The U.S. Centers for Disease Control and Prevention is expected to update its guidance for COVID-19 control in the community, including in schools, in the coming days, according to sources familiar with the plan.
A preview of the plans obtained by CNN shows that the updated recommendations are expected to ease quarantine recommendations for people exposed to the virus and de-emphasize 6 feet of social distancing.
The agency is also expected to de-emphasize regular screening testing for COVID-19 in schools as a way to monitor the spread of the virus, according to sources who were briefed on the agency's plans but were not authorized to speak to a reporter.
Instead, it says it may be more useful to base testing on COVID-19 community levels and whether settings are higher-risk, such as nursing homes or prisons.
The changes, which may be publicly released as early as this week, were previewed to educators and public health officials. They are still being deliberated and are not final.
In a statement to CNN, the agency said, "The CDC is always evaluating our guidance as science changes and will update the public as it occurs."
As part of the expected changes, the CDC would also soon remove a recommendation that students exposed to COVID-19 take regular tests to stay in the classroom.
The strategy, called "test to stay," was recommended by the agency in December, during the first Omicron wave, to keep unvaccinated kids who were exposed but didn't have symptoms in the classroom instead of quarantining at home.
Test-to-stay was resource-intensive for schools, and some districts had voiced concerns about having enough money to continue, one source said.
In schools and beyond, the agency will no longer recommend staying at least 6 feet away from other people as a protective measure. Instead, the new guidelines aim to help people understand which kinds of settings are riskier than others because of things like poor ventilation, crowds and personal characteristics like age and underlying health.
The CDC is also set to ease quarantine requirements for people who are unvaccinated or who are not up-to-date on their COVID-19 vaccines. Currently, the agency recommends that people who aren't up-to-date on their shots stay at home for at least five days after close contact with someone who tests positive for COVID-19. Going forward, they won't have to stay at home but should wear a mask and test at least five days after exposure.
People who are sick with COVID-19 should still isolate, the agency is expected to say.
The agency also plans to re-emphasize the importance of building ventilation as a way to help stop the spread of many respiratory diseases, not just COVID-19. It plans to encourage schools to do more to clean and refresh their indoor air.
Sources say the tweaks reflect both shifting public sentiment toward the pandemic -- many Americans have stopped wearing masks or social distancing -- and a high level of underlying immunity in the population. Screening of blood samples suggests that as December, 95% of Americans have had COVID-19 or been vaccinated against it, reducing the chances of becoming severely ill or dying if they get it again.
The CDC's recommendations are not legally binding. Many cities, states and school districts will review them but may ultimately follow different strategies.
One example of this is masks in schools.
More than 200 million people -- about 60% of the total population -- live in a county with a "high COVID-19 community level" where the CDC warns of a risk of strain on the health care system and recommends universal indoor masking.
Yet most schools have kept masks optional for students this year. Among the top 500 K-12 school districts, based on enrollment, about 98% do not require masks, according to the data company Burbio's school policy tracker.
Still, the agency's guidance continues to be important as a baseline. When cities or states try to go beyond what the CDC recommends, they may face pushback.
The-CNN-Wire
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Arguably, COVID-19 has caused the most unprecedented global health crisis since the 1918 H1N1 pandemic. The virus was originally identified in Wuhan, China, in December 2020. Over two yearson, it is estimated that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has infected 572 million individuals and caused over 6.3 million deaths worldwide[1]. The magnitude of turmoil the virus has created is so severe that additional hospitals (for example, Nightingale in Central London) have been constructed to support the incredible demands placed upon healthcare systems across the world.
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is classified to be a part of the Coronaviridae family[2]. There are multiple coronavirus strains, ranging in clinical severity; from the common cold to severe acute respiratory distress syndrome (SARS) and Middle Eastern respiratory distress syndrome (MERS). Genomically, SARS-CoV-2 is a single-stranded, positive-sense, enveloped virus. It possesses a variety of membranous glycoproteins that attribute to its pathogenic nature, for example, the spike (S) glycoprotein[3]. Over the past few months, the S-glycoprotein has created anxiety for the scientific community and public because it has shown the ability to mutate, resulting in highly contagious strains. The clinical significance of the new strains is that there is a reducedthreshold for infectivity, thus vulnerable individuals are at a greater risk of contracting the virus and becoming critically unwell.
Whilst it is acknowledged amongst the scientific community and public that SARS-CoV-2 affects the respiratory system, the virus has shown the ability to quickly disseminate throughout the body affecting multiple organs[4].
The nervous system is subdivided into two parts: the central nervous system (CNS) and the peripheral nervous system (PNS)[5]. The CNS consists of the brain and spinal cord. The peripheral nerves reside outside of the brain and spinal cord, that is, cranial nerves I-XII which supply the head/neck, and spinal nerves which supply the motor, sensory, and autonomic function of the rest of the body. This review aims to discuss and explain the neurological complications seen in COVID-19.
At the start of the pandemic, most literature published on the neurological complications of COVID-19 were small case reports/series[6-7]. Over a year on, there is now a plethora of scientific evidence available detailing various neurological complications observed in patients infected with SARS-CoV-2. The virus has been shown to affect both the central and peripheral nervous systems, with a range of clinical impacts[8]. It has been theorized that the pathophysiological mechanisms of COVID-19 on the nervous system are caused by entry into host cells via viral glycoproteins, which then results in a widespread inflammatory response of the immune system and vasculature[9-10]. However, it is appreciated that more research needs to be done to fully understand this.
The aim of this literature review was to identify the different neurological complications associated with COVID-19 infection.The methods were to find the most relevant, appropriate literature on this subject.
A search strategy was adopted to yield papers using the PubMed database. Specific words were searched in combinations, for example COVID-19, Common Neurological, Neuroinflammatory, Neurovascular, and Neuropsychiatric. In addition to using results from the database, other resources including website pages were searched.
For ease of review and relevance, a Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) strategywas adopted (Figure1)[11].
Duplicate results were removed initially, followed by a screening of the literature by title and abstract. The aim of this initial screening process was to identify papers that specifically fit into the question at hand. A large amount of literature yielded during the initial search result was irrelevant (for example, focusing on a different bodily system).
Following this, the literature was assessed for eligibility, with full text being screened. There is a large number of individual case reports/reviews available on specific neurological complications, therefore, one to twoarticles were chosen on specific topics that were felt to be clearest in conveying results.Overall, there was a good amount of relevant literature; providing the platform to write this review.
