Ataxias Neuro Condition Detailed

You might also like

Download as pptx, pdf, or txt
Download as pptx, pdf, or txt
You are on page 1of 80

Neurology

Because studying
the way of the mind
will literally blow
your own mind!
CONTENTS
Anatomy and Function of Cerebellum

Definition of Ataxia

Causes of ataxia

Different types of ataxia

Assessment

Treatment

CEREBELLUM

The cerebellum is located in the
area of the hindbrain which is
located at the back of the brain,
underlying the occipital and
temporal lobes of the cerebral
cortex



lies in front of the pons, behind
the brain stem. The cerebellum
is comprised of small lobes and
receives information from the
balance system of the inner ear,
sensory nerves, and the
auditory and visual systems.
STRUCTURES OF THE CEREBELLUM
There are three functional subdivisions of the
cerebellum:
A. The flocculonodular lobe is called the
vestibulocerebellum or "archicerebellum."
B. The spinocerebellum (paleocerebellum) includes the
anterior lobe and paramedian lobules.
C. The neocerebellum(pontocerebellum) makes up the
lateral hemispheres.

1. Archicerebellum: Main function is the
maintenance of equilibrium. Connected to the
vestibular apparatus through the vestibulo-cerellar and
cerebello-vestibular tracts.

o If lesions are present it will lead to disturbance of
equilibrium of the
body which is manifested by unsteadiness,
such as:
oHypotonia
- Standing: excessive swaying (truncal ataxia)
- Walking: wide-base or staggering (drunken-gait)




2. Spinocerebllum: Main function is the maintenance
and control of muscle tone. Connected to the spinal cord
through the ventral and dorsal spinocerebellar tracts which
gets feedback of propeuception impulses.
o If lesions are present, it will lead to disturbance of the
muscle tone


3. Neocerebellum: Recent part of development and
forms most of the bulk of the hemispheres. Its main
function is control muscle coordination and regulation of the
fine delicate voluntary motor activity.

o if lesions are present, it will lead to incoordination
of voluntary motor activities in the form of:
1. Nystagmus: involuntary eye movement.
2. Dysarthria: in the form of staccato speech (explosive,
interrupted speech).
3. Nodding of the head.
4. Titubation of the trunk and nodding of the head (the act
of staggering)
5. Intention kinetic tremors in the extremities.
6. Deviation of the body towards the affected side in
unilateral lesions or zigzag gait in bilateral lesions.
7. Asynrgia (lack of coordination between multiple joints)
8. Hypotonia.

The cerebellum is the part of the brain most responsible for
balance, posture, and the coordination of movement
subconsciously. The cerebellum does not initiate
movements but contributes to precision, accurate timing of
movement and learning of motor skills.

The cerebellum plays a vital role in the integration,
regulation, and coordination of motor processes.

Damage to this region can result in loss of balance, loss of
coordinated movements, hypotonia, and errors in
movement when attempting to produce a specific response.

The cerebellum is concerned with at least three major
functions:
1. The first function is an association with movements that are
properly grouped for the performance of selective responses
that require specific adjustments. This is also referred to as
synergy of movement.
2. The second function includes the maintenance of upright
posture with respect to ones position in space.
3. The third function concerns the maintenance of the tension or
firmness also refers to the muscle tone.


ATAXIA
Definition : Incoordination of voluntary motor activity
with or without dis-equilibration in the absence of
motor weakness.
o Result from defective timing of sequential contractions of agonist
and antagonist muscles due to disturbance in the smooth
performance of voluntary motor acts.
o Movements erratic in speed, range, force, and timing due to
absence of cerbellar inhibitory and modulating influences.
o Ataxia may affect limbs, trunk, gait, may be acute onset ,episodic or
progressive
Ataxia includes:
o Asynergia: defective coordination between parts, as muscles or
limbs, that normally act in unity.
o Dysdiadochokinesia: Inability to make alternating movements
exhibiting a rapid change of motion.
o Dysarthria : is a motor speech disorder. The muscles become weak,
move slowly, or not move at all.
o Wide based stance and gait characterized by staggering and
impaired tandem walking.
o Trunk instability -falls in any directions.
o Dysmetria: inability to judge distance of an object.

