Diffuse Brain Edema Research Articles

CAR-T Cells for the Treatment of Central Nervous System Tumours: Known and Emerging Neurotoxicities

The advent of chimeric antigen receptor (CAR)-T cells has recently changed the prognosis of relapsing/refractory diffuse large B-cell lymphomas, showing response rates as high as 60 to 80%. Common toxicities reported in the pivotal clinical trials include the cytokine release syndrome (CRS) and the Immune effector Cell-Associated Neurotoxicity Syndrome (ICANS), a stereotyped encephalopathy related to myeloid cell activation and blood–brain barrier dysfunction, presenting with a distinctive cascade of dysgraphia, aphasia, disorientation, attention deficits, vigilance impairment, motor symptoms, seizures, and diffuse brain oedema. The tremendous oncological efficacy of CAR-T cells observed in systemic B-cell malignancies is leading to their growing use in patients with primary or secondary central nervous system (CNS) lymphomas and in patients with solid tumours, including several CNS cancers. Early studies conducted in adult and paediatric patients with solid CNS tumours reported a distinct profile of neurotoxicity referred to as Tumour inflammation-associated neurotoxicity (TIAN), corresponding to local inflammation at the tumour site manifesting with focal neurological deficits or mechanical complications (e.g., obstructive hydrocephalus). The present review summarises available data on the efficacy and safety of CAR-T cells for solid and haematological CNS malignancies, emphasising known and emerging phenotypes, ongoing challenges, and future perspectives.

Outcome of Methanol Toxicity Outbreak In Saudi Arabia: Case Series Study.

Introduction Methanol poisoning is an acute medical emergency. If not recognized in time and treated properly, it can lead to a considerable magnitude of morbidity as well as mortality. This article aims to report cases of methanol toxicity, focusing on clinical presentation, management, and outcomes. Method Nine ICU-admitted patients with confirmed positive serum methanol levels wereanalyzed in a case series at King Fahad General Hospital in Jeddah, Saudi Arabia, between November 2022 and January 2023. Results Among the nine patients admitted to the ICU due to methanol poisoning, the majority were middle-aged males, with two females included. Gastrointestinal symptoms were seen in two-thirds of patients, while three patients required immediate mechanical ventilation due to a low Glasgow Coma Scale. Severe metabolic acidosis was observed in most cases. All patients received sodium bicarbonate and hemodialysis, with six patients also receiving fomepizole. However, two patients in the study with low initial low Glasgow Coma Scale (GCS), severe metabolic acidosis, and diffuse brain edema, did not survive. One patient reported acute complete vision loss. Conclusion This case series highlights the importance of promptly recognizing and managing methanol toxicity in ICU settings. The clinical presentation of methanol toxicity can be challenging, and early diagnosis and treatment are crucial to prevent irreversible damage.

Brainstem and upper cervical cord involvement in a patient with posterior reversible encephalopathy syndrome: Neuro-images.

Posterior reversible encephalopathy syndrome (PRES) is a clinicoradiological syndrome with acute heterogeneous neurological symptoms. It is usually preceded by hypertension or chemotherapy. Brain magnetic resonance imaging (MRI) shows vasogenic edema over the cortex and subcortex of parieto-occipital lobes. Involvement of the brainstem, basal ganglia, and spinal cord is rare. Here we described an 18 years old woman with a history of systemic lupus erythematosus who was admitted due seizure and impaired consciousness. She had a mean arterial pressure of 160 and previously received cyclophosphamide. She had a unique involvement of diffuse bilateral asymmetric brain edema over the upper cervical cord, brainstem, cerebellum, thalami, basal ganglia, frontotemporal, and parieto-occipital lobes. She was diagnosed with PRES and after the treatment vasogenic edema vanished completely. When it is clinically applicable, physicians should consider PRES as the differential diagnosis of vasogenic edema over the upper cervical cord, cerebellum, and brainstem.

