Aneurysmal bone cyst (ABC) is a non-cancerous bone tumor composed of multiple varying sizes of spaces in a bone which are filled with blood. The term is a misnomer, as the lesion is neither an aneurysm nor a cyst. It generally presents with pain and swelling in the affected bone. Pressure on neighbouring tissues may cause compression effects such as neurological symptoms.The cause is unknown. Diagnosis involves medical imaging. CT scan and X-ray show lytic expansion lesions with clear borders. MRI reveals fluid levels.Treatment is usually by curettage, bone grafting or surgically removing the part of bone. 20–30% may recur, usually in the first couple of years after treatment, particularly in children.It is rare. The incidence is around 0.15 cases per one million per year. Aneurysmal bone cyst was first described by Jaffe and Lichtenstein in 1942. Signs and symptoms
The afflicted may have relatively small amounts of pain that will quickly increase in severity over a time period of 6–12 weeks. The skin temperature around the bone may increase, a bony swelling may be evident, and movement may be restricted in adjacent joints.Spinal lesions may cause quadriplegia and patients with skull lesions may have headaches. Sites
Commonly affected sites are metaphyses of vertebra, flat bones, femur and tibia. Approximate percentages by sites are as shown:
Skull and mandible (4%)
Spine (16%)
Clavicle and ribs (5%)
Upper extremity (21%)
Pelvis and sacrum (12%)
Femur (13%)
Lower leg (24%)
Foot (3%)

Causes
Aneurysmal bone cyst has been widely regarded a reactive process of uncertain cause since its initial description by Jaffe and Lichtenstein in 1942.
The effects on the NMDA complex are dose-dependent; the product appears to enhance receptor activation at low concentrations, while inhibiting it when consumed in higher amounts, which counters the excessive activation of NMDA receptors in the context of alcohol withdrawal.The product also increases the endogenous production of taurine.Ethanol and benzodiazepines act on the central nervous system by binding to the GABAA receptor, increasing the effects of the inhibitory neurotransmitter GABA (i.e., they act as positive allosteric modulators at these receptors). In alcohol use disorder, one of the main mechanisms of tolerance is attributed to GABAA receptors becoming downregulated (i.e. these receptors become less sensitive to GABA). When alcohol is no longer consumed, these down-regulated GABAA receptor complexes are so insensitive to GABA that the typical amount of GABA produced has little effect, leading to physical withdrawal symptoms; since GABA normally inhibits neural firing, GABAA receptor desensitization results in unopposed excitatory neurotransmission (i.e., fewer inhibitory postsynaptic potentials occur through GABAA receptors), leading to neuronal over-excitation (i.e., more action potentials in the postsynaptic neuron). One of acamprosates mechanisms of action is the enhancement of GABA signaling at GABAA receptors via positive allosteric receptor modulation. It has been purported to open the chloride ion channel in a novel way as it does not require GABA as a cofactor, making it less liable for dependence than benzodiazepines.