SIDS - Preventative measures

New study finds infant hearing test results may predict sudden infant death syndrome

One of the greatest medical mysteries of our time has taken a leap forward in medical understanding with new study results announced by Dr. Daniel D. Rubens of Children's Hospital and Regional Medical Center in Seattle. Rubens' study published in July, 2007 in Early Human Development found all babies in a Rhode Island study group who died of Sudden Infant Death Syndrome (SIDS) universally shared the same distinctive difference in their newborn hearing test results for the right inner ear, when compared to infants who did not have SIDS. This is the first time doctors might be able to identify newborns at risk for SIDS by a simple, affordable and routine hearing test administered shortly after birth. In the study, medical records and hearing tests of 31 babies who died from SIDS in Rhode Island were examined and compared to healthy babies. Rhode Island has a particularly robust database of newborn hearing test data.

The cause of SIDS, known around the world as "crib death" and "cot death," has eluded physicians and grieving parents for centuries. Responsible for many previously unexplainable deaths of infants usually two to four months old and striking boys more than girls, SIDS causes tragic, sudden death in approximately 1 in 1,000 newborns world-wide, making it the largest cause of death in young infants. In the United States approximately 3,600 deaths each year were attributed to SIDS from 1992-1999, according to an April, 2004 article in Archives of Pediatric and Adolescent Medicine. Death occurs during sleep, seemingly with no warning and no previous symptoms. Changes in infant care have been promoted including the "Back to Sleep" program discouraging sleeping on the stomach, and avoiding exposure to cigarette smoke. Various causes have been suggested, including disturbances in respiratory control and infant overheating, but to date nothing has proven conclusive.

It is known that the inner ear contains tiny hairs that are involved in both hearing and vestibular function. Rubens proposes that vestibular hair cells are important in transmitting information to the brain regarding carbon dioxide levels in the blood. He postulates that injury to these cells will disrupt respiratory control, playing a critical role in predisposing infants to SIDS.

The SIDS infants in Rubens' study showed a consistent four point lower score in their standard newborn hearing tests, across three different sound frequencies in the right ear, when compared to babies that didn't die from SIDS. Additionally, healthy infants typically test stronger in the right ear than the left. However, in each of the SIDS cases studied, the right ear tested lower than the left, reversing the test results of healthy babies.

"This discovery opens a whole new line of inquiry into SIDS research," said Rubens. "For the first time, it's now possible that with a simple, standard hearing test babies could be identified as at risk for SIDS, allowing preventative measures to be implemented in advance of a tragic event." He urges further research, adding "We must now fully explore all aspects of inner ear function and SIDS, and analyze testing frequencies higher than those currently tested by newborn hearing screen centers."

Previous groundbreaking SIDS research at Seattle Children's Hospital and Regional Medical Center took place during the 1970's, when Dr. Bruce Beckwith was one of the first researchers to describe features of SIDS that can identify cases during autopsy, distinguishing SIDS deaths from other causes of infant death. Beckwith is highly recognized in the body of SIDS research, making his work among the most significant earlier published findings about the condition. "It has been my great privilege to follow in Dr. Beckwith's footsteps with this new discovery that creates the possibility of identifying SIDS infants before tragedy strikes," said Rubens. "Each new breakthrough brings us closer to making SIDS a condition of the past."

Children's Hospital and Regional Medical Center of Seattle
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Erectile dysfunction: Reducing the risk

Prevent smoking to reduce risk of erectile dysfunction

Men who smoke cigarettes run an increased risk of experiencing erectile dysfunction, and the more cigarettes smoked, the greater the risk, according to a study by Tulane University researchers published in the American Journal of Epidemiology.

A team of researchers led by Jiang He, Professor of Epidemiology at the Tulane University School of Public Health and Tropical Medicine, examined the association between cigarette smoking and erectile dysfunction in a 2000-2001 study in China involving 7,684 men. The researchers used questionnaires to assess the status of cigarette smoking and erectile dysfunction. Those surveyed were men between the ages of 35-74 who did not have vascular disease.

The team found that there was a significant statistical link between the number of cigarettes that men smoked and the likelihood they would experience erectile dysfunction. The association between smoking and erectile dysfunction was even stronger in participants with diabetes. An estimated 22.7 percent of erectile dysfunction cases among Chinese men might be attributable to cigarette smoking, says the study.

Although erectile dysfunction is not a life-threatening condition, it compromises well-being and quality of life. The Tulane study results suggest that smoking prevention should be an important approach for reducing the risk of erectile dysfunction.

Tulane University
http://www.brightsurf.com/news/headlines/31865/Prevent_smoking_to_reduce_risk_of_erectile_dysfunction.html

Milk and butter may help prevent asthma

Full fat milk and butter may help prevent asthma

Young children who regularly eat products containing milk fat are less likely to develop asthma, concludes a study in Thorax.

Researchers assessed the food consumption of 2,978 Dutch children aged 2 years and related this to asthma symptoms at age 3.

