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Syncope - Fainting - Passing out
The following is included as a story of interest and a chance to explain the functional approach to dis-ease.
It is not a case study nor is it a patient testimonial or an advertisement, as they are not allowed within Australian licensing guidelines.
Vasovagal Syncope
Or the problem of consistently fainting while eating.
A patient complained that for the last few years she was having enormous difficulty with swallowing. Often during a meal she would ‘pass out’, her record was five times during a meal, literally ‘face planting’ onto her plate. It was very distressing for her and everyone around her. They would hold onto her while she ate waiting for the ‘drop’. Even swallowing her own saliva while walking around could lead to a fall and an injury. On one occasion, she had a fall down a flight of stairs. Driving was a problem as she had to pull over to have a drink of water, prepare herself for an episode of unconsciousness, recover and drive off as if nothing had happened.
Vasovagal Syncope is a very interesting phenomena. Basically the nervous system doesn’t coordinate properly allowing a temporary drop in blood pressure to the brain. It then shuts down leading to unconsciousness. For some inexplicable reason the blood needed to pump up to the brain tends to pool in the legs.
It is known to occur for a variety of common reasons such as:
Standing still in the hot sun
Heat exposure
Seeing blood or having an injection
Fear
Straining at the stool
There is a variation of it, called Micturition Syncope where older men ‘pass out’ while urinating. Cough Syncope is another version of it.
Anyway the lady who ‘swallows’ to initiate this phenomena was typical in some ways and very different in others. She had been to multiple physicians without any hope of a treatment. The usual medical advice for this problem is to ‘work around it’ i.e., there isn’t any medication or therapy utilised as ‘best practice’. It is usually a matter of putting up with it.
From another point of view this problem is a lack of fine coordination of the haemodynamics that we all normally have. Basically, the receptors that convey messages of how much pressure the heart must pump in various situations, or the vascular response of the lower limbs, is not working properly, or both. Either way the Nervous System is dysfunctional but not pathologic. Vasovagal Syncope won’t kill someone by itself. Of course, if the environment is dangerous, passing out could end up being fatal!
This patient’s history was unremarkable and did not give any clues as to the source of her issue. A bank of tests to do with her Autonomic Nervous System revealed enough aberrant or unusual findings to start to get an idea as to what might be going on with her.
The Carotid Sinus Reflex was sluggish and largely unresponsive compared to normal. This is a test that requires measurement of the Heart Rate before and after light finger pressure upon the carotid sinuses in the neck. The occulo-cardiac reflex was similar. Gentle pressure upon the closed eyeball also affects the Heart Rate. This also was slow to respond and didn’t vary as much as normal.
More generally the evaluation of Eye Movements using Saccadometry showed a poor cerebellar control.
Dynamic Visual Acuity Testing showed a poor Vestibulo-occular Reflex.
Force Plate Analysis also showed ocular deficiency and poor proprioception integration.
Together these findings led to a formulation of a treatment regimen which included:
Spinal Adjustments which are proven to stimulate the Frontal Cortex of the Brain
Low Level Electrical Stimulation of the tongue to gently stimulate the Brain Stem
Sensory-motor integration procedures using Laser Guided Targets and Hand-eye coordination and timing techniques.
Observing Saccades and Pursuits.
Also home exercises were emphasised utilising:
Gargling
Singing loudly
Standing on one foot while brushing teeth with eyes closed.
Gaze stabilisation exercise
Deep Knee Bends (squats)
After 5 consultations in one month we were happy to hear that the problem of fainting with swallowing was completely gone. At a one year follow up phone call the patient said the problem had not returned.
A very interesting presentation.
This document is incomplete as new knowledge about this topic is rapidly improving.
Concussion - Traumatic Brain Injury - Whiplash
Concussion, Traumatic Brain Injury, and Whiplash are complex medical conditions often leading to a Post-Concussive Syndrome (PCS). PCS is characterised by symptoms persisting for more than three months after the initial injury. Diagnosis primarily relies on the patient history and includes assessments such as SCAT 5, VOMS (Vestibular Oculomotor Screen), Buffalo Treadmill Fatigue index, Concussion Balance Test (COBALT), and the King-Devic Test.
