The Neuroscience on the Web Series: CMSD 642 Neuropathologies of Swallowing and Speech CSU, Chico, Patrick McCaffrey, Ph.D

Chapter 11. Dysarthria: Definition and Description; Etiology

According to Darley, Aronson and Brown (1975), dysarthria is a speech disorder resulting from a weakness, paralysis, or incoordination of the speech musculature that is of neurological etiology. There are several different types of dysarthria. All result from damage to the central or peripheral nervous system that impairs the transmission of neural messages to the muscles involved in speech. In contrast to apraxia which affects the brain's capacity to produce the "programs" necessary for coordinated motor movements, dysarthria results from an inability to send the proper messages to the musculature. While apraxia affects articulation and, to some extent, prosody, dysarthria can impair all processes involved in speech production including respiration, phonation, articulation, resonance and prosody. Based on etiology, Darley, Aronson and Brown (1969), identified six different types of dysarthria. These include four forms of the disorder which are caused by damage to upper motor neurons. They are spastic, hyperkinetic, hypokinetic, and ataxic dysarthria. Spastic dysarthria results from lesions to the pyramidal tract, while both hypokinetic (substantia nigra) and hyperkinetic (basal ganglia) dysarthria occur when the extrapyramidal tract is damaged. Cerebellar lesions cause ataxic dysarthria. Flaccid dysarthria results from damage to lower motor neurons (cranial nerves). Mixed dysarthria, the sixth type described by Darley, et al., occurs when both upper and lower motor neurons are involved. Etiology Upper Motor Neurons vs. Lower Motor Neurons Upper motor and lower motor neurons are part of the somatic (alpha and gamma) motor system. The other major motor system controls smooth muscles (e.g arteries) and glands. A review of the difference between upper and lower motor neurons may make it easier to understand the causes of the various types of dysarthria. Upper motor neurons carry information from brain centers that control the muscles of the body. The pyramidal tract, which is a most important upper motor neuron tract transmits messages directing voluntary motor movements. It is primarily facilitatory (Duffy, 1995). The extrapyramidal tract consists of neurons that regulate involuntary/automatic movements. The neurons found in the cerebellum play an important role in the coordination and smoothness of movements required for speech. Although they carry messages intended for the muscles of the body, upper motor neurons cannot exit the central nervous system. For this reason, they synapse with lower motor neurons which are able to pass outside the central nervous system (cns) and carry information directly to the muscles. In order to reach the muscles of the body, motor commands generated in the cns must travel along the axons of upper motor and lower motor neurons. The pyramidal tracts are a type of first order neuron. They are unable to leave the central nervous system. The pyramidal tract is the most direct of the upper motor neuron tracts; the extrapyramidal tract also consists of upper motor neurons. As upper motor neurons must remain inside the neuraxis, they synapse with neurons of another type called lower motor neurons which can carry messages to the muscles of the rest of the body. Lower motor neurons, a type of second order neuron, are cranial and spinal nerves. The cell bodies of these neurons are located in the neuraxis, but their axons can leave the central nervous system and synapse with the muscles of the body. All lower motor neurons are either spinal or cranial nerves. All spinal nerves are lower motor neurons. Because they are mixed nerves all have a motor aspect. However, not all cranial nerves have a motor component. Some of the cranial nerves contain only sensory fibers and therefore cannot be classified as lower motor neurons. For example, CN I, the olfactory nerve, CN II the optic nerve, and CN VIII, the auditory nerve, do not have motor components. Lower motor neurons are sometimes called the final common pathway for neural messages traveling to the muscles of the body because these nerves are the only route by which information from any of the upper motor tracts can use to reach the periphery. Thus, when lower motor neurons are damaged, the parts of the body that they innervate are deprived of input from the pyramidal and extrapyramidal tract including cerebellar pathways. Thus, voluntary, automatic and reflexive movements are all affected. Upper motor neuron dysarthria can be due to dyskinesa, hypertonia or hyperreflexia (spastic). Lower motor neuron dysarthria can be due to atrophy, hypotonia or hyporeflexia (flaccid).   The Pyramidal Tract This group of upper motor neuron fibers carries messages for voluntary motor movement to the lower motor neurons in the brain stem and spinal cord. Approximately 80% of the cell bodies of the pyramidal tract are located on the precentral gyrus of the frontal lobe which is also known as the motor strip. Particularly large cells located here whose axons are part of the pyramidal tract are called pyramidal cells. Approximately 20% of the pyramidal tract fibers also originate in the postcentral gyrus of the parietal lobe, in Brodmann's areas 1, 2, and 3. Regardless of the location of their cell bodies, pyramidal tract fibers descend from the cortex in a fan-shaped distribution which converges inside the internal capsule (FitzGerald, 1996). This tract is direct and monosynaptic, meaning that the axons of its neurons do not syapse with other cells until they reach their final destination in the brain stem or spinal cord. These direct connections between the cortex and the lower motor neurons allow messages to be transmitted very rapidly from the central nervous system to the periphery. The fibers of the pyramidal tract that synapse with spinal nerves sending information about voluntary movement to the skeletal muscles form the corticospinal tract. These axons are among the longest in the central nervous system, as some of them travel all the way from the cortex to the