Symptoms of temporal lobe lesions

When the temporal lobes are damaged, there are disturbances in the functions of the listed analyzers and efferent systems, and disorders of higher nervous activity are manifested by disorientation in the external environment and incomprehension of speech signals (auditory agnosia).

With lesions of the temporal lobes, motor disorders are expressed insignificantly or are absent. Attacks of vestibular-cortical systemic dizziness often occur. Astasia-abasia may appear (as with lesions 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 upper quadrant hemianopsia. The main symptoms of loss and irritation of the temporal lobes are associated with a violation of the analyzer function.

Frequent signs of temporal pathology are hallucinations and epileptic seizures with various auras: olfactory (irritation of the hippocampal gyrus), gustatory (foci near the insular lobule), auditory (superior temporal gyri), vestibular (closure of three lobes - temporal, occipital, parietal). With damage to the mediobasal sections, visceral auras (epigastric, cardiac, etc.) are often observed. Foci deep in the temporal lobe can cause visual hallucinations or auras. General convulsive seizures with loss of consciousness are more often observed when foci are localized in the region of the poles of the temporal lobes. Irradiation of irritation to the temporal zone causes paroxysmal disorders of higher nervous activity.

Paroxysmal mental disorders associated with temporal lobe pathology include various changes in consciousness, which are often defined as dream-like states. During an attack, the patient's surroundings seem completely unfamiliar ("never seen", "never heard") or, conversely, long seen, long heard.

Temporal automatism is associated with disturbances of orientation in the external environment. Patients do not recognize the street, their house, the layout of the rooms in the apartment, and perform many seemingly 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 minor epileptic seizures when these lobes are damaged. These seizures are limited to short-term loss of consciousness without motor disturbances (unlike minor seizures of frontal origin).

The temporal lobes (especially their medio-basal sections) are closely connected with the hypothalamus of the diencephalon and the reticular formation, therefore, when the temporal lobes are damaged, vegetative-visceral disorders very often occur, which will be discussed in the section on damage to the limbic part of the brain.

Damage to the temporal lobe, the posterior part of the superior temporal gyrus (Wernicke's area) causes sensory aphasia or its varieties (amnestic, semantic aphasia). Disorders in the emotional sphere (depression, anxiety, emotional lability and other deviations) are also common. Memory is also impaired. W. Penfidd (1964) believes that the temporal lobes are even the "memory center". However, the memory function is carried out by the entire brain (for example, praxis, i.e. "memory" for actions, is associated with the parietal and frontal lobes, "memory" for recognizing visual images - with the occipital lobes). Memory is especially noticeably impaired in cases of damage to the temporal lobes due to the connections of these lobes with many analyzers. In addition, human memory is largely verbal, which is also associated with the functions of the temporal lobes of the brain.

Syndromes of local damage of the temporal lobes

I. Inferomedial regions (amygdala and hippocampus)

1. Amnesia

II. Anterior pole (bilateral injuries)

1. Kluver-Bucy syndrome
   • visual agnosia
   • oral exploratory behavior
   • emotional disturbances
   • hypersexuality
   • decreased physical activity
   • "hypermetamorphosis" (any visual stimulus distracts attention)

III. Inferolateral sections

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

IV. Upper lateral sections

1. Dominant hemisphere
   • "Pure" verbal deafness
   • Sensory aphasia
2. Non-dominant hemisphere
   • sensory amusia
   • sensory aprosody
3. Bilateral injuries
   • Auditory agnosia
   • Contralateral superior quadrant hemianopsia

V. Non-localized lesions

1. Auditory hallucinations
2. Complex visual hallucinations

VI. Epileptic phenomena (mainly inferomedial)

1. Interictal manifestations (items 1-6 below, plus a. or b.)

1. Excessive affectation
2. Tendency to transcendental experiences ("cosmic vision")
3. Tendency to detail and thoroughness
4. Paranoid ideas
5. Hypersexuality
6. Abnormal religiosity
   • Left hemisphere epileptic foci
   1. Tendency to form unusual ideas
   2. Paranoia
   3. A sense of foreknowledge of one's destiny
   • Right hemisphere epileptic foci
   1. Emotional disturbances (sadness, elation)
   2. Using the defense mechanism of denial

2. Ictal manifestations

1. Gustatory and olfactory hallucinations
2. Visual and other sensory illusions (deja vu, etc.)
3. Psychomotor seizures (various temporal lobe partial complex seizures)
4. Vegetative disorders

I. Inferomedial regions (amygdala and hippocampus)

Memory impairment (amnesia) is one of the most characteristic manifestations of damage to the temporal lobe, especially its lower medial parts.

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

II. Anterior pole (bilateral injuries)

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

III. Inferolateral sections

Dominant hemisphere lesions, leading to foci in the left temporal lobe in right-handed people, manifest symptoms of transcortical sensory aphasia. With a lesion located in the posterior temporal region with involvement of the lower parietal lobe, the ability to determine the "name of objects" is lost (amnestic or nominal aphasia).

Damage to the non-dominant hemisphere, in addition to deterioration of non-verbal mnemonic functions, is accompanied by deterioration in the recognition of facial emotional expression.

