Putting 'CSF-Shift Edema' Hypothesis to Test: Comparing Cisternal and Parenchymal Pressures After Basal Cisternostomy for Head Injury.

BACKGROUND: Increased brain edema in head injury is due to shift of cerebrospinal fluid (CSF) from cisterns at high pressure to brain parenchyma at low pressure. By opening basal cisterns and decreasing the increased cisternal pressure, basal cisternostomy (BC) results in reversal of CSF shift from parenchyma to cisterns, leading to decreased brain edema. Though the CSF-shift edema hypothesis is based on pressure difference between cisterns and brain parenchyma, the relationship of these pressures has not been studied. METHODS: A prospective clinical study was conducted from November 2018 to March 2020 including adult patients with head injury who were candidates for standard decompressive hemicraniectomy (DHC). All patients had neurological assessment and head computed tomography preoperatively and postoperatively. All patients underwent BC with DHC. Postoperatively, parenchymal and cisternal pressures and neurological condition were monitored hourly for 72 hours. RESULTS: Nine (5 men, 4 women) patients with head injury (mean age, 45.7 years; range, 25-72 years) underwent DHC-BC. Median Glasgow Coma Scale score of patients at admission was 8 (range, 4-14), and median midline shift on computed tomography was 8 mm (range, 7-12 mm). There was a significant difference between opening (25.70 ± 10.48 mm Hg) and closing (11.30 ± 5.95 mm Hg) parenchymal pressures (t9 = 3.963, P = 0.003). Immediate postoperative cisternal pressure was 1-11 mm Hg and was lower than immediate postoperative parenchymal pressure in all except 1 patient. Postoperatively, if cisternal pressure remained low, parenchymal pressure also decreased, and patients showed clinical improvement. Patients showing increased cisternal pressure showed increased parenchymal pressure and clinical worsening. CONCLUSIONS: Our study supports the CSF-shift edema hypothesis. Following DHC-BC, cisternal pressure is lowered to near-atmospheric pressure, and its relationship to parenchymal pressure predicts the future course of patients by reversal or re-reversal of CSF shift.

Low Risk of Traumatic Intracranial Hematoma Expansion with Factor Xa Inhibitors without Andexanet Reversal.

BACKGROUND: Andexanet alfa, a novel anticoagulation reversal agent for factor Xa inhibitors, was recently approved. Traumatic intracranial hemorrhage presents a prime target for this drug. The Novel Antidote to the Anticoagulation Effects of Factor Xa Inhibitors study established the efficacy of andexanet alfa in reversing factor Xa inhibitors. However, the association between anticoagulation reversal and traumatic intracranial hemorrhage progression is not well understood. The objective of this study was to determine progression rates of patients with traumatic intracranial hemorrhage on factor Xa inhibitors prior to hospitalization who were managed without the use of andexanet alfa. METHODS: A retrospective cohort study was performed between 2016 and 2019 at a single institution. An institutional traumatic brain injury (TBI) registry was queried. Patients with recorded use of apixaban or rivaroxaban <18 hours before injury were included. The primary study outcome was <35% increase in hemorrhage volume or thickness on repeated head computed tomography (CT) scans. RESULTS: We identified 25 patients meeting the inclusion criteria. Two patients were excluded because of a lack of necessary CT data. Twelve patients (52%) were receiving apixaban, and 11 were (48%) on rivaroxaban. On admission CT scan, 14 patients had subdural hematoma, 6 had traumatic intraparenchymal hemorrhage, and 3 had subarachnoid hemorrhage. Anticoagulation reversal was attempted in 17 patients (74%), primarily using 4-factor prothrombin complex concentrate. Twenty patients (87%) were adjudicated as having excellent or good hemostasis on repeat imaging. CONCLUSIONS: Our results indicate that patients on factor Xa inhibitors with complicated mild TBI have a similar intracranial hemorrhage progression rate to patients who are not anticoagulated or anticoagulated with a reversible agent. The hemostatic outcomes in our cohort were similar to those reported after andexanet alfa administration.

Early risk stratification of in hospital mortality following a ground level fall in geriatric patients with normal physiological parameters.

