Meningitis in Children - I.V. Bohadelnikov 2005

Sequelae of Purulent Meningitis in Children

Observation of children who have suffered Purulent meningitis, the consequences of the past infection, as well as their follow-up care and rehabilitation, constitute an essential branch of pediatrics.

At the present stage, the consequences of meningitis in children are characterized predominantly by disorders in the neuropsychiatric and emotional-affective spheres.

Post-meningitic neurological and psychological impairments in children depend on several factors:

1. The age at which the child contracted meningitis. The younger the child during the illness, the more severe its consequences.

2. The Etiology of meningitis. This is due to differences in the Pathogenesis of meningitis of various etiologies. For example, auditory nerve damage is most frequently observed in pneumococcal and Haemophilus influenzae meningitis, whereas in serous meningitis, the asthenic syndrome is more pronounced and prolonged, and myalgia may occur.

3. The state of The Nervous system prior to the onset of meningitis (presence of residual organic symptoms). Children with no prior signs of nervous system damage primarily exhibit mild neurological disorders, whereas those with a pre-morbid cerebral residual-organic Background predominantly experience moderate to severe consequences of the disease.

4. The severity of the infectious process during the acute period of meningitis.

5. The timeliness and aggressiveness of the Treatment administered to the patients.

Depending on the age at which the child suffered from meningitis, the following forms of neurological and psychological disorders are distinguished:

a) dysontogenetic — this form is characterized by delayed development and formation of various neurological and mental Functions;

b) encephalopathic — this form involves nervous system damage of varying types and severity.

Neurological and psychological disorders following meningitis are classified as mild, moderate, and severe.

Mild disorders:

- Minimal Brain dysfunction

- Asthenic syndrome

Moderate disorders:

- AUTONOMIC DYSFUNCTION SYNDROME

- Speech development delay

- Psychological development delay

- Organic psycho-syndrome

- Compensated Hydrocephalus

Severe disorders:

- "Active" (progressive) hydrocephalus

- Sensorineural Hearing loss or deafness

- Symptomatic Epilepsy

- Apalactic syndrome

- Blindness

Mild impairments:

Minimal brain dysfunction (MBD) refers to dysontogenetic forms of residual-organic lesions of the nervous system in children. Most commonly, it occurs when meningitis develops against a residual-organic background. The medical history of such children often indicates neuroinfections, brain Hypoxia, and TRAUMATIC BRAIN INJURIES sustained during the ante- or intra-natal period. Prior "minimal" lesions result in weakness and immaturity of a particular functional system, albeit with a sufficient degree of compensation. Subsequent meningitis decompensates the prior residual state, causing the functional system to become blocked in its further development.

The Diagnosis of "minimal brain dysfunction" is established in cases where nervous system disorders of a residual-organic nature do not reach the threshold of any specific nosological form of nervous system pathology. MBD manifests merely at the level of individual symptoms or syndromes (pyramidal-cerebellar insufficiency, attention deficits, and unspecified behavioral disorders). The manifestations of MBD following meningitis exhibit specific dynamics and Clinical Features depending on the acuity of the process. Over time, the severity of MBD symptoms gradually diminishes.

A characteristic feature of MBD post-meningitis is the combination of symptoms reflecting minimal organic insufficiency of the nervous system and psyche, coupled with increased fatigability in the child. These symptoms are particularly exacerbated by emotional, intellectual, or physical stress, as well as by changes in climatic conditions or alterations in the child's daily environmental routine.

Electroencephalographic (EEG) examination of such children typically reveals that the Electroencephalogram remains within age-norm limits, though minor alterations in voltage and frequency rhythms may be observed. Occasionally, slow-wave activity or spike potentials are recorded.

