Newsletter – June 2016

The June 2016 Newsletter of the Trigeminal Neuralgia Association Australia has been emailed to our members.

This edition contained:

  • A special message by the outgoing president of the TNAA, Irene Wood, reflecting on support the association has provided to people touched by trigeminal neuralgia.
  • Details of the discounts available in the Entertainment Book, a fundraising initiative of the TNAA.
  • Report summary – Bacteria, Gut Organisms Linked To Health, Autism, Schizophrenia, Depression, Diabetes, Allergies And Obesity by Xavier La Canna
  • Report summary – Opening paths to novel analgesics: the role of potassium channels in chronic pain by Christoforos Tsantoulasemail, Stephen B. McMahon
  • A report from our regional conference in Adelaide with summaries of the presentations:
    • Dr Tom Wilkinson – The Overlap Of Symptoms Between Trigeminal Neuralgia And TMD And How To
      Make A Differential Diagnosis.
    • Prof Paul Rolan: Clinical Pharmacologist; Consultant Physician; Medicines Developer; Pain Physician
    • Dr Andrew Zacest: Neurosurgeon – Surgical Option Of Trigeminal Neuralgia
    • Dr Michael Conlon: Senior Research Scientist, CSIRO Food & Nutrition – Gut Microbes and Human Health: How Your Diet Affects Your Microbes
  • A report from our Sydney support group meeting. This contained a summary of the symptoms, challenges and remedies of attendees.

We’re Fundraising with Entertainment Book

The Trigeminal Neuralgia Association of Australia is fundraising with the Entertainment Book in 2016.

The Entertainment Book comes with the Gold Card and vouchers, and contains over $20,000 worth of valuable ‘up to 50% off’ and ‘2-for-1’ offers for many of the best restaurants, cafés, arts, attractions, hotels, travel, shopping and much more.

Alternatively, The Entertainment Digital Membership puts the same value into your Apple or Android device, allowing you to conveniently search for special offers.

Editions are available for each Australian capital city and many regional areas.

The Book and Digital Memberships are on sale now at, ready to use from April, 2016.

20% of each membership sold directly supports our efforts to advocate for TN patients and empower our members with information and support.

Thank you for your support.

tnaa entertainment book

Newsletter – May 2016

The May 2016 Newsletter of the Trigeminal Neuralgia Association Australia has been emailed to our members.

This edition contained:

  • The obituary published in the New York Times, reflecting on the life of Dr. Peter J. Jannetta, Pioneering Neurosurgeon on Facial Pain, dying at 84.
  • Details of our AGM and Regional Conference on 4 June in Sydney.
  • The nomination form for TNAA executive committee positions.
  • Details of our fundraising initiative with Entertainment Books.
  • Report summary – Nonparalytic botulinum molecules for the  control of pain by Mangione, Antonina S.; Obara, Ilona;  Maiarú, Maria; Geranton, Sandrine M.; Tassorelli, Cristina;  Ferrari, Enrico; Leese, Charlotte; Davletov, Bazbek; Hunt,  Stephen P..
  • Details of the most common side effects of Lyrica.
  • Reports from our Brisbane, Sydney CBD and Melbourne support group meetings. These contain summaries of the symptoms, challenges and remedies of attendees.
  • Details of our Adelaide Regional Conference on 21 May 2016.

Newsletter – April 2016

The April 2016 Newsletter of the Trigeminal Neuralgia Association Australia has been emailed to our members.

This edition contained:

  • Irene Wood’s resignation letter from the role of President of the Trigeminal Neuralgia Association Australia.
  • Details of our fundraising initiative with Entertainment Books.
  • Report summary – Diet affects autoinflammatory disease via gut microbes.Trigeminal Neuralgia surgery by Kim J. Burchiel.
  • Report summary – pain management for the elderly by the World Health Organisation.
  • Reports from our Mackay, Gold Coast, Adelaide, Toongabbie, Sunshine Coast. These contain summaries of the symptoms, challenges and remedies of attendees.
  • The registration form for the regional conference on 21 May in Adelaide.

Newsletter – March 2016

The March 2016 Newsletter of the Trigeminal Neuralgia Association Australia has been emailed and/or posted to our members.

