What could be a pathology of the right temporal lobe. Signs of damage to the temporal lobe
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Temporal lobe lesion
Damage to the temporal lobe (the right hemisphere in right-handed people) is not always accompanied by severe symptoms, but in some cases symptoms of prolapse or irritation are detected. Quadrant hemianopsia is sometimes an early sign of damage to the temporal lobe of the cortex; its reason lies in partial damage to the fibers of the Graciole bundle. If the process is progressive, it gradually transforms into complete hemianopia of the opposite lobes of vision.
Ataxia, as in the case of frontal ataxia, leads to disturbances in standing and walking, expressed in this case as a tendency to fall backward and sideways (to the side opposite the hemisphere with the pathological focus). Hallucinations (auditory, gustatory and olfactory) are sometimes the first signs of an epileptic seizure. They are actually symptoms of irritation of the analyzers located in the temporal lobes.
Unilateral dysfunction of sensitive areas does not, as a rule, cause significant loss of taste, olfactory or auditory sensitivity, since the cerebral hemispheres receive information from the peripheral perceptive apparatuses of both sides. Attacks of dizziness of vestibular-cortical origin are usually accompanied by a feeling of a violation of the patient’s spatial relationships with the objects around him; dizziness is often accompanied by sound hallucinations.
The presence of pathological foci in the left temporal lobe (in right-handed people) leads to severe disorders. When a lesion is localized in Wernicke's area, sensory aphasia occurs, for example, which leads to loss of the ability to perceive speech. Sounds, individual words and entire sentences are not attached by the patient to concepts and objects known to him, which makes establishing contact with him almost impossible. At the same time, the speech function of the patient himself is impaired. Patients with lesions localized in Wernicke's area retain the ability to speak; Moreover, they even show excessive talkativeness, but their speech becomes incorrect. This is expressed in the fact that words necessary in meaning are replaced by others; the same applies to syllables and individual letters. In the most severe cases, the patient's speech is completely incomprehensible. The reason for this complex of speech disorders is that control over one’s own speech is lost. A patient suffering from sensory aphasia loses the ability to understand not only other people's speech, but also his own. As a consequence, paraphasia occurs - the presence of errors and inaccuracies in speech. If patients suffering from motor aphasia are more irritated by their own speech errors, then people with sensory aphasia are offended by those who cannot understand their incoherent speech. In addition, when Wernicke's area is affected, reading and writing skills are impaired.
If we conduct a comparative analysis of speech dysfunctions in pathologies of various parts of the cerebral cortex, then we can confidently say that the least severe lesions are the posterior part of the second frontal gyrus (associated with the inability to write and read); then there is a lesion of the angular gyrus, associated with alexia and agraphia; more severe - damage to Broca's area (motor aphasia); and finally, damage to Wernicke's area has the most serious consequences.
It is worth mentioning a symptom of damage to the posterior part of the temporal and lower part of the parietal lobes - amnestic aphasia, which is characterized by loss of the ability to correctly name objects. During a conversation with a patient suffering from this disorder, it is not immediately possible to notice any deviations in his speech. Only if you pay attention does it become clear that the patient’s speech contains few nouns, especially ones that define objects. He says "a sweet that goes into tea" instead of "sugar", claiming that he simply forgot the name of the item.
The rationale for an isolated speech disorder is as follows: a certain field is formed, localized between the cortical centers of hearing and vision (B.K. Sepp), which is the center of the combination of visual and auditory stimulation in the child. When a child begins to understand the meaning of words, they are compared in his mind with a visual image of an object that is simultaneously shown to him. Subsequently, the names of objects are deposited in the above-mentioned associative field when improving speech function. Thus, when this field is damaged, which is, in fact, associative pathways between the fields of visual and auditory gnosis, the connection between the object and its definition is destroyed.
Methods for studying aphasia:
1) checking the understanding of speech addressed to the person under study by suggesting the execution of simple commands - violations of the sensory function of speech are identified; deviations can be caused by both damage to Wernicke's area and apraxic disorders;
2) studying the speech of the patient himself - attention is paid to the correctness and volume of vocabulary; at the same time, the motor function of speech is examined;
3) study of the reading function - the ability to perceive written speech is tested;
4) study of the patient’s ability to write - the presence of a paragraph is revealed;
5) identifying the presence of amnestic aphasia in the patient (it is proposed to name various objects).
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Parietal lobe lesionLesions of the occipital lobe of the cerebral cortex
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Temporal lobe damage (TCL). The temporal lobe (TL) is the most vulnerable anatomical formation of the brain in TBI - 35%-45% of all cases. This is explained by the particularly frequent application of a traumatic agent to the temporal region, damage to the VD by the counter-impact mechanism in almost any localization of the primary application of force, anatomical conditions (thin scales of the temporal bone, the location of the main mass of the lobe in the middle cranial fossa, limited partially by sharp bone-dural protrusions, direct adjoining the brain stem, passing through the temporal region of the largest branches of the middle meningeal and middle cerebral arteries). As a result, it is in the VD that contusion lesions with brain crushing and intracerebral hematomas are usually located; more often than in other zones, epidural hematomas form here; Subdural hematomas are also common.
Clinic of damage to the temporal lobe.
General cerebral symptoms with VDP are not fundamentally different from those with damage to other lobes of the brain (they are described in detail in the article “ Frontal lobe damage”): quantitative changes in consciousness from moderate stupor to deep coma; headache with nausea, dizziness, vomiting; congestion in the fundus; psychomotor outbursts, etc.
Among the local signs of VDP, the phenomena of sensory aphasia dominate - from difficulty understanding complex turns of addressed speech to the complete loss of analysis of both audible and one’s own speech, which is figuratively referred to as “verbal okroshka”. In intermediate degrees of sensory aphasia, literal and verbal paraphasias are observed; tests of auditory-speech memory, alienation of the meaning of words, recognition and reproduction of similar-sounding phonemes in syllables and words help. With damage to the angular gyrus, located at the junction with the parietal and occipital lobes, i.e., the zone that integrates auditory, visual and sensory afferentation, the phenomena of alexia, agraphia, and acalculia develop. The described symptoms are observed with VDP of the dominant, usually left, hemisphere. Damage to similar zones of the subdominant (right) hemisphere causes a violation of the recognition and reproduction of “primary signal” sounds - household, street, natural noises, as well as familiar melodies, intonation and emotional structure of speech, which can be checked if the general condition of the victim allows.
