Ross Hauser, MD Reviews Cervical Spine Instability and Potential Effects on Brain Physiology

Ross Hauser, MD.

Cervical spine instability can significantly impact a patient’s life. Yet, the accurate diagnosis of cervical spine instability and the ability of doctors to get to the root cause of the patient’s problems is still perplexing to many health care providers with the end result that a patient is not being helped. We see many people who have had many MRIs, CT scans, and x-rays, and hearing a different clinician give another explanation for their symptoms. Then with no immediate answers, the patient is thrust into a myriad of medications, treatments, and surgeries without relief. Eventually, the patient goes to pain management and is placed on long-term narcotics. Often the families and even spouses do not understand because the person “looks normal” but the person is “off,” or not the “same person.” Brain Physiology is how the brain works, disrupted brain physiology is how the brain may not work correctly. In this review article, a brief description is offered of how cervical spine instability can impact brain physiology.

Cervical Spine Instability Potential Effects on Brain Physiology

All vascular (blood supply) and nerve tracks that travel to and from the brain go through the neck; as such cervical structural changes (a change in the curvature of the neck) including instability can potentially affect brain physiology and give symptoms. These symptoms may including headaches, vision changes, brain fog, dizziness, weakness, drop attacks, and imbalance. The cause of neurological issues that arise in cervical instability is unclear. One cause could be cervical instability affecting brain physiology.

The flow of nerve impulses are disrupted primarily by one of four mechanisms:

• (1) direct compression or irritation by a structure such as a vertebral bone or muscle spasm pressing on the nerves,
• (2) interruption in its own nutrition through disruption of arterial blood flow, (the nerves are not being fed),
• (3) blockage of cerebrospinal fluid flow, (a problem of blood outflow from the brain) or
• (4) hindrance of venous drainage, which is also associated with number 3 and is important in understanding how instability, especially in the neck, can disrupt nervous system transmission of impulses. The following mechanisms can explain these mechanisms in affecting brain physiology in patients with cervical instability.

Carotid sheath compression – Low blood flow to the brain (Ischemia) can lead to drop attacks, brain fog, and other symptoms

What are we seeing in this image? An ultrasound of the neck shows the three main structures in the carotid sheath. The internal jugular vein, the Vagus Nerve, the carotid artery.

There are many important structures in the neck such as nerves, arteries, veins, and lymphatics. Due to this, instability in this area can cause serious consequences. The carotid sheath encases the carotid artery, jugular vein, vagus nerve, and the sympathetic plexus of nerves. The carotid sheath is located behind the sternocleidomastoid muscle in the deep cervical fascia of the neck. The carotid sheath begins above the sternum and first rib, extending to the base of the skull. The glossopharyngeal nerve, accessory nerve, and hypoglossal nerve enter the superior section of the carotid sheath briefly. (9) The Carotid artery runs right in front of vertebra C1, consequently, the styloid process of C1 can compress the carotid artery. (3) Instability of the cervical spine can cause compression on the carotid sheath due to its proximity. The cervical compression can cause arterial ischemia (inadequate blood flow to the brain). (8) Low blood flow to the brain can have grave consequences. Ischemia can lead to drop attacks, brain fog, and other symptoms. (7)

Companion articles on this website explain in greater detail the possible consequence and symptoms caused by carotid artery, jugular vein, vagus nerve, and sympathetic plexus of nerves compression.

• Can cervical spine instability cause cardiovascular-like attacks, heart palpitations, and blood pressure problems?
  • In this article, I review how symptoms of chest pain, racing heartbeat, panic attacks, fainting, near-fainting episodes, and anxiety may be coming from a problem in the cervical spine causing compression on the nerves, arteries, and veins that are all part of the cardiovascular system.
•  Symptoms and conditions of cervical spine compression causing internal jugular vein stenosis
  • In this article, I discuss the cases of people who have been searching for possible answers to their understanding of jugular vein compression. We see many patients with intracranial hypertension who come to our center because they have a constellation of symptoms like head pressure, brain fog, eye pain, glaucoma, vision problems, and many others that indicate the root cause may involve their internal jugular vein being compressed in the upper cervical spine.

