UpToDate: Dynamic Cervical Magnetic Resonance Imaging

Dynamic Cervical Magnetic Resonance Imaging

Dynamic MRI is useful to determine more accurately the number of levels where the spinal cord is compromised, and to better evaluate narrowing of the canal and intramedullary high-intensity signal (IHIS) changes. New information provided by flexion-extension MRI might change our strategy for CSM management 1).

Imaging of the cervical spine in functional positions has so far been limited to conventional Cervical spine x ray examinations or the scarcely available open magnetic resonance imaging (MRI). An MRI compatible positioning device allows MRI examinations in various positions and even in motion. In combination with high-resolution T2-weighted MRI it allows detailed functional imaging of the cervical spine and nerve roots.

The combination of a mechanical positioning device and a high-resolution 3D T2-weighted sequence (SPACE) on a conventional 1.5 T MRI allows kinematic imaging of the cervical spine as well as high-resolution imaging in the end positions, even in the presence of metal implants. In this proof of concept study a good visualization of narrowing of the spinal canal in functional positions could be achieved, showing the potential of MRI in functional positions for clinical and research applications 2).

The Dynamic Cervical Magnetic Resonance Imaging demonstrated a major number of findings and spinal cord compressions compared to the static exam. The dynamic exam is able to provide useful information in these patients, but Nigro et al., suggested a careful evaluation of the findings in the extension exam since they are probably over-expressed 3).

It is useful in correlating symptoms with the dynamic changes only noted on dMRI, and has reduced the incidence of misdiagnosis of myelopathy4).

In a study of Pratali et al., Dynamic cervical MRI was obtained using a standard protocol with the neck in neutral, flexion, and extension positions. The morphometric parameters considered were anterior length of the spinal cord (ALSC), posterior length of the spinal cord (PLSC), spinal canal diameter (SCD) and spinal cord width (SCW). Two observers analyzed the parameters independently, and the inter- and intra-observer reliabilities were assessed by the intraclass correlation coefficient (ICC).

18 patients were included in the study and all completed the dynamic MRI acquisition protocol. The inter- and intra-observer reliabilities demonstrated “almost perfect agreement” (ICC > 0.9, p < 0.001) for ALSC and PLSC in all positions. The SCD had inter- and intra-observer reliability classified as “almost perfect agreement” (ICC: 0.83-0.98, p < 0.001 and ICC: 0.90-0.99, p < 0.001, respectively) in all positions. The SCW had inter- and intra-observer reliability classified as “substantial agreement” (ICC: 0.73-0.94, p < 0.001 and ICC: 0.79-0.96, p < 0.001, respectively) in all positions. ALSC and PLSC in neutral, flexion and extension positions from the present study were significantly greater compared to the measurements previously published (P < 0.001).

The dynamic MRI protocol presented was safe and may allow a more complete evaluation of variations in the cervical spine in patients with CSM than traditional MRI protocols. The morphometric parameters based on this protocol demonstrated excellent inter- and intra-observer reliabilities 5).

References

1)

Zhang L, Zeitoun D, Rangel A, Lazennec JY, Catonné Y, Pascal-Moussellard H. Preoperative evaluation of the cervical spondylotic myelopathy with flexion-extension magnetic resonance imaging: about a prospective study of fifty patients. Spine (Phila Pa 1976). 2011 Aug 1;36(17):E1134-9. doi: 10.1097/BRS.0b013e3181f822c7. PubMed PMID: 21785299.

2)

Gerigk L, Bostel T, Hegewald A, Thomé C, Scharf J, Groden C, Neumaier-Probst E. Dynamic magnetic resonance imaging of the cervical spine with high-resolution 3-dimensional T2-imaging. Clin Neuroradiol. 2012 Mar;22(1):93-9. doi: 10.1007/s00062-011-0121-2. Epub 2011 Dec 23. PubMed PMID: 22193978.

3)

Nigro L, Donnarumma P, Tarantino R, Rullo M, Santoro A, Delfini R. Static and dynamic cervical MRI: two useful exams in cervical myelopathy. J Spine Surg. 2017 Jun;3(2):212-216. doi: 10.21037/jss.2017.06.01. PubMed PMID: 28744502; PubMed Central PMCID: PMC5506301.

4)

Kolcun JP, Chieng LO, Madhavan K, Wang MY. The Role of Dynamic Magnetic Resonance Imaging in Cervical Spondylotic Myelopathy. Asian Spine J. 2017 Dec;11(6):1008-1015. doi: 10.4184/asj.2017.11.6.1008. Epub 2017 Dec 7. Review. PubMed PMID: 29279758; PubMed Central PMCID: PMC5738303.

5)

Pratali RR, Smith JS, Ancheschi BC, Maranho DAC, Savarese A, Nogueira-Barbosa MH, Herrero CFPS. A Technique for Dynamic Cervical Magnetic Resonance Imaging Applied to Cervical Spondylotic Myelopathy: A Reliability Study. Spine (Phila Pa 1976). 2018 Jun 26. doi: 10.1097/BRS.0000000000002765. [Epub ahead of print] PubMed PMID: 29952883.

UpToDate: Retrograde VentriculoSinus Shunt

Retrograde VentriculoSinus Shunt

A retrograde ventriculosinus (RVS) shunt is a watertight connection that delivers excess cerebrospinal fluid(CSF) to the superior sagittal sinus (SSS) against the direction of blood flow. This method of CSF shunting utilizes the impact pressure (IP) of the bloodstream in the SSS to maintain the intraventricular pressure (IVP) more than the sinus pressure (SP) regardless of changes in posture or intrathoracic pressure (ITP) and discourages stagnation and clotting of blood at the venous end of the connection. It also utilizes collapse of the internal jugular vein (IJV) in the erect posture to prevent siphonage.

Since the 1950‘s, hydrocephalus can be treated with cerebrospinal fluid shunts, usually to the peritoneal cavityor to the right cardiac hearth atrium. However, due to their siphon effect, these shunts lead to non-physiological cerebrospinal fluid drainage, with possible co-morbidity and high revision rates. More sophisticated shunt valvesystems significantly increase costs and technical complexity and remain unsuccessful in a subgroup of patients. In an attempt to obtain physiological cerebrospinal fluid shunting, many neurosurgical pioneers shunted towards the dural sinuses, taking advantage of the physiological antisiphoning effect of the internal jugular veins. Despite several promising reports, the ventriculosinus shunts did not yet become standard neurosurgical practice.


