本態性振戦

関: benign essential tremor、familial tremor

WordNet

being or relating to or containing the essence of a plant etc; "essential oil"
absolutely necessary; vitally necessary; "essential tools and materials"; "funds essential to the completion of the project"; "an indispensable worker" (同)indispensable
basic and fundamental; "the essential feature"
shake with seismic vibrations; "The earth was quaking" (同)quake
shaking or trembling (usually resulting from weakness or stress or disease)
an involuntary vibration (as if from illness or fear) (同)shudder
a small earthquake (同)earth tremor, microseism

PrepTutorEJDIC

『絶対必要な』,欠くことのできない / 『本質の』,本質的な / (植物・薬剤などの)エキスの,精の / (…に)不可欠の要素;(…の)主眼点,要点《+『of』+『名』》
(地面などの)震動,揺れ / (恐怖・興奮などによる体・手足の)震う,身震い

Wikipedia preview

出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2013/05/08 15:18:55」(JST)

wiki en

[Wiki en表示]

Essential tremor (ET) is a progressive neurological disorder of which the most recognizable feature is a tremor of the arms or hands that is apparent during voluntary movements such as eating and writing.^[1] This type of tremor is often referred to as "kinetic tremor." The tremor may also occur in the head (neck), jaw and voice as well as other body regions, with the general pattern being that the tremor begins in the arms and then spreads to these other regions in selected patients. Women are more likely to develop the head tremor than are men.^[2]^[3] Other types of tremor may also occur, including postural tremor of the outstretched arms, intentional tremor of the arms and rest tremor in the arms.^[4] Some patients may have unsteadiness and problems with gait and balance that are above and beyond that due to normal aging.^[5]^[6] In addition to these motor problems, a variety of non-motor features have recently been linked with ET. These include anxiety and depressive symptoms as well as cognitive difficulty.^[7] Recent studies have demonstrated that late-onset ET (onset > age 65) may be associated with an increased risk of developing dementia.^[8] ET is one of the most common neurological diseases, with a prevalence of approximately 4% in persons age 40 and older and considerably higher among persons in their 60s, 70s, 80s, and 90s.^[9]^[10] Aside from enhanced physiological tremor, it is the most common type of tremor and one of the most commonly observed movement disorders.^[11] Essential tremor was also previously known as "benign essential tremor", but the adjective "benign" has been removed in recognition of the sometimes disabling nature of the disorder. Although essential tremor is often mild, patients with severe tremor have difficulty performing many of their routine activities of daily living.^[12]^[13]

Signs and symptoms [edit]

Essential tremor generally presents as a rhythmic tremor (4–12 Hz) that is present only when the affected muscle is exerting effort (in other words, it is not present at rest). Any sort of physical or mental stress will tend to make the tremor worse, often creating the false impression that the tremor is of psychosomatic origin.

Tremor intensity can worsen in response to fatigue, strong emotions, low blood sugar, cold, caffeine, lithium salts, some antidepressants or other factors. It is typical for the tremor to worsen in "performance" situations, such as when writing a cheque for payment at a store or giving a presentation.

ET-related tremors do not occur during sleep, but patients sometimes complain of an especially coarse tremor upon awakening that becomes noticeably less coarse within the first few minutes of wakefulness.

In mild cases, ET can manifest as the inability to stop the tongue or hands from shaking, the ability to sing only in vibrato, and difficulty to do small precise tasks such as threading a needle. Even simple tasks like cutting in a straight line or using a ruler can range from difficult to impossible, depending on the severity of the condition. In disabling cases, ET can interfere with a person's ability to perform tasks of daily living, including feeding, dressing, and activities of personal hygiene.

People with ET can sometimes have problems with word finding and can't articulate themselves effectively even with preparation. A person with ET may become shy, withdrawn, pessimistic, anxious and also have difficulties concentrating. It is common for those with ET to be embarrassed by the condition even though it is out of their control.

