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)

Distinguishing epileptic events from nonepileptic paroxysmal neurologic events represents a common diagnostic challenge. Syncope, either cardiac or noncardiac, can appear similar to atonic and even convulsive seizures. Breath holding and benign paroxysmal vertigo in children may be confused with epilepsy. Classic migraine, transient global amnesia, and transient ischemic attacks may resemble epileptic seizures. Sleep disorders, including nocturnal movements, parasomnias, and narcolepsy also may resemble epileptic seizures. Most movement disorders are distinguished easily from epilepsy; however, paroxysmal dyskinesias may resemble atonic or reflex seizures. The correct diagnosis can be established and appropriate treatment can be instituted by relying on routine and prolonged EEG, EKG, and sleep studies, when appropriate.
 ...
PMID:Differential diagnosis of seizures. 827 29

The frequency of some episodic psychic symptoms (dysmnesic, perceptual, and experiential) was determined in a 2,500-subject general population sample. Correlations with some risk factors eventually associated with nervous system dysfunctions (seizure history, head injury, car accident, hospitalization, febrile illness, and birth injury) were calculated. Subjects with one or several risk factors were more likely to report episodic psychic phenomena in daily life. Significant correlations of episodic psychic phenomena with sleep disorders, headache, allergies, and a history of learning disabilities were observed. We propose that some subclinical dysfunctions can be associated with the appearance of episodic psychic phenomena in otherwise normal subjects.
 ...
PMID:Episodic psychic symptoms in the general population. 842 45

Circadian modulation of seizure threshold is subjected to a multitude of periodical, aperiodical and stochastical influences. Epilepsies on the other hand influence the biological rhythms themselves. Epileptic seizures are activated during transient sleep stages. Nocturnal seizures lead to severe sleep disorders and therefore to hypersomnia. Partial and generalized epilepsies have a different sleep profil even without seizure manifestation. Finally antiepileptic drugs may interfere with circadian rhythms. Knowing the chronobiological context a differentiation of epileptic seizures from nonepileptic parasomnias may succeed more easily. To ensure the appropriate diagnostical proceeding multichannel EEG should be used in every polysomnography with neurological topics.
 ...
PMID:[Interaction of epileptic seizures and biological rhythms]. 858 62

Narcolepsy is a rare sequela of brain injury. We report the case of a 27-yr-old male with post-traumatic narcolepsy who was successfully treated with methylphenidate. This patient sustained moderate brain injury from a motorcycle accident. Subsequently, he manifested the classic tetrad of narcolepsy: cataplexy, excessive daytime sleepiness, sleep paralysis, and hypnogogic hallucinations. There was no premorbid seizure or sleep disorder. There was no family history of sleep disorders. Polysomnography and Multiple Sleep Latency Test confirmed the diagnosis of narcolepsy. Sleep latency (time to sleep onset), rapid eye movement sleep latency (time from sleep onset to rapid eye movement sleep onset), and mean multiple sleep latency were all pathologically shortened (2.5, 66, and 1.2 min, respectively). Twenty-four hour electroencephalographic monitoring and magnetic resonance imaging of the brain were normal, as were serum chemistries. Treatment with caffeine was unsuccessful. He was then started on methylphenidate, 10 mg twice daily, which was increased to 30 mg twice daily over a 4-mo period. Cataplexy and excessive daytime sleepiness started to improve 1 mo after adjustments in methylphenidate dosing. Six months after the initiation of methylphenidate therapy, the patient is completely asymptomatic.
 ...
PMID:Successful treatment of post-traumatic narcolepsy with methylphenidate: a case report. 864 41

Sleep deprivation increases the risk of recurrent seizures in epileptic patients. We identified 10 patients with recurrent seizures and sleep disruption related to obstructive sleep apnoea. Two patients were treated with positional therapy and the remaining eight patients were treated with continuous positive airway pressure. Three of the patients became seizure free and a fourth patient had a greater than 95% reduction in seizure frequency following only the initiation of therapy for the sleep apnoea. Three of these four patients responding to therapy, had a state-dependent seizure pattern. Two of the four responders did not exhibit the typical body habitus for obstructive sleep apnoea. Three additional patients improved in seizure frequency with change in anticonvulsant medication and treatment of the obstructive sleep apnoea. The remaining three patients had less than 50% reduction in seizure frequency with treatment of the obstructive sleep apnoea. These results indicate sleep disruption caused by sleep apnoea may increase the seizure frequency in some epileptic patients. Regardless of body habitus, epilepsy patients should be questioned carefully for a history of sleep disturbance and state dependence to their seizures. Treatment of sleep disorders in this population may lower the frequency of recurrent seizures.
Seizure 1996 Mar
PMID:Improvement of epileptic seizure control with treatment of obstructive sleep apnoea. 877 57