50 RVS shunts were successfully implanted using valveless shunting catheters. There were no problems related to incorrect CSF drainage or sinus thrombosis. The results indicated arrest of the hydrocephalic process, normalization of the IVP and proper shunt function 1).

In 2016 Oliveira et al., published 3 consecutive cases who had previously undergone VPS revision and in which peritoneal space was full of adhesions and fibrosis. RVSS was performed as described by Shafei et al., with some modifications to each case. All 3 patients kept the same clinical profile after RVSS, with no perioperative or postoperative complications. However, revision surgery was performed in the first operative day in 1 out of 3 patients, in which the catheter was not positioned in the superior sagittal sinus. They propose that in cases where VPS is not feasible, RVSS may be a safe and applicable second option. Nevertheless, the long-term follow-up of patients and further learning curve must bring stronger evidence 2).


Baert et al., from the Department of Neurosurgery of Ghent University Hospital, Belgium implanted the retrograde ventriculosinus shunt, as advocated by El-Shafei, in 10 patients. They reports on the operation technique and long-term outcome, including 4 patients in whom this shunt was implanted as a rescue.

Implantation of a ventriculosinus shunt proved to be a feasible technique, warranting physiological drainage of cerebrospinal fluid. However, only in 3 out of 14 patients, functionality of the retrograde ventriculosinus shunt was maintained during more than 6 years follow-up. In there opinion, these shunts fail because present venous access devices are difficult to implant correctly and get too easily obstructed. After discussing possible causes of this frequent obstruction, a new dural venous sinus access device is presented.

An easy to implant and thrombogenic-resistant dural venous sinus access device needs to be developed before ventriculosinus shunting can become general practice 3).

1)

El-Shafei IL, El-Shafei HI. The retrograde ventriculosinus shunt: concept and technique for treatment of hydrocephalus by shunting the cerebrospinal fluid to the superior sagittal sinus against the direction of blood flow. Preliminary report. Childs Nerv Syst. 2001 Aug;17(8):457-65; discussion 466. PubMed PMID: 11508534.
2)

Oliveira MF, Teixeira MJ, Reis RC, Petitto CE, Gomes Pinto FC. Failed Ventriculoperitoneal Shunt: Is Retrograde Ventriculosinus Shunt a Reliable Option? World Neurosurg. 2016 Aug;92:445-453. doi: 10.1016/j.wneu.2016.05.038. Epub 2016 May 27. PubMed PMID: 27237416.
3)

Baert E, Dewaele F, Vandersteene J, Hallaert G, Okito Kalala JP, Roost DV. Treating Hydrocephalus with Retrograde VentriculoSinus Shunt Prospective Clinical Study. World Neurosurg. 2018 Jun 25. pii: S1878-8750(18)31313-5. doi: 10.1016/j.wneu.2018.06.097. [Epub ahead of print] PubMed PMID: 29953953.

UpToDate: Giant Prolactinoma

Giant prolactinoma

Their definition should be restricted to pituitary adenomas with a diameter of 40 mm or more, significant extrasellar extension, very high prolactin concentrations (usually above 1000 µg/L), and no concomitant GH or ACTH secretion.

Epidemiology

They represent only 2-3 % of all prolactinomas.

Giant prolactinoma are rare tumours. They are much more frequent in young to middle-aged men than in women with a male to female ratio of about 9:1. 1) 2).

Symptoms

Endocrine symptoms are often present but overlooked for a long period of time and diagnosis is eventually made when neurological complications arise from massive extension into the surrounding structures, leading to cranial nerve palsy, hydrocephalus, temporal lobe epilepsy or exophthalmos.

Prolactin concentrations are usually in the range of 1,000 to 100,000 µg/L, but may be underestimated by the so-called ‘high dose hook effect’.

Males

Sexual dysfunction is a hallmark of prolactinomas in males. Tumors that co-secrete prolactin and LH are extremely rare and and only a case reported in an adult male. In this case, normal testosterone was maintained by intact LH levels even in the face of the highest prolactin level reported to date 3).

Treatment

As in every prolactinoma, dopamine agonists are the first-line treatment allowing rapid alleviation of neurologic symptoms in the majority of the cases, a significant reduction of tumour size in three-fourths; of the patients and PRL normalization in 60-70%. These extensive tumours are usually not completely resectable and neurosurgery has significant morbidity and mortality. It should therefore be restricted to acute complications such as apoplexy or leakage of cerebrospinal fluid (often induced by medical treatment), or to patients with insufficient tumoral response or progression. Irradiation and temozolomide are useful adjuvant therapies in a subset of patients with aggressive/invasive tumours which are not controlled despite combined medical and surgical treatments. Because of these various challenges, it needs a multidisciplinary management in expert centres 4).

Case series

In 42 cases, male patients accounted for 71.4% of this series and were relatively younger (35.70±2.42 vs. 52.00±3.55 years, p=0.0011) and harbored bigger tumors (14.57 vs. 7.74 cm3, p=0.0179) compared to females. Almost all of these tumors showed suprasellar extension (97.6%) and cavernous sinus invasion (92.9%). Dopamine agonist represented an efficient method to control PRL concentrations (98.8%) and reduce tumor burdens (81.2 %). PRL normalization was detected in 13 out of the 27 patients initially treated with bromocriptine (BRC) whereas none of the 14 patients with first-line operation gained a normalization of PRL concentration after surgery. Although there was no reliable predictor of tumor response, First PRL reduction was a predictive criterion for the nadir PRL level during the long-time period of follow-up for first-line bromocriptine treatment. In conclusion, patients with giant prolactinomas did not gain more benefits from initial surgery. Dopamine agonist (BRC) should be first-line treatment for giant prolactinomas whereas operation merely served as a remedy for acute compression symptoms and dopamine agonist resistance. Consecutive monitoring of serum PRL levels in the early stage of initial BRC treatment is useful for evaluation of therapeutic effect and further therapeutic decision 5).


16 patients (43.7 % women); mean age at diagnosis: 42.1 ± 21 years. The most frequent presentation was compressive symptoms. The delay in diagnosis was higher in women (median of 150 months vs. 12 in men; p = 0.09). The mean maximum tumor diameter at diagnosis was 56.9 ± 15.5 mm, and mean prolactin levels were 10,995.9 ± 12,157.8 ng/mL. Dopamine agonists were the first-line treatment in 11 patients (mean maximum dose: 3.9 ± 3.2 mg/week). Surgery was the initial treatment in five patients and the second-line treatment in six. Radiotherapy was used in four cases. All patients but one, are still with dopamine agonists. After a mean follow-up of 9 years, prolactin normalized in 7/16 patients (43.7 %) and 13 patients (81 %) reached prolactin levels lower than twice the upper limit of normal. Mean prolactin level at last visit: 79.5 ± 143 ng/mL. Tumor volume was decreased by 93.8 ± 11.3 %, and final maximum tumor diameter was 18.4 ± 18.8 mm. Three patients are actually tumor free. Giant prolactinomas are characterized by a large tumor volume and extreme prolactin hypersecretion. Multimodal treatment is frequently required to obtain biochemical and tumor control 6).