BACKGROUND: The purpose of this study was to identify risk factors of mortality for geriatric patients who fell from ground level at home and had a normal physiological examination at the scene. METHODS: Patients aged 65 and above, who sustained a ground level fall (GLF) with normal scene Glasgow Coma Scale (GCS) score 15, systolic blood pressure (SBP) > 90 and <160 mmHg, heart rate ≥ 60 and ≤100 beats per minute) from the 2012-2014 National Trauma Data Bank (NTDB) data sets were included in the study. Patients' characteristics, existing comorbidities [history of smoking, chronic kidney disease (CKD), cerebrovascular accident (CVA), diabetes mellitus (DM), and hypertension (HTN) requiring medication], injury severity scores (ISS), American College of Surgeons' (ACS) trauma center designation level, and outcomes were examined for each case. Risks factors of mortality were identified using bivariate analysis and logistic regression modeling. RESULTS: A total of 40,800 patients satisfied the study inclusion criteria. The findings of the logistic regression model for mortality using the covariates age, sex, race, SBP, ISS, ACS trauma level, smoking status, CKD, CVA, DM, and HTN were associated with a higher risk of mortality (p < .05). The fitted model had an Area under the Curve (AUC) measure of 0.75. CONCLUSION: Cases of geriatric patients who look normal after a fall from ground level at home can still be associated with higher risk of in-hospital death, particularly those who are older, male, have certain comorbidities. These higher-risk patients should be triaged to the hospital with proper evaluation and management.

Ratio of Optic Nerve Sheath Diameter to Eyeball Transverse Diameter by Ultrasound Can Predict Intracranial Hypertension in Traumatic Brain Injury Patients: A Prospective Study.

BACKGROUND: Measuring optic nerve sheath diameter (ONSD), an indicator to predict intracranial hypertension, is noninvasive and convenient, but the reliability of ONSD needs to be improved. Instead of using ONSD alone, this study aimed to evaluate the reliability of the ratio of ONSD to eyeball transverse diameter (ONSD/ETD) in predicting intracranial hypertension in traumatic brain injury (TBI) patients. METHODS: We performed a prospective study on patients admitted to the Surgery Intensive Care Unit. The included 52 adults underwent craniotomy for TBI between March 2017 and September 2018. The ONSD and ETD of each eyeball were measured by ultrasound and computed tomography (CT) scan within 24 h after a fiber optic probe was placed into lateral ventricle. Intracranial pressure (ICP) > 20 mmHg was regarded as intracranial hypertension. The correlations between invasive ICP and ultrasound-ONSD/ETD ratio, ultrasound-ONSD, CT-ONSD/ETD ratio, and CT-ONSD were each analyzed separately. RESULTS: Ultrasound measurement was successfully performed in 94% (n = 49) of cases, and ultrasound and CT measurement were performed in 48% (n = 25) of cases. The correlation efficiencies between ultrasound-ONSD/ETD ratio, ultrasound-ONSD, CT-ONSD/ETD ratio, and ICP were 0.613, 0.498, and 0.688, respectively (P < 0.05). The area under the curve (AUC) values of the receiver operating characteristic (ROC) curve for the ultrasound-ONSD/ETD ratio and CT-ONSD/ETD ratio were 0.920 (95% CI 0.877-0.964) and 0.896 (95% CI 0.856-0.931), respectively. The corresponding threshold values were 0.25 (sensitivity of 90%, specificity of 82.3%) and 0.25 (sensitivity of 85.7%, specificity of 83.3%), respectively. CONCLUSION: The ratio of ONSD to ETD tested by ultrasound may be a reliable indicator for predicting intracranial hypertension in TBI patients.

Intracranial Subdural Hematoma after Spinal Anesthesia: Report of Two Cases with different Outcomes

Spinal anesthesia is a technique commonly used for local anesthesia and in obstetric surgeries. Rarely, the formation of an intracranial subdural hematoma (SDH) may result from spinal anesthesia, constituting a serious condition that often leads to severe neurological deficits. The presentation and course of this pathology may occur in a completely different way, which makes its diagnosis and management difficult. In the present article, the authors report two cases of patients with intracranial SDH after spinal anesthesia with completely different presentations and outcomes, demonstrating the variability of the manifestations of this condition. A quick review of key points of its pathophysiology, symptomatology, diagnosis, and treatment was also performed.

