Rise In Intracranial Pressure Research Articles

Modelling midline shift and ventricle collapse in cerebral oedema following acute ischaemic stroke.

In ischaemic stroke, a large reduction in blood supply can lead to the breakdown of the blood-brain barrier and to cerebral oedema after reperfusion therapy. The resulting fluid accumulation in the brain may contribute to a significant rise in intracranial pressure (ICP) and tissue deformation. Changes in the level of ICP are essential for clinical decision-making and therapeutic strategies. However, the measurement of ICP is constrained by clinical techniques and obtaining the exact values of the ICP has proven challenging. In this study, we propose the first computational model for the simulation of cerebral oedema following acute ischaemic stroke for the investigation of ICP and midline shift (MLS) relationship. The model consists of three components for the simulation of healthy blood flow, occluded blood flow and oedema, respectively. The healthy and occluded blood flow components are utilized to obtain oedema core geometry and then imported into the oedema model for the simulation of oedema growth. The simulation results of the model are compared with clinical data from 97 traumatic brain injury patients for the validation of major model parameters. Midline shift has been widely used for the diagnosis, clinical decision-making, and prognosis of oedema patients. Therefore, we focus on quantifying the relationship between ICP and midline shift (MLS) and identify the factors that can affect the ICP-MLS relationship. Three major factors are investigated, including the brain geometry, blood-brain barrier damage severity and the types of oedema (including rare types of oedema). Meanwhile, the two major types (stress and tension/compression) of mechanical brain damage are also presented and the differences in the stress, tension, and compression between the intraparenchymal and periventricular regions are discussed. This work helps to predict ICP precisely and therefore provides improved clinical guidance for the treatment of brain oedema.

Intracranial pressure is elevated at 24 h post‐stroke in mice

AbstractBackgroundIt has long been assumed that post‐stroke intracranial pressure (ICP) elevation occurs because of large infarct and edema volumes. However, we have repeatedly shown ICP elevation at 24 h post‐stroke in the presence of little to no edema in rats. Biological processes are often conserved across species and types of injury. Therefore, we aimed to determine if an ICP rise occurs at 24 h post‐stroke in the presence of small infarct and edema volumes in mice.MethodsMice were randomized by random number table to either photothrombotic stroke or sham surgery (n = 15). Epidural ICP was recorded using a fiber optic catheter at 1 h post‐stroke (baseline) and between 23 and 24 h post‐stroke.ResultsICP was significantly higher at 24 h compared to baseline in stroke animals (n = 6; 10.71 ± 6.45 mmHg vs. 3.74 ± 2.20 mmHg, respectively; p = 0.03). ICP at 24 h was also significantly higher in stroke mice compared to sham (n = 6; 3.45 ± 1.43 mmHg; p = 0.02). There was no change in ICP in sham mice (p = 0.9). Edema volumes in stroke animals were small (0.04 ± 0.04 mm3) and unlikely to have caused significant ICP elevation.ConclusionThis study provides evidence of an edema‐independent ICP elevation following small ischemic stroke in mice. The occurrence of this rise supports our findings in other species and suggests it is caused by a previously undescribed mechanism.

Developing a porcine model of severe traumatic brain injury induced by high amplitude rotational acceleration

IntroductionIt is unclear which pathophysiological processes initiate and drive dynamic cerebrovascular autoregulation (CA) impairment as seen in traumatic brain injury (TBI). This is not solely attributable to raised intracranial pressure (ICP), but also results from local tissue damage. Research questionIn order to investigate CA disturbing processes, a porcine model is needed that mimics severe TBI as seen in humans. This model requires high amplitude rotational acceleration. Material and methodsA customized device was built to produce a rotational impulse with high amplitude and short pulse duration. Following preparatory tests on cadaver piglets, six piglets of six weeks old were sedated, ventilated and subjected to rotational impulses of different magnitudes. The impulse was immediately followed by installment of invasive monitoring of ICP, PbO₂, Laser Doppler Flowmetry and arterial blood pressure. TBI was further characterized by magnetic resonance brain imaging. ResultsThe current setup enabled to reach sagittal head rotational maximal acceleration magnitudes up to 30 krad/s2. Half of the animals had an increase in ICP, measured shortly after the impulse. It has proved impossible so far to produce a sustained rise in ICP as seen in human severe TBI. MRI showed no anatomical abnormalities which would confirm severe TBI. Discussion and conclusionThe challenge to build a porcine model in which severe TBI with ICP raise and MRI changes as seen in humans can be reliably reproduced is still ongoing. It might be that higher peak rotational accelerations are needed.

