Neurology Movement Disorders CM
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| Most Common type of tremor | action tremor: arise when attempting to maintain a fixed position. Putting a screw in an eyeglass
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| Two types of tremors | physiologic, essential
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| Slower frequency physiologic tremor, common later in life | Action Tremor: Essential
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| Essential tremors plus family hx | Familial tremor
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| First line therapy for Essential tremors | Beta-adrenergic blockers (eg propanolol). Can also use Primidone,Tranquilizers,alcohol
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| Intention tremor is AKA | Ataxic Tremor. Absent at rest, and at the start of a movement. Increases when fine adjustements are required. AKA Dysmetria.
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| Pathology of Dysmetria | Disease of the cerebellum or its connections. Medication usually ineffective
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| slow writhing purposeless movements usually involving the hands, tongue and face. Most commonly seen in children with cerebral palsy or as the result of kernicterus or hypoxia. | athetosis (kids with cerebral palsy often have this).
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| from Greek for dance. Involuntary, irregular jerky movements. Can cause continuous movements. Can be the result of untreated streptococcal infection (Sydenham's chorea), pregnancy (chorea gravidarum) or Huntington's disease.UNPREDICTABLE | Chorea
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| : onset of tics 2 - 13 years. Involuntary whistles, grunts and coughs and may exhibit echolalia (repetition of just heard speech) and coprolalia (uncontrolled use of offensive language). | Tourette's Syndrome
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| Treatment for Tics | Haloperidol or pimozide but often limited by side-effects.
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| Hemiballismus | Violent Flinging Movements. Unilateral hemiballismus is usually the result of an infarct in the contralateral subthalamic nucleus of Luys.
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| Shock-like contraction of a group of muscles. Irregular in rhythm and amplitude. It may involve a restricted group of muscles or be generalized. | Myoclonus
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| Common causes of myoclonus | anoxic damage, spinal cord injury, uremia, hepatic encephalopathy or evidence of a number of other rare neurologic syndromes.
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| Torticollis is the most common type of | Dystonia
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| Maintenance of a persistent extreme posture in one or more joints | Dystonia (focal). Writer's cramp, blepharospasm are other examples
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| _______ has revolutionized the treatment of Dystonia | Botulinum toxin
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| Characteristics of Parkinson's Dz | Rest Tremor (pill rolling tremor), cogwheeling, rigidity, bradykinesia, difficulty initiating movements, masked facies, stooped posture and shuffling gait, disturbance of postrual reflexes. Mean onset age 58.
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| Pathophysiology of Parkinson's Dz | Degeneration of the nigrostriatal pathway, raphe nuclei, locus ceruleu and the motor nucleus of the vagus. Neurochemically, there is a dramatic loss of dopamine containing neurons which leads to rationale for tx
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| Treatment of PD | L-dopa: carbidopa Combination (sinemet). 80% of pts significantly improve. Treats akinesia, not so much tremor
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| role of carbidopa | Carbidopa inhibits the conversion of dopa to dopamine, allows it to stay circulating and get across the BBB.
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| AE's of L-Dopa/carbidopa | nausea, vomiting, confusion, peak dose dyskinesias and on-off phenomenon.
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| Other tx for PD | Dopamine agonists, Amantadine (anti-flu medicine that may increase dopamine release), anticholinergic drugs (more effective for tremor), MOA B inhibitors, COMT
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| What breaks down dopamine? | MOA B
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| What is Deprenyl? | a MOA B inhibitor
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| How does huntington's dz first present? | symptoms often begin with psychiatric disorder (immaturity, impulsivity, and depression) later apathy and dementia.
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| What determines the age onset of Huntington's? | Length of CAG repeats. Increases every generation, so it occurs earlier and ealier in life
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| If a parent has huntington's, child has | 50% chance of getting it. 100% penetrance; will get it if they live long enough if in fact they have the gene
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| Dopamine excess is associated with which dz? | Huntington's
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| Treatment for Huntington's? | Dopamine receptor blockers such as neuroleptics (haloperidol, chlorpromazine), Dopamine Reserve Depleters
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| Huntington's is | Autosomal Dominant
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| Wilson's is | Autosomal Recessive. Parents are only carriers.
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| Onset of wilson's | neurologic sx in the second or third decades
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| Kayser-Fleischer rings and wing beating are associated with? | Wilson's Dz. (ring is from a deposition of copper)
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| Pathophysiology of Wilson's | caused by impaired copper handling. Changes in the CNS include brownish discoloration of some of the basal ganglia and a proliferation of protoplasmic astrocytes (Alzheimer Type II cells).
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| High copper foods | liver; chocolate; mushrooms; shellfish; nuts
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| Sulfurated potash with meals is used to | prevent copper absorption
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| Populations at higher risk for Tardive Dyskinesia | Young black men, elderly white women
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| Signs of Tardive Dyskinesia | Abnormal buccal-lingual movements (tongue thrusting and chewing). Head movements including head turning and bobbing can also occur. Less commonly there are also abnormal limb movements.
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| Causes of Tardive Dyskinesia | Iatrogenic disorder from long-term treatment with neuroleptics (especially high potency like haloperidol, but less commonly atypicals. Can be caused by metoclopramide, amphetamines, L-dopa. May be the result of dopamine receptor supersensitivity
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| Treatment of Tardive Dyskinesia | Stop offending drug. Most successful agent: tetrabenazine. Vit. E has also been used with questionable success.
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