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19. Precht W, Strata P (1980) On the pathway mediating optokinetic responses in vestibular
nuclear neurons. Neuroscience 5:777
20. Carleton SC, Carpenter MB (1984) Distribution of primary vestibular fi bers in the brainstem
and cerebellum of the monkey. Brain Res 294:281
21. Ikeda K, Kobayashi T (1967) Mechanisms and origin of so-called whiplash injury. Clin Surg
22:1655
22. le Boy R, Pompeiano O (1981) Convergence and interaction of neck and macular vestibular
inputs on vestibulospinal neurons. J Neurophysiol 45:852
23. Mc Nab I (1982) Acceleration extension injuries of the cervical spine, vol II. The Spine/WB
Saunders, Philadelphia, p 515
24. Ommaya AK, Fass F, Yarnell P (1968) Whiplash injury and brain damage: an experimental
study. JAMA 204:285
25. Baloh RW, Jenkins HA, Honrubia V, Yee RD, Law GY (1979) Visual-vestibular interaction
and patients with cerebellar atrophy. Neurology 29:116
26. Nagao S (1983) Effects of vestibulocerebellar lesions upon dynamic characteristics and adap-
tation of vestibulo-ocular and optokinetic responses in pigmented rabbits. Exp Brain Res
53:498
27. Waespe W, Cohen B, Raphan T (1984) Dynamic modifi cation of the vestibuloocular refl ex by
the nodulus and uvula. Science 228:199
28. Hasegawa T, Kato I, Harada K, Ikarashi T, Yoshida M, Koike Y (1994) The effect of uvulo-
nodular lesions on horizontal optokinetic nystagmus and optokinetic after nystagmus in cats.
Acta Otolaryngol Suppl 511:126
29. Miles FA, Fuller JH (1974) Visual tracking and the primate fl occulus. Science 189:1000
A. Salami et al.
251
D.C. Alpini et al. (eds.), Whiplash Injuries,
DOI 10.1007/978-88-470-5486-8_24, © Springer-Verlag Italia 2014
24.1 Introduction
Internuclear ophthalmoplegia (INO) is a well recognisable disorder of horizontal
eye movements, and it is a common fi nding in neurological disorders [ 1 ]. INO is
due to a functional impairment of the medial longitudinal fascicle (MLF) ipsilateral
to the medial rectus paresis. Generally INO is characterised by the impairment of
adduction of the eye on the side of the impaired MLF and abduction overshoot. The
electro-oculographic saccadic and gaze nystagmus patterns are typical.
In whiplash injuries, ocular motor disturbances are frequent also in those
patients in whom a head trauma did not occur [ 2 – 4 ]. In rare cases [ 5 ] eye movement
disorders are characterised by ocular conjugate movement impairment sometimes
as typical INO, sometimes as isolated abducens palsy.
With a certain frequency, we observed “atypical” abducting ophthalmoplegia pat-
tern, characterised by bilateral impairment of the velocity of the abducting eye [ 6 – 8 ].
This fi nding was described by Lutz [ 9 ], who proposed the existence of an abduc-
tion paresis of prenuclear origin (posterior internuclear ophthalmoplegia, pINO).
D. C. Alpini (*)
ENT-Otoneurology Service , IRCCS “Don Carlo C. Gnocchi” Foundation , Milan , Italy
e-mail: dalpini@dongnocchi.it
A. Cesarani
Department of Clinical Sciences and Community Health , University of Milan ,
Milan , Italy
Audiology Unit , IRCCS “Ca’ Granda” Ospedale Maggiore Policlinico , Milan , Italy
e-mail: antonio.cesarani@unimi.it
E. Merlo
ENT Department , Azienda Ospedaliera Ospedale di Circolo di Busto Arsizio,
Saronno e Tradate , Milan , Italy
Department of Otolaryngology , Tradate Hospital ,
Piazza 24 Maggio, 1, 21049 Tradate Varese , Italy
2 4
Abducting Interocular Ophthalmoplegia After Whiplash Injuries
D. C. Alpini , A. Cesarani , and E. Merlo
252
As his basic neuroanatomical assumptions were erroneous, the existence of this
kind of INO remained controversial, and papers in the literature are quite rare.
