I. Problem/Condition.

A movement disorder is an abnormality of movement, defined as either abnormal involuntary movements (hyperkinetic movement disorders) or disruption/poverty of normal movements (hypokinetic movement disorders) with a CENTRAL nervous system etiology. The key is that neurologists define movement disorders very strictly, as ALS patients or diabetic neuropathy patients will have abnormalities of their movements, but these are neuromuscular disorders because they have a peripheral nervous system cause.

II. Diagnostic Approach.

A. What is the differential diagnosis for this problem?

Two classes: Hyperkinetic movement disorders and hypokinetic movement disorders.

  • Hyperkinetic movement disorders (too much movement)

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    Can be acquired or hereditary, long differential of causes, see chapter on Ataxias


    Huntington’s disease or Tardive dyskinesia


    Focal (torticollis, blepharospasm, writer’s cramp), segmental, or generalized

    Can have acute or tardive drug-induced dystonia


    Many causes, ranging from brain to spinal cord, from acquired to hereditary

    One of the most common in the hospital setting is post-anoxic myoclonus

    Hospitalized patients may also have restless legs syndrome, one of the most common movement disorders, which may be undiagnosed


    Tourette’s syndrome


    Primary neurologic causes: Essential tremor or Parkinson’s disease

    Secondary causes: medications, toxicity/poisoning, severe stress

  • Hypokinetic movement disorders (overall problem is not enough movement)

    Bradykinesia/ Parkinsonism

    Idiopathic Parkinson’s Disease

    Parkinson’s Plus Syndromes / Atypical Parkinsonism

    Corticobasal ganglionic degeneration (CBGD)

    Progressive supranuclear palsy (PSP)

    Multiple Systems Atrophy (MSA)

    Dementia with Lewy Bodies (DLB)

    Drug-induced Parkinsonism

B. Describe a diagnostic approach/method to the patient with this problem.

  • Describe what the dominating abnormal movement looks like.

  • Decide if it is overall a hyperkinetic or hypokinetic problem.

  • Is the problem newly acquired (i.e. during hospital stay)? If so, look for an underlying cause (medications, stroke, illicit drugs, etc.)

  • If hyperkinetic, determine which problem it is based on the criteria in next section.

  • If hypokinetic, then the patient has a form of Parkinsonism. For full details, see that chapter, but briefly:

    If you have ANY of these features within 3 years of onset of motor symptoms, suspect an atypical variant of Parkinson’s disease: prominent instability/falls, hallucinations, freezing, dementia, severe dysautonomia.

    Absence of these features plus asymmetric and insidious onset of symptoms suggests idiopathic Parkinson’s disease.

    New/abrupt onset during the hospitalization suggests vascular or drug-induced Parkinsonism.

  • If tardive (drug-induced) movement disorder, please note that these disorders:

    Are 100% iatrogenic and the #1 most frequent single diagnostic code for which physicians are sued in the United States.

    Are caused by potent dopamine-blocking drugs, which are used for their anti-emetic side effects (Metoclopramide, lesser degree promethazine) and for their antipsychotic properties (typicals like haloperidol, thorazine but also atypicals like risperidone, olanzapine – the only antipsychotics that are not described to cause tardive dyskinesia are quetiapine and clozapine).

    Can occur as early as a few days of taking a new medication (particularly if IV).

    Reversal of the abnormal movement can take months after stopping the offending drug.

Diagnostic pearls for the hospitalist:

  • RLS and essential tremor are thought to be the most common movement disorders in the general population.

  • The most common cause of new tremor in the hospital is drug or stress-induced.

  • Remember that most primary neurologic movement disorders disappear with sleep, the exceptions being periodic limb movement disorder and rare movement disorders like palatal myoclonus.

1. Historical information important in the diagnosis of this problem.

  • Was the movement disorder ever present before the hospitalization?

  • Is there a task-specific component of the movement disorder? Certain tremors or dystonia occur with specific activities such as handwriting only or holding a cup only,

  • Was the onset of the movement disorder sudden/abrupt or slowly progressive?

  • Is there a history of new medication (in particular: anti-emetic or anti-psychotic usage)?

  • Is there a family history of similar abnormal movements?