The underlying pathology of these conditions often involves damage to the brain's myelin sheaths due to rotational forces, or direct trauma to the brain tissue from rapid acceleration and deceleration. This physical disruption can affect synapses and small blood vessels. The brain's consistency, akin to jelly, makes it particularly susceptible to such injuries.
Neuro-inflammation following the initial injury is a critical aspect to address. Without intervention, it can lead to persistent production of inflammatory cytokines by the glial tissue. Recent advancements have identified biomarkers for this inflammation.
Prof. Carrick, a renowned expert in the field, emphasises the uniqueness of each concussion and the importance of tailored treatment approaches. He advocates for a patient-centric strategy, prioritising dysautonomia and adjusting treatments based on individual responses. His methodology underscores the significance of careful observation and the necessity to alter treatment plans swiftly if positive outcomes are not observed.
He stated:
“great question! Each person is different and each concussion is different. What works well in one situation does not in another. Having said that, dysautonomia of any variety always gets my maximum attention in concert with the patient wish list. I find that I must understand the individuality of the patient and the consequences of each functional performance or therapy to that person. As a consequence my therapeutic approach is most likely different for each patient. Understand the person and the consequences of a treatment. Low and slow is oftentimes faster than quick. Do it again if there is anything left. All treatments must have positive consequences so observe-treat-observe. If you are not making positive changes or things are going a bit South, then you need to change treatment immediately or pack them off to a colleague”.
PCS manifests in three subtypes:
Physiological PCS, impacting the Autonomic Nervous System and altering cerebral blood flow;
Vestibulo-ocular PCS, affecting the vestibular and oculomotor systems; and
Cervicogenic PCS, involving cervical spine dysfunction, muscle trauma, and somatosensory dysfunctions. These subtypes can coexist, and their presentations may vary depending on factors like habituation, re-injury, and co-morbidities.
A comprehensive assessment of the patient's Autonomic Nervous System, brain cortex, cerebellum, cervical spine, vestibular system, brain stem, cranial nerves, muscle stretch reflexes, sensory system, saccadic and pursuit systems, and balance is crucial for an accurate diagnosis.
Identifying the primary problem area—be it cervical, vestibular, ocular, or brain-related—is essential for effective treatment. Techniques like Smooth Pursuit, Dynamic Visual Acuity Test, Smooth Pursuit Neck Torsion Test, and various reflex tests are employed to pinpoint the affected system.
Rehabilitation strategies for PCS are multifaceted. The approach to treatment remains a subject of ongoing research, particularly regarding the effectiveness of enhancing weak functions versus developing new functions in expectation of transference.
Cervicogenic, Physiological and Vestibulo-ocular presentations can be treated as a whole for the purpose of this discussion.
Clinical treatment always includes vestibular stimulation. Home treatments are guided by assessing the patient's balance ability, with a focus on proprioception, visual inputs, and vestibular contributions.
The treatment of PCS is a holistic process, requiring a nuanced understanding of each patient's unique condition and a multifaceted approach to therapy.
It often involves:
Vestibular Stimulation which can be achieved in many ways and the use of Multi Axis Rotating Chairs is becoming popular. Its vestibular stimulation when rolling in the sagittal plane is unachievable by any other means and therefore, offers a unique opportunity for the nervous system to ‘reset’, adapt and develop.
Peripheral Nerve Stimulation done in a way to evoke a somato-sensory potential also hasn’t any comparison to the activities of daily living. It is a unique stimulation which also encourages the homeostatic mechanisms to ‘tune up’.
Spinal adjustments are similar in that, done judiciously, they improve the quality and quantity of spinal receptor afferent activity.
With PCS causing imbalance, a guide to choosing useful adjunctive and home treatment can be assumed by assessing the breakdown of the patients ability to balance.
Human balance is achieved by a combination of proprioception, visual and vestibular inputs in specific ratios.
When standing on a firm surface the Visual component contributes 10%, Vestibular input 20% and Proprioception 70%.
Comparing this to a perturbed surface, i.e. a soft surface, the Visual component contributes 20%, the Vestibular component 70% and the Proprioception component 10%.