References

1)

Shrivastava RK, Arginteanu MS, King WA, Post KD. Giant prolactinomas:clinical management and long-term follow up. J Neurosurg. 2002;97:299–306. doi: 10.3171/jns.2002.97.2.0299.
2)

Corsello SM, Ubertini G, Altomare M, Lovicu RM, Migneco MG, Rota CA, Colosimo C. Giant prolactinomas in men: efficacy of cabergoline treatment. Clin Endocrinol. 2003;58:662–670. doi: 10.1046/j.1365-2265.2003.01770.x.
3)

Tamagno G, Daly AF, Deprez M, Vroonen L, Andris C, Martin D, Beckers A. Absence of hypogonadism in a male patient with a giant prolactinoma: a clinical paradox. Ann Endocrinol (Paris). 2008 Feb;69(1):47-52. Epub 2007 Dec 20. PubMed PMID: 18082643.
4)

Maiter D, Delgrange E. The challenges in managing giant prolactinomas. Eur J Endocrinol. 2014 Feb 17. [Epub ahead of print] PubMed PMID: 24536090.
5)

Lv L, Hu Y, Yin S, Zhou P, Yang Y, Ma W, Zhang S, Wang X, Jiang S. Giant Prolactinomas: Outcomes of Multimodal Treatments for 42 Cases with Long-Term Follow-Up. Exp Clin Endocrinol Diabetes. 2018 Jun 25. doi: 10.1055/a-0597-8877. [Epub ahead of print] PubMed PMID: 29940665.
6)

Andujar-Plata P, Villar-Taibo R, Ballesteros-Pomar MD, Vidal-Casariego A, Pérez-Corral B, Cabezas-Agrícola JM, Álvarez-Vázquez P, Serramito R, Bernabeu I. Long-term outcome of multimodal therapy for giant prolactinomas. Endocrine. 2016 Oct 4. PubMed PMID: 27704480.

UpToDate: Coil price

Coil price

Patients with aneurysmal subarachnoid hemorrhage who require coiling had higher charges than patients who could be treated by clipping. The benefits of apparent decrease in length of stay in the endovascular group were offset by higher procedure price and cost of consumables. There was no significant difference in clinical outcome at 6 months.

Zubair Tahir et al., from the Department of Neurosurgery, Aga Khan University Hospital, Karachi Pakistan proposed a risk scoring system to give guidelines regarding the choice of treatment considering size of aneurysm and resource allocation 1).

Simple cost-saving policies can lead to substantial reductions in costs of neurointerventional procedures while maintaining high levels of quality and growth of services 2).

The coil prices used for intracranial aneurysm embolization has continued to rise despite an increase in competition in the marketplace. Coils on the US market range in list price from $500 to $3000. The purpose of a study from Gandhoke et al., from the Department of Neurological Surgery University of PittsburghPennsylvania was to investigate potential cost savings with the use of a price capitation model.

The authors built a clinical decision analytical tree and compared their institution’s current expenditure on endovascular coils to the costs if a capped-price model were implemented. They retrospectively reviewed coil and cost data for 148 patients who underwent coil embolization from January 2015 through September 2016. Data on the length and number of coils used in all patients were collected and analyzed. The probabilities of a treated aneurysm being ≤/> 10 mm in maximum dimension, the total number of coils used for a case being ≤/> 5, and the total length of coils used for a case being ≤/> 50 cm were calculated, as was the mean cost of the currently used coils for all possible combinations of events with these probabilities. Using the same probabilities, the authors calculated the expected value of the capped-price strategy in comparison with the current one. They also conducted multiple 1-way sensitivity analyses by applying plausible ranges to the probabilities and cost variables. The robustness of the results was confirmed by applying individual distributions to all studied variables and conducting probabilistic sensitivity analysis.

Ninety-five (64%) of 148 patients presented with a rupture, and 53 (36%) were treated on an elective basis. The mean aneurysm size was 6.7 mm. A total of 1061 coils were used from a total of 4 different providers. Companies A (72%) and B (16%) accounted for the major share of coil consumption. The mean number of coils per case was 7.3. The mean cost per case (for all coils) was $10,434. The median total length of coils used, for all coils, was 42 cm. The calculated probability of treating an aneurysm less than 10 mm in maximum dimension was 0.83, for using 5 coils or fewer per case it was 0.42, and for coil length of 50 cm or less it was 0.89. The expected cost per case with the capped policy was calculated to be $4000, a cost savings of $6564 in comparison with using the price of Company A. Multiple 1-way sensitivity analyses revealed that the capped policy was cost saving if its cost was less than $10,500. In probabilistic sensitivity analyses, the lowest cost difference between current and capped policies was $2750.

In comparison with the cost of coils from the authors’ current provider, their decision model and probabilistic sensitivity analysis predicted a minimum $407,000 to a maximum $1,799,976 cost savings in 148 cases by adapting the capped-price policy for coils 3).

References

1)

Zubair Tahir M, Enam SA, Pervez Ali R, Bhatti A, ul Haq T. Cost-effectiveness of clipping vs coiling of intracranial aneurysms after subarachnoid hemorrhage in a developing country–a prospective study. Surg Neurol. 2009 Oct;72(4):355-60; discussion 360-1. doi: 10.1016/j.surneu.2008.11.003. Epub 2009 Jul 17. PubMed PMID: 19616277.
2)

Kashlan ON, Wilson TJ, Chaudhary N, Gemmete JJ, Stetler WR Jr, Dunnick NR, Thompson BG, Pandey AS. Reducing costs while maintaining quality in endovascular neurosurgical procedures. J Neurosurg. 2014 Nov;121(5):1071-6. doi: 10.3171/2014.7.JNS14236. Epub 2014 Aug 29. PubMed PMID: 25170667.
3)

Gandhoke GS, Pandya YK, Jadhav AP, Jovin T, Friedlander RM, Smith KJ, Jankowitz BT. Cost of coils for intracranial aneurysms: clinical decision analysis for implementation of a capitation model. J Neurosurg. 2018 Jun;128(6):1792-1798. doi: 10.3171/2017.3.JNS163149. Epub 2017 Aug 25. PubMed PMID: 28841115.