This review will initially focus on the most common benign neurological complications of COVID-19, followed by the more serious ones observed. Complications involving the central and peripheral nervous system will be discussed, along with neuropsychiatric effects as they sit on the border between neurological and psychiatric disease. For completeness, some of the rarest and most interesting neurological complications documented will be reviewed.
It is arguable that the most common benign neurological-related complications of COVID-19 documented within scientific literature are anosmia and/or ageusia (the loss of smell and/or taste)[7, 12-13]. Whilst it is appreciated that coronaviruses commonly cause a loss of smell and/or taste, these symptoms were originally not promoted to be a headline feature of SARS-CoV-2s symptomatology. Indeed, it was not until two months after the arrival of the virus into the United Kingdom that the government and National Health Service promoted the importance of these symptoms to the public[14].
The olfactory system is derived from the nervous system[15]. Its embryological origin consists of the olfactory epithelium (PNS) and olfactory bulb (CNS). Pathophysiologically, it is thought that COVID-19s spike protein interacts with angiotensin-converting enzyme 2 (ACE2), and transaminase protein serine 2 (TMPRSS2) receptors on olfactory neurons[16-17]. This interaction between the S-protein with olfactory receptors creates difficulty for odors to bind to the neuroepithelial cells, causing a loss of smell. The gustatory system is also closely related to the nervous system[18]. Gustatory cells are supplied by cranial nerves VII, IX, and X, and the sense of taste is expressed within the tongue and palate. Again, it is thought that the SARS-CoV-2 spike glycoprotein possesses neuroinvasive properties in that it binds to ACE2 receptors on the oral mucosa. This leads to an inflammatory cascade within the mucosal cells, disrupting the tongue and palate receptors that help relay taste signals to the CNS.
With regard to the prevalence of these two symptoms, a systematic review and meta-analysis published by Agyeman et al.[19]reported that approximately 40% and 38% of patients diagnosed with COVID-19 experienced some degree of alteration to their sense of smell and taste respectively. This statistic highlights how common these symptoms can be within the general population. In saying this, literature has identified an increased prevalence of anosmia/ageusia in younger patients, and the exact reason for this is yet to be understood. Younger patients infected with COVID-19 tend to experience more benign complications, regardless of the bodily system[20]. This contrasts with the elderly cohort who unfortunately tend to become more critically unwell[21].
A large proportion of individuals infected with SARS-CoV-2 experience anosmia/ageusia temporarily, with the average length of time being seven days from symptom onset[22]. Nevertheless, there is documentation within literature indicating that some patients suffer from these symptoms for extended periods -- i.e., weeks/months, with a few experiencing a chronic loss of their sense of taste/smell that has not returned to normal[23-24].
Another neurological symptom of COVID-19 that is often seen as a complication for many, is a headache. The pathophysiological mechanism of the virus to cause headaches is complex. Irritation of the meninges caused by viral proteins, pro-inflammatory cytokines, and hypoxia all contribute to the sensation of headache. Whilst this symptom usually subsides within a week, there is unfortunately a cohort of patients who require ongoing help from primary care physicians to help deal with debilitating headaches (such as migraines) that occur for a long time after initial infection[25].
Even though the most common complications are often thought to be the most benign, they should not be ignored. The literature has highlighted that these symptoms can cause a significant impact on patient quality of life, and thus overall wellbeing.
Whilst most patients infected with COVID-19 do not develop any serious complications requiring medical treatment, there is a proportion that unfortunately does. One of the more prevalent severe neurological complications seen in patients with COVID-19 is cerebrovascular events, resulting in neurological deficits[26-28]. To highlight this, the literature identifies the prevalence of cerebrovascular accidents (CVAs) in patients who are COVID positive to be as high as 6%[29]. This section will look at both arterial and venous CVAs observed in COVID-19 patients.
Arterial CVAs can be broadly split into ischemic strokes and hemorrhagic strokes[30]. Arterial CVAs most commonly affect the elderly cohort and those with relevant risk factors, i.e., overweight/obesity, hypertension, hyperlipidemia, and diabetes[31]. The available literature reports cases of COVID-19 patients experiencing both types of strokes (ischemic and hemorrhagic). The commencement of anticoagulation therapyhas been shown to increase the risk for the development of hemorrhagic events in patients with COVID-19[32-33]. In contrast, immobility and hypercoagulability seen in COVID-19 patients are thought to contribute to the development of ischemic stroke[34-36]. The development of a hypercoagulable state in COVID-19 patients is due to the widespread inflammatory processes COVID-19 causes within the vasculature, often referred to as a cytokine storm. This is where the virus causes the body to produce high levels of inflammatory and pro-coagulative factors, including CRP, D-dimer, IL-6, and fibrinogen. The resultantis often observed laterin the disease process, and by this point, patients are already admitted into secondary care[26].
The symptoms of arterial CVAs in patients who are non-sedated/non-intubated present with are identical to non-COVID stroke symptoms. This includes but is not limited to, sudden-onset hemiparesis, hemisensory loss, diplopia/hemianopia, ataxia, and speech problems[36]. Following a detailed history of symptoms and relevant neurological examination, patients receive the appropriate investigations. This includes routine blood tests (e.g., FBC, U&Es, LFTs, d-dimer, CRP), electrocardiogram to check for atrial fibrillation, and appropriate imaging, such as diffusion-weighted MRI brain or CT-head. The results of the investigations are necessary to determine the nature of the CVA, and what treatment pathway to begin.
If a transient ischemic attack (TIA) is suspected, the ABCD2 scoring system can be used which helps physicians determine the risk of developing a stroke following a TIA. The treatment for TIAs is variable, however, most patients are given an antiplatelet medication such as aspirin and should be ideally seen by a stroke physician within 24 h for further management[37]. Regarding the treatment of ischemic strokes, patients should be admitted immediately to a stroke unit for further workup and may receive either medical (thrombolysis) or surgical (thrombectomy) intervention, followed by preventative management including anticoagulation, and blood pressure/cholesterol management[38]. Hemorrhagic strokes are often managed through surgical intervention. For the more severe COVID-19 patients where respiratory function is also compromised, escalation to the ICU is often needed for further monitoring due to the risk of deterioration[27, 39].
For COVID-19 patients who are intubated with an endotracheal tube and/or heavily sedated, it is much more difficult to appreciate when aCVA has occurred[40]. This often means patients go for longer periods undiagnosed. As mentioned earlier, patients who are admitted into hospital, particularly those that go to the ICU, are at a significantly higher risk for the development of a CVA.
