Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028738 (nystagmus)
 7,431 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Phenytoin toxicity may result from intentional overdose, dosage adjustments, drug interactions, or alterations in physiology. Intoxication manifests predominantly as nausea, central nervous system dysfunction (particularly confusion, nystagmus, and ataxia), with depressed conscious state, coma, and seizures occurring in more severe cases. Cardiac complications such as arrhythmias and hypotension are rare in cases of phenytoin ingestion, but they may be seen in parenteral administration of phenytoin or fosphenytoin. Deaths are unlikely after phenytoin intoxication alone. A greatly increased half-life in overdose due to zero-order pharmacokinetics can result in a prolonged duration of symptoms and thus prolonged hospitalization with its attendant complications. The mainstay of therapy for a patient with phenytoin intoxication is supportive care. Treatment includes attention to vital functions, management of nausea and vomiting, and prevention of injuries due to confusion and ataxia. There is no antidote, and there is no evidence that any method of gastrointestinal decontamination or enhanced elimination improves outcome. Activated charcoal should be considered if the patient presents early; however, the role of multiple-dose activated charcoal is controversial. Experimental studies have proven increased clearance rates, but this effect has not been translated into clinical benefit. There is no evidence that any invasive method of enhanced elimination (such as plasmapheresis, hemodialysis, or hemoperfusion) provides any benefit. This article provides an overview of phenytoin pharmacokinetics and the clinical manifestations of toxicity, followed by a detailed review of the various treatment modalities.
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PMID:Phenytoin poisoning. 1617 88

Sodium azide poisonings occur very rarely. The mechanism of sodium azide toxic effect has not yet been fully explained. Despite the lack of an explicit procedure for the cases of sodium azide poisonings, in vitro tests and rare case reports suggest that treatment with antidotes for cyanide poisoning victims can be effective. This study describes two cases of suicidal sodium azide ingestion. Case 1. 30-year-old male ingested ca. 180 mg of sodium azide. On admission to hospital, within 4 hours from poisoning, the man complained of dizziness and anxiety. Physical examination revealed horizontal nystagmus, flapping tremor, HR 135/min. In laboratory tests, higher blood concentration of lactates (3 mmol/l) was detected, as well as lower potassium concentration (3.4 mmol/L) and increased transaminase activity (ALT 74 U/l, AST 90 U/l). Electrocardiographic tests showed a negative T wave in limb lead III. Other results were within normal. As the patient ingested a toxic dose of sodium azide, he was treated according to the therapy prescription for cyanide poisoning (amyl nitrite inhalation followed by intravenous administration of sodium nitrite and sodium thiosulphate). ECG record of the last day of hospitalization (7th day of treatment) showed negative T waves in lead III, V4-V6. He was discharged from hospital in good condition. Case 2.23-year-old male ingested 10 g of sodium azide 1.5 hours prior to admission to hospital. At the beginning, the patient's condition was good, but it changed to critical state within the first hours of hospitalization. He developed a deep coma, respiratory and circulatory insufficiency, metabolic acidosis, cardiac dysrrhythmias and anuria. Cardiac activity monitoring showed alternating tachycardia (140 beats per minute) and bradycardia (48 beats per minute), numerous additional supraventricular and ventricular extrasystoles and sinus dysrrhythmia. Cardiac arrest (asystolia) occurred twice, the second incident with fatal outcome. The patient received supportive therapy, he was also treated according to the therapy prescription for cyanide poisoning. Circulatory disturbances observed in both cases have been described in literature as symptoms of sodium azide poisoning. However, available literature data are scarce and lack systematization, most of them coming from several decades ago. The lack of patient's consent for detailed examination of circulatory system and liver made it impossible to gather further knowledge on the subject. The efficacy of treatment with antidotes for cyanide poisoning has not been unequivocally determined for this kind of intoxication.
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PMID:[Sodium azide--clinical course of the poisoning and treatment]. 1772 2