Hypertonic saline versus mannitol in treatment of diffuse brain edema in patients with moderate and severe traumatic brain injury

Hypertonic saline versus mannitol in treatment of diffuse brain edema in patients with moderate and severe traumatic brain injury

Cerebral Autoregulation and Cardiovascular Physiology Dysfunction in Traumatic Brain Injury Cases: A Brief Review

Introduction: Traumatic brain injury (TBI) is one of the leading causes of death and disability in the early years of life. Post-TBI physiological alterations vary across adult and pediatric patients and severity. This disease affects the quality of life of most people. Acute hemiparesis can cause cognitive impairments. It may also impact mood, memory, and decision-making. Furthermore, parasympathetic dysfunction and sympathetic activation appear to contribute to cardiac injury via modulation of the myocardial inflammatory response via acetylcholine receptors.
 Purpose: This review aims to explain the neuronal response and cardiac dysfunction after traumatic brain injury cases.
 Methods: The review used Pubmed and Google Scholar to search for articles on traumatic brain injury, neuronal response, and cardiac biomarkers. The articles were chosen for their language, publishing, content, exposure, and outcome. The main reference is obtained from up to 79 articles that meet the inclusion requirements.
 Results: TBI can cause localized brain injury or diffuse brain injury from physical trauma such as diffuse axonal injury or brain edema. Repeated concussions raise the likelihood of chronic neurological, cognitive, and behavioral issues. Stress-induced catecholamine surges and inflammatory mediator production in response to trauma may also endanger cardiac disturbances. ECG changes in patients with severe traumatic brain injury are associated with cardiac dysfunction. Cardiac enzymes can be used as a diagnostic tool and indicate the patient's prognosis.
 Conclusion: Cerebral autoregulation and cardiac physiological responses have a synergistic relationship in maintaining tissue homeostasis in patients with traumatic brain injury. Patients with TBI may experience cardiac dysfunction as a result of the body’s exaggerated systemic response to brain injury.

Paroxysmal sympathetic hyperactivity following acute diffuse brain swelling due to traumatic brain injury: a case report with good clinical outcome

BackgroundParoxysmal sympathetic hyperactivity (PSH) may occur after acquired brain injury. The clinical presentation of PSH results from increased sympathetic overdrive, including transient paroxysms of tachycardia, hypertension, hyperventilation, hyperthermia, dystonic posturing, and excessive sweating. The exact pathophysiology of PSH, however, remains unclear, and no definitive treatment is available. Herein, the authors report a case of PSH in a male patient who experienced acute brain swelling after acquired head injury, for which a good clinical outcome was achieved due to multimodal treatment. The ensuing discussion also addresses the pathophysiology of PSH.Case presentationAn 18-year-old man was transported to the authors’ hospital after experiencing a traumatic brain injury. On admission, computed tomography revealed cerebral herniation due to diffuse brain edema in the left parietal lobe. Emergency decompressive craniotomy and internal decompression were performed. After surgery, anti-edema therapy (glycerol and mannitol) was continued. Ten days postoperatively, PSH was diagnosed in accordance with the PSH assessment score (20 points). Vecuronium, fentanyl, morphine, propofol, dexmedetomidine, and a calcium channel blocker were administered; however, the drug effect was insufficient. Thirty-two days postsurgery, the patient gradually recovered from the adrenergic symptoms of PSH, and head computed tomography performed 32 days after surgery revealed improvement in diffuse brain edema. Ultimately, the patient fully recovered and lived independently at home.ConclusionsConsidering the pathophysiology of PSH, cerebral contusion, acute brain swelling, and secondary mechanisms of brain injury may trigger sympathetic nerve-enhancing regions and cause hyperexcitation of the sympathetic nervous system, resulting in PSH. The outcome of the present case demonstrates that PSH can be reversed if it is identified early and before it becomes irreversible, that is, post the development of hypoxic encephalopathy or widespread brain damage. Appropriate management, including decompression craniotomy for brain swelling and multidisciplinary treatment, leads to good clinical outcomes.

Dramatic demise of a pregnant woman in third trimester after presenting with persistent headache: An iatrogenic

A 31-years-old patient, pregnant at 32 weeks of gestation presented to our triage unit with complaint of gradually progressive persistent headache that started 1 day earlier and was unresponsive to all analgesics. Her history was insignificant for any major medical or surgical events and the pregnancy course was smooth as well. Her lab results and obstetric ultrasound were reassuring. During magnetic resonance imaging examination, the patient suddenly deteriorated after giving her an inhalational anaesthesia for sedation. She became unconscious. She was intubated, mechanically ventilated, and put-on cardiovascular support. Brain imaging then revealed Brain Stem (BS) herniation and diffuse brain oedema. She was announced dead with intrauterine foetal death. A late diagnosis of cerebral venous thrombosis was established. This caused BS herniation through increased intracranial pressure, which was iatrogenically augmented by administering inhalation anaesthesia. Keywords: cerebral vein; thrombosi; thrombophilia; pregnancy; headache; magnetic resonance imaging; brain stem herniation.

