Many chronic complaints do not begin in the body, but in the nervous system.

Pain, exhaustion, concentration problems, migraines, or depressive moods are often the result of disrupted neural communication—that is, faulty regulation in the brain.

Parkinson’s disease (PD) is a progressive neurodegenerative disorder that primarily affects motor control. Typical symptoms include tremor, muscle rigidity, slowed movements (bradykinesia), and balance difficulties. In addition, non-motor symptoms such as sleep disturbances, mood changes, autonomic dysfunction, and cognitive impairments are common.

What happens in the brain in Parkinson’s disease

– Degeneration of dopaminergic neurons in the substantia nigra → dopamine deficiency in the striatum

– Disruption of basal ganglia networks → impaired motor control and motor planning

– Altered cortical and subcortical connectivity affecting motor, cognitive, and emotional networks

– Accumulation of alpha-synuclein (Lewy bodies) → neuronal dysfunction

– Neurotransmitter imbalances (acetylcholine, noradrenaline, and serotonin) contributing to non-motor symptoms

– Progressive network dysregulation → decline in motor function, cognition, and processing speed

Prevalence

Parkinson’s disease is the second most common neurodegenerative disorder after Alzheimer’s disease and primarily affects people over the age of 60. Men are slightly more frequently affected. Worldwide, approximately 1% of the population over 60 years of age lives with Parkinson’s disease.

Neuromodulation in Parkinson’s disease

Neuromodulation, particularly non-invasive brain stimulation techniques, is increasingly being investigated as a supportive therapy to improve motor and cognitive functions in Parkinson’s disease. Clinical studies show improvements in gait, balance, mood, and sleep.

The therapeutic benefit varies individually but is often greater when combined with movement therapy or cognitive rehabilitation.

How neuromodulation works in Parkinson’s disease

– Regulates cortical excitability and enhances neuronal plasticity

– Supports motor networks → improved gait, balance, and coordination

– Reduces rigidity and bradykinesia

– Supports cognitive functions and emotional stability

– Strengthens neuroplasticity → facilitates adaptation and response to therapeutic processes

Multiple sclerosis (MS) is a chronic inflammatory autoimmune disease in which the immune system attacks the central nervous system. Inflammation, demyelination, and neurodegeneration lead to motor, sensory, and cognitive impairments such as muscle weakness, spasticity, fatigue, coordination difficulties, visual disturbances, and concentration problems. The course of the disease varies individually and can significantly affect quality of life.

What happens in the nervous system in multiple sclerosis

– Demyelination: damaged myelin sheaths slow down or block electrical signal transmission → impaired motor function, sensory processing, and cognition

– Axonal degeneration: progressive loss of nerve fibers contributes to long-term disability

– Chronic inflammation: immune-mediated damage to myelin and neurons

– Network disruptions: impaired communication between brain regions affects movement planning, perception, and cognitive performance

Prevalence

Multiple sclerosis primarily affects young adults and occurs more frequently in women. Worldwide, more than 2.8 million people are living with MS. The disease is more common in regions farther from the equator.

Neuromodulation in multiple sclerosis

Non-invasive neuromodulation shows promising effects in improving motor and cognitive functions and in reducing fatigue. Although outcomes vary individually and long-term effects are still under investigation, many patients report noticeable functional improvements.

How neuromodulation works in multiple sclerosis

– Reduction of mental and physical fatigue

– Improvement of mobility, coordination, and motor networks

– Enhancement of attention, working memory, and cognitive performance

– Support of neuronal reorganization, which can enhance physical and cognitive therapy processes

Dementia is a progressive neurological syndrome that leads to a decline in memory, thinking, behavior, and everyday functional abilities. Commonly affected domains include short-term memory, language, executive function, and spatial orientation.

The most common form is Alzheimer’s disease, followed by vascular dementia, dementia with Lewy bodies, and frontotemporal dementia. Progressive loss of function leads to increasing dependency and poses significant emotional and organizational challenges for both affected individuals and their families.

What happens in the brain in dementia

– Loss of synaptic function and increasing neuronal degeneration, particularly in the hippocampus, prefrontal cortex, and parietal regions

– Accumulation of pathological proteins such as beta-amyloid and tau

– Disruption of key neurotransmitter systems (acetylcholine, glutamate, dopamine)

– Reduced cerebral blood flow and decreased metabolic activity

– Disruption of functional connectivity between cortical and subcortical networks

Prevalence

Worldwide, more than 55 million people are living with dementia, with approximately 10 million new cases each year. Prevalence increases markedly with age; 30–50% of people over the age of 85 are affected. Dementia is one of the most common causes of care dependency in older age.

Neuromodulation in dementia

Neuromodulation represents a promising non-pharmacological complementary approach. Clinical studies report improvements of 20–40% in attention, working memory, language, and executive functions, particularly in early and moderate stages of the disease and when combined with cognitive training.

How neuromodulation works in dementia

– Increases cortical excitability in hypoactive areas, for example in the dorsolateral prefrontal cortex

– Promotes synaptic plasticity and supports learning and memory processes

– Improves regional cerebral blood flow and glucose metabolism

– Stabilizes functional connectivity within key brain networks

– Supports neuroprotective processes that may contribute to a potential slowing of disease progression

Depression develops as a result of a profound dysregulation of the brain, nervous system, and metabolism. Affected individuals experience loss of drive, persistent low mood, loss of interest, exhaustion, sleep disturbances, or emotional numbness. Chronic stress, trauma, hormonal changes, and genetic factors often play a contributing role.

