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Many brain insults, including TBI, stroke and encephalitis, may be associated with “early seizures” in the first week after the insult. These seizures are not spontaneous (unprovoked), but are directly caused by the initial insult. Late unprovoked (i.e., spontaneously recurrent seizures), may follow weeks, months or years later.
Our question is: May such early seizures also occur after a status epilepticus and is there literature on this (both for patients and SE models)?
We do typically observe early seizures in different SE models (e.g., pilocarpine, kainate) in rats. They occur with a peak frequency at 3-5 days following SE (if the SE was effectively interrupted after 60-120 min) and then subside. Late seizures occur earliest after about 7 days but often later.
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Dear researchers,
I received an invitation from clinical neurology and neuroscience journal to be part of there editorial team. And I'm wondering if it is a serious journal to be part of?
Cordially,
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The journal “Clinical Neurology and Neuroscience” is published by "Science Publishing Group", a publisher mentioned in the Beall’s list (https://beallslist.net/). This is a red flag. But there are more:
-Indexing info mentions Eurasian Scientific Journal Index, which is a known example of a misleading metric (http://flakyj.blogspot.com/search/label/SciencePG)
-Contact info mentions a US location while it is based in Pakistan https://en.wikipedia.org/wiki/Science_Publishing_Group
-I think 970 USD is too much for a basically nonindexed journal https://www.sciencepublishinggroup.com/journal/apcs?journalid=271
So, though it all looks misleadingly professional I would stay away from this one.
Best regards.
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I'm looking for a simple scale, that evaluate children motor handicap in general, not specific to only one affection.
Thank you,
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The gross motor function classification system
level 1 patients are vambulatory in all settings
level2 patients walk without aid but have limitation in community settings
level 3 patients walk with aid
level 4 require wheelchair
level 5 fully dependant for mobility
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Sleep problems can be seen in patients with Parkinson's disease. Can it be about serotonin?
In mice, ablation of the raphe and no production serotonin increases wakefulness and impairs the homeostatic response to sleep deprivation.(DOI:https://doi.org/10.1016/j.neuron.2019.05.038)
Even in the absence of depression, the CSF levels of 5-I-HAA of patients with Parkinson’s disease are lower than those of age-matched controls.
( DOI: 10.1176/jnp.2.1.88 )
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Thank you for great articles. They gave me a new perspective about PD.
I want to suggest an article: Serotonergic dysregulation is linked to sleep problems in Parkinson's disease (doi:10.1016/j.nicl.2018.03.001)
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I have to apologize as I have recently retired from a 30 year history in clinical neurology, and am rusty on organic synthesis. As we know the acid catalyzed ester synthesis (Fisher) is an equilibrium rxn. Have people used molecular sieves 3A to adsorb one of the products, water, to force the rxn towards completion? I have contemplated placing 3A in a Soxhlet extractor and adding this to one of the ports in the rxn flask, a condenser in the other; I would add 3A to a cup in the Soxhlet and as it fills and drains water should be removed. I am using EtOH and will form the ethyl ester of my carboxylic acid. Since water and EtOH form an azeotrope I don't see a Dean-Stark device as effective. Is this thinking correct? Many thanks.
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You're efforts have succeeded. You have taught me new chemistry, and I am much appreciative. This looks like an excellent approach. As a member of the ACS I simply have access to their journals, and Tet/Tet Letters might be one, but I don't recall that being an ACS journal. Searching the specific chemical I couldn't find anything except the old literature. I wish I had a librarian. Doing what I am doing, I don't have access to online university services, e.g. their library. Yes, the discussions did expand quite a bit. Initially it was a simple comment but I let my aspirations loose, seeking more information, and did not formulate the issues as concisely as I should. That, too, has taught me something. "Be more concise." Finally, I see that I simply have to save my documents as a jpg file and they will attach. Thank you for you're excellent contributions. The very best to you.
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Within three years, a patient with a desminopathy (Thr341Pro DES mutation) was found to have a 17% increase in the level of C4 complement components to 0.41 g / l (Norm 0.1-0.4 g / l).
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Dear Yosvany Castillo! Thank you very much for your answer. Over the past 2 years in this patient with desminopathy (Thr341Pro DES mutation in the heterozygous state), the C4 level of the complement component decreased to 0.36 g/l without taking medications.
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I recently read an article regarding the use of melatonin as a neuroprotective agent using acute ethanol exposure for 1 day and it had good results, I want to know if exists an article using functional food pre ethanol treatment
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Great question.
First, I would suggest this paradigm: Ethanol toxicity manifests primarily from ROS build up downstream of hepatic inability to process aldehyde fast enough. Protective agents would feature those most able to ramp up the ARE system. Nrf2 activators would figure highly. Sulforaphane is the canonical example. A wide range of polyphenols convey benefit, including anthocyanin.
Resveratrol and curcumin are examples that hit additional pathways involving autophagy and inflammatory reduction. Some of these compounds compete with alcohol and aldehyde to some degree for catabolism. AMPK stimulation is another pathway. Any senolytics, also, is likely to help.
Ethanol itself causes very few problems compared to aldehyde. Ethanol ---(alcohol dehydrogenase)--> Acetaldehyde ---> (acetaldehyde dehydrogenase) --> Acetate. Protective agents would be those that inhibit alcohol dehydrogenase while increasing the activity of acetaldehyde dehydrogenase.
General re polyphenols
Plenty of specific articles.
Here's many:
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Verapamil, A calcium channel blocker is used for prophylaxis of cluster headache. Verapamil is a vasodilator. What is its mechanism in preventing headache ?
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According to classic theory, a migraine attack is initiated by cerebrovascular spasm followed by extracranial vasodilatation. Results of recent studies support this theory and suggest that cerebral blood flow during the initial phase of migraine symptoms is, in fact, decreased and this decrease probably leads to ischemia and hypoxia. Cellular hypoxia, in turn, can cause an increase in the flow of calcium from the extracellular fluid to the intracellular space, resulting in calcium overload and cellular dysfunction. Because calcium-channel blockers selectively inhibit the intracellular influx of calcium ions, investigators have begun evaluating the efficacy of these agents for migraine prophylaxis. Nimodipine, a calcium-channel blocker that exhibits selective effects on cerebral vessels, seems to offer protection against the cerebral ischemia and hypoxia presumed to be operative during migraine attacks.
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According to researches, appendix might has connection with Parkinson's Disease but consequences are conflict. One study says, appendix removal reduces risk of PD but another study says that it increases.
Uncovering a Link Between the Appendix and Parkinson Disease Risk
doi:10.1001/jama.2019.9041
Thank you!
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For more information see the below link:
Have any one, any information about "Cold-evoked potentials (CEP) for brain mapping"?
what is your idea about this machine:
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It would relate well to the "submersion hypothesis" (it's not a thing, but if you google it, there are some studies I've replicated. Also to the p300 wave, as well as the idea of electromagnetic theories of using a Dirac Delta for determining the state of a Laplacian channel (or a 'black-box' in a circuit diagram).
