Intracranial Hypertension Group Research Articles

Correlation between the Optic Nerve Sheath Diameter Measurement and Intracranial Hypertension Tomographic Findings from a Colombian Hospital

Abstract Objective In the present study, we aimed at determining the correlation between tomographic findings of intracranial hypertension and ultrasound measurement of the optic nerve sheath diameter (ONSD). Methods Observational, descriptive, prospective, cross-sectional pilot study. The present research was performed in a tertiary hospital in Cali, Colombia, from March 2019 to October 2019. Twenty-five patients constituted the intracranial hypertension group, and 25 patients without intracranial hypertension constituted the control group. Ultrasound measurements of the ONSD were assessed using a Sonosite Turbo (SonoSite Inc., Bothell, WA, USA) ultrasound. The computed tomography (CT) images obtained from each patient diagnosed with intracranial hypertension were available in the software of the hospital. The primary outcome was the ultrasound measurement of the ONSD. Results The ONSD values of the right eye of the intracranial hypertension group ranged from 5.2 to 7.6 mm, and the ONSD of the left eye ranged from 5.3 to 7.3 mm. The global ONSD values, obtained from the average between the right and left eye, were recorded between 5.25 and 7.45 mm. Overall, our study indicated that ultrasound measurements of the ONSD were effective in differentiating a group with intracranial hypertension, previously diagnosed by CT scan images, from patients without this condition. According to the ROC curve, the optimal cutoff point for detecting intracranial hypertension was 5.2 mm. Conclusions Ultrasound measurements of the ONSD correlated with the measurements obtained from CT scan images, suggesting that the ultrasound technique can be efficient in identifying patients with intracranial hypertension and valuable in cases when CT scan images are not an available option.

Investigation of intracranial pressure in intensive care unit patients with delirium assessed by bedside ultrasound

To explore the changes of intracranial pressure in intensive care unit (ICU) patients during the occurrence and evolution of delirium by using bedside ultrasound to measure the optic nerve sheath diameter (ONSD) to evaluate intracranial pressure. A retrospective observational study was conducted. Adult patients who developed delirium during hospitalization in the general ICU of Beihai People's Hospital from October 2020 to November 2021 were enrolled, and patients who did not have ultrasonographic ONSD records within 24 hours after the diagnosis of delirium were excluded. The ONSD measured before delirium was recorded as ONSD0, the ONSD measured within 24 hours of the onset of delirium recorded as ONSD1, and the ONSD reexamined after ONSD1 recorded as ONSD2. Patients were divided into intracranial hypertension group (ONSD1 > 5 mm) and normal intracranial pressure group (ONSD1 ≤ 5 mm) according to the size of ONSD1. According to the outcome of delirium, the patients were divided into cured, improved, and non-improved groups. The reduction ratio of ONSD2 to ONSD1 in the three groups were calculated and compared. Pearson correlation test was used to analyze the correlation between fluid balance and ONSD changes after delirium. There were 43 patients, including 40 cases in the intracranial hypertension group (the incidence rate was 93.0%), 3 cases in the normal intracranial pressure group, 23 cases were cured, 13 cases were improved, and 7 cases were not improved. In the intracranial hypertension group, 11 cases had ONSD0 and ONSD1 records, and ONSD1 was significantly higher than ONSD0 [mm: 5.88±0.61 vs. 5.34±0.57, 95% confidence interval (95%CI) -0.85 to -0.23, P = 0.003]. The reduction ratio of ONSD2 to ONSD1 in the cured group was significantly higher than that in the improved group and the non-improved group [(12.04±6.20)% vs. (5.68±4.10)%, (0.17±3.96)%; 95%CI were 2.37 to 10.33, 6.41 to 17.31, P values were 0.003 and 0.000, respectively]. The correlation analysis showed that the reduction ratio of ONSD2 to ONSD1 was negatively correlated with fluid balance (r = -0.42, 95%CI was -0.66 to -0.10, P = 0.012). The incidence of intracranial hypertension in ICU delirium patients is high. A more pronounced decrease in intracranial pressure predicts a better delirium outcome. Dynamic ONSD measurement can provide valuable information for the prevention and treatment of delirium.

Diagnosis of idiopathic intracranial hypertension - the importance of excluding secondary causes: A systematic review.

