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Basal Ganglia Diseases: more books (74)

Parkinson disease: An entry from Thomson Gale's <i>Gale Encyclopedia of Science, 3rd ed.</i> by Jordan P. Richman, 2004
Effects of verbal working memory deficits on metaphor comprehension in patients with Parkinson's disease [An article from: Brain and Language] by L. Monetta, M.D. Pell, 2007-04-01
Variable foreperiod deficits in Parkinson's disease: Dissociation across reflexive and voluntary behaviors [An article from: Brain and Cognition] by A.J. Jurkowski, E. Stepp, et all 2005-06-01
Comparison of patients with Parkinson's disease or cerebellar lesions in the production of periodic movements involving event-based or emergent timing [An article from: Brain and Cognition] by R.M.C. Spencer, R.B. Ivry, 2005-06-01
Sound lateralization in Parkinson's disease [An article from: Cognitive Brain Research] by J. Lewald, S.N. Schirm, et all 2004-11-01
Activation of conflicting responses in Parkinson's disease: evidence for degrading and facilitating effects on response time [An article from: Neuropsychologia] by S.A. Wylie, J.C. Stout, et all 2005-01
Cognitive sequence learning in Parkinson's disease and amnestic mild cognitive impairment: Dissociation between sequential and non-sequential learning ... [An article from: Neuropsychologia] by H. Nagy, S. Keri, et all 2007-01
Impaired dimensional selection but intact use of reward feedback during visual discrimination learning in Parkinson's disease [An article from: Neuropsychologia] by R. Swainson, D. SenGupta, et all
Verbal episodic memory declines prior to diagnosis in Huntington's disease [An article from: Neuropsychologia] by the Predict-HD investigators of the Huntington Stu, 2007-01
The implicit sequence learning deficit in patients with Parkinson's disease: A matter of impaired sequence integration? [An article from: Neuropsychologia] by J.G. Smith, J. McDowall,
Frontostriatal circuits are necessary for visuomotor transformation: Mental rotation in Parkinson's disease [An article from: Neuropsychologia] by M.M. Amick, H.E. Schendan, et all

lists with details

Basal Ganglia.html
which is compromised by neurodegenerative diseases that involve the basalganglia. Two such diseases, Parkinson s disease and Huntington s chorea,
http://www.unifr.ch/biochem/DREYER/BG.html

Extractions: The Basal Ganglia are a group of Functionally Related Nuclei located bilaterally in the Inferior Cerebrum, DienCephalon and MidBrain. The SubThalamic Nucleus is located in the DienCephalon, and the Substantia Nigra is located in the MidBrain. The Nuclei in the Cerebrum are collectively called the Corpus Striatum (Stripped Body) and include the Caudate Nucleus (Tail) and Lentiform Nucleus (Lens Shaped). They are the Largest Nuclei of the Brain and occupy a large portion of the Cerebrum. ( View Image ). The Basal Ganglia play an important role in planning and coordinating motor movements and posture. Complex Neural connections link the Basal Ganglia with the Cerebral Cortex.The major effect of the Basal Ganglia is to inhibit unwanted muscular activity and disorders of the Basal Ganglia result in exaggerated, uncontrolled movements. PATCH-MATRIX COMPARTMENTS AND STRIATOPALLIDAL AND STRIATONIGRAL SYSTEMS
CNS - Diseases Of Motor Function
degenerative disease involving. basal ganglia cortex. Huntington s Disease.Etiology. DA inhibitory function in the Substantia Nigra is normally inhibited
http://www.mercer.edu/pharmacy/faculty/holbrook/dss2a2.html
Media Contact Mindy Baxter 214-648-3404 Melinda.baxter@email
The researchers decided to study basal ganglia neurons and dopamine early symptoms of wellstudied degenerative diseases of the basal ganglia like
http://www.swmed.edu/home_pages/epidemi/gws/dopamine.htm

