Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0012833 (dizziness)
 9,689 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 70-year-old patient treated with oxcarbazepine experienced severe hyponatremia. The patient used oxcarbazepine (600 mg twice a day) concomitantly with diuretics (torasemide 10 mg and indapamide 1.25 mg once per day), perindopril, an angiotensin-converting enzyme inhibitor, and amlodipine, a Ca(2+) channel blocker. The patient complained of a nausea, malaise, diplopia, drowsiness, apathy, decreased diuresis (creatinine clearance - 41.51 ml/min), and exacerbation of epileptic seizures. Sodium concentration in the plasma was 113 mmol/l. The patient was hospitalized. It was suggested that a decrease in plasma sodium concentration was caused by oxcarbazepine used together with diuretics for six months. Oxcarbazepine-induced hyponatremia is reported in 22.2-50% of patients, although symptoms are present only in 5.9% of patients. The most common symptoms of central nervous system injury, experienced by patients, are drowsiness, dizziness, decreased cognitive function, coordination impairment, etc. Physicians not always in time pay proper attention to undesirable antiepileptic drug-induced effects, which can be dangerous.
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PMID:[A case of severe hyponatremia in a patient suffering from epilepsy and using oxcarbazepine]. 1696 31

This single-center analysis evaluated the efficacy of oxcarbazepine monotherapy in children and adolescents. A retrospective chart review identified 60 patients (male=33, female=27) aged 6 months to 17.8 years (mean age 8.2+/-4.7 years) with partial onset epilepsy receiving oxcarbazepine monotherapy. The range of oxcarbazepine dose was 6-71 mg/kg/day (mean 26.3+/-11.4 mg/kg/day). The duration of therapy ranged from 3 months to 8 years (mean duration 16.7+/-14.3 months). Fifty-one patients (85%) achieved>or=50% reduction in seizure frequency, and 25 of 60 patients (42%) achieved seizure freedom. Ten patients (16.67%) reported adverse events including drowsiness, aggressive behavior, ataxia, dizziness, diplopia, and leg cramps. No hyponatremia or skin rash was observed. Twenty-four patients were switched from carbamazepine to oxcarbazepine monotherapy. In these patients carbamazepine was discontinued because of incidence of adverse events, poor seizure control, or both. Seventy-nine percent of patients switched from carbamazepine to oxcarbazepine monotherapy had >or=50% reduction in seizure frequency, and 37.5% became seizure-free. These findings suggest that oxcarbazepine monotherapy is effective and well tolerated in children and adolescents with partial epilepsy.
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PMID:Oxcarbazepine monotherapy in children and adolescents: a single-center clinical experience. 1699 94

We report a case with a unilateral sudden sensorineural hearing loss caused by an infarction of brainstem and cerebellum. The patient was a 74-year-old male presented with a sudden onset of hearing loss and tinnitus in the right ear and dizziness. Steroid was administered on suspicion of idiopathic sudden deafness. However, the initial symptoms were deteriorated approximately 2 weeks later. He newly complained of the numbness of the right face and double vision, and he was transferred to our hospital for further evaluation. Neurological examination demonstrated horizontal nystagmus, diminution in the right facial sensation, right peripheral facial palsy, right hearing loss and cerebellar ataxia. Urgent MRI disclosed fresh infarctions of the right middle cerebellar peduncle and cerebellum localized in the territory of anterior inferior cerebellar artery. In general, idiopathic sudden deafness and Meniere's disease are frequent diagnosis in cases of sudden hearing loss with vertigo, but these symptoms may rarely be caused by cerebrovascular disorder. In patients with risk factors for arteriosclerosis, cerebrovascular disorder should be taken into consideration even if idiopathic sudden deafness may be suspected clinically. We emphasize the diagnostic importance of careful observation on neurological findings and early detection of radiological abnormalities on MRI.
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PMID:[Unilateral sudden deafness as a primary symptom of brainstem and cerebellar infarction]. 1705 10

