LookSmart - Article Search For " Akinetic Mutism" Results for + akinetic mutism from FindArticles (showing 1 4 of 4), About. Jointhe Zeal community and help build the + akinetic mutism Directory Topic. http://www.findarticles.com/cf_0/PI/search.jhtml?isp=FA&cat=ref&cat=health&key=+
Neurological Disorders: Brain Diseases: Akinetic Mutism Conditions and Diseases Neurological Disorders Brain Diseases Information on Conditions and Diseases, Neurological Disorders, BrainDiseases, akinetic mutism and much more Treasure Coast Health. http://www.puredirectory.com/Health/Conditions-and-Diseases/Neurological-Disorde
Free Online ICD9/ICD9CM Codes And Medical Dictionary akinetic mutism Mutism, Akinetic Akinetic Autism Coma Vigil Coma Vigilans akinetic mutisms Autism, Akinetic Vigil, Coma Vigils, Coma A syndrome http://icd9.chrisendres.com/index.php?action=dictdtl&recordid=351
Akinetic Mutism From Linkspider UK Health Directory akinetic mutism by Linkspider UK, akinetic mutism links and AkineticMutism topics from our Health directory. Helping you find what http://linkspider.co.uk/Health/ConditionsandDiseases/NeurologicalDisorders/Brain
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Extractions: , Volume 35, No. 190, June 1997. The Locked-In-Syndrome (L.I.S.) is a rare neurological disorder which often puzzles the doctor. It may occur at any time during daily life. It tests our knowledge and illustrates the limitations on what we can achieve. It poses a medical and economic problem but, above all, a human one. The first description of a state resembling L.I.S. occurs in literature. In 1884, Alexander DUMAS in The Count of Monte Christo Medical books talked about this syndrome only in 1941. In 1947, for the first time, a neurologist and a neuro-surgeon diagnosed a case of Locked-In-Syndrome. Their study cited an injury to the vertebral artery resulting from a stroke to brainstem following a manipulation of the cervical vertebrae by a chiropractor. In 1966, the term "Locked-In-Syndrome" was introduced by PLUM and POSNER. Literally, this term means "locked in the interior". PLUM and POSNER defined the Locked-In-Syndrome as supranuclear motor disefferentation which produces a paralysis of the four limbs and of the last cranial nerves while not interfering with consciousness. The paralysis of the motor pathways hinders oral or gestural communication. Other names were proposed such as : ventral pontine syndrome, state of supranuclear motor disefferentation, false coma by cerebro-medullary spinal disconnection.
What Is Akinetic Mutism?...... Neither is MGH or MGH Neurology responsible for the content of any articles or replies.No messages are screened for content. What is akinetic mutism? . http://neuro-www.mgh.harvard.edu/forum_2/MultipleSclerosisF/6.18.998.18AMWhatisA
Extractions: This Web Forum is not moderated in any sense. Anyone on the Internet can post articles or reply to previously posted articles, and they may do so anonymously. Therefore, the opinions and statements made in all articles and replies do not represent the official opinions of MGH and MGH Neurology. Neither is MGH or MGH Neurology responsible for the content of any articles or replies. No messages are screened for content. This article submitted by tigger_sm on 6/18/99.
