Blood supply to the thalamus, clinical symptoms of infarction and related mechanisms

The blood supply of the thalamus, clinical symptoms of infarction and its related mechanisms must be collected! Move the small bench and study together!

Deep in each of our brain hemispheres is an oval gray matter complex, about 3 cm × 1.
5 cm in size, roughly the size
of a small red date.

The actual thalamus is not a complete whole, but is made up of
countless neuronal nuclei clusters.
I believe that the first contact with the form of the thalamus in the textbook will be confused, what is this?

To say complex, human understanding of the thalamus is now far more than the few divisions drawn in textbooks, and the thalamus can now be divided into more than 120 nuclear groups to perform different physiological functions
.

However, in general, clinicians do not need to fully master
these complex divisions and functions.
Today, we will come and go to extract the essence, remove the false and the true, and use the most practical and simple way to talk about the blood supply to the thalamus and the clinical manifestations of common thalamic damage in different parts of the thalamus.
.
.

MRI location of the thalamus

Admittedly, almost all clinicians' initial understanding of the thalamus begins on CT or MRI
.
In our most common head MRI, the location of the thalamus is shown below:

At the level of this common MRI in the image above, the thalamus is located on either side of the midline, and the red part in the middle of the image above is the thalamus
.

Blood supply to the thalamus

Click on the picture above to zoom in, and if you look closely, there are 4 major blood supplies to the thalamus

Zooming in, let's take a look at the blood supply range
of these 4 arteries in the figure above.

Below is a flat pattern diagram
.

Let's take a look at a three-dimensional pattern diagram to understand the origin, shape and distribution
of these four arteries from another perspective.

Thalamic nodular artery thalamic infarction

Cerebral infarction in this area can be clinically manifested as impaired consciousness, psychiatric symptoms, etc
.
Fluctuating altered levels of consciousness, impaired memory, learning, personality changes, apathy, executive dysfunction, neglect, apraxia.
.
.

Parathalamic median thalamic infarction

The clinical presentation of cerebral infarction in this area is similar
to that of thalamic nodular arteries.
Mainly there is a decrease in the level of consciousness, a decrease in memory and learning ability, disorientation, aphasia, apathy, agitation, etc.
.
.

Hypolateral thalamic thalamic infarction

This site is the clinical manifestations of thalamic syndrome that we are very familiar with in our clinic, and it is also the most typical symptom
in thalamic cerebral infarction.
The main clinical manifestations are contralateral hemisensory impairment, hemiplegia, hemiataxia, thalamic pain
.

Hemilateral sensory impairment does not need much explanation, the posterior ventrolateral nucleus and the posterior ventromedial nucleus are in this area, and patients often have complete numbness
of the lateral part, hemilateral limb, and hemilateral trunk.

Hemiplegia, most of the hemiplegia caused by cerebral infarction in this area occurs when the infarct area is slightly larger, and hemiplegia is generally not serious
.
I personally understand that hemiplegia is not directly damaged by the pyramidal tract, but that this part of the thalamus is adjacent to the pyramidal tract, and the infarction is larger edema, inflammatory reaction, etc.
affect the pyramidal tract
of the inner capsule.
Therefore, hemiplegia caused by this site is generally not serious and is easy to recover
.

Hemiaxial ataxia, hemisensory ataxia, this does not need much explanation
.

Thalamic pain generally does not occur immediately after cerebral infarction, and most patients gradually appear and worsen
during the recovery period of infarction.
Patients are often in pain, have a persistent burning sensation on the side, and what is even more distressing is that once this symptom appears, the treatment effect is very poor
.

Posterior choroidal thalamic infarction

Cerebral infarction in this area is rarely involved alone, often accompanied by damage
to other sites.

The lateral and medial geniculate bodies are included in this site, so the clinical symptoms of patients mainly include visual field defects, sensory impairment, aphasia, memory loss.
.
.

Wu Chuanjie said

In thalamic infarction, the most classic is ischemia in the innervation area of the sublateral hypothalamic artery, resulting in a typical clinical manifestation of
thalamic syndrome.

However, it is not that damage to other parts of the thalamus is uncommon, but the symptoms of other parts are mostly manifested as psychiatric symptoms, cognitive changes, etc.
, which are not typical, and many other parts of the injury will have similar clinical manifestations
.

The clinical symptoms of thalamic infarction and its related mechanisms are explained in detail

1.
Infarction of the medial thalamus

The medial part of the thalamus, dominated by the dorsal medial nucleus, belongs to the neothalamus, which has extensive connection loops with the prefrontal cortex, frontal orbital cortex and Yingye neocortex, which are involved in emotions and visceral responses
accompanying emotions.

