Questions related to Clinical Neurology
I always hear about some myths in neurology, and mostly about stroke but I want to know what myths other diseases have.
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.
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!
I'm looking for a simple scale, that evaluate children motor handicap in general, not specific to only one affection.
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 )
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.
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).
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
Verapamil, A calcium channel blocker is used for prophylaxis of cluster headache. Verapamil is a vasodilator. What is its mechanism in preventing headache ?
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
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.
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?
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.
It seems we have no treatment disease-modifying for PD.
That's been supposed for rasagiline, but no scientific evidence so far
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.
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?
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?
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.
olfactory, sleep disorder, orthostatic hypotension, excessive saliva, constipation, vision problems, gastrointestinal problems
subcortical aphasia and recovery pattern ( especially in patients with CAPSULO GANGLIONIC BLEEED)
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.
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
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 ?,
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.
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.
Dr. Grandhi V Ramalingayya
male patient following botox for blepharospasm , now having fatiguable ptosis..
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?
I understand that neuroleptics block dopaminergic transmission. However I don't really understand the mechanism behind how it can cause movement disorders.
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.
Grandhi V Ramalingayya
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.
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?
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?
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????
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?
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?
can any one give me a drug or chemical can be used in induction of neuropathic pain (mice) either than chemotherapeutic agents or Suramin?
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
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?
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).
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...
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?
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?
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?
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.
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.
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?
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?
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.
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?
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?
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?
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)
- synesthetes are more susceptible to mental disorders (http://archpsyc.jamanetwork.com/article.aspx?articleid=491098, http://hms.harvard.edu/news/harvard-medicine/uncommon-sense)
- various links between creativity and synesthesia (http://www.tandfonline.com/doi/abs/10.1207/s15326934crj1001_1#.U5lcKvmSzfI), creativity and schizophrenia (http://scholar.google.de/scholar?q=schizophrenia+creativity&btnG=&hl=en&as_sdt=0%2C5&as_vis=1)
- increased intensity of perceptual experiences or hypersensitivity can be used as in indicator of schizophrenia
- strong visual imagery (http://www.sciencedirect.com/science/article/pii/S1053810007000566)
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?
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)?
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?
I would like to know the frequency (percentage) of each location (periventricular, cerebellar, spinal, etc).
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.
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?
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?
I had a patient, female 43 years old. Her headache has lasted for 6 years diagnosed as a migraine headache.the brain MRI and lab data was normal. her headache is triggered by eating foods especially foods containing lipids and relieved by drinking sour tasted liquids and none of medicines in migraine is effective.
Recently a 65 year old patient was brought by ambulance to our ER with 90 min of new hemiplegia and aphasia without any identification and inability to tell her name. No contraindications were identified on physical exam and CT but impossible to exclude. Would you give IV thrombolysis?