Case History of Diagnostic Disorder – Cerebellar Ataxia
Kenneth Wong PT 840 Differential Diagnosis & Intervention in Clinical Neurology
Overview of the Disorder
Cerebellar ataxia is a condition characterized by difficulties in movement and coordination, usually without clear weakness in musculature. Afflicted patients experience losses in balance, leading to functional limitations and worsened quality of life. Though some damage to the cerebellum is implied, the exact etiology can be manifold among patients, as trauma may be concentrated solely to that structure or be diffuse while involving other neural structures; in the latter scenario, a patient’s outlook may be worse. This is due to the cerebellum’s importance in working in concert with other neurological structures to sequence movements in afferent and efferent pathways
(Hall, 2011). The impairments can range from dysarthria characterized by a lack of rhythm to unintelligible communication because of slurring and slowness. Aside from speech, patients’ limbs may have significant difficulty in movements, manifested into predictable signs that include dysmetria, decomposition of movement, and a kinetic tremor (Manto, 2013). Correlated to these motor deficiencies, ambulation may be challenging, as patients’ steps may be staggered without a distinct cadence, with demonstrable difficulties in initiation and stopping. Moreover, patients will have gait deviations that tie closely to the level of balance deficiency (Morton & Bastian, 2003) .
Pathology
The causes for cerebellar ataxia are varied, ranging from brain tumors, chemical toxicity, infection, stroke, and degenerative diseases. An etiological differentiation exists between whether a patient’s condition was hereditary or acquired. Some diseases that comprise the former’s category include the autosomal dominant cerebellar ataxias (ADCAs), such as spinocerebellar ataxia type I (SCA1). In SCA1, progressive ataxia combines with impairment to other neurological systems, leading to additional cognitive impairments, spasticity, and sensory neuropathy; the ATXN1 gene is directly targeted by a mutation (Spinocerebellar ataxia type 1.2011). While the cerebrum and concomitant cognitive function remain whole, later declines will be seen in muscle atrophy and in sensory disturbances (Manto, 2013). Other diseases with genetic components are autosomal recessive and heterogeneous in nature, including Friedreich’s ataxia (FRDA).
In this disease, the condition typically presents early in age via a GAA repeat in the FXN gene; aside from cerebellar degeneration, the spinal cord and peripheral nerves are affected, leading to typical cerebellar signs in addition complications that include loss of tendon reflexes and scoliosis (Friedreich's ataxia fact sheet.2014). Finally, hereditary causes for cerebellar ataxia may be X-linked disorders. These include mitochondrial disease that typically presents with other neurological dysfunctions that include deafness, myopathy, and ophthalmoplegia (Bargiela et al., 2015).
In contrast, an acquired cause could be sudden in onset, progressing rapidly; a stroke directed to the cerebellum may injure one of three arteries (superior cerebellar, anterior inferior cerebellar, and posterior inferior cerebellar) that provide its blood supply, yielding differing presentations. For instance, damage to the superior cerebellar artery leads to dysmetria of the ipsilateral upper extremity and unsteadiness while ambulating (Umphred, 2007). Drug intoxication by ethanol may also result in cerebellar ataxia; the specific etiology of this condition results from predominant atrophy in the anterior superior vermis, a medial structure of the cerebellum (Sullivan, Deshmukh,
Desmond, Lim, & Pfefferbaum, 2000) . In postmortem studies of human alcoholic brains, neuronal loss has been found in the cerebellum, resulting in decreased brain weight and white matter loss (Alfonso-Loeches & Guerri, 2011) . Another acquired cause of cerebellar ataxia could be traumatic brain injury (TBI), possibly from motor vehicle accidents. A TBI typically occurs with corresponding damage to other structures; in one case series, one patient experienced multiple skull fractures and subarachnoid hemorrhage in addition to cerebellar hemorrhage (Sartor-Glittenberg & Brickner, 2014) .
