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Biomedical subjects

J Gert van Dijk

Publications and source records attributed to J Gert van Dijk.

At least 19 recordsLinked to original sources
PubMed2006

The "posture second" strategy: a review of wrong priorities in Parkinson's disease.

Falls are common in Parkinson's disease. It remains difficult to predict these falls, presumably because clinical balance tests assess single components of postural control, whereas everyday fall mechanisms are typically more complicated. A substantial proportion of everyday falls appears to occur while Parkinson patients attempt to perform multiple tasks at the same time. Furthermore, little attention is generally paid to the possible contribution of cognitive impairments to falls. The importance of mental dysfunction is supported by the fact that cognitive loading while walking or balancing can lead to marked deteriorations in postural performance, and there is some evidence to suggest that such "dual tasking" is particularly difficult for elderly persons with dementia or depression. We examined what strategies Parkinson patients used when a basic walking task became increasingly challenging by adding additional tasks (both motor and cognitive). Most patients could perform a simple "dual task" test: simultaneously walking and answering simple questions. However, as the walking task became more complex, patients' performance began to deteriorate. Interestingly, this was reflected not only by failure to answer questions, but also by an increasing number of blocks in motor performance (walking and balancing). This behaviour was different from that of both young and elderly controls, who appeared to sacrifice performance on the cognitive task in order to optimise their gait and balance ("posture first" strategy). Preliminary evidence suggest that impaired multiple task performance is associated with a two-fold increased risk of sustaining falls in daily life. We conclude that Parkinson patients are less inclined than healthy persons to maintain a safe gait. Instead, Parkinson patients use a "posture second" strategy and treat all elements of a complex task with equal priority, which in daily life may go at the expense of maintaining balance and lead to falls.

Accidental Falls↗
PubMed2006

Decreasing pain in electrical nerve stimulation.

OBJECTIVE: Do large stimulation electrodes reduce pain in nerve conduction testing? METHODS: Fourteen healthy subjects (6 men, 22-42 years) blinded for study design underwent 8 H-reflex studies, using a large (36 x 36 mm) or a small (6 x 6 mm) electrode, placed on either the patella or the popliteal fossa; either site could be used for the cathode or the anode. Stimulation intensity was adjusted to obtain M- and H-waves. Intensity and other characteristics of pain were noted, as were M- and H-wave parameters. RESULTS: Pain was felt strongest near the smaller electrode when two sizes were used. Large electrodes reduced pain without compromising H- or M-waves. CONCLUSIONS: Large stimulation electrodes reduce pain. SIGNIFICANCE: The results apply for tests relying on amplitude measurements.

Adult↗
PubMed2006

Startle syndromes.

Startle syndromes consist of three heterogeneous groups of disorders with abnormal responses to startling events. The first is hyperekplexia, which can be split up into the "major" or "minor" form. The major form of hyperekplexia is characterised by excessive startle reflexes, startle-induced falls, and continuous stiffness in the neonatal period. This form has a genetic basis: mutations in the alpha1 subunit of the glycine receptor gene, GLRA1, or related genes. The minor form, which is restricted to excessive startle reflexes with no stiffness, has no known genetic cause or underlying pathophysiological substrate. The second group of startle syndromes are neuropsychiatric, in which excessive startling and various additional behavioural features occur. The third group are disorders in which startling stimuli can induce responses other than startle reflexes, such as startle-induced epilepsy. Diagnosis of startle syndromes depends on clinical history, electromyographic studies, and genetic screening. Further study of these disorders may enable improved discrimination between the different groups.

Humans↗
PubMed2006

Altered skin-temperature regulation in narcolepsy relates to sleep propensity.

