neurological deficits

2

Phineas Gage is one of the most famous patients in the history of neuroscience. He was 25 years old when he experienced a serious accident at his work place, where a tamping iron was shot through his head - entering under his eye socket at exiting through the top of his head - after an explosive charge went off. The tamping iron was over a metre long, and after exiting Gage’s head landed 25m away. 

Initially Gage collapsed and went into minor convlusions, but recovered quickly and was able to speak after a few minutes. He walked with little assistance to an ox-cart and was brought to a nearby physician. Initially the physician did not believe his story because he was in such good condition, but was convinced when: 

Mr. G. got up and vomited; the effort of vomiting pressed out about half a teacupful of the brain, which fell upon the floor.

Gage exhibited a number of dramatic behavioural changes following the accident. Harlow, the physician who initially treated Gage, described this change “He is fitful, irreverent, indulging at times in the grossest profanity (which was not pre­vi­ous­ly his custom), manifesting but little deference for his fellows, impatient of restraint or advice when it conflicts with his desires”. However the surgeon Henry Jacob Bigelow described his condition as improving over the course of recovery, stated he was “quite recovered in faculties of body and mind”. This may have been early evidence of neural plasticity. This recovery was also reported by a physician who knew Gage while he lived in Chile, who described his ability to hold on a full time job as a Concord coach driver, a job that required exceptional social skills.

Gage’s neurological deficits following his traumatic brain injury is thought to have been exaggerated and distorted over the course of history, to the point that he is often portrayed as a ‘psychopath’. Scientific analysis of the historical accounts of Gage’s life following his accident, namely by the psychologist Malcolm Macmillan, find that these distorted accounts are most likely untrue, and that Gage made a very good recovery.

Post-mortem analysis of the Gage case concluded that it was the left frontal lobe that was damaged in the accident, although further neurological damage may have resulted from infection. Combined examination of the Phineas Gage case with the other famous cases of Tan and H.M. have concluded that social behaviour, memory, and language are dependent on the co-ordination of a number of different brain areas rather than a single region.

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Middle aged man, walking with an open pocket knife, trips on a wire, and inadvertently impale himself with the knife. Alert, oriented, no neurological deficits, small amount of venous bleeding (blood in the picture is clotted). Trauma system entry straight to OR. The knife was found to be penetrating 13 mm into the temporal lobe. Missed any major structures and vasculature. 45 minute surgery. Got to see him the day after, and he is walking, talking, absolutely no neurological deficits. He is one lucky son of a bitch.

Supporting the damaged brain

A new study shows that embryonic nerve cells can functionally integrate into local neural networks when transplanted into damaged areas of the visual cortex of adult mice.

(Image caption: Neuronal transplants (blue) connect with host neurons (yellow) in the adult mouse brain in a highly specific manner, rebuilding neural networks lost upon injury. Credit: Sofia Grade, LMU/Helmholtz Zentrum München)

When it comes to recovering from insult, the adult human brain has very little ability to compensate for nerve-cell loss. Biomedical researchers and clinicians are therefore exploring the possibility of using transplanted nerve cells to replace neurons that have been irreparably damaged as a result of trauma or disease. Previous studies have suggested there is potential to remedy at least some of the clinical symptoms resulting from acquired brain disease through the transplantation of fetal nerve cells into damaged neuronal networks. However, it is not clear whether transplanted intact neurons can be sufficiently integrated to result in restored function of the lesioned network. Now researchers based at LMU Munich, the Max Planck Institute for Neurobiology in Martinsried and the Helmholtz Zentrum München have demonstrated that, in mice, transplanted embryonic nerve cells can indeed be incorporated into an existing network in such a way that they correctly carry out the tasks performed by the damaged cells originally found in that position. Such work is of importance in the potential treatment of all acquired brain disease including neurodegenerative illnesses such as Alzheimer‘s or Parkinson’s disease, as well as strokes and trauma, given each disease state leads to the large-scale, irreversible loss of nerve cells and the acquisition of a what is usually a lifelong neurological deficit for the affected person.

In the study published in Nature, researchers of the Ludwig Maximilians University Munich, the Max Planck Institute of Neurobiology, and the Helmholtz Zentrum München have specifically asked whether transplanted embryonic nerve cells can functionally integrate into the visual cortex of adult mice. “This region of the brain is ideal for such experiments,” says Magdalena Götz, joint leader of the study together with Mark Hübener. Hübener is a specialist in the structure and function of the mouse visual cortex in Professor Tobias Bonhoeffer’s Department (Synapses – Circuits – Plasticity) at the MPI for Neurobiology. As Hübener explains, “we know so much about the functions of the nerve cells in this region and the connections between them that we can readily assess whether the implanted nerve cells actually perform the tasks normally carried out by the network.” In their experiments, the team transplanted embryonic nerve cells from the cerebral cortex into lesioned areas of the visual cortex of adult mice. Over the course of the following weeks and months, they monitored the behavior of the implanted, immature neurons by means of two-photon microscopy to ascertain whether they differentiated into so-called pyramidal cells, a cell type normally found in the area of interest. “The very fact that the cells survived and continued to develop was very encouraging,” Hübener remarks. “But things got really exciting when we took a closer look at the electrical activity of the transplanted cells.” In their joint study, PhD student Susanne Falkner and Postdoc Sofia Grade were able to show that the new cells formed the synaptic connections that neurons in their position in the network would normally make, and that they responded to visual stimuli.

The team then went on to characterize, for the first time, the broader pattern of connections made by the transplanted neurons. Astonishingly, they found that pyramidal cells derived from the transplanted immature neurons formed functional connections with the appropriate nerve cells all over the brain. In other words, they received precisely the same inputs as their predecessors in the network. In addition, they were able to process that information and pass it on to the downstream neurons which had also differentiated in the correct manner. “These findings demonstrate that the implanted nerve cells have integrated with high precision into a neuronal network into which, under normal conditions, new nerve cells would never have been incorporated,” explains Götz, whose work at the Helmholtz Zentrum and at LMU focuses on finding ways to replace lost neurons in the central nervous system. The new study reveals that immature neurons are capable of correctly responding to differentiation signals in the adult mammalian brain and can close functional gaps in an existing neural network.