ET is generally progressive in most cases (sometimes rapidly, sometimes very slowly), and can be disabling in severe cases.^[14]^[15]^[16]

Cause [edit]

The underlying etiology is not clear but many cases seem to be familial.^[17] It has been estimated that approximately one-half of the cases are due to a genetic mutation and the pattern of inheritance is most consistent with autosomal dominant transmission. No genes have been identified yet but genetic linkage has been established with several chromosomal regions.^[18]^[19] A number of environmental factors, including toxins, are also under active investigation and these may play a role in disease etiology.^[20] In terms of pathophysiology, clinical, physiological and imaging studies point to an involvement of the cerebellum and/or cerebellothalamocortical circuits.^[21] Recent postmortem studies have demonstrated the presence of degenerative changes in the ET brain, with these changes including Purkinje cell axonal swellings and Purkinje cell loss in the majority of cases and brainstem Lewy bodies in the remainder. These studies suggest that the disease is both heterogeneous and degenerative. In other words, ET might be a family of degenerative diseases rather than a single disease.^[22]^[23]

However, emerging research based on brain autopsies of 50 deceased ET patients (as of December 2009), showed clear degenerative and pathological abnormalities, including "messy" neurofilaments which can impede nerve impulses. Research by Dr. Elan Louis and colleagues revealed that 80% of autopsied brains also exhibited changes within the cerebellum particularly to neurons that produce GABA, a major inhibitory neurotransmitter. Further analysis showed elevated levels of two neurotoxins, lead and harmane, a heterocyclic amine. Heterocyclic amines (HCA) are chemicals found in some foods. Harmane has been detected in coffee and cigarettes (see: http://www.ncbi.nlm.nih.gov/pubmed/21776263), but is especially prevalent in meats that have been barbecued or exposed to high heat.

Another research^[24] indicates there is a strong link between essential tremor in males and the amount of meat consumed, but the exact mechanism is yet unknown.

Changes in the cerebelleum could also be mediated by alcohol consumption. Purkinje cells are especially susceptible to ethanol excitotoxicity.^[25] The impairment could lead to the abnormal cerebellar circuitry seen in essential tremor and suggests that alcohol may also work as an exacerbating agent in the pathology of this disease.

Chronic ethanol consumption results in a loss of Purkinje cell synapses. However, these synapses are regained following a period of recovery that includes gradual weaning off of ethanol. Continued consumption of ethanol inhibits the recovery of synapses.^[26] This impairment of Purkinje synapses is a component of cerebellar degradation that could underlie essential tremor.^[25]

Chronic alcohol abuse has also been linked to other movement disorders such as myoclonus, ataxia, and dyskinesia.^[25]

Diagnosis [edit]

Usually the diagnosis is established on clinical grounds. Tremors can start at any age, from birth through advanced ages (senile tremor).^[27]^[28] Any voluntary muscle in the body may be affected, although the tremor is most commonly seen in the hands and arms and slightly less commonly in the neck (causing the patient's head to shake), tongue, and legs. A resting tremor of the hands is sometimes present.^[29]^[30] Tremor occurring in the legs might be diagnosable as Orthostatic Tremor.

ET does sometimes occur in combination with other neurological disorders such as dystonia. In addition, there may be a link between ET and Parkinson's disease, with one study showing ET patients having an approximately 4 times greater likelihood of developing Parkinson's disease.^[31]^[32]^[33] Essential tremor also tends to co-occur with Orthostatic Tremor.

Treatment [edit]

There is no recognised cure for essential tremor. Many of the treatments available are to lower the severity of the condition. These may include:

Medication [edit]

The two most recommended medications are: the beta-blockers propranolol and the antiepileptic primidone.^[34]

Self-medication with small amounts of alcohol has been shown to give short term relief from tremor,^[35] although this form of self-medication is not recommended due to an increased risk of alcohol dependence or abuse.^[36] However other alcohol groups such as 1-octanol are being researched to provide relief from essential tremor without providing the intoxication or toxicity that ethanol does.^[37]

Gabapentin may be helpful in the treatment of essential tremor.^[38]

A trial of the benzodiazepine-anticonvulsant Clonazepam (Klonopin, Rivotril) was found not to be an effective treatment;^[39] however, it is still recommended in some cases.^[40]

Topiramate has also been cited as a possible pharmaceutical treatment.

