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  • A new-onset seizure in late life is frequently a symptom of an underlying brain disease or injury, but may not need to be treated with medications, if no cause is found. Recurrent seizures can be prevented with medications. Newer antiepileptic drugs are better tolerated.

  • Parkinson disease and other common movement disorders seen in older patients are diagnosed clinically and can be effectively managed medically.

  • Peripheral neuropathy is common in older adults, and diabetes is the most common cause in the United States. Several medications are approved by the FDA for the treatment of painful diabetic neuropathy.

  • New onset of headaches in older adults should prompt a search for a secondary cause, including brain tumor, systemic illness, temporal arteritis, or medication-induced causes.

Note: Stroke has a dedicated chapter elsewhere in the Geriatrics Nursing Review Syllabus.

Neurologic diseases and disorders are increasingly common with advancing age. The most prevalent neurologic disorders include Alzheimer disease (AD) and related dementias, gait disorders, cerebrovascular disease, epilepsy, Parkinson disease (PD), and peripheral neuropathy. In the United States, almost half (40%–50%) of the population >85 years old suffer from dementia, and a similar percentage of hospitalized patients of this age have a gait disorder caused by a neurologic condition. Other U.S. population data include the following: 7.5% of adults 60–79 years old and 15% of those ≥80 years old have had a stroke, 1% of adults >60 years old and 3% of those >80 years old have been diagnosed with PD, 3% of adults by age 75 and close to 10% of the nursing-home population have epilepsy, and up to 10% of adults >65 years old have some signs of a peripheral polyneuropathy. This chapter will cover epilepsy in older adults, PD and other movement disorders, and other common neurologic conditions, including neuromuscular disorders, myelopathy, and headaches.

Individual neurologic disorders in older adults can be challenging to differentiate, given that it is common for a patient to have more than one such disorder or sequela when examined. Pharmacologic treatment of neurologic disorders must account for the unique metabolism of older adults and the potential for drug-drug interactions. Furthermore, because neurologic disorders add substantially to the burden of functional dependency, acknowledging the psychosocial aspects of these conditions is vital in constructing treatment plans to improve functional abilities and quality of life.


A seizure is caused by excessive and synchronous discharges of cortical neurons producing a transient disruption of normal brain function. Recurrent seizures are the defining feature of epilepsy. Seizures are broadly classified as partial or generalized, depending on whether the seizure discharges involve only a portion of the cortex or the entire cortex. Partial seizures are subdivided on the basis of whether the seizure is associated with impaired consciousness. Simple partial seizures do not impair consciousness, but complex partial seizures do. Most commonly, simple partial seizures involve focal rhythmic motor twitching. Complex partial seizures are often preceded by an aura, followed by loss of awareness and responsiveness typically manifested as staring off into space. Automatisms and other minor motor manifestations can occur with complex partial seizures. After the event, patients display postictal confusion and amnesia for the seizure. Generalized seizures involve the entire cortex and typically cause tonic-clonic convulsions (ie, generalized tonic-clonic, or “grand mal,” seizures). A seizure may start as a complex partial seizure and secondarily progress into a generalized seizure. In critical care settings, a generalized seizure may manifest as a nonconvulsive continuous seizure (ie, nonconvulsive status epilepticus) in which a patient shows persistent alteration in mental status without convulsive movements.

The incidence of epilepsy follows a bimodal pattern with respect to age, with an initial peak within the first year of life and a second peak after the age of 60. The annual incidence of epilepsy peaks at 135 per 100,000 in those >80 years old. Secondary causes of seizures, ie, those with an underlying discernible cause, are more common among older adults. In this demographic group, about 70% of new-onset seizures are secondary. Common causes include cerebrovascular disease, space-occupying lesions, brain trauma, neurodegenerative diseases, and alcohol withdrawal. It is estimated that cerebrovascular disease causes 50% of known causes of late-onset seizures, with tumors, trauma, and degenerative dementias each causing 10%–20% of cases. Cortical or hemorrhagic strokes are more likely to cause seizures than other types of stroke. AD increases the risk of seizures, although seizures in AD are relatively uncommon, occurring in 2%–5% of patients. Seizures in AD are seen more often in advanced stages of dementia and in young-onset AD. The incidence of partial epilepsy (which frequently has an underlying cause) increases in older adults, whereas the incidence of primary generalized epilepsy (generally idiopathic or genetic) is more common in pediatric populations.

It is important that older adults with new-onset seizures undergo diagnostic evaluation to exclude an underlying treatable condition. The neurologic history and examination should aim to clinically characterize the seizure and localize its source, as well as to elicit other signs of a focal lesion or a metabolic disturbance (eg, uremia, hepatic failure). Blood studies (comprehensive metabolic panel, magnesium, calcium), brain imaging (MRI is preferable to CT), and electroencephalography play important roles. Brain imaging should be obtained with and without contrast to identify and characterize structural brain lesions.

Once the appropriate evaluation has been done, the decision to begin an antiepileptic drug should be made carefully to maximize benefit and minimize risk. On average, 30% of patients with a single unprovoked seizure have another seizure, but 70% do not. The presence of a focal brain abnormality on brain imaging or epileptic changes on an electroencephalogram (EEG) raises the likelihood of recurrence and should prompt consideration of pharmacologic therapy. If a patient has a second unprovoked seizure, then the probability of further seizures increases to 70%, and pharmacologic therapy should generally be initiated.

There have been only 3 randomized, double-blind, comparative clinical trials in older adults with newly diagnosed epilepsy. In a Department of Veterans Affairs (VA) study that compared lamotrigine, gabapentin, and carbamazepine, seizure control was similar among these 3 drugs, but carbamazepine was significantly less well tolerated than the other 2. Discontinuation rates due to adverse events were 12% with lamotrigine, 22% with gabapentin, and 31% with carbamazepine in this 52-week study. Two other trials compared lamotrigine to carbamazepine. As in the VA trial, both drugs effectively prevented recurrent seizures, but lamotrigine was significantly better tolerated. This difference in tolerability was not found in a third study in which a controlled-release form of carbamazepine and flexible dosing design were used. Several of the other newer antiepileptic drugs have been examined in open-label trials in older populations, including studies with oxcarbazepine, levetiracetam, and low-dose topiramate. These agents have demonstrated good seizure control and tolerability. Thus, there is growing evidence that use of one of the newer antiepileptic drugs described above is preferred to the use of older antiepileptic drugs in the older population because of improved tolerability and compliance (SOE=A).