Venous insufficiency

Venous insufficiency is a restriction of venous outflow from the brain and spinal cord usually due to an occlusion of the veins in the head and neck. The structure of the misaligned craniocervical joint can obstruct nearby anatomy such as the jugular foramen. (3) A restricted jugular foramen could put pressure on important vasculature. The vasculature is small and most likely to be compressed at the craniocervical junction (C0-C1). This vein compression obstructs blood flow back to the heart, thereby causing venous insufficiency. (4) The jugular vein is frequently narrowed in patients with increased intracranial hypertension. Narrowing of the jugular veins has been documented in patients between the lateral mass and styloid process of C1. (3) Most cerebral venous drainage is through the internal jugular vein. (4)

The cerebrospinal venous system drains cerebrospinal fluid containing neural waste products out of the brain. (4) Venous insufficiency can cause an accumulation of this excess cerebrospinal fluid and toxic metabolites in and around the brain. (2) Blocked vasculature around the brain has been indicated in up to 90% of cases of intracranial hypertension. (2,5) It has been suggested there is a brain-wide route for removing waste and water from the brain. (13)

The brain’s lymphatic drainage is similar to venous drainage. An obstruction or compression could cause problems to arise in the CSF flow. Failure of the brain’s lymphatics may cause neurodegenerative and neuroimmunological diseases. (13)

It might be crucial for toxic waste solutes of the brain to be cleared. A hallmark of dementia is pathologic accumulations of these toxic waste solutes. There have been reports of reduced glial lymphatic (glymphatic – waste disposal) function that may be instrumental in conditions such as dementia. Venous insufficiency may be a predisposing factor for inner ear disorders.  (13, 25) Venous insufficiency can be caused by cervical instability as loose structures slip and occlude the veins and lymphatics around the head and neck. (25)

In my review article: Venous insufficiency – Chronic Cerebrospinal Venous Insufficiency and neurologic-like problems,  I discuss symptoms and conditions of Chronic Cerebrospinal Venous Insufficiency outside of a primary neurological disorder such as diagnosis of Multiple Sclerosis. At our center we do not treat these diseases, we treat craniocervical instability, upper cervical spine instability, cervical spine instability, or problems related to neck pain and loss of cervical spine curvature that may share common symptoms and characteristics of neurological-like and vascular-like disorders.

 Venous insufficiency – What are we seeing in this image?

Depicted is a conventional view of the intake and outtake of cerebrospinal fluid flow. There are four ventricles of the brain. This is what they do.

• The ventricles are filled with cerebrospinal fluid. The cerebrospinal fluid protects the Central Nervous System by acting as a protective fluid barrier against head impact.
• Beyond this the ventricles
  • produce cerebrospinal fluid
  • create the flow of the cerebrospinal fluid to collect debris and waste in the brain
  • flushes out the waste-filled cerebrospinal fluid
• We see that the flow of the cerebrospinal fluid starts in the center portion of the brain at the Lateral Ventricle, flows down towards the cerebellum at the base rear of the skull, and then moves in a counter-clockward manner around the brain to the front of the brain and eventually down the front of the brain towards the spinal column.

What are we seeing in this image? The blockage of fluid flow in the brain and its consequence

On the left, we see the damaging effects of the clogged brain, the cerebrospinal fluid and waste disposal symptoms of the brain are backed up. We see obstruction of arteries and veins by the misplaced C1 vertebrae and accompanying cervical spine instability. The obstruction prevents fluids in and fluids out of the brain.  Ultimately there will be an accumulation of cerebrospinal fluid in various parts of the brain including the frontal lobe. This will eventually lead to the destruction of brain neurons and brain tissue. This can be an underlying cause of severe brain fog and mental decline in people with cervical instability. On the right side is a healthy brain with the proper flow of fluids in and out.

In my article Brain Toilet Obstruction (BTO), use this analogy of a clogged toilet to describe the problems of a brain that is not draining its toxic fluids and replenishing its clean fluids properly. We will discuss the problems these waste products from brain neuron activity may cause and what happens when these fluids back up and cannot be flushed out of the brain. We will also discuss what would happen to your brain cells in this situation of a clogged and backed-up brain toilet. What type of symptoms you may develop. What kind of conditions may present themselves.