Asthma at age 3 was lower in children who consumed full cream milk and butter daily than in those who did not. Similarly, wheeze was lower in children who consumed milk products (including yoghurt and chocolate milk) and butter daily than in those who did not. Daily consumption of brown bread was also associated with lower rates of asthma and wheeze.

Children who consumed fruit juice and vegetables daily had lower asthma rates than other children, but these differences were not statistically significant.

These results provide evidence for a beneficial association between daily consumption of products containing milk fat and the development of asthma and wheeze in young children, say the authors. Various components of the products involved could play a role, such as different fatty acids, but also antioxidants or other micronutrients, they suggest.

British Medical Journal (BMJ)
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Hyperthyroidism - Clinical Features

Hyperthyroidism

Clinical Features and Associated Disorders

Although new-onset adulthood seizures are rarely related to hyperthyroidism, the seizure incidence among thyrotoxic patients ranges from 1 to 9 percent. Movement disorders, such as tremor (usually enhanced physiological tremor) and choreoathetosis, as well as upper motor neuron signs, including spasticity, hyperreflexia, clonus, and Babinski's signs, may also be observed.

Peripheral neurological features include cranial and peripheral neuropathies, as well as neuromuscular junction and muscle disturbances . Ocular features include lid lag, stare, widened palpebral fissures, extraocular muscle dysfunction with diplopia, and optic nerve compression with visual impairment.
Eyelid retraction manifests in several ways: (1) Stellwag's sign, a staring expression with infrequent blinking; (2) Dalrymple's sign, a widened palpebral fissure due to retraction of both the upper and lower lids; (3) von Graefe's sign, a larger than normal portion of visible sclera with downward eye movement; (4) Joffroy's sign, a lack of frontalis muscle contraction with upgaze; and (5) Moaubius' sign, sympathetic overactivity-induced exophthalmos with resultant limited convergence.

Although reports of a distal sensorimotor polyneuropathy in thyrotoxic patients are rare, improvement of the neuropathic features with attainment of the euthyroid state indicates that these features are manifestations of hyperthyroidism. Myasthenia gravis (MG) can be associated with hyperthyroidism, although some of the reported cases may have been secondary to coincident MG. Also, when bulbar weakness responds to treatment of the hyperthyroid state, it is more likely related to hyperthyroidism. When MG co-exists with thyrotoxic myopathy, the clinical findings do not differ from those in euthyroid patients, although the patients may be weaker due to the co-existence of two motor disorders. Thyrotoxic myopathy is characterized by the gradual onset of proximal limb weakness, which may be accompanied by myalgias, easy fatigability, and prominent atrophy. Although the muscular atrophy may be severe, most patients remain ambulatory. Shoulder girdle muscles can be more severely affected than the hip girdle muscles, with prominent atrophy and scapular winging. Distal limb muscles are also affected, the facial muscles may be affected, and, rarely, bulbar and ocular muscles are involved.

Thyroid-associated ophthalmopathy refers to the exophthalmos and ocular muscle dysfunction associated with thyroid disease. It is seen in most patients with Graves' disease but is also seen in 5 percent of patients with Hashimoto's thyroiditis. It is not correlated with the onset of Graves' disease, having been reported to precede (rarely), occur concomitantly with, or develop after its treatment. It also does not correlate with the level of circulating thyroid hormone and may occur in euthyroid patients or in patients with hypothyroid Graves' disease. When it is prominent, thyroid-associated ophthalmopathy may cause exposure keratopathy (due to marked proptosis), as well as optic nerve compression. Thyrotoxic periodic paralysis refers to recurrent attacks of flaccid paralysis of the limbs and trunk (the oculobulbar muscles are usually spared or involved to a lesser degree) due to secondary hypokalemia.

Differential Diagnosis.

The differential diagnosis of thyrotoxicosis includes other hypermetabolic disorders, euthyroid hyperthyroxinemia, and nonthyroidal causes. Occasionally, recognition that myopathic features are due to thyrotoxicosis can be difficult, especially if the myopathy is the presenting feature (rare), when exophthalmos is minimal, or when an apathetic state is present. When it is present, the observation of hyperreflexia is helpful, because this feature is not observed in other metabolic myopathies. Thyrotoxic myopathy with pronounced muscular atrophy should be differentiated from progressive muscular atrophy by the presence of fasciculations and more profound weakness in the latter. When thyrotoxic myopathy involves the ocular and bulbar musculature, it must be differentiated from MG. In thyrotoxic myopathy, rapid muscle fatigue and recovery with rest is not appreciated, a response to anticholinesterases is not observed, and decrement is not apparent on EMG; in MG, ocular and bulbar muscle involvement is more pronounced and atrophy is not present. Polymyositis should also be considered and is differentiated by EMG and muscle biopsy.

Evaluation.

