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(Aghan & Burke)
Multiple Sclerosis III
Parkinson's Disease IV
Visual Form Agnosia
Cerebral Palsy IV
(Labbadia & Taplin)
Multiple Sclerosis IV
Cerebellar Ataxia II
Huntington's Disease III
Smooth Pursuit II
Progressive Supranuclear Palsy
Postural Control II
Parkinson's Disease III
Huntington's Disease II
Phantom Limb III
Vestibular Rehabilitation and Concussion
Cerebral Palsy III
Multiple Sclerosis II
Myofascial Referred Pain
Seizure - Cortical Related
Visual Cortical Neurons
Learning to Dance - Observation vs Action
Restless Leg Syndrome
Grand Mal Seizure
Cerebral Palsy II
Duchenne Muscular Dystrophy
Basal Ganglia II
Saccadic Eye Movement
Shaken Baby Syndrome
Parkinson's Disease II
Alcohol & Cerebellum
(Leach & McManus)
Phantom Limbs II
Cerebellum & Motor Learning
Motor Unit Adaptation
Aging Nervous System
Dance & the Brain
Enteric Nervous System
Golgi Tendon Organs
Vestibular Occular Reflex
Cerebellar Ataxia II
The cerebellum is undeniably an essential structural component of the human brain. Nearly half of the total neurons in the brain are located in the cerebellum alone. Its function is largely associated with the coordination of fine motor movements, postural control and maintenance, and motor learning and skill acquisition. That being said, any form of damage to this complex structure results in varying degrees of impaired motor ability that may present in different ways. A common result of cerebellar lesion is a condition known as cerebellar ataxia. Ataxia comes from the greek word, "a taxis", meaning "without order or incoordination" . Cerebellar ataxia often presents with very disordered, uncoordinated movement patterns and can ultimately affect speech as well.
Location of the Cerebellum
Also known as the "little brain", the cerebellum is located subcortically at the back of the brain, posterior to the brainstem at the level of the 4th ventricle. It is connected to the dorsal aspect of the stalk of the brainstem through bundlings of fibers known as the inferior, middle, and superior cerebellar peduncles. 
Figure 1 - Illustration of the cerebellum.
Figure 2 - the cerebellum and its various structures.
Two Major Parts:
1) Three Deep Nuclei of the Cerebellum [3, 5]
The three deep nuclei of the cerebellum are the main source of output from the cerebellum.
This receives input from the vermis as well as afferent input regarding proximal somatosensation, auditory input, and some visual input
Its output is to the vestibular nuclei and the
Receives input from the intermediate hemispheres as well as afferent cerebellar spinal, somatosensory, auditory, and visual input
Its output is to the contralateral magnocellular
and to the ventrolateral nucleus of the
Receives input from the lateral hemisphere and from afferents coming from the cerebral cortex
Its output is to the contralateral parvocellular red nucleus and to the ventrolateral nucleus of the thalamus.
Figure 3 - image showing the three functional regions along with the output nuclei.
2) Extensive infoldings and fissures make up the cerebellar cortex, whose gray matter contains almost all of the neurons found in the cerebellum. The cerebellum accounts for more than half of all the brains neurons 
Most texts will agree that there are three distinct layers of the cerebellar cortex [3, 8]
Figure 4 - 3 layers of the cerebellar cortex and their respective cell/fiber types.
Outermost molecular layer
This layer contains stellate and basket cells, as well as inhibitory interneurons
it also contains the axons of granule cells known as parallel fibers, as well as the dendrites of the
Middle purkinje cell layer
This layer contains the cell bodies of Purkinje cells and is only one cell thick
Purkinje cells are the main output fiber from the cerebellum
Innermost granular layer
This layer contains an estimated 10^11 granule cells that are small and densely packed 
, the main source of input into the cerebellum, synapse onto granule cells within this layer
Golgi cells, which have inhibitory action on the synapse between granule cells and mossy fibers, are also found in this layer
, which originate in the inferior olive and carry somatosensory, visual, and cerebral cortical input, pass through the granule and Purkinje cell layer and will synapse onto Purkinje dendrites within the molecular layer
How the Cerebellum is Divided
Two primary fissures run mediolaterally to divide the cerebellum into 3 main lobes :
Figure 5 - the three lobes of the cerebellum.
