Otogenic brain abscesses: causes, symptoms, diagnosis, treatment

An abscess is a cavity filled with pus and separated from surrounding tissues and organs by a pyogenic membrane.

Classification of otogenic brain abscesses

Based on the time of occurrence, otogenic abscesses are usually divided into early and late. Late abscesses are those that form after 3 months.

Early abscesses go through a series of successive stages in their development:

• purulent-necrotic encephalitis:
• formation of a pyogenic capsule;
• manifestations of abscess;
• terminal stage.

Late abscesses are divided according to their clinical course into rapidly developing, slowly developing and asymptomatic.

Pathogenesis of otogenic brain abscesses

Otogenic brain abscesses occur in close proximity to the site of infection and are most often localized in the temporal lobe and cerebellum.

In the early stage of encephalitis (first 1-3 days), a local inflammatory reaction occurs around the blood vessels. The development of encephalitis is associated with swelling of the brain tissue and the formation of a necrotic area. In the late stage of encephalitis (4-9 days), important histological changes are observed, such as maximum swelling of the brain tissue, an increase in the size of necrosis, and the formation of pus. Fibroblasts form a reticular network around the inflammation zone, which serves as a precursor to the collagen capsule.

In the early stage (days 10-13) of capsule formation, the collagen network is compacted and the necrotic center is isolated from the surrounding brain matter. Apparently, this process is crucial in protecting the surrounding tissue from damage. In the late stage of capsule formation (days 14 and later), the abscess has five distinct layers:

• necrotic center;
• peripheral zone of inflammatory cells and fibroblasts;
• collagen capsule:
• area of newly formed vessels;
• area of reactive gliosis with edema.

It takes 2 weeks for a well-formed capsule to develop.

Factors influencing capsule formation include the type of pathogen, the source of infection, the state of the body's immune system, the use of antibiotics and glucocorticoids.

Symptoms of otogenic brain abscesses

The clinical manifestations of an abscess depend on its location and volume, the virulence of the pathogen, the immune status of the patient, the presence of cerebral edema, and the severity of intracranial hypertension. An abscess is an acute inflammatory process that usually develops rapidly, which is the main difference from other intracranial space-occupying lesions. The symptoms of an abscess develop in no more than two weeks, and often in less than one week.

A characteristic feature of a late abscess is the presence of a well-defined capsule. Clinical manifestations of late abscesses are very diverse and are determined by the localization of the pathological focus and its size. The leading symptoms of late abscesses can be considered to be the manifestation of intracranial hypertension with the appearance of ophthalmological and radiological signs of a pathological volumetric formation in the cranial cavity.

The most serious complication of a brain abscess is the rupture of the purulent cavity into the path of the cerebrospinal fluid and especially into the ventricles of the brain.

There are initial, latent and obvious stages of abscess development.

In the initial stage, the main symptom is headache. It may be hemicranial, but most often it is diffuse, constant and resistant to treatment. If there is a significant increase in intracranial pressure, the headache is accompanied by nausea and vomiting. Increased intracranial pressure, together with the mass effect caused by the abscess, can lead to a disturbance in the level of consciousness: from moderate confusion to the development of coma. The state of consciousness is the single most important prognostic factor. The duration of this stage is 1-2 weeks.

Further, during 2-6 weeks of development of the latent stage, obvious symptoms of brain damage are not observed, but the patient's well-being is often altered. Mood worsens, apathy develops, general weakness and increased fatigue are noted.

The overt stage lasts on average 2 weeks. If the patient is not closely monitored, the initial stage goes unnoticed, and the overt stage is recognized late.

Diagnosis of otogenic brain abscesses

Physical examination

During a physical examination of a patient in the obvious stage of the disease, four groups of symptoms can be distinguished: general infectious, general cerebral, conductive and focal.

The first group includes general weakness, loss of appetite, constipation, and weight loss. Body temperature is usually normal or subfertile, ESR is elevated, leukocytosis is moderate without significant changes in the leukocyte count. Half of the patients may experience episodic irregular increases in body temperature to 39°C and above.

General cerebral symptoms are caused by increased intracranial pressure. These include headache, vomiting without preceding nausea, stiff neck, Kernig's sign. Unlike meningitis, bradycardia is observed due to pressure on the medulla oblongata. More often than with meningitis, congestive optic discs are detected during fundus examination. Meningism is present in 20% of patients. Edema of the optic nerve papillae is associated with intracranial hypertension and is detected in 23-50% of patients.

Compression of the conduction systems and subcortical nuclei occurs as a result of dislocation of brain tissue. Contralateral hemiparesis and paralysis are noted. Cranial nerves may suffer. Paresis of the oculomotor and facial nerves develops according to the central type. The central innervation of the upper group of facial muscles is bilateral, therefore, with paresis of the lower group of muscles, the facial function of the forehead muscles is preserved. Pyramidal symptoms are noted.

