Michael Okun's banner
Michael Okun's profile picture

Michael Okun

@MichaelOkun39,612 subscribers

Author, The Parkinson’s Plan, a NY Times Bestseller and 14 other books, Medical Advisor Parkinson’s Foundation, Distinguished Professor UF Fixel Institute

Shorts

Can serotonin syndrome trigger dancing eyes? Apparently the answer is (rarely) YES. Do you know the 5 'Aspen' tips to differentiate the opsoclonus myoclonus syndrome from other causes ? We frequently think of the syndrome in association w/ autoimmune and also paraneoplastic (causes), however we need to think bigger. A nice reminder provided by Fernanda Lustosa Cabral Gomez and colleagues in Movement Disorders Clinical Practice. Key Points: - Serotonin syndrome: cause is excessive serotonergic activity in the central and peripheral nervous system. - The cause is usually medication use or drug interactions. - The authors show a case w/ serotonin syndrome. - He was on fluoxetine, lithium, amitriptyline, and clonazepam. - Bupropion was then added. - Clues to the underlying diagnosis in this case were "flushing, diaphoresis, tachycardia, tachypnea, opsoclonus, spontaneous myoclonic jerks, and stimulus sensitive myoclonus." - How did they treat it? Stop psychotropic medications and added diazepam. Resolved in a few days. My take: Here are my top 5 'Aspen' tips to differentiate 'dancing eyes' from other syndromes: 1 - Examine the eye movements and remember the eye movements in opsoclonus: Multidirectional → Horizontal + Vertical + Torsional + Oblique; there is no intersaccadic interval (continuous bursts) 2 - Conjugate (no dissociation between the eyes) 3- Eye movements are triggered or worsened by fixation and voluntary gaze holding 4 - Associated neurological signs: myoclonus, cerebellar signs, encephalopathy (paraneoplastic, parainfectious, autoimmune) 5 - Flutter is flat (horizontal); opsoclonus is omnidirectional and ongoing. More tips: Opsoclonus-myoclonus syndrome: look for all the potentially associated features including: myoclonus, opsoclonus, and occasionally ataxia, encephalopathy, and tremor. The eyes are the key: look for saccadic intrusion characterized w/ uninterrupted bursts of conjugate eye movements. The authors remind us to think about the eye movements as "chaotic, arrhythmic, and multidirectional." In young kids think neuroblastoma. In adults think paraneoplastic (automimmune), parainfectious, or idiopathic. Cancers are present in 60% of adults. The authors remind us that "toxins and drugs are rare causes." They also remind us not to forget about "cocaine, amitriptyline, phenytoin, venlafaxine, cefepime, scorpion venom, organophosphates, lithium toxicity and their case that was serotonin syndrome." So when you see dancing eyes, here is the plan: veni, vidi, vici – I came, I saw, I conquered. Parkinson's Foundation Norman Fixel Institute for Neurological Diseases #Parkinson Movement Disorders Clinical Practice

Can serotonin syndrome trigger dancing eyes? Apparently the answer is (rarely) YES. Do you know the 5 'Aspen' tips to differentiate the opsoclonus myoclonus syndrome from other causes ? We frequently think of the syndrome in association w/ autoimmune and also paraneoplastic (causes), however we need to think bigger. A nice reminder provided by Fernanda Lustosa Cabral Gomez and colleagues in Movement Disorders Clinical Practice. Key Points: - Serotonin syndrome: cause is excessive serotonergic activity in the central and peripheral nervous system. - The cause is usually medication use or drug interactions. - The authors show a case w/ serotonin syndrome. - He was on fluoxetine, lithium, amitriptyline, and clonazepam. - Bupropion was then added. - Clues to the underlying diagnosis in this case were "flushing, diaphoresis, tachycardia, tachypnea, opsoclonus, spontaneous myoclonic jerks, and stimulus sensitive myoclonus." - How did they treat it? Stop psychotropic medications and added diazepam. Resolved in a few days. My take: Here are my top 5 'Aspen' tips to differentiate 'dancing eyes' from other syndromes: 1 - Examine the eye movements and remember the eye movements in opsoclonus: Multidirectional → Horizontal + Vertical + Torsional + Oblique; there is no intersaccadic interval (continuous bursts) 2 - Conjugate (no dissociation between the eyes) 3- Eye movements are triggered or worsened by fixation and voluntary gaze holding 4 - Associated neurological signs: myoclonus, cerebellar signs, encephalopathy (paraneoplastic, parainfectious, autoimmune) 5 - Flutter is flat (horizontal); opsoclonus is omnidirectional and ongoing. More tips: Opsoclonus-myoclonus syndrome: look for all the potentially associated features including: myoclonus, opsoclonus, and occasionally ataxia, encephalopathy, and tremor. The eyes are the key: look for saccadic intrusion characterized w/ uninterrupted bursts of conjugate eye movements. The authors remind us to think about the eye movements as "chaotic, arrhythmic, and multidirectional." In young kids think neuroblastoma. In adults think paraneoplastic (automimmune), parainfectious, or idiopathic. Cancers are present in 60% of adults. The authors remind us that "toxins and drugs are rare causes." They also remind us not to forget about "cocaine, amitriptyline, phenytoin, venlafaxine, cefepime, scorpion venom, organophosphates, lithium toxicity and their case that was serotonin syndrome." So when you see dancing eyes, here is the plan: veni, vidi, vici – I came, I saw, I conquered. Parkinson's Foundation Norman Fixel Institute for Neurological Diseases #Parkinson Movement Disorders Clinical Practice

