Wakefield childcare early learning center: Wakefield Child Care Early Learning Center

Wakefield Child Care Early Learning Center

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About the Provider

Little Sunshine’s Playhouse And…

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Little Sunshine’s Playhouse And Preschool – Colorado Springs CO Child Care Center

Description: Wakefield Childcare Center offers a variety of programs for infants through children age twelve. The daily schedule of child initiated and teacher guided activities are designed to encourage maximum growth in each child. It is our goal to provide environments and daily schedules that are stimulating, challenging, and supportive of each child’s needs, as each child is unique. A wide range of activities are offered daily to allow each child the freedom to explore their environment and select activities from a variety of areas.

Additional Information: Provider First Licensed on: 12/27/94;

Program and Licensing Details

• License Number:
  CCCB-06830
• Capacity:
  46
• Age Range:
  6 weeks to 12 years
• Enrolled in Subsidized Child Care Program:
  No
• Type of Care:
  Pre-School Program
• District Office:
  New Hampshire Dept of Health and Human Services – Child Care Licensing Unit
• District Office Phone:
  (603) 271-4624 (Note: This is not the facility phone number. )
• Licensor:
  Diana Carney

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Management of patients in the recovery period of ischemic stroke uMEDp

The principles of secondary prevention of ischemic stroke are considered, which include lifestyle changes, therapeutic correction of vascular risk factors (taking antihypertensive and antithrombotic drugs, statins) and, in some cases, surgery. The need for the earliest possible start of preventive measures is emphasized. Depending on the type and severity of existing neurological disorders, the expediency of individual selection of various rehabilitation programs and their combination with various drugs (for the treatment of depression, cognitive impairment, pelvic disorders, spasticity) is noted. Using Actovegin as an example, the possibilities of neurometabolic therapy in the recovery period and secondary prevention of ischemic stroke are analyzed.

Drawing. Stages of the post-stroke period

Introduction

Acute cerebrovascular accident (ACV) is one of the most important medical and social problems. The incidence of stroke is 2.5-3 cases per 1,000 population per year, and post-stroke disability is one of the first places among all causes of disability – 3.2 per 10,000 population [1]. According to the national registry, 31% of patients after a stroke need constant care, and 20% cannot walk on their own. About 20% of surviving patients are able to return to their previous work. At the same time, the risk of recurrent stroke after the first stroke is 26 and 39% over the next five and ten years, respectively [1–3].

The tactics of managing patients with ischemic stroke is largely determined by the characteristics of neurological (motor, sensory, cognitive and emotional) disorders. Depending on the severity of the existing disorders, it is enough for some patients to be observed at the outpatient clinic at the place of residence and follow the recommendations for secondary prevention of ischemic stroke, other patients need to undergo rehabilitation at home, in a polyclinic or specialized centers. The most active recovery of motor functions occurs in the first three months after a stroke, which is why rehabilitation measures are of particular importance during this period (figure) [4–6].

Basic principles of rehabilitation

Rehabilitation includes a set of measures aimed at restoring impaired functions. The mechanisms of compensation for impaired function are based on the phenomenon of neuroplasticity. Neuroplasticity, as defined by the World Health Organization, is the ability of cells of the nervous system to regenerate, change anatomically and functionally [7, 8]. Rehabilitation programs should be developed individually for each patient, taking into account neurological disorders. The latter depend on the location and features of the stroke.

The effectiveness of rehabilitation treatment is determined by the time of the start of rehabilitation measures, their adequacy, regularity and duration. We need a comprehensive and interdisciplinary approach, active involvement in the rehabilitation process of both the patient himself and his relatives. The most important factors affecting the effectiveness of rehabilitation measures are the volume and localization of the lesion in relation to functionally significant cerebral zones [4–6, 9, 10].

