Download Citation on ResearchGate | Merritt tratado de neurología / [editado por] Lewis P. Rowland | Traducción de: Merritts-textbook of neurology Ed. rev. de. Tratado de neurología / H. Houston Merritt. Article with Request Full-text Paper PDF. Citations Merritt tratado de neurología / [editado por] Lewis P. Rowland. 3 Fisioterapeuta do Serviço de Fisioterapia do Centro de Reabilitação Umarizal / Divisão de Medicina de Reabilitação HC .. Merritt: tratado de neurologia.
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Luciano Bruno de Carvalho Silva1, Lucia Figueiredo Mourão2, Ariovaldo Armando Silva3, .. In Merritt: Tratado de Neurologia. ed. Rio. Epilepsia não é uma doença: proposta para uma nova estrutura da epilepsia dentro da classifcação .. In Merritt HH. Tratado de Neurologia. Rio de Janeiro. Rowland LP. Merritt: tratado de neurologia. Rio de Janeiro ischemia in Mongolian gerbils. I. Light microscopic observations. (Brazil): Guanabara Koogan .
Several types of treatment for bruxism have been investigated, such as occlusal splints, medication, and psychological treatment, but they are ineffective 24, Recently, the local injection of botulinum toxin BTX has been successfully used to treat various movement disorders 26, BTX is a potent biological toxin also called neurotoxin.
It is produced by the anaerobic bacterium Clostridium botulinum 28, which has a paralytic effect by inhibiting the release of acetylcholine at the neuromuscular junction BTX is a safe and effective treatment for many forms of neurological disorders 28, Botulinum toxin type A BTX-A is a toxin scientifically recognized as being the most potent and has a longer-lasting effect.
It is extensively used for treating bruxism in patients with disabilities The injection of BTX-A in patients with CP reduces muscle spasticity, lower lip trauma, and bruxism and improves mouth opening and the ability to perform oral hygiene The goal of this study was to conduct a literature review about the treatment of bruxism with the use of BTX in patients with CP.
The database searches were performed using the keywords "cerebral palsy," "bruxism," "botulinum toxin," and "botulinum toxin A. Little first described CCE as a disease with various causes and characterized mainly by muscle rigidity.
In , it established the relationship between this clinical picture and its intercurrences with childbirth 34, Freud suggested CP expression, which later was confirmed by Phelps, in a group of children who had severe motor disorders due to CNS injury CP is the most common form of chronic motor incapacity that begins in childhood The incidence of NPCE has remained constant in recent years, with a prevalence of 2.
In developing countries, the incidence is higher, reaching 7 per 1, live births.
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In Brazil, it is estimated that there are 30,—40, new cases each year 1. The etiology of CP is variable and can occur during the prenatal, perinatal, or postnatal period Causes at presentation can be congenital, genetic, inflammatory, infectious, anoxic, traumatic, and metabolic 1. According to Rotta , the main etiological factors in the prenatal period are infections and parasitic diseases such as syphilis, rubella, toxoplasmosis, cytomegalovirus, herpes simplex virus, and HIV.
Congenital infections may reach the fetus via the placenta, causing serious lesions Some medications, such as thalidomide, have toxic and teratogenic effects Exposure to X-rays for both diagnostic and therapeutic purposes has risks because it interferes with the development of the cerebral parenchyma 14, Metabolic disorders of pregnant women, malnutrition produces reduction in brain growth , and pregnancy toxemia are causes of CP In addition, direct trauma to the abdomen or sitting falls among pregnant women are important factors Anemia during pregnancy, cord circulation, placental abruption, uterine bleeding during pregnancy, eclampsia, and hypotension are causes of brain injuries The genetic and chromosomal abnormalities, although rare, can occur at this stage The factors that occur in the perinatal period during or shortly after birth 15 may contribute to CP These events can be intracranial hemorrhage, hypoxic-ischemic encephalopathy, encephalopathy by hyperbilirubinemia, and periventricular leukomalacia.
