Symptoms of frontal lobe involvement
Last reviewed: 23.04.2024
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Central paralysis and paresis occur when the foci are localized in the precentral gyrus. Somatic representation of motor functions approximately corresponds to that for skin sensitivity in the postcentral gyrus. Because of the large extent of the precentral gyrus, focal pathological processes (vascular, tumor, traumatic, etc.) usually affect it not all, but in part. Localization of the pathological focus on the outer surface causes predominantly paresis of the upper limb, mimic muscles and tongue (lingvofacreobacterial paresis), and on the medial surface of the gyrus - predominantly the paresis of the foot (central monoparesis). Paresis of the eye in the opposite direction is associated with the lesion of the posterior part of the middle frontal gyrus ("the patient looks at the lesion"). Less often, in cortical foci, there is a paresis of the gaze in the vertical plane.
Extrapyramidal disorders in the lesions of the frontal lobes are very diverse. Hypokinesis as an element of parkinsonism is characterized by a decrease in motor initiative, aspontaneity (restriction of motivation to arbitrary actions). Less often, lesions of the frontal lobes cause hyperkinesis, usually during the execution of arbitrary movements. It is possible and rigidity of the muscles (more often with deep foci).
Other extrapyramidal symptoms are grasping phenomena - involuntary automatic seizure of objects applied to the palm (Yanishevsky-Bekhterev reflex), or (which is observed less often) obsessive desire to grasp the object appearing before the eyes. It is clear that in the first case, the cause for an involuntary motor act is the effects on the skin and kinesthetic receptors, in the second - visual irritations associated with the functions of the occipital lobes.
When lesions of the frontal lobes reflexes of oral automatism are animated. You can cause proboscis and palmar-chin (Marinescu-Radovici), less often nasolabial (Astvatsaturov) and distant-oral (Karchikian) reflexes. Sometimes there is a symptom of "bulldog" (Yanishevsky's symptom) - in response to a touch to the lips or mucous membrane of the oral cavity, any object of the patient clenches jaws convulsively.
When the fore parts of the frontal lobes are damaged in the absence of paresis of the limbs and facial musculature, one can see the asymmetry of innervation of facial muscles in emotional reactions of the patient - the so-called "mimic paresis of the facial musculature", which is explained by the violation of the frontal lobe connection with the visual tubercle.
Another sign of frontal pathology is a symptom of confrontation or resistance, which appears when the pathological process is localized in the extrapyramidal sections of the frontal lobes. With passive movements, there is an involuntary tension of the antagonist muscles, which creates the impression of a patient's conscious resistance to the actions of the examinee. A particular example of this phenomenon is the symptom of the closing of the eyelids (Kochanovsky's symptom) - the involuntary tension of the circular muscle of the eye with the closing of the eyelids when the researcher attempts to lift the upper eyelid of the patient passively. It is usually observed on the side of the pathological focus in the frontal lobe. The same involuntary contraction of the occipital muscles with a passive tilt of the head or extension of the lower limb in the knee joint may create a false impression of the patient having a meningeal symptom complex.
The connection of the frontal lobes with the cerebellar system (frontal-bridge cough path) explains the fact that in their defeat there are disorders of coordination of movements (frontal ataxia), which is manifested mainly by trunk ataxia, inability to stand and walk (astasia-abasia) with the deviation of the body into the opposite hearth lesion side.
The cortex of the frontal lobes is an extensive field of the kinesthetic analyzer, therefore lesions of the frontal lobes, especially of the premotor zones, can cause frontal apraxia, for which the incompleteness of actions is characteristic. Frontal apraxia arises from the violation of the program of complex actions (their purposefulness is lost). The defeat of the posterior part of the lower frontal gyrus of the dominant hemisphere leads to the appearance of motor aphasia, and the posterior part of the middle frontal gyrus leads to "isolated" agraphy.
Very peculiar changes in the sphere of behavior and psyche. They are spoken of as "frontal psyche". In psychiatry, this syndrome was called Apatiko-Abulic: the sick, as it were, are indifferent to the environment, they have a reduced desire to carry out arbitrary actions (motivation). At the same time, there is almost no criticism of their actions: patients are prone to flat jokes (moria), they are often benign even in a serious condition (euphoria). These mental disorders can be combined with untidiness (manifestation of frontal apraxia).