Idiopathic intracranial hypertension is characterized by increased intracranial pressure without any pathological findings on neuroimaging, except for signs of high intracranial pressure. Before diagnosing idiopathic intracranial hypertension secondary causes of increased intracranial pressure should be excluded. to characterize the phenotype of patients with secondary intracranial hypertension and to identify possible risk factors for secondary intracranial hypertension. We have systematically searched the PubMed database. The publications were analyzed according to the patient phenotype, age, gender, comorbidities, body mass index/weight status, and additional medication. The results are summarized in four categories: medication, infection, hormonal induced intracranial hypertension and miscellaneous groups of diseases related to sIH. We identified 105 eligible papers which included 272 cases. There were 49.6% pediatric cases. Among the adult group,70.9% were women. A total of 40.4% of all cases were obese or overweight, 27% among adults and 13.4% among pediatric cases. Increased BMI and recent weight gain, anemia, renal diseases and hypertension were the most frequent comorbidities related to sIH. Among sIH patients, 40.4% were obese or overweight; two thirds were women. We recommend that even patients with a typical IIH phenotype should be screened for secondary causes.

Idiopathic Intracranial Hypertension is Associated with a Higher Burden of Visible Cerebral Perivascular Spaces: The Glymphatic Connection.

Research suggests a connection between idiopathic intracranial hypertension and the cerebral glymphatic system. We hypothesized that visible dilated perivascular spaces, possible glymphatic pathways, would be more prevalent in patients with idiopathic intracranial hypertension. This prevalence could provide a biomarker and add evidence to the glymphatic connection in the pathogenesis of idiopathic intracranial hypertension. We evaluated 36 adult (older than 21 years of age) patients with idiopathic intracranial hypertension and 19 controls, 21-69 years of age, who underwent a standardized MR imaging protocol that included high-resolution precontrast T2- and T1-weighted images. All patients had complete neuro-ophthalmic examinations for papilledema. The number of visible perivascular spaces was evaluated using a comprehensive 4-point qualitative rating scale, which graded the number of visible perivascular spaces in the centrum semiovale and basal ganglia; a 2-point scale was used for the midbrain. Readers were blinded to patient diagnoses. Continuous variables were compared using a Student t test. The mean number of visible perivascular spaces overall was greater in the idiopathic intracranial hypertension group than in controls (4.5 [SD, 1.9] versus 2.9 [SD, 1.9], respectively; P = .004). This finding was significant for centrum semiovale idiopathic intracranial hypertension (2.3 [SD, 1.4] versus controls, 1.3 [SD, 1.1], P = .003) and basal ganglia idiopathic intracranial hypertension (1.7 [SD, 0.6] versus controls, 1.2 [SD, 0.7], P = .009). There was no significant difference in midbrain idiopathic intracranial hypertension (0.5 [SD, 0.5] versus controls, 0.4 [SD, 0.5], P = .47). Idiopathic intracranial hypertension is associated with an increased number of visible intracranial perivascular spaces. This finding provides insight into the pathophysiology of idiopathic intracranial hypertension, suggesting a possible relationship between idiopathic intracranial hypertension and glymphatic dysfunction and providing another useful biomarker for the disease.

MRI of the optic nerve sheath and globe in cats with and without presumed intracranial hypertension.

The study aimed to: (1) test MRI repeatability of measurements of optic nerve sheath diameter (ONSD), optic nerve diameter (OND) and eye globe transverse diameter (ETD); (2) investigate the associations between the OND, ONSD and ETD; (3) assess whether these measurements are affected by age or body weight; and (4) test the association between ONSD, OND, ETD and ONSD:ETD ratio with presumed intracranial pressure (ICP) status. This was a retrospective and blinded study where patients were allocated to presumed normal or intracranial hypertension groups based on MRI findings. The ONSD and ETD were measured and recorded. Interclass correlation coefficient (ICC) was calculated to investigate interobserver agreement. Data were analysed using the Pearson correlation coefficient, two-sample t-test and general linear model ANOVA. Seventy-seven cats were included, 62 with presumed normal ICP and 15 with presumed intracranial hypertension. The ICC showed moderate-to-good reliability for all measurements. Positive correlations were identified for: (1) ETD and weight; (2) ONSD and age; (3) OND and age; (4) ONSD and ETD; (5) ONSD:ETD ratio and presumed ICP status; and (6) ONSD and presumed ICP status. No difference was detected between the presumed normal and intracranial hypertension groups and ONSD, as well as ONSD:ETD ratio and presumed ICP status when patient age was considered. The measurement of the ONSD and the ONSD:ETD ratio on T2-weighted MRI might not be reliable as non-invasive tests for diagnosing intracranial hypertension in cats.

