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The effects of drug-related dysgeusia can often be reversed by stopping the patient's regimen of the taste altering medication. In one case, a forty-eight-year-old woman who was suffering from hypertension was being treated with valsartan. Due to this drug's inability to treat her condition, she began taking a regimen of eprosartan, an angiotensin II receptor antagonist. Within three weeks, she began experiencing a metallic taste and a burning sensation in her mouth that ceased when she stopped taking the medication. When she began taking eprosartan on a second occasion, her dysgeusia returned. In a second case, a fifty-nine-year-old man was prescribed amlodipine in order to treat his hypertension. After eight years of taking the drug, he developed a loss of taste sensation and numbness in his tongue. When he ran out of his medication, he decided not to obtain a refill and stopped taking amlodipine. Following this self-removal, he reported experiencing a return of his taste sensation. Once he refilled his prescription and began taking amlodipine a second time, his taste disturbance reoccurred. These two cases suggest that there is an association between these drugs and taste disorders. This link is supported by the "de-challenge" and "re-challenge" that took place in both instances. It appears that drug-induced dysgeusia can be alleviated by reducing the drug's dose or by substituting a second drug from the same class.
Approximately one half of drug-related taste distortions are caused by a zinc deficiency. Many medications are known to chelate, or bind, zinc, preventing the element from functioning properly. Due to the causal relationship of insufficient zinc levels to taste disorders, research has been conducted to test the efficacy of zinc supplementation as a possible treatment for dysgeusia. In a randomized clinical trial, fifty patients suffering from idiopathic dysgeusia were given either zinc or a lactose placebo. The patients prescribed the zinc reported experiencing improved taste function and less severe symptoms compared to the control group, suggesting that zinc may be a beneficial treatment. The efficacy of zinc, however, has been ambiguous in the past. In a second study, 94% of patients who were provided with zinc supplementation did not experience any improvement in their condition. This ambiguity is most likely due to small sample sizes and the wide range of causes of dysgeusia. A recommended daily oral dose of 25–100 mg appears to be an effective treatment for taste dysfunction provided that there are low levels of zinc in the blood serum. There is not a sufficient amount of evidence to determine whether or not zinc supplementation is able to treat dysgeusia when low zinc concentrations are not detected in the blood.
If a cause can be identified for a burning sensation in the mouth, then treatment of this underlying factor is recommended. If symptom persist despite treatment a diagnosis of BMS is confirmed. BMS has been traditionally treated by reassurance and with antidepressants, anxiolytics or anticonvulsants. A 2016 Cochrane review of treatment for burning mouth syndrome concluded that strong evidence of an effective treatment was not available. Other treatments which have been used include atypical antipsychotics, histamine receptor antagonists, and dopamine agonists.
Treatment requires treating the underlying condition with dental treatments, physical therapy, and passive range of motion devices. Additionally, control of symptoms with pain medications (NSAIDs), muscle relaxants, and warm compresses may be used.
Splints have been used.
BMS is benign (importantly, it is not a symptom of oral cancer), but as a cause of chronic pain which is poorly controlled, it can detriment quality of life, and may become a fixation which cannot be ignored, thus interfering with work and other daily activities. Two thirds of people with BMS have a spontaneous partial recovery six to seven years after the initial onset, but in others the condition is permanent. Recovery is often preceded by a change in the character of the symptom from constant to intermittent. No clinical factors predicting recovery have been noted.
If there is an identifiable cause for the burning sensation (i.e. primary BMS), then psychologic dysfunctions such as anxiety and depression often disappear if the symptom is successfully treated.
At-home treatments include desensitizing toothpastes or dentifrices, potassium salts, mouthwashes and chewing gums.
A variety of toothpastes are marketed for dentin hypersensitivity, including compounds such as strontium chloride, strontium acetate, arginine, calcium carbonate, hydroxyapatite and calcium sodium phosphosilicate. Desensitizing chewing gums and mouthwashes are also marketed.