Additionally, cerebellar tumors may be a primary cause, with higher rates of prevalence in children as opposed to adults, although prognosis for adults tends to be worse because the cancer may be more aggressive. Chronic conditions may include nutritional disorders such as vitamin B12 or vitamin E deficiencies. Multiple sclerosis is another acquired cause for ataxia; lesions in the cerebellum that are mediated by the immune system, with symptoms showing up between 10-50% of cases (Marsden & Harris, 2011) .
Clinical Manifestations & Differential Diagnosis
Cerebellar ataxia may be manifested distinctly in recognizable sign of dysmetria, or an inability to scale the distance a movement will make, as patients may overshoot or undershoot targets, typically seen in performance of a finger-to-nose (FTN) test. The former is known as hypermetria, and it is more pronounced when the movement is made quickly with increased inertia, while the latter, known as hypometria is typically produced with slower movements (Umphred, 2007). Dysmetria may occur in both proximal and distal joints, as patients may take varying paths between successive attempts.
In addition, patients may exhibit a disordered coordination between the head, trunk, and legs while having difficulties in multi-joint movements, known as dyssynergia. Specifically, the issue stems from a lack of range for those limbs or an inability to move in the desired direction. Patients will have problems with sequencing segments to move in succession, because they are unable to compensate for torques among limbs that interact with others during movement (Marsden & Harris, 2011) .
Oculomotor deficiencies may occur with these patients. Saccades can be slowed and dysmetric, leading to choppy pursuit when trying to follow a target (Umphred, 2007).
In progressive disorders, a downbeat nystagmus may present that leads to an illusion of oscillation of the surroundings (Marsden & Harris, 2011) . The most common form of nystagmus is gaze-evoked nystagmus, where it occurs towards the end ranges of lateral or vertical gaze. Moreover, the vestibule-ocular reflex suppression could be impaired or absent, meaning patients cannot maintain steady vision during rapid movements of the head and body (Manto, 2013).
With respect to generating force, they may find it difficult to coordinate rapidly alternating movements. Known as disdiadochokinesia, this condition causes impairments in actions that include quickly switching between supination and pronation or shifting from plantar flexion and dorsiflexion. Patients will demonstrate slower speeds with these actions and may have inconsistent patterns. It has been thought that disdiadochokinesia is caused by an inability to coordinate the timing of stopping the agonist muscle before firing the antagonist (Umphred, 2007). Another symptom is a loss of check and rebound; patients will receive an isometric resistance to a limb such as the forearm. When the force is released, there is pronounced displacement of that body part that might cause a loss of balance or injury (Manto, 2013). Associated with these broader motions, precise gripping actions that require maintenance of a constant level of force may be difficult for cerebellar ataxic patients. For instance, handwriting is typically affected, as patients will produce more errors with increased oscillations, with increased writing times (Fujisawa
& Okajima, 2015) .
Patients may also exhibit a kinetic tremor that presents only during initiating of voluntary muscle movement, antithetical to the resting tremor seen in Parkinson’s disease. These tremors are usually seen more often in proximal musculature and will typically occur in low frequencies (Manto, 2013). A subset of a kinetic tremor is an intention tremor; this occurs towards the termination of movement whereby a person will use visual feedback to correct movements to reach a target.
Another symptom is more of a compensatory measure; patients will break down multi-joint movements into simpler steps, a phenomenon known as movement decomposition. For instance, if patients are asked to touch a tester’s finger in front of them, they may first flex a shoulder before extending an elbow, as opposed to performing it in one fluid motion. Often there are errors associated with directions and rates if patients engage in slow multi-joint movements due to this lack of synergy (Grimaldi &
Manto, 2012) .
Patients will also typically demonstrate a wide base of support with increased body sway due to postural instability both in static and dynamic positions. Moreover, they will have difficulty in righting themselves after being perturbed via diminished postural responses. While moving extremities, they will also have poor control of equilibrium. The amount of sway will decrease depending on the region of damage; anterior cerebellar lobe damage is characterized by high velocity and low amplitude anterior to posterior postural sway, while vestibulocerebellar damage leads to low frequency but high amplitude sway without a usual direction (Umphred, 2007).