The incidence of adverse effects and drug-drug interactions increases with age. This is particularly true with the older antiepileptic drugs, such as phenobarbital, carbamazepine, phenytoin, and valproate. For example, phenobarbital can cause cognitive adverse effects, phenytoin can cause ataxia, carbamazepine can cause hyponatremia, and valproate can cause weight gain, tremors, and parkinsonism. Many of the older antiepileptic drugs, including phenobarbital, phenytoin, and carbamazepine, are potent inducers of the cytochrome P450 system, which increases the risk of drug-drug interactions. Also, each of these 3 agents has been associated with increased bone loss with age. Finally, changes in hepatic function or binding protein levels in older adults can alter the metabolism of older antiepileptic drugs, active drug levels, and risk of adverse effects. Clinical pharmacists can help to resolve complex issues of drug interactions, dosages, and adverse events, especially when using older antiepileptic drugs.

Antiepileptic drug doses are best started at low levels and increased very slowly in older adults to avoid problematic adverse effects. Older adults may have difficulty with adherence to antiepileptic drug schedules for a variety of reasons. It is particularly important when treating older adults to involve caregivers so that the goals of treatment, adverse events, and monitoring of response are understood. Final medication dose is determined by consideration of both seizure control and adverse events. Ideally, drug doses are increased to a level that eliminates seizures but does not result in adverse effects. Some antiepileptic drugs do not require laboratory monitoring. Common causes of breakthrough seizures in individuals known to be epileptic are systemic infections, metabolic disturbances, sleep deprivation, and medication noncompliance. Providers should consider discontinuing antiepileptic drugs if a patient has not had a seizure for ≥2 years, particularly if the original seizure was a single or poorly characterized event and if a recent EEG does not show epileptic activity.


A simple definition of movement disorder is the presence of abnormal involuntary movements. These movements result not from weakness or sensory deficits but from dysfunction of the extrapyramidal motor systems. Movement disorders can be classified as hypokinetic (paucity of movement) or hyperkinetic (excessive movement). The hypokinetic movement disorders include PD and the related Parkinson-plus syndromes (eg, multiple system atrophy, progressive supranuclear palsy). Hyperkinetic movement disorders include conditions that produce chorea (eg, Huntington disease), dyskinesias (eg, tardive dyskinesias), dystonia, and tremor (eg, essential tremor). Movement disorders are especially common among older adults.

Parkinson Disease (PD)

PD is a progressive neurodegenerative disease that results in neuronal dysfunction and neuronal loss in pathways of the brainstem, basal ganglia, and cerebral cortex. The pathologic hallmark of the disease is the Lewy body, an intracellular inclusion body originally found in dopaminergic neurons of the substantia nigra. These neurodegenerative changes cause a constellation of clinical signs, including tremor at rest, bradykinesia, rigidity, and postural instability. As the disease progresses, neurodegeneration and Lewy body pathology extends into the cortex (limbic region and neocortex), causing neuropsychiatric and cognitive symptoms (ie, PD with dementia).

The incidence and prevalence of PD increase with age. Prevalence rates in the United States rise from 1% of the population at age 60 to 3% at age 80. Aging, environmental factors, and genetics are thought to be involved in the pathogenesis of PD. Risk factors associated with increased risk of PD include exposure to pesticides, welding as a profession, exposure to manganese, age, and family history. Smoking and caffeine consumption have been associated with decreased risk. A small proportion of PD cases (5%–10%) are the result of a causative genetic mutation, while a larger proportion of patients may have inherited a susceptibility gene that increases risk. Approximately 10 genes have been associated with PD, either as causative mutations or susceptibility genes. Idiopathic PD (ie, parkinsonism not attributable to strokes, medications, or other primary causes) most commonly appears clinically between the ages of 50 and 79 years. Dementia in PD occurs in 30%–40% of PD patients and is more common with longer duration of disease, more severe motor symptoms, an akinetic-rigid presentation, and older age of onset of motor symptoms.

Diagnosis of PD

Recent clinical diagnostic criteria continue to highlight the central role of the motor signs of PD and the importance of the physical examination in making a clinical diagnosis. To make a diagnosis of PD, there should be evidence of parkinsonism, defined as the presence of bradykinesia in combination with either resting tremor, rigidity, or both. The term bradykinesia describes either a slowness in initiating movement (ie, a paucity of spontaneous movements) or slow movements themselves. This can be manifested clinically as reduced frequency and amplitude of fine finger movements, decreased facial expression or blinking, and micrographia (small handwriting). The tremor of idiopathic PD is generally asymmetric, involving one hand more than the other, and has a slow frequency (usually 4–6 Hz). It is present at rest and typically resolves or decreases with active, purposeful movement. Muscular rigidity is usually readily evident on passive movement of a limb when the patient is relaxed. Passive movement may demonstrate a smooth resistance (“lead pipe” rigidity) or superimposed ratchet-like jerks (ie, “cogwheel” phenomenon, which is caused by tremor superimposed on the rigidity). The fourth cardinal motor feature of PD is impaired postural reflexes, which can be elicited with a pull test (pulling a standing patient backward and assessing his or her ability to maintain balance). Impaired postural balance is a feature present later in the course of idiopathic PD; the presence of early postural imbalance and frequent falls often signals a Parkinson-plus syndrome.

Additional clinical features that are supportive of a diagnosis of idiopathic PD include a clear improvement in motor symptoms with dopaminergic medications and a loss of the sense of smell. Standardized tests are available to quantify a patient’s olfactory function (eg, University of Pennsylvania Smell Identification Test [UPSIT]). However, loss of sense of smell is not specific to PD and can be seen in other neurodegenerative disorders (including AD), or in those with paranasal sinus disease or a history of head trauma. Recent studies using the UPSIT demonstrated sensitivities of 78%–84% and specificities of 68%–83% in differentiating patients with PD from healthy controls, depending on age and gender. Of note, similar sensitivities and specificities have been seen in patients with Alzheimer disease as compared with healthy controls, using the UPSIT. It is appropriate to refer patients to a neurologist with movement disorder expertise if atypical features are present or the diagnosis is unclear.