Dural sinus volume in children with syndromic craniosynostosis and intracranial hypertension.

Intracranial hypertension is a major concern in children with syndromic craniosynostosis (sCS). Cerebral venous hypertension caused by cerebral venous outflow obstruction is believed to contribute to intracranial hypertension. The authors therefore hypothesized that cerebral venous volume would be increased in those children with sCS and intracranial hypertension. In a case series of 105 children with sCS, of whom 32 had intracranial hypertension, cerebral MRI techniques were used to quantify the volume of the superior sagittal sinus, straight sinus (StrS), and both transverse sinuses. Linear regression showed that total cerebral venous volume increased by 580.8 mm3 per cm increase in occipitofrontal head circumference (p < 0.001). No significant difference was found between the intracranial hypertension group and the nonintracranial hypertension group (p = 0.470). Multivariate ANOVA showed increased StrS volume (as a proportion of total volume) in the intracranial hypertension group (8.5% vs 5.1% in the nonintracranial hypertension group, p < 0.001). Multivariate logistic regression showed that a 100-mm3 increase in StrS volume is associated with increased odds of having intracranial hypertension by 60% (OR 1.60, 95% CI 1.24-2.08). Although intracranial hypertension was not associated with total cerebral venous volume increase, it was associated with an isolated increase in StrS volume. Hence, it is unlikely that general cerebral venous outflow obstruction is the mechanism of intracranial hypertension in sCS. Rather, these findings indicate either a central cerebral vulnerability to intracranial hypertension or a mechanism involving venous blood redistribution.

Repeatability of ultrasound examination of the optic nerve sheath diameter in the adult cat: comparison between healthy cats and cats suffering from presumed intracranial hypertension.

The objectives of this study were to test: (1) the repeatability of ultrasonographic examination of the optic nerve sheath diameter (ONSD) in the cat; (2) the association between the ONSD and age, sex and body weight in healthy cats; and (3) the difference in the ONSD between healthy cats and those suffering from presumed intracranial hypertension (ICH). This study had a prospective, blinded, observational cross-sectional study design. Two groups of animals were considered: healthy cats (group A) and cats with a diagnosis of presumed ICH (group B). The ONSD was evaluated, measured and compared between the two groups via an ultrasonographic transpalpebral approach. Repeatability of the procedure was evaluated through the intraclass correlation coefficient (ICC). Data were statistically compared using the Student's t-test and linear regression analysis. A strong inter- and intraobserver ICC indicating good repeatability was observed. The interobserver ICC was 0.965 (P <0.05) for the right eye and 0.956 (P <0.05) for the left eye. The intraobserver ICC was 0.988 (P <0.05) and 0.984 (P <0.05) for the right and left eyes, respectively. In healthy cats the mean ± SD ONSD was 1.23 ± 0.11 mm (range 1-1.47 mm) and 1.23 ± 0.10 (range 1-1.4 mm) for right and left eyes, respectively. The ONSD was not related to sex or weight; a weak relationship was observed with age. In group B, the mean ONSD was 1.68 ± 0.13 mm (range 1.5-1.9 mm) and 1.61 ± 0.15 mm (range 1.4-1.9 mm) for the right and left eyes, respectively. In group B, the ONSD was statistically significantly larger than in group A, the healthy cats (P <0.001). The transpalpebral ultrasonographic technique is a non-invasive, feasible and reproducible method to measure ONSD both in healthy cats and in cats suffering from suspected ICH.

Study on the feasibility of optic nerve subarachnoid width in qualitative diagnosis of intracranial hypertension

