21. Volume 64 January - December 1941 akinetic mutism with an epidermoid cyst of the 3rd ventricle. H . Cairns, RC . Oldfield , JB . Pennybacker and D . Whitteridge. Pages 273 290. http://www3.oup.co.uk/jnls/supplements/braini/hdb/Volume_64/Issue_04/640273.sgm.

Volume 64: January - December 1941 Issue 4: December 1941 Abstract Akinetic mutism with an epidermoid cyst of the 3rd ventricle H Cairns RC Oldfield JB Pennybacker and D Whitteridge Pages: Part of the OUP Brain WWW service General Information Click here to register with OUP. This page is maintained by OUP admin Last updated 13 May 97 Part of the OUP Journals World Wide Web service Oxford University Press, 1997

22. Conditions And Diseases: Neurological Disorders: Brain Diseases: Akinetic Mutism Information on Conditions and Diseases, Neurological Disorders, BrainDiseases, akinetic mutism and much more Treasure Coast Health. http://treasurecoasthealth.com/treasurecoasthealth.php/Health/Conditions_and_Dis

Find Doctors on the Treasure Coast Select Specialty Ambulatory Care Anesthesiology Cardiology Dermatology Emergency Medicine Endocrinology Family Practice Gastroenterology Hematology/Oncology Infectious Diseases Internal Medicine Maxillofacial Surgery Neonatology Nephroology Neurology Neurosurgery Obstetrics/Gynecology Ophthalmology Orthopedic Surgery Otolaryngology Pathology Pediatics Physical Medicine Plastic Surgery Podiatry Psychiatry Psychology Pulmonary Radiation Oncology Radiology Rheumatology Surgery Thoracic Surgery Urology Vascular Surgery Select City Sebastian Palm Bay Vero Beach Fort Pierce Okeechobee Port St. Lucie Jensen Beach Stuart Palm City Hobe Sound Loxahatchee MENU Home Doctor Directory Health Resources Women Only ... About Us Conditions and Diseases: Neurological Disorders: Brain Diseases: Akinetic Mutism http://www.nutrisystem.com We have helped millions of people lose weight for more than 30 years. Lose up to 10 lbs. in your first month! Medicine Net - An article about akinetic mutism, what it is, the cause and symptoms. WorldMedicus - A description of akinetic mutism, with synonyms, related subjects and a link to reviews and editorials.

23. The Locked-In-Syndrome By Philippe VAN EECKHOUT, Speech Therapist-Hospital PitiĆ PLUM and POSNER emphasize the confusion that sometimes arises betweenthe LIS and akinetic mutism. There are however different conditions http://www.club-internet.fr/alis/page_13gb.html

previous page The Locked-In-Syndrome by Philippe VAN EECKHOUT ( 1997) Federation of Neurology, Professor AGID, Professor LYON-CAEN; Department headed by Professors RANCUREL and PHILIPPON. , 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.

24. Akinetic Mutism Eerste Vorige Volgende Laatste Index Tekst. Dia 24 van 33. http://coo.med.rug.nl/summerschools/neurology/presentaties/Haaxma/sld024.htm

25. Mediofrontal Akinetic Mutism Eerste Vorige Volgende Laatste Index Tekst. Dia 23 van 33. http://coo.med.rug.nl/summerschools/neurology/presentaties/Haaxma/sld023.htm

26. Brain Injury Glossary A A glossary of terms used for brain injury, AZ.Category Health Conditions and Diseases Brain Diseases...... akinetic mutism A condition of silent, alert-appearing, immobility that characterizescertain subacute or chronic states of altered consciousness. http://www.waiting.com/glossarya.html

