Symptoms of frontal lobe lesions

Central paralysis and paresis occur when foci are localized in the precentral gyrus. Somatic representation of motor functions approximately corresponds to that for cutaneous sensitivity in the postcentral gyrus. Due to the large extent of the precentral gyrus, focal pathological processes (vascular, tumor, traumatic, etc.) usually affect it partially rather than all of it. Localization of a pathological focus on the outer surface causes mainly paresis of the upper limb, facial muscles, and tongue (linguofaciobrachial paresis), and on the medial surface of the gyrus - mainly paresis of the foot (central monoparesis). Paresis of gaze in the opposite direction is associated with damage to the posterior part of the middle frontal gyrus ("the patient looks at the lesion"). Less often, with cortical foci, paresis of gaze in the vertical plane is observed.

Extrapyramidal disorders in frontal lobe lesions are very diverse. Hypokinesis as an element of parkinsonism is characterized by decreased motor initiative, aspontaneity (limited motivation for voluntary actions). Less often, hyperkinesis occurs in frontal lobe lesions, usually during voluntary movements. Muscle rigidity is also possible (more often in deep foci).

Other extrapyramidal symptoms are grasping phenomena - involuntary automatic grasping of objects placed on the palm (Janiszewski-Bechterew reflex), or (which is observed less often) an obsessive desire to grasp an object appearing before the eyes. It is clear that in the first case the reason for the involuntary motor act is the impact on the skin and kinesthetic receptors, in the second - visual stimuli associated with the functions of the occipital lobes.

When the frontal lobes are affected, the reflexes of oral automatism are activated. It is possible to evoke the proboscis and palmar-chin (Marinescu-Radovići), less often the nasolabial (Astvatsaturova) and distant-oral (Karchikyan) reflexes. Sometimes the "bulldog" symptom (Yaniszewski's symptom) is encountered - in response to touching the lips or the mucous membrane of the oral cavity with some object, the patient convulsively clenches the jaws.

In case of damage to the anterior parts of the frontal lobes with the absence of paresis of the limbs and facial muscles, one can notice an asymmetry in the innervation of the facial muscles during the patient’s emotional reactions – the so-called “mimic paresis of the facial muscles”, which is explained by the disruption of the connections between the frontal lobe and the thalamus.

Another sign of frontal pathology is the symptom of counter-intention or resistance, which appears when the pathological process is localized in the extrapyramidal parts of the frontal lobes. During passive movements, involuntary tension of the antagonist muscles occurs, which creates the impression of conscious resistance of the patient to the actions of the examiner. A particular example of this phenomenon is the symptom of closing the eyelids (Kokhanovsky's symptom) - involuntary tension of the orbicularis oculi muscle with closing of the eyelids when the examiner tries to passively lift the patient's upper eyelid. It is usually observed on the side of the pathological focus in the frontal lobe. The same involuntary contraction of the occipital muscles during passive tilting of the head or extension of the lower limb at the knee joint can create a false impression of the presence of a meningeal symptom complex in the patient.

The connection of the frontal lobes with the cerebellar systems (fronto-pontocerebellar tract) explains the fact that when they are damaged, there are disorders of movement coordination (frontal ataxia), which is manifested mainly by truncal ataxia, the inability to stand and walk (astasia-abasia) with a deviation of the body to the side opposite the lesion.

The frontal cortex is a vast field of the kinesthetic analyzer, therefore damage to the frontal lobes, especially the premotor zones, can cause frontal apraxia, which is characterized by incompleteness of actions. Frontal apraxia occurs due to a violation of the program of complex actions (their purposefulness is lost). Damage to the posterior section of the inferior frontal gyrus of the dominant hemisphere leads to the development of motor aphasia, and damage to the posterior section of the middle frontal gyrus leads to "isolated" agraphia.

Changes in the behavioral and psychic spheres are very peculiar. They are referred to as "frontal psyche." In psychiatry, this syndrome is called apathetic-abulic: patients are seemingly indifferent to their surroundings, their desire to perform voluntary actions (motivation) is reduced. At the same time, there is almost no criticism of their actions: patients are prone to flat jokes (moria), they are often good-natured even in a serious condition (euphoria). These mental disorders can be combined with untidiness (a manifestation of frontal apraxia).

