Personalised Brain training for mind and soul
Neurofeedback and Kaiser Neuromaps – an advanced qEEG brain map – have numerous applications to neuro-degenerative conditions. These are evidence-based through peer-reviewed research, and the process is medication-free, non-invasive and enjoyable.
Personalised Brain Training – qEEG brain map-based neurofeedback training – has been shown to provide the following:
– reducing symptom severity
– structural improvements of the brain including myelination, microglial function
– ameliorating motor symptoms and sensory integration
– restoring life quality
– improving sleep, depression, anxiety and sense of self, as well as other concomitant mental health issues
– neurofeedback training has the potential to slow down the actual and perceived progress of various conditions by virtue of its positive structural effects (e.g. promoting myelination) and simultaneous palliative effect
Neurodegenerative Conditions include Parkinson’s, Alzheimer’s and Huntington’s Disease; MND / ALS; Dementia with Lewy Bodies (DLB) and Multiple Sclerosis. Many of these can lead to dementia.
Neurofeedback training is an evidence-based, non-specific, complementary therapy. It is drug-free and non-invasive.
With a Kaiser Neuromap, we can see vulnerabilities to comorbid mental health conditions as well as:
— neuromarkers for early detection, e.g. Alzheimer’s, Dementia with Lewy Bodies (DLB), Parkinson’s Disease
— while not a diagnostic tool, qEEG- based Kaiser Neuromaps can show an early indication of possible dementia onset
— this can be confirmed via fMRI or other testing that is usually only performed in more advanced stages
— helps patient plan, make lifestyle changes, gain interoceptive awareness of own perception vs that of others
— enables patient to remain functional for longer
— reduces perception mismatches between client and environment
— improves manageability of disease progress.
Neurofeedback improves quality of life, sensory integration, motor skills, movement initiation and balance in Parkinson’s Disease.
Peer-reviewed research shows the following effects in neurofeedback applications to Parkinson’s Disease:
– improved motor symptoms, on a par with other therapies such as rTMS – while being non-invasive and drug-free
– improvement in life quality
– increased sensory integration in 10-12 sessions
– reduced symptom severity
General (non-PD specific) effects of neurofeedback training include:
– overall increased fine motor skills
Chronic Pain is another application for neurofeedback, where studies have demonstrated its efficacy.
Subjectively, PD sufferers find neurofeedback training calming, reassuring and report an improved sense of feeling being part of their body.
Hallucinations are a frequent occurrence in dementia sufferers – 80% of DLB (Dementia with Lewy Bodies) patients experience visual hallucinations, and these are complex visual, animate and often involve people. They are also a feature in other forms of dementia.
Research on audio-visual hallucinations in Schizophrenia patients have found that Neurofeedback training can produce significant results in reducing treatment resistant auditory verbal hallucinations. In 30% of cases antipsychotic medication has little or no effect. Psychotropic medication use in general can have undesirable side effects and is contentious.
Hallucinations have cortical sources – there are specific brain areas responsible for visual mental imagery, and research shows that the phenomenon as experienced by dementia sufferers correlates with decreased gray matter volume in various prefrontal, motor and visual association areas. Interestingly, the brain areas affected are differ by form of dementia, such as DLB versus Parkinson’s.
This suggests that treatment could be improved without side effects.
Research funded by Parkinson’s UK regarding hallucinations is currently focused on CBD and anti-sickness pills, and possibly other drugs. Neurofeedback training is drug-free and non-invasive complementary therapy.
White matter tracts are information superhighways connecting various brain regions and make up c.50% of our brain volume. White matter abnormalities in various forms of dementia, including DLB, Alzheimer’s and Parkinson’s, and mTBI (mild traumatic brain injury) are well documented, and these contribute towards cognitive decline.
With neurofeedback, we can train white matter tracts. This seminal study indicates that we can improve myelination with neurofeedback training. It has been further corroborated since, notably with regard to efficiency.
The ability of white matter disruption to contribute towards cognitive decline to the extent that dementia results is known since the 1980s when the term “White Matter Dementia” was coined. Various pathologies, including Parkinson’s, Alzheimer’s, Huntington’s, ALD and MS (Multiple Sclerosis) are significantly characterised by white matter disruption. In fact, the involvement of white matter disruption in these neurodegenerative pathologies has been asserted with a certainty that contrasts with the evolution of attempts to define the various ‘diseases’ at times.
