Internal capsule, corpus callosum, basal ganglia... Lesion symptoms and location diagnosis diagram

*Only for medical professionals to read and reference Quick Collection! Symptoms, location and diagnosis of internal capsule lesions The internal capsule is a dense place of ascending and descending fibers in the cerebral hemisphere
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The internal capsule is very important in localization and diagnosis, because the area here is narrow, the ascending and descending fibers gather compactly, and the incidence rate is high, and the most common is cerebrovascular disease
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1.
Symptoms of internal capsule lesions There are three main groups of symptoms in internal capsule lesions, namely hemiplegia, hemianopia and hemisensory disturbance, which are clinically called "triple-bias syndrome"
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❖ Hemiplegia: ipsilateral equal central hemiplegia occurs on the opposite side of the lesion, that is, the facial and tongue paralysis and paralysis of the upper and lower limbs on the opposite side of the lesion are on the same side, and the paralysis of the upper and lower limbs is equal, manifested as increased muscle tension, Tendon hyperreflexia and positive pathological reflexes
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❖ Hemibody sensory disturbance: that is, the sensory disturbance on the opposite side of the lesion, including the depth and lightness of the head and face
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❖ hemianopia: homotropic hemianopia occurs in the visual field opposite to the lesion
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2.
Localization of internal capsule lesions The internal capsule is an extremely important anatomical structure, where a large number of nerve conduction fibers pass through, the thalamus and caudate nucleus are located medially, and the lentiform nucleus is located laterally
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If a horizontal section of the internal capsule is made in the middle of the striatum (as shown in the figure), it can be seen that the internal capsule is in the shape of a curved ruler, and its tip is medial, located between the caudate nucleus and the thalamus, which is called the knee of the internal capsule
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The anterior part of the knee of the internal capsule is bent forward and outward, located between the lentiform nucleus and the caudate nucleus, called the forelimb of the internal capsule (frontal part)
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The posterior part of the knee of the internal capsule is curved posteriorly and outwardly, between the lentiform nucleus and the thalamus, and is called the posterior limb of the internal capsule (occipital)
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Damage to different parts of the internal capsule can produce a variety of clinical symptoms
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The most common etiologies are intra-capsular intracerebral hemorrhage caused by rupture of the lenticulostriate artery, cerebral infarction at the origin of the middle cerebral artery system, and space-occupying lesions in the deep cerebral hemisphere
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❖ Internal capsule forelimb lesions: The internal capsule forelimb contains ascending thalamofrontal fibers and thalamo-striatal fibers; descending frontal-pontine fibers, frontal thalamic fibers, and striatal-thalamic fibers
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Cerebellar ataxia of the contralateral limb may occur when lesions in the forelimb of the internal capsule occur
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Such as bilateral lesions may appear emotional disturbance, involuntary crying and laughing
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❖ Internal capsule knee lesions: Cortical brainstem bundles pass through the internal capsule knee.
In this lesion, central paralysis of the lateral and hypoglossal nerves may occur, and motor nerves of other cranial nerves are not damaged
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Bilateral internal capsule knee lesions present bilateral motor paralysis of cranial nerves and pseudobulbar (bulbar) palsy.
The patient presents with hoarseness, choking on drinking water, dysphagia, presence of gag reflex, strong crying and laughter, and mandibular reflex.
Hyperactivity, orbicularis oris muscle reflex and palmar mandibular reflex were positive
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❖ Lesions of the hindlimb of the internal capsule: The hindlimb of the internal capsule can be divided into three parts: the bean mound, the posterior part of the lentiform nucleus and the lower part of the lentiform nucleus
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The lumenoid contains the corticomedullary tract mixed in it, as well as the corticospinal tract, the cortico-red nucleus tract, and the posterior thalamic radiation; the posterior part of the lentiform nucleus is located in the middle part of the hindlimb of the internal capsule, above the lateral surface of the thalamus, behind the lentiform nucleus, It contains the retrothalamic radiation; the lower part of the lentiform nucleus is located on the ventral side of the posterior lentiform nucleus, mainly including the auditory radiation, the optic radiation and the temporo-occipital bridge
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When the anterior lesion of the hind limb of the internal capsule occurs, the upper and lower extremity hemiplegia on the opposite side of the patient will appear
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Symptoms and localization diagnosis of corpus callosum lesions Because the function of the corpus callosum is not fully understood, the clinical significance and localization diagnosis of its damage are not well understood
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1.
