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Critics of this concept argue that there are no quality studies showing that headaches in patients with SLE differ from those in the general population. A detailed definition of the term lupus headache is lacking, since the terms "severe" and "persistent" are not quantified. Narcotic analgesics are not recommended for migraines or other common headache types. Other definitions from the IHS do not include responsiveness to treatments as a diagnostic criterion. Migraine patients are typically adult women around age 40, a demographic group in which SLE is also more common.
Some (but not all) studies have shown an association between (migraine) headaches in SLE and associated Raynaud's phenomenon and/or anti-cardiolipin antibodies.
Further studies are needed however to prove the underlying assumption that cerebral vasospasm causes migraines in lupus patients.
There is no specific treatment for NDPH. Often they are treated similar to migraines.
A number of medications have been used including amitriptyline, gabapentin, pregabalin, propranolol, and topiramate. There are no prospective placebo controlled trials of preventive treatment. In those with migrainous features treatment may be similar to migraines.
Opiates, or narcotics, tend to be avoided because of their side effects, including the development of medication overuse headaches and potential for dependency. NDPH is often associated with medication overuse. To avoid the development of medication overuse headaches, it is advised not to use pain relievers for more than nine days a month.
NDPH, like other primary headaches, has been linked to comorbid psychiatric conditions, mainly mood and anxiety and panic disorders. The spectrum of anxiety disorders, particularly panic disorder, should be considered in NDPH patients presenting with psychiatric symptoms. Simultaneous treatment of both disorders may lead to good outcomes.
Medications within the tetracycline family, mexiletine, corticosteroids and nerve blocks are being studied. Occipital nerve block have been reported to be helpful for some people. 23/71 people had undergone a nerve block for their severe headache. The NDPH-ICHD group responded to the nerve block much more often (88.9%) than the NDPH with migraine features (42.9% responded to nerve block).
Most patients have persistent headaches, although about 15% will remit, and 8% will have a relapsing-remitting type. It is not infrequent for NDPH to be an intractable headache disorder that is unresponsive to standard headache therapies.
Lithium, methysergide, and topiramate are recommended alternative treatments, although there is little evidence supporting the use of topiramate or methysergide. This is also true for tianeptine, melatonin and ergotamine. Valproate, sumatriptan and oxygen are not recommended as preventative measures. Botulinum toxin injections have shown limited success. Evidence for baclofen, botulinum toxin, and capsaicin is unclear.
The other primarily recommended treatment of acute attacks is subcutaneous or intranasal sumatriptan. Sumatriptan and zolmitriptan have both been shown to improve symptoms during an attack with sumatriptan being superior. Because of the vasoconstrictive side-effect of triptans, they may be contraindicated in people with ischemic heart disease.
Management of neuropsychiatric lupus is similar to the management of neuropsychiatric disease in patients without lupus. Treatment depends on the underlying causes of a patient’s disease, and may include immunosuppressants, anticoagulants, and symptomatic therapy.
Primary headache syndromes have many different possible treatments. In those with chronic headaches the long term use of opioids appears to result in greater harm than benefit.
Tension-type headaches can usually be managed with NSAIDs (ibuprofen, naproxen), acetaminophen or aspirin. Triptans are not helpful in tension-type headaches unless the person also has migraines. For chronic tension type headaches, amitriptyline is the only medication proven to help. Amitriptyline is a medication which treats depression and also independently treats pain. It works by blocking the reuptake of serotonin and norepinephrine, and also reduces muscle tenderness by a separate mechanism. Studies evaluating acupuncture for tension-type headaches have been mixed. Overall, they show that acupuncture is probably not helpful for tension-type headaches.
It is important to recognize early that these drugs are causing DIL like symptoms and discontinue use of the drug. Symptoms of drug-induced lupus erythematosus generally disappear days to weeks after medication use is discontinued. Non-steroidal anti-inflammatory drugs (NSAIDs) will quicken the healing process. Corticosteroids may be used if more severe symptoms of DIL are present.
Tension headaches that do not occur as a symptom of another condition may be painful, but are not harmful. It is usually possible to receive relief through treatment. Tension headaches that occur as a symptom of another condition are usually relieved when the underlying condition is treated. Frequent use of pain medications in patients with tension-type headache may lead to the development of medication overuse headache or rebound headache.
As of 2013 tension headaches affect about 1.6 billion people (20.8% of the population) and are more common in women than men (23% to 18% respectively). Despite its benign character, tension-type headache, especially in its chronic form, can impart significant disability on patients as well as burden on society at large.
