An effusion can cause conductive hearing loss if it interferes with the transmission of vibrations of middle ear bones to the vestibulocochlear nerve complex that are created by sound waves.Early-onset OME is associated with feeding of infants while lying down, early entry into group child care, parental smoking, lack, or too short a period of breastfeeding and greater amounts of time spent in group child care, particularly those with a large number of children. These risk factors increase the incidence and duration of OME during the first two years of life. Chronic suppurative otitis media
Chronic suppurative otitis media (CSOM) is a chronic inflammation of the middle ear and mastoid cavity that is characterised by discharge from the middle ear through a perforated tympanic membrane for at least 6 weeks. CSOM occurs following an upper respiratory tract infection that has led to acute otitis media. This progresses to a prolonged inflammatory response causing mucosal (middle ear) oedema, ulceration and perforation. The middle ear attempts to resolve this ulceration by production of granulation tissue and polyp formation. This can lead to increased discharge and failure to arrest the inflammation, and to development of CSOM, which is also often associated with cholesteatoma. There may be enough pus that it drains to the outside of the ear (otorrhea), or the pus may be minimal enough to be seen only on examination with an otoscope or binocular microscope. Hearing impairment often accompanies this disease.
A lower motor neuron lesion is a lesion which affects nerve fibers traveling from the lower motor neuron(s) in the anterior horn/anterior grey column of the spinal cord, or in the motor nuclei of the cranial nerves, to the relevant muscle(s).One major characteristic used to identify a lower motor neuron lesion is flaccid paralysis – paralysis accompanied by loss of muscle tone. This is in contrast to an upper motor neuron lesion, which often presents with spastic paralysis – paralysis accompanied by severe hypertonia. Signs and symptoms
Muscle paresis or paralysis
Fibrillations
Fasciculations – caused by increased receptor concentration on muscles to compensate for lack of innervation. Hypotonia or atonia – Tone is not velocity dependent. Hyporeflexia - Along with deep reflexes even cutaneous reflexes are also decreased or absent. Strength – weakness is limited to segmental or focal pattern, Root innervated patternThe extensor plantar reflex is usually absent. Muscle paresis/paralysis, hypotonia/atonia, and hyporeflexia/areflexia are usually seen immediately following an insult. Muscle wasting, fasciculations and fibrillations are typically signs of end-stage muscle denervation and are seen over a longer time period. Another feature is the segmentation of symptoms – only muscles innervated by the damaged nerves will be symptomatic. Causes
The most common causes of lower motor neuron injuries are trauma to peripheral nerves that serve the axons, and viruses that selectively attack ventral horn cells.