Cluster headaches have an incidence of 1–3 per 10,000 with a 2.5:1 male-to-female gender ratio. Although not life threatening, the impact of the attacks on the individual patient can result in tremendous pain and disability. The pathophysiology of the disease is unclear, but it is known that the hypothalamus, the brainstem, and genetic factors, such as the G1246A polymorphism, play a role. A distinction is made between episodic and chronic cluster headaches. In a controlled setting, we treated 29 patients with cluster headaches (13 with chronic cluster and 16 with the episodic form), who had been refractory to conventional treatments, with a low dose of ketamine (an NMDA receptor antagonist) i.v. over 40 min to one hour every 2 weeks or sooner for up to four times. It was observed that the attacks were completely aborted in 100 % of patients with episodic headaches and in 54 % of patients with chronic cluster headaches for a period of 3–18 months. We postulated neuroplastic brain repair and remodulation as possible mechanisms.
Fifty-seven CH patients according to ICHD-II-criteria participated in a single-blinded, semi-randomized, placebo-controlled, crossover inpatient study, and 102 CH attacks were treated with 100% oxygen delivered by demand valve oxygen (DVO), O2ptimask or simple mask (15 liters/min) or placebo delivered by DVO for 15 minutes. Primary endpoint: Two-point decrease of pain on a five-point rating scale within 15 minutes.
Episodic cluster headache is characterized by abnormalities in tyrosine metabolism (i.e. elevated levels of dopamine, tyramine, octopamine and synephrine and low levels of noradrenalin in plasma and platelets.) It is unknown, however, if such biochemical anomalies are present and/or constitute a predisposing factor in chronic cluster headache. To test this hypothesis, we measured the levels of dopamine and noradrenaline together with those of elusive amines, such as tyramine, octopamine and synephrine, in plasma of chronic cluster patients and control individuals.
If you do create your own setup, you will need to purchase a regulator appropriate for the tank you are using. Different tank types use different regulators due to tank pressures. 0-25 lpm regulators for E tanks are readily available online. In addition to this, you will need to purchase a mask and oxygen hose (clear tubing).
If you are not currently under medical care, it is feasible to get oxygen directly from a reputable oxygen supplier. Welding oxygen is also pure and typically comes from the same source as medical oxygen. The key difference between medical and non-medical oxygen relates more to the chain of custody of the oxygen tank (cylinder) and requirements regarding purging the tank prior to filling. You can always ask your oxygen supplier to purge your tanks before filling.
Setting up your tank properly is important to avoid any errant spillage of oxygen. The simple solution is checking your setup before opening the valve to make sure all hose connections are tight and that your regulator is firmly attached to the cylinder. Then open the tank valve slowly and set the regulator at a low flow setting, ie. 5 lpm. Listen and feel for any leaks around the regulator and hose connections. If you hear oxygen leaking anywhere but at the mask itself, close the tank valve and correct it. When using oxygen, take extra care not to allow the oxygen to flow freely for any extended period. Always turn oxygen off at the tank valve, not with the regulator.
There’s a lot of buzz on social media about a rather unconventional treatment for migraine. Some patients are choosing to treat migraine by ear piercing. More specifically, a daith piercing, which is a piercing of the innermost cartilage fold just above the opening to the ear canal. The theory is that an acupuncture point located here, when pierced, produces the same pain relief results as acupuncture.
Therapeutic agents that block the calcitonin gene–related peptide (CGRP) signaling pathway are a highly anticipated and promising new drug class for migraine therapy, especially after reports that small-molecule CGRP-receptor antagonists are efficacious for both acute migraine treatment and migraine prevention. Using XenoMouse technology, we successfully generated AMG 334, a fully human monoclonal antibody against the CGRP receptor. Here we show that AMG 334 competes with [125I]-CGRP binding to the human CGRP receptor, with a Ki of 0.02 nM. AMG 334 fully inhibited CGRP-stimulated cAMP production with an IC50 of 2.3 nM in cell-based functional assays (human CGRP receptor) and was 5000-fold more selective for the CGRP receptor than other human calcitonin family receptors, including adrenomedullin, calcitonin, and amylin receptors.