The device seems, based of their data, applicable in determining the change in threshold of a person over certain periods of their life.
However, I imagine your use for it would be along the lines of sending an impulse to see how the nerves respond in different areas of the brain and tying it in to see if it co-correlates with other measures.
My suggestion would be to combine it with an EEG and/or fMRI and see if the differences on each data set line up in any way. My imagination leads me to think that perhaps the forehead and brainstem have both a higher sensitivity and power-band together, arising from a common cause of higher-neural-activity-density. But that's an educated guess.
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There is a trend now that people are searching a way to exceed in their capability and are willing to try anything that transforms to the realm of super human, it is not a science fiction anymore! I heard a person being interviewed by BBC 5 radio, a cyborg person, a bio-mechanical "person", he mentioned his wife did the same and they keep their connection all the time through internet without speaking.
Research also shows more than 20% of UK university students do take cognitive enhancement smart drug like Modafinil which normally is prescribed to people with ADD problem.
I am wondering why people keep doing all these to get some extra intelligence but loosing all their self confidence not to mention their humanity or soul, you can say, is it worth it? Where is humanity going? What is the fate of humanity if such trend is being kept encouraged ?
REFERENCE
  1. http://www.bbc.co.uk/programmes/articles/1g2gNvk4Gc4MwYqhtQ8KNlf/meet-the-cyborgs-five-people-who-have-modified-their-bodies-with-tech
  2. https://www.theguardian.com/education/2017/may/10/universities-do-more-tackle-smart-drugs-say-experts-uk-exams
© RG: Samuel Lakew
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Leonid V Vladimirov , you are right, it is hard to believe. I think it won't be long we will start asking people whether they are human or cyborg unless we afraid how they might react to that. May be we can stop this thing if we are aware of what is happening and what damage it might cause.
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If we can record our memories in the present we can save them forever.
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Check out the International Journal of Dream Research, Heidelberg University, Germany, online. (IJoDR)
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Mild pressure feeling in the head, not painful but just very aggravating and feeling really strange. Feeling like having an extreme brain fog and like a fuzzy head/ a constant cloud over the brain.
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Brain Fog, feelings of dissociation, mild feeling of head fulness are commonly seen in someone who has a history of Sleep Apnea Syndrome. I certainly would recommend doing a CT of the brain to make sure there is no abnormality of the temporal lobes which can cause complex partial/temporal lobe epilepsy. I am a neurologist and have come across many patients with symptomology like yours. thanks.
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how can we differentiate them ?
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Essential tremor can be seen at resting or during any movements, but intention tremor, also known as cerebellar tremor, can be observed when the extremity approaches a certain object. For example, in finger to nose test, the amplitude of intention tremor increases as the finger approaches the nose.
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I have read about multiple sclerosis and I was very surprized that no medication is available for this disease!
Mayo Clinic stated " There's no cure for multiple sclerosis. However, treatments can help speed recovery from attacks, modify the course of the disease and manage symptoms"
Is it true? Which drugs are recommended for this condition?
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The range of symptomatic MS medications is endless, as is its list of symptoms.
As long as MS remains defined by unexplained neurological dysfunctions, no causal treatment is possible. Things are different for the direct venous damages to the brain and the indirect venous damages to the spinal cord shown at www.ms-info.net. But, unfortunately, there is only a minority of physicians willing to deal with these complex issues.
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The question is with reference to a patient suffering from differential body temperature, her right side (particularly the hand) occasionally being substantially colder than the left.
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we see this kind of phenomenon not very rarely in patients with multiple sclerosis. the mechanism is thought to be damage to the intermediate horn that contains the nuclei of the sympathetic nerves. the sympathetic nerves determine the tone of the arterioles. therefore, very unusual phenomenon have been noted in patients with multiple sclerosis. they can have intermittent discoloration of the skin on one of the body, they can have sweating that is restricted to one arm or a leg and sometimes they can have half of their torso that is erythematous, mild edematous and xerodermia. if this patient does not have MS then you can look at the sympathetic chain dysfunction on the affected side. thanks.
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I always hear about some myths in neurology, and mostly about stroke but I want to know what myths other diseases have.
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The immune system is NOT an intrinsic part of the Nervous System.
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It seems we have no treatment disease-modifying for PD. 
That's been supposed for rasagiline, but no scientific evidence so far
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Melatonin, at high doses (800 mg/day), works very well in Parkinson, and lacks any adverse effects. 
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Hello, colleagues.
I know a family with epileptic phenotype, which looks very similar to Severe Myoclonic Epilepsy of Infancy (so called «Dravet syndrome»). Mother had febrile convulsions in her childhood. Now first (F, 19) and fifth (M, 1) children have relative severe phenotypes, which are similar to each other. Second, third and fourth children are seizure-free, no any problems. They did NGS-genetic test «Epileptic panel» for 200+ genes in fifth child, but nothing interesting was found (at least SCN1A gene was found «normal»). All children are from the same father.
Phenotype shortly: GTCS every 1 — 2 weeks, absences, myoclonus, mental impairment (not very hard), ataxia. First and fifth children have similar phenotypes.
Does anyone interested in carrying out the investigations on this family? They need help in setting the exact diagnosis, but the doctors here in Russia can't make a decision, as well as don't want to make any OMICS-investigations.
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you can email  me at  luismi.aras@apoyodravet.eu  we can speak about some european researchers interested in gen-hunter  (also in dravet)
Dr Aras father of a 12 year old dravet girl CEO apoyodravet (promoting dravet research
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A progressive neurological disease caused by contamination of cerebrospinal fluid with blood, leading to deposits of iron on the brain & spinal cord
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There are 2 different types of Superficial Sideroses, one is Superficial Siderosis "of the central Nervous System", and the other is "Cortical" Superficial Siderosis, commonly seen in Cerebral Amyloid Angiopathy patients. If you're interested in the latter, you'll find ressources in the attached RG project ; Imaging biomarkers of hemorrhagic small vessel disease. Best regards 
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Is there any chance that dyslipidemia has any causative chance for generating neurodegeneration?
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Dear Sayam,
Thanks for an interesting question. As many of our colleagues has discussed that dyslipidemia is a modifiable risk factor in the development of dementia and cardiovascular diseases. Mr Sedat has already provided the details of few articles.
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My neighbour has a parrot & he wants to cut the claw
and he asked me to sedate the bird; what is the best drug to be used???
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Dear Dr. Hussain,
For the above scenario, use Diazepam to induce sedation and if the sedation is prolonged then antagonize the effect of diazepam by using Flumazenil.
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What is the difference between an AD and a seizure. Can we consider an AD synonymous to a seizure?
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Thank you Dr Josep & Dr Jordi
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Since an Operation two years ago a Patient suffers from the impression that he is still in a room after he had left it.  He feels body sensations, for instance as if he still would sit on the chair and sees images of what he saw in the room before. The impressions last for hours and days and are very disturbing in the daily functioning. There is no evidence for other psychotic symptoms. He is aware that his symptoms are distorted impressions. In his MRT is no abnormality.