Cerebroasthenic syndrome (CAS) is quite frequently observed in children following meningitis. As a rule, it manifests 2–3 weeks after hospital discharge and is characterized by heightened irritability, mild excitability, and rapid fatigability. Children frequently complain of headaches, particularly when fatigued. Clinical observations reveal emotional lability, Sleep disturbances, neurotic syndromes (such as tics and enuresis), autonomic dysfunctions driven by rapid fatigability, as well as impaired memory, attention, and work capacity—though without a decline in intellect—ultimately leading to reduced academic performance at school.

The electroencephalogram in CAS corresponds to age-appropriate norms, or alternatively, reveals dysfunction within associative structures alongside a reduction in the functional activity of the brain.

Children with MBD and CAS following neuroinfection require regular neurological follow-up and, when necessary, consultations with a psychiatrist, medical psychologist, and speech therapist. It is essential to establish a protective regime for these children, which includes a calm and supportive home environment, adequate sleep, sufficient time spent outdoors, the avoidance of physical and mental overexertion, and, if required, an additional day off during the school week.

Moderate Disorders of the nervous system and psyche:

Speech development delay is observed in children who contracted meningitis at an early age, before their speech function was fully established.

The child's speech development stalls at the developmental stage corresponding to the age at which they contracted meningitis. Concurrently, The Structure of speech (phonetics, grammar, vocabulary) remains unaltered and matches the child's previous developmental milestone. In such cases, the realization of expressive (outer) speech is inhibited to a greater extent than that of receptive (inner) speech. The child understands the speech of those around them, but their vocabulary is limited and poorly operationalized. The child exerts considerable effort to recall the necessary word. Grammatical constructions appear late in sentences. The Regulation of the articulatory aspect of speech is delayed, presenting as delayed dyslalia. The child mispronounces sounds, transposes them within syllables, and employs " idiosynchratic" sounds. Nevertheless, despite the delayed formation and realization of motor speech, sensory speech is typically preserved. The child understands speech and communicates using their own expressive means (words, syllables, gestures, facial expressions).

Psychological developmental delay refers to a lag in the age-appropriate maturation rate of functional systems such as sensory, motor, cognitive, and emotional-communicative. A distinction is made between generalized and partial psychological developmental delay.

In generalized psychological developmental delay, all spheres of the psyche remain structurally intact, yet lag behind in their sequential developmental stages.

In partial psychological developmental delay, There is a delayed maturation of functional systems rooted in the partial underdevelopment of one or more domains. For instance, localized underdevelopment of brain structures responsible for the speech system leads to primary underdevelopment with stable speech defects, resulting in a secondary delay in the child's psychological development.

Following meningitis, the generalized form of psychological function developmental delay is most predominantly observed. The child's behavior alters—they may become irritable or lethargic, passive, drowsy, and tearful. Reactions of emotional frustration intensify; the child may throw tantrums, cry, and display aggression. However, these reactions are unstable and quickly subside after a period of rest.

Play and learning activities also become less productive. The child fails to adhere to the rules of a game and forgets their role-playing position. Task execution is dominated by deficits in attention concentration and altered productivity. As fatigue mounts, the child entirely loses The ability to concentrate and process the content of the task, becoming incapable of applying previously acquired academic skills (writing, reading, arithmetic). Furthermore, cognitive activity is insufficient, and the inquisitive phase characterized by "what, where, and why" questions is delayed. The gaze of a younger child is frequently wandering; they struggle to focus on objects and have difficulty directing their attention during play and actions. Manipulative and imaginative play is characterized by the correct use of toys, but the child fatigues rapidly, particularly during the early convalescence period. Additionally, the meaningful content of play may be lost, with the child aimlessly handling toys and surrounding objects.

During role-playing games, the child fails to maintain their assigned role, becomes easily distracted, disrupts other children, impairs interpersonal relationships, and exhibits aimless behavior. Some children fail to recognize danger, thereby exposing themselves to life-threatening situations (climbing to heights, running into traffic, etc.). Children lack awareness of their own behavior, fail to maintain appropriate social boundaries during communication, and can be overly intrusive, demanding, and restless.