What happens in the brain in depression

– Reduced activity in the prefrontal cortex → decreased drive and impaired decision-making

– Overactivity of the stress system → inner restlessness and sleep disturbances

– Dysregulated reward system → loss of interest and reduced motivation

– Reduced neuroplasticity → impaired regeneration of the nervous system

– Imbalance of the neurotransmitters serotonin, dopamine, and noradrenaline

Prevalence

Depression is among the most common disorders worldwide. Approximately 15–20% of people experience at least one depressive episode during their lifetime. Women are more frequently affected; stress, genetic factors, and trauma increase the risk.

Neuromodulation as an additional therapeutic option

Neuromodulation offers a scientifically validated approach to gently regulate neuronal activity. It can be used as a complementary treatment alongside psychotherapy and pharmacological interventions—particularly in cases of therapy-resistant symptoms. Clinical studies show improvements in mood, sleep, drive, and emotional stability.

How neuromodulation works in depression

– Activation of the prefrontal cortex → greater clarity and emotional stability

– Strengthening of the reward system → increased motivation and positive affect

– Harmonization of the stress axis → improved sleep and reduced inner tension

– Promotion of neuroplasticity → facilitated neural regeneration

– Regulation of serotonin and dopamine

Failed Back Surgery Syndrome (FBSS) describes persistent or worsening back pain following spinal surgery, even when the procedure was technically successful. Affected individuals often continue to experience back and leg pain, numbness, muscle weakness, or functional limitations. FBSS highlights that not only mechanical factors play a role, but also dysregulation of the nervous system.

What happens in the nervous system in FBSS

– Nerve root compression: recurrent or persistent irritation of peripheral nerves

– Neuropathic mechanisms: altered pain processing due to scar-related trauma

– Disrupted cortical processing: changes in the somatosensory cortex and prefrontal cortex

– Central sensitization: increased pain sensitivity in the spinal cord and brain

– Neuroinflammation and impaired pain modulation within the central nervous system

Prevalence

Chronic back pain affects 51–84% of adults at some point in their lives. After spinal surgery, 10–40% of patients develop FBSS. The more complex the surgical procedure, the higher the risk. The consequences have a substantial impact on mobility, quality of life, and mental health and may lead to long-term functional limitations.

Neuromodulation in FBSS

Neuromodulation can achieve significant pain relief in 60–75% of cases, even in long-standing, therapy-resistant conditions. Improvements are commonly observed in:

– Pain intensity

– Mobility and daily functioning

– Mood and psychological stability

– Reduced dependence on medication

How neuromodulation works in FBSS

– Reorganizes dysfunctional pain networks and reduces central sensitization

– Normalizes brain activity in motor and sensory areas

– Strengthens descending pain control mechanisms and reduces medication requirements

– Improves mood, functional capacity, and psychosocial resilience

Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease affecting both upper and lower motor neurons. It leads to increasing muscle weakness, paralysis, and ultimately respiratory failure.

In a subset of affected individuals, cognitive and behavioral changes also occur, often overlapping with frontotemporal dysfunction. Disease progression is typically rapid and highly disabling.

What happens in the brain in ALS

– Degeneration of upper and lower motor neurons with loss of voluntary muscle control

– Cortical hyperexcitability contributing to excitotoxic neuronal damage

– Glutamate-mediated neurotoxicity and pronounced oxidative stress

– Neuroinflammation involving microglia and astrocytes

– Secondary network disruptions in brainstem and spinal circuits affecting motor function and reflexes

Prevalence

ALS affects approximately 2–5 individuals per 100,000 population per year. Disease onset most commonly occurs between the ages of 40 and 70, with a slightly higher prevalence in men.

Around 5–10% of cases are familial and associated with known genetic mutations, while the majority occur sporadically.

Neuromodulation in ALS

Scientific evidence for non-invasive brain stimulation (NIBS) in ALS is limited but is an area of increasing research interest. Some studies report 10–20% improvements in motor function, spasticity, or a potential slowing of functional decline, particularly in early stages of the disease.

Effects vary depending on stimulation protocols and individual disease progression.

How neuromodulation works in ALS

– Reduction of cortical hyperexcitability in the motor cortex

– Support of remaining motor networks and potential delay of functional loss

– Possible improvements in mood, fatigue, and quality of life

– Short-term effects that require repeated or continuous treatment sessions

Alzheimer’s disease is a progressive neurodegenerative disorder and the most common cause of dementia. It is characterized by progressive memory loss, cognitive decline, and behavioral changes that increasingly impair daily functioning, independence, and quality of life over time.

What happens in the brain in Alzheimer’s disease

– Deposition of beta-amyloid plaques and tau protein tangles → loss of synaptic function

– Neuronal cell death and cortical atrophy, particularly in the hippocampus and association cortices

– Disrupted functional connectivity in memory, attention, and executive networks

– Impaired neurotransmission, especially within the cholinergic system and glutamatergic signaling pathways

– Progressive network disintegration affecting cognition, behavior, and spatial orientation

Prevalence

Alzheimer’s disease affects approximately 5–8% of individuals over the age of 65, with prevalence increasing markedly in older age groups. Women are affected more frequently than men. Disease risk is influenced by genetic factors (e.g., APOE-ε4), vascular risk factors, and environmental influences.