Does anyone have informations about a similar case? Is it possible that the perecptions are a result of the Operation and have an neurological reason?
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Hallo Anthony, thanks a lot for your interesting Input. Until now all physical examinations were negativ. Tomorrow the Patient will come again and we will do further tests.
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Phantom eye symptoms seem to occur relatively frequently after enucleation as reported by our group (Sörös P, Vo O, Husstedt IW, Evers S, Gerding H. Phantom eye syndrome: Its prevalence, phenomenology, and putative mechanisms. Neurology 2003; 60: 1542-1543). What is your experience? 
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See the article from the American Academy of  Opthalmology at https://www.aao.org/eye-health/news/phantom-eye-syndrome-after-surgery
Also a literature review in The Scientific World Journal at https://www.hindawi.com/journals/tswj/2014/686493/
This review has 57 references and is probably a good place to begin.
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Perfusion MRI shows more detailed area of infarct bone
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Perfusion MRI is the best way to evaluate hip at children with LCP between 4 and 8 years. Before 4 years old or after 8 years (age of onset) the treatment don't change very much the final result (after Salter and Harring opinion) and perfusion MRI isn't really necessary at first visit.
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We encountered a serious case with HSV positive encephalitis. After three weeks treatment with Acyclovir, we did again a lumbar punction. The PCR turned out to be still positive. Is there anyone with experience of doing a LP after three weeks of treatment?
We are desperately seeking for information to be able to put these results in the right perspective.
Thanks
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a recent description of Acyclovir resistance in herpes simplex virus type I encephalitis and way to analyzes ACV-resistance
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olfactory, sleep disorder, orthostatic hypotension, excessive saliva, constipation, vision problems, gastrointestinal problems
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 You can review Nonmotor symptoms in LRRK2 G2019S Associated Parkinson´s Disease. PLoS One 2014;9(10) Carles Gaig and cols.
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subcortical aphasia and recovery pattern ( especially in patients with CAPSULO GANGLIONIC BLEEED)
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thanks a ton. 
Regards
Asha
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I am writing a case study as part of my degree. the case study looks at a patient with a left sided CVA with right sided hemiplegia. I have to try and include in the case study why injuries on one side of the brain affects the opposite side, but I am struggling to find much solid information.
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clinical neuroanatomy (7th edition)  richard S. snell
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I have a TN patient whose pain is well controlled with 600mg of carbamazepine. She started it a month ago, she is on 600mg for 10 days. However, patient is complaining of severe nausea. Is there anything I she or I can do to minimize this (before switching to oxcarbazepine)?
Thanks a lot
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Thank you all for your kind answers. The patient took ranitidine which significantly reduced her problems.
Once again thanks a lot!
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 A man now 80 years old presents progressive ataxia amb pendular nystagmus wich began at age 75. A extensive study was negative. He doesn't present malabsorption and diarrhea, Two month ago vomited freqüently  and ataxia got worse . Transglutaminase and endomisium antibodies were negative, Recent duodenal biopsy is compatible with celiac disease (MARSH 3), amb HLA-DQ2 is positive. Slight improvement with gluten free diet. 
This case, a silent seronegative celiac disease with clinical neuroloy over age 75,is a exception, or is not a true celiac disease, or instead, may be a possible cause of some idiophatic ataxias ?, 
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Indeed well established, well known - refer to Hajdivassalou's work from Sheffield. AV
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As described in the very recent case report by New England Journal of Medicine (Case 2-2017), the chelation therapy would increase the serum copper concentration and cause the worsening of neurological symptoms in Wilson's disease. I would like to have a discussion on the potential risk of the standard therapy with D-penicillamine.  
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A clinical deterioration occurs after the start of chelating therapy very often. This is a temporary phenomenon.Usually, the dose of D-penicillamine should be lowered slightly for few weeks/months and then again increased to maximum tolerated (within acceptable therapeutic).
Also, I have had some experience with Trientine and there was the same problem.
It is well known and expected, so all we can do is to warn patient about it and to titrate dosage...
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Dear Researchers,
We are working on post-menopause related dementia and AD.
We have noticed that, in post-menopuase women no therapeutic intervention is approved for memory impairment except the donepezil (which is also not an effective therapy when considered only post-menopause women population).
Most clinical reports support the fact that the prevalence and incidence of Alzheimer's Disease (AD) high in women, especially in post-menopause women (due to hormonal loss) as compared to men.
Whether, all cognitive impairment problems of menopause women are related to mild cognitive impairment or in later stages all cases will lead to AD?
Can we see AD post menopause women as separate entity and as a homogenous study population?
Also, if anybody knows, please help us with differential root causes of pathology underlying AD in men and Women.
Thanking you,
Best Regards,
Dr. Grandhi V Ramalingayya
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Thanks for the information provided...
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male patient following botox for blepharospasm , now having fatiguable ptosis..
causes?
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Dear colleague:
In my opinion it can be still a side effect of Botox, I would try to wash out botox at least six months. It is rare and far the possibility of co-existence of Myasthenia and blepharospasm. Also EMG/RNS was normal. Kind regards.
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14-year-old girl  presented with permanent neurological
disorder impairing motor skills, comprehension,
and memory. She began to have an epileptiform seizures.
ECG is shown in Figure below
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Dear Dr.Tatiyana, 
Sincere thanks and deep appreciation should be expressed to you for your reply and discussion.
Definitely, I agree with you, all  this family's females including, the mother, sisters, and the affected girl who met the main diagnostic criteria of Rett syndrome in your case,all of them need to have a comprehensive genetic analysis, however, according to some studies, the prognostic value of such analysis of genotype is limited, besides, normal results will not exclude the diagnosis as it mainly based upon the clinical presentation, actually, more specific studies are required to find out and detect the genotype-phenotype correlation.
In addition to what you mentioned, mother can be either a carrier or a mosaic for the mutation of MECP2 gene, putting into our account that the mutation of MECP2 is not present in all cases of Rett syndrome regardless of its forms,  the typical and the atypical ( The non-classic ), that is why the cornerstone of the diagnosis for Rett syndrome is mainly the clinical presentation ( Clinical features) and then the follow up of its progression such as the girl above who met the diagnostic criteria  based upon her clinical characteristics, however, some cases of RTT can only be diagnosed by retrospective process.
Although, most cases of RTT are female, there are 57 rare cases of male with RTT with MECP2 mutation present in 65% of those cases according to  2015 systematic review study.
Indeed, it is a very interesting case, and it would be very appreciated to you Dr.Tatiyana  if you keep us updated in regard to your interesting case.
Respectfully yours.
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This young patient presented with altered level of consciousness and rigidity. Sodium was normal. He improvedid gradually. Now having all4 limb spasticity and tongue fasciculations. EMG genioglossal denevation. What does MRI show?
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Pontine haemorrhage. AVM/Cavernous malformation?
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I understand that neuroleptics block dopaminergic transmission. However I don't really understand the mechanism behind how it can cause movement disorders. 
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As Jordj wrote.