Extractions: Media Contact: Mindy Baxter melinda.baxter@email.swmed.edu BRAIN CELL DAMAGE UNDERLYING GULF WAR SYNDROME CAUSES ABNORMAL BRAIN DOPAMINE PRODUCTION, STUDY SHOWS DALLAS Sept. 14, 2000 In a study released today, researchers say they have found a strong link between brain cell loss on the left side of the brain in sick Gulf War veterans and abnormal over-production of dopamine, a neurotransmitter chemical important in such conditions as degenerative brain diseases. The UT Southwestern Medical Center at Dallas study, published in the American Medical Associations Archives of Neurology , links brain cell loss in the left basal ganglia of sick Gulf War veterans with out-of-control production of a brain neurotransmitter chemical called dopamine. With fewer total brain cells, the remaining dopamine-producing cells become over-responsive and produce too much dopamine. This finding gives increased importance to our earlier brain scan evidence of brain damage in these veterans," said Dr. Robert Haley, professor of internal medicine and holder of the U.S. Armed Forces Veterans Distinguished Chair for Medical Research, Honoring Americas Gulf War Veterans. Showing that the degree of brain cell injury directly affects the level of brain dopamine production indicates that the brain damage is having a real effect on these veterans brain function and is not just a coincidental finding. In the June issue of Radiology , UT Southwestern researchers reported that sick Gulf War veterans had 9 percent fewer brain cells in the left basal ganglia than healthy veterans. Previous research has shown that brain damage in the left basal ganglia causes a dramatic increase in dopamine production, while brain damage in the right basal ganglia has less effect.
ScienceDaily -- Browse Topics: Health/Conditions_and_Diseases/Neurological_Disor
Conditions and diseases Neurological Disorders Brain diseases basal ganglia Search Models of Information Processing in the basal ganglia
http://www.sciencedaily.com/directory/Health/Conditions_and_Diseases/Neurologica

Extractions: Text Size A A A Front Page ... Brain Diseases : Basal Ganglia Skin Cancers Growing In Young People - A Case For Prevention (August 13, 2005) full story Habit Leads To Learning, New VA/UCSD Study Shows (July 28, 2005) full story Virtual Trip To The Heart Of 400 Million Years Old Microfossils (July 25, 2005) full story Specific Regions Of Brain Implicated In Anorexia Nervosa, Finds Univ. Of Pittsburgh Study (July 8, 2005) Biological Psychiatry , University of Pittsburgh researchers found an over-activity of dopamine receptors in the basal ganglia, an area known to play a role in how people learn from experience and make choices. full story Canadian Study Demonstrates New Approach To Achieving Diabetes Control (June 16, 2005) full story Mass Production Of Human Papillomavirus Could Lead To Gains Against Cervical Cancer (June 14, 2005) full story Love May Be A Lateralized Brain Function, Like Speech; Links Seen To Stalking, Suicide, Clinical Depression, Even Autism
[WinFlash] Q1=What Is The General Role The Basal Ganglia Play In
^o diseases of the basal ganglia can be described as disruptions of the neurochemicalinteractions between basal nuclei. Q9=What are the definitions of the
http://www.openwindow.com/ftp/neuro4.fls

