This chapter discusses the various forms of tremor and their characteristics. Section 2.1 defines the conditions under which a tremor is present. Section 2.2 describes the possible origins of tremor. Finally, a small overview on the characteristics of pathological tremors is provided in Section 2.3.
Tremors can be categorized by the conditions under which tremor is activated (Rubchinsky, Kuznetsov, Wheelock, & Sigvardt, 2007) (Smaga, 2003) (Deuschl, Bain, & Brin, 1998). The first category is rest tremors, which are active when there is no voluntary muscle activation. The amplitude of rest tremor reduces with activity. The second category is postural tremors, which are active when a body part is held in a position where muscle activity is required. The third category is kinetic tremors. This category of tremors includes simple kinetic tremor and intention tremor. Simple kinetic tremor occurs when a limb is moved voluntarily. Intention tremor is active when a body part is moved to a specific target and the amplitude of intention tremor increases as the target gets closer. A tremor can have more than one condition under which it is active.
2.2 Tremor origins
Several tremor origins are possible (Grimaldi & Manto, Tremor: From Pathogenesis to Treatment, 2008) (Ahmed & Sweeney, 2002) (McAuley & Marsden, 2000). These origins are mechanical resonances, feedback (or reflex) oscillators and central oscillators. These three origins will be described in more detail.
2.2.1 Mechanical properties and resonances
The mechanical properties of a limb segment determine its dynamics. These mechanical properties cannot initiate a tremor, but they determine the motions resulting from input forces. A limb segment of the human body has viscous and elastic properties, allowing the limb segment to be modeled as a mass-spring-damper system (Grimaldi & Manto, Tremor: From Pathogenesis to Treatment, 2008). Figure 1 shows an example of the response of a mass-spring-damper system to an applied vibration. Figure 1 illustrates that a system has a tendency to oscillate with larger amplitude at some frequencies than others. The largest amplitude is found at the natural frequency, which is determined by the mass and the stiffness of the system. A higher stiffness increases the natural frequency and a higher mass reduces the natural frequency. The amplitude at the natural frequency is affected by the damping ratio, which is determined by the mass, damping and stiffness of the system.
Figure 1 Example of damped forced vibration.M is the amplitude ratio bewteen input and output, ω is the frequency of the driving motion, ωn is the natural frequency and ζ is the damping ratio. (Meriam & Kraige, Engineering mechanics)
As a result of the dynamics of a limb segment, tremor generators at frequencies beyond the natural frequency of the limb segment needs far more power to result in notable tremor. Some natural frequencies of limb segments are: 25-27 Hz for a finger, 9 Hz for a wrist and 2 Hz for an elbow (McAuley & Marsden, 2000).
A limb segment can resonate with muscle activation as well as with vibrations originating from connected limb segments. The term mechanical resonance is used in this report to indicate that the source of the oscillation lies in another limb segment.
Mechanical resonance by itself does not involve muscle activation and thus does not result in EMG activity. However, when a limb is oscillating due to resonances, the muscles are passively stretched, which can result in reflexive activity.
2.2.2 Feedback oscillators
Feedback oscillations occur in a loop between the muscle and the central nervous system, for example in the loop between the muscle and spinal cord or in the loop between muscle and cerebellum, and they occur because of reflexes. A reflex is defined as an involuntary response to a stimulus. An example of a stretch reflex is the patellar reflex, where a physician taps the tendon just below the patella resulting in stretch of the muscle which produces a reflex in which the muscle contracts.
When the stretch reflex is regarded as an under damped negative feedback loop, oscillations with a period of double the loop time may occur. Such oscillations may result in synchronized activity of EMG and tremor at this frequency. Taking the travelling time of the signals and the muscle activation time into account, the loop time for a stretch reflex in the finger is about 50ms (Marsden, 1978) and would thus tend to result in a tremor frequency of 10Hz (McAuley & Marsden, 2000).