Neurofeedback can positively affect white matter growth. In healthy patients, this growth was faster than the rate of neurodegeneration in neurodegenerative conditions. Research has yet to confirm that this works for these conditions specifically.
This approach is non-specific and holistic – we are treating the brain as a whole, and not with regard to a particular condition. Indeed, defining a neurodegenerative pathology is in itself a challenge – Parkinson’s diagnostic criteria have evolved substantially in recent decades and are still subject to debate and expansion, as is the definition of a disease itself. In vivo, that is, before a post mortem examination, Parkinson’s is largely ascertained on the basis of symptoms. It would seem logical to aim therapy at these symptoms, rather than, say, chase a ‘cure’ for an ill-defined phenomenon (is it strictly, and only, dopaminergic neuron death?). This differentiation in approach is important as funding criteria for research into ways to ameliorate the condition often utilise this to the detriment of alternatives. As a result, neurofeedback is sadly neglected in the quest for helping people with neurodegenerative conditions.
Neurofeedback has been shown to help with primary and secondary symptoms in Parkinson’s; it is a non-specific, complementary therapy that is non-invasive and medication-free.
White matter decline is measurable with DTI (Diffusion Tensor Imaging) even before the onset of cognitive decline. The mechanisms by which damage occurs varies by pathology. However any intervention that improves these connections should have a positive effect on the person, both structurally and cognitively. Counteracting this trend in a non-invasive, medication-free and enjoyable manner seems a worthy cause.
The search for a ‘cure’ of different neurodegenerative conditions which lead to dementia is strongly focused on the defining feature – e.g. amyloid beta production in Alzheimer’s, and dopaminergic neurons in Parkinson’s. Addressing symptoms is often seen as a secondary endeavour, with regard to time, prestige, funding and resources. Daniel Webster has spent time working in palliative care and high-support living and rehabilitation facilities. He found that ameliorating life quality can lead to at least a perceived slowdown in the progression of a condition. There is also a possibility that symptom reduction can actually impede a worsening of the condition, and certainly worthy of further research.
Subjective feedback by dementia clients is very encouraging. Research into this aspect of dementia, and how neurofeedback can be applied to slow, arrest and potentially reverse disease progression, is a worthwhile endeavour. Please contact Daniel directly to support initiatives in this regard.
It has recently been shown that neurofeedback training led to cognitive improvements in Multiple Sclerosis (MS) patients, and that this corresponded to improved functional connectivity in key motor and salience networks. Increased fractional anisotropy (FA) was observed, which correlated with cognitive improvement.
MS is a neurodegenerative condition that adversely affects axonal myelination. FA is among other a measure of myelination, so the result that neurofeedback can make positive changes in this condition is very encouraging.
A study with sufferers of Huntington’s Disease, another neurodegenerative condition, showed that cognitive and motor skills improved and that these changes related to improved functional connectivity in key brain regions, again a conclusion that neuroplasticity can be induced despite the presence of neurodegeneration.
“The idea of Neurofeedback is very interesting and the evidence [above] shows great potential. Larger studies would be needed to fully understand the potential and safety of this method for people with Parkinson’s before we could share it with our community.” –Researcher Katherine Fletcher (PhD) of Parkinson’s UK
Reverse enquiries, from persons affected by Parkinson’s to charities seeking to represent their cause, could accelerate the inclusion of neurofeedback into research programmes funded by them, and awareness raising of a complementary therapy that has already been shown to produce positive effects on primary and secondary (e.g. mental health) symptoms, thus benefiting more people, in a timely manner.
Currently, few, if any, research aggregators (e.g. charities) make any mention of neurofeedback as a complementary therapy approach while admitting openness to exploring it should persons affected by the various conditions approach them. Unfortunately, the lack of mention reduces the propensity and likelihood of such reverse enquiries. To break this cycle, the opportunity exists to directly fund, or engage in, neurofeedback training for sufferers of neurodegeneration and/or dementia.
The “larger studies” needed per Parkinson’s UK (above quote) also appear to face volunteer shortages, and at the time of writing (24 July 2022), five studies face the risk of being shut down as a result, with potentially millions of pounds of research funding (and donations) going to waste. The hope of “larger studies” being conducted with regard to neurofeedback thus seems a very distant prospect.
