Hemiparesis

Last updated
Hemiparesis
Specialty Neurology
Symptoms Loss of motor skills on one side of body
Causes Stroke

Hemiparesis, also called unilateral paresis, is the weakness of one entire side of the body ( hemi- means "half"). Hemiplegia, in its most severe form, is the complete paralysis of one entire side of the body. Either hemiparesis or hemiplegia can result from a variety of medical causes, including congenital conditions, trauma, tumors, traumatic brain injury and stroke. [1]

Contents

Signs and symptoms

Different types of hemiparesis can impair different bodily functions. Some effects, such as weaknesss or partial paralysis of a limb on the affected side, are generally always to be expected. Other impairments can appear, upon external examination, to be unrelated to the limb weakness, but are nevertheless also caused by damage to the affected side of the brain. [1]

Loss of motor skills

People with hemiparesis often have difficulties maintaining their balance due to limb paralysis, leading to an inability to properly shift body weight. This makes performing everyday activities, such as dressing, eating, grasping objects, or using the bathroom, more difficult. Hemiparesis with origin in the lower section of the brain creates a condition known as ataxia, a loss of both gross and fine motor skills, which often manifests as a staggering and stumbling gait. Pure motor hemiparesis, a form of hemiparesis characterized by one-sided weakness in the leg, arm, and face, is the most commonly diagnosed form of hemiparesis. [1]

Pusher syndrome

Pusher syndrome is a clinical disorder following left- or right-sided brain damage, in which patients actively push their weight away from the non-hemiparetic side to the hemiparetic side. This is in contrast to most stroke patients, who typically prefer to bear more weight on their nonhemiparetic side. Pusher syndrome can vary in severity and leads to a loss of postural balance. [2] The lesion involved in this syndrome is thought to be in the posterior thalamus on either side, or in multiple areas of the right cerebral hemisphere. [3] [4]

A diagnosis of pusher syndrome includes observation of three behaviours. The most obvious one is the patient’s regularly occurring (not just occasional) tendency to spontaneously hold a body posture in which the torso is longitudinally tilted toward the paretic side of the body. The second is the patient’s use of the nonparetic extremities including abduction and extension of the extremities of the non-affected side, to help in the push toward the affected (paretic) side, resulting in an abnormal lateral tilt of the body axis. The third is that, when a care provider tries to realign the patient’s body to an upright posture, the patient spontaneously pushes back against the attempt, feeling this normal posture to be off balance. [2]

The pusher syndrome is present in 10.4% of patients with acute stroke and hemiparesis, [5] and may increase the time needed for physical rehabilitation. The Copenhagen Stroke Study found that patients who presented with ipsilateral pushing took an average of 3.6 additional weeks to reach the same functional outcome, as measured by the Barthel Index, compared with acute-stroke and hemiparesis patients who did not engage in ipsilateral pushing. [5]

Pushing behaviour demonstrates that these patients’ perception of their body posture in relation to gravity has been altered. They experience their body as oriented "upright" when the body is actually tilted to the side of the brain lesion. At the same time, their processing of visual and vestibular inputs when determining the subjective visual vertical seems to be normal. When they are sitting, the pushing presents as a strong lateral lean toward the affected side. When they stand up, the pushing creates a highly unstable situation as they are unable to support their body weight on the weakened lower extremity. The resulting increased risk of falls must be addressed with therapy aimed at correcting their altered proprioceptive perception of vertical. [2]

Pusher syndrome is sometimes confused with hemispatial neglect, and the two terms are sometimes (incorrectly) used interchangeably. Some older theories suggested that hemispatial neglect is what leads to pusher syndrome. [2] However, hemispatial neglect occurs mostly when there is a right-hemisphere lesion, and one study found that pusher syndrome is also present in patients with left hemisphere lesions (which generally also lead to aphasia). [6]

Neglect and aphasia are not the cause of pusher syndrome, although both are highly correlated with it (possibly because the brain structures associated with these syndromes are close to each other). [2]

Physical therapists treating patients with pusher syndrome focus on motor learning strategies that reduce its ill effects, such as the use of verbal cues, consistent feedback, and practice correcting orientation and shifting weight, [7] for example sitting with their stronger side next to a wall and repeatedly leaning towards the wall, thus gradually re-training the brain to recognize true vertical. [2]

A physical-therapy approach for patients with pusher syndrome debuted in 2003 suggests that the visual control of vertical upright orientation, which is undisturbed in these patients, is the most important intervention. In sequential order, treatment is designed to enable patients to realize their altered perception of vertical, use visual aids for feedback about body orientation, learn the movements necessary to reach proper vertical position, and maintain vertical body position while performing other activities. [2]

