76 results on '"Rodnitzky RL"'
Search Results
2. Impaired navigation in drivers with Parkinson's disease.
- Author
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Uc EY, Rizzo M, Anderson SW, Sparks JD, Rodnitzky RL, and Dawson JD
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- 2007
- Full Text
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3. Driving with distraction in Parkinson disease.
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Uc EY, Rizzo M, Anderson SW, Sparks JD, Rodnitzky RL, and Dawson JD
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- 2006
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4. Impaired visual search in drivers with Parkinson's disease.
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Uc EY, Rizzo M, Anderson SW, Sparks J, Rodnitzky RL, and Dawson JD
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- 2006
5. Visual dysfunction in Parkinson disease without dementia.
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Uc EY, Rizzo M, Anderson SW, Qian S, Rodnitzky RL, and Dawson JD
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- 2005
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- View/download PDF
6. A randomized, placebo-controlled trial of coenzyme Q(10) and remacemide in Huntington's disease
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Kieburtz, K., Koroshetz, W., Mcdermott, M., Beal, Mf, Greenamyre, Jt, Ross, Ca, Shoulson, I., Cudkowicz, Me, Sexton, P., Skeuse, C., Rosas, D., Jenkins, B., Rosenblatt, A., Sherr, M., Hersch, S., Cellar, J., Guttman, M., Brown, C., Como, Pg, Marshall, F., Demarcaida, Ja, Zimmerman, C., Marder, K., Moskowitz, C., Polanco, C., Beltre, J., Shannon, K., Jaglin, Ja, Niederman, F., Ashizawa, T., Hunter, C., Hauser, R., Walker, A., Gauger, L., Hahn, Ma, Delgado, H., Dawson, T., Siemers, E., Seeberger, L., Dingmann, C., Dubinsky, R., Gray, C., Weiner, Wj, Rodriguez-Batemen, D., Albin, Rl, Wernette, K., Harrison, M., Rost-Ruffner, E., Paulsen, J., Rodnitzky, Rl, Dobson, J., Vining, L., Suchowersky, O., Pantella, C., Saint-Hilaire, Mh, Furtado, J., Martin, W., Wieler, M., Walker, F., Hunt, V., Lynn Raymond, Almqvist, E., Rubin, A., Blair, B., Marek, K., Caplan, K., Baker, D., Brocht, A., Casaceli, C., Orme, C., Rudolph, A., Rumfola, L., Schifitto, G., Shinaman, A., Sulimowicz, K., Watts, A., Eapen, S., Zhang, L., and HUNTINGTON STUDY GRP
7. Progress in combating levodopa-induced dyskinesia.
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Rodnitzky RL
- Published
- 2004
8. Amantadine's role in the treatment of levodopa-induced dyskinesia.
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Rodnitzky RL and Narayanan NS
- Subjects
- Antiparkinson Agents adverse effects, Humans, Levodopa adverse effects, Parkinson Disease drug therapy, Amantadine therapeutic use, Antiviral Agents therapeutic use, Dyskinesia, Drug-Induced drug therapy
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- 2014
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9. Prefrontal dopamine signaling and cognitive symptoms of Parkinson's disease.
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Narayanan NS, Rodnitzky RL, and Uc EY
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- Acetylcholine metabolism, Animals, Cognition Disorders etiology, Humans, Parkinson Disease complications, Parkinson Disease pathology, Prefrontal Cortex pathology, Signal Transduction, Cognition Disorders metabolism, Dopamine metabolism, Parkinson Disease metabolism, Prefrontal Cortex metabolism
- Abstract
Cognitive dysfunction is a common symptom of Parkinson's disease (PD) that causes significant morbidity and mortality. The severity of these symptoms ranges from minor executive symptoms to frank dementia involving multiple domains. In the present review, we will concentrate on the aspects of cognitive impairment associated with prefrontal dopaminergic dysfunction, seen in non-demented patients with PD. These symptoms include executive dysfunction and disorders of thought, such as hallucinations and psychosis. Such symptoms may go on to predict dementia related to PD, which involves amnestic dysfunction and is typically seen later in the disease. Cognitive symptoms are associated with dysfunction in cholinergic circuits, in addition to the abnormalities in the prefrontal dopaminergic system. These circuits can be carefully studied and evaluated in PD, and could be leveraged to treat difficult clinical problems related to cognitive symptoms of PD.
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- 2013
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10. Upcoming treatments in Parkinson's disease, including gene therapy.
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Rodnitzky RL
- Subjects
- Animals, Clinical Trials as Topic trends, Genetic Therapy methods, Humans, Treatment Outcome, Antiparkinson Agents therapeutic use, Genetic Therapy trends, Parkinson Disease genetics, Parkinson Disease therapy
- Abstract
Progress is being made in the development of three categories of therapy for Parkinson's disease: (1) Symptomatic, (2) Neuroprotective, (3) Neurorestorative. Evolving approaches to symptomatic therapy, already in clinical trials, include the use of adenosine 2(A) antagonists, novel glutamate antagonists, and serotonin receptor antagonists, the latter for the therapy of Parkinson's psychosis and/or levodopa-induced dyskinesias. Examples of promising neuroprotective therapies under evaluation include the administration of creatine, urate-inducing compounds, calcium channel blockers, and pioglitazone, a peroxisome proliferator-activated receptor agonist. Cell-based restorative therapies are not the subject of this presentation, but various forms of gene therapy have shown promise in human Parkinson's disease trials. These protocols typically involve gene transfer into the CNS through the use of viral vectors. Currently, the most advanced studies of this technique involve delivery of an adeno-associated viral vector encoding glutamic acid decarboxylase into the subthalamic nucleus. This treatment has shown modest benefit in early clinical trials. Other gene therapies, in various stages of human clinical trials, include gene transfer for the production of trophic factors, for aromatic amino acid decarboxylase alone, and most recently, a lentiviral vector transfer of an enzymatic dopamine "factory" consisting of three essential enzymes required for production for this neurotransmitter., (Copyright © 2011 Elsevier Ltd. All rights reserved.)
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- 2012
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11. Cerebellar pathology and essential tremor: did Dr. Purkinje leave any fingerprints?
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Rodnitzky RL
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- Female, Humans, Male, Cerebellum pathology, Essential Tremor pathology, Purkinje Cells pathology
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- 2011
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12. Juvenile parkinsonism: epidemiology, diagnosis and treatment.
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Thomsen TR and Rodnitzky RL
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- Adolescent, Age of Onset, Antiparkinson Agents adverse effects, Diagnosis, Differential, Humans, Young Adult, Antiparkinson Agents therapeutic use, Parkinsonian Disorders diagnosis, Parkinsonian Disorders drug therapy, Parkinsonian Disorders epidemiology, Parkinsonian Disorders etiology
- Abstract
Juvenile parkinsonism, with onset prior to age 21 years, is a relatively rare syndrome. It is caused by a group of heterogeneous entities that can present with a clinical picture similar to idiopathic Parkinson's disease or manifest parkinsonism as part of a spectrum of other signs. Diagnostic testing is guided by the presenting symptoms and aimed at uncovering potentially reversible and/or treatable causes. If an underlying condition is found, treatment is tailored accordingly. Otherwise, treatment is symptomatic and relies on medications commonly employed to treat idiopathic Parkinson's disease. Juvenile parkinsonism patients tend to be plagued by treatment-induced complications, so caution must be employed.
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- 2010
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13. Impaired Curve Negotiation in Drivers with Parkinson's Disease.
