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261
but to soft tissue. Almost nine of ten whiplash sufferers had some degree of muscle
spasm [ 7 ].
In particular, these patients had decreased ability to relax the trapezius muscles.
Such a fi nding raises the question of whether cervical muscular dysfunction causes
ongoing excess loading of the zygapophyseal joints, yielding the clinical picture of
chronic whiplash, or whether muscle dysfunction is an attempt by the body to splint
a subtly injured cervical spine.
Several theories about musculoskeletal pain syndromes such as WAD suggest
that pain and muscle activity interact and may contribute to the chronicity of symptoms. Studies using electromyography (EMG) have demonstrated abnormal muscle
activation patterns of the upper trapezius muscles in the chronic stage of WAD
(grade II) [ 8 ].
Concerning chronic treatment of whiplash-associated (WA) pain, the most com-
monly prescribed pharmacological agents are the same: oral muscle relaxants and
nonsteroidal anti-infl ammatory drugs. Also in these cases, paracetamol has to be
preferred. However, the effectiveness of these drugs in chronic patients is limited by
their systemic therapeutic effect and unfavourable side effects. Physical interventions such as mobilisation, manipulation and exercises have proved benefi cial for
pain and dysfunction at least in the major part of the patients. Anyway, in chronic
WA pain, the only treatment that has clearly shown benefi t is radiofrequency neurotomy [ 9 ].
The potential benefi ts of relaxing selected neck muscles [ 10 ] with botulinum
toxin type-A (BTX-A) for the treatment of muscle pain in WA chronic head and/or
neck pain have been investigated by Freund et al. [ 11 , 12 ].
BTX-A ( Bot ox ® ) is a neurotoxin and is effective for treating a variety of disorders
of involuntary muscle contraction, including spasticity, cervical dystonia, blepharospasm and hemifacial spasm. It inhibits neuromuscular signalling by blocking the
release of acetylcholine at the neuromuscular junction. The biological effects of the
toxin are transient with normal neuronal signalling returning within approximately
3–6 months postinjections. The injection technique used for the neck is based on
experience with cervical dystonia. The sites chosen are chiefl y in the large superfi cial muscles, specifi cally, the splenius capitis, rectus capitis, semispinalis capitis
and trapezius. These muscles can easily be palpated in most individuals and can be
injected without sophisticated techniques. Most patients exhibit tender areas in the
larger muscles, often in conjunction with tight bands or knots. The neurotoxin
effects are thought to act only upon motor nerve endings, while sensory nerve fi bres
are spared from such effects. Thus, analgesic effects are likely to occur, not as a
result of blocking afferent sensory fi bres at the site of injection but rather from secondary effects that may be attributed to muscle paralysis, improved blood fl ow and
release of fi bres under compression by abnormally contracting muscles. The primary action may affect alpha and gamma motoneuron function in the muscle spindles resulting in lower muscle tone. BTX-A treatment is potentially a painful
procedure [ 13 ]. It is contraindicated in the presence of infection at the injection
site(s) and in individuals with known hypersensitivity to any ingredient in the formulation. Individuals with peripheral motor neuropathic diseases or neuromuscular
25 Pharmacological Treatment of Whiplash-Associated Disorders (WAD)
262
functional disorders should receive BTX-A treatment with caution. BTX-A should
also be used with caution in patients receiving aminoglycosides or other agents
interfering with neuromuscular transmission.
BTX-A injections are not a curative treatment. BTX-A provides a temporary
paralytic effect and requires repeated injections to continue the benefi cial effects.
The duration of effect is longer with the initial injection and progressively gets
shorter with repeated injections for most dystonic disorders. It is not known at this
time whether BTX-A can be readministered indefi nitely or if the effectiveness will
wear off over time.
