الفهرس 
Anatomical and Physiological Aspects of The BrainOnly 14 pages are availabe for public view
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Abstract
The brain can be injured in many different ways. The type of injury can affect just one or several parts of the brain which are responsible for different functions. Each brain injury is unique, so that symptoms can vary widely. Acute brain injury may be traumatic or non traumatic. Acute brain injury, whatever its cause, is associated with short- and long-term morbidity and mortality.
Traumatic brain injury (TBI) may be blunt head injuries, penetrating head injuries, and blast head injuries. Also, traumatic brain injury may be mild, moderate, or severe. A Glasgow Coma Score (GCS) of 13 to 15 is considered mild, 9 to 12 moderate, and GCS of 8 or less severe.
Non traumatic brain injuries include vascular brain injuries (acute ischemic stroke, intracerebral hemorrhage and subarachinoid hemorrhage), hypoxic-ischemic brain injury, toxic-metabolic brain injury, inflammatory brain injury and Infectious brain injury (Infectious encephalitis)
The examination of brain injured patient should begin with an assessment of vital signs. Not only this allows evaluation of the stability of the patient, it also provides clues to the etiology of the patient’s unresponsiveness e.g. hyperthermia can be seen in midbrain hemorrhage and infection. Similarly, hypertension can be secondary to increased intracranial pressure, or indicative of posterior reversible encephalopathy syndrome (PRES). Hypotension can point toward sepsis or progression to brain death.
The primary goal of the neurologic examination in brain injured patient is to localize the lesion and narrow the differential diagnosis. The examination should proceed in a stepwise fashion and be familiar to the neurologist because of constant repetition. In the process of the comprehensive neurologic examination, the depth of coma should be determined using a coma scale. The Glasgow Coma Scale (GCS) is the most common of such scales.
Head tomography is essential upon suspicion of brain injury and must be the first image requested. It is performed in a few seconds, is available in most emergency services and has good sensitivity to detect bleeding (subarachnoid hemorrhage, subdural hematoma, epidural hematoma, or intraparenchymal hematoma), hydrocephalus, tumors and extensive brain infarcts. On suspicion of meningitis, carry out head tomography whenever possible prior to performing lumbar puncture, since herniation of the brain stem is a real possibility in the presence of intracranial hypertension.
Brain injury is divided into 2 discrete periods: primary and secondary. The primary brain injury is the physical damage to the brain (tissue, vessels). The secondary brain injury is the result of a complex process, following and complicating the primary brain injury in the ensuing hours and days. Secondary brain injuries include cerebral edema, hydrocephalus, intracranial hypertension, vasospasm, excitotoxicity, infection, and seizures.
Optimization of oxygenation and cerebral blood flow are essential. Blood pressure should be sufficient to maintain cerebral perfusion pressure (CPP) >60 mmHg and vasopressers can be used safely, especially when iatrogenic hypotension occurs with sedation. Normalization of blood pressure in patients with chronic hypertension in whom the autoregulatory curve has shifted to the right should be avoided, unless other considerations exist, namely acute intracranial hemorrhage where BP lowering decreases hematoma expansion.
Addressing venous outflow obstruction with upright midline head positioning is a critical initial step. Head of the bed should be maintained at 30°, and the patient’s head should remain in midline positioning without jugular compression to promote venous return. Head elevation in excess of 45° should be avoided to avoide excessive CPP reduction.
The primary goal of intracranial hypertension management is to maintain intracranial pressure (ICP) <20 mmHg and CPP >60 mmHg. While elimination of the cause of elevated ICP remains the definitive approach, there are maneuvers that should be used to decrease ICP urgently. The maneuvers include the following stepwise protocol: surgical decompression, sedatives, CPP optimization, osmotherapy, hyperventilation, high-dose pentobarbital therapy, and hypothermia.
Rapid administration of intravenous recombinant tissue-type plasminogen activator (r-tPA) to appropriate patients remains the mainstay of early treatment of acute ischemic stroke. Timely restoration of blood flow in ischemic stroke patients is effective in reducing long term morbidity.
Herpes virus-related encephalitis can be treated with a potentially effective antiviral therapy. The administration of acyclovir (within 48 hours of the onset of symptoms) at a dose of 10 mg/kg intravenously thrice per day for 14 days (21 days in immunocompromised patients) reduces both the mortality rate and long-term severe neurological complications in patients with herpes simplex encephalitis (HSE).
Therapeutic measures in hepatic encephalopathy include ammonia lowering regimens suchas lactulose and non absorbable antibiotics (neomycin, rifaximin or metronidazole) , intracranial pressure monitoring and management, correction of the coagulopathy, flumazenil to counteract any endozepine action , hyperventilation (if patient is too sedated), normo- or mild hypothermia, renal replacement therapy if renal failure occurs as a result of hepatorenal syndrome.