This edition contained:

  • Information about our upcoming conference in Adelaide.
  • Report summary – Trigeminal Neuralgia surgery by Kim J. Burchiel.
  • Report summary – pain management for the elderly by the World Health Organisation.
  • Reports from our Melbourne, Toongabbie, Brisbane and  Sydney CBD support group meetings. These contain summaries of the symptoms, challenges and remedies of attendees.

Newsletter – February 2016

The February 2016 Newsletter of the Trigeminal Neuralgia Association Australia has been emailed and/or posted to our members.

This edition contained:

  • Information about our Facebook page at
  • Report summary – Comparison of Tolerability and Adverse Symptoms In Oxcarbazepine And Carbamazepine In The Treatment of Trigeminal Neuralgia and Neuralgiform Headaches Using The Liverpool Adverse Events Profile (AEP)
  • Report summary – Carbamazepine and Folic Acid In  Trigeminal Neuralgia Patients
  • Our postal address has changed to PO Box 157, North Richmond NSW 2754, Australia.
  • Reports from our Sunshine Coast, Mackay, Sydney CBD, Adelaide, Gold Coast, Brisbane and Melbourne support group meetings. These contain summaries of the symptoms, challenges and remedies of attendees.

Exercise Is Good For the Brain

By:Jeanna Bryner, LiveScience Managing Editor

This article first appeared in the May, 2010 edition of the TNAA newsletter. To read our newsletter, please visit: Newsletters

Working out on a treadmill isn’t just good for the body, it’s good for the brain, according to a new study,the latest to weigh in on the cognitive benefits of exercise.
Regular exercise speeds learning and improves blood flow to the brain in monkeys, the study found. The researchers suspect the same would hold true for humans.

While there is ample evidence of the beneficial effects of exercise on cognition in other animal models, such as the rat, it has been unclear whether the same holds true for people, said study researcher Judy Cameron, a psychiatry professor at Pitt School of Medicine. Testing the hypothesis in monkeys can provide information that is more comparable to human physiology.
For one, monkeys exercise like people, in that they love getting on a treadmill (well sort of like us), and they won’t run all night as rats would do if provided with a running wheel, Cameron said.

“Second, monkeys, like people, have well-developed cerebral cortices and that is the part of the brain used in cognition. Rats have a much less developed cortex, so again monkeys are more analogous to people,” Cameron told Live Science.
Cameron and colleagues trained adult female cynomolgusmonkeys to run on a human-sized treadmill at 80 percent of their individual maximal aerobic capacity for one hour each day, five days a week, for five months. This regimen is equivalent to what is recommended for improving the fitness of middle-aged people.

Another group of monkeys remained sedentary, meaning they sat on the immobile treadmill, for a comparable time.
Half of the runners went through a three-month sedentary period after the exercise period. In all groups, half of the monkeys were middle-aged (10 to 12 years old) and the others were more mature (15 to 17 years old). Initially, the middle-aged monkeys were in better shape than their older counterparts, but with exercise, all the runners became more fit.
During the fifth week, the monkeys completed cognitive tests in which they had to choose which covered objects contained a food reward underneath. Monkeys that exercised were twice as fast at this task as those who didn’t exercise.

However, later in the testing period, learning rate and performance was similar among the groups, which could mean that practice at the task will eventually overshadow the impact of exercise on cognitive function, Cameron said.
Brain tissue samples revealed that mature monkeys that ran had a greater volume of blood vessels compared with middle-aged runners or sedentary animals. (These blood vessels deliver oxygen and nutrients to the brain.) But those blood flow changes reversed in monkeys that were sedentary after exercising for five months.

The results agree with previous studies in this area. A recent review highlighted that exercisers learn faster, remember more, think clearer and bounce back more easily from brain injuries, such as a stroke. Some of these brain benefits are thought to arise out of the mild stress that exercise induces, which triggers the brain to protect against neuron damage.
In addition, it could just be an effect of blood flow. “Physical exercise increases blood flow to the brain,” Cameron said. “Blood delivers nutrients and oxygen, and this may be a large part of why exercise increases cognitive function.”
She suspects the benefits could be two-fold for humans. “The monkeys were more alert and engaged as well as improved cognitive function in the first task they were tested in,” Cameron said. “We expect that people would show similar effects of exercise. In addition, if over time people are more alert and engaged it would be likely that they would learn more from that alone.