25.3 Whiplash-Associated Equilibrium Disturbances (WAED)
Whiplash injury is a very common cause of vertigo and dizziness. The physiopathological mechanisms of this kind of injury can be explained from the effect of forces
applied to the head and the neck during the collision. In the fi rst phase, the force
applied to the rear end of the car during the collision results in a forward acceleration of the body while the head is pushed backwards from inertial forces causing a
cervical hyperextension. In the second phase, which always occurs because of the
effect of inertial forces, the head is pushed forward with subsequent hyperfl exion of
the neck. The whole duration of these phases is about 20 ms. This is the reason for
the lack of activation of neck neuromuscular protective refl exes, whose latency is
about 50 ms. During neck hyperextension the elongation of cervical rachidian tissues may even reach 5 cm [ 14 ].
The vestibular system is frequently involved in whiplash injuries; lesions may
involve labyrinth and central vestibular organs and pathways.
Three lesion levels of the vestibular system can be distinguished: (1) labyrinth
and organ damage, (2) central vestibular and oculomotor system damage (3) and
both involvement of the peripheral and central vestibular systems. Table 25.1
reports the classifi cation of post-traumatic vertigo (from [ 12 ], modifi ed).
The prerequisites for successful pharmacological treatment of WAEDs are the ‘4
Ds’: correct diagnosis, correct drug, appropriate dosage and suffi cient duration.
First, a correct diagnosis , on the basis of the patient history, clinical examination
and laboratory investigations; second, the correct drug —only a few have been
Table 25.1 Causes of post-traumatic vertigo
Damage site
Lesions
Physiopathology
Labyrinth Labyrinthine lesions, temporal bone
fractures, concussive trauma, haemorrhagia
Otolith displacement
Maculae—semicircular canals Round—oval window rupture
Perilymphatic fi stula
Vestibular nerve Axonotmesis neurotmesis Concussion—haemorrhage
Brainstem
cerebellum
Concussion haemorrhage ischemia Neurotransmitter release
Cervical rachis Whiplash syndrome Vascular—proprioceptive
E.A. Pallestrini et al.
263
proven in controlled trials to be effective in a suffi ciently large sample of patients,
but experience can suggest appropriate drug choice for every specifi c patient ; third,
an appropriate dosage —often the initial dose is too low or too high so that the treat-
ment is either ineffective or not well tolerated; and fourth, a suffi cient duration —
often drugs are either given for too long, such as antivertiginous agents (e.g.
dimenhydrinate), which delay central compensation and may cause drug dependence, or not long enough.
In the child, pharmacological treatment of vestibular post-traumatic disorders is
essentially symptomatic for the early and effi cient development of compensatory
mechanisms. The main aspects of treatment are related essentially to the dosages
and the frequency and duration of drug administration for each case. The choice of
substance is based on the clinical experience of the physician and on knowledge of
the pharmacological characteristics of the different categories of drugs [ 15 ].
In the elderly, pharmacological treatment of post-traumatic vertigo shows particular aspects linked to the aging processes. Several factors such as relative
enhancement of fat tissue, the reduction of body mass, decreased hepatic and kidney functions and the diminution of serum albumin infl uence drug pharmacokinetic
properties (absorbency, tissue distribution, metabolism, sensibility and clearance).
We can distinguish therapies for vertigo spells, chronic unsteadiness or relapsing
vertigo.
25.4 Vertigo
Vestibular sedative drugs should be employed immediately after head-neck trauma
and continued for a few days.
In benign positional vertigo (BPV) drug treatment should principally support
rehabilitative training because neck pain and muscular stiffness and spasm make
diffi cult vestibular physical treatment in the early stage of the disease
Symptomatic therapy involves vestibular suppressor and antiemetic drugs.
Among the vestibular suppressor drugs, antihistamines, phenothiazines and benzodiazepines are the most widely used.
Antihistaminic drugs (dimenhydrinate, fl unarizine, cinnarizine, hydroxyzine,
betahistine, astemizole) act on the synapses between the fi rst and the second neurons, on the reticular formation, on the vestibular dopaminergic pathways and on
H1 receptors. The pharmacological effect is vestibule suppressive with inhibition of
positional nystagmus.