TYPES :
1. Cerebellar ataxia.

2. Sensory ataxia.

3. Vestibular ataxia.

4. Combined ataxia.

5. Hysterical ataxia.

CEREBELLAR ATAXIA
Causes:

I. Herido familial:

1. Friedreich's ataxia:
o It occurs in the 1st decade of life. Gradual onset and slowly progressive
course. Progressive damage to the nervous system resulting in
symptoms ranging from gait disturbance and speech problems to heart
diseases.

o Positive family history is common as it is inherited as an autosomal
recessive disease (caused by having two copies of a faulty gene, one
inherited from each parent).

o Pathologically there is degeneration of:
Cerebellum specially the archicerebellum & the spinocerebellar tracts.
Pyramidal tracts.
Posterior columns.
Peripheral nerves.
It presents with:
- Progressive cerebellar ataxia mainly of the archi cerebellar type i.e. disturbance
of equilibrium in the form of gait disturbance and truncal ataxia.

- Diminished or lost deep reflexes with positive Babinski sign. The loss of reflexes
is due to the degeneration of the peripheral nerves, posterior columns and
cerebellum.

- The positive Babinski sign is due to pyramidal lesion. Stock and glove
hyposthesia with lost ankle reflex and preserved knee reflex due to
degeneration of the peripheral nerves.

- Impairment of superficial and deep sensations (movement, position
and vibration), due to degeneration of the posterior columns.

- Skeletal deformities

- Congenital heart disease and E.C.G. changes.
Autosomal Recessive Cerebellar Ataxia
2. Marie's Ataxia

1. It occurs in the 2nd and 3rd decades of life. Gradual onset and
slowly progressive course.
2. Caused by bilateral cortical atrophy of the cerebellum.
3. Positive family history is common as it is inherited as an
autosomal dominant disease
o (Caused by having one copy of the faulty gene, inherited
from only one of the parents).


Pathologically there is degeneration of:
- Cerebellum specially the neo-cerebellum (dentate nucleus).
- Pyramidal tracts.

It presents with:
o Progressive manifestations of neocerebellar degeneration.
o tremors of the extremities.
o Staccato speech.
o Nystagmus.
o exaggerated deep reflexes.
o positive Babinski sign due to pyramidal tract degeneration.
o Mental Impairments
o Ocular nerve paralysis
o Mental Impairment

Gait:
Zigzag or stamping gait.
Wide BOS gait (drunker gait).
Deviation towards affected side.


MRI of a patient with autosomal dominant
cerebellar ataxia
II. Symptomatic:

1. Congenital:
Basilar impression.
Arnold Chiari syndrome.

2. Infective:
Encephalitis
Cerebellar abscess or tuberculoma.

3. Vascular:
Superior, middle and inferior cerebellar artery occlusion.

4. Toxic:
- Alcohol.
- Barbiturates: are drugs that act as CNS depressants.
- Hydantoins: or glycolylurea a colorless solid that arises from the reaction
of glycolic acid and urea.

5. Neoplastic:
- Medulloblastoma (tumour of the vermis).
- Astrocytoma (tumour of the hemisphere).

6. Transient ischemic attack:
Caused by a temporary decrease in blood supply to part of
your brain, most TIAs last only a
few minutes. Loss of coordination and other signs and
symptoms of a TIA are temporary.

7. Stroke:
When the blood supply to a part of your brain is interrupted or
severely reduced, depriving
brain tissue of oxygen and nutrients, brain cells begin to die.


III. Idiopathic: Delayed cortical cerebellar degeneration in old
age.




Clinical picture of cerebellar ataxia:

Early symptoms of ataxia can include:
poor coordination in the arms and legs
Dysarthria :staccato speech
Walking may become difficult or even impossible

1. Incoordination of movements of different muscles in the form of:

a) Nystagmus in the eyes
b) Staccato speech.
c) Nodding of the head.
d) Titubation of the trunk.
e) Kinetic tremors of the limbs.

