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*For reference of medical professionals only, read the collection quickly! In order to become an excellent neurologist, it is essential to learn the basics of cranial anatomy.
The author has also taken a lot of detours in this regard.
After continuous study, the author summarizes the basic knowledge of cranial anatomy as follows.
It's easy to understand (the course of the neurotic masters is inevitably a little confusing to the clinical novice), I hope it will be helpful to my colleagues
.
Due to the large amount of content and the large amount of information, the author divides all the content into 3 phases to explain
.
In the last issue, we introduced the structure, function and clinical manifestations of brain parenchyma and cerebral blood vessels after damage.
In this issue, we continue to introduce the second part: brainstem, cerebellar blood supply and clinical manifestations of infarction
.
1.
Brainstem blood supply and its common syndromesFigure 1 Surface view (ventral) of the brainstem blood supply area (Figure source, Professor Cheng Xin's PPT) Yellow PCA supplies the base of the temporal lobe, occipital lobe and most of the midbrain and thalamus; dark purple The paracentral branch of the basilar artery supplies the middle pons; the light purple peripheral branches of the basilar artery supply both sides of the pons; the green SCA supplies the upper half of the cerebellum and the upper part of the pontine tegment; the blue AICA supplies the lower anterior part of the cerebellum, pompoms, pons, and pontine tegment Lower part; cyan PICA supplies the inferior posterior part of the cerebellum and the dorsolateral medulla oblongata; red paravertebral artery branches and anterior spinal arteries supply the middle medulla oblongata; pale red vertebral artery collaterals supply both sides of the medulla oblongata
.
(1) Midbrain Figure 2 Midbrain blood supply (Figure Yuan, Professor Cheng Xin's PPT) Figure 3 Midbrain - Nuclei (purple) and conduction tracts (pink) at the plane of the superior colliculus (Figure Yuan, Professor An Hongwei's PPT) 1 , Weber syndrome (oculomotor cross palsy syndrome/cerebral peduncle syndrome) damage site: the ventral cerebral peduncle (oculomotor nerve and pyramidal tract)
.
Damaged blood vessels: PCA interpeduncular branch or PchA
.
Clinical manifestations: oculomotor nerve cross palsy, i.
e.
a.
Ipsilateral oculomotor nerve palsy: ptosis, eyeball oblique outward and downward (superior oblique muscle innervated by the trochlear nerve moves the eyeball outward and downward), eyeball up, down, Adduction disorder, mydriasis, disappearance of light reflex, diplopia; b.
Contralateral central facial and tongue paralysis, limb paralysis
.
If bilateral cerebral peduncles are infarcted, the "Mickey Mouse ear sign" can be seen on MRI, which means bilateral cortical brainstem/cortical nucleus tract damage: bilateral paralysis, tongue, pharynx, articulation, and swallowing movement disorders, unable to speak ( Complete pseudobulbar palsy) and bilateral corticospinal tract damage: quadriplegia, bilateral pathological signs
.
Figure 4 Cerebral peduncle syndrome (Weber) (Figure Yuan, Professor An Hongwei's PPT) 2.
Benedit syndrome (oculomotor and extrapyramidal cross syndrome, erythronucleus syndrome) damage blood vessels: basilar artery interpeduncular branch or brain Posterior arterial blockage or blockage of both
.
Core features: ipsilateral oculomotor nerve palsy + contralateral involuntary movements
.
Clinical manifestations: Ipsilateral oculomotor nerve palsy with mydriasis (interruption of oculomotor nerve root fibers in the midbrain), contralateral decreased sense of touch, vibration, position, and discrimination (medial lemniscus damage), hyperkinesia (tremor).
, chorea-like movements, athetosis, due to damage to the red nucleus), rigidity (damage to the substantia nigra)
.
Fig.
5 Benedit syndrome (PPT by Prof.
An Hongwei) 3.
Claude syndrome (crossed oculomotor and erythronucleus syndrome, inferior erythronucleus syndrome) lesion site: red nucleus of midbrain tegmental, oculomotor The nerves and cerebellum combine with the arm/superior cerebellar peduncle
.
Involved vessels: PCA deep perforators
.
The core feature is the oculomotor nerve + upper cerebellar peduncle (you can piggyback a little red nucleus)
.
