Ataxia

For other uses, see Ataxia (disambiguation).

of movement, particularly in the extremities. There is

overshooting with nger to nose testing, and heel to shin
testing; thus, dysmetria is evident.[2] Impairments with
alternating movements (dysdiadochokinesia), as well as
dysrhythmia, may also be displayed. There may also be
tremor of the head and trunk (titubation) in individuals
with cerebellar ataxia.[2]

Ataxia (from Greek - [a negative prex] + - [order] = lack of order) is a neurological sign consisting
of lack of voluntary coordination of muscle movements.
Ataxia is a non-specic clinical manifestation implying
dysfunction of the parts of the nervous system that coordinate movement, such as the cerebellum. Several pos- It is thought that dysmetria is caused by a decit in the
sible causes exist for these patterns of neurological dys- control of interaction torques in multijoint motion.[4] Infunction. Dystaxia is a mild degree of ataxia.[1]
teraction torques are created at an associated joint when
the primary joint is moved. For example, if a movement
required reaching to touch a target in front of the body,
exion at the shoulder would create a torque at the elbow,
1 Types
while extension of the elbow would create a torque at
the wrist. These torques increase as the speed of move1.1 Cerebellar
ment increases and must be compensated and adjusted
for to create coordinated movement. This may, thereThe term cerebellar ataxia is used to indicate ataxia that fore, explain decreased coordination at higher movement
is due to dysfunction of the cerebellum. The cerebel- velocities and accelerations.
lum is responsible for integrating a signicant amount of
neural information that is used to coordinate smoothly
Dysfunction of the vestibulocerebellum
ongoing movements and to participate in motor plan(occulonodular lobe) impairs the balance and
ning. Although ataxia is not present with all cerebelthe control of eye movements. This presents itself
lar lesions, many conditions aecting the cerebellum
with postural instability, in which the person tends
do produce ataxia.[2] People with cerebellar ataxia may
to separate his/her feet upon standing, to gain a
have trouble regulating the force, range, direction, velocwider base and to avoid titubation (bodily oscillaity and rhythm of muscle contractions.[3] This results in
tions tending to be forward-backward ones). The
a characteristic type of irregular, uncoordinated moveinstability is therefore worsened when standing with
ment that can manifest itself in many possible ways,
the feet together, regardless of whether the eyes
such as asthenia, asynergy, delayed reaction time, and
are open or closed. This is a negative Rombergs
dyschronometria. Individuals with cerebellar ataxia could
test, or more accurately, it denotes the individuals
also display instability of gait, diculty with eye moveinability to carry out the test, because the individual
ments, dysarthria, dysphagia, hypotonia, dysmetria and
feels unstable even with open eyes.
dysdiadochokinesia.[2] These decits can vary depending
on which cerebellar structures have been damaged, and
Dysfunction of the spinocerebellum (vermis and
whether the lesion is bilateral or unilateral.
associated areas near the midline) presents itself
with a wide-based drunken sailor gait (called trunPeople with cerebellar ataxia may initially present with
cal ataxia),[5] characterised by uncertain starts and
poor balance, which could be demonstrated as an instops, lateral deviations, and unequal steps. As a reability to stand on one leg or perform tandem gait. As
sult of this gait impairment, falling is a concern in
the condition progresses, walking is characterized by a
patients
with ataxia. Studies examining falls in this
widened base and high stepping, as well as staggering
[2]
population
show that 74-93% of patients have fallen
and lurching from side to side. Turning is also probat
least
once
in the past year and up to 60% admit to
lematic and could result in falls. As cerebellar ataxia
[6][7]
fear
of
falling.
becomes severe, great assistance and eort are needed
to stand and walk.[2] Dysarthria, an impairment with articulation, may also be present and is characterized by
scanning speech that consists of slower rate, irregular
rhythm and variable volume.[2] There may also be slurring of speech, tremor of the voice and ataxic respiration. Cerebellar ataxia could result with incoordination

Dysfunction of the cerebrocerebellum (lateral

hemispheres) presents as disturbances in carrying
out voluntary, planned movements by the extremities (called appendicular ataxia).[5] These include:
intention tremor (coarse trembling, accentu1

