Physical Medicine and Rehabilitation Clinics of North America
Autonomic Nervous System Dysfunction After Spinal Cord Injury
Section snippets
Autonomic nervous system anatomy
The ANS has two components or divisions that may be disrupted as a result of damage to the spinal cord, the parasympathetic nervous system (PNS) and the sympathetic nervous system (SNS). The enteric nervous system, also considered a division of the ANS, is not directly disrupted after SCI. The level and extent of injury to the spinal cord determines the dysfunction that occurs. A thorough understanding of the anatomy is important in predicting the types of alterations in function that will
Autonomic nervous system physiology
The autonomic nervous system regulates all essential physiologic components of circulation including heart rate, stroke volume, and vascular resistance, which, in turn, determine arterial blood pressure and cardiac output. The autonomic nervous system regulates these functions in response to feedback from afferent pathways by affecting the force and frequency of cardiac contraction and vasodilation or vasoconstriction. Other influences have a role in the final physiologic state, including
Autonomic nervous system control of thermoregulation
Thermoregulatory responses depend on cold and warm sensors in the hypothalamus and the skin but also on input from mesencephalic, medullary, spinal, and intra-abdominal temperature sensors [2], [10]. Afferent fibers from the peripheral receptors with cell bodies in the dorsal root ganglia enter the spinal cord and ascend contralaterally to the medial lemniscus and the thalamus and then project further to the hypothalamus [2], [11]. The preoptic area of the hypothalamus controls the thermal
Alterations in autonomic nervous system function after spinal cord injury
Spinal cord injury results in a reduction or lack of autonomic control that is directly related to the level of injury. Spinal cord injury interrupts the connections between the supraspinal regulatory centers and the effector organs and interferes with both afferent and efferent signal transmission. Many of the major cardiovascular functions are associated with segmental outflow from several levels, such as the outflow to the heart or the splanchnic outflow. Sympathetic control of blood vessels
Cardiovascular alterations immediately after spinal cord injury
In the first few minutes after SCI, there is a disruption in central sympathetic control caused by interruption of the descending pathways that travel in the spinal cord. Animal studies have found that within seconds to minutes after injury, there is a systemic pressor response that results from a burst of sympathetic activity and outflow of adrenaline from the adrenal glands [25]. In the feline model of SCI, compression of the cervical spinal cord causes a brief increase in both systolic and
Summary
The autonomic nervous system plays a key role in the regulation of many physiologic processes mediated by supraspinal control from centers in the CNS. Spinal cord injury is associated with alterations in autonomic regulation, with level of injury playing a key role in the subsequent derangements that occur. Above T1, SCI causes a complete disruption of the sympathetic pathways and results in a variety of problems including bradycardia, neurogenic pulmonary edema, arrhythmias, and hypotension.
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2021, HeartRhythm Case ReportsCitation Excerpt :This is followed by spinal shock syndrome, which is the period after injury characterized by a marked reduction or abolition of sensory, motor, or reflex function of the spinal cord below the level of injury. Additionally, deficits in the autonomic nervous system include an extended period of neurogenic shock characterized by hypotension, bradycardia, and hypothermia.6 Neurogenic shock is primarily caused by a disrupted sympathetic flow to the heart and the vessels, while the parasympathetic influence is preserved.
Cervical cord injury complicated by acute mesenteric ischemia
2021, Trauma Case ReportsCitation Excerpt :In AD, a noxious stimulus triggers an unregulated sympathetic cascade, leading to focal vasoconstriction [3]. Classically, if the neurological level of injury is at or above T6, this vasoconstriction can involve the splanchnic vessels and lead to progressive hypertension [4], predisposing patients to NOMI. Experimentally, it has been shown that mesenteric blood flow is markedly diminished in rats 3 days after a T3-spinal cord injury [5].