Classification of pusher syndrome

Individuals who present with pusher syndrome or lateropulsion, as defined by Davies, vary in their degree and severity of this condition and therefore appropriate measures need to be implemented in order to evaluate the level of "pushing". There has been a shift towards early diagnosis and evaluation of functional status for individuals who have had a stroke and presenting with pusher syndrome in order to decrease the time spent as an in-patient at hospitals and promote the return to function as early as possible. [8] Moreover, in order to assist therapists in the classification of pusher syndrome, specific scales have been developed with validity that coincides with the criteria set out by Davies' definition of "pusher syndrome". [9] In a study by Babyar et al., an examination of such scales helped determine the relevance, practical aspects and clinimetric properties of three specific scales existing today for lateropulsion. [9] The three scales examined were the Clinical Scale of Contraversive Pushing, Modified Scale of Contraversive Pushing, and the Burke Lateropulsion Scale. [9] The results of the study show that reliability for each scale is good; moreover, the Scale of Contraversive Pushing was determined to have acceptable clinimetric properties, and the other two scales addressed more functional positions that will help therapists with clinical decisions and research. [9]

Causes

The most common cause of hemiparesis and hemiplegia is stroke. Strokes can cause a variety of movement disorders, depending on the location and severity of the lesion. Hemiplegia is common when the stroke affects the corticospinal tract. Other causes of hemiplegia include spinal cord injury, specifically Brown-Séquard syndrome, traumatic brain injury, or disease affecting the brain. A permanent brain injury that occurs during the intrauterine life, during delivery or early in life can lead to hemiplegic cerebral palsy. As a lesion that results in hemiplegia occurs in the brain or spinal cord, hemiplegic muscles display features of the upper motor neuron syndrome. Features other than weakness include decreased movement control, clonus (a series of involuntary rapid muscle contractions), spasticity, exaggerated deep tendon reflexes and decreased endurance.[ citation needed ]

The incidence of hemiplegia is much higher in premature babies than term babies. There is also a high incidence of hemiplegia during pregnancy and experts believe that this may be related to either a traumatic delivery, use of forceps or some event which causes brain injury. [10] There is tentative evidence of an association with undiagnosed celiac disease and improvement after withdrawal of gluten from the diet. [11]

Other causes of hemiplegia in adults include trauma, bleeding, brain infections and cancers. Individuals who have uncontrolled diabetes, hypertension or those who smoke have a higher chance of developing a stroke. Weakness on one side of the face may occur and may be due to a viral infection, stroke or a cancer. [12]

Common

Mechanism

Movement of the body is primarily controlled by the pyramidal (or corticospinal) tract, a pathway of neurons that begins in the motor areas of the brain, projects down through the internal capsule, continues through the brainstem, decussates (or cross midline) at the lower medulla, then travels down the spinal cord into the motor neurons that control each muscle. In addition to this main pathway, there are smaller contributing pathways (including the anterior corticospinal tract), some portions of which do not cross the midline.[ citation needed ]

Because of this anatomy, injuries to the pyramidal tract above the medulla generally cause contralateral hemiparesis (weakness on the opposite side as the injury). Injuries at the lower medulla, spinal cord, and peripheral nerves result in ipsilateral hemiparesis.[ citation needed ]

In a few cases, lesions above the medulla have resulted in ipsilateral hemiparesis:

Diagnosis

Hemiplegia is identified by clinical examination by a health professional, such as a physiotherapist or doctor. Radiological studies like a CT scan or magnetic resonance imaging of the brain should be used to confirm injury in the brain and spinal cord, but alone cannot be used to identify movement disorders. Individuals who develop seizures may undergo tests to determine where the focus of excess electrical activity is. [18]

Hemiplegia patients usually show a characteristic gait. The leg on the affected side is extended and internally rotated and is swung in a wide, lateral arc rather than lifted in order to move it forward. The upper limb on the same side is also adducted at the shoulder, flexed at the elbow, and pronated at the wrist with the thumb tucked into the palm and the fingers curled around it. [19]

Assessment tools

There are a variety of standardized assessment scales available to physiotherapists and other health care professionals for use in the ongoing evaluation of the status of a patient's hemiplegia. The use of standardized assessment scales may help physiotherapists and other health care professionals during the course of their treatment plant to:[ citation needed ]

Some of the most commonly used scales in the assessment of hemiplegia are:

The FMA is often used as a measure of functional or physical impairment following a cerebrovascular accident (CVA). [21] It measures sensory and motor impairment of the upper and lower extremities, balance in several positions, range of motion, and pain. This test is a reliable and valid measure in measuring post-stroke impairments related to stroke recovery. A lower score in each component of the test indicates higher impairment and a lower functional level for that area. The maximum score for each component is 66 for the upper extremities, 34 for the lower extremities, and 14 for balance. [22] Administration of the FMA should be done after reviewing a training manual. [23]

This test is a reliable measure of two separate components evaluating both motor impairment and disability. [25] The disability component assesses any changes in physical function including gross motor function and walking ability. The disability inventory can have a maximum score of 100 with 70 from the gross motor index and 30 from the walking index. Each task in this inventory has a maximum score of seven except for the 2 minute walk test which is out of two. The impairment component of the test evaluates the upper and lower extremities, postural control and pain. The impairment inventory focuses on the seven stages of recovery from stroke from flaccid paralysis to normal motor functioning. A training workshop is recommended if the measure is being utilized for the purpose of data collection. [26]

The STREAM consists of 30 test items involving upper-limb movements, lower-limb movements, and basic mobility items. It is a clinical measure of voluntary movements and general mobility (rolling, bridging, sit-to-stand, standing, stepping, walking and stairs) following a stroke. The voluntary movement part of the assessment is measured using a 3-point ordinal scale (unable to perform, partial performance, and complete performance) and the mobility part of the assessment uses a 4-point ordinal scale (unable, partial, complete with aid, complete no aid). The maximum score one can receive on the STREAM is a 70 (20 for each limb score and 30 for mobility score). The higher the score, the better movement and mobility is available for the individual being scored. [28]

Treatment

Treatment for hemiparesis is the same treatment given to those recovering from strokes or brain injuries. [1] Health care professionals such as physical therapists and occupational therapists play a large role in assisting these patients in their recovery. Treatment is focused on improving sensation and motor abilities, allowing the patient to better manage their activities of daily living. Some strategies used for treatment include promoting the use of the hemiparetic limb during functional tasks, maintaining range of motion, and using neuromuscular electrical stimulation to decrease spasticity and increase awareness of the limb. [29] [30]

At the more advanced level, using constraint-induced movement therapy will encourage overall function and use of the affected limb. [31] Mirror Therapy (MT) has also been used early in stroke rehabilitation and involves using the unaffected limb to stimulate motor function of the hemiparetic limb. Results from a study on patients with severe hemiparesis concluded that MT was successful in improving motor and sensory function of the distal hemiparetic upper limb. [32] Active participation is critical to the motor learning and recovery process, therefore it's important to keep these individuals motivated so they can make continual improvements. [33]
Also speech pathologists may work to increase function for people with hemiparesis. [34]

Treatment should be based on assessment by the relevant health professionals, including physiotherapists, doctors and occupational therapists. Muscles with severe motor impairment including weakness need these therapists to assist them with specific exercise, and are likely to require help to do this. [35]

Medication

Drugs can be used to treat issues related to the Upper Motor Neuron Syndrome. Drugs like Librium or Valium could be used as a relaxant. Drugs are also given to individuals who have recurrent seizures, which may be a separate but related problem after brain injury. [36] Intra-muscular injection of botulinum toxin A is used to treat spasticity that is associated with hemiparesis both in cerebral palsy children and stroke in adults. It can be injected into a muscle or more commonly muscle groups of the upper or lower extremities. Botulinum toxin A induces temporary muscle paralysis or relaxation. The main goal of botulinum toxin A is to maintain the range of motion of affected joints and to prevent the occurrence of fixed joint contractures or stiffness. [37] [38] A randomized trial pointed out that individualized homeopathic medication in addition to the standard physiotherapy might have some effect in post-stroke hemiparesis. [39]

Surgery

Surgery may be used if the individual develops a secondary issue of contracture, from a severe imbalance of muscle activity. In such cases the surgeon may cut the ligaments and relieve joint contractures. Individuals who are unable to swallow may have a tube inserted into the stomach. This allows food to be given directly into the stomach. The food is in liquid form and instilled at low rates. Some individuals with hemiplegia will benefit from some type of prosthetic device. There are many types of braces and splints available to stabilize a joint, assist with walking and keep the upper body erect.[ citation needed ]

Rehabilitation

Rehabilitation is the main treatment of individuals with hemiplegia. In all cases, the major aim of rehabilitation is to regain maximum function and quality of life. Both physical and occupational therapy can significantly improve the quality of life.

