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 23,468 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sixty-four patients received systemic alpha-interferon (10 million units subcutaneously daily) and 63 received systemic acyclovir (5 mg/kg body weight intravenously thrice daily) in a randomized study of acute herpes zoster. Start of healing, complete healing, development of new skin lesions in the primarily affected and in other dermatomes, and degree and duration of pain were evaluated. Both drugs proved equally clinically efficient without statistically different findings between the two groups; herpes zoster neuralgia was not prevented by either interferon or acyclovir therapy. Minor clinical side effects occurred slightly more frequently during interferon treatment and included fever and nausea. Transient and moderate leukopenia was observed in nearly all patients in the interferon group.
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PMID:Treatment of herpes zoster. Recombinant alpha interferon versus acyclovir. 328 47

Methyl-GAG, a polyamine synthesis inhibitor, was prospectively evaluated in the treatment of advanced renal adenocarcinoma. Twenty-five patients with measurable disease received methyl-GAG weekly at a starting dose of 500 mg/m2 iv, with dose escalation by 50 mg/m2/week (maximum dose, 825). All 25 patients are evaluable for response. Four of these patients (16%) achieved responses including three partial responses and one complete response, with a median duration of 9 weeks (range, 4--15). Nine patients (36%) remained stable and 12 (48%) had progressive disease. In the four responders, regression of disease occurred within the first 4 weeks of therapy. Toxic effects were generally mild and included nausea or vomiting (68%), myalgia (44%), mucositis (40%), neuralgia (40%), weight loss (32%), diarrhea (24%), skin rash (8%), leukopenia (8%), and genital ulcers (4%). We conclude that methyl-GAG has clear, albeit limited, activity against renal adenocarcinoma.
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PMID:Phase I--II trial of methyl-GAG in the treatment of patients with metastatic renal adenocarcinoma. 722 67

The surgical treatment of greater occipital neuralgia often involves diagnostic anesthetic blockade, followed by chemical or surgical ablation of the greater occipital nerve. The anatomy of this region was studied in microdissections of 2 cadaver specimens. The diagnosis and management of a series of 5 patients with greater occipital neuralgia is discussed. Two patients were treated with atlanto-epistrophic ligament decompression of the C2 dorsal root ganglion and nerve; four patients had C2 ganglionotomy performed. All patients in this series had immediate complete relief of pain following surgery. Patients were followed for a mean of 24 months (range 7-33 months). One patient had a recurrence of her original pain after 26 months following atlanto-epistrophic ligament decompression and required re-operation in the form of bilateral C2 ganglionotomy. All patients experienced transient nausea and dizziness in the several days following surgery. One patient had an incisional cerebrospinal fluid leak. Microsurgical C2 gangliotomy is advocated as the preferred surgical treatment of greater occipital neuralgia of idiopathic origin.
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PMID:Surgical treatment of greater occipital neuralgia: an appraisal of strategies. 775 28

The objective of this study was to assist clinicians in the diagnosis of the occipital neuralgia syndrome by describing its clinical characteristics. Bibliographies and clinical descriptions of occipital neuralgia syndrome were identified through a review of literature published between 1966 and 1993. A prospective case series was performed by the authors in a university emergency department during a 1-year period. Patients with unilateral aching pain of the head, coupled with pain in the distribution of the occipital nerve, Tinel's sign, and relief of pain after local anesthetic injection, were included. Patients rated pain relief on a 10-point scale. Twelve patients met the criteria for occipital neuralgia and were included in the study. All patients reported at least 80% decrease of pain after injection, and 42% had complete relief. Clinical features, other than headache, that were common in patients included tinnitus in 33%; scalp paresthesia, 33%; nausea, 42%; dizziness, 50%; and visual disturbances, 67%. Occipital neuralgia is a benign extracranial cause of headache, and it may be confused with other more serious headache syndromes. Recognition depends on an understanding of the symptoms along with a careful history and physical examination. Local anesthetic injections produce significant relief of the headaches and can aid in the diagnosis of the syndrome.
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PMID:Occipital neuralgias: clinical recognition of a complicated headache. A case series and literature review. 1033 22