Mechanical loading results in a change in reflex oscillation frequencies (Berthoz and Metral, 1970). A higher limb inertia results in lower accelerations and thus in slower movements, so the movement is detected later by the muscle spindles which results in an increased delay before the reflex is induced (McAuley & Marsden, 2000). Mechanical loading will thus directly influence the power spectrum of the EMG when reflexes are active.
2.2.3 Central oscillators
There are also tremors which are not affected by changes in stiffness and mass, and do not depend on the length of the loop. An example is such a tremor is orthostatic tremor (see section 2.3.***). Therefore it is believed that these tremors are produced by a central oscillator, which is an oscillating neural network within the central nervous system (Grimaldi & Manto, Tremor: From Pathogenesis to Treatment, 2008). Oscillators in the central nervous which are also present in healthy subjects are those involved in motions like walking or cycling.
2.2.4 Central nervous system
The central nervous system (CNS), which consists of the brain and the spinal cord, receives information, integrates that information and controls the human body. Figure 2 shows the parts of the CNS involved in tremor genesis and the pathways between them.
Figure 2 Pathways that are involved in tremor genesis
Peripheral nervous sytem: MNα/MNγ (α and γ motor neuron), Ia (Ia and II*** afferent fiber from muscle spindles), Golgi (Ib afferent fiber from Golgi tendon organs)
Brainstem: RN (red nuclei), mf (mossy fibers), cf (climbing fibers), IO (inferior olivary nucleus)
Cerebellum: CC (cerebellar cortex), CN (cerebellar nuclei)
(Adapted from (Grimaldi & Manto, Tremor: From Pathogenesis to Treatment, 2008))
The purpose of showing this figure is not so much to describe all aspects of human motor control nor to identify the role of each part of the CNS, but to give an indication of all the possible loops and pathways involved in tremor genesis. In some subsections of section 2.3***, parts of the CNS are mentioned which are affected in certain disorders. ***verwijzen naar studie materiaal over motor control?***
The simple stretch reflex as described in section 2.2.2*** involves only the muscle spindles (Ia afferent fiber), the spinal cord and the alpha motor neuron.
2.3 Different forms of pathological tremor
For each of the disorders discussed in this section the following information will be presented: the symptoms of the tremor, the frequency range of oscillation of the tremor, the prevalence, the etiology, the pathology and the possible treatments. In most cases there are different frequencies reported for a disorder. These different frequencies indicate that there is no consensus in literature on a specific frequency range for each disorder (Accardo, Chiap, Marino, Lanzafame, & Bramanti, 2010). Prevalence numbers for tremor are largely unavailable, however an attempt is made to sort the pathological tremors by prevalence.
2.3.1 Essential tremor
Symptoms
Essential tremor (ET) is a kinetic tremor which mainly affects hands and forearms and may include a postural component in more severe cases (Louis, 2005). ET may also involve the head, neck and voice and less occasionally the trunk, legs and facial structures (Rubchinsky, Kuznetsov, Wheelock, & Sigvardt, 2007) (Louis, 2005). The tremor which affects the head and neck appears as a yes-yes or no-no head movement (Smaga, 2003). ET is slowly progressive and can become very disabling (Louis, 2005) (Rubchinsky, Kuznetsov, Wheelock, & Sigvardt, 2007). The amplitude of ET increases with stress, fatigue, and certain drugs (Smaga, 2003).
Frequency range of oscillation
The frequency of oscillation of ET has been reported to be between 4 Hz and 12 Hz (Smaga, 2003) (Harish, Venkateswara Rao, Borgohain, Sairam, & Abhilash, 2009) (Kuks & Snoek, 2007) (Rubchinsky, Kuznetsov, Wheelock, & Sigvardt, 2007) and between 4 Hz and 8 Hz (Eidelberg & Pourfar, 2007).