2. Hypotonia and hyporeflexia of the affected muscles.

3. Gait disturbance: Wide base or drunken gait in archicerebellar lesions.

4. Positive tests: used by the neurologist to detect cerebellar ataxia.


SENSORY ATAXIA
DEFINITION : It is ataxia due to loss of the proprioceptive (deep)
sensations, resulting in poorly judged movements at any point in
their pathway.

CAUSES:
1. Peripheral nerve: peripheral neuropathy specially diabetic,
alcoholic and nutritional.
2. Posterior root: tabes dorsalis!
3. Posterior column: subacute combined degeneration.
4. Medial lemniscus: brain stem lesions.
5. Thalamus: thalamic syndrome.
6. Cortical sensory area: parietal lobe lesions.
Clinical Feature:

1. Kinetic tremors as tested by finger-to-nose or finger-to-finger tests
appear only on closure of the eyes.

2. Rhomberg's test: when the patient stands with his feet close
together & his eyes closed, his body sways & he may fall if not
supported.

3. Stamping gait: heavy strike of the ground on walking due to lost
deep sensation.

4. Deep sensory loss.

5. Hypotonia & hyporeflexia.
VESTIBULAR ATAXIA
Vestibular Ataxia is due to lesions of the vestibular division of the 8
th
nerve.

CAUSES :
1) Meniere's disease: disorder of the Inner ear, affects hearing and balance.
characterized by incidents of vertigo, Low-pitched tinnitus (ringing)
and fluctuating hearing loss.
2) Labyrinthitis: form of unilateral vestibular dysfunction, caused by viral
infection.
3) Acoustic neuroma: Intracranial tumor of the Myelin-forming cells of the
Vestibulocochlear Nerve (8th cranial nerve).

Clinical Feature:
1. Vertigo, tinnitus, deafness.
2. Vestibular nystagmus: involuntary eye movements in relation to head
movements.
3. Impaired tests for vestibular function.

HYSTERICAL ATAXIA
Hysterical ataxia: Weakening of the muscle sense and increased
sensibility of the skin, in hysteria.

Clinical Feature:
A loss of control over voluntary movements in walking or standing, although
the involved muscles function normally when the person is lying or sitting.

FRONTAL ATAXIA
Frontal ataxia (also known as gait apraxia)
is observed when tumors, abscesses, cerebro vascular accidents and
normal pressure hydrocephalus effect the frontal area.
Clinical features
o Patient has difficulties standing erect
o Even with use of support, patient tends to lean towards
hyperextension
o Patient's legs are in scissors-cross position during walking and there
is incoordination between the legs and trunk
o Ataxia is accompanied by frontal dementia, urinary incontinence,
frontal release signs and perseveration.

Clinical Differences Between Basic Types of Ataxia


Assessment of Ataxia
1. History taking
2. Cognitive function
3. Speech assessment
4. Muscle tone assessment
5. Deep tendon reflexes
6. Muscle power
7. ROM
8. Muscle length
9. Long and round measurement
10. Sensory assessment
11. Coordination assessment
12. Balance
13. Posture
14. Gait

Muscle tone Assessment

Clinical Feature:
Hypotonia, some cases normal.

Explanation:
Consider the feedback pathways of the cerebellum. The efferent connections of
the reticular formation to the cerebellar cortex ( part of an automatic
regulatory mechanism) complete a feedback circuit linking these two
important structures for the regulation of posture and muscle tone. Disruption
of any component of this network can lead to significant motor deficits such
as, a disorder of movement on the side of the body ipsilateral to the lesion
emerges. The two types of such cerebellar disorders that have been described
include ataxia (i.e., errors in the range, rate, force, and direction of movement
resulting in loss of muscle coordination in producing smooth movements) and
hypotonia (i.e., diminution of muscle tone).


