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*Only for medical professionals' reference to read the cause is unexpected! At the 14th Annual Meeting of Neurologists of the Chinese Medical Doctor Association (CNA 2021), Professor Qian Shuxia from the Department of Neurology, Jiaxing Second Hospital, Zhejiang Province, brought us the title "From a case of central vertigo to see mutual aid The wonderful lecture on "The Diagnosis and Treatment Ideas for Disorders", there are not many people who are ruthless, and go straight to the case
.
Case review Patient Liu, female, 65 years old
.
Main complaint: Unsteady walking for 6 years
.
History of present illness: The patient gradually developed unsteady walking 6 years ago, persisted and gradually worsened, accompanied by a little dizziness, which has nothing to do with postural changes, ignorance of rotation, nausea, vomiting, numbness of the limbs, hallucinations, delusions or unresponsiveness, no difference in urination
.
Past history: He has a history of "epilepsy" and has been taking a very small dose of phenytoin 0.
1g bid* for more than 50 years since childhood
.
Physical examination: Consciousness, normal orientation, memory, calculation ability, symmetrical forehead lines, nasolabial folds, middle tongue extension, free eye movement, spontaneous nystagmus (-), negative head shaking test, limb muscle strength level 5 , Normal muscle tone, bilateral Pap's sign (+), sit-up test (+), bilateral finger-nose, rotation, heel-knee-tibial test (+), standing blood pressure (-), cardiopulmonary abdominal examination ( -)
.
Auxiliary examination: cranial MRI: cerebellum atrophy, no brain stem atrophy
.
Figure 1: The patient’s brain MRI nystagmus: gaze-induced nystagmus (+), with gross nystagmus seen in the horizontal direction
.
Figure 2: Patient Nystagmus Checklist (MMSE): 29/30 points.
How to locate and qualitatively diagnose localized diagnosis: middle-aged and elderly women with chronic onset, progressive progression, unstable walking, denial of family genetic history Physical examination: difficulty in sitting up, gaze-induced nystagmus (+), bilateral Pap's sign (+), bilateral finger-nose and heel-knee tibial tests (+), combined with imaging findings for structural atrophy of the cerebellum, consider positioning In the cerebellum and bilateral pyramidal tract damage
.
Qualitative diagnosis: combined with localized diagnosis, the initial diagnosis of the patient is considered as chronic vestibular syndrome (CVS)
.
Chronic Vestibular Syndrome (CVS): is a group of symptoms with chronic dizziness/vertigo/walking instability as the main symptoms, usually with persistent vestibular system dysfunction (visual concussion, nystagmus, gait instability), lasting several months to several months Years of clinical syndrome, CVS clinical includes: 1.
Uncompensable unilateral vestibular disease; 2.
Chronic bilateral vestibular disease; 3.
Cerebellar degenerative disease; 4.
Posterior fossa tumor; 5.
Persistent postural perception Dizziness (PPPD)
.
Vestibular disease includes primary vestibular disease and secondary vestibular disease, combined with the patient's physical examination and auxiliary examinations are temporarily not considered
.
No tumor was found in the cranial fossa after imaging, so the posterior fossa tumor was not considered
.
The patient's dizziness and walking instability have nothing to do with posture, so PPPD is not considered temporarily .
A middle-aged and elderly woman in the patient has imaging evidence of cerebellar atrophy, and physical examination also confirmed cerebellar damage.
Therefore, cerebellar degenerative disease cannot be ruled out
.
What is the next consideration for cerebellar degenerative diseases? Cerebellar degenerative diseases include: congenital hereditary ataxia, degenerative ataxia, and acquired ataxia
.
1 Congenital hereditary ataxia AD inheritance: such as SCA, paroxysmal ataxia (EA), etc.
; AR inheritance: Friedreich ataxia, ataxia-telangiectasia, etc.
; X-linked cerebellar ataxia: including Adrenal leukodystrophy (ALD), fragile X-related tremor/ataxia syndrome (FXTAS), etc.
; mitochondrial cerebellar ataxia: including myoclonic epilepsy with broken red-edge fiber (MERRF) syndrome, mitochondrial encephalomyopathy lactic acidosis and stroke-like episodes (MELAS) and so on
.
