Introduction
Meningitis is an acute inflammatory condition. It affects the three lining layers of brain and spinal cord called the meninges. They form the protective coat around the delicate and important structures of central nervous system. An infection, possibly viral or bacterial to these meninges can cause severe damage to the nervous system and can be fatal if not attended immediately. Though it can affect anyone despite gender, age or race, kids are more prone to development of meningitis. As many of the early signs can be very mild, negligible and confusing with other diseases, chances are high that they are neglected or wrongly diagnosed. The disease can get worse so fast that even death can happen if not proper treatment is not given as soon as possible.
Signs & symptoms
Signs and symptoms of meningitis can develop within hours or days and may include:
- Confusion
- Fever
- Headache
- Numbness in your face
- Sensitivity to light
- Stiff neck, difficulty to lower chin to chest
- Stomach problems or vomiting
- Severe headache with nausea or vomiting
- Difficult to concentrate
- Seizures
- Excessive sleep or a hard time waking up
- Lack of appetite & thirst
- Skin rashes (in meningococcal meningitis)
Symptoms of meningitis in infants
In infants, meningitis symptoms may include:
- High fever
- Crying that’s constant and gets louder when you hold the baby
- Baby seems overly sleepy, sluggish, or inactive
- Stiff neck or body
- Bulge on the soft area on the top of the baby’s head
- Does not feed properly
- Crankiness
Causes
Meningitis almost always results from a bacterial or viral infection that begins somewhere else in your body, like ears, sinuses, or throat.
Less common causes of meningitis include:
- Autoimmune disorders
- Cancer medications
- Syphilis
- Tuberculosis
Meningitis can be classified according to the infection.
- Bacterial meningitis
It’s an extremely serious illness and a medical emergency. It can be fatal and lead to brain damage if not managed quickly.
Many strains of bacteria can cause bacterial meningitis. The most common ones among them are:
Streptococcus pneumoniae (pneumococcus)
Neisseria meningitidis (meningococcus)
Listeria monocytogenes (in older people, pregnant women, or those with immune system problems)
A bacterium called Haemophilus influenzae type b (Hib) was a common cause of meningitis in babies and young children until the Hib vaccine became available for infants. There are also vaccines for Neisseria meningitidis and Streptococcus pneumoniae. Experts recommend that all children get them, as well as all adults who are at a higher risk for the disease.
In many cases, bacterial meningitis starts when bacteria get into the bloodstream from the sinuses, ears or throat. The bacteria travel through the bloodstream to the brain.
The bacteria that cause meningitis can spread when infected people cough or sneeze.
- Viral meningitis
Viral meningitis is more common than the bacterial but less serious in most cases. A number of viruses can trigger the disease, including those which cause diarrhoea.
- Fungal meningitis
Fungal meningitis is much less common than the bacterial or viral forms. Healthy people rarely get it. People with a compromised immune system, are prone to such infection.
- Parasitic meningitis
Parasitic meningitis is also rare. It’s caused by parasites that usually affect animals. Humans get it from eating animals like snails, slugs, snakes, fish, or poultry that are infected by parasites or their eggs. The risk is higher with raw or undercooked foods. This type of meningitis is not contagious.
- Amoebic meningitis
Amoebic meningitis is a rare, usually fatal infection by a single-celled bug called Naegleria fowleri. This amoeba lives in soil or warm, fresh water, but not salt water. People typically get it from swimming in water where the amoeba lives, not drinking it. Amoebic meningitis isn’t contagious.
- Non-infectious meningitis
Non-infectious meningitis is caused by diseases like lupus or cancer, or after a head injury, brain surgery, or by taking certain medications. It isn’t contagious.
- Chronic meningitis
Chronic meningitis has similar symptoms as acute meningitis, but develops over a couple of weeks. It results from infections with a fungus or the mycobacteria that cause tuberculosis. These organisms get into the tissue and fluid surrounding your brain to cause meningitis.
