Correlation of cardiac arrhythmias with brainstem compression in patients with intracerebral hemorrhage.

Neurogenically caused cardiac arrhythmias and their correlation to lesions within the central nervous system were examined prospectively in 54 patients with spontaneous intracerebral hemorrhage. All patients were examined neurologically daily for 3 weeks, with special attention given to signs of brainstem compression resulting from transtentorial herniation. Electrocardiograms were continuously recorded over an average of 5 days. A significant correlation was established between the clinical manifestations of brainstem compression and sinus arrhythmias, multifocal premature ventricular contractions, couplets, and ventricular tachycardias. An explanation for this correlation may be found in the localization of the autonomous cardiovascular centers in the hypothalamus and brainstem. Transtentorial herniation frequently leads to a bilateral lesion of these structures. However, the cardiac arrhythmias are only a partial phenomenon within a complex cardiovascular reaction.

Quantitative and cytoarchitectural studies of the entorhinal region and the hippocampus of New Zealand black mice.

New Zealand Black (NZB) mice were suggested as an animal model for human dementia. We performed quantitative and cytoarchitectural studies of the entorhinal region and the hippocampus of 10 NZB mice and compared the results with those for a control group of 10 Carworth Farm Webster (CFW) mice. No cytoarchitectural disturbances were observed in the entorhinal cortex and hippocampus of the NZB mice. We, however, found a reduced density of nerve cells in the entorhinal region as well as in the CA1 and CA3 regions of the Ammon's horn in NZB mice. Since the entorhinal region is an important link between sensory and association cortices and the limbic system which seems to play an important role in learning and memory, the present findings may be a cause of learning and/or memory deficits in the NZB mice. The undisturbed cytoachitecture of the entorhinal cortex suggests that the reduced cell sensity in NZB mice is rather an acquired lesion than a developmental malformation and, therefore, indicates therapeutic studies on memory and learning deficits in NZB mice.

Cardiac arrhythmias in subarachnoid haemorrhage.

In this prospective study 52 patients with spontaneous subarachnoid haemorrhage were examined with respect to cardiac arrhythmias and their relationship to cerebral lesions. A continuous ECG was registered over an average of five days. Sinus tachycardia was the most frequently recorded arrhythmia, followed by multifocal ventricular extrasystoles, couplets, frequent supraventricular extrasystoles, non-sustained ventricular tachycardia, asystolia and sinus arrhythmia. A significant correlation was found between the clinical manifestation of a midbrain syndrome and sinus arrhythmia, and multifocal ventricular extrasystoles. This correlation points to the autonomic cardiovascular centres as the structures involved.

[Neurogenic cardiac arrhythmias in acute intracranial increase in pressure (recurrent hemorrhage in subarachnoid hemorrhages)]. / Neurogene kardiale Arrhythmien bei akutem intrakraniellem Druckanstieg (Nachblutungen bei Subarachnoidalblutungen).

Neurogenic cardiac arrhythmias during 5 cases of subarachnoid rebleeding in 4 patients were analyzed by using long-term ECG (Holter). The initial onset of rebleeding was characterized by an abrupt decrease of heart rate from 93.3 +/- 7.85 (beats/min) to 63.3 +/- 14.6 (beats/min). This was immediately followed by pronounced tachycardia of 163.0 +/- 20.9 (beats/min) and subsequently, alterations of the P wave, ST depression with an increase in T wave amplitude. Frequent premature ventricular contractions, couplets, and self-terminating episodes of ventricular tachycardia for 2-8 minutes were observed during 2 episodes of rebleeding, an idioventricular rhythm in one case. The ECG returned to normal in the 3 non-lethal cases. Pathogenetically, the initial heart rate decrease with varying P wave configuration can be explained through activation of the baroreceptor reflex. Elevated intracranial pressure causes a blood pressure increase thus stimulating the baroreceptors and consequently, the afferent and efferent tracts of the vagus nerve. The sympathicotonus appears to have a modulating effect.

Direct evidence of hypertension and the possible role of post-menopause oestrogen deficiency in the pathogenesis of berry aneurysms.

