Parkinsonism refers to the combination of bradykinesia (slowness of movement) and rigidity. It is the defining feature of Parkinson’s disease (PD) and other disorders of the extrapyramidal system such as progressive supranuclear palsy (PSP), multisystem atrophy (MSA), and corticobasal degeneration (CBD). A patient with parkinsonism may describe their problem as slowness or stiffness, but may also say that they have no energy or that they are weak. Parkinsonism is often attributed to fatigue, normal aging, or depression for months or years, and a patient with parkinsonism may only come to neurological attention after developing a tremor or gait impairment. The following are the important elements of the history in patients with parkinsonism.
Age of onset
Parkinsonism is generally a problem of older patients. Symptoms beginning before the age of 40 suggest an early-onset or familial variant of PD, a toxin- or medication-related process, or Wilson’s disease.
Pace of onset
Most forms of parkinsonism become clinically apparent over a course of months to years. Examples include PD, MSA, and PSP. Apoplectic symptom onset is exceptionally rare, and is usually due to bilateral caudate, putaminal, or thalamic infarcts.1 Symptoms that develop over days to weeks may be due to drug-induced parkinsonism (a condition that may also develop over several years). Rapid progression over several weeks to months is most typical of Creutzfeldt–Jakob disease.
Presence of tremor
Asymmetric resting hand (or less likely, foot) tremor strongly suggests a diagnosis of PD. Other tremors that are characteristic of PD include resting jaw or lip tremors. Tremor is usually absent in atypical forms of parkinsonism – when present, it is often mild, symmetric, and occurs with action rather than with rest. Large-amplitude action or intention tremors are more typical of Wilson’s disease. Chapter 14provides a more detailed discussion of the evaluation and treatment of tremor.
Gait dysfunction and falls
Almost all patients with parkinsonism eventually develop gait abnormalities, usually as a later feature of the disease. Gait difficulty at or shortly after symptom onset suggests PSP. Common descriptions of gait abnormalities in parkinsonism include stiff-leggedness, shuffling, slowness, and walking with a lack of arm movement.
Parkinson’s disease is usually asymmetric in its early stages. As the disease advances, however, both sides become involved, and most patients eventually develop more symmetric deficits. With the additional exception of CBD, most other forms of parkinsonism are relatively symmetric.
Autonomic dysfunction including dry mouth, decreased perspiration during exercise, lightheadedness, fainting, constipation, and urinary retention is prominent in MSA, and may be more impressive than either rigidity or bradykinesia. Autonomic symptoms are also common in PD, but do not usually bring the patient to clinical attention.
Ataxic symptoms including clumsiness, frequent spilling of food or liquids, and dropping things are common in MSA. These symptoms are often much more prominent than extrapyramidal ones, and patients are often referred for cerebellar strokes and tumors or hereditary ataxic disorders.
Medications and toxins
Dopamine antagonists used as antipsychotics and the promotility agent metoclopramide are the most commonly identified precipitants of drug-induced parkinsonism. Drugs of abuse are sometimes “cut” with substances that precipitate parkinsonism. Other uncommon toxins that may produce parkinsonism include manganese and carbon monoxide.
There are a number of genetic mutations, inherited in both autosomal dominant and recessive fashions that may produce familial forms of PD.2 Huntington’s disease (autosomal dominant) and Wilson’s disease (autosomal recessive) are among the more common inherited forms of parkinsonism. In most patients, however, the family history is noncontributory.
Memory loss and behavioral changes affect approximately 25–30% of patients with PD, but are not usually prominent at disease onset.3 Dementia with Lewy bodies, Huntington’s disease, PSP, and CBD are causes of parkinsonism that may initially present as dementia.
Activities of daily living
It is often helpful to ask the patient if it takes them more time to get ready in the morning, whether it is more difficult to turn over or get out of bed, and whether they have difficulty eating. Asking about activities of daily living, while not necessarily helpful in differentiating among the various forms of parkinsonism, helps to determine disease severity and guides treatment initiation.