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Uc EY, Rizzo M, Dastrup E, Sparks J, Anderson SW, Rodnitzky RL, and Dawson JD
- Published
- 2009
14. From essential tremor to Klinefelter through Fragile X, an unexpected journey.
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Harlow TL, Rodnitzky RL, and Gonzalez-Alegre P
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- Aged, Fragile X Syndrome complications, Fragile X Syndrome diagnosis, Humans, Male, Tremor diagnosis, Klinefelter Syndrome complications, Klinefelter Syndrome diagnosis, Tremor etiology
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- 2008
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15. Isolated high-frequency jaw tremor relieved by botulinum toxin injections.
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Gonzalez-Alegre P, Kelkar P, and Rodnitzky RL
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- Adult, Electromyography drug effects, Female, Humans, Injections, Intramuscular, Jaw Diseases diagnosis, Jaw Diseases physiopathology, Masseter Muscle drug effects, Masseter Muscle physiopathology, Tremor diagnosis, Tremor physiopathology, Voice Disorders diagnosis, Voice Disorders physiopathology, Botulinum Toxins, Type A therapeutic use, Jaw Diseases drug therapy, Tremor drug therapy, Voice Disorders drug therapy
- Abstract
Jaw tremor can be seen as a component of various neurological disorders such as essential tremor, Parkinson's disease, dystonia, branchial myoclonus, hereditary geniospasm, task-specific tremor, and Whipple's disease, as well as in normal situations such as shivering, and subclinical physiological jaw tremor. In most of these conditions, the jaw tremor is usually associated with tremor or other abnormal involuntary movements affecting additional body parts, and its frequency is lower than 12 Hz. Schrag and colleagues reported a patient with a high-frequency idiopathic jaw tremor, and they speculated it could be related to orthostatic tremor affecting the masseter muscles. We encountered a similar patient with intermittent rapid focal jaw tremor that was successfully treated with botulinum toxin injections to the masseters., ((c) 2006 Movement Disorder Society.)
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- 2006
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16. Predictors of weight loss in Parkinson's disease.
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Uc EY, Struck LK, Rodnitzky RL, Zimmerman B, Dobson J, and Evans WJ
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- Aged, Disability Evaluation, Disease Progression, Female, Follow-Up Studies, Hallucinations diagnosis, Humans, Male, Middle Aged, Reference Values, Retrospective Studies, Risk Factors, Lewy Body Disease diagnosis, Parkinson Disease diagnosis, Weight Loss
- Abstract
The objective of this study was to examine the change of body weight (BW) among Parkinson's disease (PD) patients and controls over years and determine the predictors of weight loss among PD patients. Studies on weight loss in PD studies are cross-sectional, have a short follow-up, or lack in clinical detail. We examined the percentage of BW change over years among 49 PD patients and 78 controls. The controls were from another study on longitudinal evolution of BW and body composition in the elderly. We determined the BW, Hoehn and Yahr (HY) stage, and dyskinesia status of 49 consecutive nondemented PD patients with symptom duration of 6.1 +/- 0.7 years (mean +/- SEM) and ascertained their BW at the time of diagnosis and 2.4 +/- 0.2 years before the diagnosis from medical records. We collected data again 7.2 +/- 0.5 years after the first visit. The PD group lost 7.7% +/- 1.5% of BW over the entire symptomatic period (13.1 +/- 0.8 years), while the control group lost only 0.2% +/- 0.7% of BW over 9.9 +/- 0.1 years; weight loss was clinically significant (>5%) in 55.6% of PD patients vs. 20.5% of the controls (both P values < 0.001, adjusted for sex, baseline age, and observation period duration). PD patients lost weight in both the early and advanced phases. While worsening of parkinsonism was the most important factor, age at diagnosis, emergence of visual hallucinations, and possibly dementia were also associated with weight loss. We demonstrated significant weight loss in PD patients compared to controls over approximately 1 decade. Neurodegeneration involving both motor and nonmotor systems may be associated with weight loss in PD., ((c) 2006 Movement Disorder Society.)
- Published
- 2006
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17. Efficacy and safety of botulinum type A toxin (Dysport) in cervical dystonia: results of the first US randomized, double-blind, placebo-controlled study.
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Truong D, Duane DD, Jankovic J, Singer C, Seeberger LC, Comella CL, Lew MF, Rodnitzky RL, Danisi FO, Sutton JP, Charles PD, Hauser RA, and Sheean GL
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- Adult, Aged, Antibody Formation, Disability Evaluation, Dose-Response Relationship, Drug, Double-Blind Method, Drug Evaluation, Female, Follow-Up Studies, Humans, Male, Middle Aged, Pain Measurement methods, Patient Satisfaction, Prospective Studies, Time Factors, Torticollis immunology, United States, Botulinum Toxins, Type A therapeutic use, Neuromuscular Agents therapeutic use, Torticollis drug therapy, Treatment Outcome
- Abstract
Botulinum toxin type A (Dysport) has been shown in European studies to be a safe and effective treatment for cervical dystonia. This multicenter, double-blind, randomized, controlled trial assessed the safety and efficacy of Dysport in cervical dystonia patients in the United States. Eighty patients were randomly assigned to receive one treatment with Dysport (500 units) or placebo. Participants were followed up for 4 to 20 weeks, until they needed further treatment. They were assessed at baseline and weeks 2, 4, 8, 12, 16, and 20 after treatment. Dysport was significantly more efficacious than placebo at weeks 4, 8, and 12 as assessed by the Toronto Western Spasmodic Torticollis Rating Scale (10-point vs. 3.8-point reduction in total score, respectively, at week 4; P < or = 0.013). Of participants in the Dysport group, 38% showed positive treatment response, compared to 16% in the placebo group (95% confidence interval, 0.02-0.41). The median duration of response to Dysport was 18.5 weeks. Side effects were generally similar in the two treatment groups; only blurred vision and weakness occurred significantly more often with Dysport. No participants in the Dysport group converted from negative to positive antibodies after treatment. These results confirm previous reports that Dysport (500 units) is safe, effective, and well-tolerated in patients with cervical dystonia., (Copyright 2005 Movement Disorder Society.)
- Published
- 2005
- Full Text
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18. Drug-induced movement disorders in children and adolescents.
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Rodnitzky RL
- Subjects
- Acute Disease, Adolescent, Age Factors, Child, Humans, Incidence, Risk Factors, Dyskinesia, Drug-Induced physiopathology, Psychotropic Drugs adverse effects, Psychotropic Drugs therapeutic use
- Abstract
The use of psychotropic medication among children and adolescents is increasing with a concomitant increase in the incidence of drug-related movement disorders. This class of adverse reactions to medications can be divided into those that are acute in onset, others that are continuous as long as the offending drug is administered, and a final category consisting of symptoms that are persistent, even after the causative agent has been discontinued. Within these three categories, this review discusses the epidemiology, risk factors, clinical features and treatment of acute dystonic reactions, drug-induced parkinsonism, neuroleptic malignant syndrome, serotonin syndrome, acute akathisia, and the tardive syndromes. In addition, drugs that commonly cause tremor, chorea, or myoclonus are included.
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- 2005
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19. Moyamoya-induced paroxysmal dyskinesia.