Treatment of PD

Patients who are functionally disabled by tremors, bradykinesia, or rigidity should be offered pharmacologic treatment. Drug therapy is effective in reducing these symptoms but does not improve postural instability or nonmotor symptoms of PD. Patients who respond well to initial pharmacologic treatment are generally well managed by primary care providers, but those with advanced disease or suboptimal response to drug therapy may benefit from referral to neurologists with movement disorder expertise and who are familiar with the increasing variety of available treatments. Nonpharmacologic therapy should include a regular exercise program. Many older adults benefit from a course of physical therapy aimed at restoring their confidence in walking and maintaining balance, often with instruction in PD-focused physical therapy programs (eg, the “Training BIG” program) or symptom-focused therapy (eg, for coping with disabling freezing episodes). Physical therapists can also help, when needed, with selection of appropriate canes or walkers. A home visit by an occupational therapist can help to evaluate safety and equipment needs in the home, such as appropriate placement of wall rails, grab bars, and other such assistive devices that reduce the risk of falling.

Levodopa therapy for PD motor symptoms: The most effective pharmacologic treatment of patients with PD is levodopa combined with carbidopa (SOE=A). Levodopa is converted to dopamine in both the CNS and the periphery via dopa decarboxylase. Peripheral conversion is reduced by combining levodopa with carbidopa (a dopa decarboxylase inhibitor), which does not cross the blood-brain barrier. This formulation decreases adverse events associated with peripheral conversion. Treatment usually begins with a half tablet of the immediate-release 25/100 combination (ie, 25 mg carbidopa to 100 mg levodopa) administered every 8–12 hours. Every 1–2 weeks, the dose can be increased by one-half tablet, to reach a dosage of one full tablet three times a day (commonly 30 minutes before meals). The duration of action of this formulation is typically 4 hours. If disabling bradykinesia, rigidity, or resting tremor is still present, the dosage can be gradually increased further, with cautious observation for adverse events. Older adults, particularly those who are cognitively impaired, rarely tolerate total levodopa doses >1,000 mg/d. Additional formulations include a “controlled-release” form (available as 25/100 and 50/200) that generally requires a slightly higher total daily dose than immediate-release, and an “extended-release” form, which is dosed at 1.5–2 times higher than immediate-release. To convert from immediate-release to extended-release, the prescriber should use the conversion table in the manufacturer’s labeling. Common adverse events of levodopa-carbidopa include nausea, abdominal cramping, orthostatic hypotension, and visual hallucinations.

Managing PD symptoms with medications becomes more challenging as the disease progresses, because the therapeutic window narrows, making it difficult to control motor symptoms without undesirable adverse effects. After 5 years of treatment for PD, up to 50% of patients develop motor fluctuations or dyskinesias (involuntary choreiform movements). PD patients are commonly described as “on” (symptoms well controlled), “on with dyskinesias” (symptoms controlled but complicated by dyskinesias), or “off” (parkinsonism not well controlled). End-of-dose “off” symptoms are common and can be treated by increasing the dosing frequency of levodopa to every 3–4 hours or by adding an enzyme inhibitor such as rasagiline or entacapone (described below) to increase the duration of action of levodopa. Peak dose “on” dyskinesias are common and are treated by increasing the interval between levodopa doses or lowering the total daily dose of dopaminergic medications. The incidence and severity of dyskinesias can be reduced by introducing a dopamine agonist (described below) early in the treatment of PD, either as monotherapy or in combination with levodopa when daily dosages exceed 400 mg/d. This is an important consideration in patients <75 years old who are expected to have a long duration of disease and treatment. An intestinal gel form of carbidopa-levodopa is available for continuous administration via a pump through a percutaneous endoscopic gastrostomy (PEG)-jejunum tube for treatment of motor fluctuations in advanced PD.

Other medications for PD motor symptoms: Medications other than levodopa that can be used to treat PD motor symptoms include enzyme inhibitors, amantadine and anticholinergic medications, and dopamine agonists. Enzyme inhibitors include the catechol-O-methyl-transferase (COMT) inhibitor entacapone. COMT inhibitors block breakdown of levodopa, thereby increasing its bioavailability at the synapse. Entacapone increases the duration of action of levodopa, resulting in greater “on” time for a given dose of levodopa, but it can also exacerbate dyskinesias (SOE=A). Adverse events of COMT inhibitors are similar to those of levodopa. A second class of enzyme inhibitors are the monoamine oxidase B (MAO-B) inhibitors, which also block one of the enzymes responsible for dopamine breakdown. Rasagiline is a newer selective MAO-B inhibitor that has been approved by the FDA as early monotherapy or as adjunct therapy (SOE=A). Selegiline, an older MAO-B inhibitor, was shown in controlled trials to delay the need for additional antiparkinsonian agents (SOE=A). A neuroprotective role of MAO-B inhibitors in PD has been investigated but not established. Although chemically related to nonselective monoamine oxidase inhibitors, the selective MAO-B inhibitors, rasagiline and selegiline, do not require dietary restrictions. MAO-B inhibitors are generally well tolerated, although some patients can experience adverse events, including nausea, insomnia, confusion, or anxiety. Other medications used to treat motor symptoms of PD include amantadine and anticholinergic medications such as trihexyphenidyl. Amantadine, which has multiple pharmacologic properties, can provide mild improvement in PD motor symptoms and decreased dyskinesias (SOE=B). Older adults, especially with impaired renal clearance, can develop confusion and hallucinations with amantadine. Anticholinergic medications can modestly improve some PD symptoms, but adverse events such as dry mouth, urinary retention, and confusion outweigh benefits in most older adults.