Vertebrobasilar insufficiency

Vertebrobasilar insufficiency is poor blood flow to the back portion of the brain or decreased circulation to the brainstem. The vertebral and basilar arteries supply blood to many vessels in the posterior circulation of the brain. The basilar artery is joined to the brainstem. Compression of the basilar artery has been shown to cause cranial nerve palsies and ischemic (stroke-like) events. The intracranial part of the vertebral arteries and their branches supply the medulla with blood. The vertebral arteries then join the basilar artery and the pons (the grouping of nerve fibers at the back of the neck manages sensation and motor function. The pons receives their blood supply from those and their branches.

The consequences of undiagnosed Vertebrobasilar insufficiency can be severe. Occlusions of these arteries cause approximately a fifth of all strokes. Vertebrobasilar insufficiency leads to an intermittently oxygen-starved brain (transient ischemia). Symptoms of Vertebrobasilar insufficiency include dizziness, headaches, swallowing difficulties, vomiting, blindness, double vision, dilated eyes, drooping eyelids, ataxia, weakness, and imbalance of legs. Drop attacks (sudden fall due to loss of proper limb function), mental confusion, paresthesia, and tinnitus are also reported. (7, 14)

More than 60% of Vertebrobasilar insufficiency patients experience dizziness. Most patients experience multiple symptoms at once for minutes at a time due to transient ischemia. (7, 11) Vertebrobasilar insufficiency should be suspected if positional dizziness is accompanied by neurological symptoms. Rotational occlusion of the vertebral artery may induce transitory ischemia.(11) Sudden occlusions of the vertebral and basilar arteries can cause ischemic damage and severe clinical deficits. (14) Instability at the craniocervical junction could cause vertebrobasilar insufficiency by causing these occlusions. Symptoms of VBI were reproducible with rotational head movement; showing that rotational vertebral occlusion is an important cause. (15)

An Angiograph demonstrated the compression of the vertebral artery. These occlusions occurred at the C2 level. Tendons may cause rotational occlusion. (15) With instability, tendons and bones are more mobile than they should be. Patients with cervical instability are prone to occlusions by the structures in the neck.

In my article Treating Vertebrobasilar insufficiency, vertebrobasilar artery insufficiency, rotational vertebral artery occlusion syndrome, or Bow Hunter Syndrome, I discuss the complexity and challenges of cervical neck instability treatment and the controversies and confusions surrounding the diagnosis of vertebrobasilar insufficiency, also called vertebrobasilar artery insufficiency, rotational vertebral artery occlusion syndrome, or Bow Hunter Syndrome. The fact that this one diagnosis or description of symptoms is known by at least four diagnostic names should be evidence enough that patients and their doctors are sometimes not sure what they are dealing with.

Pseudotumor cerebri

Intracranial hypertension is a more recent descriptive term of pseudotumor cerebri. Pseudotumor cerebri is typically explained as a diagnosis mimicking symptoms a of brain tumor. “Pseudotumor” means “fake tumor” when you add cerebri it becomes “fake brain tumor.”

• The shared symptoms of Pseudotumor cerebri and brain tumor or lesion are:
  • nausea, poor eating
  • loss of vision
  • tinnitus
  • headaches
  • neck pain or stiffness
  • cognitive difficulties

This is explained further in my article Cervical Spine Instability, Vein blockage, fluid build up, and intracranial hypertension. Here the problem of intracranial hypertension once determined, and, after a myriad of tests ruled out brain injury, stroke was ruled out, initial testing may have looked for causes in blood clots, infection, and tumors. Once tests ruled those out as causes of your diagnosis of intracranial hypertension, you then got an updated diagnosis of idiopathic intracranial hypertension, which means no one knows why you have intracranial hypertension. When CSF circulation is blocked, excess fluid begins to increase pressure, thus compressing the brain. The compression of the brain causes neuron cell death leading to brain atrophy. (6)

Normal cerebrospinal fluid (CSF) pressure inside the head (intracranial pressure) is <15mmHg. An intracranial pressure measuring above 15mmHg is considered intracranial hypertension and at this point that the person may get the diagnosis of pseudotumor cerebri (6).

When one considers pseudotumor cerebri, or idiopathic intracranial hypertension, which is increased intracranial pressure for no apparent reason, it makes sense to consider cervical instability. The condition causes moderate to severe headaches that often originate behind the eye and are worse with eye movements because the condition can cause swelling in the optic nerve and even blindness. Ringing in the ears that pulses in time with your heartbeat (pulsatile tinnitus), nausea, vomiting, or dizziness are common symptoms. Of course neck, shoulder, and back pain are common and many have other visual symptoms including blurred or dimmed vision, photopsia, or seeing light flashes, again because of the optic nerve swelling.