Prevalence
ET is the most common movement disorder (Ahmed & Sweeney, 2002) (Smaga, 2003). Prevalence ranges from 410 to 3920 cases per 100,000 persons, to as high as 5050 per 100,000 in persons older than 60 years (Smaga, 2003). Since up to 50 percent of persons suffering from ET are unaware of it, the true prevalence is probably higher (Smaga, 2003) (Rubchinsky, Kuznetsov, Wheelock, & Sigvardt, 2007).
Etiology
The etiology of ET is unknown. Often the patient has a positive family history of tremor (Ahmed & Sweeney, 2002). In 60% of the cases ET is an inherited disorder (Smaga, 2003). Age is another risk factor, where the age of onset is usually after 50 years. It also appears that ethnicity is a risk factor. Several studies showed that Caucasians show higher prevalence than African-Americans (Louis, 2005).
Pathology
The pathology of ET is largely unknown, but it is often associated with the olivocerebellar system (Kuks & Snoek, 2007) because of presence of lesions in the cerebellum, pons and thalamus (Rubchinsky, Kuznetsov, Wheelock, & Sigvardt, 2007).
Treatment
Options for treatment of ET are rest, beta blockers, and primidone (Mysoline). Alcohol ingestion appears to decrease the tremor. When the disability caused by ET is small, no treatment is performed since the side effects of the medication can outweigh the benefits (Ahmed & Sweeney, 2002).
2.3.2 Parkinsonian tremor
Symptoms
Parkinsonian tremor (PT) is a symptom of Parkinson's disease (PD). 80 to 90 percent of patients develop PT during the course of PD (Smaga, 2003). PT typically shows as a resting tremor in the forearms and up to 20% of PD patients also exhibit postural or kinetic tremor (Rubchinsky, Kuznetsov, Wheelock, & Sigvardt, 2007). Other symptoms of PD are rigidity, bradykinesia and impaired postural reflexes (Smaga, 2003). The amplitude of PT increases with stress and diminishes with voluntary movement (Smaga, 2003). Onset of PD is usually after the age of 60 (Van den Eden, et al., 2003).
Frequency range of oscillation
The frequency of oscillation of PT has been reported to be between 4 Hz and 6 Hz (Smaga, 2003), 4 Hz and 5Hz (Eidelberg & Pourfar, 2007), 3 Hz and 8 Hz (Harish, Venkateswara Rao, Borgohain, Sairam, & Abhilash, 2009), and 3 Hz and 7 Hz (Rubchinsky, Kuznetsov, Wheelock, & Sigvardt, 2007). Proprioceptive feedback appears to modify the frequency of the tremor (Pollock & Davis, 1930; Hassler, 1970; Rack and Ross, 1986) uit SP***) (Burne, 1987). Apparently there is no consensus on the frequency of oscillation of PT.
Prevalence
PT has a prevalence of 102-190 cases per 100,000 population in Western countries (Rubchinsky, Kuznetsov, Wheelock, & Sigvardt, 2007).
Etiology
The etiology of PD is yet unknown. Usually there is no family history (Ahmed & Sweeney, 2002).
