Symptoms of parietal lobe lesions

The parietal lobe is separated from the frontal lobe by the central sulcus, from the temporal lobe by the lateral sulcus, and from the occipital lobe by an imaginary line drawn from the upper edge of the parieto-occipital sulcus to the lower edge of the cerebral hemisphere. On the outer surface of the parietal lobe, there is a vertical postcentral gyrus and two horizontal lobes - the superior parietal and inferior parietal, separated by a vertical sulcus. The part of the inferior parietal lobule located above the posterior section of the lateral sulcus is called the supramarginal gyrus, and the part surrounding the ascending process of the superior temporal sulcus is called the angular gyrus.

The afferent pathways of cutaneous and deep sensitivity end in the parietal lobes and postcentral convolutions. Here, the analysis and synthesis of perceptions from the receptors of superficial tissues and organs of movement are carried out. When these anatomical structures are damaged, sensitivity, spatial orientation, and regulation of purposeful movements are impaired.

Anesthesia (or hypoesthesia) of pain, thermal, tactile sensitivity, disorders of joint-muscular sense appear with damage to the postcentral convolutions. Most of the postcentral convolution is occupied by the projection of the face, head, hand and its fingers.

Astereognosis is the failure to recognize objects when palpating them with the eyes closed. Patients describe individual properties of objects (for example, rough, with rounded corners, cold, etc.), but cannot synthesize the image of the object. This symptom occurs with lesions in the superior parietal lobe, near the postcentral gyrus. When the latter is affected, especially its middle part, all types of sensitivity for the upper limb are lost, so the patient is unable not only to recognize an object, but also to describe its various properties (false astereognosis).

Apraxia (a disorder of complex actions with preservation of elementary movements) occurs as a result of damage to the parietal lobe of the dominant hemisphere (in right-handed people - the left) and is detected in the functioning of the limbs (usually the upper). Foci in the region of the supramarginal gyrus (gyrus supramarginalis) cause apraxia due to the loss of kinesthetic images of actions (kinesthetic or ideational apraxia), and lesions of the angular gyrus (gyrus angularis) are associated with the disintegration of the spatial orientation of actions (spatial or constructive apraxia).

A pathognomonic symptom of parietal lobe damage is a disorder of the body scheme. This is expressed by non-recognition or distorted perception of parts of one's body (autotopagnosia): patients confuse the right half of the body with the left, cannot correctly show the fingers of the hand when the doctor names them. Less common is the so-called pseudopolymelia - a sensation of an extra limb or another part of the body. Another type of body scheme disorder is anosognosia - non-recognition of the manifestations of one's disease (for example, the patient claims that he moves his paralyzed left upper limb). Note that body scheme disorders are usually observed with damage to the non-dominant hemisphere (the right - in right-handed people).

When the parietal lobe is affected in the area that borders the occipital and temporal lobes (fields 37 and 39 are young formations in phylogenetic terms), the symptoms of higher nervous activity disorders are combined. Thus, the shutdown of the posterior part of the left angular gyrus is accompanied by a triad of symptoms: finger agnosia (the patient cannot name the fingers of the hands), acalculia (counting disorder) and disturbance of right-left orientation (Gerstmann syndrome). These disorders may be accompanied by alexia and symptoms of amnestic aphasia.

Destruction of the deep parietal lobe results in inferior quadrant hemianopsia.

Symptoms of irritation of the postcentral gyrus and parietal lobe are manifested by paroxysms of paresthesia - various skin sensations in the form of crawling ants, itching, burning, electric current (sensory Jacksonian seizures). These sensations arise spontaneously. With foci in the postcentral gyrus, paresthesia usually occurs in limited areas of the body (usually on the face, upper limb). Skin paresthesia before epileptic seizures is called somatosensory auras. Irritation of the parietal lobe behind the postcentral gyrus causes paresthesia on the entire opposite half of the body at once.

