back-pain

Injectable Therapy for Migraine (Onabotulinumtoxina A)

Injectable Treatments and Preventive Therapies for Migraine

Migraine is a neurological condition that causes severe throbbing pain, usually on one side of your head.

Migraine episodes are pretty common. According to a 2018 studyTrusted Source, they affect around one out of six Americans, most commonly women. Migraine is more than just a “bad headache.” If you have episodes, you may experience a multitude of symptoms that can substantially affect your life, including:

  • depression
  • anxiety
  • fatigue
  • stress
  • anger and apprehension

There are many treatments for migraine. One kind, injectable medications, can both stop and prevent migraine episodes. Let’s cover injections for migraine — their types, mode of administration, side effects, and other helpful info.

Preventive migraine injection medication brands

The following injectable CGRP inhibitors are Food and Drug Administration (FDA) approved for the prevention of migraine:

  • eptinezumab (Vyepti)
  • erenumab (Aimovig)
  • fremanezumab (Ajovy)
  • galcanezumab (Emgality)

OnabotulinumtoxinA Mechanism Overview

OnabotulinumtoxinA has proven its efficacy in reducing the number of headache days in chronic migraine (CM) patients. The usual paradigm includes 31 pericranial injection sites with low dose (5 U) per site. The aim of this study is to present the results obtained using a simpler injection protocol of onabotulinumtoxinA, with injection sites targeted to pericranial myofascial sites of pain.

OnabotulinumtoxinA contains 900-kDa BoNTA protein complex consisting of the 150-kDa botulinum neurotoxin and several nontoxic, neurotoxin-associated proteins (NAPs). The NAPs are thought to play a role in the pharmacologic actions of the neurotoxin, including structural stability of the neurotoxin,15 protection from proteolysis,16 and/or binding kinetics.17 OnabotulinumtoxinA acts on peripheral nerve terminals to interfere with specific events in the synaptic vesicle cycle. Briefly, at nerve terminals, synaptic vesicles undergo fusion to the cell membrane and are recycled. Vesicles containing neurotransmitters and neuropeptides destined for synaptic release undergo docking, priming, and fusion with the neuronal membrane.18 These steps require the crucial formation of the protein assembly SNARE complex (soluble N-ethylmaleimide-sensitive fusion-attachment protein receptor) (Fig. 1, top panel).19 Vesicular contents include small molecules in small synaptic vesicles (eg, acetylcholine and glutamate), or neuropeptides in large dense core vesicles (eg, calcitonin gene-related peptide [CGRP], pituitary adenylate cyclase activating peptide 38 [PACAP 38], and Substance P). Large dense core vesicle cargo include proteins and receptors (eg, transient receptor potential cation channel subfamily V member 1 [TRPV1], transient receptor potential cation channel subfamily A member 1 [TRPA1], purinergic receptor P2X ligand-gated ion channel 3 [P2X3], etc.) whose insertion into the lipid bilayer of the synaptic membrane is critical for proper pain signaling.20, 21 In some cases, vesicles fuse with the nerve terminal membrane through constitutive exocytosis,22 which is a housekeeping function. In other cases, fusion of synaptic vesicles with nerve terminal membrane is SNARE mediated. SNARE ability to regulate exocytosis is most commonly associated with electrical activity in the nerve. Synaptic vesicles that have fully fused with the membrane then undergo recycling and the process begins again.