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Mictruition: A case of Failure to expel urine
1.
I am a 64-year-old male and I have been force to catheterize at least three times a
day since laser reduction surgery for a benign prostatic hyperplasia in late 2012. I
believe my swollen prostate had existed for several years pinching my urethra and
causing prolonged urine retention over a long time span. This more than likely had
put a stress on my urinary bladder (through urethral blockage) until by late 2012
while I had a strong urge to void virtually no urine flowed despite a conscious effort
to void. Thus, I review micturition as the neurobiological function that has impacted
adversely my life and attempt to address what has disrupted this function; a
problem that thus far 4 urologist have attempted to comprehend, with only one
suggesting a probable cause: a degraded detrusor muscle of the urinary bladder.
Micturition has several parts that control the bladder; the pontine mictruition
center, the sympathetic circuit in the lumbar area and the parasympathetic circuit in
the sacral area. The later triggers voiding and the former results in urine storage.
The pontine mictruition center in the pons and an area in the prefrontal cortex
regulate voluntary urinating. A description of how the neuronal pathways work
follows to answer part 2 of assignment: the sympathetic to store, the
parasympathetic to expel (P for you know what) and the voluntary pathways to
empty the bladder.
2.
The sympathetic pathway descends from the pons and hypothalamus through the
lower thoracic/upper lumbar discs, out through pre-vertebral ganglions, which send
axons into the bladder wall and internal bladder sphincter. These axons disinhibit
expansion of stretch muscles to permit urine storage and innervate the internal
sphincter muscle to contract to hold in urine. This permits bladder, a capacity up to
500ml) to withstand pressure as the bladder fills up to 300 to 350 cc of urine. On
average at the 260ml level, afferent nerve pathways send pressure (increase action
potentials) signal or urge up through the spinal cord and pons to trigger voiding.
These pathways also have c nerve fibers that sense chemical changes in the bladder
up through the spine and to the pons; they also transmit pain signals from the
bladder. From the video of this course, it is explained in the course that there are
urine storage level deviations of pressure that generate urine urge and detrusor
contraction. Thus, low urine amount from hyper anxiety can trigger low urine
voiding due greater sensitivity to lower pressure leading to greater signal
innervations. Or higher urine amount during sleep is possible due to greater stretch
in the bladder wall cause by greater inhibition signal strength through the
sympathetic pathway on the stretch muscles of bladder wall resulting in longer
stretch to delay urge sensation to higher pressure and contraction of detrusor
muscle. In converse, the internal sphincter is uninhibited, open, with hyper anxiety
and innervated, closed, during sleep state. Finally, as the bladder fills, the
sympathetic pathway connects with the motor axon, in the lumbar disc, and sends
excitation signals out to to the external striated sphincter muscle to maintain
contraction.
Once the increase firing to void is transmitted back through the lumbar disc and
spinal column and up to the Pons, midbrain (PariacqueductalGray) and orbital
prefrontal cortex (The orbital medial prefrontal area (social mores) in turn
regulates the PAG), the parasympathetic pathway is then engaged to empty the
bladder. These upper structures activate the parasympathetic pathway when
conditions are safe and socially acceptable. The sensory innervations travel through
the spinal cord and into the sacral disc where axons travel out to the ganglions near
the bladder and innervate the detrusor muscle to contract the bladder wall and
disinhibit the internal sphincter to release urine. Concurrently, there is an
interneuron in the sacral dorsal horn connecting to the motor pathway, receiving
this action potential from the parasympathetic pathway and transferring a signal to
disinhibit the external sphincter in bladder neck so urine is released. These signals
continue until the bladder is completely empty and are stimulated by sensations
(flow increases volume) through the urethra and abdominal and pelvic voluntary
contractions.
I am inserting two diagrams to illustrate these coordinated sympathetic ,
parasympathetic and somatic (motor) pathway( pudendal nerve) that are
innervated by upper brain structures periaqueductal gray(PAG) and pontine
mictruition center.