Potassium-containing toothpastes are common; however, the mechanism by which they may reduce hypersensitivity is unclear. Animal research has demonstrated that potassium ions placed in deep dentin cavities cause nerve depolarization and prevent re-polarization. It is not known if this effect would occur with the twice-daily, transient and small increase in potassium ions in saliva that brushing with potassium-containing toothpaste creates. In individuals with dentin hypersensitivity associated with exposed root surfaces, brushing twice daily with toothpaste containing 5% potassium nitrate for six to eight weeks reduces reported sensitivity to tactile, thermal and air blast stimuli. However, meta analysis reported that these individuals' subjective report of sensitivity did not significantly change after six to eight weeks of using the potassium nitrate toothpaste.
Desensitizing toothpastes containing potassium nitrate have been used since the 1980s while toothpastes with potassium chloride or potassium citrate have been available since at least 2000. It is believed that potassium ions diffuse along the dentinal tubules to inactivate intradental nerves. However, , this has not been confirmed in intact human teeth and the desensitizing mechanism of potassium-containing toothpastes remains uncertain. Since 2000, several trials have shown that potassium-containing toothpastes can be effective in reducing dentin hypersensitivity, although rinsing the mouth after brushing may reduce their efficacy.
Studies have found that mouthwashes containing potassium salts and fluorides can reduce dentine hypersensitivity, although rarely to any significant degree. , no controlled study of the effects of chewing gum containing potassium chloride has been made, although it has been reported as significantly reducing dentine hypersensitivity.
Nano-hydroxyapatite (nano-HAp) is considered one of the most biocompatible and bioactive materials, and has gained wide acceptance in dentistry in recent years. An increasing number of reports have shown that nano-hydroxyapatite shares characteristics with the natural building blocks of enamel having the potential, due to its particle size, to occlude exposed dentinal tubules helping to reduce hypersensitivity and enhancing teeth remineralization.
For this reason, the number of toothpastes and mouthwashes that already incorporate nano-hydroxyapatite as a desensitizing agent is increasing.
Succinyl choline, phenothiazines and tricyclic antidepressants causes trismus as a secondary effect. Trismus can be seen as an extra-pyramidal side-effect of metoclopromide, phenothiazines and other medications.
In-office treatments may be much more complex and they may include the application of dental sealants, having fillings put over the exposed root that is causing the sensitivity, or a recommendation to wear a specially made night guard or retainer if the problems are a result of teeth grinding.
Other possible treatments include fluorides are also used because they decrease permeability of dentin "in vitro". Also, potassium nitrate can be applied topically in an aqueous solution or an adhesive gel. Oxalate products are also used because they reduce dentin permeability and occlude tubules more consistently. However, while some studies have showed that oxalates reduced sensitivity, others reported that their effects did not differ significantly from those of a placebo. Nowadays, dentin hypersensitivity treatments use adhesives, which include varnishes, bonding agents and restorative materials because these materials offer improved desensitization.
Low-output lasers are also suggested for dentin hypersensitivity, including GaAlAs lasers and . They are thought to act by producing a transient reduction in action potential in C-fibers in the pulp, but Aδ-fibers are not affected.
In order for successful treatment of abrasion to occur, the aetiology first needs to be identified. The most accurate way of doing so is completing a thorough medical, dental, social and diet history. All aspects needs to be investigated as in many cases the cause of abrasion can be multi-factorial. Once a definitive diagnosis is completed the appropriate treatment can commence.
Treatment for abrasion can present in varying difficulties depending on the current degree or progress caused by the abrasion. Abrasion often presents in conjunction with other dental conditions such as attrition, decay and erosion however the below treatment is for abrasion alone. Successful treatment focuses on the prevention and progression on the condition and modifies the current habit/s instigating the condition.
If the aetiology of abrasion is due to habitual behaviours, the discontinuation and change of habit is critical in the prevention of further tooth loss. The correct brushing technique is pivotal and involves a gentle scrub technique with small horizontal movements with an extra-soft/soft bristle brush. Excessive lateral force can be corrected by holding the toothbrush in a pen grasp or by using the non-dominant hand to brush. If abrasion is the result of an ill-fitting dental appliance, this should be corrected or replaced by a dental practitioner and should not be attempted in a home setting.