Neurologic signs and symptoms are common in acute malarial infection. However, after the parasites have been cleared from the blood and patients recover full consciousness, neurologic or psychiatric symptoms may occur or recur within 2 months after the acute illness. This phenomenon is called "postmalaria neurologic syndrome" (PMNS). We present a 50-year-old man who returned from the Republic of Malawi and soon developed Plasmodium falciparum malaria. Cerebral malaria, renal failure, hepatic failure, diffuse intravascular coagulation with thrombocytopenia, and upper gastrointestinal bleeding were noted during the acute stage. He was admitted to the infectious diseases ward and treated for 3 weeks. He was free from clinical general symptoms and parasites in blood smear when discharged. However, 2 weeks after discharge, he began to experience severe headache, dizziness, diplopia, mild hand tremor, unsteady gait, and easy falling. When readmitted to the neurologic ward, he presented with irritability, delirium, visual hallucination, and strange behavior. Neurologic examination was normal except for mild general weakness and evident truncal ataxia when walking. Brain magnetic resonance imaging revealed no structural lesions, and electroencephalography showed diffuse cortical dysfunction. Cerebral spinal fluid profile exhibited cytoalbuminologic dissociation. Brain single photon emission computed tomography showed diffuse cerebral parenchymal disorder. Nerve conduction studies revealed early sensory predominant polyneuropathy. The unsteadiness persisted for the initial 2 weeks of hospitalization until corticosteroid was administered. Intravenous methylprednisolone (80 mg/day) was continued for 3 days, followed by oral prednisolone (45 mg/day). His unsteadiness improved gradually after medication, and he absconded from the hospital on the 9th day of corticosteroid treatment with clear consciousness and free ambulation. The manifestation of PMNS is diverse and may present as an acute confusional state or psychosis, generalized seizure, fine tremors, cerebellar syndromes, postural hypotension, or malarial polyneuritis. Although the neurologic syndrome is primarily self-limited in most cases, corticosteroid may be beneficial in reversing PMNS.
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PMID:Postmalaria neurologic syndrome: a case report. 1711 25

Whiplash-associated disorders are characterized by multiple physical complaints after a flexion-extension trauma to the neck. They are difficult to treat, and they often result in great impact on the patient's quality of life. In this paper, the comprehensive treatment of a patient with whiplash-associated disorders is presented. The purpose is to highlight the importance of accurate diagnosis and appropriate treatment plans to improve patients' quality of life. This 23-year-old woman experienced a traffic accident which caused severely painful neck disability, numbness over bilateral upper limbs, dizziness, double vision and loss of balance. Among these symptoms, dizziness was the problem that bothered the patient most. She received a comprehensive rehabilitation program including physical modalities, trigger point injections for relief of pain, as well as a vestibular rehabilitation program, which included exercises challenging and improving her balance function, head-eye coordination exercise, visual-ocular control exercise and sensory substitution-promoting exercises. She resumed her previous full-time work after 3 weeks of treatment. This successfully treated case illustrates the importance of correct diagnosis and appropriate treatment for patients who suffer from whiplash-associated disorders.
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PMID:Vestibular rehabilitation in a patient with whiplash-associated disorders. 1718 55

Oxcarbazepine is an antiepileptic drug that has been approved by the US FDA and is indicated for use as monotherapy or adjunctive therapy in the treatment of partial seizures in adults and children aged over 4 years. The aim of this report is to investigate the results of clinical trials in order to ascertain the efficacy and safety of oxcarbazepine for use in bipolar disorder and schizoaffective disorder. Oxcarbazepine is a keto-congener of carbamazepine with fewer side effects and drug interactions. Orally administrated oxcarbazepine is rapidly and completely absorbed and has a half-life of 9 h. Currently, there is a lack of controlled clinical trials studying the use of oxcarbazepine. In light of controlled and open-label prospective studies, it may be useful for manic symptoms in the treatment of bipolar and schizoaffective patients. Case reports, retrospective and prospective studies suggest that oxcarbazepine might have prophylactic efficacy and long-term benefit for these patients. In addition, owing to its lower propensity for drug interactions and side effects, it may be useful in the treatment of refractory patients with bipolar and schizoaffective disorder. However, most of the trials have relevant methodological shortcomings. The side-effect profile of oxcarbazepine is similar to carbamazepine, but the severity of these effects appears to be slightly less. The symptoms that are most frequently associated with the use of oxcarbazepine are asthenia, headache, dizziness, somnolence, nausea, diplopia and skin rash. Isolated cases of hyponatremic coma have been reported, thus electrolyte abnormalities should be closely monitored. Oxcarbazepine is now a generic drug, but the metabolite licarbazepine and other related compounds, such as eslicarbazepine, are currently being studied under controlled conditions and might become useful therapies for bipolar and schizoaffective disorder in the future.
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PMID:Oxcarbazepine in the treatment of bipolar and schizoaffective disorders. 1756 45

