CRANIO-CERVICAL TRAUMATOLOGY AND VERTIGO - UniTBv
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Bulletin of the Transilvania University of Braşov
Series VI: Medical Sciences • Vol. 12 (61) No. 1 – 2019
https://doi.org/10.31926/but.ms.2019.61.12.1.5
CRANIO-CERVICAL TRAUMATOLOGY
AND VERTIGO
L.G. MĂRCEANU 1* E. BOBESCU1, 2
Abstract: The traumatic pathology of the head and neck is often
associated with peripheral or central vertiginous manifestations. These are
due either to direct or indirect traumatic damage of the temporal bones -
the labyrinth's place - (involving direct damage to the middle or inner ear,
or by affecting the cervical vascularization or the osteo-muscular skeleton
of the cervical area. The secondary psychopathological reactions
associated with this type of traumatology may also be the secondary
source of vertigo. This article reviews the clinical forms of vertigo that may
occur as an immediate or delayed consequence of cervical and cranial
traumatic pathology, with their particular diagnostic and modalities of
therapy.
Key words: cranio-cervical traumatology, vertigo, diagnosis
1. Introduction broad groups: one clinical forms with
onset of immediate vertigo (less than 24
The traumatic pathology of the head hours) and disorders causing vertigo with
and neck is frequently associated with relatively late onset, (after at least 24
peripheral, central and / or mixed hours). In this second group, the
vertiginous manifestations, due to either vertiginous manifestations that occur late
direct injury to cerebral parenchyma and after the acute CCT episode, include
/ or skull bones (the temporal bones are some pathological processes whose signs
the labyrinth's center) or consequences settle slowly, few weeks after the trauma
of complex cervical lesions with the [15], [11], [22].
interest of regional cervical blood vessels. IMMEDIATE VERTIGO: Paroxysmal
The vertigo occurring in the context of benign positional vertigo (VPPB),
cranio-cervical traumatology (CCT), and labyrinth contusion, Temporal bone
can be classified, by the onset, into two fracture, Perilimphatic fistula /
1 Department of Medical and Surgical Specialties,
Faculty of Medicine, “Transilvania” University, Brasov, Romania;
2 Departmentof Cardiology, Clinic County Emergency Hospital Brasov.
* Corresponding author: luigi-geo.marceanu@unitbv.ro10 Bulletin of the Transilvania University of Braşov. Series VI • Vol. 12 (61) No.1 - 2019
Semicircular channels dehiscence, and auditory manifestations. The diagnosis
rupture of round window membrane. resides through the reproduction of
LATE VERTIGO: post-traumatic symptomatology by the classic Dix
labyrinthitis, post-traumatic inner ear Halpike and Roll Test maneuvers, which
hydrops, cervicogenic "vertigo" and indicate the typical and asymmetrical
cervical vessel damage (after WHIPLASH), affection of several semicircular
post-traumatic vestibular epilepsy, post- channels, sometimes bilateral
traumatic migraine, vertigo from involvement. They are resistant to
posttraumatic intracranial hematoma and treatment, require repeated classical
diffuse axonal lesions, post- CCT otolithic repositioning maneuvers,
psychogenic vertigo (the old “sd.post- depending on the affected channel
concussion”) [14], [22]. (Epley, Semont, BBQ etc), and sometimes
the reeducation of residual instability due
2. Main Clinical Forms to remanent secondary otolithic sd. (by
vestibular kinetic therapy and cerebral
In these cases, vertigo occurs in compensatory medication), [2], [15], [18],
relationship and after CCT, in a patient [22].
who has not had any previous balance
disorder of this type. In this context, the 2.2. Vertigo from traumas of temporal
following pathological entities can be bones and its complications:
described in the order of frequency of
occurrence: Labyrinth contusions: it is manifested
by a reversible fluctuation of the ear-ear
2.1. Post-traumatic benign postural vestibular function. Common, even after
traumatic vertigo minor CCT, is generated by spasm and
microhaemorrhage in the labyrinth bone.
