#upper motor neuron lesion

[mcatmemoranda]

Mechanisms of nerve injury – The major mechanisms of upper extremity peripheral nerve injury are compression, transection, ischemia, inflammation, neuronal degeneration, and radiation exposure.

●Diagnostic testing

•Electromyography and nerve conduction studies are useful for identifying and classifying peripheral nerve disorders affecting the upper extremity.

•Magnetic resonance imaging of the cervical spine is useful to identify disc herniation or degeneration and the degree of nerve root compression as well as to exclude the possibility of a mass lesion.

•Neuromuscular ultrasound can be helpful in assessing individual peripheral nerves in patients who present with an unusual upper extremity mononeuropathy.

•Laboratory testing and cerebrospinal fluid analysis are generally reserved for patients with conditions associated with an inflammatory, infectious, or endocrine source.

●Median neuropathies

•Carpal tunnel syndrome is the most common upper extremity mononeuropathy. Typical symptoms include pain or paresthesia in a distribution that includes the median nerve territory, with involvement of the lateral portion of the hand. The symptoms are typically worse at night and characteristically awaken affected individuals from sleep.

•Less common median nerve syndromes include entrapment where the median nerve passes through the pronator teres muscle and injury to the anterior interosseous nerve that branches at the elbow.

●Ulnar neuropathy – Ulnar neuropathy at the elbow is the second most common compression neuropathy affecting the upper extremities. Symptoms include sensory loss and paresthesias over digits 4 and 5 and weakness of the interosseous muscles of the hand in severe cases.

●Radial nerve syndromes – With compression of the radial nerve at the spiral groove, the triceps retains full strength, but there is weakness of the wrist extensors (ie, wrist drop), finger extensors, and brachioradialis. Sensory loss is present over the dorsum of the hand and may extend up the posterior forearm. With posterior interosseous neuropathy, forearm pain and weakness of finger dorsiflexion is typical.

●Proximal neuropathies – Several uncommon proximal focal neuropathies of the upper extremity typically present with pain and sensorimotor impairment. These include suprascapular neuropathy, long thoracic neuropathy, axillary neuropathy, spinal accessory neuropathy, and musculocutaneous neuropathy.

●Brachial plexopathy – The brachial plexus is vulnerable to trauma and may be affected secondarily by disorders involving adjacent structures. Most brachial plexus disorders show a regional involvement rather than involvement of the entire brachial plexus.

●Cervical radiculopathy – Cervical radiculopathy is a common cause of both acute and chronic neck pain. Most radiculopathies arise from nerve root compression due to cervical spondylosis and/or disc herniation. Lower cervical roots, particularly C7, are more frequently affected by compression.

●Other syndromes – Additional uncommon peripheral nerve syndromes affecting the upper extremities include focal amyotrophy, mononeuropathy multiplex, multifocal motor neuropathy (MMN), and zoster radiculoganglionitis.

[sioraiocht]

~ @strxngetimes || Gets a little medical thing from Charlie ~

"Doctor Strange -" Charlie rushes to catch up with him, stethoscope swinging around her neck as she tries to grab his attention. "Hi - I'm Doctor Jenkins, I'm new." She extends her hand to try and shake his. "I'll be brief, I promise - I’m concerned about this patient who’s presented to the ER tonight with a burn to his hand. I triaged and found out that his hand was numb, he hadn't even felt the burn. In fact, he's been experiencing progressive weakness and sensory deficits that were initially dismissed as anxiety by his doctor. I examined him, found hyperreflexia in the lower extremities and a positive Babinski sign, which would point to an upper motor neuron lesion. I’m concerned about his spinal cord - I think potentially a tumor or cervical myelopathy." Eyes give him a pleading look. "I would really appreciate your professional opinion."

[coruscantguard]

me and my silly little symptoms that indicate i have an upper motor neuron lesion (this makes no sense i have never had an injury beyond stubbing my toe)

[aunstudies]

15/05/2020; 61/100 days of productivity:

I think today is the last official day of teaching of second year. I went over hypertension guidelines, and I tried making a concise flowchart but as you can see it’s moving about all over the place. I had a webinar on neurology and differentiating between upper and lower motor neuron lesions, and then a webinar on headaches. I practised some of my flashcards and did some practice sba questions.

Today would have been my last day at my gp practice. In my clinical group, we wanted to do something to show our gratitude. So we decided to get some pizzas delivered to the practice to say thank you for having us, and also for the work they’ve been doing over the past few months during the pandemic. I phoned them up so they knew to expect a delivery, and it was so heartwarming to hear their happiness. 

[doctorfiction]

The protagonist in my speculative fiction novel needs to have a problem that will eventually incapacitate him but starts with very subtle changes that become more apparent over time. I was thinking seizures, but that doesn't seem very subtle. Any ideas?

Actually, seizures are an excellent choice for what you are trying to accomplish. Seizures run the gamut from nearly imperceptible to impossible to ignore.

Let’s start with a definition of the term seizure, progress quickly through the different types, their etiologies (causes) and how they manifest, and finish up with a seizure disorder appropriate to your genre and protagonist.

Simply put, a seizure is an abrupt, abnormal electrical disturbance of the brain resulting in an aberrant motor (muscle) or sensory (thought or sensation) response.