TFTs can confirm thyrotoxicosis, typically demonstrating an elevated free T4 , total T4 , T3 RU, free thyroxine index (FTI), free T3 , total T3 , and a suppressed (usually undetectable) TSH. A normal or elevated TSH in the face of unequivocal clinical thyrotoxicosis should raise suspicion for a TSH-secreting pituitary adenoma. Other laboratory features may include anemia, hypokalemia, hypercalcemia, and an elevated erythrocyte sedimentation rate. Roughly half of hyperthyroid patients demonstrate EEG changes, most commonly generalized slowing or excessive fast activity, both of which resolve with attainment of the euthyroid state. Magnetic resonance imaging (MRI) with gadolinium may demonstrate the characteristic features of thyroid ophthalmopathy including multiple extraocular muscle (EOM) involvement, smooth margins gradually tapering into the tendon insertions, and uniform enhancement when contrast is administered. These features are readily displayed with fat saturation techniques that de-emphasize intraocular fat. Optic nerve impingement may also be visualized with a similar approach. MRI may also be useful in ruling out orbital pseudotumor, Tolosa-Hunt syndrome, orbital lymphoma, Wegener's granulomatosis, and orbital aspergillosis.

When co-existent MG is considered, acetylcholine receptor antibodies in response to edrophonium (Tensilon) may be helpful in its evaluation. Although the Tensilon test may be normal in MG (false-negative result) and may lead to improvement of dysthyroid orbitopathy (false-positive result), patients with thyrotoxic bulbar features typically do not have immunological, electrophysiological, or pharmacological evidence of MG.

Management.

Almost all of the clinical features of thyroid dysfunction, with the exception of thyroid-associated ophthalmopathy, resolve once the euthyroid state is achieved. , Medical treatment of thyrotoxicosis includes the use of beta blockers; antithyroid, anti-inflammatory, and immunosuppressive drugs; radioactive iodine-131; and iodine-containing compounds. Beta blockers, in addition to decreasing the beta adrenergic-mediated features of thyrotoxicosis, may decrease the peripheral conversion of T4 to T3 . Beta blockers are also useful in the prophylactic treatment of TPP while attainment of the euthyroid state is awaited. A typical dosage regimen is propranolol, 40 mg four times daily. In hyperthyroid patients with co-existent MG, beta blockers should be used cautiously because of their neuromuscular blocking properties. Higher grade orbital features typically require either systemic corticosteroids (with or without cyclosporine), irradiation, or orbital decompression, yet some believe surgery is rarely indicated because the dysthyroid orbitopathy usually spontaneously arrests before a serious degree of ophthalmopathy has been reached. One of the most frequent complications of thyroid surgery is recurrent laryngeal nerve paralysis. A more limited surgery involving partial lid suturing may be required to protect the cornea.

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Hyperthyroidism

 HYPERTHYROIDISM

Pathogenesis and Pathophysiology

Thyroid hormones affect mitochondrial oxidative capacity, protein synthesis and degradation, tissue sensitivity to catecholamines, muscle fiber differentiation, and capillary growth. Excess thyroid hormone produces accelerated muscle protein catabolism and enhanced lysosomal protease activity, and interferes with the anabolic effects of insulin on muscle. Despite this understanding, the exact pathophysiology of thyrotoxic myopathy remains unknown. CNS observations include elevated rates of cerebral circulation, faster posterior dominant rhythms, alterations in the sensitivity of some brain enzymes and neurotransmitter systems, and altered metabolic responses. At present, the specific pathophysiological processes causing these manifestations remain unknown. It has been proposed that alterations in central and peripheral beta-adrenergic tone may be responsible for hyperthyroid-related tremor and chorea, and that brisk tendon reflexes may reflect faster muscle contraction and relaxation times.

Epidemiology and Risk Factors

Hyperthyroidism is more common in women than in men (10:1 ratio) and often shows a strong familial predisposition. During pregnancy, hyperthyroidism occurs more commonly than hypothyroidism, with an incidence ranging from 0.05 to 0.2 percent, most commonly related to Graves' disease, acute (i.e., subacute) thyroiditis, toxic nodular goiter, and toxic adenoma. The incidence of low-birth-weight infants is significantly increased, and neonatal mortality is slightly increased.

Clinical Features and Associated Disorders

The general clinical features of thyrotoxicosis:
Subjective - Impaired concentration and memory, emotional lability, nervousness, irritability, palpitations, heat intolerance, increased sweating and appetite, weight loss, frequent defecation, menstrual abnormalities, insomnia, headaches;
Objective - Impaired attention span and memory, hypervigilance, systolic flow murmurs, skin changes (warm, moist, smooth), EKG changes (sinus tachycardia, atrial fibrillation), psychiatric problems (depression, mania, bipolar disorder, manic psychosis), chorea, thyrotoxic penodic paralysis, thyroid storm, ocular features.

Neuropsychiatric signs include impaired attention, concentration, and memory, as well as emotional lability, nervousness, hypervigilance, lethargy, depression (i.e., apathetic hyperthyroidism), mania, psychosis, insomnia, and agitated delirium. Apathetic hyperthyroidism most frequently occurs in the elderly, lacks the usual hyperadrenergic features, and may easily be confused with depression or dementia.

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