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Gonzalez-Alegre P, Ammache Z, Davis PH, and Rodnitzky RL
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- Adolescent, Adult, Female, Humans, Moyamoya Disease complications, Neurologic Examination, Chorea etiology, Moyamoya Disease diagnosis
- Abstract
Moyamoya disease (MMD) is an uncommon intracranial vasculopathy that typically presents with ischemic or hemorrhagic stroke. Persistent choreoathetosis has been identified as a rare early manifestation of MMD. We present 2 patients with paroxysmal dyskinesia as the initial symptom of MMD, one resembling paroxysmal kinesigenic dyskinesia (PKD) and the other paroxysmal non-kinesigenic dyskinesia (PNKD). We also review the cases of moyamoya-induced chorea reported previously, none of which resembled PKD or PNKD. We hypothesize that both hormonal and ischemic factors may be implicated in the pathogenesis of these abnormal involuntary movements. These cases suggest that MMD should be included in the differential diagnosis of PKD and PNKD., (Copyright 2003 Movement Disorder Society)
- Published
- 2003
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20. The midlatency auditory evoked potential P50 is abnormal in Huntington's disease.
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Uc EY, Skinner RD, Rodnitzky RL, and Garcia-Rill E
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- Acoustic Stimulation, Adult, Case-Control Studies, Electroencephalography methods, Female, Humans, Male, Middle Aged, Evoked Potentials, Auditory physiology, Huntington Disease physiopathology, Reaction Time physiology
- Abstract
The P50 (or P1) potential is a midlatency auditory evoked response, believed to be partially generated by the cholinergic pedunculopontine nucleus (PPN) neurons that give rise to the ascending reticular activating system (RAS). We compared the P50 potential in 11 Huntington's disease (HD) patients and 13 normal controls using a paired click stimulus paradigm. HD patients exhibited a P50 potential with reduced amplitude and increased latency to the first stimulus of the pair (first P50 potential), suggesting impaired ascending reticular activating system function, which may contribute to sleep disorders seen in HD. Sensory gating, measured as the percent ratio of the second P50 potential amplitude to the first P50 potential amplitude, was reduced at 250 and 500 ms interstimulus intervals (ISI), which may be related to disordered attention and anxiety in HD.
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- 2003
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21. Albuterol improves response to levodopa and increases skeletal muscle mass in patients with fluctuating Parkinson disease.
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Uc EY, Lambert CP, Harik SI, Rodnitzky RL, and Evans WJ
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- Aged, Albuterol pharmacology, Analysis of Variance, Area Under Curve, Drug Therapy, Combination, Female, Humans, Male, Middle Aged, Muscle, Skeletal physiology, Parkinson Disease physiopathology, Pilot Projects, Statistics, Nonparametric, Albuterol therapeutic use, Levodopa therapeutic use, Muscle, Skeletal drug effects, Parkinson Disease drug therapy
- Abstract
Animal studies indicate that beta(2)-adrenergic receptor agonists enhance transport of levodopa across the blood-brain barrier. Preliminary studies showed improved response to levodopa in patients with Parkinson disease (PD) who were given albuterol as adjunctive therapy. Beta(2)-adrenergic agonists may offer additional benefits to PD patients via their skeletal muscle anabolic effects, particularly those who experience decreased muscle strength and weight loss. Nondemented, fluctuating PD patients receiving levodopa but not experiencing severe dyskinesias underwent the following tests at baseline and 14 weeks after treatment with albuterol sulfate (4 mg four times a day, orally): Unified Parkinson's Disease Rating Scale motor, tapping, and stand-walk-sit tests every 30 minutes between 8 am and 5 pm; body composition analyses using whole-body plethysmography and computed tomography of the thigh; muscle strength tests; and the Parkinson's Disease Questionnaire (PDQ-39). Results were analyzed using paired t-tests (2 tailed), repeated-measures analysis of variance, and the Wilcoxon signed-rank test. Seven of 8 enrolled patients completed the study; 1 patient withdrew because of headache and anxiety. The area under the curve for all-day UPDRS motor scores improved by 9.8 +/- 9.1% (mean +/- standard deviation; P < 0.05) and tapping improved by 7.6 +/- 8.1% (P < 0.05). The effect was more pronounced when only the response to the first levodopa dose (area under the curve, 8-11 am) was analyzed: 13.0 +/- 9.8% and 9.8 +/- 9.6% respectively. Thigh muscle cross-sectional area increased significantly as measured by computed tomography (5.3 +/- 3.2%, P < 0.01), as did fat-free mass by whole-body plethysmography combined with total-body water determination (9.5 +/- 2.9%, P < 0.05). There was no significant improvement in the stand-walk-sit test, muscle strength tests, other UPDRS sections, daily OFF time, or PDQ-39. Four patients were rated as having a mild global improvement (+1 point) on a -3 to +3-point scale, and 3 of them chose to continue albuterol beyond the termination of the study. The mean heart rate increased from 78.3 +/- 9.3 beats/minute to 85.6 +/- 8.7 beats/minute (P < 0.05). No laboratory abnormalities or electrocardiographic changes were induced by albuterol in any subject. This open-label pilot study suggests that albuterol increases muscle mass and improves the therapeutic response to levodopa in patients with fluctuating PD. A double-blind, placebo-controlled study is needed to confirm the effects and safety profile of beta(2)-agonists in PD.
- Published
- 2003
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22. Traumatic internal carotid artery dissection associated with taekwondo.
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Pary LF and Rodnitzky RL
- Subjects
- Adult, Amaurosis Fugax etiology, Aphasia, Wernicke etiology, Brain Damage, Chronic etiology, Headache etiology, Humans, Magnetic Resonance Imaging, Male, Paresis etiology, Carotid Artery Injuries etiology, Carotid Artery, Internal, Dissection etiology, Infarction, Middle Cerebral Artery etiology, Martial Arts injuries
- Published
- 2003
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23. Tremor in children.
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Uddin MK and Rodnitzky RL
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- Child, Craniocerebral Trauma complications, Craniocerebral Trauma diagnosis, Endocrine System Diseases complications, Endocrine System Diseases diagnosis, Essential Tremor etiology, Essential Tremor therapy, Humans, Metabolic Diseases complications, Metabolic Diseases diagnosis, Parkinsonian Disorders complications, Parkinsonian Disorders diagnosis, Tremor etiology, Tremor therapy, Essential Tremor diagnosis, Tremor diagnosis
- Abstract
Tremor in childhood, beginning in the neonatal period, is more common than generally appreciated. Although some tremor disorders in children (eg, essential tremor) also affect adults, others (eg, shuddering, jitteriness, spasmus nutans, and vitamin B12-deficiency tremor) are seen exclusively in children. This review covers the etiology, clinical features, and treatment of the major tremor syndromes in children, and when appropriate, makes comparisons with similar disorders in adults.
- Published
- 2003
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24. Drug-induced movement disorders in children.
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Rodnitzky RL
- Subjects
- Central Nervous System Agents therapeutic use, Child, Dyskinesia, Drug-Induced etiology, Humans, Mental Disorders drug therapy, Central Nervous System Agents adverse effects, Dyskinesia, Drug-Induced diagnosis, Dyskinesia, Drug-Induced prevention & control
- Abstract
The increased use of stimulants, antipsychotic agents, and antidepressant drugs in children by primary care physicians, psychiatrists, and neurologists has inevitably led to increased numbers of pediatric patients manifesting the side effects of these agents, many of which are movement disorders. Unlike the isolated abnormal involuntary movements associated with drugs prescribed for epilepsy or asthma, movement syndromes (eg, acute dystonic reaction, neuroleptic malignant syndrome, serotonin syndrome, tardive dyskinesia) associated with psychotropic drugs are complex, difficult to recognize, and potentially seriously disabling. Accurate clinical identification of these drug-induced syndromes is critical to engaging the proper therapeutic intervention for them.
