Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0040822 (tremor)
 18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In recent years there are a considerable increase in alcohol consumption in Taiwan, which may have been accompanied by increased incidence of alcohol-related physical disease. This study was designed for an understanding of neurological problems in chronic alcoholic patients. One hundred and five cases of chronic alcoholics with neurological problems were collected. All had taken more than 100 g alcohol daily for more than 8 years. They were all males, with a mean age of 47.0 +/- 1.3 years, mean daily alcohol consumption of 185.1 +/- 9.0 g (mean +/- S.E.). These chronic alcoholic patients showed various neurological problems. Patients showing typical clinical features of alcoholic neurological disease are now rather rare. Most of the patients had manifestations of more than one problems: polyneuropathy (74.3%), alcoholic tremor (37.1%), hallucinosis (30.5%), myopathy (26.7%), head injury (24.8%), withdrawal seizures (18.1%), Wernicke encephalopathy (15.2%), paranoia (13.3%), and stroke (15.2%). Furthermore, we divided all the patients into 5 categories, they were: encephalopathy, 59 cases (56.2%); stroke, 16 cases (15.2%); cerebellar degeneration, 12 cases (11.4%); neuropathy, 78 case (74.3%); and myopathy, 28 cases (16.7%). The daily alcohol consumption and duration of daily drinking were different significantly (p less than 0.05) among five different syndrome categories.
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PMID:Neurological problems in chronic alcoholics. 165 33

Two cases of basal ganglia calcification involving the globus pallidus are presented. Both patients had cognitive dysfunction, temporal lobe-like symptoms (including amnestic state, perceptual distortions, or complex visual hallucinations), and myoclonus. Patient 1 manifested depression, auditory hallucinations, anxiety, paranoia, and postural tremor; patient 2 manifested multifocal dystonia with dystonic tremor. These cases supplement other reports of psychotic features and dementia associated with pallidal pathology. Additionally, the phenomena encountered in these cases are considered in light of recent advances in our understanding of basal ganglia functional pathways. These cases afford a potential pathophysiological window to the possible role of the globus pallidus in these neuropsychiatric conditions. In concert with other recent findings, these cases suggest specific pathway involvement in hallucinations, paranoia, depression, myoclonus, and dystonia. Further research will indicate if these pathways play a role in schizophrenia, mood disorders, and anxiety disorders.
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PMID:Neuropsychiatric disorders, myoclonus, and dystonia in calcification of basal ganglia pathways. 801 2

Methamphetamine, called meth, crystal, or speed, is a central nervous system stimulant that can be injected, smoked, snorted, or ingested orally; prolonged use at high levels results in dependence. Methamphetamine (MA) is a derivative of amphetamine, which was widely prescribed in the 1950s and 1960s as a medication for depression and obesity, reaching a peak of 31 million prescriptions in the United States in 1967. Until the late 1980s, illicit use and manufacture of MA was endemic to California, but the MA user population has recently broadened in nature and in regional distribution, with increased use occurring in midwestern states. An estimated 4.7 million Americans (2.1% of the U.S. population) have tried MA at some time in their lives. Short- and long-term health effects of MA use include stroke, cardiac arrhythmia, stomach cramps, shaking, anxiety, insomnia, paranoia, hallucinations, and structural changes to the brain. Children of MA abusers are at risk of neglect and abuse, and the use of MA by pregnant women can cause growth retardation, premature birth, and developmental disorders in neonates and enduring cognitive deficits in children. MA-related deaths and admissions to hospital emergency rooms are increasing. Although inpatient hospitalization may be indicated to treat severe cases of long-term MA dependence, optimum treatment for MA abusers relies on an intensive outpatient setting with three to five visits per week of comprehensive counseling for at least the first three months. The burgeoning problems of increased MA use must be addressed by adequate treatment programs suitable for a variety of user types.
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PMID:History of the methamphetamine problem. 1090

