Article Text

Botulinum toxin type A in the treatment of upper limb spasticity among patients with traumatic brain injury
  1. GIOVANNI PAVESI,
  2. RODOLFO BRIANTI,
  3. DORIANA MEDICI,
  4. PATRIZIA MAMMI,
  5. ANNA MAZZUCCHI,
  6. DOMENICO MANCIA
  1. Institute of Neurology, Univrsity of Parma. Parma, Italy
  1. Dr Giovanni Pavesi, Laboratorio di Elettromiografia, Azienda Ospedaliera di Parma, Monoblocco, Via Gramsci 14, 43100 Parma, Italy.

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We studied the efficacy and safety of botulinum toxin A (BTX-A) injections in patients affected by upper limb spasticity secondary to traumatic brain injury, in an open labelled trial.

Increased stretch reflexes, hypertonia, flexor spasms, and abnormal cocontraction are often associated with muscular contractures, causing many clinical manifestations in patients with traumatic brain injuries.

Botulinum toxin A (BTX-A) produces a dose related weakness of skeletal muscles by impairing the release of acetylcholine at the neuromuscular junction. Therapeutic intramuscular injections of BTX-A are a major advance in the treatment of focal dystonia, and show promise in spasticity of varying aetiology.1

The aim of this study was to evaluate the efficacy and safety of BTX-A treatment on disorders of muscular tone after traumatic brain injuries, in an early phase of rehabilitation, when retractions are still avoidable.

We examined six patients affected by severe traumatic brain injury (Glasgow coma scale<8). The mean age was 24.5 (range 18–42) years; spasticity had been present for a mean of 4.5 (range 4–6) months,. One of the patients was in a vegetative state. The table shows the clinical data.

Clinical data and results

Upper limb muscles were injected with BTX-A (Botoxr, Allergan) in all six patients In all, nine injections were carried out; three patients received only one injection (patients 2, 3, and 5), and the other three patients (1, 4, and 6) were reinjected after a variable lapse of time (1.5, 6, and 3.5 months later respectively). The mean dose of toxin injected for each treatment was 96 U. The toxin was injected by means of an EMG needle electrode guidance (Dantec 13R18), to improve the selectivity of treatment.

Target muscles for injections (table) were chosen on clinical judgement of muscle spasms or increased tone and then identified by EMG recording of active movements or stretch induced activity. Fixed muscular contractures and articular calcifications were assumed as criteria for exclusion from the trial; in doubtful cases, anaesthetic nerve block was performed before BTX-A treatment.

Each subject was assessed by a specialist in psychical medicine and a neurologist in a baseline evaluation and at fixed intervals after treatment (one week, one, three, six, and 12 months).

Outcome measurements were the modified Ashworth scale for grading muscle spasticity; joint angle measurements by means of a goniometer (range of movement); clinical evaluation of postural improvements, voluntary movements, and changes in limb function. The treated limbs were put in casts to prevent contractures after the injections; in some patients, additional medical treatment, such as lioresal, was given. The mean follow up was 10 (range 4–19) months.

The table shows the results. Improvements in modified Ashworth scale, joint range of movement, and clinical evaluation were found in all six patients. The modified Ashworth scale gain was one degree in four patients, two degrees in one patient, and three degrees in the other patients. Improvements in arm function for activities of daily living were obtained in five of the six patients. In particular, in two patients (2 and 5) the reduction in spasticity led to a significant improvement in fine movements of the dominant hand, so that writing became possible. Reduced spasticity in one patient (4) enabled hand held utilisation of walking devices; in another two patients (3 and 6), it made for independence in dressing and eating. Clinical benefit started after two to three days and peaked in about three weeks. Three patients did not need a second injection; the other three patients were reinjected after varying times. Patient 1 had right biceps and brachioradialis muscle injection in the first session and a reinjection of the biceps muscle after 1.5 months; spasticity was reduced, mainly in the wrist and finger joints. The follow up of this patient was interrupted after four months. Patient 1 is still in a vegetative state. Three patients (1, 2, and 5) had pain arising from muscle spasms, which was relieved by BTX-A treatment.

These preliminary data show that BTX-A treatment is effective in reducing spasticity in selected patients with focal upper limb muscular tone disorders secondary to traumatic brain injuries. Spasticity, as measured by means of the modified Ashworth scale, was reduced and range of movement increased in five of the six patients. Greater facility in nursing care and reduced disability were found in all the subjects. The effects of a single injection were long lasting and only three patients needed a second injection. The treatment in the early phases of the muscular tone disorders seemed to be a critical factor. The pain secondary to muscle spasms was relieved by BTX-A treatment in our patients; the pain arising from capsular and synovial tissues, mainly at the elbow joint, was unaffected.

Previous studies have shown comparable results in spasticity secondary to stroke, multiple sclerosis, degenerative diseases, and cerebral palsy. Few reports are available for patients with traumatic brain injury, dealing only with isolated cases or small samples of patients with lower limb spasticity.2-3 To our knowledge, only one paper deals with a large population of patients with traumatic brain injuries4; most of these patients (12 out of 21) were chronically affected, (that is, spasticity had lasted for more than one year), and one of the acute patients had experienced a penetrating brain injury. The results obtained in the remaining eight acute patients were similar to ours.

In our patients, the changes were not strictly limited to the muscles injected; the treatment of proximal arm muscles invariably had a positive effect also on finger movement. A local toxin diffusion or an indirect permissive action could be hypothesised; however, action mechanisms other than the peripheral one for BTX-A cannot be ruled out5 .

The treatment was completely safe and none of the patients complained of weakness due to the BTX-A injection.

Several points deserve further study: the choice of muscles, the number of injections, the dilution of the drug, and, in particular, the selection of patients. Furthermore, it is very important to define a clear goal for therapy for each patient. Double blind, placebo controlled, multicentre trials are warranted to provide answers for the aforementioned questions.

References

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