Acrocallosal syndrome (also known as ACLS) is a rare autosomal recessive syndrome characterized by corpus callosum agenesis, polydactyly, multiple dysmorphic features, motor and mental retardation, and other symptoms. The syndrome was first described by Albert Schinzel in 1979.

It is associated with "GLI3".

Acrocallosal syndrome (ACLS, ACS, Schinzel-Type, Hallux-duplication) is a rare, heterogeneous [3] autosomal recessive disorder first discovered by Albert Schinzel (1979) in a 3-year-old boy . To inherit ACLS, one gene copy from each parent must contain a mutation somewhere in the KIF7 gene and be passed on to the child [3]. Characteristics of this syndrome include absence or poor development of the area connecting the left and right parts of the brain, an abnormally large head, increased distance between facial features (eyes), poor motor skills, mental retardation [2], extra fingers and toes, many facial deformities [3], and cleft palate [5]. This is considered a rare disorder and is placed on the NIH Office of Rare Diseases (fewer than 200,000 cases) rare disease list [8]. Lifespan may range from stillbirth to normal expectancy depending on pregnancy complications and severity of the disorder [2,3,5]. In mild cases, the subjects have been shown to live relatively normal lives, but with developmental delays [2].

An individual may feel or hear a "pop" in their knee during a twisting movement or rapid deceleration, followed by an inability to continue participation in the sport and early swelling from hemarthrosis. This combination is said to indicate a 90% probability of rupture of the anterior cruciate ligament.

An individual may experience instability in the knee once they resume walking and other activities, and they may feel their knee is "giving out". Loss of full range of motion, and discomfort along the joint line are also common symptoms of an ACL injury.

Cardiac arrest is preceded by no warning symptoms in approximately 50% of people. For those who do, they have non specific symptoms such as, new or worsening chest pain, fatigue, blackouts, dizziness, shortness of breath, weakness, and vomiting.

When the arrest occurs, the most obvious sign of its occurrence will be the lack of a palpable pulse in the person experiencing it (since the heart has ceased to contract, the usual indications of its contraction such as a pulse will no longer be detectable). Certain types of prompt intervention can often reverse a cardiac arrest, but without such intervention the event will almost always lead to death. In certain cases, it is an expected outcome of a serious illness where death is expected.

Also, as a result of inadequate blood flow to the brain (cerebral perfusion), the patient will quickly become unconscious and will have stopped breathing. The main diagnostic criterion to diagnose a cardiac arrest (as opposed to respiratory arrest which shares many of the same features) is lack of circulation; however, there are a number of ways of determining this. Near-death experiences are reported by 10–20% of people who survived cardiac arrest.

Low body temperature results in shivering becoming more violent. Muscle mis-coordination becomes apparent. Movements are slow and labored, accompanied by a stumbling pace and mild confusion, although the person may appear alert. Surface blood vessels contract further as the body focuses its remaining resources on keeping the vital organs warm. The subject becomes pale. Lips, ears, fingers, and toes may become blue.

Anterior cruciate ligament injury is when the anterior cruciate ligament (ACL) is either stretched, partially torn, or completely torn. Injuries are most commonly complete tears. Symptoms include pain, a popping sound during injury, instability of the knee, and joint swelling. Swelling generally appears within a couple of hours. In approximately 50% of cases other structures of the knee such as ligaments, cartilage, or meniscus are damaged.

The underlying mechanism often involves a rapid change in direction, sudden stop, landing following jumping, or direct contact. It is more common in athletes, particularly those who participate in alpine skiing, soccer, football, or basketball. Diagnosis is typically by physical examination and maybe support by magnetic resonance imaging (MRI).

Prevention is by neuromuscular training and core strengthening. Treatment recommends depend on desired level of activity. If there will be low levels of future activity, bracing and physiotherapy may be sufficient. In those with high activity levels, arthroscopic repair via anterior cruciate ligament reconstruction is often recommended. Surgery, if recommended, is generally not carried out until the initial inflammation from the injury has resolved.

As of 2009, about 200,000 people are affected per year in the United States. In some sports, females have a higher risk while in others, both sexes are equally affected. Without surgery, in those with a complete tear, many are unable to play sports and develop osteoarthritis.

As the temperature decreases, further physiological systems falter and heart rate, respiratory rate, and blood pressure all decrease. This results in an expected heart rate in the 30's at a temperature of .