Symptoms of frontal lobe irritation are manifested by epileptic seizures. They are diverse and depend on the localization of foci of irritation.
Jacksonian focal convulsive attacks occur as a result of irritation of individual sections of the precentral gyrus. They are limited to one-sided clonic and tonic-clonic seizures on the opposite side in the musculature of the face, upper or lower limb, but may subsequently generalize to a general convulsive fit with loss of consciousness. When the upper part of the lower frontal gyrus irritates, there are attacks of rhythmic masticatory movements, smacking, licking, swallowing, etc. (opercular epilepsy).
Adverse seizures are a sudden convulsive turn of the head, eyes and whole body into the opposite pathological focus. The attack can result in a general epileptic seizure. Adverse seizures indicate the localization of epileptic foci in the extrapyramidal sections of the frontal lobe (the posterior sections of the median frontal gyrus are fields 6, 8). It should be noted that turning the head and eyes aside is a very common symptom of convulsive seizures and it indicates the presence of foci in the opposite hemisphere. When the cortex is destroyed in this zone, the head is rotated toward the location of the focus.
General convulsive (epileptic) seizures without visible focal symptoms occur when the poles of the frontal lobes are affected; they are manifested by a sudden loss of consciousness, muscle cramps on both sides of the body; often bite the tongue, foam from the mouth, involuntary urination. In a number of cases, it is possible to determine the focal component of the lesion in the post-operative period, in particular the temporary paresis of the extremities on the opposite side (Todd's paralysis). An electroencephalographic study can reveal interhemispheric asymmetry.
Attacks of frontal automatism are complex paroxysmal mental disorders, behavioral disorders in which patients unconsciously, unmotivated, automatically perform coordinated actions that can be dangerous to others (arson, murder).
Another type of paroxysmal disorders with lesions of the frontal lobes is small epileptic seizures with a sudden turn off of consciousness for a very short time. The patient's speech is interrupted, objects fall out of the hands, there is less continuation of the movement (for example, walking) or hyperkinesis (more often myoclonia). These short-term failures of consciousness are explained by close connections of the frontal lobes with the midline structures of the brain (subcortical and stem).
When the base of the frontal lobe is affected, homolateral anosmia (ambusia), amblyopia, amaurosis, Kennedy syndrome (atrophy of the nipple on the side of the focus, on the opposite side - stagnation on the fundus).
The described symptoms show that when lesions of the frontal lobes are observed mainly disorders of movement and behavior. There are also vegetative-visceral disorders (vasomotor, respiration, urination), especially with foci in the medial parts of the frontal lobes.
Syndromes of local injuries of the frontal lobes
I. Precentral gyrus (motor area 4)
- Face area (one-sided damage - transient disturbance, bilateral - permanent)
- Dysatria
- Dysphagia
- Hand area
- Contralateral weakness, awkwardness, spasticity
- Leg area (paracentral lobe)
- Contralateral weakness
- Apraxia walk
- Urinary incontinence (prolonged with bilateral injuries)
II. The medial departments (F1, girdle gyrus)
- Akinesia (bilateral akinetic mutism)
- Perseverations
- Gag reflex in hand and foot
- Syndrome of someone else's hand
- Transcortical motor aphasia
- Difficulties in initiating the movements of the contralateral arm (doctor's help may be required)
- Bilateral ideomotor apraxia
III. Lateral sections, premotor region
- Average frontal gyrus (F2)
- Deterioration of contralateral saccades
- Net agraphy (dominant hemisphere)
- Contralateral weakness of the shoulder (mainly lead and arm lift) and hip muscles plus apraxia of the limbs.
