Introduction

The somatic motor system controls voluntary movement, locomotion and posture. The motor system is the output organ for all conscious communications. The motor system is complex and it includes sophisticated control systems with many loops, most of which are integrated with one another. The motor system includes a large degree of redundancy, and it has a high degree of plasticity. Therefore, motor systems can be reorganized through expression of neural plasticity, and such reorganization can be activated by new or differing use (exercise), changing demands or injury. Expression of neural plasticity can also cause symptoms and signs of disease.

Disorders of the motor system may cause negative phenomena such as loss of voluntary movement and strength of fine motor control, muscle spasm, tremor, twitches and synkinesis, involuntary movements (chorea, athetosis) and deficits in coordination (ataxia), or positive phenomena such as increased reflexes and increased tone. Reorganization and change in function that are primarily aimed at compensating for deficits may cause symptoms and signs that are not directly related to the primary injury.

Understanding the function of motor systems is a challenge. It is an even greater challenge to understand the causes of various symptoms and signs of injury and diseases that affect the motor systems of the spinal cord and brain. We will therefore devote a part of this chapter to describing the basic organization and function of the motor system.

Introduction

Symptoms and signs of disease related to nerves can be a direct result of changes in the function of the axons themselves, or the symptoms and signs can result from subsequent changes in the function of more central structures through changes in procession of information or from expression of neural plasticity. Disorders of nerves (neuropathy) can therefore present many different, often complex, symptoms. Neuropathy of sensory nerves can give pain, cause paresthesia and other abnormal sensations and functions and cause expression of neural plasticity with subsequent re-organization of CNS structures. Neuropathy of motor nerves can give paresis, paralysis and abnormal muscle activity. Pathologies of motor nerves, the neuromuscular junctions (muscle endplates) or muscles themselves mostly result in reduced, or loss of, function (paresis or paralysis). Disorders of muscles and motor nerves can also cause re-organization of neural circuits in the CNS including the motor cortex through expression of neural plasticity. Interruption of mixed nerves can affect motor function indirectly when proprioceptive nerve fibers are affected because of change of proprioceptive input to the spinal cord or to cranial nerve motor circuits. (Disorders of cranial nerves are discussed in Chapter 6.)

Nerve disorders can initiate changes in the function of CNS structures through expression of neural plasticity; these changes develop gradually and may persist even after healing of the nerve injuries. The CNS changes may be permanent or reversible, with or without intervention.

Introduction

This chapter concerns disorders of cranial nerves and the vestibular system. Disorders of cranial nerves include paresis and paralysis of motor nerves such as facial palsy, and hyperactivity of motor nerves such as hemifacial spasm (HFS). Trigeminal and glossopharyngeal neuralgia (TGN and GPN) are hyperactivity of sensory systems that results in pain (neuralgia). Disorders of cranial nerves such as HFS, TGN and GPN are known as “vascular compression disorders” because they can be effectively cured by moving a blood vessel off the respective cranial nerve root (microvascular decompression (MVD) [109, 111]. The pathophysiology of HFS is discussed in detail in this chapter because it serves as a model of other hyperkinetic disorders. The pathophysiologies of other disorders that can be cured by MVD are also discussed. Other disorders of nerves such as those that are caused by inflammation and injuries of nerves are discussed in Chapter 2.

The vestibular system provides proprioceptive input to the motor system via the vestibulospinal tract, and this input aids in voluntary body movements as well as in automatic functions like keeping posture, as was discussed in Chapter 5. In this chapter, we will discuss disorders that are associated with the vestibular system such as benign paroxysmal vertigo (BPPV). A disorder of the vestibular system that is associated with vascular compression of the vestibular nerve (DPV) will also be discussed in this chapter. Ménière's disease affects both the vestibular and the auditory system.

This and the following chapter deal with concepts that are not NEURON-specific but instead pertain equally well to any tools used for neural modeling.

Why model?

In order to achieve the ultimate goal of understanding how nervous systems work, it will be necessary to know many different kinds of information:

• The anatomy of individual neurons and classes of cells, pathways, nuclei, and higher levels of organization.

• The pharmacology of ion channels, transmitters, modulators, and receptors.

• The biochemistry and molecular biology of enzymes, growth factors, and genes that participate in brain development and maintenance, perception and behavior, learning and forgetting, health and disease.

But while this knowledge will be necessary for an understanding of brain function, it isn't sufficient. This is because the moment-to-moment processing of information in the brain is carried out by the spread and interaction of electrical and chemical signals that are distributed in space and time. These signals are generated and regulated by mechanisms that are kinetically complex, highly nonlinear, and arranged in intricate anatomical structures.

Much of the flexibility of NEURON is due to its use of a built-in interpreter, called hoc (pronounced “hoak”), for defining the anatomical and biophysical properties of models of neurons and neuronal networks, controlling simulations, and creating a graphical user interface. In this chapter we present a survey of hoc and how it is used in NEURON. Readers who seek the most up-to-date list of hoc keywords and documentation of syntax are referred to the online Programmer's Reference (see link at http://www.neuron.yale.edu/neuron/docs/docs.html). This can also be downloaded as a pkzip archive for convenient offline viewing with any WWW browser. The standard distribution for MSWindows includes a copy of the Programmer's Reference which is current as of the date of the NEURON executable that it accompanies (see the “Documentation” item in the NEURON program group).

NEURON's hoc is based on the floating point calculator by the same name that was developed by Kernighan and Pike (1984).