Functionally, a patient may find it difficult to ambulate because of high variability in spatiotemporal parameters. During gait, patients with cerebellar ataxia will tend to have increases in stride width and a reduction in cycle duration compared to healthy controls (Martino et al., 2014). In addition, stride lengths will be reduced, as foot placement and swing through are not as uniform. Cerebellar ataxic patients have a tendency for increased temporal variability in fast and slow walking speeds, but normal for preferred walking speeds (Schniepp et al., 2012). It has been found that those individuals will have significant changes in intersegmental coordination associated with and inability to adjust for perturbations of balance, while concurrent cognitive tasks during ambulating may also cause impairment because of the cerebellum’s involvement in memory (Ilg & Timmann, 2013) . Stopping and turning at increased speeds will also present as major challenges.
Finally, patients with cerebellar ataxia will find it difficult to learn new motor behaviors such as balance recovery or novel gait patterns; they are forced to use other means to handle new task demands, including consciously thinking about movements.
Motor learning driven by the cerebellum is usually successive, as repeated practice will rectify learned errors. With poorer automatic adaptive abilities, individuals will find it difficult to walk in different surfaces (wet versus dry). Moreover, cerebellar ataxic patients will learn movements more slowly because of a lack of predictive control; they may have unimpaired abilities to make reactive changes but fail to make feed-forward or predictive corrections (Bastian, 2006).
Four distinct categories must be examined before a diagnosis can made for ataxia:
1) topological level of nervous system involvement; 2) focal versus non-focal extension;
3) progression rate; and 4) age of onset (Manto, 2013). If other nervous structures are involved, then compensatory mechanisms may be precluded from being used in the rehabilitative process. Moreover, if a condition is hereditary, there is an expectation that a patient will worsen over time and have decreased recovery potential. Tests to be used in the upper extremity include the aforementioned FTN test, alternating supination- pronation test, and hand or finger-tapping test. For the lower extremity, the movement of the heel on the contralateral shin and the dorsiflexion-plantar flexion tests are useful.
Tests should be performed bilaterally and with multiple trials. Tests should also be conducted under eyes opened and eyes closed conditions, as visual feedback may improve quality of movement. Balance measures should also be used, including the Berg
Balance Scale (BBS), Mini-Best Test, and Romberg Test.
Specific standardized rating scales for cerebellar ataxia severity have been developed to evaluate as well as assess the progression of the disease. They can also be used as outcome measures to determine the benefit of therapeutic interventions. One is the Scale for the Assessment and Rating of Ataxia (SARA), shown to be applicable for a heterogenic group of individuals. Divided into eight items yielding a maximum of 40 points, SARA’s internal validity, inter-rater reliability, and test-retest reliability were proven in a study of 64 ataxic patients (Weyer et al., 2007). It has gained preference among clinicians for its brevity. An erstwhile standard known as the International
Cooperative Ataxia Rating Scale (ICARS) has demonstrated good inter-rater reliability (Storey, Tuck, Hester, Hughes, & Churchyard, 2004) ; it is comprised of 19 items divided into four subscales based on the premise that different anatomical regions of the cerebellum house separate functions: 1) posture and gait; 2) limb ataxia; 3) dysarthria; 4) oculomotor disorders; a maximal score of 100 represents the most severe cerebellar dysfunction (Manto, 2013). Though valid, ICARS has been shown to have redundancies between sections (Schmitz‐hübsch et al., 2006).