The posterolateral fissure separates the flocculonodular lobe from the posterior lobe
The flocculonodular lobe is folded up on the inferior aspect of the cerebellum
The primary fissure separates the posterior lobe from the anterior lobe
There are two furrows that run longitudinally to distinguish three important regions :
The vermis is the elevated ridge that runs down the midline of the cerebellum
Just lateral to either side of the vermis are the cerebellar hemispheres, which are separated into intermediate (also called paravermal) and lateral portions
With the previous two points in mind, the cerebellum can be divided further into 3 functional divisions:
This area includes both the vermis and the intermediate hemispheres and receives the majority of its input from the
Figure 6 - Somatotopic mapping of the spinocerebellar region.
. The spinocerebellum integrates sensory input with motor commands to produce adaptive motor coordination . It also contains some level of somatotopic mapping. This means that afferent input to the spinocerebellum from different parts of the body are kept segregated. As Figure 8 shows, face and trunkal regions of the body are located more medially within the anterior and posterior lobes of the vermis, whereas input from distal limbs are located laterally in paravemal regions. The vermis is responsible for proximal limb and trunk coordination, some
. The vermis receives somatosensory, auditory, visual, and some vestibular input. Sensory afferents travel through the inferior peduncle to the vermis where information is processed in the cortical region of the vermis. Output from the vermis travels primarily through the fastigial nucleus, which then has output to the vestibular nuclei as well as the reticular formation [5, 8]. The intermediate hemispheres, also referred to as the paravermis, are involved primarily in distal limb coordination. This area receives somatosensory input from the limbs. Its output is to the interposed nucleus, which then sends projections via the lateral
tracts to control distal muscles of the limbs and digits [5, 8].
This functional region is the oldest part of the cerebellum and involves primarily the flocculonodular lobe, which consists of flocculi located more laterally and a central nodulus, and its output to the lateral vestibular nuclei. The function of the vestibulocerebellum is to regulate some level of tone, assist in balance and gait, and influence eye movements via the
[5, 8, 13].
This region involves the lateral hemispheres and the dentate nuclei. Its input is coming primarily from the cerebral cortex via
and its output is sent to motor, premotor, and prefontal cortices via the dentate nucleus. Functionally, this region is responsible for the timing and planning of movements, primarily in the extremities. There is also some level of cognitive function regarding the assessment of movement. Skilled movement is often a result of activity within this region [5, 8, 13].
Input & Output Pathways
The following two tables from the text
Neuroanatomy through Clinical Cases
do a great job at concisely summarizing the input and output pathways to and from the cerebellum.
To summarize, the bulk of input to the cerebellum and output from the cerebellum travel through the superior, middle, and inferior cerebellar peduncles.
Input from the
via climbing fibers, as well as from dorsospinocerebellar, cuneocerebellar, and vestibular pathways all travel through the inferior cerebellar peduncle.
Corticopontocerebellar projections will input to the cerebellum via the middle cerebellar peduncle.
Afferent input from the spinal cord traveling through the ventral and rostral spinocerebellar pathways will input to the cerebellum via the superior cerebellar peduncle.
Ouput from the vermis heading to the reticular formation and vestibular nuclei will exit the cerebellum via the inferior cerebellar peduncle. Output from the functional region known as the vestibulocerebellum will leave through this peduncle as well.
Output from the vermis heading to the ventrolateral nucleus of the thalamus as well as the tectum of the
will do so through the superior cerebellar peduncle. Output from the lateral and intermediate hemispheres will also leave through this peduncle.
No output from the cerebellum is thought to travel through the middle cerebellar peduncle.
