Monoplegia | |
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Damage to the motor cortex can induce monoplegia. | |
Specialty | Neurology |
Causes | Stroke, cerebral palsy, direct physical trauma to the affected limb, central nervous mass lesion, tumor, hematoma, or abscess, migraine, epilepsy, head or spinal trauma, brachial neuritis, neonatal brachial plexus paralysis, Brown Sequard, peripheral neuropathy, plexopathy, traumatic peroneal neuropathy, paralytic poliomyelitis, spinal muscular atrophy, seizures |
Differential diagnosis | Hemiplegia, paraplegia, quadriplegia |
Monoplegia is paralysis of a single limb, usually an arm. Common symptoms associated with monoplegic patients are weakness, numbness, and pain in the affected limb. Monoplegia is a type of paralysis that falls under hemiplegia. While hemiplegia is paralysis of half of the body, monoplegia is localized to a single limb or to a specific region of the body. Monoplegia of the upper limb is sometimes referred to as brachial monoplegia, and that of the lower limb is called crural monoplegia. Monoplegia in the lower extremities is not as common of an occurrence as in the upper extremities. Monoparesis is a similar, but less severe, condition because one limb is very weak, not paralyzed. For more information, see paresis.
Many conditions that cause paraplegia or quadriplegia begin as monoplegia. Thus, the diagnosis of spinal paraplegia must also be consulted. In addition, multiple cerebral disorders that cause hemiplegia may begin as monoplegia. [1] Monoplegia is also frequently associated with, and considered to be the mildest form of, cerebral palsy.
There are a number of symptoms associated with monoplegia. Curling of the hands or stiffness of the feet, weakness, spasticity, numbness, paralysis, pain in the affected limb, headaches, and shoulder pain are all considered to be symptoms of monoplegia. Patients of monoplegia typically feel symptoms of weakness and loss of sensation in the affected extremity, usually an arm. Despite these symptoms, the extremity with paralysis continues to maintain a strong pulse.
While chronic progressive brachial monoplegia is uncommon, syringomyelia and tumors of the cervical cord or brachial plexus may be the cause. The onset of brachial plexus paralysis is usually explosive where pain is the initial feature. Pain localizes to the shoulder but may be more diffuse, or could be limited to the lower arm. Pain is severe and often described as sharp, stabbing, throbbing, or aching. The duration of pain, which is constant, varies from a span of several hours to 3 weeks. [2] As the pain subsides, weakness usually appears. In addition, chronicle progressive weakness of one leg suggests a tumor of the spinal cord of the lumbar plexus. Fever is often the first symptom of lumbar plexus paralysis, followed by pain in one or both legs. The pain has an abrupt onset and may occur in a femoral or sciatic distribution. Weakness may develop concurrently with pain or be delayed for as long as 3 weeks. [2] Furthermore, a monomeric form of spinal muscular atrophy, affecting only one leg or arm, should be considered when progressive weakness is not accompanied by sensory loss. [1]
Some potential causes of monoplegia are listed below.
Specifically, monoplegia in the lower extremities is typically caused by Brown Sequard syndrome and hematomas in the frontoparietal cortex near the middle that could produce a deficit such as this, but this is a very uncommon occurrence.
In monoplegia, the spine and the proximal portion of nerves are usually the abnormal sites of limb weakness. [1] Monoplegia resulting from upper extremity impairments following a stroke occurs due to direct damage to the primary motor cortex, primary somatosensory cortex, secondary sensorimotor cortex, sensorimotor cortical areas, subcortical structures, and/or the corticospinal tract. [4] It is often found that impairments following stroke are either caused by damage to the same or adjacent neurological structures. [4] A combination of these impairments is more likely than just one in isolation. [4] Damage to the corticospinal system results in an inability to activate muscles with enough force or in a coordinated manner, which can lead to paresis, loss of fractional movement, and abnormal muscle tone. [4] Damage to the somatosensory cortical areas causes loss of somatosensation which results in an impaired ability to monitor movement. [4]
Considering monoplegia as it relates to cerebral palsy, in premature infants, the most common cause of cerebral palsy is periventricular hemorrhagic infarction. In term infants, the underlying causes are often cerebral malformations, cerebral infarction, and intracerebral hemorrhage. [1] Delayed crawling or walking are the usual concerns that arise in infants with paralysis of the limb. In these cases, abnormalities of the legs are the main focus of the attention. [1]