Intracranial bleeding can result from mechanical factors caused by compression of the head in the birth canal Hypoxia is the most significant cause of CP due to lesions that are produced in the cerebral cortex and subcortex, the basal nucleus, and the cerebellum. During the perinatal period, the degree of acute asphyxia of the newborn can be evaluated by using the Apgar score Premature dislocation of the placenta and cervical isthmus incontinence are important factors responsible for prematurity.
Another factor considered is severe icterus of the newborn, which is responsible for bilirubin encephalopathy; if left untreated, bilirubin encephalopathy can produce devastating cortical lesions 14, Postnatal factors occur between birth and 5 years Postnatal causes can be infections e.
The incidence of the causes varies according to geographic location and the availability of medical care 1, Classification CP is classified according to motor involvement and the topographic taxonomy indicating the ends involved 38 is still a matter of controversy in the literature According to the affected area, CP is classified into monoplegia, hemiplegia, diplegia, and quadriplegia Monoplegia is extremely rare and is characterized by the involvement of only one member an arm or leg In hemiplegia, one side of the body is affected with the relevant amendments to the lesion suffered, where the arm is more affected than the leg.
They are considered at high risk for the development of partial convulsions. This type of CP is associated with vascular malformations in the brain and limited intraventricular hemorrhage in infancy Most are able to walk independently or with assistance. In quadriplegia, all four of the patient's limbs are affected, and the trunk and the oromotor musculature are involved. Most of these individuals have some degree of intellectual deficiency in addition to motor dysfunction.
These patients are at high risk for seizures and sensory disabilities. This type of CP has been associated with suffocation and severe intraventricular hemorrhage in premature infants The clinical classification of CP can be divided into spastic, athetoid, ataxic, and mixed 5.
As for motor impairment, the spasticity presents characteristics of the first motor neuron lesion abnormal motor patterns, hyperreflexia, muscle weakness, reduced dexterity, and tremors 8, hypertonia, and the presence of the Babinski sign with probable injury of the pyramidal system in the cerebral cortex motor The movement of the extremities is made slowly and with great effort, and resistance to passive movements and abnormal motor patterns may not manifest clinically The hypertonia is responsible for the imbalance between the agonist and antagonist muscles.
Before that, it promotes an exaggerated increase in the tonus of the extensor muscles, inhibiting the flexor muscles, or otherwise increases the tone of the flexor muscles and inhibition of extensor Spasticity is present in most of the cases of CP 8, The spastic form presents clinically as tetraparesis, hemiparesis, or diparesis Spastic tetraparesis is the most severe form of CP, owing to severe motor involvement of four members and the association with mental retardation and seizures Clinical manifestations may be observed at birth and are accentuated with the development of the child The increased tone and spasticity in all extremities, decrease of spontaneous movements, living reflexes, and plantar response extension are observed at neurological examination Patients with CP of the tetraparesis type have facial hypertonia, little mime, upper lip retraction, lingual tension sometimes accompanied by tongue projection, open bite, bruxism, and ogival palate.
Patients still have slow or shallow breathing, favoring an open mouth position and mouth breathing together with difficulty swallowing, dysphagia, absence of chewing, sucking hampered by muscle tension, and not allowing the effective labial sealing These patients have difficulty in controlling the head because of the involvement of the upper limbs.
These patients have frequent pulmonary infections and upper airway In spastic diparesis or diplegia or Little's disease, spasticity predominates in the lower limbs, less severely affecting the upper limbs.
The most common causes are prematurity with or without intraventricular hemorrhage and hydrocephalus.
Longitudinal assessment of grip strength using bulb dynamometer in Duchenne Muscular Dystrophy
An adductor spasm is responsible for the leg and sharp spasticity can interfere with walking. The individual's intelligence and language are often unaffected The diplegic form is less severe than the tetraparetic form The prognosis for typical intellectual development is excellent, being minimal the probability of seizures. Severe spastic diplegia is characterized by atrophy due to disuse, impaired growth of the lower extremities, and disproportionate growth with normal development of the upper trunk The hemiparesis hemiplegia spastic elapses of an injury of the corticospinal system of a cerebral hemisphere In this clinical pattern, movement disorders are observed in a hemibody The causes are stroke in the intrauterine period or during childbirth.