STUDY OBJECTIVES: In healthy subjects, sleep propensity increases when the distal skin temperature increases relative to the proximal skin temperature. This increase results from increased blood flow in the skin of the extremities and is, among other factors, controlled by the hypothalamic circadian clock, as is sleep. Because narcolepsy is characterized by hypothalamic alterations, we studied skin temperature in narcoleptic patients in relation to their characteristically increased sleep propensity during the day. DESIGN: Distal and proximal skin temperature and their gradient (DPG) were measured during a Multiple Sleep Latency Test. This allowed temperature to be studied during wakefulness, at sleep onset and during sleep. SETTING: Tertiary narcolepsy referral center in a university hospital. PATIENTS: Fifteen unmedicated narcolepsy patients with cataplexy and 15 controls. INTERVENTIONS: None. MEASUREMENTS AND RESULTS: In subjects in the waking state, DPG was higher in narcoleptics than in controls throughout the day (time by group interaction, p < .0001), due to increased distal skin temperature and decreased proximal skin temperature. The increase in DPG was related to a shorter subsequent sleep-onset latency (p = .02). Once asleep, narcoleptics maintained their elevated distal skin temperature and DPG (p < .0001), whereas proximal skin temperature increased to reach normal levels. CONCLUSIONS: This is the first demonstration of a dramatic alteration of daytime skin temperature control in narcolepsy. Even awake narcoleptic patients showed a DPG higher than that which healthy controls achieve when asleep. This observation suggests that hypocretin deficiency in narcolepsy affects skin-temperature regulation and invites further examination. Skin-temperature control might ultimately even have therapeutic implications for the alleviation of narcoleptic symptoms.

Adult↗
PubMed2006

Syncope in adults: terminology, classification, and diagnostic strategy.

Syncope is a relatively common clinical syndrome that is a subset of a broader range of conditions that cause transient loss of consciousness (TLOC). Other TLOC conditions include seizures, concussions, and intoxications. However, despite frequent confusion in the medical literature, syncope is and should be clearly distinguished from those other causes of TLOC by virtue of its pathophysiology; specifically, syncope is the result of self-terminating inadequacy of global cerebral nutrient perfusion, while the other forms of TLOC have different etiologies. Unfortunately, the diagnostic evaluation of syncope remains for the most part poorly managed and inefficient. Careful history-taking, physical examination, and judicious use of tests can not only increase the diagnostic yield of the evaluation, but also increase patient safety and reduced overall healthcare costs.

Adult↗
PubMed2006

Focusing on vigilance instead of sleepiness in the assessment of narcolepsy: high sensitivity of the Sustained Attention to Response Task (SART).

STUDY OBJECTIVE: The severity of narcolepsy is commonly measured with the Multiple Sleep Latency Test (MSLT), focusing on the tendency to fall asleep. A neglected but perhaps equally important complaint is impaired performance in the waking state. We evaluated the Sustained Attention to Response Task (SART) for the quantification of vigilance in narcolepsy. DESIGN: The SART involves withholding key presses to 1 in 9 target stimuli. In the present study, it was administered prior to each of 5 MSLT sessions in a 1-day study. The Epworth Sleepiness Scale was administered to measure subjective sleepiness. SART and MSLT results (number of errors and sleep latency) were compared using Receiver Operator Curves, sensitivity, and specificity. SETTING: Tertiary narcolepsy referral center in a university hospital. PATIENTS: Fifteen untreated narcoleptics and 15 matched controls. INTERVENTIONS: None. MEASUREMENTS AND RESULTS: The area under the receiver operating curve was 0.97 for the MSLT and 0.95 for the SART. Sensitivity and specificity for the MLST were 80% and 100% using a cutoff point of 5 minutes. For the SART, these values were 87% and 100%, using a 5-error cutoff. The SART and MSLT showed no correlation with each other or with the Epworth Sleepiness Scale. CONCLUSIONS: The SART, measuring attention, was abnormal as often as the MSLT, measuring sleepiness. The inability to remain vigilant during the day may be the most serious complaint in narcolepsy, since it impairs performance. The SART is valid in this respect, is easy to administer, and takes little time.

Adult↗
PubMed2005

Unconscious confusion--a literature search for definitions of syncope and related disorders.

BACKGROUND: Imprecise definitions of syncope and related conditions appear common in the medical literature. To investigate the scope of the problem we systematically searched for definitions in high-ranking medical journals. METHODS: Literature review of articles on 'syncope', 'neurocardiogenic syncope', 'neurally mediated syncope', 'orthostatic intolerance', and 'orthostatic hypotension' with these keywords in the title, mainly published in the ten journals with the highest impact in the fields of cardiology, internal medicine, and neurology. RESULTS: Syncope, neurocardiogenic syncope, neurally mediated syncope, orthostatic intolerance, and orthostatic hypotension were defined in only 41%, 34%, 26%, 38%, and 48% of papers respectively. Definitions, when given, differed considerably among papers. Orthostatic hypotension was most frequently defined, with an increase in number and consistency of definitions after publication of a consensus in 1996. CONCLUSIONS: Syncope and related conditions proved to be infrequently and inconsistently defined in current medical literature. The lack of consistent terminology is likely to harm medical education, research, and patient care. There is a strong need for a systematic terminology for syncope and related conditions.

