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Query: UMLS:C0018681 (headache)
 56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Neuroaugmentative and neuromodulation therapy continues to expand. New applications are being found for existing technology, such as the use of SCS therapy in the treatment of head pain. The potential impact of existing therapies is enhanced by new discoveries as exemplified by the availability and demonstrated efficacy of different pharmacologic agents and combinations of agents in intrathecal therapy [39]. Increased attention is being paid to cortical stimulation, including motor cortex stimulation and deep brain stimulation. We must, however, not let our fascination for gadgets betray sound sense. The role of psychosocial factors in the outcome of more "objective" and measurable problems, such as spasticity and tremor versus pain, remains an open area of investigation. Although psychologic issues may not be as prevalent in the amelioration of such problems, they may influence the patient's overall level of satisfaction with the therapy and improvement in quality of life.
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PMID:Psychologic evaluation for patients undergoing neuroaugmentative procedures. 1456 42

Although much work is yet to be done in this area, nine general conclusions can be derived: 1. Local site-of-injection side effects from botulinum toxin injections are rare, assuming proper technique is used. 2. The two most common medication-related side effects from botulinum toxin orofacial injections are alterations in salivary consistency and inadvertent weakness of the swallowing, speech, and facial muscles. These complications are injection site-specific (eg, more common with lateral pterygoid injections and palatal and tongue muscle injections) and dose-dependent problems. These problems are bothersome but are not contraindications for the therapy if it is needed. 3. The data presented in this article are mostly case series-based and open trial-based information that is promising, but randomized, blinded, controlled trials are needed to establish the true efficacy of this method for the orofacial motor and pain disorders. 4. The novice should begin with injection of muscles he or she can inject with low risk of incorrect placement. The hard-to-find muscles should be avoided when starting out. The novice clinician should inject and dissect a few cadavers to improve injection technique. 5. The general latency for botulinum toxin type A is 1 week, its duration is 2 to 3 months, and it is recommended that injection be done no more than once every 12 weeks to avoid development of antibodies against the toxin. 6. Depending on the target muscle, injection dose is 10 to 50 U of Botox type A per site with a total dose of 200 U in the masticatory system. More than this can be used (400 U maximum) if other sites in the head and neck are included in the injection protocol. 7. Regarding injecting painful muscles that do not exhibit palpable muscle hardness or EMG-determined spasticity or observable involuntary movements but have chronic myofascial trigger points or the patient localizes them as the site of their chronic daily headache pain, botulinum toxin injections might be helpful used in this manner, but conclusive data for this controversial application of botulinum toxin are still missing. 8. Hemifacial spasm has the largest number of open-label, clinical trials, some of which have a 10-year follow-up. The conclusions reached by all of these reports is that treatment of hemifacial spasm with repeated injections of botulinum toxin has been highly successful and that the dose and relative effect of the injections are stable over time. 9. Although EMG-guided injection may be useful, EMG is neither practical nor needed in most situations for orofacial injections because most of the orofacial muscles are easily palpable muscles or have definitive bony landmarks to help with the localization process.
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PMID:The management of oromandibular motor disorders and facial spasms with injections of botulinum toxin. 1458 34

The diagnosis and management of pain in the patient with traumatic brain injury (TBI) can be difficult in light of the limitations imposed by the cognitive, language, and behavioral deficits. With patients in the acute rehabilitation setting, one must be vigilant for the often subtle signs and symptoms of pain. Causes more commonly seen in the population with TBI as a consequence of the injury itself include dysautonomia, neuropathic pain, spasticity, and heterotopic ossification. Headaches may be a consequence of TBI or associated with it for other reasons. Sources of pain associated with TBI include deep venous thrombosis and others. The reader is reminded that patients with TBI are subject to all the causes of pain that affect the general population.
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PMID:Clinical caveats on medical assessment and treatment of pain after TBI. 1473 29

Botulinum toxins are, as a group, among the most potent neuromuscular toxins known, yet they are clinically useful in the management of conditions associated with muscular and glandular over-activity. Botulinum toxins act by preventing release of acetylcholine into the neuromuscular junction. While botulinum toxin type A is commonly available, different manufacturers produce specific products, which are not directly interchangeable and should not be considered as generically equivalent formulations. Type B is also available in the market. Each formulation of botulinum toxin is unique with distinct dosing, efficacy and safety profiles for each use to which it is applied. Botulinum toxin type A is the treatment of choice based on its depth of evidence in dystonias and most other conditions. Botulinum toxin type A is established as useful in the management of spasticity, tremors, headache prophylaxis and several other neurological conditions. Active research is underway to determine the parameters for which the type B toxin can be used in these conditions, as covered in this review. Botulinum toxin use has spread to several fields of medicine.
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PMID:Botulinum toxins: pharmacology and its current therapeutic evidence for use. 1474 21