Neuromodulation in Alzheimer’s disease

Non-invasive brain stimulation (NIBS) has demonstrated improvements of approximately 10–30% in memory performance, attention, and other cognitive functions in individuals with mild to moderate Alzheimer’s disease. Effects are variable and typically time-limited but may be enhanced when combined with cognitive training or behavioral therapy.

How neuromodulation works in Alzheimer’s disease

– Activation of hippocampal–prefrontal networks to support memory and learning

– Improvement of attention and executive functions through dorsolateral prefrontal stimulation

– Stabilization of mood and behavior via modulation of limbic circuits

– Promotion of neuroplastic processes with temporary improvements in cognitive function

– Requirement for repeated or maintenance sessions to stabilize therapeutic effects

Attention-deficit/hyperactivity disorder (ADHD) is a neurodevelopmental disorder characterized by persistent patterns of inattention, hyperactivity, and impulsivity. Symptoms typically begin in childhood but may persist into adulthood, significantly affecting academic, occupational, and social functioning.

What happens in the brain in ADHD

– Underactivity of the prefrontal cortex (DLPFC, medial PFC) → reduced top-down control, impaired planning, and self-regulation

– Dysregulation of the basal ganglia (caudate nucleus, putamen) → altered motor control and reward processing

– Reduced activity of the anterior cingulate cortex → diminished conflict monitoring and error detection

– Disruption of fronto-striatal and fronto-parietal networks → impairment of attention and executive functions

– Neurotransmitter dysfunction (dopamine, noradrenaline) → attentional deficits and impulsivity

Prevalence

ADHD affects approximately 5–7% of children and 2–5% of adults worldwide. Diagnosis is more common in boys during childhood, while ADHD in adults is often underdiagnosed. Comorbidities such as learning difficulties, anxiety disorders, or affective disorders are common.

Neuromodulation in ADHD

Non-invasive brain stimulation (NIBS) has shown improvements of approximately 10–30% in attention, working memory, and impulse control in clinical studies. Effectiveness depends on age, symptom severity, and stimulation parameters, and is particularly pronounced when neuromodulation is combined with behavioral therapy or cognitive training.

How neuromodulation works in ADHD

– Improvement of attention and focus through stimulation of the dorsolateral prefrontal cortex

– Reduction of impulsivity and hyperactivity via modulation of fronto-striatal circuits

– Enhancement of working memory and executive functions through prefrontal network activation

– Cumulative effects with repeated sessions to stabilize symptom improvement

Post-stroke encephalopathy describes cognitive, emotional, and behavioral impairments that occur as a consequence of a stroke. It results from direct neuronal damage as well as from widespread network alterations in affected and functionally connected brain regions.

Symptoms may involve attention, memory, executive functions, and emotional regulation, significantly limiting independence in everyday life.

What happens in the brain in post-stroke encephalopathy

– Focal neuronal loss in the infarct area with subsequent diaschisis in remote brain regions

– Altered cortical excitability and reduced synaptic plasticity in peri-infarct and contralesional areas

– Disrupted functional connectivity within fronto-parietal, motor, and limbic networks

– Neuroinflammation and oxidative stress with secondary neuronal damage

– Network-related deficits in attention, memory, and executive functions

Prevalence

Cognitive and behavioral impairments affect approximately 30–50% of stroke survivors. Risk is higher in older patients and in cases of large or cortical infarctions.

Deficits may persist long term, leading to functional dependency, reduced quality of life, and increased burden on caregivers.

Neuromodulation in post-stroke encephalopathy

Non-invasive brain stimulation (NIBS) is increasingly used as a complementary therapy in the rehabilitation of cognitive and motor deficits after stroke. Clinical studies report improvements of approximately 10–30% in attention, memory, executive functions, and motor performance, particularly when combined with targeted rehabilitation or cognitive training.

How neuromodulation works in post-stroke encephalopathy

– Increases cortical excitability in peri-infarct and contralesional brain regions

– Promotes functional connectivity across disrupted motor, cognitive, and limbic networks

– Supports neuroplasticity and network reorganization

– Improves cognitive functions and enhances the effects of rehabilitative training

– Cumulative effects with repeated sessions for more sustained improvements

Anxiety disorders are among the most common mental health conditions and are characterized by excessive fear, persistent worry, and heightened physical stress responses. The most common forms include generalized anxiety disorder, panic disorder, social anxiety disorder, and specific phobias.

Symptoms include inner restlessness, concentration difficulties, sleep disturbances, muscle tension, and physical stress reactions. If left untreated, anxiety can significantly impair well-being, relationships, and overall quality of life.

What happens in the nervous system in anxiety

– Overactivity of the amygdala → heightened threat perception and emotional overload

– Reduced function of the prefrontal cortex → impaired regulation of emotions and anxiety responses

– Disrupted communication between the cortex, amygdala, and cingulate networks

– Neurotransmitter imbalance (serotonin, GABA, noradrenaline)

– Increased autonomic activity → symptoms such as palpitations, sweating, tremor, and muscle tension

Prevalence

Anxiety disorders affect more than 300 million people worldwide. Lifetime prevalence ranges between 15 and 30%, with higher rates in women and in individuals with depression, chronic pain, or traumatic experiences.

