Concussion: A Primer for GPs
Good evening everybody and welcome to this evening’s Concussion: A Primer for GPs webinar. My name is Samantha and I will be your host. We are joined by our presenters this evening, Associate Professor Antonio Di Ieva and Dr Rowena Mobbs, and our facilitator Dr Tim Senior.
Before we jump in I would like to make an Acknowledgement of Country. We recognise the traditional custodians of the land and sea on which we live and work and we pay our respects to Elders past and present.
Okay. I would to formally introduce our presenters for this evening now. Associate Professor Antonio Di Ieva is a consultant neurosurgeon with 18 years of experience in brain and spine surgery. He is an Associate Professor at Macquarie University, full Professor of Neurosurgery in Italy and Associate Professor of Neuroanatomy in Austria with main interests in neuro-oncology and TBI. Professor Di Ieva is an Australian Research Council Future Fellow and Head of Computational Neurosurgery Lab at Macquarie University.
Dr Rowena Mobbs is a Cognitive Neurologist with over a decade of experience in managing behavioural and cognitive changes in dementia and patients with mild traumatic brain injury. She has a PhD on cell death in compressive myelopathy. Rowena leads the Dementia and Concussion Clinics at Macquarie Health Neurology, working within a multidisciplinary team. She is passionate about concussion prevention and management. Rowena was appointed to Macquarie University Hospital as Senior Lecturer and is Visiting Neurologist at Mater Hospital.
And our facilitator this evening, Dr Tim Senior. Tim is a GP at the Tharawal Aboriginal Corporation in South Western Sydney. He is also an RACGP Medical Advisor for the National Faculty of Aboriginal and Torres Strait Islander Health and Senior Lecturer in General Practice and Indigenous Health at UWS. So welcome, Antonio, Rowena and Tim, and I will hand over to Tim now who is going to take us through our learning outcomes for this evening.
Dr Tim Senior:
Thank you very much, Sammi. Good evening everyone. I hope you are all keeping well and looking after each other. So these are the learning outcomes this evening. I am at home and there are big night roadworks going on outside my house, so if you hear all sorts of strange noises, it well be that. Just let us know if it sounds awful. This is what we hope to achieve tonight, the learning outcomes which is educational speak for what we are going to get out of tonight. So by the end of this activity, we should be able to classify concussion and traumatic brain injury with special attention on the physiopathological mechanisms related to concussion. We should be able to utilise the Sport Concussion Assessment Tool, characterise signs and symptoms related to concussion and its management. We should be able to be aware of the importance of neuroimaging-related research. We should be able to institute immediate headache management pathways and coordinate care. And we should be able to identify risk factors for headache disorders and cognitive overlaps post head trauma. So I will hand over to Associate Professor Antonio Di Ieva.
Associate Professor Antonio Di Ieva:
Good evening, everyone. Thank you very much for tonight’s presentation and thanks Tim and thanks Sam and thank you everyone for being here at this hour. I would like to introduce you to the universe of concussion, which is a multidimensional universe in which it is useful to say that the general practitioner is the central hub of a network, which is a very complex network formed by several physicians, surgeons and health carers.
From a historical perspective it is quite interesting I was looking for the definition of concussion in this book published in 1535. It is the first book in which there is a definition of neurotraumatology and management of trauma and traumatic brain injury, and of course there is not a really clear definition about concussion. Although the author of this book, Berengario da Carpi was refining some symptoms which are related to minor head injury like a headache or dizziness which could be related to concussion as we know it nowadays.
So in terms of definition, we will use some slides to define it. Concussion is a brain injury and is defined as a complex pathophysiological process affecting the brain, induced by biomechanical forces. So concussion may be caused either by a direct blow to the head, face, neck or elsewhere on the body with an “impulsive” force transmitted to the head. Or, concussion typically results in the rapid onset of short impairment of neurologic function that resolves spontaneously. However, in some cases the symptoms and signs may evolve over a number of minutes to hours. Concussion may result in neuropathological changes but the acute clinical symptoms largely reflect a functional disturbance rather than a structural injury and as such, no abnormality is seen on standard structural neuroimaging studies. This is a very important point that we will discuss later on in terms of neuroimaging when neuroimaging is requested. Or, concussion results in a graded set of clinical symptoms that may or may not involve loss of consciousness. Resolution of the clinical and cognitive symptoms typically follows a sequential course. However, it is important to note that in some cases, post-concussive symptoms may be prolonged.
So in this slide you can see the definition of traumatic brain injury and you will know that the most used scoring system is the Glasgow Coma Scale which scores between three which is the minimal score because one point is given to each domain of analysis which is the motor response, the eye response and the verbal response, to 15 which is the maximum score. According to the GCS, we can classify traumatic brain injury as a mild TBI when the GCS scored between 13 and 15. This is related to posttraumatic amnesia generally lasting less than one day and if there is a loss of consciousness, it is either between zero and 30 minutes. A moderate TBI is defined when a GCS is between nine and 12, and a severe TBI is between three and eight. Of course if this is a patient in a coma, who in general has a PTA longer of seven days with a loss of consciousness more than 24 hours, because of course the patient is in a coma.
