Biomedical subjects
A Fumal
Publications and source records attributed to A Fumal.
Induction of long-lasting changes of visual cortex excitability by five daily sessions of repetitive transcranial magnetic stimulation (rTMS) in healthy volunteers and migraine patients.
We have shown that in healthy volunteers (HV) one session of 1 Hz repetitive transcranial magnetic stimulation (rTMS) over the visual cortex induces dishabituation of visual evoked potentials (VEPs) on average for 30 min, while in migraineurs one session of 10 Hz rTMS replaces the abnormal VEP potentiation by a normal habituation for 9 min. In the present study, we investigated whether repeated rTMS sessions (1 Hz in eight HV; 10 Hz in eight migraineurs) on 5 consecutive days can modify VEPs for longer periods. In all eight HV, the 1 Hz rTMS-induced dishabituation increased in duration over consecutive sessions and persisted between several hours (n=4) and several weeks (n=4) after the fifth session. In six out eight migraineurs, the normalization of VEP habituation by 10 Hz rTMS lasted longer after each daily stimulation but did not exceed several hours after the last session, except in two patients, where it persisted for 2 days and 1 week. Daily rTMS can thus induce long-lasting changes in cortical excitability and VEP habituation pattern. Whether this effect may be useful in preventative migraine therapy remains to be determined.
[Medication overuse headache].
Medication overuse headache (MOH) insidiously evolves from episodic migraine or tension-type headache because of overconsumption of analgesics, ergotamine or triptans. It affects 1-2% of the general population, but 15-20% of patients attending specialized headache centers. The precise neurobiologic mechanisms underlying this complication of episodic headaches are not well understood. Abnormalities of central monoaminergic systems have been suggested and substance dependence is more frequent in personal and family histories of affected subjects. In a recent FDG-PET study of 16 migraineurs with MOH before and after analgesics withdrawal we found a persistent hypometabolism of the medial orbitofrontal cortex, comparable to the one described after withdrawal in substance abuse. The orbitofrontal cortex plays a pivotal role in drive, decision-making and drug dependence. We postulate that its hypoactivity predisposes certain migraineurs to MOH and to relapse after withdrawal. There is no unique management strategy for these patients, but medication withdrawal is a prerequisite for the effectiveness of preventive treatments and headache improvement.
Efficacy of coenzyme Q10 in migraine prophylaxis: a randomized controlled trial.
Riboflavin, which improves energy metabolism similarly to coenzyme Q10 (CoQ10), is effective in migraine prophylaxis. We compared CoQ10 (3 x 100 mg/day) and placebo in 42 migraine patients in a double-blind, randomized, placebo-controlled trial. CoQ10 was superior to placebo for attack-frequency, headache-days and days-with-nausea in the third treatment month and well tolerated; 50%-responder-rate for attack frequency was 14.4% for placebo and 47.6% for CoQ10 (number-needed-to-treat: 3). CoQ10 is efficacious and well tolerated.
Hypothalamic stimulation in chronic cluster headache: a pilot study of efficacy and mode of action.
We enrolled six patients suffering from refractory chronic cluster headache in a pilot trial of neurostimulation of the ipsilateral ventroposterior hypothalamus using the stereotactic coordinates published previously. After the varying durations needed to determine optimal stimulation parameters and a mean follow-up of 14.5 months, the clinical outcome is excellent in three patients (two are pain-free; one has fewer than three attacks per month), but unsatisfactory in one patient, who only has had transient remissions. Mean voltage is 3.28 V, diplopia being the major factor limiting its increase. When the stimulator was switched off in one pain-free patient, attacks resumed after 3 months until it was turned on again. In one patient the implantation procedure had to be interrupted because of a panic attack with autonomic disturbances. Another patient died from an intracerebral haemorrhage that developed along the lead tract several hours after surgery; there were no other vascular changes on post-mortem examination. After 1 month, the hypothalamic stimulation induced resistance against the attack-triggering agent nitroglycerin and tended to increase pain thresholds at extracephalic, but not at cephalic, sites. It had no detectable effect on neurohypophyseal hormones or melatonin excretion. We conclude that hypothalamic stimulation has remarkable efficacy in most, but not all, patients with treatment-resistant chronic cluster headache. Its efficacy is not due to a simple analgesic effect or to hormonal changes. Intracerebral haemorrhage cannot be neglected in the risk evaluation of the procedure. Whether it might be more prevalent than in deep-brain stimulation for movement disorders remains to be determined.
[Tension-type headache].