Simply.
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Clinical experience regarding this question is welcome. Thank you.
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not quite answer you seek but Nuedexta is a wonderful therapeutic option for Chorea and the neuropsychiatrist sequel aesthetic of HD
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Literature says the conventional acetylcholinesterase inhibitors (e.g. Donepezil) or HRT is not that effective in treating the post menopause associated dementia in women.However, the aged women population is gradually increasing world wide with this cognitive dysfunction and the resulting affected day to day QOL.
Can anybody has the experience with this post menopause associated dementia please share any effective treatment strategy other than HRT and AChE inhibitors.
Thanking You,
Best Ragards,
Grandhi V Ramalingayya
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Dear Grandhi,
the bold answer is that there is no treatment for dementia whatever the category of patients. Ache inhibitors have some short-term effect in patients with Lewy body disease but fail to show any efficacy otherwise. Other therapeutic strategies like cognitive training have not shocn yet convincing proofs of efficacy. We have so far only small measures like lowering vascular profile (hypertension, diabetes) in order to reduce the vascular part of dementia and suggesting to patients to do regular physical exercise and maintain social activities.
best
Christophe
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As a PT, I work with patients with Post-concussion syndrome.  (I have noticed multiple patients with this diagnosis have excessive chest, upper trapezius and accessory muscle use while breathing, which may have to do with the high incidence of neck pain and headaches in this population, but want to see if anyone else has noticed this). I also wonder if this is due to the hits to the head which may interfere with C3,4,5; which may involve inhibiting diaphragm at some time during their injury. I do not believe there is research on this yet.
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I realize this thread is somewhat older, but will offer some input.  There is a potentially far less sexy explanation...anxiety.  The strongest predictor of postconcussion syndrome is preexisting psychiatric symptoms, and anxious breathing presents just as you're describing.  Depending on the population you work with, the removal from work/school/athletics/etc. that accompanies the acute recovery process commonly progresses to anxiety and other symptoms unrelated to any specific underlying pathology.  Even if they did not have a preexisting condition, the anxiety can result from the concussion as a stressful event.  There is strong evidence suggesting that the physiological effects of concussion are strongest acutely, but then give way to psychological and psychosocial influences.  This does not mean the symptoms aren't real, it just means their etiology may not be underlying damage from the brain injury per se.  The Buffalo Treadmill Test from Leddy et al. offers a nice way to try and tease out whether lingering symptoms have a physiological basis or not.  
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I am interested in treatment, rate of progression.
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I want use Beta amyloid 25-35 as a neurotoxin for SHSY5Y cells.Although in articles 10 microM of it for 24h is used and cell viability of them decreased approximately  20% but in my experiments with two bath from different company even in 200 microM of it  , there was no decrease in cell viability. my protocol is: Briefly, Aβ25–35 was initially dissolved in double-distilled water to 1 mM. The peptide solution was divided into aliquots and stored at −20°C. Before use, the Aβ25–35 solution was incubated at 37°C for 7–10 days to form aggregated diffusible oligomers, then diluted in medium to the indicated concentration. When I treated cells with BA i tested 10% and 2% FBS in media and both of them has the same result. what  is your recommendation?
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Maybe your peptide is too aggregated and your cells are not able to internalize it?
I had the same problem in the past, but with abeta 1-42...
Take a look at this article: "Oligomer-specific Abeta toxicity in cell models is mediated by selective uptake"  http://www.ncbi.nlm.nih.gov/pubmed/18602001
Hope it helps!
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APACHE IV scoring has been implemented for about 8 months.  A recurrent issue is when patients without much chronic health history, but very poor neurological recovery after cardiac arrest are scoring to be very likely to recover.  Is this a known issue or do we need to tweak our calculations in EHR?
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Consider that APACHE is about survival which does not imply neurological recovery.
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Typically we try to place ventricular drain to drain and measure the Intracranial pressure in severe head injury.However newer avenues have shown placing cisternal drain may have ripple effect on the outcome.Can it be a mirror to the intrabrain pressure????
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I agree with Dr. Khan. Cerebral spinal fluid (CSF) pressure is varies among different compartments. In one of our patients with a rare inherited metabolic disease (MSUD), the CSF pressure was markedly elevated especially in the compartments surrounding the optic nerves. The patient was successfully treated with fenestration of the optic nerve sheets before getting blind (see publication below). This is a nice example of elevated CSF pressure restricted to certain compartments in the central nervous system.
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More than expected head dropped myasthenia onset are patient with Parkinson disease (25%) and majority of myasthenia onset in patient with Parkinson disease is head dropped (more tan 60%). We think that it may be due to fatigability associated to cervical rigidity. What do you think?
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I agree with comments above.  You need to look for a paraspinous myopathy.  The etiology of which is not known but may be related to hyperextension injury of neck muscles, which could occur with increased weakness from MG or altered posture from PD.  From a therapy perspective you need to assess if this is MG or not.
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It has been known for a long time now that cotinine, a metabolite of nicotine, is a nootropic and more importantly, is somewhat neuroprotective for PD and AD.  It is also known that cotinine is well tolerated by human subjects and has none of the negative side effects of nicotine itself.  Given today's great concern regarding both PD and AD, how can it be that research on this compound, very closely approximating a "silver bullet" if you will, is not being conducted with great intensity by NIH and/or the pharma industry?  Why does this seemingly magical solution to so many problems sit on the side while less practicable molecules get to dance?  
I don't get it. There is tons of research supporting this but not much is happening.  Why?
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Yes, Paul, I agree.  I was being a bit hyperbolic and put "silver bullet" in quotes for that very reason.  Thanks for the links; I read one of them previously.  I have read much on this and chatted with someone very active in research in this area.  The question still stands:  Why is this going nowhere?
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can any one give me a drug or chemical can be used in induction of neuropathic pain (mice) either than chemotherapeutic agents or Suramin?
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Hi,
some of the chemicals has been used for development of experimental neuropathic pain, like capsaicin, CFA, Formalin, carragenan
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It has been noticeable in our practise that a lot of children develop low to mediate grade of fever post epileptic seizures. this is more obvious after long or recurrent motor seizures. i was wondering what is the exact mechanism that can explain such an observation
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In addition to the suggestions above one can speculate that the  hypothalamic temperature setpoint is increased  by unknown  circulating "substances" and or neural input. we have limited knowledge   about the control of the temperature setpoint - just think about  cyclic hotflushes during menopause. 
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Children and adults with MECP2 duplication syndrome have a wide variety of seizures, but one of the most frequently observed looks like classic "infantile spasms" of West Syndrome However, these are occurring in individuals ranging from a few years old to their 20s and 30s. Most discussions of infantile spasms is about infants, have other adults been described with infantile spasms?
