Supra pontine lesions e.g.
Alzheimer or stroke patients. These conditions will lead to less inhibition of bladder control. It is important to understand that aging will cause atrophy of the cortex and can therefore also cause less control of the bladder function. This might not directly be associated with pathology but occur as part of the normal aging process. High lesions will mostly cause over activity of the bladder but coordinated voiding with normal urethra.
Diverse neurologic conditions:
Parkinson’s disease gives a diffuse dysfunction of the neurologic system because of degeneration of primarily the dopaminergic neurons. Dopamine deficiency in the substantia nigra accounts for the classical motor features of the disease. This leads to resting tremors and slow onset of movements. This condition will only cause lower urinary tract dysfunction after many years and there is a slow progression in the disease. Treatment must always take into consideration that the condition might deteriorate and that the patient might lose proper motor activity of the hands and later not be able to self-catheterize. Treatment decisions must take into account the progression of the disease. If lower urinary tract symptoms develop early then Multiple System Atrophy (MSA) must be considered. Voiding dysfunction occurs in 35-75% of patients. It normally consists of frequency, urgency, nocturia and urge incontinence. Urodynamically they normally have detrusor overactivity. Generally they have coordinated sphincters although sporadic involuntary activity of the striated muscle might occur as shown by EMG measurements without any true obstruction.
Multiple Sclerosis (MS)
Multiple Sclerosis is a progressive disease affecting young and middle aged people with twofold predilection for females. The primary lesion is neural demyelination with axon sparing and it is possibly immune mediated. Demyelination often affects the corticospinal and reticulospinal columns of the spinal cords. Therefore voiding and sphincteric dysfunction is common. Voiding symptoms will be present in 50-90% of patients. Detrusor overactivity with striated sphincter dyssynergia is the most common finding. Detrusor areflexia might also be present. Up to 15% of patients might present with the urinary symptoms before the primary neurologic diagnosis of Multiple Sclerosis is made.
Multiple System Atrophy (MSA)
This is a progressive degenerative neurologic disease that is characterized by combination of Parkinsonism, cerebellar ataxia and autonomic failure. In this condition the lower urinary tract function will be affected fairly soon after the start of the disease. Therefore, aggressive rehabilitation for the urinary tract dysfunction is often not indicated and not very satisfactory. The cause of the disease is unknown and it is a progressive neurodegenerative condition with a life expectancy of a mere 9 years. The so called Shy-Drager syndrome is possibly the end stage of the disease.
Spinal cord damage
Spinal cord damage, as in spinal cord injuries, spina bifida patients and compression of the spinal cord due to disc compression, tumors or cysts as well as cauda equina lesions can all lead to different types of fallout of the bladder and sphincter control. These patients will normally end up having treatment in a center for neurologic rehabilitation. It is important to have a high index of suspicion for cauda equina lesions or spinal cord compression in patients that develop new symptoms of lower urinary tract dysfunction, especially if it is associated with fallout in the lower extremities. It is normally caused by central disc compression at the level of L5 or S1 where the cauda equina is central in the spinal space before it exits through the foramina. Cauda Equina syndrome is characterized by perineal sensory loss, loss of both anal and bladder voluntary sphincters and sexual responsiveness. They have acontractile detrusor muscle and no bladder sensation. These patients will have to be evaluated urgently to prevent permanent damage. Even with emergency decompression, permanent detrusor areflexia is common. Complete spinal cord lesions below T6 will normally give detrusor over activity with smooth sphincter synergia and striated sphincter dyssynergia. Sensory loss will also be present below the lesion. Lesions above T6 might have smooth muscle sphincter dyssynergia as well, because of sympathetic damage. Treatment of spinal cord injuries should aim to create a lowpressure system and emptying with clean intermittent catheterization. A complication of the above T6 lesions is Autonomic Hyperreflexia. This is characterized by an acute autonomic response (primarily sympathetic) causing headache, hypertension and flushing of the body above the lesion. Avoidance of stimuli in susceptible patients is important and sublingual nifedipine either as prophylactic or therapeutic treatment seems very effective. Dosage of 10- 20 mg might be used as it prevents smooth muscle contraction through calcium channel blockade. Transverse myelitis is a rapidly developing condition affecting motor, sensory and sphincter function. It will mostly stabilize in 2-4 weeks and recovery is usually complete.
Peripheral Nerve Damage
Peripheral nerve damage is normally associated with diseases like diabetes, herpes virus infection, Guillain-Barre Syndrome and surgical trauma to pelvic plexus during radical surgery to the pelvic organs. In obstructed labor, minor damage can happen to the innervation of the lower urinary tract. This will normally lead to atonic or hypoactive function of the detrusor or sphincter muscle. Fortunately, damage to the pelvic plexus is often transient and temporary measures are strongly advised in the initial period. The condition will stabilize and function will return spontaneously to the pelvic plexus. Correction of the under lying neurologic damage is almost never possible.
The true incidence of lower urinary tract symptoms in the acquired immunodeficiency syndrome is not known. The whole spectrum of dysfunctions can be present in these patients but seems to be in the more advanced stages of the disease. Treatment principles are the same as other neurological conditions.
This syndrome presenting in young women below 30 presenting with acute retention and often have polycystic ovarian disease. A classical EMG finding of the sphincter was described by Fowler characterized by the inability to relax the sphincter. It is in the absence of demonstrable neurologic disease and very susceptible to neuromodulation therapy.