Mental disorders The main symptom of corpus callosum damage is mental disorders
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Patients often manifested as inattention, lack of persistence, memory loss, intellectual disability, mental retardation, decreased autonomous activities, personality changes and psychotic-like performance
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Some people think that the anterior 2/3 of the corpus callosum is mainly damaged by psychomotor symptoms, and the posterior 1/3 of the corpus callosum is mainly damaged by psychosensory symptoms
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2.
Apraxia The lesions of the anterior 1/3 of the corpus callosum cause apraxia, mainly left hand apraxia
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Apraxia is caused by lesions on the inferior parietal margin of the left hemisphere (the dominant hemisphere in the right-handed)
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Since the commissural fibers from the left supramarginal gyrus pass through the corpus callosum to reach and innervate the supramarginal gyrus of the right hemisphere, the cortical or subcortical lesions of the left supramarginal gyrus cause apraxia of both limbs
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The lesions also tend to expand to the precentral gyrus, resulting in paralysis of the right limb and apraxia of the left limb
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When the corpus callosum has lesions, the commissural fibers are interrupted, so that the supramarginal gyrus of the right hemisphere is separated from the influence of the left hemisphere, thus causing left apraxia
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In the same way, left-sided apraxia can also occur in the upper gyrus of the right hemisphere (see the figure below)
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This also means that there cannot be a separate clinical manifestation of right limb apraxia
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Figure: Three possible lesions causing left-hand apraxia (when the left hemisphere is the dominant hemisphere): 1.
Left hemisphere center semiovale lesions cause right hemiplegia and left hand apraxia; 2 and 3 lesions are in the corpus callosum and right hand, respectively 3.
Pseudobulbar palsy in the center of the hemisphere and semiovale, causing left-hand apraxia , and the fibers from the internal capsule to the head and face motor center of the right cerebral hemisphere cortex all pass through the middle of the corpus callosum, so when the middle of the corpus callosum is damaged, these fibers can be blocked at the same time, resulting in pseudobulbar palsy symptoms
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Therefore, when a patient with right hemiplegia has symptoms of pseudobulbar palsy, it may be the corpus callosum damage (as shown in the figure below)
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4.
Speech and motor ataxia Fibers in the anterior 1/3 of the corpus callosum connect the motor speech center and the corresponding area on the opposite side
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The fibers in the middle 1/3 and the anterior 1/3 of the small part connect the motor synaesthesia and the application center and the corresponding area on the opposite side
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The posterior 1/3 of the fibers connect the visual and auditory areas on both sides
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Therefore, when the corpus callosum has lesions, it can cause symptoms such as ataxia of speech and movement
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Symptoms and localization of limbic (systemic) lesions 1.
Korsakoff syndrome Korsakoff syndrome can be caused when the medial limbic circuit (Papez circuit) is disrupted or involved
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The medial limbic loop, also known as the emotional memory loop
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From the medial side of the brain to the diaphragm (paraolfactory area and inferior corpus callosum) → the deep fibrous cingulate tract of the cingulate gyrus → hippocampus → hippocampus → fornix → mammillary body → papillary thalamic tract → prethalamic nucleus → prethalamic radiation → internal capsule → cingulate gyrus (see picture below)
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Mammillary body → papillary tegmental bundle → midbrain tegmental and reticular activation system → medial forebrain bundle (MFB) → hypothalamus, diaphragm
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The semi-circle is the main place for the transformation of electrical information, and the hippocampus is the main part of the transformation and storage of recent memory information
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Double hippocampal damage or circuit disruption results in Korsakoff syndrome
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The main manifestations are obvious recent memory impairment, fiction, anterograde amnesia, and loss of orientation; more common in hemorrhagic upper cortical encephalitis (Wernicke encephalopathy), brain trauma, alcoholism, herpes simplex encephalitis, primary arachnoid Inferior hemorrhage and tumor in the area
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Due to the involvement of the hippocampus, mammillary body, temporal lobe, cingulate gyrus, and fronto-orbital surface
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2.
