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Harvey Williams Cushing
Published in Kieran Walsh, Medical Education, 2016
Harvey Williams Cushing (1869–1939) was an America neurosurgeon and educator. He was the first to describe Cushing’s syndrome and the Cushing reflex. His was a life of medical learning and teaching. He developed an interest in science as a schoolboy and learned surgery under the supervision of William Stewart Halsted. After retiring from surgery, he worked as professor of neurology at Yale.
Cardiovascular physiology
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2015
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
The rigid cranium forms a fixed volume containing the parenchyma, cerebrospinal fluid and the blood. Within the cranial vault, changes in the volume of any one component will alter the other components of cranial contents (Monro–Kellie hypothesis). The Cushing reflex describes the rise in arterial blood pressure that tends to maintain cerebral blood flow in the presence of a raised intracranial pressure. The mechanism of this reflex is stimulation of sympathetic neurons in the medulla by brainstem compression (the arterial baroreceptor reflex then also produces a bradycardia).
Vomiting in Neurological Disorders
Published in John Kucharczyk, David J. Stewart, Alan D. Miller, Nausea and Vomiting: Recent Research and Clinical Advances, 2017
What actually triggers the pressor response is still unknown. Cushing17 stressed ischemia of the medullary centers as the essential stimulus for the resultant pressor response known as the Cushing reflex. Others emphasize the role of baroreceptors in this pressor response.18 Elevated tissue pressure in association with a supratentorial mass is maximal next to the mass and follows a gradient, sparing the brain stem initially.19 Similarly, there are regional disparities in vascular responsiveness in such cases with dysautoregulation confined initially to regions adjacent to the mass. In cases of generalized intracranial hypertension without brain herniation, the vasomotor tone of the lower brain stem is preserved until cerebral blood flow is reduced to ischemic levels. When a mass lesion produces compression or distortion of the brain stem, however, pressor responses occur at relatively low levels of intracranial pressure (ICP), suggesting that brain stem distortion is a powerful stimulus for vasomotor responses from the lower brain stem as opposed to local tissue pressure and ischemia.11,12 Thompson and Malina20 believe that this reduced threshold of the lower brain stem centers for these vasomotor responses is the result of loss of tonic inhibition of lower centers from axial distortion of the brain stem. They demonstrated pressor responses at very low levels of intracranial hypertension when there was a pressure gradient through the brain stem. Possibly, a combination of diminished blood flow, uncoupling of metabolism, and brain stem distortion interrupts the modulation of the vomiting center by higher centers.
Single clip: An improvement of the filament-perforation mouse subarachnoid haemorrhage model
Published in Brain Injury, 2019
Jianhua Peng, Yue Wu, Jinwei Pang, Xiaochuan Sun, Ligang Chen, Yue Chen, Jiping Tang, John H. Zhang, Yong Jiang
The classic endovascular perforation model of SAH was performed as previously described (9). Briefly, the mice were placed in a supine position, and a midline incision was made on the neck. The connective tissue between the salivary glands was separated by blunt dissection. By dissecting the intramuscular spaces, the right common carotid artery (CCA) was exposed. Next, the CCA was mobilized cranially to the bifurcation. After separating the digastric muscle posterior belly, the hyoideum and external carotid artery (ECA) were exposed. The ECA was ligated as far cranially as possible, and prearrange one ligation for the filament around the ECA stump. Next, the pterygopalatine artery (PPA) and internal carotid artery (ICA) were traced. Once the ICA and PPA were clearly observed, microclips (Roboz Surgical Instrument Co., Inc., Gaithersburg, USA) were placed at the ICA and CCA respectively (avoid touching the nearby hypoglossal nerve and carotid body). Next, an arteriotomy was performed on the distal part of the ECA stump. A 5–0 prolene filament (Ethicon, Somerville, NJ, USA) was advanced via the ECA into the bifurcation, and the insertion site was closed with the prearranged ligation. After the clips were removed, the ECA stump was adjusted as a cranial direction. The filament was gently pushed forward (~ 12 mm) until the ICP rises. The Cushing reflex further indicated the successful induction of SAH. Subsequently, the filament was immediately withdrawn, and the ECA was ligated by closing prearranged ligation consecutively. Finally, the skin wound was sutured (Figure 1c). The sham-operated animals received the same procedure except for perforation.