Other [edit]

Memantine is a drug that is currently being researched for its potential ameliorative effects on essential tremor. Memantine is not as potent as ethanol at decreasing tremor intensity or locomotion. However, memantine exhibits neuroprotective effects. Memantine treatment results in a significantly higher reduction in caspase-3 positive neurons.^[41]

Surgical treatments (which are generally reserved for the most severe cases) include thalamotomy and deep brain stimulation.^[42]^[43]^[44]

Minor cases of ET can be treated with physical therapy and development of the muscles in the sections of the body that are severe in their shaking.

Mild cases of ET which are not affecting activities of daily life may not require any treatment. Use of wrist weights and avoiding triggers such as caffeine may be helpful.

Support groups [edit]

The International Essential Tremor Foundation (IETF) provides information, services and support to individuals and families affected by essential tremor (ET).^[45] The organization encourages and promotes research in an effort to determine the causes, treatment and ultimately the cure for ET. The IETF is a worldwide organization dedicated to meeting the needs of those whose daily lives are challenged by ET. IETF, an international non-profit 501(c)(3) organization that derives its support entirely from its membership and the general public, was founded in 1988 and is guided by a board of directors and a medical advisory council. The organization's membership consists of patients, physicians, educators, parents, relatives and volunteers who provide education, community services and funding to help support tremor research.

The National Tremor Foundation (NTF), founded in 1992, is a British friendly organisation based in Essex, England, an affiliate of the International Tremor Foundation, which was founded in 1988.^[46] The organisation's primary work is production of a quarterly informational newsletter. The NTF also maintains a list of ITF medical advisors, and facilitates the formation of self-help groups. NTF was granted charitable status in 1994.

Research [edit]

Harmaline-induced tremor [edit]

Harmaline is a widely used model of essential tremor (ET) in rodents.^[47] Harmaline is thought to act primarily on neurons in the inferior olive(IO). Olivocerebellar neurons exhibit rhythmic excitatory action when harmaline is applied locally.^[47] Additionally, when harmaline is administered to lesioned IOs, little to no tremors are observed, reinforcing harmalines’ specificity for inferior olive connections.^[48] The treatment of harmaline results in higher levels of caspase-3 immunoreactivity in Purkinje, granule and inferior olive cells, suggestive of harmaline-mediated apoptosis.^[41] Harmaline also increases the concentration of glutamate in cerebellar nuclei which disrupts normal NMDA-mediated down-regulation of glutamate release.^[49] Together, these interferences likely give rise to essential-tremor like behavior that is likely a result of diseregulation of glutamatergic circuitry within the cerebellum.^[49]

Ethanol mechanisms [edit]

Ethanol is effective at decreasing tremor intensity and locomotion.^[41] Ethanol-mediated effects are not observed on tremor frequency and peak location.^[41] Additionally, ethanol is able to reduce caspase-3 induced apoptosis though not without an increased loss of neurons in the cerebellum and olivary nucleus.^[41] Ethanol has been shown to decrease levels of glutamate in the cerebellar nuclei which had been pre-treated with harmaline.^[49] Furthermore, ethanol directly reduces hyperactivity of the climbing fiber-Purknije cell synapse by acting on glutamatergic receptors.^[50] Ethanol may reduce tremor by dampening the overexcitation of glutamatergic pathways involving deep cerebellar nuclei which may also reduce levels of caspase-3 induced apoptosis.

Octanol mechanism [edit]

Different alcohols exert similar ameliorative effects on harmaline-induced tremors, though to different degrees. Different isomers of octanol vary in efficacy when it comes to antagonizing harmaline-mediated tremors. These effects are likely mediated in the inferior olive, specifically at low-threshold calcium channels (LTCC) which have been shown to modulate the rhythmic firing of cells in this area.^[51] Octanol, specifically by binding to LTCCs of IOs, behaves in an antagonistic fashion on the spike discharges from Purkinje cells. The most potent isomers: (+)2-octanol, (-)2-octanol and 4-octanol, followed by 4-octanol, and lastly, 1-octanol.^[48] Both the magnitude and duration of the tremor are dependent on the octanol isomer. Differences in solubility does not appear to account for the disparity between isomers.^[48] The first clinical trial of 1-Octanol in essential tremor was first conducted by Bushara etal and published in 2002, 2004. This showed the safety of 1-octanol and its efficacy in reducing tremor in patients diagnosed with essential tremor.^[52]^[53]

