Microphone: Converts the sound waves into electrical energy
Mixed hearing loss: It is a hearing loss where both conductive and sensorineural losses occur at the same time.
Mastoid – Hard, boney structure behind the ear. The mastoid process is a conical prominence projecting from the undersurface of the mastoid portion of the temporal bone. It is located just behind the external acoustic meatus, and lateral to the styloid process. Its size and form vary somewhat; it is larger in the male than in the female.
The term “mastoid” is derived from the Greek word for “breast,” a reference to the shape of this bone. The temporal bone contains another protrusion, the styloid process, located in close proximity to the mastoid process. The styloid process also serves as a point of attachment for muscles and has a distinctive pointed shape akin to that of a stylus, explaining the origins of the name.
This part of the skull projects from the temporal bone and is roughly pyramidal or conical in shape. One important role for this bone is as a point of attachment for several muscles – the splenius capitis, longissimus capitis, digastric posterior belly, and sternocleidomastoid. These muscles are one reason the mastoid process tends to be larger in men, because men have bigger muscles as a general rule and thus require larger points of attachment.
Mastoid Surgery – Surgical procedure to remove infection from the mastoid bone. Mastoiditis is the result of an infection that affects the skull behind the ear. Specifically, it is an inflammation of mucosal lining of mastoid antrum and mastoid air cell system inside mastoid process, the portion of the temporal bone of the skull that is behind the ear which contains open, air-containing spaces. It is usually caused by untreated acute otitis media (middle ear infection) and used to be a leading cause of child mortality. With the development of antibiotics, however, mastoiditis has become quite rare in developed countries. It is treated with medications, and sometimes surgery. If untreated, the infection can spread to surrounding structures, including the brain, causing serious complications. Some common symptoms and signs of mastoiditis include pain, tenderness, and swelling in the mastoid region. There may be ear pain (otalgia), and the ear or mastoid region may be red (erythematous). Fever or headaches may also be present as well as eye twitching or uncontrolled blinking. Infants usually show nonspecific symptoms, including anorexia, diarrhea, or irritability. Drainage from the ear occurs in more serious cases, often manifest as brown discharge on the pillowcase upon waking. In one extreme case in the United States the pillow would stick to the child’s head upon rising in the morning. Two mastoidectomies were required to cure the child and left her hearing impaired with ringing and balance issues.
Mastoiditis with subperiostal abscess
The diagnosis of mastoiditis is clinical—based on the medical history and physical examination. Imaging studies provide additional information; The standard method of diagnosis is via MRI scan although a CT scan is a common alternative as it gives a clearer and more useful image to see how close the damage may have gotten to the brain and facial nerves. Planar (2-D) X-rays are not as useful. If there is drainage, it is often sent for culture, although this will often be negative if the patient has begun taking antibiotics. Exploratory surgery is often used as a last resort method of diagnosis to see the mastoid and surrounding areas.
The pathophysiology of mastoiditis is straightforward: bacteria spread from the middle ear to the mastoid air cells, where the inflammation causes damage to the bony structures. Streptococcus pneumoniae, Streptococcus pyogenes, Staphylococcus aureus, Haemophilus influenzae, and Moraxella catarrhalis are the most common organisms recovered in acute mastoiditis. Organisms that are rarely found are Pseudomonas aeruginosa and other Gram-negative aerobic bacilli, and anaerobic bacteria. P. aeruginosa, Enterobacteriaceae, S. aureus and anaerobic bacteria ( Prevotella, Bacteroides, Fusobacterium, and Peptostreptococcus spp. ) are the most common isolates in chronic mastoiditis. Rarely, Mycobacterium species can also cause the infection. Some mastoiditis is caused by cholesteatoma, which is a sac of keratinizing squamous epithelium in the middle ear that usually results from repeated middle-ear infections. If left untreated, the cholesteatoma can erode into the mastoid process, producing mastoiditis, as well as other complications.
Prevention and treatment
In general, mastoiditis is rather simple to prevent. If the patient with an ear infection seeks treatment promptly and receives complete treatment, the antibiotics will usually cure the infection and prevent its spread. For this reason, mastoiditis is rare in developed countries. However, the rise of “superbugs” that are resistant to conventional antibiotics increases the risk that ear infections will worsen into mastoiditis. Most ear infections occur in infants as the eustachian tubes are not fully developed and don’t drain readily.
In the United States the primary treatment for mastoiditis is administration of intravenous antibiotics. Initially, broad-spectrum antibiotics are given, such as ceftriaxone. As culture results become available, treatment can be switched to more specific antibiotics directed at the eradiaction of the recovered aerobic and anaerobic bacteria. Long-term antibiotics may be necessary to completely eradicate the infection. If the condition does not quickly improve with antibiotics, surgical procedures may be performed (while continuing the medication). The most common procedure is a myringotomy, a small incision in the tympanic membrane (eardrum), or the insertion of a tympanostomy tube into the eardrum. These serve to drain the pus from the middle ear, helping to treat the infection. The tube is extruded spontaneously after a few weeks to months, and the incision heals naturally. If there are complications, or the mastoiditis does not respond to the above treatments, it may be necessary to perform a mastoidectomy: a procedure in which a portion of the bone is removed and the infection drained.
Attack triangle in mastoidectomies
With prompt treatment, it is possible to cure mastoiditis. Seeking medical care early is important. However, it is difficult for antibiotics to penetrate to the interior of the mastoid process and so it may not be easy to cure the infection; it also may recur. Mastoiditis has many possible complications, all connected to the infection spreading to surrounding structures. Hearing loss is likely, or inflammation of the labyrinth of the inner ear (labyrinthitis) may occur, producing vertigo and an ear ringing may develop along with the hearing loss, making it more difficult to communicate. The infection may also spread to the facial nerve (cranial nerve VII), causing facial-nerve palsy, producing weakness or paralysis of some muscles of facial expression, on the same side of the face. Other complications include Bezold’s abscess, an abscess (a collection of pus surrounded by inflamed tissue) behind the sternocleidomastoid muscle in the neck, or a subperiosteal abscess, between the periosteum and mastoid bone ( resulting in the typical appearance of a protruding ear). Serious complications result if the infection spreads to the brain. These include meningitis (inflammation of the protective membranes surrounding the brain), epidural abscess (abscess between the skull and outer membrane of the brain), dural venous thrombophlebitis (inflammation of the venous structures of the brain), or brain abscess.
In the United States and other developed countries, the incidence of mastoiditis is quite low, around 0.004%, although it is higher in developing countries. The most common ages affected are 2 months – 13 months, as it is during that age that ear infections are most common. Males and females are equally affecte
Ménière’s Disease – An inner ear disorder that can affect both hearing and balance and is usually associated with vertigo (feeling like you’re spinning when you’re really not), hearing loss, roaring tinnitus, and the sensation of fullness in the ear. Ménière’s disease is a disorder of the inner ear that can affect hearing and balance to a varying degree. It is characterized by episodes of vertigo, low pitched tinnitus, and hearing loss. The hearing loss has a fluctuating then permanent nature, meaning that it comes and goes, alternating between ears for some time, then becomes permanent with no return to normal function. It is named after the French physician Prosper Ménière, who, in an article published in 1861, first reported that vertigo was caused by inner ear disorders. The condition affects people differently; it can range in intensity from being a mild annoyance to a chronic, lifelong disability. Signs and symptoms
Audiograms illustrating normal hearing (left) and unilateral low-pitch hearing loss associated with Ménière’s disease (right).