General Medical Management
Ataxia may be managed via different means, depending on the causes. For instance, if alcohol or another toxin is implicated, then detoxification is an important step to initially treat (Ramirez‐Zamora, Zeigler, Desai, & Biller, 2015) . Among inherited conditions, drugs such as Vitamin E may be provided to patients experiencing ataxia because of a metabolic deficiency caused by a mutation of a transfer protein on a chromosome. However, current literature suggests that other pharmacological interventions have not demonstrated clinical effectiveness to treat hereditary ataxias, although secondary features of the condition including depression and Parkinsonism may be addressed with conventional medicinal standards (Revuelta & Wilmot, 2010) . One case study found that transcranial magnetic stimulation for a 62 year old with probable idiopathic late-onset cerebellar ataxia resulted in improvements in a timed up-and-go test, in addition to kinematic variables such as gait speed and stride duration variability
(Farzan et al., 2013). Still, physical therapy has emerged as the primary means to restore or reduce symptoms, whereby interventions are meant to activate and demand control mechanisms that challenge patients in maintaining control and to coordinate multiple joints. Further, patients would benefit from training to use visual, somatosensory, and vestibular inputs to preserve patient abilities to react to unforeseen situations and avoid falls. Some principles that are important in training include the ability to train small amounts of movements for numerous repetitions and to make the movements have functional relevance with activities of daily living.
Implications for PT
It is important to note that not all the tests used to test for cerebellar signs are specific to etiologies solely cerebellar in nature; they are merely sensitive. In addition, the potential benefit of PT depends on the nature of the lesion. For instance, ataxias degenerative in origin will be difficult to manage because the entire cerebellum is affected; continual deterioration is expected over time. In contrast, damage from a stroke to an isolated section of the cerebellum bodes well for recovery because of neuroplasticity and the ability for supplemental structures to compensate; in this scenario, dramatic improvement can be attained. Depending on the level of deterioration, patients may be suggested to replace multi-joint movements with slower movements with sequential single joint movements or to train themselves with more cognitive strategies to adjust to different movement conditions.
Regarding the specific PT program to adhere to, therapists may couple clinical interventions with a detailed home exercise program. One study found that significant improvements were seen in the Dynamic Gait Index (DGI) as well as better stride lengths and walking speed following a 6-week training period utilizing exercises designed to challenge dynamic and static balance (Keller & Bastian, 2014) . If free standing and walking is not feasible, treadmill training with weight support via a harness has been shown to possibly contribute to an increase in walking ability in a formerly non- ambulatory ataxic subject (Cernak, Stevens, Price, & Shumway-Cook, 2008) . Further, videogame training has been shown to provide an advantageous motivational factor to promote compliance while simulating realistic activities; improvements in the SARA for posture and gait were seen in one case study (Ilg et al., 2012).
Case Scenario & Recommended PT Program
The patient is a 25 year-old female who was referred to physical therapy after being diagnosed with FRDA. She complains that around a year ago, she began to lose coordination of her hands eat, write and complete other activities of daily living. She also felt a loss of sensation in her lower extremities, with problems initiating movement and in balance. Progressive difficulties led to issues with ambulating in a straight line and multiple falls. She indicates that she tires easily and is often short of breath. The patient is currently an office worker at an architectural firm who lives with her boyfriend in a 5th floor apartment with elevator access. She would like to return to her normal activities at home and community, including walking without falling and being productive at work again.
The initial part of the physical therapy program will begin with a review of the patient’s medical history and profile; in this scenario, she offers additional information that she has DM II. A thorough subjective assessment will then be conducted, whereby the location of symptoms will be ascertained with the details listed in the excerpt above.
Next an objective examination will be conducted; her postural assessment reveals a slight postural tremor and it appears she has a right thoracic scoliosis and bilateral pes cavus.
In addition her sitting and standing balance are both poor in static and dynamic conditions, requiring moderate assistance to maintain. In her systems review, integumentary and cardiovascular functions are unimpaired. Her gross muscle strength in the bilateral upper and lower extremities is 4/5 on a MMT while ROM is within functional limits for upper and lower extremities, though she demonstrates some tightness in her bilateral hamstring groups and heel cords. Her light touch sensation is diminished in her right lower extremity. Knee and ankle jerk reflexes are also diminished at 1+. The patient exhibits bilateral cerebellar signs of dysmetria, disdiadochokinesia, and intention tremor in her upper extremities. She demonstrates considerable difficulty in gait, using a wide base of support without a steady cadence and consistency in her steps. Her transfer from sit <-> stand requires min assist while supine <-> sit requires close supervision due to significant difficulties in maintaining her balance. Her vital signs reveal a resting heart rate of 90 BPM and a blood pressure of 110/80. Her BBS score is 21, with significant usage of upper extremities for transferring and an inability to reach in a balanced fashion; her SARA score is 19.