    If yes, strong AD inheritance pattern occurs in: essential tremor, hereditary spinocerebellar ataxias, and familial Parkinson’s disease (almost exclusively onset < age 50)

  • Are there any associated non-motor features? Associated neurologic features may lead you toward a specific diagnosis:

    Vision/hearing problems can be seen with some of the spinocerebellar ataxias

    Loss of smell can be seen with Parkinson’s disease

    REM-sleep behavior disorder can be seen with all forms of Parkinsonism

    Dysautonomia can be seen with Parkinson’s disease or MSA

    Constipation is seen in >80% of Parkinson’s patients

2. Physical Examination maneuvers that are likely to be useful in diagnosing the cause of this problem.

  • Movement disorder specialists stress the importance of the phenomenology, which means a description of the movement problem, because these disorders are defined by their clinical features.

  • If considering Parkinsonism, it is essential to check muscle tone (with patient relaxed, move hand up/down to check tone around the wrist and move forearm up/down to check tone around the elbow). Tone is increased in all forms of Parkinsonism.

  • Assess for tremor. Tremor is a rhythmic movement and may occur at either rest, posturallly (have patients hold arms out in front of them), or with action (do finger to nose task). See tremor chapter for more details; postural/action tremor is an essential tremor while a tremor at rest is Parkinson’s disease. Tremor is frequently absent in atypical Parkinsonism (usually more rigidity/bradykinesia).

  • If the movement is NOT rhythmic, then distinguish between a brief rapid jerk (myoclonus) or writhing and irregular (chorea).

  • Perform a gait exam: unstressed (normal walking), heel, toe, and tandem (tightrope). Parkinson’s patients have decreased arm swing on the side where their symptoms are dominant. Gait is often affected in movement disorders but an isolated gait abnormality can have many causes (neurologic or non-neurologic).

  • Limb ataxia is assessed by finger-to-nose and heel-to-shin tasks.

3. Laboratory, radiographic and other tests that are likely to be useful in diagnosing the cause of this problem.

TSH (as hyperthyroidism can cause tremor). Severe B12 deficiency or severe hyper/hypoglycemia can cause movement disorders, so checking B12/HbA1C could be considered . If movement disorder is acute onset, get imaging to look for a structural cause (stroke, tumor, etc.), and preferred is magnetic resonance imaging (MRI). If the onset is gradual or progressive, then neurologic imaging is less useful as the diagnosis is clinical and therefore not as reliant on ancillary testing.

C. Criteria for Diagnosing Each Diagnosis in the Method Above.

Diagnosing the different types of movement disorders is a clinical diagnosis. Each movement disorder below, in turn, has its own differential diagnosis. A description of the movement and supporting /differentiating associated findings for each movement are listed below, in effort to help narrow the diagnosis. Again, all acute onset movement disorders should have an investigation for a precipitating agent (medication, toxin, metabolic, etc.).

  • Hyperkinetic movement disorders (too much movement)


    Coordination problem: Limb ataxia is dysmetria on finger-to-nose or heel-to-shin. Truncal ataxia is wobbling movement of trunk when sitting/standing. Gait ataxia is wide-based gait, usually with staggering and inability to tandem walk.

    Usually from disorders of the cerebellum, affects balance/coordination. Extent of cerebellar involvement will determine if ataxia is in limbs, trunk, gait, or combinations of those.

    Acute causes include infectious, vascular, or metabolic disturbance, ethanol ingestion, and thiamine deficiency. Chronic causes are more likely resulting from inherited/genetic syndromes, paraneoplastic disorders and/or mass effect; and are occasionally seen in Parkinsonism, MS, and B12 and Vitamin E deficiency.

    Pure gait ataxias are rare, and if you see it, you should make sure that it is not a sensory ataxia (pseudo-ataxia caused by severe sensory/proprioceptive loss in the legs from causes like diabetic neuropathy.


    Irregular dance-like movement, usually small amplitude, can be mistaken for nervousness/fidgeting.

    Differentiate from simple fidgeting by assessing ability to sustain posture of the part of body involved (i.e. hold tongue protruded for 5 seconds or hold hands outstretched without twitching for 10 seconds).

    Two main causes are Huntington’s disease (family history) or Tardive dyskinesia (i.e. history of antiemetic or antipsychotic use).

    Remember tardive dyskinesia only means late effect of a drug and NOT where the movement is. It just happens that TD most commonly affects the oro-bucco-lingual area, but technically this adverse effect of medications can cause chorea in any part of the body.


    Forced alteration of posture caused by involuntary (centrally mediated) muscle contraction.

