Rehabilitation of comatose patients
At present, there are very few researchers in Japan and abroad who provide long-term treatment and expert guidance for patients in cerebral coma, vegetative state, and minimally conscious state in rehabilitation centers. Professional rehabilitation guidance is provided for patients in this area. Early rehabilitation is as important as treatment for comatose patients, and many can regain consciousness, write, talk, and have a full-time job.
It is important to assess the outcome of brain function recovery in coma patients.
50% of patients in a coma have some functional activity.
30% of patients with severe impairment recovered slowly.
There are three subscales of prediction: each of them can be used independently. (1) response to the environment (e.g., visual, auditory); (2) motor response, (including head control, limb control); and (3) communication and swallowing response (e.g., yes/no, articulation, comprehension); these three sublevels are also scored by subtracting 7 points. An average score of 1 indicates no response on all levels. Taking visual representation as an example, the four levels are: 1=no response. 2=blink response to light and startling movements. 3Q2s are fixation gaze. 4R2s are fixation gaze.
I. Mechanism of recovery after brain injury
A, the concept of neural repair that is based on
1, the concept of brain plasticity: brain plasticity (brain plasticity) concept is a common phenomenon of living organisms, the human brain has a high degree of plasticity is not due to regeneration, but due to dynamic functional reorganization or the result of adaptation. Specific rehabilitation training is necessary, therefore, this theory is also called relearning theroy.
2. Morphological basis of brain plasticity: morphologically, it is true that the cells of the central nervous system cannot regenerate after death. The latest research on brain plasticity in old age also proves that, even in old age, although there is degeneration or death of neurons, dendrites and so on may still increase. When the brain innervates part of the dead nerve, the abundant axons of the surviving cells can replace the lost axons through the long shoots of the lateral branches, etc.
3, the physiological basis of brain plasticity: in terms of physiology, some neurons can be compensated by functional reorganization of neighboring intact neurons, or by lower-level central nervous system parts. In addition, local damage can also be compensated by mechanisms such as loss of neural hypersensitivity and activation of latent pathways and synapses.
Second, brain plasticity-related factors
Brain plasticity refers to the fact that the central nervous system can be reorganized from within through structural and functional adjustments to adapt to changes after injury. Functional reorganization can be divided into two aspects: intra-systemic reorganization and extra-systemic reorganization. Intra-systemic reorganization is the same or different levels of compensations that occur within the same system. For example. There is compensation by the tissue surrounding the lesion, or by structures above or below the lesion; inter-systemic reorganization is compensation by another system that is functionally completely different, for example, there is skin touch instead of vision, etc.
Factors related to brain plasticity rows: divided into two parts: functional reorganization and clinical practice.
(i) Functional reorganization includes.
(1) Intra-systemic functional reorganization: (1) axonal collateral long buds; (2) loss of neural hypersensitivity; (3) activation of latent pathways and synapses; (4) alteration of ion channels; (5) compensation of peri-lesional tissues; (6) compensation of lower or higher parts; (7) action of neurotrophic factors and certain genes.
(2) Inter-system functional reorganization: (i) compensation of the contralateral cerebral hemisphere; (ii) activation of latent pathways and synapses of different systems; (iii) behavioral compensation generated by different systems.
(2) Clinical practice: including external facilitators: (i) neurotrophic factors given from outside; (ii) gene therapy and neural transplantation; (iii) drugs to promote brain function recovery; (iv) functional recovery training; (v) environment; and (vi) constant electric field.
Third, the factors affecting plasticity and functional recovery
1, ultra-early: generally refers to 48 hours after the injury, ultra-early recovery of brain coma patients is very difficult to achieve. However, it can be based on clinical performance, and the more timely and earlier, the better the prognosis outcome.
2, early: 3 days to 1 month, including the acute phase (within 1 month of injury) and early recovery (1 month to 3 months of injury). The internal factors affecting recovery in this period are mainly neuroanatomical and neurophysiological aspects.
3, the middle and late stage: from 1 month to 12 months, it takes 2 – 6 months to recover the middle stage, 6 months to 2 years for the late stage of recovery. The role of internal factors begins to diminish in this period, ① mainly for axonal long shoots, functional compensation of brain tissues around the part of the lesion and/or contralateral cerebral hemisphere, and continued activation of latent pathways and synapses, etc.; ② the role of external factors begins to increase, in addition to drugs for nutrition and promotion of brain function recovery, such as nerve growth factor and ganglioside, and insistence on persistent use of cortical microcirculation expansion drugs every year, ③ correct and comprehensive integrated rehabilitation and the influence of environmental, psychological and social factors are particularly important, especially purposeful and planned rehabilitation treatment, which is increasingly significant for functional recovery.