Clival SubduralHematoma after Drainage of Concomitant Intracranial and Spinal Cord Subdural Hematomas ­ Rare Case Report

Concomitant traumatic spinal cord and intracranial subdural hematomas associated with a retroclival hematoma are very uncommon. Their pathophysiology is not totally elucidated, but one hypothesis is the migration of the hematoma from the head to the spine. In the present case report, the authors describe the case of a 51-year-old man presenting with headache, nauseas and back pain after a head trauma who presented with intracranial and spinal cord subdural hematomas. Drainage was performed but, 1 week later, a retroclival subdural hematoma was diagnosed. The present paper discusses the pathophysiology, the clinical presentation, as well as the complications of concomitant traumatic spinal cord and intracranial subdural hematomas associated with a retroclival hematoma, and reviews this condition.

Is repeat head CT necessary in patients with mild traumatic intracranial hemorrhage.

BACKGROUND: Patients with traumatic intracranial hemorrhage (TIH) frequently receive repeat head CT scans (RHCT) to assess for progression of TIH. The utility of this practice has been brought into question, with some studies suggesting that in the absence of progressive neurologic symptoms, the RHCT does not lead to clinical interventions. METHODS: This was a retrospective review of consecutive patients with CT-documented TIH and GCS ≥ 13 presenting to an academic emergency department from 2009 to 2013. Demographic, historical, and physical exam variables, number of CT scans during admission were collected with primary outcomes of: neurological decline, worsening findings on repeat CT scan, and the need for neurosurgical intervention. RESULTS: Of these 1126 patients with mild traumatic intracranial hemorrhage, 975 had RHCT. Of these, 54 (5.5% (4.2-7.2 95 CI) had neurological decline, 73 (7.5% 5.9-9.3 95 CI) had hemorrhage progression on repeat CT scan, and 58 (5.9% 4.5-7.6 95 CI) required neurosurgical intervention. Only 3 patients (0.3% 0.1-0.9% 95 CI) underwent neurosurgical intervention due to hemorrhage progression on repeat CT scan without neurological decline. In this scenario, the number of RHCT scans needed to be performed to identify this one patient is 305. CONCLUSIONS: RHCT after initial findings of TIH and GCS ≥ 13 leading to a change to operative management in the absence of neurologic progression is a rare event. A protocol that includes selective RHCT including larger subdural hematomas or patients with coagulopathy (vitamin K inhibitors and anti-platelet agents) may be a topic for further study.

The Effect of Cerebrovascular Stenosis on -Peri-Hematoma Cerebral Perfusion and Clinical Outcomes in Patients with Supratentorial Spontaneous Intracerebral Hemorrhage.

BACKGROUND Many factors are associated with the cerebral hypoperfusion after spontaneous intracerebral hemorrhage (sICH), however, the effect of cerebrovascular stenosis on peri-hematoma cerebral blood flow (CBF) and 90-day poor outcomes in patients with spontaneous intracerebral hemorrhage is still unclear. MATERIAL AND METHODS From September 2016 to March 2017, we prospectively collected data on adults with supratentorial spontaneous intracerebral hemorrhages. Using the Propensity Score model, we compared the peri-hematoma CBF and 90-day poor outcomes (mRS ≥3) in the stenosis group and the control group. RESULTS Before matching, a total of 116 patients were included in this study, 25 patients in the stenosis group and 91 patients in the control group. After matching, the patients in the stenosis group had a higher absolute decrease of CBF (p=0.003), higher relative decrease of CBF (p=0.016), and higher incidence of 90-day poor outcomes (p=0.041) than the control group. With subgroup analysis, the patients with Glasgow Coma Scale from 13 to 15 (p=0.035), hematoma in the cerebral lobe (p=0.003), mean arterial pressure lower than 120 mm Hg (p=0.003), absolute decrease of CBF higher than 15 mL/100 g per minute (p=0.007), and relative decrease of CBF higher than 30% (p=0.020) had poorer outcomes. CONCLUSIONS In our series, the stenosis of main cerebral vessels decreased the peri-hematoma CBF and increased the rate of 90-day poor outcomes. Despite higher Glasgow Coma Scale, the evaluation of cerebral perfusion in patients with sICH is needed, especially for the patients with hematoma in the cerebral lobe and lower mean arterial pressure; and treatments to keep adequate cerebral perfusion are needed.