Damage to the posterior third of the inferior temporal gyrus causes the development of amnestic aphasia, although this symptom after TBI can also act as a general cerebral one, especially in older people.
Deep traumatic processes (hematomas, contusion lesions) cause contralateral homonymous hemianopsia: lower quadrant - with selective damage to the visual pathway running above the lower horn of the lateral ventricle, and upper quadrant - when this path is damaged under the lower horn.
A whole range of symptoms can occur with damage to the medial part of the VD, which develops not only during the primary traumatic impact, but also as a result of herniation into the tentorial opening of the gyrus near the seahorse with its hook in the case of a volumetric increase in the VD. Irritation of the ancient cortex causes disruptions in the regulation of visceral and autonomic functions, which is manifested by both subjective (feelings of heaviness, discomfort, weakness, heart palpitations, heat, etc.) and objective symptoms (heart rhythm disturbances, angiotic attacks, flatulence, hyperemia or pallor of the integument, etc.). The background of the patient’s mental state changes in the form of a predominance of negative emotions, often of the type of constrained depression. Along with this, paroxysms of fear, anxiety, melancholy, and foreboding may occur. The most noticeable to the patient are disturbances of taste and smell in the form of perverted perception and deception.
Medial temporal injuries in TBI often manifest exclusively as epileptic seizures or their equivalents. The latter may include olfactory and gustatory hallucinations, sensory-visceral paroxysms, vestibular attacks, states of “previously seen”; Classic “streams of memories” are relatively rare in temporal lobe epilepsy. Epileptic discharges are also possible when the convexital sections of the VD are damaged; then simple or complex (with extended speech) auditory hallucinations act as equivalents or auras.
Secondary stem symptoms are woven into the clinical picture of UDP more than with any other localization. Basically, we are talking about dislocations of the oral part of the trunk in cases of increasing the volume of the VD - with massive edema, hematomas, cysts of traumatic origin. The diencephalon and midbrain are displaced contralaterally from the pathological focus, are injured on the opposite edge of the tentorium, and secondary dysgemia often develops in the brainstem and axonal damage to the conduction systems. Acute displacements and deformation of the trunk at the time of TBI are extremely life-threatening. With subacute or slowly growing dislocations, there are more opportunities for therapeutic measures; the doctor’s increased attention to the dynamics of brainstem symptoms is necessary (see article “Midbrain syndrome in TBI”). A number of vegetative and visceral disorders of the same type as medial-temporal disorders occur when diencephalic structures are displaced, and disturbances in sleep rhythm, thermoregulation, and vascular microcirculation are also observed; hormetonic convulsions develop. Of the secondary symptoms in VDP, the pons and medulla oblongata syndromes and craniobasal symptoms are less common and less pronounced.
Diagnosis of damage to the temporal lobe.
VDP is based on an analysis of the mechanism of TBI, a combination of primary focal and secondary cerebral symptoms. It must be remembered that in the conditions of emergency diagnosis of TBI, the doctor often fails to recognize damage to the right (subdominant) AC, and the presence of general cerebral and brainstem symptoms can generally lead the diagnosis down the wrong path. Here, invaluable help is provided by the use of modern imaging methods such as CT and MRI, and in their absence, echoencephalography. X-rays of the skull and EEG retain their value. Lumbar puncture should be performed with maximum precautions (danger of herniation!). If you suspect the formation of a hematoma, you should refrain from lumbar puncture.
Treatment of damage to the temporal lobe.
Depressed fractures, supra- and intrathecal hematomas of temporal localization require surgical intervention as soon as the diagnosis is established. The operation should be performed for large intracerebral hematomas (maximum diameter<4см) и очагах контузионного размягчения объемом не только свыше 50 см 3 , но и более мелких, если они сочетаются с отеком мозга и вызывают значительное смещение ствола. При отсутствии угрожающих клинических симптомов и инструментальных данных больному с ВДП должна быть назначена дегидратирующая, седативная, вазоактивная, противосудорожная, противовоспалительная и другие виды терапии в зависимости от показаний.
Prognosis for damage to the temporal lobe.
The prognosis of UDP is favorable in most cases if it is possible to avoid the dangers of general trauma and those specific to UDP (bleeding from large arteries, dislocations of the brain stem) in the acute period. Disability in the residual period of TBI can be caused by recorded defects of higher cortical functions - sensory aphasia, alexia, agraphia, acalculia; paresis of the limbs - with damage to the VD to the depth of the internal capsule; hemianopic defects, usually partial; epileptic syndromes. Timely and systematic rehabilitation measures and rational anticonvulsant therapy are important.
Posterior parts of the frontal lobes are responsible for motor functions. Movements of the face, arm, and hand originate in the motor cortex of the convexital surface of the frontal lobe, and movements of the leg and foot originate in the cortex of the medial surface of the frontal lobe. Voluntary movements are ensured by the integration of motor and premotor zones (fields 4 and 6); if both zones are damaged, central paresis of the muscles of the face, arms and legs on the opposite side of the body develops. There is also an accessory motor area in the posterior part of the superior frontal gyrus. Damage to this zone and the premotor zone is accompanied by the appearance of a grasping reflex on the opposite side; Bilateral damage to this area leads to the development of a sucking reflex.
Defeat in field 8 disrupts the rotation of the head and eyes in the opposite direction and the coordination of movements of the hands. Damage to areas 44 and 45 (Broca's area) of the dominant hemisphere leads to loss of expressive speech, dysarthria and impaired speech fluency, as well as apraxia of the tongue, lips and, rarely, the left hand. The remaining portions of the frontal lobes (areas 9 to 12), sometimes called the prefrontal areas, have less specific functions. They are responsible for planning motor acts and, more importantly, for controlling behavior. With their extensive damage, the needs and motivations, emotional control, and personality of the patient change; these changes, although mild, are often more noticeable to family members than to the doctor when examining the patient’s mental status.
