spasticity

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Spasticity is a condition in which certain muscles are continuously contracted. It usually occurs in people with damage to the upper motor neurons, which are nerves in the brain and spinal cord that control movement. Common causes of damage to the upper motor neurons include:

• Cerebral palsy - Damage to the motor areas of the developing brain before or shortly after birth. This can lead to muscle spasms and stiffness, especially in the legs.
• Multiple sclerosis - The immune system attacks the myelin sheaths that insulate nerve fibers in the brain and spinal cord. This can disrupt signals from the brain to the muscles and cause spasticity.
• Spinal cord injury - Trauma that damages the spinal cord can sever or compress the upper motor neurons, resulting in spasticity below the level of the injury.
• Stroke - A blood clot or hemorrhage in the brain can damage upper motor neurons and lead to spasticity, typically on one side of the body.

The main features of spasticity include:

• Hypertonia - Muscle tone that is too high, resulting in muscles that are stiff, tense and resistant to passive movement.
• Clonus - Rapid, involuntary muscle contractions that lead to twitching or jerking movements. Clonus is often triggered by quick motions or vibrations near the muscle.
• Muscle spasms - Spontaneous, involuntary muscle contractions that can range from mild twitches to severe, painful contortions. Spasms are often triggered by stimulation or movement and can interfere with voluntary movement and daily activities.
• Contractures - Muscles that remain permanently shortened and tense, which can cause joint deformities and mobility issues over time.
• Exaggerated reflexes - The tendon reflexes, such as the knee-jerk reflex, are overly responsive and can trigger muscle spasms.
• Pain - The constant muscle tension and spasms associated with spasticity frequently lead to pain, which can be quite severe. Pain management is an important part of spasticity treatment.

The main goals of spasticity treatment are: relax muscles, reduce pain, prevent complications and improve mobility and function. Treatment options include physical therapy, medications, injections and surgery.

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Topic Highlights:-

1. Spasticity is a debilitating motor disorder causing an abnormal increase in muscle tone.
2. Injury or damage to a part of the spinal cord or brain that controls muscle movement is the main cause of spasticity.
3. Spasticity comes in two types: flexor and extensor.
4. This visual presentation explains the etiology of spasticity, its pathophysiology, clinical assessment, and various management options.
5. The presentation also contains a section on the management of spasticity in children.

Transcript:-
Spasticity refers to an abnormal, involuntary and velocity-dependent rise in muscle tone that does not coordinate with other muscles. It is a complex motor disorder caused due to damage or injury to a part of the brain or spinal cord that controls muscle movements. Spasticity was first described by Little in the year 1843.

The condition may sometimes present itself after an injury and may be static or dynamic in nature. It is usually debilitating, making the patients very much dependant on others for their day-to-day activities.

Spasticity usually occurs secondary to some trauma related to the brain or spinal cord, or as a complication to conditions such as cerebral palsy, multiple sclerosis, tumor, or stroke. It can also be attributed to some neurodegenerative diseases that affect the upper motor neuron, pyramidal pathway that controls the voluntary movements and extrapyramidal pathway that controls the autonomic movements. Spasticity may also be the result of disturbed transmissions in the afferent and the efferent input that is connected to the alpha motor neuron. Injury to the nerves of the brain or spinal cord can change the inhibitory and excitatory signals to the motor neuron.

The injury could also result in other changes such as denervation super sensitivity (oversensitive nerves), deafferentation (loss of sensory input due to injury or destruction of sensory nerve fibers), adrenoleukodystrophy (inherited, progressive brain damage resulting from accumulation of very long chain fatty acids), phenylketonuria (a genetic disorder characterized by inability of the body to utilize the amino acid phenylalanine), central collateral sprouting or disinhibition of the nerves. Spinal cord mediated spasticity involves polysynaptic pathways whereas cortical-mediated spasticity involves increased excitability of monosynaptic responses.

The exact pathophysiology of spasticity is still not very well understood. Many theories are proposed to explain the increased muscle tone. This includes changes in reticulospinal pathway (a pathway that regulates muscle tone by modulating the stretch reflex), sensory as well as motor neurons.

The muscle spindle is connected to the afferent limb of the sensory neurons that are located in the dorsal root ganglion of the spinal cord. The impulses that travel from the muscle spindles to the sensory neuron, through the afferent limb, bring about the stretch reflex, from where they are transmitted to the grey matter of the spinal cord. Here, the sensory neuron maintains synaptic response with the motor neuron. The cell body of the motor neuron is present in the anterior horn of the spinal cord and from there the efferent limb of the stretch reflex runs through the anterior spinal root and reaches the muscle fibers where it elicits a contractile response.

