The Treatment Diagnosis

, Antonio Cesarani² and Guido Brugnoni³

(1)

“Don Carlo Gnocchi” Foundation, Milano, Italy

(2)

UOC Audiologia Dip. Scienze Cliniche e Comunità, Università degli Studi di Milano, Milano, Italy

(3)

Istituto Auxologico Italiano, Milano, Italy

Abstract

This chapter is aimed to provide those who plan rehabilitation (usually a medical doctor) or perform rehabilitation (usually a physiotherapist), the minimal clinical elements necessary to prepare both a customized rehab planning and eventual modifications of the planned treatment. In fact, the protocols we propose in the following chapters are based on some common aspects of the considered diseases, but it is well known that rehab has to be as customized as possible.

Treatment diagnosis is specifically aimed to prepare a pharmaco-rehab plan. Instrumental tests may be useful to refine the diagnosis but not strictly necessary. Furthermore, it is a specific choice of the authors to highlight clinical (also called bedside) tests to allow vertigo and dizziness rehab as cost-effective as possible.

3.1 Introduction

This chapter is aimed to provide those who plan rehabilitation (usually a medical doctor) or perform rehabilitation (usually a physiotherapist) the minimal clinical elements necessary to prepare both a customized rehab planning and eventual modifications of the planned treatment. In fact, the protocols we propose in the following chapters are based on some common aspects of the considered diseases, but it is well known that rehab has to be as customized as possible.

Furthermore, it is also possible that the patient is evolved, or involved, during the time between rehabilitation planning and beginning of treatment. Spontaneous or drug-induced evo-involution may be sometimes predictable, sometimes not; thus it is necessary that both the doctor and the physiotherapist have a common clinical approach to the patient in order to ameliorate doctor–patient–physiotherapist communication and, consequently, the treatment of the patient itself.

In the previous chapter, we highlighted the difference between lesion, impairment and disability. Thus, the evaluation of the patient needs to identify the combination of these three aspects in each patient. Clinical tests are used to prepare the so-called treatment diagnosis. This kind of diagnosis is different from etiologic or pathogenetic diagnosis. They have to be formulated before rehab proposal, and this kind of diagnosis is not in the scope of this book, and for them we suggest specific papers [1–4].

Treatment diagnosis is specifically aimed to prepare a pharmaco-rehab plan. Instrumental tests may be useful to refine the treatment diagnosis but not strictly necessary. Furthermore, it is a specific choice of the authors to highlight clinical (also called bedside) tests to allow vertigo and dizziness rehab as cost-effective as possible.

3.2 Case History

Case history is often the key of a correct medical diagnosis and an effective rehab.

The first diagnostic task is to differentiate between vertigo and dizziness or unsteadiness (VDU), ruling out the many varieties of specific dizziness.

Generally speaking, VDU is the awareness of some dysfunction in the balance mechanisms, that is, a dysfunction in the balance mechanisms becomes a conscious experience. The sensation is characterized by feelings of “spatial disorientation”, whereof the illusion of false movement is the most characteristic. According to Bisdorff et al. [5], the following descriptions can be transposed into the corresponding medical terms:

Vertigo: “a feeling that things are spinning or moving around”
Dizziness: “a feeling of being light-headed, ‘swimmy’or giddy”
Unsteadiness: “feeling unsteady, about to lose balance”

Vertigo is strictly linked with a spinning sensation around the head. The basic impression is the sensation of loss of stable subjective relationship with the environment. In this way less typical sensations must be included and are called “atypical” vertigo. On the other hand, syncopes, blackout, drop attacks, odd sensations in the head, etc. have to be denied as primary “vertigo” sensations, but they can accompany true vertigo. Vertigo is very similar to what is experienced on a carrousel.

Dizziness may result from disturbances of integrating structures within the central nervous system. Dizziness is sometimes confused with unsteadiness and the term is often used popularly. It includes a multitude of symptoms related to the vestibular system or other aspects of the nervous system. Dizziness may be applied to physical, emotional or intellectual disturbances, which common denominators are the sensation of loss of stability and a disruption of the pattern in which the individual is aware of her/his surrounding and its relationship to her/him, whether these refer to her/his physical orientation in space, her/his emotional equilibrium or intellectual clarity. Dizziness is very similar to what is experienced on a boat or when drunk.