Neuromodulation in anxiety disorders

Neuromodulation can significantly reduce anxiety. Clinical studies report improvements of 30–80%, with high response rates in certain patient groups. Individuals often report greater calmness, improved emotional regulation, better focus, and fewer physical stress reactions, with minimal side effects.

How neuromodulation works in anxiety

– Reduces overactivity of the amygdala and limbic structures

– Strengthens the prefrontal cortex → improved control over emotional responses

– Normalizes neurotransmitter activity, particularly GABA and serotonin

– Improves neuronal connectivity → greater emotional stability and mental clarity

Fibromyalgia is a chronic pain syndrome characterized by widespread muscle and joint pain, fatigue, sleep disturbances, concentration difficulties (“fibro fog”), and increased sensitivity to touch and pressure.
The underlying cause is altered stimulus processing within the central nervous system: pain signals are amplified and insufficiently regulated.

What happens in the brain in fibromyalgia

– Abnormal pain processing → increased activity in pain-related brain regions such as the insula, cingulate cortex, and somatosensory cortex

– Reduced inhibition of descending pain control systems → diminished endogenous pain suppression

– Neurotransmitter imbalance → lower levels of serotonin, dopamine, and noradrenaline; elevated levels of substance P and glutamate

– Autonomic dysfunction → impaired stress regulation and disrupted sleep architecture

– Neuroinflammation and reduced neuroplasticity → heightened stimulus sensitivity and chronification of symptoms

Prevalence

Fibromyalgia affects approximately 2–4% of the global population, with a significantly higher prevalence in women. The condition typically begins in adulthood and frequently co-occurs with depression, anxiety disorders, and other chronic illnesses.

Symptoms substantially impair quality of life, daily functioning, and work capacity.

Neuromodulation as a modern supportive approach in fibromyalgia

Neuromodulation is a non-pharmacological approach that is particularly helpful when medication-based treatments are insufficient or cause side effects. Clinical studies show:

– 30–60% reduction in pain

– Improved sleep quality

– Enhanced mood and cognitive performance

– Greater functional capacity in daily life

How neuromodulation works in fibromyalgia

– Normalizes hyperactive pain networks in the brain and spinal cord

– Restores balance between excitatory and inhibitory neurotransmission

– Promotes neuroplasticity → long-term improvement in stimulus processing

– Improves mood and mental clarity → addresses common comorbid symptoms such as depression and fibro fog

Neurodevelopmental disorders are neurological conditions that arise from atypical brain development and typically become apparent in early childhood. They affect cognition, behavior, emotions, and social functioning and often accompany affected individuals throughout their lives.

The most common neurodevelopmental disorders include autism spectrum disorder (ASD), attention-deficit/hyperactivity disorder (ADHD), intellectual disabilities, communication disorders, and specific learning disorders. Clinical presentation varies widely and requires long-term, individualized support.

What happens in the brain in neurodevelopmental disorders

– Atypical synaptic development and neuronal maturation, affecting the structure and efficiency of neural circuits

– Imbalance between excitatory and inhibitory neurotransmission (E/I balance), particularly involving glutamate and GABA

– Abnormal functional and structural connectivity, such as local hyperconnectivity and reduced long-range connections

– Altered activity of key brain networks, including the prefrontal cortex, default mode network, and fronto-striatal circuits

– Neurotransmitter dysregulation (dopamine, serotonin, acetylcholine), influencing attention, mood, and behavior

Prevalence

Neurodevelopmental disorders affect an estimated 15–20% of children worldwide. Autism spectrum disorders occur in approximately 1–2% of the population, while ADHD affects about 5–7% of school-aged children.

Comorbid symptoms across multiple domains are common, amplifying the impact on education, social participation, and mental health.

Neuromodulation in neurodevelopmental disorders

Neuromodulation is increasingly investigated as a complementary intervention, particularly to support attention, emotional regulation, and cognitive control. Studies report improvements of approximately 15–30% in attention, working memory, emotional stability, and social behavior, especially in individuals with ASD and ADHD.

How neuromodulation works in neurodevelopmental disorders

– Increases cortical activity in underactive regions (e.g., prefrontal cortex, temporoparietal junction)

– Stabilizes the excitatory–inhibitory balance

– Promotes neuroplastic processes and learning capacity

– Strengthens functional connectivity between disrupted networks

– Supports adaptive functions such as attention, behavior, and social interaction

Migraine is a neurological disorder characterized by recurrent attacks of severe, often pulsating headaches. These attacks are frequently accompanied by nausea, sensitivity to light or sound, and in some cases visual disturbances (aura).

Migraine is a highly burdensome condition that can significantly limit quality of life and everyday functioning.

