Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0917816 (mental retardation)
 15,867 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The data emerging from our study are the following: the presence of an identifiable cause is important: complications like tuberous sclerosis or signs of marked cerebral damage represent an adverse risk factor for IE. The presence of epilepsy among relatives, evidence of pre- or perinatal cerebral damage, mental retardation, and early onset, long periods of uncontrolled seizures before starting an adequate therapy and frequency of seizures appear to be indicative of an adverse prognosis, since differences between the two groups of responsive or unresponsive patients are statistically significant. On the contrary, the occurrence of febrile convulsions in the past history does not seem to have an adverse prognosis. Temporal lobe epilepsy and IS bear the worst prognosis. ME, CPS, GTCS, SPS, LGS and PM have a progressively better outcome in responsiveness to AEDs. Concerning therapy in patients with IE, studies indicate the results of high dose monotherapy appear to be equal or better than with polypharmacy. Because of the gravity of the situation, trials with unconventional drugs have been performed, but it is too early to draw definite conclusions about the long-term usefulness of most of them. In conclusion, our data indicate that the appearance of an IE can be predicted utilizing the above mentioned criteria, considered either alone or in combination. The issue of IE remains undoubtedly an important one among the group of convulsive disorders. Further studies considering a greater number of patients and new therpeutic strategies are to be recommended.
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PMID:Intractable epilepsy: etiology, risk factors and treatment. 329 46

From a group of 66 patients with the Lennox-Gastaut syndrome, 12 whose manifestations had started after the 6th year of life were selected for study. These patients were observed clinically and electroencephalographically for an average period of 2.5 years. We concluded that the late-onset syndrome can: occur after a long interval between diffuse encephalopathy and the first clinical manifestations, with or without previous alterations in psychomotor development; be associated from the onset with serious mental retardation; exhibit simple, complex and mixed seizures similar to those observed in the early form. These patients can also: suffer complex and mixed epileptic seizures previously unreported; paroxysmal interictal EEG abnormalities that overlap those of the early form; and spike-slow wave complexes in the EEG that can be actived by hyperpnea. Our results demonstrate that the incidence of LGS after 6 years of age does not necessarily imply a lower frequency of organic antecedents, or better neuropsychomotor development up to the onset of the syndrome or the presence of a higher rate of nonspecific seizures (generalized or partial seizures, and mainly those with elaborate symptomatology). The critical and encephalographic expression of the syndrome, which is secondary and starts after the 6th year of age, may depend at least in part on the age when diffuse encephalopathy started.
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PMID:Secondary late-onset Lennox-Gastaut syndrome: a critical view. 646 53