4.Posterior period: usually refers to 1 year later. In this period, the lesion of brain tissue has been stabilized; ① the recovery of function mainly relies on the compensation of the healthy side of the brain and the activation of latent pathways and synapses; ② the role of external factors such as neurotrophic drugs is mainly to prevent recurrence; ③ the training of functional recovery also shifts from focusing on the function of the affected side of the body to training the compensation of the healthy side of the body or the application of apparatus.
Second, the recovery process of motor disorders after brain injury
I. After brain injury, according to the site and degree of injury, there are different clinical manifestations, the most common of which is movement disorders, which is also an important factor affecting the quality of life. In the past 10 years, although it has been noted that other factors are equally important to the quality of life of patients, but at least for several years, restoring or improving motor function is still the first task of rehabilitation treatment after brain injury.
1. Manifestations of motor impairment after brain injury: 1) increased or decreased muscle tone; 2) lack of voluntary movement; 3) inability to
can complete. Selective movement; 4) can not resist gravity movement; 5) can not carry out functional activities; 6) can not complete the fine movement; 7) can not complete the movement of different speeds.
2, typical movement patterns of patients after brain injury.
Upper limbs: ① flexion pattern: scapular girdle: retraction, lifting; shoulder joint: posterior extension, abduction, external rotation; elbow joint: flexion; forearm: rotation back. ②extension pattern: scapular girdle: forward extension; shoulder joint: forward flexion, abduction, internal rotation; elbow joint: extension; forearm: rotation forward.
Lower limbs: ① flexion mode: hip: forward flexion, abduction, external rotation; knee: flexion; ankle: dorsiflexion, valgus; hip: posterior extension, adduction, internal rotation; ② extension mode: knee: extension; ankle: toe flexion, valgus
Second, the recovery process of movement disorders.
(I), recovery forms.
1.Spontaneous recovery: It refers to the natural remission of the disease after the onset of the disease without the intervention of any therapeutic factors (such as drugs, surgery, rehabilitation training, etc.), and the function is recovered to varying degrees. It is generally believed that spontaneous recovery is mostly in the early stage after the onset of the disease, and its possible mechanism has 2 aspects, one is the role of local factors, including the subsidence of edema around the lesion; reflex spasm of the blood vessels localized and around the lesion, or even the recanalization after atresia; generally not open certain collateral circulation can be recanalized, or the collateral circulation can be formed naturally, etc. There is not enough evidence to prove the role played by the above factors in long-term functional recovery. Another aspect is the role of brain plasticity.
2, therapeutic recovery: there are many studies on therapeutic recovery, and many researchers have successively described the sequence of recovery of motor function, especially Brunnstrom’s recovery 6 stages is most representative.
Table 4-1 Stages of recovery of limb function after brain injury.
Staging Upper extremity Lower extremity
Stage I Soft paresis, no voluntary movements Soft paresis, no voluntary movements
Phase II Presence of spasticity and co-movement, flexion pattern Presence of spasticity and co-movement, extension pattern
Spasticity and co-movement, extension mode first, extension mode second, flexion mode second
Stage III Can cause co-movement at will (e.g., spasticity plus) Can cause co-movement at will (spasticity plus)
weight), hooked hand grasp, no random extension or relaxation
Stage IV Disengagement from co-movement (spasticity reduced) Disengagement from co-movement (spasticity reduced)
(1) Hand touching sacrococcygeal area (1) Sitting flexion >900
(2) Anterior flexion of upper extremity 900, elbow extension (2) Sitting position, ankle dorsiflexion
(3) Bending elbow 900, forearm rotation anterior/posterior ⑶ Sitting position, knee flexion followed by slight knee extension
(4) Lateral thumb abduction and relaxation (4) Standing, knee flexion first, then slight knee extension
(5) Small range of finger movements
Phase V Independent or dissociated movement (spasticity basically disappears) Independent or dissociated movement (spasticity basically disappears)
Staging Upper extremity Lower extremity
(1) Extremity abduction 900, elbow extension
(2) Upper extremity abduction >1800, elbow extension Standing
(3) forearm rotation forward/backward in the extended elbow position (1) hip extension, knee flexion
(4) Hand grasping cylindrical and spherical objects (2) Ankle dorsiflexion
(5) Random extension of fingers in different ranges (3) Knee extension
Phase VI Coordinated movement (spasticity basically disappears) Coordinated movement (spasticity basically disappears)
(1) Upper extremity abduction 900 (1) Standing position, knee extension, hip abduction
(2) Double upper limb abduction 1800 (2) Sitting position, knee flexion, calf rotation
(3) Elbow position, forearm rotation anterior/posterior rotation (3) Sitting position, foot inversion/extrusion
(B), recovery time and process: the recovery after brain injury varies greatly among individuals, including complete recovery of function or leaving a serious disability, and the time and process of recovery is related to the nature of the injury (ischemia, hemorrhage, trauma), the degree of injury, the site, and also the patient’s age, physical quality and other factors. For example, the recovery of most craniocerebral injuries occurs within the first 6 months after acute damage and can last until 1 or 2 years after the injury, and also after 2 years with varying degrees of recovery. Among them, the recovery of somatic motor function occurs earliest and fastest. It peaks within 3 months of brain injury, speech reaches its optimal state 6 months after injury, and recovery of sensorimotor skills is later, often peaking at 12 months. In recent years, new ideas have emerged that the recovery process from brain injury has no end point, but only a gradual slowing of the recovery rate. For those patients with craniocerebral injury who are left with lifelong physical and cognitive disabilities, it is still possible to acquire some new function or to adapt to a new environment through continuous learning and training.
