Findings suggest that singing and painting interventions may reduce pain and improve mood, quality of life, and cognition in patients with mild AD, with differential effects of painting for depression and singing for memory performance.
Background: Cluster headache (CH) is a relatively rare disease and episodic CH is more frequent than chronic CH. Few studies have described the characteristics of patients with chronic CH. Methods: This was a descriptive study carried out by eight tertiary care specialist headache centres in France participating in the Observatory of Migraine and Headaches (OMH). From 2002 to 2005, OMH collected data from 2074 patients with CH, of whom 316 had chronic CH. From January to June 2005, 113 patients with chronic CH were interviewed using standardised questionnaires during a consultation. Results: The male to female ratio was 4.65:1. Median age was 42 years. The majority of patients were smokers or former smokers (87%). 46% had primary chronic CH (chronic at onset) and 54% secondary chronic CH (evolving from episodic CH). Most patients had unilateral pain during attacks and 7% had sometimes bilateral pain during an attack. 48% reported a persisting painful state between attacks. Symptoms anteceding pain onset (mainly discomfort/diffuse pain, exhaustion, mood disorders) and auras were reported by 55% and 20% of patients, respectively. The functional impact of chronic CH was estimated as severe by 74% of patients, and 75.7% suffered from anxiety, as assessed by the Hospital Anxiety and Depression scale. There was no substantial difference in clinical presentation between primary and secondary CH. Discussion: This study confirms the existence of auras and interictal signs and symptoms in patients with chronic CH, and male sex and smoking as CH risk factors. Primary and secondary chronic CH appear equally prevalent. Male sex does not appear to favour the shift from episodic to chronic CH.
Chronic cluster headache (CCH) is a disabling primary headache, considering the severity and frequency of pain attacks. Deep brain stimulation (DBS) has been used to treat severe refractory CCH, but assessment of its efficacy has been limited to open studies. We performed a prospective crossover, double-blind, multicenter study assessing the efficacy and safety of unilateral hypothalamic DBS in 11 patients with severe refractory CCH. The randomized phase compared active and sham stimulation during 1-month periods, and was followed by a 1-year open phase. The severity of CCH was assessed by the weekly attacks frequency (primary outcome), pain intensity, sumatriptan injections, emotional impact (HAD) and quality of life (SF12). Tolerance was assessed by active surveillance of behavior, homeostatic and hormonal functions. During the randomized phase, no significant change in primary and secondary outcome measures was observed between active and sham stimulation. At the end of the open phase, 6/11 responded to the chronic stimulation (weekly frequency of attacks decrease >50%), including three pain-free patients. There were three serious adverse events, including subcutaneous infection, transient loss of consciousness and micturition syncopes. No significant change in hormonal functions or electrolytic balance was observed. Randomized phase findings of this study did not support the efficacy of DBS in refractory CCH, but open phase findings suggested long-term efficacy in more than 50% patients, confirming previous data, without high morbidity. Discrepancy between these findings justifies additional controlled studies (clinicaltrials.gov number NCT00662935).
Deep brain stimulation of the posterior hypothalamus is a therapeutic approach to the treatment of refractory chronic cluster headache, but the precise anatomical location of the electrode contacts has not been clearly assessed. Our aim was to study the location of the contacts used for chronic stimulation, projecting each contact centre on anatomic atlases. Electrodes were implanted in a series of 10 patients (prospective controlled trial) in the so-called 'posteroinferior hypothalamus' according to previously described coordinates, i.e. 2 mm lateral, 3 mm posterior and 5 mm below the mid-commissural point. The coordinates of the centre of each stimulating contact were measured on postoperative computed tomography or magnetic resonance imaging scans, taking into account the artefact of the electrode. Each contact centre (n=10; left and right hemispheres pooled) was displayed on the Schaltenbrand atlas and a stereotactic three dimensional magnetic resonance imaging atlas (4.7 tesla) of the diencephalon-mesencephalic junction for accurate anatomical location. Of the 10 patients with 1-year follow-up, 5 responded to deep brain stimulation (weekly frequency of attacks decrease >50%). In responders, the mean (standard deviation) coordinates of the contacts were 2.98 (1.16) mm lateral, 3.53 (1.97) mm posterior and 3.31 (1.97) mm below the mid-commissural point. All the effective contacts were located posterior to the hypothalamus. In responders, structures located <2 mm from the centres of effective contacts were: the mesencephalic grey substance (5/5), the red nucleus (4/5), the fascicle retroflexus (4/5), the fascicle longitudinal dorsal (3/5), the nucleus of ansa lenticularis (3/5), the fascicle longitudinal medial (1/5) and the thalamus superficialis medial (1/5). The contact coordinates (Wilcoxon test) and the structures (Fisher's exact test) were not significantly different between responders and non-responders. These findings suggest that failure of deep brain stimulation treatment in cluster headache may be due to factors unrelated to electrode misplacement. They also suggest that the therapeutic effect is probably not related to direct hypothalamic stimulation. Deep brain stimulation might modulate either a local cluster headache generator, located in the hypothalamus or in the mesencephalic grey substance, or non-specific anti-nocioceptive systems.
Background: Since pre‐incisional peritonsillar infiltrations of local anesthetic solutions have been suggested to reduce postoperative pain after tonsillectomy, we compared the efficacy of either pre‐ or postoperative local anesthetic infiltration upon post‐tonsillectomy pain.Methods: After the induction of general anesthesia, 68 consecutive healthy patients, ranging in age from 8 to 65 years, were randomly allocated to either receive peritonsillar infiltration with 0.25% bupivacaine (group 1) or normal saline (group 2) before incision. A third group (group 3) had their peritonsillar region infiltrated with 0.25% bupivacaine after the completion of surgery but before the patients were awakened from anesthesia. All the patients were treated in the same way in the postoperative period: NSAIDs were given intravenously to adults and rectally to children. Acetaminophen was given intravenously or rectally (children aged < 15 yr) if additional analgesic support was requested by the patient. Additional acetaminophen consumption was recorded daily. Pain scores were assessed on every patient with the use of a visual analogue scale (VAS) at rest, 1, 5, 9, 13, 17, 21 and 36 h after surgery, and also on swallowing during the first postoperative day.Results: Global VAS pain scores were lower in the groups treated with bupivacaine infiltration during the first 24 h after surgery (P < 0.05). Supplementary analgesic consumption was lower in group 3 than in group 2 during the 0–9 h interval immediately following surgery (P < 0.05). There were no statistically significant differences for any other parameters between the 3 groups.Conclusion: These results suggest that the timing of peritonsillar infiltration with bupivacaine is not of clinical importance and does not affect the quality of postoperative analgesia in patients undergoing tonsillectomy.
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