Extractions: [WinFlash] Q1=What is the general role the basal ganglia play in motor activity? A1=* Translates the desire to move into action ^* Planning, initiation, and termination of movements, especially those with a complex cognitive dimension. Q2=Be able to identify and label components of the basal ganglia on a diagram. A2=* Striatum (caudate nucleus and putamen) (aka corpus striatum, neostriatum) ^* Lenticular nucleus (putamen and globus pallidus) ^* Globus pallidus (internal segment = medial segment; external = lateral) (aka pallidum) ^* Substantia nigra (pars compacta and pars reticulata) ^* Subthalamic nucleus ^* (Also part of the basal ganglia circuitry are the neocortex, ventral anterior, ventral lateral, and centromedian nuclei of the thalamus) Q3=What are the primary afferent structures of the basal ganglia, the major sources of inputs to the afferent structures, and the neurotransmitters involved? A3=* Striatum is primary afferent structure ^* Inputs to striatum: neocortex (except primary visual and auditory cortices); substantia nigra pars compacta; and centromedian nucleus of the thalamus ^* Neurotransmitters: neocortex and thalamus = excitatory glutamate; substantia nigra = dopamine (excitatory and inhibitory) Q4=What is the direction of information flow through the basal ganglia? A4=* Striatum project to internal and external globus pallidus segments and project to substantia nigra pars reticulata ^* External globus pallidus project to subthalamic nucleus ^* Subthalamic nucleus project to internal globus pallidus Q5=What are the primary efferent structures of the basal ganglia and their neurotransmitters? A5=* Internal segment of globus pallidus and substantia nigra pars reticulata project to centromedian, ventral anterior, and ventral lateral thalamic nuclei, which then project to the pre-central gyrus and frontal lobe. ^* Neurotransmitters: internal globus pallidus = inhibitory GABA; substantia nigra = GABA Q6=What are major diseases of the basal ganglia and the consequent changes in basal ganglia circuitry and function? A6=* Huntington's - bilateral degeneration of striatal neurons; hyperkinetic and eventually distonia; autosomal dominant gain-of-function mutation ^* Parkinson's - bilateral substantia nigra degeneration; hypokinetic Q7=What are various basal ganglia diseases? A7=o General = movement disorders ^o Hyperkinetic = involuntary, spontaneous, uncontrollable, and relatively rapid ^o Hypokinetic = inability or slowness to initiate voluntary movements; increased muscle tone, paucity of spontaneous movements ^o Distonia = spontaneous assumption of unusual fixed postures lasting seconds to minutes Q8=What are the four basal ganglia fundamentals from Haines? A8=o Damage to, or disorders affecting, the basal ganglia lead to movement disorders and possibly changes in cognition, perception, and mentation. ^o Anatomically and functionally segregated into parallel circuits that process different types of information. ^o Function primarily through disinhibition (release of inhibition). ^o Diseases of the basal ganglia can be described as disruptions of the neurochemical interactions between basal nuclei. Q9=What are the definitions of the following terms: bradykinesia, rigidity, tremor, postural instability, chorea, athetosis, ballism, dystonia, tics, and tardive disorders? A9=* Bradykinesia - extreme slowness of movements and reflexes ^* Rigidity - resistance to passive movements (by examiner) ^* Tremor - rhythmic, regular, involuntary movement, usually of the limb ^* Postural instability - tendency to fall due to delayed proximal relfexes ^* Chorea - disease featuring involuntary, uncontrollable, purposeless movements of body and face, often with marked incoordination of the limbs ^* Athetosis - marked by continuous slow movements, expecially of the extremities; related to chorea, but with more writhing, sinuous movements ^* Ballism - extreme proximal chorea with characteristic swinging, jerking limb movements ^* Dystonia - disordered fixed postures of limbs ^* Tics - involuntary movements or vocalization characterized by brief, frequent, irregular, and purposeless contractions of several functionally related muscle groups ^* Tardive disorders - twitching of the face and tongue and involuntary motor movements of the trunk and limbs, due to prolonged use of antipsychotic drugs Q10=What are the cardinal features of Parkinsonism? A10=* Tremor, rigidity, bradykinesia, impaired postural reflexes (40% get dementia) Q11=What is the primary differential diagnosis of Parkinson's disease? A11=* Infectious: von Economo's encephalitis, a sequelae only experienced during great influenze epidemics, can cause a Parkinson-like syndrome ^* Vascular: ischemic injury to substantia nigra pars compacta ^* Drug-induced: reserpine, alpha-methyl dopa, some antipsychotics ^* MPTP use: homemade Demerol derivative was actually MPTP, which is converted to MPP+ by MAO, which leads to substantia nigra death ^* Other: benign essential tremor, progressive supranuclear palsy, multisystem atrophy, olivopontocerebellar atrophy Q12=What are the cardinal features of essential tremor? A12=* Postural and terminal movement (e.g. writing, holding a spoon, etc) tremor most prominent in the upper extremities ^* Begins unilaterally, eventually bilateral because it gets progressively worse ^* PET shows overly-excited cerebellum ^* Treatment: beta-blockers, anticonvulsants, surgery to destroy the VIM thalamus to destroy connection to cerebellum Q13=What are the cardinal features of Huntington's disease? A13=* Personality change, chorea, dementia, dysarthria, abnormal eye movements, athetosis, dystonia, rigidity Q14=What are the cardinal features of Wilson's disease? A14=* Dystonic hands and face, tremor, dysarthria, rigidity ^* Young person with dystonia has WD unless proven otherwise Q15=What are the cardinal features of Ballism? A15=* Involuntary movement affecting the proximal limb musculature, manifested as jerking, flinging movements of the extremity ^* Usually one-sided = hemiballismus Q16=What are the cardinal features of Tourette's syndrome? A16=* Multiple motor and/or phonic tics which fluctuate in type and frequency, present for more than one year ^* Tic types: face > head/shoulder > arm >> leg/trunk Q17=What are the cardinal features of dystonias? A17=* Fixed postures of limbs or muscle groups ^* Types: generalized - childhood onset; focal/segmental - adult onset Q18=What are the cardinal features of tardive disorders? A18=* "the great mimic" ^* dyskinesia (usually oral/buccal - chewing, tongue thrusting), chorea, dystonia, tics, akathisia (Stedman's - akathisia = syndrombe characterized by an inability to remain in a sitting posture, with motor restlessness and a feeling of muscular quivering) ^* caused by long-term neuroleptics; limit dosing to prevent, can't do much when they start Q19=What are the pathologies of Ballism and Parkinson's, Huntington's, and Wilson's diseases? A19=* Ballism - caused by a lesion of, or near, the contralateral subthalamic nucleus ^* Parkinson's - substantia nigra pars compacta neuronal cell death ( small clonic => moderate clonic => large clonic Q66=How can epileptic syndromes be classified? A66=* Localization-related epilepsies ^o Aka partial epilepsies ^o Idiopathic partial epilepsies (genetic) ^* Benign rolandic epilepsy ^* Benign childhood epilepsy with occipital paroysms ^* Familial temporal lobe epilepsy ^* Autosomal dominant nocturnal frontal lobe epilepsy ^o Symptomatic/cryptogenic partial epilepsy ^* Temporal lobe epilepsy ^* Frontal lobe epilepsy ^* Parietal lobe epilepsy ^* Occipital lobe epilepsy ^* Generalized epilepsies ^o Idiopathic ^* Childhood absence epilepsy ^* Juvenile absence epilepsy ^* Juvenile myoclonic epilepsy ^* Epilepsy with grand mal seizures on awakening ^* Benign neonatal familial convulsions ^* Benign myoclonic epilepsy in infancy ^* Epilepsy with seizures precipitated by specific modes of activation - reading epilepsy ^o Symptomatic/cryptogenic ^* Infantile spasms ^* Lennox Gastaut syndrome ^* Epilepsy with myoclonic absences ^* Epilepsy with myoclonic astatic seizures ^* Undetermined epilepsies ^o Landau-Kleffner syndrome ^o Epilepsy with continuous spike waves during slow wave sleep ^o Severe myoclonic epilepsy in infancy Q67=When should treatment be initiated for seizures? A67=* With single unprovoked seizure, do not treat, because most will not recur ^* Remote symptomatic causes have a higher recurrence risk, but may also just be observed if MRI and EEG are normal ^* Patients with a remote cause and a history of acute symptomatic seizures should be treated, because they have a 100% recurrence rate ^* Because there is a 20% chance that patients will be refractory to medical treatment, those patients should be considered for surgery Q68=What are the appropriate anti-epileptic drugs for different types of seizures/epilepsies? A68=* Partial epilepsy - male = phenytoin (hirsutism); female or adolescent = carbamazepine ^* Avoid valproate in pregnant women and individuals with family history of spina bifida ^* Primary generalized (idiopathic) - valproate ^* Partial seizures and generalized tonic-clonic - topiramate is an add-on ^* Partial seizures - neurontin is an add-on Q69=What is convulsive status epilepticus and how is it treated? A69=* Status epilepticus - 1) continuous seizure lasting >30 minutes; or 2) two or more sequential seizures within 30 minutes ^* Treat acutely with lorazepam (rapid onset, but short half-life) first and then phenytoin (slow onset, long half-life) in saline (not D5W, because precipitates) ^* Fosphenytoin is a good replacement for phenytoin because it is less alkaline Q70=What is the general basis for choosing a particular anticonvulsant for initiating epilepsy therapy? A70=* Selection based mainly on seizure type, not cause Q71=What generally is the main difference between a first-line and second-choice anticonvulsant when either drug would be suitable for the patient, but one is generally preferred to start treatment? A71=* A drug is generally first line because of better relative safety, not necessarily greater efficacy Q72=What is the general value of, or needs for, monitoring anticonvulsant drug serum levels? A72=* Checking serum levels allows monitoring for noncompliance (no drug in serum, patient isn't taking meds) Q73=In the context of long-term drug treatment of epilepsy, what is the most frequent cause of apparent "lack of efficacy?" A73=* Noncompliance Q74=What brain neurotransmitter seems to be the "target" of anticonvulsant action, in one way or another, depending on the anticonvulsant? A74=* Gamma-aminobutyric acid Q75=What are the normally preferred first and second drug(s) for generalized tonic-clonic seizures, absence seizures, and partial/focal seizures? A75=* Tonic-clonic seizures - 1 = phenytoin; 2 = phenobarbital ^* Absence seizures - 1 = ethosuximide; 2 = valproic acid ^* Partial/focal seizures - 1 = phenytoin; 2 = carbamazepine Q76=What are the most serious toxicities or adverse responses, as well as the more common side effects, of phenytoin, carbamazepine, phenobarbitol, valproic acid, ethosuximide, and clonazepam? A76=* Phenytoin - extensive gingival hyperplasia (UNIQUE); aggrevates absence seizures; CNS (ataxia, vertigo, diplopia, nystagmus); hematologic (folate, vit K def) ^* Carbamazepine - agranulocytosis, aplastic anemia (UNIQUE); dizziness, GI upset; vit K dependent bleeding ^* Phenobarbitol - sedation; vit K dependent bleeding; tolerance is common ^* Valproic acid - GI distress, weight gain (appetite stimulation); hepatotoxicity (IMPORTANT); alopecia (UNIQUE); teratogenic (IMPORTANT); thrombocytopenia ^* Ethosuximide - headache; dizziness; GI distress ^* Clonazepam - sedation; tolerance; seizure exacerbation when drug discontinued Q77=What anticonvulsant(s) is/are important for long-term treatment of "metabolic autoinduction?" A77=* Phenytoin and carbamazepine are autoinducers Q78=Which three anticonvulsants are hepatic inducers and which is a hepatic inhibitor? A78=* Hepatic inducers: phenytoin, carbamazepine, phenobarbitol (barbiturates, OCP's, rifampin, warfarin, theophyline) ^* Hepatic inhibitor: valproic acid (cimetidine) Q79=What is the most common mechanism of interactions between common anticonvulsants (e.g. phenytoin and barbiturates, primidone, valproic acid, carbamazepine)? A79=* Hepatic induction Q80=What is currently the "most often recommended" pharmacologic approach to managing status epilepticus? A80=* Initially IV benzodiazepine (e.g. lorazepam (ATIVAN)) ^* Follow-up with IV phenytoin (DILANTIN) Q81=What are the benefits and limitations of using IV benzodiazepine or phenytoin alone for treating status epilepticus? A81=* Benzodiazepine - fast-acting, so effects gone quickly, allowing recurrence ^* Phenytoin - enters brain slowly, so delayed onset; very alkaline, so irritating to veins (overcome with newer fos-phenytoin) Q82=What precautions must be taken, for both the mother and newborn, when phenytoin or phenobarbital is administered to pregnant women? A82=* Vitamin K and folate supplementation Q83=What region of the body is the main source of behavior? A83=* Brain Q84=How was the fact that the brain is the source of behavior first determined and what techniques have been used to establish brain-behavior linkages? A84=* First established with naturally-occurring lesions (e.g. war injuries) ^* Other - surgical lesions; electrical stimulation studies; neuropsychological test batteries; biochemical measures (e.g. CSF); neuroendocrine challenge tests; psychophysiological measures (e.g. EEG); brain imaging (e.g. CT, MRI, PET); genetic studies (e.g. gene expression or knock-outs) Q85=What are behavior and how does abnormal behavior develop? A85=* Normal - the "final common manifestation" of perceptions, cognitive processes, affective regulation, and behavioral outputs. ^* Abnormal - dysregulation of any of the aspects of normal behavior. Q86=How are the various behavioral functions (e.g. perception, cognition, affect/mood, and behavior) mediated and regulated in the brain? A86=* Mediated - various types of message transmission (e.g. electrical and neurochemical) ^* Regulated - genetic influences on neurotransmitter storage and release Q87=What is the limbic system, its important components, and the normal behaviors regulated by its components? A87=* Limbic system - collection of nuclei and tracts that are intimately related to behavioral expression in animals and man ^* Components - amygdala, hippocampus, medial forebrain bundle, septal regions, hypothalamus, and anterior cingulate cortex ^* Behaviors - pain/pleasure; reward/reinforcement; aggression; fear; appetite/satiety; taste; autonomic regulation; chronobiological rhythm; sleep; libido; short-term memory/learning; concentration; psychomotor regulation; prosody; separation/bereavement; maternal behavior Q88=Are limbic networks stable or plastic and why is this important? A88=* As with other parts of the brain, the limbic networks are plastic and consequently constantly influenced and modified by developmental, psychological, and social experiences. Q89=Why is the "mind-body" dichotomy outdated and unscientific? A89=* Because the brain is plastic and...
Brain Anatomy: Basal Ganglia
It is involved in movement coordination and cognition. Major diseases of thebasal ganglia include Huntington s disease and Parkinson s disease .
http://biology.about.com/b/a/181982.htm