The most common chronic treatment method is the use of medicine. Many people try to seek pain relief from analgesic medicines (commonly termed pain killers), such as aspirin, acetaminophen, aspirin compounds, ibuprofen, and opioids. The long term use of opioids; however, appears to result in greater harm than benefit. Also, abortive medications can be used to "stop a headache once it has begun"; such drugs include ergotamine (Cafergot), triptans (Imitrex), and prednisone (Deltasone). However, medical professionals advise that abuse of analgesics and abortive medications can actually lead to an increase in headaches. The painkiller medicines help headaches temporarily, but as the "quick fix" wears off, headaches become more re-current and grow in intensity. These "rebound headaches" can actually make the body less responsive to preventive medication. The conditions keep worsening if one takes paracetamol, aspirin and non-steroidal anti-inflammatory drugs (NSAIDs) for 15 days a month or more. Therefore, analgesic and abortive medications are often advised for headaches that are not chronic in nature.
In general, any patient who has frequent headaches or migraine attacks should be considered as a potential candidate for preventive medications instead of being encouraged to take more and more painkillers or other rebound-causing medications. Preventive medications are taken on a daily basis. Some patients may require preventive medications for many years; others may require them for only a relatively short period of time such as six months. Effective preventive medications have been found to come from many classes of medications including neuronal stabilizing agents (aka anticonvulsants), antidepressants, antihypertensives, and antihistamines. Some effective preventive medications include Elavil (amitriptyline), Depakote (valproate), Topamax (topiramate), and Inderal (propranolol).
The most common medicines used to treat chronic (daily) headaches are called prophylactic medicines, which are used to prevent headaches. Such preventative medication is taken on a daily basis, even when a person may not have a headache. Prophylactic medicines are recommended for chronic headache patients because varied experiments prove that the medications "reduce the frequency, severity, and disability associated with daily headaches". A majority of the prophylactic medications work by inhibiting or increasing neurotransmissions in the brain, often preventing the brain from interpreting pain signals.
Preventative medicines include gabapentin (Neurontin), tizanidine (Zanaflex), fluoxetine (Prozac), amitriptyline (Elavil), and topiramate (Topamax). In testing, gabapentin was found to reduce the number of headache days a month by 9.1%. Tizanidine was found to decrease the average frequency of headaches per week, the headache intensity, and the mean headache duration. Through studies, Fluoxetine resulted in better mood ratings and "significant increases in headache-free days". Despite being associated with depression, antidepressants, such as amitriptyline, have been found to effectively treat "near-daily headaches" and numerous chronic pain conditions as well as improving mood and sleep—two possible triggers for chronic headache sufferers. One study found that the headache frequency over a 28-day period lowered for chronic headache patients on topiramate. Another medication to prevent headaches is botulinum toxin type A (BoNTA or BOTOX), which is given by injection instead of being taken orally. In a clinical study of botulinum toxin type A, patients participating in the 9-month treatment period with three treatments experienced headache frequency decreases up to 50%. As with all medications, the preventative medications may have side effects. Since different people respond to drugs differently, chronic headache sufferers may have to go through a "trial-and-error" period to find the right medications. The previously mentioned medicines can improve headaches, but physicians recommend multiple forms of treatments.
Antinuclear antibodies are usually positive in drug induced Lupus. Anti-Neutrophil Cytoplasmic antibodies (ANCA) can also be positive in association with certain drugs. Furthermore, Anti-Histone antibodies can also be positive in drug induced lupus.
Anti-Histone antibodies are positive in up to 95% of patients with drug induced lupus. DIThe most common medications associated with drug induced lupus are hydralazine, procainamide, isoniazid, methyldopa, chlorpromazine, quinidine, and minocycline.
MOH is common and can be treated. The overused medications must be stopped for the patient's headache to resolve. Clinical data shows that the treatment of election is abrupt drugs withdrawal, followed by starting prophylactic therapy. However, the discontinuation of overused drugs usually leads to the worsening of headache and the appearance of drug withdrawal symptoms (that greatly depend on the previously overused drugs and typically last from two to ten days and that are relieved by the further intake of the overused medication), which might reinforce the continuation of overuse. Where physical dependence or a rebound effect such as rebound headache is possible, gradual reduction of medication may be necessary. It is important that the patient's physician be consulted before abruptly discontinuing certain medications as such a course of action has the potential to induce medically significant physical withdrawal symptoms. Abruptly discontinuing butalbital, for example, can actually induce seizures in some patients, although simple over the counter analgesics can safely be stopped by the patient without medical supervision. A long-acting analgesic/anti-inflammatory, such as naproxen (500 mg twice a day), can be used to ease headache during the withdrawal period. Two months after the completion of a medication withdrawal, patients suffering from MOH typically notice a marked reduction in headache frequency and intensity.
