REHABILITATION OF MODERATE TO SEVERE TBI: MOVEMENT DISORDERS: DRUG-INDUCED, DYSTONIA, MYOCLONUS  

Drug-Induced Disorders are usually caused by the pre- or postsynaptic dopamine antagonists or CNS stimulants, which are frequently prescribed following TBI, such as anticonvulsants, tricyclic antidepressants, antipsychotics, and neuroleptics. Drug-induced movement disorders include:

  • Chorea, due to valproic acid, particularly if taken with phenytoin, in patients with severe TBI and severe epilepsy (Lancman, et al 1994)
  • Dystonia, due to metoclopromide and neuroleptics, usually within 5 days; withdrawal of drug resolves movement disorder
  • Parkinsonism, due to dopamine-depleting agents, metoclopramide or clebopride, usually within 3 months; bradykinesia and symmetrical tremor distinguish it from non-drug-induced parkinsonism; tremor may be controlled with propranolol
  • Dyskinesia, due to phenytoin or combination phenobarbital/valproic acid therapy which increases the free fraction of phenytoin

Dystonia - Repetitive, sustained twisting movements of variable speed of almost any body part. Muscle tone varies between hypertonia, which can be aggravated by voluntary movements, and hypotonia, which can occur during sleep. Onset is within minutes or years of injury, and risk factors include hemiparesis, evidence of striatal damage, and dysfunction of the lenticulothalamic neuronal circuit (Lee, et al 1994). Superficial sensory stimulation, such as holding the side of the head or abducting the thumb, can suppress or abolish movement.

     There are various classifications for dystonia:

  • Athetotic dystonias are slow; Myoclonic dystonias are shocklike
  • Dystonic spasm is brief movement; Dystonic posture may last from minutes to hours
  • Early onset dystonia, which usually resolves; Delayed dystonia, which is usually persistent (Silver and Lux, 1994).
  • Focal dystonia involves a single body part. Segmental dystonia involves 2 or more contiguous regions of the body.  Botulinum toxin is the treatment of choice, although the effects may be temporary. Levodopa and anticholinergic medications may be effective, but are not well tolerated following TBI. Muscle relaxants and, in severe cases, dopamine-depleting agents have been used, but may cause side effects such as tardive dyskinesia.
    • Cranial dystonia may involve the lingual and pharyngeal structures. Blepharospasm, brief contractions of the orbicularis oculi, is one form

    • Spasmodic dystonia involves the larynx
      • Characterized by a strained or breathy vocal quality
      • Treated by injection of botulinum toxin into the vocalis complex

    • Oromandibular dystonia involves the lower facial muscles
      • Signs include trismus, retraction of the corners of the mouth, protrusion of the tongue, jaw opening, jaw tightening, or tics
      • Treatment includes
        • Submental injection of botulinum toxin, the first line of therapy, which may result in ptosis
        • Clonazepam, lorazepam, baclofen, and trihexiphenidyl, which have cognitive side effects
        • Myectomy of the orbicularis, facial nerve sectioning, and brow lift, which may result in complications such as exposure keratitis, ptosis, and eyelid necrosis

    • Cervical dystonia (spasmodic torticollis) is a form of nuchal dystonia
      • Usually involves twisting of the head, but may involve head movements toward one shoulder, flexion, or extension
      • May cause pain
      • Treatment includes
        • Botulinum toxin injection; dysphagia is the most common side effect
        • Relaxation techniques and physical therapy to prevent contractures
        • Diazepam, lorazepam, clonazepam, cyclobenzaprine, and carbamazepine, with varying results

    • Hemidystonia following TBI
      • Can occur between 14 months and 29 years postinjury due to aberrant neuronal sprouting
      • May present during nonrapid eye movement sleep
      • Treatment involves thalamotomy (for mild or transient relief) and electrical stimulation of the ventroposterolateral nucleus of the thalamus

Myoclonus

  • Characterized by sudden and irregular, or rhythmic muscle jerks due to metabolic, toxic, and hypoxic disturbances or sudden stimuli
  • Types include:
    • Positive myoclonus, which involves active contraction of muscle
    • Negative myoclonus, which involves collapse of muscle tone
    • Palatal myoclonus
      • May be unilateral or bilateral, but is rarely associated with contractions of other body parts
      • Produces a clicking noise that can be heard by the patient and others
      • Due to lesions of the cerebello-rubro-olivary tract
      • May be relieved by clonazepam or carbamazepine
    • Posthypoxic myoclonus
      • Associated with cerebellar ataxia, dementia, postural and gait disturbances, and seizures
      • Principal therapy is clonazepam alone or in combination with carbamazepine, valproic acid or primidone; may be treated with 5-hydroxytryptophan; if tremor is also present, may be treated with propranolol
    • Cortical myoclonus may be treated with sodium valporate in combination with clonazepam
    • Brain-stem myoclonus may be treated with clonazepam

Based on information in Medical Rehabilitation of Traumatic Brain Injury, L.J. Horn and N.D. Zasler, eds. St. Louis, MO, Mosby, 1996, except for information where other papers are cited.