Diagnosing pressure in the brain

• Motion Arterial Obstruction Mapping – by doing B-mode and color duplex high-resolution doppler ultrasound of the head and neck in various positions and motions, brain arterial obstructions can be mapped. The obstructions can be inside the cranial cavity, at the neck, or the craniocervical junction.

Duplex ultrasound is a test to see how blood moves through your arteries and veins.

• Motional Venous Obstruction Mapping – by doing the same procedure on the venous drainage of the brain, the places of brain venous obstruction can be discovered. Venous obstructions are typically at the craniocervical junctions or in the neck.
• Optic Nerve Measurements – increased intracranial pressure (hypertension) can be seen by swelling of the optic nerves under high-resolution ultrasound. Optic nerve diameters of >5 mm are indicative of an intracranial pressure greater than 20 mmHg.

• Cine phase-contrast MRI – imaging of the brain and brainstem in the supine and upright positions. This can show obstructions of cerebrospinal fluid (CSF) flow, as well as the accumulations of CSF in various parts of the brain and brainstem, compressing these structures and, thus, damaging them.

If the cerebrospinal fluid can’t drain, it will cause pressure to increase and cause optic nerve damage and brain neuron death. Cerebrospinal fluid blockage causes damage to the brain. (14) This damage to the brain affects intellect, focusing, problem-solving, concentration, and higher cognitive function. Patients with intracranial hypertension have anatomically different brains (dural venous sinuses). (5)

Blocked vasculature around the brain has been indicated in up to 90% of cases of pseudotumor cerebri. (2,5) Compression from structures in the neck may be a cause of pseudotumor cerebri. The compression may cause occlusion in the cerebrospinal fluid outflow from the brain, building up pressure. The cause of this compression is most likely instability of the cervical spine. If the cervical spine is corrected and restabilized, the symptoms go away.

Optic nerve sheath diameter can be due to increased intracranial pressure

Increased optic nerve sheath diameter can be due to increased intracranial pressure causing optic damage. (1) The damage causes the optic nerve to swell. Relieving the obstruction of the cerebrospinal fluid typically relieved pseudotumor cerebri symptoms.  (3)  Intracranial hypertension may cause axonal damage. (16) It has been suggested that neuropathic pain disorders may be associated with axonal polyneuropathy (damage to axons (nerve fibers) of peripheral nerves) and compression neuropathy.

What does this image suggest? In this ultrasound image, the swelling of the optic nerve is clear compared to a normal optic nerve. A common but not as commonly diagnosed cause of swollen optic nerve and problems of vision is increased intracranial pressure from cervical spine instability.

The traditional treatments of spinal fluid shunts and optic nerve sheath fenestration (operation to reduce swelling on optic nerve) never explain why the cerebrospinal pressure is high. Anyone who has unexplained vision changes should consider upper cervical instability as a cause.

Dilation of blood vessels

Hyperemia is an increase in local blood flow in response to neuron activity.  When brain activity increases, hyperemia occurs to provide active neurons with nutrients.  The brain is nourished by fresh blood flow from the arteries throughout. The blood circulates through and then goes out the brain via veins. Neurons produce waste from metabolic activity. This waste must also go out veins. The brain utilizes approximately a fifth of the body’s oxygen supply as well as consuming nearly a fourth of the glucose.   To keep brain perfusion constant, brain blood vessels adjust tone via autoregulatory mechanisms when systemic blood pressure varies. Loss of hyperemic response is thought to be associated with neuropathological disorders such as Alzheimer’s disease, hypertension, and ischemia. Functional hyperemia may protect against such conditions. When the visual cortex of the brain is activated, blood flow increases up to 65% to meet the metabolic demand of neurons. It has been observed that capillaries, arterioles, and arteries dilate in response to neuron activity.  Capillaries actively dilate in response to sensory stimulation. When the capillaries fail, the arterioles are capable of dilating in response to stimulation. A large fraction of vascular resistance is in the capillaries in the brain. Small changes to the capillary would lead to large changes in blood flow.  The vertebral artery passes through the transverse foramen and across the posterior arch of C1. Transcranial Doppler studies have shown up to 20% dilated blood vessel (vasodilation) of the diameter of the middle cerebral artery in crisis, on the painful side of the head during a migraine, and up to 11% vasodilation in the meningeal artery. This shows there is vasodilation in the brain during migraine attacks (10) Rotational vertebrobasilar insufficiency has been shown in patients with rotational stenosis of the contralateral vertebral artery at C1-C2. (18) Instability of the cervical spine can have serious consequences to the blood supply of the brain.

