Cerebral edema is commonly present in a variety of neurological injuries. Thus, determining a definitive contribution of cerebral edema to the neurological status of an affected person can be challenging. Close bedside monitoring of a person's level of consciousness and awareness of any new or worsening focal neurological deficits is imperative but demanding, frequently requiring admission into the intensive care unit (ICU). Cerebral edema with sustained increased intracranial hypertension and brain herniation can signify impending catastrophic neurological events which require immediate recognition and treatment to prevent injury and even death. Therefore, diagnosis of cerebral edema earlier with rapid intervention can improve clinical outcomes and can mortality, or risk of death.
Diagnosis
Cerebral edema
Cerebral edema | Diagnosis
Close monitoring of a person's level of consciousness; awareness of any new or worsening focal neurological deficits; Immediate recognition of Cerebral edema and brain herniation Close bedside monitoring of a person's level of consciousness and awareness of any new or worsening focal neurological deficits is imperative but demanding, frequently requiring admission into the intensive care unit (ICU) Determining a definitive contribution of cerebral edema to the neurological status of an affected person can be challenging. diagnosis of cerebral edema earlier with rapid intervention can improve clinical outcomes and can mortality, or risk of death.
who is elwyn roy king?
user
A fighter ace in the Australian Flying Corps (AFC) during World War I
assistant
has he been a part of any other war?
user
Yes - World War II
assistant
how did he die?
user
cerebral oedema
assistant
did he get a military funeral service?
user
Yes - his funeral service was attended by hundreds of mourners from the military and civil aviation world
assistant
did an air staff chief attend it?
user
Yes - Sir Charles Burnett
assistant
the flying corps that king served, when was it formed?
user
1912
assistant
do they provide trainings?
user
Yes - they conduct both pilot and mechanic training
assistant
what are the causes of the disease king had?
user
Brain injuries from ischemic stroke, subarachnoid hemorrhage, traumatic brain injury etc
assistant
how can we diagnose it?
user
Diagnosis of cerebral edema relies on the following:
Cerebral edema | Diagnosis
Diagnosis is based on symptoms and physical examination findings and confirmed by serial neuroimaging (computed tomography scans and magnetic resonance imaging). The treatment of cerebral edema depends on the cause and includes monitoring of the person's airway and intracranial pressure, proper positioning, controlled hyperventilation, medications, fluid management, steroids. Extensive cerebral edema can also be treated surgically with a decompressive craniectomy. Cerebral edema is a major cause of brain damage and contributes significantly to the mortality of ischemic strokes and traumatic brain injuries. As cerebral edema is present with many common cerebral pathologies, the epidemiology of the disease is not easily defined.
Cerebral edema | Introduction
Serial neuroimaging (CT scans and magnetic resonance imaging) can be useful in diagnosing or excluding intracranial hemorrhage, large masses, acute hydrocephalus, or brain herniation as well as providing information on the type of edema present and the extent of affected area. CT scan is the imaging modality of choice as it is widely available, quick, and with minimal risks. However, CT scan can be limited in determining the exact cause of cerebral edema in which cases, CT angiography (CTA), MRI, or digital subtraction angiography (DSA) may be necessary. MRI is particularly useful as it can differentiate between cytotoxic and vasogenic edema, guiding future treatment decisions.
Cerebral edema | Imaging
The incidence of this disorder should be considered in terms of its potential causes and is present in most cases of traumatic brain injury, central nervous system tumors, brain ischemia, and intracerebral hemorrhage. For example, malignant brain edema was present in roughly 31% of people with ischemic strokes within 30 days after onset.
Cerebral edema | Introduction
Cerebral edema is commonly present in a variety of neurological injuries. Thus, determining a definitive contribution of cerebral edema to the neurological status of an affected person can be challenging. Close bedside monitoring of a person's level of consciousness and awareness of any new or worsening focal neurological deficits is imperative but demanding, frequently requiring admission into the intensive care unit (ICU). Cerebral edema with sustained increased intracranial hypertension and brain herniation can signify impending catastrophic neurological events which require immediate recognition and treatment to prevent injury and even death. Therefore, diagnosis of cerebral edema earlier with rapid intervention can improve clinical outcomes and can mortality, or risk of death.
Cerebral edema | Diagnosis
Clinical signs of cerebral edema, such as focal neurological deficits, papilledema and decreased level of consciousness, if temporally associated with recent hemodialysis, suggest the diagnosis. A computed tomography of the head is typically done to rule-out other intracranial causes. MRI of the head has been used in research to better understand DDS.
Dialysis disequilibrium syndrome | Diagnosis
Cerebral edema is excess accumulation of fluid (edema) in the intracellular or extracellular spaces of the brain. This typically causes impaired nerve function, increased pressure within the skull, and can eventually lead to direct compression of brain tissue and blood vessels. Symptoms vary based on the location and extent of edema and generally include headaches, nausea, vomiting, seizures, drowsiness, visual disturbances, dizziness, and in severe cases, coma and death. Cerebral edema is commonly seen in a variety of brain injuries including ischemic stroke, subarachnoid hemorrhage, traumatic brain injury, subdural, epidural, or intracerebral hematoma, hydrocephalus, brain cancer, brain infections, low blood sodium levels, high altitude, and acute liver failure.
Cerebral edema | Introduction
As cerebral edema is present with many common cerebral pathologies, the epidemiology of the disease is not easily defined. The incidence of this disorder should be considered in terms of its potential causes and is present in most cases of traumatic brain injury, central nervous system tumors, brain ischemia, and intracerebral hemorrhage.
Cerebral edema | Epidemiology
Epidural hematoma (EDH) is a rapidly accumulating hematoma between the dura mater and the cranium. These patients have a history of head trauma with loss of consciousness, then a lucid period, followed by loss of consciousness. Clinical onset occurs over minutes to hours. Many of these injuries are associated with lacerations of the middle meningeal artery. A "lenticular", or convex, lens-shaped extracerebral hemorrhage that does not cross suture lines will likely be visible on a CT scan of the head. Although death is a potential complication, the prognosis is good when this injury is recognized and treated.