Unfortunate Case of Hypoglycemia Induced Seizures Resulting in Anoxic Encephalopathy

Background: Severe hypoglycemia in patient with diabetes mellitus can manifest as seizures and coma, most commonly occurring after excessive insulin administration. Clinical Case: A 35-year-old woman with uncontrolled type 1 diabetes mellitus on basal-bolus insulin, complicated by gastroparesis, hypoglycemia unawareness, and frequent hypoglycemic episodes due to a tendency to give more than the recommended amount of insulin, who presented with seizures and diffuse brain edema as severe manifestations of profound hypoglycemia. Hemoglobin A1c was 7.3% but patient had wide variation in blood glucose (40- 300 mmol/L) on her glucometer. Patient had initially self-treated overnight hypoglycemic symptoms by drinking soda and then fell asleep without re-checking her blood sugar. She was then unresponsive in the morning. Patient’s husband reported that there was no glucagon at home since he used the last one and did not refill. On EMS arrival, patient had a blood glucose of 25, for which she received dextrose and glucagon with improvement of blood glucose but no change in mentation. En route to the hospital, patient developed tonic-clonic seizures and decerebrate posturing. She received Ativan and was intubated for airway protection. On exam, she had bilateral dilated sluggishly reactive pupils, eyes opened spontaneously but did not track, and limbs moved spontaneously but there was no purposeful movement. Initial CT head without contrast showed significant diffuse brain edema. Repeat MRI brain with and without contrast showed bilateral basal ganglia diffusion restriction with associated T2 and FLAIR hyperintense signal, suggestive of toxic-metabolic etiology including hypoglycemia. Video EEG showed findings consistent with anoxic encephalopathy. Patient received IV mannitol and IV dexamethasone for cerebral edema and Keppra for seizure prophylaxis, but was unable to be weaned from the ventilator and had to undergo tracheostomy and PEG tube placement, and was eventually discharged to inpatient rehabilitation. Conclusion: This case highlights the dangers of accidental overcorrection of high blood sugar with short-acting insulin and not appropriately treating hypoglycemia, which can lead to irreversible brain injury due to prolonged hypoglycemia. This unfortunate case highlights the importance of educating patients with diabetes mellitus on insulin how to appropriately manage low sugars to avoid such outcomes.

Prognostic Factors for Pediatric Acute Encephalopathy Associated with Severe Brain Edema

Background and Objective: Acute encephalopathy is a life-threatening brain dysfunction in children, often associated with a preceding infection and diffuse noninflammatory brain edema. At present, the role of decompressive craniectomy (DC) over the swollen area of the brain is unclear. The risk factors for predicting clinical deterioration also need clarification. Methods: A retrospective study of pediatric patients admitted between 2015 and 2019 with acute cerebral encephalopathy was carried out. Patients were classified according to: (1) the preceding pathogens, (2) the syndromic classification, and (3) the extent of brain edema. The syndromic classification is a relatively new classification of acute encephalopathy proposed in 2016 and divides patients into 3 groups: those with systemic inflammatory reactions or “cytokine storms” (group 1), those with status epilepticus but no cytokine storm (group 2), and others (group 3). Glasgow Outcome Scale (GOS) scores of 1–3 were defined as unfavorable, while a GOS score of 4 or 5 was defined as a favorable outcome in this study. DC was performed for select patients with life-threatening signs of brainstem compression. Results: Nineteen patients (mean age: 23.3 months) were included in the study, 8 (42.1%) of whom had an unfavorable outcome. There was no significant correlation between the types of pathogens and outcome. Unfavorable outcomes were observed in significantly more patients in group 1 (87.5%) than group 2 (14.3%) and group 3 (0%). There was a significant association between diffuse brain edema and unfavorable outcomes (72.7%). Neurosurgical DC was performed in 2 patients to alleviate life-threatening brainstem compression: one with a cytokine storm and diffuse bilateral brain edema, and the other with prolonged status epilepticus causing diffuse right-sided brain edema. The GOS score was 3 and 4, respectively. Conclusion: The risk factors for clinical deterioration in pediatric acute encephalopathy were evaluated based on a variety of classifications, including the new syndromic classification. Laboratory features of cytokine storms and radiological evidence of diffuse brain edema were associated with unfavorable outcomes. The role of surgical decompression is still controversial and should be assessed on a case-by-case basis.