Pathology
PD is characterized by the severe degeneration of dopaminergic neurons in the basal ganglia (Grimaldi & Manto, Tremor: From Pathogenesis to Treatment, 2008) (Rubchinsky, Kuznetsov, Wheelock, & Sigvardt, 2007), which are the main source of the neurotransmitter dopamine. The location of the oscillator remains unknown, but there is a consensus on the existence of a central tremor generator in PT (Rubchinsky, Kuznetsov, Wheelock, & Sigvardt, 2007). There are several hypotheses, but the most frequently proposed one is the basal ganglia-thalamo-cortical loop hypothesis (Burne, 1987). ***uitleg in http://www.ncbi.nlm.nih.gov/pubmed/8511438
***"A basal ganglia-thalamus-cortical loop has most frequently been proposed. Implicit in this theory is the notion that the central oscillator would determine tremor amplitude and frequency by periodic inputs to the motor neurons through descending motor pathways [reviewed by Young (24)]." (Burne, 1987)
Treatment
To compensate for the lack of dopamine, dopaminergic therapy can be applied to PD patients, which results in improved motor behavior. However, dopaminergic therapy loses its effectiveness over time and although adjusting the medication can recover the effectiveness, 10 to 20 percent of PD patients have to undergo surgical treatment (Rubchinsky, Kuznetsov, Wheelock, & Sigvardt, 2007). The most common procedure is the placement of a deep brain stimulator (Benabid, 2003)(***uit SP). ***DBS uitleggen***boek G&M***. Although risks are involved, the advantage of a deep brain stimulator is that its actions do no permanent damage, so adjustment of location and signal intensity is possible. Is some cases a thalamotomy is performed, in which case a part of the thalamus is surgically destroyed, which causes irreversible damage (Hua, Garonzik, Lee, & Lenz, 2003).
2.3.3 Cerebellar tremor
Symptoms
Cerebellar is an intention tremor, which may include a postural tremor of the trunk and neck (Smaga, 2003) (Tremor fact sheet, 2006). Symptoms which may also be present are dysarthria (speech problems), nystagmus (rapid rolling of the eyes) and gait problems (Tremor fact sheet, 2006).
Frequency range of oscillation
The frequency of oscillation of cerebellar tremor is reported to be less than 5 Hz (Smaga, 2003), between 3 and 5 Hz (Seeberger, 2005)(***SP) and between 2.5 Hz and 4 Hz (Charles, Esper, Davis, Maciunas, & Robertson, 1999) The possible postural tremor has a higher frequency of up to 10 Hz (Charles, Esper, Davis, Maciunas, & Robertson, 1999).
Prevalence
No prevalence numbers could be found for cerebellar tremor.
Etiology
Cerebellar tremor is caused by stroke, brainstem tumor, multiple sclerosis (Smaga, 2003) and degenerative diseases of the cerebellum (Seeberger, 2005). Cerebellar tremor can also result from chronic alcoholism or overuse of some medicines (Tremor fact sheet, 2006).
Pathology
The cerebellum is involved in movement in the following ways:
- Receptors like muscle spindles send information to the cerebellum which allows the adjustment of the movement.
- The motor cortex sends the muscle activation command also to the cerebellum (called efferent copy), so the cerebellum can send short loop corrections back to the cortex during the movement.
- The cerebellum can send a motor sequence plan of learned movements to the motor cortex which allows for fast complicated movements.
Cerebellar tremor is probably caused by the dysfunction of one or more of these mechanisms (Seeberger, 2005).
Treatment
Several types of medication have some benefit on cerebellar tremor, but little studies have been performed on their effectiveness. Deep brain stimulation and thalamotomy have also successfully been used on cerebellar tremor patients (Seeberger, 2005).
2.3.4 Enhanced physiologic tremor
Symptoms
Enhanced physiologic tremor is a strengthening of physiologic tremor to more visible levels. All the mechanisms discussed in section 2.2** are believed to be involved in the genesis of physiological tremor. The contribution of each of these mechanisms depends on the body part under consideration, its position and the action in which it is involved (Rubchinsky, Kuznetsov, Wheelock, & Sigvardt, 2007).
Frequency range of oscillation
The frequency of oscillation for enhanced physiological tremor is reported to be 8 to 12 Hz (Deuschl, Bain, & Brin, 1998)
Prevalence and etiology
Physiologic tremor can be enhanced by stress and fatigue, by taking stimulants and other drugs, by withdrawal from drugs or alcohol, and during certain medical conditions in which elevated thyroid hormones levels or low glucose levels are present. Physiological tremor also becomes more pronounced with age (Rubchinsky, Kuznetsov, Wheelock, & Sigvardt, 2007). Since these causes are very common, enhanced physiological tremor is probably experienced by everybody at some point.