Ménière’s often begins with one symptom, and gradually progresses. However, not all symptoms must be present for a doctor to make a diagnosis of the disease. Several symptoms at once is more conclusive than different symptoms at separate times. Other conditions can present themselves with Ménière’s-like symptoms, such as syphilis, Cogan’s syndrome, autoimmune disease of the inner ear, dysautonomia, perilymph fistula, multiple sclerosis, acoustic neuroma, and both hypo- and hyperthyroidism.
The symptoms of Ménière’s are variable; not all sufferers experience the same symptoms. However, so-called “classic Ménière’s” is considered to have the following four symptoms:
- Attacks of rotational vertigo that can be severe, incapacitating, unpredictable, and last anywhere from minutes to hours, but generally no longer than 24 hours. For some sufferers however, prolonged attacks can occur, lasting from several days to several weeks, often causing the sufferer to be severely incapacitated. This combines with an increase in volume of tinnitus and temporary, albeit significant, hearing loss. Hearing may improve after an attack, but often becomes progressively worse. Nausea, vomiting, and sweating sometimes accompany vertigo, but are symptoms of vertigo, and not of Ménière’s.
- Fluctuating, progressive, unilateral (in one ear) or bilateral (in both ears) hearing loss, usually in lower frequencies. For some, sounds can appear tinny or distorted, and patients can experience unusual sensitivity to noises.
- Unilateral or bilateral tinnitus.
- A sensation of fullness or pressure in one or both ears.
Some may have parasitic symptoms, which aren’t necessarily symptoms of Ménière’s, but rather side effects from other symptoms. These are typically nausea, vomiting, and sweating which are typically symptoms of vertigo, and not of Ménière’s. Vertigo may induce nystagmus, or uncontrollable rhythmical and jerky eye movements, usually in the horizontal plane, reflecting the essential role of non-visual balance in coordinating eye movements. Sudden, severe attacks of dizziness or vertigo, known informally as “drop attacks,” can cause someone who is standing to suddenly fall. Drop attacks are likely to occur later in the disease, but can occur at any time.
There is an increased prevalence of migraine in patients with Ménière’s disease.
Ménière’s disease is idiopathic, but it is believed to be linked to endolymphatic hydrops, an excess of fluid in the inner ear. It is thought that endolymphatic fluid bursts from its normal channels in the ear and flows into other areas, causing damage. This is called “hydrops.” The membranous labyrinth, a system of membranes in the ear, contains a fluid called endolymph. The membranes can become dilated like a balloon when pressure increases and drainage is blocked. This may be related to swelling of the endolymphatic sac or other tissues in the vestibular system of the inner ear, which is responsible for the body’s sense of balance. In some cases, the endolymphatic duct may be obstructed by scar tissue, or may be narrow from birth. In some cases there may be too much fluid secreted by the stria vascularis. The symptoms may occur in the presence of a middle ear infection, head trauma, or an upper respiratory tract infection, or by using aspirin, smoking cigarettes, or drinking alcohol. They may be further exacerbated by excessive consumption of salt in some patients. It has also been proposed that Ménière’s symptoms in many patients are caused by the deleterious effects of a herpes virus. Herpes viridae are present in a majority of the population in a dormant state. It is suggested that the virus is reactivated when the immune system is depressed due to a stressor such as trauma, infection, or surgery (under general anesthesia). Symptoms then develop as the virus degrades the structure of the inner ear.
Ménière’s disease affects about 190 people per 100,000. Recent gender predominance studies show that Ménière’s tends to affect women more often than men Age of onset typically occurs in adult years, with prevalence increasing with age.
Doctors establish a diagnosis with complaints and medical history. However, a detailed otolaryngological examination, audiometry, and head MRI scan should be performed to exclude a vestibular schwannoma or superior canal dehiscence which would cause similar symptoms. Some of the same symptoms also occur with benign paroxysmal positional vertigo (BPPV), and with cervical spondylosis (which can affect blood supply to the brain and cause vertigo). There is no definitive test for Ménière’s; it is only diagnosed when all other causes have been ruled out. If any cause had been discovered, this would eliminate Ménière’s disease, as by its very definition, as an exclusively idiopathic disease — it has no known cause.
Ménière’s disease had been recognized as early as 1860s, but it was still relatively vague and broad at the time. The American Academy of Otolaryngology-Head and Neck Surgery Committee on Hearing and Equilibrium (AAO HNS CHE) set criteria for diagnosing Ménière’s, as well as defining two sub categories of Ménière’s: cochlear (without vertigo) and vestibular (without deafness).
In 1972, the academy defined criteria for diagnosing Ménière’s disease as:
- Fluctuating, progressive, sensorineural deafness.
- Episodic, characteristic definitive spells of vertigo lasting 20 minutes to 24 hours with no unconsciousness, vestibular nystagmus always present.
- Usually tinnitus.
- Attacks are characterized by periods of remission and exacerbation.
In 1985, this list changed to alter wording, such as changing “deafness” to “hearing loss associated with tinnitus, characteristically of low frequencies” and requiring more than one attack of vertigo to diagnose. Finally in 1995, the list was again altered to allow for degrees of the disease:
- Certain – Definite disease with histopathological confirmation
- Definite – Requires two or more definitive episodes of vertigo with hearing loss plus tinnitus and/or aural fullness
- Probable – Only one definitive episode of vertigo and the other symptoms and signs
- Possible – Definitive vertigo with no associated hearing loss
Several environmental and dietary changes are thought to reduce the frequency or severity of symptom outbreaks. It is believed that since high salt diets cause water retention, it can lead to an increase (or at least preventing the decrease) of fluid within the inner ear, although the relationship between salt and the inner ear is not fully understood. High-salt intake is thought to alter the concentrations of fluid in the inner ear and Ménière’s episodes could be accelerated by high-salt binges. Recommended salt intake is often around one to two grams per day. Diuretics have traditionally been prescribed to facilitate a low-salt diet although there is no definite supportive evidence.
Additionally, patients may be advised to avoid alcohol, caffeine, and tobacco, all of which can aggravate symptoms of Ménière’s. Many patients will have allergy testing done to see if they are candidates for allergy desensitization, as allergies have been shown to aggravate Ménière’s symptoms.
Both prescription and over-the-counter medicine can be used to reduce nausea and vomiting during an episode. Included are antihistamines such as meclozine or dimenhydrinate, trimethobenzamide and other antiemetics, betahistine, diazepam, or ginger root. Betahistine, specifically, is of note because it is the only drug listed that has been proposed to prevent symptoms due to its vasodilation effect on the inner ear.
The antiherpes virus drug acyclovir has been used with some success to treat Ménière’s Disease. The likelihood of the effectiveness of the treatment was found to decrease with increasing duration of the disease, probably because viral suppression does not reverse damage. Morphological changes to the inner ear of Ménière’s sufferers have also been found in which it was considered likely to have resulted from attack by a herpes simplex virus. It was considered possible that long term treatment with acyclovir (greater than six months) would be required to produce an appreciable effect on symptoms. Herpes viruses have the ability to remain dormant in nerve cells by a process known as HHV Latency Associated Transcript. Continued administration of the drug should prevent reactivation of the virus and allow for the possibility of an improvement of symptoms. Another consideration is that different strains of a herpes virus can have different characteristics which may result in differences in the precise effects of the virus. Further confirmation that acyclovir can have a positive effect on Ménière’s symptoms has been reported.
