Symptoms of temporal lobe damage

With lesions of the temporal lobes, the functions of the listed analyzers and efferent systems are disturbed, and disorders of higher nervous activity are manifested by disorientation in the external environment and misunderstanding of speech signals (auditory agnosia).

In lesions of the temporal lobes, motor disorders are not very pronounced or absent. Often there are attacks of vestibular cortical system dizziness. Perhaps the appearance of astasia-abasia (as in the defeat of the frontal lobe) with a tendency to fall in the opposite direction. Foci in the depth of the temporal lobes cause the appearance of an upper quadrant hemianopsia. The main symptoms of loss and irritation of the temporal lobes are associated with a violation of the function of the analyzers.

Frequent signs of temporal pathology are hallucinations and epileptic seizures with various auras: olfactory (irritation of the hippocampal gyrus), taste (foci near the islet segment), auditory (upper temporal gyrus), vestibular (three lobes - temporal, occipital, parietal). When lesions of the mediobasal areas often observed visceral auras (epigastric, cardiac, etc.). Foci in the depth of the temporal lobe may cause visual hallucinations or auras. General convulsive attacks with loss of consciousness are more often observed when the foci are localized in the region of the temporal lobe poles. Irradiation of irritation in the temporal zone causes paroxysmal disorders of higher nervous activity.

Paroxysmal disorders of the psyche in the pathology of temporal lobes include various changes in consciousness, which are often defined as sleep-like states. During an attack, the surroundings appear to patients completely unfamiliar ("never seen", "never heard") or vice versa - long seen, long heard.

Temporal automatism is associated with impaired orientation in the external environment. Patients do not recognize the street, their home, the arrangement of rooms in the apartment, commit many outwardly aimless actions. The connections of the temporal lobes with the deep structures of the brain (in particular, with the reticular formation) explain the occurrence of small epileptic seizures when these lobes are affected. These seizures are limited to short-term deenergia of consciousness without motor disorders (in contrast to small seizures of frontal origin).

The temporal lobes (especially their medio-basal sections) are closely related to the intermediate brain cavernum and the reticular formation, so vegetation-visceral disorders quite often arise in the lesions of the temporal lobes, which will be discussed in the section on lesions of the limbic part of the brain.

Lesions of the temporal lobe, posterior part of the upper temporal gyrus (the Wernicke zone) cause the appearance of sensory aphasia or its varieties (amnestic, semantic aphasia). Quite often disorders in the emotional sphere (depression, anxiety, lability of emotions and other deviations). The memory is also broken. W. Penfidd (1964) believes that temporal lobes are even a "center of memory". However, the memory function is performed by the entire brain (for example, praxis, ie, "memory" for actions, associated with parietal and frontal lobes, "memory" for recognition of visual images - with occipital lobes). Memory in the lesion of the temporal lobes is particularly disturbed due to the association of these lobes with many analyzers. In addition, the memory of a person is largely verbal, which is also associated with the functions primarily of the temporal lobes of the brain.

Syndromes of local lesions of the temporal lobes

I. Lower medial divisions (amygdala and hippocampus)

1. Amnesia

II. Anterior pole (bilateral injuries)

1. Kluver-bushy (Kluver-strongucy) syndrome
   • visual agnosia
   • oral-research behavior
   • emotional disorders
   • hypersexuality
   • reduction in motor activity
   • "Hypermetamorphosis" (any visual stimulus distracts attention)

III. Lower-lateral departments

1. Dominant hemisphere
   • Transcortical sensory aphasia
   • Amnestic (nominal) aphasia
2. Non-dominant hemisphere
   • Deterioration of recognition of facial emotional expression.

IV. Upper-laterals

1. Dominant hemisphere
   • "Pure" verbal deafness
   • Sensory aphasia
2. Non-dominant hemisphere
   • sensory amusement
   • sensory aposthody
3. Bilateral damage
   • Auditory agnosia
   • Contralateral upper quadrant hemianopsia

V. Non-localized damage

1. Auditory hallucinations
2. Complex visual hallucinations

VI. Epileptic phenomena (mainly lower medial)

1. Interictal manifestations (below items 1 to 6, plus a. Or b.)

1. Excessive affectation
2. Propensity to transcendental experiences ("cosmic vision")
3. Propensity to detail and detail
4. Paranoid Ideas
5. Hypersexuality
6. Abnormal religiosity
   • Left hemisphere epileptic foci
   1. Propensity to form unusual ideas
   2. Paranoia
   3. Feeling of foresight of your destiny
   • Right hemispheric epileptic foci
   1. Emotional disorders (sadness, high spirits)
   2. Use of the defensive mechanism of negation