The most common disabling consequences of a stroke include movement disorders in the form of central paresis of varying severity. In the presence of movement disorders, early activation of the patient is of great importance. It allows you to avoid many complications of immobility, such as thrombophlebitis, bedsores, hypostatic pneumonia. Motor rehabilitation in the early recovery period affects the further activation of patients, reduces spasticity, improves walking functions, trains stability, increases exercise tolerance, and masters various household skills. Motor rehabilitation includes kinesiotherapy, therapeutic exercises, and, if possible, daily walks. If necessary, assistive devices are used (walkers, canes, wheelchairs, etc.) [4–6, 11]. Currently, new technologies are being actively used: biofeedback using electromyography, vertical tables, walking simulators, rehabilitation complexes for restoring the motor functions of the upper limbs [4].

An important area of ​​neurorehabilitation is the correction of spasticity, which develops in more than half of patients who have had a stroke and have movement disorders. In addition, therapeutic exercises, selective massage, positional treatment, neuromuscular electrical stimulation, physiotherapy methods are used to prevent the formation of contractures. With generalized spasticity, muscle relaxants are prescribed (tizanidin, tolperisone, baclofen), with local spasticity, botulinum toxin preparations.

In the post-stroke period, various trophic disorders also often develop: arthropathy of the joints of paretic extremities, bedsores, and muscle atrophy. Arthropathy can cause the formation of contractures. As a result of a significant limitation of the volume of active and passive movements due to pain in the joints, the recovery of motor functions slows down. For the treatment of arthropathy, heat therapy, vacuum or turbulent massage, and therapeutic exercises can be used.

It is necessary to remember about one more frequent complication of the acute and early recovery periods of a stroke – falls with bone fractures. Medical staff and relatives should carefully monitor patients who are at high risk of falling; drugs that cause drowsiness, decreased concentration, and weakness in the paretic leg should not be prescribed to such patients [4-6].

No less significant and common are post-stroke speech disorders, which are divided into aphasia and dysarthria. Of particular importance in the treatment of speech disorders are classes with a speech therapist-aphasiologist. The effect of these classes is more pronounced in the early stages after an ischemic stroke, so speech restoration classes should be started as early as the first three weeks. At the outpatient stage of rehabilitation, classes are held two or three times a week for 45–60 minutes. In addition to individual lessons, group lessons are also very effective, improving the communicative function of speech [12, 13].

A significant number of stroke patients have cognitive impairment, and in 6-32% of patients they reach the degree of dementia. To assess cognitive functions, a neuropsychological study is carried out. Cognitive impairment can be caused not only by a previous ischemic stroke, but also by a previous stroke with a stroke clinic or by the type of “silent” heart attack / hemorrhage. Pre-stroke asymptomatic or oligosymptomatic brain damage may also be associated with diffuse changes in the white matter of the brain as a result of chronic cerebrovascular insufficiency and (or) a concomitant neurodegenerative disease, most often Alzheimer’s disease [14]. The need for timely diagnosis of cognitive impairment is due to the fact that cognitive impairment can significantly reduce the effectiveness of rehabilitation, the quality and life expectancy of the patient, and also negatively affect the patient’s adherence to therapy. To improve memory and other cognitive functions, patients with mild and moderate cognitive impairments are recommended to perform systematic exercises to train memory and attention (cognitive training), take neurometabolic and vasotropic drugs. In severe cognitive impairment reaching the degree of dementia, cerebral acetylcholinesterase inhibitors (donepezil, galantamine, rivastigmine) and the non-competitive NMDA receptor antagonist to glutamate memantine are used.

Approximately 30-40% of patients in the post-stroke period develop depression, which is also recognized as a risk factor for recurrent strokes, myocardial infarction and is associated with an increase in mortality during the first ten years after a stroke. The presence of depression in the first six months after a vascular accident is a risk factor for the occurrence of cognitive impairment and dementia in the future [15]. Like post-stroke cognitive impairment, post-stroke depression reduces the effectiveness of ongoing rehabilitation measures. It has been shown that emotional disorders most often develop in the early recovery period of a stroke. To diagnose depression in patients who have had an ischemic stroke, you can use the Beck Depression Scale, the Hamilton Depression Scale, the Wakefield Depression Self-Assessment Scale, etc. Treatment of post-stroke depression includes individual selection of antidepressants (tricyclic, tetracyclic, selective serotonin reuptake inhibitors) and cognitive psychotherapy [15 , 16].