There is currently no specified treatment for individuals suffering from otodental syndrome. Considering that there are many possible genetic and phenotypic associations with the condition, treatment is provided based on each individual circumstance. It is recommended that those affected seek ear, nose & throat specialists, dental health specialists, and facial oral health specialists immediately; in order to determine potential treatment options.
Common treatment methods given are:
- Dental treatment/management – which can be complex, interdisciplinary and requires a regular follow up. Tooth extraction(s)and if needed, medications may be administered for pain, anxiety, and anti-inflammation. The affected individual is usually placed on a strict and preventative dental regiment in order to maintain appropriate oral hygiene and health.
- Endodontic treatment – individuals consult with an endodontist to analyze the individuals dental pulp. Typically endodontic treatment proves to be difficult due to duplicated pulp canals within the affected teeth. There may be a need for multiple extractions as well. Dental prosthesis and/or dental implants may be necessary for individuals that lack proper oral function, appearance, and comfort.
- Orthodontic treatment – given the predicament of the size and location of the affected oral area, molars and canines, orthodontic treatment is generally required in order treat any problems associated with the individuals bite pattern and tooth appearance.
- Hearing aids – in some cases affected individuals will suffer from hearing imparities and it may be necessary for hearing aid use.
The functional prognosis is mostly good with those that suffer from otodental syndrome. Appropriate dental treatment, hearing aids, and visitation to necessary specialists are recommended. Quality of life may be affected by psychological and functional aspects. It is also recommended that genetic counseling be given to families that have or may have this condition.
Treatment of opioid tolerance and Opioid-Induced Hyperalgesia (OIH) differs but it may be difficult to differentiate these two conditions in a clinical setting where most pain assessments are done through simple scale scores. The treatment for OIH may be challenging because an inadequate number of quality studies exists possibly due to the complexity in diagnosis of OIH and challenges in working with patients on chronic opioids. Currently there is no single best treatment method for OIH and clinicians are advised to choose an appropriate therapy based on the unique clinical scenario and history of each patient.
One general treatment option is to reduce or discontinue the dose of opioid to see if OIH is improved. Opioid sparing or opioid switching, which is replacing the current opioid with another pharmacological agent such as morphine or methadone, has been reported to be effective in some studies but this may also increase the sensitivity to pain according to some case reports. Ketamine, a NMDA antagonist, has been shown to prevent the extended use of opioid in post-operative hyperalgesia when it is infused in a small amount perioperatively along with the opioid but there are also studies that show ketamine being ineffective in modulating hyperalgesia. Addition of the NSAID, especially some COX-2 inhibitors, or acetaminophen is also suggested as a possible treatment option.
Two small randomized controlled trials (RCTs) and one larger RCT (86 subjects) tested glutamine in the prevention of platinum treatment-induced neuropathy and showed promise. As of September 2013 a larger, placebo-controlled trial is running.
A 2013 systematic review of the use of acetyl-L-carnitine, glutamine, vitamin E, glutathione, vitamin B6, omega-3 fatty acids, magnesium, calcium, alpha lipoic acid and n-acetyl cysteine as anti-CIPN adjuvants concluded that "currently no agent has shown solid beneficial evidence to be recommended for the treatment or prophylaxis of CIPN."
A 2006 systematic review and a 2005 review by the UK Health Protection Agency each evaluated the evidence for various medical, psychological, behavioral, and alternative treatments for EHS and each found that the evidence-base was limited and not generalizable. The conclusion of the 2006 review stated: "The evidence base concerning treatment options for electromagnetic hypersensitivity is limited and more research is needed before any definitive clinical recommendations can be made. However, the best evidence currently available suggests that cognitive behavioural therapy is effective for patients who report being hypersensitive to weak electromagnetic fields."