Seizures can be caused by fever, head trauma, brain bleeding, chemical imbalance, drug/alcohol use, or a space-occupying lesion (a brain tumor or growing mass of any kind). For fiction purposes, we will be concentrating on the space-occupying lesions and how they affect Neurons ( the cells that allow the brain to send and receive information).

Motor neurons: The brain uses these to make muscles move.

Sensory neurons: This is how the brain receives information from the body    and the outside world.

Seizures are classified into two general types: Generalized and Focal (Partial).

**When identifying seizure types, the terms Focal and Partial are interchangeable.**

Generalized seizures tend to involve all areas of the brain. This category includes a number of subtypes:

Tonic-Clonic: Formerly referred to as a gran mal (French for great evil); this is what most people visualize when they hear the word seizure. The subject is on the ground, unresponsive, arms and legs jerking. The patient may drool or suffer incontinence (loss of bowel/bladder control). The episode lasts from a few seconds to several minutes. The event is dramatic and frightening to bystanders and the subject.

Absence: The subject stares into space as if ignoring you. These seizures last only a few seconds and are more common in the young.

Atonic: Sometimes called “drop-out” seizures, these are characterized by muscle weakness. The subject generally remains alert, but the muscles go weak and they drop what they are holding and may fall to the ground. These also are of short duration. 

There are other subtypes of Generalized seizures, but the focus of our attention in this post is limited in scope and will deal primarily with the subtler and more fiction-worthy Focal variety.

Focal seizures are so named because they occur in a specific region of the brain and produce symptoms (at least initially) limited (focal) to that area.

The subject may have an altered mental status, but unlike a Generalized seizure, they are usually conscious and often aware and terrified by the manifestations of the seizure. We will explore two types of Focal seizures:

Complex Focal Seizures: These can cause blank stares, lip-smacking, pill rolling movements and laughing, crying, or screaming for no reason. This type of seizure is interesting and does have some obvious uses as a fiction vehicle.

Simple Focal Seizure: These seizures affect how we perceive our surroundings and can cause motor (movement) disorders or changes in mood or emotion. This type is especially well-suited to fiction. The following are a few of the possible symptoms: 

                         Isolated involuntary twitching of fingers

                         Blank stares

                         Hallucinations: seeing, smelling and hearing things that are not there or morphing things that are there into something else. 

                        Déjà vu sensations

                        Sudden mood or emotional changes

                        Dilated pupils

Seconday Generalized Seizure: This is a type of Focal seizure that spreads to the entire brain and can cause gran mal whole-body seizures. It can be because of multiple affected areas.

The inside of the skull is a closed space. When something foreign occupies that space, it exerts pressure on whatever structure is nearby. If the pressure becomes great enough, it will alter the signal passing through the Neurons causing a Focal abnormality. The nature of the abnormality depends on what part of the brain is sending or receiving the signal.

Now that you have a very basic idea of the nature of Focal (partial) seizures, let’s apply the principles to fiction.

For Example:

A young environmental scientist is taking water samples near an abandoned chemical plant. He is surprised to find tiny tadpole-like organisms swimming in the toxic runoff. The small creatures are whipping their tails and actually break the surface of the water. As he moves closer, there is a marked increase in activity. As he bends down to take a sample, one of the small red- brown creatures lands on his upper lip. Startled, he inhales deeply and feels a burning sensation in his nose. He sneezes, the sensation passes, and he returns to collecting samples. On the ride home, he develops an intense headache and ringing in his ears. He blows his nose many times, but cannot clear the noxious smell of the polluted water. Over the next several weeks, the headaches increase and he notices that he has developed an intermittent facial tic and an occasional uncontrollable twitching of his right index finger. He finds that he has difficulty forming words and misinterprets road signs and speech.

When he is found mumbling and walking in circles in the laboratory parking lot, his research partner takes him to the emergency room where a CT Scan reveals multiple small growths in various areas of his brain.

He is admitted to the hospital for further testing. That night, he complains to the nurse that he feels like “things” are crawling under his skin. She summons the on-call doctor who finds him naked on the floor having a gran mal seizure, his body covered with a red-brown rash.

Doctor Fiction expects someone to write this book and will look for it on the NYT Bestseller list next fall.

[sweetmoxiety]

Behind This Mask is A Desperate Heart (Part 2)

Hospital AU

AU Summary: A fall. A single fall. It may seem like nothing until it’s all consuming. What happens when the doctors struggle to diagnosis the disease responsible for Virgil’s rapid deterioration?

Characters: Virgil, Logan, Patton, Roman, and very brief mention of Sympathetic!Deceit and Remy.

Pairings: Logince & Moxiety

Warnings: Discussion of anatomy and very brief, sympathetic deceit.

Word Count: 1865

Chapter 1 | Chapter 2 | Chapter 3 | Chapter 4 | Chapter 5 |

     Virgil’s fingers curled around the stiff fabric resting in his palms as he meandered towards the white door frame. Twisting the iron knob as he went and shutting the heavy door behind him, Virgil pressed his back against the wooden plank, eyes fixed on the gown in his tight clutch.

     One breath. Two breaths. By the third breath, Virgil had rested the white fabric across the sink’s rounded edge before slowly discarding his ebony attire beside the gown. With his attire stowed precariously on the sink, Virgil reached for the dotted, white hospital gown.   