Both vertigo and dizziness may be spontaneous or provoked by movement of the head and/or the body, thus presenting as acute sudden unpredictable attacks.

Unsteadiness is the awareness that movement such as capability to maintain the desired steady gait or high-energy movement is not performed correctly. Unsteadiness is strictly correlated to dynamic interaction with the environment.

While patients may feel vertigo or dizziness even if lying supine or sitting, unsteadiness is perceived when walking, frequently out of one’s own home [6].

Spontaneous Vertigo and Dizziness attacks cannot be treated by means of rehab.

In rehab planning, it is important to pay particular attention also to the following aspects:

Vertigo or dizziness or unsteadiness. It is important to note which is the main symptom or if there is a particular and/or recurrent sequence between vertigo/dizziness and unsteadiness. For example, after a whiplash injury, dizziness appears when the patient removes the collar performing normal activities, while vertigo appears during rotation or backward and forward movement of the head and unsteadiness accompanies daily life movements. In vestibular neuritis, spontaneous vertigo is the onset symptom but chronic dizziness and unsteadiness lead to functional impairment and/or to disability.
Onset of the symptoms, e.g. immediately after a whiplash, or the day after, or when collar is removed, or after a cervical physiotherapy session, in the morning rather than in the evening, etc.
Direction of vertigo rotation or the side of prevalent unsteadiness.
Remission/provocation with particular position of the head/neck.
Combination with spine pain and stiffness, with brachial paraesthesias, with neurovegetative symptoms such as nausea and vomiting, with cognitive symptoms such as amnesia and attention disturbances and with auditory symptoms such as hearing loss and tinnitus.
Loss of consciousness associated with spontaneous or provoked vertigo/dizziness.
Headache and/or migraine immediately after vertigo attack or in the following days/weeks/months.
Temporal distance between any first medical visit and symptom onset.
Temporal onset of each symptom and reciprocal combination.
Frequency of spontaneous attacks.
Intensity that can be quantified on a decimal Visual Analogue Scale (VAS).
Duration: continuing, sub-continuing, transient and recurrent.
Temporal correlation with hearing disturbances: no hearing disturbances, hearing symptoms before, during, after vertigo attacks, etc.

During anamnesis the modality by which the patient tells her/his own history can suggest to the clinician some other characteristics, such as anxiety, restlessness or depression. Sometimes specific psychometric scales can be used, but they are generally boring and not well accepted by the subject. During anamnesis the examiner can, if necessary, simply evaluate attention disturbances with easy temporal orientation (number of the present day, etc.), cultural (name of the popes, etc.), memory (series of numbers, etc.) and logic reversal ability tasks.

Minimal case history information to be collected

Onset main symptom (vertigo dizziness or unsteadiness)

Main symptom at the moment of the rehab planning and the beginning of rehab

Symptoms to be spontaneous or provoked

3.3 Clinical Examination

In the previous chapter, we showed that human balance control is mainly based on orientation and coordination control:

1.a Body segments orientation
1.b Orientation with respect to the environment
2.a Coordination of the environment exploration (mainly through oculomotion and visual field stabilization)
2.b Coordination of the navigation into the environment

Orientation and coordination are the complex, dynamic, instant-by-instant interaction of:

Visual field stabilization, through head-to-trunk stabilization and the so-called Balance Ocular Reflex (BOR)

Antigravity static (posture) or dynamic (gait) control through the so-called Balance Spinal Reflex (BSR)

Due to the same lesion, in each specific patient, these aspects of balance control may be differently impaired and leading, or not, to specific disabilities. Thus it is necessary for each patient to collect specific information about these different aspects.

According to the MCS model, clinical examination may start evaluating the basic elements (M) of the balance control, then investigating main balance functions (C) and, at least, documenting aspects connected with cognition and behaviour (S).

