Attention is aroused however when the patient is found to collide with pieces of furniture, to fall over objects, and to experience difficulty in finding his way around. They may try to walk through a wall or through a closed door on his way from one room to another. Suspicion is still further alerted when they begin to describe people and objects around them which, as a matter of fact, are not there at all. Thus we have the twin symptoms of anosognosia (or lack of awareness of defect) and confabulation, the latter affecting both speech and behaviour. Anton syndrome may be thought of ideally as the opposite of blindsight, blindsight occurring when part of the visual field is not consciously experienced, but some reliable perception does in fact occur. Causes
Why patients with Anton syndrome deny their blindness is unknown, although there are many theories. One hypothesis is that damage to the visual cortex results in the inability to communicate with the speech-language areas of the brain. Visual imagery is received but cannot be interpreted; the speech centers of the brain confabulate a response.Patients have also reported visual anosognosia after experiencing ischemic vascular cerebral disease. A 96-year-old man, who was admitted to an emergency department complaining of a severe headache and sudden loss of vision, was discovered to have had a posterior cerebral artery thrombosis with consequent loss of vision. He adamantly claimed he was able to see despite an ophthalmologic exam proving otherwise.
Calcium is tightly regulated by the parathyroid hormone (PTH). In response to low calcium levels, PTH levels rise, and conversely if there are high calcium levels then PTH secretion declines. However, in the setting of absent, decreased, or ineffective PTH hormone, the body loses this regulatory function, and hypocalcemia ensues. Hypoparathyroidism is commonly due to surgical destruction of the parathyroid glands. Hypoparathyroidism may also be due to autoimmune problem. Some causes of hypocalcaemia are as follows:

Mechanism
Physiologically, blood calcium is tightly regulated within a narrow range for proper cellular processes. Calcium in the blood exists in three primary states: bound to proteins (mainly albumin), bound to anions such as phosphate and citrate, and as free (unbound) ionized calcium; all of these forms are ionised. Only the unbound calcium is physiologically active. Normal blood calcium level is between 8.5 and 10.5 mg/dL (2.12 to 2.62 mmol/L) and that of unbound calcium is 4.65 to 5.25 mg/dL (1.16 to 1.31 mmol/L). Diagnosis
Because a significant portion of calcium is bound to albumin, any alteration in the level of albumin will affect the measured level of calcium. A corrected calcium level based on the albumin level is: Corrected calcium (mg/dL) = measured total Ca (mg/dL) + 0.8 * (4.0 - serum albumin [g/dL]). Since calcium is also bound to small anions, it may be more useful to correct total calcium for both albumin and the anion gap. Management
Management of this condition includes:
Intravenous calcium gluconate 10% can be administered, or if the hypocalcaemia is severe, calcium chloride is given instead.