The serious consequences of a stroke include chronic pain syndrome, which is neurogenic in nature only in some cases and is directly related to damage to the central nervous system. In most cases, post-stroke pain is due to musculoskeletal dysfunction due to insufficient physical activity and changes in the motor stereotype. A significant contribution to the formation of post-stroke pain syndrome is also made by spasticity and emotional disturbances, as already mentioned above.

One of the most dangerous complications of stroke is dysphagia. The presence of dysphagia can lead to the development of aspiration pneumonia, as well as disruption of normal fluid and food intake. Early rehabilitation measures (installation of a nasogastric tube, special exercises, intrapharyngeal stimulation) allow avoiding these consequences [4].

Secondary prevention of ischemic stroke

Prevention of recurrent stroke plays an important role for patients who have had stroke. As you know, the maximum risk of recurrent ischemic stroke is noted in the first days after stroke, so preventive measures should be started as early as possible. Prevention of recurrent ischemic stroke includes lifestyle modification, the use of drugs and, if necessary, the use of surgical methods of treatment [17, 18].

It is recommended to quit smoking or reduce the number of cigarettes smoked, which can significantly reduce the risk of recurrent ischemic stroke (slowly, over two to four years) and myocardial infarction [19]. Stopping alcohol intake or significantly reducing its amount also reduces the risk of repeated strokes.

After an ischemic stroke, it is important for patients to increase physical activity, including systematically receiving aerobic exercise (30-40 minutes three to four times a week), which improves the state of the cardiovascular system [17, 18]. In the presence of a neurological defect that makes walking difficult, the patient should regularly perform a set of physical exercises under the supervision of a specialist in physical therapy.

To reduce the risk of recurrence of ischemic stroke, it is necessary to follow a low-cholesterol diet: reduce the total intake of fats and easily digestible carbohydrates (sugar, confectionery), saturated fatty acids (animal fats, butter, eggs). On the contrary, it is advisable to include in the diet products enriched with polyunsaturated fatty acids (vegetable oils, fish, seafood), fiber and complex carbohydrates. In case of arterial hypertension, the intake of table salt should be reduced to 2.4 g per day, and for a more significant reduction in blood pressure – up to 1.5 g per day [17, 18].

Normalization of blood pressure is one of the most effective areas of secondary prevention of ischemic stroke. Several large studies have shown that blood pressure control not only reduces the likelihood of a recurrent stroke, but also helps to reduce the severity and rate of progression of post-stroke cognitive impairment. The choice of an antihypertensive drug depends on the clinical features of arterial hypertension, individual tolerance and comorbidity of the patient [18].

According to generally accepted recommendations, the target is a blood pressure level of less than 140/90 mm Hg. Art. However, it is necessary to reduce blood pressure gradually, taking into account individual tolerance and patient characteristics. As is known, against the background of long-term uncontrolled arterial hypertension, the reactivity of cerebral vessels changes, and a rapid decrease in blood pressure can lead to cerebral hypoperfusion. The risk of cerebral hypoperfusion is also extremely high in patients with hemodynamically significant stenosis of the main arteries of the head.

You should also be careful and, in the absence of an immediate threat to the life and health of the patient, refrain from active antihypertensive therapy in the first hours and days after a cerebral ischemic event. This is due to the fact that in the most acute period, the rise in blood pressure may be a compensatory response of the cardiovascular system to cerebral ischemia. A decrease in blood pressure in this case threatens to aggravate neurological symptoms.

With concomitant diabetes mellitus and renal failure, it is necessary to control the level of glucose in the blood, and regularly take hypoglycemic drugs. In such patients, blood pressure should be maintained at less than 130/80 mm Hg. Art.

