Frontal lobe syndrome is a clinical symptom complex that occurs mainly with bilateral damage to the frontal lobes of the brain. The components of the syndrome are disorders of praxis, emotional-volitional sphere, behavior, speech disorders, posture and walking are possible. It is diagnosed according to clinical data, nosology verification is carried out using cerebral neuroimaging (CT, MRI), studies of cerebral circulation. Therapeutic tactics in the frontal symptom complex is determined by the etiology of the lesion, may include drug therapy (appointment of vascular, neuroprotective, psychotropic drugs), neurosurgical treatment (removal of a tumor, hematoma) with subsequent rehabilitation.
ICD 10
F07.0 Personality disorder of organic etiology
General information
Active study of the frontal parts of the brain began in the 70s of the XIX century. Researchers in this field have encountered a number of contradictions. It turned out that the “shutdown” of the frontal lobes is not accompanied by a gross disorder of the motor, sensory, reflex sphere, which led some scientists to conclude that there is no definite functional significance of these cerebral structures. Subsequent study of the issue revealed significant changes in behavior, the psycho-emotional sphere in the defeat of the frontal cortex zones, which allowed the latter to be attributed to the apparatus responsible for the implementation of higher mental functions. Confirmation of this statement is the significant development of the frontal parts of the human brain in comparison with the animal brain.
Causes
The frontal areas of the brain are considered to be the youngest and less differentiated cerebral divisions with a high interchangeability of components, therefore, a pronounced frontal lobe syndrome is observed only with extensive bilateral lesion. The cause of pathological changes are:
- Traumatic brain injuries. Damage to the frontal zones during TBI are quite common, they are the result of a forehead blow or an anti-shock injury to the back of the head. Posttraumatic intracerebral hematomas cause compression of cerebral tissues, epi- and subdural hematomas — compression of the cortex. Direct damage to neurons and interneuronal connections occurs when the brain is bruised.
- Strokes. Blood supply to the frontal lobes is carried out by the anterior and middle cerebral arteries. Violation of the passage of blood through these vessels or their branches causes the development of ischemic stroke — neurons die due to acute hypoxia. When the vessels of this basin are ruptured, a hemorrhagic stroke occurs with hemorrhage into the brain tissues.
- Vascular anomalies. Arterio-venous malformations are dangerous by local expansion of the vessel, thinning and breakthrough of its wall. The blood spilled as a result of the rupture is organized into a hematoma. As the latter increases, compression and death of neurons occur, causing frontal lobe syndrome.
- Tumors. Germinating frontal tissues, cerebral neoplasms cause their destruction and/ or compression. The function of frontal neurons is gradually lost. Clinically, the frontal symptom complex manifests itself with a large tumor size, its spread to the opposite lobe.
- Degenerative diseases. Progressive atrophic processes with frontal lesions are noted in Pick’s disease, frontotemporal dementia, and corticobasal degeneration. Violation of frontal functions occurs due to degenerative changes and subsequent apoptosis of nerve cells, their replacement by glial and connective tissue elements.
Pathogenesis
The frontal divisions perform integrative and regulatory functions that provide complex behavioral reactions, programming and implementation of a sequence of actions. The defeat of the structures of the frontal lobes, their connections with other cerebral departments leads to the disintegration of conscious activity — ideatory apraxia. Complex actions are replaced by simpler, familiar, automated, uncontrollably repetitive ones. The ability to evaluate the result of an action is lost, there is no motivation.
Side effects are disinhibited, there is no purposefulness of behavior. Impulsiveness of reactions, violation of control cause antisocial behavior. The defeat of the posterior frontal parts of the dominant hemisphere leads to the emergence of dynamic aphasia, the Broca’s center leads to the development of efferent motor aphasia. Extensive damage to the frontal lobes is accompanied by a violation of the cortical coordination of skeletal muscle tone, which leads to a loss of consistency of muscle contractions necessary to maintain posture and movements.
Classification
The frontal lobe includes several zones that differ in their functional purpose. The predominance of one or another frontal symptom complex depends on the localization of the lesion. This criterion formed the basis of the classification used in clinical neurology, according to which the frontal lobe syndrome is divided into:
- Apraxic. It is determined when the premotor cortex is affected. Disorders of the organization of complex movements and actions prevail in the clinical picture, articulation disorders (dysarthria), acalculia occur a second time.
- Apathetic-abusive. It is observed in pathology of the convexital zones of the prefrontal region. The clinic is dominated by lack of initiative, apathy, lack of will (abulia). It is characterized by a lack of interests, desires, inability to initiate any action aimed at satisfying basic needs.
- The syndrome of mental disinhibition. It develops during pathological processes in the mediobasal parts of the frontal lobe. Typically disinhibited behavior without taking into account social and ethical norms, logorrhea, carelessness, foolishness, sometimes aggressiveness.
Symptoms
A slight degree of defeat is manifested in a decrease in the interests of the patient, his inattention, inactivity. Isolated frontal lobe syndrome is not accompanied by paresis, sensitive disorders. The usual simple actions are completely preserved, difficulties arise when it is necessary to perform a complex multicomponent action, a given sequence of movements. Purposeful activity is interrupted by side impulsive actions. For example, seeing the bell button, the patient unconsciously presses it, realizing the habitual movement under the influence of a momentary impulse. Similarly, when cooking soup, the patient can put any inedible object that comes to hand into the pot.
