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Causes of Brainstem Death

发布时间:2017-03-15
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Discuss the causes of brainstem death and those parts of the brainstem that keep you alive. The brainstem is a key region for automatic neurological coordination with many vital roles. Descending from the diencephalon, to the spinal cord; the brainstem consists of the midbrain, superiorly, the pons and the medulla oblongata, inferiorly (Fig.1). The brainstem is responsible for providing a conduit for neurones between the spinal cord and the higher centres of the forebrain, as well as containing the "important nuclei of cranial nerves III through XII" (Snell, 2010). The brainstem also takes charge of reflex centres important for sustaining life, this role and the pathology that puts it at risk being the focus of this essay.

The control ventilation is a function the brainstem undertakes to maintain life.  Ventilation has two constituents to its control: voluntary and automatic. The voluntary regulation originates in the cerebral cortex (St. John, 1998), whereas the automatic control comes from specific nuclei within the Pons and Medulla. The automatic component is responsible for maintaining constant ventilation when the cortex is undertaking other tasks and during sleep. It is also responsible for the homeostasis of blood gases, with sensory input from the periphery as well as its own sensory function.

The medullary respiratory centre comprises of two areas: the ventral (VRG) and dorsal (DRG) respiratory groups (Fig. 2). "The dorsal respiratory group of neurons, are located in the ventrolateral portion of the nucleus solitarius" (Smith and DeMyer, 2003) and contains neurones involved in control of inspiration. A ventrolateral column within the medulla, extending from the facial nucleus (Feldman et al, 2003) into the spinal cord near to the level of C1, represents the VRG. It contains the nucleus ambiguus and nucleus retroambigualis and is involved in the control of both inspiration and expiration.

The DRG is made up predominantly of "'pre-motor' bulbospinal neurones" (St. John, 1998) which terminate within the spinal cord at the levels of the phrenic and intercostal motor neurones. However, these have been shown to have a less important role as lesions of this area have presented insignificantly (Ballanyi and Ruangkittisakul, 2009).

It appears the more significant area is the VRG which contains a variety of neurone types. Some are bulbospinal and exert similar control to the DRG (St. John, 1998). Others travel within the cranial nerves, particularly the vagus and glossopharyngeal nerves, to co-ordinate muscles in the head and neck also involved in respiration. There are also neurones travelling exclusively within the brainstem. At the rostral end of the VRG is a particularly important area involved in generation of respiratory rhythm, the pre-Bötzinger complex (pre-Böt).  It has been suggested that, due to the profound effect lesions in this region has on respiration, that neurones from this area have a pacemaker capacity (Feldman et al, 2003).

Within the pons, associated to the nucleus parabrachialis medialis and Kolliker-Fuse nucleus (St. John, 1998; Spyer and Gourine, 2009), is the 'pneumotaxic centre' (PC). This rostral pontine section contains a mixture of inspiratory, expiratory and phase-spanning neurones which communicate with the VRG via the pontine reticular formation. It has been shown to exert some effect on respiratory rhythm generation as the rhythm becomes very erratic after transection of the ponto-medullary junction, as shown in Figure. 3.

As already stated, the brainstem is also responsible for maintaining homeostasis. A change in blood-gas composition is detected in the carotid and aortic bodies, by glomus cells, and fed back to the brainstem via the glossopharyngeal and vagus nerve respectively. These peripheral chemoreceptors are mostly sensitive to O2 concentration, whereas the CO2/pH-sensitive chemoreceptors are mostly found within the brainstem and are known as central chemoreceptors (Feldman et al, 2003). The CO2/pH sensitivity reflects "the adequacy of breathing relative to metabolism" and so has a greater effect on respiration with just "1-mm Hg increase in PCO2 increases ventilation by 20%-30%". Central chemoreceptors can be found within: the nucleus tractus solitarius; locus ceruleus; the midline medullary raphe; the retrotrapezoid nucleus; the pre-Böt; and, the regions lying just beneath the ventral medullary surface; and are defined as areas which "exhibit an excitatory response to an increase in CO2 or H+ concentration" (Ballantyne and Scheid, 2000) to increase motor output. Mechano-sensors and proprioceptors within the associated muscles and the lung wall, also act to inhibit inspiration, to ensure the lungs aren't over inflated, causing damage to them. (Spyer and Gourine, 2009).

Closely related to the respiratory centres of the brainstem are the nuclei controlling cardiovascular function, another component vital to life. The function of the respiratory system is maintaining gas concentrations in the body, and this must be facilitated by the cardiovascular system. "Respiratory and cardiovascular rhythms are regulated synergistically to ensure adequate ventilation-perfusion," (Spyer and Gourine, 2009). This means that the control centres for both systems communicate to environmental challenges to homeostasis are dealt with and return the body back to normal. For example, if the body was to become hypoxic, chemoreceptors would evoke a change in both systems, increasing ventilation and heart rate, to reverse this change (Nicholls and Paton, 2009).

The Nucleus tractus solitarius (NTS) is fundamental to autonomic cardiovascular regulation, and is, as already stated, associated with the DRG (Hirooka, 2008). Other areas involved are the rostral ventrolateralmedulla (RVLM); nucleus ambiguus; and the midline raphe nuclei of the medulla, the parabrachial nucleus of the pons; and the periaqueductal gray area of the midbrain (Topolovec et al, 2004, Kong et al, 2007). Of these, perhaps the most important in cardiovascular control are the RVLM, nucleus ambiguus and the NTS.