Hemiplegic migraine (HM) is a rare variety of migraine with aura characterized by the presence of a motor weakness during the aura. Hemiplegic migraine has two main forms according to the familial history: patients with at least one first- or second-degree relative who has aura including motor weakness have familial hemiplegic migraine (FHM); patients without such familial history have sporadic hemiplegic migraine (SHM). The prevalence of HM is one in 10,000 with FHM and SHM being equally frequent. Typical HM attacks include a motor weakness that is always associated with other aura symptoms, the most frequent being sensory, visual and speech disorders. In addition, basilar-type symptoms occur in up to 70% of the patients. Severe attacks may occur in FHM as well as in SHM with prolonged hemiplegia, confusion, coma, fever and seizures. The clinical spectrum also includes permanent cerebellar signs (nystagmus, ataxia, dysarthria) and less frequently various types of seizures and intellectual deficiency. FHM is the only variety of the autosomal dominant migraine and all three know genes encode ion-transporters. A genetic diagnosis is now possible by screening the three known genes involved in FHM (CACNA1A, ATP1A2 and SCNA1). Prognosis is usually good. Treatment is similar to approaches used in other varieties of migraine with aura, excepted for triptans that are contraindicated in MHF/MHS. Based on new pathophysiological insight, preventive treatments by various antiepileptic agents seem promising.
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PMID:[Familial and sporadic hemiplegic migraine]. 1840 71

Carbamazepine (CBZ) is a commonly used antiepileptic agent. Common toxic effects include neurological abnormalities; ataxia, seizures, coma, cardiorespiratory problems; dysrhythmias; conduction disorders; respiratory depression; and eye abnormalities, such as nystagmus and ophthalmoplegia. Carbamazepine is highly protein bound. There is no antidote for the medication. Carbamazepine is not removed effectively through conventional hemodialysis. Supportive measures and charcoal hemoperfusion have been regarded as efficient treatment methods. We herein report a 17-year old girl to whom continuous venovenous hemodiafiltration lacking the albumin-enhance after suicidal overdose of CBZ was performed. We suggest continuous venovenous hemodiafiltration lacking the albumin-enhance as an alternative emergency treatment modality for cases who had ingested CBZ in toxic levels.
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PMID:Management of a severe carbamazepine overdose with continuous venovenous hemodiafiltration. 2015 17

Hyperemesis gravidarum can impair correct absorption of an adequate amount of thiamine and can cause electrolyte imbalance. This study investigated the neurological complications in a pregnant woman with hyperemesis gravidarum. A 29-year-old pregnant woman was admitted for hyperemesis gravidarum. Besides undernutrition, a neurological examination disclosed weakness with hyporeflexia, ophthalmoparesis, multidirectional nystagmus and optic disks swelling; the patient became rapidly comatose. Brain MRI showed symmetric signal hyperintensity and swelling of periaqueductal area, hypothalamus and mammillary bodies, medial and posterior portions of the thalamus and columns of fornix, consistent with Wernicke encephalopathy (WE). Neurophysiological studies revealed an axonal sensory-motor polyneuropathy, likely due to thiamine deficiency or critical illness polyneuropathy. Sodium and potassium supplementation and parenteral thiamine were administered with improvement of consciousness state in a few days. WE evolved in Korsakoff syndrome. A repeat MRI showed a marked improvement of WE-related alterations and a new hyperintense lesion in the pons, suggestive of central pontine myelinolysis. No sign or symptom due to involvement of the pons was present.
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PMID:Neurological complications in hyperemesis gravidarum. 2172 Sep 1