Following the examination, an assessment will determine that the patient has a problem list that includes functional limitations in gait and ADL due to poor balance and coordination. The patient has primary impairments in: motor control, gait, locomotion, balance, posture, muscle performance, and sensation. She currently is functionally limited in some aspects of self-care, home management, and community activities. PT goals would be to improve transfers to independent, enable ambulation, and to improve bilateral lower and upper extremity strength. In addition, more general goals would be to increase overall endurance and aerobic capacity, improve postural control, and provide knowledge of behaviors that will foster healthy habits. Therapeutic interventions would include gait training, balance training, exercises to strengthen musculature, and instructions to preserve energy. Specific exercises to use include: static standing on one leg, climbing stairs, whole body movements, fall prevention and recovery, and movements to treat and prevent contracture. Sessions would focus on training that calls for increasing demands and progression, either from static to dynamic or simple to complex joint movements. In case studies that demonstrated considerable progress in patients with cerebral ataxia following TBI, the following were used: manual resistance to trunk in various antigravity postures, tandem gait, braiding, and toe walking, and sitting on unstable surfaces (Sartor-Glittenberg & Brickner, 2014) .
Patient prognosis is determined to be fair because of the patient’s motivation in resuming activities and in becoming more functional; however, the progressive nature of her disease may preclude significant improvements. An assistive device such as a straight cane may be provided as necessary to help prevent falls, with suggestions of environmental modifications to reduce difficulties in movement. The patient will be seen six weeks of intensive training of three sessions of one hour each per week. After the training program, the patient will be re-evaluated with the BBS and SARA scales to determine whether she has improved.
Phase 1 (Weeks 1-2)
1. Warming up a. An initial phase to increase endurance of large lower extremity muscles in
a safe position will be beneficial for aerobic conditioning. Patient will
perform approximately 20 minutes of stationary cycling on a recumbent
bike at 70-85% of maximal heart rate to improve cardiovascular endurance
(Maring & Croarkin, 2007) .
2. Balance Training
a. Static sitting on a stable surface
i. The patient will sit on the edge of the mat in short sitting with the
trunk unsupported. She will be asked to hold this position for as
long as possible. Emphasis will be made to encourage usage of the
core musculature to maintain upright and avoid compensatory
movements.
b. Standing on a stable surface (performed in the parallel bars for safety)
i. The patient will stand with feet together, arms across chest, and
without slow head movements. This will be performed with eyes
open and held for 10 seconds.
ii. The patient will stand in a semi-tandem stance and arms across her
chest. This will be performed with a narrow base of support and
held for ten seconds.
iii. The patient maintains a unilateral stance with arms across the
chest. This will be held as long as possible with eyes open for both
legs.
3. Strengthening: a. Supine hip bridges – the patient will lift herself off the mat using her
gluteal muscles. This will be performed for three sets of 10 repetitions.
b. Sit to stand from the mat – the patient will come into a standing position
with as little upper extremity support as possible. Performed for three sets
of 12-15 repetitions with full ROM and slow pace.
c. Sidelying clamshells with resistance band resistance – the patient will be
lying on her side with a green resistance band around her knees. She will
raise the top leg out into abduction for three sets of 10 repetitions before
switching sides.