Recurrent reflex syncope in idiopathic intracranial hypertension patient resolved after lumbar puncture: pathogenetic implications

BackgroundIdiopathic intracranial hypertension is a disease characterized by increased intracranial cerebrospinal fluid volume and pressure without evidence of other intracranial pathology. Dural sinuses are rigid structures representing a privileged low-pressure intracranial compartment. Rigidity of dural sinus ensures that the large physiologic fluctuations of cerebrospinal fluid pressure associated with postural changes or to Valsalva effect cannot be transmitted to the sinus. An abnormal dural sinus collapsibility, especially when associated with various anatomical sinus narrowing, has been proposed as a key factor in the pathogenesis of idiopathic intracranial hypertension. This pathogenetic model is based on an excessive collapsibility of the dural sinuses that leads to the triggering of a self-limiting venous collapse positive feedback-loop between the cerebrospinal fluid pressure, that compresses the sinus, and the increased dural sinus pressure upstream, that reduces the cerebrospinal fluid reabsorption rate, increasing cerebrospinal fluid volume and pressure at the expense of intracranial compliance and promoting further sinus compression. Intracranial compliance is the ability of the craniospinal space to accept small volumetric increases of one of its compartments without appreciable intracranial pressure rise. In idiopathic intracranial hypertension, a condition associated with a reduced rate of CSF reabsorption leading to its volumetric expansion, a pathologically reduced IC precedes and accompanies the rise of ICP. Syncope is defined as a transient loss of consciousness due to a transient cerebral hypoperfusion characterized by rapid onset, short duration, and spontaneous complete recovery. A transient global cerebral hypoperfusion represents the final mechanism of syncope determined by cardiac output and/or total peripheral resistance decrease. There are many causes determining low cardiac output including reflex bradycardia, arrhythmias, cardiac structural disease, inadequate venous return, and chronotropic and inotropic incompetence. Typically, syncopal transient loss of consciousness is mainly referred to an extracranial mechanism triggering a decrease in cardiac output and/or total peripheral resistance. Conversely, the association of syncope with a deranged control of intracranial compliance related to cerebral venous outflow disorders has been only anecdotally reported.Case PresentationWe report on a 57-year-old woman with daily recurrent orthostatic hypotension syncope and idiopathic intracranial hypertension-related headaches, which resolved after lumbar puncture with cerebrospinal fluid subtraction.ConclusionsA novel mechanism underlying the triggering of orthostatic syncope in the presence of intracranial hypertension-dependent reduced intracranial compliance is discussed.

Photoreceptor Damage in Terson Syndrome.

To describe photoreceptor damage in patients with Terson syndrome as a potential cause for inconsistent clinical outcomes. Clinical evaluation and retinal imaging in six patients. Four patients were female and two male, with an average age of 46.8 years (SD 8.9). Four patients suffered aneurysmal subarachnoid haemorrhage, one vertebral artery dissection, and one superior sagittal sinus thrombosis. In 11 eyes, we observed a consistent pattern of outer retinal damage within the central macula affecting the ellipsoid zone and the outer nuclear layer, indicating photoreceptor damage. Areas of photoreceptor damage showed poor spatial correlation with intraocular haemorrhage, particularly sub-internal limiting membrane haemorrhage. The observed retinal abnormalities demonstrated incomplete recovery over long-term follow-up 3.5 to 8 years post-haemorrhage, irrespective of surgical or conservative treatment strategy, and had variable impact on the patients' visual function. The observations suggest that photoreceptor damage in Terson syndrome likely represents a distinct manifestation of this condition, which could be caused by transient ischaemia resulting from disturbed choroidal perfusion secondary to acute rise in intracranial pressure.

Optic Nerve Sheath Diameter as a Predictor of Raised Intracranial Pressure Findings on Orbital Ultrasound

BACKGROUND
 Several studies have found an association between raised intracranial pressure (ICP) and optic nerve sheath diameter (ONSD) in conditions with severe head injury and intracranial bleeding. Idiopathic intracranial hypertension is also a cause of elevated ICP. Because the meninges and subarachnoid space around the optic nerve are continuous, a rise in ICP can be detected with an increase in ONSD. The objectives of this study were to correlate Optic Nerve Sheath Diameter (ONSD) with features suggestive of raised intracranial pressure on CT / MRI of the Brain and describe the features suggestive of raised intracranial pressure on CT/MRI Brain in clinically suspected patients.
 METHODS
 This was a case control study carried out in the Department of Radio-diagnosis at MGMCRI for suspected raised intracranial pressure evaluation. All these patients were subjected to ultrasound examination of the eye and the optic sheath diameter was measured while the patients were in supine posture. ONSD was measured on Mind ray DC8, and/or GE S7 Expert using High frequency linear probe on the closed upper eyelid with adequate aqueous gel as a coupling agent. ONSD was also measured in Philips 1.5T MRI and Ge optima 128 slice CT. Patients were followed up on whether they were treated surgically or medically and if they developed clinical signs of raised ICP such as headache, vomiting, raised blood pressure, double vision, confusion or loss of consciousness.
 RESULTS
 The raised ICP was observed in 30.67 % of study patients and the optic nerve sheath distension was observed in 37.33% of patients. The diagnostic accuracy of determining the optic nerve sheath diameter was equal such as area under curve, sensitivity and specificity as 0.833, 66.67% and 100 % respectively in both methods.
 CONCLUSIONS
 ONSD has emerged as an interesting option for measuring intracranial hypertension in brain-injured states, owing to its simplicity, non-invasive nature, and accessibility.