     With the loose-fitted gown lightly brushing against his knees, Virgil noticed an abrupt tremble in his hands. To steady his shaking grasp, he clung to the upper   edges of the bathroom sink as his gaze became transfixed on the mirror. His scanning eyes discerned the dangling of his bangs over charcoal eye shadow, his lips curled into a pout, and the oscillatory movements of his hands.

     Grumbling, he let his grip falter from the sink and head hang low. He needed a moment. He needed a moment before seizing his clothes and emerging into his hospital suite. Frowning, Virgil shifted as his fingers trembled above the door knob. Twisting the knob and letting the door creak open meant that there really was something wrong with him.

     “Mr. Poole?” A soft knock vibrated against the wooden frame.

     “Oh- uh, yeah. Sorry,” snapping out of it, Virgil yanked open the door.

     “I was going to assess some of your motor and sensory skills,” Logan allowed Virgil to pass him and perch cross-legged on the bed’s edge, but Virgil’s twitchy hands didn’t allude him.

     “Go ahead, doc.”

     “I’m going to start by testing your reflexes with a patellar reflex test, but I’m going to need you to situate your legs so that they’re dangling over the edge of the bed,” Logan slid his fingers into a set of thin, cyan gloves.

    Virgil huffed, untangling his legs, and letting his feet hang.

    With gloved digits, Logan skimmed his cold fingertips across Virgil’s lower leg in search for the band of tissue extending down from the patella. A few more calculating touches under Virgil’s shin, and Logan identified the patellar tendon and femoral nerve. And with a short reflex hammer, Logan struck the tendon…. Virgil’s muscles convulsed.

    “Clonus,” Logan noted, scribbling the result onto a plastic clipboard in raven ink, “let’s try testing your musculocutaneous nerve.”

    “Could you flex at the elbow for me?” Logan requested as a means to identify Virgil’s bicep tendon.

     Virgil nodded, complying as Logan watched and palpated the antecubital fossa.

     “You can relax your arm now,” Logan attentively took Virgil’s arm into his grasp with his thumb over the tendon to strike with the reflex hammer. Again, more contractions.

     “Is that normal?” Virgil wore a half-frown.

     “Well, no-,” Logan paused, laying his pen across his clipboard, “a normal reaction generates an easily observed shortening of the muscle. In your case, your muscles repetitively shortened after a single stimulation, which suggests that a pathologic process is affecting peripheral nerves that results in a reflex that is abnormal.”

     “...huh?”

     “Your muscles convulsed, which suggests there is condition affecting your nerves, but with hand tremors present, that was to be expected.”

     “Any idea what it is yet?”

    “Without more testing it’s hard to say, but I postulate the issue lies within your upper motor neurons. These are the neurons that carry motor information down the spinal cord to the lower motor neurons. The information that is sent from these neurons to the lower motor neurons signals muscles to contract, thus they are the source of voluntary movement. Increased muscle tone, reflexes, and weakness would all point to lesions on your upper motor neurons, but without more testing, we cannot be sure.”

    “I see.”

“Speaking of such testing, I’m going to begin evaluating your muscle tone and then your gait.”

     Virgil nodded, glance cast to the side.

    “To start, I’m going to need you to relax for me again,” Logan clinically solicited.

    To begin testing Virgil’s upper extremity muscle tone, Logan passively rolled the joints in Virgil’s wrist and upper arm to test for rigidity. Finding some resistance, Logan apacely scrawled it onto Virgil’s charts.

    “Could you lie flat on your back now?”

    “Uh, sure,” Virgil swung his legs over the mattress as he slanted back.

    “Now, I’m going to need you to relax,” Logan repeated, pressing his palm above Virgil’s bare ankle. Moving to Virgil’s lower leg, Logan slipped his palm under his patient’s relaxed knee to suddenly bend the shin to test lower extremity muscle tone. More resistance.

    “Hmm,” Logan nodded mostly to himself, “to test your gait, I’m going to need you to walk away from me and then back towards me.”

    “Okay..,” Virgil sat up, shifting his frame so his feet brushed against the tile floor.

     Planting his feet on the ground, Virgil strolled from the bed to the farthest wall before ambling back in the direction of the doctor. And during this process, Logan took note of Virgil’s stance, stability, and leg stiffness. He watched Virgil’s leg swings and arm swings observantly. His eyes inspected Virgil’s degree of knee bending and his rate and speed only to note a decreased left arm swing.

    “Unsteady gait,” Logan jotted down.

    “I take it that’s bad?” Virgil plopped back onto the bed, picking at his black nail polish.

    “It just means a walking abnormality is present.”

    “And?”

    “And that could be caused by underlying conditions or injuries.”

    “Does that mean it could be something like Parkinson’s disease?” Virgil’s heart rate quickened.

    “It’s possible,” Logan admitted, “but we just can’t be sure with the little testing we’ve done.”

    “My blood test can help though, right? That’s what you said earlier.”

    “It’ll help us determine a diagnosis, but it’s likely the storm will delay it a couple days,” Logan glanced at Virgil apologetically, but it came off mechanically, “Anyhow, it seems optimal to take a short break from testing now.”

    Collecting up his clipboard, Logan stood in the door frame, “And in the meantime, a nurse will periodically check up on you.”

    “Okay…,” Virgil sighed.