To correct dyslipidemia, patients who have had an ischemic stroke are prescribed statins for a long time under the control of the level of liver enzymes and creatine phosphokinase in the blood. These drugs significantly reduce the likelihood of recurrent ischemic stroke and other ischemic events [17, 18]. An indicator of the effectiveness of lipid-lowering therapy is the level of low-density lipoprotein, which in patients with a history of ischemic stroke should be less than 1.8 mmol / l.

In non-cardioembolic stroke, antiplatelet agents have been shown to reduce the risk of recurrent stroke. They reduce platelet aggregation, prevent their fixation on an atherosclerotic plaque and, as a result, prevent the formation of a blood clot. Acetylsalicylic acid (ASA) at a dose of 75–325 mg/day, clopidogrel at a dose of 75 mg/day, a combination of 25 mg of ASA and 200 mg of sustained release dipyridamole have proven antiplatelet activity. The CAPRIE study showed that taking 75 mg of clopidogrel reduced the incidence of stroke, myocardial infarction and acute vascular death to a greater extent than taking 325 mg of ASA, so clopidogrel is considered to be more effective than ASA [20]. According to the ESPS-2 and ESPRIT studies, the efficacy of the combination of 200 mg sustained release dipyridamole and 25 mg ASA twice daily was superior to that of ASA and comparable to that of clopidogrel [21, 22]. Thus, this combination can be used as an alternative to ASA or clopidogrel monotherapy in patients without concomitant coronary heart disease.

In cardioembolic stroke in patients with atrial fibrillation, intraventricular thrombus, artificial valve or valvular heart disease, anticoagulants are used for secondary prevention. The vitamin K antagonist warfarin is the gold standard for anticoagulant therapy. The appointment of this drug is associated with certain difficulties in dose titration and its correction depending on the international normalized ratio. When taking warfarin, the international normalized ratio should be measured once every two weeks and maintained in the range from 2 to 3. Currently, in patients with non-valvular atrial fibrillation, new oral anticoagulants have proven their effectiveness in preventing ischemic stroke, which do not require monitoring of the international normalized ratio: direct thrombin inhibitor dabigatran, factor Xa inhibitors rivaroxaban and apixaban [23, 24]. These drugs are much more convenient to use compared to warfarin and are not inferior to it in terms of effectiveness in preventing ischemic stroke. The advantage of these drugs in terms of safety profile should be noted, since they cause intracranial bleeding significantly less frequently.

In case of severe stenosis (narrowing of 70–99% of the diameter) of the internal carotid artery on the side of the hemisphere concerned, surgical treatment is recommended in the early stages (but no later than six months from the moment of ischemic stroke): carotid endarterectomy or stenting. For patients with moderate (50 to 69%) stenosis of the internal carotid artery, surgical treatment has a slight advantage over conservative methods [17, 18].

Neurometabolic Therapy

As noted above, the restoration of neurological functions after stroke is due to the plasticity of the nervous tissue: the functional restructuring of neurons with the formation of new dendrites, synapses and neuronal networks. For the purpose of metabolic support of these processes, the so-called neurometabolic drugs (Actovegin, Ceraxon, choline alfoscerate, etc.) are widely used. They contribute to the regression of both cognitive and other neurological disorders, and also allow for more effective neurorehabilitation.

Currently, there is a positive clinical experience with the use of the neurometabolic drug Actovegin in the recovery period of ischemic stroke. Actovegin is a highly purified hemodialysate obtained by ultrafiltration from the blood of calves. The drug contains low molecular weight biologically active compounds: oligopeptides, amino acids, nucleosides, intermediate products of carbohydrate and fat metabolism, as well as trace elements (sodium, calcium, phosphorus, magnesium and copper). The experiment shows that the use of Actovegin promotes the transfer of anaerobic glycolysis processes into more energetically beneficial aerobic glycolysis. At the same time, Actovegin does not increase the oxygen demand of cells [25, 26]. Due to the insulin-like effect, the drug increases the transmembrane transport of glucose into the cell without affecting insulin receptors. It is assumed that it takes part in the activation of glucose carriers present in the membrane. An increase in glucose transport occurs under the action of inositol phosphate oligosaccharides, which are part of Actovegin [25, 26].