    Though not meriting its own chapter here, this is one of the most common movement disorders seen in the hospital due to an acute side effect of dopamine blocking drugs, aka acute dystonic reaction.

    Focal (torticollis, blepharospasm, writer’s cramp), segmental (contiguous body parts affected like head and neck), or generalized.


    Fast jerk/twitch is positive myoclonus; fast loss of tone is negative myoclonus (asterixis).

    In inpatient setting, can see myoclonus from any severe metabolic disturbance or post-hypoxic/post-code (which incidentally is one of the strongest predictors for poor prognosis of neurologic recovery after a code event) and is commonly mistaken for seizure activity.

    Many causes, ranging from brain to spinal cord, from acquired to hereditary.

    Restless Leg Syndrome, crawling or uncomfortable feeling with Urge to move limbs, Rest is worse, Getting up or moving improves, and Evenings worsen symptoms(URGE). Usually accompanied by Periodic Limb Movement Disorder characterized by repetitive stereotyped movement of legs during sleep.


    Motor, vocal, or both (Tourette’s is defined as motor and vocal tics for at least one year).

    Can be simple or complex.

    Tend to come in clusters, as patient can suppress them for a time then will occur in a burst.


    Rhythmic, oscillatory movement.

    Is either at rest, postural, or with action depending on what brings out the tremor.

    Drug-induced tremors are almost exclusively postural/action enhanced physiologic tremors (high frequency but low amplitude).

    Stress makes all forms of tremor worse.

  • Hypokinetic movement disorders

    Bradykinesia/ Parkinsonism

    Idiopathic Parkinson’s Disease – see chapter for full details, but briefly, need 2 of 4 cardinal symptoms (rest tremor, rigidity, bradykinesia, gait imbalance). Therefore, rest tremor alone is insufficient, and 30% of Parkinson’s patients never develop tremor anyway (why rigidity is the most critical determining factor). Gait imbalance (especially leading to falls) is a late feature. Symptoms almost always asymmetric at onset

    Parkinson’s Plus Syndromes / Atypical Parkinsonism – all forms are more rapidly progressive and less responsive to medications that idiopathic Parkinson’s disease and almost all lack tremor. Suspect this disease state when there is Parkinsonism but also has features unusual for idiopathic Parkinson’s disease (key one for each bolded below).

    Corticobasal ganglionic degeneration (CBGD) – bradykinesia, rigidity but also prominent apraxia, often to the extent that one limb is completely out of volitional control (alien limb phenomenon).

    Progressive supranuclear palsy (PSP) – bradykinesia, rigidity but prominent eye movement problems: supranuclear gaze palsy (when patient cannot initiate movements on their own but oculocephalic maneuver shows that ability to make those movements is intact) and/or apraxia of eyelid opening (physically able to but cannot seem to keep eyelids open) which lead to early/frequent falls.

    Multiple Systems Atrophy (MSA) – bradykinesia, rigidity (usually extreme axial rigidity) but severe dysautonomia and/or cerebellar dysfunction (ataxia described above), often also has early falls.

    Dementia with Lewy Bodies (DLB) – key is presence of early dementia. By definition, Parkinsonism and dementia coincident in onset within one year of each other. This is different from Parkinson’s disease with dementia, which is usually motor symptoms for 10 years then developing dementia. Also, frequently has associated visual hallucinations, prominent fluctuations, and neuroleptic sensitivity.

    Secondary and drug-induced Parkinsonism – symmetric parkinsonian symptoms at onset, history of commonly offending drugs (metoclopramide, antipsychotics). Secondary Parkinsonism is caused by tumors and strokes; some suggest ruling out these (with imaging) prior to diagnosing patient with idiopathic Parkinsonism.

    Will be less likely to respond to levodopa/carbidopa.

D. Over-utilized or “wasted” diagnostic tests associated with the evaluation of this problem.

Computed tomography (CT) and MRI are useful in evaluating for secondary causes of movement disorders in proper clinical context and especially in the acute setting, but are not otherwise necessary for establishing a diagnosis.

III. Management while the Diagnostic Process is Proceeding.

A. Management of Clinical Problem Movement Disorders.

Since most causes in the inpatient setting are secondary, treatment should be aimed at removing offending drug or correcting underlying metabolic disturbance (i.e. treating the cause not just the symptom).

Most common inpatient movement disorders:

1. Acute dystonic reaction from an antipsychotic or antiemetic. Treat by stopping the offending medication and give benztropine 1mg IV or diphenhydramine 25-50mg IV.