Abduction INO differs from abducens nerve palsy in several aspects, such as
absence of strabismus and diplopia in the primary position and adduction nystagmus of the contralateral eye [ 10 – 14 ].
The aim of this chapter is to report the frequency of abducting INO that occurred
in a group of patients after whiplash injuries without head trauma and to discuss
possible etiopathogenic mechanisms.
24.2 Material and Methods
Twenty-three consecutive subjects were investigated: 16 women and seven men
with mean ages of, respectively, 31.35 and 34.7 years (from 16 to 70 years).
Eye movements were recorded in DC by a computerised Nicolet Biomedical
Nystar electro-oculograph, using monocular electrodes. Eye movements were elicited by means of a semicircular LED bar, and the following tests were performed:
• Horizontal and vertical random saccades from 6° to 32°
• Sinusoidal 0.2 and 0.4 Hz horizontal smooth pursuit and 0.2 vertical smooth
pursuit
• 400/s bidirectional horizontal OKN and 200/s vertical OKN
The following parameters were calculated:
• Saccades: delay, accuracy, number, performance index, and mean velocity at
each amplitude
• Smooth pursuit: gain, DC offset, total harmonic distortion, and maximum
velocity
• OKN: number of beats, frequency, maximum velocity, and gain
• Sinusoidal provoked nystagmus (0.5 Hz at 11.5 and 5.75°/s2) in the dark (VOR)
and in the light (VVOR): nystagmus frequency and mean slow phase velocity
(SPV) and VVOR gain (VVOR-SPVNOR-SPV)
24.3 Results
The presence of bilateral abducting eye slowing was evaluated comparing accuracy,
performance index and saccadic eye velocity with the normal values previously
calculated in a group of 25 normal adults. No patients showed slowing of the adducting eye or another pattern like typical INO.
Horizontal saccades revealed slowing of the abducting eye in eight patients
(ABD) (34.7 %): two men and six women with mean ages of 35.87 years (from 16
to 58 years).
The mean age of the group of patients without abducting slowing was 33.67 years
(from 19 to 70 years).
In Table 24.1 the distribution of altered neurological tests is shown. The percent-
ages of altered tests regarding patients with abducting eye slowing are referred to
alterations of parameters other than eye velocities, such as latency, accuracy, offset,
and directional preponderance.
D.C. Alpini et al.
253
Horizontal saccades are altered in 62.5 % of ABD patients versus 20 % of the
other group. All the other ocular motor tests are altered in the same manner in the
two groups of patients (with exception of VVOR).
24.4 Discussion
Internuclear ophthalmoplegia can be attributed to a lesion of the MLF between the
levels of the third and sixth nucleus [ 15 ]. It has been assumed that the lesion affects
axons arising from cells in the paramedian pontine reticular formation (PPRF), but
this is not an accepted explanation for every case. In fact the impairment of movement is variable, the most severe lesions causing complete loss of adduction beyond
the midline during contralateral gaze; in some cases the impairment also affects the
convergence mechanism, while in others convergence is normal.
Cogan [ 14 ] divided INO into anterior and posterior types according to whether
the convergence was normal or not, while Lutz [ 9 ] divided INO into anterior and
posterior according to whether the medial or the lateral rectus muscle was paralysed. If convergence is still possible, it seems to be diffi cult to distinguish monolateral INO of abduction from abducens paralysis, while bilateral abducting INO
may refer only to a lesion of the internuclear fi bres.
There has been little agreement on the location of the responsible lesion and the
pathophysiological explanation of abducting INO. Some authors [ 16 ], rejecting the
existence of a prenuclear abduction paresis, attributed such cases to the pontine
involving the abducens nerve along its infranuclear intrapontine course. Others [ 17 ]
postulated decreased excitation of the lateral rectus motor neurons due to a lesion of
prenuclear structures, that is, aberrant “pyramidal tract” fi bres to the abducens
nucleus or the connection between the PPRF and the ipsilateral abducens nucleus.
An impaired inhibition of the antagonistic medial rectus muscle was discussed by
Collard et al. [ 18 ] suggesting an MLF lesion contralateral to the paretic eye.
