Motor Deficits Associated with Chronic Traumatic Encephalopathy (CTE)


Chronic traumatic encephalopathy (CTE) is a progressive degenerative neurological disease caused by a history of repetitive subconcussive head trauma, which results in a wide range of motor, cognitive, and behavioral deficits. This article will focus primarily on the motor deficits associated with CTE. Injuries that lead to CTE are most commonly sustained through contact sports such as boxing, football, mixed martial arts, and hockey, but the condition has also been observed in military veterans and survivors of domestic violence. Symptoms of motor deficits and mental confusion were first observed in retired professional boxers; thus, the condition was initially known as dementia pugilistica, or "punch-drunk". Clinical manifestations of the disease closely resemble those of parkinsonism, amyotrophic lateral sclerosis (ALS), cerebellar ataxia, and tauopathic dementias such as Alzheimer's disease.

Functional Anatomical Review and Input/Output Pathways of Affected Structures

Motor Cortex

The motor cortex is located in the frontal lobe and consists of the primary motor cortex, located on the precentral gyrus; the premotor cortex, which can be subdivided into the lateral premotor cortex, the cingulate motor cortex, and the frontal eye fields; the supplementary motor area; and the association cortex. The primary motor cortex is organized somatotopically, with each region representing control of movement of a particular body segment. Somatotopic mapping of the motor cortex is illustrated by the homonculus.
The primary motor cortex also has a columnar organizational pattern, with cells within each column influencing common synergistic muscles to create a certain movement. Tactile and proprioceptive input to the primary motor cortex comes both directly from the thalamus and indirectly from the cerebellum and basal ganglia via the thalamus. It has outputs to the corticospinal pathway which ultimately innervate the alpha motoneurons of distal musculature, and it is the primary executor of movement. Premotor and supplementary motor areas are more involved in the planning and preparation of movement.

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Somatotopic organization of the primary motor cortex.
Somatotopic organization of the primary motor cortex.


The cerebellum is located just beneath the occipital and temporal lobes of the cerebral cortex. Its function is to modify and correct errors in motor commands from descending pathways in order to produce accurate movements; thus, it is critical for maintenance of posture and balance, coordination of voluntary movement, motor learning, and cognitive function. The cerebellum is comprised of the cerebellar deep nuclei and the cerebellar cortex. The deep nuclei - the fastigial, interposed, red, dentate, and vestibular nuclei - are the sole output centers of the cerebellum via Purkinje cells, which receive input from mossy fibers and climbing fibers. Consequently, damage to these nuclei will have the same effect as a total cerebellar lesion. The cortex is the area of the cerebellum which receives input primarily from vestibular receptors and proprioceptors. It can be divided into the flocculonodular, anterior, and posterior lobes, as well as regions of the vermis, the intermediate zone, and the lateral hemispheres.

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Substantia Nigra

The substantia nigra is one of the major output structures of the midbrain associated with the basal ganglia. It can be divided into two components: the pars compacta and the pars reticulata. Of particular interest to the control of voluntary movement is the pars compacta, which contains the dopaminergic neurons that form the nigrostriatal pathway connecting the substantia nigra to the striatum. Dopamine released from these neurons both inhibits the indirect pathway, which inhibits movement, and excites the direct pathway, which facilitates movement. Thus, these neurons play a critical role in the initiation and facilitation of voluntary movement.

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Chronic Traumatic Encephalopathy


One finding that has been consistent across all cases of CTE is that individuals with this condition had been involved in some form of high impact contact sport or another activity or circumstance that put them at a constant high risk for head injury. Different from post-concussive symptoms, however, individuals who develop CTE typically sustain multiple lower impact blows to the head which create microtrauma that may present with few to no concussive symptoms at the time of the injury. Instead, the damage initiates the gradual degeneration and death of neurons in various brain structures that may only be observed years post-trauma. The exact mechanism is still unclear, but somehow the damage initiates a cascade of events that trigger continual apoptotic degeneration that progresses throughout the individual's lifetime and in proportion to the severity and frequency of the trauma. This is thought to be due largely to the accumulation of tau protein deposits - the same protein responsible for certain types of dementia such as Alzheimer's disease.


A prominent feature of individuals with CTE is a reduction in overall brain mass due to neuronal atrophy. Atrophy is especially notable in the frontal lobe (the location of the motor cortex) and the parietal lobes. Cases also consistently present with enlarged lateral and third ventricles due to the degeneration of surrounding structures, as well as a fenestrated cavum septum pellucidum. Scarring and degeneration has also been observed in the cerebellar tonsils, as well as a loss in pigmentation indicating a degeneration of neurons in the substania nigra. Additionally, significant tau protein deposits have been found throughout the brain.

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Individuals with CTE often present with parkinsonian symptoms, which include bradykinesia or akinesia, resting tremor, rigidity, postural instability, and difficulty initiating voluntary movement. These symptoms are caused by a degeneration of the dopaminergic neurons in the pars compacta of the substantia nigra that facilitate movement.