Brain damage caused by chlorfenapyr poisoning: a case report and literature review

Introduction: Chlorfenapyr poisoning is uncommon, but fatal, and is often ignored. Chlorfenapyr inhibits ATP production in the mitochondrial of lipid-rich organs such as the brain. The initial symptoms of chlorfenapyr poisoning are not serious and are usually ignored; fever and unconsciousness are the main signs. Patients often die of brain damage, and survivors often present toxic leukoencephalopathy. Case report: We report a case of a 15-year-old female who swallowed 10 mL of 10%chlorfenapyr, and was subjected to gastric lavage one hour after ingestion. The patient felt no discomfort on the first and second day after lavage and went to school. On the third day, the patient complained of a headache and rested at home. On the fourth day, the patient still complained of headache, and the condition progressed to confusion and fever; therefore, the patient was admitted to the emergency room and underwent hemoperfusion. Cerebral CT revealed diffuse brain edema. The patient died on the fourth day because of central fever, brain hernia, and brain dysfunction. Conclusion: Chlorfenapyr poisoning is fatal, even in small doses. Patients suspected of chlorfenapyr poisoning should be closely observed and promptly treated by hemoperfusion.

Acute necrotizing encephalopathy and myocarditis in a young patient with COVID-19

A 33-year-old woman, previously healthy was admitted with generalized status epilepticus. Four days before, she had developed generalized fatigue, fever, headache, and nasal congestion. On hospital arrival, she was comatose (Glasgow coma scale 5 [E1/V1/M3]), febrile (38.6°C), tachycardic (145/min) with a blood pressure of 100/60 mm Hg, and tachypneic (35/min) with hypoxemia (pulse oximetry 80%). She was emergently intubated and started on mechanical ventilation and received IV midazolam and valproic acid for seizure control. Chest x-ray showed mild edema. The initial blood test results showed elevated myocardial enzymes; high-sensitivity troponin-I, 2,210 pg/mL; probrain natriuretic peptide, 992 pg/mL; creatine phosphokinase, 1858 mcg/L; and creatine kinase-MB, 22.5 ng/mL. Blood count revealed a white blood cell count of 14550/μL with absolute lymphopenia of 0.92/μL. C-reactive protein and erythrocyte sedimentation rate levels were high, whereas procalcitonin and lactic acid were normal. ECG showed sinus tachycardia and diffuse ST segment elevation. Bedside echocardiography showed diffuse myocardial dyskinesia with low left ventricular ejection fraction (29%) and small pericardial effusion. Head CT showed diffuse brain edema.

Bradypsychia and Urinary Incontinence Secondary to Frontal-Lobe High Grade Astrocytoma

Background: Lower urinary tract symptoms (LUTS) are complaints that characterized by two symptoms, an overreactive symptoms such as frequency and urgency, and outlet obstruction symptoms such as difficulty urinating and weak urinary flow. Neurologic diseases such as diabetes mellitus are well-known causes of LUTS, however LUTS secondary to an intracranial mass lesion has been very rarely described in the literature. Case Report: 52-year-old woman came to Neurology outpatient clinic with difficulty in communicating. The patient's family said that the patient often did not connect to talk for approximately 3 months. Patients also often wet in the bed in the last 1 month. CT Scan with contrast revealed intracranial lesions in the right frontal lobe and diffuse brain edema, most likely high-grade astrocytoma Discussion: Lower urinary tract symptoms (LUTS) are very common in men. There are many causes of LUTS, such as neurologic, anatomic, inflammatory, infection, psychogenic, and idiopatic. Intracranial tumors rarely cause LUTS, but the pathophysiology is clearly known. Andrew and Nathan were the first researchers to report a frequency, urgency, and urinary incontinence syndrome that caused mass in the frontal lobe and anteromedial parts of the frontal lobes including the cingulate girus in 1964. Maurice-Williams also reported a serial case in which 7 of 50 patients with tumors the frontal lobe is associated with LUTS. Conclusion: Frontal lobe mass are an uncommon cause of LUTS. If the person with LUTS has no known cause, then the neurological cause must be considered. Symptoms such as bradypsychia (slowness of thought or mental activity), decreased motivation, and intracranial mass symptoms must be considered in order to determine the cause of LUTS.