The main clinical manifestation is ipsilateral oculomotor nerve palsy + contralateral ataxia
.
Some books also have a little tremor
.
The picture below shows the lesion pattern of Claude syndrome.
The lesion is mainly at the level below the red nucleus, involving the upper cerebellar peduncle, and the red nucleus is not the main affected object
.
Figure 6 Figure source ANDs (1 is the red nucleus, 2 is the upper cerebellar peduncle, the two are not at the same level, 2 is the main involved site, stained dark) Figure 7 Claude syndrome (Figure source ANDs) 4, Parinaud syndrome ( Tetrasoid syndrome, midbrain tectum syndrome) lesion location: the lesion is located in the midbrain tectum
.
Clinical manifestations: It is characterized by inability to move vertically in both eyes, dilated or unequal pupils on both sides, disappearance of light response, and presence of accommodation reflex
.
There are three cases of binocular vertical movement disorder: 1.
Paralysis of both eyes up and down; 2.
Paralysis of both eyes up and down; 3.
Paralysis of both eyes down
.
Common causes: intracranial tumors, such as pineal tumors, corpus callosum tumors, midbrain tumors, and vascular lesions caused by damage to the cortical tectal tract
.
Figure 8 Parinaud syndrome (Professor An Hongwei's PPT) (2) ponsFigure 9 Blood supply to the pons (Professor Cheng Xin's PPT) Figure 10 Common pontine syndromes (Professor Cheng Xin's PPT) 1.
Foville syndrome (Fauville syndrome, basal medial pontine syndrome, inferior pontine tegmental syndrome) Lesion site: medial basal pons (green part in Figure 10)
.
Involved vessel: parapontine median artery
.
Involvement: pyramidal tract, medial lemniscus, lateral optic center/medial longitudinal tract, abducens nerve, facial nerve
.
Clinical manifestations: contralateral central hemiplegia, contralateral hemiparesis, inability to abduct the eyeball (gazing paralysis to the side of the lesion, looking to the opposite side of the lesion), ipsilateral peripheral facial paralysis (lower motor neuron palsy)
.
Figure 11.
Transverse section of the pons - through the facial colliculus (inferior level) (Figure source Neurology Medical Network) 2.
Millard-Gubler syndrome (basolateral pontine syndrome) Lesion site: basolateral pons (yellow part of Figure 10)
.
Involved vessels: short circumflex branch of the basilar artery, which can also originate from AICA
.
Involvement: pyramidal tract, abducens nerve, facial nerve, medial lemniscus, spinothalamic tract
.
Clinical manifestations: contralateral central hemiplegia, inability to abduct the eyeball on the side of the lesion, ipsilateral peripheral facial paralysis (lower motor neuron palsy), and sensory disturbance on the contralateral side
.
Figure 12 Millard-Gubler syndrome (image source ANDs) 3, Raymond-Cestan syndrome (pontine tegmental syndrome) lesion site: the tegmental section of the upper trigeminal nerve section of the pons (blue part in Figure 10)
.
Involved vessels: The long circumflex branch of the basilar artery, also originating from the superior cerebellar artery
.
Involvement: vestibular nucleus, abducens nucleus + medial longitudinal tract, facial nerve nucleus, middle cerebellar peduncle, inferior cerebellar peduncle, spinal trigeminal nucleus + spinothalamic tract, medial lemniscus
.
Clinical manifestations: binocular gaze palsy (looking to the opposite side of the lesion), ipsilateral peripheral facial paralysis, ipsilateral cerebellar ataxia, crossed (pain and temperature) sensory disturbance, contralateral hemiparesis sensory disturbance
.
Figure 13 Transverse section of the pons (Source Neurology Medical Network) 4.
Tucked-in syndrome, also known as de-efferent state lesions: bilateral pontine base lesions
.
Involved vessels: mainly seen in bilateral occlusion of the basilar artery and pontine branches
.
