Types Of Brain Injury Vigilance and agitation for Frontal akinetic mutism. akinetic mutism is differentfrom the Minimally Responsive State because the lack of movement and http://www.biausa.org/Pages/types_of_brain_injury.html
Extractions: A direct blow to the head can be great enough to injure the brain inside the skull. A direct force to the head can also break the skull and directly hurt the brain. This type of injury can occur from motor vehicle crashes, firearms, falls, sports, and physical violence, such as hitting or striking with an object. A rapid acceleration and deceleration of the head can force the brain to move back and forth across the inside of the skull. The stress from the rapid movements pulls apart nerve fibers and causes damage to brain tissue. This type of injury often occurs as a result of motor vehicle crashes and physical violence, such as Shaken Baby Syndrome. `Traumatic brain injury is an insult to the brain, not of a degenerative or congenital nature but caused by an external physical force, that may produce a diminished or altered state of consciousness, which results in an impairment of cognitive abilities or physical functioning. It can also result in the disturbance of behavioral or emotional functioning. These impairments may be either temporary or permanent and cause partial or total functional disability or psychosocial maladjustment.
Transplantation - UserLogin First, the initial presentation of akinetic mutism with a brief episode ofblepharospasm akinetic mutism is a profoundly reduced conscious state but, http://www.transplantjournal.com/pt/re/transplantation/fulltext.00007890-2003041
Extractions: Background. Muromonab-CD3 (OKT3), a mouse monoclonal antibody directed against human T lymphocytes, is a potent immunosuppressive agent used to reverse and more recently to prevent allograft rejection, mostly in cardiac transplant recipients. Neurotoxicity from OKT3 usually manifests itself as a transient aseptic meningitis and remains uncommon. Methods. The authors describe a dramatic neurologic syndrome after orthotopic heart transplant characterized by akinetic mutism, blepharospasm, anomic aphasia, and delirium. Results. Magnetic resonance imaging (MRI) showed meningeal enhancement and single-photon emission computed tomography (SPECT) showed markedly reduced tracer uptake. Discontinuation of OKT3 resulted in resolution of this neuropsychiatric syndrome and reversal of abnormalities on neuroimaging that coincided with normalization of CD3+ lymphocyte count. Conclusions. In the initial posttransplant period, it remains difficult to attribute encephalopathic signs to toxicity of immunosuppressive drugs. However, MRI and cerebral perfusion studies may help support the diagnosis. More precise characterization of the prevalence of OKT3-associated encephalopathy could come from prospective SPECT studies.
UAB Health System: Patient Stories - Chris Wilson akinetic mutism is a state in which a person is unspeaking (mute) andunmoving (akinetic). A person with akinetic mutism has sleepwaking cycles but, http://www.uab.edu/stories/wilson.html
Extractions: Chris and his wife Angela, a nurse, had been married almost nine years, had a three-year-old son and a second son on the way at the time of the accident. In this interview with Chris, his wife and some of his therapists from UAB's Spain Rehabilitation Center , we unfold the story of an accident that changed his life, and the teamwork that led him on the road to recovery.
AKINETIC MUTISM Abulia milder on spectrum of akinetic mutism, with reduced impulse to act, slowresponses (lack of initiative spontaneity) http://www.uwo.ca/cns/resident/pocketbook/approach/akineticmutism.htm
Extractions: AKINETIC MUTISM aka Coma Vigil Definition State of consciousness with preserved awareness, retention of ability to move and speak but failure to do so (immobile and mute but eyes open, follows environment, but not respond to commands) - ie. no deficit in effectors of movement or speech (like a global apraxia of interaction) Localization 1. Frontal lobe - usually bilateral medial frontal (especially cingulate gyrus) 2. Basal ganglia - ventral striatum, globus pallidus 3. Fornix / limbic system 4. Thalamus - medial nuclei 5. Diffuse white matter disease (eg. leukoencephalopathy) Differential Diagnosis 2. Apathy - dull emotional tone, able to verbalize this lack of interest - both #1 and #2 are localized to bilateral medial frontal 3. Depression - flat affect, apathetic (see #2); ? left frontal or anterior temporal Catatonia - may have posturing and stereotypy, even bouts of excitement (can respond to benzodiazepines) 5. Extrapyramidal muteness - inability to act due to increased tone and akinesia (parkinsonism) - from basal ganglia disease (incl. neuroleptic malignant syndrome)
Tentative Anatomoclinical Classification (1941) under the name of akinetic mutism. It concerns those subjects in whom It would appear therefore that the syndrome of akinetic mutism may result 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.
Coma And Other Disorders Of Consciousness - Introduction akinetic mutism with an epidermoid cyst of the 3rd ventricle A clinical andpathologic study of akinetic mutism Neurology (Minneap.) 10 (1960) 1020. http://sommeil.univ-lyon1.fr/articles/jouvet/hcn_69/contents.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 and of reactivity , will lead to another definition borrowed from psychophysiology. According to this definition, consciousness is that central nervous process which gives significance to a stimulus from the external environment. We can thus understand by consciousness that function of the nervous system which is concerned with the perceptual experience of information from the environment and from our own body (Alajouanine 1957). The multiple disintegration of consciousness observed in coma can therefore be defined as the absence, in the patient, of objective clinical (or paraclinical) signs of appreciation of his environment. It is this behavioural deficiency that the clinician explores by simple means: failure to rouse a comatose patient by calling his name or applying a painful stimulus.