Well the problem is that where it is a concussion over here. And there is not a very well standardised way to define, to use the GCS in concussion because there are other definitions that a GCS above 15 can be defined as a minimal TBI. The problem is that concussion, and in general concussion is the one related to sports because it is the most typical one although concussion can happen also in falls or in other kinds of injury. In this case the sports concussion falls between a minimal and mild on the Glasgow Coma Scale. Because remember the patient can have a 15 on GCS but could also have a 14 because they maybe lose a score, one single point, because he is confused when you ask something.
In terms of epidemiology, concussion in sport has been reported between 0.1 and 21.5 cases for every one thousand athletic exposures, with the lowest incidence in swimming and diving and the highest one in junior ice hockey and American football. Of course this shows that these are clearly North American phenomenon for these kinds of sports and also with the publisher living over there. And by the age of 10, one in five children, this means 51 thousand children in Australia will sustain a concussion and present with acute post-concussion symptoms. So these kind of studies show that concussion and mild traumatic brain injury is very well presented in kids, especially before 14 years of age.
With regards to physiopathology there are quite interesting research aspects which can justify the symptoms that we see in these patients. Unlike more severe TBIs, the disturbance of brain function from concussion is related more to dysfunction of brain metabolism rather than to structural injury or damage. The current understanding of the underlying pathology of concussion involves a paradigm shift away from a focus on anatomic damage to an emphasis on neuronal dysfunction involving a complex cascade of ionic, metabolic and physiological events. Clinical signs and symptoms of concussion such as poor memory, speed of processing, fatigue and dizziness result from this underlying neurometabolic cascade.
In animal and human studies, MTBI can alter the brain’s physiology for hours to years, setting into motion a variety of pathological events. As one example, in some experiments on animals, after an initial increase in glucose metabolism, there is a subsequent reduced metabolic state which may persist for up to four weeks after injury. Though these events are thought to interfere with neuronal and brain function, the metabolic processes that follow concussion are reversible in a large majority of affected brain cells; however a few cells may die after the injury.
Cerebral blood flow is relatively reduced for unknown reasons, so it looks like a kind of ischemia, of course much less relevant than ischemia itself, but a loss of glucose can also cause a kind of energy crisis and a vessel spasm in the small vessels can cause a migraine and headache which is a topic that will be discussed by Dr Mobbs later on. Along with this process the activity of mitochondria may be reduced which causes the cells to rely on anaerobic metabolism to produce energy, increasing the levels of lactate.
So you can see the concussion can involve neurons as well as glial cells and the concussion can release some biomarkers from these cells in the cerebral spinal fluid as well as in the blood. So of course in the last years we have looked for specific biomarkers of a concussion. And here there is a synthesis of the most known biomarkers coming from the body of the cell neurone or from the axon or from the glial cells. But the important thing is that we trying to quantify these biomarkers and relate it to concussion but unfortunately there is not really translational clinical application so far. So it is more in the research setting.
Evaluation. Signs and symptoms. The somatic symptoms are like for example headache, cognitive dysfunction like feeling like in a fog, or emotional symptoms like lability. Physical signs include loss of consciousness and amnesia. Some behavioural changes have been reported like irritability or cognitive impairment like slowed reaction times. Or even there is sleep disturbance sometimes like drowsiness and insomnia.
On-field or sideline evaluation of acute concussion – when a player shows any features of concussion it is a very, very important thing because these should be evaluated by a physician or other licensed healthcare provider onsite using standard emergency management principles and particular attention should be given to excluding a cervical spine injury. The appropriate disposition of the player must be determined by the treating healthcare provider in a timely manner. If no healthcare provider is available, the player should be safely removed from practice or play and urgent referral to a physician arranged. Once the first aid issues are addressed an assessment of the concussive injury should be made using the SCAT5 which is an assessment tool we will see later on in the next slides. The player should not be left alone following the injury and serial monitoring for deterioration is essential over the initial few hours following injury. A player with diagnosed concussion should not be allowed to return to play on the day of injury. This is the most important point.
So the SCAT5, the sports concussion assessment tool has been done by assessment of experts who agreed to put together these tests and the last one is the version number five from 2007. It is important to understand that first of all, the SCAT5 is designed by physicians for physicians and licensed healthcare professionals. It takes time, not less than 20 to 30 minutes in general so it cannot be done in the correct way in less than 10 minutes. And if there is no physician or healthcare professional, the sports players or the people around should use the Concussion Recognition Tool 5, the CRT5. Another important point, is the SCAT5 has been designed for athletes aged 13 years or older, whereas for children aged 12 years or younger, please you should use another version which is the child SCAT5.
In the next slides there are some examples you can download for free on the website here in the PowerPoint presentation. And you can see that if you read the instructions it is impossible to be wrong following the SCAT5 which is 20 to 30 minutes long, but it is not that difficult. So step one is recognising red flags, because if there are one or more of these red flags like seizures, convulsion or double vision or weakness or tingling of the arms or the legs, these are worrisome things that could suggest that there is something more serious than a concussion itself. Then step two, the observable signs. If you have weakness in the signs or for example you saw a video or someone else told you. Then there is a memory assessment with a very weak and easy question about memory. Then there is a quantification and scoring system for the GCS by means of the scoring between three and 15 on the three different domains and here are the domains. And there is the cervical spine assessment which should be done always, because it is very important to assess if there is also a cervical injury.