Pathophysiology
Most cases of meningitis are caused by an infectious agent that has colonized or established a localized infection elsewhere in the host. Potential sites of colonization or infection include the skin, the nasopharynx, the respiratory tract, the gastrointestinal (GI) tract, and the genitourinary tract. The organism invades the submucosa at these sites by circumventing host defences (e.g., physical barriers, local immunity, and phagocytes or macrophages).
An infectious agent (i.e., a bacterium, virus, fungus, or parasite) can gain access to the CNS and cause meningeal disease via any of the 3 following major pathways:
- Invasion of the bloodstream (i.e., bacteraemia, viremia, fungemia, or parasitaemia) and subsequent hematogenous seeding of the CNS
- A retrograde neuronal (e.g., olfactory and peripheral nerves) pathway (e.g., Naegleria fowlerior Gnathostoma spinigerum)
- Direct contiguous spread (e.g., sinusitis, otitis media, congenital malformations, trauma, or direct inoculation during intracranial manipulation)
Invasion of the bloodstream and subsequent seeding is the most common mode of spread for most agents. This pathway is characteristic of meningococcal, cryptococcal, syphilitic, and pneumococcal meningitis.
Rarely, meningitis arises from invasion via septic thrombi or osteomyelitic erosion from infected contiguous structures. Meningeal seeding may also occur with a direct bacterial inoculate during trauma, neurosurgery, or instrumentation. Meningitis in the new-born may be transmitted vertically, involving pathogens that have colonized the maternal intestinal or genital tract, or horizontally, from nursery personnel or caregivers at home.
Local extension from contiguous extracerebral infection (e.g., otitis media, mastoiditis, or sinusitis) is a common cause. Possible pathways for the migration of pathogens from the middle ear to the meninges include the following:
- The bloodstream
- Preformed tissue planes (e.g., posterior fossa)
- Temporal bone fractures
- The oval or round window membranes of the labyrinths
The brain is naturally protected from the body’s immune system by the barrier that the meninges create between the bloodstream and the brain. Normally, this protection is an advantage because the barrier prevents the immune system from attacking the brain. However, in meningitis, the blood-brain barrier can become disrupted; once bacteria or other organisms have found their way to the brain, they are somewhat isolated from the immune system and can spread.
When the body tries to fight the infection, the problem can worsen; blood vessels become leaky and allow fluid, WBCs, and other infection-fighting particles to enter the meninges and brain. This process, in turn, causes brain swelling and can eventually result in decreasing blood flow to parts of the brain, worsening the symptoms of infection.
Depending on the severity of bacterial meningitis, the inflammatory process may remain confined to the subarachnoid space. In less severe forms, the pial barrier is not penetrated, and the underlying parenchyma remains intact. However, in more severe forms of bacterial meningitis, the pial barrier is breached, and the underlying parenchyma is invaded by the inflammatory process. Thus, bacterial meningitis may lead to widespread cortical destruction, particularly when left untreated.
Replicating bacteria, increasing numbers of inflammatory cells, cytokine-induced disruptions in membrane transport, and increased vascular and membrane permeability perpetuate the infectious process in bacterial meningitis. These processes account for the characteristic changes in CSF cell count, pH, lactate, protein, and glucose in patients with this disease.
Exudates extend throughout the CSF, particularly to the basal cisterns, resulting in the following:
- Damage to cranial nerves (e.g., cranial nerve VIII, with resultant hearing loss)
- Obliteration of CSF pathways (causing obstructive hydrocephalus)
- Induction of vasculitis and thrombophlebitis (causing local brain ischemia)
Intracranial pressure and cerebral fluid
One complication of meningitis is the development of increased intracranial pressure (ICP). The pathophysiology of this complication is complex and may involve many proinflammatory molecules as well as mechanical elements. Interstitial oedema (secondary to obstruction of CSF flow, as in hydrocephalus), cytotoxic oedema (swelling of cellular elements of the brain through the release of toxic factors from the bacteria and neutrophils), and vasogenic oedema (increased blood brain barrier permeability) are all thought to play a role.