Cerebellar Ataxia: A Closer Look
Cerebellar ataxia is a neurological disorder in which damage to the cerebellum through various means results in abnormality of execution of voluntary movement or lack of coordination. Ataxia literally means "lack of order", so this condition involves a degree of disorder between contractions of agonist and antagonist muscles, often leading to poor coordination and control of ones balance, posture, gait, and fine motor skill . Knierem highlights how ataxia is a rather general term and manifests itself most typically in one of two ways :
1. Disturbance of posture and gait
Patients have lost the ability to maintain postural control because cerebellar circuits responsible for fine motor control have been compromised. Normally, vestibular afferent input to the cerebellum is transformed into precise muscle movements that help prevent excessive sway and imbalance. This is compromised in patients
with vestibulocerebellar lesions. In order to make up for the loss of fine postural control, patients will develop compensatory movement strategies that will manifest
as abnormal gait and stance. This can include what is known as
, where the patient has a very wide-based, unsteady gait where the patient walks as if he/she is intoxicated. Truncal ataxia is typically a result to lesions in the vermal portions of the cerebellum .
2. Decomposition of movement
With cerebellar dysfunction, the patient often looses their ability to coordinate movement smoothly. Instead, their movements are broken down into very simple patterns that are pieced together separately instead of occurring all at once . This is a common characteristic of what is known as
, which results typically from lesions in the intermediate and lateral hemispheres of the cerebellum . More will be said about cerebellar lesions in the following section.
Causes of Cerebellar Ataxia
Causes of Cerebellar Ataxia can generally be grouped into two categories :
1. Hereditary causes
Figure 9 - various causes for hereditary and acquired ataxia.
Cases of cerebellar ataxia (CA) are often a result of an inherited gene that is expressed at some point in the persons life. Figure 9 shows the various types of autosomal recessive and dominant forms of hereditary CA as well as forms of acquired CA. Of the hereditary forms, Friedreich's Ataxia is the most common. One study reports that of the hereditary ataxias, 2-5 out of every 100,000 cases have Friedreich's ataxia . A separate study looking at prevalence of Friedreich's ataxia patients against Autosomal Dominant Spinocerebellar Ataxia patients revealed that patients who actually showed ataxic symptoms due to gene expression more frequently had the Friedreich's form when tested . Friedreich's ataxia is most commonly expressed in adolescence and is characterized by gait ataxia, dysmetria, dysdiadocokinesia, muscle weakness, sensory loss, and areflexia .
Cases of cerebellar ataxia are also caused by things like autoimmune diseases, stroke, trauma, infection from toxins, etc. . Alcohol, specifically ethanol, is a large proponent regarding toxic causes of cerebellar ataxia . Alcohol has been shown to have both direct and indirect affects in causing CA; ethanol interacts directly with neurochemical receptors when it crosses the blood brain barrier. It is thought that ethanol impairs motor coordination by increasing the tonic inhibition of granule cells through activity on the GABA-A receptor . Indirect affects of alcohol are typically due to brain injury as one's propensity for falls are increased when intoxicated.
These things often cause cerebellar lesions and will manifest themselves differently depending on the site of the lesion. As was mentioned previously, the cerebellum is divided mediolaterally into three lobes--an anterior lobe, a posterior lobe, and a third flocculonodular lobe.
The anterior lobe is receiving sensory information from the spinal cord through the spinocerebellar, cuneocerebellar, and trigeminocerebellar tracts. This sensory input is mainly associated with information from muscular, joint, and cutaneous mechanoreceptors. Information from the motor cortex is also projecting to the anterior lobe through the pontine nuclei. The anterior lobe has strong influence on head, neck, and proximal limb musculature as well as distal musculature. Lesions in the anterior lobe will thus result in what is called an
anterior lobe syndrome
, in which coordination of the lower limbs is severely impaired. Patients with an anterior lobe syndrome typically present with truncal ataxia. As mentioned previously, this manifests as a wide-based, drunken gait. Anterior lobe syndromes can also result in speech impairments and upper limb ataxia in its more progressive stages [2, 14].