Thomke et al. [ 13 ] demonstrated that the lesion is ipsilateral to the abduction
paresis at the upper pons or midbrain level. They also showed the existence of a
fasciculus near the MLF specifi c for inhibition of medial rectus. They stated that
ABD ophthalmoplegia is due to impaired inhibition of medial rectus tonic resting
activity following interruption of this para-MLF fasciculus.
In our opinion, despite the controversy about the physiopathology of abducting
ophthalmoplegia, the term of “abducting interocular ophthalmoplegia” is preferable
rather than the classical “internuclear”. In our experience this pattern is not rare, and
Table 24.1 Percentages
of pathological tests in
patients with (ABD) and
without (no-ABD) abducting
interocular ophthalmoplegia
ABD (%)
No-ABD (%)
Horizontal saccades 62.5 20
Vertical saccades 25 26.6
Horizontal smooth pursuit 37.5 40
Vertical smooth pursuit 25 33.3
Horizontal OKN 25 20
Vertical OKN 0 6.6
VOR 37.5 40
VVOR gain 25 66.6
24 Abducting Interocular Ophthalmoplegia After Whiplash Injuries
254
if monocular ENG recording is routinely performed, it describes a third of the
patients suffering vertigo and/or dizziness after whiplash injuries, even without
minor or major head trauma.
In Fig. 24.1 a case of abducting interocular ophthalmoplegia following whiplash
is showed. The involved parameters are peak velocities/movement amplitude ratio
(the butterfl y diagram) and the percentages of accuracy, comparing abducting and
adducting movements.
Fig. 24.1 A case of abducting interocular ophthalmoplegia following whiplash
D.C. Alpini et al.
255
The PI (performance index) refers to patient peak velocities compared to normal
values previously stored in the programme.
It is interesting to reveal that neuro-otological differences in the two groups of
patients concern, in an opposite way, horizontal saccades and VVOR. In fact in the
ABD group, horizontal latencies or adducting accuracies (parameters different from
those correlated to abducting eye slowing) were altered in 62.5 % versus 20 % of
the other subjects, while VVOR was normal in 75 % and altered in 66.6 % of noABD patients.
In no case was adducting slowing recorded, and we know only one paper in the
literature describing INO after whiplash without head trauma [ 6 ].
If we hypothesise a brainstem lesion with para-MLF involvement due to neck
hyperextension, there will be no need to exclude the possibility of the neurologically most frequently occurring adducting ophthalmoplegia. Our cases are not misdiagnosed bilateral abducens palsy as described either on the basis of the clinical
considerations reported in the introduction or on the basis of ophthalmological
examination excluding abducens palsy.
In our opinion abducting interocular ophthalmoplegia has to be considered a
disorder of ocular coordination correlated to head-eye, according to Treleaven et al.
and Montfoort et al. [ 19 , 20 ], and/or head-neck coordination disorders, according to
Kongsted at al. and Treleaven et. al. [ 21 , 22 ], caused by whiplash. It must not neces-
sarily be correlated to a brainstem lesion.