These are the most common forms of Changes are only functional, auditory and
post-traumatic vertigo (occurring in over vestibular, usually unilateral (non-
28% of CCT) [16]. It is due to the persistent sensorineural and / or
traumatic detachment of the macula unilateral hearing loss), successive to a
otholites and their possible migration recent CCT. Treatment consists of
into the semicircular channels. It usually instrumental surveillance, cochlear
occurs in the first 24 hours after CCT, but vasodilators, corticoids, non-ototoxic
onset may sometimes delayed 5-10 days. broad spectrum antibiotics (if there are
It is manifested by the appearance of also infected cranio-facial lesions).
vertigo with nystagmus at sudden Classically, there are no detectable bone
changes of the head position. The access lesions, there are actually lesions of
time is short (up to 30 seconds), stops at vestibular sensory neuroepithelial or
rest, repeats frequently during a day, for cochlear (isolated or associated, in
weeks, often accompanies by vegetative varying degrees and complexities).
manifestations, but without associated Labyrinth contusion may also be
produced by cranial fractures, but not ofL.G. MĂRCEANU et al.: Cranio-cervical Traumatology and Vertigo 11 labyrinth, or other CCT, without line of the injured labyrinth (acute serous or fracture (Cranial transversal-oblique bacterial labyrinthitis are common), but cranial fractures, which penetrate the in a normal evolution the vertiginous temporal rock perpendicular, produce manifestations tend to spontaneously major inner ear lesions (hemorrhagic regress. The ap-pearance of central intralabirinthyc lesions, especially of the cerebral compensation (manifested by membranous labyrinth, communications the disappearance of spontaneous with subarachnoid and lymphatic spaces nystagmus) is all the more rapid since the and pneumolabirinth). Other CCT may destruction of the labyrinth was more interest the inner ear by accidental complete, and as the individual is penetration (crossing the middle ear), younger or his bed mobilization is earlier, which also leads to its destruction. and the central neurological lesions are Symptomatology: destructive less severe [2], [19]. Treatment is usually peripheral vestibular syndrome (violent conservative. Prophylactic antibiotics are vertigo with nausea and vomiting, axial administered for about 4 weeks. and segmental deviations, spontaneous Miringototomy and insertion of a horizon-rotating nistagmus to the healthy eardrum ventilation tube may be part) along with classical otoscopic signs indicated, especially for serous otitis, (othoragia, cerebrospinal leakage, which persists after one month [2], [22]. haemotympanum, neurosensoryal or Vestibular therapy: Spontaneous mixed hearing loss, lesions of external installation of the central compensation auditory chanel) occurring in CCT context. phenomenon is usually expected (in Important: In a patient with CCT and about 2-4 weeks the patient becomes encephalic damages, spontaneous asymptomatic). If the vertiginous nystagmus occurs only if its con- manifestations persist, it shows that sciousness is partially preserved. In the there are functional relicvates of the superficial coma there is only the slow injured vestibule, which blocks the phase of nistagmatic beats, and in the installation of the central compensation. case of a deep come, spontaneous Labyrinthtotomy can be solution nystagmus will be absent. Investigating (which complements the incomplete the presence of nystagmus in a comatose destruction of the labyrinth) or unilateral is done by practicing the cold heat vestibular neurotomy. Take into account stimulation manoevra, with water at 4 C of the surgical decision, the actual degree (Frazer technique). Water is totally of dis-ability caused by vertigo and the contraindicated in the case of lesions of state of the hearing function (a normal the eardrum or CAE, and using high- cochlea denied a surgical labyrinth resolution temporal bone CT, cerebral destruction) [2], [15], [22]. MRI, and classical cochleovestibular Infection of the bone (acute investigations transcend the diagnosis. labyrinthitis) can occur by otogenic origin Evolution: It is dominated by the or meningogenic. In the initial serous prognosis of neurological lesions and the phase, can use corticoids and possibility of microbial superinfection of vasodilators, and the evolution towards
12 Bulletin of the Transilvania University of Braşov. Series VI • Vol. 12 (61) No.1 - 2019
purulent form attracts the surgical otolithic manifestations. Thus