Later on there is some background information to be taken by the physician and this is not just epidemiology information about the athlete, but also about things like if he already had a concussion in his life. And step two is a symptom evaluation. It is very important to understand that this is given to the athlete, so the athlete takes this part in his hands, or her hands, starts to read loudly the first paragraph over here and later on starts to assess all these symptoms if there are or not headaches, pressure in the head, neck pain and things like that, scoring in a subjective way between zero and six. And this an assessment which can be done at baseline, for example before the concussion before playing or post-injury. When the test is done and is given back to the physician and the doctor can check the number of symptoms between zero and 22, and the severity score which is a score between zero and 122 scoring the maximal score for each domain or each symptom.
There are some other stats in the cognitive domain, the cognitive screening includes the orientation questions, some memory questions, some words to be remembered and repeated over time. And the other tasks like the digits backwards and the months in reverse order. This domain is just to check the concentration and again these things can be scored with a yes or no if the patient was able to give the numbers or the months in the reverse order.
This is specifically by the GP because they have to check the neurological function, if there is dysfunction from a neurological point of view, or even check the balance examination. Last but not least there is delayed recall in which the doctor is asking the athlete if he remembers the words which were repeated before. And this gives the last score. At this point is the decision part in which the doctor is putting together a severity of symptoms and the number of symptoms and all these are just to put together an evaluation. Remember that there is no score which is a cut off to decide if the patient has a concussion or not. Scoring on the SCAT should not be used as a stand-alone means to diagnose concussion because there is more follow-up needed which is designed to give to athlete concussion injury advice. So try to understand if the concussion was there or not, giving some recommendations like avoid alcohol, avoid sleeping tablets and things like that. And moreover, trying to have a quantitator to be compared in case the patient shows up again with some worsening of some symptoms. And so the SCAT baseline in the first concussion or after a few hours or few days can easily depict which domain is more affected and where the management should go.
Remember that the SCAT5 is for doctors and healthcarers so if there no doctor this is a much easier version and basically everyone can ask these kind of questions and assess the level of concussion. In an emergency room or office by medical personnel the SCAT5 can be still given to the athlete, but of course we can do minimally things like checking balance and eventually decide even if neuroimaging is requested or not.
So the investigations. Just remember that if you ask for a CT scan, it is because you already are suspicious of something more suspicious like a fracture or some brain swelling or some facial injury. So basically the take home message is that a CT scan does not give any information at all on a simple concussion. Unfortunately even MRI is not able to depict any information. Remember that MRI is able to depict some micro-bleeding for example but a normal concussion has no structural changes in the brain itself. This means that metabolic change happening in the brain after concussion cannot be detected in a structural and architectural MRI, for example T1 and T2 sequences. So basically, this MRI will most likely be negative. Having said that, you ask for an MRI if you suspect or you find a focal neurological deficit or some worsening symptoms or prolonged disturbance of a conscious state. Having said that, there are a lot of research tools like functional MRI trying to quantify and characterise the connections of the brain if there some specific features which could be related to concussion. And there are other technologies that we will see in the last slides about the research aspects of concussion.
More regular investigations like for example Balance Error Scoring System of if the doctor or specialist sports physician has force plate technology, they can quantify and characterise the balance of the patient. The eye tracking system can be used by checking the visual movement of the eye and the saccades. Other tests can be given and there are other experimental things like genetic testing the markers. For example the Apolipoprotein E4 is deemed related to the some dementia and cognitive disturbances. And some people who have this genetic mutation might have a higher susceptibility of a concussion. These might justify why simple concussion effects some people more than others. Also these are a research tool because there is insufficient evidence for routine clinical use.
Neuropsychological assessment is something important which should not be done alone but a neuropsychologist can check the baseline and the difference after concussion and eventually can also check if there are other baseline problems like depression for example.
So to management. Remember that a concussion is in general a self-limiting and benign problem because the majority of concussed people, almost up to 90% resolve in a short time, less than 10 days. But this time can be longer in children or kids.
The first cornerstone is physical rest. No training, no playing exercise or weights, especially the day of the concussion itself. And there is cognitive rest which is very important, especially for kids, like no television, extensive reading or video games. But there is a question mark here because there is not very strong evidence that cognitive rest is really recommended in kids in order to recover faster.
So expect gradual resolution in less than seven days, or seven to 10 days. It is very important to try to understand how the patient or the kid will be able to return to school or to play again. So the return to play strategy has to be used, and there is a slide about that.
In terms of pharmacotherapy we use medication just for prolonged symptoms or just to help with sleep disturbances and anxiety or headache for example. But there are other modifiers like antidepressants that should not be used at the beginning because this could mask some important symptoms related to the concussion.