IV. Upper lateral sections

Damage to this area (the posterior part of the superior temporal gyrus, Wernicke's area) in the dominant hemisphere leads to the loss of the ability to understand speech ("pure" verbal deafness). In this connection, control over one's own speech also falls away: sensory aphasia develops. Sometimes, when the left (speech-dominant) hemisphere is damaged, voice perception and phoneme discrimination (phoneme identification) are more impaired in the right ear than in the left.

Damage to these areas in the non-dominant hemisphere leads to impaired discrimination of non-verbal sounds, their pitch and tonality (sensory amusia), as well as to deterioration of fine discrimination of emotional vocalizations (sensory aprosody).

Bilateral damage to both primary auditory areas (Geschli's gyrus) can lead to auditory agnosia (cortical deafness). Auditory agnosia develops.

Involvement of the optic loop (around the temporal horn of the lateral ventricle) may cause contralateral superior quadrant hemianopsia or complete homonymous hemianopsia. Bilateral lesions involving the occipital association cortex may cause object agnosia.

Aesthetic evaluation of visually perceived objects may be impaired by damage to the right temporal lobe.

V. Non-localized lesions

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

VI. Epileptic phenomena (mainly inferomedial).

Personality and mood changes as persistent interictal manifestations in patients with temporal epilepsy reflect the influence of either the underlying disease that has damaged the temporal lobe or the influence of epileptic discharges on the deep limbic structures of the brain. Such changes include: excessive affectation, a tendency toward transcendental experiences ("cosmic vision"), a tendency toward detail and thoroughness, affective rigidity and paranoid ideas, hypersexuality, abnormal religiosity. In this case, left-hemisphere foci cause ideational disorders to a greater extent, and right-hemisphere foci cause emotional-affective disorders.

Ictal manifestations are quite varied. Auditory, olfactory and gustatory hallucinations are usually the initial symptom (aura) of an epileptic seizure. Olfactory aura can also be caused (less commonly) by a frontal lobe seizure.

Visual hallucinations here are more complex (deja vu, etc.) than with stimulation of the visual (occipital) cortex.

Temporal lobe partial complex seizures are very diverse. Automatisms - non-convulsive motor manifestations of seizures - are almost always accompanied by impaired consciousness. They can be perseverative (the patient repeats the activity that he began before the seizure) or manifest themselves in new actions. Automatisms can be classified as simple (for example, repetition of such elementary movements as chewing and swallowing) and interactive. The latter are manifested by coordinated acts that reflect the active interaction of the patient with the environment.

Another type of seizure is the temporal lobe "syncope." The latter is manifested by the patient falling as if he were fainting (with or without the typical aura of a temporal seizure). Consciousness is usually lost and in the postictal period the patient is usually confused or stunned. In each of these types of automatisms the patient has amnesia for what happened during the seizure. The convulsive discharges in such seizures usually extend beyond the temporal lobe in which they began. Before the motor activity in the seizure, the initial sign in the form of a typical "fixed gaze" is very characteristic.

Epileptic "drop attacks" can also be observed in partial seizures of extratemporal 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 the non-dominant (right) temporal lobe. In contrast, postictal aphasia is typical for foci in the dominant temporal lobe.

Dystonic posturing in the arm or leg contralateral to the corresponding temporal lobe may be observed in complex partial seizures. They are presumably due to the spread of seizure 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, indicate ictal involvement of other brain structures. Such seizures often become secondarily generalized.

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

The content of consciousness during a seizure may be disrupted by deja vu, forced thinking, depersonalization, and disturbances in time perception (the illusion of accelerated or slowed down flow of events).

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

A. List of syndromes detected with damage to the right, left and both temporal lobes.

I. Any (right or left) temporal lobe.

1. Impaired olfactory identification and discrimination
2. Paresis of the contralateral lower face during spontaneous smiling
3. Visual field defect, especially in the form of homonymous incongruent upper quadrant hemianopsia.
4. Increased hearing threshold for high-frequency sounds and auditory inattention to the contralateral ear.
5. Decreased sexual activity.

II. Non-dominant (right) temporal lobe.

1. Deterioration of non-verbal mnemonic functions
2. Deterioration of discrimination of non-verbal sounds, their pitch and tonality, deterioration of discrimination of emotional vocalization.
3. Impaired discrimination of olfactory stimuli.
4. Visual perception defect.

III. Dominant (left) temporal lobe.

1. Deterioration of verbal memory
2. Impaired phoneme identification, especially in the right ear
3. Dysnomia.

IV. Both temporal lobes.

1. Global amnesia
2. Kluver-Bucy syndrome
3. Visual agnosia
4. Cortical deafness.
5. Auditory agnosia.

B. Epileptic phenomena characteristic of the temporal localization of the epileptic focus.

I. Anterior pole and internal part (including hippocampus and amygdala) of the temporal lobe.

1. Epigastric discomfort
2. Nausea
3. Initial "stopped look"
4. Simple (oral and other) automatisms
5. Vegetative manifestations (paleness, hot flashes, rumbling in the stomach, dilated pupils, etc.) More often encountered with an epileptic focus in the right temporal lobe.
6. Fear or panic
7. Confusion
8. Deja vu.
9. Vocalization.
10. Respiratory arrest.

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

1. Mood swings
2. Auditory hallucinations
3. Visual 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 arrest (epileptic focus in the inferior temporal gyrus of the dominant hemisphere).

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

1. Dystonic postures in opposite limbs
2. Decreased motor activity in opposite limbs during automatism.

[ 1 ], [ 2 ]