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- 2003
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25. Juvenile parkinsonism.
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Uc EY and Rodnitzky RL
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- Child, Humans, Parkinsonian Disorders genetics, Parkinsonian Disorders metabolism, Parkinsonian Disorders etiology
- Abstract
Juvenile parkinsonism (JP) is a clinically and etiologically heterogeneous entity. Unlike in the adult form, secondary causes, hereditary and metabolic conditions, are the predominant causes of JP. Idiopathic Parkinson's disease is very rare in this age group. In most cases of JP, parkinsonism is accompanied by other neurologic features, such as dystonia, cognitive impairment, seizures, oculomotor and visual dysfunction, and ataxia. Systemic findings, such as liver dysfunction or hepatosplenomegaly, may be present depending on the cause. This review article describes the clinical characteristics, classification, genetic basis, pathophysiology, biochemistry, pathology, and treatment of JP.
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- 2003
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26. Childhood dystonia.
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Uc EY and Rodnitzky RL
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- Child, Genetic Predisposition to Disease, Humans, Dystonia diagnosis, Dystonia drug therapy, Dystonia genetics
- Abstract
Childhood dystonias are a heterogeneous group of disorders with strong inherited basis. This review describes the clinical characteristics, classification, genetic basis, pathophysiology, biochemistry, pathology, and treatment of dystonias, including the primary dystonias, the dystonia-plus syndromes, secondary dystonias, and heredodegenerative disorders. Conditions discussed in detail include idiopathic torsion dystonia, dopa-responsive dystonia, Wilson's disease, myoclonus dystonia, rapid-onset dystonia parkinsonism, neurodegeneration with brain iron accumulation (Hallervorden-Spatz syndrome), mitochondrial dystonias, Niemann-Pick type C, and neuroacanthocytosis.
- Published
- 2003
- Full Text
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27. Head and neck muscle spasm after radiotherapy: management with botulinum toxin A injection.
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Van Daele DJ, Finnegan EM, Rodnitzky RL, Zhen W, McCulloch TM, and Hoffman HT
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- Aged, Female, Humans, Injections, Intramuscular, Male, Middle Aged, Pain Measurement, Treatment Outcome, Botulinum Toxins, Type A administration & dosage, Botulinum Toxins, Type A therapeutic use, Head and Neck Neoplasms radiotherapy, Neck Muscles drug effects, Neck Muscles radiation effects, Neuromuscular Agents administration & dosage, Neuromuscular Agents therapeutic use, Pain drug therapy, Pain etiology, Radiotherapy adverse effects, Spasm drug therapy, Spasm etiology
- Abstract
Objective: To introduce the concept of neck muscle pain and spasm after radiotherapy and its treatment with botulinum toxin A., Design: Case series., Setting: Ambulatory patients at a tertiary care medical center., Patients: Individuals who had undergone primary or adjuvant radiotherapy for treatment of carcinoma of the head and neck were asked about painful spasms of the neck musculature. A volunteer sample was used. If they desired treatment with botulinum toxin A, they were included in the study., Intervention: Patients received botulinum toxin A injections to the affected sternocleidomastoid muscle(s) in 1 or 2 locations., Outcome Measure: Subjective pain relief., Results: Four of 6 patients with painful tightness of the neck who received botulinum toxin A injections to the sternocleidomastoid muscle achieved pain relief., Conclusions: A subset of patients with irradiation-induced cervical muscle spasm benefit from treatment with botulinum toxin A injections. Further study is needed to more clearly define the entity and treatment.
- Published
- 2002
- Full Text
- View/download PDF
28. Drug-induced movement disorders.
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Rodnitzky RL
- Subjects
- Acute Disease, Akathisia, Drug-Induced diagnosis, Akathisia, Drug-Induced etiology, Akathisia, Drug-Induced therapy, Chronic Disease, Dyskinesia, Drug-Induced diagnosis, Dyskinesia, Drug-Induced etiology, Dyskinesia, Drug-Induced therapy, Humans, Neurotoxicity Syndromes diagnosis, Neurotoxicity Syndromes therapy, Drug-Related Side Effects and Adverse Reactions, Neurotoxicity Syndromes etiology
- Published
- 2002
- Full Text
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29. Neuropathology of two members of a German-American kindred (Family C) with late onset parkinsonism.
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Wszolek ZK, Gwinn-Hardy K, Wszolek EK, Muenter MD, Pfeiffer RF, Rodnitzky RL, Uitti RJ, McComb RD, Gasser T, and Dickson DW
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- Aged, Aged, 80 and over, Chromosomes, Human, Pair 2 genetics, Female, Genetic Linkage, Genetic Predisposition to Disease genetics, Germany ethnology, Humans, Longitudinal Studies, Male, Parkinsonian Disorders genetics, Pedigree, United States, Brain pathology, Parkinsonian Disorders pathology
- Abstract
We present genealogical and longitudinal clinical observations and autopsy findings of a previously reported kindred, Family C (German-American), with late-onset autosomal dominant parkinsonism with evidence for linkage on chromosome 2p13. The clinical phenotype includes the cardinal features of idiopathic Parkinson's disease. In addition, postural tremor and dementia are detected in some individuals. Two members of the kindred, one affected and one unaffected have recently come to autopsy. The unaffected family member was an 82-year-old woman whose brain showed only mild age-related pathology and no evidence of subclinical Lewy body disease. In contrast, the affected family member was an 83-year-old man whose brain had neuronal loss, gliosis and Lewy bodies in the substantia nigra and other monoaminergic brain stem nuclei, as well as the basal forebrain and amygdala. Lewy bodies and Lewy neurites had a distribution typical of cases of idiopathic Parkinson's disease. Thus, the clinical and pathological findings in this family with autosomal dominant parkinsonism are similar to those of sporadic Parkinson's disease.
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- 2002
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30. Linking clinical variables to health-related quality of life in Parkinson's disease.
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Chrischilles EA, Rubenstein LM, Voelker MD, Wallace RB, and Rodnitzky RL
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- Aged, Cross-Sectional Studies, Female, Humans, Male, Middle Aged, Health Status, Mental Health, Parkinson Disease physiopathology, Parkinson Disease psychology, Quality of Life
- Abstract
Objective: Identify the point-in-time relationship between Parkinson's disease (PD) signs and symptoms and measures of health-related quality of life (HRQL)., Background: Clinical measures used in PD assessments traditionally emphasize physical signs and symptoms. We hypothesized that these measures would be strongly associated with the physical function dimensions of HRQL that reflect mental symptoms., Design/methods: A cross-sectional study of 193 neurology clinic PD patients employed self-administered in-clinic and take-home questionnaires and in-person clinical examinations and interviews., Results: The variance explained by PD physical signs and symptoms was substantial for physical function, but only modest for all other HRQL dimensions. Mental symptoms explained a larger proportion of variance than physical symptoms for 12 of the 14 HRQL measures., Conclusion: PD patients' well-being, general health perceptions, health satisfaction and overall HRQL are strongly influenced by mental health symptoms and more weakly influenced by physical symptoms. Clinical evaluation of PD patients should include mental health and self-reported HRQL assessment.