     With Virgil taken care of, Logan strode down the long, achromatic hallway with his clipboard pressed up against his chest and his framed eyes fixed on the nurse’s station. His shoes squeaking against newly polished floors captured the attention of patients and doctors alike. And as he passed Dr. Whittaker reviewing a patient’s extensive charts, Logan offered him a polite smile.

     Now standing over the cubed nurse’s station, Logan watched as Patton’s fingers built a bridge between words, “Salutations, Patton.”

     Tearing his gaze from the new monitor, Patton grinned, “Hello, Logan.”

     “I’d appreciate it if you could check up on Virgil Poole for me before your shift ends in a couple hours. Maybe take a neurological history for me?” Logan didn’t waste time with idle chatter.

     “Sure thing,” Patton’s eyes and nose crinkled, “I’ll pay him a visit.”

     “Thanks Pat- ...Oh, Great,” Logan frowned, turning on his heel at the mere sight of Dr. Wilson’s poised approach.

     “Trying to avoid me, spectacles?” Dr. Wilson tsk’d.

     “Attempting to,” Logan muttered under his breath.

     Feigning an offended gasp, Dr. Wilson placed his palm over his chest.

     “But you adore our little chats, Lo,” he purred, inching close enough to Logan to count the careless stippling of freckles across his cheeks.

     “How are you, Roman?” Patton kindly interjected, fingers resting atop black keys.

     Flustered, Logan glanced down and away. He didn’t deny it.

     “Much better now that Lo’s back,” Roman grinned wide like a Cheshire cat.

     “I was only gone a week.”

     “And a terrible week it was.”

---

     Virgil peered out the frosted-over window through slats in the flimsy blinds, watching as specks of snow colored the road in ivory as the chilly air of the ceiling vent caressed his exposed skin.

    “Mr. Poole?”

     Virgil exhaled, shifting on the mattress to face the doorway, “more testing?”

    “Just here to collect a neurological history if that’s alright,” one of Patton’s palms rested against the door frame while the other seized a clipboard.

    “Go ahead, I guess,” Virgil raised his downcast eyes and shrugged slightly.

    “I can come back later,” instantly noticing Virgil’s hunched posture, Patton shifted his feet to retreat.

    “No- it’s fine. Ask away,” Virgil peered up before picking again at the remaining flecks of nail polish clinging to his nails.

    “Okay..,” Patton reluctantly stepped into the darkened room, brows knitted into a frown, “Do you have a history of head injury or seizures?”

    “No,” Virgil brushed away unattached, onyx, polish particles onto the stiff sheets.

    “Have you ever had surgery involving the nervous system?” Patton continued, pen tip pressed against papers shoved under the board’s metal clip.

    “No.”

    “Have you ever been treated for a neurological problem?”

     Another ‘no.’

     “Have you ever had a serious injury?”

     “If it matters, I broke my leg when I was nine,” Virgil rested his head in his now unbusy palm, gaze flitted to his crossed legs.

     “How were you treated?” Patton momentarily glanced up from the charts.

     “The doc had me wear a cast and use crutches for six weeks,” Virgil shrugged. He had been sketching - sketching wolves and bluishly radiant moons in the aged tree flourishing by his hinged, bedside window when he fractured his femur. Dropping his pen from the branch had sealed Virgil’s destiny as his balance departed with his attempt to capture it.

     “Do you have any residual effects from breaking your leg?”

     “..No.”

     Another scribble from Patton.

     “Do you have any other medical problems?”

     “Uh,” Virgil paused hesitantly, peering up to inspect Patton’s expression, “...anxiety.”

     “What about prescriptions?” Patton inquired, tilting his head, “are you currently taking any prescribed or over the counter medications?”

     “No.”

     Sighing, Patton scrawled the same answer in black pen on Virgil’s messy charts, “Could you tell me about your family’s medical history?”

     “Dad died of a heart attack and mom’s out of the picture,” Virgil huffed bluntly, shrugging with his eyes.

     “Any brothers, sisters, or cousins?” Patton donned a half-frown.

     “Nope, no, and no,” Virgil mumbled, missing the distraction that unwinding the threads of his coal-colored hoodie brought him.

    “Aunts? Uncles?”

    “Not that I know about.”

    “Oh..,” Patton frowned.

    “That all you need?” Virgil cleared his throat.

    “Uh-,” Snapping out of his haze, Patton replied, “yeah.”

    “That’s all I need,” He quickly clarified, rubbing the back of his neck.

     As Patton turned on his heel to leave, his steps faltered. He was incapable of halting his thoughts from sprinting painfully back in time to Remy. Shaking his head, Patton stopped in his footsteps and shifted to face Virgil, “Do you, uh, have anyone that will visit you? ”

    “What?” Virgil tilted his head, shoulders visibly slumping once he processed the question.

    Patton knew it wasn’t his right to pry, but he asked anyway.

    “I’m sorry,” Patton rapidly backtracked, “I- I really shouldn’t have asked.”

    “It’s whatever,” Virgil huffed, looking at his bare nails.

    “I could come and check up on you occasionally if you’d like,” Patton rushed through his words.

    “Uh-,” Virgil angled his head, unsure of what to make of the offer, “...sure.”