I. Manifestations of damage to any (left or right) frontal lobe
A. Contralateral spastic hemiparesis or hemiplegia
B. Mild euphoria, increased talkativeness, a tendency to make vulgar jokes, tactlessness, difficulties in adaptation, lack of initiative
B. With an isolated prefrontal lesion there is no hemiplegia; a grasping reflex may occur on the opposite side
D. When the medial orbital areas are involved - anosmia
II. Manifestations of damage to the right frontal lobe
A. Left-sided hemiplegia
B. Symptoms, as in paragraphs. 1B, C and D
B. Confusion in acute injuries
III. Manifestations of damage to the left frontal lobe
A. Right hemiplegia
B. Motor aphasia with agraphia (Broca’s type), impaired speech fluency with or without apraxia of the lips and tongue B. Apraxia of the left hand
D. Symptoms, as in paragraphs. 1B, C and D
IV.
A. Double hemiplegia
B. Pseudobulbar palsy
B. With prefrontal damage: abulia, dysfunction of the sphincters of the bladder and rectum or, in the most severe version, akinetic mutism, inability to concentrate and solve complex problems, rigidity of thinking, flattery, mood lability, personality changes, various combinations of disinhibited motor activity, grasping and sucking reflexes, gait disturbances.
34. Syndromes of damage to the parietal lobe.
This share is limited anteriorly by Rolandic groove, below - the Sylvian fissure, behind there is no clear border with the occipital lobe. In the postcentral gyrus (fields 1, 3 and 5) the somatosensory pathways from the opposite half of the body end. However, destructive lesions in this area lead predominantly to disruption of the differentiation of sensations (articular-muscular sense, stereognosis, localization of irritations); a violation of primary sensitivity (“cortical sensory syndrome”) develops only with significant damage to the lobe.
In addition, with bilateral one-time irritation, the patient perceives irritation only on the unaffected side.
With extensive damage to the parietal lobe In the non-dominant hemisphere, the patient ignores his hemiplegia and hemianesthesia and may not even recognize the left limbs as his own (anosognosia). It is also possible to ignore the left half of your body (when grooming and dressing) and your surroundings. Significant difficulties arise in copying figures and drawings and constructing objects (constructive apraxia). These disorders are observed very rarely and with left-sided brain damage.
In case of damage to the angular gyrus In the dominant hemisphere, the patient may lose the ability to read (Alexia). With extensive damage, in addition, the ability to write (agraphia), count (acalculia), recognize fingers (finger agnosia) and distinguish between the right and left sides of the body is lost. This combination of symptoms is known as Gerstmann syndrome. Ideomotor and ideational apraxia (loss of acquired motor skills) develop with damage to the lower parts of the left parietal lobe.
Manifestations of damage to the parietal lobe can be summarized as follows:
I. Manifestations of damage to any (right or left) parietal lobe
A. “Cortical sensory syndrome” (or total hemianesthesia for extensive acute white matter lesions)
B. Mild hemiparesis, unilateral atrophy of the limbs in children
B. Homonymous hemianopsia or inferior quadrant hemianopsia
D. Reduced attention to visual stimuli (visual inattention - English) and sometimes anosognosia, ignoring the opposite side of the body and the environment (this combination of symptoms refers to amorphosynthesis and is more significant with damage to the right hemisphere)
D. Disappearance of optical-kinetic nystagmus when the drum with black and white stripes is rotated in the direction of the lesion
E. Ataxia in the limbs on the opposite side in rare cases
II. Manifestations of damage to the parietal lobe of the dominant (left in right-handed) hemisphere; Additional symptoms include:
A. Speech disorders (especially alexia)
B. Gerstmann syndrome (see above) Gerstmann syndrome is characterized by five main features:
1. Dysgraphia/agraphia: difficulties in the ability to write;
2. Alexia/visual aphasia: difficulty reading;
3. Dyscalculia / acalculia: difficulty learning or understanding mathematics;
4. Finger agnosia: inability to distinguish fingers;
5. Right-left disorientation.
B. Tactile agnosia (bilateral astereognosis)
D. Bilateral ideomotor and ideational apraxia
III. Manifestations of damage to the parietal lobe of the non-dominant (right in left-handed) hemisphere
A. Constructive apraxia
B. Loss of topographic memory
B. Anosognosia and apractognosia. These disorders can occur with damage to either hemisphere, but are more often observed with damage to the non-dominant hemisphere
D. If the posterior parts of the parietal lobe are damaged, visual hallucinations, visual distortion, increased sensitivity to irritations or spontaneous pain are possible.
35. Syndromes of damage to the temporal lobe.
Manifestations of unilateral or bilateral temporal lobe lesions can be summarized as follows:
I. Manifestations of damage to the temporal lobe of the dominant (left) hemisphere
A. Impaired understanding of words during conversation (Wernicke's aphasia)
B. Amnestic aphasia C. Impaired reading and writing from dictation
D. Impaired reading and writing music
D. Right upper quadrant hemianopsia
II. Manifestations of damage to the frontal lobe of the non-dominant (right) hemisphere
A. Impaired perception of visual non-verbal materials
B. Inability to appreciate spatial relationships in some cases
B. Impaired speech modulation and intonation
III. Manifestations of damage to any (left or right) temporal lobe
A. Auditory illusions and hallucinations
B. Psychosis and delirium
B. Contralateral superior quadrant hemianopsia
G. Delirium in acute injuries
IV. Manifestations of bilateral lesions
A. Korsakovsky (amnestic) syndrome (hippocampal structures)
B. Apathy and indifference
B. Increased sexual and oral activity (the combination of symptoms listed in paragraphs B and C constitutes Kluver-Bucy syndrome)
D. Inability to recognize familiar melodies
D. Facial agnosia (prosopagnosia) in some cases.
36. Syndromes of damage to the occipital lobe.
Medial surface of the occipital lobe separated from the parietal lobe by the parieto-occipital sulcus; on the lateral surface there is no such clear boundary from the posterior parts of the temporal and parietal lobes. On the medial surface, the most significant is the calcarine gyrus, which runs from front to back, in which the geniculate-calcarine tract ends.
