Home About us Contact | |||
Orthostatic Tremor (orthostatic + tremor)
Selected AbstractsOrthostatic tremor in progressive supranuclear palsyMOVEMENT DISORDERS, Issue 8 2007Rob M. A. de Bie MD Abstract Patients with orthostatic tremor (OT) can be classified as having "primary OT," with or without postural arm tremor but no other abnormal neurological features, or "OT plus." We describe a patient with OT, with postural tremor of the arms and restless legs syndrome (RLS), who developed features typical of progressive supranuclear palsy (PSP). PSP can be accompanied by OT. © 2007 Movement Disorder Society [source] Orthostatic tremor arises from an oscillator in the posterior fossaMOVEMENT DISORDERS, Issue 2 2001Y.R. Wu MD Abstract We tested the hypotheses that orthostatic tremor is generated by a central oscillator and that the tremor is expressed through spinal Ib interneurons. Six patients with orthostatic tremor were examined. The tremor was reset by electrical stimulation over the posterior fossa at intensities that were below the threshold for a motor evoked potential (MEP) but was not reset by transcranial magnetic stimulation over the motor cortex that did produce an MEP. It is argued that the oscillator involves the cerebellum or brainstem. The inhibition of voluntary EMG produced by stimulation over tendons, which has been attributed to effects from Golgi tendon organs (GTO), was not modulated in synchrony with the tremor. We were unable to demonstrate, therefore, that the tremor is expressed through GTO interneurons with this method. © 2001 Movement Disorder Society. [source] The pathophysiology of tremorMUSCLE AND NERVE, Issue 6 2001Günther Deuschl MD Abstract Tremor is defined as rhythmic oscillatory activity of body parts. Four physiological basic mechanisms for such oscillatory activity have been described: mechanical oscillations; oscillations based on reflexes; oscillations due to central neuronal pacemakers; and oscillations because of disturbed feedforward or feedback loops. New methodological approaches with animal models, positron emission tomography, and mathematical analysis of electromyographic and electroencephalographic signals have provided new insights into the mechanisms underlying specific forms of tremor. Physiological tremor is due to mechanical and central components. Psychogenic tremor is considered to depend on a clonus mechanism and is thus believed to be mediated by reflex mechanisms. Symptomatic palatal tremor is most likely due to rhythmic activity of the inferior olive, and there is much evidence that essential tremor is also generated within the olivocerebellar circuits. Orthostatic tremor is likely to originate in hitherto unidentified brainstem nuclei. Rest tremor of Parkinson's disease is probably generated in the basal ganglia loop, and dystonic tremor may also originate within the basal ganglia. Cerebellar tremor is at least in part caused by a disturbance of the cerebellar feedforward control of voluntary movements, and Holmes' tremor is due to the combination of the mechanisms producing parkinsonian and cerebellar tremor. Neuropathic tremor is believed to be caused by abnormally functioning reflex pathways and a wide variety of causes underlies toxic and drug-induced tremors. The understanding of the pathophysiology of tremor has made significant progress but many hypotheses are not yet based on sufficient data. Modern neurology needs to develop and test such hypotheses, because this is the only way to develop rational medical and surgical therapies. © 2001 John Wiley & Sons, Inc. Muscle Nerve 24: 716,735, 2001 [source] Successful thalamic deep brain stimulation for orthostatic tremorMOVEMENT DISORDERS, Issue 13 2008Jorge Guridi MD Abstract We report a patient with severe orthostatic tremor (OT) unresponsive to pharmacological treatments that was successfully controlled with thalamic (Vim, ventralis intermedius nucleus) deep brain stimulation (DBS) over a 4-year period. Cortical activity associated with the OT revealed by EEG back-averaging and fluoro-deoxi-glucose PET were also suppressed in parallel with tremor arrest. This case suggests that Vim-DBS may be a useful therapeutic approach for patients highly disabled by OT. © 2008 Movement Disorder Society [source] Dopaminergic deficit is not the rule in orthostatic tremor,MOVEMENT DISORDERS, Issue 12 2008Jean-Marc Trocello MD Abstract Involvement of the dopaminergic system in orthostatic tremor is controversial. The aim of this study was to detect possible dopaminergic denervation in primary orthostatic tremor (OT). Twelve consecutive patients with a firm diagnosis of primary orthostatic tremor were compared with age-matched normal controls. All the patients had a neurological examination, surface polymyography, and quantification of striatal dopamine transporters with 123I-FP-CIT SPECT imaging. There was no significant difference in 123I-FP-CIT SPECT findings between controls and patients with OT. Longstanding primary orthostatic tremor is not necessarily associated with 123I-FP-CIT SPECT abnormalities, as 8 of our patients had more than a 10-year history of OT. Primary orthostatic tremor without dopaminergic denervation remains a valid entity, although representing only a subtype of high-frequency OT. A new role may emerge for 123I-FP-CIT SPECT in distinguishing between patients whose symptoms will be restricted to OT throughout the disease course and patients at an increased risk of developing PD. © 2008 Movement Disorder Society [source] Orthostatic tremor in progressive supranuclear palsyMOVEMENT