02-13 akinetic mutism represents the emptying out of consciousness, a state in whichthere is not much point in anything. This talk will outline the columnar 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
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Akinesia For example, a person in coma is akinetic. For another example, akinetic mutismis a condition in which a person is both mute and akinetic. http://www.psyweb.com/Glossary/akinesia.jsp
Access To Articles : Nature The end state is akinetic mutism, a kind of waking coma. Before people startedplaying with Predictors, akinetic mutism was very rare, http://www.nature.com/nature/journal/v436/n7047/full/436150a.html
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News@nature The end state is akinetic mutism, a kind of waking coma. The fact that someindividuals descend into akinetic mutism whereas others do not just http://www.nature.com/news/2005/050704/full/436150a.html
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The Journal Of Trauma: Injury, Infection, And Critical Care - UserLogin akinetic mutism. Neurology. 1958;8238242. Context Link. 12. French JD.Brain lesions associated with prolonged unconsciousness. Arch Neurol Psychiat. http://www.jtrauma.com/pt/re/jtrauma/fulltext.00005373-200503000-00032.htm
Arousal And Gating In Neurology Of Impaired Consciousness attend hyperkinetic mutism, akinetic mutism, or temporal lobe seizures. such as the crude form of attention in akinetic mutism; the uncontrolled, http://www-users.med.cornell.edu/~jdvicto/scpl00.html
Vol.8 - 6. Diagnosis, Treatment And Care Of VCJD Patients Return to top of page 1 IBD3 tab 9 2 Dysaesthesiae unpleasant abnormal sensations3 akinetic mutism - paralysis and inability to speak 4 IBD3 tab 9 http://www.bseinquiry.gov.uk/report/volume8/chaptee2.htm
Extractions: On 21 March 1996, the CJDSU circulated to all neurologists in the UK a description of the clinical and pathological features of the new phenotype. The clinical features of the new phenotype of CJD described in the circular were as follows: An early age of onset or death (average 27.6 years, range 18-41 years). A prolonged duration of illness (average 13.1 months, range 7.5-24 months). A predominantly psychiatric presentation including anxiety, depression, withdrawal and progressive behavioural changes. The first evidence of neurological involvement in four patients was dysaesthesiae in the limbs and/or face. Development of a cerebellar syndrome with problems with gait and limb muscle coordination after a period of weeks or months. Development of forgetfulness and memory disturbance, often late in the clinical course, which progressed to severe cognitive impairment and a state of akinetic mutism
Vol.8 - 3. Establishment Of The CJD Surveillance Unit 4 akinetic mutism impairment of voluntary muscle movement, including the lossof speech 5 EEG - electroencephalogram - the recording of electrical http://www.bseinquiry.gov.uk/report/volume8/chapterc.htm
Extractions: The work of the CJDSU was reviewed by the MRC Allen Committee, chaired by Professor Ingrid Allen, which met four times between 1991 and 1995. This Committee was established on the basis of concerns raised by Professor Allen at a meeting of the MRC Coordinating Committee for Research on Spongiform Encephalopathies in Man (The Murray Committee; see vol. 2: Science ) in October 1990. She considered that the design of Dr Will's study could mean that atypical features of dementia, like those exhibited by patients developing CJD as a result of treatment with human growth hormone, might fall outside the study. A Clinical Subcommittee was therefore established to coordinate and facilitate studies relating to the epidemiological monitoring and neuropathological definition of human SEs, to monitor patients at risk of iatrogenic infection and to apply new methodologies and technologies to refine the definition and improve diagnosis of SEs. The Allen Committee had powers to co-opt relevant experts when necessary. Dr Will was a co-opted member of the group.
Extractions: Vol. 44 No. 4, April 1987 Featured Link E-mail Alerts ARTICLE Article Options Send to a Friend Readers Reply Submit a reply Similar articles in this journal Literature Track Add to File Drawer Download to Citation Manager PubMed citation Articles in PubMed by Devinsky O Rottenberg DA Articles that cite this article Contact me when this article is cited O. Devinsky, W. Lemann, A. C. Evans, J. R. Moeller and D. A. Rottenberg
APPROACH TO A PATIENT IN COMA akinetic mutism is similar to the vegetative state, except, these patients havelittle spontaneous or induced movements. Catatonic patients are mute with 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.
¥Ø¿ýºKn10-2 Baclofeninduced Reversible akinetic mutism Current diagnosis of baclofen-inducedakinetic mutism is based on clinical history and the findings of EEG. http://www.neuro.org.tw/mag4-2.htm
Extractions: ²Ä¤Q¤@¤G¨÷²Ä¤G´ÁºKn Spinal Muscular Atrophy: From Animal Model to Potential Treatments Ming-Shiun Tsai , Sue-Hong Wang , Li-Kai Tsai , and Hung Li Institute of Molecular Biology, Academia Sinica, Taipei, Taiwan; Jen-Teh Junior College of Medicine, Nursing and Management, Miaoli, Taiwan; Department of Neurology, National Taiwan University Hospital, Taipei, Taiwan Abstract- Spinal muscular atrophy (SMA) is an autosomal recessive disease characterized by degeneration of the anterior horn cells of the spinal cord leading to muscular paralysis and atrophy. SMA is the second commonest genetic cause of death in childhood affecting approximately 1 in 10,000 live births, but no effective treatment is currently available. Due to gene deletions, mutations, or conversions, the telomeric copy of the survival of motor neuron (SMN) gene is abnormal in more than 96% of patients with clinically typical SMA. The identification of SMN-interacting protein strongly suggests that it is involved in the assembly of the spliceosome, processing of pre-mRNA splicing, transcription, and metabolism of ribosomal RNA. Mouse models of human SMA have been established through a combination of knockout and transgenic techniques. These SMA-like mice genotypically and phenotypically mimic SMA