How to Live Well with Chronic Disease

by David S. Sobel M.D.
Mind Body Health :

This article first appeared in the May, 2010 edition of the TNAA newsletter. To read our newsletter, please visit: Newsletters

To live well with chronic conditions you need to learn skills for managing three areas:
•Your illness and symptoms
•Your normal daily activities
•Your emotions

Managing Your Illness
Any illness is a learning experience. You may not even know you have a pancreas gland until you’re told you have diabetes. To manage a chronic illness, you need to become an expert in your disease. This doesn’t mean you become a doctor, but you need to learn enough about your condition and how your body reacts so you can take action to minimize disability and complications.

Be an Active Partner
Learn about your medical condition. What makes it worse or better? What action plan should you take if symptoms flare? What are the warning signs that you should get professional medical help? What can you expect from medical care and what must you do for yourself?

There may be specific skills you need to learn: how to measure your blood sugar if you are diabetic, how to properly use an inhaler if you have asthma, how to exercise safely with a heart or lung condition, (“how TN medication should be taken!” – Irene Wood)

Learn how to prepare for a medical visit – what questions to ask about medical tests, medications, and surgery.

Learn to Cope with Symptoms
Most chronic disease symptoms wax and wane. When symptoms are bad, take some consolation in knowing that “this will pass.” Learn and practice the proven techniques for dealing with pain, tension, depression, anxiety and insomnia.

The Role the brain plays in pain – The Mind Body Syndrome

This article first appeared in the May, 2010 edition of the TNAA newsletter. To read our newsletter, please visit: Newsletters

The concept of Mind Body Syndrome (MBS) or Tension Myositis Syndrome (TMS) is based on the theory that – “Your body is producing pain because it’s manifesting unresolved stress, possibly from your childhood, or from stressful events in your adulthood, or from your present circumstances, and as a result of your personality traits (which affects how you respond to stress and how much pressure you tend to put upon yourself). Your mind has twisted your body into pain as a way to avoid some of the emotions that are inside you.” – Dr. H. Schubiner

Excerpt from “The Structural Model of Personality” by Kendra Cherry

According to the founder of psychoanalytic theory Sigmund Freud – the mind can be divided into two main parts:

1. The conscious mind includes everything that we are aware of. This is the aspect of our mental processing that we can think and talk about rationally.A part of this includes our memory, which is not always part of consciousness but can be retrieved easily at any time and brought into our awareness. Freud called this ordinary memory the preconscious.

2. The unconscious mind is a reservoir of feelings, thoughts, urges, and memories that outside of our conscious awareness. Most of the contents of the unconscious are unacceptable or unpleasant, such as feelings of pain, anxiety, or conflict. According to Freud, the unconscious continues to influence our behaviour and experience, even though we are unaware of these underlying influences.
Sigmund Freud’s psychoanalytic theory – the personality is composed of three elements – known as the id, the ego and the superego – they work together to create complex human behaviours.

The Id

The id is the only component of personality that is present from birth. This aspect of personality is entirely unconscious and includes of the instinctive and primitive behaviours. According to Freud, the id is the source of all psychic energy, making it the primary component of personality. Id is driven by the pleasure principle, which strives for immediate gratification of all desires, wants, and needs. If these needs are not satisfied immediately, the result is a state anxiety or tension. The id is very important early in life, because it ensures that an infants needs are met. If the infant is hungry or uncomfortable, he or she will cry until the demands of the id are met.

However, immediately satisfying these needs is not always realistic or even possible. If we were ruled entirely by the pleasure principle, we might find ourselves grabbing things we want out of other people’s hands to satisfy our own cravings. This sort of behaviour would be both disruptive and socially unacceptable. According to Freud, the id tries to resolve the tension created by the pleasure principle through the primary process, which involves forming a mental image of the desired object as a way of satisfying the need.

The Ego

The ego is the component of personality that is responsible for dealing with reality. According to Freud, the ego develops from the id and ensures that the impulses of the id can be expressed in a manner acceptable in the real world. The ego functions in both the conscious, preconscious, and unconscious mind.
The ego operates based on the reality principle, which strives to satisfy the id’s desires in realistic and socially appropriate ways. The reality principle weighs the costs and benefits of an action before deciding to act upon or abandon impulses. In many cases, the id’s impulses can be satisfied through a process of delayed gratification–the ego will eventually allow the behaviour, but only in the appropriate time and place.

