Dysmetria

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Dysmetria
Specialty Neurology

Dysmetria (English: wrong length) is a lack of coordination of movement typified by the undershoot or overshoot of intended position with the hand, arm, leg, or eye. It is a type of ataxia. It can also include an inability to judge distance or scale. [1]

Contents

Hypermetria and hypometria are, respectively, overshooting and undershooting the intended position. [2] [3]

Presentation

Associated diseases

Dysmetria is often found in individuals with multiple sclerosis (MS), amyotrophic lateral sclerosis (ALS), and persons who have had tumors or strokes. Persons who have been diagnosed with autosomal dominant spinocerebellar ataxia (SCAs) also exhibit dysmetria. [4] There are many types of SCAs and though many exhibit similar symptoms (one being dysmetria), they are considered to be heterogeneous. [4] Friedreich's ataxia is a well-known SCA in which children have dysmetria. [5] Cerebellar malformations extending to the brainstem can also present with dysmetria. [6]

Causes

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. [7] 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.[ citation needed ]

According to the research article cited above, motor control is a learning process that utilizes APPGs. [8] 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. [8]

There are two types of cerebellar disorders that produce dysmetria, specifically midline cerebellar syndromes and hemispheric cerebellar syndromes. Midline cerebellar syndromes can cause ocular dysmetria, a condition in which the eyes can not track an object properly and either overshoot (ahead of the object )or undershoot (lagging behind the object). Ocular dysmetria also makes it difficult to maintain fixation on a stationary object. Hemispheric cerebellar syndromes cause dysmetria in the typical motor sense that many think of when hearing the term dysmetria.[ citation needed ]

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.

Anatomy

The cerebellum is the area of the brain that contributes to coordination and motor processes and is anatomically inferior to the cerebrum. [9] [7] 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. [9] [10] After the visual information has been translated into spatial information, the cerebellum must use this information to perform the motor task. [5] If there is damage to any pathways that connect the pathways, dysmetria may result.[ citation needed ]

Motor

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. [7]

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. [8] There have been varying theories as to the makeup of the cerebellum, which controls this process. 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. Other models, which apply mostly in robotic applications, propose that the cerebellum acquires an "inverse model of the motor apparatus". [8] More recent research in electrophysiology has shown modular structures in the spinal cord known as "motor primitives". [8] Based on the APG model, modules of APG are the features that control motor learning. [8] The entire process is a positive feedback loop. Inhibitory input is transmitted and received from various components of the cortex, including the cerebellar nucleus, a motor cortical cell and Purkinje cells. [8] Purkinje cells send the inhibitive information by obtaining learning information from parallel fibers of granule cells. This model of APGs is useful in that it effectively describes the motor learning process. [8]

Motor primitives are another proposed module of motor learning. [8] This information was found by electrical stimulation of the lumbar spinal cord in rats and frogs. [8] 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. Different movements are learned from different levels of activation. These findings led researchers to believe that these same motor primitives could be found in the cerebellum. [8]

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." [8] The authors have generated a model of adjustable primitive pattern generator (APPG), which is basically a group of parallel APGs summed together. [8]

The APPG model is a vector sum of all the inputs of the APG, which are units of position, velocity and time. [8] Granule cells send information from the spinal cord and the motor cortex which in turn translates the information in a process called state mapping. [8] The final model of the APPG becomes linear upon the vector summation of the information from the neurons and muscles. [8] 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. [8]

Saccadic

Saccades 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. [11] A person depends profoundly on the ability of the accuracy of these movements. [11] 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]

Diagnosis

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]

Cerebellar patients encounter difficulties to adapt to unexpected changes of the inertia of the limbs. [12] This can be used to increase dysmetria and confirm a diagnosis of cerebellar dysfunction. Patients also show an abnormal response to changes in damping. These findings confirm a role of the cerebellum in predictions. [13]

Treatments

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. Frenkel exercises treat dysmetria. [ citation needed ]