Syncope is defined as a temporary interruption of cerebral perfusion with a sudden and transient loss of consciousness and spontaneous recovery. Approximately one third of the population experiences syncope at least once during a lifetime. Presyncopal signs and symptoms, including weakness, headache, blurred vision, diaphoresis, nausea, and vomiting are sometimes present for seconds or minutes prior to loss of consciousness. After syncope, the patients may present with persisting drowsiness, headache, dizziness, nausea, but not usually confusion. Causes of syncope have been categorized as cardiovascular, non-cardiovascular, and unexplained. Cardiovascular causes can be subdivided into structural heart disease, coronary heart disease, and arrhythmia. Non-cardiovascular causes include neurological, metabolic, psychiatric and other disorders.Orthostatic hypotension - one of the most frequent causes of syncope - has manifold etiologies comprising various neurological and internal diseases. Orthostatic hypotension usually can be attributed to an impairment of peripheral vasoconstriction or to a reduction of the intravascular volume. Signs and symptoms, including the above prodromi are often present just after rising from a supine or sitting position. Frequently, blood pressure decreases significantly without an increase in heart rate. Autonomic cardiovascular modulation is often reduced. Many of the patients with "unexplained" syncope experience neurally mediated (i. e. neurocardiogenic or vasovagal) syncope. In these patients, cardiovascular control may be stable for an extended period of time during orthostatic stress, then there is a sudden decrease in blood pressure and heart rate. Neurocardiogenic or neurally mediated syncope can be associated with painful or emotionally stressful situations such as anxiety or fear, with prolonged standing or specific trigger situations such as micturition, defecation, coughing or sneezing, visceral or carotid sinus stimulation, or with trigeminal or glossopharyngeal neuralgia. So far, the mechanisms of neurocardiogenic syncope are not completely understood. The passive 60 degrees to 70 degrees head-up tilt test is useful for the diagnosis of orthostatic and neurally mediated syncope. The sensitivity of the test can be improved by additional pharmacological provocation, e. g. by isoproterenol, or by increased orthostatic stress using lower body negative pressure stimulation. For the treatment of syncope one should first consider non-pharmacological options. Patients with orthostatic hypotension should avoid rapid changes of the body position from supine to standing, as well as high room temperature or other situations inducing peripheral vasodilatation. An increased intake of sodium and fluids, mild physical exercise or so-called postural counter-maneuvers can improve orthostatic tolerance. Among the drugs recommended for pharmacologic treatment are mineralocorticoids (e. g. fludrocortisone), vasoconstrictor agents (e. g. ephedrine, midodrine), adenosine receptor blockers (theophylline) and beta2-blockers (propanolol), anticholinergic agents, e. g. scopolamine or disopyramide, and negative cardiac inotropes, e. g. beta1-adrenergic blockers or disopyramide. Serotonin reuptake inhibitors (e. g. fluoxetine, sertraline), alpha2-adrenergic agonists (clonidine), central nervous system stimulants such as methylphenidate or phentermine are thought to be beneficial in specific cases. Cardiac pacemakers often seem to be recommended without adequate indication. The antidiuretic, V2-receptor specific, vasopressin analogue desmopressin increases the intravascular volume. Erythropoietin improves anemia and red blood cell decrease and augments blood pressure and cerebral oxygenation. In postprandial hypotension, octreotide, a somatostatin analogue, prostaglandin inhibitors such as indomethacin or ibuprofen, as well as metoclopramide or two cups of coffee per day might be beneficial.
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PMID:[Syncope - a systematic overview of classification, pathogenesis, diagnosis and management]. 1182 26

The aim of the study was to consider Kimmerle anomaly (ponticulus posterior of the atlas) as an anatomic variant, which can cause a set of clinical symptoms and signs. A hundred and eight patients, 58 females and 50 males at the age of 18-59 years (M. 36.9 years, SD = 9.6) with radiologically verified Kimmerle anomaly were examined. A control group comprised 40 healthy subjects at the similar age range. The diagnosis of headaches was based on the criteria proposed by the IHS. A character of headaches, their localization, frequency, duration, number of days with headaches per year, circumstances associated with their onset and concomitant symptoms were evaluated. All the patients were subjected to electrophysiological studies (ENG, EEG and VEP). The results were statistically analyzed using a SPSS/PC+ computer system. It was revealed that clinical symptoms and signs in Kimmerle anomaly occurred most frequently in the third and fourth decade of life (65% of cases). These were most often tension-type headaches (50% of cases with headaches), vascular headaches (26% of cases) and neuralgia (24% of cases). Intensity of headaches was high. Headaches were accompanied by other complaints like vertigo (59% of cases) and in one third of cases--nausea. About 10% of patients also suffered from vomiting, paresthesia, dizziness, short periods of loss of consciousness. Sporadically--tinitus, drop attack, and vegetative symptoms. In cases without pain the most frequent signs were short periods of loss of consciousness, dizziness, and also nausea and dizziness. The EEG examination revealed pathology in 40% of patients with Kimmerle anomaly. The ENG examination in more than 33% of anomaly cases showed injury in the central part of vestibular system. Improper answers were reported in about 75% of the patients during the VEP examination.
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PMID:[Clinical symptoms and signs in Kimmerle anomaly]. 1242 70

