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*Only for medical professionals to read for reference ipsilateral oculomotor nerve palsy + contralateral cerebellar ataxia=? This article will take you through a case to give you a comprehensive understanding of the middle cerebral infarction syndrome, which will be of great help to your clinic.
Case introduction: A 68-year-old male patient had diplopia and instability when walking 10 days ago.
He was walking tilted to the right, and his right limbs were awkwardly moving and gradually worsened, accompanied by a drooping left eyelid.
Ignoring the rotation of the object, no crooked mouth, no drinking water, choking, difficulty swallowing, no numbness or weakness of the limbs.
Past history: 3 years of previous diabetes history, oral medication (the specific medication is unknown), and no blood glucose monitoring.
Nervous system examination: Consciousness, fluent speech, and normal cognition.
The left eyelid is drooping, the left pupil is 4mm in diameter, and the reflection of light is slow.
The right pupil has a diameter of 3mm and is sensitive to light reflection.
The left eye is laterally oblique, and adduction, upper vision, and lower vision are restricted.
The right eye moved fully in all directions without nystagmus.
Physical examination of the remaining cranial nerves was negative.
The depth and sensation of the bilateral limbs are symmetrical, the muscle strength of the limbs is grade 5, the right finger nose test, rotation test, heel-knee tibial test (+), physiological reflexes exist, and pathological reflexes are not elicited.
Soft neck.
Core symptoms: right cerebellar ataxia + left oculomotor nerve palsy.
▎Locating the cerebellar ataxia transmission pathway The efferent fibers from the cerebellum pass through the upper foot of the cerebellum, cross at the Wernekink commissure, and project to the thalamus after the contralateral red nucleus (dentate nucleus-red nucleus-thalamic tract ).
It is transmitted from the thalamus to the motor and premotor areas of the cerebral cortex (thalamic cortical tract).
The impulse sent from the cerebral cortex passes through the pontine nucleus to the cerebellar cortex (cortex-pontine-cerebellar tract), thus forming a loop.
Cerebellar ataxia can be divided into the following three situations: ▎ Right cerebellar ataxia and left oculomotor nerve palsy occur in patients with oculomotor nerve palsy, which are cross (consider ipsilateral oculomotor nerve palsy + symmetrical cerebellum Sexual ataxia), the above analysis can be located at the midbrain level.
▎ Qualitative diagnosis: The patient is elderly male with acute onset, sudden symptoms, and signs of focal neurological deficits.
There are risk factors for diabetes in the past.
There were no high-density signs on the admission cranial CT, and the possibility of ischemic stroke-midbrain infarction was considered.
For this reason, perfect cranial MRI was confirmed as acute midbrain infarction.
Final diagnosis: midbrain infarction (Claude syndrome).
Cranial MRI showed: DWI and T2WI high signal Claude syndrome in the paramedian area of the midbrain.
French psychiatrist and neurologist Claude first described ipsilateral oculomotor nerve palsy and contralateral inability to coordinate movements in 1912.
The syndrome he named-Claude syndrome.
Damage to the midbrain structure includes the ipsilateral oculomotor nerve bundle, red nucleus and upper foot of the cerebellum.
The midbrain-superthalamic level ▎The midbrain-superthalamic level maps the image to the anatomical atlas: the involved structures include the left red nucleus, the oculomotor nerve, the oculomotor nerve subnucleus and part of the reticular structure.
A question is raised: the red nucleus is located at the level of the midbrain quadriga, and the upper foot of the cerebellum is located on the upper dorsal side of the pons, and the red nucleus tract of the cerebellum moves from the back to the front to the top (see the figure below).
The presence of contralateral cerebellar ataxia can be explained by red nucleus involvement (crossover has occurred).
The fibers that pass through the dentate nucleus to the upper foot of the cerebellum have not yet crossed, and the upper foot of the cerebellum is affected by ipsilateral cerebellar ataxia.
With regard to Claude syndrome, the main involvement should be the red nucleus, or the cerebellar red nucleus bundle that has crossed to the opposite side through the upper foot of the cerebellum, rather than the upper foot of the cerebellum.
Other types of middle cerebral infarction syndrome▎Weber syndrome (cerebral foot syndrome) ① Ocular nerve root fiber: ipsilateral oculomotor nerve palsy, pupil dilation; ②Cortical bridge: contralateral ataxia; ③Cortical nuclear tract: Contralateral supranuclear facial and tongue paralysis; corticospinal tract: contralateral spastic hemiplegia; substantia nigra: dyskinesia (Parkinson's syndrome).
▎Benedikt syndrome (red nucleus syndrome) oculomotor nerve root fibers: ipsilateral oculomotor nerve palsy, pupil dilation; medial colliculus: ipsilateral touch, position, vibration, and discrimination; red nucleus: contralateral limb Dance, dexterity and ataxia; substantia nigra: contralateral rigidity, tremor.