Intracranial hemorrhage | Epidural hematoma
Finding the optimal head position in persons with cerebral edema is necessary to avoid compression of the jugular vein and obstruction of venous outflow from the skull, and for decreasing cerebrospinal fluid hydrostatic pressure. The current recommendation is to elevate the head of the bed to 30 degrees to optimize cerebral perfusion pressure and control the increase in intracranial pressure. It is also worth noting that measures should taken to reduce restrictive neck dressings or garments as these may lead to compression of the internal jugular veins and reduce venous outflow.
Cerebral edema | Positioning
Cerebral edema is a severe complication of acute brain injuries, most notably ischemic stroke and traumatic brain injuries, and a significant cause of morbidity and mortality.
Cerebral edema | Outcomes
Computed tomography (CT) and MRI scanning will show damaged area in the brain, showing that the symptoms were not caused by a tumor, subdural hematoma or other brain disorder. The blockage will also appear on the angiogram.
Cerebral infarction | Diagnosis
Subdural and epidural hematomas are serious conditions and should be immediately diagnosed and treated by a physician. Hematomas may not show the full extent of the problem initially after the head injury, but it may be revealed after comprehensive medical evaluation and diagnostic test. Diagnostic test may include: blood test, x-ray, computed tomography scan (CT/CAT scan), electroencephalogram (EEG), and magnetic resonance imaging (MRI). The two most important diagnostic tests are the CT scan and the MRI. The CT scan reveals evidence of blood within the skull, fractures, and signs of compression on the brain from the hematoma. The MRI is a more thorough evaluation of injuries to the brain tissue.
Sports-related traumatic brain injury | Diagnosis in sports
Diagnosis of a cerebral vascular accident begins with a general neurological examination, used to identify specific areas of resulting injury. A CT scan of the brain is then used to identify any cerebral hemorrhaging. An MRI with special sequences called diffusion-weighted MR imaging (DWI), is very sensitive for locating areas of an ischemic based stroke, such as a watershed stroke. Further diagnosis and evaluation of a stroke includes evaluation of the blood vessels in the neck using either Doppler ultrasound, MR-angiography or CT-angiography, or formal angiography. An echocardiogram may be performed looking for a cardiac source of emboli. Blood tests for risk factors also may be ordered, including cholesterol levels, triglyceride levels, homocysteine levels, and blood coagulation tests.
Watershed stroke | Diagnosis
Nutritional support is necessary in all patients with acute brain injury. Enteral feeding, or through mouth via tube, is the preferred method, unless contraindicated. Additional attention must be placed on the solute concentration of the formulations to avoid free water intake, decreased serum osmolality, and worsening of the cerebral edema. Elevated blood glucose, or hyperglycemia, is associated with increased edema in patients with cerebral ischemia and increases the risk of a hemorrhagic transformation of ischemic stroke. Maintaining a normal blood glucose level of less than 180 mg/dL is suggested. However, tight glycemic control of blood glucose under 126 mg/dL is associated with worsening of stroke size.
Cerebral edema | Nutrition
An increase in cerebral water content is called cerebral edema and it usually results from traumatic brain injury (TBI), subarachnoid hemorrhage (SAH), intracerebral hemorrhage (ICH), subdural hematoma, ischemic stroke, brain tumors, infectious disorders and intracranial surgery. Cerebral edema may result in compromised regional cerebral blood flow (CBF) and intracranial pressure (ICP) gradients which could lead to death of the affected. Increased ICP leads to increased intracranial volume. Unmonitored ICP leads to brain damage by global hypoxic ischemic injury due to reduction in cerebral perfusion pressure (CPP) which is found by subtracting the ICP from mean arterial pressure(MAP), cerebral blood flow, and mechanical compression of brain tissue due to compartmentalized ICP gradients.
Osmotherapy | Cerebral edema
The crucial step in the evaluation of stroke patients is to obtain brain imaging to ascertain the type and characteristics of the stroke. In this regard, non-contrast CT of the head is the imaging modality of choice. Ischemic changes may classify as acute, subacute, and chronic, depending on the time in which they present after the onset of stroke. CT scan can also rule out intracranial hemorrhage.[18] If an intracranial hemorrhage is present, aneurysmal rupture should be investigated given its association with arterial vasospasm resulting in stroke.[3] Anterior cerebral artery strokes could be missed on imaging studies depending on their location or size.
Anterior cerebral artery syndrome | Diagnosis
Cerebral edema is a present with many common cerebral pathologies and risk factors for development of cerebral edema will depend on the cause. The following were reliable predictors for development of early cerebral edema in ischemic strokes.
Cerebral edema | Risk Factors
The use of specific MRI techniques has allowed for some differentiation between the mechanisms.
Cerebral edema | Combined types of cerebral edema
Diagnosis can be confirmed by CT Scan or MRI for advanced investigations.
Middle cerebral artery syndrome | Diagnosis
Computed tomography (CT) has become the diagnostic modality of choice for head trauma due to its accuracy, reliability, safety, and wide availability. The changes in microcirculation, impaired auto-regulation, cerebral edema, and axonal injury start as soon as a head injury occurs and manifest as clinical, biochemical, and radiological changes. An MRI may also be conducted to determine if someone has abnormal growths or tumors in the brain or to determine if the patient has had a stroke. Glasgow Coma Scale (GCS) is the most widely used scoring system used to assess the level of severity of a brain injury. This method is based on objective observations of specific traits to determine the severity of a brain injury.
Head injury | Diagnosis
Intracranial pressure (ICP) and its management is a fundamental concept in traumatic brain injury (TBI). The Brain Trauma Foundation guidelines recommend ICP monitoring in individuals with TBI that have decreased Glasgow-Coma Scale (GCS) scores, abnormal CT scans, or additional risk factors such as older age and elevated blood pressure. However, no such guidelines exist for ICP monitoring in other brain injuries such as ischemic stroke, intracerebral hemorrhage, cerebral neoplasm. Clinical researches have recommended ICP and cerebral perfusion pressure (CPP) monitoring in any persons with cerebral injury who are at risk of elevated intracranial pressure based on clinical and neuroimaging features.
Cerebral edema | Intracranial pressure monitoring
Posterior reversible encephalopathy syndrome (PRES) is a rare clinical disease characterized by cerebral edema. The exact pathophysiology, or cause, of the syndrome is still debated but is hypothesized to be related to the disruption of the blood-brain barrier. The syndrome features acute neurological symptoms and reversible subcortical vasogenic edema predominantly involving the parieto-occipital areas on MR imaging. PRES in general has a benign course, but PRES-related intracranial hemorrhage has been associated with a poor prognosis.