Without medical intervention, the cycle of decreasing CSF, worsening cerebral oedema, and increasing ICP proceeds unchecked. Ongoing endothelial injury may result in vasospasm and thrombosis, further compromising CSF, and may lead to stenosis of large and small vessels. Systemic hypotension (septic shock) also may impair CSF, and the patient soon dies as a consequence of systemic complications or diffuse CNS ischemic injury.
Cerebral oedema
The increased CSF viscosity resulting from the influx of plasma components into the subarachnoid space and diminished venous outflow lead to interstitial oedema. The accumulation of the products of bacterial degradation, neutrophils, and other cellular activation leads to cytotoxic oedema.
The ensuing cerebral oedema (i.e., vasogenic, cytotoxic, and interstitial) significantly contributes to intracranial hypertension and a consequent decrease in cerebral blood flow. Anaerobic metabolism ensues, which contributes to increased lactate concentration and hypoglycorrhachia. In addition, hypoglycorrhachia results from decreased glucose transport into the spinal fluid compartment. Eventually, if this uncontrolled process is not modulated by effective treatment, transient neuronal dysfunction or permanent neuronal injury results.
Cytokines and secondary mediators in bacterial meningitis
Key advances in understanding the pathophysiology of meningitis include insight into the pivotal roles of cytokines (e.g., tumour necrosis factor alpha [TNF-α] and interleukin [IL]-1), chemokines (IL-8), and other proinflammatory molecules in the pathogenesis of pleocytosis and neuronal damage during occurrences of bacterial meningitis.
Increased CSF concentrations of TNF-α, IL-1, IL-6, and IL-8 are characteristic findings in patients with bacterial meningitis. Cytokine levels, including those of IL-6, TNF-α, and interferon gamma, have been found to be elevated in patients with aseptic meningitis.
The proposed events involving these inflammation mediators in bacterial meningitis begin with the exposure of cells (e.g., endothelial cells, leukocytes, microglia, astrocytes, and meningeal macrophages) to bacterial products released during replication and death; this exposure incites the synthesis of cytokines and proinflammatory mediators. This process is likely initiated by the ligation of the bacterial components (e.g., peptidoglycan and lipopolysaccharide) to pattern-recognition receptors, such as the Toll-like receptors (TLRs).
TNF-α and IL-1 are most prominent among the cytokines that mediate this inflammatory cascade. TNF-α is a glycoprotein derived from activated monocyte-macrophages, lymphocytes, astrocytes, and microglial cells.
IL-1, previously known as endogenous pyrogen, is also produced primarily by activated mononuclear phagocytes and is responsible for the induction of fever during bacterial infections. Both IL-1 and TNF-α have been detected in the CSF of individuals with bacterial meningitis. In experimental models of meningitis, they appear early during the course of disease and have been detected within 30-45 minutes of intracisternal endotoxin inoculation.
Many secondary mediators, such as IL-6, IL-8, nitric oxide, prostaglandins (e.g., prostaglandin E2 [PGE2]), and platelet activation factor (PAF), are presumed to amplify this inflammatory event, either synergistically or independently. IL-6 induces acute-phase reactants in response to bacterial infection. The chemokine IL-8 mediates neutrophil chemoattractant responses induced by TNF-α and IL-1.
Nitric oxide is a free radical molecule that can induce cytotoxicity when produced in high amounts. PGE2, a product of cyclooxygenase (COX), appears to participate in the induction of increased blood-brain barrier permeability. PAF, with its myriad biologic activities, is believed to mediate the formation of thrombi and the activation of clotting factors within the vasculature. However, the precise roles of all these secondary mediators in meningeal inflammation remain unclear.