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Atlanto-axial Subluxation

Atlas - First Cervical Vertebrae 

Axis - Second Cervical Vertebrae

Atlanto-Axial Joint - The joint between the 1st and 2nd Cervical Vertebrae

This joint is unique compared to other vertebrae joints, in that there is no disc between the atlas and axis. Instead it is supported and stabilised by ligaments. The main purpose of this joint is to enable the patient to move their head from side to side. 

What is a AA subluxation?

AA subluxation is essentially a disruption in the alignment of the Atlas and Axis. This means that the joint becomes unstable and results in excessive movement of the neck.

What problems does this cause?

As a result of this type of subluxation the nerves that form the spinal cord, which runs through the vertebral column can become compressed resulting in neurological deficits and neck pain.

How does it occur?

Trauma to the neck such as forced flexion of the head causing ligament/vertebrae damage can result in this condition. However, it is often congenital and usually arises from an abnormality in the Axis either due to a issue with the supporting ligaments or because the Dens ( a projection of the Axis that fits with the Atlas) is malformed or absent. 

How common is this congenital abnormality?

This type of abnormality is most common in toy breeds such as: Yorkshire Terriers, Chihuahua’s, Pomeranians and Pekingese. It usually occurs within the first year of life.

What are the symptoms?

Neck pain - yelping and crying when lifted or touched in the neck/head region

Ridgity of the neck - A reluctance to flex the neck or move, eat and drink

Paraparesis/Paresis - Resulting in the patient being anything from non-ambulatory or ataxic

How is the condition diagnosed?

Radiographs - Lateral, Ventro-dorsal and Oblique views are recommended.

MRI - This will allow assessment of spinal cord damage. 

CT - This will allow visualisation of bone deformity in regards to the vertebrae. 

What are the treatment options?

Conservative - Often only offered to patients with mild clinical signs. It includes cage rest for 4-6 weeks and often the patients are put in a neck brace for this time to allow fibrous scar tissue to form and stabilise the joint. 

Surgical - The main aims of surgery are to relieve compression of the spinal cord and stabilise the joint permanently. If the dens is malformed or damaged, it may have to be removed. The recommended surgical approach is ventrally, as it allows arthrodesis (fusion) of the atlanto-axial joint. A cancellous bone graft is placed in the joint and pins or screws are placed across the joints. A head brace is then put in place and should remain on for 4-6weeks.

Nursing considerations

Avoid flexion of the neck - this will cause further compression of the spinal cord and may result in severe neurological issues.

Gentle Physiotherapy - Often these patients do not move either due to fear of pain or they are unable to because of the spinal cord compression. Therefore physiotherapy is important to maintain muscle tone and blood flow to the limbs

Feeding Tubes - Dependent of the neurological condition of the patient a feeding tube may be the best course of action to ensure they are maintaining hydration status and meeting their RER.

Supportive Bedding - Patients that have limited movement are prone to bed sores therefore padded supportive bedding is essential. The use of donut bandages around boney joints may be needed.

Prevention of Urine Scalding - Using inco pads to soak up urine and regular baths to get urine off skin will be needed.

Being aware of complications - Further displacement of the dens (as a result of surgical failure or neck flexion) into the spinal canal can lead to diaphram paralysis, respiratory failure and death. Thus monitoring of Res rate and effort is a must.

What is the prognosis? 

The prognosis depends on the degree of spinal cord trauma and neurological deficits present before treatment. Mild clinical signs result in a good prognosis whereas prognosis for dogs with paralysis is guarded, although recovery is possible with successful surgery.

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A 5 month old girl with alobar holoprosenceohaly. This condition was diagnosed prenatally in utero and understandably resulted in severe enlargement of the child’s head. The child was oriented to sound, able to move all extremities and responded to external stimuli, however the long term prognosis for this condition is poor as it is typically fatal in the neonatal period.

A True Trainwreck:

It’s been an exceptionally long time since I’ve shared one of my “vignettes” from the emergency department. Over the summer, I have had many exciting moments in the ED, but this is by far the most memorable.

One particularly busy night, we get a call from EMS that they’re bringing us a pt in his mid 50s with a probable inferior STEMI. His vitals were normal with the possible exception of borderline hypertension. ASA was given, but no NTG was given due to possible posterior involvement.

We start getting ready for the incoming patient, expecting a quick turnover to cath lab. I don’t think anyone anticipated what happened over the next several hours.

As soon as the pt rolls into the ED, I could tell something wasn’t right. He was pale, extremely diaphoretic, and less responsive than EMS made him sound. This wasn’t any fault of their own, apparently he had just started this as the ambulance pulled up to the hospital. His vitals somehow were still normal, but he still looked sick as can be. Our EKG also confirmed an inferior MI, with significant ST depression in V1/V2, which is suspicious for posterior involvement, and he also had some possible signs of RV involvement. So, we get the ball rolling. The cath lab was activated, the cardiologist was called, and paperwork was getting its due diligence. From what we could get from the patient he had a hx of well controlled HTN, but otherwise no significant medical hx except for a remote appendectomy. He did smoke, however.

So, everything seems to be progressing as expected. The cardiologist is on their way, the patient’s vitals are stable, and he was looking slightly improved. We didn’t have labs back, but at that point his CXR was normal as well. The physician needed to go check on another patient on the other side of the ER, so I stayed in the room with the nurses just to keep an eye on the patient.

Well…for all of you new followers out there, I have the privilege of being the owner of my very own black cloud which always chooses the most inopportune moments to make its appearance. About two minutes after the physician left the room, the patient suddenly becomes obtunded, slumps over in his bed, and then of course the monitor shows him going into a pretty impressive v-fib.