447 Haptoglobin Treatment to Improve Outcome After Aneurysmal Subarachnoid Haemorrhage: A Consensus Perspective on Clinical Translation

Abstract Aim Aneurysmal subarachnoid haemorrhage (aSAH) is a devastating form of stroke with an unmet need to improve outcome. This study focusses on the development of intrathecal haptoglobin supplementation as a treatment by reviewing current knowledge and progress and arriving at a Delphi-based global consensus regarding the role of extracellular haemoglobin and research priorities for clinical translation of haemoglobin-scavenging strategies. Method A narrative review of the topic by searching PubMed with relevant keywords and through discussions with leading expert in the field of aSAH. A modified Delphi processes. Four virtual meetings were held, two prior to starting, and two during the first round. Otherwise, the study was conducted electronically. Results Clinicians (n = 72) and scientific experts (n = 28) from five continents participated in the Delphi study. Microvascular spasm, iInflammation, microvascular spasm, and initial intracranial pressure rise were deemed the most important pathophysiological pathways determining outcome. Extracellular haemoglobin was thought to play an important role mostly in iron toxicity, oxidative stress, nitric oxide homeostasis and inflammation. While useful, there was consensus that further preclinical work was not a priority, with most believing the field to be ready for early phase trial. The highest priorities were related to confirming haptoglobin’s anticipated safety, individualized versus standard dosing, timing of treatment, pharmacokinetics, pharmacodynamics and outcome measure selection. Conclusions These results highlight the pressing need for early phase trials of intracranial haptoglobin for aSAH, and the immense value of early input from clinical disciplines on a global scale during the early stages of clinical translation.

The Role of Substance P Within Traumatic Brain Injury and Implications for Therapy.

This review examines the role of the neuropeptide substance P within the neuroinflammation that follows traumatic brain injury. It examines it in reference to its preferential receptor, the neurokinin-1 receptor, and explores the evidence for antagonism of this receptor in traumatic brain injury with therapeutic intent. Expression of substance P increases following traumatic brain injury. Subsequent binding to the neurokinin-1 receptor results in neurogenic inflammation, a cause of deleterious secondary effects that include an increased intracranial pressure and poor clinical outcome. In several animal models of TBI, neurokinin-1 receptor antagonism has been shown to reduce brain edema and the resultant rise in intracranial pressure. A brief overview of the history of substance P is presented, alongside an exploration into the chemistry of the neuropeptide with a relevance to its functions within the central nervous system. This review summarizes the scientific and clinical rationale for substance P antagonism as a promising therapy for human TBI.

ICP during head movement: significance of the venous system.

It is thought that the internal jugular veins (IJV) are the primary route for cranial venous outflow in supine position and the vertebral venous plexus when upright. Previous studies have noted a greater increase in intracranial pressure (ICP) when subjects turn their head in one direction compared to the other, but no clear cause had been investigated. We hypothesised that in the supine position, head turning and consequently obstructing the IJV draining the dominant transverse sinus (TVS) would lead to a greater rise in ICP compared to turning to the non-dominant side. A prospective study in a large-volume neurosurgical centre. Patients undergoing continuous ICP monitoring as part of their standard clinical management were recruited. Immediate ICP was measured in different head positions (neutral, rotated to the right and left) when supine, seated, and standing. TVS dominance was established by consultant radiologist report on venous imaging. Twenty patients were included in the study, with a median age of 44 years. Venous system measurements revealed 85% right-sided vs 15% left-sided dominance. Immediate ICP rose more when head turning from neutral to the dominant TVS (21.93mmHg ± 4.39) vs non-dominant side (16.66mmHg ± 2.71) (p= <0.0001). There was no significant relationship in the sitting (6.08mmHg ± 3.86 vs 4.79mmHg ± 3.81, p = 0.13) or standing positions (8.74mmHg ± 4.30 vs 6.76mmHg ± 4.14, p =0.07). This study has provided further evidence that the transverse venous sinus to internal jugular system pathway is the likely primary venous drainage when supine; and quantified its effect when head turning on ICP. It may guide patient-specific nursing care and advice.