References
1. Bronstein AM, Rudge P, Gresty MA, Boulay G, Morris J (1990) Abnormalities of horizontal
gaze. Clinical, oculographic and magnetic resonance imaging fi ndings. II. Gaze palsy and
internuclear ophthalmoplegia. J Neurol Neurosurg Psychiatry 53:200–207
2. Baker RS, Epstein ADD (1991) Ocular motor abnormalities from head trauma. Surv
Ophthalmol 35:245–267
3. Wenngren BI, Pettersson K, Lowenhielm G, Hildingsson C (2002) Eye motility and auditory
brainstem response dysfunction after whiplash injury. Acta Otolaryngol 122(3):276–283
4. Hildingsson C, Wenngren BI, Bring G, Toolen G (1989) Oculomotor problems after cervical
spine injury. Acta Orthop Scand 60:513–516
5. Shifrin LZ (1991) Bilateral abducens nerve palsy after cervical spine extension injury. A case
report. Spine 16:374–375
6. Jammes JL (1989) Bilateral internuclear ophthalmoplegia due to acute cervical hyperextension
without head trauma. J Clin Neuroophthalmol 9:112–115
7. Lee J, Flynn JT (1985) Bilateral superior oblique palsies. Br J Ophthalmol 69:508–513
8. Hopf HC, Thomke F, Gutman L (1991) Midbrain vs. pontine medial longitudinal fasciculus
lesions: the utilization of masseter and blink refl exes. Muscle Nerve 14:326–330
9. Lutz A (1923) Ueber die Bahnen der Blickwendung und deren Dissocierung. In: Sanders
EACM (ed) Syndromes of the medial longitudinal fasciculus. Klin Monatsbl Augenh 70:
213–235
10. Sanders EACM, De Keizer RJW, Zee DS (1987) Eye movement disorders. MartinusNijhoff/
Dr W Junk, Dordrecht
11. Kommerell G (1975) Internuclear ophthalmoplegia of abduction. Arch Opthalmol 93:
971–980
12. Larmande AM (1969) La para1ysie supranuc1eaire du VI (dite ophta1mop1egie intemu-
cleaireposterieure). Arch d’Ophtalmol 29:521–530
24 Abducting Interocular Ophthalmoplegia After Whiplash Injuries
256
13. Thornke F, Hopf HC, Kramer G (1992) Internuclear ophthalmoplegia of abduction: clinical
and electrophysiological data on the existence of an abduction paresis. J Neurol Neurosurg
Psychiatry 55(2):105–111
14. Cogan DG, Kubik CS, Smith WL (1950) Unilateral internuclear ophthalmoplegia; report of
eight clinical cases with one postmortem study. Arch Ophtalmol 44:783
15. De Keizer RJW, Zee DS (1987) Eye movement disorders. In: Eye Movement Disorders
(Monographs in Ophthalmology) Sanders EACM, De Keizer RJW, Zee DS (eds) Martinus
Nijhoff/Dr W Junk, Dordrecht, p 186
16. Bakheit AM, Behan PO, Melville ID (1991) Bilateral internuclear- ophthalmoplegia as a false
localizing sign. J R Soc Med 84:627–630
17. Sanders EACM (1987) Syndromes of the medial longitudinal fasciculus. In: Sanders EACM,
De Keizer RJW, Zee DS (eds) Eye movement disorders. MartinusNijhoff/Dr W Junk,
Dordrecht, p 183
18. Collard M, Eber AM, Streicher D, Rohmer F (1979) L’ophtalmoplegieintemucleaireposterie
ure-existe- t-elle? A propos de onze observations avec oculographie. Rev Neurol 135:
293–312
19. Treleaven J, Jull G, Grip H (2011) Head eye co-ordination and gaze stability in subjects with
persistent whiplash associated disorders. Man Ther 16(3):252–257
20. Montfoort I, Van Der Geest JN, Slijper HP, De Zeeuw CI, Frens MA (2008) Adaptation of the
cervico- and vestibulo-ocular refl ex in whiplash injury patients. J Neurotrauma 25(6):
687–693
21. Kongsted A, Jørgensen LV, Leboeuf-Yde C, Qerama E, Korsholm L, Bendix T (2008)
Are altered smooth pursuit eye movements related to chronic pain and disability following
whiplash injuries? A prospective trial with one-year follow-up. Clin Rehabil 22(5):469–479
22. Treleaven J, Jull G, LowChoy N (2006) The relationship of cervical joint position error to
balance and eye movement disturbances in persistent whiplash. Man Ther 11(2):99–106
D.C. Alpini et al.
Part IV
Treatment
259
D.C. Alpini et al. (eds.), Whiplash Injuries,
DOI 10.1007/978-88-470-5486-8_25, © Springer-Verlag Italia 2014
25.1 Introduction
The term ‘whiplash’ has been used to describe a mechanism of injury and the
various clinical manifestations as a consequence of the injury. Moreover, signs and
symptoms have been designated the ‘whiplash syndrome’. In 1995, the Quebec
Task Force (QTF) on Whiplash-Associated Disorders (WAD) adopted the following
defi nition of whiplash: ‘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’[ 1 ].
Whiplash patients can be classifi ed according to severity of signs and symptoms.