In this study we report an individual of Wilson's disease associated with olfactory paranoid syndrome and idiopathic thrombocytopenic purpura. The initial symptom of this female patient was olfactory paranoia at age 17. Although that psychiatric symptom was well controlled under pharmacological treatment for two years, she developed olfactory paranoia as well as sialorrhea, dysarthria and finger tremor at age 20. A year later rigidity was also present in the extremities. At age 23, idiopathic thrombocytopenic purpura was found based on hematological examinations. Because her extrapyramidal symptoms were progressive, she was referred to our department to evaluate her neurologic condition. She was diagnosed as having Wilson's disease based on (1) the presence of Kayser-Fleischer rings, (2) extrapyramidal signs, and (3) a decreased level of serum copper and ceruloplasmin. T2 and FLAIR images of brain MRI showed hyperintense lesions in the putamen, thalamus and pontine tegmentum. Diffusion-weighted images also showed hyperintense lesions in the thalamus and pontine tegmentum. The biopsy specimen of the liver revealed chronic hepatitis with copper accumulation. Since D-penicillamine treatment was initiated, she has shown no olfactory paranoia and exacerbation of ITP. Her gait disturbance has also improved. Olfactory paranoia and ITP are rare clinical complications of Wilson's disease. Further analysis may warrant consideration of the pathophysiological mechanism of the psychiatric, hematological and neuroradiological condition seen in Wilson's disease.
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PMID:[Wilson's disease associated with olfactory paranoid syndrome and idiopathic thrombocytopenic purpura]. 1463 19

The evidence that Adolf Hitler might have suffered from incapacitating syphilis is reviewed. Rumors that he acquired syphilis from a prostitute at the age of 20 years, with possible re-infection during World War I, can no longer be verified. Evidence is that he was sexually rather inactive throughout his life. Suggestions that Hitler's cardiac lesion and complaints such as transitory blindness, tremor of his left arm and leg, recurring abdominal pain and a skin lesion of the leg were of syphilitic aetiology cannot be supported. Hitler's progressive mental and physical deterioration after 1942, his growing paranoia, fits of rage, grandiosity and symptoms of possible dementia would fit in neurosyphilis. There are, however, also other explanations for his terminal syndrome, and evidence that repeated clinical examinations did not show the characteristic signs of dementia paralytica or tabes dorsalis, swings the balance of probability away from tertiary syphilis.
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PMID:Did Adolf Hitler have syphilis? 1706 46

Two patients with essential tremor who had no psychiatric history developed symptoms of psychosis (visual hallucinations, paranoia, and vivid dreams) 3 days after starting topiramate (25 mg BID) for tremor control. All adverse symptoms resolved several days after topiramate was discontinued.
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PMID:Topiramate-induced psychosis in patients with essential tremor: report of 2 cases. 1677 20