Cerebellar Hematoma Location: Implications for the Underlying Microangiopathy.

BACKGROUND AND PURPOSE: Spontaneous cerebellar intracerebral hemorrhage (ICH) has been reported to be mainly associated with vascular changes secondary to hypertension. However, a subgroup of cerebellar ICH seems related to vascular amyloid deposition (cerebral amyloid angiopathy). We sought to determine whether location of hematoma in the cerebellum (deep and superficial regions) was suggestive of a particular hemorrhage-prone small-vessel disease pathology (cerebral amyloid angiopathy or hypertensive vasculopathy). METHODS: Consecutive patients with cerebellar ICH from a single tertiary care medical center were recruited. Based on data from pathological reports, patients were divided according to the location of the primary cerebellar hematoma (deep versus superficial). Location of cerebral microbleeds (CMBs; strictly lobar, strictly deep, and mixed CMB) was evaluated on magnetic resonance imaging. RESULTS: One-hundred and eight patients (84%) had a deep cerebellar hematoma, and 20 (16%) a superficial cerebellar hematoma. Hypertension was more prevalent in deep than in patients with superficial cerebellar ICH (89% versus 65%, respectively; P<0.05). Among patients who underwent magnetic resonance imaging, those with superficial cerebellar ICH had higher prevalence of strictly lobar CMB (43%) and lower prevalence of strictly deep or mixed CMB (0%) compared with those with deep superficial cerebellar ICH (6%, 17%, and 38%, respectively). In a multivariable model, presence of strictly lobar CMB was associated with superficial cerebellar ICH (odds ratio, 3.8; 95% confidence interval, 1.5-8.5; P=0.004). CONCLUSIONS: Our study showed that superficial cerebellar ICH is related to the presence of strictly lobar CMB-a pathologically proven marker of cerebral amyloid angiopathy. Cerebellar hematoma location may thus help to identify those patients likely to have cerebral amyloid angiopathy pathology.

Do Intracerebral Hemorrhage Nonexpanders Actually Expand Into the Ventricular Space?

BACKGROUND AND PURPOSE: The computed tomographic angiography spot sign as a predictor of hematoma expansion is limited by its modest sensitivity and positive predictive value. It is possible that hematoma expansion in spot-positive patients is missed because of decompression of intracerebral hemorrhage (ICH) into the ventricular space. We hypothesized that revising hematoma expansion definitions to include intraventricular hemorrhage (IVH) expansion will improve the predictive performance of the spot sign. Our objectives were to determine the proportion of ICH nonexpanders who actually have IVH expansion, determine the proportion of false-positive spot signs that have IVH expansion, and compare the known predictive performance of the spot sign to a revised definition incorporating IVH expansion. METHODS: We analyzed patients from the multicenter PREDICT ICH spot sign study. We defined hematoma expansion as ≥6 mL or ≥33% ICH expansion or >2 mL IVH expansion and compared spot sign performance using this revised definition with the conventional 6 mL/33% definition using receiver operating curve analysis. RESULTS: Of 311 patients, 213 did not meet the 6-mL/33% expansion definition (nonexpanders). Only 13 of 213 (6.1%) nonexpanders had ≥2 mL IVH expansion. Of the false-positive spot signs, 4 of 40 (10%) had >2 mL ventricular expansion. The area under the curve for spot sign to predict significant ICH expansion was 0.65 (95% confidence interval, 0.58-0.72), which was no different than when IVH expansion was added to the definition (area under the curve, 0.66; 95% confidence interval, 0.58-0.71). CONCLUSIONS: Although IVH expansion does indeed occur in a minority of ICH nonexpanders, its inclusion into a revised hematoma expansion definition does not alter the predictive performance of the spot sign.