The diagnosis of tension-type headache (TTH), a heterogeneous syndrome, is mainly based on the absence of typical features found in other headaches such as migraine. However TTH is the most common headache as about 80 percent of the general population suffer from episodic TTH and 3 percent have chronic TTH (CTTH). The underlying pathophysiology is complex. The present consensus is that peripheral pain mechanisms most likely play a role in infrequent and frequent episodic TTH whereas central pain mechanisms play a more important role in CTTH. Ibuprofen (800 mg) is currently the leading choice for the treatment of acute TTH because of its very good gastro-intestinal tolerance, followed by sodium naproxen (825 mg). Tricyclic antidepressants are the most widely used first-line therapeutic agents for CTTH (amitriptyline is the most widely used). Other preventive treatments such as relaxation, muscular biofeedback and behavioural (cognitive) techniques have also showed efficacy. It is demonstrated that the combination of stress management therapy and a tricyclic is more effective in CTTH than either behavioral or drug treatment alone.
The syndrome of transient headache with neurological deficits and CSF lymphocytosis (HaNDL): electrophysiological findings suggesting a migrainous pathophysiology.
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[Genetics of migraines: from ionic channels to single nucleotide polymorphisms?].
Our knowledge about migraine pathogenesis has increased exponentially over the last decade and this greatly due to the advances in genetics. In familial hemiplegic migraine (FHM), the findings of mutations in the CACNA1A gene (19p13), coding for the pore-forming subunit (alpha1A) of neuronal voltage-dependent P/Q-type calcium channels (FHM1), and in the ATP1A2 gene (1q21-23), encoding the alpha2-subunit of the Na+, K+ ATPase ionic pump (FHM2) have focused attention on central nervous system ionic channels and helped to better understand FHM pathophysiology. A dysfunction of these channels modifies neuronal excitability (favouring spreading depression), chemical neurotransmission and, indirectly, neuronal metabolism. These channels may represent targets for novel anti-migraine drugs, which underscores their importance for the frequent forms of migraine (without or with aura). Studies of gene associations, neuromuscular transmission, cerebellar functions, neuronal excitability and metabolism and certain drug effects suggest indeed that ionic channels play a pathogenic role in migraine with aura patients. However, in the majority of patients they are probably not the sole culprit, since most of the frequent forms of migraine seem to have a more complex genetic predisposition based on a number of single nucleotide polymorphisms. The challenge for the next decade is to establish correlations between the geno- and the phenotype of migraine patients which needs more frequent and focused genetic studies and a more precise phenotype, based on clinical as well as on neurophysiologic and metabolic data.
Excitability of visual V1-V2 and motor cortices to single transcranial magnetic stimuli in migraine: a reappraisal using a figure-of-eight coil.
We used transcranial magnetic stimulation (TMS) with a figure-of-eight coil to excite motor and visual V1-V2 cortices in patients suffering from migraine without (MO) (n = 24) or with aura (MA) (n = 13) and in healthy volunteers (HV) (n = 33). Patients who had a migraine attack within 3 days before or after the recordings were excluded. All females were recorded at mid-cycle. Single TMS pulses over the occipital cortex elicited phosphenes in 64% of HV, 63% of MO and 69% of MA patients. Compared with HV, the phosphene threshold was significantly increased in MO (P = 0.001) and in MA (P = 0.007), but there was no difference between the two groups of migraineurs. The motor threshold tended to be higher in both migraine groups than in HV, but the differences were not significant. In conclusion, this study shows that two-thirds (64.86%) of patients affected by either migraine type present an increased phosphene threshold in the interictal period, which suggests that their visual cortex is hypoexcitable.
Effects of repetitive transcranial magnetic stimulation on visual evoked potentials in migraine.