Dopamine agonists may be used initially as monotherapy to treat motor symptoms of PD, or may be added to levodopa when its dosage exceeds 400 mg/d. The agents may be particularly useful for younger PD patients with milder disease and no signs of dementia (SOE=A). Slow upward titration of dopamine agonists is required to reduce the occurrence of common adverse effects such as nausea, sleepiness, orthostatic hypotension, and hallucinations. When compared with levodopa, dopamine agonists are less effective in controlling motor symptoms and are associated with more adverse events. However, early use of dopamine agonists can delay the emergence of levodopa-induced dyskinesias (SOE=A). Commonly used dopamine agonists include ropinirole, pramipexole, and rotigotine transdermal patch. All dopamine agonists, and to a lesser extent levodopa, have been associated with sudden sleep attacks in which patients may doze off abruptly while driving. Additionally, dopamine agonists have been associated with compulsive behaviors such as pathologic gambling. Patients should be warned of these rare but potentially serious adverse events, and clinicians should ask about these behaviors during routine follow-up visits.

Nonmotor Symptoms of PD

Nonmotor symptoms are common in PD and can be a target of treatment. These include urinary incontinence, constipation, drooling, seborrhea, anxiety, depression, visual hallucinations, sleep disorders, and cognitive impairment. PD patients are also at higher risk of melanoma and may benefit from screening for the condition and counseling about sun exposure. For PD patients who develop visual hallucinations or delusions, dopaminergic regimens should be reviewed and doses reduced. If symptoms are severe, the addition of low-dose clozapine may be considered, because this atypical antipsychotic agent is least likely to exacerbate PD motor symptoms. However, clozapine requires frequent laboratory monitoring to look for neutropenia. Pimavanserin, a new medication with a different mechanism of action, has been FDA approved for treatment of psychosis (hallucinations and delusions) in patients with PD. Pimavanserin improved psychosis without worsening motor function in patients with PD and does not require laboratory monitoring. PD patients who develop dementia symptoms can be treated with a cholinesterase inhibitor. Rivastigmine has been FDA approved for treatment of the dementia associated with PD (SOE=A).

“Parkinson-plus” Syndromes

“Parkinson-plus” or parkinsonian syndromes are a group of disorders with some motor features of PD (eg, bradykinesia, rigidity, postural imbalance) but that also have additional distinct and distinguishing features atypical for idiopathic PD. As a group, these disorders are much less responsive to pharmacologic treatment with dopaminergic medications than idiopathic PD. The parkinsonian syndromes described in some detail below include multiple system atrophy (MSA) and progressive supranuclear palsy (PSP). Other Parkinson-plus syndromes include dementia with Lewy bodies; corticobasal degeneration; vascular parkinsonism, in which small-vessel ischemic strokes in the basal ganglia produce parkinsonism; and medication-induced parkinsonism, in which dopamine-receptor blocking medications (typically antipsychotic or antiemetic drugs) produce parkinsonism.

Multiple System Atrophy

A histopathologic understanding of 3 parkinsonian syndromes, olivopontocerebellar atrophy, Shy-Drager syndrome, and striatonigral degeneration, has permitted these overlapping syndromes to be included within the rubric of one disease called multiple system atrophy (MSA). MSA produces degeneration in 3 distinct neuronal systems, the basal ganglia, cerebellum, and autonomic nervous system. MSA is characterized by parkinsonism, autonomic failure (eg, severe orthostatic hypotension, constipation, incontinence, erectile dysfunction, impaired sweating or temperature control), and cerebellar dysfunction (eg, ataxia, dysmetria). Other features that can accompany MSA are upper motor neuron signs, severe dysarthria, stridor, dystonia, and restless legs syndrome. The diagnosis is clinical, and MSA can initially be indistinguishable from idiopathic PD, but the degree of autonomic dysfunction, disappointing response to levodopa, and cerebellar signs all support a diagnosis of MSA. The mean age of onset for MSA is 55 years; it is slightly more common in men, and it progresses to death in approximately 7 years on average. MSA accounts for approximately 3% of cases of parkinsonism. Orthostatic hypotension is often the most disabling symptom of MSA. Nonpharmacologic management of autonomic dysfunction includes eating small meals, arising to standing position slowly, using compressive elastic stockings, and increasing salt and fluid intake. Medications may be needed to treat severe orthostatic hypotension and include midodrine, fludrocortisone, and droxidopa (SOE=A). Use of these medications may result in supine hypertension, which requires close blood pressure monitoring and medication adjustments. Levodopa may initially help with some symptoms of rigidity and bradykinesia, but the improvement is not as significant as in idiopathic PD, and dopamine replacement may worsen orthostatic hypotension.

Progressive Supranuclear Palsy

Progressive supranuclear palsy (PSP) accounts for approximately 4% of cases of parkinsonism. PSP is marked by an akinetic-rigid form of parkinsonism with early loss of postural balance causing frequent falls (afflicted persons typically fall backward). As the disease progresses, supranuclear gaze palsy (described below) becomes apparent, and patients eventually develop spasticity, dystonia, dysarthria, dysphagia, and a subcortical-frontal dementia. Usual age of onset is the late 50s or early 60s. The disease typically progresses rapidly, with marked incapacity occurring within 3–5 years and death within 6–8 years, generally as a result of aspiration, infection, or complications of immobility. Progressive supranuclear palsy derives its name from progressive impairments of voluntary, vertical gaze. Most patients develop eye movement restrictions approximately 3–4 years into the disease course. Patients are unable to voluntarily look up or down, with down gaze impairment more specific for PSP. Resting tremor is typically absent, and the rigidity is more pronounced in the neck and trunk (axial rigidity). Patients with PSP often have a fixed facial expression due to facial dystonia that causes them to keep their eyebrows elevated in a look of surprise or furrowed in a persistent scowl. The dysarthria of PSP is distinct from that of PD, with mixed spastic (strangled) and hypophonic features. Gait is disturbed early in the course, and falls are frequent in most patients. Cognition, particularly involving executive function or judgment, is often affected, and personality changes may arise as well. Treatment with levodopa may partially reduce the rigidity, but the dramatic response to levodopa seen in patients with early PD is lacking.