decision under the cover of antibiotics manifestations such as vertigo (rotary
[2], [10]. sensations) and linear motion sensations
The chronicisation of the labyrinthytis with instability are triggered by position
(especially the otogenic variant) is often changes, CAE pressure, Valsalva
associated with the ossification of the maneuver, or strong sounds (Tullio
membrane labyrinth with the subsequent phenomenon). Considering the fluid
appearance of the signs of the post CCT communication with the cochlear
inner ear otic hydrops. The mechanism is compartment, there is also a fluctuating
by scar, typical after severe damage to “positional” hypoacusias (ascertained by
the membrane labyrinth and appears late the Frazer positional audiometry test). It
(after years). It seems to be predisposed describes the positive sign of the fistula
to those, all with Sd of broad vestibular (when the digital CAE pressure closure on
aqueduct - preexisting [3]. Treatment: it the same side as FP produces vertigo and
is common to the Meniere sd. [14] nystagmus), which unfortunately is rarely
found in daily practice. Diagnosis is
2.3. Vertigo in post-traumatic perilim- difficult, requires high resolution CT and
phatic fistula: if FP is very symptomatic, a possible
middle ear surgery will be followed by FP
Perilimphatic Fistula (FP) is a plugging.
posttraumatic dehiscence at the site of Evolution: some FPs spontaneously
round or oval windows or a labyrinthic cured in about 6-12 months, but only in
semicircular canal through which a the mucosa part, the subjacent bony
communication between the remaines beant; some may become
perilimphatic fluid compartment of the infected (evolution to suppurative
inner ear and the middle ear is made. FP labyrinthitis and meningitis in repetition).
is a functional, transient and recurrent These require traceability and
vestibular dysfunction. prophylactic antibiotic treatment in any
FP may occur after a hyper or possible new otitic or IACRS episode.
hypopressive bruise transmitted to the Paroxysmal vertigo can continue months
vestibule, either from the cerebrospinal and years after CCT, while cochlear
space (“explosive type"), or from the function also degrades. In this case the
outside, via the Eustache tube treatment is surgical by plugging the
(“implosive type”) during a blast, scarlet bone of FP.
or even cough or strong sneezing The Tullio phenomenon may occur in
(“microtraumatism”). posttraumatic circumstances that lead to
Symptomatology: FP produces inner the appearance of a FP, or which lead to
ear fluids disturbances and intra- an abnormal anatomical continuity
labirinthic pressure, with abnormal between the middle ear and the otolithic
stimulation of the vestibular macula and macula. It is manifested by vertigo
cupulas, resulting in either canallith or triggered by intense low-frequency
sounds (otolithic stimuli). Patients accuseL.G. MĂRCEANU et al.: Cranio-cervical Traumatology and Vertigo 13
are vertigo, body instability, and contact with cerebral hemispheres).
oscilopsies when passing trucks, Diagnosis requires skull TC, MRI and
compressors, etc. (when low-frequency neurosurgery exam, the treatment
sounds are transmitted directly to consisting of emergency evacuation of
otolithic zones). the hematoma, especially if the patient
Treatment is again the cause of the also has consciousness disorders. In the
Tullio phenomenon (ie FP plugging or absence of these, temporary treatment
restoration of the modified bone chain of with cortisone may favor spontaneous
middle ear) [2], [8], [14]. resorption of the hematoma [2], [14],
[22].
2.4. Vertigo in post-traumatic Pure deceleration forces can cause
intracranial hematoma and brain diffuse axonal lesions [14].
diffuse axonal lesions Mechanism: small areas of bleeding
(petechial haemorrhage) and disruption
The cerebral traumatic context is not of neuronal circuits (axonal lesions).
always obvious, especially since it may Significant effects of these diffuse
take several weeks or months to install microlesions do not occur in patients
the intracranial hematoma. After a CCT, with CCT who have reported no loss of
the intracranial hematoma can develop consciousness. A loss of consciousness of
either on the brain surface, extracerebral at least 30 minutes seems to be
(with extradural variants - directly under necessary for a significant effect
the cranial axis with rapid or subdural associated with this type of cerebral
evolution - in contact with the brain, lesion [1]. Diagnosis necessarily requires
after a few weeks) or intracerebral. angio- MRI.