Uptodate: Intracranial Subependymoma

Intracranial Subependymoma

Intracranial subependymomas are rare, mostly incidentalomas and therefore did not receive much attention in previous literature.

Many supratentorial subependymomas appear to be centered in the cortex or subcortical white matter. Therefore, a lack of ventricular involvement does not exclude subependymoma from the differential diagnosis.

By being classified as benign grade I in the World Health Organization Classification of Tumors of the Central Nervous System, they are given a special status compared to the other ependymal tumors. Tumor recurrences are a rarity, spinal “drop metastases” do not occur. While etiological, pathological and therapeutic characteristics have been subject of several publications over the last few decades and have meanwhile been well studied, the imaging characteristics are much less well received 1).

Epidemiology

They occur in middle to late adulthood.

Representing approximately 10% of ependymal tumors, subependymomas most often “present” as incidental autopsy findings in the brains of the elderly.

Most frequently they arise in the fourth ventricle (50-60%), followed by the lateral ventricle (30-40%), and less frequently in the septum pellucidum and spinal cord 2) 3).

Intraparenchymal subependymomas are extremely rare; only 6 cases have been reported in English literature. All of them were located in the supratentorial region 4) 5) 6) , and there has been only one report of infratentorial subependymoma 7)

see Subependymoma of the fourth ventricle

Histology

Subependymomas are small, discrete tumors of adults lying most often at the foramen of Monro or the fourth ventricle. It is composed of clusters of ependymal and astrocyte-like cells in a dense fibrillary stroma. It is typically attached to a ventricular wall and the most common site is the fourth ventricle.

Histologically, the tumor may be either compact or microcystic, but extensive microcystic change is rarely reported.

The histogenesis of subependymomas is still a matter of debate, with candidates including subependymal glia, astrocytes, ependymal cells, or some mixture of these cells. A recent theory hypothesizes that they originate from tanycytes, which are cells normally located in the subependymal zone 8).

Clinical features

They are likely to remain asymptomatic throughout life and some were found by autopsy. If symptomatic, tumor location and size are critical factors for presentation.

Diagnosis

Subependymomas have typical image morphologic characteristics that differentiate them from tumors of other entities, however, the rare subgroup of histopathological mixtures of subependymomas with ependymal cell fractions has no distinctly different imaging properties.

Knowing the imaging characteristics of subpendymoma and their differential diagnoses is of particular importance in order to be able to decide between the necessity of follow-up controls, an early invasive diagnosis or, depending on the entity, tumor resection.

KEY POINTS:

· Subependymomas have typical imaging characteristics that are clearly distinguishable from other entities.. · Increased incidence in middle/ older aged men, most frequent localization: 4th ventricle..

· Symptomatic subependymomas, often located in lateral ventricles, are usually characterized by hydrocephalus..

· Radiological identification of mixed subependymoma with ependymal cell fractions is not possible..

· Image based differentiation from other entities is important for the procedure.. 9).

Treatment

The surgical aims are the maximal safe tumoral resection, the decompression of neural elements, and establishment of a pathological diagnosis and the restoration of normal CSF pathways. As subependymomas are low-grade lesions with low rates of cell proliferation and a benign clinical course, complete surgical removal is usually curative.

Case series

33 patients with subependymoma, including 4 patients with a mixture of subependymomas with ependymal cell fractions in terms of imaging and clinical aspects and with reference to a current literature review.

Subependymomas have typical image morphologic characteristics that differentiate them from tumors of other entities, however, the rare subgroup of histopathological mixtures of subependymomas with ependymal cell fractions has no distinctly different imaging properties.

Knowing the imaging characteristics of subpendymoma and their differential diagnoses is of particular importance in order to be able to decide between the necessity of follow-up controls, an early invasive diagnosis or, depending on the entity, tumor resection.

KEY POINTS:

· Subependymomas have typical imaging characteristics that are clearly distinguishable from other entities.. · Increased incidence in middle/ older aged men, most frequent localization: 4th ventricle..

· Symptomatic subependymomas, often located in lateral ventricles, are usually characterized by hydrocephalus..

· Radiological identification of mixed subependymoma with ependymal cell fractions is not possible..

· Image based differentiation from other entities is important for the procedure.. 10).


With the SEER-18 registry database, information from all patients with intracranial subependymoma diagnosed during 2004-2013 were extracted, including age, sex, race, occurrence of surgery, extent of primary surgery, receipt of radiation, tumor size, and follow-up data. Age-adjusted incidence rates, overall survival, and cause-specific survival were calculated. Cox proportional hazards model was used for both univariate and multivariate analyses.

Four hundred sixty-six cases were identified. The overall incidence of intracranial subependymoma is 0.055 per 100,000 person-years (95% confidence interval, 0.05-0.06). Through multivariate analysis, age <40 years (hazard ratio [HR], 0.21; P = 0.03), female sex (HR, 0.34; P = 0.03), location within ventricles or near brainstem (HR, 0.49; P = 0.04), and occurrence of surgery (HR, 0.50; P = 0.02) were significant independent positive prognostic factors. Receipt of radiation did not show a significant relationship.

Clinical factors such as younger age, female sex, and location within ventricles or near brain stem demonstrated positive relationship with overall survival. For treatment options, surgery remains a mainstay option. No support for radiation therapy was identified 11).


Forty-three cases of pathologically confirmed, surgically treated intracranial subependymoma were identified. Thus in this patient population, subependymomas accounted for approximately 0.07% of intracranial tumors (43 of an estimated 60,000). Radiologically, 79.1% (34/43) of intracranial subependymomas were misdiagnosed as other diseases. Pathologically, 34 were confirmed as pure subependymomas, 8 were mixed with ependymoma, and 1 was mixed with astrocytoma. Thirty-five patients were followed up for 3.0 to 120 months after surgery. Three of these patients experienced tumor recurrence, and one died of tumor recurrence. Univariate analysis revealed that shorter progression-free survival (PFS) was significantly associated with poorly defined borders. The association between shorter PFS and age < 14 years was almost significant (p = 0.51), and this variable was also included in the multivariate analysis. However, multivariate analysis showed showed only poorly defined borders to be an independent prognostic factor for shorter PFS (RR 18.655, 95% CI 1.141-304.884, p = 0.040). In patients 14 years of age or older, the lesions tended to be pure subependymomas located in the unilateral supratentorial area, total removal tended to be easier, and PFS tended to be longer. In comparison, in younger patients subependymomas tended to be mixed tumors involving the bilateral infratentorial area, with a lower total removal rate and shorter PFS.