Potential effects on the autonomic nervous system 

Ganglions are the ‘brains’ of nerves. The superior (jugular) ganglion and inferior (nodose) ganglion are close to the craniocervical junction. As they are so close, cervical instability can cause structural damage to the nodose ganglion; the most important part of the vagus nerve. This can cause damage to the nerve (neuropathy).

• In the nodose ganglion, the nerve cells and proteins, these essential components of a well-functioning autonomic nervous system, can be destroyed by vagal nerve compression.

In this image upper cervical instability is seen as the structural cause of vagus nerve destruction at the nodose ganglion.

The right vagus nerve innervates the sinoatrial (SA) node of the heart; controlling pulse. The left vagus nerve innervates the atrioventricular (AV) node; controlling the electrical impulses to the SA node. A connection between nodose ganglion degeneration and coronary vasospasm has been recognized. (12)

What are we seeing in this image?

This is a simple diagram of a complex upper cervical vertebra – the vagus nerve – baroreceptor connection. The vagus, along with the glossopharyngeal nerve, run just in front of the upper cervical vertebrae (atlas and axis) and branch out to innervate (sends and receives nerve signals) the receptors in the carotid sinus and aortic arch that control blood pressure. When atlanto-axial instability is present, blood pressure issues (along with heart rate and rhythm problems) can occur because of impairment in the vagus and glossopharyngeal nerve function.

Vagal neuropathy (vagopathy) is indicated in disorders of the autonomic nervous system (ANS). (20)  High frequency of tachycardia (high heart rate) correlated to the number of degenerated neurons in the nodose ganglion. Respiratory and heart irregularities were more frequent in animals with more vagus nerve lesions and a number of degenerated neurons in their nodose ganglia. (12)  Sensory vagus nerve fibers reside in the nodose ganglion. Compression of the nodose ganglion can lead to dysregulation of the immune system which could, in turn, cause systemic body inflammation, autoimmune disease, and decreased immune function. Compression of the cervical sympathetic ganglion can lead to damage of the vagus nerve and atrophy. The cervical sympathetic ganglion is a component of the ANS and innervates the face and head. (24)

It is consequently responsible for some cases of facial pain, migraines, and autonomic nervous system disorders. It has been shown that neurological symptoms are secondary to instability-related repeated micro-injuries to the nerves. (21)  Vagopathy can also affect the gastrointestinal (GI) tract. One vagus nerve neuron innervates thousands of GI neurons. One indicator of cervical instability leading to vagopathy is a deviated uvula. A lesion to the vagus nerves pharyngeal branch can cause the uvula to deviate to the side opposite of the injury. (9)

In this video, Dr. Hauser explains the tell-tale sign of deviated uvula

• Go to a mirror, shine a flashlight into your mouth and go “ahhh.” If your uvula deviates to the side, we call that a deviated uvula which is one of the biggest signs that the vagus nerve is not functioning correctly.

One of the ways that we objectively document that a person has vagus nerve problems or disrupted or blocked signals from the vagus nerve is by looking at the uvula at the back of the soft palate. When we ask the patient to say “ahhh,” the uvula (the small finger-like tissue that hangs at the back of the soft palate (often mistaken for the tonsils)) should remain centered in the throat.

