Vestibular rehabilitation Bascharage
The semicircular canals detect the amplitude of angular rotation of the head in all three spatial dimensions. The otolith organs are sensitive to the vertical (saccule) or horizontal (utricle) linear acceleration of the head in space, and detect its inclination to gravity.
In addition to vestibular inputs, these nuclei receive visual and proprioceptive inputs. The vestibular nuclei are therefore not simply relays of information from the inner ear, but true centers of sensory-motor integration. Central vestibular neurons then project to the oculomotor nuclei to stabilize gaze, or to the medulla to stabilize posture.
Vestibular rehabilitation
Vestibular rehabilitation is a speciality of physiotherapy that provides relief for patients suffering from pathologies of the vestibular system, including :
- Central Nervous System disorders
- Balance disorders
- Walking disorders
- The inner ear
These various pathologies manifest themselves as sensations of vertigo (rotatory, linear, imbalance or oscillopsia).
In medicine, the term vertigo refers to an illusion of movement, usually rotatory, which can be compared to that experienced after turning rapidly on a merry-go-round, and results from an asymmetry of activity in the left and right vestibular nuclei. In pathology, it reflects a dysfunction of the vestibular system. In everyday language, patients often use the word vertigo to describe any instability. But the term vertigo must be distinguished from the notion of instability (lack of balance). These dizzinesses are usually associated with nausea, vomiting or other falls.
Depending on the pathology diagnosed, the liberatory maneuver will be performed to treat the seizures. The patient will also be given a range of advice and exercises, followed by rehabilitation to prevent relapses.
To better meet your expectations in vestibular physiotherapy, our Pôle Équilibre & Santé practice in Bascharage is equipped with video-nystagmoscopy (a tool for measuring vestibular symmetry or asymmetry). This vestibular instrument is connected to specialized computer software called FramiGest. We have also acquired a rotatory chair in order to carry out the necessary assessments and offer optimal rehabilitation for vertigo and instability.
The main pathologies treated by vestibular physiotherapy are :
- BPPV (Benign Paroxysmal Positional Vertigo)
- Vestibular neuritis (Neuronitis Vestibularis)
- Meniere’s disease
- Balance and gait disorders
BPPV, or Benign Positional Paroxysmal Vertigo, is one of the most common causes of vertigo. It is a good example of paroxysmal inner ear dysfunction.
Posterior canal positional vertigo
Pathophysiology :
The pathophysiology is now well established, and involves pathology of the posterior semicircular canal, itself secondary to damage to the utricular macula. This lesion is characterized by the detachment of otoconia from the utricular macula, which are deposited in the most sloping part of the labyrinthine cavity, i.e. on the ampulla of the posterior canal. This detachment may be traumatic, viral, infectious or degenerative in origin.
Symptoms:
The patient then complains of intense rotatory vertigo related to head movements which presents three particularities:
- It is triggered only when the head changes position in space.
- It is very violent and can cause nausea and vomiting.
- Short duration (less than one minute)
Diagnosis :
The head positions that trigger vertigo are most often those of the head in extension, or when the patient lies down in bed at night, or goes from lying down to sitting up in the morning. This vertigo recurs each time the patient returns his or her head to the same position, but its intensity diminishes, reflecting the patient’s fatigability. Questioning is therefore immediately very evocative. However, only a clinical examination will confirm the diagnosis.
The examination must be performed under VNG. It consists in performing positioning maneuvers. In practice, the patient sits cross-legged on the bed and is quickly moved from the sitting position to the lateral decubitus position on the side that triggers the vertigo, with head in the air and turned at 45°.
After a latency of a few seconds, nystagmus and rotatory vertigo are triggered. After about ten seconds, nystagmus and vertigo stop if the head is held in the same position. Returning to the sitting position again triggers nystagmus, this time beating in the opposite direction, which is also accompanied by a rotatory sensation. Repetition of these maneuvers leads to a gradual reduction in nystagmus and vertigo. Vertigo and nystagmus are therefore tiring.
Diagnosis of vertigo is therefore based on both questioning and clinical examination.
Evolution :
The BPPV attack recurs over a period of 3 weeks to one month. After this period, the attacks fade away, leaving the patient with a feeling of discomfort and, above all, apprehension when returning to the trigger position. Patients often suffer from feelings of instability and drunkenness, often unbearable in everyday life.
Processing :
Treatment depends on the patient’s stage of development. If the patient consults a physiotherapist trained in vestibular rehabilitation, such as your physiotherapist in Bascharage, at the time of an attack or during a relapse, the treatment is based on kinesitherapy maneuvers. Two types of maneuver have proven effective:
- The liberatory maneuver: This involves vigorously mobilizing the patient’s head to displace the cupulo or canalolithiasis. This maneuver often leads to recovery from positional vertigo. It can be repeated in a subsequent session if positional vertigo is still present. If positional vertigo resists two or three well-executed manoeuvres, the practitioner should question the diagnosis of BPPV. Under no circumstances should these maneuvers be repeated iteratively. However, it is not uncommon to see patients in consultation who have undergone more than 10 maneuvers and allege permanent feelings of inebriation.