To determine the significance of hypertension in the pathogenesis of berry aneurysms, 113 patients with subarachnoid haemorrhage (SAH) and verified aneurysm and 63 patients with SAH without aneurysm were compared. Of those patients with angiographically verified aneurysms, 61.9% were found to have elevated blood pressure (greater than 160/95 mmHg) and 19.5% showed electrocardiographic signs of left ventricular hypertrophy (SV1 + RV5 (6) greater than 3.5 mV). The percentages for patients without aneurysm were 36.5% and 6.4% respectively. A significant correlation was found between anterior aneurysms and left ventricular hypertrophy (P less than 0.01). The mean Sokolow index values were also significantly elevated in cases of aneurysm (P less than 0.01). There was a complementary relationship between the extent of left ventricular hypertrophy and the percentage of females with regard to localization of an aneurysm and age group. The predominance of females in the total aneurysm population, in the 50- to 59-year-old age group, and among patients with internal carotid aneurysms indicates that a sex-specific hormonal factor may also play a role in the pathogenesis of aneurysms in addition to hypertension. The collagen wasting commonly observed in bone and skin in the post-menopausal period due to decreased oestrogen levels could possibly be responsible for the formation of aneurysms in the proximal segments of the cerebral arteries, as occurs in various connective tissue diseases.

Blood distribution in computer cranial tomograms after subarachnoid hemorrhage with and without an aneurysm on angiography.

This is a comparative study of the blood distribution in computer cranial tomograms after spontaneous subarachnoid hemorrhage in 51 patients with saccular aneurysms and 34 patients with no evidence of a source of bleeding in cerebral panangiography. There was often less blood observed at all sites when aneurysms were not present. This was, however, significant only in the interhemispheric fissure, the Sylvian cisterns, the parietal sulci as well as intracerebrally. Thus, 79.4% of patients without an aneurysm were in grades I and II of the Hunt and Hess scale as opposed to 47.0% of those patients with evidence of an aneurysm.

[Incidence of ventricular arrhythmia relative to the QT interval in spontaneous intracranial hemorrhages]. / Häufigkeit von Kammerarrhythmien in Abhängigkeit vom QT-Intervall bei spontanen intrakraniellen Blutungen.

A prospective study was done in 54 patients with acute spontaneous intracranial haemorrhage, 27 of them with subarachnoid bleeding and 27 with primary intracerebral haemorrhage. The frequency of ventricular arrhythmias was registered by continuous long-term ECG and the incidence of QT prolongation by daily standard ECG registration. Prolongation of frequency-corrected QT-interval (QTc) developed in 9 patients with subarachnoid haemorrhage and in 10 with intracerebral haemorrhage. For assessment of time-relation between QT-interval and ventricular arrhythmias the results of corresponding long-term ECG and standard ECG were used and two groups were defined: group A (149 tapes) = QTc less than or equal to 450 ms, group B (43 tapes) = QTc greater than 450 ms. In group B singular frequent ventricular extrasystoles, couplets and non-persistent ventricular tachycardias occurred more frequently though not significantly so. Persistent ventricular tachycardias occurred significantly more frequently in group B (14% vs. 1%, P less than 0.01). In three tapes of group B, all of them with QTc prolongation of more than 550 ms persistent ventricular tachycardias with typical "torsade de pointes " morphology were seen. The results show that QTc prolongation of more than 450 ms occurs in a third and significant ventricular arrhythmia in nearly half of patients with spontaneous intracranial haemorrhage. Persistent ventricular tachycardias occur almost only in cases of QTc-prolongation. Pronounced QTc prolongation of more than 550 ms is rare. However, it can give rise to torsade de pointes and ventricular fibrillation.

Recurrent torsade de pointes type ventricular tachycardia in intracranial hemorrhage.

Two out of 72 cases of intracranial hemorrhage-induced polymorphous ventricular tachycardia with typical Torsade de Pointes morphology are presented. Both patients had marked QTc prolongation more than 550 ms. In one patient (QTc: 669 ms) Torsade de Pointes degenerated into fatal ventricular fibrillation. Even though polymorphous Torsade de Pointes type ventricular tachycardia is rare during the clinical course of intracranial hemorrhage, attention should be given to the QT interval. QTc prolongation more than 550 ms may carry a high risk of Torsade de Pointes type ventricular tachycardia and ventricular fibrillation.