Difficulty speaking, sluggish thinking, and amnesia start to appear; inability to use hands and stumbling are also usually present. Cellular metabolic processes shut down. Below , the exposed skin becomes blue and puffy, muscle coordination very poor, and walking almost impossible, and the person exhibits incoherent or irrational behavior, including terminal burrowing (see below) or even stupor. Pulse and respiration rates decrease significantly, but fast heart rates (ventricular tachycardia, atrial fibrillation) can also occur. Atrial fibrillation is not typically a concern in and of itself. Major organs fail and clinical death occurs.

Ventricular fibrillation is a cause of cardiac arrest and sudden cardiac death. The ventricular muscle twitches randomly rather than contracting in a co-ordinated fashion (from the apex of the heart to the outflow of the ventricles), and so the ventricles fail to pump blood around the body - because of this, it is classified as a cardiac arrest rhythm, and patients in V-fib should be treated with cardiopulmonary resuscitation and prompt defibrillation. Left untreated, ventricular fibrillation is rapidly fatal as the vital organs of the body, including the heart, are starved of oxygen, and as a result patients in this rhythm will not be conscious or responsive to stimuli. Prior to cardiac arrest, patients may complain of varying symptoms depending on the underlying cause. Patients may exhibit signs of agonal breathing, which to the layperson can look like normal spontaneous breathing, but it is in fact a sign of hypoperfusion of the brainstem.

It has an appearance on electrocardiography of irregular electrical activity with no discernable pattern. It may be described as 'coarse' or 'fine' depending on its amplitude, or as progressing from coarse to fine V-fib. Coarse V-fib may be more responsive to defibrillation, while fine V-fib can mimic the appearance of asystole on a defibrillator or cardiac monitor set to a low gain. Some clinicians may attempt to defibrillate fine V-fib in the hope that it can be reverted to a cardiac rhythm compatible with life, whereas others will deliver CPR and sometimes drugs as described in the advanced cardiac life support protocols in an attempt to increase its amplitude and the odds of successful defibrillation.

Sudden cardiac arrest (SCA) and sudden cardiac death (SCD) occur when the heart abruptly begins to beat in an abnormal or irregular rhythm (arrhythmia). Without organized electrical activity in the heart muscle, there is no consistent contraction of the ventricles, which results in the heart's inability to generate an adequate cardiac output (forward pumping of blood from heart to rest of the body). There are many different types of arrhythmias, but the ones most frequently recorded in SCA and SCD are ventricular tachycardia (VT) or ventricular fibrillation (VF).

Sudden cardiac arrest can result from cardiac and non-cardiac causes including the following:

Pulseless electrical activity (PEA), also known as electromechanical dissociation, refers to cardiac arrest in which the electrocardiogram shows a heart rhythm that should produce a pulse, but does not. Pulseless electrical activity is found initially in about 55% of people in cardiac arrest.

Under normal circumstances, electrical activation of muscle cells precedes mechanical contraction of the heart (known as "electromechanical coupling"). In PEA, there is electrical activity, but the heart either does not contract or there are other reasons this results in an insufficient cardiac output to generate a pulse and supply blood to the organs. While PEA is classified as a form of cardiac arrest, significant cardiac output may still be present which may be determined and best visualized by bedside ultrasound.

Cardiopulmonary resuscitation (CPR) is the first treatment for PEA, while potential underlying causes are identified and treated. The medication epinephrine may be administered. Survival is about 20%.

Pulseless electrical activity leads to a loss of cardiac output, and the blood supply to the brain is interrupted. As a result, PEA is usually noticed when a person loses consciousness and stops breathing spontaneously. This is confirmed by examining the airway for obstruction, observing the chest for respiratory movement, and feeling the pulse (usually at the carotid artery) for a period of 10 seconds.

Ventricular fibrillation (V-fib or VF) is when the heart quivers instead of pumping due to disorganized electrical activity in the ventricles. It is a type of cardiac arrhythmia. Ventricular fibrillation results in cardiac arrest with loss of consciousness and no pulse. This is followed by death in the absence of treatment. Ventricular fibrillation is found initially in about 10% of people in cardiac arrest.

Ventricular fibrillation can occur due to coronary heart disease, valvular heart disease, cardiomyopathy, Brugada syndrome, long QT syndrome, electric shock, or intracranial hemorrhage. Diagnosis is by an electrocardiogram (ECG) showing irregular unformed QRS complexes without any clear P waves. An important differential diagnosis is torsades de pointes.

Treatment is with cardiopulmonary resuscitation (CPR) and defibrillation. Biphasic defibrillation may be better than monophasic. The medication epinephrine or amiodarone may be given if initial treatments are not effective. Rates of survival among those who are out of hospital when the arrhythmia is detected is about 17% while in hospital it is about 46%.