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 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In August 2002, 65 cases of Loa-associated neurological Serious Adverse Events were reported after ivermectin treatment. The first signs, occurring within the 12-24 hours following treatment, included fatigue, generalized arthralgia, and sometimes agitation, mutism, and incontinence. Disorders of consciousness, including coma, generally appeared between 24 and 72 hours, and showed a rapid variation with time. The most frequent objective neurological signs were extrapyramidal. The patients presented with haemorrhages of the conjunctiva and of the retina. Biological examinations showed a massive Loa microfilaruria, the passage of Loa microfilariae into the cerebrospinal fluid, haematuria, and an increase in the C-reactive protein, all of which have been correlated with the high intensity of the initial Loa microfilaraemia. Eosinophil counts decreased dramatically within the first 24 hours, and then rose again rapidly. Electroencephalograms suggested the existence of a diffuse pathological process within the first weeks; the abnormalities disappearing after 3-6 months. Death may occur when patients are not properly managed, i.e. in the absence of good nursing. However, some patients who recovered showed sequelae such as aphasia, episodic amnesia, or extrapyramidal signs. The main risk factor for these encephalopathies is the intensity of the initial Loa microfilaraemia. The disorders of consciousness may occur when there are >50,000 Loa microfilariae per ml. The possible roles of co-factors, such as Loa strains, genetic predisposition of individuals, co-infestations with other parasites, or alcohol consumption, seem to be minor but they should be considered. The mechanisms of the post-ivermectin Loa-related encephalopathies should be investigated to improve the management of patients developing the condition.
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PMID:Clinical picture, epidemiology and outcome of Loa-associated serious adverse events related to mass ivermectin treatment of onchocerciasis in Cameroon. 1497 61

Outcome studies on traumatic brain injury (TBI) have shown that functional status can be predicted by demographic, injury severity, and trauma-related factors. Concurrent cognitive functions as one of the determinants of functional outcome is less documented. This study evaluated the effects of concurrent neuropsychological measures on functional outcome 1 year after injury. Neuropsychological data, employment status, self-reported fatigue, and the Glasgow Outcome Scale-Extended (GOSE) were collected from 115 persons with TBI (ranging from mild to severe) at 3 and 12 months postinjury. Principal components analysis was conducted with the neuropsychological measures and three components emerged. Multiple regression analysis, controlling for demographic and injury severity related factors, was used to test the effects of cognitive components at 12 months on functional outcome (GOSE). One year after injury, 64% were categorized as "good recovery" and 36% as "moderate disability" according to GOSE. Good functional recovery depended on shorter duration of posttraumatic amnesia, less fatigue, absence of intracranial pathology, higher education, and better performance on cognitive measures. The predictive values of Verbal/Reasoning and Visual/Perception components are supported; each added significantly and improved prediction of functional outcome. The Memory/Speed component showed a near-significant relationship to outcome.
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PMID:Cognitive recovery and predictors of functional outcome 1 year after traumatic brain injury. 1960 3

Topiramate is a highly effective drug in migraine prophylaxis and is considered a first-line treatment. The evidence for the efficacy of topiramate is based upon the results of several large, randomized, double-blind, placebo-controlled trials. Adverse events (AEs) are common and require discontinuation of the treatment in about 20-25% of patients, but they are rarely severe. There are reviews regarding topiramate-related AEs representing a large number of patients treated in controlled trials. The most common AEs are weight loss, dizziness, somnolence, abnormal thinking, fatigue, ataxia, confusion, paresthesias, impaired concentration, nervousness, amnesia, and language difficulties. The development of cough has never been reported as an AE during topiramate prophylaxis for migraine. We present 3 cases in which the prophylactic treatment for migraine with topiramate was discontinued due to the onset of primary intractable coughing.
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PMID:Topiramate-induced intractable cough during migraine prophylaxis. 1975 66