When infarction occurs in the parathalamic median artery supplying the medial part of the thalamus, the main clinical symptom is acute stroke-like onset, manifested as fluctuating consciousness impairment, amnesia, apathy, and may be accompanied by oculomotor nerve palsy, vertical gaze disorder, etc
.
Patients mostly start with drowsiness, with transient impaired consciousness, accompanied by varying degrees of decreased consciousness, lasting for different periods of time, and those with large infarction areas have a longer
duration.
Excessive drowsiness, disorientation and other symptoms may be related to
damage to the dorsomedial nucleus or the anterior thalamic nucleus.

Patients with bilateral thalamic infarction have thalamic infarction due to the sudden interruption of the blood supply to the medullary plate core and the central median nucleus of the bilateral thalamus, which interrupts the connection between the reticular ascending activation system of the midbrain, and then thalamic infarction syndrome, which is manifested as consciousness disorders of varying severity and inhibitory changes
on EEG.
Neuropsychiatric disorders appear after a short period of consciousness impairment, mainly manifested as cognitive function and behavioral abnormalities, disorientation, apathy, often fiction, prominent forgetting of recent events, and lack of
will.
Transient neglect and loss
of drawing and transcription ability may occur in the main lesion.
These dysfunctions may be related to
impaired central nucleus, plate nucleus, and partial dorsomedial nuclear ischemia.

Through the collation and analysis of clinical cases, it is proved that the contact damage between the large cell part of the dorsomedial nucleus and the frontal lobe can lead to delusions and fiction
.

Damage to the dorsal medial nucleus and anterior nucleus of the thalamus can produce severe memory loss, personality changes, inhibition and decreased initiative, and time-place disorientation, which may be caused
by the projection of this area to the orbitofrontal cortex and the interruption of the cingulate gyrus due to the interruption of ischemic injury.

Studies have found that damage to the papillary body thalamic tract adjacent to the dorsomedial nucleus and obstruction of the connection between the thalamic nucleus and the hippocampus can also cause memory impairment
.
Signs of medial thalamic infarction are often ocular alignment and ocular movement disorders
.
Orthostatic gaze paralysis is also one of the important manifestations of the disease, which can coexist with upward paralysis, downward paralysis, or upper and lower visual paralysis, which is caused
by impaired medial longitudinal tract and eye movement pathways.
Among them, the upper visual paralysis is caused by damage to the dorsal side of the upper end of the medial longitudinal bundle, and the lower visual paralysis is caused by
the damage to the ventral part.
In addition, patients with parathalamic median artery infarction may also have involuntary movements, asymmetry of healthy reflexes, and Babinski's sign
.

2.
Posterolateral thalamic infarction

The posteriolateral thalamic nucleus group includes the dorsolateral nucleus of the thalamus, the posterior ventrolateral nucleus, the posterior medial ventral nucleus and the occipital nucleus, which are mainly supplied by the thalamic geniculate artery
.
When the thalamic geniculate artery infarction, causing posterolateral ventrolateral hypochemia of the thalamus, damaging the fibers of the medial thalamus and spinal thalamic tract, sudden or gradual development of the lesion of the contralateral body numbness, can be followed by hemisensory loss, that is, sensory stroke, manifested as hemisphere, not including the face of the half, face and hand or facial sensory disorders
.
When the infarct is large and the lesion involves the corticospinal tract of the posterior ventrolateral nucleus of the thalamus and the hindlimbs of the nearby internal capsule, sensorimotor stroke occurs, manifested as contralateral central hemiparesis and hemisensory impairment, and speech, cognitive function and behavior are normal
.

The appearance of thalamic syndrome is caused by infarction involving the primary sensory nucleus in the thalamic structure posterolateral ventral nucleus, posterior ventromedial nucleus, medial geniculate body, occipital nucleus and central middle nucleus, resulting in large infarcts in the thalamic geniculate artery supply area, and one or more of the following symptoms
may occur 。 (1) Contralateral hemibody sensory impairment, accompanied by "thalamic pain" (posterolateral abdominal nucleus damage); (2) transient or persistent mild contralateral weakness, chorea-like or athetoid (extravertebral involvement); (3) somatomatic ataxia (the connection between the ventrolateral nucleus of the thalamus and the red nucleus and the cerebellar dentate nucleus is affected); (4) hemidystonia, thalamic hand or hemichorea-like movements (bean nucleus involvement); (5) Contralateral affective facial paralysis (impaired thalamus-globus pallidus-facial nerve pathway).