Autonomic Nervous System↗
PubMed2004

Syncope.

Syncope is a syndrome consisting of a relatively short period of temporary and self-limited loss of consciousness caused by transient diminution of blood flow to the brain (most often the result of systemic hypotension). Syncope comprises part of a subset of clinical conditions in which loss of consciousness is transient. Other conditions in this group, which are not syncope and should be clearly distinguished from syncope, include, for example, seizure disorders, posttraumatic loss of consciousness, and cataplexy. Recent surveys indicate that syncope accounts for approximately 1% of emergency department visits in Europe, although older reports from the United States placed this number closer to 3%. The reported prevalence of syncope in the population varies: 15% of children before the age of 18 years; 25% of a military population aged 17 to 26 years; 16% and 19%, respectively, in men and women aged 40 to 59 years; and up to 23% in a nursing home population older than 70 years. The highest frequency of syncope occurs in patients with cardiovascular comorbidity and older patients in institutional care settings. The causes of syncope are numerous and, not infrequently, multiple factors may contribute. The diagnostic evaluation is benefited by availability of a detailed medical history and reports of eyewitnesses. In this context, the physician must consider the classification of the causes of syncope, and address the most likely causes first. The principal groups of causes may be summarized as: (1) neurally mediated reflex syncope (eg, vasovagal faint, carotid sinus syndrome); (2) orthostatic (postural) syncope; (3) cardiac arrhythmias; (4) structural cardiac and pulmonary causes; and (5) cerebrovascular disorders (rare). In addition, conditions that may mimic syncope but are not true syncope (eg, psychogenic pseudosyncope) must be considered. Only after a definitive cause is established can appropriate treatment be initiated. In this regard, the syncope evaluation is facilitated by maintaining an organized diagnostic approach. The practitioner should avoid wasteful use of short-term ambulatory electrocardiographic recordings (eg, Holter monitors) and rarely positive neurologic tests (eg, electroencephelography, head magnetic resonance imaging/computed tomography) in the absence of head trauma or evident neurologic signs. In many medical centers the evaluation of patients with syncope is haphazard, and may be substantially enhanced by establishment of a multidisciplinary syncope evaluation unit or team.

Diagnosis, Differential↗
PubMed2004

Corticospinal excitability during laughter: implications for cataplexy and the comparison with REM sleep atonia.

Cataplexy is usually seen as rapid eye movement (REM) sleep atonia occurring at an inopportune moment. REM sleep atonia is the result of postsynaptic inhibition, i.e. inhibition of alpha motor neurones. Although this may explain the suppression of H-reflexes during REM sleep, cataplexy and laughter, it is not the only explanation. Presynaptic inhibition, in which afferent impulses are prevented from reaching motor neurones, is an alternative. Testing H-reflexes and magnetic-evoked potentials (MEPs) helps to tell them apart: in postsynaptic inhibition MEPs and H-reflexes change in tandem, while H-reflexes may decrease independent of MEPs with other inhibition modes. We studied motor inhibition during laughter, the strongest trigger for cataplexy. H-reflexes were evoked every 2 s in the soleus muscle in 10 healthy subjects watching comical video fragments. MEPs were evoked when H-reflexes decreased during laughter, and, as a control, when subjects did not laugh. Pairs of MEPs and the immediately preceding H-reflexes were studied. Compared with the control condition, laughter caused mean MEP area to increase by 60% (P=0.006) and mean H-reflex amplitude to decrease by 33% (P=0.008). This pattern proves that postsynaptic inhibition cannot have been the sole influence. The findings do not prove which mechanisms are involved; one possibility is that the decrease in H-reflex amplitude was the result of presynaptic inhibition, and that cortical and/or spinal facilitation accounted for increased MEPs. Regardless, the pattern differs fundamentally from the reported mechanism of REM sleep atonia. Existing scanty data on cataplexy suggest a pattern of H-reflexes and MEPs similar to that during laughter, but this needs further study.

Arousal↗