Recent technical developments allow the recording of a patient's oxygen saturation (SpO2) simultaneously with intensive long-term EEG monitoring (LTM). Clinically significant information from this enhanced multi-system physiological monitoring device can contribute to more accurate diagnoses in patients referred for LTM. This report covers the technical usage of combined SpO2/EEG recordings in a small group of patients. Clinically, the findings on the SpO2 monitor helped to define the diagnosis in many of these patients. In a few, the SpO2 changes were diagnostic in their own right and prompted referral to our Sleep Disorders Laboratory. From a research aspect, the details of the morphology and timing of the oxygen desaturations and EEG show several interesting relationships with respect to the dynamics of seizure semiology and respiratory physiology.
 ...
PMID:Technical implementation and clinical findings/results of monitoring oxygen saturation in patients referred for long-term EEG monitoring. 902 Aug 2

The disease is named after George H. Whipple who, in 1907, was the first to describe an intestinal "lipodystrophy". Although Whipple's disease is generally recognized as a multisystem chronic granulomatous disease, primarily involving the digestive system, it can also appear as a primary neurological disorder in rare cases. Most often it is manifested with loss of weight, diarrhea, malabsorption, abdominal pain, lymphadenopathy, cardiopathy, hyperpigmentation and hypotension. The presence of periodic acid-Schiff (PAS)-positive macrophages in biopsy specimens (not only jejunal) and demonstration of "Whipple's bacilli" visible by electron microscopy, are diagnostic signs of active Whipple's disease. Whipple's disease confined to the CNS is rare. It is rarely found in the differential diagnosis of patients with progressive neurological deterioration. The most common neurological picture includes progressive dementia, external ophalmoplegia, myoclonus, seizures, ataxia, hypothalamic dysfunction (sleep disorders, hyperphagia, polydipsia) and meningitis. Oculofacial-skeletal myorhythmia as a movement disorder, associated with Whipple's disease, is reported. Fulminant course of cerebral Whipple's disease is unusual and unfavourable. The confusing and nonspecific clinical appearance is typical for primary CNS involvement. It has recently been suggested that CNS involvement occurs in all cases, although only 10-20% of patients may show it. The CNS is the most common site of disease relapse. The CT scans and MRI of the brain are often normal, but may show cortical/subcortical atrophy, hydrocephalus, focal or intracerebral mass lesions. The cerebrospinal fluid can sometimes contain PAS-positive macrophages. Brain biopsy is suggested as a diagnostic method in cases of high suspicion of CNS Whipple's disease. However, the lesions are frequently inaccessible and false negative. Without extended antibiotic therapy, the course of Whipple's disease is lethal. Now, the prognosis is good, although the optimal antimicrobial regimen is not clearly established. Initial parenteral therapy (tetracycline, penicilline, streptomycine, chloramphenicol, ampicilline) and peroral long-term treatment with trimetoprime-sulphametoxasole, are recommended. As CNS relapse of Whipple's disease may occur after several years, long-term treatment should include antibiotics that are able to cross the blood-brain barrier. The CNS relapse, in contrast to the systemic ones, is resistant to the treatment. Appropriate therapy instituted earlier in the course of the disease is associated with a better neurological outcome. Early recognition can be critical in Whipple's disease because of irreversible neurological sequelae seen later in the course of this potentially treatable condition. In cases with high clinical suspicion in which Whipple's disease cannot be diagnosed with procedures such as jejunal biopsy, antibiotic therapy is recommended. Recovery of an established neurological deficit may rarely occur. Longterm follow-up studies would help to identify the optimal antibiotic regimen and duration of treatment.
 ...
PMID:[Neurologic disorders in Whipple's disease]. 910 28