Betahistine interferes with the diamine oxidase prolonging histamine action; it
has a moderate agonist activity on H1 receptors and a strong activity as an H3
antagonist. Betahistine inhibits neurons of the lateral vestibular nuclei [ 16 ] and
increases the basilar and cochlear fl ow in animal models. Betahistine has vasodilatative effects on stria vascularis, on spiral ligament and on vertebrobasilar circulation [ 17 ]. Betahistine improves microcirculatory fl ow of the inner ear and central
vestibular system, and this can explain the positive effects in the treatment of paroxysmal peripheral vertigo, modulating effect on cerebral and labyrinthine circulation.
25 Pharmacological Treatment of Whiplash-Associated Disorders (WAD)
264
Astemizole has a strong inhibitory action on vertigo and nystagmus, and it is
interesting from a clinical point of view because it crosses the blood-cerebrospinalencephalic barrier only in a minimal concentration; for this reason this drug has
very low sedative effects, and therefore its main action is on the peripheral vestibular system [ 18 ].
Phenothiazines (promethazine, thiethylperazine, prochlorperazine) are very
effective in decreasing acute vertiginous symptoms and vegetative side effects.
Pharmacological effects on the vestibular system are the inhibition of peripheral
cholinergic inputs, inhibition of H1 receptors in vestibular nuclei and an effect on
the bulbar chemoreceptor trigger zone. Phenothiazines have important side effects
on the extra pyramidal system, on pressure control mechanisms and on prolactin
secretion. For these reasons phenothiazines should be administrated carefully especially in the elderly.
Scopolamine shows strong anticholinergic activity on brainstem, reticular for-
mation and vestibular nuclei. This drug cannot be used in patients suffering from
glaucoma, prostatic hypertrophy and heart diseases [ 19 – 21 ].
Benzodiazepines (diazepam, lorazepam, clonazepam, etc.) enhance GABAergic
inhibitory properties of vestibulocerebellum on vestibular nuclei and activate the
internuclear inhibitory pathways. They are also active on glycinergic pathways, on
substantia nigra, on the limbic system and on cholinergic activatory reticular formation. The fi nal effect is the inhibition of the vestibulo-oculomotor refl ex and nystagmus. Benzodiazepines have inhibitory effects on breathing and blood circulation
and for these reasons should be carefully administered in elderly patients.
Propranolol has been successfully employed in the treatment of whiplash injury-
related vertigo. This drug reduces hypertonicity of spinal muscles lowering the discharge frequency of neuromuscular
fusicellular endings, with a subsequent diminution of cervical pain [ 22 ].
25.5 Chronic Unsteadiness and Relapsing Vertigo
Damage to the vestibular apparatus due to whiplash injuries produces acute symptoms, which gradually improve as central compensation occurs. The aim of the
pharmacological strategy in peripheral vestibular lesions is to improve CNS restorage mechanisms; for this reason vestibulo-suppressive drugs, even if effective in
reducing vertigo and imbalance, worsen the CNS compensation and should be
administered only in the fi rst stage of the disease. On the other hand with the
employment of CNS excitatory drugs or drugs with decompensating effects during
rehabilitative training, compensation processes will be stimulated with acceleration
of healing.
Among drugs which enhance compensation processes, the amphetamines,
ginkgo biloba and calcium antagonists are the most used [ 23 – 25 ]. Amphetamines
theoretically could be employed in the treatment of peripheral vestibular lesions
based on their positive effects on compensation processes. Their use is limited
because of signifi cant side effects. Pemoline and fi pexide belong to this category of
E.A. Pallestrini et al.
265
drugs and are particularly interesting for their limited side effects; pemoline affects
dopamine turnover and has few peripheral effects; fi pexide affects the reticular for-
mation and shows dopamine-like effects. Ginkgo biloba enhances postural and
locomotor balance and oculomotor function recovery in experimental unilateral
vestibular lesions.
