Many patients affected by "idiopathic" fecal incontinence have evidence of either a neurogenic or muscular injury, and some patients remain truly idio-pathic without clear identifiable cause for sphincteric dysfunction. The peripheral nervous system is divided into the somatic and autonomic portions with sensory and motor nerve fibers. Autonomic nerve fibers normally supply the gastrointestinal, bladder, sexual, and cardiovascular functions. Neuropathies can be functionally selective so that sensory, motor, or autonomic function can be involved separately or in various combinations. Disease process consists of generalized polyneuropathies, with symmetric distribution on the two sides of the body, or focal and multifocal neuropathies in which involvement is localized. Focal and multifocal neuropathies involving the nerves of the pelvis and the polyneuropathies with autonomic impairment commonly induce bowel, bladder, and sexual dysfunction.
Diabetes mellitus is the most common cause of polyneuropathy in developed countries. Diabetic neuropathy is a chronic symmetrical sensorimotor polyneuropathy that usually begins after years of hyperglycemia and is frequently associated with autonomic neuropathy and bowel, bladder, and sexual dysfunction. Severe diabetic autonomic neuropathy (DAN) is almost always associated with insulin-dependent diabetes. Symptoms of autonomic involvement include impairment of sweating and of vascular reflexes, constipation, nocturnal diarrhea and fecal incontinence, atonic bladder, sexual impotence, and occasionally postural hypotension. The pathogenetic mechanism of the constipation is uncertain, but autonomic neuropathy causing parasympathetic denervation is likely to be implicated. Diarrhea typically occurs at night or after meals, is a more troublesome complication of diabetes, and may be an isolated symptom of autonomic dysfunction. It is usually chronic, but it is intermittent and alternates with bouts of constipation or normal bowel movements. Reduced resting anal tone induced by sympathetic autonomic neuropathy and loss of rectal sensation may play a role in the nocturnal fecal incontinence . The upper gastrointestinal tract symptoms that consist of heartburn, dysphagia, and bloating may sometimes occur in diabetic patients in addition to bowel dysfunctions.
Neuropathy due to deposition of amyloid-a pro-teinaceous substance in different tissues and in particular in peripheral nerve-can occur in patients with benign plasma-cell dyscrasia or in multiple myeloma, Waldenstrom's macroglobulinemia, or non-Hodgkin's lymphoma . The neuropathy is of the small-fiber type, with a predominant loss of pain and temperature sensation early in the course of the illness and a later involvement of motor functions and sensory modalities subserved by large myelinated fibers. Autonomic involvement is another early characteristic of amyloidotic neuropathy. Anhidrosis, loss of papillary light reflexes, vasomotor paralysis with orthostatic hypotension, and alternating diarrhea and constipation are frequent in the course of the illness. Amyloidosis can also present with reduced urinary flow and infrequent voiding with reduced bladder contractility and an increased postvoiding urine volume. Uncoordinated contractions of the small bowel have been demonstrated in patients affected by familiar amyloidotic neuropathy, mainly resulting in diarrhea, but sometimes constipation may alternate with diarrhea. Diarrhea and steatorrhea are prominent in primary amyloidosis.
Constipation or, occasionally, paralytic ileus and bladder dysfunction with urine retention occurs in 20-30% of patients affected by Guillain-Barré syndrome . This inflammatory disease occurs in all ages and both genders. A mild respiratory or gastrointestinal infection, surgical procedure, or viral exanthemas precede the symptoms by 1-3 weeks in 70-80% of patients. The major clinical manifestation is weakness of proximal and distal muscles of the limbs, trunk, and intercostals, and neck muscles, which evolves symmetrically over a period of several days. The weakness can progress to total motor paralysis, with death from respiratory failure. The hyperactivity or hypoactivity of sympathetic and parasympathetic fibers can induce severe disturbances of autonomic function. Sinus tachycardia and less often bradycardia with cardiac arrhythmias, fluctuating hypertension and hypotension, loss of sweating ability, or facial flushing are frequent in the course of the disease.
Vitamin B12 deficiency may arise from inadequate oral intake, deficiency of intrinsic factors, various malabsorption disorders, resection of the stomach, or terminal ileum, inducing various neurological symptoms including peripheral neuropathy, myelopathy, altered mental status, and optic neuropathy . Subacute combined degeneration of the spinal cord and distal peripheral neuropathy are the main neurological consequences of vitamin B12 deficiency. Most patients with pernicious anemia and neurological dysfunction show, therefore, a mixed myelopathic or neuropathic clinical picture. Symmetrical numbness and paraesthesia of lower limbs and gait ataxia are the commonest presenting complaints. Weakness is sometimes found but is always accompanied by sensory lower-limb abnormalities. A small number of patients have symptoms of auto-nomic dysfunction with fecal and urinary incontinence.
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