Clonic convulsions are irregular short-term spasms, which are characterized by a rapid change in periods of contraction and relaxation of skeletal muscles. Occur against the background of epilepsy, cerebral damage of an infectious, neurodegenerative, toxic or other nature. The cause of convulsive paroxysms is confirmed by laboratory tests, genetic tests, neuroimaging methods, EEG. The basis of therapeutic correction is the use of anticonvulsants, resistant variants require a solution to the issue of neurosurgical care.
Isolated clonic seizures are more common in focal forms of genuin (idiopathic) epilepsy. The attack occurs due to abnormal excessive activity of neuronal structures. The epileptic focus of partial paroxysms is limited to individual parts of the brain, and the attack becomes generalized when the excitation wave spreads rapidly to both hemispheres.
Partial seizures are often observed in frontal epilepsy, combined with head turns, dystonic hand placement, hypermotor automatisms. Complex focal seizures with loss of consciousness and secondarily generalized paroxysms in the defeat of the frontal lobes are found much less frequently. Before clonic spasms, a number of patients develop a somatosensory aura in the form of paresthesia throughout the body.
The basis of myoclonic epilepsy of infancy (Drave's syndrome) is encephalopathy with polymorphic convulsive seizures. In children under one year old, the pathology begins with febrile paroxysms with a focal component, which disrupts mental development. After 3-5 years, hemiclonic convulsions appear, changing the side of the lesion even during one attack. An important symptom of the disease are myoclonic paroxysms, gradually increasing in intensity and frequency.
Some infections in early childhood are accompanied by convulsions. Their occurrence is due to nonspecific encephalopathic reactions, which are based on edema and swelling of the brain, diapedetic hemorrhages. Even minor organic changes in the central nervous system, allergization contribute to the development of seizures. Short-term hypoxia of the brain against the background of coughing explains convulsions in whooping cough.
Clonic convulsions are often present in the clinical picture of SARS - influenza, parainfluenza, adenovirus infection. Seizures can be defined at the onset of the disease, at the height of the rash during the peak (with measles, chickenpox) or as a delayed complication. Convulsions occur without precursors and last 2-3 minutes, they are easily stopped. Frequent seizures threaten the formation of an epileptic focus.
Convulsions of a clonic nature occur with diffuse damage to the gray matter of the brain. Prion origin is Creutzfeldt-Jakob disease, and subacute sclerosing encephalitis is a slow infection caused by the measles virus. In the first case, rapidly progressive dementia, ataxia are stated. Later, clonic spasms occur, provoked by a loud sound or other stimuli.
The course of subacute sclerosing encephalitis has a number of similar features. First, mental disorders increase, the emotional sphere suffers. Then movement disorders join in the form of convulsive twitches of individual muscles, hyperkinesis, and atactic syndrome. Vision is impaired up to blindness, spastic paresis, urinary incontinence are noted. The disease is characterized by high mortality.
Other diseases are also manifested by clonic paroxysms and mental retardation. Lysosomal storage disease, Tay-Sachs disease, is neurodegenerative. It develops against the background of a genetic breakdown of the enzyme that utilizes gangliosides in the central nervous system. For pathology, convulsive twitches, developing into epileptic attacks, rapid progression of visual and hearing impairments, mental retardation are typical.
Alpers-Huttenlocher syndrome has a similar inheritance (according to an autosomal recessive type), in which a mutation of the gene encoding mitochondrial DNA polymerase is observed. The disease is manifested by convulsive syndrome, blindness, progressive dementia. Pathology can begin with coordinating disorders; in the later stages, liver failure is typical. Focal clonic seizures are insensitive to therapy, sometimes taking a status course.
The genesis of the convulsive syndrome in non-progressive encephalopathies (tuberous sclerosis, Down syndrome) is unknown. Diseases are accompanied by mental retardation, hypotension, myoclonus. The latter are combined with partial, generalized or unilateral clonic convulsions. The most common types of seizures in children with tuberous sclerosis are infantile spasms, which are often unresponsive to anticonvulsants.
Convulsive syndrome can be considered as a non-specific response of the still immature brain of a newborn to the impact of adverse factors. Familial and idiopathic neonatal convulsions (“fifth day seizures”) are benign. The former are inherited in an autosomal dominant fashion and occur predominantly during sleep. Short clonic seizures are associated with apnea, oral automatisms, and ocular symptoms.
The occurrence of idiopathic neonatal seizures is associated with zinc deficiency. They are detected in full-term newborns in the form of a single episode of multifocal or focal paroxysms lasting from 2 hours to 3 days. Clonic convulsions may be accompanied by short-term apnea and cyanosis; they do not affect the development of the child. They are resistant to drugs, but go away on their own, do not recur.
Clonic convulsions are manifested by toxic lesions of the central and peripheral nervous system caused by chemical compounds. Poisonous substances affect the motor neurons of the motor pathways or neuromuscular synapses, disrupting the balance of neurotransmitters and electrolytes inside the cells, which provokes the generation of excitatory impulses. The cause of seizures are various intoxications and poisonings:
Sometimes it is possible to suggest the cause of clonic seizures clinically - according to the anamnesis and neurological examination. At the same time, attention is paid to the time and circumstances of the development of the attack, its nature, the presence of concomitant symptoms. But in most cases, an accurate diagnosis is established based on the results of additional procedures:
In the diagnosis, the neurologist is assisted by related specialists. A characteristic sign of Tay-Sachs disease - a red spot on the retina - is determined by an ophthalmoscopy by an ophthalmologist, hereditary pathology requires the involvement of a geneticist. It is necessary to differentiate clonic convulsions with paroxysmal conditions of a different origin: stereotyped movements, syncope, pseudoconvulsions.
Severe and prolonged convulsions require mandatory medical intervention. In case of generalized clonic seizures, before the arrival of the ambulance team, the patient is laid on a flat surface with a pillow under his head, unfasten tight clothing, and provide free access to air. It is not recommended to resist involuntary movements. The remaining paroxysm is stopped by the introduction of anticonvulsants.
Treatment of clonic seizures is largely symptomatic, aimed at alleviating the patient's condition by reducing the frequency and severity of seizures. Etiotropic and pathogenetic therapy for most of the described diseases has not been developed, so the emphasis is on supportive treatment. Depending on the clinical situation, medicines of the following groups are used:
Complex therapy of the underlying disease involves the use of physical methods - electrical muscle stimulation, massage, therapeutic exercises. Neuropsychological rehabilitation plays an important role in cognitive impairment. A promising direction in the treatment of hereditary diseases is targeted gene therapy, the possibilities of which are still being studied.
Drug-resistant clonic seizures are sometimes treated with neurosurgery. In children and adults, cortical and subpial resections of epileptogenic foci, functional hemispherectomy, and uncoupling operations are practiced. This leads to a reduction in the number of seizures and a rapid improvement in the quality of life. The development of tumor-like formations in individuals suffering from tuberous sclerosis requires consideration of the advisability of adjuvant radiotherapy.