Some of the paleospinothalamic fibers peel off in the brain stem, connecting with the reticular formation or midbrain periaqueductal gray, and the remainder terminate in the intralaminar nuclei of the thalamus.Pain-related activity in the thalamus spreads to the insular cortex (thought to embody, among other things, the feeling that distinguishes pain from other homeostatic emotions such as itch and nausea) and anterior cingulate cortex (thought to embody, among other things, the affective/motivational element, the unpleasantness of pain), and pain that is distinctly located also activates primary and secondary somatosensory cortex.Spinal cord fibers dedicated to carrying A-delta fiber pain signals, and others that carry both A-delta and C fiber pain signals to the thalamus have been identified. Other spinal cord fibers, known as wide dynamic range neurons, respond to A-delta and C fibers, but also to the much larger, more heavily myelinated A-beta fibers that carry touch, pressure and vibration signals. Ronald Melzack and Patrick Wall introduced their gate control theory in the 1965 Science article "Pain Mechanisms: A New Theory". The authors proposed that the thin C and A-delta (pain) and large diameter A-beta (touch, pressure, vibration) nerve fibers carry information from the site of injury to two destinations in the dorsal horn of the spinal cord, and that A-beta fiber signals acting on inhibitory cells in the dorsal horn can reduce the intensity of pain signals sent to the brain.
Primary aldosteronism will cause metabolic alkalosis and hypokalaemia, but hypertension will be present and serum renin will be low
EAST syndrome, though neurological features will predominate
Renal cysts and diabetes syndrome can cause hypomagnesaemia and hypocalcuria, but is distinguished by early onset chronic kidney disease and an autosomal dominant inheritance pattern of renal cysts and/or diabetes

Treatment
Most asymptomatic individuals with Gitelman syndrome can be monitored without medical treatment. Dietary modification of a high salt diet incorporated with, potassium and magnesium supplementation to normalize blood levels is the mainstay of treatment. Large doses of potassium and magnesium are often necessary to adequately replace the electrolytes lost in the urine. Diarrhea is a common side effect of oral magnesium which can make replacement by mouth difficult but dividing the dose to 3-4 times a day is better tolerated. Severe deficits of potassium and magnesium require intravenous replacement. If low blood potassium levels are not sufficiently replaced with replacement by mouth, aldosterone antagonists (such as spironolactone or eplerenone) or epithelial sodium channel blockers such as amiloride can be used to decrease urinary wasting of potassium.In patients with early onset of the disease such as infants and children, indomethacin is the drug of choice utilized to treat growth disturbances. Indomethacin in a study by Blanchard et al. 2015 was shown to increase serum potassium levels, and decrease renin concentration. Adverse effects of indomethacin include a decrease in the glomerular filtration rate, and gastrointestinal disturbances.Cardiac evaluation is promoted in the prevention of dysrhythmias and monitoring of QT interval activity.