About Brain Injury A Glossary of Terms Beginning with "A" Please wait one moment while the glossary loads. Abnormal Aneurysm Aspiration Abscess ... Articulation Click on a letter to access terms or click the "on" button to browse entire glossary. A B C D ... W Or Go To: Intracranial Pressure Understanding Coma Rancho Los Amigos Scale/ The Levels of Coma Objectives of Neurosurgery ... A Guide to Brain Anatomy Abnormal - Not average, typical or usual; not normal. [Click Here to Return to List] Abscess - A localized collection of pus in a cavity. [Click Here to Return to List] Abstract Concept - A concept or idea not related to any specific instance or object and which potentially can be applied to many different situations or objects. Persons with cognitive deficits often have difficulty undestanding abstract concepts. [Click Here to Return to List] Abstract Thinking - Being able to apply abstract concepts to new situations and surroundings. [Click Here to Return to List] Acalculia - The inability to perform simple problems of arithmetic. [Click Here to Return to List] Accident - See Terms and Definitions Related to Insurance . With respect to prevention of injuries caused by motor vehicles, the preferred term is "crash", rather than accident, so as not to suggest that the event was unavoidable.

27. 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

Creutzfeldt-Jakob Disease and How Speech Therapy Can Help 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. Title References Home

28. 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

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.

29. WebGuest - Open Directory : Health : Conditions And Diseases : Neurological Diso Sites Medicine Net An article about akinetic mutism, what it is,the cause and symptoms. WorldMedicus - A description of akinetic http://directory.webguest.com/index.cgi/Health/Conditions_and_Diseases/Neurologi

Browse thru 1000's of books about health, mind and body: About Us Privacy Statement Acceptable Use Policy Legal Notices ... Contact Us the entire directory only in Top Health Conditions and Diseases Neurological Disorders ... Brain Diseases : Akinetic Mutism Sites: Medicine Net - An article about akinetic mutism, what it is, the cause and symptoms. WorldMedicus - A description of akinetic mutism, with synonyms, related subjects and a link to reviews and editorials. Last update: 16:04 PT, Wednesday, April 3, 2002 Help build the largest human-edited directory on the web. Submit a Site Open Directory Project Become an Editor

30. Directory :: Look.com akinetic mutism (2) Sites. Medicine Net An article about akineticmutism, what it is, the cause and symptoms. WorldMedicus http://www.look.com/searchroute/directorysearch.asp?p=594553

31. 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/

APPROACH TO A PATIENT IN COMA Anthony Murro, M.D. Department of Neurology Medical College of Georgia Augusta, Georgia 3091 Contents Introduction How to identify coma States related to coma Clinical evaluation ... Outline - Evaluation of coma Introduction Coma is a challenging medical emergency. There is a broad differential diagnosis, complex physical exam, and the urgent need to diagnose and treat potentially reversible disease. This article describes an approach to the diagnosis and treatment of a patient in coma. How to identify coma 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.

32. Healthlink Template Test','Agglutinins','Air Pollution','Air Pollutions','Radioactive Air Pollution','RadioactiveAir Pollutions','akinetic mutism','Akinetic Autism','Akinetic http://healthlink.mcw.edu/search/text-search-fulllist.php?UTI

33. Clinical Symptoms Of Human TSEs illness duration; Dementia; Myoclonus; Pyramidal EEG changes; Dysphasia;Cerebellar EEG changes; akinetic mutism; Primitive reflexes; Cortical http://w3.aces.uiuc.edu/AnSci/BSE/Human_TSEs_Clinical_Symptoms.htm