Extractions: Display Latest Headlines Read Archives powered by Movable Type Advertisement Most Popular Biology Prefixes and Suffixes Biology Science Fair Project Ideas Anatomy of the Brain - Organs of the Body Biology - Articles ... Biology Prefixes and Suffixes - A What's Hot Land Biomes: Temperate Grasslands Biology Prefixes and Suffixes - zoo Land Biomes: Savannas Anatomy of the Brain - Substantia Nigra ... New York Times Company Hurricane Katrina About's Hurricane Blogs NY Times Coverage Where to Donate Exclusive: One Family's Story ... How to Explain to Kids Related Topics Animals / Wildlife Chemistry Physics Geology ... Environmental Issues Headlines Grasshopper Suicide Scientists have discovered that parasitic hairworms cause their host to...
Basal Ganglia
In current usage, the phrase basal ganglia means the caudate nucleus, When they are altered say in disorders like Huntington disease or Wilson
http://www.sci.uidaho.edu/med532/basal.htm
Basal Ganglia Cerebrovascular Disease Topic - Unified Search Environment
basal ganglia Cerebrovascular Disease MSH/MH/D020144 MSH/EP/D020144 VascularDiseases, basal ganglia MSH/EN/D020144 MSH/EN/D020144 MSH/EN/D020144
http://www.use.hcn.com.au/portals/shared/subject.`Basal Ganglia Cerebrovascular