Cinnarizine and fl unarizine [ 26 ] selectively block calcium entry into peripheral
vestibular system cells (especially cristae cells); both these drugs show antihistaminic and anticholinergic activities. In the peripheral vestibular system, calcium
antagonists modulate neurotransmitter release. Flunarizine interferes in ACh release
and enhances compensation processes. In elderly patients, these drugs should be
administered carefully for its Parkinson’s-like effects after prolonged treatment [
27 ].
In the elderly where CNS reorganisation after vestibular damage is less effective,
drugs with positive effects on compensation, as well as haemorrheologic and neuroactive drugs, should be used. Drugs which increase CNS neurotransmitter storage
will be also useful in these patients [ 28 ]. In particular, neuroactive drugs are
employed for their actions on CNS neurotransmitters, while vasoactive substances
improving blood macro- and microcirculation enhance CNS metabolism.
Neuroactive substances can be classifi ed as drugs not specifi cally acting on vestibular neurotransmitters and drugs specifi cally acting on vestibular neurotransmitters
(Tables 25.2 and 25.3 ).
Among the neuroactive drugs which are not specifi cally active on vestibular neurotransmitters, citicoline has dopaminergic and serotonergic activities and reduces
platelet aggregability. Deanol and oxiracetam have cholinergic action; piracetam, a
GABA derivative, has strong dopaminergic and mild GABAergic activities and
improves cerebral ATP synthesis; this drug accelerates compensation phenomena
and is well indicated in vertigo due to a brainstem disinhibition [
29 ] and in post-
traumatic vestibular lesions. Protirelin is a TRH derivative; this drug’s main effect
is on the cholinergic neurotransmitter system and it shows secondary effects on the
dopaminergic, noradrenergic and serotonergic systems.
Table 25.2 Neuroactive drugs not specifi cally acting on vestibular neurotransmitters
Metabolic enhancers Citicoline, deanol, piracetam, oxiracetam, ginkgo biloba,
protirelin, l -acetylcarnitine
Neurotrophics Gangliosides
Excitants Amphetamines, fi pexide, pemoline
Antidepressants Tricycles IMAO, sulpiride
Anticonvulsants Carbamazepine
Myorelaxants β-blockers Baclofen
Table 25.3 Neuroactive drugs specifi cally acting on vestibular neurotransmitters
Antihistamines Flunarizine, cinnarizine, hydroxyzine, astemizole, betahistine,
diphenhydramine, dimenhydrinate
Phenothiazines Promethazine, thiethylperazine, prochlorperazine
Benzodiazepines
Scopolamine
25 Pharmacological Treatment of Whiplash-Associated Disorders (WAD)
266
Among alpha -blockers, dihydroergotoxine, an alkaloid derivative, has vascular
and metabolic activities enhancing alpha-adrenoceptor blocking activity.
Dihydroergotoxine also has a dopaminergic activity and inhibits the specifi c cerebral phosphodiesterase response in c-AMP metabolism. Their use is however limited to selected cases. Nicergoline is an ergot derivative with actions on dopamine
turnover, on cerebral blood fl ow and on cerebral glucose consumption; this drug
enhances neurotransmitter storage, and for this reason its employment seems to be
interesting in post-traumatic vertigo of central origin especially in the elderly.
Drugs active on the microcirculatory system have been found to have multiple
actions on the neurotransmitter system, on cerebral fl ow and on cerebral metabolism with limited side effects. Among these substances bufl omedil [ 30 ] has alpha-
blocking, antiaggregant and haemorrheologic properties and a calcium antagonist
effect. This drug acts to diminish cerebral oxygen consumption. Pentoxifylline has
different pharmacological properties; the main one is the improvement of erythrocyte deformability (through an ATP improvement) and the diminution of blood viscosity (through a diminution of fi brinogen). This drug reduces platelet aggregation
by acting on membrane phosphodiesterases, reducing thromboxane synthesis and
improving at the same time the synthesis of prostacyclin. Pentoxifylline reduces
platelet adhesiveness to the vessel wall and results in delaying the thrombogenic
action. Among calcium antagonists, nimodipine improves dopa’s inhibiting action.