The ego also discharges tension created by unmet impulses through the secondary process, in which the ego tries to find an object in the real world that matches the mental image created by the id’s primary process.

The Superego

The superego is the aspect of personality that holds all of our internalised moral standards and ideals that we acquire from both parents and society- our sense of right and wrong. The superego provides guidelines for making judgments. According to Freud, the superego begins to emerge at around age five.

There are two parts of the superego:
1.  The ego ideal includes the rules and standards for good behaviours. These behaviours include those which are approved of by parental and other authority figures. Obeying these rules leads to feelings of pride, value, and accomplishment.

2.  The conscience includes information about things that are viewed as bad by parents and society. These behaviours are often forbidden and lead to bad consequences, punishments, or feelings of guilt and remorse.

The superego acts to perfect and civilize our behaviour. It works to suppress all unacceptable urges of the id and struggles to make the ego act upon idealistic standards rather that upon realistic principles. The superego is present in the conscious, preconscious, and unconscious.

What happens when the ego cannot deal with the demands of our desires, the constraints of reality, and our own moral standards? According to Freud, anxiety is an unpleasant inner state that people seek to avoid. Anxiety acts as a signal to the ego that things are not going right.

The Mind Body Syndrome/ Tension Myositis Syndrome theorise that this conflict, this emotional strain, this “energy” has to come out somehow – it needs to be expressed. So it comes out in the body as emotional symptoms such as anxiety, depression, panic or worry; in physical symptoms such as pain, headaches, migraine etc. These symptoms are real but caused by underlying emotional contents.

What happens in the brain when emotion symptoms are activated? The Amygdala, the autonomic nervous system, the sympathetic nervous system (the fight or flight reactions) and sensory neurons are also activated. This result in a cycle of information and stimulations and reactivations which could continue into days, month or years. The other thing that happens now is – Trigger comes into play. Trigger can be food, time of day, weather, place etc. Part of TMS/ MBS treatment is to recognise these triggers and getting rid of them. How?

In the conscious part of the brain (the frontal lobe ) is the dorsolateral prefrontal cortex. Studies have shown that when the dorsolateral prefrontal cortex is activated it can inhibit the autonomic nervous system; this provides the break in the link of the vicious cycle that causes Tension Myositis Syndrome /MBS.

The physical symptoms and emotional symptoms are real,but they are caused by stress, emotional reactions to stress that are built up from childhood into adulthood, exacerbated by our own personality factors. By changing our understanding about what the problem is, having hope, having a positive expectation (that you can get better) – you can take control of this whole situation through working mainly in the mind i.e. – activating the dorsolateral prefrontal cortex. Break the link between the emotional reactions and the physical and emotional symptoms that have occurred.
– “ The Role the brain plays in pain: Dr. H. Schubiner.”

Please note: the above are my notes – any error is strictly mine – Irene Wood.

How does gabapentin relieve neuropathic pain?

by Marshall Devor
Pain. 2009 Mar;142(1-2):13-6.

This article first appeared in the April, 2010 edition of the TNAA newsletter. To read our newsletter, please visit: Newsletters

The question of gabapentin’s analgesic mechanism, and that of its congener pregabalin, is important because both drugs have proven analgesic efficacy in a variety of neuropathic pain conditions, they are widely prescribed and their molecular target is a novel one. Knowledge of the mechanism of action can contribute to our overall understanding of pain mechanisms, and can serve as an important guide to the development of improved analgesic agents. For this reason I write to comment on a topical review of the subject published recently in Pain [3]. The review was written by Charles Taylor, a key player in making gabapentin a success and undoubtedly an authority on the topic. Specifically, I would like to point out what I consider a serious lacuna in Dr. Taylor’s review, and one that also characterizes a good deal of thought in our field, well beyond the specific subject of gabapentin.