A 32-year-old man developed an extremely rare subdural hematoma after syringosubarachnoid shunting for syringomyelia. He presented with a 4-year history of neck pain and spastic paraparesis resulting from T-7 and T-8 vertebral body fracture suffered in a traffic accident at age 22 years. Magnetic resonance imaging revealed syringomyelia between the craniocervical junction and the T-10 level. The symptoms were slowly progressive, and a syringosubarachnoid shunting was performed. His spasticity improved after surgery, but he developed orthostatic headache 7 days after surgery. Magnetic resonance imaging of the brain demonstrated a thin subdural hematoma over the right cerebral convexity. The subdural hematoma resolved spontaneously within a week with conservative treatment. Vigorous cerebrospinal fluid outflow observed during surgery presumably lowered the pressure in the syrinx cavity, leading to significant but transient intracranial hypotension and consequently the formation of subdural hematoma.
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PMID:Subdural hematoma caused by intracranial hypotension after syringosubarachnoid shunting--case report. 1560 Feb 82

While pain is a common problem in multiple sclerosis (MS) patients, it is frequently overlooked and has to be asked for actively. Pain can be classified into 4 diagnostically and therapeutically relevant categories. 1. PAIN DIRECTLY RELATED TO MS: Painful paroxysmal symptoms like trigeminal neuralgia or painful tonic spasms are treated with carbamazepine as first choice, or lamotrigine, gabapentin, oxcarbazepine and other anticonvulsants. Painful "burning" dysaesthesia, the most frequent chronic pain syndrome, are treated with tricyclic antidepressants or carbamazepine, further options include gabapentin or lamotrigine. While escalation therapy may require opioids, the role of cannabinoids in the treatment of pain still has to be determined. 2. PAIN INDIRECTLY RELATED TO MS: Pain related to spasticity often improves with adequate physiotherapy. Drug treatment includes antispastic agents like baclofen or tizanidine, alternatively gabapentin. In severe cases botulinum toxin injections or intrathecal baclofen merit consideration. Physiotherapy and physical therapy may ameliorate malposition-induced joint and muscle pain. Moreover, painful pressure lesions should be avoided using optimally adjusted aids. 3. Treatment-related pain can occur with subcutaneous injections of beta interferons or glatiramer acetate and may be reduced by optimizing the injection technique and by local cooling. Systemic side effects of interferons like myalgias can be reduced by paracetamol or ibuprofen. 4. Pain unrelated to MS such as back pain or headache are frequent in MS patients and may be worsened by the disease. Treatment should be follow established guidelines. In summary, a careful analysis of the pain syndrome will allow the design of the appropriate treatment plan using various medical and non-medical options and thus will help to ameliorate the patients' quality of life.
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PMID:[Therapy of pain syndromes in multiple sclerosis -- an overview with evidence-based recommendations]. 1588 Mar 5

Botulinum toxin type A (BTX-A) is best known to neurologists as a treatment for neuromuscular conditions such as dystonias and spasticity and has recently been publicized for the management of facial wrinkles. The property that makes botulinum toxin type A useful for these various conditions is the inhibition of acetylcholine release at the neuromuscular junction. Although botulinum toxin types A and B (BTX-A and BTX-B) continue to find new uses in neuromuscular conditions involving the somatic nervous system, it has also been recognized that the effects of these medications are not confined to cholinergic neurons at the neuromuscular junction. Acceptors for BTX-A and BTX-B are also found on autonomic nerve terminals, where they inhibit acetylcholine release at glands and smooth muscle. This observation led to trials of botulinum neurotoxins in various conditions involving autonomic innervation. The article reviews the emerging use of botulinum neurotoxins in these and selected other conditions, including sialorrhea, primary focal hyperhidrosis, pathological pain and primary headache disorders that may be of interest to neurologists and related specialists.
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PMID:Expanding use of botulinum toxin. 1599 Jan 16