Decompressive craniectomy following severe traumatic brain injury with an initial Glasgow coma scale score of 3 and 4

BackgroundDecompressive craniectomy formed as surgical management option for severe traumatic brain injury (TBI). Few studies that follow the TBI patients with a Glasgow coma scale (GCS) score of 3 or 4. Decompressive craniectomy was avoided in these patients due to the poor outcomes and the worse functional recovery. Clinical presentationTwo patients were presented in our case series. The first one suffered of severe TBI following an aggression with a Glasgow coma scale (GCS) score of 3/15 and bilaterally dilated unreactive pupils. A brain CT-scan showed right frontal fracture, bifrontal hematoma contusion, a fronto-temporo-parietal acute subdural hematoma (SDH) with a thickness of 14 mm on the right side, traumatic subarachnoid hemorrhage, with 20 mm of midline shift to the left side, diffuse brain edema. The second one presented with severe TBI following an automobile accident with a GCS score of 4/15 and isoreactive pupils. A brain CT-scan showed bilateral fronto-temporal fracture, diffuse brain hematoma contusion, traumatic subarachnoid hemorrhage, right extradural hematoma (EDH) and bilateral fronto-temporo-parietal acute subdural hematoma (SDH) more important in the right side. Discussion and conclusionOur case series suggest that the wide adequate decompressive craniectomy in patients with severe TBI and GCS score of 3 or 4 can be performed and useful to obtain good long-term neurological outcomes with a good functional recovery. The rapidity of the surgical indication decision can be option to obtain the better neurological outcomes.

Role of Cisternal Drainage in Patients with Traumatic Brain Injury Undergoing Decompressive Craniectomy

The effect of decompressive craniectomy (DC) on survival and functional outcome in traumatic brain injuries (TBI) is far from satisfactory. Additional modalities including cisternal drainage (CD) that provides good control of refractory intracranial pressure (ICP) intraoperatively need careful scrutiny.
 Two centre retrospective superiority study with one centre offering only standard decompressive craniectomy (DC) i.e. Group 1 and the other centre supplementing cisternal drainage (CD) to standard DC i.e. Group 2 was conducted. Consecutive patients with traumatic brain injury with signs of brain herniation or CT scan showing mass lesion or diffuse brain edema or midline shift or with GCS less than 9 or rapid fall in GCS over 2 points with persistently raised ICP of 25 mmHg over 15 minutes between August 2012 and July 2017 were included. The primary outcome was rating on Glasgow Outcome Scale (GOS) at 6 months post operatively, with GOS (1-3) categorized as ‘Unfavorable’ and GOS (4,5) as ‘Favorable’.
 Patients either received DC alone (Group 1=73 patients, 48.7%) or DC with CD (Group 2=77 patients, 51.3%). 107 (71.3%) severe, 36 (24%) moderate, and 7 (4.7%) mild head injuries cases received 72 unilateral and 78 bilateral DC. GOS 1 was observed in 32 DC only group (43.8%) and 22 DC plus CD group (28.6%) (p=0.052), an absolute risk reduction of 15.2% was found. Outcome (favorable sun favorable) against all strata of head injury severity, predominant radiological feature, laterality of surgery, and patient characteristics across the two groups were statistically not significant, however the groups were statistically significantly different on age and GCS at presentation (p=0.016 & 0.034 consecutively).
 Distinct survival benefit in patients with traumatic brain injury receiving cisternal drainage during decompressive craniectomy did not translate to better functional outcome.

