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spasms, frequency, and other stuff
  Hi. I'm a 20 yr old female who's had some urological problems for about 5 years now. my general complaints are: frequency, leakage(directly after voiding, prior to voiding, excersize..basically whenever,) spasms in my bladder (one urologist also thinks i have spasms in my external urethral sphincter,) and also a very uncomfortable sensation in my bladder. It's not "painful" but more like someone is sitting on me or pressing their hand down on my bladder. when i am driving i also have that "sitting on a golf ball" feeling. I can't stand for a doctor to press on my bladder becuase it is very tender.I never ever feel empty. i can't even remember what that kind of relief is like. i only know when i can't hear the stream anymore, i'm done (hopefully) When this first came on, it was much worse. I could have spent each day in the bathroom! i felt the urge constantly, but when i would try to void, i couldn't, but as soon as i gave up, there was leakage. some history: i used to be an avid drug user. cocaine, marijuana, LSD, cheeva, etc...and the problem first started after a sad cocaine binge.in fact, i only had the problem when i was using a mind-altering substance. A few urologists suggested i may have damaged some nerve endings with the cocaine, or possibly a "mini-stroke" I have been sober for 4 years now, and have since seen many urologists, neurourologists, had all the urodynamic testing done, ruled out MS, tried all the meds, even physical therapy with a device that sent electric signals to the muscles. i don't intake any caffeine,i do kegels (my muscles are still very weak.) i'm just very frustrated and want to DO something.please, if you have any suggestions, know anyone doing research about possible cocaine-bladder connections, new info, new meds, new anything.....i'd really appreciate it.
Dear Kat
Thanks you for your questions.
It seems you have been worked up fairly extensively.  With your symptom complex I would image you have been evaluated for interstitial cystitis.  
There is an article which supports the possible connection between cocaine abuse and neurological deficits.  Please see abstract below.    The treatment for bladder spasms secondary to a neurological lesion is the same no matter what the cause and entails; anticholinergic medications, urodynamic testing and possible clean intermittent catherization.

Majewska MD .
Clinical Trial Branch, National Institute on Drug Abuse, Rockville, MD
Cocaine addiction as a neurological disorder: implications for
treatment. [Review] [124 refs]
NIDA Research Monograph. 163:1-26, 1996.
Clinical and preclinical studies provide convincing evidence for persistent neurological/psychiatric impairments and possible neuronal
degeneration associated with chronic cocaine/stimulant abuse. These impairments include multifocal and global cerebral ischemia, cerebral hemorrhages, infarctions, optic neuropathy, cerebral atrophy, cognitive impairments, and mood and movement disorders. These findings may encourage the placement of stimulant addiction into the category of organic brain disorders. Functional and microanatomical anomalies in the frontal and temporal cortex as well as other brain regions may be
responsible for certain aspects of phenomenology and neuropsychopathology that are characteristic of stimulant polydrug
addictions. These may include broad spectrum of deficits in cognition, motivation, and insight; behavioral disinhibition; attention deficits; emotional instability; impulsiveness; aggressiveness; depression; anhedonia; and persistent movement disorders. Although it is still debated whether the hypofrontality and other brain anomalies observed in stimulant abusers are a consequence or an antecedent of drug abuse, this debate seems purely academic and irrelevant with respect to the importance of compensating for these deficits in the development of treatment strategies. The neuropsychiatric impairments accompanying stimulant abuse may contribute to the very high rate of relapse in addicts that can take place after long periods (years) of abstinence. It is possible that the neurological deficits present in stimulant addicts, whether they are primary or secondary to stimulant abuse, are responsible for perpetual drug abuse which may be a form of self-medication (Weiss et al. 1991, 1992). In this context, addiction to stimulants, once fully developed, may represent a true biological dependency on drugs that temporarily compensate for existing neurological deficits. The concept of self-medication by drug addicts is supported by major theories of biological psychiatry. While a majority of drug addicts are polydrug users, there seems to be a preference for a particular type of drug among different populations of addicts. Addicts
who experience distress, anxious dysphoria, and turbulent anger prefer the calming actions of opiates, whereas addicts with preceding attention deficit disorder, depression, or bipolar disorder often prefer stimulants (Khantzian 1985). Figure 1 presents conceptual relationships between brain damage and cocaine/stimulant abuse. More clinical studies are needed to establish unequivocally the epidemiological relationships between preexisting neurological deficits-resulting either from genetic, developmental, traumatic, or neurotoxic factors- and vulnerability to drug addictions. Nonetheless, deducing from the results of preclinical
studies, it is conceivable that individuals with neurological deficits associated with attention deficit disorder, developmental
neuroanatomical abnormalities, lead poisoning, alcoholism, posttraumatic brain lesions, and PTSD may be more vulnerable to stimulant addiction.
This notion has significant empirical support as preclinical studies have shown that animals with lesioned prefrontal cortex became
supersensitive to cocaine (Schenk et al. 1991) and animals with lesions at the amygdala, VTA, or raphe nuclei manifest more rapid acquisition of amphetamine self-administration than control rats (Deminiere et al. 1989). The above arguments, postulating neuropathology as an intrinsic component of stimulant addiction, should be taken into consideration
with the caveat that the clinical manifestations of the disease are heterogenous and addicts may express varying stages and degrees of the disease as determined by environmental and genetic factors. Therefore, it is likely that stimulant addicts who have less advanced
neuropathology may recover spontaneously after detoxification with proper nutritional and psychotherapeutic support if they can sustain abstinence. (ABSTR [References: 124]
  More individualized care is available at the Henry Ford Hospital and its urban campuses by calling  (1 800 653 6568). We can also arrange local accommodations through this number if this is your need. Please bring any physicians
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