoing invasive ICP monitoring: preliminary results. J Neurosurg. 2018 Jun;128(6):1653-1660. doi: 10.3171/2016.11.JNS152268. Epub 2017 Aug 8. PubMed PMID: 28784032.
2)

Cardim D, Robba C, Donnelly J, Bohdanowicz M, Schmidt B, Damian M, Varsos GV, Liu X, Cabeleira M, Frigieri G, Cabella B, Smielewski P, Mascarenhas S, Czosnyka M. Prospective Study on Noninvasive Assessment of Intracranial Pressure in Traumatic Brain-Injured Patients: Comparison of Four Methods. J Neurotrauma. 2016 Apr 15;33(8):792-802. doi: 10.1089/neu.2015.4134. Epub 2015 Dec 17. PubMed PMID: 26414916; PubMed Central PMCID: PMC4841086.
3)

Koskinen LD, Malm J, Zakelis R, Bartusis L, Ragauskas A, Eklund A. Can intracranial pressure be measured non-invasively bedside using a two-depth Doppler-technique? J Clin Monit Comput. 2016 Mar 14. [Epub ahead of print] PubMed PMID: 26971794.
4)

Padayachy LC. Non-invasive intracranial pressure assessment. Childs Nerv Syst. 2016 Sep;32(9):1587-97. doi: 10.1007/s00381-016-3159-2. Review. PubMed PMID: 27444289.
5)

Flanders TM, Lang SS, Ko TS, Andersen KN, Jahnavi J, Flibotte JJ, Licht DJ, Tasian GE, Sotardi ST, Yodh AG, Lynch JM, Kennedy BC, Storm PB, White BR, Heuer GG, Baker WB. Optical Detection of Intracranial Pressure and Perfusion Changes in Neonates With Hydrocephalus. J Pediatr. 2021 May 15:S0022-3476(21)00447-9. doi: 10.1016/j.jpeds.2021.05.024. Epub ahead of print. PMID: 34004191.

Intracranial dural arteriovenous fistula clinical features

Intracranial dural arteriovenous fistula clinical features

Clinical features of DAVF vary depending on their location, arterial supply, degree of arteriovenousshunting, and most importantly, their venous drainage pattern 1) 2) 3) 4)

DAVF lacking cortical vein drainage (CVD) may be asymptomatic, or present with symptoms related to increased dural sinus blood flow, such as pulsatile tinnitus, the latter particularly common for transverse sinus and sigmoid sinuses lesions.

Generalized central nervous system symptoms that may be related to venous hypertension or cerebrospinal fluid malabsorption, while resulting cranial nerve palsy, are often because of an arterial steal phenomenon or occasionally mass effect from an enlarged arterial feeder.

In addition, cavernous sinus dural arteriovenous fistula may present with orbital symptoms, including chemosisproptosisophthalmoplegia, and decreased visual acuity.

DAVF with CVD typically have more aggressive clinical presentations, including the sudden onset of severe headacheseizures, nonhemorrhagic neurological deficit (NHND), and intracranial hemorrhage, including intraparenchymal, subarachnoid, and subdural hematoma.

In a meta-analysis, Lasjaunias et al 5) reviewed 195 cases of DAVF and found that focal neurological deficits were related to the presence of associated cortical venous drainage (CVD) and venous congestion in the affected vascular territory. Less common aggressive presentations include brain stem or cerebellar dysfunction secondary to venous congestion, parkinsonism-like symptoms, extra-axial hemorrhage in the cervical spine, as well as cervical and upper thoracic myelopathy.

DAVF with extensive arteriovenous shunting, particularly in the setting of dural sinus thrombosis, can result in impaired venous drainage from the brain and the global venous hypertension. This can lead to cerebral edema, encephalopathy, and cognitive decline 6).


Pulsatile tinnitus is the most common presenting symptom of a DAVF. Cortical venous drainage with resultant venous hypertension can produce intracranial hypertension, and this is the most common cause of morbidity and mortality and thus the strongest indication for Intracranial dural arteriovenous fistula treatment.

DAVFs may also cause global cerebral edema or hydrocephalus due to poor cerebral venous drainage or by impairing the function of the arachnoid granulations, respectively. Other DAVF symptoms/signs include headaches, seizures, cranial nerve palsies, and orbital venous congestion.


Leptomeningeal venous drainage can lead to venous hypertension and intracranial hemorrhage.

The majority of patients presented with non-aggressive symptoms. 18% presented with intracranial hemorrhage: all the hemorrhages occurred in high-grade DAVFs 7).

see Dural arteriovenous fistula presenting as an acute subdural hemorrhage.


Only 4 cases of DAVF causing syncope have been reported, all in combination with other neurological symptoms. In comparison, they report a unique case of DAVF presenting solely with recurrent syncope, a previously undocumented finding in the literature. The case adds to other reports of nonspecific DAVF presentations and highlights the importance of considering this etiology 8).


1)

Gandhi D, Chen J, Pearl M, Huang J, Gemmete JJ, Kathuria S.Intracranial dural arteriovenous fistulas: classification, imaging findings, and treatment.AJNR Am J Neuroradiol. 2012; 33:1007–1013. doi: 10.3174/ajnr.A2798.
2)

Sarma D, ter Brugge K.Management of intracranial dural arteriovenous shunts in adults.Eur J Radiol. 2003; 46:206–220.
3)

Houser OW, Campbell JK, Campbell RJ, Sundt TMArteriovenous malformation affecting the transverse dural venous sinus–an acquired lesion.Mayo Clin Proc. 1979; 54:651–661.
4) , 5)

Lasjaunias P, Chiu M, ter Brugge K, Tolia A, Hurth M, Bernstein M.Neurological manifestations of intracranial dural arteriovenous malformations.J Neurosurg. 1986; 64:724–730. doi: 10.3171/jns.1986.64.5.0724.
6)

Miller TR, Gandhi D. Intracranial Dural Arteriovenous Fistulae: Clinical Presentation and Management Strategies. Stroke. 2015 Jul;46(7):2017-25. doi: 10.1161/STROKEAHA.115.008228. Epub 2015 May 21. PMID: 25999384.
7)

Signorelli, F. et al. Diagnosis and management of dural arteriovenous fistulas: A 10 years single-center experience Clinical Neurology and Neurosurgery , Volume 128 , 123 – 129
8)

Sheinberg DL, Luther E, Chen S, McCarthy D, Starke RM. Recurrent Syncope Caused by a Dural Arteriovenous Fistula: A Case Report and Review of the Literature. Neurologist. 2021 Mar 4;26(2):62-65. doi: 10.1097/NRL.0000000000000322. PMID: 33646991.
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