So you ask the patient if he feels well and if they feel fine or not they can quantify it. Maybe they do not really feel 100%. In that case you ask why they do not feel 100% and you can give again the SCAT5 to see which is the domain where they are losing some points.
This is a very pragmatic way to understand when the athlete or kid or concussed patient can go back to or return to play protocol. Imagine that every one of these is a tier in which there is a stage in activity with a functional exercise and an objective. So tier one where there is no activity at all and if the patient is able to handle a very good recovery from doing nothing, the day after they can start some light aerobic exercise, doing some walking or swimming, trying to increase the heart rate. And if he passes this tier he can go to sport-specific exercise and so on. So if you see there is 24 hours per step and in total in five or six days, the patient should be able to return to play or to return to school. If the patient gets stuck in one of these tiers, in one of these steps, he has to be there until he does pass the objective. And this makes it a little bit longer, the recovery itself.
So the only thing we have some evidence of is that same day return to play, the answer is no, because one concussion is a problem and multiple concussions is a major problem, especially when they are happening in a very short period of time. The patient can come back to play if they remain asymptomatic, if they are confident to go back. And there are the questions, should he use a helmet or head gear and there is not a lot of evidence about that.
The problems start when the patient has symptoms for a period of time longer than 10 days. So we are talking about 10% to 15% of these patients. In these cases though, sending most of them to a concussion clinic is very, very useful because this patient is a much more complex patient who has to managed in a multidisciplinary fashion. So neurologists or neurosurgeons or other healthcarers can help in the management assessment of difficult concussion cases.
Again, the psychological assessment can be important in that case, because the psychologist can assess the multifactorial problems related to the baseline of the patient or if the problems are related to the concussion itself.
Remember that there are some modifying factors which are factors which can modify the management, the decision making and the prognosis. For example, the symptoms factors. If there are a lot of concussion or the concussion lasted more than 10 days, or they were not quite as severe, or if the patient had some loss of consciousness longer than one minute. These are all modifying factors which give you a lower threshold to give much more aggressive management of the concussion itself.
Related to that is the big topic of the chronic traumatic encephalopathy because it looks like the more concussion can cause some precipitation for proteins which like the topology of Parkinson’s or Alzheimer’s disease. Unfortunately we do not know that much because the only way to diagnose the CTE now days is doing a brain autopsy. So we do not know the real incidence in athletic populations. But of course this is a big deal because especially when in the rugby league or some big leagues in the States, there was a big discussion about these entities which were not recognised or acknowledged.
In terms of prevention, we do not know if the protective equipment helps for concussion. For sure it helps to avoid facial and head injury and TBI, but about concussion we are not sure if a helmet can really help. Sometimes it can help but it can even facilitate a degree of concussion.
And there are other issues to be considered, like changing the behaviour on the playing ground, like for example avoiding aggression and violence, promoting fair play and respect.
In terms of research I already mentioned some tools that we are trying to use like functional MRI which is the image here. There is a lot of research in terms of biomedical injury because we are trying to understand if a helmet helps or not, or which kind of device could prevent all the problems related to concussion. We use in the research setting EEG and magnetoencephalography, and these give us some information about the connections of the brain. We use sometimes also eye-tracking as I mentioned to you before, or advanced imaging to check the stiffness of the brain, how the brain tissue amplifies the waves after concussion or how the molecules will move in the axon in the brain to see if there is a difference after the concussion. This imaging is called a DTI, diffusion tensor imaging which is a quite advanced MRI which is used now days for concussion, but again it is much more of a research aspect than a clinical collection of things to be done every time.
So there are some references here which you can find useful to keep going in detail with this topic. And my acknowledgements to several people, but especially to Michael Cusimano who was my supervisor during my fellowship for three years in Toronto who opened to me not just the world of neurosurgery, but also this universe of concussion from the clinical point of view and a research setting. Thank you very much.
Dr Rowena Mobbs:
Okay so an approach to headaches. So this is a really common condition as Antonio has well spoken about and also we would recognise that many people have had a concussion. If you ask patients and spend the time, many of them have quite some numbers of years of exposure to repeated head trauma so I think it is a very important issue particularly as children may be more effected and the elderly and females so we need to really all work together to understand this condition more. And look closely, it is necessarily a mild traumatic brain injury as far as the patient’s experience of course, it can be quite impactful for their life.
So we have set up a concussion clinic at Macquarie now to help work in an interdisciplinary fashion and do some more research. There has been 50 million dollars released by the Federal Government towards further traumatic brain injury research and we are certainly happy to be part of that effort if we can. And so concussions can be sustained in many ways as we have talked about. Falls can occur, particularly in conditions of Parkinsonian nature that I would see such as Lewy Body disease or Parkinson’s or epilepsy, or misadventure of course. And we are perhaps seeing less sporting concussions recently with the pandemic and more of these other sorts. Military comes to mind of course, particularly blast injury and we are typically talking about patients who have experienced over one thousand impacts if they are involved in a blast situation.
