The motor output is amplified due to the missing limb; therefore, the patient may experience the overflow of information as pain. The patient contains repressed memories from previous motor commands of clenching the hand and sensory information from digging their nails into their palm. These memories remain due to previous neural connections in the brain. Phantom limb syndrome
The term "phantom limb" was coined by physician Silas Weir Mitchell in 1871. For many years, the dominant hypothesis for the cause of phantom limbs was irritation in the peripheral nervous system at the amputation site (neuroma). By the late 1980s, Ronald Melzack had recognized that the peripheral neuroma account could not be correct, because many people born without limbs also experienced phantom limbs. According to Melzack the experience of the body is created by a wide network of interconnecting neural structures, which he called the "neuromatrix".Pons and colleagues (1991) at the National Institutes of Health (NIH) showed that the primary somatosensory cortex in macaque monkeys undergoes substantial reorganization after the loss of sensory input.Hearing about these results, Vilayanur S. Ramachandran hypothesized that phantom limb sensations in humans could be due to reorganization in the human brains somatosensory cortex. Ramachandran and colleagues illustrated this hypothesis by showing that stroking different parts of the face led to perceptions of being touched on different parts of the missing limb. Later brain scans of amputees showed the same kind of cortical reorganization that Pons had observed in monkeys.Maladaptive changes in the cortex may account for some but not all phantom limb pain.
Besides, nearly all kinds of distributive shock such as septic shock, neurogenic shock, anaphylactic shock, drug and toxin-induced shock, endocrine shock can turn out into refractory vasodilatory shock when the original shock becomes more severe.The most common cause of vasodilatory shock is sepsis. Except sepsis, other causes comprise severe acute pancreatitis, post cardiopulmonary bypass vasoplegia and other triggers for a systemic inflammatory response syndrome. Low serum calcium values might take a role in vasodilatory shock. Pathophysiology
In the cases of cardiogenic shock resulting from heart failure or acute hemorrhagic shock caused by a large volume of blood loss, the body constricts peripheral vessels to reverse the low arterial pressure that causes inadequate tissue perfusion. With vasodilatory shock, it is difficult for the peripheral vascular smooth muscle to constrict. In refractory vasodilatory shock, peripheral vascular smooth muscle responds poorly to therapy with vasopressor drugs.Vasopressin deficiency may play an important role in vasodilatory shock. In refractory vasodilatory shock, the patient has both vasopressin secretion deficit and an advanced resistance to vasopressin-induced blood-pressure changes. Some have hypothesized that patients with vasopressin deficiency, including a decrease in baroreceptor stimulation, appear to have impaired autonomic reflexes. Tone may be inhibited by atrial stretch receptors and vasopressin release may be inhibited by nitric oxide or high circulating levels of norepinephrine.Vasodilatory shock is often involved with the dysfunction of physiologic compensatory mechanisms such as the sympathetic nervous system, vasopressin arginine system and renin-angiotensin aldosterone system. Diagnosis
The definition of refractory shock or vasodilatory shock varies.