The net result of the above processes is vascular endothelial injury and increased blood-brain barrier permeability, leading to the entry of many blood components into the subarachnoid space. In many cases, this contributes to vasogenic oedema and elevated CSF protein levels. In response to the cytokines and chemotactic molecules, neutrophils migrate from the bloodstream and penetrate the damaged blood-brain barrier, producing the profound neutrophilic pleocytosis characteristic of bacterial meningitis.
Genetic predisposition to inflammatory response
The inflammatory response and the release of proinflammatory mediators are critical to the recruitment of excess neutrophils to the subarachnoid space. These activated neutrophils release cytotoxic agents, including oxidants and metalloproteins that cause collateral damage to brain tissue.
Pattern recognition receptors, of which TLR A4 (TLRA4) is the best studied, lead to increase in the myeloid differentiation 88 (MyD88)-dependent pathway and excess production of proinflammatory mediators. At present, dexamethasone is used to decrease the effects of cellular toxicity by neutrophils after they are present. Researchers are actively seeking ways of inhibiting TLRA4 and other proinflammatory recognition receptors through genetically engineered suppressors.
Bacterial seeding
Bacterial seeding of the meninges usually occurs through hematogenous spread. In patients without an identifiable source of infection, local tissue and bloodstream invasion by bacteria that have colonized the nasopharynx may be a common source. Many meningitis-causing bacteria are carried in the nose and throat, often asymptomatically. Most meningeal pathogens are transmitted through the respiratory route, including Neisseria meningitidis (meningococcus) and S pneumoniae (pneumococcus).
Certain respiratory viruses are thought to enhance the entry of bacterial agents into the intravascular compartment, presumably by damaging mucosal defences. Once in the bloodstream, the infectious agent must escape immune surveillance (e.g., antibodies, complement-mediated bacterial killing, and neutrophil phagocytosis).
Subsequently, hematogenous seeding into distant sites, including the CNS, occurs. The specific pathophysiologic mechanisms by which the infectious agents gain access to the subarachnoid space remain unclear. Once inside the CNS, the infectious agents likely survive because host defences (e.g., immunoglobulins, neutrophils, and complement components) appear to be limited in this body compartment. The presence and replication of infectious agents remain uncontrolled and incite the cascade of meningeal inflammation described above.
Diagnosis
Medical history
Physical examination
Blood tests to find bacteria
CT or MRI scans of your head to find swelling or inflammation
Spinal puncture or spinal biopsy
Treatments
Treatment depends on the type of meningitis
Bacterial meningitis needs treatment with antibiotics from broad-spectrum to specific. Corticosteroids ease inflammation.
Viral meningitis usually goes away on its own without treatment. Bed rest and hydrating fluids are usually advised. Discomforts are managed symptomatically.
Antifungal medications can treat fungal meningitis.
Prognosis
Prognosis of meningitis depends on the cause. Untreated bacterial meningitis has a very high death rate. Even with appropriate treatment, the death rate from bacterial meningitis is about 15-20%, with a higher death rate associated with increasing age. The type of bacteria makes a difference, with pneumococcal and Listeria meningitis associated with higher death rates than meningococcal meningitis. Patients who survive may be left with long term disabilities such as deafness, blindness, seizures, paralysis, impaired mental status and loss of limbs. Viral meningitis, on the other hand, is associated with a very good prognosis and generally leads to a full recovery.Many bacterial meningitis types are now preventable with vaccines, such as Haemophilus influenza type b (Hib), meningococcus serogroups A, B, C, W135 and Y, and pneumococcus.
Complications
Meningitis can cause severe complications in adults and children, especially if not taken treatment immediately. Possible complications include:
- Seizures
- Brain damage
- Loss of hearing
- Memory problems
- Learning problems
- Difficulty to walk
- Kidney failure
- Shock
- Coma
- Death
Disease & Ayurveda
Mastishkajwara & mastishkaavarana sotha
Nidana
Kapha-Pitta vitiating food and regimen
Bhootabhishanga-external factors like germ infestation, infection etc.