2. Ictal manifestations

1. Taste and olfactory hallucinations
2. Visual and other deceptions of the senses (deja vu, etc.)
3. Psychomotor seizures (a variety of temporomandibular partial complex seizures)
4. Vegetative disorders

I. Lower medial divisions (amygdala and hippocampus)

Memory impairment (amnesia) refers to the most characteristic manifestations of lesions of the temporal lobe, especially its lower median parts.

Bilateral damage to the deep sections of the temporal lobe (both hippocampi) leads to global amnesia. When the left temporal lobe is removed and seizures from the left temporal lobe develop, a deficit of verbal memory develops (which always becomes more noticeable when the hippocampus is involved). Damage to the right temporal lobe results in a memory impairment predominantly in non-verbal information (faces, senseless figures, smells, etc.).

II. Anterior pole (bilateral injuries)

Such damage is accompanied by the development of the Kluver-Bussey syndrome. The latter is rare and manifests apathy, indifference to decreased motor activity, mental blindness (visual agnosia), increased sexual and oral activity, hyperactivity to visual stimuli (any visual stimulus distracts attention).

III. Lower-lateral departments

The lesions of the dominant hemisphere, leading to foci in the left temporal lobe in right-handers, are manifested by symptoms of transcortical sensory aphasia. With a focus located in the posterior regions of the temporal region involving the lower part of the parietal lobe, it is possible to determine the "name of the objects" (amnestic or nominal aphasia).

The defeat of the non-dominant hemisphere, in addition to the deterioration of non-verbal mnestic functions, is accompanied by a deterioration in the recognition of mimic emotional expression.

IV. Upper-laterals

The defeat of this area (the posterior part of the upper temporal gyrus, the Wernicke region) in the dominant hemisphere leads to a loss of the ability to understand speech ("pure" verbal deafness). In connection with this, control over one's own speech falls out: sensory aphasia develops. Sometimes, when the left hemisphere is dominant in speech, the perception of voice and the discrimination of phonemes (identification of phonemes) are more violated in the right ear than in the left ear.

The defeat of these departments in the non-dominant hemisphere leads to violation of discrimination of non-verbal sounds, their height and tonality (sensory amusia), as well as to the deterioration of fine discrimination of emotional vocalization (sensory apoptosis).

The bilateral injuries of both primary auditory regions (Gesheli convolution) can lead to auditory agnosia (cortical deafness). The auditory agnosia develops.

The involvement of the visual loop (around the temporal horn of the lateral ventricle) can cause contralateral upper quadrant hemianopsia or complete homonymous hemianopsia. Bilateral injuries involving the occipital associative cortex can cause agnosia of objects.

Aesthetic evaluation of visually perceived objects can be disrupted if the right temporal lobe is damaged.

V. Non-localized damage

Auditory hallucinations and complex visual hallucinations (as well as olfactory and taste), as well as autonomic and respiratory symptoms in the form of distinct clinical signs are observed mainly in the picture of aura of epileptic seizures.

VI. Epileptic phenomena (mainly lower medial).

Changes in personality and mood as persistent interictal manifestations in patients with temporal epilepsy reflect the influence of either the underlying disease that caused damage to the temporal lobe or the effect of epileptic discharges on the deep limbic structures of the brain. Such changes include: excessive affectation, a tendency to transcendental experiences ("cosmic vision"), a tendency to detail and circumstance, affective rigidity and paranoid ideas, hypersexuality, abnormal religiosity. At the same time left hemisphere foci mostly cause ideator disorders, and right hemisphere foci are emotionally affective.

Ictal manifestations are very diverse. Auditory, olfactory and taste hallucinations are usually the initial symptom (aura) of an epileptic fit. The olfactory aura can also be caused (more rarely) by the lobedolevy fits.

Visual hallucinations here are more complex (deja vu, etc.) than when stimulating the visual (occipital) cortex.

The temporo-partial partial complex seizures are very diverse. Automatisms - non-convulsive motor manifestations of seizures - are almost always accompanied by a disturbance of consciousness. They can be perseverative (the patient repeats the activity that he started before the seizure) or manifests new actions. Automatisms can be classified into simple (for example, the repetition of such elementary movements as chewing and swallowing) and interactive. The latter are manifested by coordinated acts, in which the active interaction of the patient with the environment is reflected.

