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)

Forty patients (33 male, 7 female) with refractory epilepsy were randomized to receive ascending weekly doses of adjunctive remacemide hydrochloride in a b.i.d. or q.i.d. regimen, or placebo for up to 1 month. Assessments included routine physical examination and laboratory tests, recording of adverse events and seizure frequency, and neuropsychological tests. Trough plasma concentrations of concomitant AEDs were measured at weekly intervals. Trough plasma concentrations of remacemide and its desglycinyl metabolite were measured before each dose increment, and complete 24-hour profiles were measured at steady state following administration of 600 mg day(-1)and 1200 mg day(-1). A daily dose of 1200 mg was well tolerated in a q.i.d. regimen and up to 800 mg was well tolerated in a b.i.d. regimen. The most common adverse events were dizziness, diplopia, dyspepsia and abdominal pain. On some occasions, these were considered to be related to raised concentrations of concomitant AEDs. No adverse effects were observed on seizure frequency. Neuropsychology tests revealed no significant changes. Remacemide and the desglycinyl metabolite demonstrated dose proportional pharmacokinetics over the dose range tested.
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PMID:Remacemide hydrochloride: a placebo-controlled, one month, double-blind assessment of its safety, tolerability and pharmacokinetics as adjunctive therapy in patients with epilepsy. 1116 51

Spontaneous intracranial hypotension (SIH) is typically manifested by orthostatic headaches that may be associated with one or more of several other symptoms, including pain or stiffness of the neck, nausea, emesis, horizontal diplopia, dizziness, change in hearing, visual blurring or visual field cuts, photophobia, interscapular pain, and occasionally face numbness or weakness or radicular upper-limb symptoms. Cerebrospinal fluid (CSF) pressures, by definition, are quite low. SIH almost invariably results from a spontaneous CSF leak. Only very infrequently is this leak at the skull base (cribriform plate). In the overwhelming majority of patients, the leak is at the level of the spine, particularly the thoracic spine and cervicothoracic junction. Sometimes, documented leaks and typical clinical and imaging findings of SIH are associated with CSF pressures that are consistently within limits of normal. Magnetic resonance imaging of the head typically shows diffuse pachymeningeal gadolinium enhancement, often with imaging evidence of sinking of the brain, and less frequently with subdural fluid collections, engorged cerebral venous sinuses, enlarged pituitary gland, or decreased size of the ventricles. Radioisotope cisternography typically shows absence of activity over the cerebral convexities, even at 24 or 48 hours, and early appearance of activity in the kidneys and urinary bladder, and may sometimes reveal the level of the leak. Although various treatment modalities have been implemented, epidural blood patch is probably the treatment of choice in patients who have failed an initial trial of conservative management. When adequate trials of epidural blood patches fail, surgery can offer encouraging results in selected cases in which the site of the leak has been identified. Some of the spontaneous CSF leaks are related to weakness of the meningeal sac, likely in connection with a connective tissue abnormality.
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PMID:Spontaneous intracranial hypotension. 1130 18

A 54-y-old man ingested 2 g of bulk laboratory diazepam and was treated with activated charcoal, enhanced diuresis and flumazenil infusion. The treatment resulted in awakening, but the patient had drowsiness, dysarthria, diplopia, and dizziness for 9 d. Blood levels of diazepam and its main metabolite, nordiazepam, were obtained for 1 mo. The half-lives in this benzodiazepine overdose were longer than those seen with therapeutic doses. Benzodiazepines should not be readministrated when patients awake after suicide attempts.
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PMID:Diazepam poisoning with one-month monitoring of diazepam and nordiazepam blood levels. 1138 64

