Hi everyone,
I'm currently a PTA (physical therapy assistant) student in an Intro to neurology course, I was just wondering whether someone could give me a general guide to UMN vs LMN lesions. My understanding as it stand consists of:
The Upper Motor Neuron Lesions:
- Occurs in the CNS
- Result in high muscle tone (hypertonicity):
> Including Rigidity, such as lead pipe rigidity, cogwheel rigidity, Spasticity (clasp knife), and they are velocity dependent
- Voluntary muscle movements:
> Synergy between muscle groups
- Reflexes:
> Clonus, positive Babinski, Hyper reflexive, exaggerated cutaneous response
The Lower motor Neuron Lesions:
- Occurs in the PNS
- Results in low muscle tone:
> Flaccidity, not velocity dependent
- Voluntary muscle movements:
> Weak or absent
-Reflexes:
> Hypo reflexive, and decreased cutaneous sensitivity
P.S. I am 19 y/o sophomore, undergrad, and would appreciate any tips from anyone that's a health care practitioner, I appreciate all the help I can get
Hi everyone,
big neuroanatomy exam in a few days, would love it if someone could explain this concept to me in a simple fashion. I just can't grasp this idea of below, above, or at the level of lesions which annoys me. Also any tips for the exam would be great!
Thank you
I've been revising for my med school exams and found that patients with cerebellar lesions present with decreased tone and reduced/absent reflexes. These are both symptoms of damage to lower motor neurones yet the cerebellum is in the brain. Shouldn't these patients present with increased tone and hyperreflexia?
Upper motor neuron lesion can cause spastic paralysis. Lower motor neuron lesions can cause flaccid paralysis. A stroke is considered as a upper motor lesion.
If this is correct, how is it then that flaccid paralysis can be manifested after a stroke?
The flaccid paralysis could initially be explained by spinal chock, and would then later on turn into a spastic paralysis. But some stroke patients, as i understand it, does not regain function of the affected limb even after many years.
This is something me and my SO haven't been able to get our minds around for quite some time now and would really appreciate an answer from you educated redditors at meddit.
51F, 5’9, thin, white, USA. never-smoker, non-drinker; no prescriptions; unintended weight loss of now 28lbs since January, oxygen desats started in January w/ exertion, suddenly worsening in the past few weeks, worse every day - now on continuous oxygen. Several new-onset symptoms the past month - among other things, her neurologist says bulbar weakness and upper and lower motor neuron signs (see below). Reposted bc it got buried last time. X-post for visibility.
I’ve posted here and on other med subs for advice on my mom for awhile now. I hope everyone that’s seen it knows how grateful I am (and my mom is too!) for all the help. Things seem to have gotten FUBAR quickly at this point and we find ourselves in a totally unexpected situation.
In addition to mom’s chronic respiratory failure (now on continuous oxygen - (she can't even stand up without it plummeting), she began having alarming symptoms a few weeks ago: towards the end of the day - late afternoon/evening - her speech becomes slurred, slower, and her voice volume gets very quiet - she can’t talk much because it wears her out.
Additionally, starting in the late afternoon and evenings she has a hard time keeping her head upright and she begins drooling constantly, and has to have a towel with her.
She didn’t think much of it at first, was so focused on the oxygen she thought she was just fatigued. But now it’s getting obvious to everyone around her.
Her pulmonologist said he thought that it could be respiratory muscle weakness causing her problems and ordered her a PFT with MIP and MEP (done) and a sniff test day after tomorrow.
PFT in January was normal. This one was not. DLCO down, and MEP is at 40% predicted.
Same day she coincidentally had a follow up with her neurologist she has seen for past cervical spine issues. After explaining new symptoms she did a full neuro exam. Neuro verbatim said she was “extremely concerned” (Bulbar weakness, signs of both upper and lower motor neuron disease); neurologist sent an urgent referral to a neuromuscular disease specialist who happens to be in one of the best medical centers in the country (we are so blessed to live here).
They called the very next day and set her up for a back-to-back, 7am to 5pm both days 2 day evaluation next week. We looked up the doctor’s name and were shocked to see it’s with the director of the ALS Clinic in the medical center here! We were floored.
