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Medical Management of Movement Disorders

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Niranjan A, Lunsford LD, Richardson RM (eds): Current Concepts in Movement Disorder Management.
Prog Neurol Surg. Basel, Karger, 2018, vol 33, pp 41–49 (DOI: 10.1159/000480747)

Medical Management of Movement

Disorders
Marina Picillo · Renato P. Munhoz
Morton and Gloria Shulman Movement Disorders Clinic and the Edmond J. Safra Program in Parkinson’s
Disease, Toronto Western Hospital and Division of Neurology, University of Toronto, Toronto, ON, Canada

Abstract
Pharmacological treatment is the cornerstone in the management of movement disorders. Although
most available treatment options have no impact on the underlying process of each movement dis-
order, symptomatic therapies can significantly improve patient’s quality of life and level of disability.
Here, we review the current knowledge on clinical symptomatic management of Parkinson’s disease
(both early and advanced stages), essential tremor, dystonia, and chorea. Ideally, treatment should
be carried out by specialists with reasonable experience in movement disorders, as it needs to be
tailored for each patient depending on several appraisals, including but not limited to patients’
needs, compliance issues, potential side effects, caregiver support, and presence of comorbidities.
When medications fail to improve patient’s disability, stereotactic surgery is a well-established op-
tion for most of these disorders. © 2018 S. Karger AG, Basel

The rationale for most of the treatment interventions presented in this review relies
heavily on the basal ganglia biochemistry; however, the clinical management of move-
ment disorders varies widely depending on the underlying cause, predominant phe-
nomenological presentation, degree of disability, and several individual, patient-
based variables. Although cure can be eventually accomplished in selected disorders
manifesting movement disorders, in most cases, the goal of treatment is to relieve
symptoms, with no pretention of modifying the underlying pathological course.
In this chapter, we review the current practical available treatment options of the
four most common forms of movement disorders.
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Parkinson’s Disease

Parkinson’s disease (PD) is the second most common neurodegenerative disease affect-
ing more than five million people worldwide [1]. Despite significant efforts from the sci-
entific community, pharmacological management has changed little in the past decades,
and interventions able to change the progression of the disease (either neuroprotective
or disease-modifying) have yet to be introduced. Nevertheless, several treatment options
are accepted and widely available for both early and advanced stages of the disease with
the ultimate goal being improving patients’ quality of life and functionality. Indeed, treat-
ment of PD, especially in advanced stages, should be carried out by clinicians with exper-
tise in movement disorders as this disorder is a highly heterogeneous disease and treat-
ment needs to be tailored for individual patients depending on several appraisals, includ-
ing but not limited to patients’ needs, life style, compliance issues, potential side effects
(motor and nonmotor), caregiver support, and presence of cognitive decline or other
comorbidities. Several recommendations and reviews have been published so far and a
summary of medications available in PD is displayed in Table 1 [2–8].

Early Stage

In the early stage PD, the aim of the clinical management is to minimize the burden
from both motor and nonmotor symptoms of the disease, allowing patients to per-
form their activities of daily living with minimal functional disability. It is important
to acknowledge that even at these stages, a few nonmotor symptoms may precede and
accompany the manifestation of motor symptoms, further contributing to the wors-
ening of the quality of life [9]. There are currently three classes of medications used
to treat PD at early stages (to be used in either monotherapy or in combination):
monoamine oxidase B (MAO-B) inhibitors, dopamine agonists (DAs), and levodopa
(combined with either carbidopa or benserazide). Initial treatment choices typically
depend on the severity of patient’s symptoms, level of required activity, and age.

MAO-B Inhibitors
As the impact of MAO-B inhibitors (either selegiline or rasagiline) on motor symp-
toms is less significant when compared to both DAs and levodopa, they are used as a
first-line treatment when symptoms are mild. A potential disease-modifying effect of
rasagiline 1 mg has been reported by the ADAGIO study but not confirmed by addi-
tional clinical trial evidence [10].

