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There is growing evidence to suggest that physical training is beneficial for CNS health, including improved synaptic function (van Praag et al., 1999). BDNF appears to play a key role in communicating the benefits of exercise (Neeper et al., 1995; Vaynman et al., 2006; Gomez-Pinilla et al., 2008; Zoladz and Pilc, 2010; Gomez-Pinilla and Hillman 2013). In particular, BDNF is secreted as a function of activity (Lu, 2003) and its expression in the spinal cord and skeletal muscles of rodents increases after exercise (Gómez-Pinilla et al., 2001, 2002; Cuppini et al., 2007; Gomez-Pinilla et al., 2012). Similarly, basal levels of neuromuscular activity are required to maintain normal levels of BDNF in the neuromuscular system (Gómez-Pinilla et al., 2002). Recently, cultured myotubes have been shown to release BDNF when stimulated to contract, suggesting a postsynaptic origin of this neurotrophin (Matthews et al., 2009). Unfortunately, it is not clear whether skeletal muscle in vivo increases its production and/or release of BDNF through synaptic activity, muscle contraction, or a combination of both. In addition, exogenous BDNF increases the evoked release of acetylcholine (ACh) at the neuromuscular junction (NMJ) and the TrkB receptor is usually coupled to this process (Knipper et al., 1994; Mantilla et al., 2004; Garcia et al., 2010; Santafé et al., 2014). Together, these and other findings support the idea that neuromuscular activity promotes retrograde bdNF/TrkB signaling to regulate neuromuscular function (Kulakowski et al., 2011; Dorsey et al., 2012), an idea we are now testing. With normal breathing at rest, inspiration is active, but the process is passive.

The main inspiring muscle is the diaphragm, a thin dome-shaped muscle plate powered by two phrenic nerves that originate from the spinal cord high in the neck. When the diaphragm contracts, the abdominal contents are pushed down, and the vertical dimension of the chest cavity is increased. At the same time, the chest protrudes. The effect of the diaphragm is supported by external intercostal muscles that connect the neighboring ribs and fall down and forward. When these muscles contract, the ribs are pulled upwards, which increases the lateral and anteroposterior diameters of the chest. However, paralysis of the intercostal muscles alone does not seriously affect breathing, because the diaphragm is so effective. Other inspirational muscles include the neck muscles, which support inspiration during vigorous exercise. Treatment of paralysis of the phrenicle begins and ends with physiotherapy.

Patients work with physiotherapists to strengthen their diaphragm and use their rib (intercostal) and neck (scalene) muscles to help breathe. It is recommended for patients who continue to have difficulty breathing or who continue to rely on a mechanical ventilator for surgical treatment. The phrenic nerve originates from the anterior rummy from C3 to C5 and passes through the neck, heart and lungs to reach the diaphragm. Since its origin, the phrenic nerve descends vertically caudad and borders the internal jugular vein. In the neck and upper chest, the left phrenic nerve is proximal to the subclavian artery. The right phrenic nerve extends superficially to the anterior scalene muscle and to the second part of the right subclavian artery. In the chest, the right and left phrenic nerves will continue to descend anterior to the root of the lungs and between the mediastinal surface of the parietal pleura and the fibrous pericardium. The right phrenic of Venus extends laterally to the right atrium and right ventricle and continues to descend through the hiatus of the vena cava into the diaphragmatic opening at level T8. The left phrenic nerve descends before the pericardial sac of the left ventricle and ends at the central tendon of the diaphragm. [1] [2] [3] The quadriceps is a muscle of primary movement and therefore of great functional importance for patients. Although electrical stimulation of the femoral nerve is possible, it is technically difficult and reproducibility is low.11 The peripheral branches of the thigh nerve can be stimulated with flat surface electrodes on the muscle, but the part of the muscle that is activated is variable 11.

Polkey et al. 74 first described the technique of magnetic stimulation of the femoral nerve in 1996. The head of the coil is located high in the triangle of the thigh, on the side of the femoral artery (Fig. 6⇓). The strength of the quadriceps is measured in relation to the tension of the quadriceps (Qtw), with the knee bent over an extendable ankle strap connected to a transducer. Minor position adjustments are made on the coil while simultaneously monitoring the strength of the quadriceps during stimulation to determine the optimal position. Preliminary studies with a 90 mm circular coil showed no supramaximal response. Using a 45 mm rear coil, Polkey et al. However, 74 prove supramaximity in 10 healthy volunteers and 10 patients suspected of muscle weakness. In addition, Qtw fell to an average of 55% of baseline values in seven subjects who underwent a standard fatigue protocol, showing that the technique can be used to detect low-frequency quadricep fatigue. In obese subjects and those who are unable to lie completely flat, it is sometimes not possible to achieve supramaximal stimulation with this technique, and current authors are currently using two tandem magnetic stimulators to drive a 70 mm rear figure.

The phrenic nerve is actually a pair of nerves, the right and left phrenic nerves, which activate the contraction of the diaphragm that expands the chest cavity. Since the lungs adhere to the chest cavity, this expands the lungs and thus attracts air into them. The cell bodies of the motor neurons that make up the phrenic nerve are located in a longitudinal column oriented in the C3 to C5 segments of the spinal cord. The initiation of action potentials in the external intercostals lifts and widens the chest and supports inspiration. The cell bodies of motor neurons, which control the external intercostals, form a column that extends along the entire length of the thoracic spinal cord. Similarly, the motor neurons that control the internal intercostals that support the process form a separate slit. The abdominal muscles also support drainage, and the cell bodies of their motor neurons are located in the medullary segments of the lower thoracic and upper lumbar spine. The locations of these elements are shown schematically in Figure 6.6.1. Measuring the strength of peripheral muscles is also interesting in the intensive care unit. Early detection of weakness can lead to interventions to maintain or restore muscle function, thereby reducing the significant need for rehabilitation for survivors.

Recent results suggest that in survivors of acute respiratory distress syndrome, physical performance and quality of life, mainly due to muscle weakness and fatigue, are reduced up to 1 year after discharge from hospital 100. In addition, the relationship between peripheral and respiratory muscles in critically ill patients remains unknown; It is conceivable that peripheral muscle monitoring could provide an accessible marker for respiratory muscle function. However, apart from clinical examination, there are few ways to assess peripheral muscle strength, and until recently, none are independent of the patient`s effort. As mentioned earlier, the strength of the pollicis of the adductors can now be assessed in a non-thorough way in the intensive care unit using supramaximal magnetic stimulation of the ulnar nerve 75. Similarly, after magnetic stimulation of the femoral nerve 74, Qtw is a technique that can be easily adapted to the intensive care setting 101. Symptoms of diaphragmatic weakness or significant paralysis, usually bilateral, are shortness of breath when lying down, walking or diving into water to the lower chest. Bilateral diaphragmatic paralysis can lead to sleep-disordered breathing with reduced blood oxygen levels. This technique is designed to induce bilateral diaphragmatic contraction in patients in the supine position, especially mechanically ventilated patients 52. . . .