Early metabolic alterations in edematous perihematomal brain regions following experimental intracerebral hemorrhage

Wagner, Kenneth R.; Xi, Guohua; Hua, Ya; Kleinholz, Marla; Courten-Myers, Gabrielle M. de; Myers, Ronald E.

doi:10.3171/jns.1998.88.6.1058

Cited by 83 publications

(69 citation statements)

References 41 publications

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“…Both vasogenic and cytotoxic edema lead to disruption of the blood-brain barrier, sodium-pump failure, and neuronal death. 42 Controversy exists as to whether there are areas of ischemic tissue at risk around an ICH analogous to an ischemic penumbra. There is direct experimental evidence of ischemic tissue surrounding the hematoma, 43,44 and radiologic support is also available.…”

Section: Pathophysiologymentioning

confidence: 99%

Update in Intracerebral Hemorrhage

Aguilar

Brott

2011

The Neurohospitalist

127

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Spontaneous, nontraumatic intracerebral hemorrhage (ICH) is defined as bleeding within the brain parenchyma. Intracranial hemorrhage includes bleeding within the cranial vault and encompasses ICH, subdural hematoma, epidural bleeds, and subarachnoid hemorrhage (SAH). This review will focus only on ICH. This stroke subtype accounts for about 10% of all strokes. The hematoma locations are deep or ganglionic, lobar, cerebellar, and brain stem in descending order of frequency. Intracerebral hemorrhage occurs twice as common as SAH and is equally as deadly. Risk factors for ICH include hypertension, cerebral amyloid angiopathy, advanced age, antithrombotic therapy and history of cerebrovascular disease. The clinical presentation is ''stroke like'' with sudden onset of focal neurological deficits. Noncontrast head computerized tomography (CT) scan is the standard diagnostic tool. However, newer neuroimaging techniques have improved the diagnostic yield in terms of underlying pathophysiology and may aid in prognosis. Intracerebral hemorrhage is a neurological emergency. Medical care begins with stabilization of airway, breathing function, and circulation (ABCs), followed by specific measures aimed to decrease secondary neurological damage and to prevent both medical and neurological complications. Reversal of coagulopathy when present is of the essence. Blood pressure management can be key and continues as an area of debate and ongoing research. Surgical evacuation of ICH is of unproven benefit though a subset of well-selected patients may have improved outcomes. Ventriculostomy and intracranial pressure (ICP) monitoring are interventions also used in this patient population. To date, hemostatic medications and neuroprotectants have failed to result in clinical improvement. A multidisciplinary approach is recommended, with participation of vascular neurology, vascular neurosurgery, critical care, and rehabilitation medicine as the main players.

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Section: Pathophysiologymentioning

confidence: 99%

Update in Intracerebral Hemorrhage

Aguilar

Brott

2011

The Neurohospitalist

127

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“…As in traumatic brain injury, early removal of the hematoma and cellular debris, either by surgical removal of the clot or by the action of the inflammatory cells such as microglia and macrophages, help to reduce the extent of secondary damage [27,28]. Animal studies have shown that perihematoma edema can be divided into three phases: immediate (up to 24 h after hemorrhage), intermediate (from 24 h to 5 days), and late (beyond 5 days) [29]. The immediate edema results from osmotically active proteins accumulating in the extravascular compartment and can be seen on histological studies, but not on imaging.…”

Section: Pathophysiologymentioning

confidence: 99%

Intracerebral Hematoma

Kutty¹

2017

Hemorrhagic Stroke - An Update

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Intracerebral hematoma occurs in about 35/100,000 population and the incidence is likely increase over the next few decades as the population ages. The most common causes are hypertension and amyloid angiopathy. Bleeds due to these two causes are classified as primary while all other causes, such as AVM bleeds, coagulopathies, and so on, are classified as secondary. Primary tissue damage due to the intracerebral hematoma is followed by edema, neuronal damage, and secondary damage due to cellular breakdown. Basal ganglia are the most common site of intracerebral hemorrhage, accounting for nearly 50% of cases. CT scan, CT angiogram, DSA, and MRI are the investigations of choice. The initial management is medical, with control of blood pressure and antiedema measures forming the mainstay of treatment. Surgical option includes external ventricular drainage, endoscopic evacuation of hematoma, craniotomy and evacuation of hematoma, and decompressive craniectomy and is usually reserved for patients who deteriorate while on treatment.

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“…Early edema is due to the accumulation of serum proteins of the clot that contains osmotic activity [22]. Subsequently, the presence of cytotoxic and vasogenic edema leads to blood-brain barrier disturbances, sodium pump failure, and ultimately the death of neurons [23,24]. The first hours after ICH onset, the blood-brain barrier continues to be nonpermeable for larger molecules, but after 8 to 12 hours the permeability increases and therefore fosters further edema formation [20].…”

Section: Edemamentioning

confidence: 99%