Clinical manifestations: ① The reticular activation system of the cerebral hemisphere and the tegmental part of the brainstem is not damaged, so the patient is awake and has no obstacle in language comprehension; ② Because the functions of the oculomotor and trochlear nerves are preserved, he can use the up and down movements of the eyeballs to indicate; The bilateral corticospinal tracts and the cortical brainstem tracts that innervate the trigeminal nerve were damaged, and the patient presented with bilateral central paralysis, horizontal eye movement disturbance (VI), bilateral facial paralysis (VII), inability to speak, tongue, pharynx, and articulation and swallowing movement disorders (IX, X, XI), unable to turn the neck and shrug (XI); quadriplegia, with bilateral pathological reflexes, often mistaken for coma
.
A normal EEG or mild slow waves can help distinguish it from true disturbance of consciousness
.
(3) The upper layer of the medulla oblongata: the anteromedial side is the paramedian branch of the vertebral artery, and the dorsolateral side is the PICA (posterior inferior cerebellar artery)
.
Inferior level of the medulla: anteromedial is the anterior spinal artery, laterally is the vertebral artery, and dorsally is the posterior spinal artery
.
Figure 14 Figure 14 Figure 14 Figure 15 Figure 15 Figure 15 Figure 15 Figure 15 Figure 15: Neurology Medical Network Clinical manifestations: a.
Causes dizziness, vomiting, nystagmus (vestibular nucleus); b.
Ipsilateral cerebellar ataxia Disorders (cords or spinocerebellar tracts); c.
Crossed sensory disturbances (trigeminospinal and spinothalamic tracts); d.
Ipsilateral Horner's sign (reticular sympathetic descending fibers) - miosis, eye fission Small/ptosis, retraction of the eyeball, anhidrosis on the ipsilateral face; e.
choking on drinking water, dysphagia, and hoarseness (nucleus doubt)
.
Wallenberg (true bulbar palsy: damage to the nucleus doubtful) is divided into 3 types: pure medullary, medullary cerebellar, and pure cerebellar
.
In fact, only 10% are caused by PICA, 75% are caused by occlusion of one vertebral artery, and the rest are caused by occlusion of the basilar artery
.
2.
Medial medullary infarction (MMI, Dejerine) is divided into 4 types: a.
Classic triad: ipsilateral tongue muscle weakness, contralateral hemiparesis, contralateral hemiparesis deep sensory disturbance (medial lemniscus); b.
simple hemiparesis; c.
Sensorimotor stroke: no lingual paralysis, only diadic symptoms; d.
Bilateral medulla oblongata infarction (BMMI), heart-shaped infarction is seen on imaging, manifested as quadriplegia, bilateral deep sensory disturbance, dysphagia, and dysarthria
.
3.
Jackson syndrome (hypoglossal nerve cross palsy syndrome, anterior medullary syndrome or anterior olive syndrome) lesion site: the anterior and proximal suture of the medulla oblongata
.
Involved Vascular: Can be caused by occlusion of the anterior spinal artery
.
Involvement: Hypoglossal nerve, pyramidal tract
.
Clinical manifestations: ipsilateral peripheral hypoglossal nerve palsy; contralateral hemiplegia (pyramidal tract sign); cranial nerve palsies X and XI can also be seen, but there is no deep sensory disturbance caused by damage to the medial lemniscus
.
Figure 16 The upper part of the medulla oblongata (Figure source: Professor Wu Xiaoan's PPT) 2.
Blood supply to the cerebellum and clinical manifestations of infarction (1) Blood supply to the cerebellum Figure 17 Blood supply to the cerebellum (Figure source: Professor An Hongwei's PPT) a.
Superior cerebellar artery: medial branch: The upper part of the cerebellar vermis, the anterior medullary veil, etc.
; the lateral branch: the upper part of the cerebellar hemisphere; also supplies the upper part of the pontine tegmentum
.
b.
The medial and lateral branches of the anterior inferior cerebellar artery: supply the anterior lower part of the cerebellum and the pom-pom
.
In most cases, it also gives off the internal auditory artery, which supplies the inner ear (deafness and dizziness, labyrinthine stroke)
.
Also supplies the middle cerebellar peduncle/pontine arm and the lower half of the pons
.
c.
Medial and lateral branches of the posterior inferior cerebellar artery: inferior posterior part of the cerebellum (cerebellar vermis and inferior cerebellar hemisphere) and dorsolateral medulla oblongata
.