Intracranial subependymoma is a rare benign intracranial tumor with definite radiological features. Long-term survival can be expected, although poorly defined borders are an independent predictor of shorter PFS. All the features that differ between tumors in younger and older patients suggest that they might have different origins, biological behaviors, and prognoses 12).


24 pathologically proved cases of intracranial subependymomas in 17 male and seven female patients with a mean age of 48.1 years. All patients were symptomatic. CT and MR images were used to characterize the size, shape, and location of the subependymomas; the degree of hydrocephalus; tumor calcification; and the density, signal, and enhancement characteristics of the tumors.

Eighteen of 24 tumors were 3 cm or more in greatest dimension. Nineteen were lobulated, and hydrocephalus was seen in 21. Fourteen were in the lateral ventricle, and 10 were in the posterior fossa. Calcifications were present in five (all fourth ventricular) and absent in 10 (all lateral ventricular) subependymomas imaged with unenhanced CT. On 18 contrast-enhanced CT scans, five of six subependymomas with heterogeneous enhancement were in the fourth ventricle, and nine of 12 tumors with minimal or no enhancement were in the lateral ventricle. Small internal foci with a signal intensity similar to that of CSF were seen on images of all 10 lateral ventricular subependymomas obtained with both T1-weighted and T2-weighted sequences. On 13 contrast-enhanced T1-weighted images, seven of eight tumors with heterogeneous enhancement were in the fourth ventricle, and all five with minimal or no enhancement were in the lateral ventricle.

Intracranial subependymomas were seen in symptomatic middle-aged adults and showed different CT and MR imaging features, depending on their anatomic location. Calcification and heterogeneous contrast enhancement were common features of fourth ventricular subependymomas showed a lack of calcification as well as minimal or no contrast enhancement of CT and MR images 13).

1)

Kammerer S, Mueller-Eschner M, Lauer A, Luger AL, Quick-Weller J, Franz K, Harter P, Berkefeld J, Wagner M. Subependymomas – Characteristics of a “Leave me Alone” Lesion. Rofo. 2018 Jun 18. doi: 10.1055/a-0576-1028. [Epub ahead of print] PubMed PMID: 29913520.

2)

Ragel BT, Osborn AG, Whang K, Townsend JJ, Jensen RL, Couldwell WT. Subependymomas: an analysis of clinical and imaging features. Neurosurgery. 2006;58:881–890. discussion 881-890.

3)

Nishio S, Morioka T, Mihara F, Fukui M. Subependymoma of the lateral ventricles. Neurosurg Rev. 2000;23:98–103.

4)

Natrella F, Mariottini A, Rocchi R, Miracco C. Supratentorial neurenteric cyst associated with a intraparenchymal subependymoma. BMJ Case Rep. 2012;2012

5)

Hankey GJ, Davies L, Gubbay SS. Long term survival with early childhood intracerebral tumours. J Neurol Neurosurg Psychiatry. 1989;52:778–781.

6)

Shuangshoti S, Rushing EJ, Mena H, Olsen C, Sandberg GD. Supratentorial extraventricular ependymal neoplasms: a clinicopathologic study of 32 patients. Cancer. 2005;103:2598–2605.

7)

Kim Y, Lee SY, Yi KS, Cha SH, Gang MH, Cho BS, Lee YM. Infratentorial and intraparenchymal subependymoma in the cerebellum: case report. Korean J Radiol. 2014 Jan-Feb;15(1):151-5. doi: 10.3348/kjr.2014.15.1.151. Epub 2014 Jan 8. Review. PubMed PMID: 24497806; PubMed Central PMCID: PMC3909849.

8)

Sarkar C, Mukhopadhyay S, Ralte AM, Sharma MC, Gupta A, Gaikwad S, Mehta VS. Intramedullary subependymoma of the spinal cord: a case report and review of literature. Clin Neurol Neurosurg. 2003;106:63–68.

9) , 10)

Kammerer S, Mueller-Eschner M, Lauer A, Luger AL, Quick-Weller J, Franz K, Harter P, Berkefeld J, Wagner M. Subependymomas – Characteristics of a “Leave me Alone” Lesion. Rofo. 2018 Jun 18. doi: 10.1055/a-0576-1028. [Epub ahead of print] PubMed PMID: 29913520.

11)

Nguyen HS, Doan N, Gelsomino M, Shabani S. Intracranial Subependymoma: A SEER Analysis 2004-2013. World Neurosurg. 2017 May;101:599-605. doi: 10.1016/j.wneu.2017.02.019. Epub 2017 Feb 15. PubMed PMID: 28232153.

12)

Bi Z, Ren X, Zhang J, Jia W. Clinical, radiological, and pathological features in 43 cases of intracranial subependymoma. J Neurosurg. 2015 Jan;122(1):49-60. doi: 10.3171/2014.9.JNS14155. PubMed PMID: 25361493.

13)

Chiechi MV, Smirniotopoulos JG, Jones RV. Intracranial subependymomas: CT and MR imaging features in 24 cases. AJR Am J Roentgenol. 1995 Nov;165(5):1245-50. PubMed PMID: 7572512.

UpToDate: Friedreich’s ataxia

Friedreich’s ataxia

Friedreich’s ataxia (FA) is the most frequent hereditary ataxia syndrome, while painful muscle spasms and spasticity have been reported in 11-15% of FA patients.

A report describes the successful management of painful spasms in a 65-year-old woman with Friedreich’s ataxia (FA) via intrathecal baclofen(ITB) therapy following unsuccessful medical treatments.

To Kalyvas et al., knowledge, this is the third reported case in the literature. Unfortunately, the pathophysiological characteristics of muscle spasms in FA are not well explored and understood while the therapeutic mechanisms of the different treatments are rather vague. Taking into consideration the suggested spinal atrophy in FA, the clinical resemblance of FA and chronic spinal injury muscle spasms, together with the rapid ITB therapy effectiveness in alleviating FA muscle spasms, they attempted to suggest a putative pathophysiological mechanism acting at the spinal level and possibly explained by the presence of independent spinal locomotor systems producing muscle spasms. Specifically, overexcitement of these centers, due to loss of normal regulation from upper CNS levels, may result in the uncontrolled firing of secondary motor neurons and may be the key to producing muscle spasms. However, further research under experimental and clinical settings seems to be necessary 1).