In the occipital lobe perception of visual stimuli (field 17) and their recognition (fields 18 and 19) occur. In different parts of the occipital lobe, lines, shapes, movements and color are perceived. And to analyze perception (understanding what is visible), each area is connected to other areas by a widespread neural network. Like other lobes of the brain, the occipital lobe is connected through the corpus callosum to the corresponding lobe of the other hemisphere.
As noted in our article, destructive defeat one of the occipital lobes leads to contralateral homonymous hemianopsia: loss of vision in part or all of the corresponding or homonymous field (nasal field of one eye and temporal field of the other). Sometimes there may be distortion of visual objects (metamorphopsia), illusory displacement of images from one side of the visual field to the other (visual allesthesia), or persistence of a visual image after the object is removed (palinopsia).
It's also possible development of visual illusions and elementary (unformed) hallucinations, but more often they are caused by damage to the posterior parts of the temporal lobe. Bilateral damage to the occipital lobes leads to “cortical blindness,” blindness without changes in the fundus and pupillary reflexes and with preserved optokinetic reflex.
Field lesions 18 and 19 of the dominant hemisphere, surrounding primary visual field 17, lead to the inability to recognize visual objects when they are seen normally (visual agnosia); at the same time, the ability to recognize objects by tactile or other non-visual sensations is retained. Alexia, a reading disability, reflects the presence of visual verbal agnosia or “word blindness”; patients can see letters and words, but do not know their meaning, although they can recognize them by tactile sensations and hearing.
Other types agnosia, such as loss of color discrimination (achromatopsia), inability to recognize faces (prosopagnosia), visuospatial impairment or inability to perceive a scene as a whole while recognizing individual parts (simultaneous agnosia), and Balint's syndrome (inability to focus on an object in the visual field, optic ataxia and visual inattention), observed with bilateral damage to the occipital and parietal lobes.
Manifestations of damage to the occipital lobes summarized below:
I. Manifestations of damage to any (left or right) occipital lobe
A. Contralateral homonymous hemianopia, which can be central or peripheral; hemiachromatopsia (inability to distinguish colors in one field)
B. Elementary (unformed) visual hallucinations, especially in combination with epileptic seizures and migraine
II. Manifestations of damage to the left occipital lobe
A. Right homonymous hemianopsia
B. When the deep parts of the white matter or plate of the corpus callosum are involved - alexia and color naming disorder
B. Visual agnosia
III. Manifestations of damage to the right occipital lobe
A. Left-sided homonymous hemianopsia
B. With more extensive lesions - visual illusions (meta-morphopsia) and hallucinations (more often when the right lobe is affected than the left)
B. Loss of visual orientation
IV. Bilateral occipital lobe lesions
A. Cortical blindness (pupillary reactions are preserved), sometimes combined with denial of visual impairment (Anton's syndrome)
B. Loss of color perception
B. Prosopagnosia, simultaneous and other agnosias
D. Balint's syndrome (parieto-occipital border zones)
37. Syndromes of damage to the internal capsule.
Lesions in the area of the internal capsule, interrupting the pathways passing here, cause motor and sensory disorders on the opposite side of the body (sensitive conductors cross in the spinal and medulla oblongata, pyramidal ones - at their border). Foci in the area of the internal capsule are characterized by a half type of disorder, since the arrangement of fibers here, as already mentioned above, is very close.
With complete damage to the internal capsule, the so-called “three hemi syndrome” is observed: hemiplegia and hemianesthesia on the opposite side of the body and hemianopsia of opposite visual fields.
Hemiplegia, of course, has all the features of central paralysis. Usually, both upper and lower extremities are equally affected; at the same time there is a central type of paresis of the tongue and lower facial muscles. Capsular hemiplegia is especially characterized by Wernicke-Mann type contracture (see chapter on movement disorders).
Although hemianesthesia is of a half type, it is most pronounced in the distal parts of the extremities. Since the focus is located above the visual thalamus, only some types of sensitivity are lost (articular-muscular, tactile, stereognosia, subtle pain and temperature sense, etc.). Severe pain and temperature irritations cause a sharp sensation of unpleasantness with irradiation, imprecise localization, and aftereffects, i.e., hyperpathy is observed.
Hemianopsia occurs as a result of damage to the Graciole bundle, is homonymous and is observed, of course, in the visual fields opposite to the lesion (see the chapter on cranial nerves).
There are no distinct hearing disorders, despite damage to the auditory conductors; this will become clear if we recall the bidirectionality of the auditory pathways from the nuclei to the subcortical auditory centers and, therefore, the conduction of impulses from each ear to both hemispheres. With subtle research methods, it is still possible to detect some hearing loss in the ear opposite to the lesion.
Damage to the internal capsule is not always complete. More localized lesions are also often observed. With lesions in the knee and anterior posterior thigh, only hemiplegia is observed in the absence or presence of only mild sensory disturbances. When the posterior part of the hind thigh is affected, sensory disorders naturally predominate, and here, too, “three hemi syndrome” of a slightly different nature can be observed: hemianesthesia, hemianopsia and hemiataxia (as a result of loss of joint-muscular sensation). However, in these cases there are usually at least mild pyramidal disorders.
The close location of the internal capsule to the visual thalamus and the ganglia of the extrapyramidal system easily explains the addition sometimes to the capsular syndrome, for example, of thalamic pain or extrapyramidal disorders. Often there is simultaneous damage to both the large ganglia of the base and the internal capsule.
White matter of the hemispheres. Between the basal ganglia with their internal capsule and the cerebral cortex in the hemispheres there is a continuous mass of white matter (centrum semiovale), in which fibers of various directions are located. They can be divided into two main groups - projection and association.