Objective To evaluate the feasibility of optic nerve subarachnoid space in non-invasive qualitatively diagnosis of intracranial hypertension. Methods In this retrospective study,patients who received lumbar puncture from October 2009 to June 2015 were enrolled and divided into normal intracranial pressure group (41 cases) and intracranial hypertension group (39 cases). Optic nerve subarachnoid space width (SASW) behind ocular 3 mm (SASW-3),9 mm (SASW-9),and 15 mm (SASW-15) were measured on MRI and compared between groups. Chi-square test, t test and ROC analyses were used. Results SASW-3,SASW-9,and SASW-15 were (1.16±0.21), (0.98±0.21) and (0.92±0.17) mm in normal group and (1.46±0.20), (1.29±0.19) and (1.17±0.20) mm in intracranial hypertension group,respectively. According to independent samples t test,SASW-3,SASW-9,and SASW-15 of intracranial hypertension group was significant larger than those at the same measured site of normal group (P<0.01). According to MedCalc analysis,Receive operating characteristic (ROC) area was 0.849 in SASW-3 and when the cut-off value was fixes as 1.19 mm,the sensibility and specificity were 94.9% and 63.4%,respectively. ROC area was 0.849 in SASW-9 and when the cut-off value was fixes as 1.10 mm,the sensibility and specificity were 84.6% and 78.0%,respectively. ROC area was 0.824 in SASW-15 and when the cut-off value was fixes as 1.06 mm,the sensibility and specificity were 69.2% and 80.5%,respectively. Conclusion SASW-9 can be used to screen and monitor the intracranial hypertension as a non-invasive tool. Key words: Optic nerve; Subarachnoid space; Intracranial pressure; Magnetic resonance imaging

DURATION OF THE MONITORING OF INTRACRANIAL PRESSURE CONCERNING THE PRESENCE OF INTRACRANIAL HYPERTENSION

Duration of intracranial pressure (ICP) monitoring depends on the clinician`s necessity for the data that influence type and length of the management of intracranial hypertension (ICHT). On the other hand, it is also affected by the possibility of the development of the infection, which is very often fatal when it occurs in the central nervous system. A prospective study of the 32 patients with severe brain trauma (SBT) that had intracranial pressure (ICP) monitoring is presented in here. There were 22 patients with intracranial hypertension (ICHT) and 10 without it. In the ICHT group, the monitoring lasted 5.81 ± 2.70 and 4.45 ± 1.81 in the control group. We have not found a significant difference in the duration of the ICP monitoring between two groups (t = 1.71, p > 0.05). Patients with ICHT had significantly shorter survival than the control group (p = 0.04). It seems that need for prolonged monitoring of the patients with ICHT is suppressed by their shorter survival, comparing to brain-injured patients with normal intracranial pressure.

WPI-13 Lack of association of cranial lacunae with intracranial hypertension in children with crouzon syndrome and apert syndrome: a 3D morphometric quantitative analysis

ObjectivesCranial lacunae on CT is equivalent to the plain X-ray ‘copper beating’ seen in craniosynostosis. Copper beating has not been shown to correlate to intracranial hypertension (IH). However it is a purely quantitative assessment – can qualitative measurement of CT cranial lacunae more accurately predict IH in children with craniosynostosis?DesignRetrospective cohort study.Subjects18 consecutive children with Crouzon and 17 with Apert syndrome were identified.MethodsPatients were divided into IH and non-IH groups defined on an intention to treat basis. 3D software was used to analyse% of calvarial lacunae.ResultsMean age at CT scan was 380 days (range 6–1778). Of the 35 children, 21 required surgery for raised ICP (17 posterior vault expansion 2 ventriculo-peritoneal shunts (VPS), 1 spring-assisted cranioplasty and 1 fronto-orbital advancement) at mean age of 512 days (range 38–1710). Of the 21 children with raised ICP, 15 had lacunae with mean lacuna/calvarium percentage of 3% (0%–28%). Of the 14 non-raised ICP children, 8 had lacunae with mean lacuna/calvarium percentage of 2% (0%–8%). T-test demonstrated no significant difference between the 2 groups. For both groups, parietal bones were most likely to show lacunae (IH 14/21, non-IH 9/14), followed by occipital (IH 8/21, non-IH 3/14), followed by frontal (IH 6/21, non-IH 2/14).ConclusionsResults suggest that cranial lacunae, measured using quantitative 3D methods, do not predict IH, in agreement with evidence from qualitative plain skull radiograph studies.

