Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Saturday, October 22, 2011

Computerized gait analysis helps patients with brain injuries

I know this is from 2002 but before finding this I had never heard of any patients getting this kind of analysis.
http://physical-therapy.advanceweb.com/Article/Decoding-Gait.aspx

Computerized gait analysis helps patients with brain injuries

A 34-year-old mother of two, Jane was in a car accident and sustained head trauma with residual left hemiparesis. After 16 months, her gait was slow and unsteady. She couldn't walk up or down stairs without using a handrail. Although a brace did help her, she complained of pain on her lateral ankle bone because her foot turned inside the brace.

Cerebral palsy, traumatic brain injury and stroke are common types of brain injuries that frequently produce motor dysfunction of the upper motoneuron (UMN) type.1 Three factors strongly influence the clinical expression of motor dysfunction of UMN: spasticity or muscle overactivity; contracture; and impaired motor control.2,3

Treating a patient like Jane with UMN movement dysfunction can be complex, but we usually start by taking a detailed medical history, performing a physical examination and doing an evaluation in a gait laboratory.4

The physical exam usually will reveal increased tone in certain lower limb areas, but it doesn't determine contractures or motor control ability.5 In addition to performing passive range of motion and passive stretching of tissue, the examiner may observe the patient's ability to perform lower limb active functioning for the ankle, knee, hip and trunk while the patient moves. The examiner also should assess coordination and balance during this exam. At MossRehab, we often use Modified Ashworth and Tardieu scoring to quantify clinical measures of spasticity across a joint segment and document the result of a treatment.6

After the physical exam, computerized gait analysis in a laboratory helps further decode problems. In Jane's case, an equinovarus ankle foot posture during the stance phase—when one foot or leg bears most of the weight—produced an unstable ankle and base of support. Several underlying problems or a combination of them can cause this deformity; this is where computerized gait analysis comes into play.

In fact, computerized gait analysis is the mainstay of evaluation with patients with spasticity, contracture and incoordination.7 Several issues can contribute to these symptoms. For example, contracture or muscle overactivity of a combination of multiple plantar flexor muscles (gastrocnemius, soleus, long toe flexors) and ankle inverters (tibialis anterior, tibialis posterior, extensor hallucis longus, medial gastrocnemius) can contribute to ankle equinovarus. By using computerized gait analysis, the examiner can pinpoint problem areas.

Computerized gait analysis also can help pinpoint other stance problems. For example, stiff knee gait can be a result of weak knee extensors or hip flexors; muscle overactivity of the hip extensors, knee extensors or hip flexors; muscle overactivity of the hip extensor, knee extensors or ankle plantarflexors; contracture of the hip, knee or ankle; or a combination of any one of these elements.

Understanding the source and cause of these deformities is essential, particularly when spasticity or contractures coexist or if a patient has had tendon lengthening, transfer surgery or a neurotoxin injection.

Computerized gait analysis allows us to closely examine a moving patient. We can record kinematic (movement), kinetic (forces) and dynamic EMG (muscle activation) data to determine causes of the problem. In addition, many clinicians use diagnostic nerve blocks, which help differentiate a contracture from muscle overactivity. The following provides a breakdown of different computerized gait analyses8:

3-D motion analysis (kinematic). Three-dimensional motion analysis provides a quantitative description of the body as it moves. To record the movement, we place passive or active markers on the body. Passive markers reflect visible or infrared light during motion analysis. Active markers are light-emitting, but can be restrictive because wires can interfere with movement. Once we place these markers on the body, two or more specialized optoelectronic cameras track the markers as the body moves. Computerized mathematical triangulation turns the marker data into 3-D motion data. From there, this data can be processed and displayed as a function of time or as a percent of the stride period.

This analysis also can show joint angles, linear and angular velocities and acceleration. When combined with anthropometric measures and kinetic (force) data, joint moments and powers can be calculated. This will help an experienced clinician tell the cause and treatment of an abnormal problem.

Kinetics. Kinetic analysis deals with the forces that are produced during walking. It generally uses a triaxial force plate to measure ground reaction force under the feet. By recording the force, we can help determine torque on a given joint center (i.e., pelvis, hip, knee, ankle).

This movement characterizes the direction and magnitude of the external force to the joint to produce joint rotation (flexion/extension, ab/adduction, internal/external rotation). Internal forces generated primarily by muscles and to a lesser degree by tendons, ligaments and the geometry of the joint articulation (bony contact), act to control the rotation of the joints.