Another common cause is intraventricular hemorrhage.
Seizures are frequent when the lesion affects the cortex The intelligence and speech are less affected and disturbances in the articulation and rhythm may still be observed Athetoid CP, also called CP choreoathetosis or extrapyramidal CP 38, affects areas that modify or regulate movement in the extrapyramidal tract, causing involuntary movements and difficulty in voluntary movements The affected patients are characteristically hypotonic, cannot support the head, and have a higher variability of tone with rigidity and dystonia over the course of several years Changes in neurovegetative function are observed, such as arrhythmic breathing, mouth difficulty in sucking by incoordination of phonoarticulatory organs with chewing changes, and, in some cases, the presence of dysphagia Moreover, tongue protrusion and sialorrhea are present, and nutrition can become difficult.
Due to the involvement of oropharyngeal muscles, "speech" is typically affected and may be missing or indecipherable Normally, these patients have exaggerated facial mime, repeated movements of opening, intraoral sensitivity, changes in the temporomandibular joint TMJ , severe bruxism, and involuntary movements of the tongue, soft palate, or the facial musculature Epileptic seizures are uncommon, and the intellect is preserved in many patients Ataxic CP is related to impairment of the cerebellum or cerebellar pathways.
The main function of the cerebellum is to control balance and coordinate movements, and children with cerebellar lesions present ataxia Clinical manifestations are motor incoordination 5 and static and dynamic balance disorders In an ataxic clinical state, hypotonia is present and results in failure of the sequence of movements, generating some potential for tremor, postural maintenance deficiency, straightening reactions, and altered protection and balance, producing dysmetria in all actions These patients present with lingual tremor and difficulty in graduating speed, strength, and size of movements Ataxic CP is the rarest form of CP Mixed CP refers to the combination of the various manifestations of the disease, with dyskinesis and spasticity or ataxia with athetosis 48, The term is also used to describe patients who do not meet the written criteria for one of the main forms Clinical Characteristics and Oral Manifestations In addition to the motor disturbances mandatory to characterize CP, affected individuals may have other variable frequency manifestations, such as mental retardation, seizures, language disorders, visual disturbances, behavioral disorders, orthopedic disorders 2, malnutrition conditions, obesity, and hydrocephaly 4, Rev Neuroc.
The effectiveness of functional electrical stimulation for the treatment of shoulder subluxation and shoulder pain in hemiplegic patients: A randomized controlled Trial. Disabil Rehabil. Stimulation with low frequency transcuteous electric nerve stimulation increases motor function of the post-stroke paretic arm. Stand J Rehabil Med.
Almeida OP. Arq Neuropsiquiatria. Rev Bras Anestesiol. Marques AP.
Manual de Goniometria. Rev bras fisioter.
Percutaneous intramuscular neuromuscular electric stimulation for the treatment of shoulder subluxation and pain in patients with chronic hemiplegia: a pilot study. Arch Phys Med Rehabil. Duffau H. Brain plasticity: from pathophysiological mechanisms to therapeutic applications.
J Clin Neurosci. Nudo RJ.
Distonia e Discinesias
Mechanisms for recovery of motor function following cortical damage. Curr Opin Neurobiol. Albert SJ, Kesserlring J. Neurorehabilitation of stroke. J Neurol.
Poststroke spasticity management. Dobkin BH.
Strategies for stroke rehabilitation. Lancet Neurol.Caracter- therapy development. The clinical features of the most common focal dystonias are discussed in the following paragraphs.
PDF La encuadernación Bradel (Manuales prácticos Clan) ePub
Other studies have disclosed pontine angioma, gliosis in brain stem nuclei, and Lewy bodies. Lower extremity muscle strength in 6- to 8- year-old children using hand-held dynamometry. BTX is a safe and effective treatment for many forms of neurological disorders 28, The aim of this article is to provide an overview of classification, phenomenology, epidemiology, genetics, pathophysiology, neuro- psychological aspects, and treatment.
Exp Use of devices to prevent subluxation of the shoulder after stroke. Molinari GF.
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