Additionally, an electroencephalogram (EEG), will indicate a characteristic pattern of waves and spikes associated with the syndrome such as generalized 4–6 Hz polyspike and slow wave discharges. These discharges may be evoked by photic stimulation (blinking lights) and/or hyperventilation. Both a magnetic resonance imaging scan (MRI) and computed tomography scan (CT scan) generally appear normal in JME patients. However a number of quantitative MRI studies have reported focal or regional abnormalities of the subcortical and cortical grey matter, particularly the thalamus and frontal cortex, in JME patients. Positron emission tomography reports in some patients may indicate local deviations in many transmitter systems. Management
The most effective anti-epileptic medication for JME is valproic acid (Depakote).Due to valproic acids high incidence of fetal malformations, women of child-bearing age are started on alternative medications such as Lamotrigine, levetiracetam. Carbamazepine may aggravate genetic generalized epilepsies and as such its use should be avoided in JME. Treatment is lifelong. However, recent follow-up researches on a subgroup of patients showed them becoming seizure-free and off anti-epileptic drugs in due course of time. This makes this dogma questionable. Patients should be warned to avoid sleep deprivation. History
The first citation of JME was made in 1857 when Théodore Herpin described a 13-year-old boy with myoclonic jerks, which progressed to tonic-clonic seizures three months later. In 1957, Janz and Christian published a journal article describing several patients with JME. The name Juvenile Myoclonic Epilepsy was proposed in 1975 and adopted by the International League Against Epilepsy.
It is used in the Duff reaction (formylation of arenes), the Sommelet reaction (converting benzyl halides to aldehydes), and in the Delepine reaction (synthesis of amines from alkyl halides). Explosives
Hexamethylenetetramine is the base component to produce RDX and, consequently, C-4 as well as Octogen, hexamine dinitrate, hexamine diperchlorate and HMTD. Historical uses
Hexamethylenetetramine was first introduced into the medical setting in 1895 as a urinary antiseptic. However, it was only used in cases of acidic urine, whereas boric acid was used to treat urinary tract infections with alkaline urine. Scientist De Eds found that there was a direct correlation between the acidity of hexamethylenetetramines environment and the rate of its decomposition. Therefore, its effectiveness as a drug depended greatly on the acidity of the urine rather than the amount of the drug administered. In an alkaline environment, hexamethylenetetramine was found to be almost completely inactive.Hexamethylenetetramine was also used as a method of treatment for soldiers exposed to phosgene in World War I. Subsequent studies have shown that large doses of hexamethylenetetramine provide some protection if taken before phosgene exposure but none if taken afterwards. Producers
Since 1990 the number of European producers has been declining. The French SNPE factory closed in 1990; in 1993, the production of hexamethylenetetramine in Leuna, Germany ceased; in 1996, the Italian facility of Agrolinz closed down; in 2001, the UK producer Borden closed;  in 2006, production at Chemko, Slovak Republic, was closed. Remaining producers include INEOS in Germany, Caldic in the Netherlands, and Hexion in Italy.