Tag list (ask to be added): @bunny222

[expertbodylanguage]

These color-coded illustrations show the superior (dorsal) surface and the inferior (ventral) surface of the cerebellum. The cerebellar peduncles are cut to provide this view. The ventral surface of the cerebellum is the roof of the fourth ventricle. The anterior, middle, and flocculo-nodular lobes of the cerebellum are traditional anatomic subdivisions with well-described syndromes derived from lesions.  The vermis, paravermis, and lateral hemispheres are cerebellar cortical zones that have specific projection relationships with deep cerebellar nuclei (vermis with fastigial nucleus and lateral vestibular nucleus; paravermis with globose and emboliform nuclei; lateral hemispheres with dentate nucleus) which, in turn, provide neuronal feedback to specific upper motor neuronal systems that regulate specific types of motor responses.  These relationships are key to understanding how the major upper motor neuronal systems are coordinated for specific functional tasks. https://www.instagram.com/p/CaVEF-pr31Q/?utm_medium=tumblr

[albertalice920]

If you haven’t heard of Hirayama’s Disease before, you’re not alone. Hirayama’s Disease is a neurological condition that primarily affects the lower cervical cord in young males, and is classed as a rare disease. Little is known about how it works, but the good news is that it’s not as serious as it may sound. Here, we offer a brief introduction to what Hirayama’s Disease looks like.

Understanding Hirayama’s Disease

Hirayama’s Disease is a rare neurological condition that causes gradually progressive atrophy of the muscles in the arms and forearms. Also known as monomeric amyotrophy (MMA), it primarily impacts young males in their late teens and early twenties. It was first defined by Keizo Hiramaya in Japan in 1959 as juvenile muscular atrophy. Hirayama’s Disease primarily affects young males in countries like India, Sri Lanka, Japan, Taiwan, and Singapore, although there have been cases in non-Asian countries too. The disease typically progresses the fastest in the first few years before stabilizing by itself.

Symptoms for Hirayama’s Disease

Typically, Hirayama’s Disease will manifest as a sudden weakness in one or both arms, leading to difficulty performing daily activities like writing or playing games. The classic symptoms for Hirayama’s Disease include:

Weakness in the hands and/or forearms

A ‘wasted’ appearance of the hands

Tremors in the hands

Unilateral / asymmetrically bilateral muscular atrophy

Excessive sweating of the palms

Impaired palmar grasp (the reflex by which one instinctively grasps something placed in the hand)

Hypertonia (in some cases)

Mild worsening of symptoms when exposed to the cold

Slow progression in the initial years followed by spontaneous stabilization

It is the disease’s tendency to stabilize it on its own, that separates it from motor neuron disease, which it is often mistaken for. There is also no sensory impairment in the hands.

Diagnosing Hirayama’s Disease

Patients who have been exhibiting symptoms for Hirayama’s Disease should visit the clinic right away. The doctor will examine the patient’s medical history and take notes on any family history of neurological conditions, before running multiple tests including blood, stool, thyroid, and urine. The diagnosis of Hirayama’s Disease is typically by exclusion, once the doctor has ruled out other possible culprits such as motor neuron disease, brachial plexopathy, multifocal motor neuropathy, and spinal cord tumours. An MRI can also detect signs like asymmetric Spinal Cord Atrophy, upper motor neuron lesions, and forward displacement of the posterior subdural sac upon neck flexion.

Treatment for Hirayama’s Disease

Hirayama’s Disease is a self-limiting condition, as the progression stabilizes on its own after some years. In addition, regular physiotherapy can help to restore strength in the arm and hand muscles and avoid secondary problems like joint stiffness or immobility.

In short, while it may be alarming to suddenly feel your hands and arms become weaker, Hirayama’s Disease is among the least serious forms of atrophy and will in fact cease progressing on its own. With early detection and intervention, you can keep the symptoms well under control and enjoy all the activities you love.

[mcatmemoranda]

The gait associated with an upper motor neuron lesion is referred to as a spastic, scissoring gait. The patient’s legs cross over each with each step. This gait is also associated with tight hip adductors.

[neurologyteachingclub]

Corticobulbar fibres- The lower part of the face receives UMN fibres from the opposite side alone while the upper part of the face and all other motor cranial nerves get bilateral innervation For discussion of this image follow ‘Clinical neurology with KD’ podcast episode one -Approach to weakness, in Apple podcast, Spotify or Google podcast. Full notes are available on the neurologyteachingclub.com website The corticobulbar fibres arise from the lower third of the motor homunculus. They descend in corona radiata and genu of the internal capsule to reach the brainstem. In the midbrain, it is in the medial part of the cerebral peduncle. In the basis pontis, the corticobulbar fibres are intermixed with the corticospinal tract. All motor cranial nerves receive corticobulbar fibres from the bilateral motor cortex except the lower part of the face. The lower part of the face gets corticobulbar fibres only from the contralateral motor cortex. That is why the lower part of the opposite face alone is affected in lesions involving the motor cortex, corona radiata or internal capsule. The other cranial nerves are spared as they get 50% of their fibres from the unaffected side. So a patient with a right internal capsule lesion will have left hemiplegia with left upper motor neuron facial palsy as the lower face gets its upper motor neuron only from the opposite side. The left lower part of the face alone is affected, and the facial palsy is on the same side of hemiplegia. The facial deviation is to the opposite side of hemiplegia. The eye closure will be normal as the upper part has bilateral representation. All other motor cranial nerves lose 50% of their upper motor innervation, but they will be asymptomatic as the rest 50% takes up the function. #clinicalneurologywithkd #neurologyteachingclub #NTC #neurology #neurosciences #neuro #clinicalneurology #medicine #clinicalmedicine #kdpodcast #mbbs #medicos #doctors #neuroanatomy #casediscussion #medicinecase #casepresentation #medicineresidents #residency #neuroimages #NEET #finalmbbs #approachtohemiplegiapodcast #mcq #neetpg #uppermotorneuron #corticospinaltract #pyramidaltract #corticobulbartract #umnfacial https://www.instagram.com/p/CWPUQ87vtVK/?utm_medium=tumblr