Arteriovenous Fistula After Cerebral Venous Sinus Thrombosis

Thrombosis of the deep cerebral vein is a rare entity. Thrombosis of cerebral veins or dural sinus obstructs blood drainage from brain tissue, leading to cerebral parenchymal dysfunction and increased venous and capillary pressure with disruption of the blood-brain barrier. Many conditions are associated with cerebral venous sinus thrombosis. Prothrombotic conditions, malignancy, infection and head injury has been reported as risk factors for cerebral venous sinus thrombosis (CVST). Neuroimaging features of CVST include focal areas of oedema or venous infarction, hemorrhagic venous infarction, diffuse brain edema or rarely subarachnoid haemorrhage. Magnetic resonance imaging of the brain in combination with magnetic resonance venography is the most informative technique in demonstrating the presence of dural thrombus and cortical vein thrombosis.
 Bangladesh J Medicine Jan 2019; 30(1) : 35-37

Hypophosphatemia after nontraumatic intracranial hemorrhage.

The aim of this study was to assess the incidence and contributing factors of hypophosphatemia and the association with poor long-term outcome after nontraumatic intracranial hemorrhage. This was a prospective, observational study of patients with nontraumatic intracranial hemorrhage (i.e., aneurysmal or perimesencephalic subarachnoid hemorrhage, or spontaneous intracerebral or intraventricular hemorrhage) treated in the intensive care unit (ICU) at our university hospital. Plasma phosphate concentrations were measured serially in 2-day sections during the 6 day study period. The ICU mortality was recorded, 3-month and 1-year outcomes were assessed using the Glasgow Outcome Scale. One hundred patients were enrolled. The frequency of hypophosphatemia (Pi ≤ 0.65 mmol/l) was 70%. Chronic hypertension, acute hydrocephalus, and diffuse brain edema were more common in patients with hypophosphatemia compared with normophosphatemics (44% vs. 21%, P = 0.021; 59% vs. 33%, P = 0.021; and 43% vs. 13%, P = 0.004, respectively). Hypophosphatemic patients had higher maximum SOFA scores [10 (7-11) vs. 7.5 (5.75-10), P = 0.024]. Initial phosphate concentration correlated inversely with APACHE II score on admission (ρ = -0.304, P = 0.002) and SOFA score on the first ICU day (ρ = -0.269, P = 0.008). There was no difference in outcome between hypophosphatemic and normophosphatemic patients. In all five patients with severe hypophosphatemia (Pi < 0.32 mmol/l) the functional outcome was good. Hypophosphatemia was common in this patient population. The outcome was similar between hypophosphatemic and normophosphatemic patients. Chronic hypertension, acute hydrocephalus, diffuse brain edema and higher SOFA scores were more common in patients with hypophosphatemia.

Fatal Cerebral Edema With Status Epilepticus in Children With Dravet Syndrome: Report of 5 Cases.

Dravet syndrome (DS) is a well-recognized developmental and epileptic encephalopathy associated with SCN1A mutations and 15% mortality by 20 years. Although over half of cases succumb to sudden unexpected death in epilepsy, the cause of death in the remainder is poorly defined. We describe the clinical, radiologic, and pathologic characteristics of a cohort of children with DS and SCN1A mutations who developed fatal cerebral edema causing mass effect after fever-associated status epilepticus. Cases were identified from a review of children with DS enrolled in the Epilepsy Genetics Research Program at The University of Melbourne, Austin Health, who died after fever-associated status epilepticus. Five children were identified, all of whom presented with fever-associated convulsive status epilepticus, developed severe brain swelling, and died. All had de novo SCN1A mutations. Fever of 40°C or greater was measured in all cases. Signs of brainstem dysfunction, indicating cerebral herniation, were first noted 3 to 5 days after initial presentation in 4 patients, though were apparent as early as 24 hours in 1 case. When MRI was performed early in a patient's course, focal regions of cortical diffusion restriction were noted. Later MRI studies demonstrated diffuse cytotoxic edema, with severe cerebral herniation. Postmortem studies revealed diffuse brain edema and widespread neuronal damage. Laminar necrosis was seen in 1 case. Cerebral edema leading to fatal brain herniation is an important, previously unreported sequela of status epilepticus in children with DS. This potentially remediable complication may be a significant contributor to the early mortality of DS.

Successful treatment with hyperbaric oxygen therapy for severe brain edema characterized by radiological appearance of pseudosubarachnoid hemorrhage in a child.