Cerebral edema | Posterior Reversible Encephalopathy Syndrome
Computed tomography (CT scan): A CT scan may be normal if it is done soon after the onset of symptoms. A CT scan is the best test to look for bleeding in or around your brain. In some hospitals, a perfusion CT scan may be done to see where the blood is flowing and not flowing in your brain. Magnetic resonance imaging (MRI scan): A special MRI technique (diffusion MRI) may show evidence of an ischemic stroke within minutes of symptom onset. In some hospitals, a perfusion MRI scan may be done to see where the blood is flowing and not flowing in your brain.
Intraparenchymal hemorrhage | Diagnosis
Cerebral angiography and magnetic resonance imaging, family medical history, symptoms, a complete physical examination, and ultimately biopsy of the brain, are often required for the diagnosis. Also, many lab tests must be done for the diagnosis; tests may reveal anemia (a shortage of red blood cells), a high white blood cell count, a high platelet count, allergic reactions, immune complexes, antibodies (tools the body uses to fight off threats) and elevation of inflammatory markers. Another crucial part in the diagnosis of cerebral vasculitis is the use of imaging techniques. Techniques such as conventional digital subtraction angiography (DSA) and magnetic resonance imaging (MRI) are used to find and monitor cerebral involvement.
Cerebral vasculitis | Diagnosis
Autoregulation of cerebral blood flow is impaired, and is associated with anaerobic glycolysis and oxidative stress. Neuronal cell astrocytes are susceptible to these changes, and they swell up, resulting in increased intracranial pressure. Inflammatory mediators also play important role. Unfortunately, signs of elevated intracranial pressure, such as papilledema and loss of pupillary reflexes, are not reliable, and occur late in the disease process. CT imaging of the brain is also unhelpful in detecting early cerebral oedema, but is often performed to rule out intra-cerebral bleeding. Invasive intracranial pressure monitoring via subdural route is often recommended; however, the risk of complications must be weighed against the possible benefit (1% fatal haemorrhage).
Acute liver failure | Encephalopathy and cerebral edema
If the appearances are not typical, other causes for the symptoms and the imaging abnormalities need to considered before PRES can be diagnosed conclusively. In many cases there is evidence of constriction of the blood vessels (if angiography is performed), suggesting a possible overlap with reversible cerebral vasoconstriction syndrome (RCVS). Diffusion MRI may be used to identify areas of cytotoxic edema caused by poor blood flow (ischemia) but it is not clear if this prognostically relevant. Abnormal apparent diffusion coefficient is seen in about 20% of cases. In 10–25% of cases of PRES there is evidence of hemorrhage on neuroimaging.
Posterior reversible encephalopathy syndrome | Diagnosis
CAA can only be definitively diagnosed by a post-mortem autopsy. Biopsies can play a role in diagnosing probable cases. When no tissue is available for biopsy, the Boston Criteria are used to determine probable CAA cases from MRI or CT scan data. The Boston Criteria require evidence of multiple lobar or cortical hemorrhages to label a patient as probably having CAA. Susceptibility weighted imaging has been proposed as a tool for identifying CAA-related microhemorrhages.
Cerebral amyloid angiopathy | Diagnosis
An AVM diagnosis is established by neuroimaging studies after a complete neurological and physical examination. Three main techniques are used to visualize the brain and search for AVM: computed tomography (CT), magnetic resonance imaging (MRI), and cerebral angiography. A CT scan of the head is usually performed first when the subject is symptomatic. It can suggest the approximate site of the bleed. MRI is more sensitive than CT in the diagnosis of AVMs and provides better information about the exact location of the malformation. More detailed pictures of the tangle of blood vessels that compose an AVM can be obtained by using radioactive agents injected into the blood stream.
Cerebral arteriovenous malformation | Diagnosis
Early monitoring can be used to guide medical and surgical decision making and to detect potentially life-threatening brain herniation. There was however, conflicting evidence on the threshold values of ICP that indicated the need for intervention. Researches also recommend that medical decisions should be tailored to the specific diagnosis (e.g. subarachnoid hemorrhage, TBI, encephalitis) and that ICP elevation should be used in conjunction with clinical and neuroimaging and not as an isolated prognostic marker.
Cerebral edema | Intracranial pressure monitoring
Angiogram: a test that looks at the blood vessels that feed the brain. An angiogram will show whether the blood vessel is blocked by a clot, the blood vessel is narrowed, or if there is an abnormality of a blood vessel known as an aneurysm.
Intraparenchymal hemorrhage | Diagnosis
Cerebral edema is frequently encountered in acute brain injuries from a variety of origins, including but not limited to:
Cerebral edema | Causes
There are several clinical conditions in which vasogenic edema is present:
Cerebral edema | Vasogenic
CT scan (computed tomography) is the definitive tool for accurate diagnosis of an intracranial hemorrhage. In difficult cases, a 3T-MRI scan can also be used. When ICP is increased the heart rate may be decreased.
Intracranial hemorrhage | Diagnosis
The best way to confirm the diagnosis is MRI. Risk factors include anatomical abnormalities and bleeding disorders.
Spinal epidural hematoma | Diagnosis
Diagnoses of cerebrovascular disease may include: It is important to differentiate the symptoms caused by a stroke from those caused by syncope (fainting) which is also a reduction in cerebral blood flow, almost always generalized, but they are usually caused by systemic hypotension of various origins: cardiac arrhythmias, myocardial infarction, hemorrhagic shock, among others.
Cerebrovascular disease | Diagnosis
At the same time, improvement of radiographic markers, biomarkers, and analysis of clinical monitoring data is essential in treating cerebral edema. Many studies of the mechanical properties of brain edema were conducted in the 2010s, most of them based on finite element analysis (FEA), a widely used numerical method in solid mechanics. For example, Gao and Ang used the finite element method to study changes in intracranial pressure during craniotomy operations. A second line of research on the condition looks at thermal conductivity, which is related to tissue water content.