Pathology and treatment
Enhanced physiologic tremor is generally not caused by a neurological disease and is usually reversible by correcting its cause (Tremor fact sheet, 2006).
2.3.5 Psychogenic tremor
Symptoms
Psychogenic tremor can present itself as a rest tremor, action tremor and posture tremor (Tremor fact sheet, 2006) (Grimaldi & Manto, Tremor: From Pathogenesis to Treatment, 2008). Patients with psychogenic tremor have a conversion disorder, which is defined as a psychological disorder that produces physical symptoms, or suffer from another psychiatric disease (Tremor fact sheet, 2006). Psychogenic tremor cannot be attributed to any damage in the central nervous system. The characteristics of psychogenic tremor vary between patients and show fluctuations in frequency and amplitude per patient (Grimaldi & Manto, Tremor: From Pathogenesis to Treatment, 2008). The tremor greatly decreases or even disappears when the patient is distracted (Ahmed & Sweeney, 2002) (Smaga, 2003)(McAuley et al., 2004)(uit SP***). During a specific test to diagnose psychogenic tremor, the entrainment test, the patient is asked to tap his fingers on the contralateral side with a certain frequency. The clinician can then check if the frequency of the tremor affected hand shifts to the frequency that the other hand is tapping with. If the patients suffers from a psychogenic tremor the frequency will shift.
Frequency range of oscillation
The frequency of oscillation is much less stable than that of ET or PT (Rubchinsky, Kuznetsov, Wheelock, & Sigvardt, 2007). Frequency of oscillation for psychogenic tremor is reported to be between 4 to 7 Hz (Rubchinsky, Kuznetsov, Wheelock, & Sigvardt, 2007) and 4 to 10 Hz (Deuschl, Bain, & Brin, 1998).
Prevalence
No information was available on the prevalence of psychogenic tremor.
Etiology, pathology and treatment
Psychogenic tremor results from a psychiatric disease of which the etiology, pathology and treatment will not be discussed.
2.3.6 Orthostatic tremor
Symptoms
Orthostatic tremor (OT) shows a postural tremor in the legs and trunk and is relieved by sitting or walking, which results in a sensation of loss of balance and causes patients to stand with their feet wide apart (Grimaldi & Manto, Tremor: From Pathogenesis to Treatment, 2008).
Frequency range of oscillation
The frequency of oscillation of OT is reported to be between 13 Hz and 18 Hz (Grimaldi & Manto, Tremor: From Pathogenesis to Treatment, 2008) and between 14 and 18Hz (Ahmed & Sweeney, 2002).
Prevalence
OT is a rare tremor which is probably underdiagnosed (Grimaldi & Manto, Tremor: From Pathogenesis to Treatment, 2008). OT has a prevalence lower than 64 cases per 100,000 persons in the United States according to the National Institute of Health.
Etiology
OT is believed to be a variant on essential tremor (Ahmed & Sweeney, 2002) and no other clinical signs or symptoms are present (Ahmed & Sweeney, 2002) (Tremor fact sheet, 2006).
Pathology
No lesions are found using imaging techniques on patients with orthostatic tremor (Grimaldi & Manto, Tremor: From Pathogenesis to Treatment, 2008). It is presumed that orthostatic tremor had a central origin, although it is unknown which part of the brain is responsible. The brainstem has been proposed to play an important role (Rubchinsky, Kuznetsov, Wheelock, & Sigvardt, 2007).
Treatment
An anticonvulsant, clonazepam, is used in OT, as well as treatments used in essential tremor. Medications are not always effective and lose effectiveness over time (Grimaldi & Manto, Tremor: From Pathogenesis to Treatment, 2008)(Rubchinsky, Kuznetsov, Wheelock, & Sigvardt, 2007).