Hyperkinetic Movement Disorders


Chorea is a flowing, continuous, random movement that migrates from one part of the body to another. A variety of conditions are associated with chorea in older adults. The pathologic basis for chorea is dysfunction of the striatum. Huntington disease (HD) is the most common cause of chorea in adults. In HD, a patient’s family history will suggest an autosomal dominant mode of inheritance, and other family members may have a genetically confirmed diagnosis. Sometimes, however, suggestive family history is lacking, or the patient may be the first family member to display a late onset of the disease with mild features. The age of onset of HD is normally distributed around a mean age of 40 years, but there are reported cases of symptom onset as late as 75–80 years. The diagnosis of HD can be made by genetic testing of the huntingtin gene. Other causes of choreiform movements include drug-induced chorea (eg, from levodopa, antiepileptics, estrogen), which is common and optimally treated by reducing or removing the offending agent. Chorea may arise from ischemic injury to the basal ganglia (ie, vascular chorea). Idiopathic choreiform movements may occur as an isolated symptom in adults ≥60 years old, a condition termed senile chorea if other causes of chorea have been excluded. Chorea can be treated with dopamine receptor–blocking medications (eg, risperidoneOL, haloperidolOL), but possible benefit must be weighed against adverse effects, including risk of development of tardive dyskinesia (SOE=B). Two medications, tetrabenazine and deutetrabenazine, are currently approved by the FDA for treatment of chorea in HD (SOE=A) and have been used to treat other causes of chorea. These drugs block the storage and release of dopamine presynaptically. They are not associated with an increased risk of tardive dyskinesia. Patients taking tetrabenazine or deutetrabenazine need to be monitored closely for signs of depression and medication-induced parkinsonism.


Dystonia is a hyperkinetic movement disorder that results in sustained muscle contractions causing twisting movements or abnormal postures. Dystonia may occur as an isolated disorder, on a genetic basis, or as part of another movement disorder (eg, PD, corticobasal degeneration). Common focal dystonias seen in older adults include cervical dystonia (spasmodic torticollis), blepharospasm, spasmodic dysphonia, or focal hand dystonia (writer’s cramp). Medications such as anticholinergics (eg, trihexyphenidyl) or muscle relaxants (eg, baclofen) may be tried, but improvement in symptoms is typically limited and adverse effects are common (SOE=B). Botulinum toxin injections into contracted muscle can provide effective, but temporary, relief of dystonia (SOE=A).

Drug-Induced Movement Disorders

Several different types of involuntary movements can arise as a result of the use of medications. It is important to distinguish among medication effects that are acute, chronic but reversible, and chronic and irreversible. One acute effect that may occur with antipsychotic medications is an acute reaction resulting in dystonia of the mouth, tongue, or neck. If the dystonia is severe enough, treatment with intravenous diphenhydramine or lorazepam may be required, although this approach in older adults should be exercised with caution because of the risk of adverse effects. Chronic reversible drug effects include action tremor (eg, lithium, theophylline, valproic acid), parkinsonism (eg, antipsychotic or antiemetic medications), chorea (eg, antiepileptic medications, estrogen, levodopa), or dystonia (dopamine replacement therapy in PD). Chronic irreversible drug effects or tardive phenomena often begin after the medication (usually an antipsychotic medication) has been used for weeks to months; movements can include orobuccal dyskinesias, dystonia, akathisia (sensation of needing to move), myoclonus, and tics. Advanced age and duration of treatment with antipsychotic medications are the only well-established risk factors for developing tardive movement disorders. Once the diagnosis of a tardive phenomenon is established, the dosage of medication should be reduced or the medication should be discontinued. Treatment for tardive dyskinesia or tardive dystonia includes anticholinergic agents (eg, trihexyphenidylOL), valbenazine, baclofenOL, and tetrabenazineOL, all of which must be used with caution in older adults. In cases of severe tardive dystonia, intramuscular injections of botulinum toxin can reduce the frequency and severity of abnormal movements.

Essential Tremor

Essential tremor (ET) is the most common form of tremor. The tremor of ET is an action tremor and postural tremor, which is present when the limbs are in active use (eg, while writing or holding a cup). The tremor most commonly involves the arms, although the head and voice may be affected also. Other less affected areas of the body include the chin, tongue, and legs. Typically, the tremor in ET is symmetric, but it may be slightly worse in one arm than the other. The severity of the action tremor may vary significantly depending on the type of movement. The tremor disappears when the arms are relaxed, such as when the person is sitting with hands at rest in the lap, or standing with arms held at the sides. Functionally, the tremor may interfere with many daily activities, such as eating, writing, or fastening buttons. Stress or anxiety often exacerbates the tremor. The frequency of the tremor is in the range of 4–12 Hz, which is faster than the rest tremor of PD. The prevalence of ET increases with advancing age, with as many as 5% of adults >60 years old affected. The age of onset seems to have a bimodal distribution, with peaks in the teens through 20s and in the 50s through 70s. Prevalence rates among men and women are similar. Affected individuals commonly report they have an affected relative, suggesting a familial or genetic cause. Familial forms of the tremor have been linked to regions on chromosomes 2p and 3q. Familial and sporadic forms of ET have no apparent clinical differences. Alcohol may decrease the severity of ET.

The main indication for treatment of ET is functional disability due to the tremor (eg, difficulty writing, using a cup or spoon, trouble holding objects). It is important to educate the patient about exacerbating factors such as caffeine, stress, and fatigue. The first-line options for pharmacologic treatment of ET are nonselective β-blockers (propranolol, nadololOL) or primidoneOL (SOE=A). Propranolol is the only drug approved by the FDA for treatment of ET. Each of these drugs improves the severity of tremor in most patients by approximately 30%–50%. Other medications, including baclofenOL, gabapentinOL, mirtazapineOL, pregabalinOL, and topiramateOL, have been described as effective in some patients, but results have not been consistent (SOE=B/C). Occupational therapy and specialized equipment may provide complementary benefit for patients whose tremor threatens function (eg, use of weighted utensils orelectronic “tremor-cancelling” utensils). Some patients with severe, medically refractory tremor may undergo DBS. DBS stimulation in the ventral intermediate nucleus of the thalamus provides significant improvement in tremor control in most patients (SOE=A). Potential adverse events are similar to those of DBS in PD (described above). Unilateral thalamic ablations (eg, MRI-guided focused ultrasound) has been FDA approved as a treatment option for ET.