Muscle tone: Assessed by passively moving the limbs or
trunk through the normal range of movement whilst the patient
remains relaxed
1. Normal
2. Increased hypertonic due to spasticity or rigidity
3. Decreased - hypotonic

Deep Tendon Reflexes

Clinical Feature:
o Hyporeflexia

Involuntary contractions or tendon reflexes are increased in
UMNL and decreased in LMNL
6 reflexes can be tested using this grading system
Ankle, knee, biceps, supinator, tricepsand finger reflexes


Grade Grading of reflexes (Fuller, 1999)
0 Absent
Present but only with
reinforcement
1+ Present but depressed
2+ Normal
3+ Increased tone
4+ Clonus
Muscle Power
Clinical Feature:
o While muscle power may remain unaffected, fatigue in the
affected limbs can affect endurance.

Power: 0-5 scale

Group muscle testing:
o Upper limb
o Lower limb
o Trunk


ROM: Normal

Muscle length: If theres any limitation in ROM or
deformity theres going to be muscle length
shortening.

Long and round measurement: Normal



Sensory assessment
Superficial
1. Pain: Prick, Pinch
2. Temperature: Cold, Hot
3.Light touch : Cotton stroke
Deep
1. Joint Position: Instruct to close the eyes and put one limb in a
certain position and tell the patient to make the same position with
the other limb.
2. Joint movement: Demonstrate which movements you are going
to test ex: (up or down). Instruct to close the eyes and tell the
therapist what motion has been done.
3. Vibration

Cortical
1. Stereognosis: the ability to recognize an object in the absence of
vision.
2. Graphesthesia: the ability to recognize writing on the skin purely
by the sensation of touch.
3. Two-point discrimination :the ability to distinguish the points
touching the skin.
4. Tactile localization: discrimination differentiate information
received through the sense of touch.
5. Barognosis: the ability of evaluating the weight of objects
6. Sense of different texture
http://www.nottingham.ac.uk/medicine/documents/publishedassessments/nsain
structionsrevised.pdf

Coordination assessment
1. Gross motor:
o Assessment of body posture, balance and extremity movement involving
large muscle group.

2. Fine motor:
o Assessment of delicate movement concerned with utilization of small muscle
group.

3. Non-equilibrium:
o It assess both static and mobile component of movements when the body is
not an upright position.
o The test involves both gross and fine motor activities.

4. Equilibrium
o It assess static and dynamic component of posture and balance when the body
is in an upright position.
o The test involves primarily gross activities and require observation of the
body in both static and mobile posture.


Gross Motor

Walking along a straight line, foot close to foot:
o In unilateral cerebellar lesions there is deviation to the diseased side.










http://www2.pef.uni-lj.si/srp_gradiva/tgm.pdf

http://www.youtube.com/watch?v=yuVkkhpiHTA
http://www.youtube.com/watch?v=UMnbgS6Xp6I
http://motorgrowth.canchild.ca/en/gmfm/resources/gmfmscoresheet.pdf




1. Buttoning and unbuttoning
2. Following the dots



3. http://www.ehow.com/how_5655792_test-fine-motor-skills.html

Fine Motor Functions:
Visual motor
control
1.Copy a circle
2. Draw a line within a curved path
Upper Extremity
Speed &
Coordination

Sort cubes or pegs; or, string beads.
Fine Motor Test
Non Equilibrium Test

1. Finger-to-nose test : The patient brings the tip
of his forefinger from a distance onto the tip of
his nose. The test is conducted with the eyes
open then closed.

2. Finger-to-finger test : The patient brings the
tips of his forefingers from the distance of his
outstretched arms to meet each other in the
midline.

3. Finger-to-doctor's finger test : The patient
brings the tip of his forefinger from a distance
onto the tip of the doctor's forefinger.

4. Drawing a circle: the patient draws a
symmetrical circle in midair.

5. Dysdindokokinesis: The patient is asked to do
rapidly alternating movements e.g. pronation and
supination of the forearm. In cerebellar lesion there is
failure to perform the movements.


6. Rebound phenomenon : The patient, with his elbow
fixed, flexes it against resistance. When the resistance is
suddenly released the patient's forearm flies upwards
and may hit his face or shoulder.


