Errors in neuron-microglial interaction are known to lead to microglial phagocytosis of live neurons and excessive neuronal loss, potentially yielding poorer clinical outcomes. Factors that affect neuron-microglial interaction have the potential to influence the error rate. Clinical comorbidities that unfavorably impact neuron-microglial interaction may promote a higher rate of neuronal loss, to the detriment of patient outcome. This paper proposes that many common, clinically modifiable comorbidities have a common thread, in that they all influence neuron-microglial interactions. Comorbidities like traumatic brain injury, infection, stress, neuroinflammation, loss of neuronal metabolic integrity, poor growth factor status, and other factors, all have the potential to alter communication between neurons and microglia. When this occurs, microglial phagocytosis of live neurons can increase. In addition, microglia can shift into a morphological form in which they express major histocompatibility complex II (MHC-II), allowing them to function as antigen presenting cells that present neuronal debris as antigen to invading T cells. This can increase risk for the development of CNS autoimmunity, or can exacerbate existing CNS autoimmunity. The detrimental influence of these comorbidities has the potential to contribute to the mosaic of factors that determine patient outcome in some CNS pathologies that have neuropsychiatric involvement, including TBI and CNS disorders with autoimmune components, where excessive neuronal loss can yield poorer clinical outcomes. Recognition of the impact of these comorbidities may contribute to an understanding of the common clinical observation that many seemingly disparate factors contribute to the overall picture of case management and clinical outcome in these complex disorders. In a clinical setting, knowing how these comorbidities can influence neuron-microglial interaction can help focus surveillance and care on a broader group of potential therapeutic targets. Accordingly, an interest in the mechanisms underlying the influence of these factors on neuron-microglial interactions is appropriate. Neuron-microglial interaction is reviewed, and the various mechanisms by which these potential comorbidities influence neuro-microglial interaction are described.

Manual assessment of muscular function, in particular a method known as applied kinesiology (AK), is a clinical measure of neurologic function. A review of the literature reveals methodological problems with previous studies of AK as a form of neurologic assessment. Research designs that do not reflect clinical practice and principles of AK are common in the literature. Additional study is warranted to explore the potential of AK manual muscle testing as a diagnostic tool. We outline principles of AK and recommend that future research reflect more accurately the clinical practice of functional neurologic assessment and applied kinesiology.

Functional Neurologic Assessment and treatment methods common to the practice of applied kinesiology are presented. These methods are proposed to enhance neurological examination and treatment procedures toward more effective assessment and care of functional impairment. A neurologic model for these procedures is proposed. Manual assessment of muscular function is used to identify changes associated with facilitation and inhibition, in response to the introduction of sensory receptor-based stimuli. Muscle testing responses to sensory stimulation of known value are compared with usually predictable patterns based on known neuroanatomy and neurophysiology, guiding the clinician to an understanding of the functional status of the patient's nervous system. These assessment procedures are used in addition to other standard diagnostic measures to augment rather than replace the existing diagnostic armamentarium. The proper understanding of the neurophysiologic basis of muscle testing procedures will assist in the design of further investigations into applied kinesiology. Accordingly, the neurophysiologic basis and proposed mechanisms of these methods are reviewed.