The Effect of Methylphenidate on Neurological Soft Signs in ADHD
Igor Hrtanek1, Igor Ondrejka2, Ingrid Tonhajzerova3
1Department of Pharmacology, Jessenius Faculty of Medicine in Martin, Comenius University in Bratislava, Martin, Slovakia. ; Clinic of Psychiatry, Jessenius Faculty of Medicine and University Hospital in Martin, Comenius University in Bratislava, Martin, Slovakia.
Objective:
Neurological soft signs are very common in children with the attention deficit hyperactivity disorder (ADHD), and the first line medication of this disorder is methylphenidate. The aim of the study was to assess the effect of methylphenidate on the neurological soft signs in children and adolescents suffering from ADHD depending on the dose of methylphenidate.
Methods:
Thirty five patients with ADHD were investigated by the ADHD RS-IV parent version questionnaire and the Revised Neurological Examination for Subtle Signs before treatment adjustment and after four weeks of methylphenidate medication. The changes in hyperactivity symptomatology, neurological soft signs during therapy and the influence of the methylphenidate dose were statistically analyzed.
Results:
A significant decrease in hyperactivity symptomatology was found after one month of methylphenidate medication (p=0.0001) and significant decrease in neurological soft signs was demonstrated in 21 from a total of 26 items (p<0.05). Correlation analysis showed no relationship between the dose of methylphenidate and the improvement of neurological soft signs. Similarly, the improvement of ADHD symptomatology had not correlation with the improvement of neurological soft signs.
Conclusion:
The study demonstrated the positive effect of methylphenidate on neurological soft signs in which improvement occurred independently of the dose, indicating that their progress may be due to methylphenidate treatment of any dose. The unrelated effect of methylphenidate on the attention deficit hyperactivity disorder and neurological soft signs suggest that methylphenidate might be useful in the therapy of clumsy child syndrome and in ADHD treatment of non-responders.
More Related Videos
13:09Using Brain Activation nir-HEG/Q-EEG and Execution Measures CPTs in a ADHD Assessment Protocol
Published on: April 1, 2018
05:48The Adventures of Fundi Intervention Based on the Cognitive and Emotional Processing in Attention Deficit Hyperactive Disorder Patients
Published on: June 12, 2020
Related Concept Videos
01:30Attention-Deficit/Hyperactivity Disorder
Diagnostic Criteria and Symptoms
To diagnose ADHD, symptoms must manifest before age 12 and be evident across multiple settings....
01:30Cognitive Enhancers: Cholinesterase Inhibitors and NMDA Receptor Antagonists
01:24CNS Stimulants: Cocaine, Amphetamines and Cannabinoids
01:29Drugs Affecting Neurotransmitter Synthesis
01:25Adrenergic Agonists: Indirect-Acting Agents
One mechanism involves depleting stored catecholamines by displacing them from synaptic vesicles. These agents, known as "displacers," are transported into vesicles at the expense of noradrenaline. Examples include amphetamine and tyramine, which lack a catechol moiety, resulting in prolonged action, improved oral...
01:23Drugs Acting on Autonomic Ganglia: Stimulants
Ganglionic stimulants activate NM nicotinic receptors in autonomic ganglia, falling into two categories: nicotine mimetics [e.g., lobeline, dimethylpiperazine, tetramethylammonium] and muscarinic receptor agonists [e.g., muscarine, methacholine]. The first category's action is rapid and blocked by nicotinic receptor antagonists, while the second category's action is delayed and blocked by atropine-like agents. Nicotine, an alkaloid, affects the heart rate by stimulating...