Symptoms of frontal lobe irritation are manifested by epileptic seizures. They are varied and depend on the localization of the irritation foci.

Jacksonian focal seizures occur as a result of irritation of individual areas of the precentral gyrus. They are limited to unilateral clonic and tonic-clonic seizures on the opposite side in the facial muscles, upper or lower limb, but may later generalize and develop into a general seizure with loss of consciousness. When the tegmental part of the inferior frontal gyrus is irritated, attacks of rhythmic chewing movements, smacking, licking, swallowing, etc. occur (opercular epilepsy).

Adversive seizures are sudden convulsive turns of the head, eyes and the whole body in the direction opposite to the pathological focus. The attack may end with a general epileptic seizure. Adversive seizures indicate the localization of epileptic foci in the extrapyramidal parts of the frontal lobe (posterior parts of the middle frontal gyrus - fields 6, 8). It should be noted that turning the head and eyes to the side is a very common symptom of seizures and indicates the presence of foci in the opposite hemisphere. When the cortex is destroyed in this zone, the head turns in the direction of the location of the focus.

Generalized convulsive (epileptic) attacks without visible focal symptoms occur when the poles of the frontal lobes are affected; they are manifested by sudden loss of consciousness, muscle spasms on both sides of the body; biting of the tongue, foaming at the mouth, and involuntary urination are often observed. In some cases, it is possible to determine the focal component of the lesion in the post-attack period, in particular, temporary paresis of the limbs on the opposite side (Todd's paralysis). Electroencephalographic examination can reveal interhemispheric asymmetry.

Attacks of frontal automatism are complex paroxysmal mental disorders, behavioral disorders, in which patients unconsciously, unmotivatedly, automatically perform coordinated actions that can be dangerous to others (arson, murder).

Another type of paroxysmal disorders with frontal lobe lesions are minor epileptic seizures with sudden loss of consciousness for a very short period of time. The patient's speech is interrupted, objects fall out of his hands, and less often, a continuation of the movement he started (for example, walking) or hyperkinesis (more often myoclonus) is observed. These short-term loss of consciousness are explained by the close connections of the frontal lobes with the median structures of the brain (subcortical and stem).

When the base of the frontal lobe is affected, homolateral anosmia (hyposmia), amblyopia, amaurosis, and Kennedy syndrome (atrophy of the optic nerve papilla on the side of the lesion, and congestion in the fundus on the opposite side) develop.

The symptoms described show that when the frontal lobes are affected, mainly movement and behavioral disorders are observed. Vegetative-visceral disorders (vasomotor, breathing, urination) are also encountered, especially with lesions in the medial parts of the frontal lobes.

Syndromes of local damage of the frontal lobes

I. Precentral gyrus (motor area 4)

1. Facial area (unilateral damage - transient disorder, bilateral - permanent)
   • Dysarthria
   • Dysphagia
2. Arm area
   • Contralateral weakness, awkwardness, spasticity
3. Leg region (paracentral lobule)
   • Contralateral weakness
   • Apraxia of gait
   • Urinary incontinence (long-term with bilateral injuries)

II. Medial sections (F1, cingulate gyrus)

1. Akinesia (bilateral akinetic mutism)
2. Perseverations
3. Grasping reflex in the hand and foot
4. Alien hand syndrome
5. Transcortical motor aphasia
6. Difficulty initiating movements of the contralateral arm (may require medical assistance)
7. Bilateral ideomotor apraxia

III. Lateral divisions, premotor area

1. Middle frontal gyrus (F2)
   • Impairment of contralateral saccades
   • Pure agraphia (dominant hemisphere)
   • Contralateral weakness of the shoulder (mainly abduction and elevation of the arm) and thigh muscles plus apraxia of the limbs.
2. F2 dominant hemisphere. Motor aphasia

IV. Frontal pole, orbitofrontal region (prefrontal)

1. Apathy, indifference
2. Reducing criticism
3. Deterioration of goal-directed behavior
4. Impotence
5. Foolishness (moriah), disinhibition
6. Environment Dependency Syndrome
7. Apraxia of speech

