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Congenital pulmonary atresia with cerebral thrombosis and hemiplegia
occur during or because of the arrival 2tnd rise of the atriai :wTion potent,%, but Long atrioventricuiar delays during the period of electric,al recovery of the atrium. may involve serial activation of several elements thus multiplying the single junctional pause found in the normal heart.
Hunter,
A.,
and
Thrombosis
Lipscomb,
J.
and Hemiplegia.
M.: Brit.
Congenital Heart
Pulmonary
Mresia
With
Cerebral
J. 4: 124, 1942.
Cerebral manifestations in pulmonary atresia and stenosis are well recognized. They have been attributed either to paradoxical embolism, or 1-u cerebral thrombosis associated with the polycythemia. Hemiplegia and rpileptiform attacks are recorded by the authors, which lvere shown at necropsy to be SUP to cerebral thrombosis. Their transient nature may be explained by the absence of softening o-f the brain although there was such extreme distension and thrombosis of the cerebral veins. AUTHORS.
Bremer,
J. L.:
Embryologic
Transposition Study of Its
of Cause.
the Aorta and the Pulmonary Srch. Path. 34: 1016, 1942.
Artery:
An
Transposition of the aorta anil the pulmonary artery is the common facror in many anomalies of the heart, and as sigh should be the result of’ some slight and easily produced variation from the nornral course of del-clopment. Models and drawings af human hearts of 5 mm. and less show great rliCcrences in shape, especially of the bulbar region. The lower parl of the bulb is transformed into the right ventricle by the outgrowth of sinusoids, sprouting earliest ant1 most profusely from the convex surface of some acute curve. The sharpest curve in the normal bulb point,s downward and forward, and thp spongy substance of the right ventricle, therefore, is chiefly on the ventral and api& falls. In a few of the younger hearts sholvn, the sharpest curve points down\qlrd and bar+kwxrd or ~lorsslly, and in one human embryo studied, the sinusoids, whirlr are just developing, are found on the apical and dorsal walls of the ventricle. Continued growth in this .lorsal position would meet the opposition of the diaphra&~l. and the right ventrlrle would be forced ventrally. Since the left, wall of the embryonic right ventricle i-i attached to t,he interventricular canal, ventral displacement GUI bt accan~plished only by a rotary anticlockwise motion, which when transmitted to the distal bulb vvoulrl counteract the normal dextral torsion and result in transposition. The expansion of the dorsal and lateral walls at the expense of t,he central mall might also result in tlte displacement, ventrally of the supraventricular crest, the bulboatrial ledge, and the anterior tricuspid ledge, and in their intensification to form more or less complete septums across the ventricle. The ventral pouch bordered by such septums i3 not, however, the true right ventricle. Stenosis of the pulmonary Failure of the ventral sinusoids artery may depend on the efliciency of such septums. may cause the malformation or absence of the ventral interventricular septum, resulting in ( ‘ crossed transposition. ’’ of development, as all mammalian Li Overriding of the aorta ” is due to arrest emhryonie hearts pass through this stage before the final separation of the ventricles by the growth of the membranous portion of the interventricular septum. This condition has no conne&on with transposition. The main deductions of this paper rest ehiefiy on the tenuous basis of conditions and are therefore submitted as a theory rather found in a single human embryo, than as a proved exposition of the cause of the anomaly. Yet they trace the logical, mechanical effects of growth forces on an observed variation from normal, and SIIOW how these would result in transposition and its many accompanying changes in the heart. AUTHOR.
Hunter,
A.,
and
Thrombosis
Lipscomb,
J.
and Hemiplegia.
M.: Brit.
Congenital Heart
Pulmonary
Mresia
With
Cerebral
J. 4: 124, 1942.
Cerebral manifestations in pulmonary atresia and stenosis are well recognized. They have been attributed either to paradoxical embolism, or 1-u cerebral thrombosis associated with the polycythemia. Hemiplegia and rpileptiform attacks are recorded by the authors, which lvere shown at necropsy to be SUP to cerebral thrombosis. Their transient nature may be explained by the absence of softening o-f the brain although there was such extreme distension and thrombosis of the cerebral veins. AUTHORS.
Bremer,
J. L.:
Embryologic
Transposition Study of Its
of Cause.
the Aorta and the Pulmonary Srch. Path. 34: 1016, 1942.
Artery:
An
Transposition of the aorta anil the pulmonary artery is the common facror in many anomalies of the heart, and as sigh should be the result of’ some slight and easily produced variation from the nornral course of del-clopment. Models and drawings af human hearts of 5 mm. and less show great rliCcrences in shape, especially of the bulbar region. The lower parl of the bulb is transformed into the right ventricle by the outgrowth of sinusoids, sprouting earliest ant1 most profusely from the convex surface of some acute curve. The sharpest curve in the normal bulb point,s downward and forward, and thp spongy substance of the right ventricle, therefore, is chiefly on the ventral and api& falls. In a few of the younger hearts sholvn, the sharpest curve points down\qlrd and bar+kwxrd or ~lorsslly, and in one human embryo studied, the sinusoids, whirlr are just developing, are found on the apical and dorsal walls of the ventricle. Continued growth in this .lorsal position would meet the opposition of the diaphra&~l. and the right ventrlrle would be forced ventrally. Since the left, wall of the embryonic right ventricle i-i attached to t,he interventricular canal, ventral displacement GUI bt accan~plished only by a rotary anticlockwise motion, which when transmitted to the distal bulb vvoulrl counteract the normal dextral torsion and result in transposition. The expansion of the dorsal and lateral walls at the expense of t,he central mall might also result in tlte displacement, ventrally of the supraventricular crest, the bulboatrial ledge, and the anterior tricuspid ledge, and in their intensification to form more or less complete septums across the ventricle. The ventral pouch bordered by such septums i3 not, however, the true right ventricle. Stenosis of the pulmonary Failure of the ventral sinusoids artery may depend on the efliciency of such septums. may cause the malformation or absence of the ventral interventricular septum, resulting in ( ‘ crossed transposition. ’’ of development, as all mammalian Li Overriding of the aorta ” is due to arrest emhryonie hearts pass through this stage before the final separation of the ventricles by the growth of the membranous portion of the interventricular septum. This condition has no conne&on with transposition. The main deductions of this paper rest ehiefiy on the tenuous basis of conditions and are therefore submitted as a theory rather found in a single human embryo, than as a proved exposition of the cause of the anomaly. Yet they trace the logical, mechanical effects of growth forces on an observed variation from normal, and SIIOW how these would result in transposition and its many accompanying changes in the heart. AUTHOR.