Deficits are also evident within the cognitive sphere, including an insufficient level of age-appropriate knowledge and skills, a poor understanding of the environment, impaired speech development, unstable concentration, and heightened fatigability, all of which hinder the realization of the child's cognitive potential.

Apart from the aforementioned characteristics, psychological developmental delay post-meningitis is marked by premature fatigability, which further inhibits the full realization of the child's cognitive capabilities.

During the long-term convalescence period, children gradually recover the developmental pace of their psychological functions. However, this necessitates treatment for cerebroasthenic manifestations, a therapeutic and protective regimen, and a gradual reintroduction of academic tasks and social interaction.

Organic psychosyndrome belongs to the encephalopathic forms of long-term sequelae following meningitis and develops progressively during the convalescence period. It manifests predominantly during school age and is defined by impairments across various functional systems. In this condition, the child perceives environmental information only partially, analyzes it inadequately, and utilizes it in a restricted manner.

Cognitive impairment leads to learning difficulties. Such children exhibit slowed thinking, a lack of goal-directedness, an inability to promptly engage in task execution, and difficulties in regulating attention, sequential actions, and thought operations. Memory is severely compromised, particularly regarding the retention and retrieval of academic information.

In some children, an immaturity of volitional behavioral regulation predominates, making them susceptible to the motivations characteristic of younger children. Other children exhibit predominantly emotionally labile reactions marked by aggressive behavior and hysterical-type outbursts.

Behavioral and emotional disorders are unstable due to the child's heightened fatigability. Irritability accompanied by aggressive outbursts passes quickly, after which the child becomes lethargic, calm, or sometimes falls asleep. In children with CEREBROSPINAL FLUID Circulation disorders, hyperdynamic behavior tends to prevail, characterized by purposeless movements and actions, occasionally of a chaotic nature.

Vegetative dysfunction syndrome is characterized by a symptom complex of psychoemotional, sensorimotor, and autonomic disturbances. It is classified into neurocirculatory dysfunction, vegetovascular dysfunction, vegetovisceral dysfunction, and paroxysmal autonomic failure.

When in a stage of clinical symptom compensation, hydrocephalus may be asymptomatic and is diagnosed solely through supplementary examination Methods. Such children require dynamic neurological follow-up to prevent and timely treat the decompensation of hydrocephalus.

Severe nervous system and mental disorders following meningitis:

In progressive active hydrocephalus, the balance between cerebrospinal fluid production and resorption is disrupted, leading to increased intracranial pressure. External inspection reveals a progressive enlargement of HEAD dimensions. The fontanelle is widened, tense, and lacks pulsation; occasionally, cranial suture diastasis is observed, and Percussion of the head yields an altered sound (the " cracked pot" sound). The scalp becomes thinner and atrophic, with a compensatorily dilated venous network. Neurological symptoms are diverse, resulting from both the preceding meningitis and chronic intracranial Hypertension.

Cranial nerve lesions, impaired motor coordination, mental disorders, and autonomic system dysfunctions may occur. Motor impairments manifest as paresis or hyperkinesia. Young children may exhibit tremors of the hands, feet, or chin. In severe cases, children are unable to stand, sit, or hold up their heads, experience significant delays in intellectual and mental development, show slow weight gain, and present trophic disorders.

In older children, hydrocephalus is characterized by a syndrome of progressive intracranial hypertension, manifesting as headaches, nausea, vomiting at the peak of a headache, papilledema, and decreased visual acuity.

Children with progressive active hydrocephalus require a neurosurgical consultation to determine the appropriate treatment method. Dehydration therapy forms the foundation of conservative management.

Children suffering from blindness, sensorineural hearing loss, and deafness require treatment in specialized departments.

Epileptic seizures may appear within 5 or more years after recovering from meningitis. This can lead to The Development of symptomatic epilepsy with a typical Clinical presentation. Such patients require comprehensive treatment that must include anticonvulsant therapy.

Dispensing follow-up for children who have suffered from meningitis, particularly purulent forms, must be carried out for at least 2 years.