Atypical Posterior Reversible Encephalopathy Syndrome with Obstructive Hydrocephalus and Impending Tonsillar Herniation. (P6-5.030)

<h3>Objective:</h3> <h3>OBJECTIVE AND IMPORTANCE:</h3> Rhombencephalic edema with hydrocephalus has rarely been described as a manifestation of hypertensive emergency. We present an unusual case of brain edema with hydrocephalus secondary to hypertensive emergency. <h3>Background:</h3> <h3>CASE DESCRIPTION:</h3> A 33-year-old male with uncontrolled hypertension and CKD Stage IV presented to hospital with occipital headache and vomiting. His BP was 230/160. He was treated with Nicardipine infusion. CT head showed cerebellar vasogenic edema and mild tonsillar herniation with partial effacement of the fourth ventricle. MRI confirmed these findings, there was disproportionate dilatation of the lateral and third ventricles with periventricular T2 hyperintense signal consistent with transependymal CSF flow. The headache and neck pain were persistent. The patient was upgraded to Neurocritical Care Unit for monitoring and continued IV BP treatment. Given concerns for incipient tonsillar herniation, Mannitol and Hemodialysis [HD] were added to his medical treatment. After these interventions, his headache and blood pressure management improved. Two days later, CT showed significant interval improvement of hydrocephalus, cerebral edema and posterior fossa crowding. <h3>Design/Methods:</h3> N/A <h3>Results:</h3> <h3>DISCUSSION:</h3> This was an unusual case of extension of PRES to the posterior fossa, leading to hydrocephalus and a vicious cycle of worsening rise in intracranial pressure, leading to worsening refractory systemic hypertension, end organ damage, need for hemodialysis, impending tonsillar herniation and risk of death. <h3>Conclusions:</h3> <h3>CONCLUSION:</h3> This presentation and improvement were compatible with the final diagnosis of an atypical presentation of Posterior Reversible Encephalopathy Syndrome. In this case, reduction of blood pressure, hyperosmolar therapy and dialysis resulted in improvement of the symptoms as well as radiological resolution of hydrocephalus. Aggressive medical treatment was the best approach in this case, but neurosurgical intervention would have been necessary if the patient had not responded to these measures. <b>Disclosure:</b> Dr. Solano has nothing to disclose. Dr. Zafar has nothing to disclose. Dr. Newman has received personal compensation in the range of $5,000-$9,999 for serving as an Expert Witness for Clyde Bergstresser, LLC. Dr. Newman has received personal compensation in the range of $500-$4,999 for serving as an Expert Witness for Maria Rubio LLC. The institution of Dr. Newman has received research support from Albert Einstein Society.

330 Interactions of Brain, Blood, and CSF: A Novel Mathematical Model of Cerebral Edema

INTRODUCTION: Previous models of intracranial pressure (ICP) dynamics have not included flow of cerebral interstitial fluid (ISF) and changes in resistance to its flow when brain swelling occurs. METHODS: We developed a lumped parameter model which includes a representation of cerebral ISF flow within brain tissue and its interactions with CSF flow and CBF. The model is based on an electrical analog circuit with four intracranial compartments: the (1) subarachnoid space, (2) brain, (3) ventricles and (4) cerebral vasculature. We determined changes in pressure and volume within cerebral compartments at steady-state and simulated perturbations: Rapid injection into the intracranial space, hyper-and hypoventilation. We simulated changes in resistance to flow or absorption of CSF and cerebral ISF to model hydrocephalus and cerebral edema. RESULTS: The model accurately replicates features of intracranial physiology including the pressure–volume curve, increased ICP pulse pressure with rising ICP, hydrocephalus from increased resistance to CSF outflow, and changes associated with ventilation. Importantly, modeling edema with increased resistance to ISF flow mimics key features of brain swelling including elevated ICP, increased brain volume, effaced ventricles, and a contracted subarachnoid space. Similarly, decreased resistance to flow of fluid across the BBB leads to an exponential-like rise in ICP and ventricular collapse. CONCLUSIONS: The model accurately depicts the complex interactions that occur between pressure, volume, and resistances to flow in the different intracranial compartments under specific pathophysiological conditions. In modelling resistance to bulk flow of cerebral ISF, it may serve as a platform for improved modelling of cerebral edema and blood–brain barrier disruption that occur following brain injury.