Restless Legs Syndrome

Restless legs syndrome (RLS) is a condition in which a patient feels an uncontrollable urge to move the legs at night, usually accompanied by an uncomfortable and unpleasant sensation of the legs that worsens with inactivity and improves with movement. The symptoms occur while the person is awake, and symptoms may also involve the arms. The diagnosis is based on the patient’s description of the symptoms; polysomnography is not required. There may be a family history of the condition, particularly in patients with an earlier age of onset of RLS. Some patients have an associated, underlying medical disorder (eg, anemia, or renal or neurologic disease). Because iron deficiency can trigger RLS, this should be excluded with a check of serum ferritin level. RLS is 1.5 times more common in women than men, and evidence suggests that RLS prevalence increases with age. Periodic limb movements of sleep (PLMS), which entail involuntary limb movements while asleep, occurs in most (80%–90%) patients with RLS. RLS may also be seen in demented patients who may not be able to adequately describe the symptoms. Such patients may demonstrate behaviors such as rubbing or massaging of legs, increased motor activity (eg, pacing, wandering), particularly in the evening and/or with inactivity; improvement is evident with movement of the legs. Many medications may aggravate or induce RLS symptoms, such as antiemetics, antipsychotics, SSRIs, tricyclic antidepressants, and diphenhydramine. Clinicians should carefully review the medication regimens of patients with new or worsening RLS.

Several effective medications are available if pharmacologic treatment for RLS or PLMS is indicated (because of severity of symptoms or significant effects on quality of life). For example, a dopamine agonist (eg, pramipexole, ropinirole, or rotigotine, all FDA approved for treatment of RLS) about 1–2 hours before bedtime is effective in the treatment of RLS and PLMS (SOE=A). A nighttime dose of carbidopa-levodopaOL may also be effective (SOE=A) and can be used for patients who need medication infrequently (ie, for as-needed use). However, some patients describe a shift of their symptoms to daytime hours with successful treatment of symptoms at night; this problem (termed augmentation) appears more frequently when carbidopa-levodopa is used on a regular basis but can also be seen with dopamine agonists. An extended-release form of gabapentin (gabapentin enacarbil) and pregabalinOL have been shown to be effective in improving RLS symptoms (SOE=A). In a blinded, head-to-head comparison, pregabalin was as effective as the dopamine agonist pramipexole in controlling RLS symptoms but less likely to produce augmentation. RLS symptoms may improve with iron replacement in patients with iron deficiency (SOE=B). BenzodiazepinesOL and opioidsOL have also been used for RLS but likely have more adverse events in older adults than the FDA-approved agents. Dopamine agonists may cause “hangover” fatigue or sleepiness, orthostatic hypotension, confusion, or dyskinesias.


The prevalence of peripheral neuropathy in older adults has been estimated to be as high as 10%. Peripheral neuropathy can be particularly devastating in older adults, because it may cause gait impairment from sensory and motor deficits with a resulting propensity to fall. In developed countries, diabetic neuropathy is the most common form of the condition; up to 30%–60% of diabetic patients >60 years old have peripheral neuropathy. Several types of neuropathy are associated with diabetes mellitus, including a distal symmetric neuropathy; asymmetric neuropathies that may involve cranial nerves, roots, or plexi; and mononeuropathy multiplex.

The history and physical examination are the most important tools in diagnosis of a peripheral neuropathy. Questions from the history should be geared toward identifying possible causes and risk factors. If the patient is not known to be diabetic, risk factors for diabetes or insulin resistance should be assessed. The past history and review of systems may give clues to a systemic disease that could contribute to a peripheral nerve disorder. A history of gastric bypass, eating disorder, or hemodialysis could indicate a possible nutritional deficiency. A thorough medication history should be taken to look for possible causes. The social history may uncover evidence of a possible exposure, such as alcohol or an occupational toxin. The family history should include inquiries for possible genetic forms of peripheral neuropathy. The neurologic examination focuses on establishing evidence of a length-dependent loss of sensory and/or motor function that is maximal distally in the limbs, associated with decreased reflexes and atrophy in affected regions.

Electrodiagnostic studies (ie, electromyography and nerve conduction studies) are considered an extension of the neurologic examination. They may yield valuable information in classifying the neuropathy, which may help to narrow a complicated differential diagnosis. First, these studies can differentiate between lesions affecting a single nerve, a nerve root, or a peripheral polyneuropathy. Next, they can help classify a polyneuropathy as axonal, demyelinating, or mixed. This distinction is important because certain neuropathies affect nerves in characteristic ways. For instance, a diabetic neuropathy is predominantly axonal, as are many of the toxic neuropathies such as alcohol and heavy metal exposure. In contrast, the hereditary and immune-mediated neuropathies more commonly cause peripheral demyelination. Acute, atypical, rapidly progressive, or severe forms of neuropathy should be referred to a neurologist with neuromuscular medicine expertise, who may perform tests of small fiber function, tests of autonomic function, peripheral nerve biopsy, and epidermal skin biopsy.

Treatment of the neuropathy depends on the underlying cause and ranges from withdrawal of the causative agent (eg, alcohol, medications) to nutritional supplementation (in the case of nutrient deficiency), to treatment of a primary cancer (in the setting of paraneoplastic neuropathy). There is evidence that optimizing glucose control can lessen the severity of diabetic neuropathy. Topical agents such as capsaicin cream and local anesthetic medications (eg, lidocaine patch) may provide relief for some patients with peripheral neuropathy (SOE=B). Systemic treatment of neuropathic pain may include the use of tricyclic antidepressantsOL or antiepileptic medications such as gabapentin and pregabalin. Gabapentin and pregabalin are approved for use in treatment of post-herpetic neuralgia, and pregabalin is also approved for use in diabetic neuropathy and fibromyalgia (SOE=A). Two other FDA-approved medication options for use in patients with diabetic neuropathic pain are duloxetine, which is a serotonin-norepinephrine reuptake inhibitor antidepressant, and tapentadol, which also blocks reuptake of serotonin and norepinephrine and has additional agonist effects at mu-opioid receptors (SOE=A). In addition, tramadolOL, which has properties similar to those of tapentadol, and opioidsOL may be used to treat neuropathic pain (SOE=B). Combination therapy with effective medications that have different mechanisms of action are often needed to control symptoms adequately.