Info. Re: Baclofen Muscle Relaxant Email Address Reversible akinetic mutism Possibly Induced by Baclofen Devon I.Rubin, MD, and Elson L. So, MD A 76year-old man developed akinetic mutism http://neuro-www.mgh.harvard.edu/forum_2/CerebralPalsyF/6.17.9910.37PMInfo.re.Ba
Extractions: This Web Forum is not moderated in any sense. Anyone on the Internet can post articles or reply to previously posted articles, and they may do so anonymously. Therefore, the opinions and statements made in all articles and replies do not represent the official opinions of MGH and MGH Neurology. Neither is MGH or MGH Neurology responsible for the content of any articles or replies. No messages are screened for content. This article submitted by on 6/17/99. A 76-year-old man developed akinetic mutism after 3 days of receiving low-dosage baclofen. Electroencephalography showed a diffusely slow background with intermittent generalized sharp wave discharges. The condition resolved after discontinuing baclofen. To our knowledge, this is the first reported case of baclofen-induced akinetic mutism in a patient with normal renal function. The pathophysiology of this condition is unknown, but it may result from selective binding of the drug to the g-aminobutyric acid-B receptors located in the frontal lobes or thalamic nuclei, interrupting the thalamocortical limbic pathways. (Pharmacotherapy 1999;19(4):468-470)
02-13 and empirically based taxonomy for these primary disorders of consciousness, involvingcoma, persistent vegetative state, akinetic mutism, hyperkinetic mutism http://www.imprint-academic.demon.co.uk/T2000/02-13.html
Extractions: With the exception of work by Panksepp, Newman and Baars, and Damasio, there has been virtually no systematic work in consciousness theory on systems beneath the thalamus in terms of their critical participation in foundations for consciousness, although virtually everyone agrees that numerous reticular systems, particularly the core monoamine nuclei, are essential for consciousness. However, beyond notions of the ‘non-specific arousal’ functions supported in these core nuclei, the ventral brain gets very little attention and consciousness theory outside of the above noted authors. This talk will outline the columnar architecture and connectivities of PAG, its role in the organizing prototypes states of emotion, and the re-entry of PAG with the extended reticular thalamic activating system (ERTAS). At the end we will outline some potential implications of these connectivities for possible functional correlates of PAG networks that are just starting to be mapped. Over all, we will look at many lines of evidence that PAG should be conceptualized as a peri-reticular structure that has a foundational role in emotion, and in generating the meaningful organization of behavior by the brain through prototype emotional states. Cerebral Organization of Self, Two Types of Emotions and Consciousness
Tentative Anatomoclinical Classification (1941) under the name of akinetic mutism. 16 (1964) 285289. Daly, DD And JG.Loveakinetic mutism (a case report) Neurology (Minneap.) 8 (1958) 238-260. http://sommeil.univ-lyon1.fr/articles/jouvet/hcn_69/p8.html
Extractions: Handbook of Clinical Neurology Vol.3. P. J. Vinken and G. W. Bruyn , eds. North-Holland Publishing Company. Amsterdam,(1969) TABLE OF CONTENTS Introduction Physiopathological basis of coma (introductory remarks) Nervous structures necessary for consciousness Periodic physiological dissolution of consciousness: sleep and coma ... Tentative anatomoclinical classification FIGURES Select a figure Figure 1 Figure 2 Figure 3 Figure 4 Figure 5 Figure 6 Figure 7 Figure 8 Figure 9 MICHEL JOUVET Page of Michel Jouvet His articles on this server By correlating the preceding classification with anatomical observations on our own cases and others described in the literature, we have been able to distinguish four main anatomoclinical stages in prolonged coma ( Fig.8 The reactive apathic hypoperceptive syndrome The reactive hyperpathic-hypertonic aperceptivity syndrome In all the cases, the lesion is similar. There is either massive cortical involvement (Denst et al. 1958) or diffuse degenerative changes in the white matter of the cerebral hemispheres. The brainstem is intact in the majority of cases (with the exception of the pyramidal fibres which frequently show signs of degeneration). The areactive apathic normotonic aperceptivity syndrome This group concerns cases of very deep coma in which survival is usually limited to a few weeks. Perceptivity is lost (P5). Nonspecific reactions are altered (R2-R3) as well as reaction to pain (D2-D3), but autonomic reactions are normal. In most cases, there is no definite hypertonicity. Patients described by Jefferson (1952) under the name of parasomnia, by French (1952) under the name of prolonged uncounsciousness, and by Cravioto et al. (1958), and Trillet (1961), present the same symptomatology. The lesion common to all these patients is one affecting the upper part of the brainstem (mesencephalic reticular formation), but in most cases, there were also associated lesions of the cortex or white matter. It appears that total or subtotal destruction of the reticular system is responsible for the more severe losses of reactivity.