The point of this discourse is to illustrate the dynamics at play when it comes to awareness raising for neurofeedback for sufferers of neurodegeneration and its secondary (mental health) effects. There are already studies (above) demonstrating efficacy, including with regard to primary symptoms. Daniel Webster has personally witnessed its beneficial effects with his late grandfather, 99, in a palliative care setting.
Daniel Webster is offering neurofeedback training to persons suffering from Parkinson’s, and other forms of dementia or neurodegeneration, on a sponsored basis and welcomes support from donors and persons looking to benefit from it.
Neurofeedback is a form of complementary therapy and should not be seen as a replacement for conventional medicine. qEEG brain map-based neurofeedback training takes a more holistic approach to brain functioning, rather than just focusing on medical symptoms. It is not intended as a form of diagnosis nor medical intervention nor medical advice per the disclaimer.
Parkinson’s Disease is the second most common neurodegenerative disorder, after Alzheimer disease (AD).
Onset is usually characterised by motor symptoms: bradykinesia (slowness of movement), rigidity, resting tremor and instability of posture.
With regard to PD, Neurofeedback training has been shown to:
Secondary, non-motor symptoms evolve, such as cognitive impairment, depression, sleep issues (e.g. REM sleep behaviour disorder (RBD), a potential prodromal marker of PD, where paradoxically motor function is improved relative to wake state), and olfactory dysfunction.
Neurofeedback training is effective at reducing symptom severity and addressing most of these neuropsychiatric disturbances.
On a cortical level, PD involves the loss of dopaminergic neurons, accumulation of Lewy bodies, damage to neuroglial cells and demyelination of neuronal axons.
Neurofeedback training has been shown to improve myelination across white matter tracts. We can also train frequencies that pertain to glial cells, potentially improving their self-regulation.
A recent study raised the spectre of a connection between COVID-19 infection and Parkinson’s; three persons without familial history developed clinical parkinsonism within 2-5 weeks following infection requiring hospitalisation.
Alzheimer Disease (AD) is the most common neurodegenerative disorder. Similar to Parkinson’s Disease, secondary symptoms are neuropsychiatric in nature and can be addressed with neurofeedback training, helping the person to maintain their sense of self, mood regulation and sleep, and contain arising anxieties.
There are biomarkers that allow us to differentiate between Dementia with Lewy Bodies (DLB), Parkinson’s Disease, and Alzheimer Disease. A Kaiser Neuromap gives us a non-specific indication of each, that can assist early onset diagnosis and thus shape the treatment plan at an early stage.
As with other neurodegenerative disorders, physical changes in the brain affect our sensory interpretation of our surroundings, giving rise to neuropsychiatric disorders. We can become relational in our thinking, and specifically with regard to brain areas that are responsible for our interpretation of personal space and social boundaries.
Neurofeedback Personalised Brain Training aims precisely at encouraging cortical participation and help us share a reality with others, counteracting progression of major secondary, and possibly primary symptoms. Rather than promoting a ‘cure’, we are helping affected persons improve their quality of life in many ways.
The link between Alzheimer’s Disease and Herpes simplex virus type 1 (HSV1) has long been established, as summarised in this research paper from 2014. Four out of five people carry the herpes virus, with one in four being prone to physical symptoms upon periodic reactivation, e.g. blisters / cold sores occurring during times of stress and/or immunosuppression. Reactivated HSV1 has been found to cause inflammatory damage directly, probably involving increased formation of beta amyloid and AD-like P-tau changes found in HSV1-infected cell cultures. HSV1 DNA was found to be specifically localised in amyloid plaques in AD. Further links have been discovered between shared pathways of HSV1 and AD. HSV1 (herpes virus) can cross the blood-brain barrier and remain latent in the brain; combined with carriage of a type 4 allele of the apolipoprotein E gene (APOE-e4), this confers a high risk of developing Alzheimer’s Disease. Some 25-30% of the population carry this gene.
COVID-19 is of particular concern with respect to Alzheimer’s Disease. A pre-existing AD diagnosis is the single highest risk indicator of Covid infection identified thus far; the highest mortality is observed among the most elderly AD patients.
This susceptibility is partly explained by the up-regulation of ACE2R receptors in the limbic regions of AD-affected brains. It is even hypothesised that amyloid-beta is involved in fighting cerebral Covid infection, similar to an observed process with regard to alpha-synuclein in PD and Covid, a defence mechanism that might result in higher levels in the long run.