Focal neurological symptoms have the greatest diagnostic value. Focal neurological deficit is noted in 50-80% of patients, its manifestations are associated with the localization of the abscess.

Damage to the dominant temporal lobe of the brain (left in right-handed people and right in left-handed people) is characterized by sensory and amnestic aphasia. In sensory aphasia and intact hearing, the patient does not understand what is said to him. His speech becomes a meaningless set of words. This occurs due to damage to the Wernicke area in the posterior section of the superior temporal gyrus of the dominant hemisphere of the brain. The patient also cannot read (alexia) or write (agraphia). Amnestic aphasia is manifested by the fact that the patient, instead of naming an object, describes its purpose, which is associated with visual-auditory dissociation as a result of damage to the lower and posterior sections of the temporal and parietal lobes.

An abscess in the "non-leading" temporal lobe can manifest itself in mental disorders: euphoria or depression, decreased critical thinking, which often go unnoticed. That is why such a lobe is called "silent".

Pathology of any of the temporal lobes of the brain is accompanied by loss of the same visual fields of both eyes (homonymous hemnanopsia). Involvement of the cortical vestibular representation is accompanied by dizziness and ataxia with deviation of the body to the side opposite to the lesion.

Cerebellar abscess is characterized by impaired limb tone, ataxia, spontaneous nystagmus, and cerebellar symptoms. Deviation and lowering of the hand on the affected side is noted during the finger-to-finger test. Missing the mark in the direction of the affected side is observed during the index and finger-to-nose tests. The patient performs the heel-to-knee test uncertainly with the leg on the affected side, moving it further than required. Cerebellar ataxia is manifested by deviation of the body in the Romberg pose to the affected side and a "drunk" gait with deviation to the same side. Deviations of the body and limbs coincide with the direction of the fast component of nystagmus, unlike vestibular ataxia, in which deviations of the body and limbs coincide with the direction of the slow component of nystagmus. Spontaneous nystagmus is large-scale, and can be multiple in case of extensive cerebellar damage. Vertical nystagmus is an unfavorable prognostic sign. Cerebellar symptoms include the inability to perform a flank gait toward the affected cerebellar hemisphere, adiadochokinesis, and intention tremors during the finger-nose test.

In case of a brain abscess, a sudden deterioration of the patient's condition is possible. The latter is associated either with brain dislocation or with a breakthrough of the abscess contents into the subarachnoid space or into the ventricles of the brain. In case of an unfavorable course of the disease in the terminal stage, due to pronounced dislocation syndrome, anisocoria, limitation of upward gaze, loss of consciousness and disturbance of the respiratory rhythm are observed. Death occurs either against the background of increasing cerebral edema from respiratory arrest and cardiac activity, or against the background of purulent ventriculitis when pus breaks into the ventricles of the brain.

Laboratory research

In brain abscesses, moderate neutrophilic leukocytosis is observed with a shift in the leukocyte formula to the left, an increase in ESR to 20 mm/h and higher.

A spinal puncture for cerebral abscess is dangerous and quickly leads to clinical deterioration. Changes in the cerebrospinal fluid are nonspecific. The cerebrospinal fluid is transparent, flows out under pressure, has a slightly increased protein content and weakly expressed pleocytosis (up to 100-200 cells/μl). When pus breaks through into the subarachnoid space, secondary meningitis develops, characterized by corresponding changes in the cerebrospinal fluid.

Instrumental research

Radiological diagnostics is of great importance in the diagnostics of brain abscesses. Absolute radiological signs of an abscess are the contouring of calcified walls of the abscess with the presence of a level of liquid or gas in it.

When performing echoencephalography and carotid angiography, signs of an intracranial volumetric process that displaces the midline structures of the brain can be established.

Widespread use of CT and MRI is necessary for accurate diagnosis of cerebral abscess localization. CT reveals a smooth, thin, regularly contoured abscess wall that accumulates contrast agent, as well as a central area of the abscess of low density. In MRI, on T1-weighted images, the central necrosis is represented by a hypointensity zone, the capsule surrounds the necrosis zone and appears as a thin iso- or hyperintensity layer. Outside the abscess, there is a hypointensity zone, which is edema. On T2-weighted images, the same data are reproduced as a hyperintensity center, a well-differentiated hypointensity capsule, and surrounding hyperintensity edema. Based on CT and MRI data, the optimal approach to the pathological focus can be determined.

In the temporal lobe of the brain, the abscess is often rounded, and in the cerebellum, it is slit-shaped. Smooth-walled abscesses with a well-defined capsule have the most favorable course. However, the capsule is often absent, and the abscess is surrounded by inflamed and softened brain matter.

If CT and MRI are not available for diagnosis, pneumoencephalography and radioisotope scintigraphy can be used.

Differential diagnostics

Otogenic brain abscess should be distinguished from abscessing encephalitis. The formation of a delimited purulent cavity in the brain tissue is most often a consequence of encephalitis, representing one of the variants of its outcome. Differential diagnostics of late abscess should also be carried out with a brain tumor.

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