Lack of association of cranial lacunae with intracranial hypertension in children with Crouzon syndrome and Apert syndrome: a 3D morphometric quantitative analysis

PurposeCranial lacunae (foci of attenuated calvarial bone) are CT equivalents of “copper beating” seen on plain skull radiographs in children with craniosynostosis. The qualitative presence of copper beating has not been found to be useful for the diagnosis of intracranial hypertension (IH) in these patients. 3D morphometric analysis (3DMA) allows a more systematic and quantitative assessment of calvarial attenuation. We used 3DMA to examine the relationship between cranial lacunae and IH in children with Crouzon and Apert syndromic craniosynostosis.MethodsPatients were divided into IH and non-IH groups defined on an intention-to-treat basis. Pre-operative CT scans were converted into 3D skull models and processed to quantify lacunae as a percentage of calvarium surface area (LCP). This was done on individual bone and whole skull basis.ResultsEighteen consecutive children with Crouzon’s syndrome and 17 with Apert syndrome were identified. Median age at CT scan was 135 days (range 6–1778). Of the 35 children, 21 required surgery for IH at median age of 364 days (range 38–1710). Of these 21 children, 14 had lacunae with mean LCP of 3% (0–28%). Of the 14 non-IH children, 8 had lacunae with mean LCP of 2% (0–8%). LCP was not significantly different between IH and non-IH groups. Parietal bones were most likely to show lacunae (IH 14/21, non-IH 9/14), followed by occipital (IH 8/21, non-IH 3/14), and frontal (IH 6/21, non-IH 2/14).ConclusionResults suggest that cranial lacunae, measured using quantitative 3DMA, do not correlate with IH, in agreement with evidence from qualitative plain skull radiograph studies.

To Predict Visual Deterioration According to the Degree of Intracranial Hypertension in Patients with Cerebral Venous Sinus Thrombosis

Background: Visual damage is one of the most common complications of cerebral venous sinus thrombosis (CVST)-associated intracranial hypertension (IH). This study is aimed at stratifying the risk of IH-induced visual damage in an attempt to predict its deterioration and prevent high-risk patients from irreversible eyesight impairment promptly. Methods: A total of 94 patients with confirmed diagnosis of CVST were eligible for enrollment in this study. According to cerebrospinal fluid pressure at admission, the involved patients were classified into mild IH (< 250 mmH₂O), moderate IH (250–330 mmH₂O), and severe IH (≥330 mmH₂O) groups. Results: The ratio of visual deterioration in the severe IH group was 75%, which was significantly higher than in either the moderate (44.4%) or the mild groups (14.3%). As regards subjects without visual symptoms at admission, visual deterioration occurred in 9.4 ± 4.5 days after admission in the severe group while it occurred in 30.5 ± 16.8 days in the moderate group (p = 0.024). The conditional inference tree and random forest revealed that severe IH might be considered as an index of visual deterioration. Visual field defect, fading eyesight, and papilledema were significantly worse in patients with severe IH as compared to patients with mild or moderate IH, all p < 0.01. Conclusions: IH ≥330 mmH₂O may be a cut-off value to predict the deterioration of visual damage in CVST, revealing that ophthalmologic interventions should be considered in a timely manner in this condition, particularly when recanalization of cerebral venous sinus cannot be achieved within a short time.

The Effects of Induction and Treatment of Intracranial Hypertension on Cerebral Autoregulation: An Experimental Study.

Background This study aimed to analyse cerebral autoregulation (CA) during induction and treatment of intracranial hypertension (ICH) in an experimental model. Materials and Methods Landrace and Duroc piglets were divided into mild and severe ICH groups. Four or seven millilitres of saline solution was infused into paediatric bladder catheter inserted in the parietal lobe (balloon inflation). After 1.5 h, a 3% saline solution was infused via venous catheter, and 30 min later, the bladder catheter balloon was deflated (surgery). The cerebral static autoregulation (sCA) index was evaluated using cerebral blood flow velocities (CBFV) obtained with Doppler ultrasound. Results Balloon inflation increased ICP in both groups. The severe ICH group showed significantly lower sCA index values (p=0.001, ANOVA) after balloon inflation (ICH induction) and a higher sCA index after saline injection (p=0.02) and after surgery (p=0.04). ICP and the sCA index were inversely correlated (r=−0.68 and p<0.05). CPP and the sCA index were directly correlated (r=0.74 and p<0.05). Conclusion ICH was associated with local balloon expansion, which triggered CA impairment, particularly in the severe ICH group. Moreover, ICP-reducing treatments were associated with improved CA in subjects with severe ICH.

Sigmoid Sinus Diverticulum, Dehiscence, and Venous Sinus Stenosis: Potential Causes of Pulsatile Tinnitus in Patients with Idiopathic Intracranial Hypertension?