CAUSES

ated over the execution of voluntary move- positive Rombergs test. Worsening of the nger-pointing
ments, possibly involving the head and eyes as test with the eyes closed is another feature of sensory
well as the limbs and torso);
ataxia. Also, when the patient is standing with arms
peculiar writing abnormalities (large, unequal and hands extended toward the physician, if the eyes are
closed, the patients nger will tend to fall down and
letters, irregular underlining);
then be restored to the horizontal extended position by
a peculiar pattern of dysarthria (slurred sudden muscular contractions (the ataxic hand).
speech, sometimes characterised by explosive
variations in voice intensity despite a regular
rhythm).
inability to perform rapidly alternating movements, known as dysdiadochokinesia. This
could involve rapidly switching from pronation
to supination of the forearm. Movements
become more irregular with increases of
speed.[8]

1.3 Vestibular

The term vestibular ataxia is employed to indicate ataxia

due to dysfunction of the vestibular system, which in
acute and unilateral cases is associated with prominent
vertigo, nausea and vomiting. In slow-onset, chronic bilateral cases of vestibular dysfunction, these characteris inability to judge distances or ranges of move- tic manifestations may be absent, and dysequilibrium may
ment. This is known as dysmetria and is often be the sole presentation.
seen as undershooting, hypometria, or overshooting, hypermetria, the required distance
or range to reach a target. This is sometimes
seen when a patient is asked to reach out and 2 Causes
touch someones nger or touch his or her own
nose.[8]
The three types of ataxia have overlapping causes, and
the rebound phenomenon, also known as the therefore can either coexist or occur in isolation.
loss of the check reex is also sometimes seen
in patients with cerebellar ataxia. For example, when a patient is exing his or her elbow 2.1 Focal lesions
isometrically against a resistance. When the
resistance is suddenly removed without warn- Any type of focal lesion of the central nervous system
ing, the patients arm may swing up and even (such as stroke, brain tumour, multiple sclerosis) will
strike themselves. With an intact check reex, cause the type of ataxia corresponding to the site of the
the patient will check and activate the oppos- lesion: cerebellar if in the cerebellum, sensory if in the
ing triceps to slow and stop the movement.[8] dorsal spinal cord (and rarely in the thalamus or parietal

1.2

Sensory

The term sensory ataxia is employed to indicate ataxia

due to loss of proprioception, the loss of sensitivity to the
positions of joint and body parts. This is generally caused
by dysfunction of the dorsal columns of the spinal cord,
because they carry proprioceptive information up to the
brain. In some cases, the cause of sensory ataxia may
instead be dysfunction of the various parts of the brain
which receive positional information, including the cerebellum, thalamus, and parietal lobes.
Sensory ataxia presents itself with an unsteady stomping gait with heavy heel strikes, as well as a postural instability that is usually worsened when the lack of proprioceptive input cannot be compensated for by visual input,
such as in poorly lit environments.
Physicians can nd evidence of sensory ataxia during
physical examination by having the patient stand with
his/her feet together and eyes shut. In aected patients,
this will cause the instability to worsen markedly, producing wide oscillations and possibly a fall. This is called a

lobe), vestibular if in the vestibular system (including the

vestibular areas of the cerebral cortex).

2.2 Exogenous substances

Exogenous substances that cause ataxia mainly do so
because they have a depressant eect on central nervous system function. The most common example is
ethanol, which is capable of causing reversible cerebellar and vestibular ataxia. Other examples include various prescription drugs (e.g. most antiepileptic drugs
have cerebellar ataxia as a possible adverse eect),
Lithium level over 1.5mEq/L, cannabis ingestion[9] and
various other recreational drugs (e.g. ketamine, PCP
or dextromethorphan, all of which are NMDA receptor antagonists that produce a dissociative state at high
doses). A further class of pharmaceuticals which can
cause short term ataxia, especially in high doses are
the benzodiazepines.[10][11] Exposure to high levels of
methylmercury, through consumption of sh with high
mercury concentrations, is also a known cause of ataxia
and other neurological disorders.[12]

2.9

Arnold-Chiari malformation

2.3

Radiation poisoning

Ataxia can be induced as a result of severe acute radiation

poisoning with an absorbed dose of more than 30 Grays.