This is a video we will send you the link for. It illustrates a convulsive or seizure concussion in an ice hockey player and this is of course one of the sports of key focus for traumatic encephalopathy syndrome and chronic encephalopathy changes at autopsy. And we have very little literature really on the meaning of convulsive concussion and what that means as far as outcomes, but more work can be done in this field.
Recently there was a convulsive concussion for the rugby league and this was the response in the media, “We’ll give him a good 10 day break and he will be right”. I find this a little along the lines of the old attitude of come on, get up son you will be okay. And I think players are increasingly aware of that attitude and keen to look after their own health but also the community are looking at grass roots levels and what we can do better in a coordinated fashion and maybe even mandating some changes to ensure that we look after these patients very well.
So headache is of course an intrinsic part of concussion but also post-concussion syndrome and I have to admit the vast majority of my concussion patients will be beyond that two week period into the post-concussion phase just by nature of referral. Concussion is accounting for approximately 80% of all traumatic brain injuries, so very, very common. A loss of consciousness does not have to occur for a post-concussion syndrome to evolve. And the severity of the TBI at the time does not necessarily correlate with the severity of post-concussion symptoms. These symptoms are complex and common and they are very individual. Each concussion can experience tends to be a little different, with headache, dizziness, neuropsychiatric symptoms and cognitive impairment. I have mentioned the vulnerable patients, so female sex, older patients and paediatric population are more susceptible to greater frequency of concussion and severity. And there is a whole field of neurology opening up with neurohormonal research to these sorts of vulnerabilities. The recognition of PCS in children can be difficult. It is typically defined again arbitrarily as symptoms beyond four weeks. But eliciting what those symptoms are in a young child of course may be difficult. Most commonly you see post-concussion headache or posttraumatic headache in the mild TBI, but of course moderate and severe TBI patients can have that as well. We see it in whiplash, so there may be no direct impact to the head and in fact 20% of whiplash patients have cervicogenic pain evolving to migraine. And the pathophysiology is likely structural but also biochemical and neuroinflammatory and there is some really exciting work looking into this worldwide.
Here is one of these studies. So this was a study looking at the biomechanical effects of head impact. Looking at the oscillatory changes that occur. So with oscillations in the order of 20 to 40 hertz, the brain is more vulnerable to injury. It is like a bell ringing. And so it is not just a contrecoup one two, it is that repetitive vibratory effect on the brain. Of course there may be torsion and other effects. Most concussion syndrome is greatest within seven to 10 days but it may extend well beyond that. So the majority of patients have recovered by three months. But I think a large number really, 10% to 15% have symptoms beyond one year. So there is a lot of work to be done in the management of these patients.
I typically use the post-concussion scale as one of my guides. In those who have a score beyond 13 there is a much higher rate of post-concussion syndrome that will extend beyond the month. So it can be a bit of a guide and you can test that longitudinally for patients.
The headache syndromes are variable. Well, studies vary widely. Around a quarter to three quarters of patients will have a headache syndrome after concussion. Paradoxically, the headache prevalence duration and severity is greater in those with mild head injury than more severe as we mentioned. Pre-existing headaches are an ongoing risk factor for headache after trauma. The onset of headache should typically be within seven days, but really a three month latency is more likely and my own feeling is that maybe headaches syndromes can be triggered months down the track after significant levels of head trauma.
The International Headache Society classification identifies subtypes after concussion that are similar to non-traumatic headaches. Migraine and tension headaches predominate the number of these patients’ syndromes. Tension is the most frequent. Three quarters of patients have that type, but in blast injury, migraine may be more common. And many patients have more than one type of headache overlapping.
Well, tension. This can vary widely and most of us have experienced a tension headache. It can be bi-temporal, bi-frontal, generalised, unilateral, constant or intermittent. Typically associated with increased stress or screen time or late in the day. It may be dehydration. But there may be a degree of migraine overlap. It is thought that tension headache and migraine do have a spectrum. There can be a dull pressure or you know, a tightness, a tight band typically. And we need to be aware always that analgesic overuse can occur in up to 40% of posttraumatic headache actually, such as Panadol or codeine use. So ensuring a drug holiday is important.
For migraine headache, well this can vary widely. So many patients believe that a headache is a severe episode of vomiting in a dark room. But it is way more varied than that. It may be generalised or it may be lateralised or very focal like a watery effect and a focal sharp pain. It can come on very quickly almost immediately. It does not have to gradually come on. It can be a pounding or throbbing nature, photophobia but also phonophobia, the sensitivity to sounds which is more common in the Asian population. Dizziness or disequilibrium typically. You can have a migraine syndrome post trauma of pure disequilibrium without other features. Nausea, vomiting, lethargy and mental clouding. So here comes the cognitive impairment aspect and overlap with migraine. So lethargy and mental clouding are extremely common in chronic migraine, if not some of the most common symptoms. So, treating those is important for sorting the wheat from the chaff. And you will see the post-concussion symptoms scale there. The symptoms of concussion themselves and post-concussion are very similar to migraine, so it is really about good empiric management.