**Does this mean it’s likely mom has ALS? Do any other of the motor
... keep reading on reddit ➡Posting on behalf of Dr. Jarod Carter:
We need help with connections to brilliant minds with a clinical/research focus on motor neuron regeneration. More specifically, anyone with knowledge or experience working with “LOWER Motor Neuron” therapies. Our 1 year old twins, Gray and Adelaide, were diagnosed with Spinal Muscular Atrophy, Type 1. The progress that they have made in the past few months has been nothing short of incredible. The primary focus of nearly all research and therapies for spinal muscular atrophy so far has, understandably, been on stopping the nerve damage. Between Spinraza and Zolgensma (gene therapy), we’ve acquired all we can to protect their nerves from the effects of SMA. So now my focus has shifted to how we can reverse the damage that has occurred and regenerate their motor nerves ...
We know it’s been a long-held belief that once a lower motor neuron dies, it can’t be replaced or regenerated … NONSENSE! We just haven’t figured it out yet. Plenty of long-held beliefs in medicine have been completely disproven and this one will be as well. 50 years from now the statement that these motor neurons can’t be regenerated/replaced will be laughable … We want that statement to be laughable in 5 years or less.
For that, We need to connect with those around the world who are already leading the research in this area, and I’m hoping you all can help me make those connections quickly … please share this post or send it via DM to ANYONE who may be involved in this area of research/clinical application, OR Anyone who may know someone who is. Please tag us in any replies, or better yet, send a DM if you’d like to be a part helping millions around the world who suffer from nerve damage.
Sifting through thousands of research articles and trying to figure out what’s most relevant and who is truly leading the world in this area has proven more daunting and slow-moving than I expected, and I’m guessing social media will be a much faster route.
Some important details …
This is very different than regeneration of neurons in the brain… we’re looking to regenerate/replace lower motor neurons.
Also, there are some exciting things happening with stem cells and e-stim for Spinal Cord injuries, but with SMA/neuromuscular syndromes, the damage is very diffuse throughout the entire spine rather than one specific area of damage. Stem cell delivery methods of open surgical injection can work for spinal cord injuries but not for damage throughout the
... keep reading on reddit ➡
UMN deficits cause hyperreflexia, spastic paralysis etc while LMN deficits result in flaccid paralysis, weakness, loss of reflexes and tone etc....Can someone help describe how an ALS patient would present with both types of deficits? Or are LMN deficits followed by UMN deficits (or vice versa) in a sequential manner? As a third option...is the order of presentation of ALS symptoms more or less specific to each case?
So, long story short — years ago when I was 21 or 22 I was started having random dysphagia. Like oral phase, literally overnight. Neurologists cleared me, but I did get scoped by a GI doctor who did say I had acid reflux/hiatal hernia. However, I was never prescribed anything long term and it seemed like there was no concern. I was only given short term omeprazole.
Over the years I’ve always had this “dysphagia”. It gets exacerbated by stress and anxiety/OCD that I’ve had my whole life, so I just assumed it was psychosomatic - especially since it seems like I forget how to and/or coordinate a swallow. Skip to last week (a heavy period of anxiety and stress preceding) and I start getting a tickle in my throat and issues with my own saliva. For the last 5-7 days it has been a feeling of something in the back of my throat (like the airway) almost like saliva tickling. I don’t have a cough reflex triggered, but I can’t help but clear my throat or force myself to cough to try and bring something up. I’ve even noticed or perceived my voice to be gurgly or wet, but everyone I know has denied it. Last night specifically I felt like I was drowning and had a panic attack. Like no matter how much I swallowed there was what felt like an insane amount of saliva in the back of my throat. Now I feel like I’m throat clearing after drinking fluids, eating — just pretty constant throughout the day. I have also noticed that if I go to take a deep breath, I feel like I can’t do it fully, if that makes sense.
I’m still worried maybe it’s neurological, but I’m also getting stomach pressure so it feels like maybe it is acid related. On top of this, I’ve had awful congestion and seasonal allergies.
