Transient paralysis of the bladder due to wound botulism.

In the last 10 years, wound botulism has increasingly been reported and nearly all of these new cases have occurred in injecting-drug abusers. After absorption into the bloodstream, botulinum toxin binds irreversibly to the presynaptic nerve endings, where it inhibits the release of acetylcholine. Diplopia, blurred vision, dysarthria, dysphagia, respiratory failure and paresis of the limbs are common symptoms of this intoxication. Surprisingly and despite the well-known blocking action of the botulinum toxin on the autonomic nerve system, little attention has been paid to changes in the lower urinary tract following acute botulinum toxin poisoning. Here we report a case of bladder paralysis following wound botulism. Early diagnosis and adequate management of bladder paralysis following botulism is mandatory to avoid urologic complications. Accordingly, the prognosis is usually favorable and the bladder recovery complete.     

Two cases of foodborne botulism with home-preserved asparagus

Botulism is a rare but potentially fatal disease caused by toxins produced by Clostridium botulinum. We report botulism in two adult females, one of them just tasting from "bad" asparagus and the other eating the full portion. Both patients survived after intermittent mechanical ventilation and trivalent antitoxin administration. The diagnosis was confirmed by detection of botulinum toxin. Acute onset of bilateral cranial neuropathies associated with symmetric descending weakness as well as some key features of the botulism syndrome including absence of fever, symmetric neurologic deficits, the patients remaining responsive and no sensory deficits, with the exception of blurred vision, led to the clinical diagnosis in the first presenting case which was then easily made in the second. Despite the fact that amount of toxin ingested, time-to-symptom development, and time-to-recovery markedly differed in the two patients, their maximal disease severity was similar.     

Botulism toxin,bioterrorist weapon

BOTULISM AND BIOWARFARE: Botulism is a severe neuro-paralysing infection due to a toxin produced by Clostridium botulinum. The use of the botulinum toxin for terrorist aims in the form of aerosols is a perfectly credible eventuality. The botulinum toxin is the most potent toxin known; it is easy to produce and can lead to massive destruction. DEPENDING ON THE CONTAMINATION: The clinical forms of botulism depend on the mode of contamination. Botulism through inhalation can only be the result of a deliberate act using an aerosol. The clinical symptomatology is identical to that of the other forms. PREVENTION: In the case of a bio-terrorist attack with an aerosol of botulinum toxin, the subjects exposed should be vaccinated as a prophylactic measure with trivalent antitoxin vaccine (types A, B and E). This vaccine must be administered as rapidly as possible in symptomatic patients. A single case of botulism acquired by inhalation corresponds to an act of terrorism.     

Visceral Botulism – A New Form of Bovine Clostridium botulinum Toxication

There are reports of a hitherto unknown bovine disease in Germany. The symptoms are, in general, indigestion (constipation alternating with diarrhoea), non‐infectious chronic laminitis, engorged veins, oedemas, retracted abdomen, emaciation and apathy. Most cases occur during the peripartal period and often result in unexpected death. In addition, there are findings of delayed growth and wasting in heifers, as well as decreasing milk yield. Clinical and standard laboratory examinations leave the origin undisclosed. Bioassays for Clostridium botulinum, its spores and toxins in animals of affected farms revealed the presence of free botulinum toxin in the contents of the lower sections of the intestine. In two control farms without signs of the disease, the tests remained negative. This seems to support our hypothesis that long‐lasting absorption of low quantities of botulinum toxin may interfere with the neurological control of intestinal physiology. The authors propose to name this disease complex ‘visceral botulism’.     