7. Heel-to-knee test : The patient raises his leg, brings
down its heel onto the knee of his other leg & slides it
down along the shaft of the tibia.


In any of the above tests you may find:
Decomposition of movement.
Kinetic intention tremors which become more evident as the
patient's forefinger approaches the target.
Dysmetria in the form of hypermetria or hypometria.

Left Right Description
Finger to nose
Finger to therapists
Finger to finger
Alternate nose to finger
Finger opposition
Mass grasp
Pronation/supination
Rebound test of holmes
Tapping (hand)
Tapping (foot)
Pointing and past pointing
Alternate heel to knee
Toe to examiners finger
Heel on shin
Drawing a circle (hand)
Drawing a circle (foot)
Position holding (UL)
Position holding (LL)
Non-equilibrium scale
Equilibrium Test



Romberg scale
Get the patient to stand
with his feet together for
half a minute, then ask
him/ her to close his/ her
eyes.

A positive Rombergs Test
occurs when the patient
can stand with the eyes
open but falls when they
are closed.
Equilibrium test:
Grading key
1-Activity impossible

2- Can complete activity, sever impairment in performance, moderate guard
to maintain balance.

3- Can complete activity, moderate impairment in performance,, minor guard
to maintain balance .

4- Able to accomplish activity.




Grade Coordination test
Sitting with hand support
Sitting without hand support
Standing: stride in normal comfortable posture
Standing: hands elevated forward normal comfortable
Standing: hands clasped behind head
Standing: step in normal comfortable posture
Standing: normal comfortable posture with vision occluded
Standing: feet together
Standing: on heels
Standing: on toes
Standing: on one foot
Posture Assessment
Observation:
An exaggerated lumbar lordosis

An anterior pelvic tilt

Flexion at the hips

Hyperextension of the knees

Clawed toes
Gait assessment

The gait of patients with cerebellar ataxia will be unsteady
with a wide base and reeling quality. Often the patients
swing towards the side of the lesion.
o Wide-based
o Lateral instability of trunk,
o Erratic foot placement
o Decompensation of balance with tandem walking
Sensory ataxia will also result in unsteady gait but is
caused by a loss of joint position sense.
http://www.youtube.com/watch?v=FpiEprzObIU
GAITS

Cerebellar Ataxia Sensory Ataxia Frontal Ataxia
Base of Support Wide-based Narrow-based, looks
down
Wide-based
Velocity Variable Slow Very slow
Stride Irregular, Lurching Regular, path
deviation
Short, shuffling
Romberg +/- Unsteady, falls +/-
Heel to Shin Abnormal +/- Normal
Initiation Normal Normal Hesitant
Turns Unsteady +/- Hesitant, Multistep
Postural
Instability
+ +++ ++++
Falls Late event Frequent Frequent
Treatment

Physical therapy

Occupational therapy

Speech therapy

Pharmacological treatment
Physical Therapy
Rehabilitation of Ataxia
The goal of the physiotherapist in the rehabilitation of ataxia 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 physical treatment can be briefly
described as:

o Improve balance and postural stabilization against external
forces and gravitational alterations.
o Improve joint stabilization (propeuception sense) and accuracy
of limb movements.
o Develop upper extremity strength.
o Develop independent and functional gait.
o Improve quality of life for the patient by increasing
independence through daily life activities.

Breathing Exercises
Deep diaphragmatic breathing

Calisthenics exercises
o arms
push-ups
pull-ups
o Legs
calf raises
squats
lunges
o Core muscles
sit-ups
planks
bridges
Repeat the entire routine 2-3 times, 3-5 days a week.

Muscle tone Training
Neuromuscular/sensory stimulation techniques:
o (NMES) can activate hypotonic muscles, improve strength, and generate
movement in paralyzed limbs while preventing disuse atrophy


o quick stretch before:
o Rhythmic stabilization
o Isometric antagonist, relaxation, isometric contraction for agonist.
o PNF techniques

o Resistance training
o Joint approximation for propeuception sense
o Tapping to enhance muscle contraction

Plyometric exercises
Frenkels exercise

This exercises designed to help pt. compensate for the
inability to tell where their arms and legs are in space
without looking.

