**2. Physiology and pathophysiology of the lower urinary tract**

The lower urinary tract consists of two major components, the bladder and urethra. The bladder is abundant with muscarinic M2,3 receptors (contraction) and adrenergic beta 3 receptors (relaxation)12. The urethra is abundant with adrenergic alpha 1A/D receptors (contraction) and nicotinic receptors (contraction) **(Fig. 1)**. The storage and emptying functions need an intact neuraxis that involves almost all parts of the nervous system48. This is in contrast to postural hypotension, which arises due to lesions below the medullary circulation center56.

© 2012 Sakakibara et al., licensee InTech. This is an open access chapter distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. © 2012 Sakakibara et al., licensee InTech. This is a paper distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Sphincter EMG for Diagnosing MSA and Related Disorders 289

Urinary storage is dependent on the autonomic reflex arc of the sacral cord12. This reflex is tonically facilitated by the brain, particularly the pontine storage center,7,57 hypothalamus, cerebellum, basal ganglia, and frontal cortex25. In contrast, micturition is dependent on the autonomic reflex arc of the brainstem and spinal cord12. This reflex involves the periaqueductal gray12,32,78 and the pontine micturition center (PMC)6,7,12,54,63. The PMC facilitates the sacral bladder preganglionic nucleus by glutamate35, while inhibiting the sacral Onuf's nucleus by γ-amino-butyric acid (GABA) and glycine8. This reflex is regulated

Bladder (detrusor) overactivity is the major cause of urinary urgency/frequency and urgency incontinence66. In lesions above the brainstem, detrusor overactivity is considered an exaggerated micturition reflex66. This is in line with the fact that detrusor overactivity appearing after experimental stroke requires mRNA synthesis in the PMC83. The exaggeration of the micturition reflex might be brought about not only by decreased inhibition of the brain (by central cholinergic and D1 dopaminergic mechanisms); that is, it might be further facilitated by glutamatergic and D2 dopaminergic mechanisms82. Underactive detrusor (or bladder weakness) is the major cause of voiding difficulty in autonomic disorders. Underactive detrusor results from lesions in either upper or lower neurons innervating the bladder muscles, but typically occurs from lower neuron lesions.1,48 Urinary urgency incontinence and voiding difficulty in MSA result mostly from detrusor overactivity and underactive detrusor, respectively.1,48 Patients with MSA often have a combination of detrusor overactivity in the filling phase and underactive detrusor in the voiding phase; this is called detrusor hyperactivity with impaired contractile function (DHIC). DHIC presumably reflects multiple lesions in both the storage-facilitating areas (the basal ganglia, pontine storage center) and the voiding-facilitating areas (the PMC, sacral preganglionic neurons in the intermediolateral [IML] cell columns) of this disorder.23,79 In

MSA, incomplete emptying is thought to be secondary to IML involvement.

Sphincter dysfunction contributes to voiding difficulty and urinary incontinence in autonomic disorders, although less commonly than over- or underactive detrusor does. When the urethral sphincter does not relax properly during voiding bladder contraction, it is called detrusor-sphincter dyssynergia.1 Since a coordinated micturition reflex (bladder contraction with sphincter relaxation) needs an intact brainstem–sacral cord axis,12 disruption of the axis (such as lesions affecting the cervical/thoracic spinal cord) may lead to detrusor–sphincter dyssynergia. Sphincter weakness is a cause of urinary incontinence. Sphincter weakness occurs from lesions in the sacral motoneurons (Onuf's nucleus), and typically appears in women with MSA as severe stress incontinence49 or continuous urinary

**3. Physiology and pathophysiology of the lower gastrointestinal tract** 

The enteric nervous system plays the most important role in regulating the peristaltic reflex of the lower gastrointestinal tract20. Two types of myoelectrical activity or pressure changes in the colon are documented. Slow phasic pressure waves are the most common manometric

by the hypothalamus and prefrontal cortex16,25.

incontinence34.

The lower urinary tract consists of two major components, the bladder and the urethra. The bladder is mainly innervated by the parasympathetic pelvic nerve. The urethra is innervated by the sympathetic hypogastric nerve and somatic pudendal nerve, respectively. Urinary storage is dependent on the reflex arc of the sacral spinal cord. The storage reflex is thought to be tonically facilitated by the brain, particularly the pontine storage center. The storage function is thought to be further facilitated by the hypothalamus, cerebellum, basal ganglia, and frontal cortex. Central cholinergic fibers from the nucleus basalis Meynert (NBM, also called the Ch4 cell group) seem to facilitate urinary storage. Micturition is dependent on the reflex arc of the brainstem and spinal cord, which involves the midbrain periaqueductal gray (PAG) and the pontine micturition center (located in or adjacent to the locus coeruleus [LC]). The voiding function is thought to be initiated by the hypothalamus and prefrontal cortex, which overlap the storage-facilitating area. PVN: paraventricular nucleus, MPOA: medial preoptic area, A: adrenergic/noradrenergic, ZI: zona incerta, VTA: ventral tegmental area, SNC: substantia nigra pars compacta, DLTN: dorsolateral tegmental nucleus, PBN: parabrachial nucleus, IML: IML cell column, GABA: γ-aminobutyric acid, T: thoracic, L: lumbar, S: sacral (cited from ref. 41)