Monoplegia is diagnosed by a physician after a physical examination and sometimes after further neurologic examination as well. As monoplegia is fairly rare, after physical examination of a patient complaining of monoplegia, sometimes weakness of an additional limb is also identified and the patient is diagnosed with hemiplegia or paraplegia instead. [3] After neurologic examination of the limb, a diagnosis of a monoplegic limb can be given if the patient receives a Medical Research Council power grade of 0, which is a measurement of the patient's limb strength. [5] Needle Electromyography is often used to study all limbs, essentially showing the extent in each limb involvement. Furthermore, magnetic resonance imaging (MRI) is the diagnostic modality of choice for investigating all forms of hemiplegia. It is especially informative to show migrational defects in hemiplegic cerebral palsy associated with seizures. [6]
An approach called single-pulse transcranial magnetic stimulation (spTMS) has also been used to help diagnose motor deficits such as monoplegia. [5] This is done by evaluating the functional level of the corticospinal tract through stimulation of the corticospinal lesions in order to obtain neurophysiologic evidence on the integrity of the corticospinal tracts. [5] Single-pulse transcranial magnetic stimulation provides neuropsychological feedback such as motor-evoked potentials (MEPs) and central motor conduction time (CMCT). [5] This feedback can then be compared to the normal limits of patients who do not show evidence of deficits in the corticospinal tracts. [5]
There is no cure for monoplegia, but treatments typically include physical therapy and counseling to help recover muscle tone and function. Recovery will vary depending on diagnosis of temporary, partial or complete paralysis. Much of the therapies focus on the upper limb due to the fact that monoplegia in the upper limbs is much more common than in the lower limbs. It has been found that intense activity-based and goal-directed therapy, such as constraint-induced movement therapy and bimanual therapy, are more effective than standard care. Studies suggest the less affected hand could provide a template for improving motor performance of the more affected hand, and provides a strong rationale for the development of bimanual training approaches. [7] In addition to that, there is strong evidence to support that occupational therapy home programs that are goal-directed could be used to supplement hands-on direct therapy. [8]
Constraint-induced movement therapy (CIMT) is specifically targeted at upper limb monoplegia as a result of a stroke. In CIMT the unaffected arm is restrained, forcing the use and frequent practice of the affected arm. This approach to therapy is carried out during ordinary and daily activities by the affected person. It has been found that CIMT is more effective at specifically improving arm movement than a physiotherapy approach or no treatment at all. [9] This type of therapy has proved to provide an only moderate improvement in patients with monoplegia. [9] More research needs to be conducted in order to establish the lasting benefit of constraint-induced movement therapy.
Brain computer interface (BCI) systems have been proposed as a tool for rehabilitation of monoplegia, specifically in the upper limb after a stroke. [10] BCI systems provide sensory feedback in the brain via functional electrical stimulation, virtual reality environments, or robotic systems, which allows for the use of brain signals. [10] This is extremely crucial because the networking in the brain is often compromised after a stroke, leading to impaired movement or paralysis. BCI systems allow for detection of intention to move through the primary motor cortex, then provide the matched sensory stimulation according to feedback that is provided. [10] This leads to activity-dependent plasticity within the user, requiring them to pay careful attention to tasks that require the activation or deactivation of specific brain areas. [10] BCI systems utilize different sources of information for feedback, including electroencephalography (EEG), magnetoencephalography, functional magnetic resonance imaging, near-infrared spectroscopy, or electrocorticography. [10] Among all of these, the EEG signals are the most useful for this type of rehabilitation because they are highly accurate and stable. [10]
Another form of treatment for monoplegia is functional electrical stimulation (FES). It is targeted at patients who acquired monoplegia through incidents such as a spinal cord injury, stroke, multiple sclerosis, or cerebral palsy and utilizes electrical stimulation in order to cause the remaining motor units in the paralyzed muscles to contract. [11] As in traditional muscular training, FES improves the force with which the unaffected muscles contract. For less severely affected patients, FES allows for greater improvement in range of motion than traditional physical therapy. [11]
Hemiparesis, or unilateral paresis, is weakness of one entire side of the body. Hemiplegia is, in its most severe form, complete paralysis of half of the body. Hemiparesis and hemiplegia can be caused by different medical conditions, including congenital causes, trauma, tumors, or stroke.
Spasticity is a feature of altered skeletal muscle performance with a combination of paralysis, increased tendon reflex activity, and hypertonia. It is also colloquially referred to as an unusual "tightness", stiffness, or "pull" of muscles.