3.3.1 Eye Movements

In clinical practice, the investigator is in front of the patient. First, the examiner lifts suddenly her/his right thumb in front of the patient (at about 50 cm from his eyes) asking her/him to fixate it without moving her/his head, then the examiner lifts the left then the right and continues lifting alternatively as the patient continues fixating on them producing saccadic eye movements. The most important features that can be noted are the latency of the eye movements and their conjugation. Also dysmetrias can be revealed because sometimes patients are not able to fixate the thumb with only one saccade but they require adjustments of the eye movements.

Then the examiner asks to the patient to fixate on his right thumb placed at 50 cm from the patient’s eyes, during a slow continuing to-and-fro movement. In this case a smooth pursuit can be elicited. The most important feature that can be noted is the regularity of the movement that must be continuous and harmonic.

3.3.2 Vestibulo-ocular Reflex

The connections of the inner ear semicircular canals to the extraocular muscle nuclei permits the vestibulo-ocular reflex (VOR). The semicircular canals comprise three pairs of accelerometers arranged roughly in three orthogonal planes, one set on each side of the head. In humans and other erect primates, the vertical canals are large compared with those in quadrupeds, a point of some relevance in that we have greater ability to assess the horizontal than the vertical canals. Whereas the adequate stimulus is acceleration, because of the nature of the flow of fluids through narrow tubes of large radius of curvature, VIII cranial nerve carries velocity (first integral) information to the vestibular nuclei. Further integration to position occurs at a central level and this information is fed to various motor nuclei in the brainstem and cord as well as to the cerebellum and cerebral cortex.

VOR functions in three cardinal planes. Stimulation or inhibition of complementary pairs of canals results in appropriate movement of the eyes ensuring adequate foveation during head movement. The system has a wide dynamic range sufficient to stabilize a retinal image on the fovea through most movements. This is necessary as the only other oculomotor mechanism available for image stabilization is the pursuit and optokinetic system, which functions poorly above 1 Hz.

Measures of the function of individual semicircular canals are invaluable for diagnosing peripheral vestibular loss, such as superior or inferior vestibular neuritis. At present measurement of semicircular canal function relies on measures of horizontal semicircular canal responses to caloric or rotational stimulation. At the bedside, the eye movement response to brief, unpredictable, passive, horizontal head rotations (called head impulses) is an important clinical indicator of the functional state of the horizontal semicircular canals. According to the so-called Halmagyi test named also head impulse test or head thrust test, HIT or HTT) [7–10], the examiner places one hand on top of the head, the other beneath the chin, and for each impulse, moves the head abruptly through a small angle up or down (about 10–20°) with unpredictable timing, while the person attempts to maintain fixation on the earth-fixed target (usually the nose of the examiner). Changing the direction of the head movement, from horizontal to vertical, is possible to selectively activate vertical canals. Patients with bilateral loss of semicircular canal function show loss of all vertical canal responses, as well as loss of horizontal canal responses. Patients with complete unilateral loss of vestibular function, e.g. after surgery for vestibular schwannoma, show reduced or absent responses for the affected anterior, posterior and horizontal canals, leaving the responses of the healthy vertical and horizontal canals a little affected.

Otolith–ocular reflexes may be investigated by means of a modified Halmagyi test using a brisk but small translational impulse of the head. This procedure is called head heave test (HHT) [11].

One of the cardinal signs of abnormal vestibular function is nystagmus. Nystagmus (ny) is a biphasic involuntary movement of both eyes (generally) and it is constituted by a slow displacement of the eyes in a direction (slow phase of nystagmus) followed by a rapid return of the eyes in the primary position of the gaze. Nystagmus is classified as follows:

Spontaneous nystagmus. It is present without any provocative manoeuvre. Vestibular nystagmus is caused by an imbalance between the paired vestibular structures. The nystagmus is called first degree if present only when gaze is directed toward the fast phase, second degree if present in the primary position or third degree if present when the eyes are deviated in the direction of the slow phase. Removal of fixation typically enhances the nystagmus if the lesion is peripheral and the eyes drift markedly toward the deranged side (fast phase toward the healthy side). This can be seen clinically with Frenzel’s glasses that have high dioptre convergence lenses which allow a magnified view of the eyes of the patient, without the patient being able to fixate due to the blur produced by the lenses.