Syndromes of local damage to the parietal lobes

I. Postcentral gyrus

1. Elementary somatosensory disturbances
   • Contralateral decrease in sensitivity (stereognosis, muscle-joint sense, tactile, pain, temperature, vibration sensitivity)
   • Contralateral pain, paresthesia

II. Medial sections (cuneus)

1. Transcortical sensory aphasia (dominant hemisphere)

III. Lateral sections (superior and inferior parietal lobules)

1. Dominant hemisphere
   • Parietal apraxia
   • Finger agnosia
   • Acalculia
   • Right-left disorientation
   • Literal alexia
   • Alexia with agraphia
   • Conduction aphasia
2. Non-dominant hemisphere
   • Anosognosia
   • Autotopagnosia
   • Spatial disorientation
   • Hemispatial Neglect
   • Constructional apraxia
   • Apraxia of dressing

IV. Epileptic phenomena characteristic of the parietal localization of the epileptic focus.

Lesions of the parietal lobe are accompanied by various types of agnosia, apraxia and spatial disorientation.

In addition to the above, many other neurological syndromes associated with parietal localization of brain damage have been described in the literature. A rare syndrome is parietal ataxia. It develops with damage to those parts of the parietal lobe into which proprioceptive, vestibular and visual sensory flows converge, and is manifested by decomposition of movements, hyper- and hypometria, and tremor.

Muscle atrophy (especially of the arm and shoulder girdle) on the opposite half of the body is also often described, which sometimes precedes paresis in slowly progressing pathological processes.

Parietal lesions in the first three years of life are sometimes accompanied by delayed growth of bones and muscles on the opposite half of the body.

Manual and oral apraxia, hypokinesia, echopraxia, and paratonia (gegenhalten) are described.

Variants of thalamic syndrome sometimes develop with parietal damage. With processes in the posterior parietal lobe, visual disturbances in the form of visual field defects may occur. Unilateral visual neglect (neglect or inattention) may be observed without a visual field defect. Visual perception disorders (metamorphopsia) may occur with both bilateral and unilateral lesions (usually on the right). There are individual indications of the possibility of disturbances in tracking eye movements and optokinetic nystagmus, mild intellectual impairment, mental blindness, finger agnosia (in the picture of Gerstmann syndrome), disturbances in spatial orientation (the posterior parietal lobe plays a special role in visual-spatial directed attention, the ability to direct visual attention to a particular place in the surrounding space). The phenomenon of "beautiful indifference" in hemispatial neglect syndrome, deterioration in the recognition of emotional vocalizations, and depression have also been described.

I. Postcentral gyrus.

Lesions in this area are manifested by well-known somatotopically organized contralateral sensory disturbances (disturbances of stereognosis and muscle-joint sense; tactile, pain, temperature, vibration hypoesthesia) as well as contralateral paresthesia and pain.

II. Medial parts of the parietal lobe (precuneus)

The medial parts of the parietal lobe (precuneus) are directed towards the interhemispheric fissure. Lesions of this area in the left (speech-dominant) hemisphere can manifest as transcortical sensory aphasia.

III. Lateral sections (superior and inferior parietal lobules).

Damage to the dominant (left) parietal lobe, especially the gyrus supramarginalis, is manifested by typical parietal apraxia, which is observed in both hands. The patient loses the skills of habitual actions and, in severe cases, becomes completely helpless in handling this or that object.

Finger agnosia - the inability to recognize or name individual fingers in oneself or another person - is most often caused by damage to the gyrus angularis or a nearby area of the left (dominant) hemisphere. Acalculia (the inability to perform simple counting operations) has been described with damage to various parts of the cerebral hemispheres, including damage to the left parietal lobe. Sometimes the patient confuses the right side with the left (right-left disorientation). Damage to the angular gyrus (gyrus angularis) causes alexia - the loss of the ability to recognize written signs; the patient loses the ability to understand what is written. At the same time, the ability to write is also impaired, that is, alexia with agraphia develops. Here, agraphia is not as severe as with damage to the second frontal gyrus. Finally, damage to the parietal lobe of the left hemisphere can lead to the appearance of symptoms of conduction aphasia.