DAs
When a greater control of motor symptoms is necessary, DAs or levodopa should be
the options. DAs are less likely than levodopa to induce long-term dopaminergic mo-
tor complications, particularly dyskinesia, which is an advantage in younger PD pa-
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Table 1. Treatment of motor symptoms of Parkinson’s disease (adapted from Connolly and Lang [3])

Medication class Dosage Indication Adverse effect

Levodopa/Carbidopa Titrate to initial dose of 100/25 mg All motor symptoms Nausea, orthostatic hypotension,
and Levodopa/ thrice daily; max dose is variable, dyskinesia, and hallucinations
Benserazide depending on tolerability
Pramipexole* Start 0.125 mg thrice daily; max, All motor symptoms Nausea, orthostatic hypotension,
4.5 mg/day psychosis, ICDs, edema, and sleepiness
(including sleep attacks)
Ropinirole* Start 0.25 mg thrice daily; All motor symptoms Same as pramipexole
max, 24 mg/day
Rotigotine Start 2 mg/24 h; max, 16 mg/24 h All motor symptoms Same as pramipexole plus skin reactions

Entacapone 200 mg with each dose of Motor fluctuations Dark-colored urine and exacerbation of
levodopa; max, 8/day levodopa adverse effects
Tolcapone 100–200 mg thrice daily Motor fluctuations Same as entacapone, plus hepatotoxicity
resistant to entacapone
Selegiline 5–10 mg daily Early, mild motor Stimulant effect, dizziness, headache,
symptoms and fluctuations exacerbation of levodopa adverse effects
Rasagiline 0.5–1 mg daily Early, mild motor Headache, arthralgia, dyspepsia, flu-like
symptoms and fluctuations syndrome, exacerbation of levodopa
adverse effects, and constipation
Amantadine 100–300 mg daily, Dyskinesia Irritability, nightmares, purplish red,
max 400 mg daily net-like spots on the skin
Apomorphine Max 100 mg daily Motor fluctuations Same as pramipexole plus side effects
associated with infusion
Intrajejunal levodopa Max 200 mL daily Motor fluctuations Same as levodopa plus side effects
carbidopa gel (Duodopa®) associated with infusion

* Extended release formulations are available.

tients, more prone to develop dyskinesia. Therefore, DAs are usually introduced as an
initial treatment for patients younger than 60 years. However, recent evidence suggests
that disease duration may play a greater role than the timing of levodopa introduction
in fostering the development of motor fluctuations [11, 12]. Potential behavioral side
effects of DAs include impulse control disorders, usually presenting a direct relation-
ship with DAs dosage. Young, male patients with positive previous or family history
of addiction behavior seem to be more prone to develop these side effects. Currently,
DAs are available in oral (pramipexole and ropinirole) or transdermal (rotigotine) for-
mulations. DAs have been found to be variably effective also for the treatment of se-
lected nonmotor symptoms, such as depression and sleep disorders [13]. Treatment
strategies for nonmotor symptoms in PD should include optimization of dopaminer-
gic treatment prior to the addition of specific drugs (e.g., antidepressant), thus reduc-
ing the risk of side-effects associated with multi-drug therapies.
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Levodopa
Levodopa is the cornerstone of PD pharmacological management and continues to be
the most effective treatment in all stages. It is usually the first-line treatment for older
patients or for cases that are active at the time of diagnosis and, thus, need to maximize
their performances. The tendency is to keep levodopa dose low in the early stage (<500/600
mg/day) to delay motor fluctuations. To this end, when slight motor fluctuations start,
possible approach is to combine levodopa with MAO-B inhibitors or DAs [3, 5].