Research

Researchers now are testing different possibilities for treating dysmetria and ataxia. One opportunity for treatment is called rehearsal by eye movement. [14] 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. [4] In one study, researchers used visually guided stepping which is parallel to visually guided arm movements to test this treatment. [14] The patients had 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. [14] Researchers believe that prior rehearsal with the eyes might be enough for a patient with motor dysmetria as a result of saccadic dysmetria to complete a motor task with enhanced spatial awareness. [14]

Research has also been done for those patients with MS. [15] Deep brain stimulation (DBS) remains a viable possibility for some MS patients though the long-term effects of this treatment are currently under review. [15] The subjects who have undergone this treatment had no major relapse for six months and disabling motor function problems. [15] Most subjects benefited from the implantation of the electrodes and some reported that their movement disorder was gone after surgery. [15] However, these results are limiting at this time because of the small range of subjects who were used for the experiment and it is unknown whether this is a viable option for all MS patients with motor control problems. [15]

See also

Related Research Articles

Ataxia is a neurological sign consisting of lack of voluntary coordination of muscle movements that can include gait abnormality, speech changes, and abnormalities in eye movements, that indicates dysfunction of parts of the nervous system that coordinate movement, such as the cerebellum.

<span class="mw-page-title-main">Cerebellum</span> Structure at the rear of the vertebrate brain, beneath the cerebrum

The cerebellum is a major feature of the hindbrain of all vertebrates. Although usually smaller than the cerebrum, in some animals such as the mormyrid fishes it may be as large as it or even larger. In humans, the cerebellum plays an important role in motor control. It may also be involved in some cognitive functions such as attention and language as well as emotional control such as regulating fear and pleasure responses, but its movement-related functions are the most solidly established. The human cerebellum does not initiate movement, but contributes to coordination, precision, and accurate timing: it receives input from sensory systems of the spinal cord and from other parts of the brain, and integrates these inputs to fine-tune motor activity. Cerebellar damage produces disorders in fine movement, equilibrium, posture, and motor learning in humans.

Dysarthria is a speech sound disorder resulting from neurological injury of the motor component of the motor–speech system and is characterized by poor articulation of phonemes. In other words, it is a condition in which problems effectively occur with the muscles that help produce speech, often making it very difficult to pronounce words. It is unrelated to problems with understanding language, although a person can have both. Any of the speech subsystems can be affected, leading to impairments in intelligibility, audibility, naturalness, and efficiency of vocal communication. Dysarthria that has progressed to a total loss of speech is referred to as anarthria. The term dysarthria is from Neo-Latin, dys- "dysfunctional, impaired" and arthr- "joint, vocal articulation".

<span class="mw-page-title-main">Inferior olivary nucleus</span> Brain structure in the medulla that helps coordinate movement

The inferior olivary nucleus (ION), is a structure found in the medulla oblongata underneath the superior olivary nucleus. In vertebrates, the ION is known to coordinate signals from the spinal cord to the cerebellum to regulate motor coordination and learning. These connections have been shown to be tightly associated, as degeneration of either the cerebellum or the ION results in degeneration of the other.

<span class="mw-page-title-main">Cerebellar vermis</span> Structure connecting the two cerebellar hemispheres

The cerebellar vermis is located in the medial, cortico-nuclear zone of the cerebellum, which is in the posterior fossa of the cranium. The primary fissure in the vermis curves ventrolaterally to the superior surface of the cerebellum, dividing it into anterior and posterior lobes. Functionally, the vermis is associated with bodily posture and locomotion. The vermis is included within the spinocerebellum and receives somatic sensory input from the head and proximal body parts via ascending spinal pathways.