Identification of an ischemic event in patients who are intubated/sedated and not paralyzed may be observed through muscular spasticity, or abnormal limb positioning, such as elbow/wrist flexion, with internal rotation and adduction of the shoulder. Post-stroke spasticity can often take a long time to occur and is, therefore, often missed. For hemorrhagic strokes, patient pupils are regularly checked for anisocoria, i.e., unequal pupil size[41-42]. Again, this can often be subtle. Therefore, identification of CVAs in the ICU regardless of etiology is often made when patients are being weaned off sedation, and they respond in a neurologically inappropriate way[43](e.g., lack of appropriate limb movement). If this occurs, patients receive appropriate brain imaging.
The treatment of CVAs in COVID-19 patients who are intubated is based on many different factors, including overall health status, age, and suspected level of damage. For example, there have been cases where unfortunately very young patients with COVID-19 have suffered from large cerebrovascular events with suspected irreversible damage[29, 42].
The points discussed above look at neurological complications that have arisen from problems within the arterial vasculature. COVID-19 can also cause complications within the venous vasculature, again resulting in neurological deficits. Cerebrovascular complications of the venous system are much rarer than arterial. However, one of the more serious venous complications seen in COVID-19 patients is cerebral venous sinus thrombosis (CVST)[44-46]. This is where a thrombus forms within the venous vasculature of the brain, such as the superior sagittal sinus, transverse sinus, sigmoid sinus, and even the jugular foramen. The more severe CVSTs can interrupt the drainage of blood from out of the brain, which poses the risk of hemorrhagic transformation.
In contrast to arterial complications, CVSTs typically affect younger adults[45-46]. Predisposing risk factors for venous thromboses are slightly different from that of arterial. There is less focus on modifiable risk factors, and instead, hypercoagulopathies are considered more relevant. For example, pregnancy and genetic coagulopathies such as sickle cell/beta-thalassemia, place patients at a significantly higher risk. In saying this, the inflammatory and hypercoagulable state of COVID-19 causes puts patients at risk, irrespective of the clot location within the vasculature[44-46].
The symptoms of CVST patients with COVID-19 can experience include headaches, blurred vision, seizures, and loss of consciousness. Regardless of intubation status, one clinical sign that is looked for in patients with suspected CVST, is papilledema. This is because CVST can cause intracranial hypertension[46].
As with suspected arterial accidents, venous accidents are investigated through simple investigations including blood tests, electrocardiogram (ECG), and imaging including magnetic resonance (MR) or CT venogram. Treatment of venous accidents must be rapid and can either be medical (e.g., thrombolysis/anticoagulation/antiepileptics) or surgical (thrombectomy/decompressive craniotomy). Again, the direction of treatment in COVID-19 patients depends on clinical stability[44-46].
Whilst some patients with COVID-19 who experience a CVA make a full recovery, there are many cases, particularly those in the ICU, where CVAs cause devastating long-term neurological complications. A study published by Ntaios et al.[47]found that patients with COVID-19 who experienced a CVA have worse rates of morbidity/mortality, and quality of life, than non-COVID stroke patients. This was reflected through an overall lower modified Rankin scale, which measures the degree of disability post-stroke.
Cerebrovascular complications of COVID-19 are worrying. The literature available details very young patients with no cardiovascular risk factors developing such complications highlighting the viruss ability to affect anyone of any age, regardless of baseline clinical status.
COVID-19 can cause inflammation within parts of the nervous system. This can be anatomically divided into meningeal (meningitis) and brain parenchyma (encephalitis) inflammation. The latter can progress into the worrying clinical state physicians describe as encephalopathy.
The pathogenic mechanisms of COVID-19 in causing meningeal and encephalic inflammation are complex, and it must be said that meningoencephalopathy directly caused by COVID-19 is rare. As discussed in the common complications section of this review, COVID-19 can infect olfactory neuroepithelium. This can result in the retrograde transfer of virion particles into the CNS[48]. Moreover, it is thought that viral particles infect the CNS via the blood-brain barrier during the initial stage of infection. Following the penetration of the virus into the CNS, an intense inflammatory cascade resulting in meningeal/encephalic inflammation and irritation occurs[48-50]. This, coupled with hypoxia, iswhy patients with COVID-19 can present with the severe neuroinflammatory disease.
COVID patients who possess underlying co-morbidities or those who receive immunosuppression therapy (e.g., steroids) have been shown to increase the risk of opportunistic infections developing within the body, including neuroinflammatory diseases such as bacterial, fungal, or alternative viralmeningoencephalitis[51].
Regardless of whether COVID-positive individuals develop a primary or secondary neurological infection, the clinical presentation for both is roughly the same. For pure meningitis, patients can present with fevers, headaches, and neck stiffness[49]. For encephalitis, the presentation is often more severe and can progress to encephalopathy. This is defined as a widespread brain disease with resultant effects on brain structure/function[52]. Symptoms of encephalopathy which highlight the gross injury to the brain include depressed mental status, which can result in a coma. In addition to this, patients can have severe seizures due to interrupted neurological activity within the brain. In reality, both meningitis and encephalitis can occur together resulting in a devastating picture of meningoencephalitis/encephalopathy.
Investigating the neuroinflammatory complications of COVID-19 include routine blood tests, and imaging, including CT-head to identify any raised intracranial pressure (ICP)[48-49, 52]. Patient cerebrospinal fluid (CSF) may also be analyzed via lumbar puncture. The CSF analysis includes looking at the appearance of the fluid and the levels of protein, glucose, and white cell count. To identify potential bacterial infections that are secondary to COVID-19, CSF Gram stain, and microscopy, culture and sensitivity can be sent to the laboratory for further analysis. For suspected primary (COVID-19) or secondary (HSV, etc.) viral neuroinflammatory disease, viral polymerase chain reaction (PCR) can be sent to the lab. There have only been a few cases within the literature identifying patients with a positive COVID-19 PCR seen within the CSF[53-54], again, highlighting the rarity of this diagnosis.
Treatment of meningoencephalitis in COVID-19 patients depends on the causative organism. For secondary superimposed bacterial infections, IV antibiotics including ceftriaxone and vancomycin are used[55]. For meningoencephalitis where the cause is thought to be a primary infection, i.e. COVID-19, treatment is mainly supportive. This includes symptom management, such as anti-epileptics for seizure control. Occasionally, medications including hydroxychloroquine, IV methylprednisolone, and IV immunoglobulins are used for immunosuppressive control. Occasionally, IV acyclovir is also prescribed to empirically cover the risk of HSV encephalitis, even if this is not identified within CSF analysis[56].