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In my personal experience, I have often sometimes seen epileptic spasms occurring beyond the 1st or 2nd year of life, either in my patients or in patients whose EEG I have read. As mentioned above, EEG shows diferent patterns, not hypsarrytmia. Patients I have seen with later-onset or persistente spasms included: a case of tuberous sclerosis with persisting spasms (now 9 years old), a patient with Norrie disease (spasms started in adolescence), and a girl with "cryptogenic late-onset spasms" who started sezires by the age of 4. Other patients who have this type of seizures include chromomosomal abnormalities and some epileptic encephalopathies, in some cases with spasms, tonic seizures and "tonic spasms".
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The patient had SIADH. It was multi-factorial (Drugs, Colonic Irrigation, & Encephalitis). 
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I am still don't know how old the patient is!
However, if he has no further symptoms - i.e. is managing as well as he did before he became ill, I would not worry too much.  His Na has drifted down a little over the time since discharge - I suspect his is normally at the lower part of, or just below, the lab reference range.  The absolute number is not so relevant if the patient is well. 
If you wich to be cautious, you could check it in 4 weeks' time (or sooner if relevant symptoms - i.e. drowsiness, etc).  It is helpful to find out what his usual Na level is when he is well.  If indeed it is usually around 135mMol/L, this would suggest he does not have much 'osmotic control' reserve - and any of the precipitants you mention could provoke another symptomatic episode.
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A hyperactive state of the inner ear explains many of the symptoms of migraine (audiosensitivity/phonophobia, dizziness, head pressure, nausea, aura, Meniere syndrome, etc).  Could peripheral vestibular dysfunction also cause allodynia here and in other conditions?  Allodynia has been alleviated by caloric stimulation (running water at certain temperatures into the ear canal).  
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To all readers of this thread : ALLODYNIA  is not necessarily a manifestation of central sensitization,  and the idea that it is mediated by the thalamus is incorrect. I have trained under the individual who characterized the thalamic responses to visceral versus somatic pain in non-human species via electrophysiology and continued the work with neuroimaging in humans (AV Apkarian), and there is no strong evidence to even seriously consider this hypothesis. 
Only DYNAMIC MECHANICAL ALLODYNIA is indicative of SPINAL central sensitization (which is the only kind, read Clifford Woolf's work), meaning that the pressure stimulus must be moving across the skin. Direct pressure that indents the skin, which is the most common for of allodynia, is not the same animal and can co-exist with dynamic mechanical allodynia.
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81 year old women presenting generalized syncronous myoclonic jerks with a frecuency of 0.1-0.2Hz (each 5-10 seconds) since 16 hours with a perfect alertness and alfa dominant posterior rithm.. Do you believe in C3-C4??cervical*subcortical generation*? She suffered proximal humerus fracture two months ago. gait impairment, I do not know reason. (video EEG shows first proximal movement arms and legs, not distal hand muscles, no involvement of the orbicular oculi). Thank you. Dare you to say that is not epileptic, yes? DZP 5 mg no effect.. Brain and neck CT will be performed today...
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Was she on any medication previously? Or concomitantly? May be a toxic issue, e.g. combination of Tramadolol and Pregabaline for the pain following fracture may produce similar myoclonus with preserved reactivity.
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asking about using dexamethazone in intrathecal injection and its side effect
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Nervous system side effects have included convulsions, increased intracranial pressure with papilledema, vertigo, myalgia, arthralgia, malaise, headache, hiccups, and psychic disturbances.[
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I am writing an essay about the cognitive process associated with the development of dementia. Previous research states that dementia can be predicted 1-13yrs before diagnosis, is this also applicable to frontotemporal dementia?
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The best way to differentiate frontal dementias from temporal dementias is to look at neuropsychological tests of executive function and the results of functional imaging studies that measure regional cerebral blood flow.   Anomia is more common in Alzheimer's disease than in FTD, while behavioral problems indicative of a lack of frontal inhibition are more common in FTD than in AD.
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I am investigating motor control in people with cerebral palsy and the only measurement of functioning is the ADL Ashworth Scale (Bohannon and Smith, 1987) but this does not really cover patients motor control. Has anyone developed a more objective measure of motor control which does not necessary include spasticity or daily living? Specifically regarding coordinated movement for a targeted goal (e.g. moving a joystick to hit a target on a screen or picking up an object). If so how reliable are they?
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Hi Nicholas, 
I have to say I am biased as I have spent quite a bit of time developing upper extremity assessments. From all our work it the field it I came to the conclusion you can break the field of assessing motor control into two streams. One is to look at the movement, and the other is to look a functional outcomes. If your interest is Upper Extremity motor function I would advise you to consider functional outcomes.  In CP I have seen various people try to use validated standardized stroke assessments (like the Fugl Meyer Assessment) http://www.archives-pmr.org/article/S0003-9993%2809%2900484-5/abstract ,
In Dr. Prochazka's Lab we were first to automate a workstation to assess hand function, this followed by a number of interesting developments in the field such as QUEST on the robotic side developed by the Hogan group, or the AUTOCite by Peter Lum and Dr. Taub .
My personal input into this field is that I am not a huge proponent of biometric assessments (administration of kinematic data is not easy to standardize across sites, can take quite a bit of setup time per patient, as well as clinical uptake seems very slow ).  Dr. Torres above makes very good suggestions but these types of assessments are typically poorly related to functional outcomes in stroke and CP (just because a stroke patient can move significantly faster, does not mean they can perform functional tasks better – this is clear in upper extremity not so in the lower extremity).
We have worked on  upper extremity functional assessments and developed the RAHFT (Rejoyce Automated Hand Function Test). It is a validated upper extremity function test in Stoke and SCI.
The RAHFT is entirely assessed by the software on a unique joystick specifically designed to replicate ADL's ( Activities of Daily Life) and as a result it does not suffer from typical subjective clinical assessments concerns (it is fully objective). These types of tests are very meaningful for assessing ADLs. What they lack however is very high specificity (Lets take an example of how well someone can write the letter a no tests exists to assess such a specific task). In all cases the biggest tradeoff for these types of tests is how much can be assessed in the time provided (a big concern is that patients get tired during the course of the test so they are more prone to fatigue playing a role – this is a serious concerns if your patients have spasticity). Many of these tests are designed to fit into a quick clinical assessment that can give you a snapshot into the users abilities, unlike wearable sensors that might track the persons movements over a long time.
In the end I think you will need to ask yourself if you are more interested in understanding how functional a person is or how normal their movements are.
Hope this helps, 
Jan
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Traumatic brain injury, even in its mildest form, is known to result in degenerative processes including demyelination and dysmyelination of the axons over time. The shearing and tearing of the axons (primary injury) due to the acceleration and deceleration force of high velocity impact would also normally trigger off the secondary injury cascades. This includes the synaptic deregulation, cell death and axonal degeneration.  
But how quickly does these processes start (especially the demyelination of the axons) in patients with mild TBI? I am of the opinion that it will take at least a few days or weeks before such degenerative process starts. What are your thoughts?
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Dear Timothy Shea,
The "miserable minority" are those patients with mild traumatic brain injury who continue to experience prolonged cognitive deficits even after months and years, way beyond the average cutoffs (which is about 3-6 months post trauma).
