Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027497 (nausea)
 23,468 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The previously described anti-spastic effect of oxcarbazepine and 10,11-dihydro-10-hydroxycarbamazepine was found accidentally in 2 patients undergoing a double-blind comparative study for evaluation of antiepileptic effect. In this study oxcarbazepine was given orally in doses of 300-2700 mg daily to one patient with transverse myelitis and to two patients with multiple sclerosis, all of whom had clinically disabling spasticity in the form of difficulty in walking, lower limb rigidity, spastic contractions of the lower limbs and ankle clonus. Anti-spastic effect was observed at doses between 600-1200 mg daily and consisted in a substantial decrease in the above symptoms of spasticity. The anti-spastic effect appears at a dose immediately below that which produces nausea, dizziness and somnolence.
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PMID:Oxcarbazepine and spasticity: further observations. 307 37

Although cyclophosphamide pulse therapy has been reported to be beneficial for patients with chronic progressive multiple sclerosis for whom other treatment modalities are not expected to improve outcome, the experience with Japanese patients has not been shown in the literature. The reason appears due, in part, to the small size of this group and to the side effects inherent to such a large dose immunosuppressive regimen. Here, we report on 3 cases with chronic progressive multiple sclerosis who have undergone the pulse-dose cyclophosphamide treatment. The cases included 3 women, two with primary progressive multiple sclerosis (one, the classical form and the other, the spinal cord from). The 3rd case was that of myelitis-optic neuritic form and the total blindness of right eye (left side had been totally blind) was impending despite repeated corticosteroid therapies. The regimen included 600 mg/m2 intravenous cyclophosphamide per day at days 1, 2, 4, 6, 8 and infusion of totally 2,500-3,000 ml of intravenous fluid in order for avoiding hemorrhagic cystitis. The side effects were nausea, anorexia, leucopenia (10-15 days from the end of the course and the lowest value being 1,100/microliters), microscopic hematuria in one case, and alopecia in all. All the patients tolerated the therapy well. Two cases improved to a significant degree and the 3rd case with impending blindness has shown the arrest of progression. However, two of them began progressing again in one- to two-year period and the pulse-dose had to be repeated. These 3 cases have shown neurological improvements or at least arrest of the progression following the therapy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Pulse-dose cyclophosphamide therapy for chronic progressive multiple sclerosis]. 833 69

Intractable hiccup and nausea (IHN) was found in eight of 47 cases of relapsing neuromyelitis optica (NMO) (17%) but in none of 130 cases of multiple sclerosis (MS). IHN resolved with methylprednisolone. In six cases, MRI detected linear medullary lesions involving the pericanal region, the area postrema, and the nucleus tractus solitarius. Like long and centrally located myelitis, a linear medullary lesion causing IHN may distinguish NMO from MS.
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PMID:Intractable hiccup and nausea with periaqueductal lesions in neuromyelitis optica. 1627 42

Efalizumab is a recombinant humanised IgG1 kappa isotype monoclonal antibody against the CD11a molecule. Efalizumab is approved for the treatment of moderate-to-severe psoriasis and is currently administered as a weekly subcutaneous injection. Throughout October 2005, 19,000 patients were treated with efalizumab. According to the package insert that is based on 2762 subjects, the most common adverse reactions associated with efalizumab are a first dose reaction complex that includes headache, chills, fever, nausea and myalgia within two days following the first two injections. These reactions are dose-level-related in incidence and severity and were largely mild-to-moderate in severity when a conditioning dose of 0.7 mg/kg was used as the first dose. Adverse events occurring at a rate between 1 and 2% greater in the efalizumab group compared with placebo were arthralgia, asthenia, peripheral oedema and psoriasis. Efalizumab is associated with a rebound flare reaction in approximately 5% of patients when therapy is ceased. Antiefalizumab antibodies develop in approximately 5% of the subjects who were treated with efalizumab, but the clinical significance of these antibodies is unclear. Efalizumab has rare but serious haematological side effects. Immune-mediated thrombocytopenia platelet counts at or below 52,000 cells/microl have been observed in 0.3% of cases and monitoring of platelet counts monthly for the first 3 months of use and each 3 months thereafter. Reports of four cases of haemolytic anaemia diagnosed four to six months after patients started on the monoclonal antibody exist. Infrequent new onset or recurrent severe arthritis events, including psoriatic arthritis events, have been reported in clinical trials and postmarketing surveillance. Symptoms associated with a hypersensitivity reaction (e.g., dyspnoea, asthma, urticaria, angioedema, maculopapular rash) were rarely noted in the first 12 weeks of the controlled clinical studies. The overall incidence of malignancies of any kind was 1.8 per 100 patient-years for efalizumab-treated patients compared with 1.6 per 100 patient-years for placebo-treated patients. One case each of the following serious adverse reactions was observed: transverse myelitis, bronchiolitis obliterans, aseptic meningitis, idiopathic hepatitis, sialedenitis and sensorineural hearing loss. In the complete safety data from both controlled and uncontrolled studies, the overall incidence of hospitalis ation for infections was 1.6 per 100 patient-years for efalizumab-treated patients compared with 1.2 per 100 patient-years for placebo-treated patients. The rate of infection was 26% in the control group and 29% in treated cases. The most common findings on laboratory assessments in patients using efalizumab were reversible increases in lymphocyte count and total white blood cell. Efalizumab is a safe, effective, but expensive treatment for psoriasis.
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PMID:Efalizumab: a review of events reported during clinical trials and side effects. 1650 42