2.3.7 Less common tremors
Holmes' tremor, which is also known as rubral tremor, is a combination of rest and action tremors. Causes include stroke and multiple sclerosis, where it is possible that there is a delay of weeks to years before tremor occurs (Ahmed & Sweeney, 2002) (Rubchinsky, Kuznetsov, Wheelock, & Sigvardt, 2007). Lesions are most often located in the upper brain stem, thalamus and cerebellum. Holmes' tremor has a low frequency of less than 4.5 Hz (Ahmed & Sweeney, 2002) (Grimaldi & Manto, Tremor: From Pathogenesis to Treatment, 2008).
Peripheral neuropathy, which may occur when nerves from the muscles are traumatized by injury or disease, can result in an tremor which resembles ET. The tremor may be caused by severely reduced conduction velocities in the nerves, causing a time delay on the stretch reflex (Grimaldi & Manto, Tremor: From Pathogenesis to Treatment, 2008). The frequency of tremor in neuropathy would therefore probably be dependent on the conduction velocity and the nerve length, as described in section 2.***. Other symptoms are the inability to coordinate voluntary muscle movement of the affected limbs and problems with gait and balance (Tremor fact sheet, 2006) (Grimaldi & Manto, Tremor: From Pathogenesis to Treatment, 2008).
Dystonic tremor is a postural or kinetic tremor (Rubchinsky, Kuznetsov, Wheelock, & Sigvardt, 2007)(Tremor fact sheet, 2006) (Grimaldi & Manto, Tremor: From Pathogenesis to Treatment, 2008). Dystonic tremor occurs in patients suffering from dystonia, a movement disorder in which sustained involuntary muscle contractions cause twisting and repetitive motions which cause painful and abnormal postures. Reciprocal inhibition and other mechanisms involved in inhibiting reflexes on several levels of the central nervous system seem to be reduced in dystonic patients (Grimaldi & Manto, Tremor: From Pathogenesis to Treatment, 2008). When reflexes are not properly inhibited, voluntary movements become difficult due to antagonistic activity. The pathology of primary dystonia is not well understood, it is presumed that the basal ganglia are involved (Rubchinsky, Kuznetsov, Wheelock, & Sigvardt, 2007). In secondary dystonia the disorder is brought on by another identified source of brain damage, like trauma or drugs. The frequency of oscillation for dystonic tremor is reported to be 4 to 7 Hz (Rubchinsky, Kuznetsov, Wheelock, & Sigvardt, 2007) and 4 to 9 Hz (Grimaldi & Manto, Tremor: From Pathogenesis to Treatment, 2008).
Task-specific tremor is mainly active while performing very specific actions. An example of task-specific tremor is primary writing tremor, which is induced by writing or similar motor activity. The frequency of the tremor ranges from 4 to 7 Hz (Grimaldi & Manto, Tremor: From Pathogenesis to Treatment, 2008) (Rubchinsky, Kuznetsov, Wheelock, & Sigvardt, 2007).
2.4 Overview of discussed tremors
Table 1 shows all discussed forms of tremor and the conditions under which they are active. Distinction is made between characteristic activation conditions (X) and activation conditions which are not in all cases present (O).
Pathological tremor type (section 2.3)
Conditions under which the tremor is active
Table 1 Activation conditions of several tremor types (Adapted from (Rubchinsky, Kuznetsov, Wheelock, & Sigvardt, 2007))
Figure 3Figure 1 shows a speculative scheme of how different oscillators interact to produce different types of tremor.
Figure 3 TEXT*** The dashed lines and boxes indicate those mechanisms that are most uncertain.
(McAuley & Marsden, 2000)
"Peripheral mechanisms refers to those processes where the oscillatory rhythm arises peripherally, even though the primary abnormality is central. For example, a delayed antagonist burst resulting from an abnormality of cerebellar processing might act peripherally by under damping of the body part and thus increasing its mechanical oscillatory tendency."