Figure 18 Figure 18 Figure 19: Blood supply to the cerebellum (Figure source: Professor An Hongwei's PPT) Note: blue PICA: posterior inferior cerebellar artery; purple AICA: anterior inferior cerebellar artery; grey SCA: superior cerebellar artery is small in the picture above The blood supply of part of the middle cerebellar peduncle is supplied by the anterior inferior cerebellar artery, and the rest is supplied by the posterior inferior cerebellar artery.
The anterior inferior cerebellar artery supplies blood, the cerebellar layer above the upper half of the pons is supplied by the superior cerebellar artery; the medulla oblongata is basically supplied by the posterior inferior cerebellar artery
.
(2) Imaging pictures of infarction Fig.
20 Fig.
20 Fig.
21 Prof.
Tang Wei's PPTFig.
22 Fig.
22 Prof.
Tang Wei's PPT Fig.
23 SCA blood supply area: cerebellar vermis and tegmental infarction of the upper half of the pons (Photo by Professor Tang Wei PPT) (3) Clinical manifestations of infarction 1.
Posterior inferior cerebellar artery (PICA) or vertebral artery occlusion syndrome: see Wallenberg syndrome 2.
Infarction in the blood supply area of the anterior inferior cerebellar artery (AICA) (1) AICA Supply blood to peripheral and central vestibular structures, including the inner ear, lateral pons, and middle cerebellar peduncle
.
Therefore, AICA infarction usually results in peripheral and central vestibular lesions
.
(2) Patients with infarction in the AICA blood supply area mainly presented with a combination of various symptoms of dizziness/vertigo, nystagmus, hearing loss, loss of limb and facial sensation, ataxia and dysmetria
.
Difficulty walking (cerebellar ataxia), dysarthria (stuttering), vertigo, and facial weakness are common clinical manifestations of anterior inferior cerebellar artery disease/pontine infarction
.
(3) Although AICA infarction is less common than PICA infarction, AICA infarction can lead to sudden vertigo and ipsilateral sensorineural hearing loss due to ischemia of the vestibulocochlear nerve and inner ear supplied by the labyrinthine artery
.
3.
Superior cerebellar artery (SCA) infarction in the blood supply area (1) The incidence of SCA infarction is higher than that of AICA infarction, about 70% of which are embolic (mostly cardiac origin, a few arterial origin, aorta, subclavian artery) and basilar artery atherosclerotic plaque shedding), 30% are caused by thrombosis
.
(2) The clinical manifestations of SCA occlusion can cause pontine tegmental syndrome, midbrain tegmental syndrome and cerebellar syndrome, but it is generally believed that cerebellar cortical infarction is more likely to occur during SCA occlusion, and brainstem involvement is less likely
.
(3) Nystagmus occurs when the medial longitudinal tract (originating from the vestibular nucleus, connecting the eyeballs on both sides, horizontal movement of the tube and nystagmus) is involved
.
(4) Midbrain tegmental syndrome: a.
Cerebellar ataxia, poor coordination and hypotonia of the ipsilateral limb; b.
Resting tremor and chorea-like movement (red nucleus) of the upper limb on the diseased side may occur; c.
Short The circumflex artery supplies blood to the cerebral peduncle, and there is abundant anastomosis with branches from the proximal posterior cerebral artery and the anterior choroidal artery supplying the cerebral peduncle, usually without infarction
.
(5) Cerebellar syndrome: a.
Ipsilateral cerebellar ataxia, cerebellar language; b.
A small number of patients may have nystagmus, vertigo,
etc.
So far, the first two parts of the basics of craniocerebral anatomy have been introduced.
I believe that everyone has a deeper understanding of this, but if you really want to integrate it into the clinical practice, you must learn and apply it
.
In the next issue, we will introduce the content of the last part, which is also the most interesting one - small blood vessels, big problems, important perforating arteries, see you there! Special statement: In order to facilitate everyone's understanding and memory, the author uses the materials of experts and teachers collected in previous readings as materials, and there is no plagiarism and other behaviors
.
First release of the text: Neurology Channel of the Medical Community Author of this article: Guo Yanjiao 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 inaccuracies or incompleteness of the cited materials
.
Relevant parties are requested to check separately when adopting or using it as a basis for decision-making
.