Genetically-induced tremor [edit]

Genetic animal models of essential tremor utilize GABA_A receptor α1 -/- mice because of the major role GABA plays in inhibiting motor activity. Moreover, GABAA receptor α1 -/- mice produce essential-like tremors and motor impairment as seen in ET patients.^[54]

Ethanol mechanisms [edit]

Alcohol is implicated as a therapeutic agent for GABA_A receptor α1 -/- mice because of its interaction with Purkinje cells which mediate their actions via GABA transmission.^[47] GABA_A receptor α1 -/- mice respond positively to ethanol treatment. Ethanol reduces tremor activity in GABA_A receptor α1 -/- mice in a dose dependent manner. An optimum dose of 2.5 g/kg of ethanol completely suppresses tremors in GABA_A receptor α1 -/- mice.^[54] Purkinje cells in these knockout mice also exhibit a lack of GABAergic inhibitory postsynaptic potentials in response to both exogenous and endogenous GABA. The loss of GABAergic inhibition in purkinje cells likely underlies the pathological tremors observed.^[54] These ameliorative effects are thought to involve inhibition of glutamatergic transmission, though the numerous targets of ethanol make it difficult to determine the exact underlying mechanism.^[54]

References [edit]

^ Benito-Leon J, Louis ED. Clinical update: Diagnosis and treatment of essential tremor. The Lancet 2007;369:1152-1153.
^ Hubble JP, Busenbark KL, Pahwa R, Lyons K, Koller WC. Clinical expression of essential tremor: Effects of gender and age. Mov Disord 1997;12:969-972.
^ Louis ED, Ford B, Frucht S. Factors associated with increased risk of head tremor in essential tremor: A community-based study in northern manhattan. Mov Disord 2003;18:432-436.
^ Louis ED. Clinical Practice: Essential tremor. N Engl J Med 2001;345:887-891.
^ Stolze H, Petersen G, Raethjen J, Wenzelburger R, Deuschl G. The gait disorder of advanced essential tremor. Brain. November 2001;124(Pt 11):2278-2286.
^ Singer C, Sanchez-Ramos J, Weiner WJ. Gait abnormality in essential tremor. Mov Disord. March 1994;9(2):193-196.
^ Tan EK, Fook-Chong S, Lum SY, et al. Non-motor manifestations in essential tremor: use of a validated instrument to evaluate a wide spectrum of symptoms. Parkinsonism Relat Disord. September 2005;11(6):375-380.
^ Bermejo-Pareja F, Louis ED, Benito-Leon J. Risk of incident dementia in essential tremor: A population-based study. Mov Disord 2007;22:1573-1580.
^ Louis ED, Ottman R, Hauser WA. How common is the most common adult movement disorder?: Estimates of the prevalence of essential tremor throughout the world. Mov Disord 1998;13:5-10.
^ Dogu O, Sevim S, Camdeviren H, Sasmaz T, Bugdayci R, Aral M, Kaleagasi H, Un S, Louis ED. Prevalence of essential tremor: Door-to-door neurological exams in Mersin Province, Turkey. Neurology 2003;61:1804-1807.
^ Benito-Leon J, Louis ED. Essential tremor: emerging views of a common disorder. Nat Clin Pract Neurol 2006;2:666-678.
^ Bain PG, Mally J, Gresty M, Findley LJ. Assessing the impact of essential tremor on upper limb function J Neurol 1993;241:54-61.
^ Louis ED, Barnes LF, Albert SM, Cote L, Schneier F, Pullman SL, Yu Q. Correlates of functional disability in essential tremor. Mov Disord 2001;16:914-920.
^ Critchley M. Observations on essential (heredofamilial) tremor. Brain. 1949;72:113-139.
^ Busenbark KL, Nash J, Nash S, Hubble JP, Koller WC. Is essential tremor benign? Neurology. December 1991;41(12):1982-1983.