168 Elevated Intracranial Pressure is Associated With Memory Dysfunction in Intraventricular Hemorrhage Animal Model

INTRODUCTION: Survivors of nontraumatic intraventricular hemorrhage are often left with memory impairment, however, underlying mechanisms of this dysfunction remain to be elucidated. METHODS: The experimental design included two groups of Sprague Dawley rats (n=30): intraventricular hemorrhage (control) and intraventricular hemorrhage with sustained high intracranial pressures (experimental). The autologous intraventricular blood injection model was used. In the experimental group the intracranial pressure was artificially elevated. Ten days following surgery, each rat underwent Morris water maze. T test was used with a p value of &lt; 0.05 considered statistically significant. RESULTS: The average maximum intracranial pressure in the experimental group was 75.6 ± 17.5 mmHg compared to 66.5 ± 17.3 mmHg in the control group (p = 0.260). The experimental group experienced elevated intracranial pressure for two hours following induction of intraventricular hemorrhage, whereas the intracranial pressure normalized within minutes in the control group. The mean cerebral perfusion pressure tended to be lower in the experimental group (20 ± 25.6 mmHg) compared to the control group (30 ± 19.4 mmHg) (p = 0.302). In Morris water maze, the experimental group needed more time to reach the platform (37.3 ± 21.8 seconds) compared to the control group (19.7 ± 14.3 seconds) (p = 0.041). The experimental group also spent less time in 5% and 10% target quadrants, 2.4 ± 1.8 and 5.7 ± 3.9 seconds, respectively (p = 0.004) compared to the control group, 5.3 ± 2.2 and 10 ± 3 seconds, respectively (p &lt; 0.001). CONCLUSIONS: Animals who have prolonged elevated intracranial pressures following intraventricular hemorrhage perform poorly in spatial memory and learning. The authors suggest that a rise in intracranial pressure might be the driver for activating pathways responsible for subsequent memory dysfunction.

Peak appearance time in pulse waveforms of intracranial pressure and cerebral blood flow velocity.

The shape of the pulse waveforms of intracranial pressure (ICP) and cerebral blood flow velocity (CBFV) typically contains three characteristic peaks. It was reported that alterations in cerebral hemodynamics may influence the shape of the pulse waveforms by changing peaks' configuration. However, the changes in peak appearance time (PAT) in ICP and CBFV pulses are only described superficially. We analyzed retrospectively ICP and CBFV signals recorded in traumatic brain injury patients during decrease in ICP induced by hypocapnia (n = 11) and rise in ICP during episodes of ICP plateau waves (n = 8). All three peaks were manually annotated in over 48 thousand individual pulses. The changes in PAT were compared between periods of vasoconstriction (expected during hypocapnia) and vasodilation (expected during ICP plateau waves) and their corresponding baselines. Correlation coefficient (rS) analysis between mean ICP and mean PATs was performed in each individual recording. Vasodilation prolonged PAT of the first peaks of ICP and CBFV pulses and the third peak of CBFV pulse. It also accelerated PAT of the third peak of ICP pulse. In contrast, vasoconstriction shortened appearance time of the first peaks of ICP and CBFV pulses and the second peak of ICP pulses. Analysis of individual recordings demonstrated positive association between changes in PAT of all three peaks in the CBFV pulse and mean ICP (rS range: 0.32-0.79 for significant correlations). Further study is needed to test whether PAT of the CBFV pulse may serve as an indicator of changes in ICP-this may open a perspective for non-invasive monitoring of alterations in mean ICP.

Effect of sevoflurane, propofol and propofol with dexmedetomidine as maintenance agent on intracranial pressure in the Trendelenburg position during laparoscopic surgeries.

Pneumoperitoneum (PP) and the Trendelenburg position (TP) in laparoscopic surgeries are associated with rise in intracranial pressure (ICP). The optic nerve sheath diameter (ONSD) is a surrogate marker of ICP. The study aimed to evaluate the effect of sevoflurane, propofol and propofol with dexmedetomidine as maintenance agent on ICP in TP during laparoscopic surgeries. A total of 120 American Society of Anesthesiologists (ASA) physical status I/II patients, aged 18-65 years were randomly allocated into three groups: sevoflurane as group S, propofol as group P, and propofol with dexmedetomidine as group PD. The intra-abdominal pressure (IAP) was kept in the range of 12-14 mmHg and TP varied between 15°- 45° angle. The primary objective was comparison of ICP and secondary objectives were IOP, intraoperative hemodynamic and postoperative recovery characteristics among groups. The ONSD and IOP were measured in both eyes 10 min after endotracheal intubation (T0), 5 min after CO2 insufflation (T1), 5 min after TP (T2) and 5 min after deflation of gas (T3). The data were analyzed by using the Statistical Package for Social Sciences version 23. ONSD and IOP at T1 and T2 were significantly higher than T0 in all groups, but no significant difference was found among the intergroup groups. Significantly lower heart rate and mean blood pressure were observed in PD group at T1 and T2 compared to group S and group P. The rise in ICP was comparable among sevoflurane, propofol, and propofol-dexmedetomidine combination as a maintenance agent during laparoscopic surgeries in TP.