Extractions: Handbook of Clinical Neurology Vol.3. P. J. Vinken and G. W. Bruyn , eds. North-Holland Publishing Company. Amsterdam,(1969) TABLE OF CONTENTS Introduction Physiopathological basis of coma (introductory remarks) Nervous structures necessary for consciousness Periodic physiological dissolution of consciousness: sleep and coma ... Tentative anatomoclinical classification FIGURES Select a figure Figure 1 Figure 2 Figure 3 Figure 4 Figure 5 Figure 6 Figure 7 Figure 8 Figure 9
Paper Near the end of a patient s life, a condition known as akinetic mutism occurs. Akineticmutism is often found in the last stages of all dementias. http://webpages.marshall.edu/~adkins120/paper.html
Extractions: Creutzfeldt-Jakob is considered to be a transmissible dementia or transmissible spongiform encephalopathy, which means that the spread of the disease is similar to that of viruses. Further studies have shown that instead of a virus, Creutzfeldt-Jakob Disease or CJD, is considered to be caused by a proteinaceous infection agent or "prion" (Asher et al, 2000) that attacks nerve cells causing vacuolization, the formation of holes in the cell, and eventually cell death. To date there are no effective screening procedures or medications for early diagnosis or treatment (Henderson, 2000). Like other dementias, true diagnosis can only be made during autopsy.
Prions dementia; and at least two out of the following four clinical features MyoclonusVisual or cerebellar signs Pyramidal/extrapyramidal signs akinetic mutism. http://www.thedoctorsdoctor.com/diseases/prions.htm
Extractions: Background The Mad Cow Disease has struck terror in all consumers of beef. What is this microbe which is neither virus nor bacteria? Is it a new form of life or is it life? They have been termed prions and refers to an abnormal cellular protein resistant to most forms of viral inactivation. No DNA or RNA (nucleic acids fundamental to all life forms) have been found with prions. Prions is an acronym for proteinaceous infectious particles. They are the causative agents of a class of disease known as transmissible spongiform encephalopathies (TSE). Prions are a fascinating group of agents that challenge the conventional concepts of microbiology and even life. They contain no DNA or RNA and are conformational misfoldings of a normal protein. This mutated structure faciliates recruitment of other normal proteins into this abnormal structure. Prions have been implicated in several neurodegenerative diseases affecting many animals other than man. The noteriety of Mad Cow Disease, infecting cows in England, stems from the realization that the infectious agent causing the disease in the cows is the same agent causing Creutzfeld-Jakob disease in humans. Prior to this point, it was thought that each prion was species specific. Prions infect the central nervous system. Each of different prion strains have different incubation times and attack different portions of the brain.
Extractions: (advertisement) Home Specialties Resource Centers CME ... Patient Education Articles Images CME Patient Education Advanced Search Consumer Health Link to this site Back to: eMedicine Specialties Neurology Neurological Infections Last Updated: May 1, 2004 Rate this Article Email to a Colleague Synonyms and related keywords: AIDS dementia complex, ADC, HIV-1–associated cognitive/motor complex, AIDS encephalopathy, HIV encephalopathy, subacute HIV encephalitis, HIV-associated dementia complex, AIDS-related dementia, HIV dementia, acquired immunodeficiency syndrome, AIDS, human immunodeficiency virus, HIV, minor cognitive motor disorder, MCMD, highly active antiretroviral therapy, HAART AUTHOR INFORMATION Section 1 of 10 Author Information Introduction Clinical Differentials ... Bibliography
Safety Measures a typical EEG and at least 2 of the following characteristics myoclonus, visualor cerebellar signs, pyramidal or extrapyramidal signs and akinetic mutism. http://neurobio-www.uia.ac.be/neurobio/CJD/14-3-3/text.html
Extractions: CJD research at the university of Antwerp: Detection of Biochemical markers. Biochemical marker detection in cerebrospinal fluid of Creutzfeldt-Jakob disease patients. Bart Van Everbroeck, MSc, Patrick Cras, MD, PhD Lab of Neurobiology, Born Bunge Foundation, University of Antwerp, Universiteitsplein 1, 2610 Wilrijk, Belgium Tel 03 820 26 50 Fax 03 820 26 69 E-mail: bartve@uia.ua.ac.be cras@uia.ua.ac.be Introduction Creutzfeldt-Jakob disease (CJD) is a transmissible spongiform encephalopathy or prion disease. The most common type is sporadic CJD (80% of patients). Sporadic CJD is always fatal, mostly within 1 year. Other types are familial CJD, iatrogenic CJD (caused by medical treatment) and new variant CJD. Clinically, CJD can be diagnosed by the following symptoms: rapid progressive dementia, myoclonus, cerebellar signs, pyramidal or extrapyramidal signs and mutism (1). A useful clinical diagnostic test for CJD is the electro-encephalogram (EEG) that displays a typical pattern with repetitive sharp wave complexes. A positive EEG is a strong indication for CJD but a negative EEG does not exclude CJD as only 50-75% of CJD patients has a typical EEG (sensitivity = 67%, specificity = 86%) (2). At present, detection of the 14-3-3 protein in CSF is the only international consensus diagnostic test for CJD. We have implemented this immunoassay in our laboratory and would like to offer this test to our colleagues seeking help in differential diagnosis of CJD.