Prehospital Systolic Blood Pressure Is Related to Intracerebral Hemorrhage Volume on Admission.

BACKGROUND AND PURPOSE: Ultra-early blood pressure (BP) management in the prehospital setting could improve the efficacy of this treatment on attenuating intracerebral hemorrhage (ICH) expansion. We aimed to determine the association of prehospital systolic BP (SBP) with ICH volume, ultra-early hematoma growth, and the spot sign on admission. METHODS: We conducted a retrospective study of a prospective database of 219 consecutive patients with spontaneous ICH admitted to the emergency department of a tertiary stroke center during a 3-year period. Prehospital SBP and ICH volume, ultra-early hematoma growth (ICH volume/onset-to-imaging time), and presence of the spot sign on admission were prospectively recorded. Primary outcome was ICH volume on admission. Secondary outcomes included ultra-early hematoma growth and frequency of the spot sign in patients scanned within 6 hours from symptom onset (hyperacute group). RESULTS: Prehospital SBP was positively correlated with both SBP (r=0.552; P<0.001) and ICH volume (ρ=0.189; P=0.006) on admission. Patients with ICH volume above the median value presented higher prehospital SBP (172.3±35.0 versus 163.7±27.8 mm Hg; P=0.049). This association remained significant in adjusted multiple logistic regression analysis (odds ratio, 1.01 for a 1-U increase in SBP; 95% confidence interval, 1.01-1.02; P=0.018). In the hyperacute group (n=126), prehospital SBP was unrelated to ultra-early hematoma growth (ρ=0.115; P=0.203) nor the presence of the spot sign (172.2±27.6 versus 171.8±31.6 mm Hg; P=0.959). CONCLUSIONS: Prehospital SBP is correlated with SBP on admission and independently associated with ICH volume on admission. These findings support the rationale of testing whether prehospital initiation of BP-lowering attenuates ICH expansion.

Island Sign: An Imaging Predictor for Early Hematoma Expansion and Poor Outcome in Patients With Intracerebral Hemorrhage.

BACKGROUND AND PURPOSE: The aim of the study was to investigate the usefulness of the computed tomography (CT) island sign for predicting early hematoma growth and poor functional outcome. METHODS: We included patients with spontaneous intracerebral hemorrhage (ICH) who had undergone baseline CT within 6 hours after ICH symptom onset in our hospital between July 2011 and September 2016. Two readers independently assessed the presence of the island sign on the admission noncontrast CT scan. Multivariable logistic regression analysis was used to analyze the association between the presence of the island sign on noncontrast admission CT and early hematoma growth and functional outcome. RESULTS: A total of 252 patients who met the inclusion criteria were analyzed. Among them, 41 (16.3%) patients had the island sign on baseline noncontrast CT scans. In addition, the island sign was observed in 38 of 85 patients (44.7%) with hematoma growth. Multivariate logistic regression analysis demonstrated that the time to baseline CT scan, initial hematoma volume, and the presence of the island sign on baseline CT scan independently predicted early hematoma growth. The sensitivity of the island sign for predicting hematoma expansion was 44.7%, specificity 98.2%, positive predictive value 92.7%, and negative predictive value 77.7%. After adjusting for the patients' age, baseline Glasgow Coma Scale score, presence of intraventricular hemorrhage, presence of subarachnoid hemorrhage, admission systolic blood pressure, baseline ICH volume, and infratentorial location, the presence of the island sign (odds ratio, 3.51; 95% confidence interval, 1.26-9.81; P=0.017) remained an independent predictor of poor outcome in patients with ICH. CONCLUSIONS: The island sign is a reliable CT imaging marker that independently predicts hematoma expansion and poor outcome in patients with ICH. The noncontrast CT island sign may serve as a potential marker for therapeutic intervention.

Cerebrovascular Time Constant in Patients with Head Injury.

