The person serum osmolality is measured by freezing point depression and then compared with the predicted osmolality based on the persons measured sodium, glucose, blood urea nitrogen, and any ethanol that may have been ingested. The presence of a large osmolal gap supports a diagnosis of ethylene glycol poisoning. However, a normal osmolar gap does not rule out ethylene glycol exposure because of wide individual variability.The increased osmolal gap is caused by the ethylene glycol itself. As the metabolism of ethylene glycol progresses there will be less ethylene glycol and this will decrease the blood ethylene glycol concentration and the osmolal gap making this test less useful. Additionally, the presence of other alcohols such as ethanol, isopropanol, or methanol or conditions such as alcoholic or diabetic ketoacidosis, lactic acidosis, or kidney failure may also produce an elevated osmolal gap leading to a false diagnosis.Other laboratory abnormalities may suggest poisoning, especially the presence of a metabolic acidosis, particularly if it is characterized by a large anion gap. Large anion gap acidosis is usually present during the initial stage of poisoning. However, acidosis has a large number of differential diagnosis, including poisoning from methanol, salicylates, iron, isoniazid, paracetamol, theophylline, or from conditions such as uremia or diabetic and alcoholic ketoacidosis. The diagnosis of ethylene glycol poisoning should be considered in any people with a severe acidosis. Urine microscopy can reveal needle or envelope-shaped calcium oxalate crystals in the urine which can suggest poisoning; although these crystals may not be present until the late stages of poisoning.
These conditions are listed below:
Central nervous system tumor
Central pontine myelinolysis
Cerebrovascular diseases
Drug induced
Infectious or post infectious encephalopathies
Kernicterus
Metabolic
Paraneoplastic syndromes
Perinatal (during birth) cerebral injury
Peripheral or central trauma
ToxinsSecondary spasmodic torticollis is diagnosed when any of the following are present: history of exogenous insult or exposure, neurological abnormalities other than dystonia, abnormalities on brain imaging, particularly in the basal ganglia. Head positions
To further classify spasmodic torticollis, one can note the position of the head. Torticollis is the horizontal turning (rotational collis) of the head, and uses the ipsilateral splenius, and contralateral sternocleidomastoid muscles. This is the "chin-to-shoulder" version. Laterocollis is the tilting of the head from side to side. This is the "ear-to-shoulder" version. This involves many more muscles: ipsilateral sternocleidomastoid, ipsilateral splenius, ipsilateral scalene complex, ipsilateral levator scapulae, and ipsilateral posterior paravertebrals. The flexion of the neck (head tilts forwards) is anterocollis. This is the "chin-to-chest" version and is the most difficult version to address. This movement utilizes the bilateral sternocleidomastoid, bilateral scalene complex, bilateral submental complex. Retrocollis is the extension of the neck (head tilts back) and uses the following muscles for movement: bilateral splenius, bilateral upper trapezius, bilateral deep posterior paravertebrals. This is the "chin-in-the-air" version.A combination of these head positions is common; many patients experience turning and tilting actions of the head. Treatment
There are several treatments for spasmodic torticollis, the most commonly used being botulinum toxin injections in the dystonic muscle of the neck. Other treatments include sensory trick for a mild occasional twinge,  oral medications, and deep brain stimulation.