Amyotrophic Lateral Sclerosis

Amyotrophic lateral sclerosis, or ALS, is characterized by progressively worsening muscle weakness as a result of the degeneration and death of pyramidal neurons in the motor cortex. Early symptoms may include fasciculations, muscle cramps, spasticity, and muscle weakness that may cause difficulty with speech, swallowing, and chewing. Weakness can progress to the point where input to respiratory muscles is lost entirely, resulting in death. Individuals with CTE may present with symptoms and neurophysiological features associated with ALS due to the damage sustained to the frontal lobe.

Cerebellar Ataxia

Symptoms of cerebellar ataxia include incoordination of limbs, upright postural and balance deficits, dysmetria, dysdiadochokinesia, and dysarthria, as well as the hallmark cerebellar ataxic gait pattern characterized by an abnormally wide stance, staggering gait, and reduced joint angle excursions. In CTE, these symptoms are produced by the scarring and degeneration of neurons in the cerebellum.

Chronic Traumatic Encephalomyelopathy

Chronic traumatic encephalomyelopathy is a neurological disease closely associated with chronic traumatic encephalopathy that specifically affects motor neurons. This condition manifests as skeletal muscle weakness and atrophy, fasciculations, dysarthria, dysphagia, gait abnormalities, and hyperactive deep tendon reflexes.

Diagnosis and Prognosis

Currently, doctors are only able to diagnose CTE post-mortem through an autopsy due to a lack of adequate diagnostic imaging. Magnetic resonance imaging and magnetic resonance spectroscopy can provide some diagnostic information, but it is still difficult to distinguish CTE from other degenerative neurological conditions using these methods. Prognosis is generally very poor. The condition worsens progressively for the remainder of the individual's life, and is often the cause of death. Those who sustained less trauma lasting over a shorter period of time, however, will likely have less severe symptoms or slower onset.


Chronic traumatic encephalopathy remains a major concern especially for those involved in contact sports. Much research is still needed to be done to find ways to screen for early symptoms and to diagnose and treat the condition. Bringing awareness to the effects of chronic head trauma, however, emphasizes the importance of using head protection and taking preventative measures to reduce the risk of developing this condition.


  • Akinesia - no movement
  • Ataxia - movement incoordination
  • Bradykinesia - slow movement
  • Cavum septum pellucidum - cerebral spinal fluid-filled space separating the septum pellucidum
  • Dysarthria - weakness of or difficulty controlling muscles necessary for producing speech
  • Dysdiadochokinesis - impaired ability to perform rapid, alternating movements
  • Dysmetria - type of ataxia characterized by overshooting or undershooting of limb trajectory
  • Dysphagia - difficulty swallowing
  • Lateral ventricle - cerebrospinal fluid-filled cavity spanning the frontal, occipital, and temporal lobes
  • Third ventricle - cerebrospinal fluid-filled cavity between the thalamus and hypothalamus
  • Taopathy - class of neurodegenerative diseases associated with pathological aggregation of tau protein in the human brain

Suggested Readings

Neurological Consequences of Combat Sports
This article discusses CTE specifically as it applies to practitioners of combat sports like boxing and MMA.

10 NFL Players Tragically Affected by CTE
This video gives an overview of some of the ways repetitive head trauma has affected famous NFL players.


1. Which of the following is NOT a neurological structure associated with the motor deficits of CTE?
A. Cerebellum
B. Motor cortex
C. Cerebral cortex
D. Substantia nigra

2. Which of the following is a symptom associated with ALS?
A. Dysmetria
B. Hyperactive deep tendon reflexes
C. Resting tremor
D. Fasciculations

3. True or False? CTE is a neurodegenerative disease that only affects motor functioning.

4. True or False? Populations at risk for developing CTE are primarily people who have had an acute head injury such as a concussion.

5. Describe the symptoms associated with CTE.

6. Give a basic overview of how CTE is developed.

7. Describe the functional anatomy of the motor cortex, the cerebellum, and the substantia nigra.

Image URLs


Chronic Traumatic Encephalopathy : Current Sports Medicine Reports. (n.d.). Retrieved December 07, 2017, from

Galvan, A., & Wichmann, T. (2008, July). Pathophysiology of Parkinsonism. Retrieved December 07, 2017, from
Galvan, A., & Wichmann, T. (2008, July). Pathophysiology of Parkinsonism. Retrieved December 07, 2017, from
Knierim, J. (n.d.). Chapter 3: Motor Cortex. Retrieved December 07, 2017, from
Knierim, J. (n.d.). Chapter 4: Basal Ganglia. Retrieved December 07, 2017, from
Knierim, J. (n.d.). Chapter 5: Cerebellum. Retrieved December 07, 2017, from
Mckee, A. C., Cantu, R. C., Nowinski, C. J., Hedley-Whyte, E. T., Gavett, B. E., Budson, A. E., . . . Stern, R. A. (2009). Chronic Traumatic Encephalopathyin Athletes: Progressive Tauopathy After Repetitive Head Injury. Journal of Neuropathology & Experimental Neurology,68(7), 709-735.doi:10.1097/nen.0b013e3181a9d503
Rossi, F. H., Franco, M. C., & Estevez, A. G. (2013, September 11). Pathophysiology of Amyotrophic Lateral Sclerosis. Retrieved December 07, 2017, from
Saulle, M., & Greenwald, B. D. (2012, April 10). Chronic Traumatic Encephalopathy: A Review. Retrieved December 07, 2017, from