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- 2002
- Full Text
- View/download PDF
31. Safety and efficacy of NeuroBloc (botulinum toxin type B) in type A-responsive cervical dystonia.
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Brashear A, Lew MF, Dykstra DD, Comella CL, Factor SA, Rodnitzky RL, Trosch R, Singer C, Brin MF, Murray JJ, Wallace JD, Willmer-Hulme A, and Koller M
- Subjects
- Adult, Aged, Botulinum Toxins adverse effects, Botulinum Toxins, Type A therapeutic use, Disability Evaluation, Dose-Response Relationship, Drug, Double-Blind Method, Female, Humans, Male, Middle Aged, Pain Measurement, Prospective Studies, Severity of Illness Index, Torticollis physiopathology, Botulinum Toxins therapeutic use, Torticollis drug therapy
- Abstract
Objective: To determine the safety and efficacy of botulinum toxin type B (BoNT/B) in patients with cervical dystonia (CD)., Background: BoNT/B is a form of chemodenervation therapy for the treatment of patients with CD., Methods: The authors performed a 16-week, randomized, multicenter, double-blind, placebo-controlled trial of BoNT/B in patients with CD who continue to respond to botulinum toxin type A. Placebo, or 5,000 U or 10,000 U of BoNT/B was administered in two to four muscles involved clinically in CD. The Toronto Western Spasmodic Torticollis Rating Scale (TWSTRS)-Total score at week 4 was the primary efficacy measure. Clinical assessments and adverse events were recorded for treatment day 1 and at weeks 2, 4, 8, 12, and 16., Results: A total of 109 patients were enrolled randomly across all three treatment groups. The mean improvement in the TWSTRS-Total scores in each group at week 4 was 4.3 (placebo), 9.3 (5,000 U), and 11.7 (10,000 U). For the prospectively defined primary contrast (10,000 U versus placebo), highly significant differences were noted for the primary (TWSTRS-Total, baseline to week 4, p = 0.0004) and supportive secondary (Patient Global Assessment, baseline to week 4, p = 0.0001) outcome measures. Improvement in pain, disability, and severity of CD occurred for patients who were treated with BoNT/B when compared with placebo-treated patients. Overall, improvements associated with BoNT/B treatment were greatest for patients who received the 10,000-U dose. The duration of treatment effect for BoNT/B was 12 to 16 weeks for both doses., Conclusion: Botulinum toxin type B (NeuroBloc) is safe and efficacious at 5,000 U and 10,000 U for the management of patients with cervical dystonia.
- Published
- 1999
- Full Text
- View/download PDF
32. Can calcium antagonists provide a neuroprotective effect in Parkinson's disease?
- Author
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Rodnitzky RL
- Subjects
- Humans, Apoptosis drug effects, Calcium Channel Blockers therapeutic use, Neuroprotective Agents therapeutic use, Parkinson Disease prevention & control
- Abstract
Although major strides forward have been made in the symptomatic treatment of Parkinson's disease (PD), effective neuroprotective therapies have not yet been perfected. The role of calcium in neurotoxicity, and specifically in mediating the process of apoptosis, raises the possibility that calcium antagonists may have a salutary effect on conditions such as PD in which apoptosis may be the ultimate mode of cell death. Several lines of evidence support this notion including the reported effect of calcium antagonists on other human diseases involving apoptosis and animal studies demonstrating the ability of calcium antagonists to protect substantia nigra neurons from the toxin MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine). The common calcium antagonists in use for the treatment of cardiovascular diseases have the potential to modify calcium neurotoxicity in PD since they block L-type calcium channels which are predominantly responsible for regulating intracellular calcium in midbrain dopaminergic cells. The widespread use of these agents affords the opportunity to discern their effect on PD through population studies. Preliminary investigations of this type have been performed to date, suggesting that calcium antagonist use may be less common in hypertensive PD patients than in non-PD hypertensive patients. More extensive investigations of this type, and prospective studies of calcium antagonist use in PD will be required to determine if these agents truly have a salutary effect on Parkinsonism.
- Published
- 1999
- Full Text
- View/download PDF
33. The importance of formal serum iron studies in the assessment of restless legs syndrome.
- Author
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Aul EA, Davis BJ, and Rodnitzky RL
- Subjects
- Adult, Aged, Aged, 80 and over, Female, Humans, Male, Middle Aged, Retrospective Studies, Iron blood, Restless Legs Syndrome blood, Restless Legs Syndrome diagnosis
- Published
- 1998
- Full Text
- View/download PDF
34. The health burdens of Parkinson's disease.
- Author
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Chrischilles EA, Rubenstein LM, Voelker MD, Wallace RB, and Rodnitzky RL
- Subjects
- Activities of Daily Living classification, Activities of Daily Living psychology, Adaptation, Psychological, Aged, Aged, 80 and over, Costs and Cost Analysis, Cross-Sectional Studies, Disability Evaluation, Female, Humans, Male, Middle Aged, Parkinson Disease diagnosis, Parkinson Disease psychology, Patient Care Team economics, Patient Readmission economics, Quality of Life, Sick Role, Socioeconomic Factors, Cost of Illness, Parkinson Disease economics
- Abstract
Parkinson's disease (PD) is likely to have a substantial impact on an individual's health-related quality of life (HRQL), health-related resource use, and productivity. Data about the health burdens of PD by disease stage are fundamental to understanding the effectiveness of care, both from a clinical and a fiscal point of view. This study's goal was to describe the associations of patient-reported HRQL and economic characteristics with PD stage. We hypothesized that later stages of PD would be associated with poorer HRQL, greater health-related resource use, and lower work productivity than early stages of PD. We used a cross-sectional analysis to study 193 PD patients attending two hospital-based neurology clinics. Self-administered questionnaires and in-person interviews measured clinical features, functional status, general health perceptions, well-being, overall HRQL, work productivity, and health-related resource use. Consistent, strong associations were found between stage and functional status, general health perceptions, well-being, and overall HRQL even after controlling for age, gender, and comorbid conditions. Most resource use and work productivity measures were also associated with disease stage. However, physician services use was not. This study confirms that the burdens of illness are progressively higher for PD patients with early, moderate, and advanced illness. The results suggest that such important facets of the health burden as HRQL and health-related resource use may be seriously misjudged if not carefully measured but inferred from clinical observations alone.
- Published
- 1998
- Full Text
- View/download PDF
35. The usefulness of the Functional Status Questionnaire and Medical Outcomes Study Short Form in Parkinson's disease research.
- Author
-
Rubenstein LM, Voelker MD, Chrischilles EA, Glenn DC, Wallace RB, and Rodnitzky RL
- Subjects
- Activities of Daily Living, Aged, Analysis of Variance, Chi-Square Distribution, Cross-Sectional Studies, Female, Health Status, Humans, Male, Middle Aged, Psychometrics, Statistics, Nonparametric, Parkinson Disease psychology, Quality of Life, Severity of Illness Index, Surveys and Questionnaires
- Abstract
Parkinson's disease (PD) has no cure and is a progressive neurological disorder with treatment aimed at the maintenance of function and limitation of the symptoms. No extensive studies of the disease's impact on health-related quality of life (HRQoL) have been conducted. The purpose of this study was to assess the potential usefulness of the Medical Outcomes Study Short Form (SF-36) and the Functional Status Questionnaire (FSQ) in Parkinson's disease research. This cross-sectional study of 193 PD patients who visited two hospital-based neurology clinics used self-administered in-clinic and take-home questionnaires to ascertain the demographic and environmental characteristics of the subjects and to gain health profile measures from the SF-36 and the FSQ. The two health profiles provide important HRQoL information supplementary to the traditional signs and symptoms evaluated by the Unified Parkinson's Disease Rating Scale (UPDRS). Many of the HRQoL measures discriminate progressive stages of disease in this study group and distinguish those with complications of therapy from subjects without complications.
