Upper And Lower Motor Neurons Descriptive Essay

Dysarthria is a motor speech disorder resulting in impaired articulation and speech intelligibility. It interferes with verbal communication when receptive language and other means of communication may be fully intact and can diminish social interaction and quality of life. In NMDs, dysarthria can result from dysfunction of upper motor neurons, lower motor neurons, both upper and lower motor neurons, the neuromuscular junction, and muscle itself. The rehabilitation team focuses on maximizing independent communication with attention to the type of dysarthria present, the rate of progression, and patient and family goals.

Dysarthria in Motor Neuron Diseases

Motor neuron diseases often feature dysarthria of the upper and/or lower motor neuron varieties.60Dysarthria in ALS, for example, is of the mixed type, typically with prominent lower motor neuron features. Early signs of this pattern of dysarthria include slow speech rate, altered voice quality, difficulty singing, difficulty enunciating, and diminished intelligibility, resulting in decreased communication effectiveness. Speech may also sound hoarse and hypophonic, related to vocal cord and respiratory muscle weakness.

The cornerstone of rehabilitation management in progressive dysarthria is the utilization of verbal and nonverbal strategies to optimize communication throughout the course of disease progression. Speech-language pathology, neurology, physiatry, and, occasionally, otolaryngology assessments can yield comprehensive rehabilitation management strategies with these goals in mind. Of note, aggressive speech therapy per se typically does not have lasting long-term benefits in motor neuron diseases and may worsen speech impairment by causing fatigue.

In mild dysarthria, the rehabilitation team focuses on training patients and social contacts in compensatory techniques to prolong verbal communication. These can include slowing speech rate, using alternative words, spelling, repeating and overarticulating consonants, speaking face to face, using monosyllabic speech, and conserving energy by minimizing environmental noise and the distance between the patient and listeners. Importantly, developing personalized communication strategies between patient and listener can also prolong effective communication; these can include shared strategies for understanding gestures, facial expressions, and eye contact, as well as a system for confirming understanding.

Palatal lifts and palatal augmentation prostheses can be utilized to address hypernasality/hypophonia and consonant articulation, respectively, although little data exists regarding their efficacy. A retrospective review of the use of lifts and prostheses suggests that patients experience improved ease of speaking with their use.61

As dysarthria progresses, the rehabilitation team can provide augmentative and alternative communication systems. Higher-technology devices are not necessarily better for patients; device recommendations must consider patient and caregiver physical capability, education level, cognitive functional status, socioeconomic means, and general preferences. Optimally, training begins before acute need for the technology. Equipment can often be rented or acquired from charitable organizations. See Table 8-6 for a listing of augmentative communication devices.

Asynchronous communication, including the use of e-mail, message boards, and online social networks, can promote maintenance of social contacts without hindrance by slowness of speech/impaired direct in-person communication, and should also be encouraged as appropriate.

Finally, brain-computer interfaces (BCIs) are an active area of current study with much promise for use in severe dysarthria/anarthria that prevents verbal communication and co-occurs with severe motor impairment preventing other means of communication. BCIs output information from the brain directly to a computer. The use of both noninvasive (scalp recordings of electroencephalographic changes) and invasive (direct recordings from the motor cortex) devices are being investigated in ALS and other conditions resulting in severe dysarthria/anarthria.62,63

Assessment and training by occupational and adaptive technology specialists can provide technology users with individually designed accessible communication systems, mounting systems, and switches. Importantly, any technologies selected should be flexible to accommodate changes in user capabilities over time.

Dysarthria in Neuromuscular Junction Disorders

Neuromuscular junction disorders, including myasthenia gravis and the Lambert-Eaton myasthenic syndrome (LEMS), can also produce dysarthria, typically with lower motor neuron–type features and a nasal tone. In myasthenia gravis, impairment severity can fluctuate over the course of the day and with medications that alter neuromuscular junction transmission. Bulbar symptoms are presenting symptoms in 15% of individuals with myasthenia gravis and approximately 5% of individuals with LEMS. The latter statistic may be higher in practice, because the recognition of bulbar symptoms as part of LEMS is only beginning to emerge.64,65

Treatment of the underlying disorders produces resolution or improvement of dysarthria. A study of intravenous immunoglobulin in the treatment of LEMS specifically addressed bulbar function by measuring drinking times before and after therapy; there was improvement in this outcome measure after treatment.66

When dysarthria persists despite attempts at disease treatment, rehabilitation management can be employed to optimize speech quality and communication. The rehabilitation program includes patient and family education, speech therapy, and adaptive equipment as needed. Patients and families should be educated about symptoms and triggers, medication compliance, and energy conservation. Speech therapists can offer training in the control of speech rate, articulation, and interpersonal communication strategies. Augmentative communication devices and environmental modifications can also be employed. Finally, there may be a role for respiratory muscle and breathing training in enhancing intelligibility of speech in the setting of dysarthria in neuromuscular junction disorders. Such training has shown positive effects on respiratory muscle strength and endurance30; in turn, improved breath support may enhance speech volume and intelligibility.

Dysarthria in Myopathies/Muscular Dystrophies/Peripheral Neuropathies

Myopathic (congenital myopathies, mitochondrial myopathies), muscular dystrophic (myotonic dystrophy, oculopharyngeal muscular dystrophy), and peripheral neuropathic (including the hereditary peroneal muscular atrophy syndromes) conditions can also feature lower motor neuron–type or flaccid dysarthria. The general management approach to these conditions is similar to that outlined above: optimizing native verbal communication as long as feasible and facilitating continued communication via augmentative and alternative technologies, with early training.