It is characterized by “getting stuck” (perseveration) on performing a certain action: repeating a question, reading the same phrase, repeatedly squeezing the submitted hand, etc. Perseverations are most demonstrative when trying to draw a series of geometric shapes according to a sample. The first 2-3 figures can be displayed correctly, then the last figure is repeated. With more gross violations, an attempt to draw a circle leads to repeated repetition of the action with the loss of the ability to terminate it independently.
With significant pathological processes, the frontal lobe syndrome proceeds with astasia — a violation of the ability to hold a certain body position (stand, sit), abasia — the inability to walk. At the same time, in the supine position, the movements are preserved in full. Often there is a disinhibition of oral automatism, leading to the appearance of constant smacking, pulling the lips with a tube. There is a grasping reflex: the patient squeezes an object in the palm of his hand into a fist.
Pronounced apathetic-abolic syndrome is accompanied by a deep breakdown of voluntary motor activity. Patients are unable to initiate an action, for example, when thirsty, they cannot make a request or take a nearby glass of water. Active speech is sharply reduced, answers to questions are monosyllabic, echolalia is typical (repetition of the interlocutor’s phrases). A distinctive feature is the impossibility of both starting and stopping the movement. Patients do not take the object extended to them, when putting it in their hand, they tonally or repeatedly squeeze, unable to stop the action that has begun. The automatic repetition of the motor act causes the tendency of patients to constantly pull the edge of the bed, scratch the wall by the bed, touch with their fingers.
The syndrome of mental disinhibition is characterized by increased excitement, excessive speech production, motor activity. Actions are mainly aimed at satisfying biological needs, there are no moral and ethical restrictions. Patients are euphoric, constantly “making jokes”, coming up with puns, fooling around. Behavior is often devoid of common sense, may have an antisocial, aggressive nature. There is no criticism of one’s own condition.
Complications
The lack of a critical attitude to his condition, the susceptibility to impulsive actions causes social maladaptation and requires that the patient be under constant control from relatives. Apathetic-abolic frontal lobe syndrome in the absence of proper care leads to exhaustion of the body. Astasia-abasia syndrome is accompanied by repeated falls with injury to the patient, forcing him to lie in bed. Bed patients are prone to the formation of bedsores, the addition of intercurrent infections with the risk of septicemia.
Diagnostics
Diagnostic difficulties are mainly due to the mental nature of the clinical manifestations of the disease. Apathetic-abusive states resemble depression, mental disinhibition — the manic phase of bipolar disorder. Observing changes in the personality and behavior of the patient, relatives often initially turn to a psychiatrist, who directs the patient to a neurologist. Neurological examination includes:
- Assessment of neurological status. There are behavioral disorders, difficulties in performing several consecutive movements according to the instructions, perseverance of one of these movements, mirroring when performing the Head test (copying the pose of the doctor’s hands). Possible astasia in the Romberg pose, gait disorder, speech disorder. Symptoms of oral automatism, grasping reflex are revealed.
- Neuroimaging. It is of paramount importance in establishing the morphological substrate that causes the frontal lobe syndrome. CT of the brain is more informative in post-traumatic conditions, shell hematomas. Brain MRI allows you to detect post-stroke foci, tumors, degenerative changes in the frontal lobes.
- Study of cerebral hemodynamics. It is carried out if the vascular nature of the disorders is suspected. It is carried out using ultrasound Dopplerography, MRI, duplex scanning of cerebral vessels. Identifies areas of chronic cerebral ischemia, localization and nature of blood flow disorders (spasm, thromboembolism, aneurysm, AVM).
Frontal lobe syndrome is a clinical symptom complex that indicates the area of cerebral lesion, but is observed in many diseases. To establish a definitive diagnosis, it is necessary to differentiate the frontal symptoms of various etiologies. To clarify the nature of causal pathology, the features of the development of the clinical picture, concomitant symptoms help. With injuries, strokes, frontal symptoms occur acutely against the background of almost complete well-being, with tumors, degenerative processes, clinical manifestations gradually increase.
Treatment
Therapy is carried out comprehensively, combines etiopathogenetic and symptomatic treatment with subsequent rehabilitation. Neurosurgeons, speech therapists, psychiatrists, rehabilitologists, if necessary, take part in carrying out medical and rehabilitation measures. Depending on the etiology of the disease , two main methods are used in the treatment:
- Medicamental. In case of strokes, vascular, thrombolytic, and coagulant therapy are used differentially. With severe mental abnormalities (arousal, apathy), psychotropic drugs are prescribed. According to indications for intracranial neoplasms, polychemotherapy is performed. In order to restore nerve tissues as soon as possible in the post-traumatic, post-stroke period, nootropic, neuroprotective and neurometabolic pharmaceuticals are used as supportive therapy for degenerative diseases.
- Neurosurgical. An indication for surgical treatment is a frontal lobe syndrome that has arisen as a result of neoplasia, hematoma, vascular abnormality. Neurosurgical interventions are carried out with the planning of the course of the operation after accurate determination of the localization of the formation using MRI or CT. When removing tumors, microsurgical equipment is used to differentiate altered tissues from healthy ones.
Prognosis and prevention
The outcome of the disease depends on the etiology, the extent of the lesion, and the age of the patient. In young patients, recovery after TBI and neurosurgical interventions is easier than in the elderly. The regression of neurological deficit is facilitated by comprehensive rehabilitation. Progressive degenerative processes and malignant neoplasia have an unfavorable prognosis. Preventive measures consist in preventing the effects of factors that cause pathological changes in the frontal divisions. Preventive measures include the prevention of head injuries, exposure to carcinogens, cerebrovascular diseases. With regard to degenerative processes, prevention is difficult, since their etiology remains unclear.