Advanced Stage

Advanced stage PD is characterized by motor fluctuations and dyskinesias, as well as

more severe and disabling nonmotor symptoms. Motor fluctuations can present as
“end of dose” or “wearing off” phenomenon as well as “unpredictable off”. “Delayed
on” or “no on” after levodopa intake may also occur. Dyskinesias can occur as peak-
dose or biphasic (beginning and/or end of dose). Strategies for improving motor
fluctuations include increasing the dosage of dopaminergic medication, adding an-
other dopaminergic medication, levodopa dose fragmentation (i.e., dividing it into
smaller but more frequent doses), or adding a catechol-O-methyltransferase (COMT)
inhibitor or MAO-B inhibitor to prolong the effects of levodopa. Controlled-release
levodopa does not reduce the off time more than immediate-release levodopa and,
thus, it is usually only recommended for the management of nocturnal akinesia.
When oral medications fail to induce a satisfactory improvement of motor fluctua-
tions, invasive treatments should be considered. The subcutaneous infusion of apo-
morphine and intrajejunal infusion of levodopa/carbidopa intestinal gel (Duodopa®)
are well-established alternatives to stereotactic surgery for the advanced phase of the
disease. Although less invasive and challenging than brain surgery, both still require
compliance by patients and their caregivers [4, 7, 8].

COMT Inhibitors
Entacapone (a peripheral COMT inhibitor) and tolcapone (both peripheral and cen-
tral inhibitor) can be used to decrease the off time during the day, allowing and in
most times requiring a reduction of daily amount of levodopa. Tolcapone seems to be
more potent; however, it is usually used when entacapone is ineffective, since rare
cases of hepatotoxicity have occurred, requiring routine monitoring of serum trans-
aminase levels. Additional side effects of both drugs are those related to higher bio-
availability of levodopa [7, 8].

Apomorphine
Apomorphine is a dopaminergic D1/D2 receptor agonist with a short half-life
of  nearly 45 min. Apomorphine injections via Penject device administration
are  effective for a rapid relief of a sudden “off” fluctuation during the day and
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nighttime. Continuous infusion can be carried out by an apomorphine pump,
usually delivered for 12–16 h of the day. One of the main side effects related to
the infusion system are skin reactions, resulting in the formation of small nodules
[8].

Levodopa/Carbidopa Intestinal Gel

Duodopa® is a gel combination of levodopa (20 mg/mL) and carbidopa (5 mg/mL)
delivered via a portable pump directly into the duodenum through a percutaneous,
endoscopic gastrostomy [14]. A number of studies have shown a significant reduc-
tion of “off” time and an increase of “on” time, along with a reduction of dyskine-
sia. The infusion is usually used for 16 h and the nighttime is covered with con-
trolled-release levodopa formulation. Many nonmotor symptoms such as urinary
and sleep issues have also been reported to improve with this form of treatment.
Adverse events are mainly related to the device and include dislocation, obstruc-
tion, and breakage of the duodenal catheter, stoma inflammation and in rare cases,
peritonitis. Duodopa® is currently considered a good option in patients not fit for
surgery.
Finally, amantadine (100–300 mg/day) is frequently used to better control levodo-
pa-induced dyskinesia; however, long-term use in advanced PD is limited by adverse
effects, such as confusion, hallucination, and skin rash [7, 8].
Stereotactic surgery is typically considered in patients with moderate-to-severe
PD. The ideal patient is severely disabled in the “off” state but regains considerable
functionality with levodopa. In other words, in levodopa-responsive patient, the re-
sponse fluctuates and is marked by severe dyskinesias that cannot be managed with
medication adjustments [15]. Further details of patient selection, indications, and
contraindications are the main topics of another chapter in this issue of Controversies
in Movement Disorders.