Sporadic CJD (sCJD) (85% of human TSEs) Familial CJD (fCJD) (~10% of human TSEs) Fatal Familial Insomnia (FFI) GSS 6 disorders Kuru vCJD Clinical symptoms at presentation Demetia Ataxia Behavioral disturbance Demetia Ataxia Behavioral disturbance Insomnia Dementia headaches limb pains sensory or phychiatric disturbances (depression/withdrawl) dysesthesia ataxia Clinical symptoms during course of illness Rapid clinical evolution Short total illness duration Dementia Myoclonus Pyramidal EEG changes Dysphasia Cerebellar EEG changes Akinetic mutism Primitive reflexes Cortical blindness Extrapyramidal EEG changes Lower motor neuron signs Seizures Rapid clinical evolution Short total illness duration Dementia Myoclonus Pyramidal EEG changes Dysphasia Akinetic mutism Primitive reflexes Cortical blindness Extrapyramidal EEG changes Lower motor neuron signs Seizures disruption of sleep/wake cycle myoclonus sympathetic hyperactivity dementia hallucinations stupor coma hyperhidrosin pyrexia tachycardia hypertension irregular breathing ataxia myoclonus dysarthria pyramidal signs cereballar ataxia myoclonus - less common limb ataxia dysarthria nstagmus dementia parkinsonism deafness blindness gaze palsies seizures numbness Pyramidal EEG changes Extrapyramidal EEG change s ataxia dysarthria limb rigidity or rigidity no myoclonus occasionally exaggerated startled response pathologic bursts of laughter dementia in late stages sometimes late stages placid mute unresponsive death often assoc. w/ decubitus ulcers

34. BSE And CJD Linkage cerebellar involvement (% of cases), ~64, . . . depression. . . ataxia.. . involuntary movements. . . akinetic mutism. . . . . . http://w3.aces.uiuc.edu/AnSci/BSE/Human_vCJD_Linkage_to_BSE.htm

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 (

35. CJD/BSE, Monthly Statistics typical EEG and at least two of the following clinical features; myoclonus, visualor cerebellar signs, pyramidal/extrapyramidal signs or akinetic mutism. http://www.doh.gov.uk/cjd/stats/apr02.htm

A-Z site index Search Links Contact DH ... DH Home You are here: CJD/BSE Monthly statistics April 2002 CJD Key documents Committees Links ... CJD contacts MONTHLY CREUTZFELDT- JAKOB DISEASE STATISTICS Monday 2nd April 2002 The Department of Health is today issuing the latest information about the numbers of known cases of Creutzfeldt Jakob disease. This includes cases of variant Creutzfeldt Jakob disease (vCJD) - the form of the disease thought to be linked to BSE. The position is as follows: Definite and probable CJD cases in the UK: REFERRALS OF SUSPECT CJD DEATHS OF DEFINITE AND PROBABLE CJD Year Referrals Year Sporadic Iatrogenic Familial GSS *vCJD confirmed Total Total Referrals Total Deaths *As at 28th March 2002 Summary of vCJD cases Deaths Deaths from definite vCJD (confirmed): 89 Deaths from probable vCJD (without neuropathological confirmation): 18 Deaths from probable vCJD (neuropathological confirmation pending): 3 Number of deaths from definite or probable vCJD (as above): 110 Alive Number of probable vCJD cases still alive: 7 Total number of definite or probable vCJD (dead and alive): 117 The next table will be published on Tuesday 7th May 2002.

36. Virtual Naval Hospital: United States Naval Flight Surgeon Manual: Third Edition These conditions include (1) locked in syndrome, (2) psychogenic coma, (3) persistentvegetative state, (4) akinetic mutism,(5) hypersomnolence (exaggerated http://www.vnh.org/FSManual/07/07ManagementComa.html

United States Naval Flight Surgeon's Manual: Third Edition 1991: Chapter 7: Neurology Management of Coma and Unresponsiveness Naval Aerospace Medical Institute Peer Review Status: Internally Peer Reviewed The degree of drowsiness is often misrepresented on the patient'srecord. The terms obtundation, stupor, and coma are often used interchangeably. It is best to note the response the patient makes to his environment (i.e. responds to soft verbal stimuli, loud verbal stimuli,physical stimuli such as shaking, or deep painful stimuli to theextremities). Coma or absence of arousal to any external stimuli is mimicked by several other clinical conditions which should not be diagnosed as coma. These conditions include: (1) locked in syndrome, (2) psychogenic coma, (3) persistent vegetative state, (4) akinetic mutism,(5) hypersomnolence (exaggerated sleep response), and (6) brain death. All of these conditionswill look like coma and should be considered in the differential diagnosis. Locked-in syndrome is seen in brain stem infarction or metabolic conditions which cause paralysis of all four extremities without loss ofconsciousness. Generally there is preservation of eye movements and the blink reflex, and communication may be established in this manner. This may alsooccur in acute motor paralysis due to peripheral nerve or neuromuscularjunction blockade. Psychogenic coma should be considered if the patient has intact brainstem reflexes including calorics, pupillary reactions, and optokinetic nystagmus. In psychogenic coma there is an active resistance to eyelidopening and the eyes will tend to avoid looking at the examiner.