A postherpetic-neuralgia patient abruptly discontinued pregabalin. Thirty hours later, unexplained nausea, headache, and ataxia developed, progressing to delirium 8 days later. Magnetic resonance imaging indicated T2-hyperintense lesions of her splenium. Similar magnetic resonance imaging abnormalities, interpreted as focal vasogenic edema, develop in some epileptic patients after rapid anticonvulsant withdrawal. Patients with high-altitude cerebral edema have similar splenial-predominant magnetic resonance imaging abnormalities that accompany these same neurological symptoms. This case is the first to associate anticonvulsant-withdrawal splenial abnormalities with neurological symptoms, with gabapentin-type anticonvulsants, and is among the first in nonepileptic patients, suggesting that sudden anticonvulsant withdrawal alone, unaccompanied by seizures, can initiate symptomatic focal brain edema. The similarity of this syndrome to high-altitude cerebral edema suggests a possible common pathophysiology and offers potential therapies.
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PMID:Pregabalin-withdrawal encephalopathy and splenial edema: a link to high-altitude illness? 1637 25

A 78-year-old man with severe chronic obstructive pulmonary disease presented to our pain medicine clinic for treatment of post herpetic neuralgia. Pharmacotherapy with tricyclic antidepressants, anticonvulsants, tramadol and traditional analgesics had failed, primarily due to adverse drug effects, particularly sedation, dizziness and nausea. Consequently, intravenous salmon calcitonin was administered, based on evidence of efficacy in the treatment of other neuropathic pain syndromes and its relatively benign side-effects profile. The patient reported immediate and sustained improvement in his post herpetic neuralgia for over two months, without adverse effects from the calcitonin therapy.
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PMID:Salmon calcitonin in the treatment of post herpetic neuralgia. 1706 47

Carisbamate is a novel drug with neuromodulator activity that is currently under development for the treatment of epilepsy, diabetic neuropathy and neuralgia. The compound possessed a promising pharmacological profile in tests in vivo, and demonstrated broad anticonvulsant activity in preclinical studies, both elevating seizure threshold and preventing seizure spread. Carisbamate was also effective in protecting against spontaneous recurrent seizures in kainate-treated animals and in genetic models of epilepsy, and displayed antiepileptic and neuroprotective activity in the lithium-pilocarpine model of status epilepticus. In a phase I clinical trial, orally administered carisbamate demonstrated efficacy at high doses of 500 to 1000 mg. A phase II clinical trial confirmed that oral carisbamate was efficacious at a 300- to 1600-mg dose range. The preliminary evaluations of carisbamate in humans indicated complete absorption, extensive metabolism, and carbamate ester hydrolysis. The most frequently reported side effects associated with carisbamate are dizziness, headache, somnolence and nausea. In clinical trials, carisbamate did not display any significant interactions with commonly used antiepileptic drugs such as carbamazepine, valproate and lamotrigine. At the time of publication, a phase III clinical trial for carisbamate in the treatment of epilepsy was ongoing, as well as phase II trials in neuropathy and neuralgia. Data from preclinical brain injury studies with carisbamate and the analog RWJ-333369-A have also been reported. This drug profile will focus on the development of carisbamate in epilepsy.
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PMID:Carisbamate, a new carbamate for the treatment of epilepsy. 1789 91

Vagoglossopharyngeal neuralgia is a rare pathology whose atypical forms, dominated by syncopal manifestations, are still rarer. Although the territory of the vagus nerve involves, beyond the cardiovascular system, the respiratory and the digestive systems, there is no report in literature of atypical forms other than syncopal. Therefore, the authors were prompted to report the case of a patient whose vagoglossopharyngeal neuralgia was predominantly revealed by digestive symptoms. A 58-year-old patient presented with stereotypical severe digestive disturbances including nausea, vomiting and diarrhoea. High definition cranial MRI showed a neurovascular conflict between the posterior inferior cerebellar artery and the IXth and Xth nerves, on the right side. A microsurgical decompression was carried out which confirmed the vascular compression and successful transposition of the artery. One year after the surgery, the patient was free from all painful and digestive symptoms. A survey of the literature did not find any reference to digestive symptoms together with the neuralgia; only a syncopal type of cardiac symptoms related to the parasympathetic nervous system were described. The hypothesis was that the revealing digestive symptoms are linked to a similar parasympathetic mechanism, implying the visceral component of the Xth cranial nerve.
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PMID:Vagoglossopharyngeal neuralgia revealed through predominant digestive vagal manifestations. Case report and literature review. 2717 88


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