When the patient has disappearance of deep and shallow sensations, it may be caused by ischemia caused by the connection fibrous damage of the medial and lateral parts of the thalamus to the cortical sensory area, CT examination generally shows a large infarction area, and patients with disappearing of deep and shallow sensations can also develop delayed thalamic pain and mild speech fluency
.

3.
Anterolateral thalamic infarction

The main structure of the anterolateral part of the thalamus is the anterior ventral nucleus group, which is related to the mastillion body and cingulate gyrus, and the damage of this structure will inevitably affect the ability to distinguish and analyze emotional consciousness, so that the driving force of internal emotions decreases, and this part is mainly supplied by the arteries of the thalamic tubercles
.
When the thalamic nodular artery is occluded, the lesion mainly affects the ventrolateral nucleus and the dorsomedial nucleus, and the most common symptom is lack
of will.
Patients lack initiative, delay in answering or simply answering questions, have an apathetic expression, are lazy, slovenly, unresponsive, and lack interest in surrounding things
.
Patients with left-sided thalamic infarction all have speech disorders, mainly manifested as decreased active language, difficulty in finding words, and inability to fully express a sentence; naming disorders, moderately impaired language reading and comprehension, and relatively retained repetition skills; Computing and orientation are significantly reduced, and delayed memory is reduced; There is no obvious abnormality
in visuospatial perception.

According to literature reports, patients with thalamic nodular arterial infarction have reduced
blood flow in the left margin of the superior gyrus, superior gyrus, middle frontal gyrus, inferior gyrus, and the anterior and dorsal medial nuclei of the left thalamus.
Studies have found that damage to the anterior nucleus of the left thalamus can lead to language fluency impairment, in which the patient's speech fluency impairment is more severe
than the semantic fluency impairment.
In addition, it has been reported that speech fluency disorders are more attributable to frontal lobe function impairment, while linguistic fluency disorders are mainly due to the accompanying temporal lobe function damage
.
The anterior part of the thalamus contains most of the fibers that connect the thalamus and the frontal projection system, which connect the dorsomedial nucleus, zonal gyrus, and prefrontal gyrus of the thalamus, forming the limbic circuit, the Papez circuit, which plays an important role
in maintaining memory.
When this circuit is impaired, frontal lobe symptoms and amnesia are manifested, i.
e.
memory loss, impaired consciousness, drowsiness, decreased speech, etc
.
Memory impairment caused by left-sided thalamic damage has been recognized by most scholars, and there are different views on
whether right-sided thalamic damage causes memory impairment.

4.
Right thalamic infarction

Right-sided thalamic infarction is mainly manifested as thalamic neglect of the left hemisphere, and the damage to the subcortical structure produces unilateral visuospatial impairment, the mechanism is: damage to the subcortical structure (especially the thalamus), blocking the cortical-limbic system-reticular structure activation loop at the subcortical level, leading to deficits in arousal and attention, thereby inducing and producing subcortical visuospatial neglect
.
In addition, contralateral sensory impairment, hemiplegia (heavier upper limbs than lower limbs), dysarthria, asymmetry of healthy reflexes and hemilateral ataxia
can also occur.

Specific clinical manifestations of thalamic infarction

1.
Thalamic aphasia

Thalamic aphasia is a kind of subcortical aphasia, and patients often have common language disorder characteristics, which are characterized by low speech, low speech volume, and misspelling, which are considered to be the three core symptoms
of thalamic aphasia.
(1) Low speech: patients with thalamic aphasia talk in a low pitch, and even whisper in severe cases, but generally not accompanied by dysarthria; (2) Low speech volume: patients with thalamic aphasia have reduced spontaneous speech and reduced speech fluency; (3) Semantic error: Semantic error is the main feature of patients with dyslexia in cortical injury, manifested as difficulty in finding words, sometimes accompanied by misspeech
.

In addition, patients also have symptoms such as naming disorder, dyslexia, and dysphrasia, but generally have relatively good
retelling ability.
Thalamic aphasia often appears suddenly as an acute symptom or first symptom of thalamic infarction, often accompanied by signs of hemiplegia, and is mostly incomplete paresis
.

The mechanism of thalamic aphasia is not fully understood, and it is thought that the development of thalamic aphasia is related
to damage to the ventrolateral nucleus.
Damage to the ventrolateral nucleus leads to the interruption of contact between the thalamus and the frontal lobe, resulting in the loss of speech activation and regulation of the frontal language area of the thalamus, and the interruption of these contact fibers can also lead to thalamic aphasia
due to the regulation and actuating effect of the posterior inferior frontal gyrus of the dominant lateral nucleation, that is, the Broca area, and acting on the Wernicke region (posterior superior temporal gyrus) through the superior longitudinal tract.