All hell breaks loose. We’re already busy and short staffed, and it always makes these situations harder to control. A code was called, compressions were started, and the doctor comes running in the room. The patient gets shocked with no ROSC and proceeds to get intubated. He get’s epi, get’s another shock, and then has a pulse just as the cardiologist walks into the room. We all take one giant sigh of relief, and start trying to stabilize him for transport to the cath lab. His BP dropped significantly, so he was placed on levophed as well. Right after the levophed starts to hang, he arrests again. At that point, a vicious cycle beings where we get a pulse and then lose it a minute later. He gets an amiodarone bolus/drip, dopamine, and a whole lot of epi. Nothing seems to be working, and 30 minutes into this the cardiologist and ER doc begin discussing calling it. Just as it’s about to be called, we get a pulse-stronger than any of the other times. We wait a minute or so to get everything settled, and then he is whisked off to the cath lab.

Unfortunately, following the general theme of the night, the fun didn’t end there.

About 20-30 minutes later, we get an update from the cardiologist. His cath came back surprisingly not as severe as expected, with diffuse moderate vessel disease but no obvious blockage that would cause his MI. He was going to be scheduled for a CABG in the AM, but his case was still perplexing. It was suggested that maybe the clot dissolved with all the CPR he received, but the cardiologist also thought maybe a pulmonary embolism might be the cause so he sent the pt to get a CTA of his chest.   

About 5 minutes later, the scout image (basically just a CXR) of his CT is available on the computer to view, so I open it just so I won’t forget to take a look at it later. I jumped out my seat as soon as I opened it BECAUSE OF THE MASSIVE TENSION PNEUMOTHORAX HE HAD. I immediately show the ER doc, and we start running to radiology (which isn’t that far away at all), nearly crashing into the cath lab nurse who was running to the ER to grab the doctor. We get into the CT suite and, in a style reminiscent of a Grey’s Anatomy episode, the ER doctor performs a needle decompression (However, unlike Grey’s anatomy he still manages to find the time to wipe down the area with an alcohol prep). After that, instead of dragging him all the way to the ICU, he got transported to the ER for a quick chest tube and then was sent on his way to the ICU. His tension pneumo was the result of several rib fractures secondary to how much CPR he went through. 

Amazingly, and against all odds, several weeks later the patient walked out the hospital-alive. He was extremely lucky. Not many people survive cardiac arrests, even in the hospital, and especially with all of the other complicating factors. Not only that, but he walked out without a single neurological deficit.

In Emergency Medicine, we don’t get to celebrate many victories. Even though we provide the best care possible many of our most critical patients are too sick or too injured. Even for those we save, many suffer from complications and debilitating issues for the rest of their lives. To have that one patient, maybe one of the sickest I have seen in a long time, walk out of the hospital as if nothing happened is a victory that I’ll remember probably for the rest of my life. It’s the victories, no matter how small, that remind each of us how rewarding our profession is. 

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Alexandra Adams
Hello, and welcome to What's Their Problem?, the series where your favorite fictional characters get psychoanalyzed by an amateur. I use classic and beloved ...

Originally posted by desingyouruniverse

theatlantic.com
Why Some Companies Are Trying to Hire More People on the Autism Spectrum
The majority of those with autism are unemployed, but new pilot programs at big companies, such as EY and Microsoft, are discovering unexpected benefits from having "neurodiverse" colleagues.
By Bourree Lam

Found a great comment on this article by Laney Chandler. It’s wasted in a comments section, so I’m sharing it here.

So now imagine what it is like for an autistic person to work with neurotypicals. Our nervous system is structured completely differently. The challenges we face apply to essentially everyone around us.

People expect us to read non-verbal communication, but we have a neurological deficit that prevents this and yet people are not shy about chastising or rejecting us for our disability, so we are operating from a place of anxiety all the time.

The way we dress is based on sensory challenges. Many of us cannot “tune out” tactile information, so while you may put on a pair of woolly socks and find them scratchy, you soon forget about it. For many of us, when we wear certain materials, cuts, or something, we have the equivalent of someone following us, beeping loudly in our ear all day. It becomes excruciatingly painful.

People around us say one thing with their words and another with their faces - which we often cannot read. We need to verbalize things, and we are direct. We are susceptible to lies and manipulation because we have challenges in reading certain non-verbal aspects of social communication. It means we are abused and exploited many, many times, and yet, most of us continue to try and show up. Only to be told we are “too direct”.

Repetitive behaviors can have several causes. Tic disorders are extremely common, which means that many of us have repetitive movements that are of neurological origin that cannot be controlled. You think it is annoying to see someone shake or roll their head? It is much harder to endure the social scrutiny that follows an involuntary movement, not to mention pain from repetitive strain.

In other cases, repetitive movements are a natural form of self-regulation in response to a vastly different sensory system. Some people have hyposensitivities, which creates anxiety. Thus rocking may be an effort to feel where one’s body is in 3D space. We also routinely take in 2-4 times as much sensory information through the 5 standards senses, which means the world is intense and chaotic. Repetitive movement helps to ease the neurological pain we experience from that. The only analogous experience in neurotypicals is physical pain.

We generally cannot filter sensory input either, and cannot multitask. Our cognitive functioning is different - we have to focus deeply. It is how we are wired. If you startle a person on the spectrum while they are focusing, it can be extremely painful. So what you dismiss as behavior is actually an acutely difficult experience.

Temple Grandin is not the archetype for what autism is. What Grandin does is pass, whcih means that, even though she has sensory needs and experiences pain, she has learned to pass as neurotypical (as close as she can manage), by making her own needs and pain subordinate to the needs and expectations of neurotypicals. It doesn’t change her disabilities - it just hides them from your view. Many autistics do this out of fear of social punishment, rejection, etc. But that does not make it right - the problem here is that no room is made for someone with different neurological needs. Not all of us CAN pass, and the damage from passing is cumulative and devastating. Imagine having to hide who you are and sweat bullets because you are in agony in every single social encounter just so you will not be punished. It damages self-esteem. Fundamentally.

If neurotypicals can bother to learn about the differences and at least meet autistics half way in communication, a lot of the challenges would be avoided, including what you call “trouble with men.” What is actually happening is that autistics - the people with significant neurological challenges and disabilities - are being asked to shoulder the entire burden of bridging the communication gap. They are being asked to mask who they are and live in pain so that neurotypicals, already in the majority, can have a seamless experience of the world.