Cerebral edema | Research
Rarer mimics of encephalopathy are meningitis, encephalitis, Wernicke's encephalopathy and Wilson's disease; these may be suspected on clinical grounds and confirmed with investigations. The diagnosis of hepatic encephalopathy is a clinical one, once other causes for confusion or coma have been excluded; no test fully diagnoses or excludes it. Serum ammonia levels are elevated in 90% of people, but not all hyperammonaemia (high ammonia levels in the blood) is associated with encephalopathy. A CT scan of the brain usually shows no abnormality except in stage IV encephalopathy, when brain swelling (cerebral oedema) may be visible. Other neuroimaging modalities, such as magnetic resonance imaging (MRI), are not currently regarded as useful, although they may show abnormalities.
Hepatic encephalopathy | Investigations
Complete spinal imaging, X-rays, computed tomography (CT), or magnetic resonance imaging (MRI) can be used to identify infarctions on the dorsal columns. Imaging alone is often inconclusive and does not present a full analysis of the affected columns. Clinical history, blood and cerebral spinal fluid (CSF) tests can also be used to make a full diagnosis.
Posterior cord syndrome | Diagnosis
The most crutial aspect for recovery in patients with severe hematomas is rapid diagnosis and appropriate treatment. Once the clot has been removed the intracranial pressure is monitored for several days. Conditions which are also monitored after surgery are seizures, clot accumulation, and infection. If complications do occur, sometime the hematoma needs to be re-drained. Additional complications following a surgical or nonsurgical treatment may include temporary or permanent weakness, numbness, difficulty speaking, memory loss, dizziness, headache, anxiety, difficulty concentrating, seizures, and/or brain herniation. The most helpful predictors of the treatment outcome is the glasgow coma scale (GCS). This is a standardized pupil response assessment of the neurologic status of the patient.
Sports-related traumatic brain injury | Prognosis (short/long-term effects)
The modality of choice is computed tomography (CT scan), without contrast, of the brain. This has a high sensitivity and will correctly identify 98.7% of cases within six hours of the onset of symptoms. A CT scan can rule out the diagnosis in someone with a normal neurological exam if done within six hours. Its efficacy declines thereafter, and magnetic resonance imaging (MRI) is more sensitive than CT after several days.
Subarachnoid hemorrhage | Imaging
If a lumbar puncture is performed, it will show normal cerebral spinal fluid and cell counts but an increase in pressure. In one study, CT scans of patients with HACE exhibited ventricle compression and low density in the cerebellum. Only a few autopsies have been performed on fatal cases of HACE; they showed swollen gyri, spongiosis of white matter, and compressed sulci. There was some variation between individuals, and the results may not be typical of HACE deaths.
High-altitude cerebral edema | Signs and symptoms
Sometimes the lesion appearance imaged by MRI remains inconclusive. Consequently, neurosurgeons will order a cerebral angiogram or magnetic resonance angiogram (MRA). Since CCMs are low flow lesions (they are hooked into the venous side of the circulatory system), they will be angiographically occult (invisible). If a lesion is discernible via angiogram in the same location as in the MRI, then an arteriovenous malformation (AVM) becomes the primary concern.
Central nervous system cavernous hemangioma | Diagnosis
Cerebral edema has been traditional classified into two major sub-types: cytotoxic and vasogenic cerebral edema. This simple classification helps guide medical decision making and treatment of patients affected with cerebral edema. There are, however, several more differentiated types including but not limited to interstitial, osmotic, hydrostatic, and high altitude associated edema. Within one affected person, many individual sub-types can be present simultaneously. The following individual sub-types have been identified:
Cerebral edema | Classification
An X-ray computed tomography (CT) or magnetic resonance imaging (MRI) scan is necessary to characterize the extent of these tumors (size, location, consistency). CT will usually show distortion of third and lateral ventricles with displacement of anterior and middle cerebral arteries. Histologic analysis is necessary for grading diagnosis. In the first stage of diagnosis the doctor will take a history of symptoms and perform a basic neurological exam, including an eye exam and tests of vision, balance, coordination and mental status. The doctor will then require a CT scan and MRI of the patient's brain. During a CT scan, X-rays of the patient's brain are taken from many different directions.
Astrocytoma | Diagnosis
An antemortem diagnosis is often intricate considering the similarities of general neuro diagnostic profiles. To achieve a presumptive diagnosis on the live animal a multimodal approach is needed. Including the magnetic resonance imaging (MRI), computer tomography (CT), cerebrospinal liquid (CFS) analysis and immunological test. Since only the CNS is affected by the pathology, there won’t be any characteristic changes in organ systems other than the nervous system. Despite clinical examination methods, the specific diagnosis of NME depends on a postmortem, histopathological examination of the brain biopsy tissue or a necropsy.
Necrotizing meningoencephalitis | Diagnostics
Diagnosis of the disease is normally done through imaging technology such as angiograms or magnetic resonance imaging. The risk of cerebral atherosclerosis and its associated diseases appears to increase with increasing age; however there are numerous factors that can be controlled in attempt to lessen risk.
Cerebral atherosclerosis | Introduction
Diagnostic methods include: Due to positive remodeling the plaque build-up shown on angiogram may appear further downstream on the x-ray where the luminal diameter would look normal even though there is severe narrowing at the real site. Because angiograms require x-rays to be visualized the number of times an individual can have it done over a year is limited by the guidelines for the amount of radiation they can be exposed to in a one-year period. Magnetic resonance imaging has the ability to quantify the plaque anatomy and composition. This allows physicians to determine certain characteristics of the plaque such as how likely it is to break away from the wall and become an embolus.
Cerebral atherosclerosis | Diagnosis
In the treatment of traumatic brain injury (TBI), there are 4 examination methods that have proved useful: skull x-ray, angiography, computed tomography (CT), and magnetic resonance imaging (MRI). The skull x-ray can detect linear fractures, impression fractures (expression fractures) and burst fractures. Angiography is used on rare occasions for TBIs i.e. when there is suspicion of an aneurysm, carotid sinus fistula, traumatic vascular occlusion, and vascular dissection. A CT can detect changes in density between the brain tissue and hemorrhages like subdural and intracerebral hemorrhages. MRIs are not the first choice in emergencies because of the long scanning times and because fractures cannot be detected as well as CT.
