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CM Movement Disorder
Neurology Movement Disorders CM
| Question | Answer |
|---|---|
| Most Common type of tremor | action tremor: arise when attempting to maintain a fixed position. Putting a screw in an eyeglass |
| Two types of tremors | physiologic, essential |
| Slower frequency physiologic tremor, common later in life | Action Tremor: Essential |
| Essential tremors plus family hx | Familial tremor |
| First line therapy for Essential tremors | Beta-adrenergic blockers (eg propanolol). Can also use Primidone,Tranquilizers,alcohol |
| Intention tremor is AKA | Ataxic Tremor. Absent at rest, and at the start of a movement. Increases when fine adjustements are required. AKA Dysmetria. |
| Pathology of Dysmetria | Disease of the cerebellum or its connections. Medication usually ineffective |
| 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). |
| 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 |
| : 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 |
| Treatment for Tics | Haloperidol or pimozide but often limited by side-effects. |
| Hemiballismus | Violent Flinging Movements. Unilateral hemiballismus is usually the result of an infarct in the contralateral subthalamic nucleus of Luys. |
| 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 |
| Common causes of myoclonus | anoxic damage, spinal cord injury, uremia, hepatic encephalopathy or evidence of a number of other rare neurologic syndromes. |
| Torticollis is the most common type of | Dystonia |
| Maintenance of a persistent extreme posture in one or more joints | Dystonia (focal). Writer's cramp, blepharospasm are other examples |
| _______ has revolutionized the treatment of Dystonia | Botulinum toxin |
| 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. |
| 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 |
| Treatment of PD | L-dopa: carbidopa Combination (sinemet). 80% of pts significantly improve. Treats akinesia, not so much tremor |
| role of carbidopa | Carbidopa inhibits the conversion of dopa to dopamine, allows it to stay circulating and get across the BBB. |
| AE's of L-Dopa/carbidopa | nausea, vomiting, confusion, peak dose dyskinesias and on-off phenomenon. |
| 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 |
| What breaks down dopamine? | MOA B |
| What is Deprenyl? | a MOA B inhibitor |
| How does huntington's dz first present? | symptoms often begin with psychiatric disorder (immaturity, impulsivity, and depression) later apathy and dementia. |
| What determines the age onset of Huntington's? | Length of CAG repeats. Increases every generation, so it occurs earlier and ealier in life |
| 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 |
| Dopamine excess is associated with which dz? | Huntington's |
| Treatment for Huntington's? | Dopamine receptor blockers such as neuroleptics (haloperidol, chlorpromazine), Dopamine Reserve Depleters |
| Huntington's is | Autosomal Dominant |
| Wilson's is | Autosomal Recessive. Parents are only carriers. |
| Onset of wilson's | neurologic sx in the second or third decades |
| Kayser-Fleischer rings and wing beating are associated with? | Wilson's Dz. (ring is from a deposition of copper) |
| 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). |
| High copper foods | liver; chocolate; mushrooms; shellfish; nuts |
| Sulfurated potash with meals is used to | prevent copper absorption |
| Populations at higher risk for Tardive Dyskinesia | Young black men, elderly white women |
| 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. |
| 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 |
| Treatment of Tardive Dyskinesia | Stop offending drug. Most successful agent: tetrabenazine. Vit. E has also been used with questionable success. |
Created by:
ltm12