The study on the efficacy and safety of gabapentin as an add-on therapy trial was performed in 10 refractory partial seizure cases at Prasat Neurological Institute, Thailand from September 1996 to July 1998. This was an open-labeled titration dose of gabapentin starting at 600 mg/day add-on to the previously prescribed conventional antiepileptic drugs (AEDs). In cases that seizures could not be controlled, gabapentin dose was increased by 300 mg per day every two weeks until the total dose of 3,000 mg or until the side effects became intolerable. The result revealed that gabapentin reduced frequency, duration and severity of seizures and also improved the patients' activities of daily living (ADL) even at the minimum dose of 600 mg. The optimal dose of gabapentin was in the range of 600 to 1,200 mg per day. Seven patients were seizure free at the end of the study. There were some precipitating factors that interfered with the efficacy of gabapentin in some patients such as stress, menstruation, fever, and alcohol intake. Weight gain, somnolence, nystagmus, and dizziness were the major adverse events in these patients, whereas ataxia, tremor, and diplopia were found with gabapentin in a dose higher than 1,800 mg/day. These adverse events were mild and transient. No patients withdrew from the study due to adverse drug reactions. In addition, gabapentin did not alter conventional AED blood level and routine laboratory parameters. In conclusion, gabapentin was effective and well tolerated as an add-on therapy in refractory partial epileptic Thai patients.
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PMID:Efficacy and safety of gabapentin as an add-on therapy in refractory partial epileptic patients. 1146 Sep 68

The safety and efficacy of endoluminal stenting in treating atherosclerotic vertebral artery disease was evaluated in 38 vessels in 32 patients. Indications for revascularization included diplopia (n = 4), blurred vision (n = 4), dizziness (n = 23), transient ischemic attacks (n = 4), drop attack (n = 1), gait disturbance (n = 1), headache (n = 2), and asymptomatic critical stenosis (n = 1). Success (< 20% residual diameter stenosis, without stroke or death) was achieved in all 32 patients (100%). One patient experienced a transient ischemic attack (TIA) 1 hr after the procedure. At follow-up (mean, 10.6 months), all patients (100%) were alive and 31/32 (97%) were asymptomatic. One patient (3%) had in-stent restenosis at 3.5 months and underwent successful balloon angioplasty. Endoluminal stenting of vertebral artery lesions is safe, effective, and durable as evidenced by the low recurrence rate. Primary stent placement is an attractive option for atherosclerotic vertebral artery stenotic lesions. Cathet Cardiovasc Intervent 2001;54:1-5.
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PMID:Vertebral artery stenting. 1155 40

The authors describe 2 cases of posterior fosa venous infarction. A 56-year-old woman with essential thrombocytemia presented with fluctuating complaints of headache, nausea, vomiting, left-sided numbness-weakness, and dizziness and became progressively stuporous. Cranial magnetic resonance imaging (MRI) showed bilateral parasagittal fronto-parietal and left cerebellar contrast-enhancing hemorrhagic lesions. On magnetic resonance venography, the left transverse and sigmoid sinuses were occluded. The second patient, a 39-year-old woman, presented with acute onset of diplopia, numbness of the tongue, vertigo, and right-sided weakness following a gestational age stillbirth. MRI revealed lesions in the right half of midbrain and pons and in the superior part of the right cerebellar hemisphere. Digital subtraction angiography showed right transverse and sigmoid sinus occlusion. The authors suggest that one should investigate the possibility of venous infarction in the presence of posterior fossa lesions that are often hemorrhagic and are not within any arterial territory distribution but respect a known venous drainage pattern. Recognition of the observed clinical and neuroimaging features can lead to earlier diagnosis and, potentially, more effective management.
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PMID:Venous infarction of brainstem and cerebellum. 1167 84

Spontaneous intracranial hypotension (SIH) is typically manifested by orthostatic headaches that may be associated with one or more of several other symptoms, including pain or stiffness of the neck, nausea, emesis, horizontal diplopia, dizziness, change in hearing, visual blurring or visual field cuts, photophobia, interscapular pain, and occasionally face numbness or weakness or radicular upper-limb symptoms. Cerebrospinal fluid (CSF) pressures, by definition, are quite low. SIH almost invariably results from a spontaneous CSF leak. Only very infrequently is this leak at the skull base (cribriform plate). In the overwhelming majority of patients, the leak is at the level of the spine, particularly the thoracic spine and cervicothoracic junction. Sometimes, documented leaks and typical clinical and imaging findings of SIH are associated with CSF pressures that are consistently within limits of normal. Magnetic resonance imaging of the head typically shows diffuse pachymeningeal gadolinium enhancement, often with imaging evidence of sinking of the brain, and less frequently with subdural fluid collections, engorged cerebral venous sinuses, enlarged pituitary gland, or decreased size of the ventricles. Radioisotope cisternography typically shows absence of activity over the cerebral convexities, even at 24 or 48 hours, and early appearance of activity in the kidneys and urinary bladder, and may sometimes reveal the level of the leak. Although various treatment modalities have been implemented, epidural blood patch is probably the treatment of choice in patients who have failed an initial trial of conservative management. When adequate trials of epidural blood patches fail, surgery can offer encouraging results in selected cases in which the site of the leak has been identified. Some of the spontaneous CSF leaks are related to weakness of the meningeal sac, likely in connection with a connective tissue abnormality.
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PMID:Spontaneous intracranial hypotension. 1189 6