A 50-year-old female patient with Friedreich ataxia (FA) was treated successfully with an intrathecal baclofen (ITB)-delivering pump for painful spasms. This is the second reported case of FA where ITB relieved painful and disabling spasms. Berntsson et al., suggest that ITB should be considered in the treatment of disabling spasms in patients with FA 2).


Ben Smail et al.,reported a patient suffering from Friedreich’s ataxia (FA) with very painful and disabling spasms that were improved markedly by intrathecal baclofen infusion. This is the first report of an intrathecal baclofen-delivering pump implantation in an FA patient 3).

1)

Kalyvas AV, Drosos E, Korfias S, Gatzonis S, Themistocleous M, Sakas DE. Intrathecal Baclofen Therapy for Painful Muscle Spasms in a Patient with Friedreich’s Ataxia. Stereotact Funct Neurosurg. 2018 Jun 8:1-4. doi: 10.1159/000489220. [Epub ahead of print] PubMed PMID: 29886479.

2)

Berntsson SG, Holtz A, Melberg A. Does intrathecal baclofen have a place in the treatment of painful spasms in friedreich ataxia? Case Rep Neurol. 2013 Nov 21;5(3):201-3. doi: 10.1159/000356823. eCollection 2013. PubMed PMID: 24348400; PubMed Central PMCID: PMC3861848.

3)

Ben Smail D, Jacq C, Denys P, Bussel B. Intrathecal baclofen in the treatment of painful, disabling spasms in Friedreich’s ataxia. Mov Disord. 2005 Jun;20(6):758-9. PubMed PMID: 15756654.

UpToDate: Minocycline

Minocycline

Minocycline attenuates brain swelling and blood brain barrier (BBB) disruption via an iron-chelation mechanism1)

Minocycline has beneficial effects in early brain injury (EBI) following subarachnoid hemorrhage (SAH).

Minocycline treatment significantly reduced germinal matrix hemorrhage (GMH)-induced brain edema, hydrocephalus and brain damage. Minocycline also suppressed upregulation of ferritin after GMH.

Iron plays a role in brain injury following GMH and that minocycline reduces iron overload after germinal matrix hemorrhage (GMH) and iron-induced brain injury 2).


Brain iron overload is involved in brain injury after intracerebral hemorrhage (ICH). There is evidence that systemic administration of minocyclinereduces brain iron level and improves neurological outcome in experimental models of hemorrhagic and ischemic stroke. However, there is evidence in cerebral ischemia that minocycline is not protective in aged female animals. Since most ICH research has used male models, this study was designed to provide an overall view of ICH-induced iron deposits at different time points (1 to 28 days) in aged (18-month old) female Fischer 344 rat ICH model and to investigate the neuroprotective effects of minocycline in those rats. According to our previous studies, we used the following dosing regimen (20 mg/kg, i.p. at 2 and 12 h after ICH onset followed by 10 mg/kg, i.p., twice a day up to 7 days). T2-, T2⁎-weighted and T2⁎ array MRI was performed at 1, 3, 7 and 28 days to measure brain iron content, ventricle volume, lesion volume and brain swelling. Immunohistochemistry was used to examine changes in iron handling proteins, neuronal loss and microglial activation. Behavioral testing was used to assess neurological deficits. In aged female rats, ICH induced long-term perihematomal iron overload with upregulated iron handling proteins, neuroinflammation, brain atrophy, neuronal loss and neurological deficits. Minocycline significantly reduced ICH-induced perihematomal iron overload and iron handling proteins. It further reduced brain swelling, neuroinflammation, neuronal loss, delayed brain atrophy and neurological deficits. These effects may be linked to the role of minocycline as an iron chelator as well as an inhibitor of neuroinflammation 3).

Complications

Consumption of minocycline have been described among the causes associated with idiopathic intracranial hypertension 4).

A 13-year old female patient with a history of acne treated with minocycline who began with severe headache, diplopia and blurred vision. The diagnosis of pseudotumor cerebri was made, indicating the immediate antibiotic suspension and the beginning of the treatment with acetazolamide. Although the pathogenesis of pseudotumor cerebri is not fully known, an association with minocycline has been observed. This antibiotic is often used by health professionals for the management of acne, so it is important to consider its complications before being prescribed 5).

Subarachnoid hemorrhage

The molecular mechanisms underlying these effects have not been clearly identified.

SAH was induced by the filament perforation model of SAH in male Sprague Dawley rats. Minocycline or vehicle was given via an intraperitoneal injection 1 h after SAH induction. Minocycline treatment markedly attenuated brain edema secondary to blood-brain barrier (BBB) dysfunction by inhibiting NLRP3 inflammasome activation, which controls the maturation and release of pro-inflammatory cytokines, especially interleukin-1β (IL-1β). Minocycline treatment also markedly reduced the number of terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling (TUNEL)-positive cells. To further identify the potential mechanisms, we demonstrated that minocycline increased Bcl2 expression and reduced the protein expression of P53, Bax, and cleaved caspase-3. In addition, minocycline reduced the cortical levels of reactive oxygen species (ROS), which are closely related to both NLRP3 inflammasome and P53 expression. Minocycline protects against NLRP3 inflammasome-induced inflammation and P53-associated apoptosis in early brain injury following SAH. Minocycline’s anti-inflammatory and anti-apoptotic effect may involve the reduction of ROS. Minocycline treatment may exhibit important clinical potentials in the management of SAH 6).

Case series

To predict the feasibility of conducting clinical trials of acute SCI within Canada, Thibault-Halman et al., have applied the inclusion/exclusion criteria of six previously conducted SCI trials to the RHSCIR dataset and generated estimates of how many Canadian individuals would theoretically have been eligible for enrollment in these studies. Data for SCI cases were prospectively collected for RHSCIR at 18 acute and 13 rehabilitation sites across Canada. RHSCIR cases enrolled between 2009-2013 who met the following key criteria were included: non-penetrating traumatic SCI; received acute care at a RHSCIR site; age >18- <75 years, and had complete admission single neurological level of injury data. Inclusion and exclusion criteria for the Minocycline in Acute Spinal Cord injury (Minocycline), Riluzole, Surgical Timing in Acute Spinal Cord Injury Study (STASCIS), Cethrin, Nogo antibody study (NOGO) and Sygen studies were applied retrospectively to this dataset. The numbers of patients eligible for each clinical trial were determined. 2166 of the initial 2714 cases (79.8%) met the key criteria and were included in the dataset. Projected annual numbers of eligible patients for each trial was: Minocycline 117 cases; Riluzole 62 cases; STASCIS 109 cases; Cethrin 101 cases; NOGO 82 cases; and Sygen 70 cases. An additional 8.0% of the sample had a major head injury (GCS≤ 12) and would have been excluded from the trials. RHSCIR provides a comprehensive national dataset which may serve as a useful tool in the planning of multicentre clinical SCI trials 7).

