Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

When administering anticonvulsive drugs to the elderly, a number of peculiarities should be taken into consideration. Age-related changes in pharmacokinetics and drug interactions can make such treatment a complicated issue. Some of the side effects which hardly play a role among younger patients can lead to fatal consequences among the elderly. Both phenytoin (PHT), if submitted intravenously (but not in oral form), and carbamazepine (CBZ) may cause life-threatening cardiac arrhythmias. Valproate (VPA), otherwise well tolerated, seems to be less effective than CBZ and PHT in partial seizures. Cognitive dysfunction is a known side effect of barbiturates, but also seems to occur among the other drugs of first choice. In contrast to a widely held opinion, VPA, CBZ and PHT hardly differ in their effect on cognitive function if administered correctly.
 ...
PMID:[Anticonvulsant treatment in old age--principles and differential indications]. 927 44

Epileptiform discharges are found in dementia, specially in Alzheimer's disease. Most of these seizures are tonic-clonic. Triphasic waves can occur in Alzheimer's disease, although they are most often seen in metabolic disorders, particularly hepatic dysfunctions. While there is a good correlation between the severity of EEG abnormalities and cognitive impairment, epileptiform discharges or triphasic waves are not predictive factors for seizures. Finally, the EEG is often useful in the evaluation of dementia and it can aid in differentiating between a degenerative disorder and pseudo-dementia due to toxic-metabolic disorders. However, the EEG does have limitations and the most common abnormalities such as diffuse slowing are not specific and occur in many different types of dementia.
 ...
PMID:[Dementia and late epileptic seizures]. 938 Oct 38

The treatment of epileptiform abnormalities in the absence of obvious seizures has, in the past, been dismissed as "EEG cosmetics." The work on transitory cognitive impairment has highlighted the importance of asking the question: "What is a seizure?" The extent to which epileptiform discharges cause temporary or permanent impairment, profoundly influences decisions on whether to treat with antiepileptic medication or surgery.
 ...
PMID:The therapeutic dilemma: treating subtle seizures or indulging in electroencephalogram cosmetics? 942 54

Depressions of regional cerebral metabolism beyond the epileptogenic zone have been demonstrated in patients with intractable temporal lobe epilepsy. However, their clinical relevance, and the causes of prefrontal metabolic asymmetries are less well understood. We investigated 96 temporal lobe epilepsy patients by FDG-PET and neuropsychological assessment who had a corresponding unilateral temporal hypometabolism, left hemisphere speech dominance, full scale IQ of > 70 and no extratemporal lesion in MRIs. The regional glucose metabolism was determined in each patient in homologous regions including prefrontal cortex, and normalized to whole brain metabolism. Regional differences of > 10% were regarded as asymmetrical. Prefrontal metabolic asymmetries were more frequent in patients with left temporal lobe epilepsy (21 left, six right) and a history of secondarily generalized seizures. A multivariate analysis of variance revealed a main effect for prefrontal metabolic asymmetry on neuropsychological 'frontal lobe measures', including verbal and performance intelligence measures. Prefrontal metabolic asymmetry was not related to 'measures of episodic memory', presence of psychiatric symptoms or frontal interictal epileptiform discharges. We conclude that prefrontal metabolic asymmetry is associated with cognitive impairment. Patients with temporal lobe epilepsy of the left speech dominant hemisphere and a history of secondarily generalized seizures are at considerable risk of developing prefrontal metabolic asymmetry.
 ...
PMID:Prefrontal asymmetric interictal glucose hypometabolism and cognitive impairment in patients with temporal lobe epilepsy. 944 82