Klüver-Bucy syndrome This sign is also known as post-temporal lobectomy behavioral syndrome
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Klüuver-Bucy syndrome occurs when the lateral limbic circuit, dominated by the amygdala including the piriform region, is involved
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The basolateral limbic circuit (Livengston circuit) includes various connections between the orbitofrontal cortex, the anterior temporal lobe, and others with the amygdala and the dorsal nucleus of the thalamus
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Amygdala → stria terminalis → preoptic area of ​​hypothalamus → medial forebrain tract → dorsal tegmental area of ​​midbrain
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The orbitofrontal cortex and prefrontal cortex communicate with the frontotemporal neocortex, respectively
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This loop is related to cognition and memory
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Double amygdala damage, resulting in Klüiver-Bucy syndrome
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The main clinical manifestations are docile temperament, no emotional response, near-memory impairment, especially difficulty in remembering words, hypersexuality, excessive vigilance, and may have mental recognition failure, which is caused by the involvement of the anterior and lower temporal regions
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3.
Mental symptoms or dementia can be caused by damage to the limbic system, which is more serious when the hippocampus is involved
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For example, damage to the anterior temporal region, fusiform gyrus, insula, fronto-orbital surface, and cingulate gyrus may manifest as a decline in recent memory and analytical and critical abilities, stubbornness, and difficulty in taking care of oneself in life
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4.
Temporal lobe epilepsy Since the temporal lobe contains most of the limbic system, such as the nucleolus, hippocampus, and anterior temporal lobe, psychomotor epilepsy can occur, such as smell, taste, visual and auditory hallucinations, familiarity, strangeness, and dreams.
, fear, joy, confusion and forgetting
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Due to the involvement of the insula and cingulate gyrus, there may be automatisms including sucking and swallowing; a more complex dual pathological personality may also appear
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Symptoms and localization diagnosis of basal ganglia lesions The basal ganglia or striatal system is one of the components of the extrapyramidal system, which together with the vestibulo-cerebellar system constitutes the extrapyramidal system and regulates the movement of upper and lower motor neurons function
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The striatal system is the fingerprint body (caudate nucleus, lentiform nucleus), red nucleus, substantia nigra, subthalamic nucleus, collectively called the basal ganglia, and the main cortical part associated with it is the premotor area, namely area 6
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The striatum is an ancient high-level motor center
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In lower vertebrates, because the cerebral cortex has not yet occurred or is still very primitive, the pyramidal tract does not yet exist, and the striatum and thalamus are the highest motor and sensory centers
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In mammals, due to the development of the cortex and the formation of the pyramidal tract, the main motor function gradually gave way to the cortical motor area with the evolution of the race, but the striatum did not stop performing its functions, but only accepted the control of the cortical motor area.
Its function is to maintain and adjust the posture of the body, and it is responsible for semi-automatic, stereotyped, and reflexive movements, such as joint movements such as arm swinging during walking, facial expression movements, defensive responses, and eating movements
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The inhibitory impulses in the 4S, 8S and other inhibitory areas of the cortex pass through the caudate nucleus, putamen, globus pallidus, and thalamus to reach the motor area.
Once this pathway is broken, it will cause release symptoms such as chorea, athetosis and other involuntary movements
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The exact location is difficult.
Generally speaking, lesions of the neostriatum (caudate nucleus and putamen) cause chorea, athetosis, and torsional spasm, and lesions of the globus pallidus and substantia nigra cause increased muscle tone and decreased movement.
Resting tremor (such as Parkinson's disease) may also occur
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Source of this article: Neurology Medical Network Author of this article: Xuan Zhixuan Review of this article: Li Tuming, Deputy Chief Physician Responsible Editor: Mr.
Lu Li We make any promises and guarantees about the accuracy and completeness of the cited materials (if any), and do not assume any responsibility for the outdated contents, possible inaccuracy or incompleteness of the cited materials,
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