Hypothesis about the physiopathology of acute deterioration and sudden death caused by colloid cysts of the third ventricle

Hypothesis about the physiopathology of acute deterioration and sudden death caused by colloid cysts of the third ventricle

Medical Hypotheses (2004) 63, 1014–1017 http://intl.elsevierhealth.com/journals/mehy Hypothesis about the physiopathology of acute deterioration and...

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Medical Hypotheses (2004) 63, 1014–1017

http://intl.elsevierhealth.com/journals/mehy

Hypothesis about the physiopathology of acute deterioration and sudden death caused by colloid cysts of the third ventricle Abderrahmane Hamlata,*, Eduardo Pasqualinib, Brahim Askarc a

Department of Neurosurgery, CHRU Pontchaillou, Rue Henry Le Guilloux, 35000 Rennes, Cedex 2, France b Department of Neurosurgery, Buenos Aires, Argentina c Department of Neurosurgery, Military Hospital Ain Naadja, Algiers, Algeria Received 21 April 2004; accepted 27 April 2004

Summary In this paper, the authors review the mechanisms of acute deterioration and sudden death caused by colloid cysts (CCs). These dreaded events are widely recognized complications of CC, however the mechanism(s) in cause has been subject to controversy. Increased intracranial pressure (ICP) is a common event associated with many cerebral disorders, including colloid cysts, though compensatory mechanisms may allow ICP to remain at normal levels. However, a compensated system might decompensate for many factors such as intracranial haemorrhage, acute hydrocephalus, brain oedema, or an increase in sagittal sinus pressure (SSP). The sagittal sinus in adults with brain tumours appears to respond unpredictably when ICP increases and in some patients, when ICP increased the SSP increased too due to the fact that their sinuses collapse. We therefore speculate that the mechanism of acute deterioration and sudden death is a multifactorial and dynamic process, in which the increase in sagittal sinus pressure would appear to be an important element. It seems possible that acute deterioration is initiated by an increase in sagittal sinus pressure, which provokes acute brain swelling, with a series of often-irreversible events, leading to sudden death. Since the majority of cases of acute deterioration and death are due to CCs of the third ventricle, the authors suggest that surgical resection should be carried out on diagnosed CCs measuring over 1 cm, because sudden death has not been reported as having been caused by colloid cysts measuring less than this dimension. c 2004 Elsevier Ltd. All rights reserved.



Introduction Acute clinical deterioration and sudden death are well known complications of intracranial pro*

Corresponding author. Tel.: +33-2-99-28-4278x84278; fax: +33-2-99-28-4180. E-mail address: [email protected] (A. Hamlat).



cesses. They are most often caused by intracranial or intratumoural bleeding, acute hydrocephalus, brain swelling, and/or brain herniation. The incidence of sudden death caused by brain tumours ranges from 0.16% to 3.2%, and the majority of cases are due to colloid cysts (CC) of the third ventricle [5]. This dreaded event is a widely recognized complication of CC, however its mechanism has been

0306-9877/$ - see front matter c 2004 Elsevier Ltd. All rights reserved. doi:10.1016/j.mehy.2004.04.020

Hypothesis about the physiopathology of acute deterioration subject to controversy [7,4,14]. The suggested hypotheses (acute hydrocephalus, brain herniation, hypothalamic dysfunction, etc.) appear to vary and may represent only the very final stages in a more dynamic process [23]. The purpose of this report is to discuss the physiopathology of acute deterioration and sudden death occurring in patients harbouring tumours of the third ventricle.

Mechanisms and factors of increasing intracranial pressure Increased intracranial pressure (ICP) is a common event associated with many cerebral disorders, including colloid cysts. By obstructing the flow of cerebrospinal fluid (CSF), a tumour, irrespective of its size, can lead to impaired CSF absorption in the superior sagittal sinus, and increased CSF pressure [27]. With CCs, changes in ventricular fluid dynamics are possible initial etiological factors, though compensatory mechanisms (which depend in part on a reciprocal reduction in the CSF volume) may allow ICP to remain at normal levels. The buffer action of CSF on pressure is effective if the CSF absorption/secretion relationship is adequately maintained [9]. If the limits of these compensatory mechanisms (spatial compensation period) are exceeded, the ICP increases more rapidly (period of spatial decompensation) because the relationship between intracranial pressure and volume is an exponential function [12]. The primary factors controlling CSF absorption are the differences in pressure between the cortical subarachnoid spaces and the superior sagittal sinus, and the resistance to CSF flow [8,21]. The absorption/pressure relationship is a linear function of pressure, and it can be deduced that the drainage of CSF is a bulk flow phenomenon [3]. Therefore, the efficiency of intracranial spatial compensation depends on the response of sagittal sinus pressure (SSP) to the developing ICP. According to Martins and colleagues, sagittal sinus pressure (SSP) in adults with brain tumours appears to respond unpredictably when ICP increases. In most patients, SSP remained largely unaffected when ICP increased, however in some patients, when ICP increased the SSP increased too. They concluded that individuals with rapidly increasing gradients, due to the fact that their sinuses do not collapse, probably compensate more rapidly (and better) than those with collapsing sinuses and increasing ICP [18]. In hydrocephalic dogs, the difference in pressure between the sagittal sinus and

