Neurapraxia is a disorder of the peripheral nervous system in which there is a temporary loss of motor and sensory function due to blockage of nerve conduction, usually lasting an average of six to eight weeks before full recovery. Neurapraxia is derived from the word apraxia, meaning “loss or impairment of the ability to execute complex coordinated movements without muscular or sensory impairment”. This condition is typically caused by a blunt neural injury due to external blows or shock-like injuries to muscle fibers and skeletal nerve fibers, which leads to repeated or prolonged pressure buildup on the nerve. As a result of this pressure, ischemia occurs, a neural lesion results, and the human body naturally responds with edema extending in all directions from the source of the pressure. This lesion causes a complete or partial action potential conduction block over a segment of a nerve fiber and thus a reduction or loss of function in parts of the neural connection downstream from the lesion, leading to muscle weakness. Neurapraxia results in temporary damage to the myelin sheath but leaves the nerve intact and is an impermanent condition; thus, Wallerian degeneration does not occur in neurapraxia. In order for the condition to be considered neurapraxia, according to the Seddon classification system of peripheral nerve injury,  there must be a complete and relatively rapid recovery of motor and sensory function once nerve conduction has been restored; otherwise, the injury would be classified as axonotmesis or neurotmesis. Thus, neurapraxia is the mildest classification of peripheral nerve injury.
Risk Factors and genetics
An elevated risk of developing tertiary hyperparathyroidism exists when late stage kidney disease is not corrected timely. This is due to a hyperphosphatemia acting directly on the parathyroid glands. Genetically, those who have an X-linked dominant disorder that disrupts phosphate transport at the renal tubules (X-Linked hypophosphatemic rickets) and are receiving oral phosphate treatment have shown to be at high risk of developing tertiary hyperparathyroidism in the absence of secondary hyperparathyroidism. Recurring tertiary hyperparathyroidism is generally seen to be caused by incomplete parathyroidectomy without renal transplant and the risk is increased when the parathyroid tissue left after surgery is that of a nodular type.Other risk factors of tertiary hyperparathyroidism include an elevated risk of developing acute pancreatitis, mainly due to the hypercalcemia associated with the hyperparathyroidism. Other studies have shown a significant increase in the risk of developing malignancies of the urinary tract and renal system with women being more at risk. Though there is some conjecture as to the correlation between hyperparathyroidism and thyroid carcinoma development, there is however a correlation between the two, which is thought to be due to prolonged irradiation of the neck and head for parathyroid adenomas and increased parathyroid hormone.Other studies have found some correlation in the development of renal disease following parathyroidectomy. However, the mechanism for this effect remains unknown. Pathophysiology
Tertiary Hyperparathyroidism is almost always related to end stage kidney disease and a secondary hyperparathyroidism. Physiological changes due to the kidney damage adversely affect feedback loops that control secretion of parathyroid hormone.