The ICD-10 and DSM-IV do not specify any diagnostic criteria—apart from approximate answers—as a requirement for a Ganser syndrome diagnosis. Most case studies of the syndrome also depend on the presence of approximate answers and at least one of the other symptoms described by Ganser in his original paper. Usually when giving wrong answers, individuals are only slightly off, showing that the individual understood the question For instance, when asked how many legs a horse has, they might say, "five". Although subjects appear confused in their answers, in other respects they appear to understand their surroundings. Amnesia, loss of personal identity, and clouding of consciousness were among the most common symptoms apart from approximate answers.Although there is currently no uniform way to diagnose the syndrome, a full neurological and mental state examination is recommended to determine its presence as well as tests that assess malingering. In addition to mental examination, other investigations should be done to exclude other underlying causes. These include computer tomography scans (CT) or magnetic resonance imaging (MRI) scans to exclude structural pathology, lumbar puncture to exclude meningitis or encephalitis, and electroencephalography (EEG), to exclude delirium or seizure disorder.Diagnosing Ganser syndrome is challenging because of its rarity and symptom variability. The manifested symptoms may be dependent on the individuals conception of what mental illness entails, creating the possibility of a wide range of combinations of symptoms present in an individual with Ganser syndrome.
If the decrease in blood pressure is systemic (rather than occlusion of the renal artery) baroreceptors in the carotid sinus and aortic arch will be stimulated. This leads to sympathetic nerve activation, resulting in  renin secretion through β 1 -receptors. Constriction of the afferent arterioles causes a decrease in the intraglomerular pressure, reducing GFR proportionally. Renin is the main effector of the juxtaglomerular baroreceptors. Renin is secreted from granules in the JG cells, and once in the blood stream, it acts as a protease to convert angiotensinogen to angiotensin I, which is converted by angiotensin converting enzyme, to angiotensin II, which, in turn, stimulates aldosterone release. Increased aldosterone levels results in salt and water absorption in the distal collecting tubule.A decrease in volume or pressure is a nonosmotic stimulus for antidiuretic hormone production in the hypothalamus, which exerts its effect in the medullary collecting duct for water reabsorption. Through unknown mechanisms, activation of the sympathetic nervous system leads to enhanced proximal tubular reabsorption of salt and water, as well as urea (BUN), calcium, uric acid, and bicarbonate. The net result of these 4 mechanisms of salt and water retention is decreased output and decreased urinary excretion of sodium (< 20 mEq/L). The increased reabsorption of Na leads to increased water and urea reabsorption from the proximal tubules of the kidney back into the blood. In contrast, creatinine is actually secreted in the proximal tubule.