Ataxia

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. It’s

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 one’s position in space.

3. The third function concerns the maintenance of the

tension or firmness also refers to the muscle tone.

ATAXIADefinition : 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 eyesb) 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

8th 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 ATAXIAFrontal 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 erecto Even with use of support, patient tends to lean towards

hyperextensiono Patient's legs are in scissors-cross position during walking

and there is incoordination between the legs and trunko Ataxia is accompanied by frontal dementia, urinary

incontinence, frontal release signs and perseveration.

Clinical Differences Between Basic Types of Ataxia

Assessment of Ataxia1. History taking 2. Cognitive function 3. Speech assessment 4. Muscle tone assessment 5. Deep tendon reflexes6. Muscle power 7. ROM 8. Muscle length9. Long and round measurement10. Sensory assessment11. Coordination assessment12. Balance13. Posture14. 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 ReflexesClinical 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 limbo Lower limb o Trunk

ROM: Normal Muscle length: If there’s any limitation in ROM or deformity there’s going to be muscle length shortening.

Long and round measurement: Normal

Sensory assessmentSuperficial 1. Pain: Prick, Pinch

2.Temperature: Cold, Hot

3.Light touch : Cotton stroke

Deep4.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

Cortical1. 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 texturehttp://www.nottingham.ac.uk/medicine/documents/publishedassessments/nsainstructionsrevised.pdf

Coordination assessment1. 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 unbuttoning2. Following the dots

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

Fine Motor Functions:

Visual motor control

1.Copy a circle2. Draw a line within a curved path

Upper Extremity Speed & Coordination

Sort cubes or pegs; or, string beads.

Fine Motor Test

Non Equilibrium Test1. 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 scaleGet the patient to stand with his feet together for half a minute, then ask him/ her to close his/ her eyes.

A positive Romberg’s 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-basedo 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 exerciseso 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 stabilizationo 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

Frenkel’s 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 flooro 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 sidewayso Walking forward between two parallel lines 14 inches

aparto 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 unsupportedoChanging positionoStanding unsupportedoStanding with eyes closed

To improve asthenia:ostrengthening ex.

To decrease tremor:o Weight bearingo Approximationo Brief ice

Gait training:o Between parallel bareso Walk on straight line o Draw foot prints on the flooro 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). 

Actiono 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). 

Actiono 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). 

Actiono 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. 

Actiono 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. 

Actiono 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. 

Actiono 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. 

Actiono 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.pdf2. 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 rehabilitationo http://cre.sagepub.com/content/25/3/195.full.pdf+html

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

5. A Home Balance Exercise Program Improves Walking in People With Cerebellar Ataxiao http://

nnr.sagepub.com/content/early/2014/02/12/1545968314522350.full.pdf+html

6. Friedreich Ataxia: New Pathwayso 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 AtaxiaPurpose: 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

rehabilitationPurpose: 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

AbstractFriedreich 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

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