Vasospasms and heart rate variability

Atrophy of the vagus nerve (vagopathy) can cause reduced blood flow to the affected area (vasospasms). Vasospasms can affect every organ. Vasospasm can cause: high blood pressure, Bell’s Palsy, sound sensitivity manifestation, atherosclerosis, heart, lung, and kidney disease. Due to vasospasm, vagopathy can ultimately lead to organ failure. Evidence of vagal neuropathy is shown in changes in the autonomic system. A decrease in vagal activity has been expressed by decreased parasympathetic parameters of heart rate variability (HRV). The Development of autonomic neuropathy (vagopathy) is a significant factor of morality. A risk factor for sudden death is cardiac vagal denervation expressed by decreased HRV. Many peripheral and central functions are affected by vagal activity. (20)

One of the main effects of the vagus nerve is to slow heart rate by increasing the time between heartbeats. Heart rate is controlled by action potentials transmitted via the vagus nerve to the sinoatrial node of the heart, where vagus nerve-dependent acetylcholine release essentially prolongs the time to the next heartbeat, thus slowing the pulse.  HRV represents the time differences between successive heartbeats (also known as the beat-to-beat interval). When a person is functioning with a poorly functioning vagus nerve, the time between heartbeats becomes higher. The HRV is an indicator of how well the autonomic nervous system is managing day-to-day output and stress.

Ross Hauser, MD explains how monitoring HRV can be a helpful way to see how a person’s vagal tone and overall health are improving or declining. This is an objective test we have some patients monitor at home and we have a more comprehensive version that we can do in-office.

The summary transcript is below video:

Neurogenic cough

Neurogenic cough has been likened as a sign of vagopathy. (19) It has been demonstrated that compression of the vagus nerve can cause neurogenic cough, and decompression of the nerve resolved the cough. Cervical instability is usually a chronic condition that leads to persistently progressive, disabling symptoms. Even when bones are in alignment on dynamic imaging there can be instability of the spine. Cervical instability is the cause of some disorders such as Chiari malformation and basilar invagination Cervical instability is associated with cervical spondylosis, especially in older patients and those presenting with severe neurological symptoms. After stabilizing the cervical spine, it has been shown that patients make a remarkable clinical recovery immediately. Patients previously disabled by cervical instability were able to walk and do activities of daily living without assistance following stabilization of the cervical spine. (20)

A November 2021 study in the Japanese language journal Neurological Surgery (26) can offer us a wrap-up and summary of the challenges in diagnosis.

“Degenerative cervical spine diseases are caused by age-related changes in the spine and often lead to impairment of neurological function, resulting in reduced quality of life. Multiple cervical spine degenerative diseases are known, such as cervical spondylosis, cervical disc herniation, and ossification of the posterior longitudinal ligament, which often coexist in a single patient. In degenerative cervical spine disease, many lesions are noted on radiographs but are often asymptomatic; hence, caution is required in clinical practice. Therefore, for the treatment of the disease, it is important to diagnose and identify the phenomenon or location causing the disorder. For this purpose, it is important to focus on the type and extent of neurological symptoms; mechanism of nerve compression, radiculopathy or myelopathy; and presence or absence of spinal instability, static or dynamic.”

Prolotherapy as a treatment solution

Prolotherapy is the rehabilitation of an incompetent structure by the induced proliferation of new cells. Prolotherapy is used to reduce pain by improving the support and function of a joint. (22, 23) In prolotherapy, the solution is injected at the point at which ligaments attach to the bone, causing an inflammatory reaction.  This inflammation repairs the injured tissue of the joint to promote healthy tissue regeneration. Many types of pain can be treated with prolotherapy such as neck and back pain, whiplash injuries, chronic sprains, chronic tendonitis, and osteoarthritis can be treated with prolotherapy. There are different types of proliferants used in prolotherapy such as hypertonic dextrose solution, platelet-rich plasma (PRP), and stem cells. Prolotherapy triggers the inflammatory healing cascade which stimulates growth factors to heal and strengthen ligaments and tendons. An increase in glucose concentration increases DNA synthesis, cell protein synthesis, and proliferation. This stimulates an increase in ligament and tendon mass, ligament-bone junction strength, and repair of cartilage defects. Prolotherapy stimulates cells to produce growth factors that are pertinent to the repair of soft tissues. Indications for prolotherapy are repetitive sprain injury, traumatic tendon injury, or collagen deficiency. Treatments can be up to eight injections, weeks apart. These injections use small-gauge needles and up to 30mL solution of proliferant and anesthetic.