- Vestibular re-education: This consists of sessions designed to “train” the patient’s inner ear to prevent recurrences.
If the patient is seen at a distance from the crisis, a balance assessment should be performed on the equitest. This will enable us to quantify balance disorders and prescribe effective rehabilitation sessions and medical therapy.
Horizontal canal positional vertigo
This type of positional vertigo is much rarer. It most often occurs not when the patient lies down or gets up, but when he or she turns from side to side in bed.
Diagnosis :
Its diagnosis is clinically based on several types of arguments:
- It is not triggered by lateral decubitus positioning like the posterior canal, but occurs when the subject is placed in a seated position, head bent forward, which places the horizontal canals in a vertical plane.
- Induced nystagmus is horizontal and non-torsional. In this position, the direction of the rapid phase of the nystagmus indicates the diseased side.
- He rarely tires;
- Its onset latency is shorter (less than 5 s) and its duration longer (20 to 60 s).
Processing :
Treatment is based on a slightly different release maneuver: the “barbecue” maneuver.
Vestibular neuritis is a frequent cause of peripheral vertigo. It is a good example of unilateral and abrupt suppression of vestibular information involved in maintaining balance and stabilizing gaze.
Pathophysiology :
The commonly accepted pathophysiology is that of a sudden cessation of vestibular nerve activity.
This is followed by a sudden asymmetry of activity in the central vestibular nuclei on the injured and intact sides. Central vestibular neurons on the neuritis side stop discharging, while contralateral neurons have unchanged or even increased discharge activity due to inhibitory commissural pathways linking certain vestibular nuclei, such as the medial vestibular nuclei. This asymmetry of activity is responsible for rotatory vertigo, spontaneous nystagmus, balance disorders and the nausea and vomiting observed in the acute stage. Gradually, as a result of post-injury plasticity in the central nervous system (CNS), central vestibular neurons on the injured side recover normal discharge activity, while vestibular nerve neurons remain silent. In this way, a new symmetry of activity between the vestibular complexes ipsi and contralateral to the lesion will be recovered. This neuronal recovery will result in the disappearance of the vertiginous attack, spontaneous nystagmus and a return to subnormal balance.
The etiology of the condition appears to be viral. There are three main arguments in its favor:
- Epidemiological context: seasonal or family epidemics, upper respiratory tract infections in the weeks preceding the incident, concomitant cranial polyneuropathy.
- Serological tests show proteinorachy, suggestive of demyelination, or antiviral antibodies. The virus responsible cannot be identified. However, Herpex Simplex virus seems the most likely candidate.
- Histopathological studies of rocks have revealed characteristic viral lesions. Following an initial infection, the virus spreads throughout the body, then remains quiescent in the ganglia of certain cranial nerves, including the vestibular ganglia. In the event of an intercurrent disease, the virus awakens and induces an autoimmune reaction responsible for inflammation, edema and demyelination.
In some cases, a vascular etiology cannot be ruled out, especially in hypertensive subjects or those with a vascular background.
Vestibular neuritis is characterized by the sudden onset of rotatory vertigo associated with nausea and vomiting. Crucially, no auditory signs (deafness, tinnitus) are found on questioning. Given the intensity of the vertigo, it is not uncommon to find the patient in the emergency room.
Examination under videonystagmoscopy reveals spontaneous nystagmus of the peripheral type: it is horizonto-rotatory, unidirectional and reduced in amplitude and frequency during ocular fixation. The rapid phase of this nystagmus is oriented towards the healthy ear. The rest of the examination, in particular the neurological examination, was normal. The evolution is marked by a regression of vestibular symptoms. Within a few days, the rotatory sensation and neurovegetative manifestations will improve. A feeling of imbalance will persist for some time.
Immediate treatment is based on corticosteroids and antivirals. In the aftermath, careful vestibular re-education helps patients to return to normal balance, and the instability they feel disappears.
Once the acute phase is over, treatment is based on energetic mobilization of the patient. The latter is lifted as quickly as possible to promote central vestibular compensation. Gradually, other afferents from the deafferented vestibular nuclei – visual, proprioceptive and contralateral vestibular afferents – will replace the missing vestibular afferents.
Ménière’s disease is a common condition, which can be disabling due to the impact of vertigo on the patient’s professional, family and social life. This syndrome covers a wide range of etiologies, with a highly specific triad of symptoms and a highly capricious course.