Extractions: Infarction, hemorrhage, ischemia, or hypoxia of any component of the BASAL GANGLIA of the brain. Clinical manifestations may include involuntary or dyskinetic movements and hemiparesis (secondary to involvement of the INTERNAL CAPSULE). Etiologies include atherosclerosis, hypertension, inflammatory conditions (e.g., vasculitis), and emboli of arterial or cardiac origin. Lacunar infarctions frequently occur in the basal ganglia. Hemorrhages in this region are associated with hypertension, but may also result from the rupture of vascular malformations. Synonyms and Source Vocabularies:
Basal Ganglia Cerebrovascular Disease
basal ganglia Cerebrovascular Disease Medical.WebEnds.com.
http://medical.webends.com/kw/Basal Ganglia Cerebrovascular Disease

Extractions: WWW Medical.WebEnds.com Cerebrovascular Disease, Basal Ganglia; Basal Ganglia Vascular Disease; Lenticulostriate Diseases, Vascular; Lenticulostriate Vascular Diseases; Vascular Disease, Basal Ganglia; Vascular Diseases, Basal Ganglia Infarction hemorrhage ischemia , or hypoxia of any component of the BASAL GANGLIA of the brain . Clinical manifestations may include involuntary or dyskinetic movements and hemiparesis (secondary to involvement of the INTERNAL CAPSULE ). Etiologies include atherosclerosis, hypertension , inflammatory conditions (e.g., vasculitis ), and emboli of arterial or cardiac origin. Lacunar infarction s frequently occur in the basal ganglia Hemorrhage s in this region are associated with hypertension , but may also result from the rupture of vascular malformations.
Parkinson's Disease Tutorial
Parkinson s Disease. basal ganglia Animation Simulating the System UnderlyingParkinson s Disease (To view this animation, you ll need to download the
http://www.sci.sdsu.edu/multimedia/basalgang/

Extractions: Loma Linda University School of Medicine Course Coordinator: Michael Kirby, Ph.D. For the "Introduction to Motor Systems" lecture of A. Douglas Will, M.D.. Dr. Doug Will was the inspiration behind this animation, and it serves as a great help to medical students. This Shocked animation was created in collaboration with Jeff Sale . If you are interested in obtaining more information about this animation, please send email to jsale@sunstroke.sdsu.edu
Dr. Koop - Basal Ganglia Dysfunction
basal ganglia dysfunction involves dysfunction of the basal ganglia, can beassociated basal ganglia dysfunction, including Parkinson s disease,
http://www.drkoop.com/ency/93/001069.html

Extractions: Causes, incidence, and risk factors: Numerous brain disorders can be associated basal ganglia dysfunction, including Parkinson's disease Huntington's disease progressive supranuclear palsy , corticobasal degeneration, multiple system atrophy Wilson disease , and dystonia In addition, any insult to the brain can potentially damage the basal ganglia including strokes, metabolic abnormalities, liver disease, multiple sclerosis , infections, tumors, drug overdoses or side effects, and head trauma. When the basal ganglia are damaged, control over functions such as speech and movement may be impaired. Difficulties with starting movement, sustaining movement and stopping movement are all possible when this area is injured. * All Health Centers * Acne Addictions AIDS/HIV Alcohol Abuse Allergies Alternative Medicine Alzheimer's Arthritis Asthma Attention Deficit Disorder (ADHD) Backache Bipolar Affective Disorder Birth Control Blood Blood Pressure Bone/Joint/Tendon Bowel Brain Breast cancer Cancer Cerebral Palsy Cholesterol
AllRefer Health - Basal Ganglia Dysfunction
basal ganglia Dysfunction information center covers causes, prevention, symptoms, can cause basal ganglia dysfunction, including Parkinson s disease,
http://health.allrefer.com/health/basal-ganglia-dysfunction-info.html

Extractions: AllRefer Channels :: Yellow Pages Reference Health Home ... Contact Us Quick Jump ADD/ADHD Allergies Alzheimer's Disease Arthritis Asthma Back Pain Breast Cancer Cancer Colon Cancer Depression Diabetes Gallbladder Disease Heart Attack Hepatitis High Cholesterol HIV/AIDS Hypertension Lung Cancer Menopause Migraines/Headaches Osteoporosis Pneumonia Prostate Cancer SARS Stroke Urinary Tract Infection 1600+ More Conditions Alternative Medicine Health News Symptoms Guide Special Topics ... Medical Encyclopedia Go To Main Page Definition Basal ganglia dysfunction involves dysfunction of the basal ganglia, a brain region involved in motor control and movement. Numerous brain disorders can cause basal ganglia dysfunction, including Parkinson's disease Huntington's disease progressive supranuclear palsy , corticobasal degeneration, multiple system atrophy Wilson disease , and dystonia In addition, any insult to the brain can potentially damage the basal ganglia including strokes, metabolic abnormalities, liver disease
Elsevier.com - Adenosine Receptors And Parkinson S Disease
It is an essential book for researchers interested in the basal ganglia, purinebiology, and Parkinson s Disease. Audience Neuroscientists, neurologists
http://www.elsevier.com/wps/product/cws_home/673474

