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)

Lamotrigine (LTG) as both effective against a wide range of seizure types and epileptic syndromes and well tolerated drug is being used in mono--as well as in polytherapy of pharmacoresistant epilepsy. The aim of this study was to evaluate the efficacy, safety and neuropsychological functioning after LTG (mean daily dose: 316 mg) as long-term monotherapy (12 mo) in 24 young adult out-patients (22.5 ys) with newly recognised and not-previously treated epilepsy in an open, non-comparative trial. 67% of patients were responders (above 50% reduction in seizure frequency) and 42% reported seizures remission. The best were results in patients with generalised convulsive fits (87% with remission). Adverse events in the early phase of medication in 21% of patients typically concerned CNS and gastrointestinal system (headache, asthenia, insomnia, nausea, gastric aches) and resolved spontaneously without treatment discontinuation. Biochemical examinations were normal and transient leucopenia and diminishion of MCV were clinically not significant. Neurodynamic abilities, neuropsychological examination results, memory verbal and visual tests and organic evaluation in organic triada tests did not show deterioration after LTG treatment. Slight difficulties in abstractive and operative thinking and some focal symptoms of fronto-temporal origin should be considered a result of drug but also the epilepsy per se. No significant differences in latencies and amplitudes of evoked potentials (VEP, BAEP, SEP and especially ERP-300) were measured after LTG. Preliminary results obtained in this study supported good efficacy and tolerability and especially lack of unfavourable influence of LTG on neuropsychological functioning in young previously untreated patients with epilepsy.
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PMID:Long-term monotherapy with lamotrigine in newly diagnosed epilepsy in adults. 1197 53

A 68-year-old man presented with right eye pain and vertigo. Thereafter, he gradually leaned rightward, then laid down. He felt nausea and vomited. His right upper eyelid drooped and he felt dysethesia of the right hand. On neurological examination, ptosis of his right eye with slightly miotic right pupil, paresis of the right soft palate and hoarseness were noted. Arm deviation test demonstrated rightward deviation. He presented sensory ataxia of the right upper and lower extremities: finger nose test showed mild dysmetria of the right upper extremity, heel knee test demonstrated dysmetria of right lower extremity and these findings worsened when he closed his eyes. He showed mild bending of his bilateral ring and little fingers when he did rapid alternative movement. He leaned rightward when he sat and closed his eyes. Position sense of his right upper and lower extremities was decreased and sometimes he could not answer correctly when asked on which direction his finger pointed. Pinprick sensation was mildly decreased on the left side not including the face. Touch and vibration sense were normal. SEP findings on upper and lower extremity stimulation were normal. MRI of the brain showed T2 high intensity and partially T1 low intensity lesion at the right medulla (Figure). MR angiography showed no apparent lesion of major arteries such as dissection of the vertebral arteries. He complained and presented with hiccup initially. On MRI, the lesion was thought to involve the spinothalamic tract, medial lemniscus and inferior olivary nucleus. Ambiguus nucleus was in the lesion and solitary nucleus near the lesion. There is no report that seems to describe clinical features of a lesion like that in this case. Intermediate medullary infarction may present dissociated sensory disturbance like Brown-Sequard syndrome and position sensory disturbance without disturbance of vibration sense.
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PMID:[Intermediate medullary infarction: a case report]. 1609 22