Essential Tremor

Essential tremor (ET) is one of the most common movement disorders, presenting
an overall estimated prevalence ranging from 0.9 to 2.2%, even higher among people
over 65 years of age (4.6%) [16]. It is characterized by a 8–12 Hz postural and ki-
netic tremor involving the arms and less commonly the head, lower limbs, and voice,
frequently accompanied by a family history of a similar tremor. However, ET is a
heterogeneous disorder and there is little agreement among specialists regarding
both clinical definition and diagnostic criteria. Although benign in terms of its effect
on life expectancy, it often causes embarrassment and, in a smaller percentage of pa-
tients, also serious disability [15]. Moreover, symptoms are typically progressive and
potentially disabling, often forcing patients to change job or seek early retirement
[16].
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 The treatment is primarily based on pharmacological agents, although surgical in-
tervention may be an option in the most disabling cases. Pharmacotherapy may be
used to improve function or reduce the social embarrassment associated with ET, but
treatment should be tailored to the patient’s level of disability. Treatment is usually
started with one medication, but in case of partial benefit with the maximum toler-
ated dosage, additional agents may be useful. Medical management of ET include
beta-blockers, anticonvulsants and benzodiazepines, neuroleptics, and botulin toxin
type A (BTXA) injections [18–20].

Beta-Blockers
Propranolol (120–240 mg divided into three doses daily) is considered a well-estab-
lished, first-line treatment for ET [18–20]. Long-acting formulation can be used to
reduce the number of daily intakes and, thus improve compliance. The other beta-
blockers should be used as second-line treatments, considering arotinolol and sotalol
as the most effective agents [20].

Anticonvulsants and Benzodiazepines

Primidone is an anticonvulsant that is metabolized to phenylethylmalonamide (PEMA)
and phenobarbital. Several studies found that primidone effectively reduced the limb
tremor in ET, using doses from 50 to 1,000 mg/day. A variety of side effects have been
described at treatment initiation (sedation, drowsiness, nausea). In addition to propran-
olol, primidone is considered the other first-line treatment for ET, the choice between
the two depends on concurrent medical conditions and potential side effects. Unfortu-
nately, both primidone and propranolol tend to lose efficacy over time, and in addition,
their use is limited, particularly among the elderly (>70 years), due to interactions with
medications commonly used in these age group (e.g., digoxin, calcium channel blockers,
and antiarrhythmics) [18–20]. Other anticonvulsants (topiramate at doses of 25–400 mg
daily in two administrations, zonisamide, gabapentin, and phenobarbital) have been
suggested as potentially useful agents for the treatment of ET, usually well tolerated, but
less effective [19, 20]. Among benzodiazepines, alprazolam and clonazepam may also be
considered with caution due to their abuse potential and possible withdrawal symptoms
following abrupt discontinuation [18].

Neuroleptics
Although the efficacy of clozapine has been documented in reducing limb tremor, it
should be used as second-line treatment due to the well-known risk of important ad-
verse events (such as agranulocytosis and cardiac toxicity). There are insufficient or
conflicting data regarding the use of olanzapine and quetiapine in the treatment of
limb tremor in ET [18–20].
Mirtazapine, a specific noradrenergic and serotoninergic antidepressant has
been shown to be effective in reducing tremor of patients with ET in a few case
series [20].
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Botulinum Toxin Injections
Available results provide evidence of mild-to-moderate efficacy of low-dose BTXA injec-
tions in the forearm muscles of patients with upper extremity ET. Muscle weakness is
observed in 30–70% of treated patients, but the exact impact of this adverse effect on pa-
tient global functioning needs to be investigated further. BTXA may reduce head and
voice tremor associated with ET, but data are limited. BTXA injections for limb, head, and
voice tremor associated with ET may be considered in medically refractory cases [18, 20].
Combination of first- and second-line therapies may bring additional benefits. Fi-
nally, stereotactic thalamic surgery should be considered in patients with significant
disability related to ET, if the symptom is refractory or present a response that is not
functionally significant.

