Peripheral provocation of cranial autonomic symptoms is not sufficient to trigger cluster headache attacks

Cephalalgia ◽  
2017 ◽  
Vol 38 (8) ◽  
pp. 1498-1502 ◽  
Author(s):  
Maike Möller ◽  
Ame Abdu Haji ◽  
Jan Hoffmann ◽  
Arne May
Keyword(s):  
Cluster Headache ◽  
Low Frequency ◽  
Central Component ◽  
Autonomic Symptoms ◽  
Cranial Autonomic Symptoms ◽  
Peripheral Stimulation ◽  
Low Frequency Stimulation ◽  
Frequency Stimulation ◽  
Lost To Follow Up

Background Recently it has been suggested that low frequency stimulation of the sphenopalatine ganglion (SPG) may provoke cluster-like attacks in cluster headache (CH) patients. The question arises whether a robust activation of cranial autonomic symptoms is sufficient to trigger CH attacks. Methods Kinetic oscillation stimulation (KOS) of the nasal mucosa generates ipsilateral marked autonomic symptoms, among which lacrimation is quantitatively measurable. KOS was applied to 29 CH-patients, including both episodic and chronic course. We measured lacrimation at rest and during stimulation, and assessed CH attacks within 24 hours after the experiment. Results Autonomic symptoms including lacrimation were robust and significantly generated, compared to rest. Six patients were lost to follow-up, but did not develop an attack during their stay in the clinic. Of the remaining 23 patients, none developed an attack in the next 4 hours after stimulation, despite marked cranial autonomic symptoms during stimulation. Discussion Peripheral stimulation close to the SPG generated a strong parasympathetic response. However, this stimulation was not sufficient to induce CH attacks, which suggests that a central component is crucial to attack generation.

Low frequency activation of the sphenopalatine ganglion does not induce migraine-like attacks in migraine patients

Cephalalgia ◽  
2020 ◽  
Vol 40 (9) ◽  
pp. 966-977
Author(s):  
Song Guo ◽  
Katrine Falkenberg ◽  
Henrik Winther Schytz ◽  
Anthony Caparso ◽  
Rigmor Højland Jensen ◽  
...  
Keyword(s):  
Superficial Temporal Artery ◽  
Low Frequency ◽  
Temporal Artery ◽  
Sphenopalatine Ganglion ◽  
Double Blind ◽  
Autonomic Symptoms ◽  
Low Frequency Stimulation ◽  
Registration Number ◽  
Frequency Stimulation ◽  
Stimulation Of

Introduction Cephalic autonomic symptoms occur in 27‒73% of migraine patients during attacks. The role of parasympathetic activation in migraine attack initiation remains elusive. Low frequency stimulation of the sphenopalatine ganglion increases parasympathetic outflow. In this study, we hypothesized that low frequency stimulation of the sphenopalatine ganglion would provoke migraine-like attacks in migraine patients. Methods In a double-blind randomized sham-controlled crossover study, 12 migraine patients with a sphenopalatine ganglion neurostimulator received low frequency or sham stimulation for 30 min on two separate days. We recorded headache characteristics, cephalic autonomic symptoms, ipsilateral mechanical perception and pain thresholds, mean blood flow velocity in the middle cerebral artery (VMCA) and diameter of the superficial temporal artery during and after stimulation. Results Five patients (42%) reported a migraine-like attack after low frequency stimulation compared to six patients (50%) after sham ( p = 1.000). We found a significant increase in mechanical detection thresholds during low frequency stimulation compared to baseline ( p = 0.007). Occurrence of cephalic autonomic symptoms and changes in mechanical perception thresholds, VMCA and diameter of the superficial temporal artery showed no difference between low frequency stimulation compared to sham ( p = 0.533). Conclusion Low frequency stimulation of the sphenopalatine ganglion did not induce migraine-like attacks or autonomic symptoms in migraine patients. These data suggest that increased parasympathetic outflow by the sphenopalatine ganglion neurostimulator does not initiate migraine-like attacks. Study protocol: ClinicalTrials.gov registration number NCT02510742

Fatigue and damage to the masseter muscle by prolonged low-frequency stimulation in the rat

2005 ◽  
Vol 50 (12) ◽  
pp. 1005-1013 ◽  
Author(s):  
Konosuke Yamasaki ◽  
Shuitsu Harada ◽  
Itsuro Higuchi ◽  
Mitsuhiro Osame ◽  
Gakuji Ito
Keyword(s):  
Masseter Muscle ◽  
Low Frequency ◽  
Low Frequency Stimulation ◽  
Frequency Stimulation

scholarly journals MONOSYNAPTIC REFLEX RESPONSE OF INDIVIDUAL MOTONEURONS AS A FUNCTION OF FREQUENCY

1957 ◽  
Vol 40 (3) ◽  
pp. 435-450 ◽  
Author(s):  
David P. C. Lloyd
Keyword(s):  
High Frequency ◽  
Temporal Summation ◽  
Low Frequency ◽  
Stimulation Frequency ◽  
Monosynaptic Reflex ◽  
Reflex Response ◽  
High Frequency Stimulation ◽  
Low Frequency Stimulation ◽  
Frequency Stimulation ◽  
Frequency Of Stimulation