Rigidity (often called “lead-pipe” rigidity) is an increase in tone that is independent of the velocity, displacement, and direction of movement. It is the form of hypertonicity produced by extrapyramidal disease. Rigidity may affect the appendicular or axial musculature. Evaluate for appendicular rigidity at the elbow, wrist, knee, and ankle. When testing for rigidity, look for an increase in tone in response to distraction: ask the patient to rapidly tap the opposite hand or foot, trace broad circles in the air, or recite the months of the year backwards. These maneuvers may uncover rigidity that was not apparent at rest. Test for axial rigidity by examining tone in the neck and torso. With the patient sitting up straight but relaxed in a chair, grasp their head firmly by the sides and attempt to move it briskly in the anterior–posterior plane. Normally, the neck is quite loose and there will be little resistance to this movement. In a patient with axial rigidity, however, the whole trunk will move in unison with the head. One form of rigidity that is somewhat specific to PD is cogwheeling rigidity, in which a tremor is superimposed on a background of rigidity. This is most easily elicited by rotating the hand at the wrist and feeling for a ratchety resistance.
Bradykinesia, or slowness of movement, is often overlooked by primary care physicians or dismissed as a manifestation of normal aging. Masking of facial expression, reduced blinking frequency, and slowness of speech and gait are all signs of bradykinesia that may be observed without formal testing. Tests of bradykinesia should include asking the patient to rapidly tap their fingers together, alternately slap the palmar and dorsal surfaces of the hand against their thigh, and elevate the foot slightly and tap the ground with the tips of their toes. Observe for slowness, decomposition, or inability to perform these movements.
Asymmetric resting tremor is one of the findings that most reliably distinguishes between PD and other forms of parkinsonism. Chapter 14 contains a detailed discussion of the tremor of PD and other movement disorders.
The typical features of an extrapyramidal gait are a relatively narrow base, slow initiation, shortened stride length, and slow turns. A patient with PD is characteristically hunched over at the shoulders, whereas a patient with PSP tends to be hyperextended throughout the trunk. The cerebellar form of MSA may be associated with an ataxic gait. Chapter 18 contains a more detailed discussion of the gait abnormalities in patients with extrapyramidal disease.
Dysarthria is discussed in further detail in Chapter 8. It may be a useful sign in differentiating among the various forms of parkinsonism. Hypophonia and slowness of speech are the most common speech abnormalities in PD. Early spastic dysarthria suggests atypical parkinsonism, especially PSP. A high-pitched quivering dysarthria may accompany MSA.
Mental status examination
Perform a complete mental status examination (Chapter 4) in all patients with parkinsonism, as cognitive abnormalities are common in patients with extrapyramidal disease, and specific abnormalities may help to differentiate among the various disorders. Dementia in parkinsonism is usually dominated by cognitive slowing rather than by the frank memory deficits that characterize Alzheimer’s disease. Problems with processing speed and visuospatial abnormalities are the most common findings on mental status examination. Asymmetric limb apraxia is particularly suggestive of corticobasal ganglionic degeneration, and may be the presenting feature in some patients. Dementia with Lewy bodies is discussed further in Chapter 4.
Examining eye movements is essential in patients with suspected PSP, as it is often difficult to establish the diagnosis without abnormalities of saccadic movements. To test saccades, instruct the patient first to look at your nose. Next, ask them to quickly shift their gaze up, down, to the left, and to the right. Poor initiation, decreased velocity, and decreased amplitude of downward saccades are classical but not universal features of PSP. If downward saccades are absent, attempt to prove that the saccadic disorder results from supranuclear dysfunction by looking for a preserved oculocephalic reflex: quickly thrust the head in each of the four
Figure 13.1 In general, neuroimaging studies are not particularly helpful in the diagnosis of parkinsonism. In this patient with multisystem atrophy, however, atrophy of the pons and cerebellum is shown in (A), while (B) shows the pathognomonic “hot cross bun” sign in the pons (arrow).
cardinal directions and observe for an intact vestibulo-ocular response in the opposite direction.
Autonomic dysfunction is the main problem in many patients with MSA, and may also be a disabling component of PD. Testing for orthostatic hypotension is described in further detail in Chapter 9.
Laboratory and neuroimaging studies
In most cases, neuroimaging is of limited utility in evaluating parkinsonism. Brain MRI is mainly employed to exclude the possibilities of vascular parkinsonism, tumors, and hydrocephalus. Patients with rapid-onset disease should undergo diffusion-weighted imaging to look for ischemic lesions or evidence of Creutzfeldt–Jakob disease. In some cases, MRI may help to distinguish among the different forms of parkinsonism. Brain MRI of a patient with MSA may show atrophy of the pons and cerebellum and the “hot cross bun” sign (crossed T2 hyperintensities) in the pons (Figure 13.1). Huntington’s disease leads to prominent atrophy of the caudate nuclei (Chapter 14, Figure 14.1). Other neuroimaging studies including single photon emission computed tomography (SPECT) and positron emission tomography (PET) scanning are used for research purposes but are not employed routinely in the clinical setting.
