Fundamental evidence

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18 Fundamental evidence

What is functional neurology?

Functional neurology comprises the evolving body of knowledge and clinical approach concerned with the recognition, analysis, and conservative care of aberrant neurological function in the human neuraxis. The clinical application of functional neurology focuses on modulating the central integrative state of the projection systems utilised by the cortex to modulate activity throughout the neuraxis. The central integrative state of these projection systems are dependent on the processes of neural plasticity, processes which are fundamental to nervous system learning and functional change. The functional neurology approach to the management of aberrant neurological function recognises and uses the natural phenomenon of neural plasticity to evoke change in targeted functional areas of the neuraxis. This is done in order to encourage normalisation of nervous system function as far as possible. The methods utilised to evoke the neural plasticity in functional neurology tend to be conservative, non-surgical and non-pharmaceutical therapeutic interventions. Often, the functional neurologist will work in collaboration with other practitioners who do utilise pharmaceutical and surgical approaches if this is in the best interest of the patient.


Basis for neural plasticity

Neuroplasticity refers to the processes involved in the nervous system as it adjusts its functional capacities to novel contexts (Nowak et al. 2009). The processes of neuroplasticity can be expressed at two interacting levels of nervous system function such as at the level of motor or sensory representations of body parts in the cortex which corresponds to representational or map plasticity; or at the neuronal level which can involve synaptic plasticity or changes in neuron activation levels or morphology (Boroojerdi et al. 2001). In the somatosensory cortex, some forms of plasticity can occur very rapidly, within minutes to hours (Ziemann et al. 2001). For instance, cortical neurons deafferented by peripheral nerve lesion or amputation rapidly become responsive to sensory input from adjacent functioning sites (Merzenich et al. 1983; Kolarik et al. 1994; Borsook et al. 1998). In the motor cortex, neurons can also rapidly reorganise their representative maps in response to nerve lesions or ischaemic nerve block (Ziemann et al. 1998) or during motor practice (Sadato et al. 1996; Pascual-Leone et al. 1993; Butefisch et al. 2000). It is now well documented that changes in somatocortical activation can be directly linked to both direct and indirect somatosensory input from peripheral receptors including joint receptors and muscle spindle afferent projections (Ridding et al. 2001; Kaelin-Lang et al. 2002; Tinazzi et al. 2005). Several mechanisms have been suggested to explain these plastic changes in the cortex.

Functional changes

These include changes in synaptic efficacy (Hebbian plasticity) or by reducing or modifying protein synthesis and proteinase activity in nerve cells via receptor activation of immediate early genes. These processes are controlled by the central integrative state of the neuron and are thus strongly influenced by the stimulation status of the neuron.

Synaptic efficacy and unmasking of latent horizontal connections

Synaptic connections are maintained by neurons when they are active and produce activity (action potentials) in the primary neurons. These connections modulate the neurons’ output through temporal and special summation characteristics at any given moment (Hebb 1949). Mechanisms responsible for this type of plasticity include long-term potentiation (LTP) and long-term depression (LTD) (Hess & Donoghue 1996). An intriguing example of this process has been proposed as a reason for our need to sleep and dream. The Hebbian principal of synaptic maintenance due to activation also suggests that synapses or connections between inactive neurons are being constantly degraded due to spontaneous down-regulation of molecules and substrates necessary for maintenance of synaptic function. In circuits where activity levels are high these processes are refreshed by the constant activation and expression of the genes that code for the necessary substrates. Circuits that are infrequently utilised refresh their synaptic strength during sleep and dreaming (Samvat & Osiecki 2009). During sleep, the maintenance of synaptic fitness in long-term memory circuits and circuits not frequently utilised while we are awake is stimulated by spontaneous slow (delta) wave oscillations and via fast wave stimulus during the REM component of sleep (Kavanau 2002). The activation of new and old memory circuits during REM sleep may result in what we perceive as dreams (Massimini et al. 2007).

It seems that many synaptic connections that are maintained in the system have a moderate to low efficacy for individually inducing a large enough change in a neuron’s membrane potential to result in the generation of an action potential. Some of these pre-existing but semi-dormant projection fibres have been referred to as horizontal fibres. Should the firing characteristics of other more primary firing inputs to the neuron change, say through functional dysfunction, trauma or stroke, the effect of these synapses on the system become ‘unmasked’ and may change their effects on the system drastically (Durian-Smith & Gilbert 1994). The effects may be either beneficial or harmful to the individual depending on a complex set of circumstances including the functional area of the brain involved and the increase or decrease in inhibitory influences on the system. For example, in the case of a stroke, survivors typically experience an acute increase in perilesional excitability due, for the most part, to increases in excitatory neurotransmitters, followed by chronic changes that include changes in intracortical and interhemispheric inhibitory imbalances that manifest in a variety of physical symptoms that could facilitate or hinder recovery, depending on the functional systems involved (Kreisel 2006).

Immediate early gene activation of protein synthesis

It is now commonly accepted that the brain controls mental, physiological, and behavioural processes and that brain function is controlled by gene activation. It is also accepted that social, developmental, and environmental factors can alter gene expression and that alteration in this gene expression induces change in brain function (Kandel 1998). This process is accomplished by special transmission proteins called immediate early genes (IEG) which are activated by a variety of second-messenger systems in the neuron in response to membrane stimulus (Chen & Tonegawa 1997; Kaczmarek & Chaudhuri 1997). Two types of IEG responses have been recognised and include type 1 IEG responses which are specific for the genes in the nucleus of the neuron and type 2 IEG responses which are specific for mitochondrial genes (Pleasure 1992). These genes are activated by a complex interaction involving receptor stimulation and the biochemical status of the neuron.