V. Epileptic phenomena characteristic of the frontal localization of the epileptic focus.

VI. Damage to the corpus callosum (callosal syndromes)

1. Insufficiency of interhemispheric kinesthetic transfer
   • Inability to imitate the position of the contralateral arm
   • Apraxia of the left hand
   • Agraphia of the left hand
   • Constructional apraxia of the right hand
   • Intermanual conflict (alien hand syndrome)
2. Tendency to confabulate and give unusual explanations for the behavior of one's left hand
3. Double hemianopsia.

The most common manifestation of frontal dysfunction is a defect in the ability to organize ongoing cognitive and behavioral acts. Motor functions can be impaired both in the direction of hyperkinesia (motor hyperactivity) with increased distractibility by external stimuli, and in the form of hypokinesia. Frontal hypokinesia is manifested by decreased spontaneity, loss of initiative, slow reactions, apathy, and decreased facial expression. In extreme cases, akinetic mutism develops. It is caused by bilateral damage to the lower medial frontal and anterior parts of the cingulate gyrus (interruption of connections of the frontal cortex with the diencephaloneum and the ascending activating reticular formation).

Characteristic features include problems maintaining attention, the appearance of perseverations and stereotypies, compulsive-imitative behavior, mental sluggishness, and weakening of memory and attention. Unilateral inattention, affecting motor and sensory functions, most often observed with parietal damage, can also be observed after damage to the supplementary (additional motor) and cingulate (belt) areas. Global amnesia has been described with massive damage to the medial parts of the frontal lobe.

Also characteristic is the accentuation of premorbid personality traits, often the appearance of depressive disorders, especially after damage to the anterior sections on the left side. Typically, there is a decrease in criticism, hyposexuality or, conversely, hypersexuality, exhibitionism, foolishness, puerile behavior, disinhibition, moria. An increase in mood in the form of euphoria is more common with right-sided damage than with left-sided damage. Here, moria-like symptoms are accompanied by an elevated mood in combination with motor excitement, carelessness, a tendency to flat, rude jokes and immoral acts. Sloppiness and untidiness of the patient are typical (urination in the ward on the floor, in bed).

Other manifestations include changes in appetite (especially bulimia) and polydipsia, gait disturbances in the form of apraxia of walking or a “marche a petite pas” gait (walking with small, short steps and shuffling).

Precentral gyrus (motor area 4)

Varying degrees of motor paresis in the arm may be observed with posterior frontal lesions, as well as speech disorders with damage to these areas in the left hemisphere. Dysarthria and dysphagia with unilateral damage are often transient, with bilateral damage they are permanent. Impaired motor function in the leg is typical for damage to the paracentral lobe (contralateral weakness, or apraxia of walking). For the same localization, urinary incontinence is typical (long-term with bilateral damage).

Medial regions (F1, cingulate gyrus)

The so-called "anterior akinetic mutism syndrome" is characteristic of damage to the medial parts of the frontal lobe, in contrast to the "posterior" (or mesencephalic) similar syndrome. In the case of an incomplete syndrome, "frontal akinesia" occurs. Damage to the medial parts is sometimes accompanied by impaired consciousness, oneiroid states, and memory impairment. Motor perseverations may appear, as well as a grasping reflex in the hand and its analogue in the leg. "Bowing" seizures have been described, as well as such an unusual phenomenon as alien hand syndrome (a feeling of alienness of the upper limb and involuntary motor activity in it.) The latter syndrome has also been described in damage to the corpus callosum (less often - in other localizations). Transcortical motor aphasia (described only in frontal lesions) and bilateral ideomotor apraxia may develop.

Lateral divisions, premotor area

A lesion of the posterior sections of the second frontal gyrus causes paralysis of gaze in the direction opposite to the lesion (the patient "looks at the lesion"). Less severe lesions result in worsening of contralateral saccades. In the left hemisphere, close to this zone, there is an area (the upper premotor), the lesion of which causes isolated agraphia ("pure agraphia" not associated with motor aphasia). A patient with agraphia is unable to write even individual letters; a mild lesion of this area may manifest itself only in an increased frequency of spelling errors. In general, agraphia may also develop with local lesions of the left temporal and left parietal lobes, especially near the Sylvian fissure, as well as with involvement of the basal ganglia on the left.