Dystonia assessment
Dystonia in patients with cerebral coma is a relatively prominent problem that is not recognized and acknowledged by laymen. Early intervention and treatment should be given for dystonia of brain-injured limbs and trunk tonicity. The awareness of preventive reduction of increased dystonia should be enhanced.
I. Classification and classification of muscle tone
(A) Classification of muscle tone.
1. Normal tension: when moving the limb passively, there is no feeling of sudden increase or decrease of resistance
2. high tension: muscle tension increases, higher than the normal resting state muscle tension
3. low tension: muscle tension is reduced, lower than the muscle tension in the normal resting state
4. Dystonia: muscle tension disorder, or high or low, irregular alternation
(B) muscle tone grading
1, clinical grading: clinical grading of muscle tone is a quantitative assessment method, the examiner classifies it into 0-4 grades according to the limb response or resistance felt when moving the limb passively
2.Joint activity assessment: The causes and manifestations of abnormal joint range of motion are divided into two categories: decreased activity and excessive activity. The former is more common in paralyzed patients and is caused by the following main reasons.
(1) Pain in the joints and surrounding soft tissues; both active and passive activities are reduced due to pain. For example, fractures, post-surgery, prolonged bed rest in brain injury patients, etc.
(2) Muscle contracture: spasticity caused by central nervous system lesions, often with reduced active activity and basically normal passive activity, or passive activity greater than active activity, such as muscle spasm caused by brain injury.
(3) Soft tissue contracture: Both active and passive activities are reduced when the muscles around the joints, ligaments joint capsule and other soft tissues are contracted. For example, after tendon grafting, long-term immobility after paralysis.
(4) Muscle weakness: Whether it is a central nervous system lesion or peripheral nervous system injury, there is usually reduced active activity and normal passive activity, i.e., passive activity is greater than active activity.
IV. Postural management of patients in coma and vegetative state
There are three important reasons for this: the first reason is that sitting or standing has an arousing effect on the superior brainstem reticular formation; the second reason is that providing optimal posture can help reduce muscle spasm, which also gives the patient the opportunity to better express perception; the third reason is that good postural support can help prevent deformities and pressure sores.
I. Dystonia control and deformity prevention in comatose patients
1, coma and the type of hypertonia: the degree and extent of abnormal muscle tone varies with the site and area of brain injury
And different, some patients will not appear increased muscle tone, but the vast majority of patients with severe brain injury coma will appear very high muscle tone, this increase often leads to fixed deformity and contracture.
Patients in the decerebrate position usually have a somewhat worse prognosis than patients in the decorticate position. Sometimes there are patients with one side in the decortical position and the other side in the decerebrate position.
2. The significance of passive and active exercises for patients in cerebral coma
Patients in cerebral coma should not be allowed to miss a good time for recovery, and bed rest will cause the patient’s resistance to decline. Medical staff should assist the chaperone to train the patient at least once a day for passive sitting and standing or active sitting and standing, or even standing. Prolonged bed rest is detrimental to treatment and recovery. “Nurture is the early stage of the body’s recovery, when seriously ill do need to nurture 3-5 days, bed rest to facilitate the smooth vital signs, but if a single rest is not conducive to recovery. Scientific research shows that if a normal person is bedridden for 7 days, need to be “useful” after 7 rehabilitation exercise to return to a normal state.