It can be argued additional neuroinflammatory complications of COVID-19 occur in individuals who already suffer from neuroinflammatory conditions, mainly multiple sclerosis (MS). MS is a chronic immune-mediated and neurodegenerative disorder, developed by both genetic and environmental factors[57]. Common symptoms of MS include fatigue, visual disturbances, and motor/sensory impairment. Interestingly, studies have shown that patients with MS are at a higher risk of developing neurological symptom recurrence preceding or coinciding with COVID-19 infection. For example, Garjani et al.[58]identified 57% of patients experiencing an exacerbation of MS symptoms during COVID-19 infection. Whilst there is no definitive cure for MS, physicians may offer patients steroids during relapses, or disease modifying therapies (DMTs) to reduce the number of relapses. Regarding COVID-19, the literature is limited in identifying whether DMTs reduce symptom recurrence.
The overall clinical outcome for COVID-19 patients with neuroinflammatory disease depends on a multitude of factors. Whilst some patients make a full recovery, patients who fall ill may experience long-term neurological problems[59].
It is important to touch on the neuropsychiatric complications of COVID-19, because these complications sit on the border between neurological and psychiatric illness and are, therefore, relevant from a neurological perspective[60].
One of the most common neuropsychiatric complications seen in patients with COVID-19 is delirium[61]. This is often related to prolonged ICU admission and thus indirectly related to COVID-19. The literature suggests COVID-19-related delirium is more prevalent compared to non-COVID-19 delirium[62]. The etiology for this includes factors including neuroinflammation, secondary infections in combination with environmental factors. The ICU is an unfamiliar environment for many, and with the strict personal protective equipment (PPE) measures that have been put in place since the start of the pandemic, many ICU patients go long periods without seeing a human face that is not behind a mask.
The importance of delirium is that literature has associated patients with having both poorer clinical and functional outcomes[60-61]. A study published by Mcloughlin et al.[63]found that COVID- 19 patients who experienced in-hospital delirium had worse functional outcomes post-discharge, that is, they struggled more whilst doing their activities of daily living than those who did not experience delirium throughout their stay. This finding remained statistically significant (p<0.01) even after appropriate patient factor adjustments. It is thought that patients who experience delirium have worse long-term outcomes because the etiology of delirium often corresponds with other illnesses (e.g., secondary infection) that patients experience throughout their battle with COVID-19.
A more severe and rare neuropsychiatric complication of COVID-19 that has been documented is catatonia, and only a few publications have reported this[64-65]. The etiology of COVID-19 catatonia has not yet been extensively explored. Authors have theorized that this rare presentation could be iatrogenic in etiology or be caused by the severe mental stress patients must deal with whilst in the ICU.
Furthermore, a condition that some scientists have argued to have neuropsychiatric elementsis Long COVID[61]. Some researchers believe Long COVID is like functional neurological illnesses including chronic fatigue syndrome (CFS) and functional neurological disorder (FND)[66]. Neuropsychiatric symptoms patients with Long COVID might experience include depression, anxiety, and cognitive deficits[67]. Data collected from the U.Ks COVID-19 infection survey[68]estimates that around 10% of people who test positive for the virus experience Long COVID, that is, symptoms that last for greater than three months. Therefore, this complication should be discussed as it has a significant impact on many people.
Long COVID is defined as ongoing multi-organ complications and the inability to recover from symptoms for weeks to months following initial infection. The neurological symptoms of Long COVID include extreme tiredness, amnesia, dizziness, and insomnia[66]. Long COVID can have a debilitating impact on the quality of life due to the length of symptoms post-infection[69]. Therefore, this complication is extremely important.
Overall, the neuropsychiatric complications observed in COVID-19 are wide-ranging and can affect a large proportion of patients significantly.
As mentioned in the introduction, COVID-19 can affect the peripheral nervous system.
Important peripheral neurological complications observed in critically unwell COVID patients include critical illness polyneuropathies (CIP) and critical illness myopathies (CIM)[70-71]. CIP and CIM are diseases of the peripheral nerves in patients who have experienced severe trauma and/or critical illness. The literature has identified the prevalence ofperipheral neuropathies to be higher in COVID patients than in non-COVID patients. To support this statement, an observationalstudy written by Frithiof et al.[71]reported that 9.9% of COVID-19 patients developed CIN/CIM, whereas only 3.4% in the general population developed CIN/CIM.
The clinical presentations of CIM and CIN are slightly different. CIM affects the nerves supplying motor function, resulting in significant atrophy, with sensory function usually being preserved. Furthermore, CIM generally affects the proximal aspect of the limb. This contrasts with CIP, which usually affects the distal limb, and is characterized by impaired sensory function. Whilst CIP also causes weakness, the level of atrophy is usually less compared to that seen in CIM due to a degree of motor neuron preservation.
Long-term outcomes for patients with critical illness neuromyopathy (CINM) are mixed.It must be said that patient factors including age, previous mobility, and co-morbidities are very important in determining how well this disease resolves. Nevertheless, a large proportion of patients can continue to suffer from chronic neurological deficits like foot drops and sensory changes like paraesthesia or chronic painfor up to months post-discharge[72].
Treatment for CIN/CIM is mainly supportive. Early intense physiotherapy regimes are recommended to aid the restoration of baseline sensory and motor function. For patients whose glucose levels are raised, extensive dietician input and tight glucose control with insulin therapy are suggested. This is necessary because high glucose levels result in oxidative stress and free radical formation, resulting in further damage to peripheral nerves[73-74].
The above conditions primarily affect the upper and lower limbs. What is interesting is that literature has also identified a link between COVID-19 affecting peripheral nerves of the head and neck. The facial nerve (CN VII) carries motor fibers to the muscles of facial expression, parasympathetic fibers to the lacrimal and salivary glands, and special sensory fibers to supply taste to the anterior two-thirds of the tongue[75]. In facial nerve palsy, patients typically present with total unilateral paralysis of the muscles supplied by CNVII, ptosis, and lacrimal/salivary gland disturbances. COVID-19 has been identified by a number of authors to potentially cause facial nerve palsy[76]. This is thought to be due to the viruses' neuroinvasive abilities to directly infiltrate the nerve fibers.
Another associated peripheral neurological complication of COVID-19 that has been documented is trigeminal nerve (CN V) neuralgia[77]. This is where patients experience sudden, severe facial pain in the forehead, cheek, and lower jaw. However, the evidence for this association is weak.