Studies done over the use of transtympanic micropressure pulses have indicated promise with patients who had not been previously treated by gentamicin or surgery. Other studies suggest less clear results and propose that micropressure devices are simply placebos.
Sufferers tend to have high stress and anxiety due to the unpredictable nature of the disease. Healthy ways to combat this stress can include aromatherapy, yoga, t’ai chi, and meditation. Greenberg and Nedzelski recommend education to alleviate feelings of depression or helplessness.
If symptoms do not improve with typical treatment, more permanent surgery is considered. Unfortunately, because the inner ear deals with both balance and hearing, few surgeries guarantee no hearing loss.
Nondestructive surgeries include those which do not actively remove any functionality, but rather aim to improve the way the ear works Intratympanic steroid treatments involve injecting steroids (commonly dexamethasone) into the middle ear in order to reduce inflammation and alter inner ear circulation. Surgery to decompress the endolymphatic sac has shown to be effective for temporary relief from symptoms. Most patients see a decrease in vertigo occurrence, while their hearing may be unaffected. This treatment, however, does not address the long-term course of vertigo in Ménière’s disease. Danish studies even link this surgery to a very strong placebo effect, and that very little difference occurred in a 9-year followup, but could not deny the efficacy of the treatment.
Conversely, destructive surgeries are irreversible and involve removing entire functionality of most, if not all, of the affected ear. The inner ear itself can be surgically removed via labyrinthectomy although hearing is always completely lost in the affected ear with this operation. Alternatively, a chemical labyrinthectomy, in which a drug (such as gentamicin) that “kills” the vestibular apparatus is injected into the middle ear can accomplish the same results while retaining hearing. In more serious cases surgeons can cut the nerve to the balance portion of the inner ear in a vestibular neurectomy. Hearing is often mostly preserved, however the surgery involves cutting open into the lining of the brain, and a hospital stay of a few days for monitoring would be required. Vertigo (and the associated nausea and vomiting) typically accompany the recovery from destructive surgeries as the brain learns to compensate.
Physiotherapists also have a role in the management of Meniere’s disease. In vestibular rehabilitation, physiotherapists use interventions aimed at stabilizing gaze, reducing dizziness and increasing postural balance within the context of activities of daily living. After a vestibular assessment is conducted, the physiotherapist tailors the treatment plan to the needs of that specific patient.
The central nervous system (CNS) can be re-trained because of its plasticity, or alterability, as well as its repetitious pathways. During vestibular rehabilitation, physiotherapists take advantage of this characteristic of the CNS by provoking symptoms of dizziness or unsteadiness with head movements while allowing the visual, somatosensory and vestibular systems to interpret the information. This leads to a continuous decrease in symptoms.
Although a significant amount of research has been done regarding vestibular rehabilitation in other disorders, substantially less has been done specifically on Meniere’s disease. However, vestibular physiotherapy is currently accepted as part of best practices in the management of this condition.
Ménière’s disease usually starts confined to one ear, but it often extends to involve both ears over time. The number of patients who end up with bilaterial Ménière’s is debated, with ranges spanning from 17% to 75%.
Some Ménière’s disease sufferers, in severe cases, may end up losing their jobs, and will be on disability until the disease burns out However, a majority (60-80%) of sufferers will not need permanent disability and will recover with or without medical help.
Hearing loss usually fluctuates in the beginning stages and becomes more permanent in later stages, although hearing aids and cochlear implants can help remedy damage. Tinnitus can be unpredictable, but patients usually get used to it over time.
Ménière’s disease, being unpredictable, has a variable prognosis. Attacks could come more frequently and more severely, less frequently and less severely, and anywhere in between. However, Ménière’s is known to “burn out” when vestibular function has been destroyed to a stage where vertigo attacks cease.
Studies done on both right and left ear sufferers show that patients with their right ear affected tend to do significantly worse in cognitive performance. General intelligence was not hindered, and it was concluded that declining performance was related to how long the patient had been suffering from the disease.
Meningitis – Inflammation of the meninges, the membranes that envelop the brain and the spinal cord; may cause hearing loss or deafness. Meningitis is inflammation of the protective membranes covering the brain and spinal cord, known collectively as the meninges. The inflammation may be caused by infection with viruses, bacteria, or other microorganisms, and less commonly by certain drugs. Meningitis can be life-threatening because of the inflammation’s proximity to the brain and spinal cord; therefore the condition is classified as a medical emergency.
The most common symptoms of meningitis are headache and neck stiffness associated with fever, confusion or altered consciousness, vomiting, and an inability to tolerate light (photophobia) or loud noises (phonophobia). Sometimes, especially in small children, only nonspecific symptoms may be present, such as irritability and drowsiness. If a rash is present, it may indicate a particular cause of meningitis; for instance, meningitis caused by meningococcal bacteria may be accompanied by a characteristic rash.
A lumbar puncture may be used to diagnose or exclude meningitis. This involves inserting a needle into the spinal canal to extract a sample of cerebrospinal fluid (CSF), the fluid that envelops the brain and spinal cord. The CSF is then examined in a medical laboratory. The usual treatment for meningitis is the prompt application of antibiotics and sometimes antiviral drugs. In some situations, corticosteroid drugs can also be used to prevent complications from overactive inflammation. Meningitis can lead to serious long-term consequences such as deafness, epilepsy, hydrocephalus and cognitive deficits, especially if not treated quickly. Some forms of meningitis (such as those associated with meningococci, Haemophilus influenzae type B, pneumococci or mumps virus infections) may be prevented by immunization.
Signs and symptoms
Neck stiffness, Texas Meningitis Epidemic of 1911–12.
In adults, a severe headache is the most common symptom of meningitis – occurring in almost 90% of cases of bacterial meningitis, followed by nuchal rigidity (inability to flex the neck forward passively due to increased neck muscle tone and stiffness). The classic triad of diagnostic signs consists of nuchal rigidity, sudden high fever, and altered mental status; however, all three features are present in only 44–46% of all cases of bacterial meningitis. If none of the three signs is present, meningitis is extremely unlikely. Other signs commonly associated with meningitis include photophobia (intolerance to bright light) and phonophobia (intolerance to loud noises). Small children often do not exhibit the aforementioned symptoms, and may only be irritable and look unwell. In infants up to 6 months of age, bulging of the fontanelle (the soft spot on top of a baby’s head) may be present. Other features that might distinguish meningitis from less severe illnesses in young children are leg pain, cold extremities, and an abnormal skin color.
Nuchal rigidity occurs in 70% of adult cases of bacterial meningitis. Other signs of meningism include the presence of positive Kernig’s sign or Brudzinski’s sign. Kernig’s sign is assessed with the patient lying supine, with the hip and knee flexed to 90 degrees. In a patient with a positive Kernig’s sign, pain limits passive extension of the knee. A positive Brudzinski’s sign occurs when flexion of the neck causes involuntary flexion of the knee and hip. Although Kernig’s sign and Brudzinski neck sign are both commonly used to screen for meningitis, the sensitivity of these tests is limited. They do, however, have very good specificity for meningitis: the signs rarely occur in other diseases. Another test, known as the “jolt accentuation maneuver” helps determine whether meningitis is present in patients reporting fever and headache. The patient is told to rapidly rotate his or her head horizontally; if this does not make the headache worse, meningitis is unlikely.