This exercise takes about 1/2 hour and should be done 2
times daily.
Exercises are designed primarily for coordination not
for strengthening.
Commands should be given in an even, slow voice.




Avoid fatigue. Perform each exercise not more than
four times. Rest between each exercise.
Exercises should be done within normal range of
motion to avoid over-stretching of muscles.

Exercises should begin with very simple movement
and than progress to more difficult patterns.
First ex. done with eyes open than closed.

Exercise in lying:
o Starting position: lie supine with hip and knee extended, head raised
on a pillow.
o Flexion of one leg, foot kept on bed than extend it and Repeat with
other leg.
o Flexion as above with abduction, than add. and ext.
o Flexion hip and knee with heel raised from bed.
o Flexion of one leg and place the heel on the opposite knee.
o Flex both legs and extend.

Exercise in sitting:
o Starting position: sit on a chair with feet flat on the floor
o Make 2 cross marks on the floor, alternately glide the foot over the
marked cross forward, backward, left and right.
o Learn to from chair and sit again.





Exercise in standing:
These are designed to give reeducation in walking.
o Starting position: stand erect with feet 4 to 6 inches.
o Walking sideways
o Walking forward between two parallel lines 14 inches apart
o Turn to the right. complete the full turn, and then repeat to
the left.
o Walk up and down the stairs one step at a time.


Upper Extremity Exercises:
o Using a blackboard and chalk.
For example: Change a minus sign to a plus sign; copy simple
diagrams (straight lines, circles, zig-zag lines, etc.)
o improve eye-hand coordination.



The lower trace shows an attempt by a patient with cerebellar
ataxia to copy the upper trace.
Balance Exercise
To improve balance:
ositting unsupported
oChanging position
oStanding unsupported
oStanding with eyes closed

To improve asthenia:
ostrengthening ex.


To decrease tremor:
o Weight bearing
o Approximation
o Brief ice

Gait training:
o Between parallel bares
o Walk on straight line
o Draw foot prints on the floor
o Assistive devise




Dynamic Balance Training / Safety Steps

1. Side Steps:
Stand upright with your feet hip-width apart
Take a big step to the side
Go back to the original position
Repeat 20 times with each leg
2. Steps forwards
Stand upright with your feet hip-width apart
Take a big step forwards
Go back to the original position
Repeat 20 times with each leg
1. Steps backwards
Stand upright with your feet hip-width apart
Take a big step backwards
Go back to the original position
Repeat 20 times with each leg
2. Cross-Step front
Stand upright with your feet hip-width apart
Cross your legs in the front
Go back to the original position
Repeat 20 times with each leg



Strengthen Core muscles:
Basic crunches(rectus abdominals) :
o Supine with knees bent and hands behind head. Feet should be flat on the ground.
Keep a space between your chin and chest (looking diagonal towards the ceiling).

Action
o EXHALE: Raise your chest until your shoulder blades lift off the floor.
INHALE: Slowly lower back to floor.
Side plank(obliques):
o Side line position, legs straight, feet stacked. Straighten bottom arm, keeping
it in line below shoulder, and place free hand on your hip. Flex feet and
balance on sides of feet (feet are stacked).

Action
o Use abs to keep hips lifted. Hold for 30 seconds. Work up to 1-3 minutes.
crunches with twist (abs, obliques): Supine position knees bent
and hands behind head. Feet should be flat on the ground. Keep a space
between your chin and chest (looking diagonal towards the ceiling).

Action
o EXHALE: As you lift up, rotate upper body toward one side, then rotate
back to center.
INHALE: Lower your back to the floor. Alternate sides.

Standing side bends(obliques):
o Stand with legs hip-width apart, knees slightly bent. Holding ends of a
rolled-up towel, extend arms overhead in a V formation.

Action
o Lift up and out of your rib cage and reach about 10 degrees to the left
without moving your lower body. Return to start. Bend to opposite side
to complete one rep.