When an impulse is transmitted through the stretch reflex, it brings about contraction in agonist muscles. An inhibitory neuron in the spinal cord elicits relaxation in the antagonist muscles.

In healthy individuals, rapid stretching of muscles does not bring about a response beyond a particular period of time, but in patients with spasticity it brings about a prolonged response. There are changes that are introduced in the excitability of motor neurons especially that of the alpha motor neuron, interneuronal junctions and reflex pathways. The antagonistic muscle relaxation brought about by the descending pathway called Ia pathway, is also affected in spasticity due to changes in the activities of the pathway.

In addition to disturbances in the transmission of impulses from the reticulospinal system and other descending pathways to the motor and interneuronal circuits of the spinal cord, spasticity can occur due to the absence of an intact corticospinal system.

Based on the muscles involved, spasticity is of two types – flexor and extensor. In flexor spasticity, the hamstring muscle (upper back muscles of the leg) and hip flexor muscles (muscles at the upper thigh) are involved, leading to abnormal posture and movement of the hip and knee joint. Extensor spasticity involves the quadriceps (muscles on the front of the upper leg) and adductors (inner thigh muscles). The hips and knees remain straight, while the legs are very closely placed to each other, or there is crossing over at the ankles.

The signs and symptoms are related to time elapsed since the injury or disease occurrence and may increase or decrease overtime.

The general symptoms observed are

1. Hypertonicity (increased muscle tone)
2. Exaggerated deep tendon reflex (knee-jerk reflex)
3. Clonus (repeated jerky movements)
4. Scissoring of legs (involuntary crossing of the legs), and
5. Abnormal body posture – placing the shoulders, wrists or fingers at an unusual angle Changes in speech may also be observed.

Severe, long term spasticity leads to bending of joints into a set position due to abnormal muscle contraction.

Spasticity may also be accompanied by clonus, the clasp-knife phenomenon, hyperreflexia, Babinski syndrome, flexor reflexes and flexor spasms.

While assessing a patient with spasticity, it is vital to identify the muscles or the muscle groups that are affected, the effect of it on the patient – his mobility and performance of daily activities etc. Assessment of the affected muscle may be difficult as a number of muscles are present over a particular joint and not all muscles may be spastic.

A thorough recording of the patient’s history and examination, supplemented with diagnostic imaging of the head, neck and the spine areas are followed. Laboratory studies are included to eliminate the possibilities of any infections. The common laboratory studies that are performed include a complete blood count, urine culture, blood culture and examination of cerebrospinal fluid.

Muscle tone is the first parameter assessed before any tests to evaluate muscle functions. Electromyography and diagnostic blocks with local anesthesia are used to assess the spastic muscles and determine their range of motion. In infants, spasticity is diagnosed by assessing the muscle tone in supination and pronation of the upper extremities, and dorsiflexion and plantar flexion of the lower extremities.

While assessing a patient for spasticity, some of the patterns of symptoms commonly found in patients with other disorders should be considered.

Patients with cerebral palsy, trauma and stroke, commonly exhibit the following patterns in the upper extremities

1. Elbow and wrist flexion
2. Forearm pronation
3. Flexion of fingers and thumb adduction
4. Internal rotation and adduction of shoulders

Common patterns in lower extremities exhibited by patients with cerebral palsy, multiple sclerosis, trauma and stroke include

1. Ankle plantar flexion or equinovarus posture
2. Hip flexion and adduction
3. Knee flexion
4. Excessive toe flexion

It is important to perform the tests in the same pattern each time, as the test itself may be detrimental on muscle tone. While assessing upper extremities, the patient must sit so various muscle groups can be evaluated. While assessing the pronator, shoulder rotators, supinators, wrist and finger flexors, the elbow is placed at 90° of flexion, whereas for other muscle groups the elbow is completely extended. For evaluating the lower extremities, the patient is asked to lie down in a supine position. This is a useful position to assess all muscle groups except the knee flexors for which the patient is placed prone.

There are many different scales available to standardize the recordings of these diagnostic procedures. Some of them are: modified Ashworth Scale, Medical Research Council Motor Testing Scale, Spasm Frequency Scale, Global Pain Scale and the Adductor Tone Rating.

The ratio scales, measuring the parameters before and after treatment, are useful in evaluating treatment outcome. A functional outcome is the measure of improvement in the patient’s capability to execute some tasks or functions. A patient’s satisfaction measure is also included in these assessments.

There are various approaches to treat a patient with spasticity. Before treatment, it is essential to assess whether the patient requires treatment and if so, what are the results that are to be expected. It is also important to evaluate the adequate time that can be devoted by the patient and the patient’s caregivers for treatment.