Patients should avoid nonsteroidal anti-inflammatory (NSAID) medications before and after prolotherapy. NSAIDs will stop the healing inflammation cascade. Patients can use acetaminophen for pain if needed. Prolotherapy’s most common side effects are a temporary increase in stiffness and tenderness and possible bruising at the injection site. Other side effects can include nausea, headache, minor allergic reaction, and rare injuries such as hemorrhage, nerve damage, and lung collapse. This is why it is pertinent to find a competent prolotherapist. Prolotherapy is known for its effectiveness in treating chronic pain and tendinopathies. It has been shown that prolotherapy, gentle spinal manipulation, and light exercise improve chronic back pain and disability. There are studies showing promising results in the treatment of osteoarthritis.  Prolotherapy is regenerative injections that help the body to heal itself to strengthen ligaments and tendons. It is a low-risk treatment for pain that may be beneficial before surgical intervention and opioid medications. Prolotherapy can be used to stabilize the ligaments and tendons of the craniocervical junction. This strengthens the supportive soft tissue of the joints in the neck and can correct the instability. Patients’ symptoms and disability improved significantly once the spine was stabilized in multiple studies.

C2 Malrotation

Ross Hauser, MD discusses C2 Malrotation and the symptoms associated with it, as well as why we like adjustments, curve correction, and Prolotherapy to help restore spinal integrity and resolve symptoms.

Video learning points:

The malrotation of the C2 vertebrae or the axis, is often what I call the the Missing Link into what is causing a person’s symptoms.

• Rotated C2 can compress the vagus nerve that can cause digestive problems seen in some upper cervical instability patients.
• Rotated C2 can cause compression on the  glossopharyngeal nerve which can cause dysfunction of the larynx muscles and cause swallowing difficulties.
• Rotated C2 can cause compression of the spinal accessory nerve cause cramping into the sternocleidomastoid muscle or the trapezius muscle and creating a situation of torticollis.
• Rotated C2 can cause compression and obstruct right jugular vein causing increased brain pressure and problems of cognitive decline and mood disorders.
• Rotated C2 can compress the carotid sheath causing compression on  jugular veins and carotid arteries causing intracranial hypertension.