Botulinum toxin type A for the treatment of lower urinary tract disorders

Many papers report the clinical success of botulinum toxin A as a method of management of various bladder dysfunctions. The rationale was that botulinum toxin A was able to block the presynaptic release of acetylcholine from the parasympathetic efferent nerve. The efficacy might result not only from an inhibitory effect on detrusor muscle, but also some effects might be mediated by altering the afferent nerve input. This systematic literature review discusses the efficacy and safety of botulinum toxin A therapy for idiopathic detrusor overactivity, neurogenic detrusor overactivity, interstitial cystitis/painful bladder syndrome and benign prostatic hyperplasia. The information was gathered from a PubMed literature research for abstracts from recent urological meetings. Injection of botulinum toxin A appears to have a positive therapeutic effect in multiple urological conditions, such as refractory idiopathic detrusor overactivity, neurogenic detrusor overactivity, interstitial cystitis/painful bladder syndrome and benign prostatic hyperplasia. Because the United States Food and Drug Administration has approved botulinum toxin A (Botox) for injection for the treatment of urinary incontinence as a result of neurogenic detrusor overactivity (e.g. spinal cord injury, multiple sclerosis) in adults who have an inadequate response to or are intolerant of an ant cholinergic medication, the use of botulinum toxin A will spread and be a more familiar therapy in the urological arena. However, further robust evidence should be awaited. We will discuss the current use of this agent within the urological field.     

Does Laser Inactivate Botulinum Toxin?

BACKGROUND: Botulinum toxin is a popular and effective treatment for dynamic rhytids. It is a neurotoxic protein complex that exerts its effect by inhibiting acetylcholine release at the presynaptic neuromuscular junction. Nonablative resurfacing treatments have also become well liked by patients and physicians owing to the minimal downtime associated with treatment. Currently, same-day nonablative laser treatments are performed prior to botulinum toxin injection owing to the concern that the laser may inactivate it. On occasion, it may be desirable to perform nonablative laser after the botulinum toxin has been injected (ie, patient afterthought, scheduling concern). OBJECTIVE: To determine whether the use of nonablative rejuvenation laser or intense pulsed light (IPL) immediately following botulinum toxin injections has any effect on the efficacy of the botulinum toxin treatment. METHODS: Nineteen subjects received botulinum toxin injections to either the glabellar or crow's-feet areas. One side of the treated glabellar or periorbital area was treated with either VBeam laser (Candela, Wayland, MA, USA), SmoothBeam laser (Candela), CoolGlide laser (Cutera, Brisbane, CA, USA), or an IPL or radiofrequency (RF) device within 10 minutes of botulinum toxin injection. Pretreatment and 2-week post-treatment photographs were compared. RESULTS: No decrease in the efficacy of botulinum toxin denervation was observed when glabellar or perioral areas were treated with VBeam laser, SmoothBeam laser, CoolGlide laser, or an IPL or RF device within 10 minutes of botulinum toxin injection. CONCLUSION: Patients may be treated with several nonablative lasers and IPL or RF devices immediately after botulinum toxin injection without loss of efficacy or other apparent untoward effect.     

Effect of botulinum toxin A on the autonomic nervous system of the rat lower urinary tract

PURPOSE: The magnitude and duration of the effects of botulinum toxin A on acetylcholine (ACh) and norepinephrine release from the bladder and urethra of rats were measured using a radiochemical method. MATERIALS AND METHODS: Saline (sham treatment) or botulinum toxin A was injected into the bladder (50 microl.) or urethra (30 microl.) in separate groups of animals. The release of 3H-norepinephrine or 14C-choline was measured at 2 time points after injection (5 or 30 days). RESULTS: The fractional release of ACh in botulinum toxin A treated animals was significantly inhibited at higher frequencies of electrical field stimulation (20 Hz.) but not at lower frequencies (2 Hz.) 5 days after injection. However, ACh release recovered to sham injected values 30 days after toxin injection. No significant differences in the fractional release of norepinephrine from sham injected or botulinum toxin A bladders were observed. In contrast, norepinephrine release from the urethra was inhibited by botulinum toxin A for at least 30 days after injection. Similar to its effect on transmitter release in the bladder, botulinum toxin A inhibited norepinephrine release in the urethra at high (20 Hz.) but not at low (4 Hz.) electrical stimulation frequencies. CONCLUSIONS: These data indicate that the clinical effects of botulinum toxin A on the lower urinary tract may vary depending on the site of injection and level of nerve activity.     