The cerebrovascular time constant (τ) theoretically estimates how fast the cerebral arterial bed is filled by blood volume after a sudden change in arterial blood pressure during one cardiac cycle. The aim of this study was to assess the time constant of the cerebral arterial bed in patients with traumatic brain injury (TBI) with and without intracranial hematomas (IH). We examined 116 patients with severe TBI (mean 35 ± 15 years, 61 men, 55 women). The first group included 58 patients without IH and the second group included 58 patients with epidural (7), subdural (48), and multiple (3) hematomas. Perfusion computed tomography (PCT) was performed 1-12 days after TBI in the first group and 2-8 days after surgical evacuation of the hematoma in the second group. Arteriovenous amplitude of regional cerebral blood volume oscillation was calculated as the difference between arterial and venous blood volume in the "region of interest" of 1 cm(2). Mean arterial pressure was measured and the flow rate of the middle cerebral artery was recorded with transcranial Doppler ultrasound after PCT. The time constant was calculated by the formula modified by Kasprowicz. The τ was shorter (p = 0.05) in both groups 1 and 2 in comparison with normal data. The time constant in group 2 was shorter than in group 1, both on the side of the former hematoma (р = 0.012) and on the contralateral side (р = 0.044). The results indicate failure of autoregulation of cerebral capillary blood flow in severe TBI, which increases in patients with polytrauma and traumatic IH.

[Post-dural puncture headache and blood-patch: theoretical and practical approach]. / Céphalées post-brèches méningées et blood-patch: aspects théoriques et pratiques.

OBJECTIVE: To review the current research and formulate a rational approach to the physiopathology, cause and treatment of post-dural puncture headache (PDPH). DATA SOURCES: Articles published to December 2011 were obtained through a search of Medline for the MeSh terms "epidural blood-patch" and "post-dural puncture headache". STUDY SELECTION: Six hundred and eighty-two pertinent studies were included and 200 were analysed. DATA SYNTHESIS: Resulting of a dural tap after spinal anaesthesia or diagnostic lumbar puncture or as a complication of epidural anaesthesia, PDPH occurs when an excessive leak of cerebrospinal fluid leads to intracranial hypotension associated to a resultant cerebral vasodilatation. Reduction in cerebrospinal fluid volume in upright position may cause traction of the intracranial structure and stretching of vessels. Typically postural, headache may be associated to nausea, photophobia, tinnitus or arm pain and changes in hearing acuity. In severe cases, there may be cranial nerve dysfunction and nerve palsies secondary to traction on those nerves. The Epidural Blood-Patch (EBP) is considered as the "gold standard" in the treatment of PDHP because it induces a prolonged elevation of subarachnoid and epidural pressures, whereas such elevation is transient with saline or dextran. EBP should be performed within 24-48hours of onset of headache; the optimum volume of epidural blood appears to be 15-20mL. Severe complications following EBP are exceptional. The use of echography may be safety puncture. The optimum timing of epidural blood-patch, the resort of repeating procedure if the symptomatology does not disappear, the alternative to the conventional medical treatment need to be determined by future clinical trial.

Comparison between cerebral tissue oxygen tension and energy metabolism in experimental subdural hematoma.

BACKGROUND: An experimental swine model (n = 7) simulating an acute subdural hematoma (ASDH) was employed (1) to explore the relation between the brain tissue oxygenation (PbtO(2)) and the regional cerebral energy metabolism as obtained by microdialysis, and (2) to define the lowest level of PbtO(2) compatible with intact energy metabolism. METHODS: ASDH was produced by infusion of 7 ml of autologous blood (infusion rate 0.5 ml/min) by a catheter placed subdurally. PbtO(2) and microdialysis probes were placed symmetrically in the injured ("bad-side") and non-injured ("good-side") hemispheres. Intracranial pressure (ICP) was monitored in the "good-side." RESULTS: ICP, cerebral perfusion pressure (CPP), PbtO(2), glucose, lactate, pyruvate, lactate-pyruvate ratio (LP ratio), glutamate, and glycerol were recorded at baseline (60 min) and post trauma (360 min). After the creation of the ASDH, PbtO(2) decreased significantly in both the hemispheres (P < 0.001). No significant difference was found between the sides post trauma. The LP ratio, glutamate, and glycerol in the "bad-side" increased significantly over the "good-side" where the values remained within the normal limits. A PbtO(2) value below approximately 25 mmHg was found to be associated with disturbed energy metabolism in the "bad-side" but not in the "good-side." No correlation was found between the LP ratio and PbtO(2) in either hemisphere. CONCLUSIONS: PbtO(2) monitoring accurately describes tissue oxygenation but does not disclose whether the oxygen delivery is sufficient for maintaining cerebral energy metabolism. Accordingly, it may not be possible to define a threshold level for PbtO(2) below which energy failure and permanent tissue damage occurs.