This paper will review the lumbosacral spine (L1-S5). Procedures performed in the lumbosacral spine include electromyography, spinal stimulator implants, spinal infusion implants for spasticity or pain medications, sacroiliac spine injections, facet blocks, and steroid injections. Complications from these procedures include iatrogenic paraplegia or paraplegia due to transverse myelitis, intravascular penetration, dural puncture, increased pain at the injection site, increased radicular pain, increased spine pain, lightheadedness, nausea, nonspecific headache, and vomiting. Long-term complications include implant infection, implant or catheter dislodgment/kinking, and device failure. This paper provides anatomically accurate schematics of innervations of the lumbosacral spine (L1-S5) that can be used to interpret magnetic resonance images of the muscles and nerves. Cross-sectional schematics of the lumbosacral spine were drawn as they appear on imaging projections. The relevant nerves were color coded. The muscles and skin surfaces were labeled and assigned the color of the appropriate nerves. An organized comprehensive map of the motor innervation of the lumbosacral spine allows the physician to increase the accuracy and efficacy of interventional procedures. This anatomical map could also assist the electromyographer in correlating the clinical and electrophysiological findings on magnetic resonance images.
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PMID:Sectional neuroanatomy of the lumbosacral spine (L1-S5). 1789

We describe the case of a 36-year-old woman who developed acute encephalo-myelitis after acute viral hepatitis type B. She was admitted to the hospital with a history of general malaise and nausea of 5 days duration. Her serum showed high transaminase levels and positive HBs-Ag and increased IgM HBc-Ab titers. She had urinary dysfunction, myoclonus and postural tremor of her extremities. Several days later, she developed bilateral limb ataxia and alteration of consciousness. The cerebrospinal fluid examinations showed pleocytosis and increased protein. Treatment with high-dose methylprednisolone resulted in a marked improvement of the clinical and CSF examination. Magnetic resonance imaging of the brain and the spinal cord did not disclose abnormal lesions. The symptoms and clinical course were quite similar to those of acute disseminated encephalomyelitis.
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PMID:Acute encephalomyelitis associated with acute viral hepatitis type B. 1921 76

Neuromyelitis optica (NMO) is a severe inflammatory, demyelinating disease, and its clinical characteristics include recurrent optic neuritis and longitudinally extensive transverse myelitis. The NMO-immunoglobulin (Ig) G auto-antibody (Ab), which binds to the aquaporin-4 (AQP4) water channel protein, is a marker for NMO. These clinical and immunological features have been used to distinguish NMO from multiple sclerosis (MS). In 1999, Wingerchuk et al. broadened the clinical criteria for diagnosing NMO to include "negative brain magnetic resonance imaging (MRI) at onset." However, after NMO-IgG/AQP4-Ab became a supportive criterion for diagnosing NMO, patients with NMO were frequently found to have symptomatic or asymptomatic brain lesions. In 2006, Pittock et al. reported that asymptomatic brain lesions were common in NMO, and that NMO brain lesions characteristically occurred in the hypothalamus and periventricular areas, which correspond to brain regions with high levels of AQP4 expression. Furthermore, Nakashima et al. detected abnormalities on brain MRI in 71% of NMO-IgG-positive Japanese patients. Patients with NMO have unique brain lesions that are clearly different from the lesions of patients with MS. In patients with NMO, involvement of the dorsal portion of the medulla oblongata causes intractable hiccups and nausea. Some studies described a hypothalamic lesion, and hypothalamic dysfunction could cause symptomatic hypersomnia, narcolepsy, and endocrinopathies. In some patients with NMO and NMO spectrum disorder who experience blood pressure fluctuations, vasogenic edema, manifesting as posterior reversible encephalopathy syndrome, may occur. In a recent report highlighting brain MRI with contrast enhancement, the most prominent feature that appeared to be a specific finding in NMO was "cloud-like enhancement" with multiple patchy enhancing lesions with a blurred margin. Another report showed that acute, large, edematous callosal lesions with heterogeneous intensity ("marbled pattern") occasionally occur in NMO. This review presents the characteristic clinical features of NMO according to the brain MRI findings and the features that can be used to distinguish NMO from MS.
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PMID:[Clinical features of NMO according to brain MRI findings]. 2084 4