4. Coordination:
a. Upper Extremity Coordination while sitting: This routine will be
performed with both arms: 1) The patient keeps arms straight at side and
raise forward and upwards over head; 2) The patient keeps arms straight at
side and raise sideways and upwards over head; 3) The patient lifts arms
alternately with one going up as the other goes down; 4) The patient
straightens arm in front and brings tip of index finger to touch the top of
nose and repeats with other hand; 5) Begin as in #4, but the patient brings
tip of index finger to touch the ear lobe on the opposite side. Repeat with
other hand; 6) The patient lifts arms out and sideways and upwards 90°
and then bring tips of index fingers together; 7) The patient raises arms
sideways and upwards, clapping hands above the head. Then the patient
repeats the same exercise but touches the back of the hands together; 8)
The patient raises arm sideways until shoulder height. Then the patient moves the arms in circles, starting with small circles and gradually
increasing their size.
b. Lower Extremity Coordination while supine: This routine will be
performed with one leg and repeated with the other leg: 1) Hip and knee
flexion (HKF) while contralateral foot remains on the mat, followed by
hip and knee extension (HKE); 2) HKF, followed by hip abduction, hip
adduction, and then HKE; 3) HKF to 50% of ROM, followed by HKE; 4)
HKF to 50% of ROM, hip abduction, hip adduction, and then HKE; 5)
HKF to a point designated by therapist verbal command, followed by
HKE. The sequence was adapted from Frenkel’s exercises (Krasilovsky,
2015) and will be performed for three repetitions.
5. Gait Training: Patient will initially engage in pre-gait activities in parallel bars to
improve standing weight shifts and forward, lateral, and backward steps. A an 8-
inch step stool will also be presented in front of the patient; she will be instructed
to place one foot on the step and stand up before coming back down eccentrically
on that foot. This will be performed for approximately five minutes.
6. Flexibility Exercises
a. Proprioceptive neuromuscular facilitation (PNF) stretching will be used on
the hamstring group on both lower extremities. While supine, the patient
will be taken into the end range of D1 flexion pattern with the knee
extended for the lower extremity. From there, a contract-relax of the
agonistic quadriceps muscles will be performed for 7 seconds before a
passive 10 second stretch into the new range will be performed. This will be completed for three bouts. This technique uses reciprocal inhibition
that may provide excitatory input to inhibitory interneurons that synapse
onto the motorneurons of the targeted muscle (Sharman, Cresswell, &
Riek, 2006) .
Phase 2 (Weeks 3-4)
1. Warming up
a. The patient will continue to perform 20 minutes of stationary cycling, with
possible increases in intensity and resistance.
2. Balance Training
a. Dynamic sitting
i. The patient will sit on a Swiss Ball and engage in exercises that
firstly involve sitting for as long as possible without bilateral upper
extremity support. An exercise program with this device has been
shown to improve balance measures in patient populations (Seo,
Yun, Kim, & Lee, 2012) . Then, the patient will perform trunk
rotation with her hands free and perform lateral and
anterior/posterior rolling while reaching out with an outstretched
arm. Each movement will be performed for ten repetitions with
three sets each.
b. Dynamic standing
i. The patient will march in place with arms across the chest with
eyes open. She will attempt to pause as long as possible in unilateral stance and possibly progress to performance with eyes
closed. This will be done for three sets of 10-second holds.
ii. The patient will stand and perform 360 degree turns
counterclockwise and then clockwise with arms across chest and
eyes open. This will be performed for three sets with an emphasis
of a safe turning speed.
iii. The patient will stand on a foam surface and reach with her upper
extremity to targets designated by the therapist with her feet apart.
The frequency will be 10 targets for each side.