Damage to the posterior part of the third frontal gyrus in Broca's area causes motor aphasia. Incomplete motor aphasia is characterized by decreased speech initiative, paraphasia, and agrammatism.

Frontal pole, orbitofrontal cortex

Damage to these areas is characterized by apathy, indifference, aspontaneity, as well as mental disinhibition, decreased critical thinking, silliness (moria), disorders of purposeful behavior, and dependence on the immediate environment. Impotence may develop. Oral and manual apraxia are very typical for damage to the left anterior areas. When the orbital surface of the brain is involved (e.g., meningioma), unilateral anosmia or unilateral optic nerve atrophy may be observed. Foster-Kennedy syndrome is sometimes observed (decreased sense of smell and vision on one side and stagnant papilla on the opposite side).

Damage to the corpus callosum, especially its anterior parts, separating the frontal lobes, is accompanied by specific syndromes of apraxia, agraphia (mainly in the left non-dominant hand), and other rarer syndromes (see below the section “Damage to the corpus callosum”).

The above neurological syndromes can be summarized as follows:

Any (right or left) frontal lobe.

1. Contralateral paresis or incoordination of the arm or leg.
2. Kinetic apraxia in the proximal parts of the contralateral hand (premotor area lesion).
3. Grasp reflex (contralateral supplementary motor area).
4. Decreased activity of facial muscles in voluntary and emotional movements.
5. Contralateral oculomotor neglect during voluntary gaze movements.
6. Hemi-inattention.
7. Perseverations and mental torpidity.
8. Cognitive impairment.
9. Emotional disturbances (aspontaneity, decreased initiative, affective flattening, lability.
10. Impaired olfactory discrimination of odors.

Non-dominant (right) frontal lobe.

1. Instability of the motor sphere (motor program): what is designated in foreign literature by the term “motor impersistence”, which does not have a generally accepted translation into Russian.
2. Inadequate perception (understanding) of humor.
3. Disturbances in the flow of thinking and speech.

Dominant (left) frontal lobe.

1. Motor aphasia, transcortical motor aphasia.
2. Oral apraxia, apraxia of the limbs with preserved understanding of gestures.
3. Impaired fluency of speech and gestures.

Both frontal lobes (simultaneous damage to both frontal lobes).

1. Akinetic mutism.
2. Problems with bimanual coordination.
3. Aspontaneity.
4. Apraxia of gait.
5. Urinary incontinence.
6. Perseverations.
7. Cognitive impairment.
8. Memory impairment.
9. Emotional disturbances.

Epileptic phenomena characteristic of frontal localization of the epileptic focus

Frontal lobe irritation syndromes depend on its localization. For example, stimulation of Brodmann's field 8 causes deviation of the eyes and head to the side.

Epileptic discharges in the prefrontal cortex tend to generalize rapidly into a grand mal seizure. If the epileptic discharge extends to area 8, a versive component of the seizure may be observed before secondary generalization.

Many patients with complex partial seizures have frontal rather than temporal origin. The latter are usually shorter (often 3-4 sec.) and more frequent (up to 40 per day); there is partial preservation of consciousness; patients come out of the seizure without a state of confusion; characteristic automatisms are typical: rubbing of the hands and blows, finger snaps, shuffling movements of the legs or pushing them; head nodding; shoulder shrugging; sexual automatisms (manipulation of the genitals, pushing of the pelvic region, etc.); vocalization. Vocal phenomena include swearing, screaming, laughter, as well as simpler inarticulate sounds. Breathing may be irregular or unusually deep. In seizures originating from the medial prefrontal region, a tendency to mild development of epileptic status is noted.

Unusual ictal manifestations may cause erroneous overdiagnosis of pseudoseizures (so-called epileptic "pseudo-pseudo seizures", "salute" seizures, etc.). Since most of these seizures originate in the medial (supplementary area) or orbital cortex, routine scalp EEG often does not detect any epileptic activity. Frontal seizures develop more easily during sleep than other types of epileptic seizures.