Krimi-parasites
Purvaaroopa
Not mentioned
Samprapti
Causative factors for the vitiation of Kapha and Pitta along with external factors like infection leads to infection and swelling of the mastishka aavarana. Infection manisfests as aagantu jwara. Both Kapha & Pitta along with Vaata develops severe doshadushti and gets lodged in the mastishka aavarana(meninges) and sushumna(spinal cord), leading to manifestation of symptoms.
Lakshana
Jwara-Fever
Sirasoola- Headache
Manyastambha-Stiffness of neck
Gatrasadana- Fatigue
Gatrakampa- Shivering of body
Gatracheshta-Abnormal movements of body, like seizures
Divisions
Not mentioned
Prognosis
Yaapya
Chikithsa
Treatment of meningitis in Ayurveda comprises of both Jwarachikithsa and sothachikithsa. As it is mainly situated in head and neck areas, Kaphadosha is involved, when infection & fever develops, role of Pitta is eveident and as this disease affects the central nervous system, role of Vaata is obvious. As this disease involve the vitiation of all the three doshas, treatment is difficult. If not treated properly, the disease will develop into Paaka and cause fatal complications.
Ayurvedic treatment for sotha(swelling) aims mainly normalising the vitiated Kapha causing the obstruction and threreby relieving the passage of Vaata. In inflammatory conditions (Paaka) and fever (Jwara) Pitta shold also be addressed at the same time.
Samana
Mild langhana in the beginning for aamapachana
Then agnideepana with medicines and Pathya diets
Lepanam with Rookshana dravyas
Swedanam
Dhoopanam
Sodhana
After proper Aamapachana & agnideepana, virechana can be done if no fever is present. If cough & other signs of respiratory disorders are present, Vamana also will be needed. Snehana and swedana prior to each panchakarma procedure and the dietary restrictions after that should be done with precaution, checking all the indicated and contraindicated conditions in the patient.
Commonly used medicines
Varanadi kashayam
Kanchanaraguggulu
Rasnadi choornam
Brands available
AVS Kottakal
AVP Coimbatore
SNA oushadhasala
Vaidyaratnam oushadhasala
Home remedies
No home remedy is scientifically proven to cure meningitis. But some traditional methods are found effective in some cases. Intake of a balanced healthy diet will keep the inflammations away. Intake of natural anti-microbial foods like
Garlic
Olives
Cat’s claw
Chlorella
Turmeric
Soybean milk
Ginger etc. can help prevent the chance of infection.
Diet
- To be avoided
Heavy meals and difficult to digest foods – cause indigestion.
Junk foods- cause disturbance in digestion and reduces the bioavailability of the medicine
Carbonated drinks – makes the stomach more acidic and disturbed digestion
Refrigerated and frozen foods – causes weak and sluggish digestion by weakening Agni (digestive fire)
Milk and milk products – increase kapha, cause obstruction in channels and obesity
Curd – causes vidaaha and thereby many other diseases
- To be added
Light meals and easily digestible foods
Green gram, soups, honey
Freshly cooked and warm food processed with cumin seeds, ginger, black pepper, ajwain etc
Behaviour:
Protect yourself from cold climate.
Better to avoid exposure to excessive sunlight wind rain or dust.
Maintain a regular food and sleep schedule.
Check for infections if any, and take appropriate treatment on time.
Avoid holding or forcing the urges like urine, faeces, cough, sneeze etc.
Avoid a sedentary lifestyle.
Yoga
Exercises are not recommended in severe infectious conditions.
After regaining normal health, regular stretching and mild cardio exercises are advised. Also, specific yogacharya including naadisuddhi pranayama, bhujangaasana, pavanamuktasana is recommended.
Regular exercise helps improve the bioavailability of the medicine and food ingested and leads to positive health.
Yoga can maintain harmony within the body and with the surrounding system.
Pavanamuktasana
Nadisudhi pranayama
Bhujangasana
Simple exercises for lungs and heart health
All the exercises and physical exertions must be decided and done under the supervision of a medical expert only.
Research articles