The precise definition of a severe asthmatic exacerbation is an issue that presents difficulties. The term 'status asthmaticus' relates severity to outcome and has been used to define a severe asthmatic exacerbation that does not respond to and/or perilously delays the repetitive or continuous administration of short-acting inhaled beta(2)-adrenergic receptor agonists (SABA) in the emergency setting. However, a number of limitations exist concerning the quantification of unresponsiveness. Therefore, the term 'acute severe asthma' is widely used, relating severity mostly to a combination of the presenting signs and symptoms and the severity of the cardiorespiratory abnormalities observed, although it is well known that presentation does not foretell outcome. In an acute severe asthma episode, close observation plus aggressive administration of bronchodilators (SABAs plus ipratropium bromide via a nebulizer driven by oxygen) and oral or intravenous corticosteroids are necessary to arrest the progression to severe hypercapnic respiratory failure leading to a decrease in consciousness that requires intensive care unit (ICU) admission and, eventually, ventilatory support. Adjunctive therapies (intravenous magnesium sulfate and/or others) should be considered in order to avoid intubation. Management after admission to the hospital ward because of an incomplete response is similar. The decision to intubate is essentially based on clinical judgement. Although cardiac or respiratory arrest represents an absolute indication for intubation, the usual picture is that of a conscious patient struggling to breathe. Factors associated with the increased likelihood of intubation include exhaustion and fatigue despite maximal therapy, deteriorating mental status, refractory hypoxaemia, increasing hypercapnia, haemodynamic instability and impending coma or apnoea. To intubate, sedation is indicated in order to improve comfort, safety and patient-ventilator synchrony, while at the same time decrease oxygen consumption and carbon dioxide production. Benzodiazepines can be safely used for sedation of the asthmatic patient, but time to awakening after discontinuation is prolonged and difficult to predict. The most common alternative is propofol, which is attractive in patients with sudden-onset (near-fatal) asthma who may be eligible for extubation within a few hours, because it can be titrated rapidly to a deep sedation level and has rapid reversal after discontinuation; in addition, it possesses bronchodilatory properties. The addition of an opioid (fentanyl or remifentanil) administered by continuous infusion to benzodiazepines or propofol is often desirable in order to provide amnesia, sedation, analgesia and respiratory drive suppression. Acute severe asthma is characterized by severe pulmonary hyperinflation due to marked limitation of the expiratory flow. Therefore, the main objective of the initial ventilator management is 2-fold: to ensure adequate gas exchange and to prevent further hyperinflation and ventilator-associated lung injury. This may require hypoventilation of the patient and higher arterial carbon dioxide (PaCO(2)) levels and a more acidic pH. This does not apply to asthmatic patients intubated for cardiac or respiratory arrest. In this setting the post-anoxic brain oedema might demand more careful management of PaCO(2) levels to prevent further elevation of intracranial pressure and subsequent complications. Monitoring lung mechanics is of paramount importance for the safe ventilation of patients with status asthmaticus. The first line of specific pharmacological therapy in ventilated asthmatic patients remains bronchodilation with a SABA, typically salbutamol (albuterol). Administration techniques include nebulizers or metered-dose inhalers with spacers. Systemic corticosteroids are critical components of therapy and should be administered to all ventilated patients, although the dose of systemic corticosteroids in mechanically ventilated asthmatic patients remains controversial. Anticholinergics, inhaled corticosteroids, leukotriene receptor antagonists and methylxanthines offer little benefit, and clinical data favouring their use are lacking. In conclusion, expertise, perseverance, judicious decisions and practice of evidence-based medicine are of paramount importance for successful outcomes for patients with acute severe asthma.
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PMID:Acute severe asthma: new approaches to assessment and treatment. 1991 54

A 66-year-old man presented with mild amnesia, progressive fatigue, ataxia, visual hallucinations, and debility. His past medical history included right-sided carotid endarterectomy performed elsewhere 6 years previously. Cranial magnetic resonance imaging showed left parieto-occipital arteriovenous malformation-like tortous vessels, venous congestion, and ischemic areas. Cerebral angiography showed right-sided compound external carotid artery-internal jugular vein (IJV) fistula, and distal occlusion of the right IJV. Transvenous embolization via contralateral IJV was performed, and the fistula, together with fistulous portion of the distal IJV, was sealed using coils. Two years later, patient is well with normal neurologic examination findings. The presence of an arteriovenous communication after vascular surgery is a serious complication with potential long-term effects and therefore should be diagnosed and treated as promptly as possible.
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PMID:External carotid-internal jugular fistula as a late complication after carotid endarterectomy: a rare case. 2055 93

The current study sought to (1) determine the relative frequency and severity of eight symptoms in adults with cerebral palsy (CP), (2) examine the perceived course of these eight symptoms over time, and (3) determine the associations between the severity of these symptoms and psychosocial functioning. Eighty-three adults with CP completed a measure assessing the frequency, severity, and perceived course of eight symptoms (pain, weakness, fatigue, imbalance, numbness, memory loss, vision loss, and shortness of breath). Respondents also completed measures of community integration and psychological functioning. The results indicated that pain, fatigue, imbalance, and weakness were the most common and severe symptoms reported. All symptoms were reported to have either stayed the same or worsened, rather than resolved, over time. The symptoms were more closely related to social integration than to home integration, productive activity, or psychological functioning. Memory loss was a unique predictor of social integration in the multivariate context. This study highlighted several common and problematic symptoms experienced by adults with CP. Additional research is needed to identify the most effective treatments for those symptoms that affect community integration and psychological functioning as a way to improve the quality of life of individuals with CP.
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PMID:Symptom burden in individuals with cerebral palsy. 2117 51