**Figure 1.** Neural circuitry relevant to micturition.

Urinary storage is dependent on the autonomic reflex arc of the sacral cord12. This reflex is tonically facilitated by the brain, particularly the pontine storage center,7,57 hypothalamus, cerebellum, basal ganglia, and frontal cortex25. In contrast, micturition is dependent on the autonomic reflex arc of the brainstem and spinal cord12. This reflex involves the periaqueductal gray12,32,78 and the pontine micturition center (PMC)6,7,12,54,63. The PMC facilitates the sacral bladder preganglionic nucleus by glutamate35, while inhibiting the sacral Onuf's nucleus by γ-amino-butyric acid (GABA) and glycine8. This reflex is regulated by the hypothalamus and prefrontal cortex16,25.

Computational Intelligence in Electromyography Analysis – 288 A Perspective on Current Applications and Future Challenges

The lower urinary tract consists of two major components, the bladder and the urethra. The bladder is mainly innervated by the parasympathetic pelvic nerve. The urethra is innervated by the sympathetic hypogastric nerve and somatic pudendal nerve, respectively. Urinary storage is dependent on the reflex arc of the sacral spinal cord. The storage reflex is thought to be tonically facilitated by the brain, particularly the pontine storage center. The storage function is thought to be further facilitated by the hypothalamus, cerebellum, basal ganglia, and frontal cortex. Central cholinergic fibers from the nucleus basalis Meynert (NBM, also called the Ch4 cell group) seem to facilitate urinary storage. Micturition is dependent on the reflex arc of the brainstem and spinal cord, which involves the midbrain periaqueductal gray (PAG) and the pontine micturition center (located in or adjacent to the locus coeruleus [LC]). The voiding function is thought to be

PVN: paraventricular nucleus, MPOA: medial preoptic area, A: adrenergic/noradrenergic, ZI: zona incerta, VTA: ventral tegmental area, SNC: substantia nigra pars compacta, DLTN: dorsolateral tegmental nucleus, PBN: parabrachial nucleus, IML: IML cell column, GABA: γ-aminobutyric acid, T: thoracic, L: lumbar, S: sacral

initiated by the hypothalamus and prefrontal cortex, which overlap the storage-facilitating area.

(cited from ref. 41)

**Figure 1.** Neural circuitry relevant to micturition.

Bladder (detrusor) overactivity is the major cause of urinary urgency/frequency and urgency incontinence66. In lesions above the brainstem, detrusor overactivity is considered an exaggerated micturition reflex66. This is in line with the fact that detrusor overactivity appearing after experimental stroke requires mRNA synthesis in the PMC83. The exaggeration of the micturition reflex might be brought about not only by decreased inhibition of the brain (by central cholinergic and D1 dopaminergic mechanisms); that is, it might be further facilitated by glutamatergic and D2 dopaminergic mechanisms82. Underactive detrusor (or bladder weakness) is the major cause of voiding difficulty in autonomic disorders. Underactive detrusor results from lesions in either upper or lower neurons innervating the bladder muscles, but typically occurs from lower neuron lesions.1,48

Urinary urgency incontinence and voiding difficulty in MSA result mostly from detrusor overactivity and underactive detrusor, respectively.1,48 Patients with MSA often have a combination of detrusor overactivity in the filling phase and underactive detrusor in the voiding phase; this is called detrusor hyperactivity with impaired contractile function (DHIC). DHIC presumably reflects multiple lesions in both the storage-facilitating areas (the basal ganglia, pontine storage center) and the voiding-facilitating areas (the PMC, sacral preganglionic neurons in the intermediolateral [IML] cell columns) of this disorder.23,79 In MSA, incomplete emptying is thought to be secondary to IML involvement.

Sphincter dysfunction contributes to voiding difficulty and urinary incontinence in autonomic disorders, although less commonly than over- or underactive detrusor does. When the urethral sphincter does not relax properly during voiding bladder contraction, it is called detrusor-sphincter dyssynergia.1 Since a coordinated micturition reflex (bladder contraction with sphincter relaxation) needs an intact brainstem–sacral cord axis,12 disruption of the axis (such as lesions affecting the cervical/thoracic spinal cord) may lead to detrusor–sphincter dyssynergia. Sphincter weakness is a cause of urinary incontinence. Sphincter weakness occurs from lesions in the sacral motoneurons (Onuf's nucleus), and typically appears in women with MSA as severe stress incontinence49 or continuous urinary incontinence34.