Physical therapy

Physical therapy (PT) can help improve muscle strength & coordination, mobility (such as standing and walking), and other physical function using different sensorimotor techniques. [40] Physiotherapists can also help reduce shoulder pain by maintaining shoulder range of motion, as well as using Functional electrical stimulation. [41] Supportive devices, such as braces or slings, can be used to help prevent or treat shoulder subluxation [42] in the hopes to minimize disability and pain. Although many individuals with stroke experience both shoulder pain and shoulder subluxation, the two are mutually exclusive. [43] A treatment method that can be implemented with the goal of helping to regain motor function in the affected limb is constraint-induced movement therapy. This consists of constraining the unaffected limb, forcing the affected limb to accomplish tasks of daily living. [44]

Occupational therapy

Occupational therapists may specifically help with hemiplegia with tasks such as improving hand function, strengthening hand, shoulder and torso, and participating in activities of daily living (ADLs), such as eating and dressing. Therapists may also recommend a hand splint for active use or for stretching at night. Some therapists actually make the splint; others may measure your child's hand and order a splint. OTs educate patients and family on compensatory techniques to continue participating in daily living, fostering independence for the individual - which may include, environmental modification, use of adaptive equipment, sensory integration, etc.[ citation needed ]

Orthotic Intervention

Orthotic devices are one type of intervention for relieving symptoms of hemiparesis. Commonly called braces, orthotics range from 'off the shelf' to custom fabricated solutions, but their main goal is alike, to supplement diminished or missing muscle function and joint laxity. A wide range of orthotic treatment can be designed by a Certified Orthotist (C.O.) or Certified Prosthetist Orthotist (C.P.O). Orthotics may be made of metal, plastic, or composite material (such as fiberglass, dyneema (UHMWPE,) carbon fiber; etc.) and design may be changed to address many different conditions. [45]

Prognosis

Hemiplegia is not a progressive disorder, except in progressive conditions like a growing brain tumour. Once the injury has occurred, the symptoms should not worsen. However, because of lack of mobility, other complications can occur. Complications may include muscle and joint stiffness, loss of aerobic fitness, muscle spasms, bed sores, pressure ulcers and blood clots. [46]

Sudden recovery from hemiplegia is very rare. Many of the individuals will have limited recovery, but the majority will improve from intensive, specialised rehabilitation. Potential to progress may differ in cerebral palsy, compared to adult acquired brain injury. It is vital to integrate the hemiplegic child into society and encourage them in their daily living activities. With time, some individuals may make remarkable progress. [46]

See also

Related Research Articles

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.

<span class="mw-page-title-main">Tetraplegia</span> Paralysis of all four limbs and torso

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. 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.

Anosognosia is a condition in which a person with a disability is cognitively unaware of having it due to an underlying physical condition. Anosognosia results from physiological damage to brain structures, typically to the parietal lobe or a diffuse lesion on the fronto-temporal-parietal area in the right hemisphere, and is thus a neuropsychiatric disorder. A deficit of self-awareness, the term was first coined by the neurologist Joseph Babinski in 1914, in order to describe the unawareness of hemiplegia.

Hypotonia is a state of low muscle tone, often involving reduced muscle strength. Hypotonia is not a specific medical disorder, but a potential manifestation of many different diseases and disorders that affect motor nerve control by the brain or muscle strength. Hypotonia is a lack of resistance to passive movement, whereas muscle weakness results in impaired active movement. Central hypotonia originates from the central nervous system, while peripheral hypotonia is related to problems within the spinal cord, peripheral nerves and/or skeletal muscles. Severe hypotonia in infancy is commonly known as floppy baby syndrome. Recognizing hypotonia, even in early infancy, is usually relatively straightforward, but diagnosing the underlying cause can be difficult and often unsuccessful. The long-term effects of hypotonia on a child's development and later life depend primarily on the severity of the muscle weakness and the nature of the cause. Some disorders have a specific treatment but the principal treatment for most hypotonia of idiopathic or neurologic cause is physical therapy and/or occupational therapy for remediation.

The primary goals of stroke management are to reduce brain injury and promote maximum patient recovery. Rapid detection and appropriate emergency medical care are essential for optimizing health outcomes. When available, patients are admitted to an acute stroke unit for treatment. These units specialize in providing medical and surgical care aimed at stabilizing the patient's medical status. Standardized assessments are also performed to aid in the development of an appropriate care plan. Current research suggests that stroke units may be effective in reducing in-hospital fatality rates and the length of hospital stays.