The subdural hematoma can thus be
installed by performing the shape of the 2.5. Cervical vertigo (most frequent form
chronically subdural hematoma. Its after "WHIPLASH” mechanism):
favorable factors are represented by the
presence of coagulation changes (chronic Vertigo in “cervical whiplash”:
anticoagulant therapy, chronic The notion of "cervical vertigo" is quite
consumption of aspirin or other NSAIDs, confusing. It is now accepted that only a
alcoholism, chronic hepatopathy, clear and strong cervical spine injury at
hematopoiesis, etc.) and minor skull the level of cervical proprioceptors may
injuries [6]. be a possible cause of vertigo. CCT must
Symptomatology: Elderly patients with produce a real "sensory conflict" by
the above-mentioned pathology, vertigo, producing an abnormality of cervical
and chronic late-onset headache with a posture, which later -through cervical
tendency to fall backwards in the proprioceptors -will send new sensory
Romberg axial manoevra-can predict information that “contradicts” normal
cerebellum haemorrhage (or hematom), vestibular or visual information,
and with lateral fall (hematoma in generating the “vertigo” sensation. In14 Bulletin of the Transilvania University of Braşov. Series VI • Vol. 12 (61) No.1 - 2019
fact, the sensation is not vertigo, but the cervical spine C1 - C4 (with pain in the
“imbalance” That occurs always after palpation of spiny apophyses, painful
major cervical trauma, never minor one! limitation of cervical movements, etc.)
[7, 8]. the existence of strong cervical
The notion of "cervical whiplash" pathology: fracture or dilation of the
describes the damage to the neck that cervical column, muscle elongation,
followed a brutal "back" recent local surgery, recent port of
hit/collision. Mechanisms involved in the cervical minerva.
generation of post-Whiplash lesions: positive cervical imaging balance for
damage caused by severe neck osteoarticular lesion in the area (CT,
hyperextension - rupture of the anterior cervical column MRI, etc.)
longitudinal ligament, muscle Prognosis: Cervical stiffness can persist
haemorrhage and disc rupture and bulge, in 20-45% of patients. Dizziness
and occasionally even brain damage [14]. associated with whiplash occurs at 20-
Visual disturbances, as well as internal 60% and can persist for years, 75% of
ear disturbances, are classically patients are recovered for up to 1 year
attributed to vertebrobasilar artery [12], [17].
injury. The vertebral arteries can be Aspects of vertigo in post-traumatic
damaged by vertebral movement or dissection of cervical vessels:
elongation of the vertebral arteries. The Dissection of a cervical vessel is not an
origin of these sensations is probable, exceptional event in cervical
knowing the role of postural reflexes with traumatology. Following this
origin in cervical muscles, which are phenomenon, a cavity containing blood
transmitted through spinovestibular and thrombi is formed inside the wall of a
paths and contribute to stabilizing the damaged cervical artery. Coagulations
eye. It is therefore admitted that can either produce a complete
vertebral osteoarticular lesions or obstruction of the respective cervical
cervical muscles can trigger abnormal artery, or they can be trained as emboli,
proprioceptive inflows that arrive in the to the cerebral hemispheres (through the
cerebral trunk are the origin of a genuine internal carotid artery) or to the cerebral
sensory conflict, producing pseudo- or cerebral trunk (through the vertebral
vertigo sensations. It has been shown artery). In both cases, these processes
that nuchal lesions can produce true cause strokes. Any preexisting vascular
visual illusions of movement [7], [12]. So comorbidities are an unfavorable
Clinical Whiplash is similar to the old prognostic factor [6].
