A parapharyngeal abscess is a deep neck space abscess of the parapharyngeal space (or pharyngomaxillary space), which is lateral to the superior pharyngeal constrictor muscle and medial to the masseter muscle. This space is divided by the styloid process into anterior and posterior compartments. The posterior compartment contains the carotid artery, internal jugular vein, and many nerves. Signs and symptoms
Symptoms include fever, sore throat, painful swallowing, and swelling in the neck. An anterior space abscess can cause lockjaw (spasm of jaw muscle), and hard mass formation along the angle of the mandible, with medial bulging of the tonsil and lateral pharyngeal wall. A posterior space abscess causes swelling in the posterior pharyngeal wall, and lockjaw is minimal. Other structures within the carotid sheath may be involved, causing rigors, high fever, bacteremia, neurologic deficit, or a massive haemorrhage caused by carotid artery rupture. Cause
Infection can occur from:

Pharynx: acute and chronic infection of tonsil and adenoids
Teeth: dental infection occurs from lower last molar tooth
Ear: Bezolds abscess and petrositis
Other space: infection of parotid retropharyngeal space
External trauma: penetrating injuries of neck, injection of local anaesthetic

Epidemiology
Parapharyngeal abscess is more common in male than the female gender. Any age group can develop a parapharyngeal abscess but it is most commonly seen in children and adolescents. Adults who are immunocompromised are also at high risk. == References ==
As mentioned above, carisoprodol appears to have strong anxiolytic effects on its own; however, a large part of its effects also come from the fact that it is metabolized into meprobamate: at least a 25% of the carisoprodol administered will be transformed into meprobamate which means that meprobamate is 3.25× stronger than carisoprodol (although this rate varies from person to person according to their levels of CYP2C19 enzymes in their livers with some people having considerably higher levels) or, in other words, 200 mg of meprobamate (which is the lowest standard dose) is equivalent to 650 mg of carisoprodol. As such, meprobamate is believed to play a significant role in the effects of carisoprodol and meprobamates long half-life results in bioaccumulation following extended periods of carisoprodol administration. It is slightly soluble in water and freely soluble in ethanol, chloroform and acetone. The drugs solubility is practically independent of pH. History
On 1 June 1959, several American pharmacologists convened at Wayne State University in Detroit, Michigan to discuss a newly discovered structural analogue of meprobamate. The substitution of one hydrogen atom with an isopropyl group on one of the carbamyl nitrogens was intended to yield a drug with new pharmacological properties. It had been developed by Frank Berger at Wallace Laboratories and was named carisoprodol.Building on meprobamates pharmacological effects, carisoprodol was intended to have better muscle relaxing properties, less potential for addiction, and a lower risk of overdose.