Another type of seizure is the temporal lobar syncope. The latter is manifested by the fall of the patient as in a syncope (with or without a typical aura of temporal seizure). Consciousness is usually lost and in the postictal period the patient, as a rule, is confused or deafened. In each of these types of automatism, the patient amnesizes what is happening during the seizure. The convulsions in such attacks generally spread beyond the temporal lobe in which they began. Before motor activity in a fit, the initial sign in the form of a typical "stopped look" is very characteristic.

Epileptic "drop-attacks" can also occur with partial seizures of extramarine origin or in primary generalized seizures.

Ictal speech is often observed in complex partial seizures. In more than 80% of cases, the source of discharges comes from a non-dominant (right) temporal lobe. In contrast, post-aphthous aphasia is typical for focal points in the dominant temporal lobe.

Dystonic postures in the arm or leg, contralateral corresponding temporal lobe, can be observed with complex partial seizures. They are presumably due to the spread of convulsive discharges to the basal ganglia.

Clonic jerks on the face often appear ipsilateral to the temporal epileptic focus. Other somatomotor manifestations of temporal seizures (tonic, clonic, postural) appearing at subsequent stages of the seizure process indicate the ictal involvement of other brain structures. Such seizures often become secondary generalized.

Changes in mood or affect are typical of temporal seizures. The most common emotion is fear, which can develop as the first symptom of a seizure (typical of amygdala involvement). In such cases, it is accompanied by characteristic vegetative symptoms in the form of pallor, tachycardia, hyperhidrosis, pupil changes and piloerection. Sexual arousal sometimes appears in the early phases of a seizure.

The content of consciousness in a fit can be violated by the type of deja vu, forced thinking, depersonalization and violation of time perception (the illusion of an accelerated or delayed course of events).

All of the above can be summarized in another way, indicating first the list of the main neurologic syndromes of damage to temporal lobes, and then listing the epileptic phenomena characteristic for this localization.

A. List of syndromes, which are detected when the right, left and both temporal lobes are damaged.

I. Any (right or left) temporal lobe.

1. Violation of olfactory identification and discrimination
2. Paresis of the contralateral lower face with a spontaneous smile
3. Defect of the field of view, especially in the form of a homonymous, incongruent, upper-quadrant hemianopsia.
4. Increased auditory threshold for high-frequency sounds and auditory inattention to the contralateral ear.
5. Reduced sexual activity.

II. Non-dominant (right) temporal lobe.

1. Deterioration of nonverbal mnestic functions
2. Deterioration of discrimination of nonverbal sounds, their height and tonality, worsening of discrimination of emotional vocalization.
3. Deterioration of discrimination of olfactory stimuli.
4. Defect of visual perception.

III. Dominant (left) temporal lobe.

1. Impairment of verbal memory
2. Deterioration of the identification of phonemes, especially the right ear
3. Dysnomia (dysnomia).

IV. Both temporal lobes.

1. Global amnesia
2. Kluver-Buci Syndrome
3. Visible agnosia
4. Cortical deafness.
5. Auditory agnosia.

B. Epileptic phenomena, characteristic for temporal localization of epileptic focus.

I. The anterior pole and the inner part (including the hippocampus and amygdala) of the temporal lobe.

1. Epigastric discomfort
2. Nausea
3. An initial "stopped look"
4. Simple (oral and other) automatisms
5. Vegetative manifestations (pallor, hot flashes, rumbling in the abdomen, dilated pupils, etc.). More common in epileptic focus in the right temporal lobe.
6. Fear or Panic
7. Confusion of consciousness
8. Deja vu.
9. Vocalization.
10. Stop breathing.

II. The posterior and lateral part of the temporal lobe.

1. Mood Changes
2. Auditory hallucinations
3. Spotting spatial hallucinations and illusions.
4. Ictal and postictal aphasia.
5. Current ictal speech (usually with focus in the non-dominant hemisphere).
6. Ictal or postictal disorientation.
7. Ictal speech stopping (epileptic focus in the lower temporal gyrus of the dominant hemisphere).

III. Non-localized epileptic foci in the temporal lobe.

1. Dystonic postures in opposite extremities
2. Reduction of motor activity in the opposite limbs during the automatism.

[1], [2]