Coma | Imaging and testing
Hemiplegia is identified by clinical examination by a health professional, such as a physiotherapist or doctor. Radiological studies like a CT scan or magnetic resonance imaging of the brain should be used to confirm injury in the brain and spinal cord, but alone cannot be used to identify movement disorders. Individuals who develop seizures may undergo tests to determine where the focus of excess electrical activity is. Hemiplegia patients usually show a characteristic gait. The leg on the affected side is extended and internally rotated and is swung in a wide, lateral arc rather than lifted in order to move it forward.
Hemiparesis | Diagnosis
It is based on three traits eye-opening, verbal response, and motor response, gauged as described below. Based on the Glasgow Coma Scale severity is classified as follows, severe brain injuries score 3–8, moderate brain injuries score 9-12 and mild score 13–15. There are several imaging techniques that can aid in diagnosing and assessing the extent of brain damage, such as computed tomography (CT) scan, magnetic resonance imaging (MRI), diffusion tensor imaging (DTI) and magnetic resonance spectroscopy (MRS), positron emission tomography (PET), single-photon emission tomography (SPECT). CT scans and MRI are the two techniques widely used and are the most effective.
Head injury | Diagnosis
Both computed tomography angiography (CTA) and magnetic resonance angiography (MRA) have been proved to be effective in diagnosing intracranial vascular malformations after ICH. So frequently, a CT angiogram will be performed in order to exclude a secondary cause of hemorrhage or to detect a "spot sign". Intraparenchymal hemorrhage can be recognized on CT scans because blood appears brighter than other tissue and is separated from the inner table of the skull by brain tissue. The tissue surrounding a bleed is often less dense than the rest of the brain because of edema, and therefore shows up darker on the CT scan.
Intracerebral hemorrhage | Diagnosis
ESUS is a diagnosis of exclusion based on radiological and cardiological examinations. For exclusion of haemorrhagic or lacunar strokes CT or MRI imaging is needed. Both procedures also allow detection of embolic pattern of ischemic lesions. 12-lead ECG and cardiac monitoring for at least 24 h with automated rhythm detection are mandated to exclude atrial fibrillation; echocardiography (TTE and/or TEE) is used to detect other major-risk cardioembolic sources (e.g., intracardiac thrombi, or ejection fraction <30%). For imaging of both the extracranial and intracranial arteries supplying the area of brain ischaemia, examination methods like catheter, MR/CT angiography or cervical duplex plus transcranial Doppler ultrasonography are required.
Embolic stroke of undetermined source | Diagnosis
Preliminary diagnosis may be made in utero via standard ultrasound, and can be confirmed with a standard anatomy ultrasound. This sometimes proves to provide a misdiagnosis of differential diagnoses including bilaterally symmetric schizencephaly (a less destructive developmental process on the brain), severe hydrocephalus (cerebrospinal fluid excess within the skull), and alobar holoprosencephaly (a neurological developmental anomaly). Once destruction of the brain is complete, the cerebellum, midbrain, thalami, basal ganglia, choroid plexus, and portions of the occipital lobes typically remain preserved to varying degrees. Though the cerebral cortex is absent, in most cases the fetal head remains enlarged due to the continued production by the choroid plexus of cerebrospinal fluid that is inadequately reabsorbed causing increased intracranial pressure.
Hydranencephaly | Diagnosis
Cerebral edema is mainly classified into cytotoxic edema, vasogenic edema and interstitial edema. Cytotoxic edema affects both the white and gray matter and results from the swelling of cellular elements such as neurons, glia and endothelial cells. Vasogenic edema affects white matter and results from blood brain barrier (BBB) breakdown. Interstitial edema results from lack of proper cerebrospinal fluid (CSF) absorption.
Osmotherapy | Cerebral edema
Since lateral medullary syndrome is often caused by a stroke, diagnosis is time dependent. Diagnosis is usually done by assessing vestibular-related symptoms in order to determine where in the medulla that the infarction has occurred. Head Impulsive Nystagmus Test of Skew (HINTS) examination of oculomotor function is often performed, along with computed tomography (CT) or magnetic resonance imaging (MRI) to assist in stroke detection. Standard stroke assessment must be done to rule out a concussion or other head trauma.
Lateral medullary syndrome | Diagnosis
Although cerebral edema is closely related to increased intracranial pressure (ICP) and cerebral herniation and the general treatment strategies above are useful, the treatment should ultimately be tailored to the primary cause of the symptoms. The management of individual diseases are discussed separately. The following interventions are more specific treatments for managing cerebral edema and increased ICP:
Cerebral edema | Specific Measures
There are a few methods used to diagnose a head injury. A healthcare professional will ask the patient questions revolving around the injury as well as questions to help determine in what ways the injury is affecting function. In addition to this hearing, vision, balance, and reflexes may also be assessed as an indicator of the severity of the injury. A non-contrast CT of the head should be performed immediately in all those who have suffered a moderate or severe head injury. A CT is an imaging technique that allows physicians to see inside the head without surgery in order to determine if there is internal bleeding or swelling in the brain.
Head injury | Diagnosis
Examination of brain tissue is required to confirm a diagnosis of variant CJD. The following confirmatory features should be present:
Variant Creutzfeldt–Jakob disease | Definitive
The Cushing reflex often indicates compression of the brain on brain tissue and blood vessels, leading to decreased blood flow to the brain and eventually death.
Cerebral edema | Signs and symptoms
Subdural hematoma occurs when there is tearing of the bridging vein between the cerebral cortex and a draining venous sinus. At times they may be caused by arterial lacerations on the brain surface. Acute subdural hematoma are usually associated with cerebral cortex injury as well and hence the prognosis is not as good as extra dural hematoma. Clinical features depend on the site of injury and severity of injury. Patients may have a history of loss of consciousness but they recover and do not relapse. Clinical onset occurs over hours. A crescent shaped hemorrhage compressing the brain that does cross suture lines will be noted on CT of the head.
Intracranial hemorrhage | Subdural hematoma
Duret haemorrhages can be demonstrated by medical imaging techniques of CT or MRI though difficult.