Alzheimer’s Disease is viewed as a prion disease, a feature that again puts it into context with Covid-19, a coronavirus whose S1 spike protein has prion-like qualities.
Alzheimer’s Disease is the number one cause for dementia, with no known effective treatments. Finding the ‘root cause’ of this condition in order to produce a targeted cure is further complicated by the fact that the definition of what constitutes AD is somewhat circular. We define the phenomenon by its symptoms:
– Amyloid beta (Ab) plaques: Ab(40-42) oligomers are prominent in AD brains, both in soluble form, where they are more toxic, and in dense plaques, which are thought to serve as reservoirs. These oligomers can cause synaptic dysfunction, dendritic spine damage and neuronal death. Their inflammatory effect includes activation of microglia, astrogliosis, overproduction of cytokines, and dystrophy of neurites. This leads to brain atropy, often first observed in the temporal lobes. The epsilon4 allele of ApoE (e4APOE) is a genetic risk factor thought to affect Ab metabolism; 25-30% of the population have this gene. Ab oligomers can also induce the formation of Neurofibrillary Tangles (NFTs):
– P-Tau: Neurofibrillary tangles of hyperphosphorylated tau (p-tau) is another defining feature of AD. These formations occur after Ab accumulations, though they are seen in frontotemporal dementia without Ab plaques and may also be a parallel, symbiotic phenomenon accelerating disease progression. The Ab / p-tau theory however only accounts for a fraction of the structural dementia comorbidities, and treatment strategies targeting these two aspects have thus far been unsuccessful. This necessitates additional theories:
– Neuroinflammation: While unclear whether this is a consequence or cause of the condition, neuroinflammation is deemed to a major contributor towards the progression and severity of AD, possibly more so than Ab accumulation and NFTs. All three of the above aspects are addressed by another causative, or at least contributory theory:
– Viral Infection: Herpes Simplex Virus (HSV) reactivation is highly correlated with AD; causes damage to the same brain areas that are affected in AD (herpes simplex encephalitis (HSE), induced by HSV, damages the hippocampus, temporal and frontal lobes); is found (by DNA analysis) in substantially all amyloid plaques; is known to alter Ab metabolism, CA2+ homeostasis, synaptic dysfunction and apoptosis in HSV infected neuronal and glial cells. Note that this pertains to carriers of the e4APOE allele, while HSV in the brain of non-e4APOE carriers confers a much lesser risk. At least 80% of the population carries HSV, with only one fifth exhibiting symptoms (e.g. cold sores in times of stress or immunodeficiency); 25-30% of the population carry the e4APOE allele.
The last point is particularly relevant: There are multiple approaches to arresting HSV reactivation (e.g. anti-virals, such as acyclovir, and also components of seaweed(!)), which appears to be the most promising approach addressing suspected cause. It also provides a link with Covid, and an explanation for the high susceptibility of AD patients to this:
Covid, especially the S1 spike protein, has been shown to cross the blood brain barrier (BBB) and enter the brain through a number of pathways, including olfactory and vagus nerve. It has been found to reactivate latent cerebral HSV-1. Amyloid beta (Ab) (1-42) has been found to strengthen the binding of the S1 spike protein of Covid (SARS-CoV-2) to ACE2 receptors and increase viral entry. Covid also increases neuroinflammation. Further, the CA2+ dysregulation in AD facilitates passage of the Covid virus. ACE2 receptors are more prevalent in limbic regions of the brain, including brainstem and hippocampus, and importantly, they are up-regulated in AD brains, thus conferring higher susceptibility. Another possibility is that beta amyloid formation increases in response to HSV (and potentially Covid), as a defence mechanism, resulting in higher aggregation. An analogy is an observation made with influenza viruses, in particular the West Nile Virus, where alpha synuclein production increased to combat the virus (an absence thereof resulted in disastrous disease progression), leading to aggregation and thus higher Parkinson’s Disease susceptibility.
With a Kaiser Neuromap, we can identify character traits, vulnerabilities and strengths.
Different brain areas and networks govern our behaviour. For example, there are parts of our brain which control mood regulation; spatial distractibility; physiological arousal; our sense of self; self-critical thoughts; anger and emotional attachment; and there are various sources of anxiety.
A brain map shows us which brain areas are behaving immaturely, and thus expose us to vulnerabilities or mental health issues.
Rather than fitting people into categories – diagnosis – we can assess vulnerability to behaviour patterns. Every brain is different. A brain map provides a more granular approach to understanding our strengths and weaknesses.
