Borderline lobe epilepsy and borderline status epilepticus
Epilepsy is a common neurological disorder and syndrome that, despite its different etiologies, is characterized by temporary central system malfunction (manifested by different disorders of motor, sensory, consciousness, behavior, autonomic nerves, or both) due to recurrent neuronal overdischarge in the brain during the course of the disease.
The complexity of the clinical manifestations of epilepsy has given rise to a variety of classifications. An internationally harmonized classification would not only facilitate communication among clinicians, but also establish a recognized basis for clinical and basic research to jointly promote the development of epileptology. The International League Against Epilepsy (ILAE) has done a great deal of work on the classification and nomenclature of epilepsy. The International League Against Epilepsy, at its congress in Buenos Aires in 2001, presented the Diagnostic Outline of Seizures and Patients with Epilepsy, in which limbic lobe epilepsy and borderline status epilepticus were proposed among the diagnostic classification recommendations.
Marginal lobe epilepsy is classified as symptomatic (or possibly symptomatic) focal epilepsy, which is subdivided into.
1. medial temporal lobe epilepsy with hippocampal sclerosis;
2. medial temporal lobe epilepsy determined by specific etiology;
3. other types determined by location and etiology.
Hippocampal sclerosis is one of the important pathological features of limbic lobe epilepsy, mainly manifested by neuronal degeneration, atrophy and loss of neuronal cells in the hippocampus and amygdala and gliosis. The pathology of medial temporal lobe epilepsy has hippocampal sclerosis in 50% to 83% of cases. The hypothesis that the medial temporal lobe hippocampus and amygdala are the initiating points of limbic lobe epilepsy with both common pathways and amplifier effects has been proposed. However, it has been debated whether hippocampal sclerosis is a cause or a consequence of medial temporal lobe epilepsy onset, and it has been suggested that hippocampal sclerosis is the result of hypoxia after medial temporal lobe seizures.
Regardless of whether it is a cause or a consequence, pathology demonstrates that the hippocampus is only part of the medial temporal lobe that is involved. In addition to the place of hippocampal sclerosis, other parts of the medial temporal lobe have small vascular lesions, microabscesses, localized atrophic scarring, glial cell hyperplasia and neuronal degeneration. There are various causes of limbic lobe epilepsy, but perinatal and delivery disorders are considered high risk factors.
Limbic lobe epilepsy predominates in adolescents, with 62% of patients having their first seizure before the age of 15. Its clinical manifestations include.
1. symptoms of autonomic and/or psychiatric origin and certain specific sensory (e.g., smell, hearing) phenomena (including delusions). The most common is the sensation of a rush of air upward in the upper abdomen.
2. Typical symptoms of oral and gastrointestinal tract autonomic symptoms occur, often followed by other autonomic symptoms that last for more than 1 minute. There is often post-ictal confusion and post-ictal amnesia, and recovery is gradual.
In the case of amygdala-hippocampal seizures, the most common form of limbic seizures, they are characterized by rising epigastric discomfort, nausea, significant autonomic symptoms and other symptoms, including bowel movements, belching, facial pallor, facial distention, facial flushing, respiratory depression, pupil dilation, fear, panic and olfactory hallucinations.
In the case of cingulate seizures, there may be complex motor postural automatisms, autonomic symptoms and changes in mood and emotion.
In orbitofrontal seizures, motor and postural automatism are present initially, along with hallucinations and delusions and autonomic symptoms.
Features of insular cap seizures include mastication, salivation, swallowing, laryngeal symptoms, speech arrest, taste hallucinations, epigastric aura, fear, and autonomic symptoms.
Some have classified the clinical manifestations of limbic lobe epilepsy into the following seizure types.
1, sensory (taste, smell, visual, and auditory hallucinations)
2. affective (irritability, rage state, aggressive behavior, fear, panic, mania, suicidal ideation)
3, autonomic (abdominal, cardiac)
4.Memory disorders (forgetfulness, hallucinations, delusions, nostalgia for the past)
5, Automatism or psychomotor episodes (pharyngeal, mouth, simple or complex movements)
6, Hazy state of consciousness (mental confusion, etc.)