Papilloedema as a non-invasive marker for raised intra-cranial pressure following decompressive craniectomy for severe head injury.

BACKGROUND: Decompressive craniectomy is an extremely useful surgical procedure for decreasing intra cranial pressure following severe head injury. However, there is anecdotal evidence to suggest that some of these patients may continue to have raised intracranial pressure in spite of an apparently adequate Decompressive craniectomy. AIMS AND OBJECTIVES: (1) To assess whether fundoscopic findings accurately reflect changes in ICP in severe head injury. (2) To study the temporal course of fundoscopic findings in patients with severe head injury following decompressive craniectomy and to correlate fundoscopy findings with ventriculomegaly (if any) on serial Computerized tomography in these patients. MATERIALS AND METHODS: In this prospective study from November 2008 to March 2009, 32 patients severe head injury (GCS ≤8) admitted at the Department of Neurosurgery, JPN Apex Trauma Center, All India Institute of Medical Sciences, New Delhi who underwent a wide (>80 cubic cm) decompressive craniectomy with a lax duraplasty for severe head injury were subjected to fundoscopic examinations on the 1st, 3rd, 5th, 7th and 14th post operative days along with serial C.T. imaging studies to check for ventriculomegaly. Ventriculomegaly was defined as dilatation of temporal horn >2mm along with ballooning of III ventricle and/or presence of peri-ventricular lucency. Seven severe head injury patients who were conservatively managed with continuous ICP monitoring were also subjected to serial fundoscopic examinations. RESULTS: 32 patients who underwent decompressive craniectomy for severe head injury were evaluated during the study period. The age group of the patients ranged from 12 to 75 years. The mean GCS on admission was 6/15 (range 3/15-8/15). There were 12 cases of acute traumatic subdural hemorrhage and 20 cases of intracerebral contusion (frontal/temporal regions). Fundoscopic examination showed papilloedema in 81% (n=26) on the first post operative day, 66% (n=21) on the third post operative day, 28% (n=9) on the fifth post operative day, 13% (n=4) on the seventh post operative day and 6% (n=2) at 14 days post-operatively. In 4 (13%) patients papilloedema reappeared on fundoscopy after one week of surgery. Of these, only 1 (3%) patient had ventriculomegaly on CT scans. Lumbar drain was placed in 2 of these patients and resulted in prompt resolution of papilloedema. In the 7 patients who were managed conservatively and had ICP monitoring, serial fundoscopic examination were found to accurately reflect the ICP readings in all cases. No papilloedema was seen in any of the patients when ICP was below 20mm of Hg and papilloedema appeared in all cases where the ICP was ≥20mm of Hg. CONCLUSION: Fundoscopy is an extremely useful non-invasive tool to assess changes in intracranial pressure in severe head injury. Reappearance of papilloedema in the postoperative period even in the absence of ventriculomegaly indicates raised ICP and should be treated aggressively.

Traumatic interhemispheric subdural haematoma: Study of 35 cases.

The clinical and radiological findings, management, and outcomes in 35 patients with traumatic interhemispheric subdural haematoma (ISH) were reviewed retrospectively. Twenty-five patients had favourable outcomes and 10 had poor outcomes. All patients were treated conservatively for ISH. Univariate analysis found that the Glasgow Coma Scale (GCS) score (p < 0.001), hypovolemic shock (p = 0.018), skull fracture (p = 0.008), convexity or posterior fossa subdural haematoma (p = 0.008), and subarachnoid haemorrhage (SAH) were correlated with outcome (p < 0.001). Multivariate analysis showed that GCS score (p = 0.031; odds ratio [OR], 0.6; 95% confidence interval [CI], 0.3-0.9) and the presence of SAH (p = 0.023; OR, 14.2; 95% CI, 1.5-138.2) were significantly related to poor outcome. This study provides important information on the clinicoradiological findings and prognoses in patients with traumatic ISH.