Botulinum toxin A for the management of vulvodynia

Clinically, botulinum toxin A blocks the cholinergic innervation of the target tissue. Recently, it has been proved effective not only at a neuromuscular junction but also within parasympathetic or sympathetic neural synapses. Seven women with pain on genitalia that could not be controlled with conventional pain managements were enrolled in this study. Twenty to 40 U of botulinum toxin A were used in each injection. Injection sites were the vestibule, levator ani muscle or the perineal body. Repeat injections were administered every 2 weeks if the patient's symptoms had not fully subsided. In all patients, pain had disappeared with botulinum toxin A injections. Five patients needed to be injected twice; the other two patients needed only one injection. We did not observe complications related to botulinum toxin A injections, such as pain, hemorrhage, infection, muscle paralysis or other complications. The subjective pain score improved from 8.3 to 1.4, and no one has experienced a recurrence (the follow-up period was four to 24 months, with a mean follow-up of 11.6 months). Botulinum toxin A is effective in blocking nociception. Even though further investigation and well-controlled study will be necessary, we suggest that the botulinum toxin therapy would be useful and safe in managing vulvodynia of muscular or neuroinflammatory origins.     

Complications with the Use of Botulinum Toxin Type A in Facial Rejuvenation: Report of 8 Cases

The botulinum toxin A is produced by Clostridium botulinum and causes a reversible, selective muscle relaxation that leads to a temporary flattening of the mechanical component of wrinkling without the stigmata of invasive surgery. Since the end of the 1980s, this neurotoxin has been used to treat mimic facial lines with good results. Although this is considered a safe therapy, with adverse effects typically self-limited, more severe complications have been observed when it is used by nonskilled physicians or in improper dosages. This article reports eight patients treated with botulinum toxin A for aesthetic purposes who developed different complications. Treatment of the complication included the use of electrical stimulation, lymphatic drainage, antiinflammatory therapy, dipivefrine cloridrate drops, and other approaches. With specific treatment for each patient, the lengths of these complications seemed to be reduced.     

The basic science of botulinum toxin

Understanding the basic science of botulinum toxin should serve as a fundamental first step for clinical therapy. This article endeavors to cover many aspects of basic research that also have clinical import. The two principal toxins of the clostridial family, Clostridium tetani and C botulinum, are described in detail. The five clinical manifestations of botulism poisoning are also outlined, and structural aspects and the mechanism of action of botulinum toxin are then presented. Finally, the immunologic and pharmacologic principles that define the various serotypes of botulinum toxin are set forth.     

A case of type A botulism

The neurotoxin produced by Clostridium botulinum, is responsible for botulism. The clinical signs are digestive disorders, pupillar alterations, and peripheral muscular weakness. The failure of thoracic muscles is responsible for the severity of botulism. We describe a case of a 74 year old woman who presented a severe form of botulism, requiring a prolonged intensive care unit stay.     

Acute paralysis following “a bad potato”: A case of botulism

PURPOSE: Intensivists often encounter patients with respiratory failure as a result of neuromuscular disease, however, acute neuro-muscular syndromes are less common. We present a case of food borne Clostridium botulism and discuss the diagnostic and therapeutic considerations. CLINICAL FINDINGS: A 35-yr-old healthy male presented with abdominal pain and blurred vision 12 hr after ingesting a "bad" potato. During the next 17 hr, the patient demonstrated a gradual descending paralysis which ultimately resulted in no cranial nerve function and 0/5 strength in all extremities. Sensation was intact. The patient required intubation and mechanical ventilation. His blood count, biochemical profile, computerized tomography and magnetic resonance imaging of the head were normal. A lumbar puncture revealed no abnormalities. Due to the rapid deterioration and presentation of 'descending' paralysis, botulism was suspected. The patient was treated empirically with botulinum anti-toxin. Samples of blood, stool and gastric contents were cultured for the presence of Clostridium botulinum and its toxin and these tests were positive for botulinum toxin A 12 days later. The patient's neuromuscular function gradually improved over a prolonged period of time. Six and one-half months after his initial presentation, the patient was discharged home after completing an aggressive rehabilitation program. CONCLUSIONS: Botulism is a rare syndrome and presents as an acute, afebrile, descending paralysis beginning with the cranial nerves. If suspected, botulinum anti-toxin should be considered, particularly within the first 24 hr of onset of symptoms. Confirmation of the presence of botulinum requires days therefore the diagnosis and management rely on history and physical examination.     