Effective management of the syncope patient is critically dependent on excluding conditions in which altered consciousness is not due to syncope (e.g., seizure and sleep disorders) then establishing the basis for syncopal symptoms. The initial diagnostic step in syncope patients is differentiation of those individuals with normal cardiovascular status from those with structural heart disease. In the former, tilt-table testing and related studies of autonomic nervous system function are usually the most productive direction in which to proceed. In patients with structural heart disease, a functional assessment of the suspected structural disturbance (i.e., hemodynamic, angiographic, imaging as appropriate) and evaluation for susceptibility to symptomatic arrhythmias by monitoring or conventional electrophysiologic testing is appropriate. Autonomic function testing should follow if the diagnosis remains unclear. In only a few instances should specialized neurologic studies be undertaken as an initial step. The ultimate objective is always to obtain a sufficiently strong correlation between syncopal symptoms and detected abnormalities to feel confident in the diagnosis, permit an accurate assessment of prognosis, and develop an appropriate treatment plan.
 ...
PMID:Clinical approach to diagnosis of syncope. An Overview. 916 8

We examined the licensing of drivers with conditions likely to endanger the public in a State in which doctors are obliged to notify the licensing authority. During 1991, 1460 medically endorsed licenses were cancelled. A sample of 245, including all 49 with epilepsy were mostly voluntary, the twenty exceptions with retained files being drivers with epilepsy. In the same period, 115 traffic accidents were attributed to illness, with the only four (4) investigated by the licensing authority being those with licenses endorsed "epilepsy" where a seizure was responsible. Compulsory notification appeared to result in the identification of epilepsy as the important medical reason for controlling licenses, but failed to recognise sleep disorders or alcoholism, both more significant causes of traffic accidents. In those accidents attributed to illness, almost no action was taken to review the medical fitness of drivers, suggesting a reliance on doctors rather than police or road safety authorities.
 ...
PMID:Epilepsy and driving in South Australia--an assessment of compulsory notification. 921 18

These clinical guidelines, which have been reviewed and approved by the Board of Directors of the American Sleep Disorders Association, provide recommendations for the practice of sleep medicine in North America regarding the indications for polysomnography in the diagnosis of sleep disorders. Diagnostic categories that are considered include the following: sleep-related breathing disorders; neuromuscular disorders and sleep-related symptoms; chronic lung disease; narcolepsy; parasomnias; sleep-related epilepsy; restless legs syndrome; periodic limb movement disorder; depression with insomnia; and circadian rhythm sleep disorders. Whenever possible, conclusions are based on evidence from review of the literature. Where scientific data are absent, insufficient, or inconclusive, recommendations are based on consensus of opinion. The Standards of Practice Committee of the American Sleep Disorders Association appointed a task force to review the topic, the indications for polysomnography and related procedures. Based on the review and on consultation with specialists, the subsequent recommendations were developed by the Standards of Practice Committee and approved by the Board of Directors of the American Sleep Disorders Association. Polysomnography is routinely indicated for the diagnosis of sleep-related breathing disorders; for continuous positive airway pressure (CPAP) titration in patients with sleep-related breathing disorders; for documenting the presence of obstructive sleep apnea in patients prior to laser-assisted uvulopalatopharyngoplasty; for the assessment of treatment results in some cases; with a multiple sleep latency test in the evaluation of suspected narcolepsy; in evaluating sleep-related behaviors that are violent or otherwise potentially injurious to the patient or others; and in certain atypical or unusual parasomnias. Polysomnography may be indicated in patients with neuromuscular disorders and sleep-related symptoms; to assist in with the diagnosis of paroxysmal arousals or other sleep disruptions thought to be seizure-related; in a presumed parasomnia or sleep-related epilepsy that does not respond to conventional therapy; or when there is a strong clinical suspicion of periodic limb movement disorder. Polysomnography is not routinely indicated to diagnose chronic lung disease; in cases of typical, uncomplicated, and noninjurious parasomnias when the diagnosis is clearly delineated; for patients with epilepsy who have no specific complaints consistent with a sleep disorder; to diagnose or treat restless legs syndrome; for the diagnosis of circadian rhythm sleep disorders; or to establish a diagnosis of depression.
 ...
PMID:Practice parameters for the indications for polysomnography and related procedures. Polysomnography Task Force, American Sleep Disorders Association Standards of Practice Committee. 930 25


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