The rarer COVID-19 peripheral neurological complications documented within the literature are extremely interesting. A few case studies published in the U.K. have identified Guillain-Barre syndrome (GBS) as a potential post-infectious complication of COVID-19[78-79]. Even outside of the COVID world, GBS isa rare autoantibody inflammatory peripheral neurological disorder, typically caused by infection withCampylobacter Jejuni, a Gram-negative bacterium[80].
Webb et al.[79]first made the association between COVID-19 and GBS in 2020, with documentation of a 57-year-old male presenting to the emergency department with ascending paralysis one week after diagnosis with COVID-19. This eventually progressed into respiratory failure, with intubation being needed (the overall outcome of this patient has not been documented). Whilst GBS is an incredibly rare complication, clinicians should be aware of this, and if suspected, must act quickly without delaying treatment. The treatment for GBS can be with plasmapheresis which helps remove autoantibodies from the blood or with IV immunoglobulin which provides antibody replacement to help stop the autoantibodies produced from causing further nerve damage. Supportive treatment is also provided.
Another interesting peripheral neurological complication of COVID-19 is Miller-Fischer syndrome (MFS)[81-82]. Again, this disease is rare and considered to be a variant of GBS. Cases have been identified where COVID-19 patients present with diplopia due to weakening of the ocular musculature, ataxia, and reduced reflexes. As with GBS, the treatment of MFS is IV immunoglobin. Again, whilst only a few cases of this disease have been documented, it is important for clinicians to remain vigilant and to include this as part of their differential diagnosis.
Whilst it is important for clinicians to have a sound understanding of the more common neurological complications of COVID-19, it is also useful to understand rarer complications that do not directly fit into a category.
There have been some fascinating cases documented over the past year. For example, a UK-wide surveillance survey published by Varatharaj et al.[83]looked at the different neurological complications of COVID-19. It was reported that one patient presented with an opsoclonus- myoclonus syndrome (OPS); an incredibly rare neurological disorder that results in opsoclonus (rapid eye movements, occurring in any direction), myoclonus (fast involuntary muscular jerks), and ataxia. The prevalence of OPS in the general population is thought to be 0.18 cases per million[84]. A small case series analysis conducted by Emamikhah et al.[85]identified opsoclonus-myoclonus syndrome as a post-infectious complication of COVID-19, with the average symptom onset being 11 days. Whilst some clinicians believe that the presentation of OPS whilst infected with COVID-19 are separate issues, there is a school of thought that COVID-19 causes this rarity. Whilst the pathological mechanism of this is complex, it is thought to be immunologically mediated.
Another rare neurological complication seen in COVID-19 patients that might be caused directly by the virus is an isolated sixth nerve palsy[86]. It has been hypothesized that the viral proteins (e.g., spike protein) infiltrate the neurons of the abducens nerve, causing neuroinflammation. Patients with COVID-19 who develop a sixth nerve palsy show atrophy of the lateral rectus muscle. Again, this is thought to be due to the neuroinflammatory nature of the virus, resulting in ocular myopathy.
The rare neurological complications documented in patients with COVID-19 are interesting to discuss, as they highlight the viruss potential to affect the body in a multitude of ways. In the future, it would not be unreasonable to suggest that further neurological complications which have not yet been documented, will be observed.
The Hawaii Department of Health today reported 3,689 new COVID-19 infections over the past week, lower than reported the previous week, bringing the total since the start of the pandemic to 329,633.
The states seven-day average of new cases also fell to 528, down from 573 reported on July 27. DOHs daily average reflects new cases per day from July 23 to 29, which is an earlier set of days than the new infections count.
DOH also reported 21 more deaths, bringing the states coronavirus-related death toll to 1,592.
By island, there were 2,503 new infections reported on Oahu, 468 on Hawaii island, 462 on Maui, 146 on Kauai, 12 on Molokai, and two on Lanai. Another 96 infections were reported for out-of-state Hawaii residents.
Actual numbers are estimated to be at least five to six times higher since these figures do not include home test kit results.
The states average positivity rate, meanwhile, declined to 13.8% compared to 15.7% reported the previous week, representing tests performed between July 16 to Aug. 1.
There are 147 patients with COVID in Hawaii hospitals today, according to the Hawaii Emergency Management Agencys dashboard. Of the 147, 19 are in intensive care and four on ventilators.
The Healthcare Association of Hawaii reported a 7-day rolling over of 135 patients with COVID in hospitals over the past week, and an average of 23 new COVID admissions per day.
Both SARs-CoV-2 and influenza are respiratory viruses that are contagious and can affect your lungs and breathing. Patients infected with COVID or the flu can experience similar symptoms ranging from fever, cough, body aches, sore throat, runny/stuffy nose, muscle pain, headache and gastrointestinal issues.
However, COVID-19 can cause different complications from the flu, such as blood clots and multisystem inflammatory syndrome in children, according to the Mayo Clinic.
Furthermore, experts believe symptoms like loss of sense of smell and taste are specific to COVID-19, which was prevalent during the Delta wave.
The BidenHarris Administration is committed to helping people across America affected by Long COVID. In April, President Joe Biden issued a Memorandum on Addressing the Long-Term Effects of COVID-19, which called for the creation of two reports. Within 120 days, the U.S. Department of Health and Human Services (HHS), leading a whole-of-government response, developed two reports that together, pave an actionable path forward to address Long COVID and associated conditions.
The National Research Action Plan on Long COVID details advances in current research and charts a course for future study to better understand prevention and treatment of Long COVID. The Services and Supports for Longer-Term Impacts of COVID-19 report highlights resources for health care workers, and those effected by broader effects of COVID-19, including not only Long COVID but also effects on mental health and substance use, and loss of caregivers and loved ones.
Long COVID can hinder an individuals ability to work, attend school, participate in community life, and engage in everyday activities, said HHS Secretary Xavier Becerra. As our nation continues to make strides in the fight against COVID-19, these reports are critical to shine a light on Long COVIDs impact and how to match people to resources.
The Biden-Harris Administration is committed to combating and responding to the COVID-19 pandemic with the full capacity of the federal government, said HHS Assistant Secretary for Health ADM Rachel Levine. "These initial reports are an important step as HHS continues to accelerate research and programmatic support to address the consequences of the pandemic and work across sectors to ensure no one is left behind as we continue to build a healthier future.