Neurofeedback lets us train dysrythmic brain areas. With sensors comfortably fitted to the brain areas we want to train, we detect brainwave patterns real-time while watching a movie. When these patterns are inefficient, the volume drops momentarily. This is the feedback we are giving our brain, short and instantaneously.
The brain area we are training recognises this – while our conscious mind is focussed on the movie – and adjusts its behaviour to restore the normal volume. With repetition, throughout a session, learning occurs.
Meanwhile our conscious mind is solely focussed on the movie; the training process is passive in this sense.
The drop in volume is subtle, so we continue to understand the flow of the movie. No current or electrical stimulation is fed to the brain; sensors simply read brainwaves and the feedback is purely audio-visual.
Rather than engaging the conscious mind, which slows us down, we are training preconscious processes.
This equips us with the ability to live in the moment and attain our potential (if we have to resort to conscious control, we are not living in the moment).
We take a holistic approach to healthy brain self-regulation, rather than categorisation or diagnosis.
Personalised Brain Training is an advanced qEEG brain map-based approach to neurofeedback training developed by the founders of the field. Taking Othmer Method / ILF training methods further, it employs Default Network Training protocols as developed by David Kaiser.
Neurofeedback training is an evidence-based complementary therapy. Its efficacy was first demonstrated some 50 years ago, and with advances in technology, training protocols have become more efficient and the feedback method – watching movies – thoroughly enjoyable.
Neurofeedback is evidence-based. It’s first application was discovered in 1971 when it was used to resolve intractable epilepsy.
There are over 2,000 peer-reviewed research reports on PubMed demonstrating efficacy across a number of pathologies.
In the US, it is an accepted complementary treatment for many challenges.
Neurofeedback training can substantially improve the life-quality of sufferers of age-related conditions such as Alzheimer’s, Dementia, Parkinson’s, Huntington’s and Stroke victims. It has been shown to improve cognitive performance in elderly patients with mild cognitive impairment.
By targeting specific brain areas responsible for functions that are observably degenerating, neurofeedback aims to arrest and possibly reverse declines.
Specifically, white matter tracts can be trained, and comorbid mental health disorders (anxiety, depression, anger) treated.
Improving the brain’s ability to self-regulate can substantially benefit a person’s sense of well-being. Physical and emotional calming help to soothe irritability and mood swings. We can work on specific areas of the brain responsible for bodily coordination, speech and expression. With the Synchrony protocol, we aim to improve memory, focus, and through further calming produce a sense of comfort, thus reducing any anxiety. Given the organic degeneration at the root of the condition, neurofeedback training is likely to be an ongoing complement to care.
Sue Othmer, who devised the Othmer Method of Neurofeedback, discusses what it does and how it can help with age-related conditions by giving the example of own family members:
A qEEG recording takes about 45minutes for a 20 minute recording.
A cap with 19 sensors is is fitted to our head and gels inserted to ensure connectivity. The sensors only read – there is a tiny voltage on the surface of our head that these pick up. The gels are easily washed out later. This is also the last time we wear the cap (until a remap after ten sessions); training is done with single sensors.
We analyse the data with Kaiser Neuromap software which gives us a unique view into character traits and vulnerabilities.
Findings are presented in a separate one-hour conversation where we discuss the key elements.
We use a movie of choice as the feedback mechanism – our conscious mind engages with the film, and feedback is delivered by small changes in volume or picture size.
Our pre-conscious mind adapts its behaviour to preserve the more comfortable volume and picture size, and learning occurs.
Volume changes are slight, not stop-start, and the process is enjoyable.
Key is that we are interested in the movie – our conscious mind is engaged with the content, which forms the reward, and our preconscious mind – without our conscious effort – changes its behaviour in response to the feedback.
A two hour training session allows us to do 90-110 minutes of neurofeedback training during which we can work on various brain sites.
This captures an entire ultradian rhythm cycle and corresponds to the approximate duration of feature film movies.
We can start with shorter sessions as appropriate, mainly with children.
Ideally, we do two or more sessions per week to start with.
We would expect to see responsiveness within the first few sessions and remap after twenty hours or about ten sessions.
Generally, we would expect to doing twenty sessions over two months, though this can vary substantially.
We can also accommodate intensives, where we do two sessions per day over a number of days, and have had good results with these.