The prevalence of attention-deficit hyperactivity disorder (ADHD) in the USA is estimated at approximately 4-9% in children and 4% in adults. It is estimated that prescriptions for ADHD medications are written for more than 2.7 million children per year. In 2010, US poison centers reported 17,000 human exposures to ADHD medications, with 80% occurring in children <19 years old and 20% in adults. The drugs used for the treatment of ADHD are diverse but can be roughly separated into two groups: the stimulants such as amphetamine, methylphenidate, and modafinil; and the non-stimulants such as atomoxetine, guanfacine, and clonidine. This review focuses on mechanisms of toxicity after overdose with ADHD medications, clinical effects from overdose, and management. Amphetamine, dextroamphetamine, and methylphenidate act as substrates for the cellular monoamine transporter, especially the dopamine transporter (DAT) and less so the norepinephrine (NET) and serotonin transporter. The mechanism of toxicity is primarily related to excessive extracellular dopamine, norepinephrine, and serotonin. The primary clinical syndrome involves prominent neurological and cardiovascular effects, but secondary complications can involve renal, muscle, pulmonary, and gastrointestinal (GI) effects. In overdose, the patient may present with mydriasis, tremor, agitation, hyperreflexia, combative behavior, confusion, hallucinations, delirium, anxiety, paranoia, movement disorders, and seizures. The management of amphetamine, dextroamphetamine, and methylphenidate overdose is largely supportive, with a focus on interruption of the sympathomimetic syndrome with judicious use of benzodiazepines. In cases where agitation, delirium, and movement disorders are unresponsive to benzodiazepines, second-line therapies include antipsychotics such as ziprasidone or haloperidol, central alpha-adrenoreceptor agonists such as dexmedetomidine, or propofol. Modafinil is not US FDA approved for treatment of ADHD; however, it has been shown to improve ADHD signs and symptoms and has been used as an off-label pharmaceutical for this diagnosis in both adults and children. The mechanism of action of modafinil is complex and not fully understood. It is known to cause an increase in extracellular concentrations of dopamine, norepinephrine, and serotonin in the neocortex. Overdose with modafinil is generally of moderate severity, with reported ingestions of doses up to 8 g. The most common neurological effects include increased anxiety, agitation, headache, dizziness, insomnia, tremors, and dystonia. The management of modafinil overdose is largely supportive, with a focus on sedation, and control of dyskinesias and blood pressure. Atomoxetine is a selective presynaptic norepinephrine transporter inhibitor. The clinical presentation after overdose with atomoxetine has generally been mild. The primary effects have been drowsiness, agitation, hyperactivity, GI upset, tremor, hyperreflexia, tachycardia hypertension, and seizure. The management of atomoxetine overdose is largely supportive, with a focus on sedation, and control of dyskinesias and seizures. Clonidine is a synthetic imidazole derivative with both central and peripheral alpha-adrenergic agonist actions. The primary clinical syndrome involves prominent neurological and cardiovascular effects, with the most commonly reported features of depressed sensorium, bradycardia, and hypotension. While clonidine is an anti-hypertensive medication, a paradoxical hypertension may occur early with overdose. The clinical syndrome after overdose of guanfacine may be mixed depending on central or peripheral alpha-adrenoreceptor effects. Initial clinical effects may be drowsiness, lethargy, dry mouth, and diaphoresis. Cardiovascular effects may depend on time post-ingestion and may present as hypotension or hypertension. The management of guanfacine overdose is largely supportive, with a focus on support of blood pressure. Overdose with ADHD medications can produce major morbidity, with many cases requiring intensive care medicine and prolonged hospital stays. However, fatalities are rare with appropriate care.
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PMID:Overdose of drugs for attention-deficit hyperactivity disorder: clinical presentation, mechanisms of toxicity, and management. 2375 86

Herod the Great was appointed "king of Jews," to govern Judea, by the Roman Emperor and Senate. He lived from 73/74 BCE to 4 CE. He died with an illness and symptoms that have been the source of considerable speculation. Richard Strauss depicted Herod in his classic opera, "Salome." That opera was derived from a play of the same name by Oscar Wilde, which was based on an 1876 painting, "Salome Dancing Before Herod," by Gustave Moreau. The operatic Herod was afflicted with an illness characterized by dementia, hallucinations, paranoia, alcoholism (from drinking the Emperor's wine), violence, twitches, and sterility; different interpretations showed him also with falls, chills, shaking, thirst, forgetfulness, and sleepiness, for which we suggest the novel diagnosis of chronic lead intoxication (which can manifest to rheumatologists as saturnine gout). He had compatible symptoms (encephalopathy and neuromuscular abnormalities) and consumed excessive quantities of imperial wine, known to be highly contaminated with lead and likely associated with similar symptoms among Roman aristocracy. Herod's demented cruelties-an oppressive reign which including the beheading of John the Baptist-exacerbated the political climate and may have contributed to the subsequent violent 7-year revolt culminating in the destruction of the second temple. How different might history have been if Herod the Great had been abstemious?
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PMID:Did King Herod suffer from a rheumatic disease? 2873 92