Anaesthetic management of parturient posted for elective caesarean section with cerebral arteriovenous malformation

Sir, Cerebral arteriovenous malformation (AVM) has a prevalence of 0.01–0.05%.[1] We present a case of a 25-year-old primigravida at 37 weeks gestation, a known case of left frontoparietal AVM and epilepsy posted for elective cesarean section. Five years ago, she presented with weakness of the right upper and lower limbs. She was diagnosed with left frontoparietal AVM [Figures 1 and 2]. She had multiple seizure episodes and was started on T. levetiracetam 500 mg BD, T. lacosamide 200 mg BD, T. clobazam 10 mg BD, and T. phenytoin 100 mg OD.Figure 1: MR venogram showing large draining veins joining superior sagittal sinusFigure 2: MRI of the brain showing numerous flow voids along the left frontoparietal lobe and atrophy of neuroparenchyma in the left cerebral hemisphereA pre-anesthetic evaluation was done. She gave a history of seizure attacks 4 days back. She was premedicated with oral pantoprazole 40 mg and metoclopramide 10 mg 1 h before surgery and kept nil per oral for 6 h. All antiepileptic drugs were continued. In the operating room, the wedge was placed under her right hip. Standard pre-induction monitors were attached and intravenous (IV) access was secured. The cesarean section was done under general anesthesia. Rapid sequence induction was performed with IV thiopentone 5 mg/kg and rocuronium 1.2 mg/kg. The patient was intubated with a 7 mm internal diameter endotracheal tube after 1 min. Anesthesia was maintained with oxygen, air, and isoflurane. After delivery of a live female baby of 2.2 kg, IV fentanyl 2 mg/kg, midazolam 2 mg, ondansetron 4 mg, and oxytocin infusion were given. The patient was hemodynamically stable and the postoperative pain was managed with an ultrasound-guided bilateral transverses abdominis plane block. The parturient was extubated and shifted to the intensive care unit (ICU). She had an uneventful postoperative period. Cerebral AVM usually presents with intracranial hemorrhage, seizures, focal neurologic deficits, and headaches.[2] The symptoms of AVM may be mistaken with pregnancy-associated disorders such as eclampsia. computed tomography (CT) and magnetic resonance imaging (MRI) (with abdomen shielding) help to confirm the diagnosis. It is mandatory to document the neurological deficits, optimize antiepileptics, counsel regarding the potential complications, and the need for neurosurgery. The neurosurgeon and intervention radiologist were alerted regarding the patient’s delivery plan and the neurologist’s opinion was taken to optimize the antiepileptics. There are no conclusive data regarding the risk of AVM hemorrhage during pregnancy.[3,4] AVM hemorrhage during pregnancy is associated with 28% maternal and 14% neonatal mortality. Most centers prefer elective cesarean sections even though normal vaginal deliveries do not increase the risk of AVM hemorrhage. Uterine contractions during normal labor may increase the stress on the abnormal veins. Hence, if vaginal delivery is planned, epidural labor analgesia and assisted instrumental vaginal delivery are recommended. For cesarean section, general anesthesia is preferred over regional anesthesia to avoid neurological complications. cerebrospinal fluid (CSF) release with subarachnoid block causes a sudden change in the transmural pressure across the AVM predisposing it to rupture. An accidental intravascular injection of local anesthetic containing epinephrine test dose during the initiation of the test dose following epidural anesthesia could predispose to the rupture of AVM. The main aim of anesthetic management is to maintain the mean arterial and intracranial pressure within the normal range to reduce the risk of hemorrhage and cerebral hypoperfusion. Hypertensive responses to laryngoscopy and extubation should be obtunded. Thiopentone is the preferred induction agent.[5] Ketamine is avoided as it can increase blood pressure and intracranial pressure. Suxamethonium has to be avoided and a high dose of rocuronium 1.2 mg/kg is used for rapid sequence induction.[6] General anesthesia with controlled ventilation is used to keep PaCO2 at a low normal range to minimize cerebral vasodilatation and rise in intracranial pressure. Hypotension during surgery is avoided by optimal fluid resuscitation and vasopressors. Supine hypotension is avoided by the use of a wedge under the hip. Thus, multi-disciplinary care involving an obstetrician, intervention radiologist, neurologist, neurosurgeon, and obstetric anesthesiologist is required to ensure good pregnancy outcomes in these high-risk parturients. Declaration of patient consent The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.