Dr. Taylor opened his review by pointing out that gabapentin binds selectively to a Ca2+ channel subunit, Cavα2-δ, in muscle tissue and brain. After ruling out muscle as the analgesic site of action, he concluded that “Pharmacology mediated byCavα2-δ binding is confined to the brain and spinal cord …”. He proceeded to consider several possible mechanisms of action in the CNS with a strong tilt towards a fascinating new mechanism (for an analgesic drug), interference with the trafficking of Ca2+ channels from the cytoplasm to the neuronal membrane. The idea is that with fewer Ca2+ channels delivered to the membrane of synaptic terminals in the spinal cord, synaptic transmission and hence pain will be attenuated.

Pain readers should be aware, however, that gabapentin also binds to primary sensory neurons in the dorsal root ganglia (DRGs) as shown, among others, by Taylor and Garrido [4], and that it has profound effects on the electrical discharge properties of these neurons in experimental models of neuropathic pain. Specifically, gabapentin strongly suppresses the ectopic discharge that originates from the DRG following peripheral nerve injury, at doses relevant to those achieved in clinical use. The first demonstration of this suppressive effect in the peripheral nervous system (PNS) was published 10years ago by Pan et al. [2]. This was followed by several others, including a recent study in Pain by Yang etal. [6] who explored the mode whereby gabapentin suppresses neuropathic ectopia. There are good reasons for believing that ectopic discharge originating in the PNS contributes to neuropathic pain [1]. Hence, the fact that gabapentin suppresses ectopia ought to be mentionedin a review of gabapentin’s potential analgesic actions.

But my concern goes beyond the completeness of an otherwise excellent review. The issue is broader as it extends to a wide range of pharmacological studies in which agents are assumed to produce analgesia by an action on the CNS, without any consideration given to the PNS. For example, ketamine and amitriptyline are almost universally presumed to act in the CNS because they have known synaptic effects (on NMDA-type glutamate receptors and on catecholamine reuptake, respectively). However, both also stronglysuppress neuropathic ectopia in the PNS (e.g. [5], [7]). The problem is even more acute when drugs are applied intrathecally. Although many authors (and journal referees) presume that this route of delivery insures that the drug is acting in the spinal cord, it is well known that the DRG resides within the intrathecal space and is accessed by drugs injected intrathecally. One cannot presume that analgesia following spinal administration of a drug is due to a spinal action without first ruling out the possibility that the 5major analgesic action is in fact on the DRG. This issue is not just of academic interest. If drugs that are widely used in the treatment of neuropathic pain such as gabapentin and amitriptyline in fact act in the PNS, it might be possible to develop peripherally acting derivatives that fail to penetrate the blood–brain-barrier. This would yieldanalgesic agents devoid of the CNS side effects, somnolence, vertigo and nausea, that plague the drugs in current clinical use.

Article Outline : Volume 145, Issue 1, Pages 259-261 (September 2009)


REPLY: Charles P. Taylor

I would like to thank Dr. Devor for his thoughtful letter to the editor concerning my recent Topical Review in PAIN. Many of his points are important ones. I would like to reply to some of those points in detail.

Firstly, attention is drawn to the binding of gabapentin to calcium channel alpha2-delta (CaVα2δ) protein expressed in the cytosol and membranes of dorsal root ganglion cell bodies. Although this observation is clear, it is less clear that drug binding sites in the sensory ganglia or axons are important to the analgesic action of gabapentin and pregabalin. In particular, the recent paper by Annette Dolphin and colleagues [1] shows that allodynia in rat sensory nerve ligation is correlated with an increase of CaVα2δ-1protein in the plasma membrane of sensory neurons at their presynaptic endings in the spinal dorsal horn, but increases of protein that were mostly restricted to endoplasmic reticulum of sensory ganglion cell bodies and intracellular vesicles of axons. This finding suggests that functional increases of CaVα2δ-1 protein associated with allodynia are restricted mostly to presynapticregions in the spinal cord. Devor also cites the observations of Pan and colleagues [13] showing that gabapentin reduces ectopic firing of damaged sensory neurons in a partial nerve injury model. Another paper from the same group [5] demonstrated that pregabalin (but not its enantiomer) inhibited ectopic firing in neuropathic sciatic nerve. However, other investigators (e.g. Tomotoshi et al., Pfizer Nagoya, Japan, personal communication) failed to replicate this effect of pregabalin with ectopic firing caused by chronic sciatic nerve constriction and instead found no effect on ectopic firing. Therefore, the observations of Pan et al. still need additional confirmation.