3
condition is the rare fragile X-associated tremor/ataxia
syndrome.

2.9 Arnold-Chiari malformation

Arnold-Chiari malformation is a malformation of the

brain. It consists of a downward displacement of the
Vitamin B12 deciency may cause, among several neuro- cerebellar tonsils and the medulla through the foramen
logical abnormalities, overlapping cerebellar and sensory magnum, sometimes causing hydrocephalus as a result of
obstruction of cerebrospinal uid outow.
ataxia.

2.4

Vitamin B12 deciency

2.5

Hypothyroidism

Symptoms of neurological dysfunction may be the presenting feature in some patients with hypothyroidism.
These include reversible cerebellar ataxia, dementia,
peripheral neuropathy, psychosis and coma. Most of
the neurological complications improve completely after
thyroid hormone replacement therapy.[13][14]

2.6

Causes of isolated sensory ataxia

Peripheral neuropathies may cause generalised or localised sensory ataxia (e.g. a limb only) depending on
the extent of the neuropathic involvement. Spinal disorders of various types may cause sensory ataxia from
the lesioned level below, when they involve the dorsal
columns[15][16][17]

2.7

Wilsons disease is an autosomal-recessive gene disorder

whereby an alteration of the ATP7B gene results in an
inability to properly excrete copper from the body.[18]
Copper accumulates in the nervous system and liver and
can cause ataxia as well as other neurological and organ
impairments.[19]

2.11 Gluten ataxia

Gluten ataxia is a gluten-related disorder, a wide spectrum of disorders marked by an abnormal immunological
response to gluten. Like celiac disease, it is an autoimmune disease.[20] With gluten ataxia, damage takes place
in the cerebellum, the balance center of the brain that
controls coordination and complex movements like walking, speaking and swallowing.[21] Gluten ataxia is the single most common cause of sporadic idiopathic ataxia.[22]

Non-hereditary cerebellar degenera- Gluten ataxia is an immune-mediated disease triggered

by the ingestion of gluten in genetically susceptible indition

Non-hereditary causes of cerebellar degeneration include chronic ethanol abuse, head injury, paraneoplastic
cerebellar degeneration, high altitude cerebral oedema,
coeliac disease, normal pressure hydrocephalus and
cerebellitis.

2.8

2.10 Wilsons disease

Hereditary ataxias

Ataxia may depend on hereditary disorders consisting

of degeneration of the cerebellum and/or of the spine;
most cases feature both to some extent, and therefore
present with overlapping cerebellar and sensory ataxia,
even though one is often more evident than the other.
Hereditary disorders causing ataxia include autosomal
dominant ones such as spinocerebellar ataxia, episodic
ataxia, and dentatorubropallidoluysian atrophy, as well as
autosomal recessive disorders such as Friedreichs ataxia
(sensory and cerebellar, with the former predominating)
and Niemann Pick disease, ataxia-telangiectasia (sensory and cerebellar, with the latter predominating), and
abetalipoproteinaemia. An example of X-linked ataxic

viduals. It should be considered in the dierential diagnosis of all patients with idiopathic sporadic ataxia. Early
diagnosis and treatment with a gluten free diet can improve ataxia and prevent its progression. Readily available and sensitive markers of gluten ataxia include antigliadin antibodies. Immunoglobulin A (IgA) deposits
against transglutaminase 2 (TG2) in the small bowel and
at extraintestinal sites are proving to be additionally reliable and perhaps more specic markers of the whole
spectrum of gluten sensitivity. They may also hold the
key to its pathogenesis.[23]
Gluten ataxia is dened as sporadic cerebellar ataxia associated with the presence circulating antigliadin antibodies
and in the absence of an alternative etiology for ataxia.[24]

2.12 Sodium-potassium pump

Misfunction of the sodium-potassium pump may be a factor in some ataxias. The Na+
-K+
pump has been shown to control and set the intrinsic activity mode of cerebellar Purkinje neurons.[25] This sug-

gests that the pump might not simply be a homeostatic,

housekeeping molecule for ionic gradients; but could be
a computational element in the cerebellum and the brain.
Indeed, an ouabain block of Na+
-K+
pumps in the cerebellum of a live mouse results in it
displaying ataxia and dystonia.[26] Ataxia is observed for
lower ouabain concentrations, dystonia is observed at
higher ouabain concentrations.