Neuromuscular function and transmission

The neuromuscular junction (NMJ) is a chemical synapse between a motor neurone and a skeletal muscle cell. It has been the most intensively studied synapse in the body owing to its comparatively large size, relative simplicity and accessibility. Commands from the central nervous system are transmitted along motor neurone axons, resulting in the release of the neurotransmitter acetylcholine from axon terminals. The transmitter activates nicotinic cholinergic receptors located on the muscle cell membrane. These receptors are ligand-gated cation channels. Upon binding of acetylcholine, the receptor channel opens to allow mainly Na⁺ ions to enter the muscle cell, causing a partial membrane depolarization. This triggers action potentials in the muscle cell membrane, resulting in Ca²⁺ influx and muscle contraction. The structure and function of the NMJ are such that, even under the extremes of muscular exertion, the operation of the NMJ is highly reliable. This is because a large ‘safety factor’ is intrinsic to NMJ function in the sense that more neurotransmitter is released than is necessary to initiate muscle contraction. However, the normal function of the NMJ can be severely disrupted by drugs, naturally occurring toxins and disease. Myasthenia gravis, for example, is characterized by muscle weakness and easily fatigued muscles. It is an autoimmune disorder in which the body produces antibodies to the muscle nicotinic receptor protein.     

Bupivacaine-induced myotoxicity and its effect on botulinum toxin paresis

PURPOSE: To determine the effect of the coinjection of bupivacaine with botulinum toxin type A on the degree of muscular paralysis. Enhancement of paralysis could allow a decreased dose of neurotoxin treatment, thus reducing the risk for neutralizing antibody formation. METHODS: Prospective, randomized, double-blind study. Sixteen consecutive patients undergoing treatment of glabellar furrows received botulinum toxin A reconstituted with bupivacaine 0.75% to one corrugator muscle and botulinum toxin A reconstituted with nonpreserved normal saline to the contralateral muscle. Patients were evaluated on days 0 (injection day), 3, 7, 30, 60, and 90. Patients also completed a questionnaire each visit regarding their assessment of paralysis, asymmetry, and adverse effects. RESULTS: At 1 week after botulinum toxin A injection, 68.8% of the patients showed greater weakness on the bupivacaine-reconstituted side as opposed to 25.0% of patients showing greater weakness on the saline-reconstituted side. At 1 and 3 months, there was no statistical difference in weakness between the saline and the bupivacaine sides. The survey revealed that 56% of the patients had greater pain on the saline side, 31% on the bupivacaine side, and equal pain in 13%. CONCLUSIONS: Reconstituting botulinum toxin A with bupivacaine is safe, does not limit efficacy, and does not reduce the degree or relative duration of muscular paralysis. Reconstituting botulinum toxin A with bupivacaine results in faster onset of paresis, possibly due to a synergistic effect of bupivacaine induced myotoxicity. Utilizing bupivacaine may result in less pain for patients.     

Botulinum toxin for the treatment of essential blepharospasm

Twenty-six patients with essential blepharospasm were treated with botulinum toxin by injection. The onset of protractor weakness in all patients ranged from one to five days following treatment. Maximal weakness developed within 12 days. There was a variable and gradual return of protractor strength over eight to 29 weeks in most patients and, with it, a return of spasm. Twenty-five patients received some degree of functional relief following initial injection. In most patients, however, the post-injection result could not be stabilized and repeat injections have been necessary to control recurrent spasms. There was one treatment failure. Three patients treated by injection following previous neurectomy and myectomy appeared to have a reduced requirement for subsequent injections. Complications included transient ptosis in six patients and mild exposure symptoms in four patients. Extraocular muscle paresis did not occur. There were no systemic side effects from the botulinum toxin injections.     

A型肉毒毒素治疗Meige综合征的方法及效果分析

目的：探讨A型肉毒毒素治疗Mei ge综合征的方法及疗效。方法：47例患者在肌电图引导下用兼作注射器的针电极进行,在患者肌痉挛部位用A型肉毒毒素肌肉内注射,每点注射量为0.1～0.2ml（含肉毒毒素2.5～5 U）,注射点数为数点～8点。根据Cohen、Albert痉挛强度分级评估疗效。结果：注射后一般3～4天起效,疗效持续3～6个月,复发者重复注射仍有效。治疗后患者肌痉挛强度明显下降,与治疗前比较有极显著性差异（P〈0.01）;症状完全缓解和明显缓解者达89.4%,治疗前后疗效比较有极显著性差异（P〈0.01）。不良反应主要有：局部水肿、咬肌无力、眼睑下垂等,一般两周内均能恢复。结论：局部注射A型肉毒毒素治疗Meige综合征为一种安全有效、简便易行的治疗手段。     