Old age is recognized to be the commonest time in life to develop epilepsy. There is a perception that older patients are more sensitive to the deleterious cognitive effects of antiepileptic drugs (AEDs). Elderly patients (median age 70 years, range 60-88 years) taking anticonvulsant monotherapy (10 carbamazepine [CBZ], 8 sodium valproate [VPA], 5 phenytoin [PHT]) took an extra dose of their usual medication (200mg CBZ, 500mg VPA, 100mg PHT) and matched placebo each for a month in random order. The concentrations of AEDs were higher after 7 and 28 days of active treatment compared with placebo (7 days: CBZ 9.5 vs. 7.8 mg L(-1), p < 0.05; VPA 97 vs. 64 mg L(-1), p < 0.05; PHT 13 vs. 11 mg L(-1), p < 0.05; 28 days: CBZ 9.4 vs. 7.7 mg L(-1); p < 0.01, VPA 85 vs. 60 mg L(-1), p < 0.05; PHT 16 vs. 13 mg L(-1), p < 0.05). Despite these increases in concentration, there were no significant changes in attention, reaction time, finger tapping, memory, side-effect scale or sedation scoring during the active phases compared with placebo phases for the three drugs analysed together and separately. Elderly patients taking standard AEDs as monotherapy did not develop cognitive impairment when the dose was modestly increased within the target range for each drug.
Seizure 1998 Apr
PMID:Cognitive effects of anticonvulsant monotherapy in elderly patients: a placebo-controlled study. 962 8

We report three children with pure congenital hemiplegia found to have congenital bilateral perisylvian polymicrogyria (CBPP). None of our patients had the seizures, oromotor dysfunction, or cognitive impairment usually associated with CBPP. CBPP may be more common and heterogeneous than previously thought, is easily recognized by MRI, and should be included in the differential diagnosis of the young child presenting with congenital hemiplegia.
 ...
PMID:Congenital bilateral perisylvian polymicrogyria presenting as congenital hemiplegia. 963 45

Electrophysiological studies of the rodent hippocampus show that repeated seizure activity has a profound, deleterious effect on an important form of synaptic plasticity (long-term potentiation, LTP) which has been suggested to underlie memory formation. It appears that seizure activity incrementally causes an indiscriminate and widespread induction of long-term potentiation, consuming and thereby reducing overall hippocampal plasticity available for information processing. Consistent with this finding, severe deficits in a form of learning known to be mediated by hippocampal function are observed in rat subjected to repeated electroconvulsive seizures (ECS). The effect on synaptic function gradually resolves over a period of around 40 days, paralleling the time course of the transitory cognitive impairment seen following electrical seizure induction (ECT) in humans being treated for severe affective disorder. The effect is likely to be mediated by NMDA receptor activation during seizure activity, as the phenomenon can be prevented by the administration of a non-competitive NMDA receptor associated channel blocker (ketamine) immediately before seizure induction. The mechanisms described may account for the inter-ictal cognitive disturbance observed in patients suffering from poorly controlled epilepsy.
Seizure 1997 Oct
PMID:Seizures, memory and synaptic plasticity. 966 98

We present the clinical and electrographic data of 17 patients with reading-induced seizures documented with ictal video-EEG studies during provocation with language related tasks. The median age at onset was 15 years (range 11-22 years) and the male:female ratio was 2.4. Fourteen patients had no spontaneous seizures of any type while the remaining three had infrequent generalized tonic-clonic seizures during nocturnal sleep. Two distinct electroclinical ictal patterns were confirmed on video-EEG analysis. (i) Fifteen patients had reading-induced jerks which invariably involved the region of the jaw but also included the upper limbs in five of them. Ictal EEG discharges were noted in 12 patients; these were brief but varied in terms of morphology and spatial distribution, with a clear tendency for left-sided predominance. All but one of these patients had similar myoclonic seizures induced by linguistic activities other than reading, the phenomenon probably justifying the term 'language-induced epilepsy'. Some patients had evidence of transient cognitive impairment associated with the reading-induced jaw or limb jerks. Three patients had a sibling with reading epilepsy but there was no other family history of epileptic seizures. (ii) Two patients had reading-provoked paroxysmal alexia without motor symptoms, associated with prolonged focal ictal EEG abnormalities. Reading provoked a subclinical, continuous and reproducible EEG activation over the left posterior temporal area. We propose that ictogenesis in reading or language-induced epilepsy is based on the reflex activation of a hyperexcitable network that subserves the function of speech and extends over multiple cerebral areas on both hemispheres. The parts of this network responding to the stimulus may, secondarily, drive the relative motor areas producing the typical regional myoclonus. This network hyperexcitability can be genetically determined and its clinical expression is age-related.
 ...
PMID:The variants of reading epilepsy. A clinical and video-EEG study of 17 patients with reading-induced seizures. 971 4

