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Biomedical subjects

J G van Dijk

Publications and source records attributed to J G van Dijk.

At least 19 recordsLinked to original sources
PubMed2006

EEG and MRI correlates of mild cognitive impairment and Alzheimer's disease.

OBJECTIVE: To investigate whether cognitive function in the spectrum of normal aging to Alzheimer's disease is better reflected in MRI or EEG measures, or a combination of both. METHODS: Cognitive functions were tested in 33 elderly subjects: 10 with probable Alzheimer's disease, 11 with mild cognitive impairment and 12 controls. Structural brain parameters were derived from conventional MRI and a quantitative MR technique called magnetization transfer imaging. The EEG provided measures of brain function. We performed multiple linear regression analyses to relate EEG and MRI parameters to global cognition, memory, language and psychomotor speed. RESULTS: The model showed EEG alpha reactivity during eyes open to be the primary factor associated with global cognition, memory and language skills. Brain atrophy was the primary factor associated with psychomotor speed. Furthermore, EEG alpha reactivity during eyes open explained significant additional variability in psychomotor speed. CONCLUSION: EEG and MRI are each associated with different aspects of cognitive function and complement each other in their relations to psychomotor speed.

Aged↗
PubMed2006

Interobserver variation in the interpretation of SSEPs in anoxic-ischaemic coma.

OBJECTIVE: To study interobserver variation in the interpretation of median nerve SSEPs in patients with anoxic-ischaemic coma. METHODS: SSEPs of 56 consecutive patients with anoxic-ischaemic coma were interpreted independently by 5 experienced clinical neurophysiologists using guidelines derived from a pilot study. Interobserver agreement was expressed as kappa coefficients. RESULTS: Kappa ranged from 0.20 to 0.65 (mean 0.52, SD 0.14). Disagreement was related with noise level and failure to adhere strictly to the guidelines in 15 cases. The presence or absence of N13 and cortical peaks caused disagreement in 5 cases each. For recordings with a noise level of 0.25 microV or more, mean kappa was 0.34; for recordings with a noise level below 0.25 microV mean kappa was 0.74. CONCLUSIONS: Interobserver agreement for SSEPs in anoxic-ischaemic coma was only moderate. Since the noise level strongly influenced interobserver variation, utmost attention should be given to its reduction. If an artefact level over 0.25 microV remains, absence of N20 cannot be judged with sufficient certainty and the SSEP should be repeated at a later stage. SIGNIFICANCE: Because of its moderate interobserver agreement, great care has to be given to accurate recording and interpretation of SSEPs before using the recordings for non-treatment decisions.

Adult↗
PubMed2006

Syncope in migraine: the population-based CAMERA study.

OBJECTIVE: To examine the association between migraine and syncope-related autonomic nervous system (ANS) symptoms. METHODS: A population-based study among migraineurs with and without aura (n = 323) and control subjects (n = 153) was conducted. A systematic questionnaire and cardiovascular measurements during rest, while standing, and after venipuncture addressed the prevalence of syncope, orthostatic intolerance, orthostatic hypotension (OH), and the postural tachycardia syndrome (POTS) in migraineurs and control subjects. RESULTS: The lifetime prevalence of syncope in all participants was 41%, more often in women (45 vs 32%; p = 0.02). Compared with control subjects, migraineurs had a higher lifetime prevalence of syncope (46 vs 31%; p = 0.001), frequent syncope (five or more attacks) (13 vs 5%; p = 0.02), and orthostatic intolerance (32 vs 12%; p < 0.001). There was no association between ANS symptoms and the severity of migraine or migraine subtype. Cardiovascular measurements and the prevalence of POTS and OH did not differ significantly between migraineurs and control subjects. CONCLUSION: This population-based study demonstrated an elevated prevalence of syncope and orthostatic intolerance in migraineurs without clear interictal signs of autonomic nervous system dysfunction.

Blood Pressure↗
PubMed2006

Memory activation enhances EEG abnormality in mild cognitive impairment.

This exploratory study investigated EEG power changes during memory activation in patients with amnestic mild cognitive impairment (MCI). Twelve MCI patients and 16 age-matched controls underwent EEG registration during two conventional EEG conditions ('eyes closed' and 'eyes open') and three memory conditions ('word memory', 'picture memory' and 'animal fluency'). For all conditions, EEG power in the theta (4-8 Hz), lower alpha (8-10.5 Hz) and upper alpha (10.5-13 Hz) bands were expressed as percentile changes compared to 'eyes closed'. MCI patients showed significantly less decrease in the lower alpha band than controls (p=0.04) during picture memory activation. The word memory task showed a trend towards a similar effect (p=0.09). This study suggests that memory activation reveals EEG differences between MCI patients and controls while conventional EEG conditions do not.