Projection fibers connect the cerebral cortex with the underlying parts of the central nervous system and are located more or less perpendicular to the cortex. Here we meet the already familiar cortical and cortical conductors. From the cerebral cortex, from the anterior central gyrus, the tractus cortico-bulbaris and cortico-spinalis, the frontal and occipito-temporal tracts of the bridge (from the corresponding lobes), the corticothalamic tracts (from all lobes, but mainly from the frontal lobe) go downwards. In the direction of the cortex, the newly disassembled thalamo-cortical sensory conductors follow, going to the sensitive areas of the cortex: the posterior central gyrus, the parietal lobes; in the occipital lobes - visual, in the temporal - auditory conductors. A powerful bundle of projection fibers that penetrates the centrum semiovale and fan-shapedly diverges from the internal capsule to the cortex is called corona radiata, or corona radiata.
Association fibers connect various lobes and areas of the cortex within each hemisphere; here we encounter fibers of various directions and lengths. They can be short, connecting, for example, neighboring gyri; such fibers are called V-shaped. Long routes establish connections with more distant territories of their hemisphere; these include, for example, fasciculus longitudinalis superior, inferior, uncinatus, cingulum, etc. (Fig. 57).
Commissural fibers are a type of association fiber; they connect the cortex not within one hemisphere, but both hemispheres with each other. The direction of the fibers is predominantly frontal. The most powerful and important of the commissural bundles is the corpus callosum (corpus callosum).
The corpus callosum connects the lobes of the same name to each other: both frontal, parietal, etc. In addition, commissural fibers pass into the comissura anterior (anterior white commissure) and posterior. The last two spikes are related to the olfactory function.
Lesions in the centrum semiovale cause symptom complexes close to those with damage to the internal capsule. Since here the fibers of various significance diverge more widely and are not located as compactly as in the internal capsule, movement disorders can be observed more isolated from the sensory ones, and vice versa. The complete half type of lesion may also be affected, i.e. the lower limb, for example, may be more affected than the upper, etc.
38. Syndromes of damage to the hypothalamic-pituitary region.
The variety of functions of the hypothalamic-pituitary part of the diencephalon leads to the fact that when it is damaged, various
pathological syndromes, including neurological disorders of various nature, including signs of endocrine pathology, manifestations of autonomic dysfunction, emotional imbalance.
The hypothalamic region ensures interaction between regulatory mechanisms that integrate the mental, especially emotional, autonomic and hormonal spheres. Many processes that play an important role in maintaining homeostasis in the body depend on the state of the hypothalamus and its individual structures. Thus, the preoptic region located in its anterior section provides thermoregulation due to changes in thermal metabolism. If this area is affected, the patient may not be able to give off heat in conditions of high ambient temperature, which leads to overheating of the body and to hyperthermia, or the so-called central fever. Damage to the posterior hypothalamus can lead to poikilothermia, in which body temperature varies depending on the ambient temperature.
The lateral area of the gray tuberosity is recognized as the “appetite center”, and the feeling of satiety is usually associated with the location of the ventromedial nucleus. When the “appetite center” is irritated, gluttony occurs, which can be suppressed by stimulating the satiety zone. Damage to the lateral nucleus usually leads to cachexia. Damage to the gray tuberosity can cause the development of adiposogenital syndrome, or Babinski-Froelich syndrome
Adiposogenital syndrome
Autonomic dystonia may be a consequence of an imbalance in the activity of the trophotropic and ergotropic parts of the hypothalamus. Such an imbalance is possible in practically healthy people during periods of endocrine changes (during puberty, during pregnancy, menopause). Due to the high permeability of the vessels supplying blood to the hypothalamic-pituitary region, in infectious diseases, endogenous and exogenous intoxications, a temporary or persistent autonomic imbalance, characteristic of the so-called neurosis-like syndrome, may occur. It is also possible that vegetative-visceral disorders arise against the background of autonomic imbalance, manifested, in particular, by peptic ulcer disease, bronchial asthma, hypertension, as well as other forms of somatic pathology
Particularly characteristic of damage to the hypothalamic part of the brain is the development of various forms of endocrine pathology. Among neuro-endocrine-metabolic syndromes, various forms of hypothalamic (cerebral) obesity occupy a significant place (Fig. 12.6), while obesity is usually pronounced and fat deposition often occurs on the face, trunk and proximal limbs. Due to the uneven deposition of fat, the patient’s body often takes on bizarre shapes. With the so-called adiposogenital dystrophy (Babinsky-Froehlich syndrome), which can be a consequence of a growing tumor of the hypothalamic-pituitary region - craniopharyngioma, obesity occurs already in early childhood, and in the puberty period, underdevelopment of the genital organs and secondary sexual characteristics.
One of the main hypothalamic-endocrine symptoms is diabetes insipidus, caused by insufficient production of antidiuretic hormone, characterized by increased thirst and the release of large amounts of urine with low relative density. Excessive secretion of adiurecrin is characterized by oliguria, accompanied by edema, and sometimes alternating polyuria in combination with diarrhea (Parhon's disease).
Excessive production of growth hormone by the anterior pituitary gland is accompanied by the development of acromegaly syndrome.
Hyperfunction of basophilic cells of the anterior pituitary gland leads to the development of Itsenko-Cushing's disease, which is mainly caused by excess production of adrenocorticotropic hormone (LCTH) and the associated increase in the release of adrenal hormones (steroids). The disease is characterized primarily by a peculiar form of obesity. The round, purple, greasy face attracts attention. Also, the face is characterized by acne-type rashes, and in women, facial hair growth is also typical of the male type. Hypertrophy of fatty tissue is especially pronounced on the face, on the neck in the area of the VII cervical vertebra, in the upper abdomen. The patient's limbs appear thin in comparison with the obese face and torso. On the skin of the abdomen and the anterior surface of the thighs, stretch marks are usually visible, reminiscent of stretch marks of pregnant women. In addition, an increase in blood pressure is typical, amenorrhea or impotence are possible.
With severe insufficiency of the functions of the hypothalamic-pituitary region, pituitary depletion, or Simons' disease, may develop. The disease progresses gradually, and exhaustion reaches a sharp degree of severity. Skin that has lost turgor becomes dry, matte, wrinkled, the face acquires a Mongoloid character, hair turns gray and falls out, and nails become brittle. Amenorrhea or impotence occurs early. A narrowing of the circle of interests, apathy, depression, and drowsiness are noted.