Contribution/reprint/business cooperation: yxjsjbx@yxj.
org.
cn
The author has also taken a lot of detours in this regard.
After continuous study, the author summarizes the basic knowledge of cranial anatomy as follows.
It's easy to understand (the course of the neurotic masters is inevitably a little confusing to the clinical novice), I hope it will be helpful to my colleagues
.
Due to the large amount of content and the large amount of information, the author divides all the content into 3 phases to explain
.
In the last issue, we introduced the structure, function and clinical manifestations of brain parenchyma and cerebral blood vessels after damage.
In this issue, we continue to introduce the second part: brainstem, cerebellar blood supply and clinical manifestations of infarction
.
1.
Brainstem blood supply and its common syndromesFigure 1 Surface view (ventral) of the brainstem blood supply area (Figure source, Professor Cheng Xin's PPT) Yellow PCA supplies the base of the temporal lobe, occipital lobe and most of the midbrain and thalamus; dark purple The paracentral branch of the basilar artery supplies the middle pons; the light purple peripheral branches of the basilar artery supply both sides of the pons; the green SCA supplies the upper half of the cerebellum and the upper part of the pontine tegment; the blue AICA supplies the lower anterior part of the cerebellum, pompoms, pons, and pontine tegment Lower part; cyan PICA supplies the inferior posterior part of the cerebellum and the dorsolateral medulla oblongata; red paravertebral artery branches and anterior spinal arteries supply the middle medulla oblongata; pale red vertebral artery collaterals supply both sides of the medulla oblongata
.
(1) Midbrain Figure 2 Midbrain blood supply (Figure Yuan, Professor Cheng Xin's PPT) Figure 3 Midbrain - Nuclei (purple) and conduction tracts (pink) at the plane of the superior colliculus (Figure Yuan, Professor An Hongwei's PPT) 1 , Weber syndrome (oculomotor cross palsy syndrome/cerebral peduncle syndrome) damage site: the ventral cerebral peduncle (oculomotor nerve and pyramidal tract)
.
Damaged blood vessels: PCA interpeduncular branch or PchA
.
Clinical manifestations: oculomotor nerve cross palsy, i.
e.
a.
Ipsilateral oculomotor nerve palsy: ptosis, eyeball oblique outward and downward (superior oblique muscle innervated by the trochlear nerve moves the eyeball outward and downward), eyeball up, down, Adduction disorder, mydriasis, disappearance of light reflex, diplopia; b.
Contralateral central facial and tongue paralysis, limb paralysis
.
If bilateral cerebral peduncles are infarcted, the "Mickey Mouse ear sign" can be seen on MRI, which means bilateral cortical brainstem/cortical nucleus tract damage: bilateral paralysis, tongue, pharynx, articulation, and swallowing movement disorders, unable to speak ( Complete pseudobulbar palsy) and bilateral corticospinal tract damage: quadriplegia, bilateral pathological signs
.
Figure 4 Cerebral peduncle syndrome (Weber) (Figure Yuan, Professor An Hongwei's PPT) 2.
Benedit syndrome (oculomotor and extrapyramidal cross syndrome, erythronucleus syndrome) damage blood vessels: basilar artery interpeduncular branch or brain Posterior arterial blockage or blockage of both
.
Core features: ipsilateral oculomotor nerve palsy + contralateral involuntary movements
.
Clinical manifestations: Ipsilateral oculomotor nerve palsy with mydriasis (interruption of oculomotor nerve root fibers in the midbrain), contralateral decreased sense of touch, vibration, position, and discrimination (medial lemniscus damage), hyperkinesia (tremor).
, chorea-like movements, athetosis, due to damage to the red nucleus), rigidity (damage to the substantia nigra)
.
Fig.
5 Benedit syndrome (PPT by Prof.
An Hongwei) 3.
Claude syndrome (crossed oculomotor and erythronucleus syndrome, inferior erythronucleus syndrome) lesion site: red nucleus of midbrain tegmental, oculomotor The nerves and cerebellum combine with the arm/superior cerebellar peduncle
.
Involved vessels: PCA deep perforators
.
The core feature is the oculomotor nerve + upper cerebellar peduncle (you can piggyback a little red nucleus)
.