“postconccusive syndrome of CCT” but to Symptomatology: The traumatized
the neck. The clinical diagnostic criteria patient has a laterocervical pain, on the
required to associate vertigo with cervical side of the injured artery, Claudius
post-traumatic affections, and include Bernard Horner's omolateral syndrome,
[14], [22]: along with the neurological signs of the
vertigo should be associated with brain damaged by the cerebral accident
clinical signs of suffering of the highL.G. MĂRCEANU et al.: Cranio-cervical Traumatology and Vertigo 15
(including vertigo). Diagnosis is syndrome appear to be found in minimal,
determined by echographic hard or even undetectable intracerebral
examinations, Doppler of the neck, lesions through current investigation
arteriography, cervical and cranial CT. methods. Patient symptomatology
Emergency treatment is medical and associates unsystematic equilibrium
consists of control of coagulation, rest in disorders associated with emotional
bad, and treatment of stroke. disturbances occurring in post-traumatic
Evolution of arterial lesions is followed context. The treatment addresses the
by periodic Doppler examinations; total emotional, anxious and depressive
reparations occurs between 3 and 6 context, joining a typical anti-migraine
months [12], [14], [21]. treatment for headache, psychotherapy,
antidepressants, sedatives, and cervical
2.6. Post- CCT psychogenic vertigo in physiotherapeutic procedures [1].
post-traumatic intracranial Post-traumatic stress disorder (PTSD):
hematoma and diffuse axonal can determine the re-examination of CCT
lesions and vertigo [9], [14].
"Malingering" vertigo: the so-called
They include several forms of clinical "money issue" was noted, - especially for
treatment that the psychiatrist is people with head trauma, - when
responsible for: "disability" is partially correlated with the
"Factitious vertigo": or the adoption of financial incentive targeted as harm, it
the "role" of the ill persone (occurs by was found that applicants /
"vertigo" accusations after a CCT, in fact, compensation / damages recipients
people need to be in the spotlight - the report the incidence and severity of the
respondents have an unconscious need symptoms being "significantly higher"
for increased affection). than those who were not seeking or not
Psychogenic vertigo: it is directly receiving financial compensation [4],
related to psychological causes, such as [19].
depression, anxiety. Anxiety and
depression can result from traumatic 2.7. Post-traumatic Migraine
brain injuries that create a self-
perpetuating psychological reaction. It is It occurs in about 41% of CCTs.
a frequent consequence of CCT, even Associates dizziness (non-vertigo) with
benign, manifested by a subjective headache, difficult to distinguish from
syndrome that includes: instability, anxiety or tension headache [5].
capricious headache, and various Sometimes a true MAV (vertigo-migraine)
neurovegetative signs. The characteristic is formed. Respond to classic migraine
of this syndrome is that the clinical and (triptans) and BETAHISTINUM cochlear-
paraclinically examinations show the vestibular vasodilators if signs of
absence of cerebral or vestibular organic migraine vertigo (European Consensus
abnormalities. The causes of this 2016 ROMA) [12-14].16 Bulletin of the Transilvania University of Braşov. Series VI • Vol. 12 (61) No.1 - 2019
structures are affected; in the possible
2.8. Post CCT epileptic vertigo case of non-participation of the patient
(coma), the anatomical and functional
It is due to temporal lobe cerebral evaluation of the vestibular acoustic
lesions (processing the vestibular signals), organ is necessary for the purpose of
vertigo is accompanied by altered early therapy, differential diagnosis and
consciousness [23]. Typical symptom is for the aim of medico-legal evaluation.
"rapid rotation," followed by alteration of Therefore, the emergency care of these
consciousness, but this symptom has cases requires modern paraclinical
other causes potentially more frequent examinations: auditory evoked potential,
potentials (requires differential diagnosis stapedial reflex, computerized
with VPPB). Treatment is neurological: electronystagmography (ENG test),
anticonvulsant [23, 24]. videonystagmography (VNG test) and
other vestibular function tests, possible
3. Conclusions only in over-specialized medical centers.
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