The Bobath concept is an approach to neurological rehabilitation that is applied in patient assessment and treatment. The goal of applying the Bobath concept is to promote motor learning for efficient motor control in various environments, thereby improving participation and function. This is done through specific patient handling skills to guide patients through the initiation and completing of intended tasks. This approach to neurological rehabilitation is multidisciplinary, primarily involving physiotherapists, occupational therapists, and speech and language therapists. In the United States, the Bobath concept is also known as 'neuro-developmental treatment' (NDT).

<span class="mw-page-title-main">Mirror therapy</span> Treatment for some kinds of pain

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.

<span class="mw-page-title-main">Monoplegia</span> Paralysis of a single limb

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.

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.

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.

<span class="mw-page-title-main">Weber's syndrome</span> Medical condition

Weber's syndrome, also known as midbrain stroke syndrome or superior alternating hemiplegia, is a form of stroke that affects the medial portion of the midbrain. It involves oculomotor fascicles in the interpeduncular cisterns and cerebral peduncle so it characterizes the presence of an ipsilateral lower motor neuron type oculomotor nerve palsy and contralateral hemiparesis or hemiplegia.

Constraint-induced movement therapy is a form of rehabilitation therapy that improves upper extremity function in stroke and other central nervous system damage patients by increasing the use of their affected upper limb. Due to its high duration of treatment, the therapy has been found to frequently be infeasible when attempts have been made to apply it to clinical situations, and both patients and treating clinicians have reported poor compliance and concerns with patient safety. In the United States, the high duration of the therapy has also made the therapy not able to get reimbursed in most clinical environments.

Kernohan's notch is a cerebral peduncle indentation associated with some forms of transtentorial herniation. It is a secondary condition caused by a primary injury on the opposite hemisphere of the brain. Kernohan's notch is an ipsilateral condition, in that a left-sided primary lesion evokes motor impairment in the left side of the body and a right-sided primary injury evokes motor impairment in the right side of the body. The seriousness of Kernohan's notch varies depending on the primary problem causing it, which may range from benign brain tumors to advanced subdural hematoma.

<span class="mw-page-title-main">Management of cerebral palsy</span>

Over time, the approach to cerebral palsy management has shifted away from narrow attempts to fix individual physical problems – such as spasticity in a particular limb – to making such treatments part of a larger goal of maximizing the person's independence and community engagement. Much of childhood therapy is aimed at improving gait and walking. Approximately 60% of people with CP are able to walk independently or with aids at adulthood. However, the evidence base for the effectiveness of intervention programs reflecting the philosophy of independence has not yet caught up: effective interventions for body structures and functions have a strong evidence base, but evidence is lacking for effective interventions targeted toward participation, environment, or personal factors. There is also no good evidence to show that an intervention that is effective at the body-specific level will result in an improvement at the activity level, or vice versa. Although such cross-over benefit might happen, not enough high-quality studies have been done to demonstrate it.

<span class="mw-page-title-main">Athetoid cerebral palsy</span> Type of cerebral palsy associated with basal ganglia damage

Athetoid cerebral palsy, or dyskinetic cerebral palsy, is a type of cerebral palsy primarily associated with damage, like other forms of CP, to the basal ganglia in the form of lesions that occur during brain development due to bilirubin encephalopathy and hypoxic–ischemic brain injury. Unlike spastic or ataxic cerebral palsies, ADCP is characterized by both hypertonia and hypotonia, due to the affected individual's inability to control muscle tone. Clinical diagnosis of ADCP typically occurs within 18 months of birth and is primarily based upon motor function and neuroimaging techniques. While there are no cures for ADCP, some drug therapies as well as speech, occupational therapy, and physical therapy have shown capacity for treating the symptoms.

Upper motor neuron syndrome (UMNS) is the motor control changes that can occur in skeletal muscle after an upper motor neuron lesion.

<span class="mw-page-title-main">Spastic cerebral palsy</span> Cerebral palsy characterized by high muscle tone

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.

<span class="mw-page-title-main">Spastic hemiplegia</span> Medical condition

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.

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.

Pusher syndrome is a condition observed in some people following a stroke which has left them with one side weakened due to hemiparesis. Sufferers exhibit a tendency to actively push away from the unweakened side, thus leading to a loss of postural balance. It can be a result of left or right brain damage. In contrast to most stroke patients, who typically prefer more weight-bearing on their non-hemiparetic side, this abnormal condition can vary in severity and leads to a loss of postural balance. The lesion involved in this syndrome is thought to be in the posterior thalamus on either side, or multiple areas of the right cerebral hemisphere.