Tetraplegia, also known as quadriplegia, is defined as the dysfunction or loss of motor and/or sensory function in the cervical area of the spinal cord. A loss of motor function can present as either weakness or paralysis leading to partial or total loss of function in the arms, legs, trunk, and pelvis; paraplegia is similar but affects the thoracic, lumbar, and sacral segments of the spinal cord and arm function is retained. The paralysis may be flaccid or spastic. A loss of sensory function can present as an impairment or complete inability to sense light touch, pressure, heat, pinprick/pain, and proprioception. In these types of spinal cord injury, it is common to have a loss of both sensation and motor control.
The brachial plexus is a network of nerves formed by the anterior rami of the lower four cervical nerves and first thoracic nerve. This plexus extends from the spinal cord, through the cervicoaxillary canal in the neck, over the first rib, and into the armpit, it supplies afferent and efferent nerve fibers to the chest, shoulder, arm, forearm, and hand.
The pyramidal tracts include both the corticobulbar tract and the corticospinal tract. These are aggregations of efferent nerve fibers from the upper motor neurons that travel from the cerebral cortex and terminate either in the brainstem (corticobulbar) or spinal cord (corticospinal) and are involved in the control of motor functions of the body.
Klumpke's paralysis is a variety of partial palsy of the lower roots of the brachial plexus. The brachial plexus is a network of spinal nerves that originates in the back of the neck, extends through the axilla (armpit), and gives rise to nerves to the upper limb. The paralytic condition is named after Augusta Déjerine-Klumpke.
Erb's palsy is a paralysis of the arm caused by injury to the upper group of the arm's main nerves, specifically the severing of the upper trunk C5–C6 nerves. These form part of the brachial plexus, comprising the ventral rami of spinal nerves C5–C8 and thoracic nerve T1. These injuries arise most commonly, but not exclusively, from shoulder dystocia during a difficult birth. Depending on the nature of the damage, the paralysis can either resolve on its own over a period of months, necessitate rehabilitative therapy, or require surgery.
Mirror therapy (MT) or mirror visual feedback (MVF) is a therapy for pain or disability that affects one side of the patient more than the other side. It was invented by Vilayanur S. Ramachandran to treat post-amputation patients who had phantom limb pain (PLP). Ramachandran created a visual illusion of two intact limbs by putting the patient's affected limb into a "mirror box," with a mirror down the center.
A brachial plexus injury (BPI), also known as brachial plexus lesion, is an injury to the brachial plexus, the network of nerves that conducts signals from the spinal cord to the shoulder, arm and hand. These nerves originate in the fifth, sixth, seventh and eighth cervical (C5–C8), and first thoracic (T1) spinal nerves, and innervate the muscles and skin of the chest, shoulder, arm and hand.
Hypertonia is a term sometimes used synonymously with spasticity and rigidity in the literature surrounding damage to the central nervous system, namely upper motor neuron lesions. Impaired ability of damaged motor neurons to regulate descending pathways gives rise to disordered spinal reflexes, increased excitability of muscle spindles, and decreased synaptic inhibition. These consequences result in abnormally increased muscle tone of symptomatic muscles. Some authors suggest that the current definition for spasticity, the velocity-dependent over-activity of the stretch reflex, is not sufficient as it fails to take into account patients exhibiting increased muscle tone in the absence of stretch reflex over-activity. They instead suggest that "reversible hypertonia" is more appropriate and represents a treatable condition that is responsive to various therapy modalities like drug or physical therapy.
Fazio–Londe disease (FLD), also called progressive bulbar palsy of childhood, is a very rare inherited motor neuron disease of children and young adults and is characterized by progressive paralysis of muscles innervated by cranial nerves. FLD, along with Brown–Vialetto–Van Laere syndrome (BVVL), are the two forms of infantile progressive bulbar palsy, a type of progressive bulbar palsy in children.
Progressive bulbar palsy (PBP) is a medical condition. It belongs to a group of disorders known as motor neuron diseases. PBP is a disease that attacks the nerves supplying the bulbar muscles. These disorders are characterized by the degeneration of motor neurons in the cerebral cortex, spinal cord, brain stem, and pyramidal tracts. This specifically involves the glossopharyngeal nerve (IX), vagus nerve (X), and hypoglossal nerve (XII).
Diplegia, when used singularly, refers to paralysis affecting symmetrical parts of the body. This is different from hemiplegia which refers to spasticity restricted to one side of the body, paraplegia which refers to paralysis restricted to the legs and hip, and quadriplegia which requires the involvement of all four limbs but not necessarily symmetrical. Diplegia is the most common cause of crippling in children, specifically in children with cerebral palsy. Other causes may be due to injury of the spinal cord. There is no set course of progression for people with diplegia. Symptoms may get worse but the neurological part does not change. The primary parts of the brain that are affected by diplegia are the ventricles, fluid filled compartments in the brain, and the wiring from the center of the brain to the cerebral cortex. There is also usually some degeneration of the cerebral neurons, as well as problems in the upper motor neuron system. The term diplegia can refer to any bodily area, such as the face, arms, or legs.