Pathological processes in the parietal lobe of the non-dominant hemisphere (e.g., stroke) may manifest as anosognosia, in which the patient is not aware of his defect, most often paralysis. A rarer form of agnosia is autotopoagnosia - a distorted perception or failure to recognize parts of one's own body. In this case, symptoms of a distorted body scheme ("hemidepersonalization"), difficulty orienting oneself in body parts, and a sensation of the presence of false limbs (pseudomelia) are observed. Spatial orientation may be impaired. For example, the patient begins to experience difficulties in any actions that require orientation in space: the patient is unable to describe the way from home to work, cannot navigate a simple plan of the area or the plan of his own room. The most noticeable symptom of damage to the inferior parietal lobe of the non-dominant (right) hemisphere is hemispatial contralateral neglect (neglect): a distinct tendency to ignore events and objects in one half of the space contralateral to the damaged hemisphere. The patient may not notice the doctor if the latter is standing by the bed on the side opposite the hemispheric damage. The patient ignores words on the left side of the page; trying to find the center of a horizontal line, he points to it, significantly shifting to the right, etc. Constructive apraxia may occur, when the patient loses the ability to perform even elementary actions that require precise spatial coordinates. Apraxia of dressing has been described with damage to the right parietal lobe.

A lesion in the inferior parietal lobule sometimes manifests itself as a tendency not to use the hand contralateral to the lesion, even if it is not paralyzed; she shows clumsiness in performing manual tasks.

Neurological syndromes of parietal lobe damage can be summarized in another way:

Any (right or left) parietal lobe.

1. Contralateral hemihypesthesia, impairment of the sense of discrimination (with damage to the posterior central gyrus).
2. Hemispatial neglect (neglect).
3. Changes in the size and mobility of the contralateral limb, including muscle volume and growth retardation in children.
4. Pseudothalamic syndrome
5. Impaired pursuit eye movements and optokinetic nystagmus (with damage to the parietal association cortex and deep white matter).
6. Metamorphopsia.
7. Constructional apraxia
8. Parietal ataxia (retrolandic region).

Non-dominant (right) parietal lobe.

1. Constructional apraxia
2. Spatial disorientation
3. Impaired recognition of speech information
4. Affective disorders.
5. Unilateral spatial neglect.
6. Apraxia of dressing.
7. Attention disorders, confusion.
8. Anosognosia and autotopagnosia

Dominant (left) parietal lobe.

1. Aphasia
2. Dyslexia
3. Agraphia.
4. Manual apraxia
5. Constructional apraxia.

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

1. Visual agnosia.
2. Balint's (strongalint) syndrome (develops with damage to the parietal-occipital region of both hemispheres) - the patient, with normal visual acuity, can perceive only one object at a time; apraxia).
3. Gross visual-spatial disorientation.
4. Gross constructional apraxia.
5. Autotopagnosia.
6. Bilateral severe ideomotor apraxia.

IV. Epileptic paroxysmal phenomena characteristic of the parietal localization of the epileptic focus.

Sensory areas. Primary sensory area.

1. Paresthesia, numbness, rarely - pain in the opposite half of the body (especially in the hand, forearm or face).
2. Jackson's Touch March
3. Bilateral paresthesias in the legs (paracentral lobule).
4. Gustatory aura (inferior Rolandic region, insula).
5. Paresthesia in the tongue (numbness, tension, coldness, tingling)
6. Abdominal aura.
7. Bilateral facial paresthesias
8. Genital paresthesia (paracentral lobule)

Secondary sensory area.

1. Bilateral bodily (without facial involvement) paresthesias, sometimes painful.

Additional sensory area.

1. Bilateral paresthesia in the extremities.

Posterior parietal and parieto-occipital region.

1. Hallucinations.
2. Metamorphopsia (mainly with damage to the non-dominant hemisphere).
3. Photopsies.
4. Macropsia or micropsia.
5. Dizziness (this symptom may be due to involvement of the temporal lobe structures).

Speech symptoms.

1. Ictal aphasia
2. Stopping speech

Non-dominant parietal lobe.

1. Ignorance of the opposite half of the body (asomatognosia).

Poorly localizable phenomena.

1. Intra-abdominal paresthesia
2. Dizziness.

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