References

  1. 1 2 3 4 Detailed article about hemiparesis Archived 2022-02-02 at the Wayback Machine at Disabled-World.com
  2. 1 2 3 4 5 6 7 Karnath HO, Broetz D (December 2003). "Understanding and treating "pusher syndrome"". Phys Ther. 83 (12): 1119–25. doi: 10.1093/ptj/83.12.1119 . PMID   14640870.
  3. Karnath HO, Ferber S, Dichgans J (November 2000). "The origin of contraversive pushing: evidence for a second graviceptive system in humans". Neurology. 55 (9): 1298–304. doi:10.1212/wnl.55.9.1298. PMID   11087771. S2CID   19399616.
  4. Karnath HO, Ferber S, Dichgans J (December 2000). "The neural representation of postural control in humans". Proceedings of the National Academy of Sciences of the United States of America. 97 (25): 13931–6. Bibcode:2000PNAS...9713931K. doi: 10.1073/pnas.240279997 . PMC   17678 . PMID   11087818.
  5. 1 2 Pedersen PM, Wandel A, Jørgensen HS, Nakayama H, Raaschou HO, Olsen TS (January 1996). "Ipsilateral pushing in stroke: incidence, relation to neuropsychological symptoms, and impact on rehabilitation. The Copenhagen Stroke Study". Archives of Physical Medicine and Rehabilitation. 77 (1): 25–8. doi:10.1016/s0003-9993(96)90215-4. PMID   8554469.
  6. Davies PM (1985). Steps to follow: A guide to the treatment of adult hemiplegia : Based on the concept of K. and B. Bobath. New York: Springer-Verlag.
  7. O'Sullivan S (2007). "Ch. 12: Stroke". In O'Sullivan S, Schmitz T (eds.). Physical Rehabilitation (5th ed.). Philadelphia: F.A. Davis. pp. 705–769.
  8. Lagerqvist, J.; Skargren, E. (2006). "Pusher syndrome: reliability, validity, and sensitivity to change of a classification instrument". Advances in Physiotherapy. 8 (4): 154–160. doi:10.1080/14038190600806596. S2CID   145015737.
  9. 1 2 3 4 Babyar SR, Peterson MG, Bohannon R, Pérennou D, Reding M (July 2009). "Clinical examination tools for lateropulsion or pusher syndrome following stroke: a systematic review of the literature". Clinical Rehabilitation. 23 (7): 639–50. doi:10.1177/0269215509104172. PMID   19403555. S2CID   40016612.
  10. "hemiplegia in children". Children's Hemiplegia and Stroke Association (CHASA). Archived from the original on February 4, 2012.
  11. Shapiro M, Blanco DA (February 2017). "Neurological Complications of Gastrointestinal Disease". Seminars in Pediatric Neurology (Review). 24 (1): 43–53. doi:10.1016/j.spen.2017.02.001. PMID   28779865.
  12. "What is hemiplegia? | HemiHelp: for children and young people with hemiplegia (hemiparesis)". HemiHelp. Archived from the original on 2013-03-05. Retrieved 2013-03-08.
  13. Martin L (2009). "I was awake -- and could not move!". Lakesidepress.com. Retrieved 2013-03-08. Sleep paralysis, parasomnia, sleep apnea, sleep eat, parasomnias, paresthesias, dysesthesias, obstructive sleep apnea, REM, Stage 1, Sinemet narcolepsy, insomnia, cataplexy, benzodiazepines, opioids, sleepiness, sleep walking, daytime sleepiness, upper airway, CPAP, hypoxemia, UVVP, uvula, Somnoplasty, obesity, airway obstruction, EEG, electroencephalogram, Klonopine, night terrors, bruxism, parasomnias, EMG, Epworth Sleepiness Scale, BiPAP, sleep efficiency
  14. Ago T, Kitazono T, Ooboshi H, Takada J, Yoshiura T, Mihara F, et al. (August 2003). "Deterioration of pre-existing hemiparesis brought about by subsequent ipsilateral lacunar infarction". Journal of Neurology, Neurosurgery, and Psychiatry. 74 (8): 1152–3. doi:10.1136/jnnp.74.8.1152. PMC   1738578 . PMID   12876260.
  15. Song YM, Lee JY, Park JM, Yoon BW, Roh JK (May 2005). "Ipsilateral hemiparesis caused by a corona radiata infarct after a previous stroke on the opposite side". Archives of Neurology. 62 (5): 809–11. doi: 10.1001/archneur.62.5.809 . PMID   15883270.