2. Post-hypoxic myoclonus. Notoriously refractory to anti-epileptics. Tends to abate on its own as the injured hypoxic cortex either dies altogether or begins to heal. One study evaluated using propofol and found post hypoxic myoclonus ceased immediately after a single dose of IV propofol in 60/60 patients, despite no improvement in survival. Utility in that it will aid in ventilation and will help to relieve distressed family members.

3. Enhanced physiologic tremor from stress or medications. If medication-induced, can withdraw the medication and/or provide reassurance.

Otherwise, if this is a primary degenerative type movement disorder, you may want neurology consultation to guide initiation of symptomatic therapy. We will list some common treatment algorithms for each movement disorder below:

  • Ataxia. There is no available symptomatic treatment for ataxia. PT/OT for adaptive measures is the most helpful.

  • Chorea. Tardive dyskinesia may improve with cessation of dopamine blocking agent, though this often takes months and may not completely resolve. If residual/debilitating despite stopping the agent, can use tetrabenazine titrated to effect (average is 25-75mg/day). Chorea of Huntington’s disease is also effectively treated by tetrabenazine. This is unlikely to be used in the hospital as tetrabenazine is not stocked in any commercial/retail/hospital pharmacy (only available direct from manufacturer).

  • Dystonia. See above. If focal, unless you can give a patient botulinum toxin in the hospital, then pharmacotherapy primarily starts with trihexiphenidyl titrated to 2mg TID.

  • Myoclonus. Try to treat the cause, but as above, symptomatically may respond to levetiracetam, valproate, or clonazepam.

  • Restless legs syndrome: Start with dopamine agonists ropinerole (0.5-6mg) and pramipexole(.125-1.5mg); Pregabalin and Gabapentin are also efficacious and well tolerated. Oral iron may help if patient is iron deficient; SSRIs are likely to worsen symptoms.

  • Tics. Start with clonidine (0.05mg BID-0.1mgQID); dose limited by hypotension. Next can try topiramate, next can try antipsychotics like risperidone/haloperidol.

  • Tremor. See above. Postural/action tremor of essential tremor is treated with either primidone (25-250mg HS with slow titration) or propranolol (dose limited by bradycardia). Rest tremor, if part of Parkinsonism, treated as below.

  • Parkinsonism. In a younger patient (under 65), start with a dopamine agonist, either ropinirole (slow titration to 4mg TID) or pramipexole (slow titration to 0.5 TID). In older patient or intolerant to dopamine agonist, can try carbidopa/levodopa 25/100 titrating slowly to one tab TID-QID.

    Non-motor sequelae likely to be encountered in hospitalized patients:

    Orthostatic hypotension—discontinue blood pressure lowering drugs; avoid large meals, sudden changes in posture, alcohol and heat; increase fluid and salt intake; trial abdominal binding or waste high compression stockings; insufficient evidence for fludrocortisone or midodrine.

    Drug induced psychosis:

    Olanzapine should not be used for management due to unacceptable risk of motor deterioration.

    Clozapine is efficacious but should be monitored for sedation and rarely agranulocytosis, quetiapine is still investigational.

    Depression should be treated with nortriptyline and pramiprexole.

B. Common Pitfalls and Side-Effects of Management of this Clinical Problem.

Remember that Parkinson’s patients in the hospital should have their medications continued. Stopping dopaminergic therapy suddenly can lead to a withdrawal that is identical to neuroleptic malignant syndrome, which is a neurologic emergency.

The most common side effect of carbidopa/levodopa therapy is nausea, which should be treated with extra carbidopa added to each dose. Too rapid titration of dopaminergic therapy (agonists or carbidopa/levodopa) can cause sedation/confusion, which is aided by slowing titration schedule. Dopamine agonists may cause pedal edema and are known for the rare side effect of causing obsessive-compulsive behaviors (gambling, sexual behavior, eating, etc.).

Trihexyphenidyl, if used for dystonia, is an anti-muscarinic agent and therefore has anticholinergic side effects.

Anticonvulsants (i.e. levetiracetam, valproic acid, etc.) used for treatment of myoclonus do not need levels checked as treatment is aimed at abating the movement (if possible) not reaching a certain blood level.

When treating essential tremor, the typical contraindications to propranolol apply (pulmonary dysfunction, diabetes, bradycardia), so if these are present, just use primidone. The only side effect of primidone is sedation, so can go slower if this occurs.