<span class="mw-page-title-main">Spinocerebellar ataxia</span> Medical condition

Spinocerebellar ataxia (SCA) is a progressive, degenerative, genetic disease with multiple types, each of which could be considered a neurological condition in its own right. An estimated 150,000 people in the United States have a diagnosis of spinocerebellar ataxia at any given time. SCA is hereditary, progressive, degenerative, and often fatal. There is no known effective treatment or cure. SCA can affect anyone of any age. The disease is caused by either a recessive or dominant gene. In many cases people are not aware that they carry a relevant gene until they have children who begin to show signs of having the disorder.

<span class="mw-page-title-main">Romberg's test</span> Test used in an exam of neurological function for balance

Romberg's test, Romberg's sign, or the Romberg maneuver is a test used in an exam of neurological function for balance. The exam is based on the premise that a person requires at least two of the three following senses to maintain balance while standing: proprioception ; vestibular function ; and vision.

<span class="mw-page-title-main">Flocculus</span>

The flocculus is a small lobe of the cerebellum at the posterior border of the middle cerebellar peduncle anterior to the biventer lobule. Like other parts of the cerebellum, the flocculus is involved in motor control. It is an essential part of the vestibulo-ocular reflex, and aids in the learning of basic motor skills in the brain.

Cerebellar ataxia is a form of ataxia originating in the cerebellum. Non-progressive congenital ataxia (NPCA) is a classical presentation of cerebral ataxias.

Intention tremor is a dyskinetic disorder characterized by a broad, coarse, and low-frequency tremor evident during deliberate and visually-guided movement. An intention tremor is usually perpendicular to the direction of movement. When experiencing an intention tremor, one often overshoots or undershoots one's target, a condition known as dysmetria. Intention tremor is the result of dysfunction of the cerebellum, particularly on the same side as the tremor in the lateral zone, which controls visually guided movements. Depending on the location of cerebellar damage, these tremors can be either unilateral or bilateral.

Uner Tan syndrome (UTS) is a syndrome that was discovered by the Turkish evolutionary biologist Üner Tan. People affected by UTS walk with a quadrupedal locomotion and often have severe learning disabilities. Tan postulated that this is an example of "reverse evolution" (atavism). The proposed syndrome was featured in the 2006 BBC2 documentary The Family That Walks On All Fours.

Benedikt syndrome, also called Benedikt's syndrome or paramedian midbrain syndrome, is a rare type of posterior circulation stroke of the brain, with a range of neurological symptoms affecting the midbrain, cerebellum and other related structures.

<span class="mw-page-title-main">Dyschronometria</span> Inability to estimate amount of time that has passed

Dyschronometria is a condition of cerebellar dysfunction in which an individual cannot accurately estimate the amount of time that has passed. It is associated with cerebellar ataxia, when the cerebellum has been damaged and does not function to its fullest ability. Lesions to the cerebellum can cause dyssynergia, dysmetria, dysdiadochokinesia, dysarthria, and ataxia of stance and gait. Dyschronometria can result from autosomal dominant cerebellar ataxia (ADCA).

<span class="mw-page-title-main">Vestibulocerebellar syndrome</span> Medical condition

Vestibulocerebellar syndrome, also known as vestibulocerebellar ataxia, is a progressive neurological disorder that causes a variety of medical problems. Initially symptoms present as periodic attacks of abnormal eye movements but may intensify to longer-lasting motor incapacity. The disorder has been localized to the vestibulocerebellum, specifically the flocculonodular lobe. Symptoms of vestibulocerebellar syndrome may appear in early childhood but the full onset of neurological symptoms including nystagmus, ataxia, and tinnitus does not occur until early adulthood. To date, vestibulocerebellar syndrome has only been identified in three families but has affected multiple generations within them. Based on the familial pedigrees it has been characterized as an autosomal dominant disorder, although the exact genetic locus has not been identified. It has been found to be genetically distinct from other seemingly similar forms of neurological syndromes such as episodic ataxia types 1 and 2. Due to its rarity, however, little is known about specific details of the pathology or long-term treatment options. There is currently no cure for vestibulocerebellar syndrome, although some drug therapies have been effective in alleviating particular symptoms of the disorder.

