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ICD-10 R27
ICD-9 781.3
DiseasesDB 2218
MeSH D002524

Template:Search infobox Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]


Dysmetria (Greek: "difficult to measure") is a condition that describes a lack of coordination of movement typified by the undershoot and/or overshoot of intended position with the hand, arm, leg, or eye. It is sometimes described as an inability to judge distance or scale [1].

(From the Online Medical Dictionary) an aspect of ataxia, in which the ability to control the distance, power, and speed of an act is impaired. Usually used to describe abnormalities of movement caused by cerebellar disorders.

As dysmetria can refer to more than just a motor problem, an overlying definition that encompasses all forms of it is “the inability to receive and process information rapidly, to retrieve the relevant associated constructs, and to produce a well-modulated and fine-tuned response.”[2]

Hypermetria describes undershooting intended position and hypometria describes overshooting intended position [3].

The cerebellum is the area of the brain that contributes to coordination and motor processes and is anatomically inferior to the cerebrum [2] [4]. Sensorimotor integration is the brain’s way of integrating the information received from the sensory (or proprioceptive) neurons from the body, including any visual information. To be more specific, information needed to perform a motor task comes from retinal information pertaining to the eyes’ position and has to be translated into spatial information . Sensorimotor integration is crucial for performing any motor task and takes place in the post parietal cortex [3] [4]. After the visual information has been translated into spatial information, the cerebellum must use this information to perform the motor task [2][5]. If there is damage to any pathways that connect the pathways, dysmetria may result.


Motor dysmetria is the customary term used when a person refers to dysmetria. Dysmetria of the extremities caused by hemispheric syndromes is manifested in multiple ways: dysrhythmic tapping of hands and feet and dysdiadochokinesis, which is the impairment of alternating movements [5].. Damage to the cerebellum makes a person slow to orient their extremities in space [4].

Motor Control as a Learning Process

Recent research has also shed light upon a specific process that if interrupted, may be the cause of ataxia and dysmetria. According to sources cited in this article, motor control is a learning process that occurs in the synapses of Purkinje dendrites [6]. Research has shown that inhibitory synaptic connections are the primary way the learning occurs, as saturation would occur with excitatory synaptic transmission [6]. There have been varying theories as to the makeup of the cerebellum, which controls this process [6]. Some predicted that the cerebellum was an array of adjustable pattern generators (APGs), each of which generate a “burst command” with varying intensity and duration [6]. Other models, which apply mostly in robotic applications, propose that the cerebellum acquires an “inverse model of the motor apparatus [6].” More recent research in electrophysiology has shown modular structures in the spinal cord known as “motor primitives [6].”

Based on the APG model, modules of APG are the features that control motor learning [6]. The entire process is a positive feedback loop [6]. Inhibitory input is transmitted and received from various components of the cortex, including the cerebellar nucleus, a motor cortical cell and Purkinje cells [6]. Purkinje cells send the inhibitive information by obtaining learning information from parallel fibers of granule cells [6]. This model of APGs is useful in that it effectively describes the motor learning process [6].

Motor primitives are another proposed module of motor learning [6]. This information was found by electrical stimulation of the lumbar spinal cord in rats and frogs [6]. Upon the stimulation, researchers found that motor primitives are found in the spinal cord and use patterns of muscle activation to generate a specific motor output [6]. Different movements are learned from different levels of activation [6]. These findings lead researchers to believe that these same motor primitives could be found in the cerebellum [6].

These two different models combined show that it is possible that motor primitives are in the cerebellum, because, “a set of parallel arrays of APG can drive each motor primitive module in the spinal cord [6].” The authors have generated a model of adjustable primitive pattern generator (APPG), which is basically a group of parallel APGs summed together [6].

The APPG model is a vector sum of all the inputs of the APG, which are units of position, velocity and time [6]. Granule cells send information from the spinal cord and the motor cortex which in turn translates the information in a process called state mapping [6]. The final model of the APPG becomes linear upon the vector summation of the information from the neurons and muscles [6]. This model is consistent with the “virtual trajectory hypothesis” which states that the desired trajectory is sent to the spinal cord as a motor command [6].


Saccadic eye movements are the very quick, simultaneous movements made by the eye to receive visual information and shift the line of vision from one position to another [7]. A person depends profoundly on the ability of the accuracy of these movements [7].. The area of the brain that controls saccades is the superior colliculus, specifically the fastigial oculomotor region (FOR) [7].. The information is received from the retina, is translated into spatial information and is then transferred to motor centers for motor response. A person with saccadic dysmetria will constantly produce abnormal eye movements including microsaccades, ocular flutter, and square wave jerks even when the eye is at rest [5]. During eye movements hypometric and hypermetric saccades will occur and interruption and slowing of normal saccadic movement is common [5].