Aged↗
PubMed2006

Cardiovascular autonomic function tests in cluster headache.

While facial autonomic signs are prominent during cluster headache (CH) attacks, cardiovascular autonomic changes have been described in few CH patients. Cardiovascular autonomic function tests (AFT) can be used to assess general autonomic function in CH patients in different stages of the disease. We aimed to assess whether general autonomic function is changed in CH patients during a cluster period. AFT was performed both during a cluster period, but outside an actual attack, and outside a cluster period in 18 patients. Heart rate variability was studied at rest, during deep breathing, after standing up and during a Valsalva manoeuvre. Blood pressure (BP) changes were recorded at rest, during standing up and during sustained handgrip. Measurements during and outside the cluster period were compared using the paired t-test. AFT measurements revealed no significant differences between the two measurements, except for diastolic BP in rest, which was higher during the cluster period [80.3 (SD 12.2) vs. 74.8 (SD 9.0), P = 0.04]. Autonomic dysfunction during a cluster period, but outside an attack, does not include systemic cardiovascular control.

Autonomic Nervous System↗
PubMed2006

The prevalence of premonitory symptoms in migraine: a questionnaire study in 461 patients.

Migraine attacks are often preceded by premonitory symptoms. Prevalence rates of migraine patients reporting one or more premonitory symptoms show considerable variability and rates range between 12% and 79%. Sources of variability might be differences in study population or research design. Using a questionnaire, we retrospectively studied the prevalence of 12 predefined premonitory symptoms in a clinic-based population. Of 461 migraine patients, 374 (81%) responded. At least one premonitory symptom was reported by 86.9% and 71.1% reported two or more. The most frequently reported premonitory symptoms were fatigue (46.5%), phonophobia (36.4%) and yawning (35.8%). The mean number of premonitory symptoms per person was 3.2 (+/- 2.5). Women reported 3.3 premonitory symptoms compared with 2.5 symptoms in men (P = 0.01). Age, education, migraine subtype (with or without aura) and mean attack frequency had no effect on the mean number of symptoms per individual. In conclusion, premonitory symptoms are frequently reported by migraine patients. Sensitivity and specificity of premonitory symptoms for migraine need to be assessed using prospective methods.

Adult↗
PubMed2005

Recognising F-response interference as a source of increased jitter in stimulated single fibre EMG.

OBJECTIVE: To determine the source of an abnormal pattern of latency shifts leading to falsely high jitters in single fibre electromyography (SFEMG). METHODS: We observed a sudden shortening of the latency to an individual single fibre spike component followed by a gradual return to baseline values during stimulation single fibre electromyography (SFEMG) of the facial muscle. The pattern could be reproduced in healthy controls. RESULTS: The sudden decrease in latency proved to follow an additional discharge of the muscle fibre, not due to the external stimulus. This additional discharge was identified as an F-response. CONCLUSIONS: The mechanism is thought to be a higher muscle fibre conduction velocity resulting from a temporary increase in stimulus frequency, in the form of an extra impulse along the muscle fibre represented by the F-response. SIGNIFICANCE: The typical abnormal pattern should be recognised because it can falsely increase the mean jitter. We advice to increase the time base to 50 ms if this pattern is observed and to exclude the affected potentials from jitter measurements.

Algorithms↗
PubMed2005

Stress induced hypotension in pure autonomic failure.

A 47 year old woman with pure autonomic failure complained of dizziness during emotional stress. Emotional stimuli have not previously been reported to cause hypotension in patients with autonomic failure. In the patient, ambulatory blood pressure recording revealed severe hypotension (50/30 mm Hg) after a stressful event. During a tilt table test, hyperventilation was shown to cause a significant fall of blood pressure. This suggests that emotional stress can induce hypotension, probably through hyperventilation, in subjects with autonomic failure.

Autonomic Nervous System Diseases↗
PubMed2005

[Terms in use for transient loss of consciousness in the emergency ward; an inventory].