Duret haemorrhages | Diagnosis
Diagnosis of a ruptured cerebral aneurysm is commonly made by finding signs of subarachnoid hemorrhage on a computed tomography (CT) scan. If the CT scan is negative but a ruptured aneurysm is still suspected based on clinical findings, a lumbar puncture can be performed to detect blood in the cerebrospinal fluid. Computed tomography angiography (CTA) is an alternative to traditional angiography and can be performed without the need for arterial catheterization. This test combines a regular CT scan with a contrast dye injected into a vein. Once the dye is injected into a vein, it travels to the cerebral arteries, and images are created using a CT scan.
Aneurysm | Diagnosis
Cerebrospinal fluid (CSF) analysis may demonstrate elevated protein level with or without pleocytosis. Imaging including angiography may be indicated to identify dural venous sinus thrombosis as a cause of intracranial hypertension and optic atrophy.
Behçet's disease | Diagnosis
MRI scans are used in imaging the brain and can allow visualization of the optic nerve and any possible atrophy. MRI, CT, and cerebral angiography may all be used to investigate the extent and location of any vascular lesions affecting the brain. This is helpful in determining the extent of the syndrome.
Bonnet–Dechaume–Blanc syndrome | Diagnosis
Hemarthrosis is diagnosed through the methods listed below: A physical examination is the first step, the joints of the patient are moved and bent to study the functioning. Synovial Fluid analysis is another method to diagnose Hemarthrosis. It involves a small needle being inserted into the joint to draw the fluid. Reddish-colored hue of the sample is an indication of the blood being present. Imaging tests are normally done. The tests also include MRI, Ultrasound and X-ray test, which give better information about the joint inflammation.
Hemarthrosis | Diagnosis
There are various neuroimaging investigations that may detect cerebral sinus thrombosis. Cerebral edema and venous infarction may be apparent on any modality, but for the detection of the thrombus itself, the most commonly used tests are computed tomography (CT) and magnetic resonance imaging (MRI), both using various types of radiocontrast to perform a venogram and visualise the veins around the brain. Computed tomography, with radiocontrast in the venous phase ("CT venography" or CTV), has a detection rate that in some regards exceeds that of MRI. The test involves injection into a vein (usually in the arm) of a radioopaque substance, and time is allowed for the bloodstream to carry it to the cerebral veins - at which point the scan is performed.
Cerebral venous sinus thrombosis | Imaging
The diagnosis is established by a computed tomography (CT) (with contrast) examination. At the initial phase of the inflammation (which is referred to as cerebritis), the immature lesion does not have a capsule and it may be difficult to distinguish it from other space-occupying lesions or infarcts of the brain. Within 4–5 days the inflammation and the concomitant dead brain tissue are surrounded with a capsule, which gives the lesion the famous ring-enhancing lesion appearance on CT examination with contrast (since intravenously applied contrast material can not pass through the capsule, it is collected around the lesion and looks as a ring surrounding the relatively dark lesion).
Brain abscess | Diagnosis
There are several tests done to diagnose hemifacial spasm. Diagnosing a case of hemifacial spasm begins with a complete neurological exam, including an Electromyography (EMG – a test that measures and records electrical activity generated in muscle at rest and in response to muscle contraction), Magnetic resonance imaging (MRI – a test that uses magnetic waves to make pictures of structures inside the head), Computed tomography (CT scan – a type of x-ray that uses a computer to make pictures of structures inside the head), and Angiography (an x-ray exam of the blood vessels when they are filled with a contrast material).
Hemifacial spasm | Diagnosis
Intraocular hemorrhage is typically diagnosed with slit lamp examination.
Intraocular hemorrhage | Diagnosis
Neuroferritinopathy is most commonly diagnosed using MRI and other neuroimaging techniques. MRIs help identify the iron deposits in the cerebellum, basal ganglia, and motor cortex common to neuroferritinopathy. MRIs of affected individuals also show mild cerebellar and cerebral atrophy, or tissue breakdown, and gas cavity formation in the putamen. Most importantly, the MRIs show misfolded ferritin proteins and iron deposits in the glial cells of the caudate, putamen, globus pallidus, cerebral cortex, thalamus, and purkinje cells, causing neuronal death in these areas.
Neuroferritinopathy | Neuroimaging
Diagnosis is suspected based on lesion circumstances and clinical evidence, most prominently a neurological examination, for example checking whether the pupils constrict normally in response to light and assigning a Glasgow Coma Score. Neuroimaging helps in determining the diagnosis and prognosis and in deciding what treatments to give. DSM-5 can be utilized to diagnose TBI and its psychiatric sequelae. The preferred radiologic test in the emergency setting is computed tomography (CT): it is quick, accurate, and widely available. Follow-up CT scans may be performed later to determine whether the injury has progressed. Magnetic resonance imaging (MRI) can show more detail than CT, and can add information about expected outcome in the long term.
Traumatic brain injury | Diagnosis
Interstitial edema can be best characterized by in noncomunnicating hydrocephalus where there is an obstruction to the outflow of cerebrospinal fluid within the ventricular system. The obstruction creates a rise in the intraventricular pressure and causes CSF to flow through the wall of the ventricles into the extracellular fluid within brain. The fluid has roughly the same composition of CSF. Other causes of interstitial edema include but are not limited to communicating hydrocephalus, and normal pressure hydrocephalus.
Cerebral edema | Interstitial (Hydrocephalic)
Cerebral edema, if associated with coma, often necessitates admission to intensive care, artificial ventilation, and close observation. The administration of fluids is slowed. The ideal treatment of cerebral edema in DKA is not established, but intravenous mannitol and hypertonic saline (3%) are used—as in some other forms of cerebral edema—in an attempt to reduce the swelling.
Diabetic ketoacidosis | Cerebral edema
After a subarachnoid hemorrhage is confirmed, its origin needs to be determined. If the bleeding is likely to have originated from an aneurysm (as determined by the CT scan appearance), the choice is between cerebral angiography (injecting radiocontrast through a catheter to the brain arteries) and CT angiography (visualizing blood vessels with radiocontrast on a CT scan) to identify aneurysms. Catheter angiography also offers the possibility of coiling an aneurysm (see below).
Subarachnoid hemorrhage | Angiography
Diagnosis of Harlequin syndrome is made when the individual has consistent signs and symptoms of the condition, therefore, it is made by clinical observation. In addition, a neurologist or primary care physician may require an MRI test to rule out similar disorders such as Horner's syndrome, Adie's syndrome, and Ross' syndrome. In an MRI, a radiologist may observe areas near brain or spinal cord for lesions, or any damage to the nerve endings. It is also important that the clinician rules out traumatic causes by performing autonomic function tests. Such tests includes the following: tilt table test, orthostatic blood pressure measurement, head-up test, valsalva maneuver, thermoregulatory sweat test, tendon reflex test, and electrocardiography (ECG).