Many medicines, mainly with neurological purpose, interfere with the oculomotricity. The biochemistry of the oculomotor systems and thus, the mechanisms of action of these drug interferences are not completely clarified. Most medicines impair the eye movements at the level of their fine adjustment by feed-back loops implying the cerebellum. Quite often, the interferences remain asymptomatic, restricted to a saccadic pursuit, hypometric saccades or an end-point nystagmus. Sometimes however, symptoms of dizziness or oscillopsia appear, due to loss of the vestibulo-ocular reflexes efficiency. A diplopia or a blurred vision by double outline could be suggestive of an ocular motor paresis or a loss of the binocular fusion due to drugs action.
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PMID:[Oculomotor anomalies from medications]. 1771 42

A 37-year-old man presented with acute dizziness, nausea, headache and fever. Later on, he developed diplopia, swallowing difficulties, numbness and ataxia. MRI on day 6 showed hypo-intense, contrast-enhancing lesions on TI-weighted scans in the brainstem and cerebellum. Cerebrospinal fluid (CSF) findings on day 6 included pleiocytosis, a mildly-elevated protein level and mildly-decreased glucose level. CSF and blood cultures were initially negative for both bacteria and viruses. Acute disseminated encephalomyelitis (ADEM) was suspected and dexamethasone therapy was started. On day 26, a blood culture was positive for Listeria monocytogenes. The diagnosis 'Listeria rhombencephalitis' was made and the patient was treated with amoxicillin. This resulted in good recovery. In patients with a subacute onset of progressive cranial nerve dysfunction, ataxia, CSF pleiocytosis, and MRI lesions in the brainstem and cerebellum, Listeria rhombencephalitis should be considered. Early diagnosis and treatment improve the prognosis.
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PMID:[Rhombencephalitis due to Listeria monocytogenes]. 1790 63

Diabetes mellitus develops in about 10% of acromegalic patients, usually secondary to insulin resistance caused by growth hormone excess. Diabetic ketoacidosis is a result of relative insulin deficiency and is a rare feature of acromegaly. Here, we present one case of this disorder. A 57-year-old man came to the emergency room due to 2 weeks of dizziness. He also had polyuria, polydipsia, nausea, diplopia, blurred vision and dysarthria. His plasma glucose level was 32.06 mmol/L, plasma osmolarity was 322 mOsm/L, arterial pH was 7.30, level of bicarbonates was 18 mmol/L, urine ketones was 4+, and HbA1c was 14.1%. No specific cause for the development of this metabolic derangement could be found. He displayed clinical features of acromegaly during admission, which was confirmed by an elevated growth hormone level and pituitary macroadenoma shown on magnetic resonance imaging. The patient underwent total transsphenoid tumor removal 2 weeks later; plasma glucose levels became normal thereafter.
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PMID:Diabetic ketoacidosis in a patient with acromegaly. 1790 70

Lacosamide, (R)-2-acetamido-N-benzyl-3-meth- oxypropionamide, is a new chemical entity specifically synthesized as an anticonvulsive drug candidate, which appears to have a novel dual mode of action. Its pharmacokinetic characteristics have been studied in young and elderly healthy adults, as well as in adults with epilepsy or diabetic neuropathic pain. After oral administration, lacosamide is rapidly and completely absorbed. An elimination half-life of 13 hours allows for twice-daily dosing. Lacosamide has a low potential for drug-drug interactions. Both oral and intravenous formulations of lacosamide are being developed. In completed placebo-controlled clinical trials, lacosamide has demonstrated efficacy as adjunctive therapy for reduction of seizure frequency in patients with uncontrolled partial-onset seizures, and has been generally well tolerated. For patients treated with lacosamide, the most frequently reported adverse events in placebo-controlled trials include dizziness, headache, nausea and diplopia. When used as short-term replacement for oral lacosamide, intravenous lacosamide has a comparable safety profile to oral lacosamide. Results from clinical trials to date suggest that lacosamide may be a useful pharmacological treatment option for patients with partial-onset seizures.
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PMID:Lacosamide: an investigational drug for adjunctive treatment of partial-onset seizures. 1830 2


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