2 Degenerative ataxia Multiple system atrophy (MSA); primary late-onset cerebellar ataxia
.
3 Acquired ataxia: cerebrovascular disease; poisoning: alcohol, drugs (antiepileptic drugs, lithium salts, antitumor drugs, cyclosporine, metronidazole), heavy metals, organic solvents: immune-mediated: multiple Sexual sclerosis, cerebellar ataxia with anti-glutamate decarboxylase antibody, gluten ataxia, Miller-Fisher syndrome, systemic lupus erythematosus, Sjogren syndrome, Cogan syndrome, thyroiditis, paraneoplastic syndrome; infections : Abscess, cerebellitis; trauma; tumor; endocrine: hypothyroidism; structural disease: Chiari malformation, dysplasia
.
The patient has no genetic family history, and congenital hereditary ataxia can be ruled out
.
Although the patient is a middle-aged and elderly woman, the patient has never had symptoms of the autonomic nervous system for 6 years, so multiple system atrophy is not considered
.
Whether it is acquired ataxia is identified and ruled out one by one according to the midnights principle.
The patient has a history of taking phenytoin for 50 years.
Finally, it is considered that the patient is chronically poisoned by low-dose phenytoin and cerebellar ataxia
.
Diagnosis: low-dose phenytoin sodium chronic poisoning caused cerebellar ataxia Treatment: stop phenytoin sodium, change levetiracetam 0.
5g bid + ganglioside 120mg qd*7 days, the patient returned after 2 weeks, dizziness improved, finger nose In the test (-) and Pap's sign (-), the patient's dizziness and walking instability symptoms improved significantly during the half-year follow-up visit
.
Discussion: Phenytoin sodium treats epilepsy by stabilizing the function of brain cell membranes and increasing the inhibitory neurotransmitters serotonin and GABA in the brain; common side effects of phenytoin sodium: gingival hyperplasia, gastrointestinal symptoms, allergic reactions, ataxia; Acute ataxia caused by high-dose phenytoin is generally not easy to be misdiagnosed, low-dose phenytoin and structural atrophy of the cerebellum are easily misdiagnosed and mistreated as hereditary/degenerative disease; long-term use of phenytoin has been reported to cause structural atrophy of the cerebellum, which may be speculated to be The Purkinje cells and granule cells of the cerebellum are caused by the specific binding sites of phenytoin sodium
.
.
Case review Patient Liu, female, 65 years old
.
Main complaint: Unsteady walking for 6 years
.
History of present illness: The patient gradually developed unsteady walking 6 years ago, persisted and gradually worsened, accompanied by a little dizziness, which has nothing to do with postural changes, ignorance of rotation, nausea, vomiting, numbness of the limbs, hallucinations, delusions or unresponsiveness, no difference in urination
.
Past history: He has a history of "epilepsy" and has been taking a very small dose of phenytoin 0.
1g bid* for more than 50 years since childhood
.
Physical examination: Consciousness, normal orientation, memory, calculation ability, symmetrical forehead lines, nasolabial folds, middle tongue extension, free eye movement, spontaneous nystagmus (-), negative head shaking test, limb muscle strength level 5 , Normal muscle tone, bilateral Pap's sign (+), sit-up test (+), bilateral finger-nose, rotation, heel-knee-tibial test (+), standing blood pressure (-), cardiopulmonary abdominal examination ( -)
.
Auxiliary examination: cranial MRI: cerebellum atrophy, no brain stem atrophy
.
Figure 1: The patient’s brain MRI nystagmus: gaze-induced nystagmus (+), with gross nystagmus seen in the horizontal direction
.
Figure 2: Patient Nystagmus Checklist (MMSE): 29/30 points.
How to locate and qualitatively diagnose localized diagnosis: middle-aged and elderly women with chronic onset, progressive progression, unstable walking, denial of family genetic history Physical examination: difficulty in sitting up, gaze-induced nystagmus (+), bilateral Pap's sign (+), bilateral finger-nose and heel-knee tibial tests (+), combined with imaging findings for structural atrophy of the cerebellum, consider positioning In the cerebellum and bilateral pyramidal tract damage
.
Qualitative diagnosis: combined with localized diagnosis, the initial diagnosis of the patient is considered as chronic vestibular syndrome (CVS)
.
