Symptoms of meningeal syndrome

Typical objective signs of meningeal syndrome, i.e. irritation of the meninges, are Brudzinski's and Kernig's symptoms, and rigidity of the neck muscles, which are detected in the patient regardless of the cause that caused them.

Neck muscle rigidity is detected in a patient lying on his back. During passive flexion of the head, pronounced tension of the neck muscles and occipital muscles is noted, preventing the chin from being brought to the chest. Neck muscle rigidity is often combined with rigidity of the back and limb extensors. False rigidity may be present in patients with spondyloarthrosis, spondylosis of the cervical spine, and constitutional features of the skeletal system. Neck muscle rigidity may also be absent in children under 6 months of age. Neck muscle rigidity should be examined with particular care in patients with acute craniocervical trauma.

Kernig's symptom is the inability to fully extend the leg at the knee joint, bent at the hip and knee joints at an angle of 90°. In a patient with acute brain damage, Kernig's symptom may be less pronounced on the side of paresis. Passive extension of the leg at the knee joint may be difficult with diffuse muscle rigidity and joint pathology. A distinctive feature of Kernig's symptom is the occurrence of pronounced muscle rigidity (muscle contracture), which does not allow full extension.

When assessing the rigidity of the neck muscles, involuntary pulling up of the legs, their flexion at the knee and hip joints is possible, which is regarded as a positive upper Brudzinski symptom. If, when examining the Kernig symptom, flexion at the knee joint of the opposite leg is observed, this is the lower Brudzinski symptom. Bending the legs at the knee joints and pulling them to the body when pressing on the symphysis area of the pubic bones is regarded as a positive middle Brudzinski symptom.

In children, an important sign of irritation of the meninges is the "pointer dog pose" - lying on the side with the head thrown back and the knees bent, legs pulled up to the stomach. In infants, the Lesage suspension symptom is also detected: the baby, raised above the bed by the armpits, pulls his legs up to the stomach and fixes them in this position.

Meningeal symptoms are combined with intense headache, photo- and phonophobia, nausea, repeated vomiting, cutaneous hyperesthesia. The value of these signs for diagnosing irritation of the meninges in the absence of other meningeal symptoms is ambiguous, although in certain situations they precede the appearance of meningeal symptoms, occurring in the early stages of the disease. Correct interpretation of the nature and severity of cephalgia, cutaneous hyperesthesia, taking into account the overall clinical picture (the presence of signs of inflammation, previous head injury, etc.) allows us to suspect the involvement of the meninges in the pathological process and choose the correct tactics for managing the patient.

As the disease progresses, a clinical picture of a full-blown meningeal syndrome usually appears. Depression of consciousness, stupefaction, drowsiness to deep stupor and coma appear. When the brain tissue is affected, focal neurological deficit develops.

The vast majority of patients with meningitis have inflammatory and toxic manifestations of the disease: fever, hyperhidrosis, changes in the white blood cell count. The sensitivity of isolated meningeal symptoms in detecting damage to the membranes is relatively low; a combination of such signs as neck muscle rigidity, Kernig's and Brudzinsky's symptoms, fever, headache (increasing with coughing, straining), and impaired consciousness are much more significant. Interpretation of the results of the study of meningeal symptoms requires mandatory consideration of anamnestic data, the clinical picture of the disease, and paraclinical studies. In this regard, it should be noted that lumbar puncture is necessary in some patients with a clinical picture of an inflammatory disease, but in the absence of meningeal symptoms.

It should be borne in mind that with moderately expressed inflammatory phenomena in the cerebrospinal fluid, the severity of meningeal symptoms may be minimal or absent altogether, increasing with severe meningitis (>1000 cells in 1 μl of cerebrospinal fluid).

Acute development of meningeal syndrome against the background of physical or emotional stress, during the period of active wakefulness, accompanied by sudden intense headache (may occur as a blow, a sensation of boiling water spilled on the back of the head or back), may indicate spontaneous subarachnoid hemorrhage. Extensive hemorrhage may be accompanied by depression of consciousness from stupor to deep coma, development of single epileptic or serial seizures. Simultaneous occurrence of focal neurological deficit is characteristic of parenchymatous-subarachnoid hemorrhage. Meningeal syndrome in combination with confusion or depression of consciousness occurs in acute hypertensive encephalopathy. Focal neurological deficit is not characteristic of this condition. Indications of recent head or neck trauma, traces of trauma on the head in combination with meningeal symptoms and depressed consciousness are highly likely to indicate traumatic subarachnoid hemorrhage.

Meningeal syndrome may occur with volumetric lesions of the brain and its membranes (tumors, hematomas, abscesses, parasites). In this situation, both direct irritation of the meninges by the neoplasm and the effect caused by a significant increase in intracranial pressure are possible. Sometimes there is a toxic effect on the membranes. The overwhelming majority of patients have focal neurological deficit. Its severity and nature depend on the localization and size of the pathological focus. The listed conditions are also characterized by an increase in cerebrospinal fluid pressure, which is revealed during a lumbar puncture. An increased protein content in the cerebrospinal fluid is possible, as a rule, in the absence of inflammatory changes.

Dissemination of a malignant neoplasm on the meninges (carcinomatosis) can cause the development of a slowly growing meningeal syndrome. In addition, focal neurological symptoms are detected in these patients, including damage to the cranial nerves. In some cases, neurological disorders outpace other manifestations of the oncological process, even those associated with the localization of the primary lesion.

Infections accompanied by intoxication can also cause the development of meningeal syndrome (flu, salmonellosis). Careful observation of the patient with an assessment of the dynamics of his condition is of great importance for establishing the correct diagnosis in this situation; a lumbar puncture is often required to exclude true damage to the meninges (secondary meningitis).

Pseudotumor cerebri is a rare syndrome characterized by increasing intracranial hypertension, swelling of the optic disc, and oculomotor disorders (in particular, damage to the abducens nerve).

Radiation encephalopathy may develop in patients who have undergone radiation therapy for cerebral neoplasms. This condition typically involves a combination of manifestations characteristic of the underlying disease (brain tumor) and the consequences of radiation exposure (focal or multifocal symptoms, epileptiform seizures, and meningeal symptoms) that occur immediately after the course of therapy.

If the excretion of fluid from the body is impaired (for example, adrenal insufficiency, blood hypoosmolarity, hyponatremia), hyperhydration - water intoxication - may develop. Moderately expressed meningeal syndrome is combined with cramps, asthenic disorders, possibly with ascites, hydrothorax.

Pseudomeningeal syndrome occurs due to causes that impede or exclude movements in the cervical spine, knee joints, thereby simulating the presence of meningeal symptoms (muscle rigidity of the neck, Kernig's sign). Most often, it is caused by increased muscle tone (parkinsonism), paratonia (continence in extrapyramidal lesions) or orthopedic pathology (spondyloarthrosis and spondylosis, including those with severe pain syndrome).

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