PubMed Health⌕ Search

Biomedical subjects

R Bhidayasiri

Publications and source records attributed to R Bhidayasiri.

14 recordsLinked to original sources
PubMed2006

Botulinum toxin in blepharospasm and oromandibular dystonia: comparing different botulinum toxin preparations.

Amongst all regions of the body, the craniocervical region is the one most frequently affected by dystonia. Whilst blepharospasm--involuntary bilateral eye closure--is produced by spasmodic contractions of the orbicularis oculi muscles, oromandibular dystonia may cause jaw closure with trismus and bruxism, or involuntary jaw opening or deviation, interfering with speaking and chewing. Both forms of dystonia can be effectively treated with botulinum toxin injection. This article summarizes injection techniques in both forms of dystonia and compares doses, potency and efficacy of different commercially available toxins, including Botox, Dysport, Xeomin and Myobloc/NeuroBloc.

Anti-Dyskinesia Agents↗
PubMed2006

Botulinum toxin therapy of laryngeal muscle hyperactivity syndromes: comparing different botulinum toxin preparations.

Spasmodic dysphonia (SD) is a focal dystonia characterized by a strained, strangled voice. Botulinum toxin is a symptomatic treatment for SD and has become the mainstay of therapy over the last two decades. In this manuscript, we briefly review different laryngeal muscle hyperactivity syndromes, their injection techniques and toxins currently available. Adductor SD is the most common indication for botulinum toxin treatment in the larynx. All studies report similar results with regard to improvement, patient satisfaction and side effects. We describe different injection techniques to treat this disorder such as the percutaneous, transoral, transnasal, point-touch techniques. In abductor SD, a subtype of SD, the treatment is aimed at the posterior cricoarytenoid muscle. Other applications of botulinum toxin in the larynx include spasmodic laryngeal dyspnea and voice tremors. We also review injection techniques, the different toxin types used, and toxin doses.

Anti-Dyskinesia Agents↗
PubMed2006

State of the art: deep brain stimulation in Parkinson's disease.

Surgical therapy for Parkinson's disease has a long history beginning in the 1930s with empirical exploration of different brain targets, such as resection of the primary motor cortex or extirpation of the caudate. Recently, there has been a renaissance of functional neurosurgery for the treatment of advanced Parkinson's disease, particularly deep brain stimulation (DBS). To date, DBS of the globus pallidus interna and subthalamic nucleus has been reported to relieve motor symptoms and levodopa-induced dyskinesia in patients with advanced Parkinson's disease. DBS also has different advantages over pallidotomy and subthalamotomy, including reversibility, decreased risk of reoperation and decreased morbidity. In addition to well-experienced neurologists and neurosurgeons, a multidisciplinary team approach is fundamental and critical to ensure success in the DBS procedure in individual patients. With the advances in neuroimaging, neurophysiology and localization techniques, it is increasingly likely that there will be more surgical targets in the future that can also improve cardinal features of Parkinson's disease, or even nonmotor manifestations of this condition.

Deep Brain Stimulation↗
PubMed2005

Differential diagnosis of common tremor syndromes.

Tremor is one of the most common involuntary movement disorders seen in clinical practice. In addition to the detailed history, the differential diagnosis is mainly clinical based on the distinction at rest, postural and intention, activation condition, frequency, and topographical distribution. The causes of tremor are heterogeneous and it can present alone (for example, essential tremor) or as a part of a neurological syndrome (for example, multiple sclerosis). Essential tremor and the tremor of Parkinson's disease are the most common tremors encountered in clinical practice. This article focuses on a practical approach to these different forms of tremor and how to distinguish them clinically. Evidence supporting various strategies used in the differentiation is then presented, followed by a review of formal guidelines or recommendations when they exist.

Brain Diseases↗
PubMed2004

Wound botulism.

Explore the source record for details and available documents.

Botulism↗
PubMed2004

Chorea and related disorders.