References

1)

Zhao F, Xi G, Liu W, Keep RF, Hua Y. Minocycline Attenuates Iron-Induced Brain Injury. Acta Neurochir Suppl. 2016;121:361-5. doi: 10.1007/978-3-319-18497-5_62. PubMed PMID: 26463975.

2)

Guo J, Chen Q, Tang J, Zhang J, Tao Y, Li L, Zhu G, Feng H, Chen Z. Minocycline-induced attenuation of iron overload and brain injury after experimental germinal matrix hemorrhage. Brain Res. 2015 Jan 12;1594:115-24. doi: 10.1016/j.brainres.2014.10.046. Epub 2014 Oct 31. PubMed PMID: 25451129.

3)

Dai S, Hua Y, Keep RF, Novakovic N, Fei Z, Xi G. Minocycline attenuates brain injury and iron overload after intracerebral hemorrhage in aged female rats. Neurobiol Dis. 2018 Jun 4. pii: S0969-9961(18)30173-6. doi: 10.1016/j.nbd.2018.06.001. [Epub ahead of print] Review. PubMed PMID: 29879529.

4) , 5)

González Gili LO, Buffone IR, Carrara LE, Coto MB, Fortunatti EA, Dejtera M, García Elliot MF, Giacone A, Luncio AC, Masnicoff SD, Oviedo Crosta MB, Parroua M, Romano M. [Pseudotumor cerebri secondary to consumption of minocycline in a pediatric patient]. Arch Argent Pediatr. 2016 Apr 1;114(1):e78-e83. doi: 10.5546/aap.2016.e78. Epub 2016 Apr 1. Spanish. PubMed PMID: 27079408.

6)

Li J, Chen J, Mo H, Chen J, Qian C, Yan F, Gu C, Hu Q, Wang L, Chen G. Minocycline Protects Against NLRP3 Inflammasome-Induced Inflammation and P53-Associated Apoptosis in Early Brain Injury After Subarachnoid Hemorrhage. Mol Neurobiol. 2015 Jul 5. [Epub ahead of print] PubMed PMID: 26143258.

7)

Thibault-Halman G, Rivers CS, Bailey C, Tsai E, Drew B, Noonan V, Fehlings M, Dvorak MF, Kuerban D, Kwon BK, Christie S. Predicting recruitment feasibility for acute spinal cord injury clinical trials in Canada using national registry data. J Neurotrauma. 2016 Sep 14. [Epub ahead of print] PubMed PMID: 27627704.

UpToDate: HeadSense medical

HeadSense medical

HeadSense Medical develops inexpensive, easy-to-use devices for patient monitoring and diagnosis of cerebral dysfunction. The HS-1000 is the first product of the company.

The author and the developer of the device, as well as the co-founder and scientific director of the company is Surik Papyan, who is originally from Armenia and currently resides in Israel.


What are the advantages of the HS-1000 over the existing invasive and noninvasive ICP monitoring methods?

Figuratively speaking, the HS-1000 “listens” to our brains.

“The brain, just like the rest of the body, makes a noise when it works. This noise is at “low frequencies,” so we do not hear it. The sound of our circulatory system can be compared with the sounds of running water. The blood makes a different noise when it passes through too narrow or too wide vessels,” Surik Papyan explained.

We can “hear” these “sounds” only when we put a microphone in the ear canal, because of the fact that the outer ear canal, being hermetically sealed, becomes a unique resonator, something like an “organ pipe,” according to Alexander Khachunts, who is the head of the Laboratory of Psychophysiology of the National Academy of Sciences of Armenia and also took part in this project.

Just as a skilled mechanic can detect faults in a vehicle by listening to the sound of the engine, the HS-1000 can identify problems in the brain by listening to its sounds. The mathematical algorithms implemented in the device allow to dynamically measure and display the value of intracranial pressure.

The HS-1000 is equipped with a microphone, which is placed in the ear and records the mixed acoustic signal, which is formed by hemodynamic and liquorodynamic processes in the brain. It also records the air flow in the upper airways.

The acoustic signal is transmitted from the microphone to a tablet, PC or a mobile device with a special application installed. This application calculates the level of intracranial pressure and the physiological parameters needed to assess the patient’s condition. Then the results are displayed.

see more https://med.news.am/eng/news/9852/new-noninvasive-method-of-intracranial-pressure-monitoring-hs-1000-listens-to-the-brain.html


In a study a new method of Noninvasive intracranial pressure monitoring performed using algorithms to determine ICP based on acoustic properties of the brain was applied in patients undergoing invasive intracranial pressure monitoring, and the results were analyzed.

In patients with traumatic brain injury and subarachnoid hemorrhage who were undergoing treatment in a intensive neurocritical care unit, Ganslandt et al., from the Department of Neurosurgery, Klinikum Stuttgart; and Department of Neurosurgery, University of ErlangenGermanyrecorded ICP using the gold standard method of invasive external ventricular drainage or intraparenchymal monitoring. In addition, they 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.

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 values1).

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.

UpToDate: Cranioplasty timing

Cranioplasty timing

There is an increasing body of evidence in the recent literature, which demonstrates that cranioplasty may also accelerate and improve neurological recovery. Although the exact pathophysiological mechanisms for this improvement remain essentially unknown, there are a rapidly growing number of neurosurgeons adopting this concept.

Cranioplasty performed between 15 and 30 days after initial craniectomy may minimize infectionseizure, and bone flap resorption, whereas waiting > 90 days may minimize hydrocephalus but may increase the risk of seizure 1).


Communicating hydrocephalus is an almost universal finding in patients after hemicraniectomy. Delayed time to cranioplasty is linked with the development of persistent hydrocephalus, necessitating permanent CSF diversion in some patients.

Waziri et al., propose that early cranioplasty, when possible, may restore normal intracranial pressure dynamics and prevent the need for permanent CSF diversion in patients after hemicraniectomy 2).

Factors

One modifiable factor that may alter the risk of cranioplasty is the timing of cranioplasty after craniectomy. Case series suggest that early cranioplasty is associated with higher rates of infection while delaying cranioplasty may be associated with higher rates of bone resorption.

When considering ideal timing for cranioplasty, predominant issues include residual brain edema, brain retraction into the cranial vault, risk of infection, and development of delayed post-traumatic hydrocephalus.


