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Botulinum toxin use in
post traumatic cervical dystonia
and head tremor
Dr Marieta Anca-Herschkovitsch
Movement Disorder Clinic
Edith Wolfson Medical Center
Israel
Post-traumatic cervical dystonia :a subject of debate
The development of abnormal posturing of the neck or shoulder after
local injury has been termed posttraumatic cervical dystonia (PTCD).
FIRST DESCRIPTION IN 1888 BY GOWERS
Features to distinguish this disorder as a distinct clinical entity from those
of typical idiopathic cervical dystonia are :
onset and maximum disability occur very quickly after injury(hours
to days), severe pain and a fixed abnormal posture(Lang ,2003),not
influenced by sleep,poor response to BTX (Frei et al ,2004 )
In order to establish a consistent causal relationship between peripheral trauma
and movement disorder, Jankovic (1994) proposed the following criteria :
1. The injury should be severe enough to cause local symptoms persisting or
requiring medical attention for at least two weeks after the trauma;
2. The onset of involuntary movements must have occurred within one year after
the trauma;
3. The abnormal movements should be anatomically related to the site of the injury.
Moreover, the causal relationship should be supported by the absence of other
causes capable of producing the same symptoms, presence of reflex sympathetic
dystrophy and poor response to conventional treatment.
The mechanism by which dystonia may be related to posttraumatic movement disorders and CRPS is poorly understood.
*-mediated through the sympathetic nervous system- view recently called into
question (Schott, 1995 ; Baron et al., 1999 )
* -Inflammation might be involved in the development of CRPS following
injury, at least in the early stages (Birklein et al., 2001 ).
* -Peripheral mechanisms ( sensitization of peripheral nociceptors, or
ectopic or ephaptic transmission of nerve impulses) are suggested as a
possible mechanism of CRPS and post-traumatic movement disorders (Jankovic,
1994 ; Schott, 1986b , 2001 ).
However, spread to ipsilateral, axial, and contralateral muscles may occur in fixed
dystonia, as in CRPS and post-traumatic dystonia, in these cases, such peripheral
mechanisms are unlikely to explain the development of abnormal movements after
injury.
*-Impairment of interneuronal circuits at the spinal/ brainstem level and
central synaptic reorganization analogous to that following amputation could
be a possible mechanisms leading to such sequelae even after a minor
peripheral injury (van Hilten et al., 2001 ).
Controversy:
1-abnormal movements in CRPS indicate a somatoform or
malingering origin?
2-evidence for organic origin :
*-
abnormalities of reciprocal inhibition of H-reflexes, seen in typical
dystonia (Koelman et al., 1999 ; van de Beek et al., 2002a ,b ),
*-abnormal stretch reflexes (van Hilten et al., 2001 ; van de Beek et al., 2002b)
*- high prevalence of HLA-DR 13 in dystonia associated with CRPS
(van Hilten et al., 2000b )
*-changes in contra lateral thalamic perfusion on 123iodine-labeled single
photon emission computed tomography (SPECT) imaging in cases of
CRPS (Fukumoto et al., 1999 ) .
However, whether these central or peripheral changes are primary or secondary to
the clinical abnormalities remains a matter of dispute, and the finding of a HLA-DR
13 association has yet to be replicated in other studies.
Literature
*- A series of 9 patients with PTCD in whom involuntary muscle spasms and
abnormal head postures occurred within 7 days after cervical injury were treated
with botulinum toxin as necessary, and were followed up to 5 years. Based on our
observations of these cases, we propose that complex regional pain syndrome
(CRPS) could represent a variant of posttraumatic cervical dystonia that may
develop over time after the initiation of dystonia. (Frei et al,2004)
*-A retrospective study of the clinical characteristics of the 16 patients with early
post-traumatic CD (CD-PT) in comparison with the 52 patients reporting no
antecedent trauma (CD-NT) was performed( O’Riordan,2004 ).
In this comparison the CD-PT group had a significantly increased
frequency of laterocollis, significantly more reported pain and more reported
depression. Non-significant trends were noted for less responsiveness to
botulinum toxin and less use of gestes antagonistes in the CD-PT group
WHIPLASH ASSOCIATED DISORDER
• The term "whiplash" has been used to describe a mechanism of injury, and the
clinical manifestations as a consequence of the injury.
• In 1995, the Quebec Task Force on Whiplash Associated Disorders (WAD)
defined: "whiplash is an acceleration-deceleration mechanism of energy
transfer to the neck. It may result from rear-end or side-impact motor vehicle
collisions, but can also occur during diving or other mishaps. The impact may
result in bony or soft-tissue injuries (whiplash-injury), which in turn may lead
to a variety of clinical manifestations called Whiplash Associated Disorders
• The incidence of whiplash injury :between 70–200 per 100,000 inhabitants
no consensus about the natural course of the whiplash injuries .
•
It was concluded that 14 - 42 %of patients could develop chronic
complaints (over six month duration), and that 10 percent of those patients
had constant severe pain.