What happens in the brain in migraine

– Cortical hyperexcitability (CSD) → may trigger aura and amplify pain signals

– Trigemino-vascular activation → inflammatory neuropeptides such as CGRP promote pain

– Brainstem dysregulation → altered activity in pain-processing centers

– Neurotransmitter imbalance → serotonin, dopamine, glutamate

– Central and peripheral sensitization → promotes chronification and pain persistence

Prevalence

Worldwide, more than 1 billion people live with migraine, making it one of the most common neurological disorders. Women are affected significantly more often, and onset typically occurs between the ages of 15 and 49. Migraine may present in episodic or chronic forms.

Neuromodulation – a modern supportive approach in migraine

Neuromodulation is a non-pharmacological, scientifically validated option, particularly helpful for individuals who respond only partially or not at all to conventional treatments. Studies demonstrate a 20–60% reduction in attack frequency, shorter duration and lower intensity of attacks, and reduced need for medication.

Neuromodulation can be used both preventively (prophylactically) and in the acute setting.

How neuromodulation works in migraine

– Stabilizes cortical excitability → reduced likelihood of CSD

– Modulates pain sensitivity → decreased trigemino-vascular hypersensitivity

– Normalizes brainstem activity → improved endogenous pain inhibition

– Promotes neuroplasticity → reduced chronification and lower attack frequency

Epilepsy is a neurological disorder characterized by recurrent, unprovoked epileptic seizures. These seizures arise from abnormal, excessive, or synchronous electrical activity in the brain. Seizure manifestations can vary widely and may affect motor, sensory, cognitive, or autonomic functions.

Epilepsy can significantly impair quality of life, daily functioning, and mental health, even independently of the seizures themselves.

What happens in the brain in epilepsy

• Imbalance between excitatory and inhibitory networks → increased neuronal excitability
• Cortical and subcortical hyperexcitability, often involving temporal or frontal brain regions
• Altered synaptic transmission, with glutamatergic overactivity and reduced GABAergic inhibitory mechanisms
• Disrupted functional connectivity between seizure-generating regions and surrounding networks
• Neuroinflammation and gliosis, promoting chronic excitability and seizure susceptibility
• Network dysfunctions that also lead to cognitive, emotional, and behavioral changes between seizures (interictal phase)

These mechanisms underlie seizure generation, propagation, and recurrence, as well as the associated interictal symptoms.

Prevalence

Epilepsy affects approximately 0.5–1% of the global population, corresponding to around 50 million people worldwide.

The disorder can occur at any age, with higher incidence in early childhood and in older adults.

Possible causes include genetic factors, structural brain abnormalities, infections, traumatic brain injury, as well as metabolic or autoimmune diseases.

Neuromodulation in epilepsy

Non-invasive brain stimulation (NIBS) has been shown in studies to reduce seizure frequency by approximately 10–30% in selected patients. In addition, improvements in interictal symptoms such as:

• cognitive performance
  • mood
  • mental resilience

have been reported.

Effectiveness varies individually and depends, among other factors, on seizure type, target brain region, and stimulation protocol. Neuromodulation may be particularly beneficial when pharmacological treatments are insufficient or limited by side effects.

How neuromodulation works in epilepsy

• Reduction of cortical hyperexcitability through stabilization of neuronal networks
• Enhancement of inhibitory mechanisms (e.g., GABAergic activity)
• Normalization of functional connectivity between epileptogenic and non-epileptogenic regions
• Modulation of neuroinflammatory processes influencing seizure susceptibility
• Improvement of interictal cognitive and emotional symptoms, independent of seizure control

Motor neuron disease (MND) is a progressive neurodegenerative disorder affecting the upper and lower motor neurons responsible for voluntary muscle control. It leads to increasing muscle weakness, muscle atrophy, spasticity, as well as speech and swallowing difficulties. In advanced stages, respiratory insufficiency may occur.

In up to 50% of affected individuals, cognitive and behavioral changes are also observed, often overlapping with the frontotemporal dementia spectrum.

What happens in the brain in MND

– Degeneration of upper and lower motor neurons in the motor cortex, brainstem, and spinal cord

– Cortical hyperexcitability and impaired inhibitory control in early stages of the disease

– Glutamate-mediated excitotoxicity and calcium overload leading to neuronal damage

– Oxidative stress and mitochondrial dysfunction, impairing cellular energy metabolism

– Protein aggregation and neuroinflammation as drivers of progressive degeneration

– Disrupted connectivity between cortical and spinal networks, affecting motor control and coordination

Prevalence

MND affects approximately 2–5 individuals per 100,000 population per year. Disease onset most commonly occurs between the ages of 40 and 70. Men are slightly more frequently affected.

Approximately 5–10% of cases are familial and associated with genetic mutations, including SOD1, C9orf72, TARDBP, and FUS.

Neuromodulation in MND

Evidence for non-invasive brain stimulation (NIBS) in MND is currently limited but encouraging. Pilot studies report 10–20% improvements in motor function, spasticity, fatigue, and a potential slowing of functional decline, particularly in early disease stages.

Neuromodulation is used as a complementary approach and does not replace disease-modifying therapy.

How neuromodulation works in MND

– Reduction of cortical hyperexcitability and attenuation of excitotoxic stress

– Support of remaining motor neurons and compensatory cortical regions

– Improvement of spasticity and fatigue with functional relief

– Positive effects on mood and cognitive aspects, supporting quality of life

Cerebral palsy (CP) is a non-progressive neurodevelopmental disorder resulting from injury to or abnormal development of the immature brain. It primarily affects motor control, muscle tone, and posture. Typical clinical features include spasticity, muscle weakness, dystonia, and coordination impairments.