Botulinum toxin reduces anal spasm but has no effect on pain after haemorrhoidectomy

Objective  Pain following haemorrhoidectomy is due to a combination of factors including spasm of the internal sphincter, an open wound and local infection. In this study, we investigated the effect of botulinum toxin on postoperative pain following Milligan–Morgan haemorrhoidectomy.
Method  A prospective randomized controlled trial was conducted in 32 patients undergoing haemorrhoidectomy. Routine postoperative care included metronidazole and bupivacaine. Patients were also given an inter-sphincteric injection of either placebo or botulinum toxin (150 units). Maximal resting pressure (MRP) and maximal squeeze pressure (MSP) were measured postoperatively. A linear analogue score was used to assess postoperative pain. The sample size calculation was calculated to show one standard deviation difference between groups. The primary endpoint was reduction in postoperative pain.
Results  The MRP was significantly lower in the botulinum toxin group (mean 50.5 mmHg; 95% CI 39.77–61.23) compared with the placebo group (mean 64.94 mmHg; 95% CI 55.65–74.22) ( P  = 0.04) at week 6. At week 12 there was no significant difference in MRP between the two groups. In contrast MSP was significantly lower in the botulinum toxin group at weeks 6 and 12 (mean 87.1 mmHg; 95% CI 66.9–107.1) compared with the placebo group (mean 185.8 mmHg; 95% CI 134.2–237.4) at week 12 ( P  = 0.0014). There was no significant effect on overall or maximal pain scores. Median time for return to normal activities was not significantly different between groups.
Conclusion  Botulinum toxin reduces anal spasm but has no significant effect on postoperative pain.     

Botulism, a clinical diagnosis

Foodborne botulism results from the effect of a neurotoxin produced by a sporulated anaerobic bacillus called Clostridium botulinum. The mode of contamination occurs through the consumption of foodstuff, already contaminated by the neurotoxin. Following an incubation period that varies from 2 hours to 8 days, the symptoms start with intestinal problems. Then paralysis of the cranial nerve pairs sets in, classically manifested by diplopia, dysphagia, dysphonia, areactive mydriasis and ptosis. The onset of motor disorders occurs in descending order with possible involvement of the respiratory muscles, hence requiring reanimation measures and sometimes mechanical ventilation. The diagnosis of botulism is clinical. Identification of the botulinum toxin in the blood or faeces of the patients or in the contaminating food stuff confirms the diagnosis.     

Urologic applications of botox

Botulinum toxin (BTX), a neurotoxin produced by the gram-positive, rod-shaped anaerobic bacterium Clostridium botulinum, was isolated in 1897 by Belgian scientist Professor Pierre Emile van Ermengem. BTX acts by blocking the release of acetylcholine at the neuromuscular junction. As a result of this chemodenervation, a temporary flaccid paralysis ensues. Different medical disciplines have taken advantage of this temporary paralysis to treat muscular hypercontraction. BTX was first approved by the US Food and Drug Administration in 1989 for use in patients with strabismus and blepharospasm. Since then, BTX has been used to treat a number of different neuromuscular disorders. Although not approved by the US Food and Drug Administration, BTX has been used successfully in urology to treat neurogenic and non-neurogenic detrusor overactivity, detrusor-sphincter dyssynergia, motor and sensory urge, and chronic pain syndromes.     

Botulinum Toxin A in the Treatment of Chromhidrosis

Background. Chromhidrosis is an uncommon disorder characterized by secretion of colored sweat by apocrine glands, typically localized to the face or axilla. The current treatments available for chromhidrosis are time consuming and frequently ineffective.
Objective. Our purpose is to demonstrate a novel approach to the treatment of apocrine chromhidrosis.
Methods. We report a case of apocrine chromhidrosis successfully treated with botulinum toxin A (BTX-A; Botox).
Results. BTX-A therapy successfully controlled facial chromhidrosis, and the effects were visible at 19 weeks post-treatment. The therapeutic benefits may be attributed to its inhibitory effects on cholinergic stimulation, adrenergic stimulation, and substance P release, although further studies are necessary to elucidate the precise mechanism of action.
Conclusion. This report demonstrates a new therapeutic approach to patients suffering from chromhidrosis.