Transient global amnesia: what is it, causes, symptoms. treatment, prognosis

What is transient global amnesia?

Transient global amnesia (TGA) is an acute-onset temporary anterograde amnesia that usually occurs in middle-aged and older people. The disorder is often caused by particularly strenuous activity, stressful situations, or intercourse, but can also occur when migraine. Studies have not been conclusive as to whether there are risk factors for developing TGA, although some have suggested a link to prior heart disease, migraines, or hyperlipidemia history. Patients often present with repetitive questions and complete anterograde memory loss that resolves within 24 hours. As long as there is disorientation in relation to other people and location, patients do not lose self-awareness. After disappearance, symptoms rarely recur, and no other neurological disturbances are observed in this condition.

Sign and symptoms

A person with a TGA attack is almost unable to create new memories, but usually appears otherwise mentally alert and clear, possessing full knowledge of self-identification and identity of close relatives and maintaining intact perception skills and a wide repertoire of difficult learned behavior. The person simply cannot remember anything that happened outside of the last few minutes, while while the memory of events more distant in time may or may not be largely intact. The degree of amnesia is great, and during the period during which a person is aware of his condition, anxiety is often accompanied.

Causes

There are many theories regarding the true etiology of TGA, but none of them have been proven. These theories included vascular events, depression, migraine, epilepsy or psychogenic origin. Studies have confirmed and refuted arterial ischemia as a source. Vascular congestion has been considered and remains one of the leading hypotheses, although issues related to certain age groups, and the fact that it is not observed in venous thrombosis remains to be explain. In addition, the disorder rarely occurs more often than a couple of times in a patient's life. In fact, theories developed regarding the etiology of transient global amnesia do not explain all clinical aspects of the disorder to date.

Epidemiology

The incidence of TGA is about 5.2-10 / 100,000 per year in the general population. In persons aged 50 and over, the incidence increases to 23.5–32 per 100,000 per year. Most of the reported cases were in patients between the ages of 50 and 80. There is no gender difference. Although no obvious risk factors were identified, the disease was more common in patients with ischemic heart disease and a history of hyperlipidemia. No history of ischemic stroke, diabetes or arterial hypertension. Many studies have demonstrated concomitant migraines in patients, but not in all cases.

Pathophysiology

The origin of transient global amnesia is thought to be from the hippocampus, in particular CA-1 and the Sommer sector, as well as the mediobasal temporal lobe. The marked area of ​​the hippocampus is a watershed of the brain, which is particularly susceptible to the effects of various metabolic stress, possibly due to sensitivity to cytotoxic uptake or release glutaminergic substances. These areas can be affected bilaterally or unilaterally, but most often occur on the left side. However, with functional imaging, such as functional MRI, reversible defects were observed on both sides. The patient temporarily has difficulties with the formation, as well as with the restoration of new memories.

The picture observed with TGA correlates with the affected side of the brain. In bilateral cases, the patient will experience impairments in both visual-spatial and speech memory. The predominant brain lesions show an associated speech deficit.

Diagnostics

- History and physics.

Typically, patients experience severe memory loss for several hours. Patients will exhibit repetitive questions and will not remember how they got to where they are or what they did in the time immediately before the start. Often, those accompanying the patient report recent activities such as intense physical exertion, intercourse, or intense stress. Patients do not report loss of consciousness, do not lose the ability to self-identify. There are no associated neurological or other cognitive impairments. There will be no history of injury and symptoms will disappear within 24 hours of onset. The presence of active epileptic seizures excludes TGA, whether new-onset or chronic. Symptoms are absent when the patient wakes up in the morning, but occurs later in the afternoon.

Patients will not have focal neurological disorders, but they often do not remember how they got to the hospital, what they are in the hospital, or about the events of the day. Patients often have trouble remembering people or places in the past few hours and will feel disoriented as a result. Even with visual cues such as pictures taken throughout the day, they won't remember events. The patient will constantly ask the same question because he forgets that he just asked a question a few minutes ago. Symptoms will begin to improve within a few hours, and memory will slowly and almost completely recover over the next 24 hours. It was initially thought that there was complete resolution of symptoms, but later research suggests that there may be some minor residual impairment associated with the event, as well as some subclinical cognitive impairment, even after years.

- Analyzes and visualization.

The patient should be hospitalized until the amnesia disappears. Toxicology screening, alcohol levels, and basic laboratory tests, including glucose and electrolytes, should be checked. Vital signs should be checked, including oxygen saturation. Due to the possibility of a similar manifestation encephalopathy Wernickeconsider prescribing thiamine. If there are signs suggesting a repetitive or epileptic etiology, an EEG may be considered, but this is generally not recommended. MRI with diffusion-weighted imaging is necessary to exclude ischemic stroke, which in some cases may have a similar picture. However, there is no diagnostic test for TGA; rather, it is a diagnosis of exclusion.

- Differential diagnosis.

• Basilar artery thrombosis;
• Cardioembolic stroke;
• Complex partial seizures;
• Lacunar syndrome;
• Migraine options;
• Fainting;
• Temporal lobe epilepsy.

Treatment

Treatment for transient global amnesia is generally supportive. There is no specific therapy for the condition and is unnecessary. The patient should be carefully evaluated for any concomitant neurologic abnormalities or signs of head trauma that would rule out TGA as a diagnosis. The patient should be observed in the hospital until the memory deficit disappears. Intravenous thiamine should be considered. Relapses, although they do occur, are rare. Once the memory deficit has been corrected, the patient does not need any driving restrictions or other activities.

Forecast

The prognosis for "pure" TGA is very good. It does not affect mortality or morbidity and, unlike earlier understanding of this condition, TGA is not a risk factor stroke or coronary artery disease. Relapse rates have been reported in various ways, with one systematic estimate suggesting a relapse rate of less than 6% per year. Transient global amnesia "is widely regarded as a benign disease that requires no further treatment other than reassurance of the patient and family." The most important part of post-diagnosis treatment is caring for the psychological needs of the patient and his relatives. Seeing a once competent and healthy partner, brother, sister, or parent lose the ability to remember what was said just a minute ago is very upsetting, and therefore it is often the relatives who need comfort.