As of 2005, WHO recommended that people presenting with claims of EHS be evaluated to determine if they have a medical condition that may be causing the symptoms the person is attributing to EHS, that they have a psychological evaluation, and that the person's environment be evaluated for issues like air or noise pollution that may be causing problems.
Oral antibiotics of the tetracycline class such as minocycline, doxycycline, and tetracycline have been recommended for CGPD. However, their use is limited by side effects such as nausea, vomiting, and sensitivity of the skin to sunlight. Tetracycline antibiotics are not recommended for children under the age of 8 since tetracyclines are known to deposit in teeth (thereby staining them) and impair bone growth in children. The use of calcineurin inhibitor creams such as tacrolimus or pimecrolimus on the skin is controversial and results have been mixed. Certain studies have found the use of topical calcineurin inhibitors led to resolution of CGPD whereas others found incomplete resolution or prolonged symptoms. Topical azelaic acid has also been used successfully to treat CGPD.
An important factor is whether the involved tooth is to be extracted or retained. Although the pulp is usually still vital, a history of recurrent periodontal abscesses and significantly compromised periodontal support indicate that the prognosis for the tooth is poor and it should be removed.
The initial management of a periodontal abscess involves pain relief and control of the infection. The pus needs to be drained, which helps both of these aims. If the tooth is to be removed, drainage will occur via the socket. Otherwise, if pus is already discharging from the periodontal pocket, this can be encouraged by gentle irrigation and scaling of the pocket whilst massaging the soft tissues. If this does not work, incision and drainage is required, as described in Dental abscess#Treatment.
Antibiotics are of secondary importance to drainage, which if satisfactory renders antibiotics unnecessary. Antibiotics are generally reserved for severe infections, in which there is facial swelling, systemic upset and elevated temperature. Since periodontal abscesses frequently involve anaerobic bacteria, oral antibiotics such as amoxicillin, clindamycin (in penicillin allergy or pregnancy) and/or metronidazole are given. Ideally, the choice of antibiotic is dictated by the results of microbiological culture and sensitivity testing of a sample of the pus aspirated at the start of any treatment, but this rarely occurs outside the hospital setting.
Other measures that are taken during management of the acute phase might include reducing the height of the tooth with a dental drill, so it no longer contacts the opposing tooth when biting down; and regular use of hot salt water mouth washes (antiseptic and encourages further drainage of the infection).
The management following the acute phase involves removing any residual infection, and correcting the factors that lead to the formation of the periodontal abscess. Usually, this will be therapy for periodontal disease, such as oral hygiene instruction and periodontal scaling.
In a study of patients receiving oxaliplatin treatment, only 4 percent of those also receiving intravenous calcium and magnesium (ca/mg) before and after each oxaliplatin dose had to discontinue treatment due to neurotoxicity, compared to 33 percent who were receiving intravenous placebo; onset of neuropathy was also significantly delayed in the ca/mg patients, and only 22 percent of the ca/mg patients had long-term CIPN of grade 2 or worse compared with 41 percent of those on placebo. Overall, trials of ca/mg infusion suggest there are no serious harmful side effects and it may be an effective preventative therapy — the number of patients so far studied is small, however, and confident conclusions cannot be drawn.
Some practitioners believe there would be evidence indicating anxiolytics to be helpful in treating children and adults with selective mutism, to decrease anxiety levels and thereby speed the process of therapy. Use of medication may end after nine to twelve months, once the person has learned skills to cope with anxiety and has become more comfortable in social situations. Medication is more often used for older children, teenagers, and adults whose anxiety has led to depression and other problems.
Medication, when used, should never be considered the entire treatment for a person with selective mutism. While on medication, the person should be in therapy to help them learn how to handle anxiety and prepare them for life without medication.
Antidepressants have been used in addition to self-modeling and mystery motivation to aid in the learning process.