Chorea refers to irregular, flowing, non-stereotyped, random, involuntary movements that often possess a writhing quality referred to as choreoathetosis. When mild, chorea can be difficult to differentiate from restlessness. When chorea is proximal and of large amplitude, it is called ballism. Chorea is usually worsened by anxiety and stress and subsides during sleep. Most patients attempt to disguise chorea by incorporating it into a purposeful activity. Whereas ballism is most often encountered as hemiballism due to contralateral structural lesions of the subthalamic nucleus and/or its afferent or efferent projections, chorea may be the expression of a wide range of disorders, including metabolic, infectious, inflammatory, vascular, and neurodegenerative, as well as drug induced syndromes. In clinical practice, Sydenham's chorea is the most common form of childhood chorea, whereas Huntington's disease and drug induced chorea account for the majority of adult onset cases. The aim of this review is to provide an up to date discussion of this disorder, as well as a practical approach to its management.

Chorea↗
PubMed2001

Pathophysiology of slow vertical saccades in progressive supranuclear palsy.

OBJECTIVES: To investigate the relative roles of burst neurons (which generate the saccadic command) and omnipause neurons (which gate the activity of burst neurons) in the pathogenesis of slow saccades in progressive supranuclear palsy (PSP). BACKGROUND: Experimental inactivation of mesencephalic burst neurons impairs vertical but not horizontal saccades. Experimental inactivation of omnipause neurons causes slowing of both horizontal and vertical saccades. Combining saccadic with vergence movements in healthy subjects induces small, high-frequency, conjugate oscillations, which indicate that omnipause neurons are inhibited. METHODS: The authors studied seven patients with PSP, six patients with other parkinsonian syndromes, and seven age-matched control subjects. They compared vertical saccades of similar sizes made with or without associated vergence movements. They compared the speed of vertical and horizontal saccades. RESULTS: Five patients with PSP and the six patients with other parkinsonian made vertical saccades in combination with horizontal vergence; all showed conjugate horizontal oscillations (29 to 41 Hz) during 27% to 93% of saccade-vergence trials. Vertical saccades made in conjunction with vergence movements were not speeded up or increased in size compared with saccades made between equidistant targets for the PSP or parkinsonian groups. Vertical saccades were slowed more than horizontal saccades in the PSP group (p < 0.005) but not in the parkinsonian group. CONCLUSIONS: Dysfunction of omnipause neurons ("gate dysfunction") is unlikely to be the primary cause of slow vertical saccades in progressive supranuclear palsy. Deficient generation of the motor command by midbrain burst neurons is the more likely cause.

Aged↗
PubMed2001

Ocular oscillations induced by shifts of the direction and depth of visual fixation.

Shifts of the point of fixation between two targets aligned on one eye that are located near and far (Müller paradigm) stimulates a combined saccadic-vergence movement. In normal subjects, this test paradigm often induces saccadic oscillations of about 0.3 degrees at 20 to 30 Hz. We measured eye movements using the magnetic search coil technique in 2 patients recovering from viral opsoclonus-myoclonus syndrome, comparing saccadic-vergence responses to the Müller paradigm with conjugate saccades between distant targets. Both patients exhibited intermittent conjugate ocular oscillations of about 4 to 5 degrees amplitude at about 10 Hz. Combined saccadic-vergence movements induced these oscillations twice as often as did conjugate saccades. One patient also exhibited disjunctive ocular oscillations at 10 Hz while sustaining fixation on the near target. The Müller paradigm provides a useful clinical and experimental technique for inducing saccadic oscillations. The probable mechanism is that pontine omnipause neurons, which normally gate saccades, are inhibited during the sustained vergence movement that follows the saccadic component of the response to the Müller paradigm.

Adult↗
PubMed2000

A hypothetical scheme for the brainstem control of vertical gaze.