Depending on the extent and location of brain involvement, additional cognitive, sensory, and communication impairments may also be present.

What happens in the brain in cerebral palsy

– Static lesions or malformations of the developing brain leading to permanent impairment of motor networks

– Disrupted signal transmission in the primary motor cortex and corticospinal pathways → spasticity and weakness

– Involvement of the basal ganglia and cerebellum → abnormalities of muscle tone and coordination

– Impaired thalamocortical circuits → altered sensory feedback and motor planning

– Altered neuroplasticity and interhemispheric imbalance, particularly in unilateral forms

Prevalence

Cerebral palsy is the most common motor disability in childhood, affecting approximately 2–3 per 1,000 live births worldwide. Causes include perinatal hypoxia, prematurity, infections, vascular events, and structural brain malformations.

Neuromodulation in cerebral palsy

Non-invasive brain stimulation (NIBS) has demonstrated 10–30% improvements in motor function, spasticity reduction, and coordination in clinical studies, particularly when combined with physiotherapy or motor training. The greatest effects are reported when neuromodulation is applied early during rehabilitation.

How neuromodulation works in cerebral palsy

– Increases corticospinal excitability and improves voluntary motor control

– Reduces spasticity and hypertonia through modulation of inhibitory networks

– Promotes motor learning and improved coordination when combined with therapy

– Positive effects on attention, mood, and adaptive behavior

Tinnitus refers to the perception of sounds such as ringing, buzzing, or hissing without an external sound source. For many individuals, tinnitus develops into a persistent and distressing condition that can significantly impair sleep, concentration, and emotional well-being.

Over time, the constant sound and the attention directed toward it increase stress, irritability, and mental exhaustion.

What happens in the brain in tinnitus

– Hyperactivity of the auditory system due to reduced auditory input and central amplification of spontaneous neuronal activity

– Altered functional connectivity between auditory areas and limbic structures (amygdala, hippocampus)

– Maladaptive neuroplasticity in the auditory cortex leading to persistence of the phantom perception

– Activation of the stress system with increased sympathetic arousal and cortisol release

– Enhanced involvement of attentional networks, further intensifying sound perception

Prevalence

Tinnitus affects approximately 10–15% of the global population. In around 1–2% of individuals, symptoms are severe and significantly impair quality of life.

Prevalence increases with age, but tinnitus is increasingly observed in younger individuals as well, particularly due to noise exposure, chronic stress, and ototoxic medications.

Neuromodulation in tinnitus

Neuromodulation represents a non-pharmacological treatment option, especially when conventional therapies provide only limited relief. Clinical studies report a reduction in tinnitus loudness in 30–60% of patients, along with decreased stress and anxiety and improved habituation to the sound.

How neuromodulation works in tinnitus

– Reduction of hyperactivity in auditory pathways

– Attenuation of excessive limbic responses associated with stress and emotional burden

– Restoration of a more balanced network state between auditory, emotional, and attentional systems

– Promotion of adaptive neuroplasticity to support habituation

– Improvement of stress regulation and subjective symptom perception

Die Onkologie befasst sich mit der Prävention, Diagnostik und Behandlung von Krebserkrankungen, die durch unkontrolliertes Zellwachstum sowie die Fähigkeit zur Invasion oder Metastasierung gekennzeichnet sind. Krebs kann nahezu jedes Organ betreffen und geht häufig mit systemischen Auswirkungen einher.
Neben der Primärerkrankung leiden viele Betroffene unter behandlungsbedingten neurologischen, kognitiven und emotionalen Beeinträchtigungen, die die Lebensqualität, Belastbarkeit und Alltagsfunktion erheblich einschränken können.

Was im Gehirn bei onkologischen Erkrankungen passiert

• Kognitive Dysfunktion („Chemo-Brain“)
– Neuroinflammation, oxidativer Stress und gestörte Konnektivität in präfrontalen, parietalen und hippocampalen Netzwerken

• Müdigkeit (Fatigue)
– veränderte Aktivität in cortico-striatalen Schaltkreisen und im Default-Mode-Netzwerk

• Emotionale Dysregulation und depressive Symptome
– Veränderungen limbisch-präfrontaler Regelkreise

• Neuropathische Schmerzen
– periphere Nervenschädigungen und zentrale Sensibilisierung

• Gestörte Netzwerkkommunikation
– verminderte neuronale Effizienz und reduzierte kognitive Belastbarkeit

Diese Mechanismen tragen wesentlich zur neurologischen und psychischen Symptomlast bei Krebserkrankungen und deren Therapie bei.

Häufigkeit

Krebs betrifft weltweit etwa 1 von 6 Menschen, mit steigender Inzidenz im höheren Lebensalter. Zu den häufigsten Krebsarten zählen Brust-, Lungen-, Darm- und Prostatakrebs. Dank moderner Therapien nimmt die Zahl der Langzeitüberlebenden zu, viele Betroffene kämpfen jedoch langfristig mit therapiebedingten Folgeerscheinungen wie kognitiven Einschränkungen, Fatigue und neuropathischen Schmerzen.