Waiting to perform cranioplasty is important to prevent the development of devitalized autograft or allograft infections.

It is generally accepted to wait 3 to 6 months before reconstructive surgery. If there is an infected area, this waiting period can be as long as one year.

Cranioplasty is performed after craniectomy when intracranial pressure is under control for functional and aesthetic restorations and for protection, but it may also lead to some neurological improvement after the bone flap placement 3) 4) 5).

Timing of cranioplasty after decompressive craniectomy for trauma

The optimal timing of cranioplasty after decompressive craniectomy for trauma is unknown.

After decompressive craniectomy for trauma, early (<12 weeks) cranioplasty does not alter the incidence of complication rates. In patients <18 years of age, early (<12 weeks) cranioplasty increases the risk of bone resorption. Delaying cranioplasty (≥12 weeks) results in longer operative times and may increase costs 6).

Timing of cranioplasty after decompressive craniectomy for malignant middle cerebral artery infarction

Patients with malignant middle cerebral artery infarction frequently develop hydrocephalus after decompressive hemicraniectomy. Hydrocephalus itself and known shunt related complications after ventriculoperitoneal shunt implantation may negatively impact patients outcome.

A later time point of cranioplasty might lead to a lower incidence of required shunting procedures in general 7).

References

1)

Morton RP, Abecassis IJ, Hanson JF, Barber JK, Chen M, Kelly CM, Nerva JD, Emerson SN, Ene CI, Levitt MR, Chowdhary MM, Ko AL, Chesnut RM. Timing of cranioplasty: a 10.75-year single-center analysis of 754 patients. J Neurosurg. 2018 Jun;128(6):1648-1652. doi: 10.3171/2016.11.JNS161917. Epub 2017 Aug 11. PubMed PMID: 28799868.

2)

Waziri A, Fusco D, Mayer SA, McKhann GM 2nd, Connolly ES Jr. Postoperative hydrocephalus in patients undergoing decompressive hemicraniectomy for ischemic or hemorrhagic stroke. Neurosurgery. 2007 Sep;61(3):489-93; discussion 493-4. PubMed PMID: 17881960.

3)

Honeybul S, Janzen C, Kruger K, Ho KM. The impact of cranioplasty on neurological function. Br J Neurosurg. 2013;27:636–641. doi: 10.3109/02688697.2013.817532.

4)

Jelcic N, De Pellegrin S, Cecchin D, Della Puppa A, Cagnin A. Cognitive improvement after cranioplasty: a possible volume transmission-related effect. Acta Neurochir (Wien) 2013;155:1597–1599. doi: 10.1007/s00701-012-1519-6.

5)

Di Stefano C, Sturiale C, Trentini P, Bonora R, Rossi D, Cervigni G, et al. Unexpected neuropsychological improvement after cranioplasty: a case series study. Br J Neurosurg. 2012;26:827–831. doi: 10.3109/02688697.2012.692838.

6)

Piedra MP, Nemecek AN, Ragel BT. Timing of cranioplasty after decompressive craniectomy for trauma. Surg Neurol Int. 2014 Feb 25;5:25. doi: 10.4103/2152-7806.127762. PubMed PMID: 24778913; PubMed Central PMCID: PMC3994696.

7)

Finger T, Prinz V, Schreck E, Pinczolits A, Bayerl S, Liman T, Woitzik J, Vajkoczy P. Impact of timing of cranioplasty on hydrocephalus after decompressive hemicraniectomy in malignant middle cerebral artery infarction. Clin Neurol Neurosurg. 2016 Dec 9;153:27-34. doi: 10.1016/j.clineuro.2016.12.001. [Epub ahead of print] PubMed PMID: 28012353.

Update: Pupil Reactivity Score

Pupil Reactivity Score

The GCS Pupils Score (GCS-P) was described by Paul Brennan, Gordon Murray and Graham Teasdale in 2018 as a strategy to combine the two key indicators of the severity of traumatic brain injury into a single simple index.

How do I calculate the GCS-P?

The GCS-P is calculated by subtracting the Pupil Reactivity Score (PRS) from the Glasgow Coma Scale (GCS) total score:

GCS-P = GCS – PRS

The Pupil Reactivity Score is calculated as follows.

see more at http://www.glasgowcomascale.org/what-is-gcs-p/


Information about early GCS scores, pupil responses, late outcomes on the Glasgow Outcome Scale, and mortality were obtained at the individual patient level by reviewing data from the CRASH (Corticosteroid Randomisation After Significant Head Injury; n = 9,045) study and the IMPACT(International Mission for Prognosis and Clinical Trials in TBI; n = 6855) database. These data were combined into a pooled data set for the main analysis.

Methods of combining the Glasgow Coma Scale and pupil reaction data varied in complexity from using a simple arithmetic score (GCS score [range 3-15] minus the number of nonreacting pupils [0, 1, or 2]), which Brennan et al., called the GCS Pupils score (GCS-P; range 1-15), to treating each factor as a separate categorical variable. The content of information about patient outcome in each of these models was evaluated using Nagelkerke R2.

Separately, the GCS score and pupil response were each related to outcome. Adding information about the pupil response to the GCS score increased the information yield. The performance of the simple GCS-P was similar to the performance of more complex methods of evaluating traumatic brain damage. The relationship between decreases in the GCS-P and deteriorating outcome was seen across the complete range of possible scores. The additional 2 lowest points offered by the GCS-Pupils scale (GCS-P 1 and 2) extended the information about injury severity from a mortality rate of 51% and an unfavorable outcome rate of 70% at GCS score 3 to a mortality rate of 74% and an unfavorable outcome rate of 90% at GCS-P 1. The paradoxical finding that GCS score 4 was associated with a worse outcome than GCS score 3 was not seen when using the GCS-P.

A simple arithmetic combination of the GCS score and pupillary response, the GCS-P, extends the information provided about patient outcome to an extent comparable to that obtained using more complex methods. The greater range of injury severities that are identified and the smoothness of the stepwise pattern of outcomes across the range of scores may be useful in evaluating individual patients and identifying patient subgroups. The GCS-P may be a useful platform onto which information about other key prognostic features can be added in a simple format likely to be useful in clinical practice 1).

1)

Brennan PM, Murray GD, Teasdale GM. Simplifying the use of prognostic information in traumatic brain injury. Part 1: The GCS-Pupils score: an extended index of clinical severity. J Neurosurg. 2018 Jun;128(6):1612-1620. doi: 10.3171/2017.12.JNS172780. Epub 2018 Apr 10. PubMed PMID: 29631516.
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