Parkinson’s DiseaseParkinsonism is a syndrome with symptoms that are similar to Parkinson’s disease. These symptoms can include tremor, bradykinesia or slowing of motor skills, rigidity, and postural instability, resulting in poor balance. Parkinson’s disease can be the cause of Parkinsonism, but it is not the only cause. Other causes include diseases of metabolism, other neurological conditions, and toxins. Some drug side effects include the symptoms of Parkinsonism. One main type of these medications are neuroleptic antipsychotics. These drugs work by blocking dopamine receptors or depleting stored dopamine. Dopamine is essential for motor coordination, which is why the disruption of normal dopamine activity can cause movement disorders like Parkinsonism. Drug-induced Parkinsonism (DIP) is the most common movement disorder from dopamine affecting drugs. This syndrome greatly impacts the lives of patients. It is important to understand the factors that go into deciding the right balance of benefits versus risks and factor that determine adequate dosage.
This review focuses on Parkinsonism resulting from medication use, or DIP. The first study shows that gastrointestinal prokinetics, calcium channel blockers, atypical antipsychotics, and antiepileptic drugs can cause Parkinsonism. This study found that a dopamine blockage can cause changes in the basal ganglia motor circuit resulting in the syndrome. Its results showed that the syndrome does not cease with discontinued use of the drug. Another study examined Olanzapine-induced Parkinsonism. This is an atypical antipsychotic. A third study looked at neuroleptic-induced Parkinsonism and added an interesting association. People with olfactory dysfunction were more likely to develop Parkinsonism as a side effect. The previous three studies assessed occurrences in the elderly population, but a fourth study looked at two cases of drug induced Juvenile Parkinsonism which is when the onset occurs before 21 years of age.
Shin and Chung (2012) discussed how DIP is often misdiagnosed with Parkinson’s disease. This misdiagnosis is common because the signs and symptoms are very similar and almost indistinguishable. The biggest clue that someone is presenting with DIP is often found by getting a thorough medical history. Typical antipsychotics (neuroleptics), atypical antipsychotics, gastrointestinal (GI) motility drugs, calcium channel blockers, and antiepileptic drugs have been shown to cause DIP in some patients; neuroleptics being the most common. Antipsychotic drugs work by blocking the D2 receptors, which are coupled to a G protein. This inhibits the activity of enzyme adenylyl cyclase and directly inhibits cAMP formation. In the limbic system, dopamine transmission is reduced. In the striatum, GABA and encephalin-containing striatal neurons are activated. Over 80% of D2 receptors were blocked in patients with DIP (Shin and Chung, 2012). After this blockade, changes in the basal ganglia motor circuit
in the striatum in the absence of the blockade of D2 receptors are seen. This leads to disruption of GABA production and thereby the movement of motor and visual functions in the striatum of patients with DIP (Shin, Chung, 2002).
Prolonged administration of a new antipsychotic for anxiety (MDR) and depression was also shown to affect DIP (Shin and Chung, 2012). Patients with high levels of dopamine became more anxious at times, with increasing frequency even in comparison with never treatment. This could be explained by the increased dopamine production and decreased cAMP levels that occur during D6-D6 administration in healthy volunteers. The increased dopamine production appears to lead to an increased vulnerability to anxiety. Patients with moderate or no evidence of a Parkinson’s disease or dementia with DIP have a higher risk than other patients with MDR. The DIP in both Parkinson’s and non Parkinson’s patients may be a “dopamine dearth”. Patients with Parkinson’s disease have a low affinity for a dopamine receptor, called beta-aminobutyric acid (BAQ), that does not bind to the D2 receptors. DIP deficiency can cause a state of dopamine deprivation, which is a memory loss and anxiety syndrome. This is not the case among bipolar disorder (BD). In BD, anxiety-like behaviors are accompanied by increased parasympathetic tone during the dopamine receptor desensitization and decreased parasympathetic tone during the inhibitory control. This disturbance is characterized by a state of anxiety-like behavior rather than the symptoms of a DIP deficiency.
A few patients with ADHD have reported a DIP episode and have been cured of their ADHD symptoms as a result of treatment of multiple DIP deficiencies (Shin, Chung, & Zaglia, 2011). These patients were not treated with DIP (Shin et al., 2002). If this was the case, there is no reliable treatment for the DIP deficiency and DIP should not be prescribed to anyone else.
This information is incomplete and should not be relied upon for diagnosis of DIP. Many patients with bipolar disorder experience difficulties with cognitive deficits. For this reason, many individuals with DIP have taken medications that are not safe or effective for the symptomatic and symptomatic (Shin, Chung, & Zaglia, 2011).
All patients with DIP should undergo a blood monitor at least once a month (Shin, Chung, & Zaglia, 2011).
A patient should be taken out of the ED to complete a diagnosis at least once a week in the beginning of his or her lifetime, with follow-up of approximately 6 to 12 months after stopping treatment. The patient should undergo an electrocardiogram with a validated blood pressure clamp.
Individuals with DIP should receive a referral as soon as possible for the development of a DIP clinic in the community. It should also be documented and documented at the clinic. If the patient cannot be referred with the current AD team, the case would not be reviewed during follow-up by the clinician in the ER. If there are no other follow-ups necessary, the referral referral should be made, as soon as possible.
This information is not an accurate representation or an accurate reflection of all patient experiences.
Please note that some patients experience similar feelings of drugged or intoxicated in situations where such events typically do not occur in the setting or in the setting at which they occur (Shin, Chung, & Zaglia, 2012). The following information appears to be from an experience in which this would have been the case. As with many medications, some users develop very similar emotions or behaviors, which may be exacerbated due to withdrawal, sedation, and/or alcohol consumption or intoxication.
A patient must not try to make a