Second, the complications of long-term bed rest
Firstly, it causes muscle and joint contracture, which is a common symptom of coma and vegetative state disability patients.
The second leads to osteoporosis: when the limb bones do not move normally and do not bear the pressure, osteoporosis will occur after 30 hours of geocentric attraction.
Thirdly, it predisposes to venous thrombosis: as patients are bedridden or lying down for a long time, “venous and arterial thrombosis, which is the most dangerous, is always
threat.
Fourth increase the chance of recurrence: whether patients with cerebrovascular disease or other diseases bedridden patients, if timely rehabilitation is not carried out, the chances of triggering or recurrence of vascular disease will be greatly increased.
Fifth affect the quality of life: long-term bed rest leads to muscle wasting atrophy, so that patients lose a lot of physical strength and basic living ability, some irreversible joint stiffness and deformities appear.
Rehabilitation is a complex and systematic medical discipline, and rehabilitation of patients in brain coma and vegetative state in traditional medicine only emphasizes treatment over rehabilitation, and does not treat rehabilitation as a natural habit, as hospitals began to pay attention to rehabilitation programs ten years ago. Especially comatose and vegetative state patients, who are bedridden for a long time throw away their health that should belong to them.
Third, brain coma patients with five tubes of exercise: usually brain coma patients have five tubes, trachea, oxygen tube, nasal feeding tube, urinary catheter, infusion tube and other five tubes, should be early to let the patient sit, stand, get out of bed to take steps, and gradually increase the amount of activity to achieve a certain amount of exercise.
IV. Time and method of bedside exercise for patients in vegetative state.
1, the time of movement: the movement in the intensive care unit is mainly two kinds of.
(1) Lying on the side: an important posture for comatose patients.
(2) shaking the bed and sitting: sitting and standing when the bed is at an angle of 85 degrees, this position is conducive to automatic sputum excretion of patients, and sputum excretion starts after a few minutes, sitting for half an hour each time, three times a day. First, to reduce choking and coughing of sputum; second, to reduce cerebral and pulmonary pressure; third, to facilitate gastrointestinal peristalsis.
(3) hand and foot bicycle: long-term bedridden patients will have rapid bilateral limb muscle atrophy and muscle relaxation, regularly given with bedside hand and foot bicycle training, so that the patient’s double upper limbs, hands muscle, double lower limbs tibial gastrocnemius muscle function recovery, increase muscle protein synthesis, less hypoproteinemia.
(4) Acupuncture, massage: are commonly used in the clinical treatment of patients in coma and vegetative state.
(5) chest pressure, abdominal pressure treatment: become a set of treatment methods for coma, chest pressure is mainly based on the patient’s respiratory kinetics, massage rehabilitator, the hands will be pressed on both sides of the patient’s chest (and first aid when pressing the chest posture), with the patient’s respiratory kinetics, gently squeeze the chest muscles to achieve the activity of the lung muscles, conducive to the recovery of respiratory kinetics and sputum, facilitate the inhalation of oxygen and reduce asthma. Abdominal pressure: pressing the abdomen clockwise like kneading the noodles in the abdomen increases intestinal peristalsis, enhances the function of the gastrointestinal tract, facilitates excretion, and also enhances the smooth reflux of the lymphatic system and increases the immunity of the body.
(6) Standing bed training: for patients in cerebral coma and vegetative state rely on standing bed to make the patient stand up, provided that the patient’s condition is stable, the final exercise training after bedside sitting and bicycling. Patients were given standing time in the range of 5-10 minutes twice a day at first and 20 minutes twice a day thereafter. Standing training has a significant effect on the patient’s recovery of consciousness and the enhancement of physical function (7) Microwave therapy: Microwave therapy is mainly to reduce and treat lung infections. (8) Medium frequency treatment: 1. Medium frequency treatment principle: In a certain frequency range, the impedance of human tissues is inversely proportional to the frequency, that is, the impedance of human tissues to medium frequency current is lower than that to low frequency current, so medium frequency current can reach deeper parts of the tissue, and the skin feels comfortable. Medium-frequency current itself has
The IF current itself has certain therapeutic effect, and the IF current modulated by low frequency has the combined effect of low frequency and medium frequency, and the effect is better. 2. Characteristics of IF current stimulation: ① The effect on sensory nerve. ②The effect on the transverse muscle. ③The effect on local blood circulation is found to increase the blood volume after treatment.3.The effect of medium frequency treatment: ①The electrotherapy stimulates the extensor muscle belly of upper limb. ②Patients who are bedridden for a long time, poor limb mobility, possible atrophy of limb muscles, early passive activity