Memantin HCL (Ebixa) is a drug which antagonizes the effects of N-methyl-D-aspartat receptors and which is used for the treatment of acute Alzheimer patients. Plasmapheresis is a method of cleaning nonspecific extracorporeal blood and it is applied in many immunologic and toxicologic diseases. Female patient at the age of 35 was admitted to the emergency department with complaints of tendency to sleep and sensory loss. About 12 hours before her history she had taken 200 tablets of 10 mg memantin HCL (Ebixa) (2000 mg) and she was transferred to an intensive care department with the diagnosis of drug toxicity (400 mg toxic dose). Her memantin HCL (Ebixa) level in blood was 12,000 ng/mL. It was reported in her physical examination that she was unconscious, her general condition was bad, there were no cooperation and orientation, ahe hadmydriasis and reflexes of light, cornea and eyelash were bilaterally positive and she had horizontal nystagmus. Glascow Coma Scale of the patient was 6, body temperature was 37.5 degrees C and she had tachycardia (130/min) and hypertension (160/90 mmHg). Intravenous Diazepam was effective aginst recurring convulsions. Sinusoidal tachycardia was detected with electrocardiography (EKG) and respiratory alkalosis in arterial blood gases. Six cysles of plasmapheresis were aplied and in the sixth cycle the memantin HCL (Ebixa) level turned to normal. As a result of the sixth plasmapheresis the findings were normal and that is why she was discharged from the hospital. Plasmapheresis should be taken into consideration in case of drug overdose or high doses of plasmatic proteinous drug toxicities (Ref. 11).
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PMID:A memantin HCL intoxication responsive to plasmapheresis therapy. 2195 34

Lithium salts have been used in treatment of depression and bipolar disorder for more than 50 years. Neurotoxic side-effects such as nystagmus, ataxia, tremor, fasciculation, clonus, seizure and even coma have been well described in the literature. We present a case of generalised peripheral neuropathy following lithium intoxication. It is a rare presentation with delayed onset and characterised by a rapid downhill course. Diagnosis was confirmed by nerve conduction tests, which showed axonal neuropathy. Despite the profound neurological effects of this toxicity, it is readily reversible with supportive care and the prognosis is good.
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PMID:A rare neurological complication due to lithium poisoning. 2286 82

Gammabutyrolactone is included in the solvent such as wheel cleaners, pesticides, cosmetics, drugs. After ingestion GBL is converted to gamma-hydroxybutyrate. Both substances are classified as so called "club drugs" and their action is characterized by euphoria, sedation, and induction of retrograde amnesia of events. These activities were basis for the use of GHB and its lactone as rape pill. Acute poisoning with these compounds causes confusion, agitation, ataxia, nausea, vomiting, nystagmus, dyskinesia, hallucinations, coma, irregular breathing, hypothermia, bradycardia, hypotension, convulsions, respiratory paralysis and thus respiratory arrest. These substances carry a risk of development of physical addiction of the hard proceeding of abstinence syndrome. In the USA there is a ban on the sale and promotion of these compounds. In Poland despite the fact that GHB is a controlled substance, there is no regulation of GBL trading. The aim of this paper is to summarize current knowledge regarding the pharmacology, impact on the human body, toxicity, and the effects of chronic abuse of these substances.
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PMID:[Gamma-hydroxybutyrate (GHB) and its lactone (GBL) as psychoactive substances]. 2324 24