In terms of providing accommodation for a disability. autistics are being asked to accommodate neurotypicals far more than neurotypicals are being asked to accommodate autistics.

So in terms of having a “thick skin”, autistics are absorbing the rougher end of that. It is worth remembering that. Because they endure the challenge of dealing with difference in 99% of the people they meet. Likely all of their work colleagues (if they are lucky enough to get a job). And they struggle with this for their entire lives, feeling like an alien species and shut out of most of social life. A little compassion in place of a zoological taxonomy would go a long way.

Update: June 2017

So, this month has been pretty shit. No, the last two months have been shit. Actually, no. 2017 can go fuck a donkey cos it’s been fucking awful.

We’ve had a few bright spots, and they’ve been good. But, in early May, my mom had a small stroke one evening. Thankfully it was only small, and she’s more or less back to normal. She is only down on energy and stamina and has no neurological deficits or anything physical. She was lucky. Very lucky.

But then, early June, as in a couple of weeks back, I was on my way back from collecting wine when the car developed a knocking sound in the engine. I pulled over to stop at a pharmacy as planned, and has a look and couldn’t see anything obvious. So, I decided to head home, albeit slowly. By the time I was a few klicks from home, the engine was really struggling. And I just about made it home. Made a call to the insurance company’s breakdown service and they sent us a tow truck the next morning.

The mechanic then told me that the engine was done and dusted. Finished. Fucked. And that it could cost up to 5 grand to get the car back on the road. Cool story, but the car is only worth 2k at best in its current condition. So, basically we need to find a new(er) car. As cheaply as possible. Because the banks over here are a bunch of cocks and are throwing all kinds of demands for paperwork and proof of this and that, and more. I’m just waiting for them to ask for proof of penis size. On top of that, a friend who had offered to loan me enough to buy a car, suddenly pulled out and was “unable to help” but felt “very sorry”. Yeah, right.

I need a break. Seriously. I need some good luck. I need shit to start going right. Because I honestly don’t know how much worse shit can get or how much more I can take. Oh, and yes, I’m still alive. Just.

anonymous asked:

Can I ask about the possible problems and complications a patient might experience if they are in a coma longer than a few days? If someone has sustained heavy injuries (such as a severe car crash) that has caused the coma, is there a length of time that might be considered "normal" and "severe"?

Eyyo!!! I really, really need like 8-12 masterposts about coma, don’t I?

Okay, so, here’s the basics on this. It’s not the coma itself that’s the problem. It’s whatever is causing the coma that is the problem, or causing the thing that made the doctors decide to sedate until the brainwaves essentially come to zero.

I want to be clear on this: there is no such thing as a “lightswitch coma” due to injury, where the character can be “woken up” and miraculously have no ill effects. This does not happen. Do not write as though it does. It disrespects millions worldwide who are living with the aftereffects of TBIs, persistent intractable seizures, brain cancers, and other neurological diseases.

Originally posted by coooolcaat

Comas do not happen to healthy brains (unless they’re medically induced for non-neurological reasons, like poor ventilator compliance in severe respiratory failure or ARDS). They only happen to very, very, very sick brains. In pre-modern medicine days, these are things that would be fatal. In the modern medicine days, these things could usually still be fatal. Mmkay? Mmkay.

Now. You say your character entered a coma because of a car crash. That suggests that this is neurological. That suggests that your character has a significant amount of traumatic brain injury (TBI). There’s a good starter-with-links rundown on TBI here: http://www.traumaticbraininjury.com/understanding-tbi/what-are-the-effects-of-tbi/ .

By losing consciousness for > 30 mins, your character already has a severe TBI. The questions related to this are:

Will they wake up?

What deficits will they have (not might; they will have neurological deficits)?

What will their “new normal” be?

What tasks can they complete without re-learning them and what needs to be re-learned? Speech? Motor control? Skills like typing, tying shoelaces, etc? Walking? Don’t forget appropriate social interaction; many people with TBI have damage to the frontal lobe, which induces personality changes and may affect their ability to interpret and respond appropriately to social cues.  

Now, as to complications from coma: muscle atrophy happens surprisingly quickly, as do bedsores. In addition to a lot of neuro rehab, and potentially speech and occupational therapy, your character may need significant amounts of physical therapy to get back on their feet. During the initial waking-up phase, they may be extremely disoriented and even violent; this is in large part because sedation interferes with the brain’s sleep/wake cycle, and so even though they’ve been unconscious during their sedation, they haven’t been sleeping.

This got waaaay longer than I intended it to. Sorry! But I hope you have great luck and happy holidays ;)

xoxo, Aunt Scripty

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2

Multiple Sclerosis

  • is a chronic demyelinating condition, affecting white matter of brain, spinal cord and optic nerves, distribution is non-uniform
  • typical age of onset is 20-40yrs old, the course of the disease is often unpredictable, periods of remission, interspersed with acute relapses which may leave lasting neurological deficits
  • the above images show classic bilateral periventricular plaques, which appear bright on MRI
Just Another Day

Today is your last day of rotation in the SICU; and we’re sharing two patients.

Mrs M is 29 years old, she came to us yesterday, s/p MVA, s/p craniotomy. You were there today when she became unresponsive, and part of the team who revived her. You placed a central line to her right subclavian, in the process unintentionally nicking her lung. I was there when your attending surgeon explained to you, “it happens,” and I was there while you inserted a chest tube to counteract the error, you didn’t skip a beat, although I could read the devastation on your face, and slight tremor in your hand when you turned away. I stood by you, as support, when you admitted the event to the family. A known complication, but these words are of little solace even to you, right now.  I stood close to you, as we worked on our patient who went into complete heart block, respiratory arrest, then cardiac arrest, and I stood by you in support when your attending said it was time to give up, there was no coming back from the cascade of injuries and events. I listened as you argued to be more aggressive. I share your despair, as she is young, and this shouldn’t have happened, but you are human, you made a human mistake - one you would remember for the rest of your career, and although these words are of little value, the insight and memory of your mistake will one day save another patient, and help guide another resident as they are inserting a central line.  However, these words may seem empty, right now.