This assessment guides the practitioner to the most deficient components of the somatosensory systems including showing up an over compensated system. Quantitatively this is best achieved with Force Plate Analysis equipment, but it can be assessed with other methods. These results lead the clinician to focus on what to rehabilitate, such as:
Cerebellum Rehab - Gait and Balance considerations are addressed by utilising a motor program and making it unstable by adding complexity, then testing and measuring it to establish a baseline followed by multiple repetitions of it until it has improved. Similar or the same with Heal to Toe walking, Yes-Yes, No-No head movements while walking, the One leg teeth cleaning Exercise, Fast turning, Backwards walking, Fast eye movements while walking, Lunges with one foot on a soft surface, andSaccadic Eye movements.
Cortical Rehab - spacial awareness, predominantly Parietal area uses up most of the neocortical activity, memory saccades, visualisation.
Frontal Rehab - executive function, can’t start or finish jobs, low motivation. Intellectual activities use mainly the dlPFCx of the frontal lobe which is small by comparison. Sensory processing is about 70% with motor activity about 30%. Complex Sequential Finger Tapping Exercise. Saccades and Pursuits.
BG Rehab - fast decisive explosive movements, Using a Reaction Timer, Burpees with confounding, eg star jump every 2nd, then 3rd, then 4th… or Dual tasking - count backwards from 100 by 7’s.
VOR Rehab - Firstly, we must consider why is the VOR dysfunctional?
The original assault occurred to the nerve tissue. Nerves have, as a fundamental function - the transmission of impulses. Clearly, disease or damage will affect this fundamental ability. Intracortical circuits run at 3-4mS transmission speeds. The VOR is the fastest reflex in our nervous system running at 5-6mS. The next fastest reflex is 70mS so it is easy to expect that a dysfunctional nervous system is going to show up as impaired nerve transmission.
Hence, the fastest reflex stops being as fast and the result of this in the case of the VOR is a loss of the ability to fixate upon a target when the head is moving. Not complete loss, just a loss of speed and therefore, efficiency.
Why does a broken VOR matter?
Loss of the ability to fixate upon a target while moving, relatively speaking, will have initial effects followed by habituation of the resultant behaviour.
Initially, damage to the nervous system which results in a slow/dysfunctional/broken VOR will cause an instability necessitating slow and careful movement. However, this is co-morbid with other signs and symptoms from the initial injury or disease and is easily overlooked and considered ‘normal behaviour’ for someone suffering PCS.
As the nervous system habituates and the original injury heals, the dysfunctional VOR becomes established as the new ‘normal’.
Likewise the ‘instability’, from the initial response to an injury or disease, will also become learned. It then looks like poor balance, incoordination and hesitation. However, habituation of this dysfunctional fundamental ability has far reaching consequences.
The nervous system is intricately interdependent.
When the patient is imbalanced there is a threat assessment involving the Limbic system.
The Cerebellum predicts 2.5 sec in advance and alerts the Amygdala if there is a disparity for ‘threat assessment’. Imbalance consistently has the Amygdala firing to ensure survival. This engages the Hypothalamic-Pituitary-Adrenal Axis causing an increased cortisol response and eventual dysautonomia.
This is backed up by the Mid-Cingulate Cortex which also predicts motor movements in relation to behaviour - it is involved in processing information around reward-based decision making and cognitive activity associated with intentional motor control and connects to many areas including the Limbic System.
Limbic system activity inhibits Frontal Lobe activity, therefore, Reason, Emotional control, discrimination, executive function etc are diminished preventing the patient from being the ‘human’ they were pre accident. An ‘altered personality’ is a post concussion consequence .
Imbalance by itself can lead to Anxiety(30%). Consider how the ‘worry’ of falling could habituate and lead to hypervigilance.
Rehabilitation of the VOR
The Vestibulo-Ocular Reflex is a complex issue. It involves the peripheral and central vestibular systems and there is much that can influence the outcome.
The Peripheral Otolithic system can be the source of a lesion, as can the Central Vestibular connections including mixtures of both. The cerebellum modulates the central vestibular system and can affect the reflex. The vestibular system has contributory somatosensory input, so that can affect the system as well. This is a very big topic which would be titled ‘Vestibular Rehabilitation’ and much too huge for this missive.