Neuropage.com Is Your Online Resource For Neurology Behavioral neurology, Frontal lobe syndromes medial akinetic mutism, UI, billeg weakness - orbitofrontal disinhibition, Witzelsucht (compulsion to say http://www.neuropage.com/
Locked In Syndrome differential diagnosis akinetic mutism is a disorder characterized by the patientappearing to be in an awake state with open eyes, but without communication. http://www.bchealthguide.org/kbase/nord/nord472.htm
Extractions: It is possible that the main title of the report is not the name you expected. Please check the synonyms listing to find the alternate name(s) and disorder subdivision(s) covered by this report. Information on the following diseases can be found in the Related Disorders section of this report: Locked-In Syndrome is characterized by complete paralysis except for voluntary eye movements. It is usually caused by lesions in the nerve centers that control muscle contractions, or a blood clot that blocks circulation of oxygen to the brain stem. In the Locked-In Syndrome, all voluntary muscles controlling movement are paralyzed, except for those performing eye and eyelid movements. Individuals with Locked-In Syndrome are conscious, but unable to speak. However, they can learn to communicate through an eye blink code.
Extractions: Possible link between BSE and Creutzfeldt-Jacob Disease Four cases of CJD among dairy farmers in the UK occurred in 1994-5 These cases resembled typical sporadic CJD . They did, however, highlight concern about the possible transmission of BSE to humans. In 1995, Britton and Bateman identified cases (2) of CJD in teenagers that had unusually kuru-type plaques. These are normally seen in only 5% of CJD cases. Patients have behavioral and psychiatric disturbances, early and progressive ataxia (failure of muscular coordination). The new cases had extensive plaque formation and identifiable patterns of prion protein immunostaining. These cases had similarities to iatrogenic CJD associated with peripheral inoculation of prions (cadaveric growth-hormone cases) and kuru which are also characterized by progressive ataxia, behavioral and psychiatric disturbances. These patients had no recognized risk factors for CJD (iatrogenic routes or previously recognized prion gene mutations), However, they did have some familial history of dementia (Collinge Subsequently, a consistent and previously unrecognized disease pattern was identified in 10 (currently 14) other cases of CJD. Six of these were diagnosed in 1994 and four in 1995. Some of the features of the disease are different from those of classic CJD and a consideration of the medical histories, genetic analysis, possibility of increased ascertainment and other possible explanations failed to provide an adequate explanation for the pattern. This cluster is being referred to as Variant CJD (
APPROACH TO A PATIENT IN COMA The coma state should be distinguished from stupor, the persistent vegetative state,lockedin-syndrome, akinetic mutism, catatonia, pseudocoma and brain death http://www.neuro.mcg.edu/amurro/coma/
Extractions: A patient with coma has eyes closed, has no sleep-wake cycle and remains unconscious despite vigorous stimulation. Unconsciousness implies that the patient has no observable evidence of awareness of self or surroundings. Coma is caused by diffuse bilateral brain, diencephalic or brainstem disease. The coma state should be distinguished from stupor, the persistent vegetative state, locked-in-syndrome, akinetic mutism, catatonia, pseudocoma and brain death. Unlike the patient in coma, a patient with stupor temporarily regains consciousness following vigorous stimulation. If consciousness does not return within 2-4 weeks, the comatose patient enters a persistent vegetative state. Unlike coma, these patients have sleep-wake cycles, spontaneous movements, and eye opening. The patient might persist in the vegetative state for months or years. Locked-in-patients are mute and have no limb, facial or horizontal eye movements. These patients communicate through vertical eye movements and blinking. Brainstem stroke is a common cause of locked-in-syndrome.