- F2 of the dominant hemisphere. Motor aphasia
IV. The frontal pole, the orbitofrontal region (prefrontal)
- Apathy, indifference
- Reducing criticism
- Impairment of targeted behavior
- Impotence
- Foolishness (moria), disinhibition
- The syndrome of dependence on the environment
- Apraxia of speech
V. Epileptic phenomena, characteristic for the frontal localization of the epileptic focus.
VI. Damage to the corpus callosum (callosal syndromes)
- Inadequacy of interhemispheric kinesthetic transport
- Inability to mimic the position of the contralateral hand
- Apraxia of the left hand
- Agra of the left hand
- Constructive apraxia of the right hand
- Intermanual conflict (a syndrome of someone else's hand)
- Propensity to confabulation and unusual explanations of the behavior of his left hand
- Double (double) hemianopsia.
The most common manifestation of frontal dysfunction is a defect in the ability to organize current cognitive and behavioral acts. Motor functions may be disrupted both in the direction of hyperkinesia (motor hyperactivity) with increased distractibility to external stimuli, and in the form of hypokinesia. Frontal hypokinesia is manifested by a decrease in spontaneity, loss of initiative, slowing of reactions, apathy, a decrease in mimic expression. In extreme cases, akinetic mutism develops. It is caused by bilateral injuries to the inferior medial frontal and anterior regions of the cingulate gyrus (interruption of the frontal cortex with diencephalone and the ascending activating reticular formation).
Characteristic problems in retaining attention, the emergence of perseverations and stereotypes, compulsive-imitative behavior, torpidity of the psyche, weakening of memory and attention. One-sided inattention, affecting motor and sensory functions, most often observed with parietal lesions, can be observed even after damage to the complementary (additional motor) and cingular (waist) area. Global amnesia is described with massive lesions of the medial parts of the frontal lobe.
The accentuation of premorbid features of the personality is also characteristic, often the appearance of depressive disorders, especially after damage to the anterior parts on the left side. Typically, a reduction in criticism, hyposexuality or, conversely, hypersexuality, exhibitionism, foolishness, puerile behavior, disinhibition, moria. Mood swell in the form of euphoria is more common with right-sided injuries than left-sided ones. Here, morio-like symptoms are accompanied by a heightened mood combined with motor excitation, carelessness, a tendency to flat rude jokes and immoral acts. Typical slovenliness and untidiness of the patient (urination in the ward on the floor, in bed).
Of the other manifestations, there are changes in appetite (especially bulimia) and polydipsia, gait irregularities in the form of apraxia walk or gait like "marche a petite pas" (walking in small short steps with shuffling).
Precentral gyrus (motor area 4)
A different degree of motor paresis in the arm can be observed with posterior frontal injuries, as well as speech disorders in case of damage to these departments in the left hemisphere. Dysarthria and dysphagia with unilateral damage are often transient in nature, with bilateral - permanent. Violation of motor functions in the leg is characteristic for the lesion of the paracentral lobule (contralateral weakness, or apraxia walking). For the same localization, incontinence is typical (prolonged with bilateral injuries).
The medial departments (F1, girdle gyrus)
To defeat the medial parts of the frontal lobe, the so-called "anterior syndrome of akinetic mutism" is characteristic, in contrast to the "posterior" (or mesencephalic) analogous syndrome. With incomplete syndrome, there is a "frontal akinesia". The defeat of the medial divisions is sometimes accompanied by a violation of consciousness, onyroid states, memory impairments. Perhaps the appearance of motor perseverations, as well as a grasping reflex in the hand and its analog in the leg. The "bow" seizures are described, as well as an unusual phenomenon like the syndrome of the foreign hand (the feeling of alienity of the upper limb and involuntary motor activity in it.) The latter syndrome is also described in the case of a corpus callosum (less often with other localizations). Perhaps the development of transcortical motor aphasia (described only with frontal lesions), bilateral ideomotor apraxia.
Lateral sections, premotor region
The defeat of the posterior part of the second frontal gyrus causes paralysis of the gaze in the opposite side (the patient "looks at the hearth"). With less severe lesions, there is a worsening of contralateral saccades. In the left hemisphere close to this zone is located the region (upper premotornaya), the defeat of which causes isolated agraphy ("pure agraphia", not associated with motor aphasia). A patient with agrarians is not able to write even single letters; a rough violation of this area can be manifested only by an increase in the frequency of spelling errors. In general, agraphia can also develop with local lesions of the left temporal and left parietal lobe, especially near the Sylvian furrow, and also with the involvement of the basal ganglia on the left.