Congenital ornithine transcarbamylase (OTC) deficiency is the most common inborn error of urea cycle enzymes in humans. A large percentage of survivors of neonatal OTC deficiency suffer severe developmental disorders, including seizures, mental retardation and cerebral palsy. Neuropathological studies reveal ventricular enlargement, cerebral atrophy and delayed myelination, as well as Alzheimer type II astrocytosis. Using the sparse-fur (spf) mouse model of congenital OTC deficiency, studies of central cholinergic integrity revealed a developmental delay in choline acetyltransferase activity and of high-affinity [3H]-choline uptake in several brain structures. Subsequent studies of muscarinic cholinergic binding site distribution showed a widespread loss of M1 sites, consistent with cholinergic cell loss. These alterations are similar to those reported in Alzheimer's disease, suggesting that the severe cognitive dysfunction in congenital OTC deficiency may at least partly result from a muscarinic cholinergic lesion. Possible mechanisms involved in the pathogenesis of cholinergic cell loss in congenital OTC deficiency include ammonia-induced inhibition of pyruvate and alpha-oxoglutarate oxidation, resulting in decreased synthesis of acetyl CoA and a cerebral energy deficit, as well as NMDA receptor-mediated excitotoxicity. Treatment of spf mice with acetyl-L-carnitine (ALCAR) results in partial recovery of the developmental choline acetyltransferase deficit, suggesting a potential therapeutic benefit of ALCAR in congenital OTC deficiency. Other therapies currently used include ammonia-lowering strategies (using sodium benzoate or sodium phenylacetate) and, in severe cases, liver transplantation.
 ...
PMID:Evidence for a central cholinergic deficit in congenital ornithine transcarbamylase deficiency. 977 87

Adverse effects associated with antidepressant drug therapy rarely cause significant morbidity or mortality. Nevertheless, the successful management of patients with depression requires recognition of potential adverse effects that have serious consequences, which include the discontinuation of otherwise effective therapy. The aim of this overview is to highlight the more common and potentially deleterious adverse effects of both older and newer classes of antidepressant drugs. Major adverse effects attributed to the tricyclic antidepressant drugs (TCAs) include conduction defects and lethal overdose. Most worrisome with the selective serotonin reuptake inhibitor drugs (SSRIs) is the serotonin syndrome. Although rare, this syndrome can be insidious and lethal. Recent trends toward the use of medication combinations and augmentation therapies significantly enhance the risk of serotonin syndrome. Cognitive impairment also may occur, especially with the TCAs. Apathy is occasionally a problem with SSRI therapy. The syndrome of inappropriate antidiuretic hormone (SIADH) has been reported with most antidepressant drugs but appears to be more common with serotonergic agents and in elderly patients. Although seizures are uncommon in patients receiving antidepressant therapy, the risk must be understood by both the patient and the clinician. Adverse effects related to sexual function are common, especially with TCAs, SSRIs, and venlafaxine. Sexual dysfunction often leads to noncompliance and self-discontinuation of therapy. Sleep disturbances are common in patients with depression, and recent data illustrate how crucial sleep regulation is to mood. Antidepressant drugs vary in their sleep effects. Although antidepressant drugs can cause a variety of adverse effects, these drugs save lives and their benefits far exceed their risks.
 ...
PMID:Antidepressant drugs: disturbing and potentially dangerous adverse effects. 979 63


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>