Pulsatile tinnitus is experienced by most patients with idiopathic intracranial hypertension. The pathophysiology remains uncertain; however, transverse sinus stenosis and sigmoid sinus diverticulum/dehiscence have been proposed as potential etiologies. We aimed to determine whether the prevalence of transverse sinus stenosis and sigmoid sinus diverticulum/dehiscence was increased in patients with idiopathic intracranial hypertension and pulsatile tinnitus relative to those without pulsatile tinnitus and a control group. CT vascular studies of patients with idiopathic intracranial hypertension with pulsatile tinnitus (n = 42), without pulsatile tinnitus (n = 37), and controls (n = 75) were independently reviewed for the presence of severe transverse sinus stenosis and sigmoid sinus diverticulum/dehiscence according to published criteria. The prevalence of transverse sinus stenosis and sigmoid sinus diverticulum/dehiscence in patients with idiopathic intracranial hypertension with pulsatile tinnitus was compared with that in the nonpulsatile tinnitus idiopathic intracranial hypertension group and the control group. Further comparisons included differing degrees of transverse sinus stenosis (50% and 75%), laterality of transverse sinus stenosis/sigmoid sinus diverticulum/dehiscence, and ipsilateral transverse sinus stenosis combined with sigmoid sinus diverticulum/dehiscence. Severe bilateral transverse sinus stenoses were more frequent in patients with idiopathic intracranial hypertension than in controls (P < .001), but there was no significant association between transverse sinus stenosis and pulsatile tinnitus within the idiopathic intracranial hypertension group. Sigmoid sinus dehiscence (right- or left-sided) was also more common in patients with idiopathic intracranial hypertension compared with controls (P = .01), but there was no significant association with pulsatile tinnitus within the idiopathic intracranial hypertension group. While our data corroborate previous studies demonstrating increased prevalence of sigmoid sinus diverticulum/dehiscence and transverse sinus stenosis in idiopathic intracranial hypertension, we did not establish an increased prevalence in patients with idiopathic intracranial hypertension with pulsatile tinnitus compared with those without. It is therefore unlikely that these entities represent a direct structural correlate of pulsatile tinnitus in patients with idiopathic intracranial hypertension.

Increased Curvature of the Tentorium Cerebelli in Idiopathic Intracranial Hypertension.

Transverse sinus effacement is detectable on MRV examinations in almost all patients with idiopathic intracranial hypertension. This effacement of the transverse sinus is presumed to be mediated by elevation of intracranial pressure, resulting in compression and inward collapse of the dural margins of the sinus. We sought to establish whether supratentorial broad-based downward deformity of the tentorium might explain transverse sinus effacement in idiopathic intracranial hypertension. MRV examinations of 53 adult patients with idiopathic intracranial hypertension were reviewed retrospectively and compared with 58 contemporaneously acquired controls. The curvature of the tentorium with reference to a line connecting the transverse sinus laterally with the confluence of the tentorial leaves medially was calculated as a segment of a circle. The height and area of the segment and the angle subtended by the midpoint of the tentorium from the falx were calculated. The height and area of the segment described by the chord connecting the transverse sinus with the apex of the tentorial confluence and subtended midtentorial angle were greater in the idiopathic intracranial hypertension group; this finding supports the hypothesis that increased tentorial bowing is present in idiopathic intracranial hypertension. Increased bowing of the tentorium in patients with idiopathic intracranial hypertension compared with controls is a new observation, lending itself to new hypotheses on the nature and localization of elevated intracranial pressure in idiopathic intracranial hypertension. Bowing of the tentorium may play a part in distorting the contour of the transverse sinuses, resulting, at least in part, in the effacement of the transverse sinuses in idiopathic intracranial hypertension.

High-resolution transbulbar ultrasonography helping differentiate intracranial hypertension in bilateral optic disc oedema patients.

The enlargement of optic nerve sheath diameter (ONSD) has been proven to be related with raised intracranial pressure (ICP). No prospective study has been focused on utilizing retrobulbar ultrasonography in optic disc oedema patient presented to ophthalmologist. High-resolution transbulbar ultrasonography was performed in a cohort of patient presented with bilateral optic disc oedema. The subarachnoid space of optic nerve (SAS), ONSD and optic nerve diameter (OND) was measured prior to other ancillaries including lumbar puncture. Subjects were classified into increased intracranial pressure (IIP) and normal intracranial pressure (NIP) group according to the open cerebrospinal fluid pressure more than 200mm H2 0. The SAS, ONSD and OND were compared between groups and with normal control. The sensitivity of SAS or ONSD change for predicating intracranial hypertension was assessed. A total of 20 IIP, 25 NIP patients and 25 normal controls were evaluated. The mean SAS and ONSD measured in idiopathic intracranial hypertension group was significantly increased than that of NIP and controls (p<0.001), whereas the OND showed no statistic difference between each group. The sensitivities using the SAS and ONSD for differentiating increased ICP in optic disc oedema patients were 0.99 and 0.97, respectively. The enlarged SAS and ONSD measured by high-resolution transbulbar sonography are very sensitive parameters to predicate increased ICP in bilateral optic disc oedema patients.