• The common symptoms are: neck pain (88–100%), headache (54–66%
),neck stiffness, shoulder pain, arm pain/numbness, paraesthesia, weakness,
dysphagia, visual and auditory symptoms and dizziness
Mechanics of Whiplash
Hyperextension
HyperFlexion
Majority of cases, no injury can be identified
Symptoms attributed to musculo-ligamental sprain
The exact pathophysiology of WAD is uncertain but
probably involves some degree of aberrant muscle
spasms and may produce a wide range of symptoms
• Initial treatment of pain associated with whiplash usually includes oral
medications, such as muscle relaxants and nonsteroidal anti-inflammatory
drugs, agents limited by potential systemic adverse effects. Some patients
with chronic WAD may benefit from radiofrequency neurotomy.
• A new approach to treatment is the use of botulinum toxin, which acts to
reduce muscle spasms.
• Type A toxin (Botox) studied in small trials of patients with WAD has
generally been found to relieve pain and improve range of
motion(ROM).
• Preliminary data from a small trial showed that type B toxin (Myobloc)
produced almost immediate pain relief for most patients with postwhiplash headache.,
LITERATURE
It was reported a significant reduction in pain and improvement in ROM in
77.4% of patients responding significantly to a BTX-A injection in an open label
study with 31 patients, grade II WAD( Francisco Juan, 2003 ).
Patients received 50–75 units of BTX-A, and the follow-up assessment was at
week 8. BTX-A, specifically Botox®, has been studied for the treatment of WAD
and chronic neck pain. BTX type-B has been studied in patients with postwhiplash headaches( Opida CL, 2002).
The injection technique used for the neck is based on experience with cervical
dystonia. The sites chosen are chiefly in the large superficial muscles,
specifically, the splenius capitis, rectus capitis, semispinalis capitis, and
trapezius (can develop hypertrophy).
The muscles can easily be palpated in most individuals and can be injected
without sophisticated techniques and without EMG .
Personal experience
Posttraumatic painful cervical dystonia
SUBJECTS( 12 PATIENTS ) : 4 male and 8 female,age range 25-68y, 1 subject
post cervical laminectomy , 1 post head trauma, 10 post whiplash injury
ONSET of neck dystonia : few weeks to 6 months post trauma , on chronic
cervicalgia and lack of other treatment strategies efficacy
RESPONSE to Botox treatment –variable :
--mild whiplash early treated resolved in 6 mo (2 inj) in 2 patients,
--subjective/objective improvement (pain,ROM )in treatment period 2y-8y
(each3-4 months), reduction of muscle tenderness and volume,head posture
--Dynamic dystonia on treatment: 1 patient’s laterocollis shifted to
anterocollis
SIDE EFFECTS: transient dysphagia in 1 patient
DOSES of Botulinum toxin/inj : 150-300 ui BTX /400-1000 ui Dysport
SITES FOR INJECTION : trapezius,splenius capitis,sternomastoids ,paraspinal
muscles
HEAD TREMOR
*In a clinical series of 487 individuals diagnosed with ET with a mean age of
onset of 52, half of the sample had a family history of ET, half presented with
symmetrical disease and tremor affected the arms (97%), voice (62%), head or
neck (48%). ( Uitti RJ, 2007 )
* 43 patients with head tremor as the major complaint were treated with local
botulinum toxin type A (Btx A) injections into neck muscles: 29 were
classified as tremulous cervical dystonia (TCD), and 14 as head tremor without
dystonia (HT). Patients with HT received mean total doses of 400 units (U) of
Dysport (Btx A) (range, 160-560 U) distributed between the two splenius
capitis muscles. Patients with TCD received a mean total dose of 500 U
Dysport (range, 320-720 U) injected into a mean of 3 muscles (range, 2-4
muscles). The condition of all patients improved subjectively. The total on the
Tsui scale as well as pain scores decreased significantly (p < 0.05) following
treatment. Latency of onset, duration of improvement, and side effects showed
no significant difference in HT and TCD. Amplitude of HT decreased
significantly for both groups following treatment. The mean dominant peak
frequency in TCD and HT was slightly less than 5 Hz and did not change
significantly after treatment.(Poewe et al, 1997)
Personal experience
SUBJECTS(6 patients):
4 female, 2male, age 23-62 y, 2 with TCD as rotatory torticollis ,
4 with HT changing direction /axis between anteroposterior
(yes-yes) to lateral (no-no)movements
Family history –negative
Associated movement disorders- 2 patients(TS)
Treatment duration :1y-5y
Doses of botulinum toxin : 100-300 ui Botox/300-900ui Dysport
Sites for injection: splenius capitis, sternomastoid muscles, bilateral
Efficacy: improvement subjective / objective(amplitude,frequency)
Side effects: negative
Conclusion
Botulinum toxin is a safe and effective therapy
for most patients with cervical dystonia,
including posttraumatic syndromes
Botulinum toxin can safely be used to control
tremor in patients in whom other forms of
therapy have failed.
“Regarding every disease now incurable we
may entertain the hope that our powerlessness
may not be permanent, and that we, or those
who come after us , may be able to speak in
very different terms “
W.R.Gowers , 1879