Meningitis caused by the bacterium Neisseria meningitidis (known as “meningococcal meningitis”) can be differentiated from meningitis with other causes by a rapidly spreading petechial rash which may precede other symptoms. The rash consists of numerous small, irregular purple or red spots (“petechiae”) on the trunk, lower extremities, mucous membranes, conjuctiva, and (occasionally) the palms of the hands or soles of the feet. The rash is typically non-blanching: the redness does not disappear when pressed with a finger or a glass tumbler. Although this rash is not necessarily present in meningococcal meningitis, it is relatively specific for the disease; it does, however, occasionally occur in meningitis due to other bacteria. Other clues as to the nature of the cause of meningitis may be the skin signs of hand, foot and mouth disease and genital herpes, both of which are associated with various forms of viral meningitis.
A severe case of meningococcal meningitis in which the petechial rash progressed to gangrene and required amputation of all limbs. The patient, Charlotte Cleverley-Bisman, survived the disease and became a poster child for a meningitis vaccination campaign in New Zealand.
People with meningitis may develop additional problems in the early stages of their illness. These may require specific treatment, and sometimes indicate severe illness or worse prognosis. The infection may trigger sepsis, a systemic inflammatory response syndrome of falling blood pressure, fast heart rate, high or abnormally low temperature and rapid breathing. Very low blood pressure may occur early, especially but not exclusively in meningococcal illness; this may lead to insufficient blood supply to other organs. Disseminated intravascular coagulation, the excessive activation of blood clotting, may cause both the obstruction of blood flow to organs and a paradoxical increase of bleeding risk. In meningococcal disease, gangrene of limbs can occur. Severe meningococcal and pneumococcal infections may result in hemorrhaging of the adrenal glands, leading to Waterhouse-Friderichsen syndrome, which is often lethal.
The brain tissue may swell, with increasing pressure inside the skull and a risk of swollen brain tissue causing herniation. This may be noticed by a decreasing level of consciousness, loss of the pupillary light reflex, and abnormal posturing. Inflammation of the brain tissue may also obstruct the normal flow of CSF around the brain (hydrocephalus). Seizures may occur for various reasons; in children, seizures are common in the early stages of meningitis (30% of cases) and do not necessarily indicate an underlying cause. Seizures may result from increased pressure and from areas of inflammation in the brain tissue. Focal seizures (seizures that involve one limb or part of the body), persistent seizures, late-onset seizures and those that are difficult to control with medication are indicators of a poorer long-term outcome.
The inflammation of the meninges may lead to abnormalities of the cranial nerves, a group of nerves arising from the brain stem that supply the head and neck area and control eye movement, facial muscles and hearing, among other functions. Visual symptoms and hearing loss may persist after an episode of meningitis (see below). Inflammation of the brain (encephalitis) or its blood vessels (cerebral vasculitis), as well as the formation of blood clots in the veins (cerebral venous thrombosis), may all lead to weakness, loss of sensation, or abnormal movement or function of the part of the body supplied by the affected area in the brain.
Meningitis is usually caused by infection from viruses or microorganisms. Most cases are due to infection with viruses, with bacteria, fungi, and parasites being the next most common causes. It may also result from various non-infectious causes.
The types of bacteria that cause bacterial meningitis vary by age group. In premature babies and newborns up to three months old, common causes are group B streptococci (subtypes III which normally inhabit the vagina and are mainly a cause during the first week of life) and those that normally inhabit the digestive tract such as Escherichia coli (carrying K1 antigen). Listeria monocytogenes (serotype IVb) may affect the newborn and occurs in epidemics. Older children are more commonly affected by Neisseria meningitidis (meningococcus), Streptococcus pneumoniae (serotypes 6, 9, 14, 18 and 23) and those under five by Haemophilus influenzae type B (in countries that do not offer vaccination, see below). In adults, N. meningitidis and S. pneumoniae together cause 80% of all cases of bacterial meningitis, with increased risk of L. monocytogenes in those over 50 years old. Since the pneumococcal vaccine was introduced, however, rates of pneumococcal meningitis have declined in children and adults.
Recent trauma to the skull gives bacteria in the nasal cavity the potential to enter the meningeal space. Similarly, individuals with a cerebral shunt or related device (such as an extraventricular drain or Ommaya reservoir) are at increased risk of infection through those devices. In these cases, infections with staphylococci are more likely, as well as infections by pseudomonas and other Gram-negative bacilli. The same pathogens are also more common in those with an impaired immune system. In a small proportion of people, an infection in the head and neck area, such as otitis media or mastoiditis, can lead to meningitis. Recipients of cochlear implants for hearing loss are at an increased risk of pneumococcal meningitis.
Tuberculous meningitis, meningitis due to infection with Mycobacterium tuberculosis, is more common in those from countries where tuberculosis is common, but is also encountered in those with immune problems, such as AIDS.
Recurrent bacterial meningitis may be caused by persisting anatomical defects, either congenital or acquired, or by disorders of the immune system. Anatomical defects allow continuity between the external environment and the nervous system. The most common cause of recurrent meningitis is skull fracture, particularly fractures that affect the base of the skull or extend towards the sinuses and petrous pyramids. A literature review of 363 reported cases of recurrent meningitis showed that 59% of cases are due to such anatomical abnormalities, 36% due to immune deficiencies (such as complement deficiency, which predisposes especially to recurrent meningococcal meningitis), and 5% due to ongoing infections in areas adjacent to the meninges.
The term aseptic meningitis refers loosely to all cases of meningitis in which no bacterial infection can be demonstrated. This is usually due to viruses, but it may be due to bacterial infection that has already been partially treated, with disappearance of the bacteria from the meninges, or by infection in a space adjacent to the meninges (e.g. sinusitis). Endocarditis (infection of the heart valves with spread of small clusters of bacteria through the bloodstream) may cause aseptic meningitis. Aseptic meningitis may also result from infection with spirochetes, a type of bacteria that includes Treponema pallidum (the cause of syphilis) and Borrelia burgdorferi (known for causing Lyme disease). Meningitis may be encountered in cerebral malaria (malaria infecting the brain). Amoebic meningitis, meningitis due to infection with amoebae such as Naegleria fowleri is contracted from freshwater sources.
Viruses that can cause meningitis include enteroviruses, herpes simplex virus type 2 (and less commonly type 1), varicella zoster virus (known for causing chickenpox and shingles), mumps virus, HIV, and LCMV.
There are a number of risk factors for fungal meningitis including the use of immunosuppressants (such as after organ transplantation), HIV/AIDS, and the loss of immunity associated with aging. It is uncommon in those with a normal immune system. Symptom onset is typically more gradual with headaches and fever being present for at least a couple of weeks before diagnosis. The most common fungal meningitis is cryptococcal meningitis due to Cryptococcus neoformans. In Africa, cryptococcal meningitis is estimated to be the most common cause of meningitis overall where it accounts for 20-25% of AIDS-related deaths in Africa. Other common fugal agents include Histoplasma capsulatum, Coccidioides immitis, Blastomyces dermatitidis, and Candida species.