References

1. B. Bragée, et al. Signs of Intracranial Hypertension, Hypermobility, and Craniocervical Obstructions in Patients With Myalgic Encephalomyelitis/Chronic Fatigue Syndrome. Front
Neurol 11 (2020): 828 [Google Scholar]
2 Degnan AJ, Levy LM. Pseudotumor cerebri: brief review of clinical syndrome and imaging findings. American journal of neuroradiology. 2011 Dec 1;32(11):1986-93. [Google Scholar]
3. J. N. Higgins, et al. An Evaluation of Styloidectomy as an Adjunct or Alternative to Jugular Stenting in Idiopathic Intracranial Hypertension and Disturbances of Cranial Venous Outflow. J
Neurol Surg 78.2 (2017): 158–163 [Google Scholar]
4. D. S. Ruíz, et al. The Craniocervical Venous System in Relation to Cerebral Venous Drainage. Amer J Neurorad 23.9 (2002): 1500-1508
5 Farb RI, Vanek I, Scott JN, Mikulis DJ, Willinsky RA, Tomlinson G. Idiopathic intracranial hypertension: the prevalence and morphology of sinovenous stenosis. Neurology. 2003 May 13;60(9):1418-24. [Google Scholar]
6 Thompson DN, Harkness W, Jones B, Gonsalez S, Andar U, Hayward R. Subdural intracranial pressure monitoring in craniosynostosis: its role in surgical management. Child’s Nervous System. 1995 May;11(5):269-75. [Google Scholar]
7 Lima AC, Bittar R, Gattas GS, Bor-Seng-Shu E, Oliveira MD, Monsanto RD, Bittar LF. Pathophysiology and diagnosis of vertebrobasilar insufficiency: a review of the literature. International archives of otorhinolaryngology. 2017 Jul;21:302-7. [Google Scholar]
8. M. D. Schauber, et al. Cranial/cervical nerve dysfunction after carotid endarterectomy. J Vasc Surg 25.3 (1997): 481-487 [Google Scholar]
9. Darren H. Garner, et al. Anatomy, Head and Neck, Carotid Sheath. “StatPearls.” 1 st ed. StatPearls Publishing. Treasure Island, FL, US. (2020). [Google Scholar]
10 Geraud G. Vasodilatation et migraine. Revue Neurologique. 2014 Apr 1;170:A218-9 [Google Scholar]
11 Moubayed SP, Saliba I. Vertebrobasilar insufficiency presenting as isolated positional vertigo or dizziness: A double‐blind retrospective cohort study. The Laryngoscope. 2009 Oct;119(10):2071-6. [Google Scholar]
12 Yolas C, Kanat A, Aydin MD, Altas E, Kanat IF, Kazdal H, Duman A, Gundogdu B, Gursan N. Unraveling of the effect of nodose ganglion degeneration on the coronary artery vasospasm after subarachnoid hemorrhage: an experimental study. World neurosurgery. 2016 Feb 1;86:79-87. [Google Scholar]
13. P. K. Eide, et al. Magnetic resonance imaging provides evidence of glymphatic drainage from human brain to cervical lymph nodes. Sci Reports 8.7194 (2018): 1-10
14 Mattle HP, Arnold M, Lindsberg PJ, Schonewille WJ, Schroth G. Basilar artery occlusion. The Lancet Neurology. 2011 Nov 1;10(11):1002-14. [Google Scholar]
15 Kuether TA, Nesbit GM, Clark WM, Barnwell SL. Rotational vertebral artery occlusion: a mechanism of vertebrobasilar insufficiency. Neurosurgery. 1997 Aug 1;41(2):427-33. [Google Scholar]
16 Hartmann CJ, Klistorner AI, Brandt AU, Schroeder K, Kolbe R, Cohn E, Goebels N, Guthoff R, Aktas O, Hartung HP, Albrecht P. Axonal damage in papilledema linked to idiopathic intracranial hypertension as revealed by multifocal visual evoked potentials. Clinical neurophysiology: official journal of the International Federation of Clinical Neurophysiology. 2015 Oct;126(10):2040-1. [Google Scholar]
17. A. R. Nippert, et al. Mechanisms mediating functional hyperemia in the brain. The Neuroscient 24.1 (2018): 73-83
18 Dabus G, Gerstle RJ, Parsons M, Cross III DT, Moran CJ, Thompson R, Derdeyn CP. Rotational vertebrobasilar insufficiency due to dynamic compression of the dominant vertebral artery by the thyroid cartilage and occlusion of the contralateral vertebral artery at C1–2 level. Journal of Neuroimaging. 2008 Apr;18(2):184-7. [Google Scholar]
19 Honey CR, Krüger MT, Morrison MD, Dhaliwal BS, Hu A. Vagus Associated Neurogenic Cough Occurring Due to Unilateral Vascular Encroachment of Its Root: A Case Report and Proof of Concept of VANCOUVER Syndrome. Annals of Otology, Rhinology & Laryngology. 2020 May;129(5):523-7.  [Google Scholar]
20. Weissman‐Fogel I, Dashkovsky A, Rogowski Z, Yarnitsky D. An animal model of chemotherapy‐induced vagal neuropathy. Muscle & Nerve: Official Journal of the American Association of Electrodiagnostic Medicine. 2008 Dec;38(6):1634-7. [Google Scholar]
21 Goel A, Ranjan S, Shah A, Rai S, Dandpat S, Patil A, Vutha R. Adjacent-segment “central” atlantoaxial instability and C2–C3 instability following lower cervical C3–C6 interbody fusion: Report of three cases. Journal of craniovertebral junction & spine. 2020 Jan;11(1):51. [Google Scholar]
22 Goswami A. Prolotherapy. Journal of pain & palliative care pharmacotherapy. 2012 Dec 5;26(4):376-8.  [Google Scholar]
23 Dagenais S, Yelland MJ, Del Mar C, Schoene ML. Prolotherapy injections for chronic low‐back pain. Cochrane Database of Systematic Reviews. 2007(2). [Google Scholar]
24. Carcamo CR. Pulsed radiofrequency of superior cervical sympathetic ganglion for treatment of refractory migraine. Pain Medicine. 2017 Aug 1;18(8):1598-600.  [Google Scholar]
25. G. Attanasio. Chronic cerebrospinal venous insufficiency and menière’s disease: Interventional versus medical therapy. Laryngoscope 130.8 (2020): 2040-2046
26 Takeshima Y, Nakase H. Variations in Cervical Degenerative Diseases: What are the Key-points in Diagnosis?. No Shinkei geka. Neurological Surgery. 2021 Nov 1;49(6):1171-82. [Google Scholar]

5494

• Surgery
• NSAIDs
• Cortisone Shots
• R.I.C.E.