"The NTS is the primary site for integration of the chemoreceptor and baroreceptor reflexes" (Thomas et al, 2000). Baroreception allows the body to sense changes in blood pressure and the afferent fibres for this are located within the walls of the atria, aortic and carotid bodies. These afferents, along with chemoreceptive data, travel to the NTS via the vagus and glossopharyngeal nerves to exert synaptic influence on vagal output to the heart (Spyer and Gourine, 2009). It has also been suggested that there is a degree of central sensation to blood pressure within the brainstem itself (Shusterman et al, 2002). Activation of baroreceptors evokes bradycardia, reduces vascular resistance and so reverses hypertension. For this to occur, the NTS must synapse with other nuclei of the brainstem to trigger an autonomic response.

The autonomic centres concerned with cardiovascular control are RVLM and nucleus ambiguus. Sympathetic 'pre-motor' neurones originate predominantly in the RVLM. When signals come from baroreceptors, they synapse with these 'pre-motor' efferents to bring about a rise in blood pressure (Shusterman et al, 2002). This is done mostly by causing vasoconstriction and thus raises total peripheral resistance (Spyer and Gourine, 2009). The nucleus ambiguus is the crucial centre in reducing cardiac output when in a hypertensive state. This is completed by parasympathetic 'pre-motor' fibres, to produce a negative chronotropic effect on the heart, via the vagus nerves.

Another area of particular importance within the brainstem is the reticular formation (RF) (Fig. 4). Consisting of three columns and spanning the whole length of the brainstem; the RF contributes to many vital control mechanisms within the body, such as: somatic and visceral sensation; the autonomic and endocrine nervous systems; the biological clock; and consciousness (Snell, 2010). Consciousness is particularly vital in staying alive as it allows voluntary survival behaviours, directed by the cerebral cortex, to be displayed. Part of the RF, the ascending reticular activating system is responsible for activating the cortex and bringing about wakefulness (Parvizi and Damasio, 2001).

Causes of Brainstem Death

Brainstem death is the result of a major traumatic event and is defined as "a state in which there is irreversible loss of the capacity for consciousness combined with irreversible loss of the capacity to breathe spontaneously (and hence to maintain a spontaneous heart beat)" (Pallis and Harley, 1996). The causes for brainstem death can be broadly grouped into two categories, those that cause direct physical trauma to the neurones of the brainstem and disrupt their interconnections; or those causes resulting in hypoxia, leaving the neurones unable to maintain metabolism and causing injury in situ.

Physical trauma to the brainstem breaks down the intricate excitatory pathways within it, thus rendering communication between the centres of the brainstem, and the regions under their control, impossible. Often the result of a head injury, one example of this is the ponto-medullary tear (Fig. 5). This is a severance of the ponto-medullary junction and is often the result of a blunt head trauma, such as a head butt (Stan et al, 1996). The RF is one area that is likely to be damaged in such an injury, resulting in the patient falling into a deep irreversible coma. Centres for both respiratory and cardiac control could also be separated, e.g. the parabrachial nucleus.  As the patient would be unable to resume consciousness and sustain cardio-respiratory function, they would be deemed brainstem dead, and so according to UK law, legally dead.

A ponto-medullary tear is not the only cause of death as a result of head trauma. Rapid deceleration within the cranial cavity, such as that experienced during a road traffic accident, can also often result in lesions within the brainstem (Gunji et al, 2002). It must also be noted that a large lesion to the brainstem is often accompanied by massive haemorrhaging, leading to additional injury to other areas of the brainstem and is discussed later. Tumours can also have a traumatic consequence within the brainstem, damaging neurones as they infiltrate tissues (Yilmazlar et al, 2004).

Haemorrhage, as a result of head trauma, raises intracranial pressure: another major cause of brainstem death. As the dura mater does not expand, there is a constant intracranial volume. By adding to the content of the cavity, e.g. arterial haemorrhage, the pressure increases and so has a detrimental effect on the fragile nervous tissue within. As intracranial blood perfusion is inversely proportional to the cavity pressure, an increase could to lead to decreased perfusion pressure and even infarction of some key areas of the brainstem.

Another consequence of a pressure increase is herniation. This is where the increased pressure causes movement of the brain around the dural partitions and through the foramen magnum. This can cause either tension within the cerebral peduncles and midbrain or force the delicate structures against the harder ones (Hussain et al, 2008; Crippen, 2009). This means these areas can either be damaged by the physical trauma of the displacement or the resulting ischemia: as these areas cannot be adequately perfused with blood. The exact position of the origin of the raised pressure will propagate force in a certain direction (Orlando Regional Healthcare, Education and Development, 2004). One example of this is when a downward force pushes the lower medulla through the foramen magnum: a tonsillar herniation. The resultant damage will occur in the region of the brainstem containing many of the centres for CV and respiratory control and can lead to an inability to breathe without cortical innervation: Ondine's curse (Smith and DeMyer, 2003).

A stroke is where cerebral blood flow is interrupted, causing necrosis of the unperfused tissue. This can be caused by either blockage of the blood vessel or a haemorrhage causing blood flow to be diverted away. Haemorrhagic strokes can arise from a ruptured aneurism or a bleeding tumour (Yilmazlar et al, 2004) and not only diverts blood away from the tissues it should supply, but can also increase intracranial pressure, damaging other areas. Ischemic stroke is the most common form of vascular malfunction and is often caused by thrombotic accumulations blocking blood supply to critical regions (Sims and Muyderman, 2010). If such an episode was to occur in the basilar artery supplying much of the brainstem, parts of it vital to sustaining life would be permanently damaged. Occlusion or rupture of the vertebral arteries, often a result of rotational trauma in the neck, could have similar effects (Auer et al, 1994).

It is clear that the brainstem is a crucial component of the central nervous system which, if non-functional, the coordination and synchronicity of the entire body would simple fail. It is important, as a clinician to be able to not only understand its importance but, also, to appreciate the location of more indispensible areas should disease arise. By grasping the prevailing sources of brainstem pathology, rapid identification of risk to this fragile region can be made and so reduce injury.

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