Pseudosubarachnoid hemorrhage (PSAH) is a rare neuroradiological finding, particularly in pediatric patients. The appearance of PSAH is commonly associated with poor clinical outcome due to refractory cerebral edema. Recent clinical trials have favored hyperbaric oxygen therapy (HBOT) as a promising therapeutic strategy for adult patients with severe head injuries. The present report describes a pediatric case of diffuse brain edema characterized by the radiological appearance of PSAH successfully treated with HBOT. An adolescent boy collapsed unconscious following convulsion for 3-5 min with fever and headache for 2 days. A brain computed tomography (CT) scan provided an image compatible with subarachnoid hemorrhage (SAH). Lumbar puncture was conducted on admission to hospital and showed no evidence of SAH. The CT scan was again considered and eventually interpreted as PSAH. The patient received drug treatment including acyclovir and mannitol, but the condition deteriorated rapidly. HBOT was administered at 72 h post admission and the condition was clearly improved following the initial therapy. The patient was discharged with 20 sessions of HBOT and recovered completely after 1 year. The appearance of PSAH indicates severe cerebral edema refractory to treatment with conventional internal medicine. HBOT maybe an effective therapeutic strategy for this condition.

Mannitol Improves Brain Tissue Oxygenation in a Model of Diffuse Traumatic Brain Injury.

Based on evidence supporting a potential relation between posttraumatic brain hypoxia and microcirculatory derangements with cell edema, we investigated the effects of the antiedematous agent mannitol on brain tissue oxygenation in a model of diffuse traumatic brain injury. Experimental study. Neurosciences and physiology laboratories. Adult male Wistar rats. Thirty minutes after diffuse traumatic brain injury (impact-acceleration model), rats were IV administered with either a saline solution (traumatic brain injury-saline group) or 20% mannitol (1 g/kg) (traumatic brain injury-mannitol group). Sham-saline and sham-mannitol groups received no insult. Two series of experiments were conducted 2 hours after traumatic brain injury (or equivalent) to investigate 1) the effect of mannitol on brain edema and oxygenation, using a multiparametric magnetic resonance-based approach (n = 10 rats per group) to measure the apparent diffusion coefficient, tissue oxygen saturation, mean transit time, and blood volume fraction in the cortex and caudoputamen; 2) the effect of mannitol on brain tissue PO2 and on venous oxygen saturation of the superior sagittal sinus (n = 5 rats per group); and 3) the cortical ultrastructural changes after treatment (n = 1 per group, taken from the first experiment). Compared with the sham-saline group, the traumatic brain injury-saline group had significantly lower tissue oxygen saturation, brain tissue PO2, and venous oxygen saturation of the superior sagittal sinus values concomitant with diffuse brain edema. These effects were associated with microcirculatory collapse due to astrocyte swelling. Treatment with mannitol after traumatic brain injury reversed all these effects. In the absence of traumatic brain injury, mannitol had no effect on brain oxygenation. Mean transit time and blood volume fraction were comparable between the four groups of rats. The development of posttraumatic brain edema can limit the oxygen utilization by brain tissue without evidence of brain ischemia. Our findings indicate that an antiedematous agent such as mannitol can improve brain tissue oxygenation, possibly by limiting astrocyte swelling and restoring capillary perfusion.

CT scan Imaging – A Modality of Choice in Patients Having Head Injury

Introduction: Today in world of growing population and increase vehicle use, trauma is the leading cause of death in children, young and adults. Head injury is the major contributor to mortality in over half of these cases. Neuroimaging is fundamental for diagnosis and management of patients with head injury. In this new era of development computed tomography has become the primary modality of choice. The main objective of this study is to assess the utility and importance of CT scan imaging in head injury patients. Methods: This is retrospective study of one year. Out of 120 patients males were 96 and females were 24 in number. Results: Male predominance is seen in this study. Patients up to the age of 70 years were considered. 6 cases were found up to the age of 15 years. 99 cases were found of age of 16 years to 40 years. 15 cases were found above the age of 40 years. Out of 120 cases 80 patients suffered from skull fractures. Most common lesion indentified in CT was brain contusion in 42 patients followed by epidural collection in 9 cases, subdural haematoma in 19 cases, Intracerebral haematoma in 15 cases, localised brain edema in 23 cases, diffuse brain edema 10 cases and pneumocephalus 2 cases were observed. Conclusion: CT scan imaging is a prime important tool in the diagnosis of various pathological abnormalities in the patients suffering from head injury which is important for planning the initial life saving treatment.