Manifestations of Pediatric Intracranial Hypertension From the Intracranial Hypertension Registry

ObjectiveThe purpose of this study was to examine the presenting symptoms, demographics, and interventions in pediatric patients enrolled in the Intracranial Hypertension Registry. MethodsWe analyzed confirmed intracranial hypertension patients ≤18 years at the time of initial diagnosis who were enrolled in the registry. ResultsA total of 203 patients met the criteria for inclusion; 142 (70%) were considered primary intracranial hypertension. Females made up 72.5% (103 of 142) and 75.8% (47 of 61) in the primary intracranial hypertension and secondary intracranial hypertension groups, respectively. There were no clinically significant differences in age, body mass index, or opening pressure between the primary intracranial hypertension and secondary intracranial hypertension groups. Symptoms most often reported were headache and blurred vision. Bilateral optic disc edema occurred in 89.3% of primary intracranial hypertension and 78.7% of secondary intracranial hypertension patients. When divided into pre- and postpubertal status, 32.5% of patients were classified prepubertal; 77.3% of these had primary intracranial hypertension. This resulted in a female to male ratio of 1:1.04 for prepubertal and 6:1 for postpubertal primary intracranial hypertension patients. The body mass index was significantly higher in the postpubertal primary intracranial hypertension group (P = 0.0014). There was no significant difference in opening pressure. ConclusionsThe common symptoms of intracranial hypertension, including headache, optic disc edema, and vision changes, occurred with similar frequencies in our cohort to those reported in the literature. In separate subanalyses, we found significantly higher rates of obesity in postpubertal females with primary intracranial hypertension. The female-to-male ratios in the postpubertal primary intracranial hypertension and secondary intracranial hypertension groups were higher than reported in the literature.

Automated Quantitation of the Posterior Scleral Flattening and Optic Nerve Protrusion by MRI in Idiopathic Intracranial Hypertension

Subjective determination of the posterior sclera flattening and optic nerve protrusion in MRI is challenging because of the 3D nature of the globe morphology. This study aims to develop and compare quantitative measures of globe flattening and optic nerve protrusion with subjective rating, and assess relationships with papilledema grade and intraocular and CSF pressures. Data of 34 globes from 7 overweight female patients with idiopathic intracranial hypertension and 6 age- and weight-matched healthy female control subjects were assessed, as well as a subcohort of 4 of the patients with idiopathic intracranial hypertension who underwent follow-up MR imaging 2 weeks after lumbar puncture and initiation of treatment with acetazolamide. MR imaging examination included a 3D CISS sequence on 1.5T and 3T scanners with 0.6-mm isotropic resolution. Subjective ratings of globe flattening were obtained by experienced and inexperienced readers. Quantitative measures of globe flattening, nerve protrusion, and maximal deformation were derived by use of a 2D map of the distances from the globe center to the posterior wall. Contingency coefficients for globe flattening agreements with subjective rating by the experienced and inexperienced readers were 0.72 and 0.56, respectively. Mean values of the 3 deformation measures were significantly poorer in the idiopathic intracranial hypertension group, with nerve protrusion demonstrating the strongest difference (P = .0002). Nerve protrusion was most strongly associated with papilledema grade with a contingency coefficient of 0.74 (P = .01), whereas globe flattening was negatively correlated with intraocular pressure (R = -0.75, P < .0001). Maximal deformation was negatively associated with CSF opening pressure (R = -0.86, P = .0001). After treatment, only the changes in nerve protrusion and maximal deformation were significant. Automated measures of globe deformation improve reliability over subjective rating. Of the 2 globe deformation measures, nerve protrusion had the strongest predictive value for papilledema grade and had the highest sensitivity for assessment of treatment efficacy in idiopathic intracranial hypertension.