The posterior lobe contains a very large portion of the cerebellum, especially that of the lateral hemispheres. The majority of the posterior lobe represented by the lateral hemispheres is involved with learning and storage of skilled movement patterns. Lateral portions of the cerebellum are receiving extensive input from the cerebral cortex, especially the association areas containing the desired motor plan. A large portion of its output is to the motor cortex where representations for skilled movements are found. Lesions in the posterior lobe will result in a
posterior lobe syndrome
, resulting in loss of coordination in voluntary movements. Appendicular ataxia is very typical of a posterior lobe syndrome, as the patient will have a very difficult time reaching for objects in a smooth, well-coordinated manor.
is a common symptom of posterior lobe syndromes and this tremor is only present during voluntary movements, as it is not present at rest.
are also common symptoms of posterior lobe syndromes [2, 14].
The flocculonodular lobe of the cerebellum is receiving direct input from the vestibular apparatus, as well as the vestibular nuclei. This input is giving the flocculonodular lobe information regarding positioning and inertial properties of the head movements. This region is therefore able to contribute to maintaining balance and posture through output to back to the vestibular nuclei, influencing systems like the
, as well as output down to the spinal cord to influence motor neurons associated with axial musculature [8, 14]. Lesions to the flocculonodular lobe result in a
flocculonodular lobe syndrome
, where the patient has very poor control over muscles associated with posture and balance. Truncal ataxia is also common of flocculonodular lobe syndromes, especially the characterized wide base stance. Patients show what has been called a reeling trunk movement, as if they were being swayed too and fro like a boat in rough seas [2, 14].
It is important to note that lesions to the hemispheres of the cerebellum will result in ipsilateral symptoms, meaning the symptoms will appear on the same side of the body as the lesion in the particular hemisphere. Lesions involving more midline regions of the cerebellum, like those within the vermis, will manifest themselves bilaterally as is seen in truncal ataxia. It is observed, however, that patients will still fall or loose balance toward the side of the lesion [3, 10].
Treating Cerebellar Ataxia
The reality of Cerebellar Ataxia can be quite hard for most, as there is no known cure for the disease to date. Medicinal treatments for CA are still an area of research, as causes are often hereditary and will vary from person to person in its mechanisms. There are currently no U.S. Food and Drug Administration–approved medications for the treatment of CA and most medicinal treatments used are largely experimental . There are alternative treatment options, however, that can improve symptoms in some cases or at least slow the degeneration process. This often comes in the form of physical therapy. Below is a piece taken from the paper ,"Ataxia: Physical Therapy and Rehabilitation Applications for Ataxic Patients", that summarizes nicely the role of the therapist in CA treatment:
"The goal of the physiotherapist in the rehabilitation of ataxia resulting from defects in neurological structures and effecting the functions of the patient, is to improve the functional level of the patient through restorative techniques. When this is not possible, the therapist makes use of compensatory strategies to make the patient perform as independent as possible within the present functional level. The goals of restorative physical treatment can be briefly described as:
Improving balance and postural reactions against external stimuli and gravitational changes
Improving and increasing postural stabilization following the development of joint stabilization
Developing upper extremity functions
Through developing independent and functional gait, improving the life quality of the patient by increasing the patient's independence while performing daily life activities" 
A frequently used exercise routine are the Frenkel exercises, a series of repetitious exercises that progress in difficulty that the patient can perform on their own without any equipment. Frenkel exercises do, however, require a high level of mental concentration as the patient is trying to consciously improve his/her coordination. They also require that hundreds of repetitions be done over time in order to have beneficial effects for the patient in the long term [2, 7].
Because of the importance of the cerebellum in movement and the complex nature of its physiology, lesions to the cerebellum are quite severe and have no known cure. Cerebellar Ataxia is a complex disease that can result in significant impairment of movement for those impacted by it. There is hope for the ataxic patient, however, as treatments for the disease are starting to be uncovered. The benefits of physio-therapeutic treatments, especially for those in less progressive stages of CA, are still being explored by therapists.