▎Parinaud syndrome (midbrain dorsal syndrome) vertical gaze paralysis, light reflection-near reflex separation, convergent nystagmus when looking upward, eyelid retraction, reverse deflection.
The lesions involved the midbrain reticular structure, including the oral medial longitudinal fascicular mesenchymal nucleus (RIMLF) and the interstitial nucleus of Cajal (INC) and Darkschewitsch nucleus (ND) connected to it, as well as the posterior connection and (PC) (see figure below) .
▎Wernekink's commissure syndrome bilateral cerebellar ataxia, with or without extraocular muscle palsy, palatine myoclonus, and lethargy.
The lesion was located in the midbrain area in front of the midbrain aqueduct.
The involved structures are mainly Wernekink's commissure, medial longitudinal fasciculus, and reticular structure.
Midbrain hypothalamic level (lower midbrain) 1.
Corticospinal tract 2.
Medial thalamus 3.
Medial longitudinal fascia 4.
Reticulum structure 20.
Wernekink commissure 21.
Substantia nigra 22.
Inferior colliculus 23.
Trochlear nucleus 27.
Nipple body 28.
Optic beam 45.
Cerebellum mountain top 47.
Central lobule If you think this article is helpful to you, please forward it to more people in need. References: 1.
Duus neurological disease location diagnosis 2.
Rabadi MH.
Unilateral midbrain infarct presenting as dorsal midbrain syndrome.
J.
Neurol.
Neurosurg.
Psychiatry 2013 Sep;84(9).
3.
Swinkin E, Bui E.
Teaching NeuroImages: Acute Parinaud syndrome.
Neurology 2017 04 18;88(16).
4.
Witsch J, Narula R, Amin H, Schindler JL.
Mystery Case: Bilateral Claude syndrome.
Neurology 2019 09 24;93(13).
5.
Shields M, Sinkar S, Chan W, Crompton J.
Parinaud syndrome: a 25-year (1991–2016) review of 40 consecutive adult cases.
Acta Ophthalmol 2017 Dec;95(8).
Source of this article: Medical Neurology Channel Author of this article Responsible editor: Mr.
Lu Li, copyright statement.
The original text is welcome to forward to the circle of friends-End-Call for papers, welcome to submit papers to the editor’s mailbox: yxjsjbx@yxj.
org.
cn Please specify: [Submission] Hospital + Department + Name The manuscript is written in word Document format, author's remuneration favorably edit WeChat: chenaff0911
Case introduction: A 68-year-old male patient had diplopia and instability when walking 10 days ago.
He was walking tilted to the right, and his right limbs were awkwardly moving and gradually worsened, accompanied by a drooping left eyelid.
Ignoring the rotation of the object, no crooked mouth, no drinking water, choking, difficulty swallowing, no numbness or weakness of the limbs.
Past history: 3 years of previous diabetes history, oral medication (the specific medication is unknown), and no blood glucose monitoring.
Nervous system examination: Consciousness, fluent speech, and normal cognition.
The left eyelid is drooping, the left pupil is 4mm in diameter, and the reflection of light is slow.
The right pupil has a diameter of 3mm and is sensitive to light reflection.
The left eye is laterally oblique, and adduction, upper vision, and lower vision are restricted.
The right eye moved fully in all directions without nystagmus.
Physical examination of the remaining cranial nerves was negative.
The depth and sensation of the bilateral limbs are symmetrical, the muscle strength of the limbs is grade 5, the right finger nose test, rotation test, heel-knee tibial test (+), physiological reflexes exist, and pathological reflexes are not elicited.
Soft neck.
Core symptoms: right cerebellar ataxia + left oculomotor nerve palsy.
▎Locating the cerebellar ataxia transmission pathway The efferent fibers from the cerebellum pass through the upper foot of the cerebellum, cross at the Wernekink commissure, and project to the thalamus after the contralateral red nucleus (dentate nucleus-red nucleus-thalamic tract ).
It is transmitted from the thalamus to the motor and premotor areas of the cerebral cortex (thalamic cortical tract).
The impulse sent from the cerebral cortex passes through the pontine nucleus to the cerebellar cortex (cortex-pontine-cerebellar tract), thus forming a loop.
Cerebellar ataxia can be divided into the following three situations: ▎ Right cerebellar ataxia and left oculomotor nerve palsy occur in patients with oculomotor nerve palsy, which are cross (consider ipsilateral oculomotor nerve palsy + symmetrical cerebellum Sexual ataxia), the above analysis can be located at the midbrain level.
▎ Qualitative diagnosis: The patient is elderly male with acute onset, sudden symptoms, and signs of focal neurological deficits.
There are risk factors for diabetes in the past.
