Table 1: Parkinson-Like Syndromes and Their Symptoms
Identified disorder*
Sleep abnormality
Yes/no
Yes/no
Yes
Yes/no
Yes/no
No
Yes
Hallucinations
No**
No
No
No
No
No
Yes
Asymmetrical findings
Yes
No
Yes/no
No
No
Yes
Yes
Levodopa response
Yes
Yes/no
Yes/no
Yes/no
No
No
Yes
Neuropathy No * PD = Parkinson’s disease; PSP = progressive supranuclear palsy; MSA = multiple system atrophy; SND = striatonigral degeneration; OPCA = olivo-pontocerebellar atrophy; CBGD = corticobasal ganglionic degeneration; LBD = Lewy body dementia ** Hallucinations are sometimes seen in PD, but are most often due to dopamine medications; decreased dosage usually resolves the hallucinations. Note . From Western Schools, 2018. Medical management There are no known disease-modifying agents for the treatment No No Yes/no No Yes/no No
hypokinetic or experience “freezing.” Another secondary effect, increased motor fluctuations, becomes problematic later in the disease. Known as an on-off phenomenon, these fluctuations in motor performance occur as the level of active drugs in the system ramp up and then fall off. Overall, levodopa-carbidopa has been well tolerated and effective. However, its use in treating younger patients for longer periods poses an increased risk of long-term complications. Therefore levodopa-sparing strategies, which use agents such as dopamine agonists to optimize endogenous dopamine use and uptake, are being instituted early in treatment (Armstrong & Okun, 2020). Medications such as Eldepryl ® and Deprenyl ® act to optimize endogenous dopamine by slowing down its reuptake; the dopamine agonists Requip ® , Mirapex ® , and Neupro ® mimic dopamine in the brain and activate the dopamine receptors. Other medications, such as catechol-O-methyltransferase (COMT) inhibitors and anticholinergics, are used for symptomatic relief. COMT inhibitors potentiate levodopa by preventing its degradation by COMT. Anticholinergic medications reduce overactivity of acetylcholine and thus inhibit dopamine reuptake in the striatum of the basal ganglia. This medication is good for reducing tremor activity and is typically used in younger individuals. Monoamine oxidase B (MAO-B) inhibitors inhibit MAO-B, which degrades dopamine after it is released. Use of these medications lengthens the time in which dopamine remains active in the brain. Glutamate antagonists are known as dopamine agonists because they lead to the release of dopamine and decrease dopamine reuptake. A full listing of common medications used for the treatment of PD and their actions is provided in Table 2.
of PD. The cornerstone of management continues to be symptom management through levodopa therapy. Medical management also incorporates surgical procedures and referral to rehabilitation therapies. Pharmacological management Dopaminergic drugs improve motor function, reduce both the morbidity and mortality of PD, and improve quality of life (Armstrong & Okun, 2020). Levodopa was first developed in the 1960s, and when combined with carbidopa, it is the most clinically effective medication for managing the symptoms of PD. The brand names for carbidopa-levodopa are Sinemet ® , Atamet ® , and Parcopa ® . When levodopa is combined with carbidopa, it is better able to cross the blood-brain barrier and is turned into dopamine within the nerve cell. It alleviates bradykinesia and rigidity but has only minimal effect on reducing tremor. Common side effects include orthostatic hypotension, dyskinesias, hallucinations, and sleepiness. Although early symptoms of PD respond well to levodopa or carbidopa- levodopa, late-occurring motor and nonmotor symptoms respond poorly to this medication. Over time, the death of neurons in the basal ganglia leads to the need for higher and higher doses of dopaminergic drugs to obtain symptomatic relief. Because dopamine is active systemically, these higher doses lead to undesired secondary effects. One such secondary effect is dyskinesia (abnormal involuntary movement), which typically occurs at peak dose. Patients often report that they are not troubled by the dyskinesias and would rather have the dyskinesias than be Table 2: Pharmacologic Management of Parkinson’s Disease Dopamine agonists Directly stimulate dopamine receptors.
Pramipexole (Mirapex ® ), ropinirole (Requip ® ), apomorpine (Upima ® ). Entacapone (Comtan ® ), LD and entacapone (Stalevo ® ), tolcapone (Tasmar ® ). Trihexyphenidyl HCl (Artane ® ) and benztropine mesylate (Cogentin ® ), procyclidine hydrochloride (Kemadrin ® ). Selegiline hydrochloride (Eldepryl ® ), rasagiline (Azilect ® ).
COMT inhibitors
Potentiates levodopa: prevents its degradation by COMT. Reduce overactivity of acetylcholine; inhibit dopamine reuptake in the striatum; good for tremors; used in younger individuals.
Anticholinergics
MAO-B inhibitors
Inhibits MAO-B that degrades dopamine.
COMT = catechol-O-methyltransferase; MAO-B = Monoamine oxidase B Note . From Western Schools, 2018. Surgical intervention There are three common surgical procedures that can be used to treat the symptoms of PD: deep brain stimulation, pallidotomy, and thalamotomy. Deep brain stimulation involves
placing electrodes in the brain that are connected by wires to an impulse generator implanted under the skin of the chest, below the collarbone. It is unclear whether the stimulation suppresses or activates cells. This procedure is indicated when
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