Extractions: Home Site map Regional Sites Advanced Product Search ... Adenosine Receptors and Parkinson's Disease Book information Product description Audience Author information and services Ordering information Bibliographic and ordering information Book related information Submit your book proposal Other books in same subject area About Elsevier Select your view ADENOSINE RECEPTORS AND PARKINSON'S DISEASE This book is the first definitive overview on adenosine receptor antagonists and their application to the treatment of Parkinson's Disease. The effect of these novel non-dopamine drugs on vitro and in vivo systems clearly shows their potential for the treatment of this debilitating disease. This book covers how the Parkinson's disease antagonist drug, A2A, has been researched, developed, and tested. It is an essential book for researchers interested in the basal ganglia, purine biology, and Parkinson's Disease.
Fahr's Disease
Fahr s Disease is a rare degenerative neurological disorder characterized The condition is often referred to as idiopathic basal ganglia calcification
http://my.webmd.com/hw/parkinsons/nord597.asp

Extractions: You are in Choose a Topic All Conditions ADD/ADHD Allergies Alzheimer's Arthritis Asthma Back Pain Bipolar Disorder Breast Cancer Cancer Cholesterol Management Dental Depression Diabetes Epilepsy Eye Health Heart Disease Hepatitis HIV/AIDS Hypertension Men's Conditions Mental Health Migraines/Headaches Multiple Sclerosis Osteoporosis Parkinson's Sexual Conditions Stroke Weight Control Women's Conditions According to reports in the medical literature, Fahr's Disease is often familial. Familial Fahr's Disease may be transmitted as an autosomal recessive trait or, in other affected families (kindreds), may have autosomal dominant inheritance. In other instances, the condition appears to occur randomly for unknown reasons (sporadically). Some experts suggest that the condition may sometimes result from an unidentified infection during pregnancy affecting the developing fetus (intrauterine infection).
Movement Disorders
The basal ganglia send output messages to the motor cortex, A slowly progressivedisease that destroys nerve cells in the basal ganglia and thus causes
http://www.chclibrary.org/micromed/00057050.html

Extractions: Though it seems simple and effortless, normal movement in fact requires an astonishingly complex system of control. Disruption of any portion of this system can cause a person to produce movements that are too weak, too forceful, too uncoordinated, or too poorly controlled for the task at hand. Unwanted movements may occur at rest. Intentional movement may become impossible. Such conditions are called movement disorders. Abnormal movements themselves are symptoms of underlying disorders. In some cases, the abnormal movements are the only symptoms. Disorders causing abnormal movements include: Parkinson's disease Parkinsonism caused by drugs or poisons Parkinson-plus syndromes ( progressive supranuclear palsy , multiple system atrophy, and cortical-basal ganglionic degeneration) Huntington's disease Wilson's disease Inherited ataxias ( Friedreich's ataxia , Machado-Joseph disease, and spinocerebellar ataxias) Tourette syndrome and other tic disorders Essential tremor Restless leg syndrome Dystonia Stroke Cerebral palsy Encephalopathies Intoxication Poisoning by carbon monoxide, cyanide, methanol, or manganese.
Progressive Supranuclear Palsy
Progressive supranuclear palsy is a disease of middle age. Symptoms usually begin in PSP affects the brainstem, the basal ganglia, and the cerebellum.
http://www.chclibrary.org/micromed/00062040.html

Extractions: Progressive supranuclear palsy (PSP; also known as Steele-Richardson-Olszewski syndrome) is a rare disease that gradually destroys nerve cells in the parts of the brain that control eye movements, breathing, and muscle coordination. The loss of nerve cells causes palsy, or paralysis , that slowly gets worse as the disease progresses. The palsy affects ability to move the eyes, relax the muscles, and control balance. Description PSP affects the brainstem, the basal ganglia, and the cerebellum. The brainstem is located at the top of the spinal cord. It controls the most basic functions needed for survivalthe involuntary (unwilled) movements such as breathing, blood pressure, and heart rate. The brainstem has three parts: the medulla oblongata, the pons, and the midbrain. The parts affected by PSP are the pons, which controls facial nerves and the muscles that turn the eye outward, and the midbrain, the visual center. The basal ganglia are islands of nerve cells located deep within the brain. They are involved in the initiation of voluntary (willed) movement and control of emotion. Damage to the basal ganglia causes muscle stiffness (spasticity) and
HD-Iron
MRI evaluation of basal ganglia ferritin iron and neurotoxicity in Alzheimer s and The basal ganglia contain the highest levels of iron in the brain and
http://hdlighthouse.org/see/treat/ironchelate.htm