3. After my laser reduction of my enlarged prostrate, voiding was no longer
occurring as above and the urologists I have seen could not give a definitive answer.
In selecting to delve into this topic and through the videos 9.8 & 9.9, I am
overwhelmed by the complexity of mictruition. It is my suspicion that what has
gone wrong is the detrusor muscle integrity or detrusor hypertrophy. The effects of
long-term urethra blockage by my prostrate has probably cause thickening of the
bladder wall leading to non-response to the parasympathetic signal to contract
(reference “Y-Tube: Bladder Wall Thickening, “yejimarina”). Chronic blockage
results in repeated exposure for the bladder of isotonic pressure. This ongoing
pressure on the wall triggers an anabolic process, so complex I barely grasps it, that
results in fibrosis of detrusor muscle where it no longer stretches or collapses.
Other factors I realize added to detrusor non-response, I my use of anti-histamines
and opiate pills for pain which block stretch muscle receptors to the nerve firings of
the parasympathetic reflex. When my bladder fills to 275ml to 300ml I experience
acute pain, which I feel as pressure and the urge to empty, but without results,
which suggest to me the nerve firing of sympathetic reflex is active. When I am
emptying with a catheter, during this experience, I suspected maybe the laser
surgery damaged my sphincter internal muscle; yet, I often feel some muscle
contractions on the catheter. This suggests the reflex for either of two sphincter
contracting as voiding completes. Examining the complexity of mictruition has
diffused the anger I’ve felt toward the urologists’ failure to give me an explanation
or a solution of my urine retention. Adding to the receptivity of the detrusor muscle
to urine expansion pressure, neuronal signaling for the receptors of stretch muscle
cells involve varied neurotransmitter and hormones which as noted can be
degraded by medications I’ve used for allergy and for pain.
Two other consideration, I have read on prostate surgery, is that the laser surgery
may have scared the urethra or insufficient reduction of the prostrate has caused
blockage.
I come away from the knowledge imparted from this course with greater impetus to
master the episodic pain and intrusive need to catheterize three times. First and
foremost, this disruption of my everyday life pales against having any kind of spinal
rupture, brain tumor or strokes. It has been inspirational to learn how the cases
presented with neurologic challenges have found positive adaptation and mastery
or damage parts of their senses and neurobiology.
Very helpful is the discussion on how one can effect positive change by thinking
and/or acting in a positive way. While I am retired, I continue my social work
practice in part-time work with children, which continues to give me satisfaction
meaning in helping children develop. Many of the topics covered have provided
greater insight into how to help children in their development. Oppositional or
ADHD affected children can extinguish negative behaviors/attitude by using notion
that if you adopt a positive behavior it will create and positive feeling and vice versa.
The encoding of emotional memory in the experience of any trauma was clearly
explained as bonded/coupled with sensory channels (smell, sound, etc.) which is the
triggers PTSD. Thus, this underscored for me the key to helping someone recovering
from PTSD: desensitize the trauma from its negative emotion from. Particular
helpful was how deep breathing is very effective in calming a person’s anxiety or
anger and similarly with muscle relaxation technique; in both of these, voluntary
control over decreasing the body sensation of anxiety or tension affects a change in
the mind or body state.
Many of the videos addressing neurobiological disorder have added to my capacity
to help people or clients I may encounter with strokes, speech, hearing, and vision
problems. Alzheimer’s memory lost can be slowed or counteract with relying on the
cerebellum’s memory role in procedural behavior. Explaining why you have chills
with a fever or hot flashes during menopause in terms of the hypothalamus’ fixed
thermostat provided pragmatic solutions to offer.
Finally, learning how much the brain relies on oxygen and how muscle fibers and
neurotransmitters (endorphin, encephalin-pain blockers) are reinforced with
aerobic exercise validates my past positive experience with swimming and weight
lifting. I have learned that exercise shifts up the mean arterial pressure without
risks to blood vessel rupture, yet exercise increases the capacity for bathing the
brain with oxygen and nutrients. During this past year with pelvic pain I have
stopped exercising and have now restarted with weight lifting manage my pain and
loss of strength and yield a positive mood, more tolerant of pain.

