An association between injuries and involuntary movements has been suggested since the nineteenth century speculation of Parkinson, Charcot, and Gowers. When a movement disorder begins shortly after a brain injury, a cause-and-effect relationship is apparent. An association is less obvious with longer latencies after the injury and after peripheral trauma, however. In some cases, the patient
may not have noticed or reported a mild movement disorder that was present before the injury. y , y
Pathogenesis and Pathophysiology. Direct trauma to subcortical and substantia nigral neurons can result in movement disorders occurring shortly after an injury. Movement disorders occurring months following the injury have been hypothesized to be related to sprouting, remyelination, ephaptic transmission, inflammatory changes, oxidative reactions, and central synaptic reorganization. Peripheral trauma that precedes the development of a movement disorder may alter sensory input, leading to central cortical and subcortical reorganization. y
Epidemiology and Risk Factors. Movement disorders due to trauma are rare, and specific epidemiological and risk factor studies have not been performed.
Clinical Features and Associated Findings. Although head injury does not result in Parkinson's disease with pathological findings of Lewy bodies, head injury may result in a temporary exacerbation of motor function in patients with pre-existing Parkinson's disease. y Parkinsonism is a rare complication of single closed head injuries and may also occur after penetrating bullet and knife injuries of the brain stem. Repeated head injury as in the case of boxers with dementia pugilistica may result in parkinsonism in association with many other neurological signs. Parkinsonian tremor may rarely be associated with peripheral body trauma, although a direct causal relationship cannot be established. y
Postural and kinetic tremor can be due to direct traumatic lesions of the dentatothalamic circuit. Benedikt's syndrome (unilateral third nerve palsy and contralateral ataxic hemiparesis) can be associated with rest and postural and kinetic tremor. Postural-kinetic tremors of the arms, legs, or head may occur within weeks of mild head injury even without loss of consciousness. Peripheral trauma can induce tremor, which can occur along with reflex sympathetic dystrophy, dystonia, and myoclonus.y Myoclonus, dystonia, and athetosis may be present in patients with post-traumatic tremors.
Contralateral dystonia can be due to a lesion in the striatum, particularly the putamen. Causes include perinatal trauma, closed head injury (severe much more often than mild), and thalamotomy. The onset of dystonia may have a latency period from 1 month to 9 years. Spastic dystonia due to pyramidal and extrapyramidal injury and paroxysmal nocturnal dystonia are variants of post-traumatic dystonia. Often patients develop post-traumatic dystonia as a delayed sequela of severe head injury, initially characterized by coma and quadriplegia. After the patient awakens and the plegia improves, severe action dystonia develops. Minor or moderate local peripheral trauma can be associated with focal dystonia, sometimes in patients with reflex sympathetic dystrophy. Examples of peripherally induced dystonia include the following: blepharospasm after surgery on the eyelids; oromandibular dystonia after dental procedures; spasmodic dysphonia after facial injuries; cervical dystonia after neck injuries such as whiplash; and foot dystonia after stubbing a toe.
A recent report by Kraus and colleagues studied survivors of severe HI, admitted to the hospital with GCS of 8 or less. Of the 264 survivors, follow-up was obtained on 221, and 22 percent reported or showed evidence of movement disorders, half transient and half persistent. Tremor, usually kinetic, and dystonia were the most common disorders, and usually developed with a post-trauma latency of 2 to 24 months.
Chorea, choreoathetosis, and ballismus can follow blunt head trauma with injury to the striatum, subthalamic nucleus, and anterior thalamus. The onset is usually days to months following the trauma.
Action myoclonus, palatal myoclonus, and segmental myoclonus may result from head injury not associated with anoxia or epilepsy. Segmental myoclonus may also occur after spinal cord injury.
A deep, burning pain followed by persistent, involuntary, and irregular movements of the toes and feet, termed painful legs and moving toes, can be associated with minor foot and ankle injuries. Hemifacial spasm has been rarely associated with trauma. Additionally, after amputation, the remaining stump can involuntarily jerk.
Differential Diagnosis. Because the relationship between many injuries and the movement disorder may be circumstantial and retrospective, an idiopathic movement disorder is always a diagnostic consideration. The possibility of psychogenic movement disorders, which may be more common in women, should also be considered. Because movement disorders often develop several weeks or months after trauma and because patients often receive neuroleptic medications after acute injuries, drug-induced movement disorders are another possible cause.
Evaluation. Neuroimaging such as MRI and occasionally PET can demonstrate responsible brain lesions. Depending upon the case, testing to exclude other potential causes of the movement disorder such as Wilson's disease may also be appropriate.
Management and Prognosis. Post-traumatic parkinsonism may respond to dopaminergic and cholinergic medications. Post-traumatic action tremors only occasionally respond to standard medical treatment. Selected cases may benefit from botulinum toxin injections into involved muscles and ventrolateral thalamotomy. Medications are usually not helpful for dystonia associated with central and peripheral trauma, although botulinum toxin injections can produce temporary relief. y Post-traumatic chorea and choreoathetosis may respond to valproic acid and haloperidol, whereas trauma-induced cortical myoclonus can be treated with clonazepam.
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