But you see, you were also responsible for Ms. D is a 19 year old patient, who was in the next room to Mrs M. You were the resident on call earlier this morning when she was admitted for DXM overdose, and you saw her as a consult in the ER. In a roomful of doctors who were about to write her off as an intoxicated partying teenager, you noticed an ever so slight droop to her smile, and you looked beyond the intake of substances to see that her slurred speech was a serious warning sign You argued with the ER attending who was ready to turf her to rehab once her stomach was pumped. You advocated for a patient who presented with confusion, dizziness, blurred vision all commonly seen in DXM overdose, but you also advocated for a young girl who seemed to have no one else in  her corner to think outside the box. You fought for her to be admitted to the ICU when everyone else laughed at you, laughed at the waste of bed, but you fought it anyway. You didn’t gloat when the CT came back positive for stroke, but you saw her through the embolectomy that would eventually lead her to the SICU.  I stood with you as you managed her carefully, subtleties of bedside care that couldn’t be taught in any book, or any medical college.  At the end of the day she is smiling a full even smile,  her family is here, after a long trip across the country.  She is speaking, her voice very soft, but she isn’t confused any longer. She tells us that she has been experiencing odd intermittent floating sensations in her eyes, and numbness to right side for some time, but she was a sophomore in college, and she had taken the DXM to escape the peculiarities of her body, and devastation of a tough semester in school. I stood next to you, as you listened patiently to her story, and you explained to her that the embolectomy was successful, and she would likely go home in a few days, no neurological deficits.

I stood by you today, as you experienced the cataclysmic effects of a mistake, and I stood by you as you saved a life.

People often call caregivers heroes, yet we don’t often look at the lives we’ve impacted, but the ones behind the scenes that suffered at our hands, the impact tearing us apart, the impact guiding our practice with the patients we see beyond that mistake. We don’t think of ourselves as heroes, we’re just trying to make the best clinical decisions on any given day, and learn from the devastations & the patients who are eternally etched into our hearts.

 - A letter to an extraordinary Surgical Resident,  on an ordinary day. 

Everything Pt. 2

Everything Part One You MUST MUST MUST read part 1 before you read this or else you’ll be completely lost. They won’t stand alone. Also, I did my best with all of the medical stuff (disclosure: I haven’t gone to medical school so I did enough research to get me through). 

“Owen,” he heard Meredith sit beside him in the gallery where he was watching Amelia’s surgery. “Why don’t you go get some rest?”

“I’m not tired,” he answered her as he sniffled. He had sat there silently crying through the entire surgery, watching every move Stephanie made. Impressed with her skill and technique, it didn’t change the fact that it was Amelia on the table.

“Okay.”

“Why are you here?” he asked her, not accusingly, more so curious.

“To make sure you’re okay. Are you okay?” she asked him, her eyes focused on the surgery below.

“No.”

“Don’t run,” Meredith warned him. “You’ve hurt her before. And as much as I can’t stand her right now, I can’t watch that happen to her again. So, don’t pull away again.”

“She won’t want me.”

“Stop talking nonsense,” Meredith said.

“I blame myself. For this. I should have done more. I should have made her get checked out. We could’ve found this earlier. She wouldn’t be on that table.”

“Did you get checked out after the explosion?” Meredith asked him. Finally, he turned to face her. “No one got checked after the explosion because no one had any apparent injuries. Even Amelia had no idea she hit her head. So you can stop playing the blame game right now. As soon as she started showing symptoms you got her here. No one can predict a brain bleed. You did the best you could.”

“If only that were good enough.”

Meredith reached down and took ahold of Owen’s hand and didn’t let go until Amelia was rolled out of surgery.

“She’s going to be fine,” Stephanie reassured him as she came to update Owen. “I got control of the bleeder and we’ll keep monitoring her closely until she wakes up.”

Owen nodded and sat by Amelia’s bedside. “You’re going to be okay,” he said as he used the back of his hand to caress her face.

Day 3

“She hasn’t woken up!” A disheveled Owen shouted at Stephanie in the hall outside of Amelia’s room. Since her surgery, he hadn’t moved from her room. Meredith brought him food and water, knowing he wouldn’t leave. His facial hair had grown out and you could see he had worried his hair into a heap of a mess. Now there was a distinct odor being emitted from him, yet he still wouldn’t leave.

“I don’t know why she’s not waking up.”

“You don’t know?” he roared at her.

“Her CTs are clear. She didn’t have a stroke. She should be awake.”

“That’s not good enough!” he shouted.

“Dr. Hunt!” Bailey shouted and marched over to him, motioning for Stephanie to leave them. “That poor girl has been running herself ragged trying to do everything she can for Dr. Shepherd. You need to control yourself and get it together.”

Entering into her room, he pulled the chair as close as he could to maintain his vigil. “Amelia, I need you to wake up. Okay? I’m sorry this is all my fault. I should’ve paid more attention. I should’ve taken care of you. I never should have pushed you away. I’ll never do that again, I promise. It’s time to wake up now. Show me those beautiful blue eyes. It’s time to wake up.”

Day 10

“This is just sad,” Alex said as the group of them stood outside of Amelia’s room, watching Hunt as he restlessly slept in the chair beside her.

“Shut up,” Meredith slapped him.

“The dude hasn’t even had a decent shower. Have you smelled him lately?”

“You don’t know what it’s like so shut up,” Meredith scolded again.

“It’s the worst feeling in the world,” Arizona chimed in, dwelling on her experience with Callie. “Just let him be.”

Day 13

“They all just forced me into that shower. It was not appreciated at the time, but I have to admit I was starting to smell pretty ripe,” he laughed as he arranged some flowers around her room. “I bet you’re wondering what in the world we’re all doing out here. Stephanie is working around the clock trying to figure out a way to wake you up since you’re being so stubborn. Ironic thing is that you’re probably the only one who would be able to figure it out in the first place.”

He paced around the floor. “What do you want me to do here, Amelia? Haven’t I begged and pleaded enough? Why won’t you just…WAKE UP?” he shouted, tears streaming down his face.

