Transient global amnesia is a transient memory impairment for current and past events lasting up to a day. Accompanied by a loss of orientation while maintaining self-consciousness. Some temporary disturbances of higher nervous functions are possible. Diagnostics includes neurological examination, EEG, MRI, duplex scanning of cerebral vessels; if necessary, PET of the brain. It is necessary to exclude acute vascular pathology of the brain, epilepsy and intracerebral tumor. There is no specific therapy yet. The treatment of the underlying pathology is carried out; according to indications, psychotherapy.
ICD 10
G45.4 Transient global amnesia
General information
Transient global amnesia (TGA) refers to temporary (transient) memory disorders. As a rule, the duration of the attack (an attack of amnesia) does not exceed 24 hours. More often, the attack lasts 2-3 hours. It is observed mainly in middle-aged and elderly people. 75% of cases occur in the age period from 50 to 70 years. In most cases, the TGA attack is of a single nature. In some patients, repeated amnestic seizures are noted, which can have adverse consequences up to the development of persistent memory disorders.
Transient global amnesia is a fairly rare syndrome. According to some data, its occurrence does not exceed 5 episodes per 100 thousand people per year. The urgency of the problem in modern neurology is due to the fact that TGA can be a symptom of serious vascular and oncological cerebral pathology. Sometimes a first-time TGA attack acts as a clinical debut of a brain tumor.
Causes
For a long time, TGA remained a mystery to clinicians. Only thanks to the development of diagnostic methods such as MRI, PET and duplex scanning of blood vessels, researchers were able to advance in understanding the causes of transient amnesia. Minor changes in the form of hypo- or hyperperfusion, increased signal intensity were detected in the hippocampal region. Based on this, 2 main hypotheses have been put forward. According to one of them, the causes of TGA lie in the violation of blood circulation of the hippocampus and adjacent structures. Adherents of this hypothesis attribute TGA attacks to a special type of transient ischemic attack. Another hypothesis speaks of the epileptic nature of TGA and explains the occurrence of seizures by the temporary epiactivity of the focus located in the deep structures of the hippocampus..
There are many cases when TGA attacks occurred against the background of other pathological conditions. For example, in patients with migraine, after a TBI, with chronic cerebral ischemia, cerebral tumors, hypertensive crisis, severe diabetes mellitus, in the debut of subarachnoid hemorrhage. Provoking factors of TGA can be acute stressful situations, physical overstrain, extreme conditions (pain, immersion of the body in cold water, etc.).
Symptoms
The main clinical manifestation of TGA is a sudden attack of loss of the ability to remember information and what is happening at the moment (anterograde amnesia), combined with loss of memory of past events that took place both in recent years and in the distant past (retrograde amnesia). The TGA attack in most cases occurs suddenly, for no apparent reason. In some patients, the attack was observed against the background of a hypertensive crisis, migraine paroxysm.
During an episode of amnesia, the patient loses orientation in time and space. But his cognitive abilities (attention, thinking), speech, social skills are preserved. Usually, the patient recognizes relatives and friends without problems, orients himself in his own personality. Outwardly, such a person looks confused and worried. Trying to understand what is happening to him and to orient himself in his surroundings, he asks a lot of questions, but immediately forgets the answers he received.
In about 35% of cases, along with mnestic disorders, individual disorders of higher nervous functions are observed. Visual agnosia (disorder of recognition of familiar objects), auditory perception errors, mild motor aphasia, praxis disorder (lack of purposefulness in movements), motor automatism are possible. Some clinicians distinguish transient partial amnesia — an episode of disorientation and memory loss associated with professional activity. In such cases, the mnestic violations are partial in nature, the memory of current and past events is preserved.
An episode of amnesia can last from 30 minutes to 24 hours, on average 2-5 hours. After its completion, memory and all nervous functions are fully restored. Amnesia may persist for events that occurred during the TGA episode itself. The regression of symptoms begins with the restoration of long-term memory and is accompanied by a subjective improvement in the condition. Then short-term memory begins to recover and objective restoration of all impaired abilities gradually takes place.
Diagnostics
With a short-term course of TGA, its diagnosis by a neurologist is retrospective and consists in conducting a thorough interview and examination of the patient. Separate studies show that 25% of patients have a history of paroxysmal conditions: migraine attacks, fainting, epileptic paroxysms, attacks of hypersomnia. During the study of the neurological status, as a rule, deviations are not detected. There may be changes characteristic of the background pathology.
Diagnosis of TGA during an attack requires the exclusion of acute vascular pathology (TIA, ischemic and hemorrhagic stroke, subarachnoid hemorrhage). For this purpose, an MRI of the brain is urgently performed. During the period of amnesia, fixation of MRI signals of increased intensity emanating from the hippocampus region is characteristic. In the retrospective diagnosis of TGA, MRI is used to exclude a brain tumor. It often reveals diffuse changes typical of dyscirculatory encephalopathy.
Electroencephalography during an amnesic attack registers an increase in bioelectric activity mainly in the alpha-2 and beta-1 ranges. Its implementation makes it possible to exclude epilepsy. After an episode of transient global amnesia, patients have a temporary decrease in the amplitude of the cognitive evoked potential of P300, which may reflect the phase of recovery of mnestic functions. With repeated TGA, the period of reduction of P300 increases.
In many patients with an episode of amnesia, transcranial dopplerography reveals atherosclerotic changes in cerebral vessels, which may be associated with age-related changes. In some cases, the results of PET brain indicate an increase or decrease in perfusion of the left temporal lobe.
Treatment and prognosis
Specific therapy for TGA has not been developed, since its pathogenetic mechanism (ischemia or epileptic activity) is not known. It is advisable to treat background pathology: vascular, antimigrenous, neuroprotective, anticonvulsant drugs. When a tumor is detected, neurosurgeons and oncologists are engaged in further treatment of the patient. Individual patients after suffering a paroxysm need the help of a psychologist or psychotherapist.
The prognosis of TGA depends on the underlying pathology, against which an episode of amnesia occurred. Relapses are rare – with a frequency of 3% per year. They are dangerous by the formation of persistent mnestic disorders up to the development of Korsakov syndrome. Prognostically, the most unfavorable cases of TGA are those that have arisen as a result of the tumor process. In other patients who have suffered an amnesic attack, there is an increased risk of progression of cerebral circulatory insufficiency with an outcome in PNMC, ischemic stroke, vascular dementia.