So here is a typical MRI from a migraine patient where you would see specks of tiny white matter hyperintensities in the frontal regions typically and these are thought not to have a clinical significance other than to associate with migraine. That being said, I must mention that migraine has an association with stroke as you all know and if you are a smoker that is in the order of 34 times the increased risk. So that is an important question to follow up with patients.
What is migraine like? Well these are some of the quotes from patients. So they have tried many types of medications, nothing has helped. They have often gone on for decades and not really realising they were migraine, just thinking they were headaches. And suffering in silence. It is affecting their work, their life, it is greatly debilitating. And they just may not realise the options out there. So really important to recognise for the person and economically.
Migraine can occur with or without visual aura. So these are the typical scintillations or bright sparkles, fortification spectra which are the zig-zags. You might get central scotoma and you may get tunnelling or just simple blurring or obscuration. There can be severe pain and nausea and vomiting. Migraine is thought to have strong genetic elements. Often these patients, particularly with posttraumatic migraine will have a family history. It may be the mother or the father. I am yet to really understand the literature but it would seem that often on the father’s side, there may be a more severe migraine syndrome.
Migraine can extend to the brainstem and cerebellum and there may be significant disequilibrium and the nausea and vomiting of course. Recurrent attacks can result from the mild head injury, particularly if you have two concussions in a row. And the head or cervical impact itself can of course directly trigger pain. Pain can lead to tension which might lead to migraine. It is usually multifactorial. It was originally termed footballers migraine but of course this occurs in any contact or collision sport.
Other headache syndromes are seen. The TMJ dysfunction can be due to direct trauma or jarring and you can get an ipsilateral hemicranial pain resulting from that. Many patients have bruxism so you might want to treat this as part of the headache management. Occipital neuralgia can occur from a direct load to that region of the skull causing aching, pressure, stabbing. And in fact again there is evidence of treating that in chronic migraine let alone treating occipital neuralgia with a range perineural occipital injections typically. And get them to avoid massage. They often try to massage the area and that may damage the nerve further.
There can be direct trigeminal nerve injury particularly to supraorbital or infraorbital branches with a shooting allodynic pain, tingling, aching or burning, paroxysmal or constant. And of course at the site of a soft tissue injury you can have pain there, tingling and shooting pain that can persist despite apparent healing of the wound. Some patients very rarely might have a low pressure headache from CSF leak due to a dural root sleeve tear or a cribriform plate fracture. You might ask about anosmia. There is a prominent positional association with this, so it is fine when they are supine but severe when upright. And identical to a post-dural headache.
Cortical contusions can have pain much like stroke. But this is variable, it might be a generalised ache and if it extends to the sub-arachnoid space with a haemorrhage then there can be severe pain. Traumatic dissection can occur remember, so I always typically order an MRA from the arch to the Circle of Willis alongside MRB for any venous thrombosis that can occur in trauma, and a good MRI with temporal views. We look at SWI imaging too for any micro haemorrhage changes. And there are case reports of cluster headache and also autonomic dysfunction. A particular syndrome called SUNCT which is rare and occurs in women mostly. They typically brace, are pretty unilateral head pain and there is tearing associated with that. It is a case of extremus lasting for hours at a time.
Sleep is really important. So sleep disturbances are common. Remember to look for PTSD. Insomnia occurs in about a third of patients in the acute phase after TBI. They can be hypersomnolent, have insomnia, increased sleep need overall. But also we can see weight gain and depression associated with obstructive sleep apnoea or OSA contributing to migraine full stop. And there can be bruxism of course with the trauma of the event, increased anxiety around their loss of return to work or life and other factors. So I would typically look at a PSG or sleep study.
Dizziness occurs in about half of patients with concussion. It is non-specific often. It might be lightheaded or disequilibrium or a true vertigo. And I have seen patients with a functional neurological disorder in this circumstance, a conversion disorder. So consider that as a possible diagnosis. Around 25% of neurology patients have an overlap with FND. Complaints of dizziness at the time of injury and afterwards are often associated with more prolonged recovery.
Psychology. So more than half of patients have a mood of affect of disturbance. They are intolerant of noise. They get emotional. Rushes of emotion or excitement and difficulty handling crowds for example. They can be more susceptible to alcohol effects. And their family members report that they are quite irritable or more withdrawn or just not themselves. 15% to 20% meet the criteria for a psychiatric disorder such as PTSD or acute stress. And of course overlaps of PTSD in veterans are common.
So cognitive rehabilitation has been looked at particularly in Defence. It is a little controversial, but overall the results are fairly promising. But it is costly and it takes expertise. In one study, 15 patients with mild TPI who met the criteria for depression were treated with Sertraline and there was a substantial remission in depressive symptoms. So this may have a role. And like migraine, providing a serotonergic environment could be helpful. CBT has been looked at and again this may be helpful.
When do I need a neuropsychologist? We have touched on this. When it is getting a little complex and when you expect that there might be cognitive overlaps this could reflect a possible traumatic encephalopathy syndrome or a more severe spectrum of TBI tending towards moderate, mild to moderate. Or mood disturbance, or even fogginess of migraine can occur. So it helps us really define which areas of the brain are effected and in that way gives the player a very good baseline going forward. So I would typically look at this in the months after a head injury if they have not resolved. In one study 15% of patients had persistent cognitive deficit and it can be very similar to psychological illness, pain and medication overlaps. Age and baseline are considered but not all of the testing for this is well standardised. So we take it a little with a grain of salt and in the context their other investigations.
