INTRACRANIAL HEMORRHAGE AND THROMBOSIS. 

 APOPLEXY. SOFTENING OF THE BRAIN- 



Definition. Causes : Nature : intracrauial rupture, with pressure, serous 

 effusion, excessive congestion, experimental cases, anemia from pressure, 

 comparative immunity of horse, heart disease, Bright's disease, atheroma, 

 degeneration, emboli, age, blood tension, severe exertion, excitement, con- 

 cussion, insolation, venous obstruction, toxins, neoplasms. Lesions: blood 

 clots, small and multiple, large and solitary, brain absorption, cavities, cysts. 

 Symptoms : dullness, .swaying, trembling, elevation of head, turning in circle, 

 sudden fall, spasms, unequal dilated or contracted pupils, eyes turned to 

 affected side, congested or anaemic mucosae, stertor, puffing cheeks except 

 in solipeds, pulse .slow, soft, full, vomiting, stupor, coma, iinconsciousness, 

 paralysis, monoplegia, hemiplegia, sequelae. Diagnosis : sudden iincon- 

 sciousness, with little spasm, but paral}-sis, history, sign of trauma, deep 

 coma, eyes turned to one side, pupils unequal, stertor, slow breathing and 

 pulse ; from uraemia, pulmonary apoplexy, oedema or anthrax. Treatment : 

 bleeding, ice pack, snow, cold water, rest, derivatives to limbs, later purge, 

 bromides, potassium iodide, tonics, open air life. 



Defiyiition. Cerebral apoplexy has been defined as a sudden 

 loss of sensation and volnntai'}' motion, from pressure originating 

 within the cranium and followed by paralysis, often unilateral. 

 The definition is somewhat insufficient as regards tlie early symp- 

 toms as the same conditions attend on convulsions and epilep.sy 

 (haut mal), and it is only by excluding these by their character- 

 istic features of sudden seizure with clonic spasms and their inter- 

 mittent and paroxysmal habit that we reach an easy and satisfac- 

 tory distinction. Later the paralysis tends to identify the a|)0- 

 plectic attack. 



Causes and Nature. The immediate cause and essential lesion 

 of apoplexy has been generally held to be the rupture of an intra- 

 cranial artery and the formation of a considerable blood clot which 

 presses upon (and abolishes the functions of) the brain. There 

 are cases, however, in which the characteristic symptoms are 

 present, and yet a complete recovery ensues at an early date, too 

 early to allow for the absorption of a considerable clot. Moreover, 

 in fatal cases perhaps no blood clot is to be found, but in place a 

 serous effusion, or an internal conge.stion which exercised the 

 fatal pressure on the brain. So far, therefore, as clinical phe- 

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