People with Long COVID have disease symptoms that persist for weeks or months after acute COVID-19 infection. It remains difficult to measure precisely, but an estimated 7.7 to 23 million Americans have developed Long COVID, and roughly one million people may be out of the workforce at any given time due to the conditionequivalent to about $50 billion in lost earnings annually.
The National Research Action Plan on Long COVID (the Research Plan), created in coordination with 14 government departments and agencies, introduces the first U.S. governmentwide national research agenda focused on advancing prevention, diagnosis, treatment, and provision of services and supports for individuals and families experiencing Long COVID.
The Research Plan stresses four guiding principles to govern federal government data analysis work: health equity, accelerating and expanding current research, orienting the research effort to improve patient care, and partner engagement. The plan demonstrates innovation in early achievements and highlights the importance of collaboration between the public and private sectors to advance prevention, diagnosis, treatment, and provision of health care, public health, and human services for individuals experiencing Long COVID.
The Services and Supports for Longer-Term Impacts of COVID-19 Report (Services Report) outlines federal services available to the American public to address longer-term effects of COVID-19, including Long COVID and related conditions, as well as other impacts on individuals and families. It provides valuable information in three key areas:
Federal departments will continue to engage with partners, including state and local governments, on the scope and accessibility of these services to meet the needs of individuals. Engagement of nongovernmental experts, organizations, and stakeholders, including individuals affected directly by the longer-term effects of COVID-19, has played an essential role in shaping the governments response to COVID-19 and Long COVID, including the development of these reports.
As we learn more about Long COVID, the best protection remains to prevent COVID-19 in the first place by following basic public health interventions, including getting vaccinated, boosted, and wearing a mask indoors in public where the COVID-19 community level is high.
Yale University, New Haven, CT, USA
Gita A. Pathak&Renato Polimanti
Institute for Molecular Medicine Finland (FIMM), Univerisity of Helsinki, Helsinki, Finland
Juha Karjalainen,Mark Daly,Andrea Ganna&Mark J. Daly
Broad Institute of MIT and Harvard, Cambridge, MA, USA
Christine Stevens,Mark Daly,Andrea Ganna,Masahiro Kanai,Rachel G. Liao,Amy Trankiem,Mary K. Balaconis,Huy Nguyen,Matthew Solomonson,Kumar Veerapen,Samuli Ripatti,Lindo Nkambul,Mark J. Daly,Sam Bryant&Vijay G. Sankaran
Massachusetts General Hospital, Broad Institute of MIT and Harvard, Cambridge, MA, USA
Benjamin M. Neale
Analytic and Translational Genetics Unit, Massachusetts General Hospital, Boston, MA, USA
Mark Daly,Andrea Ganna,Konrad J. Karczewski,Alicia R. Martin,Elizabeth G. Atkinson,Masahiro Kanai,Kristin Tsuo,Nikolas Baya,Patrick Turley,Rahul Gupta,Raymond K. Walters,Duncan S. Palmer,Gopal Sarma,Matthew Solomonson,Nathan Cheng,Wenhan Lu,Claire Churchhouse,Jacqueline I. Goldstein,Daniel King,Wei Zhou,Cotton Seed,Mark J. Daly,Benjamin M. Neale,Hilary Finucane,F. Kyle Satterstrom&Sam Bryant
Icahn School of Medicine at Mount Sinai, New York, NY, USA
Shea J. Andrews,Laura G. Sloofman,Stuart C. Sealfon,Clive Hoggart&Slayton J. Underwood
Institute for Molecular Medicine Finland (FIMM), University of Helsinki, Helsinki, Finland
Mattia Cordioli,Matti Pirinen,Kati Donner,Katja Kivinen,Aarno Palotie&Mari Kaunisto
Icahn School of Medicine at Mount Sinai, Genetics and Genomic Sciences, York City, NY, USA
Nadia Harerimana
Centre for Bioinformatics and Data Analysis, Medical University of Bialystok, Bialystok, Poland
Karolina Chwialkowska
University of Michigan, Ann Arbor, MI, USA
Brooke Wolford
Ancestry, Lehi, UT, USA
Genevieve Roberts,Danny Park,Catherine A. Ball,Marie Coignet,Shannon McCurdy,Spencer Knight,Raghavendran Partha,Brooke Rhead,Miao Zhang,Nathan Berkowitz,Michael Gaddis,Keith Noto,Luong Ruiz,Milos Pavlovic,Eurie L. Hong,Kristin Rand,Ahna Girshick,Harendra Guturu&Asher Haug Baltzell
Institute for Molecular Medicine Finland (FIMM), Helsinki, Finland
Mari E. K. Niemi&Sara Pigazzini
University of Liege, GIGA-Institute, Lige, Belgium
Souad Rahmouni,Michel Georges&Yasmine Belhaj
CHC Mont-Lgia, Lige, Belgium
Julien Guntz&Sabine Claassen
5BHUL (Lige Biobank), CHU of Lige, Lige, Belgium
Yves Beguin&Stphanie Gofflot
Institute for Molecular Medicine Finland, University of Helsinki, Helsinki, Finland
Mattia Cordioli
Analytic & Translational Genetics Unit, Massachusetts General Hospital, Boston, MA, USA
Lindokuhle Nkambule,Lindokuhle Nkambul,Lindokuhle Nkambule&Lindo Nkambul
Stanley Center for Psychiatric Research, Broad Institute of MIT and Harvard, Cambridge, MA, USA
Lindokuhle Nkambule
Program in Medical and Population Genetics, Broad Institute of MIT and Harvard, Cambridge, MA, USA
Lindokuhle Nkambule,Konrad J. Karczewski,Alicia R. Martin,Elizabeth G. Atkinson,Masahiro Kanai,Kristin Tsuo,Nikolas Baya,Patrick Turley,Rahul Gupta,Raymond K. Walters,Duncan S. Palmer,Gopal Sarma,Matthew Solomonson,Nathan Cheng,Wenhan Lu,Claire Churchhouse,Jacqueline I. Goldstein,Daniel King,Wei Zhou,Cotton Seed,Benjamin M. Neale,Hilary Finucane,F. Kyle Satterstrom,Sam Bryant&Caroline Cusick
CHU of Liege, Lige, Belgium
Michel Moutschen,Benoit Misset,Gilles Darcis,Julien Guiot,Samira Azarzar,Olivier Malaise,Pascale Huynen,Christelle Meuris,Marie Thys,Jessica Jacques,Philippe Lonard,Frederic Frippiat,Jean-Baptiste Giot,Anne-Sophie Sauvage,Christian Von Frenckell&Bernard Lambermont
