This syndrome might be difficult to distinguish from a bilateral temporal lesion such as described above. Diagnosis
Since cortical deafness and auditory agnosia have many similarities, diagnosing the disorder proves to be difficult. Bilateral lesions near the primary auditory cortex in the temporal lobe are important criteria. Cortical deafness requires demonstration that brainstem auditory responses are
normal, but cortical evoked potentials are impaired. Brainstem auditory evoked potentials (BAEP), also referred to as brainstem auditory evoked responses (BAER) show the neuronal activity in the auditory nerve, cochlear nucleus, superior olive, and inferior colliculus of the brainstem. They typically have a response latency of no more than six milliseconds with an amplitude of approximately one microvolt. The latency of the responses gives critical information: if cortical deafness is applicable, LLR (long-latency responses) are completely abolished and MLR (middle latency responses) are either abolished or significantly impaired. In auditory agnosia, LLRs and MLRs are preserved. Another important aspect of cortical deafness that is often overlooked is that patients feel deaf. They are aware of their inability to hear environmental sounds, non-speech and speech sounds. Patients with auditory agnosia can be unaware of their deficit, and insist that they are not deaf. Verbal deafness and auditory agnosia are disorders of a selective, perceptive and associative nature whereas cortical deafness relies on the anatomic and functional disconnection of the auditory cortex from acoustic impulses. Case examples
Although cortical deafness has very specific parameters of diagnosis, its causes on the other hand can vary tremendously.
A complement receptor is a membrane-bound receptor belonging to the complement system, which is part of the innate immune system. Complement receptors bind effector protein fragments that are produced in response to antigen-antibody complexes or damage-associated molecules. Complement receptor activation contributes to the regulation of inflammation, leukocyte extravasation, and phagocytosis; it also contributes to the adaptive immune response. Different complement receptors can participate in either the classical complement pathway, the alternative complement pathway, or both. Expression and function
White blood cells, particularly monocytes and macrophages, express complement receptors on their surface. All four complement receptors can bind to fragments of complement component 3 or complement component 4 coated on pathogen surface, but the receptors trigger different downstream activities. Complement receptor (CR) 1, 3, and 4 function as opsonins which stimulate phagocytosis, whereas CR2 is expressed only on B cells as a co-receptor. Red blood cells (RBCs) also express CR1, which enables RBCs to carry complement-bound antigen-antibody complexes to the liver and spleen for degradation. a.^ B: B cell. E: erythrocyte. Endo: endothelial cell. D: dendritic cell. FDC: follicular dendritic cell. Mac: macrophage. MC: mast cell. M0: monocyte. Pha: phagocyte. PMN: polymorphonuclear leukocyte. Clinical significance
Deficits in complement receptor expression can cause disease. Mutations in complement receptors which alter receptor function can also increase risk of certain diseases. See also
Complement system
Humoral immunity
Immune system

References
External links
Complement+receptors at the US National Library of Medicine Medical Subject Headings (MeSH)