The QTF-WAD classifi cation system consists of fi ve levels: WAD 0 indicates no
complaints or physical signs; WAD I indicates neck complaints but no physical
signs; WAD II indicates neck complaints and musculoskeletal signs (such as a
decreased range of motion or muscle tenderness); WAD III and IV indicate neck
complaints and neurological signs (WAD III) or fracture/dislocation (WAD IV),
respectively. The most common presenting symptoms following an acute motor
E. A. Pallestrini • E. Castello • G. Garaventa
I Division of Otolaryngology, Head and Neck Surgery,
“San Martino” Hospital, Genoa, Italy
F. Ioppolo (
*)
Department of Physical Medicine and Rehabilitation,
“Sapienza” University, Piazzale Aldo Moro 5,
00185 Rome, Italy
e-mail: francescoioppolo@yahoo.it
F. Di Berardino
Department of Clinical Sciences and Community Health, University of Milan,
Milan , Italy
Audiology Unit, IRCCS “Ca’ Granda” Ospedale Maggiore Policlinico, Milan, Italy
2 5
Pharmacological Treatment of Whiplash-Associated Disorders (WAD)
E. A. Pallestrini, E. Castello, G. Garaventa, F. Ioppolo,
and F. Di Berardino
260
vehicle collision were neck pain (88–100 %) and headache (54–66 %). Other symptoms were neck stiffness, shoulder pain, arm pain/numbness, paraesthesia, weakness, dysphagia, visual and auditory symptoms and dizziness. In most cases, WAD
resolves quickly; 47 % of injured people return to normal activities within 4 weeks,
and only 2 % continue to be absent from pre-accident activities 1 year after injury.
Pharmacological treatment of acute WAD regards especially vertigo, dizziness,
neck pain, headache, nausea and unsteadiness. Vertigo, nausea and cervical pain are
very frequent in the acute and subacute [ 2 ] WADs; unsteadiness and diffuse (not
only cervical) spine pain are very usual in the chronic WADs [ 3 , 4 ].
25.2 Whiplash-Associated Headache and Neck Pain
The main goal of treatment must be to kill the pain in order to avoid processes of
spinal and central sensitisations that may lead to chronic pain [ 5 ].
Paracetamol at the dosage of 1 g three times a day for 7/10 days is the fi rst drug
of choice for pain relief. Paracetamol has to be preferred over other nonsteroidal
anti-infl ammatory (NSAI) drugs, even if it has to be administered at high dosages.
Paracetamol and, in general, NSAI have to be combined with muscle relaxant sub-
stances. They can be divided into: (1) drugs active on CNS (mephenesin, carisoprodol), (2) drugs with spinal actions (baclofen), (3) drugs active on the muscular
system (dantrolene) and (4) drugs active on the different systems (thiocolchicoside). f3-blockers also reduce muscular hypertonicity of cervical spine, and they can
be employed as well as proper muscle relaxant drugs. Paracetamol could be com-
bined with myorelaxants such as tizanidine, a centrally acting α2 adrenergic ago-
nist, used 2–4 mg twice a day for 7/10 days. If dizziness or true vertigo is present,
this drug in not indicated due to its central effects on brainstem and thus on vestibular nuclei. In these cases, it is better to combine paracetamol with low doses of
benzodiazepines (BDZ) like diazepam 5 mg at night time.
In presence of nausea, it is possible to use metoclopramide 10 mg twice a day for
7/10 days. In these cases, L-sulpiride at low dosage (12.5 mg twice or three times a
day) also allows a good control of nausea and dizziness; it also has a mild myorelaxant action.
WAD is considered chronic if pre-accident activity levels are not gained within
6 months. Ongoing cervical pain and reduced range of motion (ROM) associated
with chronic WAD constitute both a prognostic and a therapeutic dilemma. The
location and severity of tissue injury and the prognosis of chronic neck pain may
depend on predisposing neck pathology. In addition to peripheral input, longstanding neck pain (like other chronic pain conditions) may be associated with a
central component that can modify the pain threshold. Considerable research has
been dedicated to determine the direct and indirect roles of the zygapophyseal joints
in the generation of pain and dysfunction in whiplash injury [ 6 ].
Blocking the sensory nerves that innervate these joints reduced symptoms in
50 % of the subjects with chronic whiplash pain. However, this fi nding suggests that
no responders might have been suffering from a pathology related not to the joints
E.A. Pallestrini et al.