Movement Disorders

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Movement Disorders


Sangeeta Patel Driver and Cindy Zadikoff


GENERAL PRINCIPLES


Definition


A movement disorder is a neurologic phenomenon that affects the ability to generate or control movement.


Epidemiology


The incidence of movement disorders following severe traumatic brain injury (TBI) is 13% to 66% according to epidemiologic studies [1].


In a large study of survivors of severe TBI, posttraumatic movement disorders were reported in 22.6%, and persisted in 12.2%. The most common persisting movement disorder was tremor, followed by dystonia [2].


Movement disorders are less prevalent following mild to moderate TBI. In a survey study of mild to moderate TBI survivors, posttraumatic movement disorders were reported in 10.1%, and persisted in 2.6% [2].


Classification


Hyperkinetic disorders—characterized by excessive, abnormal involuntary movement



   Tremor


   Dystonia


   Ballism and chorea


   Tics and tourettism


   Myoclonus


   Stereotypy, hyperekplexia, and akathisia


Hypokinetic disorders—characterized by slowness or paucity of movement



   Parkinsonism


The previously listed disorders will each be discussed in more detail in subsequent sections of this chapter.


Etiology and Pathophysiology


Posttraumatic movement disorders are caused by:



  1.   Primary injury


        image   Focal contusions to the basal ganglia and associated pathways as well as cortical regions that modulate basal ganglia function indirectly


        image   Diffuse axonal injury preferentially affecting the superior cerebellar peduncles, brainstem, and subcortical regions


        image   Hemorrhage and ischemia from arterial injury caused by trauma-associated rotational forces


  2.   Secondary injury


        image   Associated hypoxia, hypotension, and cerebral edema


        image   Release of toxic cytokines and oxidative stress resulting in free radical production


        image   The restorative process of neuroplasticity including collateral sprouting and changes in neurotransmitter sensitivity [3]


General Guiding Principles for Treatment


  1.   A “start low, go slow” approach is important, as patients with TBI are particularly susceptible to adverse effects from medications.


  2.   Movement disorders cannot be treated in isolation because other sequelae of TBI such as balance or cognitive impairments may be exacerbated by standard treatments [4]. As such, the focus of treatment should be aimed at optimizing function.


  3.   Some posttraumatic movement disorders may resolve spontaneously, so it is important to withdraw medications after several months to determine whether they continue to be necessary.


HYPERKINETIC MOVEMENT DISORDERS


Tremor


Definition:


Rhythmic, oscillatory movement due to alternate or synchronous contraction of agonist and antagonist muscles [5].


Subtypes:


     image   Resting—present when body part is inactive


     image   Postural—present when maintaining body part in an antigravity position


     image   Kinetic—present when moving from one position to another


     image   Intention—only present when nearing goal of movement (“endpoint tremor”)


Epidemiology:


   10% to 20% of posttraumatic movement disorders [6].


Risk Factors:


   Prolonged coma.


Timing:


   Often appears in the first weeks after injury when voluntary movement begins to recover, but can develop years after injury [4].


Clinical Presentation:


   Temor usually occurs bilaterally, affecting the upper greater than lower extremities, and is commonly associated with ataxia of the affected limb [6,7,]. Affected limbs are evaluated in different postures, and the frequency and amplitude of tremor are described.


Differential Diagnosis:


   Seizure; rigors; tremor due to hyperthyroidism, hepatic failure, hypercapnia, or medication side effects (e.g., amiodarone, lithium, valproic acid).


Treatment:


     image   Medications—to date, there have been no studies performed to demonstrate efficacy. There are anecdotal reports of treatment with the following medications: primidone, propranolol, benzodiazepines (e.g., clonazepam), antiepileptics (e.g., carbamazepine, leviteracetam, gabapentin), glutethimide, L-tryptophan, anticholinergics, L-dopa/carbidopa, isoniazid, and botulinum toxin injections. In general, use of medications with greater potential for sedative side effects, such as benzodiazepines, should be avoided if possible. Choice of initial therapy can also be guided by tremor phenomenology (e.g., for action and posture tremor consider an antiepileptic or anticholinergic; for resting tremor consider L-dopa/carbidopa).


     image   Physical modalities—light weights on affected limb to dampen tremor.


     image   Surgery—consider at least one year after onset of tremor, if not adequately responsive to conservative measures:


          image   Deep brain stimulation (DBS): less effective for treatment of posttraumatic tremor compared to essential tremor or Parkinson’s tremor [8]. No consensus exists for the best anatomical location for stimulation.


          image   Stereotactic surgery (e.g., radiofrequency lesioning or g-knife thalamotomy): in one study, radiofrequency lesioning in the ventrolateral thalamus demonstrated tremor improvement in 88% of patients. However, there was an increase in dysarthria and/or gait disturbance in up to 90% of patients immediately post operatively and in 63% persistently [6].


