Stroke and TBI from internship 1 Correct 100%

Intraparenchymal hemorrhage (IPH) -ANSWER An intraparenchymal hemorrhage is a blood clot that develops in the brain. Intraparenchymal hemorrhage is one form of intracerebral bleeding in which there is bleeding within brain parenchyma. The other form is intraventricular hemorrhage. Intraparenchymal hemorrhage accounts for approx. 8-13% of all strokes and results from a wide spectrum of disorders. It is more likely to result in death or major disability than ischemic stroke or subarachnoid hemorrhage, and therefore constitutes an immediate medical emergency. Intracerebral hemorrhages and accompanying edema may disrupt or compress adjacent brain tissue, leading to neurological dysfunction. Substantial displacement of brain parenchyma may cause elevation of intracranial pressure and potentially fatal herniation syndromes. Intraparenchymal hemorrhage may occur suddenly without any apparent cause, according to the Mayo Clinic. In such cases, the affected individuals normally have weakened blood vessels as a result of long term hypertension. Other causes of intraparenchymal hemorrhage include tumors, anticoagulant medication and brain lesions, according to the Mayo Clinic. The Mayo Clinic notes that, as with most brain lesions, intraparenchymal hemorrhage may present with various symptoms, such as severe headache, seizures, memory loss and coma in cases that are severe. Parenchyma -ANSWER Parenchyma refers to the functional tissue in the brain that is made up of the two types of brain cell, neurons nad glial cells. Damage or trauma to the brain parenchyma often results in a loss of cognitive ability or even death. Intraventricular hemorrhage -ANSWER Intraventricular hemorrhage, also known as intraventricular bleeding, is a bleeding into the brain's ventricular system, where the cerebrospinal fluid is produced and circulates through towards the subarachnoid space. It can result from physical trauma or from hemorrhaging in stroke. Cerebral embolus (CE) -ANSWER is composed of bits of matter (blood clot, plaque) formed elsewhere and released into the bloodstream, traveling to the cerebral arteries where they lodge in a vessel, producing occlusion and infarction. The most common source of CE is disease of the cardiovascular system. Intracerebral hemorrhage (IH) -ANSWER is caused by rupture of a cerebral vessel with subsequent bleeding into the brain. Primary cerebral hemorrhage -ANSWER (nontraumatic spontaneous hemorrhage) typically occurs in small blood vessels weakened by atherosclerosis producing an aneurysm. Subarachnoid hemorrhage (SH) -ANSWER occurs from bleeding into the subarachnoid space typically from a saccular or berry aneurysm affecting primarily large blood vessels. Arteriovenous malformation (AVM) -ANSWER is another congenital defect that can result in stroke. AVM is characterized by a tortuous tangle of arteries and veins with agenesis of an interposing capillary system. The abnormal vessels undergo progressive dilation with age and eventually bleed in about 50% of cases. Clinical signs of elevating intracranial pressure (ICP) -ANSWER include decreasing level of consciousness (stupor and coma), widened pulse pressure, increased heart rate, irregular respirations (Cheyne-Stokes respirations), vomiting, unreacting pupils (cranial nerve [CN] III signs), and papilledema. Cerebral edema is the most frequent cause of death in acute stroke and is characteristic of large infarcts involving the middle cerebral artery and the internal carotid artery. Transient ischemic attack (TIA) -ANSWER the temporary interruption of blood supply to the brain. Symptoms of focal neurological deficit may last for only a few minutes or for several hours, but by definition do not last longer than 24 hours. After the attack is over there is no evidence of residual brain damage or permanent neurological dysfunction. TIAs may result from a number of different etiological factors, including occlusive episodes, emboli, reduced cerebral perfusion (arrhythmias, decreased cardiac output, hypotension, overmedication with antihypertensive medications, subclavian steal syndrome), or cerebrovascular spasm. The major clinical significance of TIA is as a precursor to susceptibility for both cerebral infarction and myocardial infarction. Approximately 15% of all strokes are preceded by a TIA, with the greatest risk of occurrence within 90 days.1 Anterior Cerebral Artery Syndrome -ANSWER is the first and smaller of two terminal branches of the internal carotid artery. It supplies the medial aspect of the cerebral hemisphere (frontal and parietal lobes) and subcortical structures, including the basal ganglia (anterior internal capsule, inferior caudate nucleus), anterior fornix, and anterior four-fifths of the corpus callosum (Fig. 15.3). Because 650 651the anterior communicating artery allows perfusion of the proximal ACA from either side, occlusion proximal to this point results in minimal deficit. More distal lesions produce more significant deficits. Table 15.1 presents the clinical manifestations of anterior cerebral artery (ACA) syndrome. The most common characteristics of ACA syndrome include contralateral hemiparesis and sensory loss with greater involvement of the lower extremity (LE) than the upper extremity (UE) because the somatotopic organization of the medial aspect of the cortex includes the functional area for the LE. Middle Cerebral Artery Syndrome -ANSWER The middle cerebral artery (MCA) is the second of the two main branches of the internal carotid artery and supplies the entire lateral aspect of the cerebral