Meningeal syndrome is a symptom complex characteristic of lesions of the cerebral membranes. It may have an infectious, toxic, cerebrospinal hypertension, vascular, traumatic, carcinomatous etiology. It is manifested by headache, muscle rigidity, vomiting, hyperesthesia, algic phenomena. The diagnostic basis consists of clinical data, the results of the study of cerebrospinal fluid. Treatment is carried out according to the etiology with antibacterial, antiviral, antifungal, antiprotozoal agents, includes symptomatic therapy, reduction of intracranial pressure.
General information
Meningeal (shell) syndrome is a common pathology faced by neurologists, infectious disease specialists, pediatricians, therapists, otolaryngologists and many other specialists. The syndrome got its name from the Latin term “meningea”, meaning the membranes of the brain. In cases where meningeal syndrome is caused by irritation of the cerebral membranes without their inflammatory changes, the definition of meningism is used in medical practice. The peak of the active study of pathology occurred at the end of the XIX century, various authors have proposed numerous specific symptoms of the disease that are still used today. Meningeal syndrome is observed at any age without gender preferences. In elderly patients, it has an erased clinical picture.
Causes
Many intracranial and polysystemic pathological processes act as etiofactors. Most often meningeal syndrome provokes inflammation of the meninges (meningitis), subarachnoid hemorrhage, traumatic brain injury. In accordance with the effect on the cerebral membranes, the etiological causes are divided into two main groups – inflammatory and non-inflammatory lesions.
Inflammatory lesions:
- Bacterial. Nonspecific – caused by meningococcal infection, hemophilic bacillus, streptococci, pneumococci, in newborns – salmonella, E. coli. Specific – arising from penetration into the shells of pathogens of tuberculosis, syphilis.
- Viral. In 75% of cases, they are provoked by enteroviruses, less often by Epstein–Barr virus, arenavirus, herpes infection, tick-borne encephalitis virus.
- Fungal. The main pathogens are cryptococci, candida, Aspergillus, histoplasma. They cause serous inflammation of the membranes with petechial hemorrhages.
- Protozoan. They are observed in toxoplasmosis, malaria.
Non-inflammatory lesions:
- Hemorrhages in the membranes of the brain. They may occur due to acute cerebral circulatory disorders, severe arterial hypertension, TBI, cerebral vasculitis.
- Intracranial hypertension. It develops due to hydrocephalus, volumetric formations (brain tumors, intracranial cyst, abscess, intracerebral hematoma).
- Intoxication. Exogenous – paint and varnish production, substance abuse, alcoholism. Endogenous – uremia, hypoparathyroidism.
- Neurotoxicosis in common infectious diseases (influenza, typhus, dysentery, ARVI).
- Carcinomatosis is the infiltration of the cerebral membranes by tumor cells in various oncological processes, including leukocyte infiltration in neuroleukosis.
Pathogenesis
Meningeal syndrome has two mechanisms of development. The first – the inflammatory process – is realized in response to the penetration of infectious agents. Infection of the cerebral membranes occurs by contact (with open TBI, osteomyelitis of the skull bones), lymphogenic, perineural, hematogenic pathways. The introduction of pathogens with blood flow is more often observed in the presence of foci of purulent infection (sinusitis, purulent otitis, mastoiditis). In encephalitis, inflammation in the substance of the brain spreads to the tissues of the membranes with the development of meningoencephalitis. The second pathogenetic mechanism is irritation of the meninges. Blood accumulations in subarachnoid hemorrhage, increased intracranial pressure, toxic substances entering the body from the outside or formed as a result of dysmetabolic processes, the vital activity of pathogenic microorganisms, tissue decay in oncological diseases have an irritating effect.
Symptoms
The shell symptom complex is formed by general cerebral manifestations and the actual meningeal symptoms. Intense diffuse cephalgia (headache), vomiting without previous nausea is typical. Vomiting is not accompanied by relief of the general condition of the patient. In severe cases, there is excitement, followed by apathy, possible epileptic seizures, hallucinations, depression of consciousness to sopor, coma. Pathognomonic symptoms characterizing meningeal syndrome include three groups of symptoms: signs of hyperesthesia, muscle-tonic manifestations, pain phenomena.