Remacemide hydrochloride is a low-affinity, non-competitive N-methyl-D-aspartic acid (NMDA) receptor channel blocker, under investigation in epilepsy. This double-blind, placebo-controlled, multicentre study assessed the safety and efficacy of remacemide hydrochloride or placebo, as adjunctive therapy, in 252 adult patients with refractory epilepsy who were already taking up to three antiepileptic drugs (including an enzyme-inducer). Patients were randomized to one of three doses of remacemide hydrochloride (300, 600 or 1200 mg /day) or placebo Q.I.D., for up to 15 weeks. An increasing percentage of responders (defined as a reduction in seizure frequency from baseline of > or =50%) was seen with increasing remacemide hydrochloride dose. At 1200 mg /day, 23% of patients were responders compared with 7% on placebo. This difference was significant (P = 0.016), as was the overall difference between treatments (P = 0.038). Adverse events: dizziness, abnormal gait, gastrointestinal disturbance, somnolence, diplopia and fatigue were mild or moderate in severity. Carbamazepine and phenytoin plasma concentrations were well controlled and maintained within target ranges, with no evidence of improved seizure control due to increases in the concentrations of these drugs. A dose-dependent, significant, increase in responders following adjunctive remacemide hydrochloride compared with placebo was observed. Remacemide hydrochloride was well tolerated.
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PMID:Remacemide hydrochloride as an add-on therapy in epilepsy: a randomized, placebo-controlled trial of three dose levels (300, 600 and 1200 mg/day) in a Q.I.D. regimen. 1194 98

In 1978, Hoffman and Brookler published an article in The Laryngoscope to challenge prevailing views on the lack of diagnostic power of certain symptoms often reported by patients to neuro-otologists. Some of these 'under-rated neuro-otological symptoms' include complaints of non-rotational dizziness, blurred and double vision, and the development of visual motion hypersensitivity in patients with balance disorders. In this review, I revisit these visual symptoms in the light of new findings from our laboratory. Double vision due to skew eye deviation can indeed occur in peripheral vestibular disease when there is a large, acute peripheral imbalance of vestibular function. It is more frequent and severe in brain stem disease. In both cases, it is explained by disruption of the torsional vestibular ocular reflex. It is usually assumed that damage to the otolith underlies the emergence of skew diplopia, but recent evidence shows that the vertical canal system is likely to be partly responsible as well. The other 'under-rated symptom' revisited here is what patients describe as dizziness when watching moving objects or whilst walking in visually busy surroundings such as supermarkets. Recent work has shown that this 'visual vertigo' emerges in patients who, in addition to suffering from a vestibular disorder, have increased visual dependence. Visual dependence denotes subjects who preferentially use vision, as opposed to vestibular or proprioceptive input, for spatial orientation and postural control. We do not know as yet what makes some vestibular patients become extremely visually dependent. However, we have provided evidence for Hoffman and Brookler's impression that visually triggered complaints should not be summarily dismissed, as they often point to an underlying vestibular disorder.
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PMID:Under-rated neuro-otological symptoms: Hoffman and Brookler 1978 revisited. 1232 95

A case is presented of a 43-year-old female patient who presented with severe dizziness, neck pain and headache. Clinical examination revealed diplopia with a horizontal gaze. Plain skull radiographs showed an enlarged sella turcica with no abnormal intracraial calcifications. Pre and post contrast axial and post contrast coronal computerised tomography scans through the sella turcica were done. An enlarged sella turcica filled with cerebrospinal fluid was demonstrated.
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PMID:Empty sella syndrome: incidental findings at computerised tomography. 1278 30


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