University of Liege, Lige, Belgium
Michel Moutschen,Benoit Misset,Gilles Darcis,Julien Guiot&Samira Azarzar
Department of Human Genetics, McGill University, Montreal, Quebec, Canada
Tomoko Nakanishi
Lady Davis Institute, Jewish General Hospital, McGill University, Montreal, Quebec, Canada
Tomoko Nakanishi,David R. Morrison,J. Brent Richards,Guillaume Butler-Laporte,Vincenzo Forgetta,Biswarup Ghosh,Laetitia Laurent,Danielle Henry,Tala Abdullah,Olumide Adeleye,Noor Mamlouk,Nofar Kimchi,Zaman Afrasiabi,Nardin Rezk,Branka Vulesevic,Meriem Bouab,Charlotte Guzman,Louis Petitjean,Chris Tselios,Xiaoqing Xue,Jonathan Afilalo&Darin Adra
Kyoto-McGill International Collaborative School in Genomic Medicine, Graduate School of Medicine, Kyoto University, Kyoto, Japan
Tomoko Nakanishi
Research Fellow, Japan Society for the Promotion of Science, Tokyo, Japan
Tomoko Nakanishi
McGill Genome Centre and Department of Human Genetics, McGill University, Montreal, Quebec, Canada
Vincent Mooser,Rui Li,Alexandre Belisle,Pierre Lepage,Jiannis Ragoussis,Daniel Auld&G. Mark Lathrop
Department of Human Genetics, Epidemiology, Biostatistics and Occupational Health, McGill University, Montreal, Quebec, Canada
J. Brent Richards
Department of Twin Research, Kings College London, London, UK
J. Brent Richards
Department of Epidemiology, Biostatistics and Occupational Health, McGill University, Montral, Qubec, Canada
Guillaume Butler-Laporte
Department of Emergency Medicine, McGill University, Montreal, Quebec, Canada
Marc Afilalo
Emergency Department, Jewish General Hospital, McGill University, Montreal, Quebec, Canada
Marc Afilalo
McGill AIDS Centre, Department of Microbiology and Immunology, Lady Davis Institute for Medical Research, Jewish General Hospital, McGill University, Montreal, Quebec, Canada
Maureen Oliveira
McGill Centre for Viral Diseases, Lady Davis Institute, Department of Infectious Disease, Jewish General Hospital, Montreal, Quebec, Canada
Bluma Brenner
Research Centre of the Centre Hospitalier de lUniversit de Montral, Montreal, Canada
Nathalie Brassard
Department of Medicine, Research Centre of the Centre Hospitalier de lUniversit de Montral, Montreal, Canada
Madeleine Durand
Department of Medicine, Universit de Montral, Montreal, Canada
Madeleine Durand,Michal Chass&Daniel E. Kaufmann
Department of Medicine and Human Genetics, McGill University, Montreal, Quebec, Canada
Erwin Schurr
Department of Intensive Care, Research Centre of the Centre Hospitalier de lUniversit de Montral, Montreal, Quebec, Canada
Michal Chass
Division of Infectious Diseases, Research Centre of the Centre Hospitalier de lUniversit de Montral, Montreal, Quebec, Canada
Daniel E. Kaufmann
MRC Human Genetics Unit, Institute of Genetics and Cancer, University of Edinburgh, Western General Hospital, Edinburgh, UK
Caroline Hayward,Anne Richmond&J. Kenneth Baillie
Center for Applied Genomics, Childrens Hospital of Philadelphia, Philadelphia, PA, USA
Joseph T. Glessner,Hakon Hakonarson&Xiao Chang
Department of Pediatrics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA
Joseph T. Glessner&Hakon Hakonarson
Vanderbilt University Medical Center, Nashville, TN, USA
Douglas M. Shaw,Jennifer Below,Hannah Polikowski,Petty E. Lauren,Hung-Hsin Chen,Zhu Wanying,Lea Davis&V. Eric Kerchberger
Centre for Genomic and Experimental Medicine, Institute of Genetics and Cancer, University of Edinburgh, Western General Hospital, Edinburgh, UK
Archie Campbell,David J. Porteous&Chloe Fawns-Ritchie
Usher Institute, University of Edinburgh, Nine, Edinburgh Bioquarter, Edinburgh, UK
Archie Campbell
University of Texas Health, Houston, TX, USA
Marcela Morris&Joseph B. McCormick
Department of Psychology, University of Edinburgh, Edinburgh, UK
Chloe Fawns-Ritchie&Chloe Fawns-Ritchie
University of North Carolina at Chapel Hill, Chapel Hill, NC, USA
Kari North
Center for Applied Genomics, The Childrens Hospital of Philadelphia, Philadelphia, PA, USA
Xiao Chang,Joseph R. Glessner&Hakon Hakonarson
Division of Human Genetics, Department of Pediatrics, The Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA
Joseph R. Glessner
WEDNESDAY 8/3/2022, 1:53 p.m.
(WFRV) The Wisconsin Department of Health Services has reported 1,573,177 total positive coronavirus test results in the state and 13,235 total COVID-19 deaths.
Unable to view the tables below?Click here.
The DHS announced an attempt to verify and ensure statistics are accurate, some numbers may be subject to change. The DHS is combing through current and past data to ensure accuracy.
Wisconsins hospitals are reporting, that the 7-day moving average of COVID-19 patients hospitalized was 534 patients. Of those,71 are in an ICU. ICU patients made up 13.5%of hospitalized COVID-19 patients.
The Wisconsin Department of Health Services reports that 10,022,229 vaccine doses and 2,597,985 booster doses have been administered in Wisconsin as of August 3.
Unable to view the tables below?Click here.
The Wisconsin Department of Health Services is using a new module to measure COVID-19 activity levels. They are now using the Center for Disease Control and Preventions (CDC) COVID-19 Community Levels. The map is measured by the impact of COVID-19 illness on health and health care systems in the communities.
The Center for Disease Control and Prevention (CDC) reports that 26 counties in Wisconsin are experiencing high COVID-19 community levels. Of those 26, two are in northeast Wisconsin: Forest and Oneida County.
30 counties in Wisconsin are experiencing medium COVID-19 community levels. Of those 30, eleven are located in northeast Wisconsin: Brown, Door, Fond du Lac, Green Lake, Langlade, Marinette, Menominee, Oconto, Shawano, Waushara, and Winnebago County.