Hyperesthesia is manifested by increased susceptibility to sounds (hyperacusis), light (photophobia), and touch. The most common musculotonic symptom is rigidity (hypertonus) of the occipital muscles, detected when trying to passively bend the patient’s head. An increase in muscle tone causes a typical position: lying on his side with his back arched, head thrown back, limbs bent and brought to the body (“the pose of a cop dog”). Reactive algic symptoms include eye soreness when moving and pressing on the eyelids, pain in the trigger points of the trigeminal nerve, Kerer points on the back of the head, in the cheekbones.
Diagnostics
Meningeal syndrome is diagnosed by specialists in the field of infectology, pediatrics, neurology, therapy. During the examination, attention is paid to the presence of meningeal posture, hyperesthesia, pain and tonic phenomena. Hypertonus of meningeal genesis is differentiated from the muscle tension accompanying myositis, sciatica. In the neurological status, characteristic changes in the reflex sphere are determined: the revival of reflexes, followed by their uneven decrease. If meningeal syndrome is associated with damage to the brain substance, then a corresponding focal neurological deficit is detected (pyramidal insufficiency, aphasia, cerebellar ataxia, facial nerve paresis). There are more than 30 clinical symptoms that help diagnose shell syndrome. The most widely used among neurologists and general practitioners are the following:
- Kernig’s symptom – in the patient’s supine position, the lower limb is passively bent in the hip and knee joints. Subsequent attempts by the doctor to straighten the leg at the knee are impossible due to the tonic contraction of the muscles flexing the shin.
- Symptoms of Brudzinsky – in the position on the back, there is an involuntary tightening of the lower extremities to the abdomen when bending the patient’s head (upper), pressing on the pubis (middle), checking the Kernig symptom (lower).
- Edelman’s symptom is the extension of the thumb on the foot when examined by the Kernig method.
- Netter’s symptom – in a sitting position with legs stretched out in bed, pressing on the knee of one leg causes the other to bend.
- Kholodenko’s symptom is bending of the knees when the doctor tries to lift the patient by the shoulders.
- Guillain’s symptom – in the patient’s position on his back with his legs straightened, compression of the muscles of the anterior surface of one thigh leads to flexion of the second leg.
- The symptom of Lessage is that when the child is held in the air in an upright position by the armpits, the legs are pulled up to the stomach. It is typical for young children.
Lumbar puncture plays an important role in the diagnosis of shell syndrome. It is contraindicated in severe intracranial hypertension, the danger of mass effect, is carried out after the exclusion of these conditions according to ophthalmoscopy and echoencephalography. Examination of the cerebrospinal fluid helps to establish the etiology of the syndrome. Turbid cerebrospinal fluid with a predominance of neutrophils indicates purulent, opalescent with an increased content of lymphocytes – the serous nature of inflammation. An admixture of blood is observed in subarachnoid hemorrhage, cancer cells – in oncological lesions.
Meningeal syndrome is differentiated by etiology. Verification of the final diagnosis is achieved with the help of bacteriological and virological examination of the cerebrospinal fluid, blood sampling, PCR studies, electroencephalography, MRI of the brain.
Treatment
A developed meningeal symptom complex requires treatment in a hospital setting. Therapy is carried out in a differentiated manner, taking into account the etiology and clinical manifestations, and includes the following areas:
- Etiotropic treatment. With bacterial etiology, antibiotic therapy is prescribed with broad–spectrum drugs, viral – antiviral agents, fungal – antimycotics. Detoxification, treatment of the underlying disease is performed. Prior to the establishment of the causative agent, etiotropic therapy is carried out empirically, after clarifying the diagnosis – in accordance with the etiology.
- Decongestant therapy. It is necessary to prevent cerebral edema, aimed at reducing intracranial pressure. It is carried out with diuretics, glucocorticosteroids.
- Symptomatic therapy. It is aimed at relieving the emerging symptoms. Hyperthermia is an indication for the use of antipyretics, arterial hypertension – hypotensive agents, repeated vomiting – antiemetics. Psychomotor agitation is stopped by psychotropic drugs, epileptic paroxysm – anticonvulsants.
Prognosis and prevention
In most cases, timely and correct treatment leads to the recovery of the patient. Residual phenomena may be observed for several months: asthenia, emotional lability, cephalgia, intracranial hypertension. An unfavorable outcome is meningeal syndrome, which accompanies severe CNS disease, lightning-fast course of the infectious process, oncopathology. Prevention of shell syndrome includes increased immunity, prevention of infectious diseases, injuries, intoxication, timely therapy of cerebrovascular and cardiovascular pathology. Specific prevention is possible in relation to meningococcal, pneumococcal infection.