EVOLUTION OF BRAIN TISSUE INJURY AFTER EVACUATION OF ACUTE TRAUMATIC SUBDURAL HEMATOMAS

Acute traumatic subdural hematoma complicated by brain parenchymal injury is associated with a 60 to 90% mortality rate. Early surgical evacuation of the mass lesion is essential for a favorable outcome, but the severity of the underlying brain injury determines the outcome, even when surgery has been prompt. The purpose of this study was to analyze tissue biochemical patterns in the brain underlying an evacuated acute subdural hematoma to identify a characteristic pattern of changes that might indicate evolving brain injury. Prospectively collected data from 33 patients after surgical evacuation of acute subdural hematoma were analyzed. Both a brain tissue oxygen tension probe and an intracerebral microdialysis probe were placed in brain tissue exposed at surgery. On the basis of the postoperative clinical course, the patients were divided into three groups: patients with early intractable intracranial hypertension, patients with evolution of delayed traumatic injury (DTI), and patients with an uncomplicated course (the no-DTI group). The overall mortality rate was 46%, with 100% mortality in the intracranial hypertension group (five patients). Mortality in the DTI group was 53% compared with only 9% in the no-DTI group (P = 0.002). There were no significant differences in the initial computed tomographic scan characteristics, such as thickness of the subdural hematoma or amount of midline shift, among the three groups. Physiological variables, as well as the microdialysate measures of brain biochemistry, were markedly different in the intracranial hypertension group compared with the other groups. Differences between the other two groups were more subtle but were significant. Significantly lower values of brain tissue oxygen tension (14 +/- 8 mm Hg versus 27 +/- 14 mm Hg) and higher dialysate values of lactate and pyruvate were documented in patients who developed a delayed injury compared with patients with uncomplicated courses (4.1 +/- 2.3 mmol/L versus 1.7 +/- 0.7 mmol/L for lactate, and 104 +/- 47 micromol/L versus 73 +/- 54 micromol/L for pyruvate at 24 h after injury). Evolution of DTI in the area of brain underlying an evacuated subdural hematoma is associated with a significant increase in mortality. Postoperatively decreasing brain tissue oxygen tension and increasing dialysate concentrations of lactate and pyruvate in this area may warn of evolving brain injury and evoke further diagnostic and therapeutic activity.

Evolution of Brain Tissue Injury after Evacuation of Acute Traumatic Subdural Hematomas

Acute traumatic subdural hematoma complicated by brain parenchymal injury is associated with a 60 to 90% mortality rate. Early surgical evacuation of the mass lesion is essential for a favorable outcome, but the severity of the underlying brain injury determines the outcome, even when surgery has been prompt. The purpose of this study was to analyze tissue biochemical patterns in the brain underlying an evacuated acute subdural hematoma to identify a characteristic pattern of changes that might indicate evolving brain injury. Prospectively collected data from 33 patients after surgical evacuation of acute subdural hematoma were analyzed. Both a brain tissue oxygen tension probe and an intracerebral microdialysis probe were placed in brain tissue exposed at surgery. On the basis of the postoperative clinical course, the patients were divided into three groups: patients with early intractable intracranial hypertension, patients with evolution of delayed traumatic injury (DTI), and patients with an uncomplicated course (the no-DTI group). The overall mortality rate was 46%, with 100% mortality in the intracranial hypertension group (five patients). Mortality in the DTI group was 53% compared with only 9% in the no-DTI group (P = 0.002). There were no significant differences in the initial computed tomographic scan characteristics, such as thickness of the subdural hematoma or amount of midline shift, among the three groups. Physiological variables, as well as the microdialysate measures of brain biochemistry, were markedly different in the intracranial hypertension group compared with the other groups. Differences between the other two groups were more subtle but were significant. Significantly lower values of brain tissue oxygen tension (14 +/- 8 mm Hg versus 27 +/- 14 mm Hg) and higher dialysate values of lactate and pyruvate were documented in patients who developed a delayed injury compared with patients with uncomplicated courses (4.1 +/- 2.3 mmol/L versus 1.7 +/- 0.7 mmol/L for lactate, and 104 +/- 47 micromol/L versus 73 +/- 54 micromol/L for pyruvate at 24 h after injury). Evolution of DTI in the area of brain underlying an evacuated subdural hematoma is associated with a significant increase in mortality. Postoperatively decreasing brain tissue oxygen tension and increasing dialysate concentrations of lactate and pyruvate in this area may warn of evolving brain injury and evoke further diagnostic and therapeutic activity.