In chronic WAD, paying attention to the patient’s age and the metabolism [ 31 ],
cinnarizine and fl unarizine may be used, at the lowest dosage possible and for the
shortest possible period. Cinnarizine has vasodilatatory, antihistamine and anticho-
linergic effects inhibiting central vestibular system activities. The main CNS action
of fl unarizine , difl uorinated derivative of cinnarizine, is blocking Ca 2+ ’s entry into
cells during hypoxia.
Sometimes post-whiplash headache, generally a tension-type headache, in prewhiplash migrainous patients may evolve into the vestibular migraine. Characteristic
features include recurrent attacks of various combinations of vertigo, ataxia of
stance and gait, photophobia and phonophobia and other brainstem symptoms,
accompanied or followed by head pressure, pain, nausea or vomiting [ 31 ]. Tricyclic
antidepressants in combination with diet gave a good response. Generally, only
drugs that are effective for treating migraine with and without aura can currently be
recommended. For the therapy of acute attacks, aspirin and an antiemetic could be
offered, whereas metoprolol (100 mg/day), topiramate (50–100 mg/day) or valproic
acid (300–900 mg/day) could be offered for prophylaxis.
Very rarely, and only after a major and complex whiplash such as rear and consequently front collision, atlantooccipital strain may lead to a central vestibular
lesion inducing downbeat nystagmus (DBN, a form of acquired nystagmus that is
characterised by slow upward drifts with downward quick phases). Patients frequently report blurred vision or oscillopsia, which increases on lateral gaze, as well
as associated unsteadiness of gait and postural imbalance. As a pathophysiological
mechanism, a tone imbalance of the central vestibular pathways subserving vertical
eye movements, including the otolithic pathways, such that DBN is often gravity
dependent, has been proposed for DBN. Baclofen and clonazepam dosage of 0.5 mg
tid or 1 mg bid, both GABA agonists, improve DBN [ 32 ].
E.A. Pallestrini et al.
267
Pharmacological therapy can be employed during rehabilitative treatment. The
aim of drug treatment is to reduce hypertonic contracture of muscles of the neck
to facilitate physiotherapeutic treatment and to improve the effi cacy of such therapy. In these cases, muscle relaxant substances may be employed. Also drugs
acting on central plasticity mechanisms may be useful (e.g. piracetam ) .
Amantadine results to be particularly useful in WA chronic unsteadiness especially when it is due to a labyrinthine damage. Amantadine [ 33 – 35 ] on one hand
reduces vestibular organ damage through an anti-glutamate action on NMDA
labyrinth receptors and on the other hand through dopaminergic mechanism
improves compensation.
In labyrinthine post-traumatic lesions (direct or indirect through labyrinth concussion or vertebral artery spasm), the preferred drugs are those with positive effects
on vestibular compensation. Vestibular suppressive drugs would be helpful initially
to improve vertigo and neurovegetative phenomena but should be avoided for long
treatments.
In post-traumatic vertigo of central origin (generally caused by vertebrobasilar
acute insuffi ciency), drugs which are active on neurotransmitter systems may be
employed together with vasoactive substances improving CNS circulation and
metabolism. In the brainstem involvement, drugs which are active on the cholinergic,
histaminergic and adrenergic neurotransmitter systems (scopolamine, cinnarizine)
are effective in reducing symptoms but can interfere with the processes of compensation. In cases exhibiting lack of cerebellovestibular control, drugs with GABAergic
actions such as benzodiazepines may be employed successfully [ 30 , 31 ].