Gaze–evoked nystagmus. It is elicited by eccentric position of the eyes that the patient has to maintain for at least 20 s. When bilateral, it is usually a sign of central disorders due to a deficit of the central gaze neural integrator localized in the medial vestibular nucleus and in the prepositus hypoglossi nucleus.

Positional nystagmus. Nystagmus may readily be induced or, if already present, modified by changes in position of the head. The conventional method is the Hallpike manoeuvre [12]. In this, the patient sits on a couch and the examiner firmly grasps the head which is turned 60° toward one shoulder. The patient is instructed to keep the eyes open and to fixate the examiner’s forehead. The patient’s head is rapidly lowered below the level of the couch and the eyes observed for any nystagmus. After an interval of 30 s, if nystagmus is not found, or after the nystagmus ceases, the patient is returned to sitting position. Again, any nystagmus is normally noted. The test is repeated if nystagmus is found to see if there is any adaptation. After this, the test is performed with the opposite ear dependent. The variables noted are latency to onset of nystagmus, its duration and adaptation, its direction and, finally, associated symptoms. If any nystagmus is found after the Hallpike manoeuvre, nystagmus has to be investigated in the supine position, in head-hanging position and with brisk turning of the head to one side while the patient is in the supine position, the so-called McClure manoeuvre [13]. Typical benign positional nystagmus indicates a peripheral dysfunction, it presents a latency and it is generally horizontal rotatory, usually geotropic, fatiguable and adaptable. Although it is generally unilateral, occasionally what seems to be bilateral benign positional nystagmus occurs.

Typical central positional nystagmus occurs in a wide variety of lesions, especially those involving the vestibulo-cerebellum. Spontaneous vertical nystagmus, either upward or downward, can often be modified by positional testing using the conventional Hallpike manoeuvre or by placing the subject supine or prone. If the nystagmus is increased in prone position, it is usually decreased lying supine. Nystagmus induced by canal stimulation can also be profoundly modified by alteration in the position of the head, due to otolith/semicircular canal interaction.

Vibration nystagmus. Mastoid or suboccipital stimulation by means of a 100 Hz vibration delivered by a specific vibration apparatus [14] evoked a nystagmus when canals or maculae are unbalanced. In whiplash patients, it is very frequent to observe nystagmus induced only by paravertebral cervical stimulation of one side, generally by the same side of more pronounced cervical muscle tension and pain, probably due to overstimulation of cervical muscle spindles.

Head shaking nystagmus. In some patients, vigorous head shaking may generate a nystagmus that is not clinically apparent. The head shaking test (HST) (20–30 full cycles at around 2 Hz followed by Frenzel’s glasses observation) is claimed to be a useful addition to the clinical vestibular examination

Cervical nystagmus. It is due to the activation of the cervico-ocular reflex (COR). It is elicited by the rotation of the subject with the head still. This provokes a stimulation of the neck muscles (stretching reflex), a stimulation of the vestibular nuclei and the elicitation of a nystagmus directed toward the opposite side of body rotation. In normal subjects nystagmus usually don’t appear; thus the gain of the COR has been calculated to be very low (about 0.1). In patients cervical nystagmus can be more easily observed especially when the labyrinth is hypofunctional. Cervical nystagmus evocation is difficult to perform as “bedside” test.

Optokinetic nystagmus. Optokinetic nystagmus (OKN) is a nystagmus elicited by the rotation of the environment with respect to the patient. It is a compensatory movement of the eyes to pursue a target displacement with more width than the visual field. It can be assessed as “bedside” test with a small stripped drum rotated in front of the patient. This is basically a pursuit task and not surprisingly correlates well with other pursuit measures.

BOR minimal tests to be performed

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