You were absolutely right that one should consider preexisting comorbidities/(maybe even age) factors and as well as neurobehavioral/ neuropsychiatric condition arising from the trauma that could adversely influence the cognitive performance of these patients. Having said that, there are many studies (Ref 1-5) that has proven that even when all these factors are accounted for, and removed from the analysis, these individuals continue to exhibit deficits in their neurocognitive functions. So what then would best explain these manifesting derangements/ impairments ?
One possible explanation may lie in the structural changes. Patients with visible injuries -complicated mild TBI (radiologically visible lesions  i.e hematoma, contusion, edema, etc) and the corresponding functional and cognitive deficits are findings that are widely accepted by scientific community. How about the wider group of mild TBI patients whose radiological findings are usually negative and discharged from the ED without even being seen by neurosurgeons and without any subsequent follow-ups? Does normal CT/ MRI in the acute stage means there isn't any injury to start with with?
Many advances imaging protocols have proven otherwise. Diffusion Tensor Imaging (DTI) studies (reference to which I will give at the end of this reply) for example are able to pick up changes to the microstructure like the axons or the white matter tracts which are usually missed by the CT/ conventional MRI sequences. Could these structural anomalies/injuries then  explain the neurocognitive impairments experienced by the "miserable minority"? I guess the answer would be affirmative (see ref 5-8). With all these new evidences of microstructural abnormalities (even at the earliest hours post trauma), we can no longer reject the patient experiences as purely psychogenic in origin, ensuring we do our due diligence. 
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For my masters in health research, I am exploring differences in factors seen as faciliators or barriers to return to work following acquired brain injury between professional/managerial and non professional/managerial jobs.
I feel I have made a novices blunder, as I am struggling to find a reference on which to base my incl/exclu criteria for professional/managerial jobs as the taxonomies i have come accross are based more on industry than career level.
I know that i want to compare careers that usually require higher level education and/ or where there is responsibility for managing others, but now Im questioning whether i should put these two catergories together.  My assumption  is that these jobs will have higher cognitive and interpersonal demands, but now I am questioning even that!  any thoughts/advice would be appreciated.
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According to the few studies and reports there is a big lack of reports in psychiatry and neurology, where medical errors and inappropriate prescribing are reported. In most countries worldwide there are no appropriate systems within health systems in terms of inappropriate prescribing detection and appropriate solutions. One of the most important question in this field is ... Who will protect patients from medical errors and inappropriate prescribing ... Clinical pharmacists and/or pharmacologists with practice in psychiatry, GPs, psychiatrists with practice with inappropriate prescribing or whole team, where all specialists will be included. On the end, it is very interesting that we do not have studies or reports on this topic in the most European countries.
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Hi Matej
The literature shows that the error rate in medication administration is about 10% (not counting errors in timing). That means about 500 errors each day for a hospital with 600 beds. The reporting rates run at 200 per year which is a tiny percentage. I have come to appreciate that it is better to concentrate on those errors that are reported than to expend energy on increasing the reporting rate. Much can be learned from each error and implementing a change to prevent the error will also prevent many of the other unreported ones. In my own hospital there is a committee dedicated to analysis of error reports and making corrective suggestions. There are two doctors, two nurses and two pharmacists. Each brings their own experience and perspective to the discussions. This could be extended to the problem of inappropriate prescribing. Multidisciplinary groups are ideal and it should be implemented through each discipline with reports back to the committee. An essential part of this kind of activity is to have the full support of the management.
Regards
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I see children who have ADHD, LD, or Autism Spectrum disorders, I usually share neurodevelopmental perspectives with parents. An 8 year old male, with early ADHD, now 8, diagnosed 2/15 with aggressive melanotic medulloblastoma,  metatstatic drops on the spine. 98% tumor removal by surgery. Any thoughts or research about embryonic factors that may suggest correlation of these two conditions?
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Thank you for the response, and the sharing of your professional experience
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There are thin lines amongst the three maladies. Could someone assist to define the gold standard in one's country in diagnosing any of such maladies thus making it easier to start treatment regime?
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Hi Howan - Indeed it is a misdiagnosis especially in the A & E context. Unless further investigated, the three "maladies" would have been known and treated easily.
Thank you Rose for pointing towards Howan's article, it is pretty enlightening indeed.
Dear Khaled, your comprehensive article on syncope and childhood epilepsy really impress me. Unfortunately, it is rare for it to be practised in my country owing to a simpler labelling of psychogenic, pseudosyncope or inorganic syncope a.k.a. psychiatric disorder. I wish it could be practised here (my country) - to be fair to all the "infected" patients.
Appreciate your kind input Muzammil - labelling and stigmatising patients without proper, elaborate or definitive PMH and others' observation is synonymous to finding them guilty without trial. Your input shed greater lights to those who are on the frontline (ED) in determining the thin line thus enabling the patients to be treated and accorded the respect they duly deserve.
Appreciate our camaraderie on this issues - thank you all.
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Today, I`ve seen a patient who has both MI and CVA at the same time! What are the possible pathophysiologic mechanisms?
what will we investigate?
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Today in our centre, a 40 year old man was admitted to cardiology department   for left sided chest pain, headache and neck pain. He had ST-T changes on  ECG. He was triaged  quickly for a coronary  angioram. Post- procedure he suffered deteriorating consciousness. CT head revealed central large subarachnoid haemorrhage. My colleagues had to reverse his heparin dosage given in angio. He was transferred for neurosurgical intervention
Learning lessons:-
History  taking and examination are very important. It is also common to find ST- T wave changes in subarachnoid haemorrhage.
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Basic concepts surrounding epilepsy in ancient Indian medicine were refined and developed during the Vedic period of 4500–1500 BC. In the Ayurvedic literature of Charaka Samhita (which dates to 400 BC—the oldest existing description of the complete Ayurvedic medical system), epilepsy is described as ‘apasmara’ which means ‘loss of consciousness’. The Charaka Samhita contains abundant references to all aspects of epilepsy including symptomatology, aetiology, diagnosis and treatment.
The ancient Indian medical system, Ayurveda, meaning science of life, is the oldest system of medicine in the world. Epilepsy is defined as Apasmara: apa, meaning negation or loss of; smara, meaning recollection or consciousness. Aura was recognized and was called Apasmara Poorva Roopa. A large number of symptoms indicative of aura were listed. Worthy of mention are subjective sensation of sounds, sensation of darkness, feeling of delusion, and dream-like state. An actual attack of Apasmara includes falling down; shaking of the hands, legs, and body; rolling up of the eyes; grinding of the teeth; and foaming at the mouth. Four major types of epilepsy based on the disturbance of doshas (humors) that govern the physiological and physiochemical activities of the body are mentioned. Apasmara is considered a dangerous disease that is chronic and difficult to treat. Several causes are mentioned. Treatment included correcting the etiological factors and dietary regimen and avoiding dangerous places that may result in injuries.