For example, because Jane's foot is turned in before it touches the ground, her ankle will be unstable or her knee will extend back once it makes contact, increasing the activation of trunk and pelvic muscles.

Electromyographic (EMG) activation patterns. In normal locomotion, opposing muscular forces control gravitational forces to yield a smooth and energy-efficient movement pattern. Efficient movement patterns depend upon a highly coordinated sequence of the timing and strength of the muscle contractions.

Because of the redundant relationship between muscles and the joints, there is no unique association between a movement and the pattern of muscle forces producing movement. For example, the tibialis anterior and the tibialis posterior can produce ankle inversion.

An EMG signal accurately indicates neurological control for muscles and joints that may be causing the deforming force. Bipolar surface electrodes secured with double-sided tape are ideal for superficial muscles. For deep muscles or to differentiate between adjacent muscles, we can insert indwelling fine wire electrodes through a hypodermic needle.

EMG recordings provide information about the timing, duration and relative strength of muscle activation. To help standardize terminology for EMG recordings, researchers have determined a timing classification for electromyographic activity:

  • No activity. Muscle is not active and, perhaps, a contracture is the cause of the posture.

  • Continuous activity. This indicates the muscle is spastic or weak.

  • Dysinergic. This shows out-of-phase activity, which means the muscle is active at the wrong time.

  • Phasic premature. This occurs when the activation is premature.

  • Phasic prolonged. The muscle will activate in a timely fashion, but with overflow.

  • Normal phasic. This classification indicates normal activation.

    Be aware and understand that walking speed affects the EMG patterns. Thus, direct comparison with normal data at a different walking velocity may not produce accurate results. In addition, when interpreting dynamic-EMG data, there may be many causes for a specific problem.

    To promote rebalancing of the joints' static and dynamic forces, interventions, such as Botox injections, phenolization of motor nerve branches and neuroorthopedic options, can reduce muscle overactivity.

    Jane significantly improved after we injected Botox in the affected muscles. She is now walking with just a cane in the park with her daughters. She can go up and down stairs and can walk at home without aids.

    Other patients will benefit from a neuroorthopedic surgical approach to promote rebalancing of static and dynamic forces across joints. However, it's crucial to clearly identify the problem. As these examples show, several causes and treatments for UMN syndrome in patients with brain injury exist. Computerized gait analysis is a great tool for unraveling an often-confusing mystery. Gait and motion analysis laboratories can help advance the clinical treatment of upper motor neuron dysfunction, resulting in an improved quality of life.

    References

    1. Esquenazi, A., & Hirai, B. (1994). Assessment and management of gait dysfunction in patients with spastic stroke or brain injury. State of the Art Reviews, 8(3), 523-533.

    2. Mayer, N. (1997). Clinicophysiology concepts of spasticity and motor dysfunction in adults with an upper motoneuron lesion. Muscle & Nerve, 6, S1-S13.

    3. Mayer, N., Esquenazi, A., & Childers, M. (1997). Common patterns of clinical motor dysfunction. Muscle & Nerve, 6, S21-S35.

    4. Mayer, N., Esquenazi, A., & Wannstedt, G. (1996). Surgical planning for upper motoneuron dysfunction: The role of motor control evaluation. The Journal of Head Trauma Rehabilitation, 11, 37-56.

    5. Ochi, F., Esquenazi, A., Hirai, B., & Talaty, M. (1999). Temporal-spatial features of gait after traumatic brain injury. The Journal of Head Trauma Rehabilitation, 14(2), 105-115.

    6. Perry, J. (1999). The use of gait analysis for surgical recommendations in traumatic brain injury. The Journal of Head Trauma Rehabilitation, 14(2), 116-135.

    7. Fuller, D.A., Keenan, M.A., Esquenazi, A., Whyte, J., Mayer, N., & Fidler-Sheppard, R. (2002, August). The impact of instrumented gait analysis on surgical planning: Treatment of spastic equinovarus deformity of the foot and ankle. Foot and Ankle International, 22, 738-743.

    8. Mayer, N., Esquenazi, A., & Keenan, M.A. (1996). Evaluation and management of spasticity, contracture and impaired motor control: Medical rehabilitation of traumatic brain injury. In. L. Horn and N. Zasler (Eds.), Medical rehabilitation of traumatic brain injury. Philadelphia: Henley & Belfus

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