Pharmacotherapy is important of course, particularly if you are managing migraine. So amitriptyline has been looked at directly in post-trauma with some evidence of resolving features. Propranolol or amitriptyline in combination can be helpful. Topiramate, valproate, Lyrica, Sandomigran and Candesartan have a rather sparse literature for posttraumatic headache. Triptans may be helpful, a Panadol/Nurofen combination or high dose aspirin. And the newest kid off the block is the CGRP antagonist which directly blocks one of the receptors on the trigeminal nerve and alters vascular response and this has almost as good evidence as Botox in migraine and could look promising for posttraumatic headache. An inpatient program of metoclopramide and intravenous dihydroergotomine can be helpful, but that is quite an intense approach and the occipital nerve block is up your sleeve to try.
Okay. We have got to be wary of analgesic overuse as I mentioned and indomethacin can be helpful too, particularly in coital headaches. In one study looking at Botox for posttraumatic headaches or those with a history of MTPI in the military, there was a response. 64% of patients reported feeling better but further studies are needed and this is some of the work we are looking at at Macquarie.
The non-pharmacotherapeutic management is so essential, providing education, basic education around concussion and post-concussion syndrome. Helping to involve family members in that support, a multidisciplinary team. And this has some evidence in the studies of course for providing better outcomes.
There are conservative approaches of gentle neck massage and we involve the physiotherapy team, Chris Wynne at MQ Health for this. Looking at B vitamins as a group. B vitamin preparation can be of assistance. Involving neurology. Looking at MRI and then we work with a team including neurosurgery and ENT as appropriate. Many patients have tinnitus overlaps to their syndrome.
I am co-director at the Australian Sports Brain Bank. So we are really interested in not only sports related exposure to concussion and sub-concussion, so they are the head impacts without symptoms, but also in sports and the non-sporting environment. The military, in farmers or those handling livestock, and in falls for example. So we are working with RPA at the Sports Brain Bank and we are studying these patients in line with neuropsychology, neuro-ophthalmology and imaging.
So it is worth mentioning too that some patients have a very prolonged syndrome after concussion. This may involve a functional overlap. There is usually very prominent emotional symptoms associated with this, and the risk factors for this small group of patients remains unclear, but no doubt a team of support in the long term is needed. And at the very least you are there to help listen and counsel your patients of course.
So in summary, just a few pearls. Post-concussion syndrome and headache disorders are common and they are complex in their installation. They require individualist care, specialist care may be useful. Women, children and older patients are more susceptible and they present their own unique challenges. So a team with experience is important. The severity of the brain injury does not correlate with the risk of developing PCS nor the prognosis. So I think there may be a role for more standardised follow up for at least sporting concussion. And there are many theories on the structural and biochemical brain changes and I think we will gain some good insights over the next decade or two regarding this. It is quite an exciting time to be in this space.
So I would like to thank everyone here tonight and also thank my team. Antonio is there. Jennifer Batchelor is our neuropsychologist on the team. Alan Pearce in neurophysiology. Clare Fraser for neuro-ophthalmology. Our neuropsychologists and imaging and Michael Buckland at RPA as well. So thank you very much, everyone and I am happy to answer questions.
Dr Tim Senior:
Thank you very much indeed. You have done a fantastic job getting through a lot of information both of you and thank you for answering some of the questions that came through in the chat box as well. Those are our learning outcomes there. We have got a bit of time for questions still, so there are two questions currently available so I will invite either of you to answer. Would the treatment for post-concussion migraine, is it any different to typical migraine? And the question is in terms of medication but I guess that is also in terms of non-medication management of migraines as well.
Dr Rowena Mobbs:
Yes, so I guess I will answer that. Thank you. So, look it is very similar. The only thing I would be a little wary of is the very somnolent patient or the very mood-disturbed patient that you may see in a post-concussion syndrome versus migraine. Of course it can occur in migraine. But I am very passionate about offering migraine therapy for these patients because I think it can make a difference. There is evidence it can and we should you know, the proof is in the pudding, so trialling these medications carefully, starting low, going slow but certainly offering that range of therapies is important.
Dr Tim Senior:
Excellent. There is another question which I think you answered in your presentation as well about Botox injections in managing migraine headaches and how helpful that is. Nerve blocks.
Dr Rowena Mobbs:
Yes. So I think Botox is really our best evidenced therapy. It has been around for decades now, not just years. It typically can improve over two thirds of patients for chronic migraine. It is well-tolerated, very localised and patients you know, may find that more easily adherent than say taking a medication routinely. And the other issue to that must be raised of using medications in sport, so of course things like propranolol, the beta-blockers or sedating medications may not go too well on the sporting field or in those sports requiring shooting for example in pentathlon. So you have just got to pick and choose a little bit. But I think Botox would be our number one treatment in migraine.