The main clinical manifestation is ipsilateral oculomotor nerve palsy + contralateral ataxia
.
Some books also have a little tremor
.
The picture below shows the lesion pattern of Claude syndrome.
The lesion is mainly at the level below the red nucleus, involving the upper cerebellar peduncle, and the red nucleus is not the main affected object
.
Figure 6 Figure source ANDs (1 is the red nucleus, 2 is the upper cerebellar peduncle, the two are not at the same level, 2 is the main involved site, stained dark) Figure 7 Claude syndrome (Figure source ANDs) 4, Parinaud syndrome ( Tetrasoid syndrome, midbrain tectum syndrome) lesion location: the lesion is located in the midbrain tectum
.
Clinical manifestations: It is characterized by inability to move vertically in both eyes, dilated or unequal pupils on both sides, disappearance of light response, and presence of accommodation reflex
.
There are three cases of binocular vertical movement disorder: 1.
Paralysis of both eyes up and down; 2.
Paralysis of both eyes up and down; 3.
Paralysis of both eyes down
.
Common causes: intracranial tumors, such as pineal tumors, corpus callosum tumors, midbrain tumors, and vascular lesions caused by damage to the cortical tectal tract
.
Figure 8 Parinaud syndrome (Professor An Hongwei's PPT) (2) ponsFigure 9 Blood supply to the pons (Professor Cheng Xin's PPT) Figure 10 Common pontine syndromes (Professor Cheng Xin's PPT) 1.
Foville syndrome (Fauville syndrome, basal medial pontine syndrome, inferior pontine tegmental syndrome) Lesion site: medial basal pons (green part in Figure 10)
.
Involved vessel: parapontine median artery
.
Involvement: pyramidal tract, medial lemniscus, lateral optic center/medial longitudinal tract, abducens nerve, facial nerve
.
Clinical manifestations: contralateral central hemiplegia, contralateral hemiparesis, inability to abduct the eyeball (gazing paralysis to the side of the lesion, looking to the opposite side of the lesion), ipsilateral peripheral facial paralysis (lower motor neuron palsy)
.
Figure 11.
Transverse section of the pons - through the facial colliculus (inferior level) (Figure source Neurology Medical Network) 2.
Millard-Gubler syndrome (basolateral pontine syndrome) Lesion site: basolateral pons (yellow part of Figure 10)
.
Involved vessels: short circumflex branch of the basilar artery, which can also originate from AICA
.
Involvement: pyramidal tract, abducens nerve, facial nerve, medial lemniscus, spinothalamic tract
.
Clinical manifestations: contralateral central hemiplegia, inability to abduct the eyeball on the side of the lesion, ipsilateral peripheral facial paralysis (lower motor neuron palsy), and sensory disturbance on the contralateral side
.
Figure 12 Millard-Gubler syndrome (image source ANDs) 3, Raymond-Cestan syndrome (pontine tegmental syndrome) lesion site: the tegmental section of the upper trigeminal nerve section of the pons (blue part in Figure 10)
.
Involved vessels: The long circumflex branch of the basilar artery, also originating from the superior cerebellar artery
.
Involvement: vestibular nucleus, abducens nucleus + medial longitudinal tract, facial nerve nucleus, middle cerebellar peduncle, inferior cerebellar peduncle, spinal trigeminal nucleus + spinothalamic tract, medial lemniscus
.
Clinical manifestations: binocular gaze palsy (looking to the opposite side of the lesion), ipsilateral peripheral facial paralysis, ipsilateral cerebellar ataxia, crossed (pain and temperature) sensory disturbance, contralateral hemiparesis sensory disturbance
.
Figure 13 Transverse section of the pons (Source Neurology Medical Network) 4.
Tucked-in syndrome, also known as de-efferent state lesions: bilateral pontine base lesions
.
Involved vessels: mainly seen in bilateral occlusion of the basilar artery and pontine branches
.