It was shown that Actovegin prevents the formation of reactive oxygen species, inhibiting oxidative stress, and has a neuroprotective effect, increasing the survival of neurons and reducing the level of apoptosis induction markers (caspase 3). Actovegin increases the survival of primary hippocampal neurons when exposed to amyloid protein.

The implementation of glycolysis in ischemic tissues under the action of Actovegin ensures the operation of other metabolic shunts, in particular alanine and ornithine, since these and other amino acids are also part of Actovegin. The inclusion of such essential amino acids as proline, leucine and ornithine in the corresponding cycles of tissue metabolism contributes to the activation of protein synthesis and a pronounced reparative (healing) effect of the drug. In addition, proline, leucine and ornithine contained in Actovegin correct the cytokine imbalance due to “inclusion” in the appropriate detoxifying cycles [27].

Actovegin also improves microcirculation in tissues, having a positive effect on the endothelium of microvessels.

Experimental studies have shown that Actovegin not only helps neurons survive the period of critical ischemia, but also reduces the negative effect of postischemic recirculation, helping to eliminate the delayed energy deficit in the cerebral cortex and hippocampus of adult rats. Taking into account the results of experimental and clinical studies, we can say that the use of this drug in the early recovery period of cerebral stroke is pathogenetically justified.

A.A. Skoromets and V.V. Kovalchuk analyzed the results of treatment of 1920 stroke patients, of which 1520 patients had an ischemic stroke. The mean age of patients with ischemic stroke (846 women and 674 men) was 62.3 years (from 36 to 80 years). The patients were hospitalized at the Department of Neurological Rehabilitation of the City Hospital No. 38 named after ON THE. Semashko from 2001 to 2005 inclusive. All of them were hospitalized in the department three times: during the first, sixth and 11th month from the onset of the disease. The degree of recovery of various functions one year after a stroke was determined using the Barthel index, the Lindmark scale and the Scandinavian stroke scale. During the rehabilitation period, patients received various neurometabolic drugs: piracetam, antioxidants, antihypoxants, vitamins, alpha-lipoic acid, etc. (11 drugs in total). Therapy with Actovegin contributed most to the restoration of impaired functions after ischemic stroke. So, in 78. 3% of patients receiving this drug, there was a “sufficient” and “complete” restoration of functions [28].

There is also evidence of the effectiveness of Actovegin in post-stroke cognitive impairment. E.A. Wooden et al. studied the dynamics of cognitive functions in 43 patients with ischemic stroke and receiving various neurometabolic therapies. Against the background of the use of Actovegin, they had a significantly more pronounced improvement in cognitive functions in the early recovery period of a stroke [29].

Considering the neuroprotective action profile of Actovegin, its probable preventive effect in relation to the onset and progression of post-stroke cognitive impairment is of greatest interest. At present, a large international randomized placebo-controlled study of the effectiveness of Actovegin in post-stroke cognitive impairment has been completed [30]. The results of the study were first presented at the 1st Congress of the European Academy of Neurology in Berlin in June 2015. After six months of treatment, a statistically significant difference was obtained in the Actovegin group relative to the placebo group in the primary endpoint – a change in the cognitive function assessment scale for Alzheimer’s disease (Alzheimer’s Disease Assessment Scale – Cognitive Subscale – ADAS-cog+). This confirms the effectiveness of the drug in terms of improving cognitive functions in patients after a stroke.

According to the generally accepted scheme, Actovegin is usually prescribed in the rehabilitation period of a stroke, depending on the severity of the neurological deficit: 5 ml (200 mg) intramuscularly or 10–20 ml (400–800 mg) intravenously for 10–20 days, then one tablet three times a day, the course of administration is at least one month.

Conclusion

A patient who has had an ischemic stroke needs constant prevention of recurrent stroke. Secondary prevention includes lifestyle modification, medications (antihypertensive and antithrombotic agents, statins) to correct vascular risk factors, and in some cases surgery.