Central facial palsy is a symptom or finding characterized by paralysis or paresis of the lower half of one side of the face. It usually results from damage to upper motor neurons of the facial nerve.
Upper motor neuron syndrome (UMNS) is the motor control changes that can occur in skeletal muscle after an upper motor neuron lesion.
Spastic cerebral palsy is the type of cerebral palsy characterized by spasticity or high muscle tone often resulting in stiff, jerky movements. Cases of spastic CP are further classified according to the part or parts of the body that are most affected. Such classifications include spastic diplegia, spastic hemiplegia, spastic quadriplegia, and in cases of single limb involvement, spastic monoplegia.
Spastic hemiplegia is a neuromuscular condition of spasticity that results in the muscles on one side of the body being in a constant state of contraction. It is the "one-sided version" of spastic diplegia. It falls under the mobility impairment umbrella of cerebral palsy. About 20–30% of people with cerebral palsy have spastic hemiplegia. Due to brain or nerve damage, the brain is constantly sending action potentials to the neuromuscular junctions on the affected side of the body. Similar to strokes, damage on the left side of the brain affects the right side of the body and damage on the right side of the brain affects the left side of the body. Other side can be effected for lesser extent. The affected side of the body is rigid, weak and has low functional abilities. In most cases, the upper extremity is much more affected than the lower extremity. This could be due to preference of hand usage during early development. If both arms are affected, the condition is referred to as double hemiplegia. Some patients with spastic hemiplegia only experience minor impairments, where in severe cases one side of the body could be completely paralyzed. The severity of spastic hemiplegia is dependent upon the degree of the brain or nerve damage.
Restorative neurology is a branch of neurology dedicated to improving functions of the impaired nervous system through selective structural or functional modification of abnormal neurocontrol according to underlying mechanisms and clinically unrecognized residual functions. When impaired, the body naturally reconstructs new neurological pathways and redirects activity. The field of restorative neurology works to accentuate these new pathways and primarily focuses on the theory of the plasticity of an impaired nervous system. Its main goal is to take a broken down and disordered nervous system and return it to a state of normal function. Certain treatment strategies are used to augment instead of fully replace any performance of surviving and also improving the potential of motor neuron functions. This rehabilitation of motor neurons allows patients a therapeutic approach to recovery opposed to physical structural reconstruction. It is applied in a wide range of disorders of the nervous system, including upper motor neuron dysfunctions like spinal cord injury, cerebral palsy, multiple sclerosis and acquired brain injury including stroke, and neuromuscular diseases as well as for control of pain and spasticity. Instead of applying a reconstructive neurobiological approach, i.e. structural modifications, restorative neurology relies on improving residual function. While subspecialties like neurosurgery and pharmacology exist and are useful in diagnosing and treating conditions of the nervous system, restorative neurology takes a pathophysiological approach. Instead of heavily relying on neurochemistry or perhaps an anatomical discipline, restorative neurology encompasses many fields and blends them together.
Alternating hemiplegia is a form of hemiplegia that has an ipsilateral cranial nerve palsies and contralateral hemiplegia or hemiparesis of extremities of the body. The disorder is characterized by recurrent episodes of paralysis on one side of the body. There are multiple forms of alternating hemiplegia, Weber's syndrome, middle alternating hemiplegia, and inferior alternating hemiplegia. This type of syndrome can result from a unilateral lesion in the brainstem affecting both upper motor neurons and lower motor neurons. The muscles that would receive signals from these damaged upper motor neurons result in spastic paralysis. With a lesion in the brainstem, this affects the majority of limb and trunk muscles on the contralateral side due to the upper motor neurons decussation after the brainstem. The cranial nerves and cranial nerve nuclei are also located in the brainstem making them susceptible to damage from a brainstem lesion. Cranial nerves III (Oculomotor), VI (Abducens), and XII (Hypoglossal) are most often associated with this syndrome given their close proximity with the pyramidal tract, the location which upper motor neurons are in on their way to the spinal cord. Damages to these structures produce the ipsilateral presentation of paralysis or palsy due to the lack of cranial nerve decussation before innervating their target muscles. The paralysis may be brief or it may last for several days, many times the episodes will resolve after sleep. Some common symptoms of alternating hemiplegia are mental impairment, gait and balance difficulties, excessive sweating and changes in body temperature.