Drug withdrawal is performed very differently within and across countries. Most physicians prefer inpatients programmes, however effective drug withdrawal may also be achieved in an outpatient setting in uncomplicated MOH patients (i.e. subjects without important co-morbidities, not overusing opioids or ergotaminics and who are at their first detoxification attempt). In the absence of evidence-based indications, in MOH patients the choice of preventive agent should be based on the primary headache type (migraine or TTH), on the drug side-effect profile, on the presence of co-morbid and co-existent conditions, on patient’s preferences, and on previous therapeutic experiences.
Following an initial improvement of headache with the return to an episodic pattern, a relevant proportion (up to 45%) of patients relapse, reverting to the overuse of symptomatic drugs.
Predictors of the relapse, and that could influence treatment strategies, are considered the type of primary headache, from which MOH has evolved, and the type of drug abused (analgesics, and mostly combination of analgesics, but also drugs containing barbiturates or tranquillisers cause significantly higher relapse rates), while gender, age, duration of disease and previous intake of preventative treatment do not seem to predict relapse rate.
MOH is clearly a cause of disability and, if not adequately treated, it represents a condition of risk of possible co-morbidities associated to the excessive intake of drugs that are not devoid of side-effect. MOH can be treated through withdrawal of the overused drug(s) and by means of specific approaches that focus on the development of a close doctor-patient relationship in the post-withdrawal period.
Treatment consists primarily of immunosuppressive drugs (e.g., hydroxychloroquine and corticosteroids). An interesting second line drug is methotrexate in its low-dose schedule. In 2011, the U.S. Food and Drug Administration (FDA) approved the first new drug for lupus in more than 50 years to be used in the US, belimumab. In addition to medicative therapy, due to the psychological and social impacts that Lupus may have on an individual, Cognitive Behavioural Therapy (CBT) has also been demonstrated to be effective in reducing stress, anxiety, and depression in lupus sufferers.
Neuropsychiatric systemic lupus erythematosus or NPSLE refers to the neurological and psychiatric manifestations of systemic lupus erythematosus. SLE is a disease in which the immune system attacks the body's own cells and tissues. It can affect various organs or systems of the body. It is estimated that over half of people with SLE have neuropsychiatric involvement.
The treatment of SLE involves preventing flares and reducing their severity and duration when they occur.
Treatment can include corticosteroids and anti-malarial drugs. Certain types of lupus nephritis such as diffuse proliferative glomerulonephritis require intermittent cytotoxic drugs. These drugs include cyclophosphamide and mycophenolate.
Hydroxychloroquine was approved by the FDA for lupus in 1955. Some drugs approved for other diseases are used for SLE 'off-label'. In November 2010, an FDA advisory panel recommended approving belimumab (Benlysta) as a treatment for the pain and flare-ups common in lupus. The drug was approved by the FDA in March 2011.
Avoiding sunlight in SLE is critical, since sunlight is known to exacerbate skin manifestations of the disease. Avoiding activities which induce fatigue is also important, since those with SLE fatigue easily and it can debilitating. These two problems can lead to people becoming housebound for long periods of time. Drugs unrelated to SLE should be prescribed only when known not to exacerbate the disease. Occupational exposure to silica, pesticides, and mercury can also worsen the disease.
Treatment largely depends upon individual disease progression and the nature of presenting symptoms. Antimalarials, corticosteroids, and other drugs may be prescribed, if deemed appropriate by the treating physician.
Of the phenomena occurring in neurosarcoid, only facial nerve involvement is known to have a good prognosis and good response to treatment. Long-term treatment is usually necessary for all other phenomena. The mortality rate is estimated at 10%
Polyarthritis is most often caused by an auto-immune disorder such as rheumatoid arthritis, amyloidosis, psoriatic arthritis, and lupus erythematosus but can also be caused by infection with an alphavirus such as chikungunya virus and Ross River virus. This condition is termed alphavirus polyarthritis syndrome. Sindbis virus, which is endemic in Northern Europe, Africa, the Middle East, and Australia, is the most widely distributed of the alphaviruses causing polyarthritis, though infection is usually mild or asymptomatic.
Most patients will maintain a diagnosis of undifferentiated connective tissue disease. However, about one third of UCTD patients will differentiate to a specific autoimmune disease, like rheumatoid arthritis or systemic sclerosis. About 12 percent of patients will go into remission.
Severe vitamin D deficiency has been associated with the progression of UCTD into defined connective tissue diseases. The presence of the autoantibodies anti-dsDNA, anti-Sm, and anti-cardiolipin has been shown to correlate with the development of systemic lupus erythematosus, specifically.