Dystonia

Dystonia is characterized by involuntary muscle contractions resulting in abnormal

movements or postures. Dystonia can affect any of the body, and may result in sus-
tained, rhythmic, or task-specific involuntary muscle contractions. Dystonia can oc-
cur on its own or be part of a syndrome [21]. Correspondingly, etiologies vary. Based
on phenomenology, a new consensus proposed a syndromic approach to guide diag-
nosis [21]. With regard to treatment, in addition to physical and supportive therapy,
oral medications and botulinum toxin sum up the current options for these cases
[22–24]. Finally, stereotactic surgery targeting the internal segment of the globus pal-
lidus has been shown to be efficacious in the treatment of primary generalized and
segmental dystonia, in both adults and children, as well as in cervical dystonia and
craniofacial dystonia that does not respond to conservative treatment with medica-
tions and botulinum toxin (BoNT) injections.
Trihexyphenidyl and other anti-cholinergics have their efficacy documented for de-
cades in reducing the severity of various forms of dystonia. Typically, the total daily dose
is limited due to peripheral and central side effects, such as vision disturbances, constipa-
tion, dry mouth, and cognitive slowing. A slow titration is recommended. Children usu-
ally tolerate higher doses than adults (8–12 mg daily for trihexyphenidyl) [22–24].
Treatment with GABAergic agents also provides some relief of dystonic symp-
toms. Benzodiazepines (clonazepam, diazepam, and lorazepam) are usually effective,
although sedation limits their dose. Oral baclofen, which activates the GABA-B recep-
tor, is also used in the treatment of dystonia. Intrathecal baclofen has been shown to
be effective in reducing associated spasticity, particularly in the legs. Most of the pa-
tients are treated with a combination of the highest tolerated dose of each medication.
In addition, patients with early onset dystonia should always be trialed with levodopa
to rule out dopa-responsive dystonia [22–24].
BoNT is safe and effective in a variety of forms of focal dystonia. By interfering with
vesicle fusion, BoNT inhibits the release of acetylcholine at the neuromuscular junction.
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Serotypes A and B are available for therapeutic purposes. Three different brands of sero-
type A and 1 brand of serotype B are commercially available in the United States (Ona-
botulinumtoxin A, Rimabotulinumtoxin B, Abobotulinumtoxin A, Incobotulinumtox-
in A). The various brands of BoNT have different dosing guidelines and storage require-
ments, and thus are not interchangeable. The most important factors in determining the
success of treatment with BoNT is the appropriate selection of muscles and accurate in-
jection of the adequate dose. Muscle selection should be based on the determination of
the primary abnormal position and knowledge of the insertion sites of the corresponding
muscles that when contracting produce the abnormal position. Electromyography guid-
ance may improve the accuracy of muscle selection and targeting [22–24].

Chorea

Chorea is a hyperkinetic movement disorder consisting of involuntary brief move-

ments that tend to flow randomly between body regions. Chorea can be caused by a
large variety of diseases including neurodegenerative diseases, metabolic diseases, and
autoimmune diseases, or can be secondary to structural changes. Therapeutic ap-
proach is prevalently symptomatic, has the goal to improve the functionality and in-
cludes medications such as dopamine-depleting agents (tetrabenazine), antipsychot-
ic drugs, benzodiazepines, glutamate antagonists [23, 24]. When choosing an inter-
vention, clinicians should consider the eventual presence of behavioral and cognitive
issues frequently associated with chorea and responsible of further disability. If pa-
tients suffer from neuropsychiatric symptoms besides chorea such as depression, psy-
chosis, aggression, or compulsive behavior, it is advisable to start with antipsychotic
drugs (off-label), such as tiapride, olanzapine, and quetiapine. On the contrary, in
patients without neuropsychiatric symptoms, tetrabenazine is suggested as the first-
line therapy. Conflicting results are available for amantadine and riluzole [23, 24].

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Dr. Renato Puppi Munhoz, MD, PhD
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Hospital, Division of Neurology, University of Toronto
399 Bathurst St., 7 Mc412
Toronto, ON Canada M5T 2S8 (USA)
E-Mail renato.munhoz@uhn.ca
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Niranjan A, Lunsford LD, Richardson RM (eds): Current Concepts in Movement Disorder Management.
Prog Neurol Surg. Basel, Karger, 2018, vol 33, pp 41–49 (DOI: 10.1159/000480747)
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