Effect of minimally invasive surgery for cerebral hematoma evacuation in different stages on motor evoked potential and thrombin in dog model of intracranial hemorrhage.

OBJECTIVE: To observe the effect of minimally invasive surgery for cerebral hematoma evacuation in different stages on motor evoked potential (MEP) and thrombin in dog model of intracranial hemorrhage. METHODS: Twenty dogs were selected to prepare the intracranial hemorrhage model, which were randomly divided into 6, 12, 18 and 24 hour groups, respectively. The animals in each group underwent a minimally invasive surgery to evacuate the cerebral hematoma after the models were prepared. Before and after procedures, Purdy score, MEP and thrombin in hematoma region were determined and compared. RESULTS: Significant decreases in Purdy score, latency of MEP and thrombin expression were observed in 6 and 12 hour groups as compared with the 18 and 24 hour groups (p<0.01). DISCUSSION: In the present experiment, we established a dog model of intracranial hemorrhage, which was minimally invasive, easy to operate, highly repeated, simulating the pathological and physiological changes of clinical hypertensive intracranial hemorrhage. Both the latency of MEP and the expression of thrombin decreased after evacuation of intracranial hematoma in early stages by minimally invasive procedures, indicating that minimally invasive procedures for cerebral hematoma in ultra-early and early stages might be more effective to limit brain injury and decrease the latency of MEP and thrombin expression.

Systematic characterization of the computed tomography angiography spot sign in primary intracerebral hemorrhage identifies patients at highest risk for hematoma expansion: the spot sign score.

BACKGROUND AND PURPOSE: The presence of active contrast extravasation (the spot sign) on computed tomography (CT) angiography has been recognized as a predictor of hematoma expansion in patients with intracerebral hemorrhage. We aim to systematically characterize the spot sign to identify features that are most predictive of hematoma expansion and construct a spot sign scoring system. METHODS: We retrospectively reviewed CT angiograms performed in all patients who presented to our emergency department over a 9-year period with primary intracerebral hemorrhage and had a follow-up noncontrast head CT within 48 hours of the baseline CT angiogram. Three neuroradiologists reviewed the CT angiograms and determined the presence and characteristics of spot signs according to strict radiological criteria. Baseline and follow-up intracerebral hemorrhage volumes were determined by computer-assisted volumetric analysis. RESULTS: We identified spot signs in 71 of 367 CT angiograms (19%), 6 of which were delayed spot signs (8%). The presence of any spot sign increased the risk of significant hematoma expansion (69%, OR=92, P<0.0001). Among the spot sign characteristics examined, the presence of > or =3 spot signs, a maximum axial dimension > or =5 mm, and maximum attenuation > or =180 Hounsfield units were independent predictors of significant hematoma expansion, and these were subsequently used to construct the spot sign score. In multivariate analysis, the spot sign score was the strongest predictor of significant hematoma expansion, independent of time from ictus to CT angiogram evaluation. CONCLUSIONS: The spot sign score predicts significant hematoma expansion in primary intracerebral hemorrhage. If validated in other data sets, it could be used to select patients for early hemostatic therapy.

Accidental traumatic head injury in infants and young children.

This article will discuss accidental head injuries in infants and young children. The first category of injury is the crushing head injury. Static forces applied slowly to the head result in multiple fractures of the skull and contusions and lacerations of the brain resulting from the bone fragments striking the brain. This article will discuss the subject of short falls in young children and the resulting head injuries. Because falls are frequent events in early life, many cases have been collected and many papers written on the subject. Study of these cases is informative about the injuries likely to occur in these falls. Most often, only a minor contact injury such as scalp bruise or laceration results. In a 2 to 3% of falls, a simple linear skull fracture occurs and the majority of these are uneventful in terms of neurological deficit or intracranial bleeding. In about 1% of the fractures, an epidural or subdural hemorrhage occurs. Each of these forms of contact hemorrhages will be discussed and illustrated. While these are relatively rare injuries, it is essential that they can be identified as consistent with an accidental mechanism so that an erroneous diagnosis of inflicted injury is not made.