^ Louis ED, Ford B, Barnes LF. Clinical subtypes of essential tremor. Arch Neurol 2000;57:1194-1198.
^ Deng H, Le W, Jankovic J. Genetics of essential tremor. Brain. June 2007;130(Pt 6):1456-1464.
^ Higgins JJ, Pho LT, Nee LE. A gene (ETM) for essential tremor maps to chromosome 2p22-p25. Mov Disord. 1997;12:859-864
^ Gulcher JR, Jonsson P, Kong A et al. Mapping of a familial essential tremor gene, FET1, to chromosome 3q13. Nature Genetics 1997;17:84-87.
^ Louis ED. Etiology of essential tremor: Should we be searching for environmental causes? Mov Disord 2001;16:822-829.
^ Louis ED, Vonsattel JP. The emerging neuropathology of essential tremor. Mov Disord 2007;23:174 - 182.
^ Louis ED, Faust PL, Vonsattel JPG, Honig LS, Rajput A, Robinson CA, Rajput A, Pahwa R, Lyons KE, Ross W, Borden S, Moskowitz CB, Lawton A, Hernandez N. Neuropathological changes in essential tremor: 33 cases compared with 21 controls. Brain 2007;130:3297-3307.
^ Shill HA, Adler CH, Sabbagh MN, Connor DJ, Caviness JN, Hentz JG, Beach TG: Pathologic findings in prospectively ascertained essential tremor subjects. Neurology 2008;70:1452-1455.
^ Louis, Elan D.; Keating, Garrett A., Bogen, Kenneth T., Rios, Eileen, Pellegrino, Kathryn M., Factor-Litvak, Pam (1 January 2008). "Dietary Epidemiology of Essential Tremor: Meat Consumption and Meat Cooking Practices". Neuroepidemiology 30 (3): 161–166. doi:10.1159/000122333. Retrieved 25 July 2011.
^ ^a ^b ^c Mostile, G.; Jankovic, J. (2010). "Alcohol in essential tremor and other movement disorders". Movement Disorders 25 (14): 2274–2284. doi:10.1002/mds.23240. PMID 20721919. edit
^ Dlugos, C. A.; Pentney, R. J. (1997). "Morphometric evidence that the total number of synapses on Purkinje neurons of old F344 rats is reduced after long-term ethanol treatment and restored to control levels after recovery". Alcohol and alcoholism (Oxford, Oxfordshire) 32 (2): 161–172. PMID 9105510. edit
^ Louis ED, Dure L, Pullman S. Essential tremor in childhood. Mov Disord 2001;16:921-923.
^ Bain PG, Findley LJ, Thompson PD, et al. A study of hereditary essential tremor. Brain. August 1994;117 ( Pt 4):805-824.
^ Cohen O, Pullman S, Jurewicz E, Watner D, Louis ED. Rest tremor in essential tremor patients: Prevalence, clinical correlates, and electrophysiological characteristics. Arch Neurol 2003;60:405-410.
^ Rajput AH, Rozdilsky B, Ang L, Rajput A. Significance of Parkinsonian manifestations in essential tremor. Can J Neurol Sci 1993;20:114-117.
^ Minen M, Louis ED (2008). "Emergence of Parkinson’s disease in essential tremor: A study of the clinical correlates in 53 patients". Mov Disord 23 (11): 1602–1605. doi:10.1002/mds.22161. PMC 2683412. PMID 18618664.
^ Yahr MD, Orosz D, Purohit DP. (2003). "Co-occurrence of essential tremor and Parkinson’s disease: a clinical study of a large kindred with autopsy findings.". Parkinsonism Relat Disord 9 (4): 225–231. doi:10.1016/S1353-8020(02)00057-3. PMID 12618058.
^ Benito-Leon J, Louis ED, Permejo-Pareja F. (April 2009). "Risk of incident Parkinson's disease and parkinsonism in essential tremor: a population-based study.". J Neurology Neurosurgery Psychiatry 80 (4): 423–5. doi:10.1136/jnnp.2008.147223. PMID 19289477.
^ Zesiewicz, TA; Elble, RJ, Louis, ED, Gronseth, GS, Ondo, WG, Dewey RB, Jr, Okun, MS, Sullivan, KL, Weiner, WJ (2011-11-08). "Evidence-based guideline update: treatment of essential tremor: report of the Quality Standards subcommittee of the American Academy of Neurology.". Neurology 77 (19): 1752–5. doi:10.1212/WNL.0b013e318236f0fd. PMID 22013182.