OBJECTIVES: To develop a hypothetical scheme to account for clinical disorders of vertical gaze based on recent insights gained from experimental studies. METHODS: The authors critically reviewed reports of anatomy, physiology, and effects of pharmacologic inactivation of midbrain nuclei. RESULTS: Vertical saccades are generated by burst neurons lying in the rostral interstitial nucleus of the medial longitudinal fasciculus (riMLF). Each burst neuron projects to motoneurons in a manner such that the eyes are tightly coordinated (yoked) during vertical saccades. Saccadic innervation from riMLF is unilateral to depressor muscles but bilateral to elevator muscles, with axons crossing within the oculomotor nucleus. Thus, riMLF lesions cause conjugate saccadic palsies that are usually either complete or selectively downward. Each riMLF contains burst neurons for both up and down saccades, but only for ipsilateral torsional saccades. Therefore, unilateral riMLF lesions can be detected at the bedside if torsional quick phases are absent during ipsidirectional head rotations in roll. The interstitial nucleus of Cajal (INC) is important for holding the eye in eccentric gaze after a vertical saccade and coordinating eye-head movements in roll. Bilateral INC lesions limit the range of vertical gaze. The posterior commissure (PC) is the route by which INC projects to ocular motoneurons. Inactivation of PC causes vertical gaze-evoked nystagmus, but destructive lesions cause a more profound defect of vertical gaze, probably due to involvement of the nucleus of the PC. Vestibular signals originating from each of the vertical labyrinthine canals ascend to the midbrain through several distinct pathways; normal vestibular function is best tested by rotating the patient's head in the planes of these canals. CONCLUSIONS: Predictions of a current scheme to account for vertical gaze palsy can be tested at the bedside with systematic examination of each functional class of eye movements.

Animals↗
PubMed2000

Vertical nystagmus in normal subjects: effects of head position, nicotine and scopolamine.

We measured gaze stability in darkness of four normal humans using the search coil technique. Subjects were tested first with their heads erect, and then with their heads positioned 180 degrees upside-down. In each position, subjects held their head stationary for one minute, and then actively performed pitch rotations for 20 sec. All subjects showed sustained chin-beating nystagmus in the upside-down position. Each subject showed a significant increase of slow-phase velocity directed towards their brow after 40 sec in the inverted versus erect position. Pitch head rotation had little effect on subsequent nystagmus, except for transient reversal in one subject. The sustained changes of vertical eye drifts induced by 180 deg change of head position suggest that otolithic factors may contribute to vertical nystagmus in normals. The subjects were retested after wearing a nicotine patch for 2 hours. In three subjects, nicotine induced brow-beating nystagmus; adopting a head-hanging position increased this nystagmus in two subjects. In a third session, subjects were tested after wearing a scopolamine patch for 2 hours; results were generally similar to the control condition. We conclude that normal subjects may show chin-beating ("downbeating") nystagmus in a head-hanging position in darkness, reflecting a normal, physiological change in otolithic inputs brought about by the head orientation.

Adult↗
PubMed1997

Cancer-related thromboembolic disease in patients with solid tumours: a retrospective analysis.

BACKGROUND: Cancer patients frequently suffer thromboembolic events. This study assessed the incidence and resource implications of cancer-related thromboembolic disease (CTD) in a single, large cancer centre. PATIENTS AND METHODS: A retrospective analysis of patients admitted with CTD and/or the complications of treatment of CTD over a two-year period has been conducted. Forty-eight patients (23 male, 25 female, median age 60 years) with a variety of solid tumours were identified. RESULTS: The initial presentations were venous thromboses (28 patients) and pulmonary embolism (20 patients). The median interval from cancer diagnosis to the initial episode of CTD was eight (range 0-112) months. Twenty-two patients suffered additional thromboses, despite maintenance warfarin anticoagulation in 18 patients. Six patients experienced anticoagulation-induced haemorrhage. Forty-one (85.4%) patients have died. The median survival from the first thromboembolic event was 8.5 months. The median inpatient stay for management of the first event was 10 (range 4-75) days, accounting for 729 inpatient days during the study period. Recurrent episodes of CTD or complications of anticoagulation resulted in 28 readmissions, accounting for 295 inpatient days. During the two-year period 1024 inpatient days were directly caused by CTD and its complications, representing 6.1% bed occupancy on our unit. CONCLUSION: This study demonstrates that CTD represents a significant cause of morbidity in cancer patients with considerable resource implications for cancer centres. Improvements in prevention and management of CTD would reduce morbidity and lead to considerable cost savings.

Adult↗