The treatment process should mainly focus on reducing pain, discomfort, frequency of spasms, and improving gait. It should help the patient get better, perform passive functions such as day-to-day activities independently and improve voluntary active motor function such as reaching for an object, grasping, moving, releasing an object, etc.

Spasticity treatment does not follow a stepped approach. Instead, a variety of treatments are used at the same time or they may be interchanged, based on the individual.

1. Preventive methods – include identifying and avoiding precipitating factors such as pressure, temperature variations, constipation, distension of the bladder, stress, infections, etc.
2. Therapeutic methods – include physiotherapy and other techniques such as cryotherapy, heat therapy, electrical stimulation, hydrotherapy, massage, sustained stretching, etc.
3. Positioning methods – Devices like orthoses, splints or casts are used to position the affected part, including positioning during seating or lying down on the bed, reducing deformity and alleviating pain.
4. Oral medications – Commonly prescribed medications include Baclofen, Benzodiazepines, Dantrolene, Tizanidine, Clonidine, Gabapentin, Lamotrigine, Cyproheptadine and Cannabinoid-like compounds among others.
5. Baclofen is a commonly used muscle relaxant that affects the spinal cord. It is a GABA agonist and inhibits the release of excitatory neurotransmitters by binding to the GABA-B receptor.
6. Tizanidine, a centrally acting α-2-adrenergic agonist, is used to reduce spasms and relax tightened muscles.
7. Benzodiazepines work by binding to the brain stem and spinal cord, increasing the affinity of GABA to the GABA-A receptor. This reduces hyperreflexia, pain and spasms. Benzodiazepines are prescribed in small doses with baclofen at bedtime to release spasms during sleep.
8. Dantrolene sodium is prescribed only if other medications are found ineffective. It is prescribed for patients with spasticity of supraspinal origin, like those with cerebral palsy. It decreases muscle tone, clonus and muscle spasm.

Injections

1. Intrathecal bolus injection of 5% phenol acts as a nerve-blocking agent that reduces pain and frequency of spasm.
2. Botulinum toxin is found to be effective in relieving individual muscles for a period of one to three months. Botulinum toxin type A or B can be used alone or as a combination therapy including both phenol and botulinum.

Surgical methods

1. Intrathecal Baclofen (ITB) – Balcofen used to treat patients with severe spasticity of the lower extremities. The drug is administered through a pump that is surgically implanted into the patient’s abdomen so that the medication is directly delivered to the spinal fluid.
2. Orthopedic Interventions – are the frequently used procedures to treat spasticity. Two types of surgical procedures are currently in use: tenotomy – lengthening or release of muscles, and tendons and procedures pertaining to bones called osteotomy. Both these procedures aim at reducing spasticity, increase the range of motion and reduce pain. Osteotomy is particularly aimed at reducing bone deformities.
3. Selective Dorsal Rhizotomy – is a procedure that involves ablation (cutting) of posterior spinal nerve roots between L2 and S1 or S2. This method is effective in alleviating spasticity in lower extremities that interfere with positioning and mobility.

Other surgical procedures that may be used include:

1. Myelotomy or Cordectomy which involves resection of some parts of the spinal cord
2. Stimulation of the spinal cord with a stimulator that is implanted percutaneously. The stimulator helps in reducing pain but does not have any effect on spasticity.
3. Stereotactic neurosurgery and cerebellar stimulation are still in the experimental stage, with success reported in some patients.

The main aim of rehabilitation is to maintain range of motion of joint and prevent muscle spasms. Stretching is the conventional treatment during rehabilitation and should be done regularly. Strengthening exercises are recommended to improve functioning of muscles in the affected limbs. Proper limb positioning in bed, chair or wheelchair is suggested to improve comfort and posture.

Neurodevelopmental Therapy – is aimed to reduce the abnormal reflexes and train the muscles to bring in normal balanced reactions. Here the patient is trained to use the affected limb, using aids, to produce normal movement patterns with or without assistance.

Proprioceptive Neuromuscular Facilitation – Like neurodevelopmental therapy, the patients are trained to use spastic muscles normally. They are trained to roll on the floor, sit, stand and walk. Here, the stronger and less spastic muscles are worked on, in turn strengthening the weaker muscles and activating them to work normally. Range of motion exercises are instructed on the stronger muscles and later to the weaker parts of the hand or foot, to increase proprioceptive feedback to the muscles.

Sensory Integration – Therapist continuously repeats a set of instructions to move the affected limb. The patient remains passive so that the instructions are registered in the brain and aid in normal movement of the limb.

There are a number of management programs for children with spasticity that aim at reducing pain and maximize functionality. The treatment options available, both medical and psychosocial methods, aim to improve short-term mobility and reduce long-term deformities of the limb and spine. Parents of spastic children should be encouraged to participate in the treatment and evaluation regimen.