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The normal process of bladder filling proceeds in silence as the bladder's walls become distended. The individual has no conscious perception of the process until the contents reach around 1,000 cc (one liter). At this point, the bladder starts signaling to the brain that the time for emptying has arrived. The brain - consciously now - keeps the bladder from emptying until the person has found the appropriate location to void. Once all is ready, the brain gives the go-ahead. The bladder contracts while at the same instant, a system of sphincters that have kept the bladder closed relaxes. A network of nerve centers including the basal ganglia insures this perfect timing, this synchrony. And it is in these basal ganglia - located deep in the brain substance - that the central malfunction of PD is located.

Specifically, the basal ganglia are part of the connections that allow the brain to keep the bladder quiet while filling. In PD the malfunction in this part of the circuit results in a bladder that contracts prematurely at low amounts of urine, much lower than 1,000 cc. This condition of unstable or irritable bladder is known as detrusor hyperreflexia, named for the muscle that contracts the bladder wall. Such premature contractions are not strong enough to directly cause the bladder to empty but create enough signaling to the brain to create a sense of a strong urge to void. Enter the symptom of urinary urgency, a sensation that a normal person may only feel if she or he had not emptied the bladder after many hours. The patient rushes to the bathroom only to empty a very small amount of urine. Since the process repeats itself over and over the visits to the bathroom become numerous both during the daytime - urinary frequency - and at night - nocturia. Urinary urgency can become so strong that if the PD patient - already burdened by slowness of movement - fails to reach a bathroom on time, she or he suffers an 'accident', something we call urge incontinence. All of these symptoms represent a abnormality in bladder filling and urologists also know them as irritative symptoms.

A patient with PD with these symptoms should seek a urological evaluation. The patient should expect a urine analysis to rule out an infection or some other inflammation of the bladder and an assessment as to whether the prostate (in the man) or the bladder neck (in the woman) may harbor the cause of the problem. These and other 'local' problems are also capable of causing premature contractions of the bladder. Even if an enlarged prostate or a sclerosed (hardened) bladder neck are found and surgery is advised, the patient should know that symptoms may persist even after a well executed operation. Currently even the most proficient of urologists cannot predict in advance the outcome of surgery. Surgery may well be indicated but the desired result may not be attained and further measures may be necessary.

In the process of managing these problems the urologist may advise additional tests known as urodynamics. Here, the bladder is instilled with a saline solution and the presence of premature contractions may be detected by a system of pressure detectors. If a cause for surgery is not found or if symptoms persist after surgery, the urologist may prescribe medications to relax the detrusor muscle of the bladder.

Tolterodine (brand name Detrol) and Oxybutinin (brand name Ditropan) are frequently prescribed. Their mechanism of action differ. Ditropan, an anti-cholinergic drug, blocks, in a relatively specific manner, a set of nerves, the cholinergic nerves, that carry impulses to the derussor muscle and the internal sphincter of the bladder. Detrol, an anti-muscarinic receptor blocker, blocks receptors for acetyl-choline along the bladder wall. While technically Detrol is an anti-cholinergic drugs, it acts more specifically on the bladder wall. Judicious use of both drugs will minimize side effects. These include, for ditropan, driness of the mouth and constipation. And for detrol, problems emptying the bladder. Those suffering from glaucoma should, before starting ditropan, point this out to their physician.

Other medications may be prescribed to overcome obstruction to the flow of urine in an attempt to indirectly 'calm' the bladder. These include terazocin (brand name Hytrin) and doxazocin (brand name Cardura). Since they can also lower blood pressure patients should avoid getting out of bed too fast since it may result in a faint.

Some PD patients may complain of straining during urination (heasitancy) and of weak urinary stream. These so-called obstructive symptoms again raise the possibility that local bladder outflow problems are present such as an enlarged prostate. But additional causes should be looked for.

Certain drugs may weaken bladder contraction. These include anti-cholinergics used in the treatment of PD such as trihexiphenydil (brand name Artane), and certain antidepressants such as amitryptilline (brand name Elavil). These drugs, like Ditropan and Detrol are anti-cholinergic drugs. However, while Detrol and Ditropan "fine-tune" the cholinergic receptors along the bladder wall or sphincter, Artane and Elavil do not. Thus Detrol and Ditropan, anti-cholinergic drugs relieve bladder symptoms in Parkinson, whereas Artane and Elavil can aggravate them. Diabetes and other conditions that affect nerve conduction may also weaken bladder contractions.

Some PD patients may experience a delay in relaxation of the sphincter at the time of bladder emptying, especially when the effect of L-dopa is waning. Finally a different form parkinsonism known as Multiple System Atrophy (the Shy Drager Syndrome) may be present and account for the delay in relaxation Whereas Parkisnon patients may exhibit frequency and urgency when emptying their bladder, Shy Drager patients may be unable to empty their bladder.

Management of obstructive symptoms involves a urological evaluation for obstruction of the bladder outflow. Potentially responsible drugs should be discontinued. Once these causes have been discounted, the urologist may use certain medications to strengthen bladder contraction. However if these measures fail patients with weak bladder emptying may require the placement of a catheter into the bladder a few times a day. This is particularly the case of patients with Shy Drager.

In summary, urinary symptoms are a frequent cause of discomfort in PD patients. The cause or causes, in each patient, must be systematically approached. Bladder and bladder outlet problems and side effects of medications should be excluded. Parkinson's disease and other forms of parkinsonism such as multiple system atrophy can also cause these symptoms. Management should be directed by an urologist with additional counseling provided by the neurologist.