OBJECTIVE: To investigate the terminology for transient loss of consciousness in use in a Dutch emergency ward and to compare it with European definitions. DESIGN: Descriptive. METHOD: The records of all consecutive patients seen during an eight-week period in the Emergency Clinic of Leiden University Medical Centre, the Netherlands, were reviewed. Patients were enrolled in one of the following Dutch terms was encountered, expressing either a specific form or a general description of non-traumatic transient loss of consciousness (TLOC): 'collaps' (collapse), 'syncope' (syncope), 'flauwvallen' (fainting), 'wegraking' (TLOC) and 'insult' (seizure). The use of these terms was compared with the definitions of the European Society of Cardiology (ESC). RESULTS: The prevalence of a non-traumatic TLOC diagnosis in the Emergency Clinic was 2.9% (123/4300). 'Collaps' was the most frequently used term (53%), followed by 'insult' (31%), 'wegraking' (11%), 'flauwvallen' (3%) and 'syncope' (2%). The term 'collaps' was found to have been used in the context of the ESC category 'syncope' (n=47), TLOC (n=5), 'no TLOC' (n=9) or for situations that could not be classified (n=4). The term 'insult' was used exclusively in the context of epilepsy and the term 'syncope' exclusively in the context of the ESC category 'syncope'. The term 'wegraking' proved to have been used in the context of the ESC category 'TLOC' (n=11), 'epilepsy' (n=1) or for situations that could not be classified (n=1). 'Flauwvallen' was used in the context of the ESC category 'syncope' (n=3) or the category 'no TLOC' (n=1). CONCLUSION: It would be advisable to give the terms mentioned above a specific meaning: reserve 'collaps' for a fall without an obvious external cause, 'wegraking' for transient loss of consciousness without a clear cause, and 'syncope' for loss of consciousness due to temporary low cerebral blood flow.

Diagnosis, Differential↗
PubMed2005

Gene dosage-dependent transmitter release changes at neuromuscular synapses of CACNA1A R192Q knockin mice are non-progressive and do not lead to morphological changes or muscle weakness.

Ca(v)2.1 channels mediate neurotransmitter release at the neuromuscular junction (NMJ) and at many central synapses. Mutations in the encoding gene, CACNA1A, are thus likely to affect neurotransmitter release. Previously, we generated mice carrying the R192Q mutation, associated with human familial hemiplegic migraine type-1, and showed first evidence of enhanced presynaptic Ca(2+) influx [Neuron 41 (2004) 701]. Here, we characterize transmitter release in detail at mouse R192Q NMJs, including possible gene-dosage dependency, progression of changes with age, and associated morphological damage and muscle weakness. We found, at low Ca(2+), decreased paired-pulse facilitation of evoked acetylcholine release, elevated release probability, and increased size of the readily releasable transmitter vesicle pool. Spontaneous release was increased over a broad range of Ca(2+) concentrations (0.2-5mM). Upon high-rate nerve stimulation we observed some extra rundown of transmitter release. However, no clinical evidence of transmission block or muscle weakness was found, assessed with electromyography, grip-strength testing and muscle contraction experiments. We studied both adult ( approximately 3-6 months-old) and aged ( approximately 21-26 months-old) R192Q knockin mice to assess effects of chronic elevation of presynaptic Ca(2+) influx, but found no additional or progressive alterations. No changes in NMJ size or relevant ultrastructural parameters were found, at either age. Our characterizations strengthen the hypothesis of increased Ca(2+) flux through R192Q-mutated presynaptic Ca(v)2.1 channels and show that the resulting altered neurotransmitter release is not associated with morphological changes at the NMJ or muscle weakness, not even in the longer term.

Acetylcholine↗
PubMed2004

Single-fiber EMG in familial hemiplegic migraine.

Twelve familial hemiplegic migraine (FHM) patients (6 with the I1811L mutation in CACNA1A, 3 with M731T mutation in ATP1A2, and 3 without known mutations) and 10 control subjects underwent single-fiber EMG. Mean jitter did not differ significantly between patients and control subjects or among patients. No blocking was found. The results suggest that neuromuscular function is normal in FHM.

Adolescent↗
PubMed2004

Diagnostic value of history taking in reflex syncope.

The medical history, in combination with the physical examination and a 12-lead electrocardiogram, plays a key role in the diagnosis and risk stratification of patients with syncope. However, diagnostic clinical criteria are not uniformly applied. In older studies, the diagnostic criteria for vasovagal or reflex syncope often included typical precipitating events and warning symptoms. More recent studies have documented that a variety of unrecognized stressors can trigger reflex syncope and that warning signs and symptoms may be minimal. A characteristic medical history (a trigger and/or prodromi) is enough to diagnose reflex syncope if the risk for a cardiac cause of syncope is low (e. g. patients < 65 yrs, without a history of heart disease and no ECG abnormalities). In elderly subjects with a higher risk of cardiac syncope, the yield of the medical history is lower. However, a prospective study of the value of the medical history for the diagnosis of syncope with long-term follow-up has not been performed.