3. Classification of tremor
3.1 By hand
***
(Smaga, 2003)
Tests ET
No specific test; rule out other problems with general chemistry profile, CBC, and thyroid function tests
(Raethjen, et al., 2004)
"We will show that robust criteria distinguishing physiologic from early stage, low amplitude pathologic tremors can be deï¬ned, whereas quantitative measures like frequency and amplitude are very sensitive to the details of the recording condition or technique and therefore need to be normalized for each individual lab."
Current diagnosis (Smaga, 2003)
3.1.1 Scheme
Figure 4 shows a scheme for evaluating tremor
Figure 4 Algorithm for evaluating tremor (Smaga, 2003)
3.1.2 No useful comparison between limb and same contralateral limb
In clinical setting it is common practice to compare a limb affected by a movement to the asymptomatic contralateral limb (ref***). By comparing the two limbs, assumptions can be made on the behavior of the symptomatic limb before the movement disorder affected the limb, and so determine the effect of the disorder. Several studies have shown that in tremor classification this method cannot be used because the tremor in two limbs are dissimilar in people without a disorder (Findley, Gresty, & Halmaygi, 1981) (Köster, et al., 1998).
3.2 Frequency analysis
***adds objective data
***different fourier transform
To transform data from the time domain to the frequency domain the Fourier transform is used. There are several forms of Fourier transforms, but the most common is the fast Fourier transform (Grimaldi & Manto, Tremor: From Pathogenesis to Treatment, 2008).
"The combination of electromyography (EMG) with kinematic sensors is widely used" (Grimaldi & Manto, Neurological Tremor: Sensors, Signal Processing and Emerging Applications, 2010)
Method used in (Timmer, Lauk, & Deuschl, Quantitative analysis of tremor time series, 1996) is applicable to accelerometer as well as to EMG data.
3.2.1 Electromyography
Electromyography (EMG) is a technique to measure electrical muscle activity and the measurement can be performed with surface electrodes and needle electrodes. Surface electrodes are applied to the skin and are considered less invasive than needle electrodes which are inserted in the muscle.
***A skeletal muscle consists of many motor units, which are all separately innervated. If they activate asynchronous smooth movements are possible, if they activate synchronous it results in a very fast motion.***
By recording the muscle activity (***actually motor unit activity) over time, an electromyogram can be produced. There is much information which can be extracted from an electromyogram, for example the burst duration of the muscle activation. Figure 5 shows burst durations in forearm muscles for several of the discussed pathological tremors (chapter***)
Figure 5 Duration of EMG bursts in forearm muscles for several pathological tremors:
PD: Parkinson's disease, ET: essential tremor, PN:
peripheral neuropathy, OT: orthostatic tremor (Grimaldi & Manto, Neurological Tremor: Sensors, Signal Processing and Emerging Applications, 2010)
***
3.2.2 Kinematic analysis
There are many types of kinematic sensors available like accelerometer, gyroscopes, tracking systems using infrared and ordinary cameras. By attaching a sensor to a limb the total mass of the limb changes and thus the dynamics (see chapter 2.***) and it is therefore important to have sensors with low masses. Accelerometers are the most commonly used kinematic sensors (Grimaldi&Manto 2008 93blz***why).
There are different types of accelerometers which work according with different components like piezoelectric, piezoresistive en capacitive components. The working principle is the same for all sensors: there is a mass attached to a component acting as a spring and damper. Because of an acceleration the mass moves, causing a deformation which is measured. An example of a piezoelectric accelerometer is depicted in Figure 6.
Figure 6 Piezoelectric accelerometer (Lecture slides WB2303: Measurement in engineering)
When the piezoelectric accelerometer is attached to the limb of a subject, the acceleration of the limb will result in a force on the piezoelectric crystal because of the inertia of the mass on top of it. The crystal will then deform, resulting in a voltage over the crystal which is proportional with the applied force. By using Newton's second law the acceleration can be calculated because the mass and the force are known. Accelerometers are nowadays often MEMS (microelectromechanical systems) so they have a very low mass.