3. Strengthening
a. Lunges – the patient will land on the heel and forefoot of one leg by
flexing the knee and hip until the other knee of the rear leg is almost in
contact with the floor, before returning to a standing position. This will be
performed for three sets of eight repetitions.
b. Sit to stand from mat with weights – the patient will hold a 10 pound
dumbbell against her chest to add resistance while performing these
squats. An emphasis will be made to have controlled motions, especially
during descent. This will be performed for three sets of 8 repetitions.
c. Heel raises – the patient will strengthen her triceps surae by holding onto a
chair and lifting her body weight off the ground. This will be performed
for three sets of 10 repetitions
4. Coordination: a. Upper Extremity Coordination while seated: The patient will perform the
routine as mentioned in Phase 1 except pausing when instructed to do so
by the therapist.
b. Lower Extremity Coordination while seated: the patient will cross the
right ankle over the left, cross the left ankle over the right. Then she will
cross the right knee over the left knee and cross the left knee over the
right; an emphasis is made to avoid excessive hip rotation. With certain
cones placed in front of her, she then is asked to touch a cone, return to a
position under the seat, before repeating for the remaining cones. This
entire routine will be performed for three repetitions.
5. Gait Training:
a. Straight line: The patient will ambulate with a narrow base of support and
arms at sides. A progression can be made to vary the head movements or
to close the eyes. This will be performed for approximately 3 minutes.
b. Turning: The patient will continue with gait with arms at sides but now
incorporate wide turns to provide dynamic elements. There could be
possible progression in increasing the angle of the turns. The patient will
perform five turns for each side.
c. Gait with perturbation: the patient will walk in on a designated track with
external perturbations provided by the therapist (i.e. pushing) to challenge
her balance. This will be performed for roughly three minutes.
6. Flexibility Exercises a. PNF stretching by using both the D1 and D2 flexion patterns may now be
incorporated to target stretching for different sides of the hamstring
groups. In addition, more emphasis could be placed on the heel cords
given the increased work in this phase of the therapy program. The usage
of contract relax with contraction of the antagonist musculature may be
implemented.
Phase 3 (Weeks 5-6)
1. Warming up
a. The patient will continue to perform 15 minutes of treadmill walking,
assuming she has progressed enough and possesses the capability of
prolonged walking.
2. Balance Training
a. Dynamic sitting on an unstable surface: while sitting on the Swiss Ball,
the patient may now march with hands on or free. Next, the patient will
perform foot circles with one leg in the air and the contralateral foot
planted to the ground. Finally, the patient may sit on a see-saw board and
alternate raising her hands and feet into the air. This routine will be
performed for five minutes.
b. Dynamic stance: the patient will stand on a wobble disc with either feet
apart or feet together. She will work on weight shifts side to side and
anterior/posterior, trunk rotation, and arm raises. This will be performed
for five minutes.
3. Strengthening: a. Squats – the patient will perform continuous body weight squats with a 10
pound dumbbell for additional weight for three sets of eight repetitions.
b. Stair negotiation – the patient will walk up steps and be encouraged to use
as little upper extremity support as possible. She will perform three sets of
ascending and descending one flight.
4. Coordination:
a. Upper Extremity Coordination while standing: the patient will perform the
routine as mentioned in phase I except in standing.
b. Lower Extremity Coordination while standing: the patient will perform the
sequence described for phase II now in a standing position for roughly
three minutes.
5. Gait Training:
a. Sideways walking: the patient will lead with one direction with arms at
sides and repeat with the opposite side. The patient may progress to
braiding, where the trailing leg will alternate between being placed in front
or behind the leading leg with each step. This will be performed for five
minutes.
b. Backwards walking: this will be performed with a normal base of support
and with arms at the sides. This will be performed for five minutes.
c. Obstacle negotiation: with cones placed on the floor, the patient will now
perform figure eights around the cones with an emphasis on avoiding
contact. Depending on how challenging this is, the patient will perform
this for eight minutes. d. Gait with a cognitive task: the patient will respond to yes-no questions at
first and progress to counting or performing arithmetic (Umphred, 2007) .
This will be performed for three minutes.
6. Flexibility Exercises
a. The PNF patterns for D1 and D2 will continue as described in phase II.
In addition, the patient will be encouraged to continue training while at home, with a focus on improving balance. A Home Exercise Program will be provided to her as seen in the next page.
Home Exercise Program
These exercises are designed to: 1) Improve your overall balance and coordination. 2) Increase neuromuscular control, strength, and endurance in the muscles around the lower extremity to reduce the risk of falls.