Clinical manifestations: ① The reticular activation system of the cerebral hemisphere and the tegmental part of the brainstem is not damaged, so the patient is awake and has no obstacle in language comprehension; ② Because the functions of the oculomotor and trochlear nerves are preserved, he can use the up and down movements of the eyeballs to indicate; The bilateral corticospinal tracts and the cortical brainstem tracts that innervate the trigeminal nerve were damaged, and the patient presented with bilateral central paralysis, horizontal eye movement disturbance (VI), bilateral facial paralysis (VII), inability to speak, tongue, pharynx, and articulation and swallowing movement disorders (IX, X, XI), unable to turn the neck and shrug (XI); quadriplegia, with bilateral pathological reflexes, often mistaken for coma
.
A normal EEG or mild slow waves can help distinguish it from true disturbance of consciousness
.
(3) The upper layer of the medulla oblongata: the anteromedial side is the paramedian branch of the vertebral artery, and the dorsolateral side is the PICA (posterior inferior cerebellar artery)
.
Inferior level of the medulla: anteromedial is the anterior spinal artery, laterally is the vertebral artery, and dorsally is the posterior spinal artery
.
Figure 14 Figure 14 Figure 14 Figure 15 Figure 15 Figure 15 Figure 15 Figure 15 Figure 15: Neurology Medical Network Clinical manifestations: a.
Causes dizziness, vomiting, nystagmus (vestibular nucleus); b.
Ipsilateral cerebellar ataxia Disorders (cords or spinocerebellar tracts); c.
Crossed sensory disturbances (trigeminospinal and spinothalamic tracts); d.
Ipsilateral Horner's sign (reticular sympathetic descending fibers) - miosis, eye fission Small/ptosis, retraction of the eyeball, anhidrosis on the ipsilateral face; e.
choking on drinking water, dysphagia, and hoarseness (nucleus doubt)
.
Wallenberg (true bulbar palsy: damage to the nucleus doubtful) is divided into 3 types: pure medullary, medullary cerebellar, and pure cerebellar
.
In fact, only 10% are caused by PICA, 75% are caused by occlusion of one vertebral artery, and the rest are caused by occlusion of the basilar artery
.
2.
Medial medullary infarction (MMI, Dejerine) is divided into 4 types: a.
Classic triad: ipsilateral tongue muscle weakness, contralateral hemiparesis, contralateral hemiparesis deep sensory disturbance (medial lemniscus); b.
simple hemiparesis; c.
Sensorimotor stroke: no lingual paralysis, only diadic symptoms; d.
Bilateral medulla oblongata infarction (BMMI), heart-shaped infarction is seen on imaging, manifested as quadriplegia, bilateral deep sensory disturbance, dysphagia, and dysarthria
.
3.
Jackson syndrome (hypoglossal nerve cross palsy syndrome, anterior medullary syndrome or anterior olive syndrome) lesion site: the anterior and proximal suture of the medulla oblongata
.
Involved Vascular: Can be caused by occlusion of the anterior spinal artery
.
Involvement: Hypoglossal nerve, pyramidal tract
.
Clinical manifestations: ipsilateral peripheral hypoglossal nerve palsy; contralateral hemiplegia (pyramidal tract sign); cranial nerve palsies X and XI can also be seen, but there is no deep sensory disturbance caused by damage to the medial lemniscus
.
Figure 16 The upper part of the medulla oblongata (Figure source: Professor Wu Xiaoan's PPT) 2.
Blood supply to the cerebellum and clinical manifestations of infarction (1) Blood supply to the cerebellum Figure 17 Blood supply to the cerebellum (Figure source: Professor An Hongwei's PPT) a.
Superior cerebellar artery: medial branch: The upper part of the cerebellar vermis, the anterior medullary veil, etc.
; the lateral branch: the upper part of the cerebellar hemisphere; also supplies the upper part of the pontine tegmentum
.
b.
The medial and lateral branches of the anterior inferior cerebellar artery: supply the anterior lower part of the cerebellum and the pom-pom
.
In most cases, it also gives off the internal auditory artery, which supplies the inner ear (deafness and dizziness, labyrinthine stroke)
.
Also supplies the middle cerebellar peduncle/pontine arm and the lower half of the pons
.
c.
Medial and lateral branches of the posterior inferior cerebellar artery: inferior posterior part of the cerebellum (cerebellar vermis and inferior cerebellar hemisphere) and dorsolateral medulla oblongata
.