- Published
- 1998
- Full Text
- View/download PDF
36. Visual dysfunction in Parkinson's disease.
- Author
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Rodnitzky RL
- Subjects
- Color Perception, Contrast Sensitivity, Dopamine physiology, Hallucinations etiology, Humans, Parkinson Disease physiopathology, Vision, Ocular physiology, Visual Acuity, Parkinson Disease complications, Vision Disorders etiology
- Abstract
Several abnormalities of visual function have been demonstrated in Parkinson's disease (PD) by both electrophysiologic and psychophysical testing. Prolonged visual evoked potential latencies and abnormal electroretinographic patterns, both of which respond to levodopa therapy, have been demonstrated in Parkinson's disease patients and in primates with experimental parkinsonism suggesting that retinal dopamine deficiency is an important factor in the pathogenesis of PD visual dysfunction. Abnormalities of color perception, especially in the blue-green axis, and of visual contrast sensitivity (VCS) have also been well documented in PD patients. Although VCS impairment is likely related to retinal dopaminergic dysfunction, the fact that this visual abnormality is orientation-specific raises the possibility of visual cortex involvement as well. Visual abnormalities in PD are usually clinically occult and not likely to be uncovered during a routine neurological examination or by ordinary high contrast visual acuity testing. The clinician must be aware, however, that several forms of disability ranging from gait freezing to visual hallucinations may be linked to an underlying impairment of visual function in Parkinson's disease.
- Published
- 1998
37. Botulinum toxin type B: a double-blind, placebo-controlled, safety and efficacy study in cervical dystonia.
- Author
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Lew MF, Adornato BT, Duane DD, Dykstra DD, Factor SA, Massey JM, Brin MF, Jankovic J, Rodnitzky RL, Singer C, Swenson MR, Tarsy D, Murray JJ, Koller M, and Wallace JD
- Subjects
- Adult, Aged, Anti-Dyskinesia Agents administration & dosage, Botulinum Toxins administration & dosage, Dose-Response Relationship, Drug, Double-Blind Method, Drug Administration Schedule, Dystonia physiopathology, Female, Humans, Male, Middle Aged, Neck Muscles drug effects, Pain Measurement, Placebos, Severity of Illness Index, Sickness Impact Profile, Treatment Outcome, Anti-Dyskinesia Agents therapeutic use, Botulinum Toxins therapeutic use, Dystonia drug therapy, Neck Muscles physiopathology, Torticollis drug therapy
- Abstract
We enrolled and treated 122 patients with idiopathic cervical dystonia in a double-blind, placebo-controlled safety and efficacy study of botulinum toxin type B (BotB). Both A-responsive and A-resistant patients were enrolled. Patients received intramuscular injections of either BotB (2,500 U, 5,000 U, or 10,000 U) or placebo. The primary outcome measure of efficacy was the Toronto Western Spasmodic Torticollis Rating Scale (TWSTRS)-Total score at 4 weeks following study drug administration. Secondary measures of efficacy were TWSTRS-Severity, -Disability, and -Pain subscale scores, and Analog Pain Assessment, Investigator Global Assessment, Patient Global Assessment, and Sickness Impact Profile scores. Duration of effect was estimated with an intent-to-treat analysis of responders. Safety measures included clinical parameters, laboratory tests, and adverse events. The primary and most of the secondary analyses indicated a statistically significant treatment effect and a dose response. BotB is safe, well tolerated, and efficacious in the treatment of cervical dystonia at the doses tested.
- Published
- 1997
- Full Text
- View/download PDF
38. Multicenter, placebo-controlled trial of cabergoline taken once daily in the treatment of Parkinson's disease.
- Author
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Hutton JT, Koller WC, Ahlskog JE, Pahwa R, Hurtig HI, Stern MB, Hiner BC, Lieberman A, Pfeiffer RF, Rodnitzky RL, Waters CH, Muenter MD, Adler CH, and Morris JL
- Subjects
- Activities of Daily Living, Adult, Aged, Aged, 80 and over, Cabergoline, Dopamine Agonists therapeutic use, Double-Blind Method, Drug Administration Schedule, Ergolines adverse effects, Ergolines therapeutic use, Female, Humans, Levodopa administration & dosage, Levodopa therapeutic use, Male, Middle Aged, Movement, Parkinson Disease physiopathology, Patient Dropouts, Placebos, Treatment Outcome, Ergolines administration & dosage, Parkinson Disease drug therapy
- Abstract
Cabergoline is a dopaminergic agonist relatively specific for the D2 receptor and much longer-acting than other dopamine agonists. We conducted a randomized, placebo-controlled, double-blind study of cabergoline in 188 levodopa/carbidopa-treated patients with suboptimally controlled Parkinson's disease (PD). The cabergoline patients had significantly better Activities of Daily Living (p = 0.032) and Motor Examination (p = 0.031) scores at the conclusion of the trial compared with the placebo group. The daily levodopa dose for the cabergoline patients decreased 18% compared with a 3% reduction for the placebo group (p < 0.001). The amount of time in the "on" state increased more in the cabergoline group (p = 0.022). The side-effect was similar to that seen with other dopamine agonists, and cabergoline was generally well tolerated. We conclude that cabergoline is an effective adjunct to levodopa for the treatment of PD.
- Published
- 1996
- Full Text
- View/download PDF
39. Localization of the gene for rapidly progressive autosomal dominant parkinsonism and dementia with pallido-ponto-nigral degeneration to chromosome 17q21.
- Author
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Wijker M, Wszolek ZK, Wolters EC, Rooimans MA, Pals G, Pfeiffer RF, Lynch T, Rodnitzky RL, Wilhelmsen KC, and Arwert F
- Subjects
- Adult, Brain Diseases pathology, Female, Gliosis genetics, Gliosis pathology, Globus Pallidus pathology, Humans, Lod Score, Male, Middle Aged, Nerve Degeneration, Pons pathology, Substantia Nigra pathology, Brain Diseases genetics, Chromosome Mapping, Chromosomes, Human, Pair 17, Dementia genetics, Parkinson Disease genetics
- Abstract
Rapidly progressive autosomal dominant parkinsonism and dementia with pallido-ponto-nigral degeneration (PPND) is a neurodegenerative disorder which begins later in life (> 30 years of age) and is characterized by rapidly progressive parkinsonism, dystonia, dementia, perservative vocalizations and pyramidal tract dysfunction. The disease is observed in a large American family that includes almost 300 members in nine generations with 34 affected individuals. In this kindred evidence for linkage to chromosome 17q21 was obtained with a maximum lod score of 9.08 for the D17S958 locus. Multilocus analysis positions the disease gene in an approximately 10 cM region between D17S250 and D17S943. Notably, the disease locus for a clinically distinct familial neurodegenerative disease named 'disinhibition-dementia-parkinsonism-amyotrophy complex' (DDPAC) was recently mapped to the same region of chromosome 17, suggesting that PPND and DDPAC may possibly originate from mutations in the same gene.
- Published
- 1996
- Full Text
- View/download PDF
40. Ranitidine-induced cranial dystonia.
- Author
-
Davis BJ, Aul EA, Granner MA, and Rodnitzky RL
- Subjects
- Aged, Humans, Male, Cranial Nerve Diseases chemically induced, Dystonia chemically induced, Histamine H2 Antagonists adverse effects, Ranitidine adverse effects
- Abstract
We report a case of cranial dystonia related to the administration of ranitidine. The symptoms started shortly after institution of treatment, resolved after discontinuation, and recurred upon repeat administration of the drug. Although there have been a few reports of abnormal involuntary movements related to other histamine2 antagonists, this is only the second reported instance due to ranitidine and the first reported instance of dystonia related to the drug. The pathophysiology of this effect is unclear, but a central cholinergic effect of this agent may be a contributing factor.