Dr Tim Senior:
Yes, excellent. We have a question from a participant who has been doing exactly this sort of work this week. She has had three patients present with tinnitus and hearing loss post head injury. So she is sending them for formal hearing tests, but anything else you would recommend in those circumstances?
Dr Rowena Mobbs:
Yes, so I think it is essential to work with the ENT specialist on this. So there can be overlaps with Meniere’s disease so we are always heightened to that, in which case you would look at a low salt diet and some anti-histamines and stress management as well as ENT watch. Of course there can be structural injury to the ears and that must be excluded, with specific views on MRI and specialist review.
Associate Professor Antonio Di Ieva:
And I would add also a CT scan, because as you know I spoke against a CT scan but sometimes this comes back as useful, for example if there is hearing loss, I would like to do a skull based high resolution CT scan to see slice by slice 1 mm thick if there is a small fracture on the petrous bone and this information can be very, very useful for the ENT surgeon as well.
Dr Rowena Mobbs:
Dr Tim Senior:
Thank you, that is really helpful. There is a question that came through earlier that you answered by text but I am not sure if everyone saw the answer and I think it is potentially important for everyone. If a patient is already on anti-depressants and then sustains a concussion, should that be withheld or continued? And I think that is a useful thing for us to know about.
Dr Rowena Mobbs:
Yes, so given depression can overlap from the actual brain injury perspective of biological depression, neurobiological depression plus the situational depression and reactive changes by being out of their sport or out of their work in these typically highly achieving individuals, I would continue the SSRI or the SNRI with expectation that would need to be maintained and not stop it because certainly there can be a withdrawal syndrome that could mix the picture and muddy the waters for a post-concussion assessment, they could have a reactive depression if we did that. However there are the exceptions of amitriptyline and mirtazapine. If the patient is somnolent she might consider a careful down-titration or cessation. I guess with mirtazapine paradoxically it can be less sedating on 30 mg rather than 15, so you might even consider a dose up if they need it, but evidence in migraine for a serotonergic stage that can assist the actual headache syndrome, so I think we should try to continue those if we can.
Dr Tim Senior:
Excellent. That is helpful. We have got a question, does a history of previous concussion increase the risk of concussion with milder head injuries in the future?
Dr Rowena Mobbs:
I think a proximate concussion, no one really knows the answer to that but say within a few months of your last concussion but particularly within a fortnight, can lead to more severe and more prolonged symptoms after the second concussion. Does that help answer?
Associate Professor Antonio Di Ieva:
I think it is a very big topic because we know that the time frames are very important because it is a metabolic problem in which neurons are trying to recover and trying to reduce the lactate, so if there is a second concussion in a very short period of time, you can increase the neuronal death. Having said that, sometimes concussion will come in even after days or weeks or months or years. Some people are most susceptible than others and this case of course we do not know the answer, but it could be related to some genetic susceptibility. I was talking about for example some genetic mutation in the E4, so we do not know. There is a lot of research about that. For sure having more concussion in a short period of time is something very bad, but also over a wide range of time could be a problem. We do not have a clear answer about that.
Wonderful. Was there any more questions, Tim? Or is that wrapping us up for the evening? Was there any more you wanted to field?
Dr Tim Senior:
There is probably just one quick one. Do non-invasive stimulators have a role to play in these types of headaches, especially in children?
Dr Rowena Mobbs:
Antonio? I defer.
Associate Professor Antonio Di Ieva:
I am not sure what is a non-invasive stimulator.
Dr Tim Senior:
Yes, we might get back to you on that question. I am just looking at another. We have had a few comments come through which I think we all recognise about that tension between what we know to be the best management of concussion and head injuries and the pressure that players and sports clubs feel to get people back playing can be pretty tough. There are a few comments around that and I think we all recognise that tension and my understanding is that the moving towards a better understanding but is certainly not perfect yet at the moment.
Dr Rowena Mobbs:
I would like to just comment that I think there is a community shift occurring of more awareness around the importance of looking after your brain in order to be the best player you can, and I think people are being more careful.
Dr Tim Senior:
Associate Professor Antonio Di Ieva:
Just on the comment about the stimulator. So with a basic stimulator. So, we do neuromodulation for pain, so supraorbital stimulator sometimes can be used and I agree with that. For example Dr Mobbs mentioned the block of the occipital nerve for occipital neuralgia. That block if it fails can be just be a previous step to neuromodulation putting a stimulator on the occipital nerve. So I agree that one of the last tiers of treatment can be neurostimulation.
Dr Tim Senior:
Excellent. Thank you very much. So on your screen now is the learning outcomes from tonight. So if you look through those, hopefully we have achieved all of those for you. We have had a few people asking about whether we will get the slides and those will be sent to you sometime after the webinar this evening. I would like to thank very much our speakers this evening for an excellent session on concussion and Sammi, over to you to close for this evening.
Wonderful, thanks Tim, and I would like just to reiterate Tim’s message and thank Antonio and Rowena again and also yourself Tim and everybody who joined us online this evening. We do hope you enjoyed session and enjoy the rest of your evening.