[science-online]

Upper motor neuron refers to the motor neurons of the cerebral cortex and their axons which terminate at the brainstem and spinal cord while the lower motor neu

[expertbodylanguage]

The oculomotor nerve (III) emerges from the ventral surface of the brain stem in the interpeduncular fossa, at the medial edge of the cerebral peduncle. In conditions of increased intracranial pressure in the anterior and middle cranial fossa, such as that caused by a tumor, edema from injury, or other space-occupying lesions, the brain stem can herniate through the tentorium cerebelli, a rigid wing of dura.  The resultant transtentorial herniation can compress the third nerve on one side that is ipsilateral fixed and dilatated pupil resulting from parasympathetic disruption and paralysis of medial gaze resulting from motor fiber disruption and compressing the cerebral peduncle on that same side, resulting in contralateral hemiparesis. The medullary pyramids contain the descending corticospinal tract fibers from the ipsilateral cerebral cortex, particularly from the motor and premotor cortex. The major crossing of the corticospinal tract takes place in the decussation of the pyramids (80%), producing the crossed, descending, lateral corticospinal tract in the spinal cord.  An infarct in the upper reaches of the anterior spinal artery or the paramedian branches of the vertebral artery can result in damage to the ipsilateral pyramid (contralateral hemiparesis); to the ipsilateral medial lemniscus (contralateral loss of epicritic somatosensory sensations such as fine, discriminative touch, vibratory sensation, and joint position sense); and the ipsilateral hypoglossal nerve (cranial nerve XII; paralysis of the ipsilateral tongue, which deviates toward the weak side when protruded).  This condition is called Dejerine's syndrome.  The hemiparesis is not spastic and is characterized by mild loss of tone, loss of fine hand movements, and a plantar extensor response (Babinski's sign). It appears that isolated damage to the pyramids does not result in spasticity.  Damage to other descending systems, from either the motor-related cortices or other upper motor neurons in the brain stem, must accompany pyramidal tract damage to produce spasticity. Thus, the term pyramidal tract syndrome, when used to describe spastic hemiplegia, is anatomically incorrect https://www.instagram.com/p/CaQIiIgL3yy/?utm_medium=tumblr

[lupine-publishers-tooaj]

Lupine Publishers | Pupil Functions in Diabetes Mellitus

Lupine Publishers | Trends in Ophthalmology Open Access Journal

Abstract

Pupil is innervated by autonomic nerve system. As a result, its dimension or actions well reflects the autonomic nervous system function. Pupillary autonomic neuropathy is considered an early symptom of the development of systemic autonomic neuropathy. Pupil tests present suitable and easy methods for evaluation of autonomic nervous system function. Most patients with autonomic nervous system disorders show data of sympathetic or parasympathetic deficits in the pupil, and these findings can be detected using a combination of clinical signs, pupillometric and pharmacological tests.

Introduction

As a circular aperture in the middle of iris, along with leading aqueus humor from posterior chamber to anterior chamber, pupil has functions like regulating the amount of light entering the orbit, increasing the focusing depth, decreasing the spheric and chromatic aberrations. Under normal circumstances pupil has a diameter between 2-6mm with an average diameter of 3 mm. In neonatal period/babyhood pupilla has a smaller diameter that reachs its normal size at around 7-8 ages. On the other hand it is observed smaller in size in the old age, related on atrophy of iris stroma (1).

The muscles in the iris stroma are responsible miosis and mydriasis of pupil. These muscles are examined in two groups. The encircling muscle fibers all around the pupil are settled in the iris and they are named as circular and sphincter muscles innervated by parasympathetic system. When they contract miosis of pupil happens. The parasympathetic nerve fibers leading to miosis start from Edinger-Westphal nucleus and end in ciliary ganglion and nerve fibers that start from ciliary ganglion end in circular muscles (Figure 1).The other muscle fibers located perpendicular to the pupil are radial (dilatator) fibers. These fibers are sympathetically innervated and lead to mydriasis. The start point of the fibers that bring sympathetic impulses to the radial muscles is posterior hypothalamus. Nerve fibers originating from this region descend from mesensephalon and pons and end in the Budge ciliospinal center which is located in between 8th cervical and 2nd thoracic spinal segments of the medulla. 2nd nerve fibers for pupil which start from this region leave the medulla especially from 1st thoracic spinal segment. After being neighbor on apex of lung while ascending, these fibers join sympathetic chain at the level of inferior cervical ganglion. Fibers passing directly through the inferior and middle cervical ganglions end in upper cervical ganglion. 3rd nerve fibers starting from the upper cervical ganglion enter the cranium with internal carotid artery and communicates with ophthalmic branch of trigeminal nerve in the cavernous sinus. Sympathetic fibers reach the radial muscles, responsible for mydriasis, through the ciliary ganglion by the nasociliary nerve and the long ciliary nerves (Figures 1-2).

