The activity of the sympathetic nervous system following severe head injury

Hörtnagl, Heide; Hammerle, A. F.; Hackl, J. M.; Brücke, Thomas; Rumpl, E.; Hörtnagl, Helmut

doi:10.1007/bf01757299

Cited by 95 publications

(51 citation statements)

References 37 publications

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“…The postulated sites of dysfunction range from the upper brainstem and diencephalon through to the anterior hypothalamus and/or other cortical and subcortical centres [5,8,9,11,13,15,[18][19][20][21][22][23][24]. Recently, the Excitatory:Inhibitory Ratio (EIR) Model [2] was proposed as an alternative disconnection theory, where paroxysms are driven by abnormal processing of afferent stimuli within the spinal cord.…”

Section: Introductionmentioning

confidence: 99%

A Critical Review of the Pathophysiology of Dysautonomia Following Traumatic Brain Injury

et al. 2007

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The management of Dysautonomia following severe traumatic brain injury (TBI) remains problematic, primarily due to an inadequate understanding of the pathophysiology of the condition. While the original theories inferred an epileptogenic source, there is greater support for disconnection theories in the literature. Disconnection theories suggest that Dysautonomia follows the release of one or more excitatory centres from higher centre control. Conventional disconnection theories suggest excitatory centre/s located in the upper brainstem and diencephalon drive paroxysms. Another disconnection theory, the Excitatory:Inhibitory Ratio (EIR) Model, suggests the causative brainstem/diencephalic centres are inhibitory in nature, with damage releasing excitatory spinal cord processes. Review of the available data suggests that Dysautonomia follows structural and/or functional (for example raised intracerebral pressure or neurotransmitter blockade) abnormalities, with the tendency to develop Dysautonomic paroxysms being more closely associated with mesencephalic rather than diencephalic damage. Many reports suggest that paroxysmal episodes can be triggered by environmental events and minimised by various but predictable neurotransmitter effects. This article presents a critical review of the competing theories against the available observational, clinical and neurotransmitter evidence. Following this process, it is suggested that the EIR Model more readily explains pathophysiological and treatment data compared to conventional disconnection models. In particular, the EIR Model provides an explanatory model that encompasses other acute autonomic emergency syndromes, accommodates 'triggering' of paroxysms and provides a rationale for all known medication effects.

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Section: Introductionmentioning

confidence: 99%

A Critical Review of the Pathophysiology of Dysautonomia Following Traumatic Brain Injury

et al. 2007

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“…1 Survivors of TBI often experience profound catecholamine surges and additional systemic complications such as hypertension, pulmonary edema, and cardiomyopathy. [2][3][4][5][6][7][8][9] Notably, endothelial dysfunction secondary to systemic inflammation and shock is widely believed to contribute to systemic complications in severe trauma, 9,10 yet there have been no studies that directly measure endothelial function in systemic blood vessels after head trauma.…”

Section: Introductionmentioning

confidence: 99%

Traumatic Brain Injury Causes Endothelial Dysfunction in the Systemic Microcirculation through Arginase-1–Dependent Uncoupling of Endothelial Nitric Oxide Synthase

Villalba

Sackheim

Nuñez

et al. 2017

Journal of Neurotrauma

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Endothelial dysfunction is a hallmark of many chronic diseases, including diabetes and long-term hypertension. We show that acute traumatic brain injury (TBI) leads to endothelial dysfunction in rat mesenteric arteries. Endothelial-dependent dilation was greatly diminished 24 h after TBI because of impaired nitric oxide (NO) production. The activity of arginase, which competes with endothelial NO synthase (eNOS) for the common substrate l-arginine, were also significantly increased in arteries, suggesting that arginase-mediated depletion of l-arginine underlies diminished NO production. Consistent with this, substrate restoration by exogenous application of l-arginine or inhibition of arginase recovered endothelial function. Moreover, evidence for increased reactive oxygen species production, a consequence of l-arginine starvation-dependent eNOS uncoupling, was detected in endothelium and plasma. Collectively, our findings demonstrate endothelial dysfunction in a remote vascular bed after TBI, manifesting as impaired endothelial-dependent vasodilation, with increased arginase activity, decreased generation of NO, and increased O 2 -production. We conclude that blood vessels have a ''molecular memory'' of neurotrauma, 24 h after injury, because of functional changes in vascular endothelial cells; these effects are pertinent to understanding the systemic inflammatory response that occurs after TBI even in the absence of polytrauma.

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“…It is worth mentioning that in a HC derived from a status epilepticus and not related to hypertensive encephalopathy, the patient may present with hypotension after the first acute hypertensive event, 5 just like the patient in question. It is also important to mention that most cases of diencephalic epilepsy associated to severe hypertension are reported in comatose patients, victims of serious traumatic brain injury; 6,7 however, the patient in question did not present a history of brain injury. Treatment with carbamazepine yields good responses, 4 with gabapentin as a second option.…”

Section: Discussionmentioning

confidence: 99%