Radiculopathy results from compression of a spinal root as it exits the spinal canal. Among older adults, this can be the result of herniated discs or osteophyte formation. Symptomatic nerve root compression may result in complaints of pain radiating down the neck, back, arm, or leg, and on neurologic examination, this can be accompanied by motor and sensory deficits as well as by diminution of reflexes in the distribution of a particular spinal root or roots. MRI imaging of the involved nerve root may determine a structural cause of radiculopathy. Progressive involvement of lumbosacral nerve roots may be seen in meningeal carcinomatosis. MRI imaging with contrast and lumbar puncture with cytology may help to make this diagnosis. An acute, immune-mediated form of polyradiculopathy is acute inflammatory demyelinating polyradiculoneuropathy (AIDP), also termed Guillain Barré syndrome. AIDP is treated with immunotherapy acutely, using either plasma exchange or intravenous immunoglobulin therapy (IVIG). Chronic inflammatory demyelinating polyneuropathy is a chronic counterpart of AIDP and requires long-term immunotherapy. Patients with diabetes may present with diabetic amyotrophy, which is a lumbosacral polyradiculitis and plexopathy that starts with subacute onset of severe neuropathic pain in the thighs, which is often asymmetric, followed by proximal muscle weakness in the legs and eventual atrophy. Referral to a neuromuscular specialist is recommended for atypical and severe cases of radiculopathy.


Myopathies are characterized by proximal limb weakness, muscle wasting, and diminished or absent reflexes. Typically, they are accompanied by an increase in serum concentrations of muscle enzymes (eg, creatine kinase), a myopathic pattern on electromyogram, and abnormalities on muscle biopsy. Older adults may attribute mild to moderate muscle weakness to aging and therefore may not immediately consult a clinician. Proximal muscle weakness, which may result in difficulty rising from a chair, climbing stairs, or washing one’s hair, is particularly likely to be falsely attributed to aging or arthritis.

The most common myopathies in older adults are polymyositis, endocrine myopathies, and toxic myopathies. Polymyositis, a disorder of skeletal muscle with diverse causes, is characterized by lymphocytic infiltration of the muscles. Muscle biopsy usually shows signs of both myocyte degeneration and regeneration. Immunotherapy with prednisone is considered the treatment of choice for polymyositis, but it should be used with caution in older adults because of adverse effects of chronic steroid use. In thyrotoxic myopathy, weakness and wasting are greatest in the pelvic girdle muscles and, to some extent, in the muscles of the shoulder region. Reflexes can be normal, and diagnosis is based on the distribution of muscle weakness in an individual with thyrotoxicosis. The myopathy improves with successful treatment of the underlying endocrine disorder. Hypothyroidism may cause a myopathy that improves with thyroid replacement therapy. Creatine kinase levels are significantly increased in the myopathy associated with hypothyroidism. Finally, several medications are known to cause myopathy, including corticosteroids, lipid-lowering agents, colchicine, and procainamide. The treatment of choice for drug-induced myopathy is cessation of the offending medication.

Motor Neuron Disease

Motor neuron disease, also called amyotrophic lateral sclerosis (ALS), is a neurodegenerative condition involving the cell bodies of both upper and lower motor neurons. It is characterized clinically by progressive weakness and wasting of skeletal muscles, often in combination with dysarthria, dysphagia, and respiratory failure. The incidence increases with age but reaches a plateau in the seventh decade of life. To date, age remains the single most clearly identifiable risk factor for this progressive and fatal disorder. Genetic causes of ALS are thought to occur in 5%–10% of patients. Four genes have been identified that can cause ALS. The gene C9ORF72 is the most common cause of familial ALS, accounting for 25%–40% of such cases. Mutations in this gene can also cause frontotemporal dementia, or a combination of ALS and frontotemporal dementia.

Patients with ALS commonly present with gait disturbance, falls, foot drop, weakness in grip, dysphagia, or dysarthria. On neurologic examination, patients may have a combination of upper motor neuron signs (eg, hyperreflexia, clonus, extensor plantar responses) and lower motor neuron signs (eg, weakness, atrophy, fasciculations). Weakness of the face, tongue, and palate are common, but extraocular muscles are usually spared. The electromyogram demonstrates findings consistent with diffuse denervation and poor recruitment of motor units. The differential diagnosis includes lesions at the level of the foramen magnum, a combination of cervical myelopathy associated with cervical and lumbar polyradiculopathies, or a motor predominant peripheral polyneuropathy in a patient with CNS lesions. The prognosis is poor with survival time averaging 2–3 years. The presence of bulbar weakness carries a poorer prognosis. Although most new cases of ALS occur in older adults, it is less common than several other neurologic disorders in this population. Therefore, gait disturbance and focal motor weakness may frequently be incorrectly attributed to the more common conditions. Older adults are also more likely to have coexisting neurologic disorders that might explain symptoms of weakness, adding to the challenge of and delay in diagnosing ALS. In one study, afflicted individuals >65 years old were diagnosed after 19 months, while those <65 years old were diagnosed after 3 months.

Treatment of ALS is primarily supportive. Riluzole, which has demonstrated modest effects on survival or time to tracheostomy (SOE=A), is in widespread use. Riluzole is thought to protect against glutamate toxicity, which may be implicated in the pathogenesis of ALS. Follow-up in a dedicated multidisciplinary ALS or muscular dystrophy clinic has also been shown to improve quality of life of ALS patients and may improve survival (SOE=B). In these settings patients may receive multidisciplinary care from a team, including a neuromuscular subspecialist; respiratory, physical, occupational, and speech therapists; and a social worker. Noninvasive support of ventilation, such as bilevel intermittent positive-airway pressure (BiPAP), has been shown to improve survival in ALS patients with respiratory compromise (SOE=A). Edaravone is a new medication approved by the FDA for treatment of ALS. It is given as an intravenous infusion for 10–14 days in a row, followed by 2 weeks off, and then this cycle is repeated. Edaravone is thought to reduce oxidative stress and was shown to slow progression of disability on an ALS scale (ALSFRS-R) in a subset of patients with milder symptoms of ALS by 33% (SOE=B). The impact of edavarone on long-term outcomes, such as quality of life and survival, is not known.