Neuromodulation bei onkologischen Erkrankungen

Nicht-invasive Hirnstimulation (NIBS) zeigt in Studien 20–40 % Verbesserungen bei krebs- und therapieassoziierten Symptomen, insbesondere in den Bereichen:

• kognitive Leistungsfähigkeit
• Müdigkeit
• depressive Symptome
• neuropathische Schmerzen

Die Effekte sind moderat, aber klinisch relevant und werden durch Krebsart, Krankheitsstadium, Stimulationsparameter und individuelle Neurobiologie beeinflusst. Besonders wirksam ist Neuromodulation in Kombination mit rehabilitativen, verhaltensbezogenen oder medikamentösen Maßnahmen.

So wirkt Neuromodulation bei onkologischen Erkrankungen

• Verbesserung kognitiver Funktionen durch Aktivierung dorsolateraler präfrontaler und parietaler Netzwerke
• Reduktion von Fatigue und Steigerung der Wachheit über cortico-striatale Modulation
• Linderung neuropathischer Schmerzen durch Normalisierung somatosensorischer und limbischer Schaltkreise
• Unterstützung der Emotions- und Stressregulation durch Stabilisierung präfrontal-limbischer Konnektivität
• Gute Verträglichkeit und Nicht-Invasivität, bei Bedarf mit wiederholten Sitzungen zur Stabilisierung der Effekte

Der Einsatz erfolgt unterstützend und gilt aktuell als off-label.

Oncology focuses on the prevention, diagnosis, and treatment of cancer, which is characterized by uncontrolled cell growth and the ability to invade surrounding tissue or metastasize. Cancer can affect almost any organ and is often associated with systemic effects.

In addition to the primary disease, many individuals experience treatment-related neurological, cognitive, and emotional impairments that can significantly limit quality of life, resilience, and everyday functioning.

What happens in the brain in oncological diseases

• Cognitive dysfunction (“chemo brain”)
  – Neuroinflammation, oxidative stress, and disrupted connectivity in prefrontal, parietal, and hippocampal networks
• Fatigue
  – Altered activity in cortico-striatal circuits and the default mode network
• Emotional dysregulation and depressive symptoms
  – Changes in limbic–prefrontal regulatory circuits
• Neuropathic pain
  – Peripheral nerve damage and central sensitization
• Disrupted network communication
  – Reduced neuronal efficiency and diminished cognitive resilience

These mechanisms contribute substantially to the neurological and psychological symptom burden associated with cancer and its treatment.

Prevalence

Cancer affects approximately 1 in 6 people worldwide, with incidence increasing markedly in older age.

Among the most common cancer types are breast, lung, colorectal, and prostate cancer.

Thanks to modern therapies, the number of long-term survivors is increasing; however, many individuals continue to struggle with long-term treatment-related sequelae such as cognitive impairment, fatigue, and neuropathic pain.

Neuromodulation in oncological diseases

Non-invasive brain stimulation (NIBS) has demonstrated 20–40% improvements in cancer- and treatment-associated symptoms in clinical studies, particularly in the areas of:

• cognitive performance
  • fatigue
  • depressive symptoms
  • neuropathic pain

The effects are moderate but clinically relevant and are influenced by cancer type, disease stage, stimulation parameters, and individual neurobiology. Neuromodulation is particularly effective when combined with rehabilitative, behavioral, or pharmacological interventions.

How neuromodulation works in oncological diseases

• Improvement of cognitive functions through activation of dorsolateral prefrontal and parietal networks
• Reduction of fatigue and enhancement of alertness via cortico-striatal modulation
• Relief of neuropathic pain through normalization of somatosensory and limbic circuits
• Support of emotional and stress regulation through stabilization of prefrontal–limbic connectivity
• Good tolerability and non-invasiveness, with repeated sessions when needed to stabilize effects

Use is supportive and is currently considered off-label.

Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease affecting both upper and lower motor neurons. It leads to increasing muscle weakness, paralysis, and ultimately respiratory failure. In a subset of affected individuals, additional cognitive and behavioral changes occur, often overlapping with frontotemporal dysfunction. Disease progression is typically rapid and highly disabling.

What happens in the brain in ALS

– Degeneration of upper and lower motor neurons with loss of voluntary muscle control

– Cortical hyperexcitability contributing to excitotoxic neuronal damage

– Glutamate-mediated neurotoxicity and pronounced oxidative stress

– Neuroinflammation involving microglia and astrocytes

– Secondary network disturbances in brainstem and spinal circuits affecting motor function and reflexes

Prevalence

ALS affects approximately 2–5 individuals per 100,000 population per year. Disease onset most commonly occurs between the ages of 40 and 70, with a slightly higher prevalence in men. About 5–10% of cases are familial and associated with known genetic mutations, while the majority occur sporadically.

Neuromodulation in ALS

Evidence for non-invasive brain stimulation (NIBS) in ALS is limited but increasingly under scientific investigation. Studies report 10–20% improvements in motor function, spasticity, or a potential slowing of functional decline, particularly in early disease stages. Effects vary depending on stimulation protocol and disease course.