Ayurvedic Management of apasmara-
Removal of etiological factor-
1. Sanshodhan chikitsa
2. Bahi Parimarjana chikitsa
3. Shanshamana chikitsa
4. Vegakaalina chikitsa
5. Rasayana Chikitsa
6. Sattvavajaya chikitsa
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Does anyone know when it became common practice to divide the Glasgow Coma Scale into severe, moderate and mild? I only find references to the original article by Teasdale and Jennett from 1974, but the three levels of severity are not mentioned there.
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you're welcome
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Thanks in advance.
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TTP is accompanied by multiple micro-thrombi affecting the CNS and other end-organs. The neurological symptoms are often flirting and variable, occurring in 70-80% of cases. the features include headache, confusion, paresis, aphasia, dysarthria, encephalopathy and coma (in 10% of cases with CNS involvement). Plasmapharesis has improved outcome significantly, reducing mortality from 90% in pre-plasmapharesis era to 10% nowadays. Plasmapharesis does not result in permanent cure after stroke. there are other prognosticating factors like severity of infarction (size of infarct), co-morbidities, presence of early interventional strategies, etc.
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Chelators, i.e. trientine and penicillamine are regarded helpful in patients with Wilson's disease, given that they may stimulate the excretion of serum copper via the urine by elevating the serum free copper levels. In Wilson's disease patients, urinary copper content had already been dangerously increased as an indicator of raised serum free copper. Increasing this toxic level of copper paradoxically devastates the clinical situation of the treated patients and push them into hemolysis or death! However, there is a chance of improvement, in case of passing the so called "copper depletion" phase, and many patients do depending on their severity of clinical situations. There is a big question mark in front of the question whether shouldn't we rationally aim at normalization of the raised serum free copper values when there is no well-designed randomized clinical trial in the field and based on the available evidence, zinc therapy can safely and effectively suffice this?
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What about hemodilaysis using chelating agents?
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Dear Colleagues, there is a 67 year old female patient with focal edema of frontal, parietal and temporal right side cerebral lobes, with slight dislocation of median brain structures on MRI, no enhancing contrast regions. Sick for 1,5 months, symptoms: fatigue, slight ataxia, slow thinking, no headache. Exam: slowliness of all types actions. No signs of compromised immunological status, no signs of infections. MRI performed twice: 25 september and 20 october, looks almost the same. Some ideas? thank you!
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Dear Dr. Olga! I'm agree with previous comments toward bad resolution of this images. As for me, I believe, that MRI with contrast is needed. Why you didn't use USD for brain vessels conditions and hydrodynamic conflict. Probably you have the local cerebral venous stasis. Perhaps after light brain trauma with slowly progressive posttraumatic amnesia. More about this investigations - http://angio-veritas.com/technologies/uzd-diahnostyka-sudyn-mozku-v-psyhonevrolohiji/?lang=en&lang=en
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I would like to administer a drug centrally into a specific brain region and then look at activation of neurons in this same region as a result via IHC staining for cFOS. However, because there may be some tissue damage due to the cannula implantation, I am wondering if staining will be an option. Anyone have any ideas?
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Sly, D J, M J McKinley, and B J Oldfield. 2001. “Activation of Kidney-Directed Neurons in the Lamina Terminalis by Alterations in Body Fluid Balance..” American Journal of Physiology. Regulatory, Integrative and Comparative Physiology 281 (5): R1637–46.
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Treatment options? Rate of progression? long term prognosis?
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The CANVAS approach model is critisiced by the effectivenes, but povides human contact therapist-patient . surely we nedded for more studies regarding the effectiveness
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The patient is 35 years old, only 4th grade of academic studies. History of alcohol and cocaine consumption. The stroke was right insulotemporoparietal. What neuropsychological tests may be appropiate for the evaluation of this patient?
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Right insulotemporal lesions may also result in changes in behavior (e.g. apathy), modification of speech prosody (e.g. flat intonation) and difficulty in detecting the emotional connotation of speech (e.g. anger, happiness). You may also want to administer a questionnaire regarding evidence of apathetic/dishinbited behavior (e.g. the FBI-Q) and present some speech samples (even short sentences) and ask the patient to identify the emotional connotation associated with each of them.
Complex problem solving and conceptual flexibility may also be affected, as already suggested, and one additional test you could administer would be the Wisconsin Card Sorting Test (although not sure if appropriate given the limited education).
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I've been thinking a lot lately about the overlap between synesthesia and schizophrenia as some characteristics of the two are quite similar (hyper-associative thinking, hypersensitivity, etc.). I'm aware that synesthesia is not a mental disorder but reading through case reports of patients with diagnosed schizophrenia, several of them also mention synesthetic experiences.
For example, when looking at the two conditions, the following research findings suggest to me a certain correlation, proneness, or similarity between the two:
- synesthetes who experience colour sensations in response to colour-neutral stimuli show increased positive and disorganized schizotypy (http://discovery.ucl.ac.uk/1314590/1/1314590.pdf)
- increased intensity of perceptual experiences or hypersensitivity can be used as in indicator of schizophrenia
Other aspects that might indicate a link between the two are vivid imagination and strong ability to form mental images/sounds/sensations/etc., increased daydreaming, etc.
Does anyone know of other similarities between the two (particularly with regard to brain structure & function) and to what extent synesthesia can become pathological?
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Any condition that causes those experiencing it distress can become a pathology or the cause of a pathology. This 'condition' synesthesia is a perception based experience and is not a pathology in itself. Creative people tend to think in these patterns and it is possible to train the mind to do this.
The most common, if not necessarily adequate way to define pathology in thought processes is where those processes cause harm to the person afflicted or if the thoughts (delusions and hallucinations) are outside the range of human experience and distressing.
Synesthesia is far more common than schizophrenia and that in itself is an indicator that it should not be considered a disease but more of a variant in human thought processes. As ever we should be ultra vigilant against pathologising different thought processes as if there is a standard model that we all should adhere to.
The human mind is a wonderful thing and should not be regimented into normal and abnormal (healthy and diseased) . Some of the greats in human history thought 'differently' to the majority.
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Are there any interactions between serotonin and dopamine in the human brain? Does serotonin up- or down-regulate dopamine? Also does dopamine modulate serotonin?
In which brain networks / pathways / regions do they interact positively and in which, do they interact negatively (if there are any interactions)?
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From a grant application I submitted a while ago (based on mostly rat studies, and a few studies with humans):
DA/5-HT interaction can be conceptualized on a system and on a neuronal level. On the neuro-anatomical level, 5-HT neurons in the raphe nuclei project to DA neurons in the VTA and substantia nigra, as well as to their targets in striatum and the PFC. The clearest evidence for the influence of 5-HT on DA signaling is that lesion of the raphe nuclei leads to increased levels of DA in the striatum and to decreased DA levels in the PFC 31. This superficially straight forward picture is complicated by the complexity of 5-HT receptor influence on DA signaling, which resists a simple association of receptor type and excitatory or inhibitory function10. While the raphe nuclei also receive projections from the VTA32, projections from DA neurons to 5-HT neurons and their targets are comparatively less developed. Consistently, reports of DA influence on 5-HT function are rare, though it has been shown that stress induced changes in 5-HT signaling required an intact DA neurotransmission in the nucleus accumbens33.