Prognosis:


   Posttraumatic tremor may decrease spontaneously within 1 year after onset [1]. However, for the majority, this tremor remains a persistent problem [7].


Dystonia


Definition:


Involuntary, simultaneous sustained—but not fixed—contraction of opposing muscles resulting in repetitive twisting movements or abnormal postures that are usually exacerbated or elicited by voluntary activity.


Subtypes:


   Focal, segmental, generalized, and hemidystonia [9].


Epidemiology:


   4.8% to 16% of posttraumatic movement disorders; occurs more commonly in men [5]. Hemidystonia is the most common subtype.


Risk Factors:


   Younger age at time of trauma (first 2 decades of life) and severe TBI [10]. Frequently preceded by, or associated with, ipsilateral hemiparesis [7].


Timing:


   Onset is likely to be delayed (1 month to 9 years), with mean latency of 20 months [9]. Initially, there is slow progression with spread over months to years followed by eventual stabilization.


Clinical Presentation:


   May occur at rest but usually exacerbated by voluntary movement. Characterized by twisting movements or involuntary postures.


Physical Examination:


   Evaluate for abnormal posture exacerbated by limb activation. Rule out other possible causes of abnormal posturing such as muscle, joint, or bone injuries, ocular or vestibular abnormalities that could lead to head or trunk tilt, and toxic or metabolic conditions (e.g., Wilson’s disease) [4].


Treatment:


     image   Medications [4]—variably effective:


          image   Anticholinergics (e.g., trihexyphenidyl)—major side effect is sedation; better tolerated in the pediatric population


          image   Tetrabenazine—major side effects include sedation, Parkinsonism, and depression


          image   Neuroleptics—often effective but may interfere with neuroplasticity and functional recovery in TBI patients; carries long-term risk of tardive dyskinesias


          image   Antiepileptics (e.g., gabapentin, carbamazepine)—can be tried, but not usually effective


          image   Benzodiazepines—ineffective as a sole agent but may be useful as adjuvant; major side effect is sedation and may interfere with neuroplasticity and functional recovery


          image   Botulinum toxin injections—effective for focal, but not generalized, dystonia


          image   Oral baclofen—major side effect is sedation


          image   L-dopa/carbidopa—may be effective in patients with dopa-responsive dystonia


          image   Physical modalities: range of motion to prevent contractures


     image   Surgery:


          image   Intrathecal baclofen pump—recommended for generalized dystonia associated with significant spasticity, but not usually beneficial for isolated dystonia. Response to oral baclofen does not necessarily predict response to intrathecal baclofen


          image   Functional stereotactic surgery—less effective for secondary dystonia (e.g., due to TBI) than for primary dystonia


          image   Deep brain stimulation—for generalized, focal, segmental, and hemidystonia. Long-term efficacy data is limited


          image   Pallidal radiofrequency lesioning (pallidotomy)—improvement may take several months to occur postoperatively


Prognosis:


   Spontaneous remission is unlikely.


Chorea, Ballism, and Athetosis


Definitions:


   Chorea: rapid unpredictable, flowing dance-like movements. Chorea occurs predominantly in the distal limbs. There have been rare case reports of a possible association with epidural and subdural hematomas.


   Ballism: repetitive, but variable, high-amplitude purposeless movement that often is characterized by jerking or flinging of an extremity. Ballism occurs predominantly in the proximal limbs.


   Athetosis: slower writhing movement of the proximal limbs, often described as “snake-like.”


Timing:


Latency of weeks to months after injury.


Treatment:


Similar to dystonia except for the following:



   Chorea: consider amantadine. Deep brain stimulation and botulinum toxin injections are not recommended.


   Hemiballism: responsive to intrathecal baclofen in a single case report [11]

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May 29, 2017 | Posted by in PSYCHIATRY | Comments Off on Movement Disorders

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