The defeat of the posterior part of the third frontal gyrus in the Broca region causes motor aphasia. With incomplete motor aphasia, there is a decrease in speech initiation, paraphasia and agrammatism.
Frontal pole, orbitofrontal cortex
For the defeat of these departments is characterized as apathy, indifference, aspontaneity, and mental disinhibition, reduced criticism, foolishness (moria), disorders of purposeful behavior, a syndrome of dependence on the nearest environment. Perhaps the development of impotence. To damage the left anterior parts is very typical oral and manual apraxia. When involving the orbital surface of the brain (for example, meningioma), one-sided anosmia or one-sided atrophy of the optic nerve can be observed. Sometimes there is Foster-Kennedy syndrome (decrease in smell and vision on one side and stagnant nipple on the opposite side).
Damage to the corpus callosum, especially its anterior parts, separating the frontal lobes, is accompanied by peculiar syndromes of apraxia, agraphia (mainly in the left non-dominant hand), and other less frequent syndromes (see the section "Damage to the corpus callosum" below)
The above neurological syndromes can be summarized as follows:
Any (right or left) frontal lobe.
- Contralateral paresis or incoordination of the arm or leg.
- Kinetic apraxia in the proximal parts of the contralateral arm (defeat of the premotor region).
- Grasping reflex (contralateral motor area).
- Decrease in activity of facial muscles in voluntary and emotional movements.
- Contralateral oculomotor neglect (oculomotor neglect) with arbitrary vizor movements.
- Heminievnim (hemi-inattention).
- Perseveration and torpidity of the psyche.
- Cognitive impairment.
- Emotional disorders (aspontaneity, decreased initiative, affective flattening, lability.
- Deterioration of olfactory discrimination of smells.
Non-dominant (right) frontal lobe.
- Instability of the motor sphere (motor program): what is designated in the foreign literature as "motor impersistence", which does not have a generally accepted Russian translation.
- Inadequate perception (understanding) of humor.
- Violations of the flow of thinking and speech.
Dominant (left) frontal lobe.
- Motor aphasia, transcortical motor aphasia.
- Oral apraxia, apraxia of the limbs with a safe understanding of the gestures.
- Violation of smoothness of speech and gestures.
Both frontal lobes (simultaneous defeat of both frontal lobes).
- Akinetichesky mutism.
- Problems with bimanual coordination.
- Aspontaneity.
- Apraxia walking.
- Urinary incontinence.
- Perseveration.
- Cognitive impairment.
- Memory impairment.
- Emotional disorders.
Epileptic phenomena, characteristic for the frontal localization of epileptic focus
Syndromes of stimulation of the frontal lobes depend on its localization. For example, stimulation of the Broadden field 8 causes deviation of the eyes and head to the side.
Epileptic discharges in the prefrontal cortex tend to rapidly generalize into a large convulsive fit. If the epileptic discharge spreads to the field 8, then before the secondary generalization, one can observe the version of the seizure component.
Many patients with complex partial seizures have not a temporal, but a frontal origin. The latter are usually shorter (often 3-4 sec.) And more frequent (up to 40 per day); there is a partial preservation of consciousness; patients get out of a fit without a confusion; Typical characteristic automatisms are typical: rubbing of hands and blows, flicks of fingers, shuffling movements with their feet or jerking them; nodding his head; shrugging shoulders; sexual automatisms (manipulation of the genitals, tremors of the pelvic region, etc.); vocalization. Vocal phenomena include curses, cries, laughter, as well as simpler, non-articulated sounds. Breathing can be irregular or unusually deep. With seizures that result from the medial prefrontal area, there is a tendency to an easy development of epileptic status.
Unusual ictal manifestations can cause erroneous overdiagnosis of pseudo-seizures (so-called epileptic "pseudo-pseudo-fits", "salute" seizures, etc.). Since most of these seizures originate from the medial (complementary area) or the orbital cortex, the usual scalp EEG often shows no epileptic activity. Frontal seizures develop more easily during sleep than other types of epileptic seizures.
