ESSENTIALS IN UNDERSTANDING HEADACHE
What causes headaches?
Headache theory has been a heavily evolving field of study. The unified theory of headache states that all headaches originate as increased nerve activity in the center of the brain at the periaquaductal grey (PAG). This increased nerve activity propagates through the brain leaving neuronal inflammation and hyperexcitability in its wake. The increased nerve activity can advance along nerve paths or in a wave-like expansion like a stone dropped in a pond. As this increased nerve activity flows over and through the brain and upper spinal cord, it activates nerves and structures that hang off the brain and spinal cord, called cranial nerves, spinal nerves and nuclei. Which structures are activated determines the symptoms of the headache.
These cranial nerves and nuclei serve major functions primarily in the head and neck but also in the stomach and intestines. The most common headaches are associated with the activation of cranial nerves 5,10 and 11 (V,X and XI), their origins in the brain stem (called nuclei), and nerves that exit from the upper spine called spinal nerves 2 and 3 (C2,C3) as well as other deep brain stem structures.
The locus coeruleus and nucleus raphe are deep brain structures adjacent to the PAG. These structures are involved in sensory integration that when activated is thought to be responsible for the throbbing as well as light and sound sensitivity associated with some headache. The locus coeruleus and raphe nucleus are also key players in the sleep initiation/ maintenance mechanism.
CN V, the trigeminal nerve, and its nucleus, trigeminal nucleus caudalis (TNC), provide the sensory and pain nerves to the face, sinuses, and temples. Its' activation causes the face, sinus and temple pain/pressure associated with headache. It also provides motor innervation to the chewing muscles and parts of the soft pallet. This is associated with jaw and some pallet pain. Due to its length and location in the brainstem, the TNC is thought to be a primary transmitter of increased nerve activity causing structure activation in headache pathophysiology.
CN X and its nuclei serves as the nausea and vomiting center as well as innervation to the GI tract. When CN X is activated it causes nausea and vomiting.
CN XI provides the nerve supply to shoulder and upper back muscles, called the trapezius, and when activated causes the shoulder and upper back pain.
Finally, the TNC extends far enough down the brainstem to stimulate the upper cervical nerves (C2 and C3). C2 and C3 innervate the muscles at the base of the head, called the suboccipital muscles directly and via the greater and lesser occipital nerves. When these nerves are activated they cause pain/pressure at the base of the head.
These are the most commonly activated brain structures in HA because of their close proximity to the PAG. However, other brain structures can be activated causing somewhat less common symptoms in HA types. These symptoms include double vision, sensitivity to smells, ringing in the ears, eye pain, redness and tearing, and throat tightness/soreness.
In some cases the increased nerve activity extends along the outer surface of the brain in an area called the cortex and meninges in what is called cortical spreading depression. This creates more complex symptoms called aura. The most common aura is bright spots in the vision called scotomata, however it can also exist as sensing smells that are not present or tingling, numbness or even temporary paralysis. There are blood vessels in this area that when activated by the increased nerve activity can cause the head pulsation associated with Migraine.
What causes this neurological process to stimulate different structures in different patients is a combination of each persons own vulnerabilities in their neurological pathways and the amount of time that these overstimulation-generated- neurological-changes have to affect the nervous system.
David Tanner D.O.
The Migraine Center
How can this be a migraine, I just have neck tension and head pressure?
Migraine begins as a marked increase in neuronal activity that starts deep within the brain. This increase propagates through the brain leaving neuronal inflammation and hyperexcitability in its wake. This process creates the symptoms that we attribute to migraine.
When this is a new, undeveloped process the neurons start in a pristine undisturbed state then abruptly escalate into an excitability and inflammatory chaos along a few select pathways. Patients' symptoms include photo/phonophobia, nausea, vomiting, and severe headache. This process can be aborted with triptans at onset and is diagnosed as episodic migraine (EM).
As this process is repeated the neurons fail to return to a baseline level of activity and involve many neurological pathways. This creates a change in patient symptoms which are typically of a dull, relentless nature. It is also associated with anxiety/depression, irritable bowel complaints, sleep problems and muscle/body pain (fibromyalgia). Symptoms combine decreasing or lost features of EM with periods of face and temple pressure as well as neck, shoulder and back of the head tension.
This may be confused with EM or chronic tension type headache (CTTH) but a more accurate diagnosis is transformed migraine (TM). This does not respond well to triptans. This is better treated with PT, deep tissue therapy, biofeedback, tizanidine, corticosteroids, burst phenergan or compazine with toradol, anticonvulsants, peripheral nerve blocks and Botox for migraine. The first step in treating head and neck is determining where a patient is on this continuum and then creating a treatment plan tailored to them.
Arguably, the greatest advances in the treatment of head and neck pain has come with the understanding that migraine is a condition with evolving symptoms and that it is related to other headaches.
David Tanner D.O.
The Migraine Center