Neurorehabilitation

CHAPTER 25


Neurorehabilitation


      I.  Background and General Principles: approximately 500 million people worldwide are disabled in some way; prevalence: one in 10 of the world population; three main groups of roughly equal size: developmental, acute, and chronic conditions; four-fifths of disabled live in developing countries; one-third are children.


    II.  Mechanisms of Functional Recovery


           A.  Artifact theories: secondary tissue effects, such as inflammation, edema, and vasospasm, may be associated with temporary changes in neurotransmitter pathways and nonspecific inhibition of neural activity (diaschisis); as innervation is regained elsewhere, so does function return to otherwise undamaged structures; examples: spinal shock or the remote effects of a cortical stroke.


           B.  Regeneration: classically regarded as confined to the peripheral nervous system; potential for regeneration within the central nervous system (CNS) may exist; animal experiments with neural trophic factors or transplantation offer an additional method of artificial tissue regeneration. Human axon growth rates can reach 2 mm/day in small nerves and 5 mm/day in large nerves.


           C.  Anatomic reorganization: after damage to higher cortical levels of control, certain functions could be taken over by a lower, subcortical level, albeit in a less sophisticated way; rather than strict hierarchical ordering, certain adjacent cortical association areas or even symmetric regions in the contralateral cerebral hemisphere might fulfill equipotential roles, or have the capacity to take over what are termed vicarious functions; greatest potential exists in the immature, developing brain.


           D.  Behavioral substitution: a person with a right hemiplegia may recover the ability to write by learning how to use the left hand; also called functional adaptation.


           E.  Pharmacologic intervention: examples: amphetamine, physostigmine, nerve growth factor, corticosteroids, 21-aminosteroids, opiate receptor antagonists, free radical scavengers


   III.  Aims of Rehabilitation


           A.  Ethical issues


                 1.  Respect for autonomy is paramount: do not ignore the disabled person’s responsibility for self-care.


                 2.  Beneficence: doing good


                 3.  Nonmaleficence: doing no harm


                 4.  Justice: ethical duty to ensure that disabled patients receive equally high standards of care and equitable distribution of resources


           B.  Management aims


                 1.  Prevent complications.


                 2.  Promote intrinsic recovery.


                 3.  Teach adaptive strategies.


                 4.  Facilitate environmental interaction.


    IV.  Management of Specific Neurologic Impairments


           A.  Cognitive impairment


                 1.  Reception by sense organs: arousal and alerting techniques (e.g., verbal, tactile, visual, oral stimulation in a patient in a vegetative state)


                 2.  Perception: training the patient in obeying commands; miming


                 3.  Discrimination: selective attention may be facilitated by performance of matching and selecting tasks.


                 4.  Organization: sorting, sequencing, and completion tasks can be practiced.


                 5.  Memory and retrieval: psychological techniques (e.g., interactive visual imagery, mental peg systems, etc.), behavioral techniques (e.g., reinforcement with partial cueing), alerting the environment (e.g., checklists, physical cues, etc.), drugs


           B.  Language and speech


                 1.  Aphasia


                      a.  Traditional aphasia therapy: rote learning; selective stimulation


                      b.  Cues or deblocking techniques


                      c.  Behavioral modification using operant conditioning: programmed instructions break tasks down into small steps, initially with the use of cues, which is later slowly faded.


                      d.  Melodic intonation or rhythm therapy: based on the belief that musical and tonal abilities are subserved by an intact right hemisphere


                 2.  Dysarthria: improving person’s awareness of deficit may allow him or her to compensate for it; specific exercises for one or two weak muscle groups; self-monitoring; use of ice or palatal training appliances.


                 3.  Dyslexia: prognosis for acquired dyslexia is generally poor; use of right-hemisphere strategies; arrangement of sentences into vertical columns; tactile presentation of material.


           C.  Aural impairment: requires full evaluation of communication; visual acuity is relevant to lipreading; hearing aids: cornerstone of therapy, but unable to overcome the common problem of auditory distortions; environmental aids (e.g., amplification devices); sensory substitution aids (for profound or total deafness; e.g., wearing a belt that converts sound into patterns of vibrotactile stimulation); direct nerve stimulation via cochlear implant; communication training.


           D.  Visual impairment


                 1.  Vision loss: magnifying devices; psychological and environmental adjustments (e.g., large-print books, radio, prerecorded “talking books,” white stick, guide dog)


                 2.  Visual agnosia: intensive visual discrimination training can improve agnosia and neglect.


                 3.  Diplopia: alternating covering each eye; prisms; surgery; botulinum toxin injection


                 4.  Oscillopsia: resistant to treatment


                 5.  Swallowing and nutrition: need direct observation; videofluoroscopy


                 6.  Dysphagia: counseling and advice on positioning, exercises, diet modification; ice may reduce bulbar spasticity; treatments: baclofen, preprandial pyridostigmine (for lower motor neuron weakness); appliances; Teflon injection of vocal cords; cricopharyngeal myotomy (controversial).


           E.  Motor impairment


                 1.  Weakness: physical therapy; variable loading with springs, fixed loads with weights, self-loading; suspension devices and hydrotherapy (for very weak muscles)


                 2.  Spasticity: stretching; drugs: benzodiazepines, baclofen, tizanidine, dantrolene (acts directly on muscle, inhibiting excitation-contraction coupling by depressing calcium release from the sarcoplasmic reticulum); botulinum toxin injection; nerve or motor point blocks; surgery: lengthening or division of soft tissues; rhizotomy, cordectomy (rare); electrical stimulation of dorsal columns


                 3.  Ataxia: use of visual, kinesthetic, and conscious voluntary pathways to compensate should be encouraged; repeated practice of exercises of increasing complexity; avoidance of fatigue; redevelopment of self-confidence.


    V.  General Prognostic Pearls After a Cerebrovascular Accident
















































Ambulation


95% of recovery occurs in 11 wk


There is generally no increase in the number of patients able to walk after 2 mo


Arm weakness


Most recovery occurs in 6 wk


There is some increase in neurologic capacity up to 3 mo


There is some functional improvement after 1 yr


Sensory recovery


Usually occurs within 2 mo


Visual field defect


Usually recovery occurs within 2 wk


Some at 3 wk


No further recovery at 9 wk


Neglect


Most recovery occurs in 10 days


Some up to 3 mo


Continence


50% of patients recover in 1 wk


Some can take up to 6 mo


Aphasia


Recovery occurs in weeks to months


Some recovery can still occur up to 1 yr, especially with comprehension


Apraxia


Recovery can occur up to 3 yrs

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Nov 10, 2016 | Posted by in NEUROLOGY | Comments Off on Neurorehabilitation

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