Harlequin syndrome | Diagnosis
Hemorrhages may be larger than in normal contusions if the injury is quite severe. This type of injury has a poor prognosis if the patient is comatose, even with no apparent causes for the coma.
Cerebral contusion | Multiple petechial hemorrhages
ALO is often a benign and unilateral condition, and extensive evaluation may not be necessary. The diagnosis may be a clinical diagnosis based on a thorough history and physical exam, and being able to exclude other diagnoses and pathology. Computed tomography (CT) or magnetic resonance imaging (MRI) may be ordered to help determine whether there is a lesion or other pathological cause present in the brain or brainstem. Electromyography may be used to aid the diagnosis.
Apraxia of lid opening | Diagnosis
Blood tests, cerebrospinal fluid examination by lumbar puncture (also known as spinal tap), brain imaging studies, electroencephalography (EEG), and similar diagnostic studies may be used to differentiate the various causes of encephalopathy. Diagnosis is frequently clinical. That is, no set of tests give the diagnosis, but the entire presentation of the illness with nonspecific test results informs the experienced clinician of the diagnosis.
Encephalopathy | Diagnosis
Computed tomography (CT) has become the diagnostic modality of choice for head trauma due to its accuracy, reliability, safety, and wide availability. The changes in microcirculation, impaired auto-regulation, cerebral edema, and axonal injury start as soon as head injury occurs and manifest as clinical, biochemical, and radiological changes. Proper therapeutic management of brain injury is based on correct diagnosis and appreciation of the temporal course of the disease process. CT scan detects and precisely localizes the intracranial hematomas, cerebral contusions, edema and foreign bodies. Even in emergency situations, when a head injury is minor as determined by a physician's evaluation and based on established guidelines, CT of the head should be avoided for adults and delayed pending clinical observation in the emergency department for children.
Computed tomography of the head | Uses
When a stroke has been diagnosed, various other studies may be performed to determine the underlying cause. With the current treatment and diagnosis options available, it is of particular importance to determine whether there is a peripheral source of emboli. Test selection may vary since the cause of stroke varies with age, comorbidity and the clinical presentation. The following are commonly used techniques: For hemorrhagic strokes, a CT or MRI scan with intravascular contrast may be able to identify abnormalities in the brain arteries (such as aneurysms) or other sources of bleeding, and structural MRI if this shows no cause.
Stroke | Underlying cause
Callosal disorders can be diagnosed through brain imaging studies or during autopsy. They may be diagnosed through an MRI, CT scan, Sonography, prenatal ultrasound, or prenatal MRI.
Agenesis of the corpus callosum | Diagnosis
Prognostics factors: Lower Glasgow Coma Scale score, higher pulse rate, higher respiratory rate and lower arterial oxygen saturation level is prognostic features of in-hospital mortality rate in acute ischemic stroke.
Cerebrovascular disease | Prognosis
The clinician should first rule out conditions with similar symptoms, such as subarachnoid hemorrhage, ischemic stroke, pituitary apoplexy, cerebral artery dissection, meningitis, and spontaneous cerebrospinal fluid leak. This may involve a CT scan, lumbar puncture, MRI, and other tests. Posterior reversible encephalopathy syndrome has a similar presentation, and is found in 10–38% of RCVS patients. RCVS is diagnosed by detecting diffuse reversible cerebral vasoconstriction. Catheter angiography is ideal, but computed tomography angiography and magnetic resonance angiography can identify about 70% of cases. Multiple angiographies may be necessary. Because other diseases (such as atherosclerosis) have similar angiographic presentations, it can only be conclusively diagnosed if vasoconstriction resolves within 12 weeks.
Reversible cerebral vasoconstriction syndrome | Diagnosis
Neurocysticerosis is diagnosed by computed tomography (CT) scan. Diagnosis may be confirmed by detection of antibodies against cysticerci in CSF or serum through ELISA or imunoblotting techniques.
Neurocysticercosis | Diagnosis
The Monroe-Kellie doctrine states that the skull is a fixed and inelastic space and the accumulation of edema will compress vital brain tissue and blood vessels. Surgical treatment of cerebral edema in the context of cerebellar or cerebral infarction is typically done by removing part of the skull to allow expansion of the dura. This will help to reduce the volume constraints inside of the skull. A decompressive hemicraniectomy is the most commonly used procedure. Multiple randomized clinical trials have shown reduced risk of death with hemicraniectomy compared with medical management. However, no individual study has shown an improvement in the percentage of survivors with good functional outcomes.
Cerebral edema | Surgery
The current understanding of the pathophysiology of cerebral edema after traumatic brain injury is incomplete. Current treatment therapies aimed at cerebral edema and increased intracranial pressure are effective at reducing intracranial hypertension but have unclear impacts on functional outcomes. Additionally, cerebral and ICP treatments have varied effects on individuals based on differing characteristics like age, gender, type of injury, and genetics. There are innumerable molecular pathways that contribute to cerebral edema, many of which have yet to be discovered. Researchers argue that the future treatment of cerebral edema will be based on advances in identifying the underlying pathophysiology and molecular characteristics of cerebral edema in a variety of cases.
Cerebral edema | Research
Most people with severe closed head injury either die or recover enough to live independently; middle ground is less common. Coma, as it is closely related to severity, is a strong predictor of poor outcome. Prognosis differs depending on the severity and location of the lesion, and access to immediate, specialised acute management. Subarachnoid hemorrhage approximately doubles mortality. Subdural hematoma is associated with worse outcome and increased mortality, while people with epidural hematoma are expected to have a good outcome if they receive surgery quickly. Diffuse axonal injury may be associated with coma when severe, and poor outcome. Following the acute stage, prognosis is strongly influenced by the patient's involvement in activity that promote recovery, which for most patients requires access to a specialised, intensive rehabilitation service.