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Every other county in Wisconsin is experiencing low COVID-19 community levels.
For more information on how the data is collected, visit theCDCs COVID-19 Community Levels data page.
Mallika Marshall, MD is an Emmy-award-winning journalist and physician who has served as the HealthWatch Reporter for CBS Boston/WBZ-TV for over 20 years. A practicing physician Board Certified in both Internal Medicine and Pediatrics, Dr. Marshall serves on staff at Harvard Medical School and practices at Massachusetts General Hospital at the MGH Chelsea Urgent Care and the MGH Revere Health Center, where she is currently working on the frontlines caring for patients with COVID-19. She is also a host and contributing editor for Harvard Health Publications (HHP), the publishing division of Harvard Medical School.
WASHINGTON, D.C. U.S. Sen. Ted Cruz (R-Texas) today introduced theCatch Up Our Kids Act of 2022,legislation that would combat K-12 learning loss that American children incurred due to school closures during the COVID-19 pandemic. Nearly every K-12 school switched to remote learning in the Spring of 2020, not returning to in-person learning until Fall 2020 at the earliest, and for many it was longer. Because of this, students fell behind in math and reading, and low-income students were the hardest hit.
The Catch Up Our Kids Act would allow parents to take back control of their childs education so children can recover from any learning loss resulting from misguided and politically driven pandemic school closures.This proposal includes a mix of tax incentives and re-allocation of some Elementary and Secondary School Emergency Relief Fund (ESSER) funding. As of June 2022, states have not spent the majority of their ESSER allotment.
About the bills Senator Cruz said:
At the start of the COVID-19 pandemic, schools across the country began to close and go virtual in order to protect the health and well-being of our kids. But while the science quickly showed that COVID-19s impact on schoolchildren was minimal, teachers unions, and liberal bureaucrats across the country were slow to return to normal. Because of this, millions of children across the country fell behind educationally an outcome far more harmful than the pandemic. This is unacceptable, but the Biden administration has done little if anything to help these kids catch up. As a father, I am personally concerned about educating the next generation. This issue is foundationally important, and the Catch Up Our Kids Act will begin to address the learning loss weve seen because of the pandemic, and get our kids back on track.
The Catch Up Our Kids Act includes the following:
Learning Loss Tax Credit:Creates a temporary 3-year Learning Loss Tax Credit of $1,200 per-child to allow the parent or legal guardian of a K-12 student to recoup actual expenses incurred for education-related activities.
Employer Reimbursement:Temporarily extends the tax provision that allows employers to reimburse an employee for certain tuition and education-related expenses on a tax-free basis to include educational expenses for employees children.
Expand 529 ESAs:Expands Education Savings Accounts (ESAs) to include homeschool expenses for a period of 3 years.
Double Coverdell Contribution Limit:Doubles the annual contribution limit for Coverdell ESAs from $2,000 to $4,000 per year for a period of 3 years.
Favorable ESA Gift Exclusion Tax Treatment:Exempts contributions to a 529 ESA and Coverdell ESA from the annual exclusion, ensuring these gifts do not trigger gift tax consequences.
Reprogram ESSER Money:Allows states to use unspent Elementary and Secondary School Emergency Relief (ESSER) funds to fund Scholarship Granting Organizations (SGOs), using ESSER money as seed money. SGOs would then be able to award parents/legal guardians scholarships.
Read the legislationhere.
American Federation for Children:Senator Cruzs bill confirms what we already knew: he is a staunch supporter of educational freedom. The COVID-19 pandemic highlighted significant problems in the way our current education system operates, and the only real answer is securing parental rights in education by expanding school choice.
Americans for Tax Reform President Grover Norquist:Democrats immorally shut down schools across the country using COVID as an excuse to do the bidding of teachers union bosses. Meanwhile, Republicans are dedicated to expanding school choice and protecting parental control in their childrens education. Sen. Cruzs bill cuts taxes for parents who did the right thing and made sure their kids were educated when their schools failed them. The bill also expands education savings accounts and empowers families to make the best education decisions for themselves. Americans for Tax Reform applauds the introduction of Senator CruzsCatch Up Our Kids Act.
American Principles Project:Since the onset of the COVID pandemic, public health officials, working hand-in-hand with teachers unions, have done terrible harm to our nations families, shutting down schools and setting students significantly behind in their education. And thanks to the monopoly our government has over education, many parents were all but powerless to help their kids. Its time for that to change.Sen. Cruzs legislation would be a welcome step towards putting parents back in charge of ensuring their children receive the best education possible. APP fully supports the Catch Up Our Kids Act, and we encourage all pro-family lawmakers to sign on as well.
Center for Urban Renewal and Education President &Founder Star Parker:The Catch Up Our Kids Act will empower parents not government to make educational decisions on behalf of their children. Millions of students suffered from ill-advised COVID lockdowns, especially children from low-income families, and this legislation will allow parents to guide the educational recovery process for their children. I am pleased to express my strong support for this timely initiative.
Concerned Women for Americas Legislative Action Committee, CWA CEO and President Penny Nance:This is the Year of the Parent, and Senator Ted Cruzs Catch Up Our Kids Act gives parents the tools they need to help their kids take ownership over learning lost during the coronavirus pandemic. The pandemic has revealed with greater clarity why choice in education really matters. We are grateful to Senator Cruz for this important bill that enables parents to have greater access and control over the money necessary to pay for educational activities that are best for their children.
FreedomWorks President Adam Brandon:Heavy-handed lockdown policies destroyed the lives and livelihoods of millions of Americans. Not the least affected are students suffering from severe learning loss due to mass school closure. Senator Ted Cruzs Catch Up Our Kids Act works to help the students whose education was upended by government lockdowns and embraces the idea that parents should be able to choose their childs best path for success.
Independent Womens Voice:School districts and unions hold all the power when it comes to education. The Catch Up Our Kids Act recognizes that the best way to effectively address the learning loss crisis we are in and get students back on track is to put power back into the hands of parents. The bill empowers parents by directing education funding towards students. We thank Senator Cruz for prioritizing parental rights and educational freedom, not bureaucratic systems and union control.
Texas Public Policy Foundation CEO Greg Sindelar:We are grateful to Senator Cruz for recognizing millions of children are behind due to school closures during the Covid-19 pandemic, and his commitment to helping every child catch up. The Catch Up Our Kids Act will help address our nations student learning loss problems by providing resources directly to parents who are looking to help their children. We fully support the Catch Up Our Kids Act and hope to see it passed quickly.
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