Between attacks, migraine patients are characterized by potentiation instead of habituation of stimulation-evoked cortical responses. It is debated whether this is due to increased or decreased cortical excitability. We have studied the changes in visual cortex excitability by recording pattern-reversal visual evoked potentials (PR-VEP) after low- and high-frequency repetitive transcranial magnetic stimulation (rTMS), known respectively for their inhibitory and excitatory effect on the cortex. In 30 patients (20 migraine without, 10 with aura) and 24 healthy volunteers, rTMS of the occipital cortex was performed with a focal figure-of-eight magnetic coil (Magstim). Nine hundred pulses were delivered randomly at 1 or 10 Hz in two separate sessions. Stimulus intensity was set to the phosphene threshold or to 110% of the motor threshold if no phosphenes were elicited. Before and after rTMS, PR-VEP were averaged sequentially in six blocks of 100zztieresponses during uninterrupted 3.1 Hz stimulation. In healthy volunteers, PR-VEP amplitude was significantly decreased in the first block after 1 Hz rTMS and the habituation normally found in successive blocks after sustained stimulation was significantly attenuated. In migraine patients, 10 Hz rTMS was followed by a significant increase of first block PR-VEP amplitude and by a reversal to normal habituation of the potentiation (or dishabituation) characteristic of the disorder. This effect was similar in both forms of migraine and lasted for at least 9 min. There were no significant changes of PR-VEP amplitudes after 1 Hz rTMS in migraineurs and after 10 Hz rTMS in healthy volunteers, nor after sham stimulation. The recovery of a normal PR-VEP habituation pattern after high-frequency rTMS is probably due to activation of the visual cortex and the dishabituation in healthy volunteers to cortical inhibition. We conclude, therefore, that the deficient interictal PR-VEP habituation in migraine is due to a reduced, and not to an increased, pre-activation excitability level of the visual cortex.
Motor and phosphene thresholds to transcranial magnetic stimuli: a reproducibility study.
OBJECTIVES: As repetitive transcranial magnetic stimulation (rTMS) is often applied on different days, it is of interest to know whether motor (MT) and phosphene (PT) thresholds are reproducible across time and whether the intensity determined on the first day can be used in subsequent sessions. METHODS: We studied MT and PT over 5 separate recordings in 10 healthy volunteers using a focal coil and a Magstim(Rapid stimulator. After the initial recording (session 1), the others (2 to 5) were performed respectively after 1 day, 7 days, 1 month and 4 months. RESULTS: Mean MT at rest were 65.30 +/- 5.54%, 65.7 +/- 7.18%, 60.4 +/- 4.27%, 61.8 +/- 4.34%, and 63 +/- 9.1% at sessions 1 to 5. Mean PT were 71.43 +/- 6.68%, 66.29 +/- 10.67%, 60.71 +/- 8.64%, 60.57 +/- 8.08%, and 68.71 +/- 15.48% at sessions 1 to 5. MT and PT were reproducible (ANOVA analysis), however, as shown by coefficients of variation, variability between the first 3 sessions exceeded 10% for MT in 3 subjects and in 4 subjects for PT. CONCLUSIONS: It seems preferable to determine thresholds and adapt output intensity of the stimulator at each rTMS session.
[Neuroborreliosis].
Lyme disease, or borreliosis, is an endemic affection in Belgium. It is transmitted by a spirochete, Borrelia burgdorferi. The particularity of the infecting genomic group, Borrelia garinii, implies that half of the reported cases of Lyme disease in our country have neurologic manifestations. Due to the marked clinical heterogeneity and the difficult serologic diagnosis, neuroborreliosis is often part of the differential diagnosis in neurology. The antibiotic treatment is necessary because it decreases the risk of more advanced stages of the disease. We hope that a vaccination will soon be available in Belgium.
[Clinical case of the month. Report of a case of antiphospholipid syndrome].
This article reports a case of Anton-Babinski syndrome, due to right middle cerebral artery thrombosis and attributed to a likely primary antiphospholipid syndrome. It is always difficult to diagnose the latter, especially in the case of our patient who had a past history of multiple venous thromboses but also a heterozygosity for the mutation of the factor V of Leyden. We reviewed the literature dedicated to the prothrombotic events linked to the presence of these antiphospholipid antibodies: the lupus anticoagulant and the anticardiolipin antibodies.
A new combined bodian-luxol technique for staining unmyelinated axons in semithin, resin-embedded peripheral nerves: a comparison with electron microscopy.
Quantitation of unmyelinated fibers (UF) in peripheral nerves has classically relied upon ultrastructural morphometry. Because this method is time-consuming, it is not typically performed in routine analysis of nerve biopsies. We applied the Bodian-Luxol technique to detect unmyelinated axons by light microscopy on semithin sections from resin-embedded nerve tissue. Estimates were compared to ultrastructural counts. The staining appeared highly specific for axons. Excellent correlation was found between optic densities and the population of UF larger than 0.5 microm. The smallest profiles detected by light microscopy had a diameter close to 0.6 microm. This new technique is not a substitute for ultrastructural quantitative morphometry of UF, as very small unmyelinated axons, especially regenerating ones, can not be reliably visualized. However, it provides a valuable light microscopic method for evaluating axonal loss among UF.