The tract of pupillary light reaction is composed of an afferent way that takes light impulse to the central nervous system, and an efferent way that takes the response to the iris muscles. This tract is composed of an arc containing four neurons. First neuron is in between retina and pretectal nucleus which is in the middle brain at the level of superior colliculus. Ganglion cells that start from retina end in this center. Light reaction starts with the excitation of retinal photoreseptors by light. Impulses, coming from temporal half of the retina by nerve fibers not crossing at the optic chiasma, reach the pretectal nucleus by passing through the optic tractus on the same side. However impulses coming from nasal half of the retina crosses in the chiasma and reach the pretectal nucleus by passing through the contralateral optic tractus. Nerve fibers responsible for light reaction leave the optic tractus and reach out the pretectal nucleus without a stop by lateral geniculate nucleus. The second neuron is the neuron that connects the pretectal nucleus, on one side, to both Edinger-Westphal nuclei. This neural tract is the reason of symmetric constriction of pupils at the same time when a light impulse is given. The third neuron starts with Edinger-Westphal nucleus. These parasympathetic nerve fibers interfere with the motor fibers that come from other nuclei of nervus occulomatorius and they reach the ciliary ganglion in orbita. The course of these fibers in the nervous occulomatorius is important. These superficial fibers that course between the brain stem and cavernous sinus are sensitive to pressure in this region. A lesion that presses on nervus occulomatorius in this region leads to 3rd cranial nerve palsy that also affects the pupil. The fibers related to pupil take part in the center of the nerve after the cavernous sinus. For this reason, even there are lesions in this area that cause external ophthalmoplegia, pupil fibers are preserved even. After the enterance of nervous occulomatorius into the orbita, the nerve fibers related to pupil leave the nerve and reach the ciliary ganglion within the inferior branch that goes to the inferior oblique muscle, while the fourth neuron starts from ciliary ganglion and ends in the circular muscles of iris. In orbita the ciliary ganglion is located in the extraocular muscle conus, just behind the eye ball. Only the nerve fibers that bring pupil’s light reaction form synapses in the ciliary ganglion, while the others don’t form any synapses while ending in their related places. Figure 1 Neural pathways related to accomodation start from retina like the fibers responsible for light reaction. Unlike the fibers related to light reaction, they reach the visual cortex by the route of chiasma, optic tractus and optic radiation. The source of the impulses that lead to accomodation is the peristriat cortex that is located in the 19th area on the superior end of calcarin fissure. The impulses that excite from here somehow activates the Edinger-Westphal nucleus. Fibers that start from Edinger-Westphal nucleus and come in orbita with nervus occulomatorus, reach the ciliary ganglion. A group of postganglionic nerve fibers that leave from here, goes to ciliary muscle for accomodation, another group goes to medial rectus muscle for convergence and another group goes to circular muscle of iris for miosis (1).

The examination of pupil reactions provides information about autonomic nerve system of the eye. In order to set out the functions of ocular autonomic nerve system, either pharmacological tests that show the denervation hypersensivity, or measurement methods like time of pupillary cycles that show the integrity of pupillary reflex arc can be used. In diabetes, there are some changes occur in pupil, as there are in all structures of the eye. In diabetic people, pupil is smaller than normal values, and its response to mydriatics is lower. The reason of pupil being smaller in diabetes is because of impairment of the balance between sympathetic and parasympathetic innervation. Being longer than the nerve trace of parasympathetic innervation makes the sympathetic innervation more vulnerable to development of sympathetic neuropathy. A neuropathy in sympathetic innervation causes the parasympathetic system become effective resulting in the pupil smaller in size. Failure in accomodation, can be seen in diabetes. Factors like infiltration of glycogen in the ciliary muscle, diabetic neuropathy or changes in lens structure can lead to failure in accomodation.

One of the methods that give some information about pupillary reflex arc is the measurement of pupillary cycle time. It practically gives information about the afferent and efferent ways of pupillary light reaction and the integrity of iris. This test is done by biomicroscope. The examination room is provided to be dark and the patient is waited at least two minutes to adapt to the darkness. The light of biomicroscope is set to be in horizontal position and 6x0.5 mm in size. The patient places his head on biomicroscope and he is looked at a small red light which is at least 5 metres away to avoid accomodation. Then the light of biomicroscope is slowly brought on the edge of the pupil to drop it on the retina. The pupil constricts by the effect of light. For this reason retina is exposed to darkness again and pupil tends to dilate again. Meanwhile again by the effect of light that is brought before, the pupil constricts and enlarges in a rhythmic process. When the rhythmic process starts, the time of 100 processes of constriction dilatation is determined by keeping a chronometer in milisecond (ms) type. The duration of this process can be determined both by a single time or by summing up 50+50 or 30+30+40 processes in order to get a total time of 100 constriction dilatation processes. While normal duration is between 850 ms and 950 ms, for applications done in specific clinics, it is better to determine the normal values of people in the same conditions who are in similar age groups (Figure 3).

It is shown that depending on the poor glisemic control of patients with diabetes melliltus, autonomic neuropathy can develop frequently and by affecting especially cardiovascular system vital complications can occur. At the same time it is found that symptoms of ocular autonomic neuropathy are the precursors of symptoms of systemic autonomic neuropathy. Pupil changes in diabetes can be grouped as below.