  16. Yamamoto S, Takasawa M, Kajiyama K, Baron JC, Yamaguchi T (2007). "Deterioration of hemiparesis after recurrent stroke in the unaffected hemisphere: Three further cases with possible interpretation". Cerebrovascular Diseases. 23 (1): 35–9. doi:10.1159/000095756. PMID   16968984. S2CID   40273792.
  17. Terakawa H, Abe K, Nakamura M, Okazaki T, Obashi J, Yanagihara T (May 2000). "Ipsilateral hemiparesis after putaminal hemorrhage due to uncrossed pyramidal tract" (PDF). Neurology. 54 (9): 1801–5. doi:10.1212/WNL.54.9.1801. PMID   10802787. S2CID   15086685.
  18. "Spastic Hemiplegia : Cerebral Palsy". OriginsOfCerebralPalsy.com. Archived from the original on 2018-01-26. Retrieved 2013-03-08.
  19. "Gait Abnormalities". The Stanford 25. Archived from the original on October 11, 2010.
  20. Fugl-Meyer AR, Jääskö L, Leyman I, Olsson S, Steglind S (1975). "The post-stroke hemiplegic patient. 1. a method for evaluation of physical performance". Scandinavian Journal of Rehabilitation Medicine. 7 (1): 13–31. doi: 10.2340/1650197771331 . PMID   1135616. S2CID   19245788.
  21. Sullivan KJ, Tilson JK, Cen SY, Rose DK, Hershberg J, Correa A, et al. (February 2011). "Fugl-Meyer assessment of sensorimotor function after stroke: standardized training procedure for clinical practice and clinical trials". Stroke. 42 (2): 427–32. doi: 10.1161/STROKEAHA.110.592766 . PMID   21164120.
  22. Sullivan SB (2007). "Stroke". In O'Sullivan SB, Schmitz TJ (eds.). Physical Rehabilitation (5th ed.). Philadelphia PA: F.A. Davis.
  23. "Fugl-Meyer Assessment of Motor Recovery after". Rehab Measures. Archived from the original on 2016-09-24. Retrieved 2013-03-08.
  24. Gowland C, Stratford P, Ward M, Moreland J, Torresin W, Van Hullenaar S, et al. (January 1993). "Measuring physical impairment and disability with the Chedoke-McMaster Stroke Assessment". Stroke. 24 (1): 58–63. doi:10.1161/01.STR.24.1.58. PMID   8418551.
  25. Valach L, Signer S, Hartmeier A, Hofer K, Steck GC (June 2003). "Chedoke-McMaster stroke assessment and modified Barthel Index self-assessment in patients with vascular brain damage". International Journal of Rehabilitation Research. 26 (2): 93–9. doi:10.1097/00004356-200306000-00003. PMID   12799602.
  26. "Chedoke-McMaster Stroke Assessment Measure". Rehab Measures. Archived from the original on 2014-10-06. Retrieved 2013-03-08.
  27. Daley K, Mayo N, Wood-Dauphinée S (January 1999). "Reliability of scores on the Stroke Rehabilitation Assessment of Movement (STREAM) measure". Physical Therapy. 79 (1): 8–19, quiz 20–3. doi: 10.1093/ptj/79.1.8 . PMID   9920188.
  28. O'sullivan S, Schmitz T (2007). Physical Rehabilitation (5th ed.). Philadelphia PA: F.A. Davis. p. 736.
  29. Knutson, Jayme S.; Fu, Michael J.; Sheffler, Lynne R.; Chae, John (November 26, 2015). "Neuromuscular Electrical Stimulation for Motor Restoration in Hemiplegia". Physical Medicine and Rehabilitation Clinics of North America. 26 (4): 729–745. doi:10.1016/j.pmr.2015.06.002. ISSN   1558-1381. PMC   4630679 . PMID   26522909.
  30. Beebe, Justin A.; Lang, Catherine E. (March 5, 2009). "Active range of motion predicts upper extremity function 3 months after stroke". Stroke. 40 (5): 1772–1779. doi:10.1161/STROKEAHA.108.536763. ISSN   1524-4628. PMC   2718540 . PMID   19265051.
  31. Sterr A, Freivogel S (September 2003). "Motor-improvement following intensive training in low-functioning chronic hemiparesis". Neurology. 61 (6): 842–4. doi:10.1212/wnl.61.6.842. PMID   14504336. S2CID   43563527.