inferior part of the spinal cord. As they descend through the brain, they form part of the posterior limb of the internal capsule. At the pyramids in the inferior part of the medulla, eighty-five to ninety percent of corticospinal fibers decussate, or cross to the other side of the brain. The remaining ten to fifteen percent continue to descend ipsilaterally. The fibers that deccussate are called the lateral corticospinal tract or the lateral pyramidal tract because they descend along the sides of the spinal cord. The uncrossed or direct fibers that synapse with spinal nerves on the ipsilateral side of the body are called the direct pyramidal tract. They may also be referred to as the ventral pyramidal tract or the corticospinal tract since they travel down the ventral aspect of the spinal cord. The spinal nerves receive only contralateral innervation from the corticospinal tract. This means that unilateral pyramidal tract lesions above the point of decussation in the pyramids will cause paralysis of the muscles served by the spinal nerves on the opposite side of the body. For example, a lesion on the left pyramidal tract could cause paralysis on the right side of the body. The fibers of the pyramidal tract that synapse with cranial nerves located in the brain stem form the corticobulbar tract. Obviously, this is the part of the pyramidal tract that carries the motor messages that are most important for speech and swallowing. Corticobulbar axons descend from the cortex within the genu or bend of the internal capsule. Almost all of the cranial nerves receive bilateral innervation from the fibers of the pyramidal tract. This means that both the left and right members of a pair of cranial nerves are innervated by the motor strip areas of both the left and right hemispheres. This redundancy is a safety mechanism. If there is a unilateral lesion on the pyramidal tract, both sides of body areas connected to cranial nerves will continue to receive motor messages from the cortex. The message for movement may not be quite as strong as it was previously but paralysis will not occur. The two exceptions to this pattern are the portion of CN XII that provides innervation for tongue protrusion and the part of CN VII that innervates the muscles of the lower face. These only receive contralateral innervation from the pyramidal tract. This means that they get information only from fibers on the opposite side of the brain. Therefore, a unilateral upper motor neuron lesion could cause a unilateral facial droop or problems with tongue protrusion on the opposite side of the body. For example, a lesion on the left pyramidal tract fibers may cause the right side of the lower face to droop and lead to difficulty in protruding the right side of the tongue. The other cranial nerves involved in speech and swallowing would continue to function almost normally as both members of each pair of nuclei still receives messages from the motor strip. Because most cranial nerves receive bilateral innervation, lesions of the upper motor neurons of the pyramidal tract must be bilateral in order to cause a serious speech problem. (The effects of the inability to protrude the tongue and of paralysis of the lower face on speech are negligible.) On the other hand, unilateral lesions of the lower motor neurons may cause paralysis. This occurs because the lower motor neurons are the final common pathway for neural messages traveling to the muscles of the body. At the level of the lower motor neurons, there is no alternative route which will allow messages from the brain to reach the periphery. Muscles on the same side of the body as the lesion will be affected. Injuries to the nuclei of the cranial nerve nuclei located in the brain stem are called bulbar lesions. The paralysis that they produce is called bulbar palsy. It is usually bi-lateral. Lesions to the axons of the cranial nerves are called peripheral lesions. As cranial nerves are lower motor neurons, both bulbar and peripheral lesions are lesions of the final common pathway (FCP), although some sourses consider the FCP to be axonal only. When bilateral lesions of the upper motor neurons of the pyramidal tract occur, they produce a paralysis similar to that which occurs in bulbar palsy. For this reason, the condition is known as pseudo-bulbar palsy. If a lesion occurs in the brain stem and damages both the nucleus of a cranial nerve and one side of the upper motor neurons of the pyramidal tract, a condition known as alternating hemiplegia may result. This involves paralysis of different structures on each side of the body. The lesioning of the nucleus of the cranial nerve will cause a paralysis of the structures served by that nerve on the same side of the body as the injury. Because the pyramidal tract provides only contralateral innervation to the spinal nerves, damage to the upper motor neurons will meanwhile cause a paralysis of different structures on the other side of the body. For example, a lesion that affected the right nucleus of the trigeminal cranial nerve and the right side of the pyramidal tract would cause paralysis of the right side of the jaw and of part of the left side of the body. Both the corticospinal and corticobulbar tracts send some axons to the pontine nuclei in the pons as they descend to synapse with lower motor neurons. These fibers that end in the pons form the corticopontine tract. This pathway carries information about the type and strength of the motor impulses generated in the cortex to the cerebellum. The copy sent to the cerebellum actually leaves the cortex before the command is sent to the muxcles. While the corticopontine fibers actually end in the pontine nuclei, second order neurons carry their message to the cerebellum via the middle cerebellar peduncle. I consider this tract to be part of the extrapyramidal system rather than a component of the pyramidal tract since it does not synapse directly with lower motor neurons.

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Other courses in the Neuroscience on the Web series: CMSD 620 Neuroanatomy | CMSD 636 Neuropathologies of Language and Cognition Copyright, 1998-2013. Patrick McCaffrey, Ph .D.