In younger patients, check for reduced serum ceruloplasmin levels or increased 24-hour urinary copper excretion diagnostic of Wilson’s disease (Chapter 14). A variety of commercial genetic studies is available to evaluate patients with familial forms of PD. Autonomic testing to document orthostatic hypotension and other autonomic abnormalities is essential to the diagnosis of MSA. Anal sphincter electromyography is often performed in an attempt to distinguish MSA from PD, but it is generally less helpful than history and autonomic testing.
Idiopathic PD is the most common form of parkinsonism. Patients usually develop the disorder between their 50s and 70s, although symptoms will begin before the age of 40 in 5–10% of patients.4 The cardinal features of PD are tremor, rigidity, and bradykinesia. Unfortunately, there is no laboratory test or neuroimaging study that definitively confirms PD, and the diagnosis must be made clinically. The features that most reliably distinguish PD from other forms of parkinsonism are asymmetric resting tremor and symptomatic improvement with levodopa.5 Because up to 30% of patients lack a tremor, a trial of levodopa is often necessary in unclear cases.5 Parkinson’s disease may be divided into three stages: an early, levodopa- responsive stage in which disability is minimal, a middle stage in which responsiveness to levodopa decreases and disability becomes more prominent, and an end stage in which the benefits from levodopa are minimal and disability becomes severe, leading to death in some cases.
Treatment of early Parkinson’s disease
Tremor is often the most prominent symptom in the early stages of PD, and some patients may have a milder, tremor-predominant form of the disease for many years. The anticholinergic agent trihexyphenidyl (started at 1 mg qd and titrated up to 2–3 mg tid as needed) is the preferred treatment for a patient with isolated or predominant tremor. Side effects of this medication include sedation and dry mouth. Other options for tremor-predominant PD include benzodiazepines such as clonazepam (0.5–1.0 mg bid) and the anticonvulsant zonisamide (50–100 mg qd).
The treatment options for a patient with symptomatic bradykinesia or rigidity include dopamine agonists, levodopa, and monoamine oxidase B (MAO-B) inhibitors. Because early exposure to levodopa theoretically increases the long-term risk for developing dyskinesias, I usually treat younger patients or those with mild disability with a dopamine agonist. The two most commonly used agents are ropinirole (starting dose 0.25 mg tid, usual effective dose 1–3 mg tid) and pramipexole (starting dose 0.125 mg tid, usual effective dose 0.5 mg tid). Side effects of these agents include nausea, vomiting, and hypotension. Excessive daytime sleepiness, sleep attacks, and compulsive behaviors such as gambling and shopping are important, but less common side effects of dopamine agonists.
Use levodopa for patients who do not tolerate dopamine agonists, do not respond to therapeutic doses after 3 months of treatment, or have at least moderate disability at presentation. Peripheral side effects from levodopa include nausea, vomiting, and orthostasis, and may be avoided by using levodopa in combination with the dopamine decarboxylase inhibitor carbidopa. Carbidopa/levodopa combinations come in 10 mg/100 mg, 25 mg/100 mg, and 25 mg/250 mg doses. I usually initiate treatment with one half of a 25 mg/100 mg pill three times a day and titrate it to a full pill three times a day over 2–3 weeks in order to avoid side effects such as confusion, hallucinations, and orthostatic hypotension. Most patients respond by the time the daily levodopa dose reaches 300–600 mg.
The MAO-B inhibitors rasagiline (1–2 mg qd) and selegiline (5 mg bid) are the third main option for treating early parkinsonism. There are two important interactions to keep in mind when prescribing MAO-B inhibitors: when combined with a selective serotonin reuptake inhibitor, they may lead to the serotonin syndrome characterized by confusion, autonomic instability, and myoclonus, and when combined with tyramine-rich foods such as red wine, aged cheese, or aged meat, they may precipitate a hypertensive crisis. Inhibitors of MAO-B may provide mild symptomatic relief. Their capacity to provide neuroprotection is of great interest but is not necessarily supported by available evidence.