DISORDERS, Issue 8 2007Rob M. A. de Bie MD Abstract Patients with orthostatic tremor (OT) can be classified as having "primary OT," with or without postural arm tremor but no other abnormal neurological features, or "OT plus." We describe a patient with OT, with postural tremor of the arms and restless legs syndrome (RLS), who developed features typical of progressive supranuclear palsy (PSP). PSP can be accompanied by OT. © 2007 Movement Disorder Society [source] Gabapentin can improve postural stability and quality of life in primary orthostatic tremorMOVEMENT DISORDERS, Issue 7 2005Julian P. Rodrigues MD Abstract Primary orthostatic tremor (OT) is characterized by leg tremor and instability on standing. High frequency (13,18 Hz) tremor bursting is present in leg muscles during stance, and posturography has shown greater than normal sway. We report on an open-label add-on study of gabapentin in 6 patients with OT. Six patients were studied with surface electromyography, force platform posturography, and a modified Parkinson's disease questionnaire (PDQ-39) quality of life (QOL) scale before and during treatment with gabapentin 300 mg t.d.s. If on other medications for OT, these were continued unchanged. Of the 6 patients, 4 reported a subjective benefit of 50 to 75% with gabapentin, 3 of whom showed reduced tremor amplitude and postural sway of up to 70%. Dynamic balance improved in all 3 patients who completed the protocol. QOL data from 5 patients showed improvement in all cases. No adverse effects were noted. Gabapentin may improve tremor, stability, and QOL in patients with OT, and symptomatic response correlated with a reduction in tremor amplitude and postural sway. The findings confirm previous reports of symptomatic benefit with gabapentin and provide justification for larger controlled clinical trials. Further work is required to establish the optimal dosage and to validate the methods used to quantify the response to treatment. © 2005 Movement Disorder Society [source] Primary orthostatic tremor is an exaggeration of a physiological response to instabilityMOVEMENT DISORDERS, Issue 2 2003Andrew Sharott BSc Abstract Primary orthostatic tremor (POT) is a rare disorder characterised by an intense sense of unsteadiness upon standing and a 16-Hz tremor in which the timing between tremor bursts in different muscles (unilateral and bilateral) remains constant. Hitherto, similar EMG activity has not been described in healthy subjects and it has been postulated that the oscillations seen in POT are primarily pathological. In this study, EMG was recorded from tibialis anterior in healthy subjects who were made unsteady through vestibular galvanic stimulation or leaning backwards. Under these conditions, a peak at approximately 16 Hz was seen in the coherence between the left and right tibialis anterior. This bilateral coherence was absent when the subjects activated the same muscles when not unsteady. These data indicate the existence of a physiological system involved in organising postural responses under circumstances of imbalance and characterised by a highly synchronised output at approximately 16 Hz. In addition, the results suggest that the core abnormality in POT may be an exaggerated sense of unsteadiness when standing still, which then elicits activity from a 16-Hz oscillator normally engaged in postural responses. © 2002 Movement Disorder Society [source] Bilaterally coherent tremor resembling enhanced physiological tremor: Report of three cases,MOVEMENT DISORDERS, Issue 2 2002John D. O'Sullivan MD Abstract The contribution of the central nervous system to tremor pathogenesis is unclear. Poor side-to-side coherence in physiological, essential, and parkinsonian tremors suggests distinct bilateral generators. By contrast, significant bilateral coherence demonstrated in orthostatic tremor and in enhanced physiological tremor (EPT) in patients with persistent mirror movements favours single or closely linked bilateral oscillators. We describe three patients (aged 21,37 years) who developed unusual bilateral postural and kinetic tremors at 6,13 Hz resembling EPT. The tremor involved all limbs, and in two cases the face or jaw, in the absence of other significant neurological features. Significant side-to-side coherence was demonstrated in each case using cross-correlation of electromyographic recordings from homologous muscle pairs. We postulate that these unusual tremors originate from a single brainstem source or from bilateral oscillators closely linked at or below this level. © 2002 Movement Disorder Society [source] Orthostatic tremor arises from an oscillator in the posterior fossaMOVEMENT DISORDERS, Issue 2 2001Y.R. Wu MD Abstract We tested the hypotheses that orthostatic tremor is generated by a central oscillator and that the tremor is expressed through spinal Ib interneurons. Six patients with orthostatic tremor were examined. The tremor was reset by electrical stimulation over the posterior fossa at intensities that were below the threshold for a motor evoked potential (MEP) but was not reset by transcranial magnetic stimulation over the motor cortex that did produce an MEP. It is argued that the oscillator involves the cerebellum or brainstem. The inhibition of voluntary EMG produced by stimulation over tendons, which has been attributed to effects from Golgi tendon organs (GTO), was not modulated in synchrony with the tremor. We were unable to demonstrate, therefore, that the tremor is expressed through GTO interneurons with this method. © 2001 Movement Disorder Society. [source] |