2.
Thalamic dementia

Thalamic dementia is a type of vascular dementia that is clinically rare
.
(1) Memory impairment: including instantaneous memory, near memory, and distant memory impairment, mainly manifested as near memory impairment; (2) Cognitive impairment: manifested as mental retardation, lack of judgment, time, place, and character orientation impairment; (3) Language disorders: slurred speech, spontaneous language reduction, volume reduction, slow speech, and silence in severe cases; (4) Abnormal mental behavior: manifested as apathy, inattention, reduced movement, and sitting
all day.

The occurrence of thalamic dementia is mainly caused by infarction leading to damage to the anterior thalamic nucleus and papillary-thalamic tract, which interrupts the round-trip fibers between the papillary body composed of the papillarythalamic tract and the prethalamic nucleus
.
At the same time, it has been pointed out that thalamic dementia may be caused
by the disruption of the pathway connecting the thalamus and the reticular structure to the frontal lobe, resulting in weakening of the frontal cortex.
It can be seen that thalamic dementia is caused
by impaired thalamus and extensive communication between the thalamus and cortex.
Therefore, when the parathalamic median artery and thalamic nodule artery infarction affects the above sites, dementia symptoms can occur
.

3.
Hypophalopheric hand

The thalamic hand often presents with contractures of the contralateral upper extremity; The wrist flexion and pronation, the hand and fingers are constantly in a characteristic posture, that is, the end of each finger joint is in an extendable position, the middle joint of each finger is flexed, and the metacarpophalangeal joint flexion makes the fingers also flex; Each finger moves slowly one by one, most finger movement disorders; Most of the wrist joints are ulnar offset; May be accompanied by resting tremor or intention tremor, chorea-like movements; Generally no sensory disturbance
.

The thalamic hand is commonly seen in unilateral parathalamic median artery infarction, especially the infarction of the main arterial trunk, resulting in damage to
the medial thalamic nucleus group and dorsomedial nucleus, midbrain foot nucleus, binding arm crossing, and inner red nucleus.
Because these thalamic nuclei are connected with extrapyramidal fibers, especially the central mesonucleus is connected with the putamen and caudate nuclei, and the red nucleus is damaged, resulting in indirect damage to the red nucleus spinal cord tract and the cerebellar dentate nucleus on the opposite side of the pontine nucleus of the red nucleus, resulting in extrapyramidal symptoms, and the production of the thalamic hand is related to
this.

4.
Episodic falls

Episodic falls are manifested as lying flat without dizziness, sudden dizziness and unstable standing when getting up and walking, sudden weakness of the lower limbs and falling, and recovery quickly after a short limb weakness, and can also be accompanied by hemiplegia, deep and shallow sensory disorders, sensory ataxia and other symptoms
.

Episodic falls may result from
infarction of the parathalamic median artery and thalamic geniculate artery.

The main function of the vestibular system is to maintain the balance of the body, and the lateral vestibular nucleus emits an important lateral vestibulospinal tract, descending on the ipsilateral anterior spinal cord until the spinal cord γ and α motor neurons as far as the cuboid segment, so as to maintain sufficient muscle tension throughout the body to maintain body balance
.

When the thalamus passes through the artery and the thalamic geniculate artery is blocked, the lesion damages the reticular nucleus of the brainstem, the midbrain cover and the red nucleus, causing obstacles to the reticular spinal tract and vestibulospinal tract of the red nucleus, so that the lower limbs cannot maintain tension and fall
.

epilogue

In recent years, the clinical symptoms and mechanisms of thalamic infarction have gradually become a research hotspot
for clinicians.
At present, the treatment of thalamic infarction is mainly drug treatment such as volume expansion, anticoagulation, nerve cell activator, etc.
, according to the size of the infarction area, dehydration drugs can be appropriately applied for treatment, and for some cases found earlier, thrombolytic drugs can be selected
.
However, the exact mechanism of clinical manifestations of thalamic infarction is still unclear, and most of the studies on thalamic infarction are retrospective and have certain limitations, and it is impossible to formulate absolutely effective treatment plans and rehabilitation plans
for different patients.
Therefore, it is necessary to conduct forward-looking multivariate analysis studies
.
By summarizing and analyzing the relationship between the clinical symptoms of thalamic infarction and related blood supply vessels, we can further understand the relevant mechanism of thalamic infarction, so as to help
clinical diagnosis and treatment.

Awesome, image anatomy map (shock is coming)

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