- Published
- 1994
- Full Text
- View/download PDF
41. Botulinum toxin enhancement of postoperative immobilization in patients with cervical dystonia. Technical note.
- Author
-
Traynelis VC, Ryken T, Rodnitzky RL, and Menezes AH
- Subjects
- Adult, Cervical Vertebrae, Dystonia complications, Female, Humans, Male, Middle Aged, Postoperative Period, Spinal Diseases complications, Spinal Diseases drug therapy, Spinal Fusion, Torticollis complications, Botulinum Toxins therapeutic use, Dystonia drug therapy, Immobilization, Spinal Diseases surgery, Torticollis drug therapy
- Abstract
Postoperative immobilization in patients with cervical dystonia requiring fusion presents a unique management problem. Two patients with severe degenerative cervical spine disease secondary to chronic repetitive motion are reported. Both required a surgical fusion and postoperative immobilization. Botulinum toxin was injected intramuscularly to assist in immobilization. The technique used is described.
- Published
- 1992
- Full Text
- View/download PDF
42. Rapidly progressive autosomal dominant parkinsonism and dementia with pallido-ponto-nigral degeneration.
- Author
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Wszolek ZK, Pfeiffer RF, Bhatt MH, Schelper RL, Cordes M, Snow BJ, Rodnitzky RL, Wolters EC, Arwert F, and Calne DB
- Subjects
- Adult, Dementia diagnostic imaging, Dementia pathology, Female, Genes, Dominant, Gliosis diagnostic imaging, Gliosis genetics, Gliosis pathology, Humans, Lewy Bodies pathology, Male, Middle Aged, Parkinson Disease diagnostic imaging, Parkinson Disease pathology, Pedigree, Tomography, Emission-Computed, Dementia genetics, Globus Pallidus pathology, Nerve Degeneration, Parkinson Disease genetics, Pons pathology, Substantia Nigra pathology
- Abstract
We describe a family with nearly 300 members over 8 generations with 32 affected individuals who have an autosomal dominant neurodegenerative disease characterized by progressive parkinsonism with dystonia unrelated to medications, dementia, ocular motility abnormalities, pyramidal tract dysfunction, frontal lobe release signs, perseverative vocalizations, and urinary incontinence. The course is exceptionally aggressive; symptom onset and death consistently occur in the fifth decade. Positron emission tomographic studies with [18F]6-fluoro-L-dopa (6FD) were performed in 4 patients and 7 individuals at risk for development of the disease. All affected subjects had markedly reduced striatal uptake of 6FD (p less than 0.001). All individuals at risk had normal striatal uptake, but high 6FD uptake rate constants were noted in 3 of the 7 studied. Autopsy findings revealed severe neuronal loss with gliosis in substantia nigra, pontine tegmentum, and globus pallidus, with less involvement of the caudate and the putamen. There were no plaques, tangles, Lewy bodies, or amyloid bodies. This kindred appears to represent a neurodegenerative disease not heretofore described. We propose the following name for this new genetic disease: autosomal dominant parkinsonism and dementia with pallido-ponto-nigral degeneration.
- Published
- 1992
- Full Text
- View/download PDF
43. Periodic, aperiodic, and rhythmic motor disorders of sleep.
- Author
-
Dyken ME and Rodnitzky RL
- Subjects
- Bruxism physiopathology, Electromyography, Extremities physiopathology, Humans, Myoclonus physiopathology, Time Factors, Movement Disorders physiopathology, Sleep physiology
- Abstract
A variety of spontaneous movements can occur during sleep. Most are unassociated with identifiable CNS pathology and are presumed to be caused by sleep-related modulation of CNS motor control systems. Individual dyskinesias occurring during sleep can be characterized not only by their frequency, rhythmicity, and anatomic predilections, but also by the stage of sleep in which they characteristically occur. Wake-pattern movement disorders improve during sleep but, contrary to common belief, they do not entirely disappear. Instead, these disorders reemerge in attenuated form, often during nonrapid eye movement sleep. The identification and proper characterization of the various sleep-related dyskinesias are greatly aided by careful polysomnographic study.
- Published
- 1992
44. Neurologic complications of drugs. Tardive dyskinesias, neuroleptic malignant syndrome, and cocaine-related syndromes.
- Author
-
Rodnitzky RL and Keyser DL
- Subjects
- Age Factors, Diagnosis, Differential, Dyskinesia, Drug-Induced diagnosis, Female, Humans, Male, Nervous System Diseases diagnosis, Neuroleptic Malignant Syndrome diagnosis, Seizures chemically induced, Seizures diagnosis, Sex Factors, Antipsychotic Agents adverse effects, Cocaine adverse effects, Dyskinesia, Drug-Induced etiology, Nervous System Diseases chemically induced, Neuroleptic Malignant Syndrome etiology, Substance-Related Disorders complications
- Abstract
Drugs, either self-administered or prescribed by physicians, can result in substantial neurologic disability in psychiatric patients. It is clear that the use of neuroleptic agents to treat psychiatric illness may result in a variety of tardive movement disorders. Most commonly, these take the form of orobuccal dyskinesias, but choreic movements of the trunk and extremities, dystonic postures, myoclonus, tics, parkinsonism, and akathisic syndromes also may occur. The choreic tardive syndromes are thought to occur more commonly in the elderly female population, but tardive variants may affect a different population. The neuroleptic malignant syndrome carries a significant mortality and remains a diagnostic and therapeutic challenge. Early detection and vigorous treatment reduces the morbidity and mortality from this condition. Stroke, seizures, and various movement disorders may complicate the illicit use of cocaine and complicate the rehabilitation of those patients dependent on its use. The unsatisfactory treatment of tardive syndromes, neuroleptic malignant syndrome, and cocaine-induced neurologic disease underscores our incomplete understanding of the neurochemistry of dopamine, the function of newly discovered dopamine receptors, and the role they play in maintaining normal emotional and motoric function. For now, awareness of the varied neurologic syndromes related to neurotransmitter-modulating agents should provide the impetus for careful use of these agents and for the continued development of improved drugs for the treatment of psychiatric disease.
- Published
- 1992
45. Thalamic ependymoma presenting as recurrent subarachnoid hemorrhage.
- Author
-
Gordon DL, Biller J, Moore SA, and Rodnitzky RL
- Abstract
We describe a 65-year-old woman who presented with recurrent subarachnoid hemorrhage due to a pathologically proven thalamic ependymoma. This is the first report of such a case. Cerebral angiography and initial imaging studies did not reveal a source of bleeding. Our case emphasizes the importance of periodically following patients with subarachnoid hemorrhage of undetermined etiology., (Copyright © 1992 National Stroke Association. Published by Elsevier Inc. All rights reserved.)