Diagnosis, Differential↗
PubMed2004

Neurophysiological tests and neuroimaging procedures in non-acute headache: guidelines and recommendations.

The use of instrumental examinations in headache patients varies widely. In order to evaluate their usefulness, the most common instrumental procedures were evaluated, on the basis of evidence from the literature, by an EFNS Task Force (TF) on neurophysiological tests and imaging procedures in non-acute headache patients. The conclusions of the TF regarding each technique are expressed in the following guidelines for clinical use. 1 Interictal electroencephalography (EEG) is not routinely indicated in the diagnostic evaluation of headache patients. Interictal EEG is, however, indicated if the clinical history suggests a possible diagnosis of epilepsy (differential diagnosis). Ictal EEG could be useful in certain patients suffering from hemiplegic and basilar migraine. 2 Recording of evoked potentials is not recommended for the diagnosis of headache disorders. 3 There is no evidence to justify the recommendation of autonomic tests for the routine clinical examination of headache patients. 4 Manual palpation of pericranial muscles, with standardized palpation pressure, can be recommended for subdividing patient groups but not for diagnosis. Pressure algometry and electromyography (EMG) cannot be recommended as clinical diagnostic tests. 5 In adult and paediatric patients with migraine, with no recent change in attack pattern, no history of seizures, and no other focal neurological signs or symptoms, the routine use of neuroimaging is not warranted. In patients with atypical headache patterns, a history of seizures and/or focal neurological signs or symptoms, magnetic resonance imaging (MRI) may be indicated. 6 If attacks can be fully accounted for by the standard headache classification [International Headache Society (IHS)], a positron emission tomography (PET) or single-photon emission computerized tomography (SPECT) and scan will generally be of no further diagnostic value. 7 Nuclear medicine examinations of the cerebral circulation and metabolism can be carried out in subgroups of headache patients for diagnosis and evaluation of complications, when patients experience unusually severe attacks, or when the quality or severity of attacks has changed. 8 Transcranial Doppler examination is not helpful in headache diagnosis. Although many of the examinations described are of little or no value in the clinical setting, most of the tools have a vast potential for further exploring the pathophysiology of headaches and the effects of pharmacological treatment.

Diagnosis, Differential↗
PubMed2003

[Initial diagnostic strategy in the case of transient losses of consciousness: the importance of the medical history].

It is estimated that almost half of the people experience a transient loss of consciousness at some time during their life. In young patients (< 35 years) the cause is mostly a reflex syncope. In older patients the common causes are orthostatic and postprandial hypotension, sinus caroticus syndrome, cardiac arrhythmias and valvular disorders. The medical history can identify a probable cause of the transient loss of consciousness in almost all young patients (< 35 years) and in the majority of older patients. A physical examination and an ECG should be performed in all patients who have experienced a transient loss of consciousness, other than those with classical vasovagal syncope, in order to exclude orthostatic hypotension and dangerous cardiac causes.

Adult↗
PubMed2003

Impaired antagonist inhibition may contribute to akinesia and bradykinesia in Huntington's disease.

OBJECTIVE: To test the hypothesis that besides impaired agonist facilitation, impaired antagonist inhibition also contributes to delayed initiation (akinesia) and slow execution (bradykinesia) of voluntary movements in Huntington's disease. METHODS: Fifteen patients with Huntington's disease and 11 age-matched controls participated in the study. The amount of agonist facilitation was measured as the increase in soleus H-reflex amplitude prior to ballistic voluntary plantar flexion (soleus contraction). Antagonist inhibition was measured as the decrease in soleus H-reflex prior to ballistic dorsiflexion (tibialis anterior (TA) contraction). The amount of agonist facilitation and antagonist inhibition was correlated with the time needed for motor initiation (reaction time) and movement execution (movement time). RESULTS: Starting 50ms prior to soleus contraction, soleus H-reflex increased in control subjects but less so in patients. Soleus H-reflexes decreased in controls 25ms prior to TA contraction, while this antagonist inhibition was completely lacking in patients. Thus, patients with Huntington's disease not only displayed reduced agonist facilitation, but impaired antagonist inhibition as well. Moreover, more impairment of antagonist inhibition correlated significantly with more severe akinesia and bradykinesia. CONCLUSIONS: Antagonist inhibition prior to and during agonist contractions is markedly impaired in Huntington's disease. This impairment might contribute to motor slowness in these patients.

Adult↗