There were no high-density signs on the admission cranial CT, and the possibility of ischemic stroke-midbrain infarction was considered.
For this reason, perfect cranial MRI was confirmed as acute midbrain infarction.
Final diagnosis: midbrain infarction (Claude syndrome).
Cranial MRI showed: DWI and T2WI high signal Claude syndrome in the paramedian area of the midbrain.
French psychiatrist and neurologist Claude first described ipsilateral oculomotor nerve palsy and contralateral inability to coordinate movements in 1912.
The syndrome he named-Claude syndrome.
Damage to the midbrain structure includes the ipsilateral oculomotor nerve bundle, red nucleus and upper foot of the cerebellum.
The midbrain-superthalamic level ▎The midbrain-superthalamic level maps the image to the anatomical atlas: the involved structures include the left red nucleus, the oculomotor nerve, the oculomotor nerve subnucleus and part of the reticular structure.
A question is raised: the red nucleus is located at the level of the midbrain quadriga, and the upper foot of the cerebellum is located on the upper dorsal side of the pons, and the red nucleus tract of the cerebellum moves from the back to the front to the top (see the figure below).
The presence of contralateral cerebellar ataxia can be explained by red nucleus involvement (crossover has occurred).
The fibers that pass through the dentate nucleus to the upper foot of the cerebellum have not yet crossed, and the upper foot of the cerebellum is affected by ipsilateral cerebellar ataxia.
With regard to Claude syndrome, the main involvement should be the red nucleus, or the cerebellar red nucleus bundle that has crossed to the opposite side through the upper foot of the cerebellum, rather than the upper foot of the cerebellum.
Other types of middle cerebral infarction syndrome▎Weber syndrome (cerebral foot syndrome) ① Ocular nerve root fiber: ipsilateral oculomotor nerve palsy, pupil dilation; ②Cortical bridge: contralateral ataxia; ③Cortical nuclear tract: Contralateral supranuclear facial and tongue paralysis; corticospinal tract: contralateral spastic hemiplegia; substantia nigra: dyskinesia (Parkinson's syndrome).
▎Benedikt syndrome (red nucleus syndrome) oculomotor nerve root fibers: ipsilateral oculomotor nerve palsy, pupil dilation; medial colliculus: ipsilateral touch, position, vibration, and discrimination; red nucleus: contralateral limb Dance, dexterity and ataxia; substantia nigra: contralateral rigidity, tremor.
▎Parinaud syndrome (midbrain dorsal syndrome) vertical gaze paralysis, light reflection-near reflex separation, convergent nystagmus when looking upward, eyelid retraction, reverse deflection.
The lesions involved the midbrain reticular structure, including the oral medial longitudinal fascicular mesenchymal nucleus (RIMLF) and the interstitial nucleus of Cajal (INC) and Darkschewitsch nucleus (ND) connected to it, as well as the posterior connection and (PC) (see figure below) .
▎Wernekink's commissure syndrome bilateral cerebellar ataxia, with or without extraocular muscle palsy, palatine myoclonus, and lethargy.
The lesion was located in the midbrain area in front of the midbrain aqueduct.
The involved structures are mainly Wernekink's commissure, medial longitudinal fasciculus, and reticular structure.
Midbrain hypothalamic level (lower midbrain) 1.
Corticospinal tract 2.
Medial thalamus 3.
Medial longitudinal fascia 4.
Reticulum structure 20.
Wernekink commissure 21.
Substantia nigra 22.
Inferior colliculus 23.
Trochlear nucleus 27.
Nipple body 28.
Optic beam 45.
Cerebellum mountain top 47.
Central lobule If you think this article is helpful to you, please forward it to more people in need. References: 1.
Duus neurological disease location diagnosis 2.
Rabadi MH.
Unilateral midbrain infarct presenting as dorsal midbrain syndrome.
J.
Neurol.
Neurosurg.
Psychiatry 2013 Sep;84(9).
3.
Swinkin E, Bui E.
Teaching NeuroImages: Acute Parinaud syndrome.
Neurology 2017 04 18;88(16).
4.
Witsch J, Narula R, Amin H, Schindler JL.
Mystery Case: Bilateral Claude syndrome.
Neurology 2019 09 24;93(13).
5.
Shields M, Sinkar S, Chan W, Crompton J.
Parinaud syndrome: a 25-year (1991–2016) review of 40 consecutive adult cases.
Acta Ophthalmol 2017 Dec;95(8).
Source of this article: Medical Neurology Channel Author of this article Responsible editor: Mr.
Lu Li, copyright statement.
The original text is welcome to forward to the circle of friends-End-Call for papers, welcome to submit papers to the editor’s mailbox: yxjsjbx@yxj.
org.
cn Please specify: [Submission] Hospital + Department + Name The manuscript is written in word Document format, author's remuneration favorably edit WeChat: chenaff0911