Syndromes of sleep and wakefulness disorders can be paroxysmal or protracted, sometimes persistent (see Chapter 17). Among them, perhaps the best studied syndrome is narcolepsy, which is manifested by an uncontrollable desire to sleep that occurs during the day, even in the most inappropriate environment. Cataplexy, often combined with narcolepsy, is characterized by attacks of a sharp decrease in muscle tone, leading the patient to a state of immobility for a period of several seconds to 15 minutes. Attacks of cataplexy often occur in patients who are in a state of passion (laughter, feelings of anger, etc.); states of cataplexy that occur upon awakening are also possible (awakening cataplexy).
39. Syndromes of damage to the thalamic region.
Thalamic syndromes
Syndromes and symptoms of lesions
lamus are highly dependent
ty from the nature of this defeat. Floor-
thalamic syndrome observed
rarely occurs. With one-sided or two-
third-party lesions of the thalamus can
the following symptoms may be detected:
1. Contralateral hypoesthesia, usually
but more pronounced on the body and
limbs than on the face. In more
the depth is significantly reduced
lateral sensitivity. Threshold of recovery
acceptance of tactile, painful and
temperature irritants usually
downgraded If it's particularly low,
then even a weak stimulus will cause
gives an unpleasant feeling in the form
radiating, burning, piercing
piercing and tearing pain (hyperpain)
tiya). Regular visual or
auditory stimuli, e.g.
melodic music, may not be
pleasant, annoying. Typical spon-
tannaya, arising without visible
causes of pain or paresthesia in
contralateral half of the body.
They often become aggravated by emotions
or fatigue. Analgesics for
this often does not bring relief.
On the contrary, anticonvulsants
parathas such as Dilantin (diphen-
nilgidantoin) may help. In pro-
otherwise, in order to try to
pain relief was carried out using stereotactic
tic destruction of the ventrocaudal
of the parvicellular nucleus of the thala-
musa (V. s. rs. core in Fig. 5.4).
2. Intention tremor or hemia-
taxia combined with choreoathetia
id movements, probably trained
caused by damage to the cerebellum
covothalamic, rubrothalamic
sky or pallidothalamic vo-
curl. Non-
common contractures involving
most often the hands (thalamic
brush).
3. Affective disorders in the form
emotional lability and ten-
dence to violent laughter or
I'm crying possibly due to
damage to the anterior nucleus and its connections
Zey with the hypothalamus or limbic
skaya system.
4. Contralateral hemiparesis, often
transient, if the internal capsule
la is involved only through peripheral
Roland region. With damage to the precentral gyrus ( gyrus precentralis) Central paralysis or paresis occurs on the opposite side of the body. They are characterized by a more local character than paralysis caused by damage to the internal capsule, and more often manifest as hemiparesis with a predominance of damage to the arm, leg or face.
Isolated monoplegia with predominant damage to the distal parts of the limb may also be observed.
When the process is localized in the upper sections of the precentral gyrus, a predominant lesion is observed in the leg, in the middle sections - in the arm, in the lower sections - in the face and tongue.
Damage to the postcentral gyrus ( gyrus postcentralis) leads to disorders of all types of sensitivity on the opposite side. The prevalence and localization of disorders are similar to movement disorders with lesions of the precentral gyrus. Monoanesthesia, mainly expressed in the distal parts of the extremities, is more often observed. Along with loss of pain, tactile and temperature sensitivity, and joint-muscular sensation, hyperpathy may be observed in the area of sensory disorders.
Frontal lobe. When the posterior part of the inferior frontal gyrus (Broca's area) of the dominant hemisphere (left in right-handed people) is damaged, efferent motor aphasia. In this case, the patient loses the ability to speak, but understands speech addressed to him, which is confirmed by the correct execution of the doctor’s commands. The patient moves his tongue and lips freely (unlike dysarthria, which is observed with bulbar or pseudobulbar palsy), but loses the skills of speech movements (praxia). Often, with the loss of speech, the ability to write is also lost - agraphia occurs. In cases of incomplete damage to Broca's area, a narrowing of the vocabulary and the appearance of speech errors (agrammatism) are noted; the patient speaks with difficulty and notices his mistakes. At the recovery stage, the patient masters the entire vocabulary, but “stumbles” on syllables, especially in words containing many consonants and many similar syllables (dysarthric phase of motor aphasia).
With an isolated lesion of the posterior part of the middle frontal gyrus of the left hemisphere (in right-handed people), which is rare, isolated agraphia may occur - loss of the ability to write. At the same time, the patient understands oral speech addressed to him and retains his reading skill. Motor aphasia and agraphia are types of apraxia. If this area is damaged, gaze paresis may develop in the direction opposite to the lesion.
With damage to the frontal lobe of both the left and right hemispheres, the appearance of frontal ataxia(from here begins the frontopontine tract, which is related to the cerebellar system). It manifests itself most strongly in the torso - in disorders of standing and walking. The patient, without paralysis, falls in an upright position (astasia) or, having difficulty staying on his feet, cannot walk (abasia).
In mild gait disorders, walking reveals instability when turning with a tendency to deviate in the direction opposite to the affected hemisphere. Frontal ataxia can also manifest itself in the extremities, most often in the form of swinging outwards with the hand opposite to the affected hemisphere during the finger-nose or finger-hammer test.
Mental disorders with damage to the frontal lobes manifest themselves in the form of disturbances in the emotional-volitional sphere, which can be divided into two main options: apathetic-abulic syndrome And psychomotor disinhibition syndrome. With apathetic-abulic syndrome, patients are passive, uninitiative, adynamic, aspontaneous. They have a narrowing range of interests, lack of will, and lack of spontaneous impulses. Psychomotor disinhibition syndrome is characterized by torpidity of thinking, talkativeness, euphoria, reaching the point of foolishness (“moria”), underestimation of the severity of one’s condition, weakening of memory and attention, lack of a critical attitude towards one’s behavior, loss of a sense of distance when communicating with others, and, less often, depression and aggressiveness. Sloppiness and a tendency to crude, flat witticisms are typical, which do not correspond to the personality and upbringing of the patient in the premorbid state. Sometimes there is a painful craving for theft (kleptomania), devoid of material meaning (theft of useless items).