Glossary of Terms
Appendicular ataxia -
characterization of cerebellar ataxia in which movements are broken down into very simple patterns that are pieced together separately instead of occurring all at once
Climbing fibers -
second fiber type carrying input to the cerebellum, but only coming from the inferior olive
Corticopontocerebellar pathways -
projections from the cortex that travel to the cerebellum via the pons
Corticospinal tracts -
pathways, including both medial and lateral portions, that carry motor commands to both the spinal cord and to the cerebellum
common symptom of posterior lobe syndromes characterized by an inability to perform rapid alternating movements
common symptom of posterior lobe syndromes in which the patient overshoots or undershoots movements involving the limbs
Inferior olive -
nucleus in the medulla that has significant projections to the cerebellum via climbing fibers and is heavily involved in the learning and timing of movements
Intentional Tremor -
common symptom of posterior lobe syndromes in which the hands shake at a broad, low frequency and will typically increase in frequency at the endpoint of a deliberate movement
Mossy fibers -
main input fiber to the cerebellum
Purkinje cells -
the main output fibers from the cerebellar cortex
Red nucleus -
nucleus located in the brainstem that plays an important role in motor coordination
Reticular formation -
collection of nuclei in the brainstem responsible for monitoring various sensory and motor functions
Rubrospinal tracts -
pathway originating in the red nucleus that carries motor information to various levels of the spinal cord, especially the cervical levels
type of eye movement in which the eyes conjugately move from one point of fixation to another with maximal speed
Smooth pursuit -
type of eye movement in which the eyes follow a moving object while keeping it focused on the retina
Spinocerebellar tracts -
includes dorsal, ventral, and rostral tracts that carry sensory and proprioceptive input from the spinal level to the cerebellum
Superior colliculus -
structure located in the midbrain that plays a large role in the control of eye movements
important mass of gray matter in the brain responsible for relaying various forms of sensory and motor information
Truncal ataxia -
characterization of cerebellar ataxia in which the patient presents with a very wide-based, unsteady gait where the patient walks as if he/she is intoxicated
Vestibulo-ocular reflex -
involuntary reflex in which activity in the vestibular canals causes rotation of the eyes in the opposite direction
1) This paper provides a closer look into some of the postural disorders associated with cerebellar ataxia and treatments for each:
Marquer, A., Barbieri, G., & Pérennou, D. (2014). The assessment and treatment of postural disorders in cerebellar ataxia: a systematic review. Annals of physical and rehabilitation medicine, 57(2), 67-78.
2) For a more detailed look at some of the work being done in terms of medicinal treatments of cerebellar ataxia, visit this paper:
Sarva, H. and Shanker, V. L. (2014), Treatment Options in Degenerative Cerebellar Ataxia: A Systematic Review. Mov Disord Clin Pract, 1: 291–298. doi:10.1002/mdc3.12057
3) This article goes more in depth into the pathophysiology behind cerebellar ataxia:
Diener, H. C., & Dichgans, J. (1992). Pathophysiology of cerebellar ataxia. Movement Disorders, 7(2), 95-109.
4) Though not discussed in this page, cerebellar ataxia does affect the oculomotor systems. This paper is helpful in understanding some of those abnormalities:
Zee, D. S., Yee, R. D., Cogan, D. G., Robinson, D. A., & Engel, W. K. (1976). Ocular motor abnormalities in hereditary cerebellar ataxia. Brain: a journal of neurology, 99(2), 207-234.
True/False & Multiple Guess
The fastigial nucleus directly outputs to the spinal cord. (True/false)
Mossy fibers are the main output fiber type from the cerebellum. (True/false)
Which one of these is considered the middle layer of the cerebellar cortex?
Granule cell layer
Purkinje cell layer
Golgi cell layer
Which of the following is NOT a role of the spinocerebellum?
All of the above are functions of the spinocerebellum
The middle cerebellar peduncle is the only peduncle that is not involved in output from the cerebellum. (True/False)
The neurotransmitter GABA is thought to have a significant correlation with cerebellar ataxia. (True/False)
According to current research, cerebellar ataxia is only inherited and is usually not acquired through other causes. (True/False)
Which of the following is not a common symptom of a posterior lobe syndrome?
There are currently no cures for cerebellar ataxia. (True/False)
The Frenkel exercises have proved an ineffective means of treating ataxic patients. (True/False)
List and briefly describe the three functional regions of the cerebellum.
Describe some of the symptoms of an anterior lobe syndrome in patients with cerebellar ataxia.