OTHER USES

known whether the improvements are due to adaptations

in the cerebellum or compensation by other areas of the
brain.[30]

The treatment of ataxia and its eectiveness depend on

the underlying cause. Treatment may limit or reduce the
eects of ataxia, but it is unlikely to eliminate them entirely. Recovery tends to be better in individuals with a
single focal injury (such as stroke or a benign tumour),
compared to those who have a neurological degenerative
condition.[27] A review of the management of degenerative ataxia was published in 2009.[28]

Decomposition, simplication, or slowing of multijoint movement may also be an eective strategy that
therapists may use to improve function in patients
with ataxia.[32] Training likely needs to be intense and
focusedas indicated by one study performed with
stroke patients experiencing limb ataxia who underwent
intensive upper limb retraining.[33] Their therapy consisted of constraint-induced movement therapy which resulted in improvements of their arm function.[33] Treatment should likely include strategies to manage diculties with everyday activities such as walking. Gait aids
(such as a cane or walker) can be provided to decrease
the risk of falls associated with impairment of balance or
poor coordination. Severe ataxia may eventually lead to
the need for a wheelchair. To obtain better results, possible coexisting motor decits need to be addressed in addition to those induced by ataxia. For example, muscle
weakness and decreased endurance could lead to increasing fatigue and poorer movement patterns.

The movement disorders associated with ataxia can be

managed by pharmacological treatments and through
physical therapy and occupational therapy to reduce
disability.[29] Some drug treatments that have been used
to control ataxia include: 5-hydroxytryptophan (5-HTP),
idebenone, amantadine, physostigmine, L-carnitine or
derivatives, trimethoprimsulfamethoxazole, vigabatrin,
phosphatidylcholine, acetazolamide, 4-aminopyridine,
buspirone, and a combination of coenzyme Q10 and
vitamin E.[28]

There are several assessment tools available to therapists and health care professionals working with patients
with ataxia. The International Cooperative Ataxia Rating
Scale (ICARS) is one of the most widely used and has
been proven to have very high reliability and validity.[34]
Other tools that assess motor function, balance and coordination are also highly valuable to help the therapist
track the progress of their patient, as well as to quantify
the patients functionality. These tests include, but are not
limited to:

Treatment

Physical therapy requires a focus on adapting activity and

facilitating motor learning for retraining specic functional motor patterns.[30] A recent systematic review suggested that physical therapy is eective, but there is only
moderate evidence to support this conclusion.[31] The
most commonly used physical therapy interventions for
cerebellar ataxia are vestibular habituation, Frenkel Exercises, proprioceptive neuromuscular facilitation (PNF),
and balance training; however, therapy is often highly individualized and gait and coordination training are large
components of therapy.
Current research suggests that, if a person is able to walk
with or without a mobility aid, physical therapy should
include an exercise program addressing ve components:
static balance, dynamic balance, trunk-limb coordination, stairs, and contracture prevention. Once the physical
therapist determines that the individual is able to safely
perform parts of the program independently, it is important that the individual be prescribed and regularly
engage in a supplementary home exercise program that
incorporates these components to further improve long
term outcomes. These outcomes include balance tasks,
gait, and individual activities of daily living. While the
improvements are attributed primarily to changes in the
brain and not just the hip and/or ankle joints, it is still un-

The Berg Balance Scale

Tandem Walking (to test for Tandem gaitability)
Scale for the Assessment and Rating of Ataxia[35]
tapping tests The person must quickly and repeatedly tap their arm or leg while the therapist monitors
the amount of dysdiadochokinesia.[36]
nger-nose testing[36] This test has several variations including nger-to-therapists nger, nger-tonger, and alternate nose-to-nger.[37]