For all exercises, do not hold your breath and count aloud the repetitions. Apply ice or a cold pack to an area after these exercises if you feel soreness.
Balance/Coordination 1. Tandem stance Objective: Improve overall balance while standing. Position: Standing in front of a chair with arms to support as needed. Procedure: Refer to Figure 1. Place one foot in front of the other. Stand for as long as tolerated. Repeat with the other foot in front. Frequency: 1-2 times per day, 3-5 times per week.
Figure 1
2. Standing on a foam surface Objective: Develop dynamic control of the muscles in the lower extremity. Position: Standing Procedure: Refer to Figure 2. Stand on the surface as long as possible, progressing to narrower bases of support or with eyes closed. Frequency: 1-2 times per day, 3-5 times per week
Figure 2 3. Sitting on an unstable surface Objective: Improve sitting balance in a dynamic position Position: Sitting Procedure: Refer to figure 3. Stabilize pelvis by engaging the abdominal muscles. Attempt to march on foot off the floor approximately 6 inches. Alternate and repeat. Frequency: 5 repetitions for each foot, 1-2 times per day, 3-4 days per week.
Figure 3
Coordination 1. Arm coordination exercise 1 Objective: Improve coordination of arms Position: Sitting Procedure: Perform the following routine as was demonstrated in therapy: 1. Keep arms straight at your side, raise it forward and upward over your head. 2. Keep arms straight at your side, raise sideways and then upward over head. 3. Keep arms at side and alternate raising one arm while the other arm lowers. 4. Straighten arm in front of you and bring tip of index finger to touch the top of your nose. 5. Straighten arm in front of you and bring tip of index finger to touch the opposite ear lobe. 6. Lift arms out and sideways and upwards 90°, then bring tips of index fingers together. 7. Raise arms sideways and upwards, clapping hands above the head. Repeat the same exercise, bringing the back of the hands together. 8. Raise arm sideways, shoulder high. Then move the arm in circles, starting with small circles and gradually increasing their size. Frequency: 1 repetition, 1-2 times per day, 3-5 times per week.
2. Leg coordination exercise 1 Objective: Improve coordination of legs Position: Sitting Procedure: Cross the right ankle over the left, cross the left ankle over the right. Then cross the right knee over the left knee and cross the left knee over the right. Frequency: 5 repetitions, 1-2 times per day, 3-5 times per week.
3. Leg coordination exercise 2 Objective: Improve coordination of legs Position: Sitting/Standing Procedure: Place a cone in front of the seat. Touch the cone with one foot and then touch the foot back under the seat. Repeat on the other leg. Frequency: 10 repetitions, 1-2 times per day, 3-5 times per week.
Strengthening
1. Lunges Objective: Strengthening the muscles around the legs to improve ability to transfer. Position: Standing Procedure: Refer to Figure 4. Take large step forward with one foot and bend at both knees as if driving back knee down toward the floor. Be aware not to let front knee go past toes. Return and repeat with other leg. Frequency: 8-10 repetitions, 1-2 times per day, 3-5 times per week.
Figure 4
2. Squats Objective: Strengthening the muscles around the gluteal and knee areas Position: Standing Procedure: While standing with feet shoulder width apart and in front of a stable support for balance assist if needed, bend your knees and lower your body towards the floor. Your body weight should mostly be directed through the heels of your feet. Return to a standing position. Knees should bend in line with the 2nd toe and not pass the front of the foot. Frequency: 8-10 repetitions, 1-2 times per day, 3-5 times per week.
Figure 5 3. Standing heel raise Objective: Strengthening the plantar flexors while weight loading Position: Standing against a chair Procedure: Refer to Figure 6. While standing and holding a chair, rise up on your toes as you lift your heels off the ground. Slowly lower yourself to the initial resting position. Once you are able to perform this easily without pain, progress to not holding onto the chair. Frequency: 10-12 repetitions, 1-2 times per day, 3-5 times per week.
Figure 6
References
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