Apologize for the long winded post, but it’s just been a rough go lately. I feel like I can’t even properly celebrate Christmas due to this. I did however set up a GI appointment (won’t see until February) and am starting therapy in a couple of weeks. Hope to see an ENT as well. At this point if it’s not MND, I’m expecting Barrett’s esophagus. I’m only 27, but I know it’s possible.
I'm writing a paper on ALS for a class. (Grad student in Speech and Language Pathology). I know very little about ALS and most of the articles I'm finding are so technical that I think I need some basic knowledge before I start researching specifics. From what I understand, ALS attacks upper and lower motor neurons, but I'm not sure exactly what the difference is between the two. So... any experts?
I’m having lower right quadrant pain off and on for the last week accompanied by a lot of gas. I just saw my Endo specialist and had an ultrasound and there are no visible lesions or endometriomas. I had extensive excision for stage 4 in August. No fever, no nausea, no diarrhea, some constipation but things are moving. Laying on my right side makes it more uncomfortable. It’s not super painful, just annoying and kind of feels like when I first felt my endometrioma that something was there kind of where my right ovary is. I was just wondering if this sounds familiar to any of you? It’s been less than a year since they suspected endo and since excision things have been SO much better. I’m just wondering if this sounds like flares you describe? I’m not on any meds to try and treat or slow regrowth yet because dim TTC. TIA!
I posted this yesterday but it was instantly deleted and doesn't seem to be getting a review... Not sure if this will work:
I was reading a passage in my textbook and the author mentioned a "motor field" while talking about the frontal eye fields. I think I know what a neuron's visual field is but a motor field is vague without any explanation. What is it?
Upper motor neuron lesion can cause spastic paralysis. Lower motor neuron lesions can cause flaccid paralysis. A stroke is considered as a upper motor lesion.
If this is correct, how is it then that flaccid paralysis can be manifested after a stroke?
The flaccid paralysis could initially be explained by spinal chock, and would then later on turn into a spastic paralysis. But some stroke patients, as i understand it, does not regain function of the affected limb even after many years.
This is something me and my SO haven't been able to get our minds around for quite some time now and would really appreciate an answer from you educated redditors at meddit.
Posting on behalf of Dr. Jarod Carter:
We need help with connections to brilliant minds with a clinical/research focus on motor neuron regeneration. More specifically, anyone with knowledge or experience working with “LOWER Motor Neuron” therapies. Our 1 year old twins, Gray and Adelaide, were diagnosed with Spinal Muscular Atrophy, Type 1. The progress that they have made in the past few months has been nothing short of incredible. The primary focus of nearly all research and therapies for spinal muscular atrophy so far has, understandably, been on stopping the nerve damage. Between Spinraza and Zolgensma (gene therapy), we’ve acquired all we can to protect their nerves from the effects of SMA. So now my focus has shifted to how we can reverse the damage that has occurred and regenerate their motor nerves ...
We know it’s been a long-held belief that once a lower motor neuron dies, it can’t be replaced or regenerated … NONSENSE! We just haven’t figured it out yet. Plenty of long-held beliefs in medicine have been completely disproven and this one will be as well. 50 years from now the statement that these motor neurons can’t be regenerated/replaced will be laughable … We want that statement to be laughable in 5 years or less.
For that, We need to connect with those around the world who are already leading the research in this area, and I’m hoping you all can help me make those connections quickly … please share this post or send it via DM to ANYONE who may be involved in this area of research/clinical application, OR Anyone who may know someone who is. Please tag us in any replies, or better yet, send a DM if you’d like to be a part helping millions around the world who suffer from nerve damage.
Sifting through thousands of research articles and trying to figure out what’s most relevant and who is truly leading the world in this area has proven more daunting and slow-moving than I expected, and I’m guessing social media will be a much faster route.
Some important details …
This is very different than regeneration of neurons in the brain… we’re looking to regenerate/replace lower motor neurons.
Also, there are some exciting things happening with stem cells and e-stim for Spinal Cord injuries, but with SMA/neuromuscular syndromes, the damage is very diffuse throughout the entire spine rather than one specific area of damage. Stem cell delivery methods of open surgical injection can work for spinal cord injuries but not for damage throughout the
... keep reading on reddit ➡