Nonsteroidal anti-inflammatory drugs (NSAIDs) are among the most commonly used agents in clinical practice. They are employed as anti-inflammatory, analgesic, and antipyretic agents for a wide spectrum of clinical conditions. Their anti-inflammatory properties are primarily due to inhibition of prostaglandin synthesis. In this paper we review the neurological effects associated with the use of NSAIDs. Acute CNS toxicity related to NSAID use is pervasive and varied. A prospective study looking at ibuprofen overdose noted that 30% of patients experience CNS effects ranging from drowsiness to coma. Case reports have identified numerous neurologic sequelae including ataxia, vertigo, dizziness, recurrent falls, nystagmus, headache, encephalopathy, and disorientation. Seizures have also been reported, mostly after overdose ingestions, but even therapeutic doses have occasionally been associated with seizures. One of the important neurologic side-effects attributed to the use of NSAIDs is aseptic meningitis. The clinical signs of drug-induced meningitis are similar to those of infectious meningitis and include fever, headache, photophobia, and stiff neck. The laboratory findings are also similar, including cerebrospinal fluid (CSF) pleocytosis of several hundred or thousand cells, mainly neutrophils, elevated levels of protein, normal or low glucose levels and negative cultures. Drug-induced meningitis is a transient disorder with an excellent prognosis. Most or all drugs used for the treatment of headache, including NSAIDs, may cause a condition known as medication overuse headache - a refractory chronic daily headache that tends to resolve following discontinuation of the analgesics. Reye's syndrome is a rare severe illness occurring mainly in children and adolescents and characterized by abnormal liver function, vomiting, and encephalopathy, with a mortality rate approaching 40%. The pathogenesis is currently unknown, but commonly the syndrome is preceded by a viral episode, with an intermediate latent period of 3-5 days. An association with aspirin use is strongly suggested. Aspirin, the classic and most commonly used NSAID, has a well-documented effect in inhibiting intravascular clotting, thus reducing the occurrence of ischemic strokes and other vascular events. NSAIDs, however, have a double impact on coagulation. On the one hand, most agents inhibit the synthesis of thromboxane in the platelets, thereby inhibiting coagulation. On the other hand, they also inhibit the production of prostacyclin by endothelial cells, resulting in a prothrombotic state. Selective inhibition of COX-2 by drugs such as rofecoxib (Vioxx) and valdecoxib (Bextra) results in specific inhibition of synthesis of prostaglandins participating in inflammation and was found to lead to vascular complications including an increased risk for stroke. The connection between inflammation and neuronal degeneration is well established. Most studies, including the prospective Rotterdam study, have found an inverse correlation between the use of NSAIDs and the risk for dementia. Two meta-analyses have found 40% and 25% reduction, respectively, in the risk of Alzheimer's disease among NSAID users. However, some large, well designed studies failed to confirm these results, and some even found that NSAID use is associated with cognitive decline. The clinical impact of NSAIDs on Parkinson's disease (PD) remains unclear. While some studies showed that chronic NSAID use is protective against PD, other studies could not confirm the existence of a significant relationship. A recent meta-analysis indicated that the use of non-aspirin NSAID, particularly ibuprofen, reduces the risk of PD by 15% while the use of aspirin did not show any effect.
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PMID:Nonsteroidal anti-inflammatory drugs exposure and the central nervous system. 2436 21

The history, symptoms, diagnosis and treatment of phencyclidine hydrochloride (PCP) intoxication, the pharmacology of PCP and the detection, identification and analysis of PCP are reviewed. The history of PCP from its synthesis in the early 1950s to the present is discussed. Intoxication with low to moderate doses of PCP resembles an acute, confusing state. High doses may cause serious neurological and cardiovascular complications and the patient is often comatose for several days. Treatment involves supportive psychological and medical measures, and acidification of the urine may further increase PCP clearance. The metabolism of PCP involves primarily hydroxylation followed by conjugation and elimination in the urine. Analysis can be accomplished by a number of instrumental methods, and several commercial test kits based on antigen-antibody interactions are available. PCP's effect on human performance and behaviour is due to its ability to alter the perception of reality in the user. PCP causes a range of effects that include hallucinations, delirium, disorientation, agitation, muscle rigidity, ataxia, nystagmus, seizures, and stupor. PCP has stimulant, depressant, hallucinogenic and analgesic effects. Which of these will be most pronounced is unpredictable and depends on the user's personality, psychological state and the environment of use. The impairment can manifest itself as over-aggressive or reckless driving behavior, or may mimic depressant effects due to PCP's anesthetic and depressant effect.
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PMID:Phencyclidine - Effects on Human Performance and Behavior. 2625 94


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