Ultrasonographic measured optic nerve sheath diameter as a bedside prognostication tool in patients with severe traumatic brain injury

Rise in intracranial pressure (ICP) after the severe traumatic brain injury (TBI) has been associated with poor outcomes in patients. Measuring ONSD on ultrasonography is an emerging noninvasive bedside tool that can reliably and rapidly detect raised ICP. 30-year-old patient sustained a head injury in a road traffic accident. On examination it was found that GCS was 7/15, 4 mm bilaterally fixed pupils, negative corneal response and ONSD was 6.38 mm on the ultrasound. The raised intracranial pressure was detected and management was immediately started. Patient was immediately taken up for surgery after a CT scan was done. This case report highlights the potential of rapidly identifying raised intracranial pressure at the patients’s bedside by measuring ONSD by ultrasonography.

Surgical decompression for malignant cerebral oedema after ischaemic stroke.

Large territory middle cerebral artery (MCA) ischaemic strokes account for around 10% of all ischaemic strokes and have a particularly devastating prognosis when associated with malignant oedema. Progressive cerebral oedema starts developing in the first 24 to 48 hours of stroke ictus with an associated rise in intracranial pressure. The rise in intracranial pressure may eventually overwhelm compensatory mechanisms leading to a cascading secondary damage to surrounding unaffected parenchyma. This downward spiral can rapidly progress to death or severe neurological disability. Early decompressive craniectomy to relieve intracranial pressure and associated tissue shift can help ameliorate this secondary damage and improve outcomes. Evidence has been accumulating of the benefit of early surgical decompression in stroke patients. Earlier studies have excluded people above the age of 60 due to associated poor outcomes; however, newer trials have included this patient subgroup. This review follows a Cochrane Review published in 2012. To assess the effectiveness of surgical decompression in people with malignant oedema after ischaemic stroke with regard to reduction in mortality and improved functional outcome. We also aimed to examine the adverse effects of surgical decompression in this patient cohort. We searched the Cochrane Stroke Group Trials Register, the Cochrane Central Register of Controlled Trials (CENTRAL; 2022, Issue 7 of 12), MEDLINE Ovid, Embase Ovid, Web of Science Core Collection, Scopus databases, ClinicalTrials.gov, and the WHO ICTRP to July 2022. We also reviewed the reference lists of relevant articles. We included randomised controlled trials (RCTs) comparing decompressive craniectomy with medical management to best medical management alone for people with malignant cerebral oedema after MCA ischaemic stroke. Two review authors independently screened the search results, assessed study eligibility, performed risk of bias assessment, and extracted the data. The primary outcomes were death and death or severe disability (modified Rankin Scale (mRS) &gt; 4) at 6 to 12 months follow-up. Other outcomes included death or moderate disability (mRS &gt; 3), severe disability (mRS = 5), and adverse events. We assessed the certainty of the evidence using the GRADE approach, categorising it as high, moderate, low, or very low. We included nine RCTs with a total of 513 participants included in the final analysis. Three studies included patients younger than 60 years of age; two trials accepted patients up to 80 years of age; and one trial only included patients 60 years or older. The majority of included trials (six) mandated a time from stroke ictus to treatment of &lt; 48 hours, whilst in two of them this was &lt; 96 hours. Surgical decompression was associated with a reduction in death (odds ratio (OR) 0.18, 95% confidence interval (CI) 0.12 to 0.27, 9 trials, 513 participants, P &lt; 0.001; high-certainty evidence); death or severe disability (mRS &gt; 4, OR 0.22, 95% CI 0.15 to 0.32, 9 trials, 513 participants, P &lt; 0.001; high-certainty evidence); and death or moderate disability (mRS &gt; 3, OR 0.34, 95% CI 0.22 to 0.52, 9 trials, 513 participants, P &lt; 0.001; moderate-certainty evidence). Subgroup analysis did not reveal any significant effect on treatment outcomes when analysing age (&lt; 60 years versus ≥ 60 years); time from stroke ictus to intervention (&lt; 48 hours versus ≥ 48 hours); or dysphasia. There was a significant subgroup effect of time at follow-up (6 versus 12 months, P = 0.02) on death as well as death or severe disability (mRS &gt; 4); however, the validity of this finding was affected by fewer participant numbers in the six-month follow-up subgroup. There was no consistent reporting of per-participant adverse event rates in any of the included studies, which prevented further analysis. Surgical decompression improves outcomes in the management of malignant oedema after acute ischaemic stroke, including a considerable reduction in death or severe disability (mRS &gt; 4) and a reduction in death or moderate disability (mRS &gt; 3). Whilst there is evidence that this positive treatment effect is present in patients &gt; 60 years old, it is important to take into account that these patients have a poorer prospect of functional survival independent of this treatment effect. In interpreting these results it must also be considered that the data demonstrating benefit are drawn from a unique patient subset with profound neurological deficit, reduced level of consciousness, and no pre-morbid disability or severe comorbidity.