A 45-year-old female was positive for anti-aquaporin-4 antibody with disturbance of consciousness, respiratory failure, and ophthalmoplegia associated with extensive brain stem involvement with intractable hiccup and nausea as an initial manifestation. Her level of consciousness and state of respiration worsened approximately one month later. There was no abnormality in the cerebrospinal fluid examination. A lesion was found in the medullary tegmentum on brain MRI. The patient received steroid pulse therapy and her level of consciousness improved the next day. However, her state of respiration worsened, and she had extensively clinical involvement of the brain stem. Her symptoms gradually improved with intravenous administration of prednisolone and intravenous immunoglobulin therapy (IVIg). The patient had almost completely recovered, but she relapsed with cervical myelitis extending over 3 vertebral segments approximately 10 months later. She underwent steroid pulse therapy, oral prednisolone, and IVIg again and improved.
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PMID:[Anti-aquaporin-4 antibody autoimmune syndrome with disturbance of consciousness, respiratory failure, and ophthalmoplegia associated with extensive brain stem involvement with intractable hiccup and nausea as an initial manifestation. A case report]. 2159 94

Neuromyelitis optica (NMO) is an inflammatory demyelinating disorder that predominantly affects the optic nerve and spinal cord; however, symptomatic brain involvement is not rare and is sometimes an initial manifestation in NMO. In this study, we investigated the characteristic features of patients with NMO with symptomatic brain involvement as the initial manifestation of disease (NMO(brain)) compared with patients with NMO who presented initially with optic neuritis or myelitis (NMO(ON/myelitis)). We retrospectively reviewed 27 consecutive Korean patients with NMO with aquaporin-4 antibodies. Patients with NMO(brain) (n=9) initially presented with intractable hiccup/nausea/vomiting and/or encephalopathy at a younger age than the patients with NMO(ON/myelitis) (n=18) (p<0.01). During the disease course, the patients with NMO(brain) continued to show more frequent symptomatic involvement of the brain than the 18 patients with NMO(ON/myelitis) (p<0.05). At the final visit, the mean age was also significantly lower in patients with NMO(brain) than in patients with NMO(ON/myelitis) (p<0.01); however, the Expanded Disability Status Scale scores, used to evaluate disease progression, were not different between the two groups. Our study suggests that patients with NMO who present initially with symptomatic brain involvement may have earlier disease onset and become disabled at a younger age compared to patients with typical NMO. Additional large scale prospective studies are warranted.
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PMID:Symptomatic brain involvement as the initial manifestation of neuromyelitis optica. 2367 42

Brainstem involvement, especially the medulla oblongata (MO), has been reported in neuromyelitis optica spectrum disorders (NMOSDs). The purpose of this study was to investigate retrospectively and compare clinical, laboratory, and imaging features of NMOSDs with and without MO lesions. A total of 170 patients with NMOSDs were enrolled, including 44 patients with MO lesions and 126 patients without MO lesions. Clinical features, laboratory tests, and magnetic resonance imaging findings among these patients were assessed. MO lesions were found in 25.9 % of the NMOSDs patients. The mean duration was 13 months. Patients with MO lesions had a higher Annualized relapse rate and Expanded Disability Status Score Scale. Headache, dizziness, nystagmus, dysarthria, intractable hiccup and nausea, choking cough or dysphagia, movement disorders, and neuropathic pain were more common in MO lesion patients. Patients with MO lesions were more frequently complicated with thyroid diseases. Multiple brain involvement, More importantly, Longitudinally extensive transverse myelitis were more frequently found in patients with MO lesions. MO lesions might be a symbol of more severe neurologic deficits and worse prognosis of NMOSDs.
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PMID:Comparative clinical characteristics of neuromyelitis optica spectrum disorders with and without medulla oblongata lesions. 2460 71


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