Redirection, reorganisation or rerouting of nerve transmission

This type of plasticity includes creation of new anatomical connections (sprouting of axons and dendrites) or elimination of existing connections or by altering synapses morphologically (Sanes & Donoghue 1997). A typical example of this type of plastic change is recovery after ischemic strokes. Mechanisms of plasticity result in reorganisation of the nervous system in such a way as to allow other parts of the CNS to take over some of the functions that were impaired from the ablative loss of neural tissue. For example, injury to cortical areas elicits a sequence of self-repair mechanisms, including redirection of tasks to other cortical areas. This reorganisation may include functional circuits far removed from the original site of injury. This injury-induced reorganisation may include enlargement of the cortical areas representative of the new circuits involved, and it may provide the neural substrate for adaptation and recovery of motor behaviour after injury (Frost et al. 2003). This type of reorganisation seems to occur spontaneously in response to injury, and training can facilitate the shift of processing from damaged parts of the CNS to more functionally intact areas. Focused rehabilitation that facilitates expression of neural plasticity is presently the most effective form of reorganisation stimulus but additional methods are under investigation and include stimulation of the cerebral cortex utilising both direct current in the form of transcranial direct current stimulation (tDCS) (Plautz et al. 2003; Schlaug & Renga 2008) and magnetic currents in the form of transcranial direct magnetic stimulation (TMS) (Khedr et al. 2005; Kim et al. 2006).

Afferent modulation of cortical function

The development and maintenance of functional projection systems of the neuraxis is dependent on the central integrative state of the neurons supporting the projection fibres of the system. This is dependent to a large degree on the afferent input and efferent output transmitted by the system. Changes in cortical activation can result from changes or attenuation of afferent information arriving in the cortex from peripheral or subcortical structures. The changes resulting from attenuation of the afferent input that are manifested both morphologically and functionally in the cortex seem to also occur at all levels within the projection system involved (Merzenich et al. 1984). For instance changes in cortical somatotopic maps in cats also show acute and chronic changes at the level of the spinal cord, dorsal columns and the thalamus following nerve transsection (Dostrovsky et al. 1976; Millar et al. 1976). Similar findings have also been found in monkeys (Merzenich et al.1981, 1983, 1984).

There is extensive evidence that alterations in motor activities which involve both afferent and efferent projection systems can induce structural and functional plasticity within the cortex, basal ganglia, cerebellum, and spinal cord in humans (Classen et al. 1998; Kelly et al. 2003; De Zeeuw & Yeo 2005; Graybiel 2005). Novel movement performance induces changes in cortical synaptic number, strength, and topography of cortical maps in the projection systems and neural assemblies involved in the performance of the movements (Montfils et al. 2005). Peripheral sensory stimulation has also been shown to induce long-lasting modulation of cortical activation and cortical motor output (Ridding et al. 2001). Cortical representation of cranial nerves has also been shown to modulate with alterations in afferent input. Hamdy et al. (1998) reported an increase in excitation levels in the pharynx cortical representation maps following short-term (10 min) stimulation of the pharynx. These changes lasted 30 minutes following the cessation of the initial stimulus. In a similar study, Ridding et al. (2000) showed that repetitive mixed nerve stimulation of the ulnar nerve increased the excitability of the cortical projections to the hand muscles of the same hand lasting at least 15 minutes longer than the stimulus. The rapid development of these plastic changes suggests that the mechanism involves unmasking or disinhibition of pre-existing weak (horizontal) projections (Boroojerdi et al. 2001).

Spinal and extremity manipulations have been postulated to exert their effects through a wide variety of anatomical, mechanical, and physiological parameters which result in modulation of mechano-receptive afferentation including somatosensory receptors, proprioception, and pain modulators. We will now look at some of the evidence that supports the effects of joint manipulation on various aspects of the neuraxis, starting with the local effects, then expanding to include segmental and suprasegmental modulatory actions that may help to explain the more wide-ranging effects we can detect following manipulation.

Korr (1975) proposed that effects of spinal manipulation on receptors in the paraspinal tissues were mediated by group I and II proprioceptive afferents. He proposed that spinal manipulation increases joint mobility by producing a barrage of impulses in muscle spindle afferents and smaller-diameter afferents, ultimately silencing facilitated gamma motor neurons. Group III and IV afferents have also been implicated as contributing to the effects of manipulation on the paraspinal structures. Studies on the spines of rats, rabbits, and cats have helped us understand the mechanical and chemical stimuli that can excite the receptive endings of sensory paraspinal neurons. The majority of afferents, including those with receptive fields in or near the facet joint capsule, responded in a graded fashion to the direction of a non-noxious load applied to the joint (Pickar & McLain 1995). Several studies have also demonstrated the effects of the manipulation on structures in the intervertebral foramina. Substantial evidence demonstrates that the dorsal roots (DRs) and dorsal root ganglia (DRG) are more susceptible to the effects of mechanical compression than are the axons of peripheral nerves (Rydevik 1992). Compressive loads as low as 10 mg applied rapidly to the DRs slightly increases the discharge of group I, II, III, and IV afferents (Howe et al. 1977). Clearly, the idea that a herniated disc could directly compress the DRs or DRG is a realistic and plausible scenario. A second scenario outlining the mechanism of involvement of a herniated intervertebral disc affecting nerve root function suggests that its effects are mediated indirectly by the release of neuroactive and immune-stimulating chemicals (McCarron et al. 1987). This mechanism would help explain the common observation that, even in the absence of compression, herniated discs are accompanied by neurological and immunological (inflammatory) findings.

Central facilitation (also called central sensitisation) refers to the increased excitability or enhanced responsiveness of dorsal horn neurons to an afferent input. Central facilitation can be manifested by increased spontaneous central neural activity, by enhanced discharge of central neurons to an afferent input, or by a change in the receptive field properties of central neurons (Cook et al. 1987

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