A parasitic cause is often assumed when there is a predominance of eosinophils (a type of white blood cell) in the CSF. The most common parasites implicated are Angiostrongylus cantonensis, Gnathostoma spinigerum, Schistosoma, as well as the conditions cysticercosis, toxocariasis, baylisascariasis, paragonimiasis, and a number of rarer infections and noninfective conditions.
Meningitis may occur as the result of several non-infectious causes: spread of cancer to the meninges (malignant or neoplastic meningitis) and certain drugs (mainly non-steroidal anti-inflammatory drugs, antibiotics and intravenous immunoglobulins). It may also be caused by several inflammatory conditions such as sarcoidosis (which is then called neurosarcoidosis), connective tissue disorders such as systemic lupus erythematosus, and certain forms of vasculitis (inflammatory conditions of the blood vessel wall) such as Behçet’s disease. Epidermoid cysts and dermoid cysts may cause meningitis by releasing irritant matter into the subarachnoid space. Mollaret’s meningitis is a syndrome of recurring episodes of aseptic meningitis; it is thought to be caused by herpes simplex virus type 2. Rarely, migraine may cause meningitis, but this diagnosis is usually only made when other causes have been eliminated.
The meninges comprise three membranes that, together with the cerebrospinal fluid, enclose and protect the brain and spinal cord (the central nervous system). The pia mater is a very delicate impermeable membrane that firmly adheres to the surface of the brain, following all the minor contours. The arachnoid mater (so named because of its spider-web-like appearance) is a loosely fitting sac on top of the pia mater. The subarachnoid space separates the arachnoid and pia mater membranes, and is filled with cerebrospinal fluid. The outermost membrane, the dura mater, is a thick durable membrane, which is attached to both the arachnoid membrane and the skull.
In bacterial meningitis, bacteria reach the meninges by one of two main routes: through the bloodstream or through direct contact between the meninges and either the nasal cavity or the skin. In most cases, meningitis follows invasion of the bloodstream by organisms that live upon mucous surfaces such as the nasal cavity. This is often in turn preceded by viral infections, which break down the normal barrier provided by the mucous surfaces. Once bacteria have entered the bloodstream, they enter the subarachnoid space in places where the blood–brain barrier is vulnerable—such as the choroid plexus. Meningitis occurs in 25% of newborns with bloodstream infections due to group B streptococci; this phenomenon is less common in adults. Direct contamination of the cerebrospinal fluid may arise from indwelling devices, skull fractures, or infections of the nasopharynx or the nasal sinuses that have formed a tract with the subarachnoid space (see above); occasionally, congenital defects of the dura mater can be identified.
The large-scale inflammation that occurs in the subarachnoid space during meningitis is not a direct result of bacterial infection but can rather largely be attributed to the response of the immune system to the entrance of bacteria into the central nervous system. When components of the bacterial cell membrane are identified by the immune cells of the brain (astrocytes and microglia), they respond by releasing large amounts of cytokines, hormone-like mediators that recruit other immune cells and stimulate other tissues to participate in an immune response. The blood–brain barrier becomes more permeable, leading to “vasogenic” cerebral edema (swelling of the brain due to fluid leakage from blood vessels). Large numbers of white blood cells enter the CSF, causing inflammation of the meninges, and leading to “interstitial” edema (swelling due to fluid between the cells). In addition, the walls of the blood vessels themselves become inflamed (cerebral vasculitis), which leads to a decreased blood flow and a third type of edema, “cytotoxic” edema. The three forms of cerebral edema all lead to an increased intracranial pressure; together with the lowered blood pressure often encountered in acute infection, this means that it is harder for blood to enter the brain, and brain cells are deprived of oxygen and undergo apoptosis (automated cell death).
It is recognized that administration of antibiotics may initially worsen the process outlined above, by increasing the amount of bacterial cell membrane products released through the destruction of bacteria. Particular treatments, such as the use of corticosteroids, are aimed at dampening the immune system’s response to this phenomenon.
CSF findings in different forms of meningitis
Type of meningitis
often > 300/mm³
|Acute viral||normal||normal or high||mononuclear,
PMNs, < 300/mm³
Blood tests and imaging
In someone suspected of having meningitis, blood tests are performed for markers of inflammation (e.g. C-reactive protein, complete blood count), as well as blood cultures.
The most important test in identifying or ruling out meningitis is analysis of the cerebrospinal fluid through lumbar puncture (LP, spinal tap). However, lumbar puncture is contraindicated if there is a mass in the brain (tumor or abscess) or the intracranial pressure (ICP) is elevated, as it may lead to brain herniation. If someone is at risk for either a mass or raised ICP (recent head injury, a known immune system problem, localizing neurological signs, or evidence on examination of a raised ICP), a CT or MRI scan is recommended prior to the lumbar puncture. This applies in 45% of all adult cases. If a CT or MRI is required before LP, or if LP proves difficult, professional guidelines suggest that antibiotics should be administered first to prevent delay in treatment, especially if this may be longer than 30 minutes. Often, CT or MRI scans are performed at a later stage to assess for complications of meningitis.
In severe forms of meningitis, monitoring of blood electrolytes may be important; for example, hyponatremia is common in bacterial meningitis, due to a combination of factors including dehydration, the inappropriate excretion of the antidiuretic hormone (SIADH), or overly aggressive intravenous fluid administration.
A lumbar puncture is done by positioning the patient, usually lying on the side, applying local anesthetic, and inserting a needle into the dural sac (a sac around the spinal cord) to collect cerebrospinal fluid (CSF). When this has been achieved, the “opening pressure” of the CSF is measured using a manometer. The pressure is normally between 6 and 18 cm water (cmH2O); in bacterial meningitis the pressure is typically elevated. The initial appearance of the fluid may prove an indication of the nature of the infection: cloudy CSF indicates higher levels of protein, white and red blood cells and/or bacteria, and therefore may suggest bacterial meningitis.
Gram stain of meningococci from a culture showing Gram negative (pink) bacteria, often in pairs
The CSF sample is examined for presence and types of white blood cells, red blood cells, protein content and glucose level. Gram staining of the sample may demonstrate bacteria in bacterial meningitis, but absence of bacteria does not exclude bacterial meningitis as they are only seen in 60% of cases; this figure is reduced by a further 20% if antibiotics were administered before the sample was taken, and Gram staining is also less reliable in particular infections such as listeriosis. Microbiological culture of the sample is more sensitive (it identifies the organism in 70–85% of cases) but results can take up to 48 hours to become available. The type of white blood cell predominantly present (see table) indicates whether meningitis is bacterial (usually neutrophil-predominant) or viral (usually lymphocyte-predominant), although in the beginning of the disease this is not always a reliable indicator. Less commonly, eosinophils predominate, suggesting parasitic or fungal etiology, among others.
The concentration of glucose in CSF is normally above 40% of that in blood. In bacterial meningitis it is typically lower; the CSF glucose level is therefore divided by the blood glucose (CSF glucose to serum glucose ratio). A ratio ≤0.4 is indicative of bacterial meningitis; in the newborn, glucose levels in CSF are normally higher, and a ratio below 0.6 (60%) is therefore considered abnormal. High levels of lactate in CSF indicate a higher likelihood of bacterial meningitis, as does a higher white blood cell count.