Pathophysiology :
The pathophysiology of this condition, first described in 1861 by Prosper Menière, is still debated today. It is likely to result from abnormalities in the functioning of endolymph resorption mechanisms, particularly those located in the endolymphatic sac. The result is endolymphatic hydrops, i.e. distension of the membranous labyrinth, the histopathological hallmark of the disease.
The characteristic features of the disease, namely the onset of vertigo and deafness, seem to be caused either by rupture of the labyrinth as a result of pressure jolts, or by these jolts themselves occurring on elastic membranous walls, in which case rupture is only secondary.
A second set of hypotheses involves physical concepts. The vertiginous attack results from endolymphatic hyperpressure linked to the progressive accumulation of endolymph in an elastic compartment. It is thought to modify the mobility of the stereocilia of the ampullary ridges and otolith macules, resulting in reduced excitability of sensory cells on the diseased side. It also causes ampullopic fluid movements, spreading from the narrowest cavities (those of the semicircular canals) to the widest cavities (utricular and saccular).
Symptoms:
- Tumarkin’s otolith catastrophe: this clinical form is characterized by violent, unpredictable, linear forward or backward thrusts that throw the patient to the ground. They occur more frequently in advanced forms of the disease. They are thought to be due to abrupt distension of the otolith membrane and acute deafferentation of the otolith system. Given the potential severity of these falls, the recommended treatment is radical surgery (vestibular neurotomy).
- Lermoyez’s vertigo or the vertigo that makes you hear: This clinical form, first described in 1919, is characterized by a transient improvement in deafness during an acute attack of vertigo. It is thought to be a chronological and temporary variant of Ménière’s disease.
Diagnosis :
- Onset of severe rotatory vertigo requiring bed rest, accompanied by intense neurovegetative signs: nausea, vomiting, sweating, diarrhea. The dizziness lasts 2 to 3 hours, leaving the patient exhausted. At the end of the attack, the patient may feel inebriated.
- Concomitant presence of unilateral auditory signs:
- Tinnitus producing a non-pulsating buzzing, hissing or whirring sensation.
- A perceptive-type deafness which, in the early stages of development, predominates in the low frequencies and shows wide fluctuations. It is often associated with an impression of a blocked ear, fullness or pressure, which regresses after the acute attack. Over time, deafness worsens, affecting all frequencies and stabilizing at a loss of 50 to 70dB. This hypoacusis is accompanied by endocochlear signs: impaired discrimination, intolerance to loud sounds, diplacousia and sound distortion.
- Terrain: patients often present a particular psychological context, including stress, anxiety, fatigue and emotional shocks. These patients are usually perfectionists, intelligent and obsessive.
- Progression of the disease: it is capricious. The frequency of vertiginous attacks is unpredictable and varies from patient to patient. It can vary from one to two attacks per week or month, or may occur only once a year or every two years.
Evolution :
Over time, the characteristics of the attack change: the vertigo becomes less violent and the rotating sensation is replaced by sensations of drunkenness, rolling and pitching. Cochlear signs may not be observed at first, or may remain isolated for some time.
Processing :
Treatment of vertiginous attacks is based on isolation and the administration of an antivertiginous, sedative and/or antiemetic medication. Background treatment is aimed at preventing recurrence of vertigo. It is subdivided into conservative or destructive, medical or surgical treatments, depending on whether they preserve or destroy vestibular function on the diseased side.
When medication is not sufficiently effective, sufferers can undergo vestibular rehabilitation. This is a physiotherapy specialty for people suffering from vertigo, dizziness and balance disorders caused by an anomaly of the vestibular apparatus. This re-education is supervised by a team specialized in balance disorders, working in collaboration with ear, nose and throat (ENT) specialists. Various exercises can be performed, using a rotating chair, eye movement devices, a trampoline, or special glasses (called Frenzel or videonystagmos-copy) to observe eye movements.
These exercises re-educate balance by reinforcing the complementary mechanisms normally involved in balance to compensate for the vestibular damage caused by Menière’s disease.
Balance depends on the integration of three types of sensory information: vestibular inputs, proprioceptive inputs and visual inputs. This sensory information is processed in the vestibular nuclei, the thalamus and various cortical areas. There is a redundancy of different sensory information at each level of the central nervous system, from the brain stem to the cortex, to promote balance during head and body movements in space.
This is achieved through a variety of habituation, substitution or sensory illusion procedures, using a combination of physical exercises and/or instrumental maneuvers such as rotating chairs, oculomotricity ramps, optokinetic target generators, posturology platforms, etc. According to the literature, the average duration of a vestibular rehabilitation program ranges from 4 to 10 weeks.
In senior patients suffering from instability, vestibular rehabilitation considerably reduces complaints and prevents falls, which are the second leading cause of death after stroke.