hemisphere (frontal, temporal, and parietal lobes) and subcortical structures, including the internal capsule (posterior portion), corona radiata, globus pallidus (outer part), most of the caudate nucleus, and the putamen (Fig. 15.4). Occlusion of the proximal MCA produces extensive neurological damage with significant cerebral edema. Increased intracranial pressures typically lead to loss of consciousness, brain herniation, and possibly death. Table 15.2 presents the clinical manifestations of middle cerebral artery (MCA) syndrome. The most common characteristics of MCA syndrome are contralateral spastic hemiparesis and sensory loss of the face, UE, and LE, with the face and UE more involved than the LE. Lesions of the parieto-occipital cortex of the dominant hemisphere (usually the left hemisphere) typically produce aphasia. Lesions of the right parietal lobe of the nondominant hemisphere (usually the right hemisphere) typically produce perceptual deficits (e.g., unilateral neglect, anosognosia, apraxia, and spatial disorganization). Homonymous hemianopsia (a visual field defect) is also a common finding. The MCA is the most common site of occlusion in stroke. BRAINSTEM LESIONS -ANSWER Symptoms of crossed anesthesia (ipsilateral facial impairments with contralateral trunk and limb involvement) typify brainstem lesions anosognosia -ANSWER is a deficit of self-awareness, a condition in which a person who suffers some disability seems unaware of the existence of their disability. results from physiological damage to brain structures, typically to the parietal lobe or a diffuse lesion on the fronto-temporal-parietal area in the right hemisphere. asomatognosia -ANSWER a form of neglect in which patients deny ownership of their limbs. apraxia -ANSWER Total or partial loss of the ability to perform coordinated movements or manipulate objects in the absence of motor or sensory impairment. Internal Carotid Artery Syndromes -ANSWER Occlusion of the internal carotid artery (ICA) typically produces massive infarction in the region of the brain supplied by the middle cerebral artery. The ICA supplies both the MCA and the ACA. If collateral circulation to the ACA from the circle of Willis is absent, extensive cerebral infarction in the areas of both the ACA and MCA can occur. Significant edema is common with possible uncal herniation, coma, and death (mass effect). Posterior Cerebral Artery Syndrome -ANSWER The two posterior cerebral arteries (PCAs) arise as terminal branches of the basilar artery and each supplies the corresponding occipital lobe and medial and inferior temporal lobe (see Fig. 15.3). It also supplies the upper brainstem, midbrain, and posterior diencephalon, including most of the thalamus. Table 15.3 presents the clinical manifestations of posterior cerebral artery (PCA) syndrome. Occlusion proximal to the posterior communicating artery typically results in minimal deficits owing to the collateral blood supply from the posterior communicating artery (similar to ACA syndrome). Occlusion of thalamic branches may produce hemianesthesia (contralateral sensory loss) or central post-stroke (thalamic) pain. Occipital infarction produces homonymous hemianopsia, visual agnosia, prosopagnosia, or, if bilateral, cortical blindness. Temporal lobe ischemia results in amnesia (memory loss). Involvement of subthalamic branches may involve the subthalamic nucleus or its pallidal connections, producing a wide variety of deficits. Contralateral hemiplegia occurs with involvement of the cerebral peduncle. Lacunar strokes -ANSWER are caused by small vessel disease deep in the cerebral white matter (penetrating artery disease). They are strongly associated with hypertensive hemorrhage and diabetic microvascular disease. Lacunar syndromes are consistent with specific anatomical sites. Pure motor lacunar 651 653stroke is associated with involvement of the posterior limb of the internal capsule, pons, and pyramids. Pure sensory lacunar stroke is associated with involvement of the ventrolateral thalamus or thalamocortical projections. Other lacunar syndromes include dysarthria/clumsy hand syndrome (involving the base of the pons, genu of anterior limb, or the internal capsule), ataxic hemiparesis (involving the pons, genu of internal capsule, corona radiata, or cerebellum), sensory/motor stroke (involving the junction of the internal capsule and thalamus), or dystonia/involuntary movements (choreoathetosis with lacunar infarction of the putamen or globus pallidus; hemiballismus with involvement of the subthalamic nucleus). Deficits in consciousness, language, or visual fields are not seen in lacunar strokes because the higher cortical areas are preserved. A hypertensive hemorrhage affecting the thalamus can also produce central post-stroke pain. Vertebrobasilar Artery Syndrome -ANSWER Vertebrobasilar Artery Syndrome The vertebral arteries arise from the subclavian arteries and travel into the brain along the medulla where they merge at the inferior border of the pons to form the basilar artery. The vertebral arteries supply the cerebellum (via posterior inferior cerebellar arteries) and the medulla (via the medullary arteries). The basilar artery supplies the pons (via pontine arteries), the internal ear (via labyrinthine arteries), and the cerebellum (via the anterior inferior and superior cerebellar arteries). The basilar artery then terminates at the upper border of the pons giving rise to the two posterior arteries (see Fig. 15.2). Occlusions of the vertebrobasilar system can produce a wide variety of symptoms with both ipsilateral and contralateral signs, b