Traumatic brain injury | Prognosis
Diagnosis is typically by CT scan or MRI. MRIs have greater sensitivity and should be used if there is a high suspicion of epidural hematoma and a negative CT scan. Differential diagnoses include a transient ischemic attack, intracranial mass, or brain abscess. Epidural hematomas usually appear convex in shape because their expansion stops at the skull's sutures, where the dura mater is tightly attached to the skull. Thus, they expand inward toward the brain rather than along the inside of the skull, as occurs in subdural hematomas. Most people also have a skull fracture. Epidural hematomas may occur in combination with subdural hematomas, or either may occur alone.
Epidural hematoma | Diagnosis
GCS helps assess many different types of head injuries and predicts how a patient will recover following a hematoma. Factors such as elevated intracranial pressure, increased patients age, and abnormal GCS results lead to a poor prognosis. The mortality rate following a hematoma could be as high as 80% and survivors many not regain the same pre-injury function. Subdural and epidural hematomas are serious injuries and recovery varies widely depending on the severity of the hematoma. Severity depends on type and location of the injury, the size of the blood collection, and how quickly treatment is obtained. Hence, it is difficult to determine when an athlete can return to sports after his/her injury.
Sports-related traumatic brain injury | Prognosis (short/long-term effects)
AFM is diagnosed by examining a person's nervous system in combination with reviewing images of the spinal cord. A doctor can examine a person's nervous system and the places on the body where he or she has weakness, poor muscle tone, and decreased reflexes. In addition, a doctor can do magnetic resonance imaging to look at a person's brain and spinal cord, do laboratory tests on the cerebrospinal fluid (CSF, the fluid around the brain and spinal cord), and may check nerve conduction (impulse sent along a nerve fiber) and response. Diagnosis of AFM requires acute onset limb paralysis and at least one gray-matter spinal-cord lesion.
Acute flaccid myelitis | Diagnosis
The diagnosis may be suspected on the basis of the symptoms, for example the combination of headache, signs of raised intracranial pressure and focal neurological abnormalities, or when alternative causes of headache and neurological abnormalities, such as a subarachnoid hemorrhage, have been excluded.
Cerebral venous sinus thrombosis | Diagnosis
Cerebral amyloid angiopathy can be presented with lobar intracerebral hemorrhage or microbleeds in the brain. The bleeding usually occurs on the surfaces of the brain in contrast with intracranial haemorrhage due to high blood pressure which occurs deep locations of the brain such as basal ganglia and pons. In lobar intracerebral bleed, computed tomography (CT) scan would show hyperdense haemorrhage area and hypodense odema around the haemorrhagic site. MRI sequence of gradient echo and Susceptibility weighted imaging(SWI) are useful in detecting microbleeds and deposition of iron on the brain cortex (cortical superficial siderosis). Other MRI indicators of CAA include white matter hyperintensities and cortical thinning.
Cerebral amyloid angiopathy | Imaging
One case series found that 37.5% (6 of 16) of ACA infarcts evaluated by CT were identifiable only after using contrast injection or angiography. If the area of hypodensity is small and localized over a sulcus, the infarct could be overlooked.[1][13] Noncontrast head CT should be quickly followed by CT angiography of the head and neck to expedite identification of intracranial large vessel occlusion. The finding of a hyperdense lesion in the ACA on CT scan aid in the diagnosis of stroke in its acute phase, particularly when it may be otherwise difficult to establish. The frequency of this sign in ACA infarcts is similar to that in the territories of the middle cerebral artery and the posterior circulation.[19]
Anterior cerebral artery syndrome | Diagnosis
Several methods exist for diagnosing a patient as having bobble-head doll syndrome. Most involve brain scans to look for swelling while some use cisternography to observe obstruction in cerebrospinal fluid (CSF) flow among ventricles. In order to try to investigate the flow dynamics of the cerebrospinal fluid, doctors utilize cisternography, which injects a radiolabeled substance into the CSF via lumbar puncture. The CSF flow is then tracked by taking pictures at incremental times. However, cisternography is declining in use with physicians who are opting to use MRI instead, to assess CSF flow. Cerebrospinal fluid flow is important in diagnosing bobble-head doll syndrome because disturbances in CSF dynamics can be contributed to blockages in the connections between ventricles such as foramen and aqueducts.
Bobble-head doll syndrome | Diagnosis
Meningitis can be diagnosed after death has occurred. The findings from a post mortem are usually a widespread inflammation of the pia mater and arachnoid layers of the meninges. Neutrophil granulocytes tend to have migrated to the cerebrospinal fluid and the base of the brain, along with cranial nerves and the spinal cord, may be surrounded with pus – as may the meningeal vessels.
Meningitis | Postmortem
These images show exactly how blood flows into the brain arteries.
Aneurysm | Diagnosis
The results of the examination are taken together to anatomically identify the "lesion". This may be diffuse (e.g., neuromuscular diseases, encephalopathy) or highly specific (e.g., abnormal sensation in one dermatome due to compression of a specific spinal nerve by a tumor deposit). General principles include: A differential diagnosis may then be constructed that takes into account the patient's background (e.g., previous cancer, autoimmune diathesis) and present findings to include the most likely causes. Examinations are aimed at ruling "out" the most clinically significant causes (even if relatively rare, e.g., brain tumor in a patient with subtle word-finding abnormalities but no increased intracranial pressure) and ruling "in" the most likely causes.
Neurological examination | Interpretation
Diagnosis can be made by a physical exam with the use of a nasal speculum or otoscope. Sometimes palpatation is used to diagnose the hematoma.
Nasal septal hematoma | Diagnosis
The extent and severity of the symptoms of cerebral edema depend on the exact etiology but are generally related to an acute increase of the pressure within the skull. As the skull is a fixed and inelastic space, the accumulation of cerebral edema can displace and compress vital brain tissue, cerebral spinal fluid, and blood vessels, according to the Monro-Kellie doctrine. Increased intracranial pressure (ICP) is a life-threatening surgical emergency marked by symptoms of headache, nausea, vomiting, decreased consciousness. Symptoms are frequently accompanied by visual disturbances such as gaze paresis, reduced vision, and dizziness. Increased pressures within the skull can cause a compensatory elevation of blood pressure to maintain cerebral blood flow, which, when associated with irregular breathing and a decreased heart rate, is called the Cushing reflex.
Cerebral edema | Signs and symptoms