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AL EMADI HOSPITAL-QATAR-DOHA AMERICAN BOARD CERTIFICATE AESTHETIC MEDICINE

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Sleepiness, tiredness and fatigue are complaints which must be thoroughly analyzed to eliminate blur and ambiguity.
Physiological sleepiness (“sleep pressure”) increases while being awake and additionally underlies the circadian rhythm with a lower threshold to fall asleep during night time.
Excessive daytime sleepiness (EDS) is considered normal only after sleep deprivation. Clinically, EDS manifests by frequents daytime napping and/or reduced alertness with automatic behavior or - in its extreme form - in recurrent attacks of sudden, uncontrollable compulsion to sleep also in inappropriate situations (= “sleep attacks”).
EDS is “objectively” addressed by measuring the mean sleep latency to four to five nap opportunities throughout the day using the multiple sleep latency test (MSLT) or the maintenance of wakefulness test (MWT).
EDS denotes both, a ready entrance into sleep as well as difficulty in staying awake during daytime or accordingly in inappropriate situations. These two partially independent aspects of EDS are separately assessed by the “passive” MSLT and the “active” MWT respectively.
For that reason the MSLT and MWT only weakly correlate with each other when tested over a broad range of patients with EDS. It is important to keep in mind, that these tests are importantly influenced by a great variety of factors such as mood, anxiety, and motivation.
“Vigilance” comprises wakefulness, alertness and attention and therefore is more than just the reciprocal to sleepiness. Cognitive performance tasks such as Steer Clear Reaction Time Test (SCRTT) or driving simulators require the complete integrity of vigilance to achieve normal results. Hypersomnia is usually broadly defined as the combination of abnormally prolonged night-time sleep (regularly >10 h) with EDS during ≥1 months.
On the other hand, the term hypersomnia has also been used in a narrower scene for the isolated abnormality of a prolonged night-time sleep need (>10 h). “Tiredness”, also in colloquial language often used for sleepiness, in a broader sense also describes the feeling of lack of energy, motivation and initiative.

These patients seek rest rather than sleep. They often cannot fall asleep when given the opportunity in spite of feeling tired, and hence, in an MSLT, do not show an abnormally short sleep latency. Furthermore, tiredness (and fatigue) as opposed to sleepiness has a mental (“central”) and physiological (bodily or “peripheral”) component, which the patients can readily distinguish. Patients with insomnia, mild sleep apnea syndrome, or depression rather suffer from mental tiredness than sleepiness during the day.
The simple subjective self-assessment using the Epworth Sleepiness Scale (ESS) quite reliably differentiates between sleepiness and mental tiredness (without sleepiness), which makes it a widely used test. The term “fatigue” is also heterogeneously used.
In physiology the “fatigue” implied a “time on task performance decrement” to describe decreasing muscle force during a sustained physical effort. In clinical medicine one distinguishes physical (“peripheral”) from mental (“central”) fatigue and the term usually denotes a chronic and more abnormal situation than tiredness.
In a broad sense “fatigue” implies a deficiency in coping satisfactorily with mental and physical work load. The chronic fatigue syndrome entails both mental as well as a physical fatigue (so called “leaden paralysis” of limbs). Depressive states are often associated with insomnia and fatigue, but there are also cases with hypersomnia rather than insomnia ( non organic hypersomnia , “atypical depression” or “hypersomnolent depression”)
Sometimes these patients have a tendency to spend much of the day lying in the bed without actually sleeping (so called clinophilia). The basic and clinical aspects of fatigu

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Marfan syndrome is a disorder of connective tissue, the tissue that strengthens the body's structures. Disorders of connective tissue affect the skeletal system, cardiovascular system, eyes, and skin.

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The term subclavian steal describes retrograde blood flow in the vertebral artery associated with proximal ipsilateral subclavian artery stenosis or occlusion, usually in the setting of subclavian artery occlusion or stenosis proximal to the origin of the vertebral artery. Alternatively, innominate artery disease has also been associated with retrograde flow in the ipsilateral vertebral artery, particularly where the subclavian artery origin is involved. Subclavian steal is frequently asymptomatic and may be discovered incidentally on ultrasound or angiographic examination for other indications, or it may be prompted by a clinical examination finding of reduced unilateral upper limb pulse or blood pressure. In some cases, patients may develop upper limb ischemic symptoms due to reduced arterial flow in the setting of subclavian artery occlusion, or they may develop neurologic symptoms due to posterior circulation ischemia associated with exercise of the ipsilateral arm.[1] Treatment has traditionally consisted of open subclavian artery revascularization, typically via carotid-subclavian bypass or subclavian artery transposition, which are generally durable procedures. Newer, less invasive options include endovascular intervention with recanalization as appropriate and angioplasty and stenting if required. The clinical relevance of subclavian steal was described in 1961 by Reivich, Holling and Roberts; however, the recognition of retrograde vertebral artery flow dates back another 100 years to Harrison and Smyth. Some papers, including a previous version of this article, advocate restricting the term subclavian steal to patients with neurologic symptoms only, but this is incorrect in view of the substantial literature using this term to describe the hemodynamic scenario of retrograde vertebral flow and proximal subclavian artery disease.

Anemia is a condition in which you don't have enough healthy red blood cells to carry adequate oxygen to the body's tissues. Having anemia may make you feel tired and weak. There are many forms of anemia, each with its own cause. Anemia can be temporary or long term, and it can range from mild to severe. See your doctor if you suspect you have anemia because it can be a warning sign of serious illness. Treatments for anemia range from taking supplements to undergoing medical procedures. You may be able to prevent some types of anemia by eating a healthy, varied diet.