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the torcular may be due to a change in the geometry of the sagittal sinus [21]. On the other hand, any increase in venous pressure at the outflow from the capillary bed leads to (brain) venostasis [24]. Although the volume/pressure curve configuration is influenced by the process responsible for intracranial hypertension and its rate of progress, the increase in ICP can be attributed to other factors such as cerebral compliance, elasticity, and ICP fluctuations. Patients with adequate compliance (adequate compensatory mechanisms for adapting to an increase in volume) are more able to tolerate increased ICP than those with decreased compliance [1,17]. Once the compensatory process fails, the pressure/volume relationship is determined primarily by brain elasticity [25]. Elasticity (or elastance) is defined as the ratio of change in pressure to change in volume (and is the opposite of compliance). Therefore the results of high elastance and low compliance are similar [22]. Compliance is probably the more commonly used term when discussing the compensating ability of the intracranial system [1]. Since Lundberg’s classic observation [16] it is well known that in patients with cerebral tumours CSF pressure is subject to marked fluctuations, of which the most important are B waves and plateau waves. This fact has also been reported in hydrocephalic patients [26] and colloid cysts [4,13,14].

Physiopathology of acute deterioration and sudden death Classically, a compensated system might decompensate for many factors such as intracranial haemorrhage, acute hydrocephalus, or brain oedema. This may also result from an increase in SSP [18], an increase in resistance to CSF flow across the absorptive channels [11], a disturbance of other factors influencing intracranial dynamics such as cardiovascular or respiratory systems [15], or occurrences of plateau waves [4]. In fact, ICP is a dynamic process, which cannot be resolved by a static (volume/pressure) relationship [21]. We can therefore speculate that the mechanism of acute deterioration and sudden death is a multifactorial and dynamic process that includes the degree and duration of pre-existing ICP, the rapidity of increase in intracranial volume, a decrease in compliance, the height and duration of pressure waves, and an increase in SSP. It seems possible that acute deterioration is initiated by an increase in sagittal sinus pressure (irrespective of its causes), which provokes acute brain swelling,

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with a series of often-irreversible events, leading to sudden death (see Table 1). Other phenomenon such as systemic response, cellular and molecular reactions of the brain, etc., should also be considered in this situation of brain stress. Since this potentially lethal complication exists in patients with colloid cysts, the treatment of asymptomatic forms has been subject to some controversy [2,10,20], although sudden death has

Table 1

not been reported as having been caused by colloid cysts measuring less than 1 cm [4,6,19,23]. We therefore suggest surgical resection of any diagnosed CCs measuring over 1 cm, even if MRI demonstrates fluid pathways through the interventricular foramen on flair MRI, because we speculate that the cause of acute deterioration and sudden death is a dynamic and multifactorial process.

Physiopathology of acute deterioration and sudden death

This hypothesis supposes that intra-cranial pressure, compensatory mechanisms, and factors that raise the intracranial pressure are not static, but rather dynamic. Thus, at any time a compensated system may deteriorate, and a system in the process of deterioration could stabilize, thus the relation between the different states is an open one.

Hypothesis about the physiopathology of acute deterioration

Conclusion We have highlighted the pathophysiology of acute clinical deterioration and sudden death. It is a multifactorial and dynamic process in which the increase in sagittal sinus pressure would appear to be an important component. Since the majority of cases of acute deterioration and death are due to CCs of the third ventricle, we suggest that surgical resection is carried out on any diagnosed CC measuring over 1 cm.

Acknowledgements We are grateful to A. Elghaziz for his help and to Ms. A. Bradley for correcting the English.

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