An assemblage of individual motoneurons constituting a synthetic motoneuron pool has been studied from the standpoint of relating monosynaptic reflex responses to frequency of afferent stimulation. Intensity of low frequency depression is not a simple function of transmitter potentiality. As frequency of stimulation increases from 3 per minute to 10 per second, low frequency depression increases in magnitude. Between 10 and approximately 60 per second low frequency depression apparently diminishes and subnormality becomes a factor in causing depression. At frequencies above 60 per second temporal summation occurs, but subnormality limits the degree of response attainable by summation. At low stimulation frequencies rhythm is determined by stimulation frequency. Interruptions of rhythmic firing depend solely upon temporal fluctuation of excitability. At high frequency of stimulation rhythm is determined by subnormality rather than inherent rhythmicity, and excitability fluctuation leads to instability of response rhythm. In short, whatever the stimulation frequency, random excitability fluctuation is the factor disrupting rhythmic response. Monosynaptic reflex response latency is stable during high frequency stimulation as it is in low frequency stimulation provided a significant extrinsic source of random bombardment is not present. In the presence of powerful random bombardment discharge may become random with respect to monosynaptic afferent excitation provided the latter is feeble. When this occurs it does so equally at low frequency and high frequency. Thus temporal summation is not a necessary factor. There is, then, no remaining evidence to suggest that the agency for temporal summation in the monosynaptic system becomes a transmitting agency in its own right.

Effects of low-frequency stimulation of the superior colliculus on spontaneous and visually guided saccades

1993 ◽  
Vol 69 (3) ◽  
pp. 953-964 ◽  
Author(s):  
P. W. Glimcher ◽  
D. L. Sparks
Keyword(s):  
Superior Colliculus ◽  
Time Course ◽  
Low Frequency ◽  
Arbitrary Point ◽  
Visually Guided ◽  
Spontaneous Movements ◽  
Low Frequency Stimulation ◽  
Frequency Stimulation ◽  
Stimulation Current ◽  
Stimulation Of

1. The first experiment of this study determined the effects of low-frequency stimulation of the monkey superior colliculus on spontaneous saccades in the dark. Stimulation trains, subthreshold for eliciting short-latency fixed-vector saccades, were highly effective at biasing the metrics (direction and amplitude) of spontaneous movements. During low-frequency stimulation, the distribution of saccade metrics was biased toward the direction and amplitude of movements induced by suprathreshold stimulation of the same collicular location. 2. Low-frequency stimulation biased the distribution of saccade metrics but did not initiate movements. The distribution of intervals between stimulation onset and the onset of the next saccade did not differ significantly from the distribution of intervals between an arbitrary point in time and the onset of the next saccade under unstimulated conditions. 3. Results of our second experiment indicate that low-frequency stimulation also influenced the metrics of visually guided saccades. The magnitude of the stimulation-induced bias increased as stimulation current or frequency was increased. 4. The time course of these effects was analyzed by terminating stimulation immediately before, during, or after visually guided saccades. Stimulation trains terminated at the onset of a movement were as effective as stimulation trains that continued throughout the movement. No effects were observed if stimulation ended 40–60 ms before the movement began. 5. These results show that low-frequency collicular stimulation can influence the direction and amplitude of spontaneous or visually guided saccades without initiating a movement. These data are compatible with the hypothesis that the collicular activity responsible for specifying the horizontal and vertical amplitude of a saccade differs from the type of collicular activity that initiates a saccade.

Natural course of untreated cluster headache: A retrospective cohort study

Cephalalgia ◽  
2017 ◽  
Vol 38 (4) ◽  
pp. 655-661 ◽  
Author(s):  
Mi Ji Lee ◽  
Hyun Ah Choi ◽  
Jong Hwa Shin ◽  
Hea Ree Park ◽  
Chin-Sang Chung
Keyword(s):  
Cluster Headache ◽  
Disease Duration ◽  
Medical Center ◽  
Natural Course ◽  
Duration Of Disease ◽  
Lost To Follow Up ◽  
Active Patients ◽  
Single Predictor ◽  
Over Time

Objective To determine the natural course of cluster headache. Methods We screened patients with cluster headache who were diagnosed at Samsung Medical Center and lost to follow-up for ≥5 years. Eligible patients were interviewed by phone about the longitudinal changes in headache characteristics and disease course. Remission was defined as symptom-free 1) for longer than twice the longest between-bout period and 2) for ≥5 years. Results Forty-two patients lost to follow-up for mean 7.5 (range, 5.0–15.7) years were included. The length of the last bout did not differ from the first one, while the last between-bout period was longer than the first one ( p = 0.012). Characteristics of cluster headache decreased over time: Side-locked unilaterality (from 92.9% to 78.9%), seasonal and circadian rhythmicity (from 63.9% to 60.9% and from 62.2 to 40.5%, respectively), and autonomic symptoms (from 95.2% to 75.0%). Remission occurred in 14 (33.3%) patients at a mean age of 42.3 (range, 27–65) years, which was not different from the age of last bouts in active patients ( p = 0.623). There was a trend for more seasonal and circadian predilection at baseline in the active group ( p = 0.056 and 0.063, respectively) and fewer lifetime bouts and shorter disease duration in patients in remission ( p = 0.063 and 0.090). Conclusions This study first shows the natural courses of cluster headache. Features of cluster headache become less prominent over time. Remission occurred regardless of age. Although no single predictor of remission was found, our data suggest that remission of cluster headache might not be a consequence of more advanced age, longer duration of disease, or accumulation of lifetime bouts.

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