My review was written prior to the appearance of the recent report of reduced ectopic firing and reduced sustained sodium currents in dorsal root ganglion neurons by Yang et al. [18]. I agree that this is potentially an important finding. It will be of particular interest to determine whether gabapentin in Yang’s model acts indirectly via binding to CaVα2δ proteins in sensory neurons, or instead acts by some other unknown mechanism that secondarily influences voltage-gated sodium channels. It appears that the site of drug action in this case must be other than “normal” voltage-gated sodium channels, since a previous paper [3] demonstrated that gabapentin had no effect on voltage-clamped sodium currents in sensory neurons, unlike lidocaine, mexiletine and carbamazepine.

Surprisingly little work has been focused on the anatomical site(s) of analgesic action of gabapentin and pregabalin within the neuraxis. One study [10] differentiated gabapentin responses in sciatic nerve constricted rats between vocalization to paw pressure (a supraspinally mediated behavior) and paw withdrawal (a spinally mediated behavior). Interestingly, vocalization (although produced by stronger paw pressure stimuli) was reduced at systemic doses of gabapentin that were 100-fold lower than those needed to suppress paw withdrawal 6responses, suggesting a potent and important drug action in the fore brain. On the other hand, a study by Carlton and Zhou [4] showed that local injection of gabapentin or pregabalin into the rat footpad attenuated late-phase behavioral responses in the formalin footpad test, indicating a peripheral site of drug action. Additional work is needed to determine whether CaVα2δ-1 protein is localized at the peripheral tactile and pain-sensitive endings of sensory neurons in the periphery.

It appears that compounds related to gabapentin by structure and pharmacology fail to act as analgesics if they are poorly penetrable across the blood–brain barrier via system L transport [2]. In particular, one potent CaVα2δ binding compound was inactive as an anticonvulsant when given systemically (it was also inactive as an analgesic, data not shown) but the same compound prevented seizures when administered intracerebrally to mice [14]. This observation suggests that the brain is an important site of action for CaVα2δ drugs, but additional experiments comparing intracerebral and spinal administration in pain-related models are needed. It is certainly possible that CaVα2δ drugs act in the periphery (for example to reduce ectopic firing in sensory neurons) but that they also act in the spinal dorsal horn, where neuropathic rats have increased density of CaVα2δ-1 protein at presynaptic endings [1] and where pregabalin decreases the frequency of glutamate miniature synaptic potentials in neuropathic rats when applied locally [16].

Furthermore, gabapentin acts when applied directly to isolated neurons of the rostroventral medulla [7], [8], and gabapentin and pregabalin reduce synaptic currents and presynaptic neurotransmitter release when applied directly to neurons of isolated entorhinal cortex [6], hippocampus [12], [17] and perhaps other fore brain areas. An additional possibility not mentioned in my recent review is that gabapentin and pregabalin promote slow-wave sleep both in animals [11] and in humans [9], presumably by an action within the brain. This could have important implications for emotional stress, anxiety and pain perception in pain patients who are partially deprived of sleep by their discomfort.

Unfortunately, it is not immediately clear which of these various sites of action of gabapentin and pregabalin are the most important for their clinical use in chronic pain. I completely agree with Dr. Devor’s point, suggesting that several papers have shown gabapentin or pregabalin to have analgesic action following intrathecal administration without proving where the drugs act. Intrathecally administered drugs could potentially act in the dorsal root ganglia, the brainstem, or even the neocortex. It will be interesting to see whether future investigations are able to shed more light on the anatomical sites of action that are most relevant to the clinically important actions of gabapentin, pregabalin and related compounds.

Reply to: How does gabapentin relieve pain? (Marshall Devor), 01 July 2009
Charles P. Taylor
PAIN® : September 2009 (Vol. 145, Issue 1, Pages 259-261

FYI: voltage-gated calcium channel alpha2-delta proteins (CaVα2-δ); voltage-gated calcium channel (CaV); calcium (Ca2+); Dorsal Root Ganglion ( DRG); central nervous system(CNS); peripheral nervous system ( PNS).