Various more specialized tests may be used to distinguish between various types of meningitis. A latex agglutination test may be positive in meningitis caused by Streptococcus pneumoniae, Neisseria meningitidis, Haemophilus influenzae, Escherichia coli and group B streptococci; its routine use is not encouraged as it rarely leads to changes in treatment, but it may be used if other tests are not diagnostic. Similarly, the limulus lysate test may be positive in meningitis caused by Gram-negative bacteria, but it is of limited use unless other tests have been unhelpful. Polymerase chain reaction (PCR) is a technique used to amplify small traces of bacterial DNA in order to detect the presence of bacterial or viral DNA in cerebrospinal fluid; it is a highly sensitive and specific test since only trace amounts of the infecting agent’s DNA is required. It may identify bacteria in bacterial meningitis and may assist in distinguishing the various causes of viral meningitis (enterovirus, herpes simplex virus 2 and mumps in those not vaccinated for this). Serology (identification of antibodies to viruses) may be useful in viral meningitis. If tuberculous meningitis is suspected, the sample is processed for Ziehl-Neelsen stain, which has a low sensitivity, and tuberculosis culture, which takes a long time to process; PCR is being used increasingly. Diagnosis of cryptococcal meningitis can be made at low cost using an India ink stain of the CSF; however, testing for cryptococcal antigen in blood or CSF is more sensitive, particularly in persons with AIDS.
A diagnostic and therapeutic conundrum is the “partially treated meningitis”, where there are meningitis symptoms after receiving antibiotics (such as for presumptive sinusitis). When this happens, CSF findings may resemble those of viral meningitis, but antibiotic treatment may need to be continued until there is definitive positive evidence of a viral cause (e.g. a positive enterovirus PCR).
Histopathology of bacterial meningitis: autopsy case of a patient with pneumococcal meningitis showing inflammatory infiltrates of the pia mater consisting of neutrophil granulocytes (inset, higher magnification).
Meningitis can be diagnosed after death has occurred. The findings from a post mortem are usually a widespread inflammation of the pia mater and arachnoid layers of the meninges covering the brain and spinal cord. Neutrophil granulocytes tend to have migrated to the cerebrospinal fluid and the base of the brain, along with cranial nerves and the spinal cord, may be surrounded with pus—as may the meningeal vessels.
Bacterial and viral meningitis are contagious. Neither are as contagious as the common cold or flu. Both can be transmitted through droplets of respiratory secretions during close contact such as kissing, sneezing or coughing on someone, but cannot be spread by only breathing the air where a person with meningitis has been. Viral meningitis is typically caused by Enteroviruses, and is most commonly spread through fecal contamination. By changing behavior to prevent the causes of transmission, infection by viruses and bacteria can be prevented.
For some causes of meningitis, prophylaxis can be provided in the long term with vaccine, or in the short term with antibiotics.
Since the 1980s, many countries have included immunization against Haemophilus influenzae type B in their routine childhood vaccination schemes. This has practically eliminated this pathogen as a cause of meningitis in young children in those countries. In the countries where the disease burden is highest, however, the vaccine is still too expensive. Similarly, immunization against mumps has led to a sharp fall in the number of cases of mumps meningitis, which prior to vaccination occurred in 15% of all cases of mumps.
Meningococcus vaccines exist against groups A, C, W135 and Y. In countries where the vaccine for meningococcus group C was introduced, cases caused by this pathogen have decreased substantially. A quadrivalent vaccine now exists, which combines all four vaccines. Immunization with the ACW135Y vaccine against four strains is now a visa requirement for taking part in the Hajj. Development of a vaccine against group B meningococci has proved much more difficult, as its surface proteins (which would normally be used to make a vaccine) only elicit a weak response from the immune system, or cross-react with normal human proteins. Still, some countries (New Zealand, Cuba, Norway and Chile) have developed vaccines against local strains of group B meningococci; some have shown good results and are used in local immunization schedules. In Africa, until recently, the approach for prevention and control of meningococcal epidemics was based on early detection of the disease and emergency reactive mass vaccination of the at-risk population with bivalent A/C or trivalent A/C/W135 polysaccharide vaccines, though the introduction of MenAfriVac (meningiococcus group A vaccine) has demonstrated effectiveness in young people and has been described as a model for product development partnerships in resource-limited settings.
Routine vaccination against Streptococcus pneumoniae with the pneumococcal conjugate vaccine (PCV), which is active against seven common serotypes of this pathogen, significantly reduces the incidence of pneumococcal meningitis. The pneumococcal polysaccharide vaccine, which covers 23 strains, is only administered in certain groups (e.g. those who have had a splenectomy, the surgical removal of the spleen); it does not elicit a significant immune response in all recipients, e.g. small children.
Childhood vaccination with Bacillus Calmette-Guérin has been reported to significantly reduce the rate of tuberculous meningitis, but its waning effectiveness in adulthood has prompted a search for a better vaccine.
Short-term antibiotic prophylaxis is also a method of prevention, particularly of meningococcal meningitis. In cases of meningococcal meningitis, prophylactic treatment of close contacts with antibiotics (e.g. rifampicin, ciprofloxacin or ceftriaxone) can reduce their risk of contracting the condition, but does not protect against future infections.
Meningitis is potentially life-threatening and has a high mortality rate if untreated; delay in treatment has been associated with a poorer outcome. Thus treatment with wide-spectrum antibiotics should not be delayed while confirmatory tests are being conducted. If meningococcal disease is suspected in primary care, guidelines recommend that benzylpenicillin be administered before transfer to hospital. Intravenous fluids should be administered if hypotension (low blood pressure) or shock are present. Given that meningitis can cause a number of early severe complications, regular medical review is recommended to identify these complications early, as well as admission to an intensive care unit if deemed necessary.
Mechanical ventilation may be needed if the level of consciousness is very low, or if there is evidence of respiratory failure. If there are signs of raised intracranial pressure, measures to monitor the pressure may be taken; this would allow the optimization of the cerebral perfusion pressure and various treatments to decrease the intracranial pressure with medication (e.g. mannitol). Seizures are treated with anticonvulsants. Hydrocephalus (obstructed flow of CSF) may require insertion of a temporary or long-term drainage device, such as a cerebral shunt.
Structural formula of ceftriaxone, one of the third-generation cefalosporin antibiotics recommended for the initial treatment of bacterial meningitis.
Empiric antibiotics (treatment without exact diagnosis) must be started immediately, even before the results of the lumbar puncture and CSF analysis are known. The choice of initial treatment depends largely on the kind of bacteria that cause meningitis in a particular place. For instance, in the United Kingdom empirical treatment consists of a third-generation cefalosporin such as cefotaxime or ceftriaxone. In the USA, where resistance to cefalosporins is increasingly found in streptococci, addition of vancomycin to the initial treatment is recommended. Empirical therapy may be chosen on the basis of the age of the patient, whether the infection was preceded by head injury, whether the patient has undergone neurosurgery and whether or not a cerebral shunt is present. For instance, in young children and those over 50 years of age, as well as those who are immunocompromised, addition of ampicillin is recommended to cover Listeria monocytogenes. Once the Gram stain results become available, and the broad type of bacterial cause is known, it may be possible to change the antibiotics to those likely to deal with the presumed group of pathogens.