There have been many studies concerning the cerebellum’s role in cognitive processes. The cerebellum is connected to other higher-order areas of the brain and is therefore thought to take part in many cognitive processes [2]. Previously there has been evidence that the cerebellum contributed to cognitive processes but with the development of functional magnetic resonance imaging (fMRI), researchers have proved that the cerebellum is associated with higher-order functions including attention, perception, and language [8] [4]. Some clinical studies have revealed that there is an association between the cerebellum and personality [5]. Researchers have also been able to find correlations between cerebellar disorders and psychosis, especially schizophrenia [5]. In particular, cerebellar cognitive affective syndrome (CCAS) is a cerebellar disorder that exhibits both motor dysfunction (including dysmetria: referred to as impaired spatial cognition), personality change, impairment of linguistic abilities, and disturbance of higher-order functions including reasoning and memory [5]. It is believed that the there are specific pathways that link not only the prefrontal cortex, superior temporal regions, posterior parietal lobes, and hippocampus to the cerebellum, but there are also very specific pathways that link the cerebellum back to these areas of the brain [5]. These loops may contribute to the cognitive properties of the cerebellum that have recently been discovered. A good definition of cognitive dysmetria, also referred to as dysmetria of thought, is “a difficulty in coordinating and monitoring the process of receiving, processing, and expressing information” [2]. Cognitive dysmetria manifests itself in association with other cerebellar disorders [5].


The actual cause of dysmetria is thought to be caused by lesions in the cerebellum or by lesions in the proprioceptive nerves that lead to the cerebellum that coordinate visual, spatial and other sensory information with motor control [4].. Damage to the proprioceptive nerves does not allow the cerebellum to accurately judge where the hand, arm, leg, or eye should move. These lesions are often caused by strokes, Multiple Sclerosis (MS), Amyotrophic Lateral Sclerosis (ALS), or tumors [9].

According to the research article cited above, motor control is a learning process that utilizes APPGs [6]. Disruption of APPGs is possibly the cause of ataxia and dysmetria and upon identification of the motor primitives, clinicians may be able to isolate the specific areas responsible for the cerebellar problems [6].

There are two types of cerebellar disorders that produce dysmetria, specifically midline cerebellar syndromes and hemispheric cerebellar syndromes [9]. Midline cerebellar syndromes can cause ocular dysmetria, which is a condition in which the pupils of the eye overshoot [9]. Ocular dysmetria makes it difficult to focus vision onto one object. Hemispheric cerebellar syndromes cause dysmetria in the typical motor sense that many think of when hearing the term dysmetria [9].

A common motor syndrome that causes dysmetria is cerebellar motor syndrome, which also marked by impairments in gait (also known as ataxia), disordered eye movements, tremor, difficulty swallowing and poor articulation [5]. As stated above, cerebellar cognitive affective syndrome (CCAS) also causes dysmetria.

Associated Diseases

Dysmetria is often found in individuals with Multiple Sclerosis (MS), Amyotrophic Lateral Sclerosis (ALS), and persons who have suffered from tumors or strokes. Persons who have been diagnosed with autosomal dominant spinocerebellar ataxia (SCAs) also exhibit dysmetria [10]. SCAs are a type of cerebellar disease that is inherited. There are many types of SCAs and though many exhibit similar symptoms (one being dysmetria), they are considered to be heterogeneous [10]. Freidrich’s ataxia is a well-known SCA in which children have dysmetria [5]. It is also closely associated with schizophrenia and autism [8].


Diagnosis of any cerebellar disorder or syndrome should be made by a qualified neurologist. Prior to referring a patient to a neurologist, a general practitioner or MS nurse will perform a finger-to-nose test [5]. The clinician will raise a finger in front of the patient and ask him to touch it with his finger and then touch his nose with his forefinger several times. This shows a patient’s ability to judge the position of a target. Other tests that could be performed are similar in nature and include a heel to shin test in which proximal overshoot characterizes dysmetria and an inability to draw an imaginary circle with the arms or legs without any decomposition of movement [5]. After a positive result in the finger-to-nose test, a neurologist will do a magnetic resonance image (MRI) to determine any damage to the cerebellum [5].


Currently there is no cure for dysmetria itself as it is actually a symptom of an underlying disorder. However, Isoniazid and Clonazepam have been used to treat dysmetria [1]. Cannabis has been used in trials in the U.K. and displayed some success, though it is not legal to use in the U.S. at this time [1].


Researchers now are testing different possibilities for treating dysmetria and ataxia. One opportunity for treatment is called rehearsal by eye movement [11]. It is believed that visually guided movements require both lower- and higher-order visual functioning by first identifying a target location and then moving to acquire what is sought after [10]. In one study, researchers used visually guided stepping which is parallel to visually guided arm movements to test this treatment [11]. The patients suffered from saccadic dysmetria which in turn caused them to overshoot their movements 3. The patients first walked normally and were then told to twice review the area that was to be walked through 3. After rehearsal with eye movements, the patients improved their motor performance [11]. Researchers believe that prior rehearsal with the eyes might be enough for a patient that suffers from motor dysmetria as a result of saccadic dysmetria to complete a motor task with enhanced spatial awareness [11].