Treatment of intermediate Parkinson’s disease
Patients with PD almost inevitably progress over a period of months to years. During the intermediate stage of PD, bradykinesia and rigidity worsen. Responsiveness to levodopa decreases, while side effects secondary to the medication increase. Motor fluctuations and the “wearing-off” phenomenon begin in the intermediate stages of PD: after several hours of symptomatic response to levodopa, the benefit disappears before the next scheduled dose is administered and the patient enters the “off” state. Address the wearing-off phenomenon by decreasing the interval between levodopa doses or by adding the catechol-O-methyltransferase (COMT) inhibitor entacapone (200 mg with each dose of levodopa) to extend the half-life of levodopa. The main side effect of entacapone is diarrhea. Liver dysfunction, a concern with the older COMT inhibitor tolcapone, is not a side effect of entacapone. Other options to treat wearing off include adding dopamine agonists or MAO-B inhibitors. Controlled-release formulations of carbidopa/levodopa are not terribly effective at extending “on” time and reducing wearing-off symptoms.6
In addition to experiencing motor fluctuations and wearing off, patients in the intermediate stage of PD also derive less benefit from each individual levodopa dose. Higher doses of levodopa, even up to a total daily dose of 1000–1200 mg, may be ineffective. It is important to determine at what times of day the patient is most symptomatic, and to make sure that the levodopa is dosed adequately in anticipation of these dips. Most patients require additional medication early in the day to get through their morning routines. Others might require more levodopa at night in order to avoid nocturnal akinesia that prevents them from getting to the bathroom. For some patients, the problem might be eating high-protein meals that interfere with the intestinal absorption of levodopa. Address this problem by instructing the patient to take their levodopa an hour before or after meals, or to eat low-protein meals in the morning. Dopamine agonists and MAO-B inhibitors may be effective as adjuncts to levodopa.
Dyskinesias secondary to long-term levodopa use also develop in the intermediate stage of PD. Dyskinesias may affect any part of the body and are usually choreiform in nature, but may take the form of any of the hyperkinetic movements (Chapter 14). Dyskinesias are generally more prominent at the time of peak levodopa effect, but may also be more pronounced in the “off” state. In some patients, decreasing the levodopa dose reduces peak-dose dyskinesias. Obviously, though, this reduces any symptomatic benefit from levodopa and increases time spent in the “off” state. Amantadine (100 mg bid–tid) may provide modest benefit in reducing dyskinesias, but should be used cautiously in older patients, as it may precipitate confusion.
Deep brain stimulation (DBS) of the subthalamic nucleus is a surgical option for patients with intermediate PD, and may improve any of the symptoms of PD, decrease the time spent in the “off” state, and reduce dyskinesias. Candidates for DBS must be selected carefully and evaluated by a multidisciplinary team. The response to DBS is generally equivalent to the maximum improvement that the patient derives from medical treatment: patients with no response to levodopa are therefore not eligible for treatment. Patients with severe cognitive impairment are also poor candidates and are usually excluded. Possible side effects of DBS include infection, hemorrhage, seizure, and misplacement of the stimulator leads, requiring reoperation. Deep brain stimulation requires frequent follow-up visits for stimulator testing and programming. Other less commonly employed surgical options include thalamotomy or thalamic DBS (for patients with disabling tremor) and pallidotomy.
Treatment of advanced Parkinson’s disease
In the advanced stage of PD, bradykinesia and rigidity worsen. Further increases in levodopa doses or addition of other symptomatic treatments for PD are generally unhelpful. Gait freezing and other forms of akinesia also become problematic in advanced PD. Falls become more frequent as postural reflexes become impaired. As a result, patients often need to use walkers or wheelchairs or become bed bound. Medical and surgical treatment of freezing gait and falls are generally ineffective. Supportive care, including management of nonmotor symptoms, becomes the mainstay of treatment at this stage. Unfortunately, many patients with later-stage PD die from pneumonia or as a result of a traumatic injury from a fall.
Treatment of nonmotor symptoms
As PD progresses, treating nonmotor symptoms becomes increasingly important. Cognitive and autonomic functions generally worsen as motor symptoms become more severe. The following are among the most important of the nonmotor symptoms of PD.