37. Creutzfeldt-Jakob Disease Surveillance System In Canada, May 2002 - Health Care in order of progression), 1 rapid progressive dementia 2 - involuntary movements(myoclonus, chorea, dystonia) 3 - akinetic mutism 4 - extrapyramidal symptoms http://www.hc-sc.gc.ca/pphb-dgspsp/hcai-iamss/cjd-mcj/cjdss-ssmcj/0502_e.html

Creutzfeldt-Jakob Disease CJD Home Page CJD-SS Family Information Physician Information ... Adobe Downloadable Document (493 KB) How to download PDF documents BULLETIN!!! Due to the recent use of new testing methods and techniques for 14-3-3 CSF protein analysis, we have noticed an increase in sensitivity of these techniques, resulting in a greater number of positive results. This phenomenon is being seen worldwide and is currently being assessed. It is therefore strongly recommended that the 14-3-3 protein analysis not be used as a screening test in the evaluation of Creutzfeldt-Jakob Disease patients, but rather as a test to be interpreted in conjunction with the overall clinical signs, symptoms and other investigations. May 2002 Highlights The 14-3-3 test must be used in conjunction with the overall clinical signs and symptoms of CJD. 121 confirmed cases of CJD identified by CJD-SS since inception. Incidence of CJD in Canada is as expected at 0.92 and 1.02 per million population.

38. Brain Diseases Brain Diseases. Back to previous level akinetic mutism Search PUBMEDfor akinetic mutism All Review Therapy Diagnosis. Auditory Diseases http://www.ohsu.edu/cliniweb/C10/C10.228.140.html

Brain Diseases Back to previous level Akinetic Mutism Search PUBMED for Akinetic Mutism: All Review Therapy Diagnosis ... Auditory Diseases, Central [2 more specific term/s, 1 more link/s] Search PUBMED for Auditory Diseases, Central: All Review Therapy Diagnosis ... Basal Ganglia Diseases [13 more specific term/s, 107 more link/s] Search PUBMED for Basal Ganglia Diseases: All Review Therapy Diagnosis ... Basal ganglia hemorrhage with hypertension, gross: U. of Utah Webpath Brain Abscess Search PUBMED for Brain Abscess: All Review Therapy Diagnosis ... Brain Damage, Chronic [1 more specific term/s, 2 more link/s] Search PUBMED for Brain Damage, Chronic: All Review Therapy Diagnosis ... Brain Diseases, Metabolic [19 more specific term/s, 25 more link/s] Search PUBMED for Brain Diseases, Metabolic: All Review Therapy Diagnosis Brain Edema Search PUBMED for Brain Edema: All Review Therapy Diagnosis ... Brain Neoplasms [4 more specific term/s, more link/s] Search PUBMED for Brain Neoplasms: All Review Therapy Diagnosis ... Tumor in the Subinsular Area: Stereotactic Volumetric Resection: NYU. Med. Ctr. Canavan Disease Search PUBMED for Canavan Disease: All Review Therapy Diagnosis ... Spongy Degeneration (Canavan Disease): Med. Coll. of Wisconsin

39. 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

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.

40. 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

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. Info. re: Baclofen muscle relaxant This article submitted by on 6/17/99. Email Address: Reversible Akinetic Mutism Possibly Induced by Baclofen Devon I. Rubin, M.D., and Elson L. So, M.D. 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)

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