Plank hold (transverse abdominals) Prone position with
palms on the floor next to your shoulders, feet and legs together, toes
down.

Action
o Lift your body up so that your arms are straight (palms below
shoulders) and weight is balanced evenly between hands and toes,
keeping body as straight as possible. Hold for 30 seconds and work up
to 1-3 minutes
Back extensions (lower back) Begin very close to a wall, facing
away from it. Pull the ball into your legs as close to your body as possible.
Keep your toes firmly on the ground and the soles of your feet flat on the
wall behind you. Straighten legs so that weight is evenly distributed
between your feet (at the wall) and the ball. Adjust the ball if necessary so
that it is under your hips. Place your hands behind your ears or across
your chest.

Action
o EXHALE: Extend from your hips- Bringing your torso upward toward
the wall as high as possible. Hold for 1-3 counts.

INHALE: Slowly return to starting position to complete one rep.



Slow Swimming on ball (lower back) Begin in
a kneeling position with the ball under your abdomen. Walk
you hands out until they touch the ground right under your
shoulders and your toes are also touching the ground. Allow
your weight to press into the ball.

Action
o Slowly raise your right arm and left leg up into the air,
balancing on the other hand and leg that are touching the
ground. Lift as high as you can, until both leg and arm are
parallel to the floor. Hold for 1-3 seconds. Slowly return to
start. Repeat with the opposite sides to complete one rep.

strengthen the upper back:
o Reverse Dumbbell flys Raise your arms to your side, bringing the
dumbbells up to shoulder level height.
o Rows with resistance band: EXHALE: Pull hands toward chest so
elbows and fists are at or near shoulder level, pinching shoulder blades
together at the end of the movement. INHALE: Slowly return to
starting position to complete one rep.
stretch tight muscles:
o Standing chest stretch (chest, shoulders) With arms straight, lift
arms up behind you while keeping your back straight and your
shoulders down.
o Torso Stretch (shoulders, latissimus dorsi) Clasp hands together
and slowly raise them above your head towards the ceiling.
o Standing quad stretch (quads, hips) Reach back and grab your
left foot in your left hand, keeping your thighs lined up next to
each other and left leg in line with the hip (not pulled back
behind you).


Neutralize Tilted Hips

Pharmacological Treatment
There are no specific drug treatments
but these are alternative treatments :
o Depression: SSRI's (Selective serotonin reuptake inhibitors)
o Dizziness/Vertigo/Nystagmus: Acetazolamide (Diamox), Ondansetron (Zofran),
Baclofen.
o Excessive daytime sleepiness: Modafinil (Provigil) or Armodafinil (Nuvigil)
o Fatigue: Amantadine, Atomoxetine (Strattera), Carnitine, Creatine
o Imbalance/ln-coordination: Amantadine, Buspirone (Buspar), Riluzole (Rilutek)
o Memory or thinking disorders: Cholinesterase inhibitors (memory drugs
approved for use in Alzheimer's disease), Memantine (Namenda)

For episodic ataxia:
Episodic Ataxia type 1: Carbamazepine, Phenytoin
Episodic Ataxia type 2: Flunarizine, Acetazolamide, and 4 aminopyridine
Articles

1. Coordinative Physiotherapy for Patients with Ataxia
o https://www.ataxia.org/pdf/Coordinative_Physiotherapy.pdf
2. Decreased ataxia and improved balance after vestibular rehabilitation
o http://oto.sagepub.com/content/130/4/418.full.pdf+html

3. Cerebellar ataxia: pathophysiology and rehabilitation
o http://cre.sagepub.com/content/25/3/195.full.pdf+html

4. Current treatment of vestibular, ocular motor disorders and nystagmus
o http://tan.sagepub.com/content/2/4/223.full.pdf+html

5. A Home Balance Exercise Program Improves Walking in People With Cerebellar
Ataxia
o http://nnr.sagepub.com/content/early/2014/02/12/1545968314522350.full.pdf+html

6. Friedreich Ataxia: New Pathways
o http://jcn.sagepub.com/content/27/9/1204.full.pdf+html

7. Rehabilitation Management of Friedreich Ataxia: Lower Extremity Force-Control
Variability and Gait Performance.
o http://nnr.sagepub.com/content/18/2/117.full.pdf+html


Article 1: A Balance Exercise Program
Improves Walking in People With
Cerebellar Ataxia
Purpose: The aim is to determine if a home balance exercise
program is feasible for improving locomotor and balance
abilities in these individuals.