The results of the CSF culture generally take longer to become available (24–48 hours). Once they do, empiric therapy may be switched to specific antibiotic therapy targeted to the specific causative organism and its sensitivities to antibiotics. For an antibiotic to be effective in meningitis, it must not only be active against the pathogenic bacterium, but also reach the meninges in adequate quantities; some antibiotics have inadequate penetrance and therefore have little use in meningitis. Most of the antibiotics used in meningitis have not been tested directly on meningitis patients in clinical trials. Rather, the relevant knowledge has mostly derived from laboratory studies in rabbits.
Tuberculous meningitis requires prolonged treatment with antibiotics. While tuberculosis of the lungs is typically treated for six months, those with tuberculous meningitis are typically treated for a year or longer. In tuberculous meningitis there is a strong evidence base for treatment with corticosteroids, although this evidence is restricted to those without AIDS.
Adjuvant treatment with corticosteroids (usually dexamethasone) has been shown in some studies to reduce rates of mortality, severe hearing loss and neurological damage in adolescents and adults from high income countries which have low rates of HIV. The likely mechanism is suppression of overactive inflammation. Professional guidelines therefore recommend the commencement of dexamethasone or a similar corticosteroid just before the first dose of antibiotics is given, and continued for four days. Given that most of the benefit of the treatment is confined to those with pneumococcal meningitis, some guidelines suggest that dexamethasone be discontinued if another cause for meningitis is identified.
Adjuvant corticosteroids have a different role in children than in adults. Though the benefit of corticosteroids has been demonstrated in adults as well as in children from high-income countries, their use in children from low-income countries is not supported by evidence; the reason for this discrepancy is not clear. Even in high-income countries, the benefit of corticosteroids is only seen when they are given prior to the first dose of antibiotics, and is greatest in cases of H. influenzae meningitis, the incidence of which has decreased dramatically since the introduction of the Hib vaccine. Thus, corticosteroids are recommended in the treatment of pediatric meningitis if the cause is H. influenzae and only if given prior to the first dose of antibiotics, whereas other uses are controversial.
A 2010 analysis of previous studies has shown that the benefit from steroids may not be as significant as previously found. The one possible significant benefit is reduction of hearing loss in survivors, and adverse neurological outcomes.
Viral meningitis typically requires supportive therapy only; most viruses responsible for causing meningitis are not amenable to specific treatment. Viral meningitis tends to run a more benign course than bacterial meningitis. Herpes simplex virus and varicella zoster virus may respond to treatment with antiviral drugs such as aciclovir, but there are no clinical trials that have specifically addressed whether this treatment is effective. Mild cases of viral meningitis can be treated at home with conservative measures such as fluid, bedrest, and analgesics.
Fungal meningitis, such as cryptococcal meningitis, is treated with long courses of highly dosed antifungals, such as amphotericin B and flucytosine. Raised intracranial pressure is common in fungal meningitis, and frequent (ideally daily) lumbar punctures to relieve the pressure are recommended, or alternatively a lumbar drain.
Untreated, bacterial meningitis is almost always fatal. Viral meningitis, in contrast, tends to resolve spontaneously and is rarely fatal. With treatment, mortality (risk of death) from bacterial meningitis depends on the age of the patient and the underlying cause. Of the newborn patients, 20–30% may die from an episode of bacterial meningitis. This risk is much lower in older children, whose mortality is about 2%, but rises again to about 19–37% in adults. Risk of death is predicted by various factors apart from age, such as the pathogen and the time it takes for the pathogen to be cleared from the cerebrospinal fluid, the severity of the generalized illness, decreased level of consciousness or abnormally low count of white blood cells in the CSF. Meningitis caused by H. influenzae and meningococci has a better prognosis compared to cases caused by group B streptococci, coliforms and S. pneumonia. In adults, too, meningococcal meningitis has a lower mortality (3–7%) than pneumococcal disease.
In children there are several potential disabilities which result from damage to the nervous system. Sensorineural hearing loss, epilepsy, learning and behavioral difficulties, as well as decreased intelligence, occur in about 15% of survivors. Some of the hearing loss may be reversible. In adults, 66% of all cases emerge without disability. The main problems are deafness (in 14%) and cognitive impairment (in 10%).
Although meningitis is a notifiable disease in many countries, the exact incidence rate is unknown. Bacterial meningitis occurs in about 3 people per 100,000 annually in Western countries. Population-wide studies have shown that viral meningitis is more common, at 10.9 per 100,000, and occurs more often in the summer. In Brazil, the rate of bacterial meningitis is higher, at 45.8 per 100,000 annually. Sub-Saharan Africa has been plagued by large epidemics of meningococcal meningitis for over a century, leading to it being labeled the “meningitis belt”. Epidemics typically occur in the dry season (December to June), and an epidemic wave can last two to three years, dying out during the intervening rainy seasons. Attack rates of 100–800 cases per 100,000 are encountered in this area, which is poorly served by medical care. These cases are predominantly caused by meningococci. The largest epidemic ever recorded in history swept across the entire region in 1996–1997, causing over 250,000 cases and 25,000 deaths.
Meningococcal disease occurs in epidemics in areas where many people live together for the first time, such as army barracks during mobilization, college campuses and the annual Hajj pilgrimage. Although the pattern of epidemic cycles in Africa is not well understood, several factors have been associated with the development of epidemics in the meningitis belt. They include: medical conditions (immunological susceptibility of the population), demographic conditions (travel and large population displacements), socioeconomic conditions (overcrowding and poor living conditions), climatic conditions (drought and dust storms), and concurrent infections (acute respiratory infections).
There are significant differences in the local distribution of causes for bacterial meningitis. For instance, while N. meningitides groups B and C cause most disease episodes in Europe, group A is found in Asia and continues to predominate in Africa, where it causes most of the major epidemics in the meningitis belt, accounting for about 80% to 85% of documented meningococcal meningitis cases.
Some suggest that Hippocrates may have realized the existence of meningitis, and it seems that meningism was known to pre-Renaissance physicians such as Avicenna. The description of tuberculous meningitis, then called “dropsy in the brain”, is often attributed to Edinburgh physician Sir Robert Whytt in a posthumous report that appeared in 1768, although the link with tuberculosis and its pathogen was not made until the next century.
It appears that epidemic meningitis is a relatively recent phenomenon. The first recorded major outbreak occurred in Geneva in 1805. Several other epidemics in Europe and the United States were described shortly afterward, and the first report of an epidemic in Africa appeared in 1840. African epidemics became much more common in the 20th century, starting with a major epidemic sweeping Nigeria and Ghana in 1905–1908.
The first report of bacterial infection underlying meningitis was by the Austrian bacteriologist Anton Weichselbaum who in 1887 described the meningococcus. Mortality from meningitis was very high (over 90%) in early reports. In 1906, antiserum was produced in horses; this was developed further by the American scientist Simon Flexner and markedly decreased mortality from meningococcal disease. In 1944, penicillin was first reported to be effective in meningitis. The introduction in the late 20th century of Haemophilus vaccines led to a marked fall in cases of meningitis associated with this pathogen, and in 2002, evidence emerged that treatment with steroids could improve the prognosis of bacterial meningitis.