Research has also been done for those patients that suffer from Multiple Sclerosis (MS) [12]. Deep brain stimulation (DBS) remains a viable possibility for some MS patients though the long term effects of this treatment are currently under review [12]. The subjects that have undergone this treatment had had no major relapse for 6 months and disabling motor function problems [12]. Most subjects benefited from the implantation of the electrodes and some reported that their movement disorder was gone after surgery [12]. However, these results are limiting at this time because of the small range of subjects that were used for the experiment and it is unknown whether this is a viable option for all MS patients that suffer from motor control problems [12].

See also


  1. 1.0 1.1 1.2 “Dysmetria,” Multiple Sclerosis Encyclopaedia, Last modified 10/16/2007, http://www.mult-sclerosis.org/dysmetria.html/
  2. 2.0 2.1 2.2 2.3 2.4 N.C. Andreasen, D.S. Oleary, T. Cizadlo, S. Arndt, K. Rezai, L.L.B. Ponto, G.L. Watkins, and R.D. Hichwa, “Schizophrenia and cognitive dysmetria: A positron-emission tomography study of dysfunctional prefrontal-thalamic-cerebellar circuitry,” Proceedings of the National Academy of Sciences of the United States of America, vol. 93, (no. 18), pp. 9985-9990, Sep 1996.
  3. 3.0 3.1 J.D. Schmahmann, “Disorders of the cerebellum: Ataxia, dysmetria of thought, and the cerebellar cognitive affective syndrome,” Journal of Neuropsychiatry and Clinical Neurosciences, vol. 16, (no. 3), pp. 367-378, Sum 2004.
  4. 4.0 4.1 4.2 4.3 4.4 J. Townsend, E. Courchesne, J. Covington, M. Westerfield, N.S. Harris, P. Lyden, T.P. Lowry, and G.A. Press, “Spatial attention deficits in patients with acquired or developmental cerebellar abnormality,” Journal of Neuroscience, vol. 19, (no. 13), pp. 5632-5643, Jul 1999.
  5. 5.00 5.01 5.02 5.03 5.04 5.05 5.06 5.07 5.08 5.09 5.10 5.11 5.12 5.13 J.D. Schmahmann, “Disorders of the cerebellum: Ataxia, dysmetria of thought, and the cerebellar cognitive affective syndrome,” Journal of Neuropsychiatry and Clinical Neurosciences, vol. 16, (no. 3), pp. 367-378, Sum 2004.
  6. 6.00 6.01 6.02 6.03 6.04 6.05 6.06 6.07 6.08 6.09 6.10 6.11 6.12 6.13 6.14 6.15 6.16 6.17 6.18 6.19 6.20 6.21 6.22 6.23 S. Vahdat, A. Maghsoudi, M.H. Hasani, F. Towhidkhah, S. Gharibzadeh, and M. Jahed, “Adjustable primitive pattern generator: A novel cerebellar model for reaching movements,” Neuroscience Letters, vol. 406, (no. 3), pp. 232-234, Oct 2006.
  7. 7.0 7.1 7.2 Y. Iwamoto and K. Yoshida, “Saccadic dysmetria following inactivation of the primate fastigial oculomotor region,” Neuroscience Letters, vol. 325, (no. 3), pp. 211-215, Jun 2002.
  8. 8.0 8.1 G. Allen and E. Courchesne, “Differential effects of developmental cerebellar abnormality on cognitive and motor functions in the cerebellum: An fMRI study of autism,” American Journal of Psychiatry, vol. 160, (no. 2), pp. 262-273, Feb 2003
  9. 9.0 9.1 9.2 9.3 Timothy C. Hain, MD, “Cerebellar Disorders,” Last modified 7/26/02, http://www.tchain.com/otoneurology/disorders/central/cerebellar/cerebellardisorders
  10. 10.0 10.1 10.2 ] M.U. Manto, “The wide spectrum of spinocerebellar ataxias (SCAs),” Cerebellum, vol. 4, (no. 1), pp. 2-6, 2005.
  11. 11.0 11.1 11.2 11.3 K.A. Crowdy, D. Kaur-Mann, H.L. Cooper, A.G. Mansfield, J.L. Offord, D.E. Marple-Horvat, “Rehearsal by eye movement improves visuomotor performance in cerebellar patients,” Experimental Brain Research, vol.146, pp. 244-247, July 2002.
  12. 12.0 12.1 12.2 12.3 12.4 J. Hooper, R. Taylor, B. Pentland, and I.R. Whittle, “A prospective study of thalamic deep brain stimulation for the treatment of movement disorders in multiple sclerosis,” British Journal of Neurosurgery, vol. 16, (no. 2), pp. 102-109, Apr 2002.

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