“I’m sorry,” filled with remorse, he rubbed circles over her hand with his thumb. “I didn’t mean to scream at you. I just don’t know what to do anymore. I don’t know who I am without you anymore. I don’t want to be this person. I’m mean and irritable and I yell at everyone. I’ve never been more in touch with my feelings, that’s for sure,” he chuckled.

“I’m desperate here.”

He sat there for a few moments before an idea struck him. “I had a sister. Megan. She was three years younger than me. Smarter than me, funnier than me, better person than me. She did everything I did. We went to med school together and that’s where we met Riggs. Nate was my best friend. And Megan loved him. And he was with her the day that we lost her. I trusted him with her, and he was like a brother to me. And he should’ve…but he didn’t. And I don’t talk about it. We all have things we don’t like to talk about. This is one of them.”
He continued to stroke her hands. “And now I’m wishing I would’ve told you sooner. There’s a lot of things I wished I would have said to you. Like all of the things I love about you. The way your mouth looks like a ducks when you’re really pondering something. The way you walk, the way you talk. You’re filter or the lack of one. I love that you have the ability to just say whatever is on your mind without thinking about any consequences. I know you’re working on it, but I love it even if it hurts sometimes. I love your intensity in an OR and your ability to take charge and command. Whenever you would tell Derek off, I used to think it was so hot,” he laughed.

“I love your confidence. I love how you are with the kids. You’re so good with them. I love your pancakes, best I’ve ever had. I love the way that you hold only my elbows when we kiss. I love how your small petite baby hands somehow seem to fit perfectly with mine. And there are more, but that’s enough for now. I love you Amelia. And I’ll spend every moment for the rest of my life telling you that. But you need to wake up first.”

Day 20

“Zola wanted me to tell you that she sold 500 boxes of Girl Scout cookies. She set the record in her troop. Although she set aside a box of the peanut butter patties because she knows those are your favorite. Those are your favorite?” he chastised. “Everyone knows Thin Mints are the best.”

Owen switched out the older flowers for newer ones and set them on the ledge behind her bed.

“And Bailey keeps growing like a weed. Pretty soon he’ll be taller than you. And Ellis just keeps looking more like Derek every day. Sometimes when she smiles she looks just like you. She has your dimples.”

He sat on the corner of her bed and takes ahold of her hand. “What are you thinking about, Amelia? What I wouldn’t love to know what you’re thinking in there. Can you hear us? Hear me? Because I just can’t understand why you’re not awake yet. We’re all here waiting for you. All you need to do is get it together and open your eyes. Come back to me. We’re getting close to 30 days. After 30 days…” he trailed off unable to finish the thought. “I wish it were me here instead of you. I’d gladly be in your place if it meant you were out in the world.”

Day 22

“Owen, why don’t you go home for awhile? Go sleep. I’ll stay with her for awhile.”

“No.”
“Owen, she wouldn’t want you to do this to yourself.”

“Shut up. We only have eight days left. I’m not leaving her. I want to be here for whatever time she has left. I need to be here for whatever’s left.”

“It’s only a couple of hours. Get some decent food; get some sleep. When she wakes up you don’t want her to see you looking all haggard and decrepit.”

“Call me if anything changes?” he asked.

“Of course.”

Owen stood and leaning over, kissed Amelia’s forehead. “I’ll be right back. I love you.”

He returned to the trailer that he had settled a few blocks away from the hospital and fell asleep as soon as his head hit the pillow. He hadn’t left the hospital much in the last 22 days. A few hours here a few hours there, but he mostly had stayed in her hospital room, showering in the lounge when he began to get tired of his own stench and filth. He didn’t think it would feel so good to be outside of those depressing gray walls and feel like a normal human being. And for a few hours he forgot everything. Forgot that Amelia would probably never wake up or if she did she would probably have so many neurological deficits that she wouldn’t even be herself anymore.

Amelia’s directive had been very clear that she didn’t want to be kept alive by machines or any other extraordinary measures for over 30 days. There had been no improvement; no change. And in 8 days, she would be let go.

Owen stepped into his shower and spent what felt like hours inside, letting the warmth radiate through his pores and try to bring his body peace. He exited the shower and began to mill about the trailer trying to find anything that wasn’t out of date. Finding a can of soup he put it into a pot and placed it onto the small burner.

His phone vibrated in his pocket, a page from Meredith. He had missed at least 10 pages from Meredith, the hospital, Stephanie, Maggie lit up on his phone. Something was going on. Pulling on the rest of his clothes, he ran back to the hospital.

Taking the elevator up to the neurological ICU floor, he couldn’t help but think that he had missed it. That he had let her down again. That he hadn’t been there for her when she left this world.

The doors to the elevator opened and he hesitated to even step off of them, not wanting to admit that she was gone. As he entered the hall he saw Stephanie around the nurses station sobbing, her head in her hands. Meredith sitting close outside Amelia’s room, also sobbing. He had missed it and he’d never forgive himself.

Tears stung his eyes as he came closer and closer. Rounding the corner to Amelia’s room, he prepared himself for what he was about to see.

“You’re late,” her voice called out to him. Shocked and stunned, his brain worked in overdrive to propel his feet forward to her.

With tears in her eyes, she reached out for him and enveloped him as he cried.

Day 30

“Dinner is served,” Owen bowed as he placed the plate of food in front of her.

She took a bite and moaned. “This is really good.”

“Thank you.” They continued to eat in companionable silence.

When they were finished, Amelia began. “I missed you. So much. Even though you were there I missed you. I need to come clean. I heard you. I heard every word you said to me. That you think I look like a duck…”

“I’m pretty sure that’s not what I said,” he laughed.

“That you love me. I definitely heard you scream at me to wake up. I’m sorry my brain was too slow to catch up. But I want you to know and understand that this was an accident. All of this everything we just went through was not your fault, okay?” When he wouldn’t meet her eyes, she forced him to. “Okay?”
“Okay,” he consented. “You heard everything?”

“Everything. One last thing to come clean about,” she said as she moved over to sit in his lap, wrapping her hands around his neck.

“What’s that?”

“I love you too.”