Myelopathy or spinal cord dysfunction can be the result of extrinsic compression of the spinal cord or intrinsic spinal cord lesions. The cervical region is affected most commonly. Intrinsic spinal cord lesions may include spinal cord tumors, vascular events (eg, infarcts or hemorrhages), or trauma (eg, central cord syndrome). Extrinsic compressive lesions are more prevalent; common causes among older adults are cervical spondylosis (with resultant osteophyte formation and degenerative disc disease), disc prolapse or herniation, rheumatoid arthritis with vertebral body subluxation, meningioma, or spinal metastases. Nearly 80% of adults ≥70 years old have radiographic evidence of osteophyte formation with some narrowing of the spinal canal, but most are asymptomatic. Cervical spinal stenosis most often arises from spondylosis but may be worsened by disc protrusion or a congenitally narrow canal. Narrowing of the cervical canal can lead to neck stiffness and pain; radicular pain, sensory loss, or weakness in the arms; and weakness with upper motor neuron signs (eg, hyperreflexia, spasticity, Babinski sign) in the legs. Narrowing of the lumbar canal may lead to lower back pain, radicular pain, sensory loss, or weakness and other lower motor neuron signs in the legs. Lumbar spinal stenosis causes neurogenic claudication, manifested by increasing pain with weakness and numbness while walking, relieved by flexion at the waist or sitting.

MRI can be helpful for diagnosis of myelopathy, but results must be viewed with caution because abnormal MRI findings are common in asymptomatic older adults. If the patient cannot tolerate MRI because of the presence of an implanted metallic object (such as a pacemaker) or severe claustrophobia, then spinal CT with intrathecal contrast may be performed. Conservative management includes activity modification, neck immobilization with a cervical collar, massage, heat treatment, physical therapy, and analgesics.


The prevalence of headaches appears to diminish with age. One study demonstrated that although 74% of men and 92% of women 21–34 years old have headaches, these proportions drop to 22% and 55% after the age of 75 years. Headache is one of the most common medical complaints in young persons, and yet one study suggests that it is only the tenth most common symptom in older women and the fourteenth most common symptom in older men. The incidence of migraine, the most common cause of headaches in younger adults, also declines with age, with only 2% of people developing their first migraine after age 50.

New-onset or persistent headaches in older adults are more likely to represent systemic illness or intracranial lesions (ie, secondary causes). In one study, 10% of headaches among younger patients represented systemic illness or intracranial lesions; in older adults, this proportion was 34%. These secondary causes include intracranial masses (eg, primary or secondary tumors, subdural hematomas), cervical spondylosis, COPD, obstructive sleep apnea, carbon monoxide poisoning, and giant cell arteritis. Brain imaging with contrast (ie, head CT or brain MRI) is indicated in older patients with new-onset or progressive headaches to exclude structural causes.

An important secondary cause of headache specific to older adults is giant cell (temporal) arteritis. This condition does not appear to develop in those <50 years old and peaks in incidence between the ages of 70 and 80. Women are affected twice as often as men. Pain may be centered at the temporal or occipital arteries. Palpation of the scalp arteries may reveal focal tenderness and nodularity. Complaints of visual changes, low-grade fever, polymyalgia, and constitutional symptoms further suggest the diagnosis. Typically, the serum sedimentation rate is significantly increased, and the diagnosis is made with a temporal artery biopsy. If the diagnosis is suspected and biopsy is planned within a few days, then corticosteroids may be started to prevent vascular complications (eg, loss of vision or stroke). In addition to structural and systemic causes of headaches, many commonly used medications may cause headaches that are dull, diffuse, and nondescript, including vasodilators (eg, nitrates), antihypertensives, antidepressant medications, and stimulants.

The common primary headache disorders can be classified into migraine (with or without aura), tension-type headaches, cluster headache, and chronic daily headaches. Migraines are headaches of moderate to severe intensity associated with nausea, vomiting, or photophobia. Half of the time they are unilateral and throbbing, but commonly the pain is bilateral. Auras, when they occur, usually precede the headache and are manifested by transient neurologic symptoms that can be localized to the cerebral cortex or brainstem. Visual phenomena are among the most common types of auras. Migraine headaches in older adults typically present as they do in younger people, but atypical presentations have been described. These include migraine auras without headache (acephalic migraine). The occurrence of an isolated visual or sensory aura in the absence of a headache can be diagnostically challenging, because it can mimic signs of a transient ischemic attack. In contrast to migraines, tension-type headaches typically are more diffuse in distribution, less severe in intensity, have a pressing or a tight quality, and are much less often associated with nausea or vomiting. Cluster headaches are much more common in men, may be associated with tearing and rhinorrhea, and are of shorter duration (15 minutes commonly but may last up to 3 hours) than migraines. They are severe in intensity and tend to recur in clusters during an interval of time (eg, within a day or within a few weeks). Chronic daily headaches are persistent, often bilateral, and have features that overlap with those of both migraine and tension-type headaches.

The treatment of migraine headaches can be categorized as either abortive (treating an attack that has already begun) or preventive. Other than various OTC preparations that contain NSAIDs, migraine-specific abortive therapies include ergotamines or triptans (eg, sumatriptan), which act by central serotonergic mechanisms. These medications are mild vasoconstrictors and thus contraindicated in patients with uncontrolled hypertension, stroke, or coronary artery disease. Generally, safety data in geriatric populations are lacking. Preventive therapies for migraine include nonselective β-blockers (eg, propranololOL), valproic acid, topiramate, tricyclic antidepressantsOL, and calcium channel blockers (eg, verapamilOL). Preventive therapies decrease the frequency and severity of migraine over time and should be considered for patients who have disabling migraine headaches ≥2 times per month. The choice of agent should be guided by an effort to avoid adverse events and drug interactions. Treatment of muscle tension headaches includes NSAIDsOL as abortive agents and low doses of tricyclic antidepressantsOL as preventive medication in chronic muscle tension headaches. Muscle relaxants, such as tizanidineOL, have shown some effectiveness in treating chronic muscle tension headaches in open-label studies but may cause sedation or confusion. Each of the medications above may be contraindicated by comorbidities or existing medication regimens. A referral to a headache specialist should be considered for patients with either cluster headaches or chronic daily headaches.


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