List the four goals of restorative physical treatment.
 Alekseeva, N., McGee, J., Kelley, R. E., Maghzi, A. H., Gonzalez-Toledo, E., & Minagar, A. (2014). Toxic-metabolic, nutritional, and medicinal-induced disorders of cerebellum. Neurologic clinics, 32(4), 901-911.
 Armutlu K. (2010). Ataxia: Physical Therapy and Rehabilitation Applications for Ataxic Patients. In: JH Stone, M Blouin, editors. International Encyclopedia of Rehabilitation. Available online:
 Blumenfeld, H. (2002). Neuroanatomy through clinical cases. Sunderland, MA: Sinauer Associates, Inc.
 BOZ, P. B., KOÇ, F., SEL, S. K., GÜZEL, A. İ., & KASAP, H. (2016). Determination of Genotypic and Phenotypic Characteristics of Friedreich's Ataxia and Autosomal Dominant Spinocerebellar Ataxia Types 1, 2, 3, and 6. Archives Of Neuropsychiatry / Noropsikiatri Arsivi, 53(2), 115-119. doi:10.5152/npa.2015.9925
 Cerebellum (Section 3, Chapter 5) Neuroscience Online: An Electronic Textbook for the Neurosciences | Department of Neurobiology and Anatomy - The University of Texas Medical School at Houston. Retrieved December 15, 2016 from
 Disorders of the Motor System (Section 3, Chapter 6) Neuroscience Online: An Electronic Textbook for the Neurosciences | Department of Neurobiology and Anatomy - The University of Texas Medical School at Houston. Retrieved December 15, 2016 from
 Das, P. (2009). Frenkel exercises for ataxic conditions. Retrieved from
 Kandel, E. R., Schwartz, H. J., Jessell, T. M. (2000). Principles of Neural Science 4th edition. New York City, NY: McGraw-Hill.
 Marsden, J., & Harris, C. (2011). Cerebellar ataxia: pathophysiology and rehabilitation. Clinical Rehabilitation, 25(3), 195-216. doi:10.1177/0269215510382495
 Reeves, A. G., Swenson, R. S. (2008). Chapter 10 - Motor System Examination. In Disorders of the Nervous System - A Primer. Retrieved from
 Sarva, H. and Shanker, V. L. (2014), Treatment Options in Degenerative Cerebellar Ataxia: A Systematic Review. Mov Disord Clin Pract, 1: 291–298. doi:10.1002/mdc3.12057
 Vasco, G., Gazzellini, S., Petrarca, M., Lispi, M. L., Pisano, A., Zazza, M., & ... Bertini, E. (2016). Functional and Gait Assessment in Children and Adolescents Affected by Friedreich’s Ataxia: A One-Year Longitudinal Study. Plos ONE, 11(9), 1-13. doi:10.1371/journal.pone.0162463
 Vilis, T. (2013). Cerebellum and Basal Ganglia. In Neurophysiology for Medicine. Retrieved from
 Young, P. A., Young, H. A., Tolbert, D. L. (2008) The Cerebellum: Ataxia. In Basic Clinical Neuroscience 2nd edition. Baltimore, MD: Lippincott Williams & Wilkins
Figure 1 -
Figure 2 & 6 - Purves, D., Augustine, G. J., Fitzpatrick, D., Hall, W. C., LaMantia, A., McNamara, J. O., White, L. E. (2008). Neuroscience 4th edition. Sunderland, MA: Sinauer Associates, Inc.
Figure 3 -
Figure 4 - Kandel, E. R., Schwartz, H. J., Jessell, T. M. (2000). Principles of Neural Science 4th edition. New York City, NY: McGraw-Hill.
Figure 5 -
Figure 7 & 8 - Blumenfeld, H. (2002). Neuroanatomy through clinical cases. Sunderland, MA: Sinauer Associates, Inc.
Figure 9 - Marsden, J., & Harris, C. (2011). Cerebellar ataxia: pathophysiology and rehabilitation. Clinical Rehabilitation, 25(3), 195-216. doi:10.1177/0269215510382495
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