Then there is the actual brain areas that have sustained damage, these form part of a network. e.g. Executive, Default Mode Network, Salience Network. The damaged areas feed into other areas that will also show signs of dysfunction as they are not getting the usual stimulation expected of normal function. The whole network is disrupted because part of the network is damaged.
Clinically, we can do a very decent job of looking at the problem globally and reacting accordingly, i.e. treat the person not the pathology.
We use head mounted lasers aimed to sequential targets on a lighted panel bearing in mind peripheral vision starts at 60deg from centre. The research suggests 15 minute exercise times with a 4000 lumen contrast, i.e. a darkened room. A normal subject will accurately perform this test at 0.4s and often a post concussion patient will struggle to achieve 1.2s, but lots of repetition will retrain the brain to improve.
As an exercise for home follow up.
Head shaking while looking at a target, as fast as possible (>100deg/sec is very fast) but not allowing the target to move will operate this reflex. Done horizontally, vertically (Yes-Yes, No-No) and in a circular movement. Start with a distant target and progress inward to arms length.
The ability for the eyes to fixate upon a target is actually reliant on three reflexes. Small movements are controlled by the Cervico-ocular Reflex, Faster movements require the Optokinetic Reflex and fast movements use the VOR. Activities of daily living use all three.
Watching a Bee moving about on a flower uses the Cervico-ocular Reflex (<30deg/Sec).
Observing a bird fly past uses the Optokinetic Reflex (30-100deg/sec).
A quick look to see if traffic is coming before crossing the road uses the VOR. (>100deg/sec)
The Cervico-ocular Reflex afferents predominantly arise from the soft tissues of the sub-occipital region. Stimulating these repeatedly will re-habituate/retrain/develop these circuits.
Small head movements will work these.
A weighted Helmet while doing small head movements will increase the afferent barrage to the oculomotor nuclei.
Wearing Pinhole Glasses and examining a complex target for detail like a ‘Where’s Wally’ picture.
Wearing a Head mounted laser and tracing a small shape in the distance.
Massage, dry needling, heat, cryotherapy, manipulation, stretching and Range of Motion exercises to the sub-occipital/cervical region will all be beneficial but less so than above. Why? Because these activities are activating only some of the complex mix of receptors that produce the afferent input. Whereas, using the reflex, uses all of the receptors and in the same proportions as to the way we have evolved and developed. Isometric exercises might be an exception because they powerfully activate the CB which is involved in the fine control of the reflexes.
The Optokinetic Reflex involves the Accessory Optic System which we have already discussed elsewhere along with the information on Collicular Remapping and the Looming Exercise. The 'Focus Builder’ App has Pursuit ‘games’ for this activity.
Clinical Treatment for PCS
Vestibular Stimulation can be achieved in many ways and the use of Multi Axis Rotating Chairs is becoming popular. It’s vestibular stimulation when rolling in the sagittal plane is unachievable by any other way and therefore offers a unique opportunity for the nervous system to ‘reset’, adapt and develop.
Peripheral Nerve Stimulation done in a way to evoke a somato-sensory potential hasn’t any comparison to the activities of daily living. It is a unique stimulation which also forces the homeostatic mechanisms to ‘tune up’.
Spinal adjustments are similar in that, done judiciously, they improve the quality and quantity of spinal receptor afferent activity.
Eye movement activities, Cognitive exercises and challenges, 19 Channel Neurofeedback, Cold Laser, Transcranial alternating current stimulation, Entrainment therapy and Proprioceptive activating activities may be utilised.
Dysautonomia is also a ‘must do’ hurdle for lasting treatment effect. It is not an unachievable goal but requires patient compliance.,
Considerations to address this may include some of the following:
Aerobic activity
O2 therapy - (Hyperbaric)
Ketogenic Diet
Vit C to bowel tolerance
CBD oil
Dietary Fasting >12hrs
Creatine supplementation 20grams/day. Magnesium 400mg/day, Co-Q10 200mg/day.(4mg/kg)
Gut Biome correction.
The goal is to achieve Autophagy of the superfluous organelles and membranous detritus left over from the injury, to stop the inflammatory cascade within the glial tissue and support the replication of new mitochondria for improved energy metabolism.
Concussion, traumatic brain injury and whiplash are serious conditions involving a multifaceted approach to treatment. The treatment is tailored to each individual and requires time and perseverance.