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Failed mictruition

  • 1. Mictruition: A case of Failure to expel urine 1. I am a 64-year-old male and I have been force to catheterize at least three times a day since laser reduction surgery for a benign prostatic hyperplasia in late 2012. I believe my swollen prostate had existed for several years pinching my urethra and causing prolonged urine retention over a long time span. This more than likely had put a stress on my urinary bladder (through urethral blockage) until by late 2012 while I had a strong urge to void virtually no urine flowed despite a conscious effort to void. Thus, I review micturition as the neurobiological function that has impacted adversely my life and attempt to address what has disrupted this function; a problem that thus far 4 urologist have attempted to comprehend, with only one suggesting a probable cause: a degraded detrusor muscle of the urinary bladder. Micturition has several parts that control the bladder; the pontine mictruition center, the sympathetic circuit in the lumbar area and the parasympathetic circuit in the sacral area. The later triggers voiding and the former results in urine storage. The pontine mictruition center in the pons and an area in the prefrontal cortex regulate voluntary urinating. A description of how the neuronal pathways work follows to answer part 2 of assignment: the sympathetic to store, the parasympathetic to expel (P for you know what) and the voluntary pathways to empty the bladder. 2. The sympathetic pathway descends from the pons and hypothalamus through the lower thoracic/upper lumbar discs, out through pre-vertebral ganglions, which send axons into the bladder wall and internal bladder sphincter. These axons disinhibit expansion of stretch muscles to permit urine storage and innervate the internal sphincter muscle to contract to hold in urine. This permits bladder, a capacity up to 500ml) to withstand pressure as the bladder fills up to 300 to 350 cc of urine. On average at the 260ml level, afferent nerve pathways send pressure (increase action potentials) signal or urge up through the spinal cord and pons to trigger voiding. These pathways also have c nerve fibers that sense chemical changes in the bladder up through the spine and to the pons; they also transmit pain signals from the bladder. From the video of this course, it is explained in the course that there are urine storage level deviations of pressure that generate urine urge and detrusor contraction. Thus, low urine amount from hyper anxiety can trigger low urine voiding due greater sensitivity to lower pressure leading to greater signal innervations. Or higher urine amount during sleep is possible due to greater stretch in the bladder wall cause by greater inhibition signal strength through the sympathetic pathway on the stretch muscles of bladder wall resulting in longer stretch to delay urge sensation to higher pressure and contraction of detrusor muscle. In converse, the internal sphincter is uninhibited, open, with hyper anxiety and innervated, closed, during sleep state. Finally, as the bladder fills, the sympathetic pathway connects with the motor axon, in the lumbar disc, and sends excitation signals out to to the external striated sphincter muscle to maintain contraction.
  • 2. Once the increase firing to void is transmitted back through the lumbar disc and spinal column and up to the Pons, midbrain (PariacqueductalGray) and orbital prefrontal cortex (The orbital medial prefrontal area (social mores) in turn regulates the PAG), the parasympathetic pathway is then engaged to empty the bladder. These upper structures activate the parasympathetic pathway when conditions are safe and socially acceptable. The sensory innervations travel through the spinal cord and into the sacral disc where axons travel out to the ganglions near the bladder and innervate the detrusor muscle to contract the bladder wall and disinhibit the internal sphincter to release urine. Concurrently, there is an interneuron in the sacral dorsal horn connecting to the motor pathway, receiving this action potential from the parasympathetic pathway and transferring a signal to disinhibit the external sphincter in bladder neck so urine is released. These signals continue until the bladder is completely empty and are stimulated by sensations (flow increases volume) through the urethra and abdominal and pelvic voluntary contractions. I am inserting two diagrams to illustrate these coordinated sympathetic , parasympathetic and somatic (motor) pathway( pudendal nerve) that are innervated by upper brain structures periaqueductal gray(PAG) and pontine mictruition center.