Traumatic brain injury (TBI) may be defined as any extracranial mechanical force to the brain that results in any period of loss of consciousness, any loss of memory for events immediately before or after the event, or any alteration in mental status at the time of the event. The major causes are automobile accidents, falls, sporting injuries, and assaults. Many soldiers returning from combat in Afghanistan and Iraq have also experienced TBI. This article provides an overview of the neuropsychiatric complications of TBI, including impairment of consciousness, posttraumatic amnesia, cognitive disorders and dementia, posttraumatic epilepsy, aphasia, depression, mania, psychosis, anxiety disorders, personality changes, aggression, behavioral dyscontrol, fatigue/apathy, and increased risk of suicide. Discussion will focus primarily on issues affecting mental health clinicians. Because mental health providers are more involved in care of chronic issues related to TBI, these issues will be discussed in more detail, although acute neuropsychiatric complications of TBI will be briefly explained.
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PMID:Neuropsychiatric complications of traumatic brain injury. 2132 64

Insulinoma, usually benign (90%), is clinically characterized by symptoms as tremulousness, tachycardia, weakness, sweating, fatigue, hunger, headache, dizziness, disorientation and unconsciousness. However rarely it has an unusual presentation. We present a case of insulinoma misdiagnosed as neurologic disease. A 48-year-old man was admitted to our Emergency Division because of car accident caused by loss of consciousness. A diagnosis of complex partial seizure was made one year before. The patient appeared pale, tachycardic, BP 130/85 mmHg. Laboratory tests showed a severe hypoglycemia (30 mg/dl). He was treated with hypertonic glucose solution and the resolution of symptoms was obtained. Dosages of insulin and C-peptide, CT-scan and RMN confirmed a diagnosis of insulinoma. Seizure disappeared after surgical excision. The diagnosis of insulinoma is sometimes delayed up to more than 20 years. Neurologic or psychiatric presentation like disorientation, personality changes, amnesia, irritability, seizures, bizarre behavior, visual difficulties, neuropathy in patients affected by insulinoma could be cause of misdiagnosis. Diagnosis of insulinoma should always be considered whenever these symptoms occur, especially if unresponsive to specific therapy. Insulinoma is curable in most cases and an early diagnosis can avoid adverse consequences including neurologic damage.
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PMID:[Complex partial seizure in patient with insulinoma: importance of early diagnosis]. 2135 8

Although a universally accepted definition is lacking, mild traumatic brain injury and concussion are classified by transient loss of consciousness, amnesia, altered mental status, a Glasgow Coma Score of 13 to 15, and focal neurologic deficits following an acute closed head injury. Most patients recover quickly, with a predictable clinical course of recovery within the first one to two weeks following traumatic brain injury. Persistent physical, cognitive, or behavioral postconcussive symptoms may be noted in 5 to 20 percent of persons who have mild traumatic brain injury. Physical symptoms include headaches, dizziness, and nausea, and changes in coordination, balance, appetite, sleep, vision, and hearing. Cognitive and behavioral symptoms include fatigue, anxiety, depression, and irritability, and problems with memory, concentration and decision making. Women, older adults, less educated persons, and those with a previous mental health diagnosis are more likely to have persistent symptoms. The diagnostic workup for subacute to chronic mild traumatic brain injury focuses on the history and physical examination, with continuing observation for the development of red flags such as the progression of physical, cognitive, and behavioral symptoms, seizure, progressive vomiting, and altered mental status. Early patient and family education should include information on diagnosis and prognosis, symptoms, and further injury prevention. Symptom-specific treatment, gradual return to activity, and multidisciplinary coordination of care lead to the best outcomes. Psychiatric and medical comorbidities, psychosocial issues, and legal or compensatory incentives should be explored in patients resistant to treatment.
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PMID:Subacute to chronic mild traumatic brain injury. 2319 72

Minor traumatic brain injury (mTBI) is a major public health problem. The Centers for Disease Control and Prevention and the National Center for Injury Prevention and Control label it a "silent epidemic." Subtle signs and symptoms of mTBI, including headache, fatigue, and memory loss, are often seen in conjunction with musculoskeletal trauma. Although sometimes evident immediately, mTBI may not manifest until patients return to work and their personal lives. In the patient with acute concurrent mTBI, skeletal management must be based on either a period of observation to rule out evolving neurologic symptoms or, when warranted, the recommendations of a neurosurgeon. Such input is particularly important when mTBI is associated with a prolonged loss of consciousness or posttraumatic amnesia. In the outpatient setting, when concern for mTBI exists weeks after an injury, familiarity with and referral to locally available mTBI specialists and programs can facilitate proper care. Armed with this knowledge, the orthopaedic surgeon has an opportunity to positively influence outcomes and help provide crucial care that extends beyond the management of musculoskeletal injuries.
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PMID:Minor traumatic brain injury: a primer for the orthopaedic surgeon. 2408 36


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