^ Lou JS, Jankovic J (February 1991). "Essential tremor: clinical correlates in 350 patients". Neurology 41 (2 ( Pt 1)): 234–8. PMID 1992367.
^ http://www.nlm.nih.gov/medlineplus/ency/article/000762.htm
^ http://neurology.jwatch.org/cgi/content/full/2004/923/1
^ http://www.uwo.ca/cns/ebn/PDFCATs/move-tremor-gabapentin-therapy.pdf
^ Thompson C, Lang A, Parkes JD, Marsden CD (1984). "A double-blind trial of clonazepam in benign essential tremor". Clin Neuropharmacol 7 (1): 83–8. doi:10.1097/00002826-198403000-00004. PMID 6367975.
^ http://www.aafp.org/afp/20051101/practice.html
^ ^a ^b ^c ^d ^e Iseri, P. K.; Karson, A.; Gullu, K. M.; Akman, O.; Kokturk, S.; Yardýmoglu, M.; Erturk, S.; Ates, N. (2011). "The effect of memantine in harmaline-induced tremor and neurodegeneration". Neuropharmacology 61 (4): 715–723. doi:10.1016/j.neuropharm.2011.05.015. PMID 21640732. edit
^ Zesiewcz TA, Elble R, Louis ED, Hauser RA, Sullivan KL, Dewey RB, Ondo WG, Gronseth GS, Weiner WJ. Practice parameter: Therapies for essential tremor. Report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology 2005;64:2008-2020.
^ Schuurman PR, Bosch DA, Bossuyt PM, et al. A comparison of continuous thalamic stimulation and thalamotomy for suppression of severe tremor. N Engl J Med. February 17, 2000;342(7):461-468.
^ Rana A.Q. An Introduction to Essential Tremor.iUniverse, Bloomington, IN 2010.
^ International Essential Tremor Foundation
^ National Tremor Foundation
^ ^a ^b ^c Miwa, H. (2007). "Rodent models of tremor". The Cerebellum 6 (1): 66–72. doi:10.1080/14734220601016080. PMID 17366267. edit
^ ^a ^b ^c Sinton, C. M.; Krosser, B. I.; Walton, K. D.; Llinás, R. R. (1989). "The effectiveness of different isomers of octanol as blockers of harmaline-induced tremor". Pflugers Archiv : European journal of physiology 414 (1): 31–36. doi:10.1007/BF00585623. PMID 2542888. edit
^ ^a ^b ^c Manto, M.; Laute, M. -A. (2008). "A possible mechanism for the beneficial effect of ethanol in essential tremor". European Journal of Neurology 15 (7): 697–705. doi:10.1111/j.1468-1331.2008.02150.x. PMID 18445025. edit
^ Carta, M.; Mameli, M.; Valenzuela, C. F. (2006). "Alcohol Potently Modulates Climbing Fiber->Purkinje Neuron Synapses: Role of Metabotropic Glutamate Receptors". Journal of Neuroscience 26 (7): 1906–1912. doi:10.1523/JNEUROSCI.4430-05.2006. PMID 16481422. edit
^ Llinás, R.; Yarom, Y. (1981). "Properties and distribution of ionic conductances generating electroresponsiveness of mammalian inferior olivary neurones in vitro". The Journal of physiology 315: 569–584. PMC 1249399. PMID 7310722. edit
^ Bushara KO, Goldstein SR, Grimes GJ, Jr., Burstein AH, Hallett M. Pilot trial of 1-octanol in essential tremor. Neurology 2004;62(1):122-124
^ Bushara, K. O.; Goldstein, S. R.; Grimes Jr, G. J.; Burstein, A. H.; Hallett, M. (2004). "Pilot trial of 1-octanol in essential tremor". Neurology 62 (1): 122–124. PMID 14718713. edit
^ ^a ^b ^c ^d Kralic, J. E.; Criswell, H. E.; Osterman, J. L.; o’Buckley, T. K.; Wilkie, M. E.; Matthews, D. B.; Hamre, K.; Breese, G. R. et al. (2005). "Genetic essential tremor in γ-aminobutyric acidA receptor α1 subunit knockout mice". Journal of Clinical Investigation 115 (3): 774–779. doi:10.1172/JCI23625. PMC 1052003. PMID 15765150. |displayauthors= suggested (help) edit