<span class="mw-page-title-main">Babinski–Nageotte syndrome</span> Medical condition

Babinski–Nageotte syndrome is an alternating brainstem syndrome. It occurs when there is damage to the dorsolateral or posterior lateral medulla oblongata, likely syphilitic in origin. Hence it is also called the alternating medulla oblongata syndrome.

<span class="mw-page-title-main">Post viral cerebellar ataxia</span> Medical condition

Post-viral cerebellar ataxia also known as acute cerebellitis and acute cerebellar ataxia (ACA) is a disease characterized by the sudden onset of ataxia following a viral infection. The disease affects the function or structure of the cerebellum region in the brain.

<span class="mw-page-title-main">Autosomal recessive cerebellar ataxia type 1</span> Hereditary ataxia that has material basis in autosomal recessive inheritance

Autosomal recessive cerebellar ataxia type 1 (ARCA1) is a condition characterized by progressive problems with movement. Signs and symptoms of the disorder first appear in early to mid-adulthood. People with this condition initially experience impaired speech (dysarthria), problems with coordination and balance (ataxia), or both. They may also have difficulty with movements that involve judging distance or scale (dysmetria). Other features of ARCA1 include abnormal eye movements (nystagmus) and problems following the movements of objects with their eyes. The movement problems are slowly progressive, often resulting in the need for a cane, walker, or wheelchair.

Dyssynergia is any disturbance of muscular coordination, resulting in uncoordinated and abrupt movements. This is also an aspect of ataxia. It is typical for dyssynergic patients to split a movement into several smaller movements. Types of dyssynergia include Ramsay Hunt syndrome type 1, bladder sphincter dyssynergia, and anal sphincter dyssynergia.

<span class="mw-page-title-main">Gómez–López-Hernández syndrome</span> Medical condition

Gómez–López-Hernández syndrome (GLH) or cerebellotrigeminal-dermal dysplasia is a rare neurocutaneous (Phakomatosis) disorder affecting the trigeminal nerve and causing several other neural and physical abnormalities. Gómez–López-Hernández syndrome has been diagnosed in only 34 people. Cases of Gómez–López-Hernández syndrome may be under-reported as other diseases share the characteristics of cerebellar malformation shown in Gómez–López-Hernández syndrome. Gómez–López-Hernández syndrome was first characterized in 1979.

<span class="mw-page-title-main">Cerebellar degeneration</span> Medical condition

Cerebellar degeneration is a condition in which cerebellar cells, otherwise known as neurons, become damaged and progressively weaken in the cerebellum. There are two types of cerebellar degeneration; paraneoplastic cerebellar degeneration, and alcoholic or nutritional cerebellar degeneration. As the cerebellum contributes to the coordination and regulation of motor activities, as well as controlling equilibrium of the human body, any degeneration to this part of the organ can be life-threatening. Cerebellar degeneration can result in disorders in fine movement, posture, and motor learning in humans, due to a disturbance of the vestibular system. This condition may not only cause cerebellar damage on a temporary or permanent basis, but can also affect other tissues of the central nervous system, those including the cerebral cortex, spinal cord and the brainstem.