Since the accelerometer uses a mass, it is also sensitive to gravity. This feature is sometimes desired, for example in digital cameras to switch between portrait and landscape or even in kinematics to determine the orientation of a limb. However, when used to record tremor the signal is corrupted by gravity and the recording shows a bias or even modulations depending on the amount of rotation involved in the tremor. These alterations would obviously also result in a affected power spectrum, so proper measures must be taken to prevent or correct for influences of gravity.
HofH
Low G accelerometers/piezoelectric detectors (Harish, Venkateswara Rao, Borgohain, Sairam, & Abhilash, 2009)
Results in (Harish, Venkateswara Rao, Borgohain, Sairam, & Abhilash, 2009)
Surface EMG and piezoresistive accelerometer (Raethjen, et al., 2004)
(Grimaldi & Manto, Neurological Tremor: Sensors, Signal Processing and Emerging Applications, 2010)
"Accelerometers are also used for intraoperative assessment of the best position to implant electrodes for deep brain stimulation (DBS) and neurophysiological monitoring of stereotactic intervention of movement disorders [28]"
***accuracy emg/accelerometer
3.2.3 Signal processing
All the steps in signal processing, from acquiring the signal to presenting the results, are susceptible of errors.
There are several factors influencing the quality of the signal to be measured i.e. the signal to noise ratio. Noise can be picked up from the environment, like the 50Hz from the mains electricity or electromagnetic fields. Poor skin contact in EMG also leads to a low signal to noise ratio. Noise can be reduced by averaging the signal (in time or frequency domain). Artifacts due to movements and other undesired phenomena like the gravitational component of an accelerometer are also pitfalls.
When the signal is converted from analog to digital, the sample rate must fulfill the Nyquist criterion to prevent aliasing. Filtering techniques like low or high pass filters can be applied to eliminated unwanted signals or noises from the measured signal. After measuring a subject's tremor, the signal is often edited through visual inspection by an expert, who looks at a graphical representation of the signal (Grimaldi & Manto, Tremor: From Pathogenesis to Treatment, 2008).
Before applying a Fourier transformation the signal is often windowed to reduce spectral leakage. Spectral leakage is caused by signals which do not have an integer number of periods in a time sample, which corrupts the frequency spectrum by showing power at frequencies which are not in the signal. There are several window functions available like Blackman, Hamming and Hanning window functions.
The frequency resolution of the power spectrum depends on the observation time. Since tremor is often non periodic, the length of the observation time is limited because techniques like Fourier transforms can only be applied to time invariant measurements. This impairment limits the frequency resolution. ***guestimation of achievable resolution
***wavelets also possible page 104
***
To investigate the relation between two signals, for example the EMG signals of two antagonistic muscles, the cross-spectral density can be calculated. By scaling the square of the cross-spectrum with the auto-spectra of the two signals, the coherence is obtained. The coherence is a value between 0 and 1 and gives an indication of a possible linear relation between the two signals. If the relationship is a nonlinear one or is there is much measurement noise, the coherence will drop.
3.3 Other methods
EEG/EMG
DBS, Local field potential
fMRI/PET
PA Studies?
***
3.4 Haptic devices
To increase the subjectivity and repeatability of a measurement, haptic devices can be used (***figure). The same sensors can be used as discussed in section 3.1 and 3.2***.
*** (Grimaldi & Manto, Tremor: From Pathogenesis to Treatment, 2008)
A subject's limb is placed on the manipulator and the subject can perform different tasks like making certain motions, applying certain forces or resisting perturbations applied by the manipulator. The manipulator has the ability to create certain environments by changing the inertia, stiffness and damping of the manipulator. By creating different conditions for the subject's limb, different characteristics can be derived from the measurement, which can help understand the functioning of the human body and may give insight into a pathology.