Chronic Vestibular Syndrome (CVS): is a group of symptoms with chronic dizziness/vertigo/walking instability as the main symptoms, usually with persistent vestibular system dysfunction (visual concussion, nystagmus, gait instability), lasting several months to several months Years of clinical syndrome, CVS clinical includes: 1.
Uncompensable unilateral vestibular disease; 2.
Chronic bilateral vestibular disease; 3.
Cerebellar degenerative disease; 4.
Posterior fossa tumor; 5.
Persistent postural perception Dizziness (PPPD)
.
Vestibular disease includes primary vestibular disease and secondary vestibular disease, combined with the patient's physical examination and auxiliary examinations are temporarily not considered
.
No tumor was found in the cranial fossa after imaging, so the posterior fossa tumor was not considered
.
The patient's dizziness and walking instability have nothing to do with posture, so PPPD is not considered temporarily .
A middle-aged and elderly woman in the patient has imaging evidence of cerebellar atrophy, and physical examination also confirmed cerebellar damage.
Therefore, cerebellar degenerative disease cannot be ruled out
.
What is the next consideration for cerebellar degenerative diseases? Cerebellar degenerative diseases include: congenital hereditary ataxia, degenerative ataxia, and acquired ataxia
.
1 Congenital hereditary ataxia AD inheritance: such as SCA, paroxysmal ataxia (EA), etc.
; AR inheritance: Friedreich ataxia, ataxia-telangiectasia, etc.
; X-linked cerebellar ataxia: including Adrenal leukodystrophy (ALD), fragile X-related tremor/ataxia syndrome (FXTAS), etc.
; mitochondrial cerebellar ataxia: including myoclonic epilepsy with broken red-edge fiber (MERRF) syndrome, mitochondrial encephalomyopathy lactic acidosis and stroke-like episodes (MELAS) and so on
.
2 Degenerative ataxia Multiple system atrophy (MSA); primary late-onset cerebellar ataxia
.
3 Acquired ataxia: cerebrovascular disease; poisoning: alcohol, drugs (antiepileptic drugs, lithium salts, antitumor drugs, cyclosporine, metronidazole), heavy metals, organic solvents: immune-mediated: multiple Sexual sclerosis, cerebellar ataxia with anti-glutamate decarboxylase antibody, gluten ataxia, Miller-Fisher syndrome, systemic lupus erythematosus, Sjogren syndrome, Cogan syndrome, thyroiditis, paraneoplastic syndrome; infections : Abscess, cerebellitis; trauma; tumor; endocrine: hypothyroidism; structural disease: Chiari malformation, dysplasia
.
The patient has no genetic family history, and congenital hereditary ataxia can be ruled out
.
Although the patient is a middle-aged and elderly woman, the patient has never had symptoms of the autonomic nervous system for 6 years, so multiple system atrophy is not considered
.
Whether it is acquired ataxia is identified and ruled out one by one according to the midnights principle.
The patient has a history of taking phenytoin for 50 years.
Finally, it is considered that the patient is chronically poisoned by low-dose phenytoin and cerebellar ataxia
.
Diagnosis: low-dose phenytoin sodium chronic poisoning caused cerebellar ataxia Treatment: stop phenytoin sodium, change levetiracetam 0.
5g bid + ganglioside 120mg qd*7 days, the patient returned after 2 weeks, dizziness improved, finger nose In the test (-) and Pap's sign (-), the patient's dizziness and walking instability symptoms improved significantly during the half-year follow-up visit
.
Discussion: Phenytoin sodium treats epilepsy by stabilizing the function of brain cell membranes and increasing the inhibitory neurotransmitters serotonin and GABA in the brain; common side effects of phenytoin sodium: gingival hyperplasia, gastrointestinal symptoms, allergic reactions, ataxia; Acute ataxia caused by high-dose phenytoin is generally not easy to be misdiagnosed, low-dose phenytoin and structural atrophy of the cerebellum are easily misdiagnosed and mistreated as hereditary/degenerative disease; long-term use of phenytoin has been reported to cause structural atrophy of the cerebellum, which may be speculated to be The Purkinje cells and granule cells of the cerebellum are caused by the specific binding sites of phenytoin sodium
.