With time the symptoms of ARFID can lessen and can eventually disappear without treatment. However, in some cases treatment will be needed as the symptoms persist into adulthood. The most common type of treatment for ARFID is some form of cognitive-behavioral therapy. Working with a clinician can help to change behaviors more quickly than symptoms may typically disappear without treatment. Also hypnotherapy may be used. In that it lessens the anxiety associated with food.
There are support groups for adults with ARFID.
In some cases Meige's syndrome can be reversed when it is caused by medication. It has been theorized that it is related to cranio-mandibular orthopedic misalignment, a condition that has been shown to cause a number of other movement disorders (Parkinon's, tourettes, and torticollis). This theory is supported by the fact that the trigeminal nerve is sensory for blink reflex, and becomes hypertonic with craniomandibular dysfunction. Palliative treatments are available, such as botulinum toxin injections.
Hormonal suppressive therapy with luteinizing hormone receptor agonists like leuprolide can be used to treat the seizure component, and are effective in most patients.
Surgery is offered if there is failure of medical therapy or rapid growth of lesion, with specific options including stereotactic thermocoagulation, gamma knife radiosurgery, and physical resection by transsphenoidal microsurgery. Surgical response is typically better when the seizure focus has been found by EEG to originate in or near the mass. The specific location of the lesion relative to the pituitary and infundibulum and the amount of hormonal disturbance at presentation can help predict risk of hypopituitarism following surgery.
Spacing is important to integrate, especially with self-modeling. Repeated and spaced out use of interventions is shown to be the most helpful long-term for learning. Viewing videotapes of self-modeling should be shown over a spaced out period of time of approximately 6 weeks.
Children can benefit from a four stage in-home treatment program based on the principles of systematic desensitization. The four stages of the treatment are record, reward, relax and review.
- In the record stage, children are encouraged to keep a log of their typical eating behaviors without attempting to change their habits as well as their cognitive feelings.
- The reward stage involves systematic desensitization. Children create a list of foods that they might like to try eating some day. These foods may not be drastically different from their normal diet, but perhaps a familiar food prepared in a different way. Because the goal is for the children to try new foods, children are rewarded when they sample new foods.
- The relaxation stage is most important for those children that suffer severe anxiety when presented with unfavorable foods. Children learn to relax to reduce the anxiety that they feel. Children work through a list of anxiety-producing stimuli and can create a story line with relaxing imagery and scenarios. Often these stories can also include the introduction of new foods with the help of a real person or fantasy person. Children then listen to this story before eating new foods as a way to imagine themselves participating in an expanded variety of foods while relaxed.
- The final stage, review, is important to keep track of the child's progress. It is important to include both one-on-one sessions with the child, as well as with the parent in order to get a clear picture of how the child is progressing and if the relaxation techniques are working.
Neutropenic vs non-neutropenic candidemia is treated differently.
An intravenous echinocandin such as anidulafungin, caspofungin or micafungin is recommended as first-line therapy for fungemia, specifically candidemia. Oral or intravenous fluconazole is an acceptable alternative. The lipid formulation amphotericin B is a reasonable alternative if there is limited antifungal availability, antifungal resistance, or antifungal intolerance.
In the US, neuroborreliosis is typically treated with intravenous antibiotics which cross the blood–brain barrier, such as penicillins, ceftriaxone, or cefotaxime. One relatively small randomized controlled trial suggested ceftriaxone was more effective than penicillin in the treatment of neuroborreliosis. Small observational studies suggest ceftriaxone is also effective in children. The recommended duration of treatment is 14 to 28 days.
Several studies from Europe have suggested oral doxycycline is equally as effective as intravenous ceftriaxone in treating neuroborreliosis. Doxycycline has not been widely studied as a treatment in the US, but antibiotic sensitivities of prevailing European and US isolates of "Borrelia burgdorferi" tend to be identical. However, doxycycline is generally not prescribed to children due to the risk of bone and tooth damage.
Discreditied or doubtful treatments for neuroborreliosis include:
- Malariotherapy
- Hyperbaric oxygen therapy
- Colloidal silver
- Injections of hydrogen peroxide and bismacine