One of the manifestations of damage to the frontal lobe is frontal apraxia(apraxia of design). At the same time, the ability to plan actions and carry out plans suffers, the sequence of actions is disrupted, and actions are often not completed. Repeated, repeated actions are typical, and their connection with the original intentions is lost.
Damage to the frontal lobe anterior to the precentral gyrus in the right hemisphere (in right-handed people) may not produce clear symptoms of damage or loss of function. In such cases, the orienting symptom may be a transient paresis of gaze in the direction opposite to the lesion (damage to the area of voluntary rotation of the eyes and head), which is clinically manifested by deviation of the eyes and head towards the lesion due to the preservation of muscle tone on the opposite side. Typically, this symptom manifests itself during acute processes in the frontal lobe (stroke, trauma).
With bilateral damage to the frontal lobes, there may be phenomena of resistance(opposition). When the doctor tries to quickly carry out passive movement with one or another limb, resistance is observed on the part of the patient. A particular manifestation of the phenomenon is the symptom of I. Yu. Kokhanovsky - the symptom of “closing of the eyelids”: when trying to lift the patient’s upper eyelid, involuntary resistance is felt.
Sometimes there may be "grasping" phenomena, expressed normally in young children. When the frontal lobes are damaged, the phylogenetically ancient grasping reflex is disinhibited and manifests itself by involuntary grasping of an object when it strokes the patient’s hand (Yanishevsky-Bekhterev reflex). In more severe cases, the patient follows with his hand the object that is approaching or moving away.
Temporal lobe. When the left temporal lobe is damaged in right-handed people (dominant hemisphere), in particular the posterior part of the superior temporal gyrus (Wernicke's area), it is noted sensory aphasia. At the same time, understanding of both oral speech, including one’s own, and written speech is lost. The patient's speech becomes incomprehensible to the same extent as if he were speaking an unknown foreign language.
Having lost control over his own speech, the patient is often excessively talkative; his speech is a meaningless set of syllables and words (“word salad”). The defect is most often not recognized, and the patient becomes annoyed with people who cannot understand him.
The patient is unable to follow the doctor’s commands, which helps distinguish sensory aphasia from motor aphasia. In milder cases, letters in a word are replaced or another word is mistakenly pronounced instead of the desired one. Such patients can perform monosyllabic commands, but perform complex tests incorrectly. The function of reading and writing is lost.
With damage to the posterior part of the temporal lobe and the lower part of the parietal lobe of the dominant hemisphere, amnestic aphasia. The patient loses the ability to name objects, although he understands their purpose. If the name is suggested, the patient confirms its correctness, but soon forgets the name of the object and, when shown, describes its functions. For example, if you show a pencil to a patient, he says: “This is for writing.”
Damage to the parietotemporal region of the dominant hemisphere can lead to semantic aphasia, in which the understanding of the semantic meaning of the order of words in a sentence is impaired (for example, brother’s father and father’s brother, etc.).
A symptom characteristic of damage to both lobes is temporal ataxia. Like the frontal one, it is more pronounced in the trunk and manifests itself in the form of a disorder in standing and walking with a tendency to fall backward and to the side opposite to the affected hemisphere. In the limb opposite to the lesion, an inward miss is observed during the finger-hammer test.
The phenomena of temporal ataxia are often combined with attacks of vestibular-cortical vertigo. It is accompanied by a feeling of a violation of the patient’s spatial relationships with surrounding objects (the cortical representation of the vestibular apparatus is located in the temporal lobe).
With lesions in the deep parts of the temporal lobe, quadrant hemianopia may be observed. The reason for its occurrence is incomplete damage to visual radiation ( radiatio optica). Progression of the process can lead to complete homonymous hemianopsia of the opposite visual fields.
In the cortex of the temporal lobes, representations of the auditory, gustatory and olfactory analyzers are determined. Unilateral destruction of these zones does not cause noticeable disorders of hearing, smell and taste due to the fact that each hemisphere is connected to the perceptive apparatus on both sides - its own and the opposite.
Parietal lobe. With damage to the left parietal lobe in right-handed people (dominant hemisphere) in the region of the marginal gyrus ( gyrus supramarginalis) arises motor apraxia: the patient loses the ability to produce complex purposeful movements in the absence of paralysis and with the preservation of elementary movements. Thus, the patient cannot fasten buttons on his own, confuses the sequence of actions, and is helpless in handling various objects and tools. The skills of symbolic movements may also be lost: gestures of threat with a finger, a military salute, etc. Typically, apraxia affects both hands, although with damage to the corpus callosum, isolated apraxia may occur in the left hand. A hint (show) does not help the patient much.
Lesions in the inferior parietal lobe on the left in right-handed people may appear constructive apraxia(spatial apraxia). The patient cannot construct a whole from parts (a figure from matches or cubes). Apraxia can be combined with sensory aphasia.
Damage to the angular gyrus ( gyrus angularis) of the dominant hemisphere can lead to alexia– loss of ability to understand what is written. At the same time, the ability to write is also lost, not reaching the level of complete agraphia, as with damage to the frontal lobe. When writing, the patient writes words, and sometimes even letters, incorrectly, to the point of complete meaninglessness of what is written. Alexia is one of the species visual agnosia.
The result of damage to the area located posterior to the posterior central gyrus is astereognosia. In its pure form, with this disorder, the patient can feel and describe the properties of an object (weight, shape, size, surface properties) located in the hand opposite the lesion. However, he cannot create a summarized image of an object and recognize it. If the posterior central gyrus is damaged, the lack of recognition of the object will be complete: due to the loss of all types of sensitivity, even individual properties and qualities of the object cannot be established.
Lesions located posterior to the inferior part of the postcentral gyrus may appear as afferent motor aphasia, caused by blockade of afferent proprioceptive impulses from the speech motor parts of the postcentral gyrus. With it, as a rule, elements of oral apraxia are observed. Control of the articular act is confusing, loses its clarity and selectivity, as a result of which the patient does not immediately find the desired positions of the tongue and lips. Word differentiation is disrupted; instead of one word, a consonant or distorted word pops up, distorting the meaning (hump-coffin, horns-mountain, mountain-bark). Repeated speech is grossly impaired, and the understanding of speech is to some extent impaired again, which is why the patient does not notice his verbal mistakes.