I super hate when people think that attention deficits and neurological problems could be solved by “trying harder to focus” or w/e

Like, I feel like some people literally can’t comprehend that hey!!! other people’s brains? They’re not like yours!! They work!! Differently!! And your experience does not apply to everyone!! Wow!

Planning a Place of Birth

This is all according to one resource, the National Institute for Health and Care Excellence. If anyone (especially midwives) have any other information and good resources on home births and birthing facilities please let me know. I’ll post what the website has as well as what I’ve seen on other resources.

Everyone should be offered the choice of planning birth at home, in a midwife-led unit or in an obstetric unit. Everyone should be informed:

  • That giving birth is generally very safe for both the pregnant person and their baby. (650 people die from pregnancy related issues every year, about half of those giving birth each year have some sort of complication)
  • That the available information on planning place of birth is not of good quality, but suggests that among those who plan to give birth at home or in a midwife-led unit there is a higher likelihood of a natural birth, with less intervention. We do not have enough information about the possible risks relating to planned place of birth.
  • That the obstetric unit provides direct access to obstetricians, anaesthetists, neonatologists and other specialist care including epidural analgesia.
  • Depending on locally available services, the likelihood of being transferred into the obstetric unit and the time this may take. Take this into consideration.
  • That if something does go unexpectedly seriously wrong during labour at home or in a midwife-led unit, the outcome for could be worse than if they were in the obstetric unit with access to specialised care.
  • That if they have a pre-existing medical condition or has had a previous complicated birth that makes them at higher risk of developing complications during their next birth, they should be advised to give birth in an obstetric unit.

I know that a lot of birthing centers do make sure that you are as safe as possible and that if things do go wrong you are transferred to emergency care quickly.

Factors to consider when planning the place of birth

1. Medical conditions that may indicate a need for obstetric care.

These conditions include:

  • Confirmed cardiac disease
  • Hypertensive disorders 
  • Asthma requiring an increase in treatment or hospital treatment
  • Cystic fibrosis
  • Haemoglobinopathies – sickle-cell disease, beta-thalassaemia major
  • History of thromboembolic disorders
  • Immune thrombocytopenia purpura or other platelet disorder or platelet count below 100,000
  • Von Willebrand’s disease
  • Bleeding disorder in the adult or unborn baby
  • Atypical antibodies which carry a risk of haemolytic disease of the newborn
  • Risk factors associated with group B streptococcus whereby antibiotics in labour would be recommended
  • Hepatitis B/C with abnormal liver function tests
  • Carrier of/infected with HIV
  • Toxoplasmosis – receiving treatment
  • Current active infection of chicken pox/rubella/genital herpes in the adult or baby
  • Tuberculosis under treatment
  • Systemic lupus erythematosus
  • Scleroderma
  • Hyperthyroidism
  • Diabetes
  • Abnormal renal function
  • Renal disease requiring supervision by a renal specialist
  • Epilepsy
  • Myasthenia gravis
  • Previous cerebrovascular accident
  • Liver disease associated with current abnormal liver function tests
  • Psychiatric disorder requiring current inpatient care

2. Other factors that may suggest needing obstetric care

Situations where there is an increased risk for parent or child:

  • Unexplained stillbirth/neonatal death or previous death related to intrapartum difficulty
  • Previous baby with neonatal encephalopathy
  • Pre-eclampsia requiring preterm birth
  • Placental abruption with adverse outcome
  • Eclampsia
  • Uterine rupture
  • Primary postpartum haemorrhage requiring additional treatment or blood transfusion
  • Retained placenta requiring manual removal in theatre
  • Caesarean section 
  • Shoulder dystocia
  • Multiple birth 
  • Placenta praevia
  • Pre-eclampsia or pregnancy-induced hypertension
  • Preterm labour or preterm prelabour rupture of membranes 
  • Placental abruption
  • Anaemia –- haemoglobin less than 8.5 g/dl at onset of labour
  • Confirmed intrauterine death
  • Induction of labour 
  • Substance misuse
  • Alcohol dependency requiring assessment or treatment
  • Onset of gestational diabetes 
  • Malpresentation – breech or transverse lie
  • Body mass index at booking of greater than 35 kg/m2
  • Recurrent antepartum haemorrhage
  • Small for gestational age in this pregnancy (less than fifth centile or reduced growth velocity on ultrasound)
  • Abnormal fetal heart rate (FHR)/Doppler studies
  • Ultrasound diagnosis of oligo-/polyhydramnios
  • Myomectomy
  • Hysterotomy

Now many health organizations, like the World Health Organization, say not to focus too much on high risk pregnancies as this causes many supposed “low risk” pregnancies to not get the level of care they need and also limits choices for “high risk” pregnancies that may be totally fine and not need obstetric care.

3. Medical Conditions that aren’t necessarily reasons to have obstetric care but may indicate further consideration

  • Cardiac disease without intrapartum implications
  • Atypical antibodies not putting the baby at risk of haemolytic disease
  • Sickle-cell trait
  • Thalassaemia trait
  • Anaemia – haemoglobin 8.5–10.5 g/dl at onset of labour
  • Hepatitis B/C with normal liver function tests
  • Non-specific connective tissue disorders
  • Unstable hypothyroidism such that a change in treatment is required
  • Spinal abnormalities
  • Previous fractured pelvis
  • Neurological deficits
  • Liver disease without current abnormal liver function
  • Crohn’s disease
  • Ulcerative colitis

4. Other factors that aren’t necessarily reasons to have obstetric care but may indicate further consideration

  • Stillbirth/neonatal death with a known non-recurrent cause
  • Pre-eclampsia developing at term
  • Placental abruption with good outcome
  • History of previous baby more than 4.5 kg
  • Extensive vaginal, cervical, or third- or fourth-degree perineal trauma
  • Previous term baby with jaundice requiring exchange transfusion
  • Antepartum bleeding of unknown origin (single episode after 24 weeks of gestation)
  • Body mass index at booking of 30–34 kg/m2
  • Blood pressure of 140 mmHg systolic or 90 mmHg diastolic on two occasions
  • Clinical or ultrasound suspicion of macrosomia
  • Para 6 or more
  • Recreational drug use
  • Under current outpatient psychiatric care
  • Age over 40 at booking
  • Fetal abnormality
  • Major gynaecological surgery
  • Cone biopsy or large loop excision of the transformation zone (LLETZ)
  • Fibroids

For more information on planning your place of birth, visit this post!