4 Other uses
The term ataxia is sometimes used in a broader sense to
indicate lack of coordination in some physiological process. Examples include optic ataxia (lack of coordination between visual inputs and hand movements, resulting
in inability to reach and grab objects) and ataxic respiration (lack of coordination in respiratory movements,
usually due to dysfunction of the respiratory centres in
the medulla oblongata). Optic ataxia may be caused by

5
lesions to the posterior parietal cortex, which is respon- [9] Inadvertent Ingestion of Marijuana --- Los Angeles, California, 2009. Retrieved 3 September 2009.
sible for combining and expressing positional information and relating it to movement. Outputs of the posterior
[10] Browne TR (May 1976). Clonazepam. A review of
parietal cortex include the spinal cord, brain stem motor
a new anticonvulsant drug. Arch. Neurol. 33 (5):
pathways, pre-motor and pre-frontal cortex, basal gan32632. doi:10.1001/archneur.1976.00500050012003.
glia and the cerebellum. Some neurons in the posterior
PMID 817697.
parietal cortex are modulated by intention. Optic ataxia
is usually part of Balints syndrome, but can be seen in [11] Gaudreault P, Guay J, Thivierge RL, Verdy I (1991).
Benzodiazepine poisoning. Clinical and pharmacologiisolation with injuries to the superior parietal lobule, as
cal considerations and treatment. Drug Saf 6 (4): 247
it represents a disconnection between visual-association
65. doi:10.2165/00002018-199106040-00003. PMID
[38]
cortex and the frontal premotor and motor cortex.
1888441.

See also
Ataxic cerebral palsy
Spinocerebellar ataxia

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EXTERNAL LINKS

[35] Schmitz-Hbsch T, du Montcel ST, Baliko L, Berciano

J, Boesch S, Depondt C et al. (June 2006). Scale
for the assessment and rating of ataxia: development
of a new clinical scale. Neurology 66 (11): 1717
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Gijn J, Wokke JH (January 1994). Measuring ataxia:
quantication based on the standard neurological examination. J. Neurol. Neurosurg. Psychiatr. 57 (1): 22
6. doi:10.1136/jnnp.57.1.22. PMC 485035. PMID
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Harrell Center. Retrieved 7 May 2012.
[38] Vallar G (July 2007). Spatial neglect, Balint-Homes and
Gerstmanns syndrome, and other spatial disorders. CNS
Spectr 12 (7): 52736. PMID 17603404.

7 Further reading
Pagon RA, Bird TD, Dolan CR, Stephens K, Adam
MP, Bird TD (1998). Hereditary Ataxia Overview
(last revision 2012). All GeneReview. PMID
20301317.
Manto M, Gruol D, Schmahmann J, Koibuchi N,
Rossi F (2013). Handbook of the Cerebellum and
Cerebellar Disorders. Springer.

8 External links
Friedreichs Ataxia Research Alliance (FARA)
Ataxia Connect Social Network
Ataxia UK, including guidelines
Brasil, Rio Grande do Sul - Associao dos Amigos,
Parentes e Portadores de Ataxias Dominantes
Canadian Association for Familial Ataxias - Claude
St-Jean Foundation
International Ataxia Awareness Day
LivingWithAtaxia Forums & Community
Overview at National Institute of Neurological Disorders and Stroke (NINDS)
Rochester Ataxia Foundation, Rochester, NY
The latest news and research on Ataxia
US National Ataxia Foundation
University of Minnesota Ataxia Center
Video demonstration of ataxic gait

7
Gluten Ataxia
Range of Neurologic Disorders in Patients With
Celiac Disease
The Cerebellum
Cerebellum and Ataxias

9 TEXT AND IMAGE SOURCES, CONTRIBUTORS, AND LICENSES

Text and image sources, contributors, and licenses

9.1

Text

Ataxia Source: http://en.wikipedia.org/wiki/Ataxia?oldid=644428974 Contributors: Eloquence, ErdemTuzun, Matusz, Heron, Edward,

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