  • 3. 3. After my laser reduction of my enlarged prostrate, voiding was no longer occurring as above and the urologists I have seen could not give a definitive answer. In selecting to delve into this topic and through the videos 9.8 & 9.9, I am overwhelmed by the complexity of mictruition. It is my suspicion that what has gone wrong is the detrusor muscle integrity or detrusor hypertrophy. The effects of long-term urethra blockage by my prostrate has probably cause thickening of the bladder wall leading to non-response to the parasympathetic signal to contract (reference “Y-Tube: Bladder Wall Thickening, “yejimarina”). Chronic blockage results in repeated exposure for the bladder of isotonic pressure. This ongoing pressure on the wall triggers an anabolic process, so complex I barely grasps it, that results in fibrosis of detrusor muscle where it no longer stretches or collapses. Other factors I realize added to detrusor non-response, I my use of anti-histamines and opiate pills for pain which block stretch muscle receptors to the nerve firings of the parasympathetic reflex. When my bladder fills to 275ml to 300ml I experience acute pain, which I feel as pressure and the urge to empty, but without results, which suggest to me the nerve firing of sympathetic reflex is active. When I am emptying with a catheter, during this experience, I suspected maybe the laser surgery damaged my sphincter internal muscle; yet, I often feel some muscle contractions on the catheter. This suggests the reflex for either of two sphincter contracting as voiding completes. Examining the complexity of mictruition has diffused the anger I’ve felt toward the urologists’ failure to give me an explanation or a solution of my urine retention. Adding to the receptivity of the detrusor muscle to urine expansion pressure, neuronal signaling for the receptors of stretch muscle cells involve varied neurotransmitter and hormones which as noted can be degraded by medications I’ve used for allergy and for pain. Two other consideration, I have read on prostate surgery, is that the laser surgery may have scared the urethra or insufficient reduction of the prostrate has caused blockage. I come away from the knowledge imparted from this course with greater impetus to master the episodic pain and intrusive need to catheterize three times. First and foremost, this disruption of my everyday life pales against having any kind of spinal rupture, brain tumor or strokes. It has been inspirational to learn how the cases presented with neurologic challenges have found positive adaptation and mastery or damage parts of their senses and neurobiology. Very helpful is the discussion on how one can effect positive change by thinking and/or acting in a positive way. While I am retired, I continue my social work practice in part-time work with children, which continues to give me satisfaction meaning in helping children develop. Many of the topics covered have provided greater insight into how to help children in their development. Oppositional or ADHD affected children can extinguish negative behaviors/attitude by using notion that if you adopt a positive behavior it will create and positive feeling and vice versa.
  • 4. The encoding of emotional memory in the experience of any trauma was clearly explained as bonded/coupled with sensory channels (smell, sound, etc.) which is the triggers PTSD. Thus, this underscored for me the key to helping someone recovering from PTSD: desensitize the trauma from its negative emotion from. Particular helpful was how deep breathing is very effective in calming a person’s anxiety or anger and similarly with muscle relaxation technique; in both of these, voluntary control over decreasing the body sensation of anxiety or tension affects a change in the mind or body state. Many of the videos addressing neurobiological disorder have added to my capacity to help people or clients I may encounter with strokes, speech, hearing, and vision problems. Alzheimer’s memory lost can be slowed or counteract with relying on the cerebellum’s memory role in procedural behavior. Explaining why you have chills with a fever or hot flashes during menopause in terms of the hypothalamus’ fixed thermostat provided pragmatic solutions to offer. Finally, learning how much the brain relies on oxygen and how muscle fibers and neurotransmitters (endorphin, encephalin-pain blockers) are reinforced with aerobic exercise validates my past positive experience with swimming and weight lifting. I have learned that exercise shifts up the mean arterial pressure without risks to blood vessel rupture, yet exercise increases the capacity for bathing the brain with oxygen and nutrients. During this past year with pelvic pain I have stopped exercising and have now restarted with weight lifting manage my pain and loss of strength and yield a positive mood, more tolerant of pain.