17,427 просмотров

Would you call a crab walk gait a functional neurological disorder? Not so fast. If you encounter someone walk with tiny, sideways shuffling steps, kinda like a crab, it could be a clue. In a striking case just published by Fraiman and colleagues, a crab walk-like helped to uncover a rare but important white matter brain disease called CSF1R-related leukoencephalopathy. Key Points: - A short-stepped laterally swaying crab-like gait may be an early sign of a higher-level gait disorder. - This disorder could originate from the brain’s motor planning centers, and not muscles or nerves. - These gait patterns may signal frontal lobe dysfunction, especially when strength, sensation and coordination remain intact. - When paired w/ behavioral symptoms and frontal white matter changes on MRI, this gait pattern may point to CSF1R-related leukoencephalopathy. - This syndrome is an underrecognized adult-onset leukodystrophy. My take: My mentor used to teach that a great neurologist always walked their patients to the examination room and in many cases he/she would clinch the diagnosis even before the door was shut and the vital signs collected. Here are 5 points that resonated w/ me about this case. 1- A strange walk might be a warning sign. Don't jump to a functional diagnosis if you see a sideways walk. 2- The brain can be the source of walking challenges even when the legs are strong. 3- White matter diseases can show up as a funny walk. Memory and speech challenges may emerge later. 4-Don’t ignore personality or speech changes. Disinhibition, apathy or trouble finding words acould point to a deeper brain condition. 5- A brain MRI and genetic test can unlock the mystery. #parkinson Parkinson's Foundation Norman Fixel Institute for Neurological Diseases

Would you call a crab walk gait a functional neurological disorder? Not so fast. If you encounter someone walk with tiny, sideways shuffling steps, kinda like a crab, it could be a clue. In a striking case just published by Fraiman and colleagues, a crab walk-like helped to uncover a rare but important white matter brain disease called CSF1R-related leukoencephalopathy. Key Points: - A short-stepped laterally swaying crab-like gait may be an early sign of a higher-level gait disorder. - This disorder could originate from the brain’s motor planning centers, and not muscles or nerves. - These gait patterns may signal frontal lobe dysfunction, especially when strength, sensation and coordination remain intact. - When paired w/ behavioral symptoms and frontal white matter changes on MRI, this gait pattern may point to CSF1R-related leukoencephalopathy. - This syndrome is an underrecognized adult-onset leukodystrophy. My take: My mentor used to teach that a great neurologist always walked their patients to the examination room and in many cases he/she would clinch the diagnosis even before the door was shut and the vital signs collected. Here are 5 points that resonated w/ me about this case. 1- A strange walk might be a warning sign. Don't jump to a functional diagnosis if you see a sideways walk. 2- The brain can be the source of walking challenges even when the legs are strong. 3- White matter diseases can show up as a funny walk. Memory and speech challenges may emerge later. 4-Don’t ignore personality or speech changes. Disinhibition, apathy or trouble finding words acould point to a deeper brain condition. 5- A brain MRI and genetic test can unlock the mystery. #parkinson Parkinson's Foundation Norman Fixel Institute for Neurological Diseases

11,129 просмотров

What bedside test do I think all healthcare providers should perform at every #parkinsons visit? 'The pull test for retropulsion,' Think of how many #falls we could 'prevent' if we performed the test and took appropriate action. Nice video from Dr. Doshi.

What bedside test do I think all healthcare providers should perform at every #parkinsons visit? 'The pull test for retropulsion,' Think of how many #falls we could 'prevent' if we performed the test and took appropriate action. Nice video from Dr. Doshi.