Figure 18 Figure 18 Figure 19: Blood supply to the cerebellum (Figure source: Professor An Hongwei's PPT) Note: blue PICA: posterior inferior cerebellar artery; purple AICA: anterior inferior cerebellar artery; grey SCA: superior cerebellar artery is small in the picture above The blood supply of part of the middle cerebellar peduncle is supplied by the anterior inferior cerebellar artery, and the rest is supplied by the posterior inferior cerebellar artery.
The anterior inferior cerebellar artery supplies blood, the cerebellar layer above the upper half of the pons is supplied by the superior cerebellar artery; the medulla oblongata is basically supplied by the posterior inferior cerebellar artery
.
(2) Imaging pictures of infarction Fig.
20 Fig.
20 Fig.
21 Prof.
Tang Wei's PPTFig.
22 Fig.
22 Prof.
Tang Wei's PPT Fig.
23 SCA blood supply area: cerebellar vermis and tegmental infarction of the upper half of the pons (Photo by Professor Tang Wei PPT) (3) Clinical manifestations of infarction 1.
Posterior inferior cerebellar artery (PICA) or vertebral artery occlusion syndrome: see Wallenberg syndrome 2.
Infarction in the blood supply area of the anterior inferior cerebellar artery (AICA) (1) AICA Supply blood to peripheral and central vestibular structures, including the inner ear, lateral pons, and middle cerebellar peduncle
.
Therefore, AICA infarction usually results in peripheral and central vestibular lesions
.
(2) Patients with infarction in the AICA blood supply area mainly presented with a combination of various symptoms of dizziness/vertigo, nystagmus, hearing loss, loss of limb and facial sensation, ataxia and dysmetria
.
Difficulty walking (cerebellar ataxia), dysarthria (stuttering), vertigo, and facial weakness are common clinical manifestations of anterior inferior cerebellar artery disease/pontine infarction
.
(3) Although AICA infarction is less common than PICA infarction, AICA infarction can lead to sudden vertigo and ipsilateral sensorineural hearing loss due to ischemia of the vestibulocochlear nerve and inner ear supplied by the labyrinthine artery
.
3.
Superior cerebellar artery (SCA) infarction in the blood supply area (1) The incidence of SCA infarction is higher than that of AICA infarction, about 70% of which are embolic (mostly cardiac origin, a few arterial origin, aorta, subclavian artery) and basilar artery atherosclerotic plaque shedding), 30% are caused by thrombosis
.
(2) The clinical manifestations of SCA occlusion can cause pontine tegmental syndrome, midbrain tegmental syndrome and cerebellar syndrome, but it is generally believed that cerebellar cortical infarction is more likely to occur during SCA occlusion, and brainstem involvement is less likely
.
(3) Nystagmus occurs when the medial longitudinal tract (originating from the vestibular nucleus, connecting the eyeballs on both sides, horizontal movement of the tube and nystagmus) is involved
.
(4) Midbrain tegmental syndrome: a.
Cerebellar ataxia, poor coordination and hypotonia of the ipsilateral limb; b.
Resting tremor and chorea-like movement (red nucleus) of the upper limb on the diseased side may occur; c.
Short The circumflex artery supplies blood to the cerebral peduncle, and there is abundant anastomosis with branches from the proximal posterior cerebral artery and the anterior choroidal artery supplying the cerebral peduncle, usually without infarction
.
(5) Cerebellar syndrome: a.
Ipsilateral cerebellar ataxia, cerebellar language; b.
A small number of patients may have nystagmus, vertigo,
etc.
So far, the first two parts of the basics of craniocerebral anatomy have been introduced.
I believe that everyone has a deeper understanding of this, but if you really want to integrate it into the clinical practice, you must learn and apply it
.
In the next issue, we will introduce the content of the last part, which is also the most interesting one - small blood vessels, big problems, important perforating arteries, see you there! Special statement: In order to facilitate everyone's understanding and memory, the author uses the materials of experts and teachers collected in previous readings as materials, and there is no plagiarism and other behaviors
.
First release of the text: Neurology Channel of the Medical Community Author of this article: Guo Yanjiao 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 inaccuracies or incompleteness of the cited materials
.
Relevant parties are requested to check separately when adopting or using it as a basis for decision-making
.
Contribution/reprint/business cooperation: yxjsjbx@yxj.
org.
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