References

  1. ↑ "dysmetria – definition of dysmetria in the Medical dictionary – by the Free Online Medical Dictionary, Thesaurus and Encyclopedia".
  2. ↑ Schmahmann JD, Weilburg JB, Sherman JC (2007). "The neuropsychiatry of the cerebellum – insights from the clinic". Cerebellum. 6 (3): 254–67. doi:10.1080/14734220701490995. PMID   17786822. S2CID   14176315.
  3. ↑ Manto M (2009). "Mechanisms of human cerebellar dysmetria: experimental evidence and current conceptual bases". J Neuroeng Rehabil. 6: 10. doi: 10.1186/1743-0003-6-10 . PMC   2679756 . PMID   19364396.
  4. 1 2 3 Manto MU (2005). "The wide spectrum of spinocerebellar ataxias (SCAs)". Cerebellum. 4 (1): 2–6. doi:10.1080/14734220510007914. PMID   15895552. S2CID   5311177.
  5. 1 2 3 4 5 6 7 8 9 Schmahmann JD (2004). "Disorders of the cerebellum: ataxia, dysmetria of thought, and the cerebellar cognitive affective syndrome". J Neuropsychiatry Clin Neurosci. 16 (3): 367–78. doi:10.1176/jnp.16.3.367. PMID   15377747.
  6. ↑ Mario Manto (2010). Cerebellar Disorders: A Practical Approach to Diagnosis and Management. Cambridge, UK: Cambridge University Press. ISBN   978-0-521-87813-5. OCLC   456170457.
  7. 1 2 3 Townsend J, Courchesne E, Covington J, et al. (July 1999). "Spatial attention deficits in patients with acquired or developmental cerebellar abnormality". J. Neurosci. 19 (13): 5632–43. doi: 10.1523/JNEUROSCI.19-13-05632.1999 . PMC   6782343 . PMID   10377369.
  8. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 Vahdat S, Maghsoudi A, Haji Hasani M, Towhidkhah F, Gharibzadeh S, Jahed M (October 2006). "Adjustable primitive pattern generator: a novel cerebellar model for reaching movements". Neurosci. Lett. 406 (3): 232–4. doi:10.1016/j.neulet.2006.07.038. PMID   16930835. S2CID   9679947.
  9. 1 2 Trillenberg P, Sprenger A, Petersen D, Kömpf D, Heide W, Helmchen C (2007). "Functional dissociation of saccade and hand reaching control with bilateral lesions of the medial wall of the intraparietal sulcus: implications for optic ataxia". NeuroImage. 36 (Suppl 2): T69–76. doi:10.1016/j.neuroimage.2007.03.038. PMID   17499172. S2CID   43241167.
  10. ↑ Indovina I, Sanes JN (October 2001). "Combined visual attention and finger movement effects on human brain representations". Exp Brain Res. 140 (3): 265–79. doi:10.1007/s002210100796. PMID   11681302. S2CID   14364368.
  11. 1 2 Iwamoto Y, Yoshida K (June 2002). "Saccadic dysmetria following inactivation of the primate fastigial oculomotor region". Neurosci. Lett. 325 (3): 211–5. doi:10.1016/S0304-3940(02)00268-9. PMID   12044658. S2CID   35443728.
  12. ↑ Manto, M.; Godaux, E.; Jacquy, J. (January 1994). "Cerebellar hypermetria is larger when the inertial load is artificially increased". Annals of Neurology. 35 (1): 45–52. doi:10.1002/ana.410350108. ISSN   0364-5134. PMID   8285591. S2CID   19328973.
  13. ↑ Leggio, M.; Molinari, M. (February 2015). "Cerebellar sequencing: a trick for predicting the future". Cerebellum (London, England). 14 (1): 35–38. doi:10.1007/s12311-014-0616-x. ISSN   1473-4230. PMID   25331541. S2CID   15713873.
  14. 1 2 3 4 Crowdy KA, Kaur-Mann D, Cooper HL, Mansfield AG, Offord JL, Marple-Horvat DE (September 2002). "Rehearsal by eye movement improves visuomotor performance in cerebellar patients". Exp Brain Res. 146 (2): 244–7. doi:10.1007/s00221-002-1171-0. PMID   12195526. S2CID   7703727.
  15. 1 2 3 4 5 Hooper J, Taylor R, Pentland B, Whittle IR (April 2002). "A prospective study of thalamic deep brain stimulation for the treatment of movement disorders in multiple sclerosis". Br J Neurosurg. 16 (2): 102–9. doi:10.1080/02688690220131769. PMID   12046727. S2CID   30644098.
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