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269
D.C. Alpini et al. (eds.), Whiplash Injuries,
DOI 10.1007/978-88-470-5486-8_26, © Springer-Verlag Italia 2014
26.1 Introduction
Recent studies highlight the fact that where there is pain in a WAD patient, there is
a rapid alteration of neck muscle functioning. It has been seen that within 24 h of
the trauma, there is an alteration in muscle control: on the contrary, there is no
proof of an automatic recovery if the pain diminishes and so special training is
necessary [ 1 , 2 ].
Physical exercise plays a major role in rehabilitating the patient, integrating him
back to a normal life. It is possible to identify some goals to be obtained in WAD
rehab:
1. Activation of the deep neck muscles (exercises with a low load)
2. Re-education of deep neck muscle resistance
3. Realignment of the activation patterns of both the deep and the superfi cial neck
muscles
4. Posture realignment, also during functional tasks
5. Readjustment of force and resistance to functional necessities (exercises with a
high load)
The basic principles of physical exercises are the segmentation, simplifi cation
and an increasing and continuous feedback. This treatment is executed with the
patient in various positions, from the supine up to the orthostatic, so as to pass from
a low workload to a more elevated one.
I. Odkvist • L.M. Odkvist
Physiotherapy , Risbrinksgatan 6a , Linkoping , Sweden
Department of Otolaryngology , University Hospital , Linkoping , Sweden
S. Negrini (
*)
Department of Clinical and Experimental Sciences , University of Brescia , Brescia , Italy
e-mail: stefano.negrini@med.unibs.it
C. Mariconda
Department of Physical Medicine and Rehabilitation , Gradenigo Hospital , Torino , Italy
e-mail: carlo.mariconda@gradenigo.it
2 6
Physiotherapy of Neck, Back and Pelvis
I. Odkvist , L.M. Odkvist , S. Negrini , and C. Mariconda
270
The motor control of the scapular girdle must not be overlooked seeing that a
variation of load distribution on the spine will negatively increase the compressive
load on the cervix vertebrae.
Scientifi c evidence [ 3 ] has been collected for a multimodal programme which
foresees:
– Explanations and reassurance for the patient
– Encouragement in activities and movement
– Pain relief
– Therapeutic exercises
– Ergonomic strategies
26.2 Orthopaedic Collar
Keeping in mind the numerous clinical variables and subjective ones of WAD, more
recent new studies highlight the importance and long-term effi cacy of a swift mobilisation and treatment of the symptoms of distortion trauma. The mobilisation is
carried out in terms of treatment and pain prevention of the disability and consequent recuperation of good specifi c muscle control.
In some cases we have noticed that immobilisation, where not clinically adequate, even if followed by rehabilitation treatment has led to a longer recovery time
and longer absences from work. This also evidently means an increase in health and
social welfare costs.
26.2.1 Physiotherapy
Decontraction is usually the very fi rst step. It can be achieved by relaxing the patient,
letting him feel confi dent with the therapist. This is easier, for example, in a good
environment, as happens in water, but for everybody it is suggested to work gradually, with the head well fi xed at the beginning resting on the table and then in the
therapist’s hands with a very good manual grasp. Many exercise techniques able to
reduce pain do exist and can be used in conjunction with decontracting and strengthening manoeuvres when one begins to remove the collar. We can mention, for
example, the McKenzie method [ 4 ], the Mézières, Souchard or Bienfait approaches,
the Sohier or Maitland technique, and so on. Obviously, The Method does not exist,
but only many useful techniques that must fi t the pathology of a single patient and
the knowledge and ability of the physiotherapist. Physiotherapy is not only muscular (and psychological) relaxation: it is also a fi rst step in returning a part of the body
to its normal daily life activities. This means that exteroception and proprioception
play a role other than the simple goal of decontraction.
The evidence suggests that physical exercises [ 5 , 6 ] may be benefi cial in the
short and long term. According to our experience, regaining enough strength to
permit not only movement but usually also the ability to sustain the head is perhaps
the most important goal when rehabilitation begins. In fact, the collar reduces
I. Odkvist et al.