Methods: A total of 14 patients with cerebellar ataxia participate
in a 6-week individualized home-based balance exercise
program and attended 5 testing sessions. Pretraining,
posttraining, and follow-up testing included a neurological
assessment, clinical gait and balance tests, and laboratory
assessments of balance and walking.

Results: Improvement in locomotor performance in people with
cerebellarataxia was observable after a 6-week home
balance exercise program.
Article 2: Decreased ataxia and improved balance after vestibular
rehabilitation
Purpose: To determine the effects of vestibular rehabilitation on gait
ataxia and balance.

Methods: Subjects were patients with chronic vertigo due to peripheral
vestibular impairments, referred for vestibular rehabilitation. They were
assessed on the Timed Up and Go test, ataxia during a path
integration test, computerized dynamic posturography, level of
vertigo, independence in activities of daily living, and psychological
locus of control. They were randomly assigned to three home
program treatment groups.

Result: Ataxia decreased significantly, and posturography scores and
time to perform Timed Up and Go improved significantly, for all
subjects.


Article 3: Friedreich
Ataxia: New Pathways
Abstract
Friedreich ataxia is a rare disorder characterized by an
autosomal recessive pattern of inheritance. The disease is
noted for a constellation of clinical symptoms, notably loss
of coordination and a variety of neurologic and cardiac
complications. More recently, scientists have focused their
research on an array of general investigations of the
underlying cellular basis for the disease, including
mitochondrial biogenesis, iron-sulfur cluster synthesis, iron
metabolism, antioxidant responses, and mitophagy.
Combined with investigations that have explored the
pathogenesis of the disease and the function of the
protein frataxin, these studies have led to insights that will
be key to identifying new therapeutic strategies for
treating the disease.
Reference
PRINCIPLE OF NEUROLOGY BY DR. HASSAN ELWAN
Physical Management in Neurological Rehabilitation. Mosby
Siegel Essential Neuroscience 2nd edition

http://en.wikipedia.org/wiki/Ataxia
http://www.merriam-webster.com/medical/dysdiadochokinesia
http://en.wikipedia.org/wiki/Dysdiadochokinesia
http://www.dartmouth.edu/~rswenson/NeuroSci/chapter_8B.html
http://www.healthline.com/human-body-maps/cerebellum
http://www.nhs.uk/Conditions/Ataxia/Pages/causes.aspx
http://www.patient.co.uk/doctor/Cerebellar-Lesions.htm
http://www.nlm.nih.gov/medlineplus/cerebellardisorders.html
http://www.mayoclinic.org/diseases-conditions/ataxia/basics/causes/con-20030428
LECTURE SLIDES.
http://dublinphysio.ie/services/neurological-physio/ataxia/
http://www.aahf.info/pdf/Berg_Balance_Scale.pdf
http://dc347.4shared.com/doc/FkjthRJR/preview.html
(jeffmann.net/NeuroGuidemaps/gait) http://cirrie.buffalo.edu/encyclopedia/en/article/112/
http://www.idahopt.com/article/calisthenics-get-stronger-without-lifting-weights/
http://www.sparkpeople.com/resource/fitness_articles.asp?id=1407&page=2
https://www.ataxia.org/pdf/Coordinative_Physiotherapy.pdf
http://internaf.org/ataxia/exercise.html
http://www.livestrong.com/article/337986-physiotherapeutic-exercises-for-cerebellar-ataxia/
http://cirrie.buffalo.edu/encyclopedia/en/article/112/
https://www.ataxia.org/pdf/Medications_for_ataxia_symptoms.pdf

You might also like