The following specific epileptic phenomena of frontal origin have been described:

Primary motor area.

1. Focal clonic jerks (jerks), more often seen in the contralateral arm than in the face or leg.
2. Stopping speech or simple vocalization (with or without salivation).
3. Jackson Motor March.
4. Somatosensory symptoms.
5. Secondary generalization (transition to a generalized tonic-clonic seizure).

Premotor area.

1. Simple tonic movements of axial and adjacent muscles with versive movements of the head and eyes to one side
2. Secondary generalization is typical.

Supplementary motor area.

1. Tonic elevation of the contralateral arm and shoulder with flexion at the elbow joint.
2. Turning the head and eyes towards the raised hand.
3. Stopping speech or simple vocalization.
4. Stopping current motor activity.

Cingulate gyrus.

1. Affective disorders.
2. Automatisms or sexual behavior.
3. Vegetative disorders.
4. Urinary incontinence.

Fronto-orbital region.

1. Automatisms.
2. Olfactory hallucinations or illusions.
3. Vegetative disorders.
4. Secondary generalization.

Prefrontal region.

1. Complex partial seizures: frequent, brief seizures with vocalization, bimanual activity, sexual automatisms, and minimal postictal confusion.
2. Frequent secondary generalization.
3. Forced thinking.
4. Aversive head and eye movements or contraversive body movements.
5. Axial clonic jerks and falls of the patient.
6. Vegetative signs.

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Corpus callosum lesions (callosal syndromes)

Damage to the corpus callosum leads to disruption of the interaction processes between the hemispheres, disintegration (disconnection) of their joint activity. Diseases such as trauma, cerebral infarction or tumor (less often - multiple sclerosis, leukodystrophy, radiation damage, ventricular shunting, agenesia of the corpus callosum), which affect the corpus callosum, usually involve interhemispheric connections of the middle sections of the frontal lobes, parietal or occipital lobes. Disruption of interhemispheric connections in itself has almost no effect on everyday life, but is detected when performing certain tests. In this case, an inability to imitate the position of one hand with the other (contralateral) is revealed due to the fact that kinesthetic information is not transferred from one hemisphere to the other. For the same reason, patients are unable to name an object that they feel with their left hand (tactile anomia); they have agraphia in the left hand; they cannot copy with the right hand the movements performed by the left (constructive apraxia in the right hand). Sometimes an "intermanual conflict" (the "alien hand" syndrome) develops, when uncontrolled movements in the left hand are initiated by voluntary movements of the right hand; the phenomenon of "double hemianopsia" and other disorders have also been described.

Perhaps the greatest clinical significance is the phenomenon of the "alien hand", which can result from combined callosal and medial frontal damage. Less often, this syndrome occurs with parietal damage (usually in the picture of paroxysmal manifestations of an epileptic seizure). This syndrome is characterized by a feeling of alienness or even hostility of one hand, involuntary motor activity in it, which is unlike any other known forms of movement disorders. The affected hand seems to "live its own independent life", involuntary motor activity is observed in it, similar to voluntary purposeful movements (palpation, grasping and even autoaggressive actions), which constantly stresses these patients. A typical situation is also when during involuntary movements the healthy hand "holds" the sick one. The hand is sometimes personified with a hostile, uncontrollable alien "evil and disobedient" force.

Alien hand syndrome has been described in vascular infarctions, corticobasal degeneration, Creutzfeldt-Jakob disease, and some atrophic processes (Alzheimer's disease).

A rare syndrome of damage to the central part of the anterior sections of the corpus callosum is the Marchiafava-Beñami syndrome, which is related to alcohol-induced damage to the nervous system. Patients suffering from severe alcoholism note in their anamnesis a periodic syndrome of alcohol withdrawal with tremors, epileptic seizures and delirium tremens. Some of them develop severe dementia. Dysarthria, pyramidal and extrapyramidal symptoms, apraxia, aphasia are characteristic. In the last stage, patients are in a deep coma. The diagnosis is made during life very rarely.

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