External links [edit]

International Essential Tremor Foundation (USA)
Tremor Action Network (USA)
National Tremor Foundation (UK)
Association APTES (France)
Leonid L. Rubchinsky et al. (2007) Tremor. Scholarpedia 2(10):1379
Brain Autopsies Reveal Abnormalities
Essential Tremor Centralized Brain Repository
Essential Tremor Info

UpToDate Contents

全文を閲覧するには購読必要です。 To read the full text you will need to subscribe.

1. 本態性振戦の薬理学的治療 pharmacologic treatment of essential tremor
2. 振戦の概要 overview of tremor
3. 本態性振戦の外科治療 surgical treatment of essential tremor
4. 心因性不随意運動 psychogenic movement disorders
5. ウィルソン病の臨床症状、診断、および自然史 clinical manifestations diagnosis and natural history of wilson disease

English Journal

Value of combined midbrain sonography, olfactory and motor function assessment in the differential diagnosis of early Parkinson's disease.

Busse K, Heilmann R, Kleinschmidt S, Abu-Mugheisib M, Höppner J, Wunderlich C, Gemende I, Kaulitz L, Wolters A, Benecke R, Walter U.SourceDepartment of Neurology, University of Rostock, Gehlsheimer Str 20, D-18147 Rostock, Germany; uwe.walter@med.uni-rostock.de.
Journal of neurology, neurosurgery, and psychiatry.J Neurol Neurosurg Psychiatry.2012 Apr;83(4):441-7. Epub 2012 Feb 22.
Objective Characteristic features of Parkinson's disease (PD) are asymmetric parkinsonian motor signs, hyposmia and substantia nigra (SN) hyperechogenicity on transcranial ultrasound. However, each of these features has limited diagnostic value as they may be present, albeit less frequently, in othe
PMID 22362921

Specificity of transcranial sonography in parkinson spectrum disorders in comparison to degenerative cognitive syndromes.

Lauckaite K, Rastenyte D, Surkiene D, Vaitkus A, Sakalauskas A, Lukosevicius A, Gleizniene R.AbstractABSTRACT:
BMC neurology.BMC Neurol.2012 Mar 8;12(1):12. [Epub ahead of print]
ABSTRACT:BACKGROUND: Hyperechogenicity of the substantia nigra (SN+), detected by transcranial sonography (TCS), was reported as a characteristic finding in Parkinson's disease (PD), with high diagnostic accuracy values, when compared mainly to healthy controls or essential tremor (ET) group. Howeve
PMID 22400906

Japanese Journal

Cortical activities associated with voluntary movements and involuntary movements.

Shibasaki Hiroshi
Clinical neurophysiology 123(2), 229-243, 2012-02
… The sensorimotor cortex (S1-M1) was shown to play an important role in generation of cortical myoclonus, essential tremor, Parkinson tremor and focal dystonia. … Cortical myoclonus is actively driven by S1-M1 while essential tremor and Parkinson tremor are mediated by S1-M1. …
NAID 120003824943

不随意運動に対する脳深部刺激療法(<特集>最新のニューロモデュレーション)

深谷親,小林一太,大島秀規,山本隆充,片山容一
脳神経外科ジャーナル 20(2), 80-86, 2011-02-20
急速に普及しつつある脳深部刺激療法は, 脳神経外科領域に新たな局面をもたらしたといえよう.脳深部刺激療法は, 異常をきたした神経ネットワークに可逆性をもって働きかけ, 修飾・制御し病態を改善させると考えられている.不随意運動症と難治性疼痛が主たる対象疾患である.特に不随意運動症では, パーキンソン病, ジストニア, 本態性振戦に対する効果は確立しているといえる.パーキンソン病では, 運動症状の日内 …
NAID 110008441004