Chughtai et al clearer with the National Overactive Bladder Evaluation (NOBLE) study (Coyne et al 2004). In this study, OAB was associated with much lower quality-of-life scores, higher scores on depression, and poorer sleep quality when compared to patient controls (Coyne et al 2004). Although OAB increases with age, it should not be considered a normal consequence of aging by patients or physicians. By using a systematic approach to diagnosing and evaluating OAB followed by instituting appropriate therapy, care providers can improve the health and quality of life of older patients with OAB. Normal bladder physiology Bladder function represents an interplay between the urinary tract and the nervous system. There are two main phases, ﬁlling and emptying. The normal bladder stores urine at a low pressure that remains lower than urethral resistance. Micturition is hallmarked by a decrease in urethral resis- tance and contractions of the detrusor muscle with resultant emptying. There is a complex interplay of neurotransmitters and receptors leading to normal bladder function. Acetylcholine, by acting on muscarinic receptors within the bladder, is the primary neurotransmitter in bladder contraction (Yamanishi et al 2001). Contraction occurs as a result of increased para- sympathetic outﬂow and relaxation of sympathetic inhibition. There are 5 known muscarinic subtypes (M1 to M5) that are distributed throughout the human body (Table 1). The muscarinic receptor subtypes are located in smooth muscle (bladder), exocrine glands, the nervous system, and the heart. M2 receptors are the predominant subtype within the healthy detrusor muscle; activation of M2 receptors inhibits sympathetically mediated detrusor relaxation. M2 receptors are also located in the heart and central nervous system (CNS). M3 receptors are responsible for detrusor smooth muscle contraction and also have an exocrine function in the salivary glands (Pontari et al 2004). The muscarinic receptor antagonists used to treat OAB may affect these receptors to varying levels. The use of muscarinic receptor antagonists Table 1 Muscarinic receptors distribution (afterYamanishi et al 2001) Muscarinic receptor Distribution M1 Brain (cortex, hippocampus), glands, sympathetic ganglia M2 Heart, hindbrain, smooth muscle M3 Smooth muscle, glands, brain M4 Brain (forebrain, striatum) M5 Brain (substantia nigra), eye 504 is associated with a spectrum of outcomes in both efﬁcacy and side-effect proﬁle. Evaluating patients with overactive bladder Patients with uncomplicated OAB can be managed by the primary care physician. The ﬁrst step is to screen for a his- tory of frequency, urgency, and incontinence. Unfortunately, many patients with OAB do not seek treatment because of embarrassment, the misconception that the problem is an inevitable consequence of aging, or that treatment options are limited. The history should focus on relevant medical, neurologic, and genitourinary symptoms that may lead to or worsen the symptoms of OAB. Neurologic conditions such as Alzheimer’s or Parkinson’s disease may affect cortical inhibitory function, which can cause or contribute to OAB (Stevens et al 2007). Conditions that affect the spinal cord (multiple sclerosis, disc herniation) may also disrupt normal micturition reﬂexes, resulting in OAB. Factors that affect the genitalia or the lower urinary tract, eg, bladder cancer, atrophic vaginitis, yeast infections, and cystitis, may lead to symptoms similar to OAB. When dealing with symptoms of OAB, it is imperative to identify causes that are easily reversed and appropriately manage these patients. In addition to a thorough history, assessment of ﬂuid intake, voiding pat- terns, and real-time symptoms should be reviewed with the aid of a patient-completed voiding diary. In this exercise the patient logs intake of ﬂuid, number of times voided, amount voided, and episodes of incontinence for at least one full day. It is important to asses for medical conditions that lead to increased production of urine during sleep, eg, diabetes mellitus, diabetes insipidus, sleep apnea, or congestive heart failure. Nocturnal polyuria is calculated as 35% of daily urine production occurring during the sleep hours. All medications should be reviewed for those that may affect urinary function, output, and so on. Diuretics, by increasing urinary output, clearly increase urinary frequency. Occasionally patients report night-time administration, a reversible cause of nocturnal polyuria. Various medications, including anticholinergics, narcotics, and calcium channel blockers, may decrease bladder contractility, leading to inability to completely empty the bladder and more frequent voiding. In addition, the use of sedatives may lead to deceased mobility and inability to get to the bathroom in time, leading to incontinence. Physical examination should include the abdominal, genitourinary, rectal, and neurologic systems. It is important during the abdominal examination to make sure the bladder Clinical Interventions in Aging 2008:3(3)