On the system level, DA/5-HT interaction is thought to be involved in adaptive behavior by signaling the long-term average rewards and the value of currently available actions. More specifically, Cools and colleagues hypothesize that tonic DA and 5-HT levels signal average reward and punishment, respectively, obtained when performing an instrumental task11. These expectations are crucial for adaptive behavior because they are the basis for the evaluation of current outcomes and because net outcome expectations (average rewards – average punishments) are thought to deter-mine response vigor/inhibition10. Intuitively, the DA/5-HT interaction is thought to calibrate out-come evaluation by providing a yardstick against which outcomes can be evaluated, and by strengthening approach or avoidance behavior depending on reward expectations.
The system level DA/5-HT interaction is also apparent in a number of patient studies. For in-stance, L-Dopa medication of Parkinson’s disease can induce psychosis, and in the area of decision making increased risk taking and impulsivity by biasing the system towards stronger response vigor (due to increased tonic DA levels) and overestimation of action values (due to stronger positive prediction errors). Interestingly, selective serotonin reuptake inhibitors and the 5-HT precursor L-Tryptophan can alleviate these undesired side effects34, supporting the view that 5-HT modulates DA action. Further evidence for DA/5-HT interaction comes from a study of combined tryptophan and tyrosine depletion, which found that tryptophan and tyrosine depletion individually reduced interference in the Stroop task, but a combined depletion did not35. In animal experiments, Winstanley et al12 investigated delay aversion after modulating both nucleus accumbens DA/NA and 5-HT neurotransmission and found that either manipulation alone had a small (if any) effect on behavior, whereas a combined manipulation shows the largest effect.
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A 25 year old man presented with an acute spinal cord syndrome. Symptoms progressed within hours starting with fluctuating hypaethesia and paresis of the right arm. After 4-5 hours patient had tetraplegia and respiratory insufficiency. After initial imaging of brain and spinal cord as well as lumbar puncture were without any pathological findings, repeated imaging confirmed a myelitis from C1 to Th1. Lumbar puncture showed 80 lymphos. We found no evidence of a (para)infectious cause, only Ana/Anti-Ro was elevated as hint for systemic autoimmune disease. Anti-AQP was negative, visual evoked potentials on intensive care unit were not conclusive.
Patient was treated with high dose methylprednisolone and plasma exchange. Which additional chemotherapeutic treatment would you suggest?
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Thanks for the answers so long:
@Yoshiyuki: spinal infarction was unlikely due to the very high spinal chord syndrome, but furthermore Imaging was highly atypical, as well as CSF analysis would not fit. Nevertheless we ruled out aortic dissection.
@Marta:
- Presence of spinal cord inflammation YES
- CSF pleocytosis YES (but rather high)
- elevated CSF IgG index YES
- gadolinium enhancement on a spinal MRI YES
- Absence of an identified CNS infection YES
- Exclusion of acute myelopathy secondary to a known underlying disease YES (only Ana/Anti-Ro was positive)
- ...spinal cord infarct and compressive myelopathies YES
@M. Houman: good answer this was one of the options we considered...
This is what J.Birnbaum from J. Hopkins answered:
...my preference for a patient who is so severely ill and has eminent jeopardy of diaphragmatic function is to treat with IV Cytoxan initially at 750mg/m2, and with monthly doses continued for 3-6 months with judicious tapering and adjustments depending on side-effects. Subsequently, oral steroid-sparing therapy wtih cellcept, 2 to 3 grams per day.
In our SLE patients, risk for relapse is Ro antibodies and NMO IgG antibodies. The presence of background rheumatic disease is an overall risk, and if the patient has anti-Ro/SS-A antibodies should ideally also undergo a lip biopsy to confirm Sjogren'ns syndrome .
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I would like to know the frequency (percentage) of each location (periventricular, cerebellar, spinal, etc).
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Looking for human or animal model evidence of neuronal/physical damage to assess the impact of poorly controlled partial onset seizures.
The clinical motto is always that one seizure is a seizure too many, but is there any physical pointer for this? I find this crucial to evaluate the burden of AED polytherapy on patients and the importance of trying new therapies in unsatisfactorily controlled patients.
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1: Fuerst D, Shah J, Shah A, Watson C. Hippocampal sclerosis is a progressive
disorder: a longitudinal volumetric MRI study. Ann Neurol. 2003 Mar;53(3):413-6.
PubMed PMID: 12601713.
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I would like to get your opinions on a patient that I have recently received. The patient is a 49 year old female. She is a known case of essential tremors for the past 35 years (positive family history of tremors, MRI and CT from a few months back completely normal). In the past four months, she has started experiencing an exacerbation of her tremors, which has started interfering with her activities of daily living. The tremors were originally only in both of her hands, however in the past 4 months, they have involved the entire upper and lower limbs, the head, tongue, lips and she has started having voice tremors as well. Along with this, in the past 2 months she has developed intense proximal muscle weakness (can't stand after sitting, can't climb stairs). When her proximal muscles are supported, the tremors seem to improve considerably and almost become lessened to the condition she was in before the acute exacerbation 4 months. This probably points that her proximal muscle weakness is responsible for some of the exacerbation of the limb tremors but still doesn't explain the head, voice, tongue and lips tremors. She is also a diabetic with well-controlled blood glucose levels, including HbA1c levels and her thyroid function tests are normal. She was started on Propranolol and is currently taking it in doses of 120 mg/day with significant improvement in tremors but not complete resolution. The patient is worried about her continuously worsening whole body tremors and proximal muscle weakness. Her reflexes are normal and power is 4 minus in the limbs. What possible differential diagnoses would you consider and how would you investigate her initially? Could this possibly be a dietary deficiency (since the patient has been trying to lose weight with on and off diet plans for several years)? Would you recommend any immediate treatment steps?
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Dear Haider,
I definitely suggest to perform an electromyographic examination. The recent strength reduction should be investigated, it could be due to a diabetic neuropathy. Also a lumbar plessopathy in diabetes is described ('can't stand after sitting, can't climb stairs'). I see that this does not explain all the complaints, but could provide more insight to find an explanation.
Best regards,
Piero
  • asked a question related to Clinical Neurology
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Actually I'm working on the spasticity measurement, and searching literature/ prior art for the same. I would be happy, if someone can provide me the following information:
1. What are the different types of spasticity and in which part of the body is it most prevalent?
2. What are the current measurement system that you have adopted during spastic measurement / rehabilitation, apart from MAS/Tardieu and any other manual analytical scales?
3. What is the difference between spastic stretch reflex and parkinson's rigidity reflex?
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Hi,
I am coming from the PD side of things too, but I can explain the difference between spasticity and parkinsonian rigor.
As opposed to rigor, spasticity is dynamic and increases with muscle elongation. Spasticity is associated with upper motor neuron lesions. Hence, the lower motor neuron pathways are intact and the muscles reflex arc works without control from higher order structures. This leads to the mentioned stretch reflex.
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