In notable distinction to many other NMDs, however, in which activity can worsen speech production, the opposite is true in myotonic dystrophy. In myotonic dystrophy, both muscle weakness and myotonia contribute to impaired articulation, and speaking loudly may provoke myotonia. Warm-up exercises with prolonged sound production may improve repetition rate and fluency of speech and decrease the myotonic component of dysarthria without producing fatigue.67 This suggests that more aggressive speech therapy with practice exercises may be of benefit in the treatment of dysarthria in myotonic dystrophy, whereas there is no evidence of beneficial effects of aggressive speech therapy in the dysarthria of most other NMDs.


The corticospinal tract is a descending tract of the spinal cord which contains bundles of axons which originate in the cerebral cortex and descend to synapse within the brainstem or spinal cord. The neurons are called "upper motor neurons". [1]



  • 60% of fibres originate from the primary motor area, the premotor area, and the supplementary motor area of the frontal lobe
  • Other fibres originate from the primary
    sensory area, the parietal cortex and the parietal operculum [1]

Course / Path

The descending corticospinal tract descends from the origin:

  • Through the corona radiata
  • Posterior half of lateral ventrical (lower limb represented by posterior fibres, face most anterior)
  • Posterior limb of internal capsule (lower limb represented by posterior fibres, face most anterior)
  • Enters midbrain through cerebral peduncle (face represented by medial fibres, foot lateral and hand in the middle
  • Enter medulla where they form medullary pyramids on either side of midline:
  1. Lateral fibres (lateral corticospinal tract) are contralateral fibres. These make up between 75-90% fibres. They descend in the posterior part of the lateral funiculus. This tract is detected through to the lumbosacral spine and fibres synapse either directly on anterior horn cells of the contralateral side to their origin (ipsilateral to their side of descent in the spinal cord), or on interneurones of layers within this same side.
  2. Anterior fibres (Anterior corticospinal tract) makes up between 10-25% of fibres. They descend ipsilaterally, however decussate near to their termination. Therefore these fibres continue to innteravate the contralateral side of the spinal cord. [2][1]

Of all corticospinal fibres approximately 20% terminate at thoracic levels, 25% at lumbosacral levels and 55% at cervical levels. Many of the fibres that originate from the motor cortex then terminate in the ventral horn of the spinal cord. [2]


Anterior Corticospinal Tract

  • responsible for the control of the proximal musculature.

Lateral Corticospinal Tract

  • responsible for the control of the distal musculature [3]
  • fine control of movements of the hand


Damage can occur to the upper motor neurones of the corticospinal tract resulting in the upper motor neurone syndrome. Damage to the upper motor neurones can result can lead to presentations of "paralysis (or paresis), hypertonia, hyperreflexia, clonus, up-going plantar reflexes (Babinski’s sign) and spasticity". [4]


Stinear et al (2007) suggested that Corticospinal Tract integrity could be used to identify the likely extent of motor recovery and may enable appropriate selection of rehabilitation strategies for individuals recovering from stroke [5]. In a further study conducted by Stinear et al (2012) they trialled the use of the PREP(predicting motor recovery) algorithm to assess the likelihood of upper limb recovery. By utilising the SAFE score (sum of the shoulder abduction and finger extension) 72 hours after stroke, Transcranial magnetic stimulation, motor
evoked potentials in affected upper limb or the Asymmetry Index (measured with diffusion-weighted MRI) they were able to predict whether there could be a complete- no recovery. It was suggested from these finding that clinicians using the PREP algorithm may be able to predict the likely extent of upper limb recovery and may be able to therefore manage of patient expectations from an earlier period.[6]

Recent Related Research (from Pubmed)





  1. MF, Connors BW, Paradiso. Neuroscience: Exploring the Brain Neuroscience: Exploring the Brain, Michael A. Paradiso. Edition 2, illustrated. Lippincott Williams & Wilkins, 2001
  2. 2.02.1Crossman AR, Neary D. Neuroanatomy: An Illustrated Colour Text. Third Edition. London: Elsevier, 2004
  3. ↑Masri OA. An Essay on the Human Corticospinal Tract: History, Development, Anatomy, and Connections. Neuroanatomy 2011; 10:1-4
  4. ↑Ivanhoe CB, Reistetter TA. Spasticity: the misunderstood part of the upper motor neuron syndrome.Am. J. Phys. Med. Rehabil. 2004; 83(10 Suppl): S3–9
  5. ↑Stinear CM, Barber PA, Smale PR, Coxon JP, Fleming MK, Byblow WD. Functional potential in chronic stroke patients depends on corticospinal tract integrity. Brain. 2007 Jan 1;130(1):170-80.
  6. ↑Stinear CM, Barber PA, Petoe M, Anwar S, Byblow WD. The PREP algorithm predicts potential for upper limb recovery after stroke. Brain. 2012 Aug 1;135(8):2527-35.
  7. ↑3D Neuroanatomy and Neurology. Neuroanatomy - The Corticospinal Tract in 3D. https://www.youtube.com/watch?v=9BaWBGRVxp8 (accessed 31/3/2016)
  8. ↑Handwritten Tutorials. Spinal Pathways 4 - Corticospinal Tract. https://www.youtube.com/watch?v=dZ5H6PesskA (accessed on 31/3/2016)

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