Disentangling psychomotor slowing produced by depression and bradykinesia secondary to PD is often challenging and in some cases requires formal neuropsychological or psychiatric evaluation. Depressive symptoms may affect as many as 50% of patients with PD, and generally parallel the severity of intellectual impairment.7 Selective serotonin reuptake inhibitors (SSRIs) are usually the first line of treatment, but must be avoided in patients who are taking MAO-B inhibitors. Tricyclic antidepressants are also helpful, but their anticholinergic properties may worsen cognitive dysfunction. Electroconvulsive therapy is often effective for treating severe depression in PD, and offers the additional benefit of temporary PD symptom relief.8
Approximately 25–30% of patients with PD develop dementia. Executive function, processing speed, and visuospatial abilities are the cognitive domains that tend to be most severely affected. Memory and language deficits may be later occurrences. Because medications used to treat PD may contribute to cognitive deficits, a trial of decreasing or discontinuing medications may help to improve symptoms. The medications used for PD in descending order of cognitive side effect likelihood (and thus the recommended sequence of discontinuation) are:
• anticholinergic agents
• MAO-B inhibitors
• COMT inhibitors
• dopamine agonists
Acetylcholinesterase inhibitors such as donepezil or rivastigmine are somewhat effective for patients with dementia associated with PD.9
Hallucinations and psychosis
Hallucinations and psychosis are features of intermediate and advanced PD. They often occur as side effects of one of the medications used to treat motor symptoms, and may lead to hospitalization or, in severe cases, institutionalization. The first step in evaluating and treating psychotic symptoms is to screen for metabolic disturbances that may cause confusion, as described in Chapter 1. Try to decrease psychoactive antiparkinsonian medications as described above. If excluding metabolic derangements and tapering medications still does not improve symptoms, consider antipsychotics with minimal extrapyramidal side effects such as clozapine (25–75 mg qd) or quetiapine (25 mg qd–qid). Although clozapine improves psychosis, it may cause agranulocytosis and, for this reason, requires frequent white blood count monitoring and registration with a clozapine provider program.
Constipation occurs in approximately half of patients with PD, and may be a disabling symptom.10 The first step in evaluating and treating constipation is to exclude treatable medical causes. Although constipation may be related to agents used for PD including anticholinergics and levodopa, discontinuing these medications usually does not help to reverse symptoms. Laxatives such as lactulose (30–45 ml tid–qid) and polyethylene glycol (17 g qd) are usually the agents of first choice. Consider referring patients with refractory symptoms to a gastroenterologist.
Oropharyngeal bradykinesia leads to difficulty with eating and swallowing pills, and puts patients at risk of aspiration. Formal swallowing studies may help to clarify the problem if there is any doubt about the presence or severity of dysphagia. Dysphagia often responds to levodopa, provided that the patient has enough residual swallowing function to take their pills. Parcopa is an orally disintegrating carbidopa/levodopa formulation that dissolves on the tongue, allowing patients with severe dysphagia access to adequate levodopa. Percutaneous enteric gastrostomy tubes may be necessary for patients with severe dysphagia.
Dysarthria affects up to 70% of patients with PD and is characterized by a slow, monotonous, hypophonic voice.11 Although dysarthria may improve initially with levodopa, as the disease progresses the response of this symptom to levodopa also decreases. Deep brain stimulation of the subthalamic nucleus is similarly disappointing. While speech therapy may help marginally, the treatment of dysarthria related to PD is often unsatisfactory and may ultimately require assistive communication devices.
Progressive supranuclear palsy
Although there is considerable clinical heterogeneity, PSP most commonly presents with bradykinesia and rigidity without tremor.12 Other common presentations include dementia, gait dysfunction, and bulbar dysfunction. It may be difficult to differentiate PSP from other forms of parkinsonism, but the following features are the most valuable in making the diagnosis:
• Prominent gait instability at disease onset. Falls and other gait disturbances that occur within the first year of disease presentation are more consistent with PSP than with any of the other extrapyramidal syndromes. Patients with PSP tend to be hyperextended at the trunk, unlike those with PD who tend to be hunched over at the shoulders.
• Spastic dysarthria. Patients with PSP may have a harsh, strangled quality to their speech or may sound robotic. Amyotrophic lateral sclerosis and the pseudobulbar state affect speech in similar ways (Chapter 8).
• Supranuclear gaze palsy or slowing of vertical saccades. This is the most specific feature for PSP, but its frequent absence at disease onset often prevents definitive diagnosis. Patients with PSP have most difficulty with looking downwards, often leading to problems with reading or with spilling food. Examination of saccadic eye movements is discussed above.