The Arthrex SpeedBridge™ is an innovative soft tissue fixation device used in the treatment of Achilles injuries. While standard anchor fixation of the tendon creates only a single point of compression directly over the anchor, the SpeedBridge enables an hourglass pattern of FiberTape® suture to be laid over the distal end of the tendon. This four-anchor construct enables a true knotless repair and a greater area of compression for the Achilles tendon on the calcaneus, improving stability and possibly allowing for earlier return to normal activities.

Primary infection with herpes simplex viruses (HSVs) is clinically more severe than recurrent outbreaks. However, most primary HSV-1 and HSV-2 infections are subclinical and may never be clinically diagnosed. Orolabial herpes Herpes labialis (eg, cold sores, fever blisters) is most commonly associated with HSV-1 infection. Oral lesions caused by HSV-2 have been identified, usually secondary to orogenital contact. Primary HSV-1 infection often occurs in childhood and is usually asymptomatic. Primary infection Symptoms of primary herpes labialis may include a prodrome of fever, followed by a sore throat and mouth and submandibular or cervical lymphadenopathy. In children, gingivostomatitis and odynophagia are also observed. Painful vesicles develop on the lips, the gingiva, the palate, or the tongue and are often associated with erythema and edema. The lesions ulcerate and heal within 2-3 weeks. Recurrences The disease remains dormant for a variable amount of time. HSV-1 reactivation in the trigeminal sensory ganglia leads to recurrences in the face and the oral, labial, and ocular mucosae. Pain, burning, itching, or paresthesia usually precedes recurrent vesicular lesions that eventually ulcerate or form a crust. The lesions most commonly occur in the vermillion border, and symptoms of untreated recurrences last approximately 1 week. Recurrent erythema multiforme lesions have been associated with orolabial HSV-1 recurrences. A recent study reported that HSV-1 viral shedding had a median duration of 48-60 hours from the onset of herpes labialis symptoms. They did not detect any virus beyond 96 hours of symptom onset.[7] Genital herpes HSV-2 is identified as the most common cause of herpes genitalis. However, HSV-1 has been increasingly identified as the causative agent in as many as 30% of cases of primary genital herpes infections likely secondary to orogenital contact. Recurrent genital herpes infections are almost exclusively caused by HSV-2. Primary infection Primary herpes genitalis occurs within 2 days to 2 weeks after exposure to the virus and has the most severe clinical manifestations. Symptoms of the primary episode typically last 2-3 weeks. In men, painful, erythematous, vesicular lesions that ulcerate most commonly occur on the penis, but they can also occur on the anus and the perineum. In women, primary herpes genitalis presents as vesicular/ulcerated lesions on the cervix and as painful vesicles on the external genitalia bilaterally. They can also occur on the vagina, the perineum, the buttocks, and, at times, the legs in a sacral nerve distribution. Associated symptoms include fever, malaise, edema, inguinal lymphadenopathy, dysuria, and vaginal or penile discharge. Females may also have lumbosacral radiculopathy, and as many as 25% of women with primary HSV-2 infections may have associated aseptic meningitis. Recurrences After primary infection, the virus may be latent for months to years until a recurrence is triggered. Reactivation of HSV-2 in the lumbosacral ganglia leads to recurrences below the waist. Recurrent clinical outbreaks are milder and often preceded by a prodrome of pain, itching, tingling, burning, or paresthesia. Individuals who are exposed to HSV and have asymptomatic primary infections may experience an initial clinical episode of genital herpes months to years after becoming infected. Such an episode is not as severe as a true primary outbreak. More than one half of individuals who are HSV-2 seropositive do not experience clinically apparent outbreaks. However, these individuals still have episodes of viral shedding and can transmit the virus to their sexual partners. Other HSV infections Localized or disseminated eczema herpeticum is also known as Kaposi varicelliform eruption. Caused by HSV-1, eczema herpeticum is a variant of HSV infection that commonly develops in patients with atopic dermatitis, burns, or other inflammatory skin conditions. Children are most commonly affected. Herpes whitlow, vesicular outbreaks on the hands and the digits, was most commonly due to infection with HSV-1. It usually occurred in children who sucked their thumbs and, prior to the widespread use of gloves, in dental and medical health care workers. The occurrence of herpes whitlow due to HSV-2 is increasingly recognized, probably due to digital-genital contact. Herpes gladiatorum is caused by HSV-1 and is seen as papular or vesicular eruptions on the face, arms, or torsos of athletes in sports involving close physical contact (classically wrestling). Disseminated HSV infection can occur in females who are pregnant and in individuals who are immunocompromised. These patients may present with atypical signs and symptoms of HSV, and the condition may be difficult to diagnose. Herpetic sycosis, a follicular infection with HSV, may present as a vesiculopustular eruption on the beard area. This infection often results from autoinoculation after shaving through a recurrent herpetic outbreak. Classically caused by HSV-1, there have been rare reports of relapsing beard folliculitis caused by type 2 HSV.[8] Neonatal HSV HSV-2 infection in pregnancy can have devastating effects on the fetus. Neonatal HSV usually manifests within the first 2 weeks of life and clinically ranges from localized skin, mucosal, or eye infections to encephalitis, pneumonitis, disseminated infection, and demise. Most women who deliver infants with neonatal HSV had no prior history, signs, or symptoms of HSV infection. Risk of transmission is highest in pregnant women who are seronegative for both HSV-1 and HSV-2 and acquire a new HSV infection in the third trimester of pregnancy. Factors that increase the risk of transmission from mother to baby include the type of genital infection at the time of delivery (higher risk with active primary infection), active lesions, prolonged rupture of membranes, vaginal delivery, and an absence of transplacental antibodies. The mortality rate for neonates is extremely high (>80%) if untreated.