This study investigated the clinical manifestations and outcomes of central nervous system (CNS) infection by enteroviruses. Cases with CNS involvement among all enterovirus-culture-positive cases from January 1995 to June 2003 were retrospectively reviewed. Among 1028 enterovirus-culture-positive cases, there were 333 cases involving the CNS. Of these, the ratio of male to female subjects was 1.78, and the mean (+/- standard deviation) age was 6.83 +/- 5.9 years; 21 were premature neonates, and 10 failed to thrive. Disease entities included 282 cases of aseptic meningitis (84.7%), 44 cases of encephalitis (13.2%), and 7 cases of encephalomyelitis/polio-like syndrome (2.1%). Of these cases, 97.9% (326/333) had fever with peak body temperature at 38.9 degrees C, 85% had headache and vomiting, 70% had meningeal signs, 64% had neck stiffness, 16.6% (55/333) had change of consciousness, 5.4% (18/333) had seizures and 5.2% (17/333) had myoclonic jerks. Mannitol was administered in 77.2% of patients (257/333), along with intravenous immunoglobulin in 6.6% (22/333). Twelve cases received ventilator support. One patient died of hand-foot-and-mouth disease, encephalitis plus cardiopulmonary failure, and 2 premature neonates died of hepatic failure, disseminated intravascular coagulation, sepsis-like syndrome and myocarditis. Eighteen had neurologic sequelae, including 7 with limb weakness, 5 with epilepsy, 2 with sixth cranial nerve palsy, 3 with cerebral palsy, 4 with psychomotor retardation, 2 with spasticity, and 1 with hearing loss. Factors associated with unfavorable outcomes (death or sequelae) included younger age (p=0.0003), higher peak white blood cell count (WBC) [p=0.0009] and skin rash (p=0.005). Younger age and higher peak WBC were poor prognostic factors of severe enterovirus CNS infection. Death was related to neonatal enterovirus infection and enterovirus 71 infection in young children.
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PMID:Clinical features and factors of unfavorable outcomes for non-polio enterovirus infection of the central nervous system in northern Taiwan, 1994-2003. 1634 42

Botulinum toxin A (btxA) is widely used for cosmetic purposes, headaches, dystonia, spasticity, pain and other on and off label uses. Despite the widespread use of btxA in women of childbearing potential, there are few data on the effects of this drug on pregnant women and the fetus. The goal of this study was to survey physicians who use btxA, to determine their experience with pregnant women. We surveyed 900 physicians who used commercially available btxA. The questionnaire asked treating physicians if they had knowingly or unknowingly injected pregnant women and what was the outcome of each pregnancy. In total, 396 physicians (44%) returned questionnaires, of whom only 12 physicians reported injecting pregnant women with btxA. Sixteen pregnant women were injected, mostly in the first trimester, and only one patient, who had prior spontaneous abortions, suffered a miscarriage. Another woman had a therapeutic abortion. All other pregnancies went to term and there were no fetal malformations. Based on this limited survey of treating physicians in the USA, btxA appears to be relatively safe for both expectant mother and fetus. We need further data, however, and we would recommend that physicians and patients carefully consider the risks and benefits before using btxA in pregnant women.
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PMID:Botulinum toxin A during pregnancy: a survey of treating physicians. 1636 10

The flexion or flexor reflex (FR) recorded in the lower limbs in humans (LLFR) is a widely investigated neurophysiological tool. It is a polysynaptic and multisegmental spinal response that produces a withdrawal of the stimulated limb and resembles (having several features in common) the hind-paw FR in animals. The FR, in both animals and humans, is mediated by a complex circuitry modulated at spinal and supraspinal level. At rest, the LLFR (usually obtained by stimulating the sural/tibial nerve and by recording from the biceps femoris/tibial anterior muscle) appears as a double burst composed of an early, inconstantly present component, called the RII reflex, and a late, larger and stable component, called the RIII reflex. Numerous studies have shown that the afferents mediating the RII reflex are conveyed by large-diameter, low-threshold, non-nociceptive A-beta fibers, and those mediating the RIII reflex by small-diameter, high-threshold nociceptive A-delta fibers. However, several afferents, including nociceptive and non-nociceptive fibers from skin and muscles, have been found to contribute to LLFR activation. Since the threshold of the RIII reflex has been shown to correspond to the pain threshold and the size of the reflex to be related to the level of pain perception, it has been suggested that the RIII reflex might constitute a useful tool to investigate pain processing at spinal and supraspinal level, pharmacological modulation and pathological pain conditions. As stated in EFNS guidelines, the RIII reflex is the most widely used of all the nociceptive reflexes, and appears to be the most reliable in the assessment of treatment efficacy. However, the RIII reflex use in the clinical evaluation of neuropathic pain is still limited. In addition to its nocifensive function, the LLFR seems to be linked to posture and locomotion. This may be explained by the fact that its neuronal circuitry, made up of a complex pool of interneurons, is interposed in motor control and, during movements, receives both peripheral afferents (flexion reflex afferents, FRAs) and descending commands, forming a multisensorial feedback mechanism and projecting the output to motoneurons. LLFR excitability, mediated by this complex circuitry, is finely modulated in a state- and phase-dependent manner, rather as we observe in the FR in animal models. Several studies have demonstrated that LLFR excitability may be influenced by numerous physiological conditions (menstrual cycle, stress, attention, sleep and so on) and pathological states (spinal lesions, spasticity, Wallenberg's syndrome, fibromyalgia, headaches and so on). Finally, the LLFR is modulated by several drugs and neurotransmitters. In summary, study of the LLFR in humans has proved to be an interesting functional window onto the spinal and supraspinal mechanisms of pain processing and onto the spinal neural control mechanisms operating during posture and locomotion.
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PMID:The lower limb flexion reflex in humans. 1638 47


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