Development of Traumatic Brain Injury Associated Intracranial Hypertension Prediction Algorithms: A Narrative Review.

Traumatic intracranial hypertension (tIH) is a common and potentially lethal complication of moderate to severe traumatic brain injury (m-sTBI). It often develops with little warning and is managed reactively with the tiered application of intracranial pressure (ICP)-lowering interventions administered in response to an ICP rising above a set threshold. For over 45 years, a variety of research groups have worked toward the development of technology to allow for the preemptive management of tIH in the hope of improving patient outcomes. In 2022, the first operationalizable tIH prediction system became a reality. With such a system, ICP lowering interventions could be administered prior to the rise in ICP, thus protecting the patient from potentially damaging tIH episodes and limiting the overall ICP burden experienced. In this review, we discuss related approaches to ICP forecasting and IH prediction algorithms, which collectively provide the foundation for the successful development of an operational tIH prediction system. We also discuss operationalization and the statistical assessment of tIH algorithms. This review will be of relevance to clinicians and researchers interested in development of this technology as well as those with a general interest in the bedside application of machine learning (ML) technology.

Pathology and Pathogenesis of Brain Lesions Produced by Clostridium perfringens Type D Epsilon Toxin.

Clostridium perfringens type D epsilon toxin (ETX) produces severe, and frequently fatal, neurologic disease in ruminant livestock. The disorder is of worldwide distribution and, although vaccination has reduced its prevalence, ETX still causes substantial economic loss in livestock enterprises. The toxin is produced in the intestine as a relatively inactive prototoxin, which is subsequently fully enzymatically activated to ETX. When changed conditions in the intestinal milieu, particularly starch overload, favor rapid proliferation of this clostridial bacterium, large amounts of ETX can be elaborated. When sufficient toxin is absorbed from the intestine into the systemic circulation and reaches the brain, two neurologic syndromes can develop from this enterotoxemia. If the brain is exposed to large amounts of ETX, the lesions are fundamentally vasculocentric. The neurotoxin binds to microvascular endothelial receptors and other brain cells, the resulting damage causing increased vascular permeability and extravasation of plasma protein and abundant fluid into the brain parenchyma. While plasma protein, particularly albumin, pools largely perivascularly, the vasogenic edema becomes widely distributed in the brain, leading to a marked rise in intracranial pressure, coma, sometimes cerebellar herniation, and, eventually, often death. When smaller quantities of ETX are absorbed into the bloodstream, or livestock are partially immune, a more protracted clinical course ensues. The resulting brain injury is characterized by bilaterally symmetrical necrotic foci in certain selectively vulnerable neuroanatomic sites, termed focal symmetrical encephalomalacia. ETX has also been internationally listed as a potential bioterrorism agent. Although there are no confirmed human cases of ETX intoxication, the relatively wide species susceptibility to this toxin and its high toxicity mean it is likely that human populations would also be vulnerable to its neurotoxic actions. While the pathogenesis of ETX toxicity in the brain is incompletely understood, the putative mechanisms involved in neural lesion development are discussed.

A computational study of metal ions interaction with amyloid-β 1–42 peptide structure in hyperpyrexia: Implications for Alzheimer disease

Given the current context of the SARS-CoV-19 pandemic, among the interfering risky factors with the Aβ peptide aggregation in the brains of Alzheimer’s disease (AD) patients can be hyperpyrexia and increased intracranial pressure (ICP). According to our hypothesis on the relationship between hyperpyrexia and cognitive decline in AD, two models of Aβ peptides were used in this study: the structure of AD amyloid beta-peptide and near-atomic resolution fibril structures of the Aβ peptide. Therefore, the binding templates were constructed for Aβ peptide regions able to bind 9 different metal ions. The fragment transformation method was used for the structural comparison between Aβ chains. Molecular dynamics simulation (MDS) was applied using the Nose-Poincare-Anderson equation to generate a theoretically correct NPT (isothermal–isobaric ensemble). The smallest dissimilarities were observed in the case of Cu+ binding potential followed by Co2+, both with similar variation. Structural changes have also occurred as a result of the dynamic simulation. All these changes suggest an aggravating factor in both hyperpyretic and AD conditions. Our findings suggest that elevated temperature and increased intracranial pressure rise the effect of peptide aggregation, by converting α-helix motif to β-sheet and random coil conformation, which are related to the formation of senile plaques in AD brains.