• Eyelid-opening apraxia. This disorder is often confused with blepharospasm, and is discussed in further detail in Chapter 7. Briefly, patients have difficulty opening their eyelids, in some cases leading to functional blindness.
• Axial rigidity. Unlike PD, rigidity is greater in the axial relative to the appendicular musculature. This results in slow head turning and difficulty with truncal stability.
There is no single neuroimaging or laboratory test that confirms the diagnosis of PSP. Rather, the diagnosis is established by suggestive clinical features and by exclusion of other extrapyramidal disorders. Patients in the early stages of PSP may derive mild benefit from levodopa, and a trial up to a total daily dose of 1000 mg is justifiable. As the disease progresses, supportive care becomes the mainstay of treatment. Physical therapy and occupational therapy are important for patients with PSP. Unfortunately, patients with PSP have a poor prognosis, surviving for 5–6 years, on average.12
Multisystem atrophy is characterized by extrapyramidal dysfunction in combination with autonomic, cerebellar, or pyramidal dysfunction. Extrapyramidal features may be the initial and often sole manifestations of MSA for many years (MSA-P subtype), in which case it may be difficult to separate MSA from PD. Other patients present with primary autonomic dysfunction including orthostatic hypotension, hypohydrosis, and sphincter dysfunction (MSA-A subtype). Finally, the initial symptoms may be cerebellar ataxia, in which case the disorder may be difficult to distinguish from an inherited spinocerebellar ataxia (MSA-C subtype). The diagnosis of MSA is usually established by clinical history and examination. Autonomic testing may help to confirm the diagnosis in patients with MSA-A. Brain MRI demonstrating atrophy of the pons and cerebellum or the “hot cross bun” sign (Figure 13.1) is often useful in patients with the MSA-P and MSA-C variants. Patients may respond to levodopa in the early stages of MSA, but this response declines as the disease progresses. The mainstays of treatment are symptomatic therapy for orthostatic hypotension (Chapter 9) and other autonomic nervous system problems, and physical therapy and occupational therapy for the cerebellar components. Unfortunately, MSA is a progressive disabling disease, with a median survival of 6–9 years.13
Corticobasal ganglionic degeneration
Corticobasal ganglionic degeneration (CBD) is an uncommon condition that is often confused with another extrapyramidal disorder such as PD or PSP, or with a primary dementing disorder.14 Similar to PD, CBD is usually characterized by asymmetric rigidity and bradykinesia. Tremor, however, is usually absent. Two important findings in CBD that are unusual at presentation in the other movement disorders are asymmetric limb apraxia (Chapter 4) and cortical sensory loss (Chapter 15). Limb apraxia may be accompanied by an unusual finding known as the “alien hand” phenomenon in which the affected limb seems to act of its own volition without the input of the patient. Many patients with CBD are demented at presentation. Unlike dementia in other extrapyramidal disorders, the dementia in CBD affects cortical function such as memory and language. Dysarthria and vertical gaze impairments may lead to confusion of CBD with PSP. Patients with CBD respond minimally to levodopa, and supportive therapy is the mainstay of treatment.
Other causes of parkinsonism
Dopamine antagonists including antipsychotics and the antiemetic metoclopramide may precipitate parkinsonism. Although symptoms tend to be relatively symmetric in drug-induced parkinsonism, almost half of patients with drug-induced PD will have a degree of asymmetry suggestive of idiopathic PD.15 Only a minority, however, will have resting tremor. Removing the offending agent may lead to mild symptomatic improvement. Treating symptoms with levodopa or with a dopamine agonist is usually not effective and should be avoided.
Parkinsonism due to cerebrovascular disease is perhaps only 5% as common as idiopathic PD.16 Although patients often have a history of prior acute ischemic stroke, this is not a requirement for diagnosis. The lower half of the body is more commonly affected in vascular parkinsonism than it is in PD, and gait disturbances are often the presenting symptoms. Tremor is usually absent, and symptoms tend to be relatively symmetric. Dementia, corticospinal tract findings such as spasticity and hyperreflexia, and urinary incontinence commonly accompany vascular parkinsonism. Unfortunately, vascular parkinsonism does not respond to levodopa, making supportive care the mainstay of treatment.
Other extrapyramidal disorders
Other common disorders leading to parkinsonism include those that have more prominent hyperkinetic features (Huntington’s disease and Wilson’s disease, Chapter 14) or dementia (dementia with Lewy bodies, Chapter 4) at onset.
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