  32. Dohle C, Püllen J, Nakaten A, Küst J, Rietz C, Karbe H (2009). "Mirror therapy promotes recovery from severe hemiparesis: a randomized controlled trial". Neurorehabilitation and Neural Repair. 23 (3): 209–17. doi: 10.1177/1545968308324786 . PMID   19074686. S2CID   14252958.
  33. Stroke in Physical Rehabilitation 2007 , p. 746
  34. "Right Hemisphere Damage". American Speech-Language-Hearing Association. Retrieved 2023-10-06.
  35. Patten C, Lexell J, Brown HE (May 2004). "Weakness and strength training in persons with poststroke hemiplegia: rationale, method, and efficacy". Journal of Rehabilitation Research and Development. 41 (3A): 293–312. doi:10.1682/JRRD.2004.03.0293. PMID   15543447. S2CID   563507.
  36. "Hemiplegia/Hemiparesis". Archived from the original on 2009-04-20. Retrieved 2014-10-02.
  37. Farag SM, Mohammed MO, El-Sobky TA, ElKadery NA, ElZohiery AK (March 2020). "Botulinum Toxin A Injection in Treatment of Upper Limb Spasticity in Children with Cerebral Palsy: A Systematic Review of Randomized Controlled Trials". JBJS Reviews. 8 (3): e0119. doi:10.2106/JBJS.RVW.19.00119. PMC   7161716 . PMID   32224633.
  38. Blumetti FC, Belloti JC, Tamaoki MJ, Pinto JA (October 2019). "Botulinum toxin type A in the treatment of lower limb spasticity in children with cerebral palsy". The Cochrane Database of Systematic Reviews. 2019 (10): CD001408. doi:10.1002/14651858.CD001408.pub2. PMC   6779591 . PMID   31591703.
  39. Dutta, Abhijit; Singh, Subhas; Saha, Subhranil; Rath, Prasanta; Sehrawat, Nisha; Singh, Navin Kumar (2022-08-29). "Efficacy of individualized homeopathic medicines in treatment of post-stroke hemiparesis: A randomized trial". Explore. 19 (2): S1550–8307(22)00160–4. doi:10.1016/j.explore.2022.08.017. ISSN   1878-7541. PMID   36115790. S2CID   251943815.
  40. Barreca S, Wolf SL, Fasoli S, Bohannon R (December 2003). "Treatment interventions for the paretic upper limb of stroke survivors: a critical review". Neurorehabilitation and Neural Repair. 17 (4): 220–6. doi: 10.1177/0888439003259415 . PMID   14677218. S2CID   23055506.
  41. Price CI, Pandyan AD (February 2001). "Electrical stimulation for preventing and treating post-stroke shoulder pain: a systematic Cochrane review". Clinical Rehabilitation. 15 (1): 5–19. doi:10.1191/026921501670667822. PMID   11237161. S2CID   1792159.
  42. Ada L, Foongchomcheay A, Canning C (January 2005). Ada L (ed.). "Supportive devices for preventing and treating subluxation of the shoulder after stroke". The Cochrane Database of Systematic Reviews. 2005 (1): CD003863. doi:10.1002/14651858.CD003863.pub2. PMC   6984447 . PMID   15674917. S2CID   10451803.
  43. Zorowitz RD, Hughes MB, Idank D, Ikai T, Johnston MV (March 1996). "Shoulder pain and subluxation after stroke: correlation or coincidence?". The American Journal of Occupational Therapy. 50 (3): 194–201. doi:10.5014/ajot.50.3.194. PMID   8822242.
  44. Wittenberg GF, Schaechter JD (December 2009). "The neural basis of constraint-induced movement therapy". Current Opinion in Neurology. 22 (6): 582–8. doi:10.1097/WCO.0b013e3283320229. PMID   19741529. S2CID   16050784.
  45. Choo, Yoo Jin; Chang, Min Cheol (2021-08-13). "Commonly Used Types and Recent Development of Ankle-Foot Orthosis: A Narrative Review". Healthcare. 9 (8): 1046. doi: 10.3390/healthcare9081046 . ISSN   2227-9032. PMC   8392067 . PMID   34442183.
  46. 1 2 "Hemiplegia (Hemiparalysis)". Healthopedia.com. 2009-04-06. Retrieved 2013-03-08.
  47. "Kingsolver, Barbara : The Poisonwood Bible". Litmed.med.nyu.edu. 2000-05-17. Retrieved 2013-03-08.
  48. "The Poisonwood Bible Barbara Kingsolver Study Guide, Lesson Plan & more". eNotes.com. Retrieved 2013-03-08.
  49. "HAERTS Announce Debut EP Hemiplegia, Out 9/17 on Columbia Records". broadwayworld.com. 2013-08-08. Retrieved 2013-10-19.