The following specific epileptic phenomena of frontal origin are described:
Primary motor area.
- Focal clonic tremors (flinches), more often observed in the opposite hand than in the face or leg.
- Stop speech or simple vocalization (with or without salivation).
- Jackson motor march.
- Somatosensory symptoms.
- Secondary generalization (transition to a generalized tonic-clonic seizure).
The premotor region.
- Simple tonic movements of the axial and contiguous musculature with versions of the head and eye in one direction
- Typical secondary generalization.
Additional motor area.
- Tonic lift of the contralateral arm and shoulder with flexion in the elbow joint.
- Turn the head and eyes toward the raised hand.
- Stop speech or simple vocalization.
- Stop the current motor activity.
Belt gyrus.
- Affective disorders.
- Automatisms or sexual behavior.
- Vegetative disorders.
- Urinary incontinence.
Frontal-orbital region.
- Automatisms.
- Olfactory hallucinations or illusions.
- Vegetative disorders.
- Secondary generalization.
Prefrontal area.
- Complex partial seizures: frequent, short seizures with vocalization, bimanual activity, sexual automatisms and minimal postictal confusion.
- Frequent secondary generalization.
- Forced thinking.
- Adverse movements of the head and eyes or the body's contraversial movements.
- Axial clonic jerks and falls of the patient.
- Vegetative signs.
[1], [2], [3], [4], [5], [6], [7]
Damage to the corpus callosum (callosal syndromes)
Damage to the corpus callosum leads to disruption of hemispheric interaction, disconnection of their joint activity. Diseases such as trauma, cerebral infarction or swelling (less often - multiple sclerosis, leukodystrophy, radiation damage, ventricular shunting, corpus callosum), which affect the corpus callosum usually involve interhemispheric connections of the middle parts of the frontal lobes, parietal or occipital lobes. Violation of interhemispheric connections in itself has almost no effect on everyday household activity, but is found when certain tests are performed. At the same time, the inability to imitate the other (contralateral) positions due to the fact that kinesthetic information is not transferred from one hemisphere to another is revealed. For the same reason, patients are not able to name an object that they touch with their left arm (tactile anomie); they have an agraphia in their left hand; they can not copy the right hand movements that are committed left (constructive apraxia in the right hand). Sometimes there is an "intermanual conflict" (syndrome of "someone else's hand"), when uncontrolled movements in the left hand are initiated by arbitrary movements with the right hand; The phenomenon of "double hemianopsia" and other violations are also described.
Perhaps the greatest clinical significance is the phenomenon of "someone else's hand," which can be the result of combined callosal and medial lesions. Less often this syndrome occurs with parietal lesions (usually in the picture of paroxysmal manifestations of epileptic seizure). This syndrome is characterized by a feeling of alienation or even hostility of one hand, involuntary motor activity in it, which is unlike any other known forms of movement disorders. The affected hand "lives its own life" as if it were, and involuntary motor activity is observed in it, similar to arbitrary targeted movements (feeling, grasping and even autoaggressive actions), which constantly stresses these patients. Typical is also the situation when, during involuntary movements, a healthy hand "holds" the patient. The hand is sometimes personified with a hostile uncontrolled alien "evil and disobedient" force.
The "foreign hand" syndrome is described in vascular infarctions, cortico-basal degeneration, Creutzfeldt-Jakob disease, and some atrophic processes (Alzheimer's disease).
A rare syndrome of damage to the central part of the anterior parts of the corpus callosum is the Marhiafava-Benjami syndrome, which refers to alcoholic lesions of the nervous system. Patients suffering from severe alcoholism, noted in the anamnesis periodic alcohol withdrawal syndrome with trembling, epileptic seizures and white fever. Some of them develop severe dementia. Dysarthria, pyramidal and extrapyramidal symptoms, apraxia, aphasia are characteristic. In the last stage, the patients are in a deep coma. The diagnosis is made during life is very rare.