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Detrusor activity
-impaired contractility
Detrusor compliance
Smooth sphincter activity
Striated sphincter activity
-impaired voluntary control,fixed tone
The fashion of neurologic lesion is dependent on
-the area(s) of the nervous system affected
-the physiologic function(s)
-whether the lesion or process is destrutive,inflammatory or irritative
Bladder outlet obstruction is associated with
-damage to intrinsic innervation of the bladder smooth muscle from the combination of pressure and ischemia
Ultrastructure changes related to bladder outlet obstruction
-increasing expression of several growth factors
-increasing COX-2
-swelling and structural destruction of the detrusor mitochondria
-increased type III/I collagen ratio
-downregulation of MMP
-upregulation of tissue inhibitors of MMP
Bladder outlet obstruction and unmyelinated C fibers
-activation of unmyelinated C fibers
Neurologic lesions above the brainstem (with rare exeptions)
-may affect micturition generally result in involuntary bladder contractions
-coordinated sphincter function (smooth and striated sphincter function synergy)
-sensation and voluntary striated sphincter function are generally preserved (sensation may be delayed or deficient)
Lesions above the brainstem and detrusor areflexia
-may occur as initial or as a permanent dysfunction
Lesions above the brainstem and UI
-may occur due to the detrusor overactivity
Complete Spinl Cord Lesions from Spinal Cord Level T6 to S2 after recover from from spinal shock
-involuntary bladder contractions
without sensation
-smooth sphincter synergy
-but striated sphincter dyssynergia
Lesions above T6 may expierence
-smooth sphincter dyssynergia
-autonomic hyperreflexia
UI and lesions between T6 to S2
-due to DO
-but may be due to BOO and overflow incontinence
Lesions below Spinal Cord Level S2
-do not manifest involuntary bladder contractions
-detrusor areflexia is initially the rule after spinal shock
-usually a residual resting sphincter tone (not the same as dyssynergia)
-is not under voluntary control
The most common causes of stroke
Thrombosis,occlusion and hemorrhage usually leading to
-ischemia and infarction usually around the internal capsule
Bladder  manifestation after the initial acute episode of stroke
-urinary retention from detrusor areflexia
The most common long term expression of lower urinary tract dysfunction after CVA is
-phasic detrusor overactivity
Bladder sensation after stroke
-generally intact
After stroke patient usually has
-urgency and frequency with detrusor overactivity
The appropriate response of patient after stroke is
-to try to inhibit the involuntary bladder contraction by forceful voluntary contraction of the striated sphincter
If forceful voluntary contraction can be accomplished
-only urgency and frequency result
-if not urgency with incontinence results
Two possible mechanisms for the incontinence associated with involuntary bladder contractions in pts who have ssustained a CVA
-impaired striated sphincter control
-lack of appreciation of bladder filling and impending bladder contraction
Smooth sphincter activity and CVA
True DSD in CVA
-does not occur
Pseudo DSD in CVA
-may occur during UDS
-EMG sphincter flare during filling cystometry that is secondary to attempted inhibition of involuntary bladder contraction by voluntary contraction of the striated sphincter
Detrusor hypocontractility or areflexia
-may persist after CVA
CVA  and functional system of classification
-failure to store secondary to bladder overactivity (specifically involuntary bladder contractions)
ICS Classification system and CVA
-overactive neurogenic detrusor function
-normal sensation
-low capacity
-normal compliance
-normal urethral closure function during storage
-during voiding phase:  normal detrusor activity,normal urethral function
Treatment of bladder dysfunction after CVA in the absence of coexisting significant bladder obstruction or significantly impaired bladder contractility
-decreasing bladder contractility
-increasing bladder capacity
Voiding dysfunction in dementia
-usually incontinence
Traumatic brain injury and voiding dysfunction
-initial period can be detrusor areflexia
Traumatic lesions above pontine micturition center ,the most frequent manifestation
-involuntary bladder contractions
-coordinated sphincter function is the role
Traumatic lesions below the pontine micturition center
- DSD may occur in addition
Brain tumor and voiding dysfunction
-urinary incontinence
-synergic smooth and striated sphincter activity

Urinary retention in brain tumor pts
-in pts with space-occurying lesions of the frontal cortex
Cerebral ataxia and voiding dysfunction
-incontinence associated with DO
-sphincter synergia
-may be detrusor areflexia and striated DSD (if involved spinal cord)
Cerebral palsy
-a nonprogressive injury of the brain
-in prenatal,perinatal or posnatal period (during the first year of life)
-that produces neuromuscular disability and/or specific symptom complex of cerebral dysfunction
Voiding dysfunction in pts with CP
-depends of localization
The most of the classic clinical motor features of Parkinson disease accounts from
-dopamine deficiency in the nigrostriatal pathway
The classic major signs of Parkinson Disease
-skeletal rigidity
D2 receptor stimulation responsible for
-reduceing of bladder capacity
-worsening of DO
Causes of parkinsonism
-multiple system atrophy
-progressive supranuclear palsy
-cortical-basal ganglionic degeneration
-vascular parkinsonism
-dementia with Lewy bodies
Signs of Parkinson disease DD from parkinsonism
-assymetry of symptoms and signs
-presence of resting tremor
-good response to levadopa
MSA multiple system atrophia includes
-striatonigral degeneration
-sporadic olivopontocerebellar atrophy
-Shy-Drger syndrome
The following suggest MSA
-urinary symptoms precede or present with parkinsonism
-urinary incontinence
-significant postvoid residual
-initial erectile failure
-abnormal striated sphincter electromyogram
Parkinson's Plus Syndromes
-5% of pts diagnosed with Parkinson disease
-early dementia
-and/or falls
-symmetric symptoms such as wide-based gait,normal eye movements
-autonomic dusfunction
-marked dysability
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