- Published
- 1992
- Full Text
- View/download PDF
46. The use of Sinemet CR in the management of mild to moderate Parkinson's disease.
- Author
-
Rodnitzky RL
- Subjects
- Carbidopa administration & dosage, Drug Administration Schedule, Drug Combinations, Dyskinesia, Drug-Induced, Humans, Levodopa administration & dosage, Levodopa pharmacokinetics, Movement, Parkinson Disease physiopathology, Patient Compliance, Patient Education as Topic, Tissue Distribution, Carbidopa therapeutic use, Levodopa therapeutic use, Parkinson Disease drug therapy
- Abstract
The pharmacokinetic advantage of controlled-release carbidopa-levodopa (Sinemet CR) is its slow dissolution and gradual absorption, resulting in more sustained plasma levodopa levels and higher plasma troughs. In patients with moderately severe disease, the benefits include less severe "wearing-off," a modest increase in daily "on" time, and fewer daily doses. Bioavailability of Sinemet CR levodopa is less than that of standard Sinemet, so a slightly higher total daily levodopa dose is required to achieve a comparable effect; but because Sinemet CR is absorbed much more slowly than is the standard preparation, dosing frequency can be reduced by up to half. For most patients, titration will be required after the transition has been made from standard to controlled-release Sinemet. The effect of Sinemet CR on dyskinesias is often difficult to predict and, in individual patients, may depend on the temporal pattern of dyskinesias being experienced. Success in using this new preparation depends on understanding its pharmacokinetic properties, judicious patient selection, and an effective program of patient education.
- Published
- 1992
47. Alteration of SEP topography in Huntington's patients and their relatives at risk.
- Author
-
Yamada T, Rodnitzky RL, Kameyama S, Matsuoka H, and Kimura J
- Subjects
- Adult, Aged, Brain Mapping, Electric Stimulation, Electroencephalography, Family, Female, Humans, Male, Median Nerve physiology, Middle Aged, Reaction Time physiology, Reference Values, Evoked Potentials, Somatosensory physiology, Huntington Disease physiopathology
- Abstract
We studied the amplitude maps of median SEP parameters in patients with Huntington's disease (HDP) and their relatives at risk (HDF). Corresponding to the small amplitude of SEP in HDP, the power (microV2) was significantly smaller at all electrodes, and the maximum power was shifted anteriorly as a result of greater reduction of the power in the parietal than in the frontal region. In HDF, significant power reduction at the parietal region resulted in a similar anterior shift of the power to that noted in HDP. In addition to the overall reduction of SEP amplitude, the field distributions of parietal N20, frontal N29 and central N60 were significantly different in HDP, as compared to the normals. The typical relationship of the frontal positive and parietal negative fields normally present at N20 latency was lost in HDP due to the loss of the frontal P20. Frontal N29 was absent. Also N60 field shifted anteriorly. In HDF, the degree of deviation was in between those of HDP and normals. These alterations of SEP amplitude, wave form and field distribution in HDP and in some of HDF may be viewed as a result of aberrant modulatory effect exerted by the non-sensory system upon the somatosensory input.
- Published
- 1991
- Full Text
- View/download PDF
48. Neuroleptic malignant syndrome in Parkinson's disease after withdrawal or alteration of dopaminergic therapy.
- Author
-
Keyser DL and Rodnitzky RL
- Subjects
- Aged, Brain metabolism, Dopamine metabolism, Dopamine Agents therapeutic use, Female, Humans, Male, Middle Aged, Dopamine Agents adverse effects, Neuroleptic Malignant Syndrome etiology, Parkinson Disease drug therapy, Substance Withdrawal Syndrome
- Abstract
Neuroleptic malignant syndrome is characterized by altered consciousness, fever, extrapyramidal signs, autonomic instability, elevated creatine kinase level, and leukocytosis. Although originally described in patients receiving neuroleptic drugs, this syndrome may also occur in patients with Parkinson's disease during withdrawal or reduction of levodopa therapy or other dopaminergic drug therapy. We have encountered three cases of neuroleptic malignant syndrome related to withdrawal of levodopa therapy. These cases illustrate the variety of circumstances in which alteration of therapy with dopaminergic drugs can cause this syndrome and the relative unfamiliarity of the neuroleptic malignant syndrome-levodopa relationship among physicians who do not treat large numbers of patients with Parkinson's disease. An understanding of the role of brain dopamine in the pathogenesis of neuroleptic malignant syndrome and an appreciation of the great variety of drugs whose manipulation can result in this potentially fatal syndrome will aid its proper and timely recognition, especially when the offending pharmacologic manipulation does not involve neuroleptic drugs.
- Published
- 1991
49. Stroke and its modification in Parkinson's disease.
- Author
-
Struck LK, Rodnitzky RL, and Dobson JK
- Subjects
- Aged, Case-Control Studies, Cerebrovascular Disorders complications, Cerebrovascular Disorders physiopathology, Female, Humans, Incidence, Iowa, Male, Myocardial Infarction complications, Myocardial Infarction epidemiology, Myocardial Infarction physiopathology, Parkinson Disease complications, Parkinson Disease physiopathology, Retrospective Studies, Risk Factors, Cerebrovascular Disorders epidemiology, Parkinson Disease epidemiology
- Abstract
Previous studies have not agreed on the incidence of ischemic stroke in persons with Parkinson's disease. There are epidemiologic and neurochemical facets of Parkinson's disease that might confer some benefit or protection against ischemic stroke. We used a case-control method to determine the lifetime history of ischemic stroke in 200 patients with Parkinson's disease and 200 controls of a similar age range. Analysis was also carried out for myocardial infarction as a marker of generalized atherosclerotic disease and for stroke risk factors. The cumulative incidence of ischemic stroke was significantly less in the patients with Parkinson's disease than in the controls, as was the cumulative incidence of myocardial infarction. Among risk factors, significantly fewer patients with Parkinson's disease used tobacco than controls. The decreased incidence of ischemic stroke in the patients with Parkinson's disease appears to be related to their less severe generalized atherosclerosis, possibly due to their lower incidence of tobacco use. In view of the known potential for dopamine to exacerbate experimental ischemic tissue damage, the possibility that the dopamine deficiency in the central nervous system of persons with Parkinson's disease confers an additional specific protective benefit against ischemic stroke cannot be excluded and requires further study.
- Published
- 1990
- Full Text
- View/download PDF
50. Circadian fluctuations of contrast sensitivity in Parkinson's disease.
- Author
-
Struck LK, Rodnitzky RL, and Dobson JK
- Subjects
- Aged, Aged, 80 and over, Humans, Middle Aged, Statistics as Topic, Circadian Rhythm, Contrast Sensitivity, Parkinson Disease physiopathology
- Abstract
Spontaneous circadian fluctuations of motor symptoms in Parkinson's disease (PD) often occur, with dysfunction typically less severe in the early morning than in the afternoon. In 23 PD patients with or without a history of circadian motor fluctuations, we studied contrast sensitivity (CS), a non-motor function, considered to be dependent on dopaminergic transmission to see if it exhibits similar circadian variability. We tested CS throughout the day at 2-hour intervals beginning at 8:30 AM. To facilitate multiple testing sessions, we used a rapid, printed, forced choice test of CS not requiring a motor response. We tested CS in 43 eyes in the PD patients and 23 eyes in 12 controls at spatial frequencies of 1.5, 3, 6, 12, and 18 cycles per degree (cpd). At 8:30 AM, CS in PD did not differ from that of controls, but at all other testing times it was significantly worse at 3 or more spatial frequencies. In PD, CS was significantly worse at 2:30 PM than at 8:30 AM at 3 and 6 cpd, but in controls it was unchanged throughout the day. Separate analysis of CS in PD patients, with and without a history of circadian change in motor symptoms, revealed no significant difference between the groups. These results suggest that in PD a non-motor dopaminergic function can exhibit circadian variability and that this pattern can exist in the absence of similar variability in motor symptoms. Circadian variability which parallels the most common pattern of motor variability in PD supports the notion that the CS abnormality in this condition is related to dopamine deficiency.
- Published
- 1990
- Full Text
- View/download PDF
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