How neuromodulation works in ALS

– Reduction of cortical hyperexcitability in the motor cortex

– Support of remaining motor networks and delay of functional loss

– Possible improvement in mood, fatigue, and quality of life

– Short-term effects requiring repeated or continuous sessions

Myalgische Enzephalomyelitis / Chronisches Müdigkeitssyndrom (ME/CFS) ist eine komplexe, multisystemische Erkrankung, die durch anhaltende körperliche und geistige Erschöpfung gekennzeichnet ist. Typisch sind post-exertionelles Unwohlsein, kognitive Einschränkungen („Gehirnnebel“), nicht erholsamer Schlaf, autonome Dysregulation sowie Schmerzen. Die Symptome lassen sich nicht vollständig durch andere Erkrankungen erklären und schwanken häufig in ihrer Intensität. ME/CFS ist mit einer erheblichen Einschränkung der körperlichen und kognitiven Belastbarkeit sowie der Lebensqualität verbunden.

Was im Gehirn bei ME/CFS passiert

– Verminderte Aktivität im präfrontalen und anterioren cingulären Kortex → kognitive Verlangsamung und mentale Erschöpfung

– Veränderte funktionelle Konnektivität innerhalb des Default-Mode-, Salienz- und fronto-parietalen Netzwerks

– Autonomes Ungleichgewicht mit reduziertem Vagaltonus und erhöhter sympathischer Aktivität → orthostatische Intoleranz und Fatigue

– Hinweise auf Neuroinflammation und Mikrogliaaktivierung in bildgebenden Studien

– Reduzierter zerebraler Blutfluss und Glukosemetabolismus in Aufmerksamkeits- und Motorkontrollarealen

– Gestörte zentrale Energie- und Belastungsregulation

Häufigkeit

ME/CFS betrifft schätzungsweise 0,2–0,8 % der Weltbevölkerung. Frauen sind etwa dreimal häufiger betroffen als Männer. Der Krankheitsbeginn liegt meist zwischen dem 20. und 50. Lebensjahr. Häufig geht der Erkrankung eine Virusinfektion, ein Immunstress oder eine längere körperliche oder psychische Belastung voraus. Die Erkrankung ist mit einer hohen Rate an langfristiger Behinderung verbunden.

Neuromodulation bei ME/CFS

Aufkommende wissenschaftliche Hinweise zeigen, dass nicht-invasive Hirnstimulation (NIBS) bei ME/CFS Verbesserungen von etwa 10–30 % in den Bereichen Müdigkeit, kognitive Leistungsfähigkeit und Schmerzsymptomatik bewirken kann. Die Effekte scheinen ausgeprägter zu sein, wenn Neuromodulation mit abgestufter Aktivierung, Tempo-Management oder kognitiven Interventionen kombiniert wird. Die Evidenzlage ist derzeit noch heterogen.

So wirkt Neuromodulation bei ME/CFS

– Modulation präfrontaler und limbischer Netzwerke zur Verbesserung von Aufmerksamkeit, Arbeitsgedächtnis und Stimmung

– Unterstützung der autonomen Regulation mit Erhöhung des parasympathischen Tonus

– Reduktion sympathischer Überaktivität und Stressantworten

– Beeinflussung neuroinflammatorischer Prozesse und Förderung neuroplastischer Anpassungen

– Verbesserungen bei Fatigue, Konzentration, Schlafqualität und emotionaler Stabilität 

A spinal cord injury (SCI) results from trauma or disease that damages the spinal cord and disrupts signal transmission between the brain and the body. This leads to loss of motor, sensory, and autonomic functions below the level of injury.

Clinical manifestations range from muscle weakness and sensory deficits to complete paralysis, chronic pain, and disturbances of bladder, bowel, and cardiovascular regulation. SCI has profound effects on mobility, independence, and quality of life.

What happens in the brain and spinal cord in SCI

– Axonal damage and demyelination resulting in impaired neuronal signal transmission

– Secondary injury cascade involving inflammation, ischemia, excitotoxicity, and oxidative stress

– Maladaptive reorganization in the spinal cord and motor cortex due to loss of afferent and efferent signals

– Interruption of motor, sensory, and autonomic pathways (corticospinal, spinothalamic, autonomic)

– Autonomic dysregulation affecting blood pressure control, thermoregulation, and cardiovascular stability

Prevalence

Worldwide, approximately 250,000–500,000 people sustain a spinal cord injury each year. The most common causes include traffic accidents, falls, sports injuries, and violence.

Affected populations include primarily young adults—especially men—as well as older individuals with increased fall risk. In many cases, lifelong medical, rehabilitative, and psychosocial care is required.

Neuromodulation in spinal cord injury

Neuromodulation is emerging as an important complementary therapy in the management of SCI. Studies indicate that targeted non-invasive stimulation can enable improvements in motor activation, sensory function, spasticity, and autonomic stability in a relevant subset of patients.

Effectiveness depends on injury level, completeness of the lesion, and stimulation parameters.

How neuromodulation works in spinal cord injury

– Activation of preserved neuronal pathways above and below the lesion

– Improvement of corticospinal and spinal network communication

– Promotion of neuroplastic reorganization to support functional recovery

– Reduction of spasticity and neuropathic pain through modulation of spinal networks

– Support of autonomic regulation, including cardiovascular, bladder, and bowel function

– Cumulative effects with repeated sessions in combination with rehabilitation