22,385 просмотров

What is the diagnosis? Opsoclonus myoclonus syndrome. This is an 'oldie but a goodie.' Teaching phenomenology of movement and neurological disorders today @VUMCneurology. This one was published in Archives of Neurology which later became JAMA Neurology. What is the differential possibilities for causes: A whole bunch of potential causes: Posterior fossa tumors, intracranial hemorrhage, stroke, central nervous system infection, acute cerebellitis, acute cerebellar ataxia, drug intoxication, Guillain-Barré syndrome, and migraine-related. If a fever, opsoclonus and ataxia think about acute infectious encephalitis or meningitis. Could be scrub typhus, mumps or tuberculous meningitis. Don't forget autominune as high on the list and remember to nail the phenomenology before rushing to the diagnosis. Perhaps also there is a neuroblastoma present. #fixelinstitute

What is the diagnosis? Opsoclonus myoclonus syndrome. This is an 'oldie but a goodie.' Teaching phenomenology of movement and neurological disorders today @VUMCneurology. This one was published in Archives of Neurology which later became JAMA Neurology. What is the differential possibilities for causes: A whole bunch of potential causes: Posterior fossa tumors, intracranial hemorrhage, stroke, central nervous system infection, acute cerebellitis, acute cerebellar ataxia, drug intoxication, Guillain-Barré syndrome, and migraine-related. If a fever, opsoclonus and ataxia think about acute infectious encephalitis or meningitis. Could be scrub typhus, mumps or tuberculous meningitis. Don't forget autominune as high on the list and remember to nail the phenomenology before rushing to the diagnosis. Perhaps also there is a neuroblastoma present. #fixelinstitute

14,762 просмотров

Videos

MichaelOkun's profile picture

Can you identify an oculogyric crisis? @ChristosGanos and colleagues teach us about the intriguing possibility that the rolling eyes we frequently see after administration of a drug, may be localized to a brain lesion network associated with a brain dopaminergic transcriptomic signature. Read about it in a new paper Brain. Key Points: - Oculogyric crises what are they? Acute episodes sustained, typically upward, conjugate deviation of the eyes. - Common cause? Acute D2-dopamine receptor blockade by a drug. - The authors used data from 14 previously reported cases of lesion-induced oculogyric crises and employed' lesion network mapping' to search for shared connections. - What was the common network? Basal ganglia, thalamic, brainstem nuclei and cerebellum. - A look at the gene expression profiles showed spatial overlap specifically with the gene coding for dopamine receptor type 2 (DRD2). - The very cool part: spatial overlap with DRD2 and DRD3 gene expression seemed to be 'specific to brain lesions associated with oculogyric crises when contrasted to lesions that led to other movement disorders.' My take: I love the use of multiple modalities to chase down a common neural network for oculogyric crises. We should keep in mind that these were cases associated with brain lesions, and as we all contribute by reporting more cases and sharing their MRI scans we will likely further refine our understanding of the network. For clinicians when you see this, look down that medication list for the 'dopamine blocker' as your first step in diagnosis. This video by Elan Louis provides a nice illustration of oculogyric crisis to help you to identify them in your practice. #Parkinsons #oculogyric

Michael Okun

15,352 просмотров • 2 лет назад

MichaelOkun's profile picture

Do you remember the case of the 'frozen addict' from recreational drug use (MPTP). Is there a 'new frozen addict syndrome' caused by methcathione (ephedrone). YES. This psychostimulant leads to release of brain catecholamines. Check out this case and video by Thayler and Gurevitch which responded to amantadine and check out the link to manganese. Key points: - Methcathione (ephedrone) can be used as a recreational drug and use has been documented in Eastern Europe and other world locations. - This chemical is synthesized by oxidation of ephedrine or pseudoephedrine w/potassium permanganate. - It is usually given IV and the 'parkinsonism' is thought to be caused by manganese. - It is unlike the MPTP frozen addict as in this case levodopa does not work to treat. - The authors point out that the syndrome tends to be more symmetrical than in idiopathic PD; the clinician should look for bradykinesia, dystonia, and gait impairment. - Check out this 41 year old case w/ a normal flurodopa PET and an abnormal MRI. - He was treated with a 5-day course of IV amantadine followed by oral amantadine. My take: It is humbling to think about the history of a recreational drug which provided one of our best overall animal models of PD (the MPTP model). Now we are observing another form of recreational drug induced parkinsonism, and this one seems to be related to manganese. It is interesting in this case to observe the response to IV and oral amantadine; which as a therapy has multiple mechanisms of action including on dopamine, acetlycholine and glutamate pathways. In the USA, we have not used IV amantadine so this will be a new trick for us. One important aspect of this case was that the clinicians resisted the urge to 'dismiss the person' as an addict or as functional case. Similar to Bill Langston's experience with the MPTP frozen addict, these authors persisted, made the diagnosis and designed and implemented a treatment. BRAVO. Remember, we will all (one day) come down with a disease or diseases and Fortuna est caeca; Fortune is blind. #Parkinsons #manganese #methcathione #ephedrone

Michael Okun

12,908 просмотров • 2 лет назад