Extractions: Cell Mol Biol (Noisy-le-grand) 2000 Jun;46(4):821-33, Cell Mol Biol (Noisy-le-grand) 2000 Jun;46(4):821-33, Bartzokis G, et al. MRI evaluation of basal ganglia ferritin iron and neurotoxicity in Alzheimer's and Huntingon's disease. Interventions aimed at decreasing brain iron levels, as well as reducing the oxidative stress associated with increased iron levels, may offer novel ways to delay the rate of progression and possibly defer the onset of AD and HD. The basal ganglia contain the highest levels of iron in the brain and post-mortem studies indicate a disruption of iron metabolism in the basal ganglia of patients with neurodegenerative disorders such as Alzheimer's disease (AD) and Huntington's disease (HD). Iron can catalyze free radical reactions and may contribute to oxidative damage observed in AD and HD brain. Magnetic resonance imaging (MRI) can quantify transverse relaxation rates, which can be used to quantify tissue iron stores as well as evaluate increases in MR-visible water (an indicator of tissue damage). A magnetic resonance imaging (MRI) method termed the field dependent relaxation rate increase (FDRI) was employed which quantifies the iron content of ferritin molecules (ferritin iron) with specificity through the combined use of high and low field-strength MRI instruments. Three basal ganglia structures (caudate, putamen and globus pallidus) and one comparison region (frontal lobe white matter) were evaluated. Thirty-one patients with AD and a group of 68 older control subjects, and 11 patients with HD and a group of 27 adult controls participated (4 subjects overlap between AD and HD controls).
Basal Ganglia Definition - Medical Dictionary Definitions Of Popular Medical Ter
basal ganglia A region consisting of 3 clusters of neurons (called the caudate Dystonia SourceMedicineNet; Huntington Disease - SourceMedicineNet
http://www.medterms.com/script/main/art.asp?articlekey=10030
Virtual Children's Hospital: Functional Anatomy Of Basal Ganglia
basal ganglia; Corpus Striatum; Striatum, Dorsal Striatum and Neostriatum Motor Tics; Parkinson s Disease. Tables. Blood Supply of basal ganglia
http://www.vh.org/adult/provider/anatomy/BasalGanglia/BasalGanglia.html

Extractions: Last Revised: May 2004 Table of Contents Definitions and Nomenclature Gross Features Neuronal Populations Connections Cortico-Striato-Thalamo-Cortical Loops Function Blood Supply Clinical Correlates Tables Blood Supply of Basal Ganglia Figures Schematic Diagram of the Direct and Indirect Corticostriate Projections Schematic Diagram of Nigrostriatal Pathway Schematic Diagram of the Direct and Indirect Striatopallidal Pathways Schematic Diagram of the Major Connections of the Basal Ganglia ... Coronal Brain Section from a Patient with Huntington's Chorea Showing Atrophy of the Caudate Nucleus This information is written primarily
Virtual Children's Hospital: Functional Anatomy Of Basal Ganglia: Clinical Corre
Disorders of the basal ganglia and the extrapyramidal system are manifested by Parkinson s Disease. This is a hypokinetic disorder characterized by
http://www.vh.org/adult/provider/anatomy/BasalGanglia/08ClinicalCorrelates.html

Extractions: Peer Review Status: Internally Peer Reviewed Disorders of the basal ganglia and the extrapyramidal system are manifested by involuntary movements that characteristically disappears in sleep. Two types of movements are associated with basal ganglia: 1) Hyperkinetic, characterized by excessive involuntary movements such as seen in chorea, athetosis, ballism, dystonia, and motor tics. 2) Hypokinetic (bradykinetic), characterized by paucity of movement, or by difficulty in initiation of movement (akinesia) as seen in Parkinson's disease. Chorea This hyperkinetic disorder is characterized by involuntary, sudden, frequent, and purposeless jerks of the extremities, head, and trunk associated with facial grimaces. The term is derived from the Greek word for "dance." The pathology in the brain is diffuse and includes the caudate nucleus ( Figure 9 ). Two clinical varieties of chorea are recognized: a benign reversible variety (Sydenham's chorea) that occurs in children as a complication of rheumatic fever, and a malignant hereditary variety (Huntington's chorea) transmitted in an autosomal dominant fashion, linked to chromosome 4, and characterized with progressive mental and cognitive deterioration. Choreic patients are often unable to sustain a hand grip (milkmaid's grip) or a protruded tongue (trombone tongue).

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