Middle Ear – Part of the ear that includes the eardrum and three tiny bones (ossicles) of the middle ear, ending at the oval window that leads to the inner ear. The mammalian middle ear contains three ossicles, which couple vibration of the eardrum into waves in the fluid and membranes of the inner ear. The hollow space of the middle ear has also been called the tympanic cavity, or cavum tympani. The eustachian tube joins the tympanic cavity with the nasal cavity (nasopharynx), allowing pressure to equalize between the middle ear and throat.
The primary function of the middle ear is to efficiently transfer acoustic energy from compression waves in air to fluid–membrane waves within the cochlea
Ordinarily, when sound waves in air strike liquid, most of the energy is reflected off the surface of the liquid. The middle ear allows the impedance matching of sound traveling in air to acoustic waves traveling in a system of fluids and membranes in the inner ear. This system should not be confused, however, with the propagation of sound as compression waves in a liquid.
The middle ear couples sound from air to the fluid via the oval window, using the principle of “mechanical advantage” in the form of the “hydraulic principle” and the “lever principle”. The vibratory portion of the tympanic membrane (eardrum) is many times the surface area of the footplate of the stapes (the third ossicular bone which attaches to the oval window; furthermore, the shape of the articulated ossicular chain is like a lever, the long arm being the long process of the malleus, the fulcrum being the body of the incus, and the short arm being the lenticular process of the incus. The collected pressure of sound vibration that strikes the tympanic membrane is therefore concentrated down to this much smaller area of the footplate, increasing the force but reducing the velocity and displacement, and thereby coupling the acoustic energy.
The middle ear is able to dampen sound conduction substantially when faced with very loud sound, by noise-induced reflex contraction of the middle-ear muscles.
The middle ear contains three tiny bones known as the ossicles: malleus, incus, and stapes. The ossicles were given their Latin names for their distinctive shapes; they are also referred to as the hammer, anvil, and stirrup, respectively. The ossicles directly couple sound energy from the ear drum to the oval window of the cochlea. While the stapes is present in all tetrapods, the malleus and incus evolved from lower and upper jaw bones present in reptiles. See Evolution of mammalian auditory ossicles.
The ossicles are classically supposed to mechanically convert the vibrations of the eardrum, into amplified pressure waves in the fluid of the cochlea (or inner ear) with a lever arm factor of 1.3. Since the area of the eardrum is about 17 fold larger than that of the oval window, the sound pressure is concentrated, leading to a pressure gain of at least 22. The eardrum is merged to the malleus, which connects to the incus, which in turn connects to the stapes. Vibrations of the stapes footplate introduce pressure waves in the inner ear. There is a steadily increasing body of evidence that shows that the lever arm ratio is actually variable, depending on frequency. Between 0.1 and 1 kHz it is approximately 2, it then rises to around 5 at 2 kHz and then falls off steadily above this frequency. The measurement of this lever arm ratio is also somewhat complicated by the fact that the ratio is generally given in relation to the tip of the malleus (also known as the umbo) and the level of the middle of the stapes. The eardrum is actually attached to the malleus handle over about a 0.5 cm distance. In addition the eardrum itself moves in a very chaotic fashion at frequencies >3 kHz. The linear attachment of the eardrum to the malleus actually smooths out this chaotic motion and allows the ear to respond linearly over a wider frequency range than a point attachment. The auditory ossicles can also reduce sound pressure (the inner ear is very sensitive to overstimulation), by uncoupling each other through particular muscles.
The middle ear efficiency peaks at a frequency of around 1 kHz. The combined transfer function of the outer ear and middle ear gives humans a peak sensitivity to frequencies between 1 kHz and 3 kHz.
The movement of the ossicles may be stiffened by two muscles. The stapedius muscle, the smallest skeletal muscle in the body, connects to the stapes and is controlled by the facial nerve; the tensor tympani muscle connects to the base of the malleus and is under the control of the trigeminal nerve. These muscles contract in response to loud sounds, thereby reducing the transmission of sound to the inner ear. This is called the acoustic reflex or Tympanic reflex.
Of surgical importance are two branches of the facial nerve that also pass through the middle ear space. These are the horizontal and chorda tympani branches of the facial nerve. Damage to the horizontal branch during surgery can lead to partial mastoid process paralysis
The middle ear of tetrapods is homologous with the spiracle of fishes, an opening from the pharynx to the side of the head in front of the main gill slits. In fish embryos, the spiracle forms as a pouch in the pharynx, which grows outward and breaches the skin to form an opening; in most tetrapods, this breach is never quite completed, and the final vestige of tissue separating it from the outside world becomes the eardrum. The inner part of the spiracle, still connected to the pharynx, forms the eustachian tube.
In reptiles, birds, and early fossil tetrapods, there is only a single auditory ossicle, the stapes. This runs directly from the eardrum to the fenestra ovalis.
The structure of the middle ear in living amphibians varies considerably, and is often degenerate. In most frogs and toads, it is similar to that of reptiles, but in other amphibians, the middle ear cavity is often absent. In these cases, the stapes either is also missing or, in the absence of an eardrum, connects to the quadrate bone in the skull, although, it is presumed, it still has some ability to transmit vibrations to the inner ear. In many amphibians, there is also a second auditory ossicle, the operculum(not to be confused with the structure of the same name in fishes). This is a flat, plate-like bone, overlying the fenestra ovalis, and connecting it either to the stapes or, via a special muscle, to the scapula. It is not found in any other vertebrates.
Mammals are unique in having three ear bones, which allow for finer detection of sound. The malleus has evolved from the articular bone of the lower jaw, and the incus from the quadrate. In other vertebrates, these bones form the joint of the jaw, but the expansion of the dentary bone in mammals has allowed those animals to develop an entirely new jaw joint, freeing up the old joint to become part of the ear. In many mammals, the middle ear also becomes protected by a bony sheath, the auditory bulla, not found in other vertebrates. This is often a separate structure, but, in humans, it is part of the temporal bone.
Disorders of the middle ear
The middle ear is hollow. If the animal moves to a high-altitude environment, or dives into the water, there will be a pressure difference between the middle ear and the outside environment. This pressure will pose a risk of bursting or otherwise damaging the tympanum if it is not relieved. If middle ear pressure remains low, the ear drum may become retracted into the middle ear. One of the functions of the Eustachian tubes that connect the middle ear to the nasopharynx is to help keep middle ear pressure the same as air pressure. The Eustachian tubes are normally pinched off at the nose end, to prevent being clogged with mucus, but they may be opened by lowering and protruding the jaw; this is why yawning or chewing helps relieve the pressure felt in the ears when on board an aircraft.
Otitis media is an inflammation of the middle ear.
Motion Sickness – Dizziness, sweating, nausea, vomiting, and generalized discomfort experienced when an individual is in motion.
Mixed hearing loss – A hearing loss which is a combination of conductive and sensorineural impairments.
Multi-channel adaptive directional microphones – an adaptive directional microphone system which can manage multiple noise sources at the same time.
Multiple directional microphones – see omni-directional microphone.
Multi-channel technology – Technology which electronically separates the incoming sound into bands and adjusts the sound intensity in each band independently. The benefit is a hearing aid that more finely tailors the frequency response and compression characteristics to each user’s unique hearing needs.
Misarticulation – Inaccurately produced speech sound (phoneme) or sounds
Motor Speech Disorders – Group of disorders caused by the inability to accurately produce speech sounds (phonemes).