Researchers Show Human Learning Altered by Electrical Stimulation of Dopamine Neurons

Stimulation of a certain population of neurons within the brain can alter the learning process, according to a team of neuroscientists and neurosurgeons at the University of Pennsylvania. A report in the Journal of Neuroscience describes for the first time that human learning can be modified by stimulation of dopamine-containing neurons in a deep brain structure known as the substantia nigra. Researchers suggest that the stimulation may have altered learning by biasing individuals to repeat physical actions that resulted in reward.

“Stimulating the substantia nigra as participants received a reward led them to repeat the action that preceded the reward, suggesting that this brain region plays an important role in modulating action-based associative learning,” said co-senior author Michael Kahana, PhD, professor of Psychology in Penn’s School of Arts and Sciences.

Eleven study participants were all undergoing deep brain stimulation (DBS) treatment for Parkinson’s disease. During an awake portion of the procedure, participants played a computer game where they chose between pairs of objects that carried different reward rates (like choosing between rigged slot machines in a casino). The objects were displayed on a computer screen and participants made selections by pressing buttons on hand-held controllers. When they got a reward, they were shown a green screen and heard a sound of a cash register (as they might in a casino). Participants were not told which objects were more likely to yield reward, but that their task was to figure out which ones were “good” options based on trial and error. 

When stimulation was provided in the substantia nigra following reward, participants tended to repeat the button press that resulted in a reward. This was the case even when the rewarded object was no longer associated with that button press, resulting in poorer performance on the game when stimulation was given (48 percent accuracy), compared to when stimulation was not given (67 percent).

“While we’ve suspected, based on previous studies in animal models, that these dopaminergic neurons in the substantia nigra - play an important role in reward learning, this is the first study to demonstrate in humans that electrical stimulation near these neurons can modify the learning process,” said the study’s co-senior author Gordon Baltuch, MD, PhD, professor of Neurosurgery in the Perelman School of Medicine at the University of Pennsylvania. “This result also has possible clinical implications through modulating pathological reward-based learning, for conditions such as substance abuse or problem gambling, or enhancing the rehabilitation process in patients with neurological deficits.”

Brain Degeneration In Huntington’s Disease Caused By Amino Acid Deficiency

Working with genetically engineered mice, Johns Hopkins neuroscientists report they have identified what they believe is the cause of the vast disintegration of a part of the brain called the corpus striatum in rodents and people with Huntington’s disease: loss of the ability to make the amino acid cysteine. They also found that disease progression slowed in mice that were fed a diet rich in cysteine, which is found in foods such as wheat germ and whey protein.

Their results suggest further investigation into cysteine supplementation as a candidate therapeutic in people with the disease.

Up to 90 percent of the human corpus striatum, a brain structure that moderates mood, movement and cognition, degenerates in people with Huntington’s disease, a condition marked by widespread motor and intellectual disability. And while the genetic mutation underlying Huntington’s disease has long been known, the precise cause of that degeneration has remained a mystery.

In a report on their discovery in the advanced online publication of Nature on March 26, the Johns Hopkins researchers, led by Solomon Snyder, M.D., tracked the degenerative process to the absence of an enzyme, cystathionine gamma lyase, or CSE.

“Usually it’s very hard, if not impossible, to develop straightforward mechanisms that explain what’s going on in a disease. What’s even harder is even if you can find a mechanism that causes a tissue to rot, usually there’s nothing you can do about it,” says Snyder, a professor of neuroscience at the Johns Hopkins University School of Medicine. “In this case, there is.”

Huntington’s disease, an inherited disorder, does its damage because of abnormal DNA coding for the amino acid glutamine. Healthy individuals have some 15 to 20 DNA “repeats” in that part of their genetic code, while Huntington’s disease gene carriers have more than 36 — and often upward of 100. Children born to a parent carrier have a 50/50 chance of inheriting the disorder, and the greater the number of repeats, the earlier the age of onset of the incurable disorder.

Bindu Diana Paul, Ph.D., a molecular neuroscientist and faculty instructor in Snyder’s laboratory, was studying mice lacking CSE, which helps make the amino acid cysteine and hydrogen sulfide that moderate blood pressure and heart function. Paul, who had previous research experience with Huntington’s disease, says she was startled to observe that her mutant mice also behaved a lot like those with the disease.

When a normal mouse is dangled upside down from its tail, it will twist and turn and try to bite the offending hand, she explains. But her CSE-knockout mice stayed relatively still and clasped their paws together — the same behavior she’d observed in mice with the rodent equivalent of Huntington’s disease. “It looked like there was a neurological deficit,” Paul says. “But nobody had looked at CSE in the brain.”

Paul and Snyder began monitoring CSE in mouse and human brain tissues and found considerably less CSE in all diseased tissues. All people carry some normal huntingtin protein made by the Huntington’s disease gene, although the protein’s function remains elusive. But people with Huntington’s disease also carry mutant huntingtin proteins. Snyder and his team saw that the mutant proteins were attaching themselves to a crucial protein responsible for turning the CSE gene on or off, which ultimately led the diseased rodent and human brain tissues to be deprived of cysteine.

To see if loss of cysteine was directly responsible for the symptoms associated with Huntington’s disease, the Johns Hopkins team turned to readily available sources of the substance in everyday foods and fed mice a cysteine-rich diet.

The results, Paul says, were striking. When those mice were dangled from their tails, they resumed struggling, although with a bit less vigor than their healthy peers. They were able to grip an object with greater strength, and they took longer to fall off a balancing apparatus than CSE-knockout mice. Their life expectancies increased one to two weeks.

Snyder and Paul say they are cautiously optimistic about the results, noting that although they suggest a possible treatment for Huntington’s disease, it’s clear that a high cysteine diet merely slows rather than halts the progression of the disease. Moreover, the results in live mice may not occur in humans.