A rare form of agnosia is autotopognosia– failure to recognize parts of one’s own body or distorted perception of it. With autotopagnosia, the patient confuses the right side with the left, feels the presence of a third arm or leg (pseudomelia), the hand may seem to him to be a direct continuation of the shoulder, and not the forearm. Lesions of the right parietal lobe can lead to a combination of autotopognosia with anosognosia– lack of awareness of one’s defect, paralysis.
Lesions of the parietal lobe at the junction with the temporal and occipital lobes in the dominant hemisphere lead to the development of Gerstmann-Schilder syndrome (acalculia - counting disorder, finger agnosia and impaired right-left orientation).
With lesions located in the deep parts of the parietal lobes, inferior quadrant hemianopsia may develop.
Occipital lobe. When the occipital lobe is damaged, visual and discoordination disorders may occur. Thus, with lesions in the area of the calcarine groove on the inner surface of the occipital lobe, loss of the opposite visual fields occurs - homonymous hemianopsia. Partial lesions of the visual projection field above sulcus calcarinus lead to quadrant hemianopsia opposite lower quadrants; lesions below the calcarine sulcus - the lingual gyrus - lead to loss of the fields of the opposite upper quadrants.
The appearance of small lesions in the area of the visual projection field can lead to the appearance of scotomas (from the Greek. skotos– darkness) – island vision defects in both opposite quadrants of the same name. Milder degrees of damage lead to loss of color sensations in opposite fields of vision and decreased vision - hemiamblyopia.
A feature of visual impairments with damage to the cortex is the preservation of macular vision even with extensive bilateral lesions of the cortex, which makes it possible to distinguish tractus hemianopia from cortical hemianopia.
Damage to the outer surface of the left occipital lobe in right-handed people (dominant hemisphere) can lead to:
– for mild lesions – to metamorphopsia, impairment of correct recognition of the contours of objects; they appear to the patient as broken and distorted;
– for more severe lesions – to visual agnosia, loss of the ability to recognize objects by their appearance. At the same time, the patient does not lose vision and the ability to recognize objects by touching or by the characteristic sounds they make.
Complete visual agnosia, when the world seems to the patient to be filled with a number of unfamiliar objects, is less common than cases of partial visual agnosia (agnosia for colors, faces, etc.).
Discoordinating disorders manifest themselves as contralateral ataxia(the function of the occipital-pontine-cerebellar pathway is impaired).
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Auditory (acoustic) agnosia. Temporal neuropsychological syndromes vary depending on the side of the lesion due to the clear lateralization of the brain mechanisms of speech functions and occur when fields 42, 22 (secondary and tertiary) of the auditory analyzer are damaged.
Types of auditory agnosia:
1. Speech acoustic agnosia. It is more often called sensory aphasia, since it is based on a violation of phonemic hearing, which provides a differentiated analysis of meaningful speech sounds. One hundred,” the severity of agnosia can vary: from a complete inability to distinguish phonemes of the native language (native speech is perceived as a set of sounds without meaning) to difficulty understanding close phonemes, rare and complex words, speech at a fast pace or pronounced in “difficult” conditions.
2. Auditory agnosia occurs when the nuclear zone of the auditory analyzer on the right is damaged. With this type of agnosia, the patient does not recognize the usual everyday, object and natural noises (creaking, the sound of pouring water, etc.).
2. Auditory agnosia occurs when the nuclear zone of the auditory analyzer on the right is damaged. With this type of agnosia, the patient does not recognize the usual everyday, object and natural noises (creaking, the sound of pouring water, etc.).
3. Arrhythmia - is expressed in the fact that patients cannot correctly “assess by ear” and reproduce rhythmic structures. When the right temple is damaged, the perception of the structural design of the rhythm as a whole is disrupted; when the left temple is damaged, the analysis and synthesis of the structure of the rhythm, as well as its reproduction, is disrupted.
4. Amusia manifests itself in a violation of the ability to recognize and reproduce a familiar or just heard melody.
5. Violations of the intonation side of speech (prosody) are expressed in the fact that patients do not distinguish intonations in the speech of others, in addition, their own speech is inexpressive: the voice is devoid of modulations and intonation diversity. This disorder is characteristic of a right temporal lesion.
6. Acoustic-mnestic aphasia. Occurs when the mediobasal parts of the cortex of the left temporal region are damaged. The patient is unable to remember even relatively small speech material due to impaired auditory-verbal memory. As a result, a secondary misunderstanding of oral speech occurs due to the weakness of hearing speech traces.
The central symptom is a decrease in memory capacity. The speed of processing verbal information also decreases.
Modality-nonspecific memory impairments. They occur when the mediobasal parts of the temporal region of the cerebral cortex are damaged.
Defects in “general memory” manifest themselves in patients with difficulties in directly retaining traces of any modality. With more massive lesions of these parts of the brain, short-term memory disorders approach the intensity of Korsakov's syndrome (fixation amnesia, mental disorientation, paramnesia).
Emotional disturbances. They occur when the mediobasal parts of the temporal cortex of the brain (limbic system) are damaged.
When the cortex of the right temporal lobe is damaged, two types of affective disorders are possible:
- paroxysms of excessively powerful emotions with a tinge of suffering (anguish, fear, horror), which may be accompanied by hallucinations and viscerovegetative changes;
- paroxysms, including the experience of derealization and depersonalization with a sharp decrease in emotionality or a euphoric background mood.
Clinical observations of patients with left temporal lesions have shown that the leading factor here is the predominance of depressive and anxious experiences with activation and motor restlessness. Against the background of constant emotional stress and anxiety, alertness, suspicion, irritability, and conflict become more and more apparent.
Impaired consciousness. Appear when the medial parts of the temporal region of the brain are damaged. In severe cases, these are drowsy states of consciousness and confusion. In milder cases - difficulties in orientation in place, time (right hemisphere); absence seizures.
