Semerau-Semyanovsky Paroxysmal Collapse

Semerau-Semyanovsky paroxysmal collapse: understanding this disease

Semerau-Siemenowski paroxysmal collapse, also known as Semerau-Siemenowski syndrome, is a rare disease that was first described by Polish physician Ludwig Semerau-Siemenowski in 1891. This condition is characterized by sudden and short-term convulsive movements of the head, neck and torso, which can occur either in response to external stimuli or for no apparent reason.

Semerau-Semyanovsky syndrome usually appears in childhood and has varying degrees of severity. For some patients, the symptoms may be so mild that they cause no particular problems, while for others they may be so intense that they interfere with normal life.

The causes of Semerau-Semyanovsky syndrome are still unknown, but it is believed that it is a hereditary disease associated with changes in genes responsible for the functioning of the nervous system. Other research suggests a possible connection between Semerau-Siemenowski syndrome and disruption of the basal ganglia, which plays an important role in regulating movement.

Although Semerau-Siemenowski syndrome has no known cure, patients may receive relief from symptoms through the use of anticonvulsants and other medications that help reduce the frequency and intensity of seizure movements.

Overall, Semerau-Siemenowski syndrome is a rare but important condition that requires further study to develop more effective treatments and improve the quality of life of patients suffering from this condition.

Semereu-Semyanovsky Paroxysmal collapse

Semerau-Semyanovsky Paroxysmal collapse is called vascular collapse (acute disruption of the blood supply to an organ) with subarachnoid hemorrhage developing on the second or third day after it. It is often characterized by the development of bilateral thrombosis of the retinal vessels and its edema, floaters before the eyes, nausea, dizziness, euphoria, and drowsiness are noted.

Blood flows to the retinal vessels from the ophthalmic vein, passing in the sella turcica of the sphenoid bone; as a result of this hemorrhage in the brain, the outflow of blood from the aorta into the ophthalmic vein is disrupted, as a result of which the flow of venous blood to the vessels of the eye increases. In the common arterial trunk, the pupils quickly dilate, spasm of the veins of the patient’s neck, arms and legs is caused, as a symptom characteristic of arterial hypertension, euchromic cyanosis and rashes on the skin in the form of “bunches of grapes” are observed. Therefore, the diagnosis is false; it is necessary to differentiate between SSPC and various forms of AGM.

Symptoms of SSCH (subarachnoid hemorrhage): * signs of poisoning [40-50% of patients]; * visual impairment and headache (60-80%); * hydrocephalus (20-30%) *; * rarely hemiplegia and other less significant symptoms. More often, the first signs occur within 1-2 days after subarachnoid hemorrhage. Then, within 24 hours, a second period begins, characterized by an increase in hydrocephalus, largely due to cerebral edema. Initially, pronounced hydrocephalic atrophy of the forebrain is observed, manifested by rigidity of the neck muscles. When water enters through the scalp sinuses between the membranes and the optic tract, abundant cerebrospinal meningeal signs are observed: headache, tension and pain in the cervical spine, mainly at the point of exit of the roots, painful palpation of the exit site of the trigeminal nerve root, positive and negative meningeal symptoms, etc. Bailey's meningeal sign is positive, Kernig's sign is positive. Hemorrhages and destruction of the retina were found in the fundus. There is compression of the optic nerve head. A temporary loss of visual function is possible in the presence of distinct congestive visual discs