Neurapraxia is very common in professional athletes, especially American football players, and is a condition that can and should be treated by a physician. Signs and symptoms
A variety of nerve types can be subjected to neurapraxia and therefore symptoms of the injury range in degree and intensity. Common symptoms of neurapraxia are disturbances in sensation, weakness of muscle, vasomotor and sudomotor paralysis in the region of the affected nerve or nerves, and abnormal sensitivity of the nerve at the point of injury. It has been observed that subjective sensory symptoms include numbness, tingling, and burning sensations at the site of the injury. Objective sensory symptoms are generally minimal in regards to touch, pain, heat, and cold. In cases of motor neuron neurapraxia, symptoms consist of flaccid paralysis of the muscles innervated by the injured nerve or nerves. Symptoms are often transient and only last for a short period of time immediately following the injury. However, in severe cases of neurapraxia, symptoms can persist for weeks or months at a time. Causes
The cause of neurapraxia is a neural lesion which causes a temporary block of nerve conduction without transection of the axon. A conduction block is classified as a 40% reduction in action potential amplitude over a short distance on the nerve, or a 50% reduction for a longer distance on the nerve. In neurapraxia, stimulation to the injured nerve results in a greater reduction in the action potential amplitude on the proximal site of the injury as opposed to the distal site.
Tumoral calcinosis is a rare condition in which there is calcium deposition in the soft tissue in periarticular location, around joints, outside the joint capsule. They are frequently (0.5–3%) seen in patients undergoing renal dialysis. Clinically also known as hyperphosphatemic familial tumoral calcinosis (HFTC), is often caused by genetic mutations in genes that regulate phosphate physiology in the body (leading to too much phosphate (hyperphosphatemia)). Best described genes that harbour mutations in humans are FGF-23, Klotho (KL), or GALNT3. A zebrafish animal model with reduced GALNT3 expression also showed HFTC-like phenotype, indicating an evolutionary conserved mechanism that is involved in developing tumoral calcinosis. Clinical features
The name indicates calcinosis (calcium deposition) which resembles tumor (like a new growth). They are not true neoplasms – they dont have dividing cells. They are just deposition of inorganic calcium with serum exudate. Children and adolescents (6 to 25 years) are the most commonly affected. The symptom that the accumulations cause is not pain but swelling around joints. They have propensity to enlarge progressively and ulcerate the overlying skin and extrude. They are most common around shoulders, hips and elbows. Laboratory evaluation reveal normal serum calcium levels and hyperphosphatemia. Rarely ALP (alkaline phosphatase – an enzyme active at sites of bone formation) may be elevated. Treatment is normalization of serum phosphate levels and resection of lesions. Surgical removal should be complete and if part of it is left, recurrence is likely to occur. Cutting through the excised calcium deposition reveals semifluid calcium suspension in albumin encapsulated by fibrous tissue.