Pupil Changes in Diabetes

Myopathic causes: The storage of glycogen in iris muscles of people with diabetes has been shown in studies. There are two main muscle groups in iris as known. Being one of these muscle groups as mentioned before, circular muscle fibers that sorround the pupil are innervated by occulomotor nerve and responsible for miosis. The other muscle group is located perpendicularly to the pupil that is innervated by sypmpathetic nerve system and responsible for mydriasis. Accumulation of glycogen in iris muscles lead to contraction disfunctions. Histologically apart from accumulation of glycogen in iris muscles, vacuoles ares seen in the iris epithelium. These vacuoles are accepted as a sign of acute diabetes and thought of originating from abnormal storage of glycogen (2).

Neuropathic causes: Pupil changes developed by neuropathic causes, can be examined under three major headings.

Optic Neuropathy: Ischemic optic neuropathy are more seen in patients with diabetes. The form of pupil change in optic neuropathy is afferent pupillary defect. The direct pupillary light reaction is weaken or lost in the eye where optic neuropathy has developed. In the other eye it is the same subject for the indirect pupillary light reflex (3-5).

Cranial Neuropathy: Pupil changes can come out depending on affected occulomotor nerve that is one of the cranial nerves. In such a case there are findings like efferent pupillary defect. There are also findings added to the table which develop depending on affected motor fibers. Parasympathetic nerve fibers taking part in the third neuron start from Edinger-Westphal nucleus and extend to the ciliary ganglion that is located in the orbita. Because of the course of nerve fibers in the occulomotor nerve, any lesion located in a region between the brain stem and cavernous sinus and presses on occulomotor nerve, leads to 3rd nerve pasly which also affects pupil. On the other hand in the lesions locating after the cavernous sinus, pupillary fibers can be preserved. After the occulomotor nerve enters the orbita, the fibers that bring the pupillary light reflex reach the ciliary ganglion within the inferior branch that goes to inferior oblique muscle. In the occulomotor nerve palsy, superior, medial and inferior recti with inferior oblique muscles are affected. However usually because of ptosis developed by affected levator palpebralis superior muscle, patients don’t complain about diplopia. Usually pupil is not affected in diabetic occulomotor nerve palsy. Nevertheless it should be kept in mind that there are also diabetic palsies in which the pupil is affected.

Autonomic Neuropathy:

a) Sympathetic

b) Parasympathetic

In long lasting diabetes, a decrease in physiological hippus and a smaller pupil in size are detected. These effects are thought to result from selective diabetic autonomic neuropathy that rather shows itself significantly more in sympathetic system than parasympathetic system. Diabetic autonomic neuropathy which is a complication of diabetes, manifests itself as pupillary disfunction in the eye. Autonomic neuropathy is asymptomatic in the early stage and it can be reversible by glisemic control in the early stages of diabetes. In order to aviod permanent pathologies, scanning of autonomic disfunction is substantial. Pupil tests would be a method for the diagnosis of such a case at the earliest time. Pfeifer et al have shown that autonomic pupil disfunction has shown itself as miosis, and they has stated that this situation was due to impairment of balance between sympathetic and parasympathetic innervation, in favor of parasympathetic system (6).

Clark has determined that there are parasympathetic denervation supersensivity with %2,5 metacolin and sympathetic denervation supersensivity with %0,5 phenylephrin in patients with diabetic retinopathy. They had also determined a significant relationship between proliferative diabetic retinopathy and autonomic neuropathy. They had found that in proliferative cases, the incidence of rate of the parasympathetic retinopathy was %36, sympathetic neuropathy was %38; where as in nonproliferative cases they were %6 and %5 respectively (7).

Cahill et al have argued that the pupil responses to the %4 cocaine were same both in diabetics and control group, and for this reason they had argued that in both groups the sympathetic tract was intact (8). In the same study they had suggested that the changes in the superior cervikal ganglion were causing denervation hypersensivity in sympathetic tracts and this was the reason for the pupillary changes in diabetics. On the other side, (9) have studied the denervation sensivity of aproclonidin. They have shown the denervation sensivity in diabetic cases and found it to be proportionate to the duration and severity of the disease (5).

Söylev et al. (10) have studied the response to diluted pilocarpine in groups of diabetic patients with or without retinopathy and in control group. They have found a response to diluted pilocarpine more in diabetic group with retinopathy, according to diabetic group without retinopathy and control group (10). At the same time they have detected that marked mydriasis developed with diluted phenylephrine in diabetic group with retinopathy, which was found significantly different comparing to the other groups.

Clark et al. (11) have detected the rate of the defect in pupillary reflex arc as %88,5 in patients with proliferative diabetic retinopathy. They have also mentioned that this result was the earliest sign of autonomic nerve disfunction (11). Pena et al. (12) emphasized that the pupillary symptoms were the earliest evidence of autonomic nerve disfunction.

In our study the pupil cycle time was found longer in diabetic cases. At the same time the rate of inability of measuring pupil cycle time was found more in the diabetic group. Pupil cycle time was found related both with the existence of diabetic retinopathy and the level of periferic retinopathy (13). As seen in all structures of eye, there are some changes in diabetes that can be seen in the pupil, too. These changes can be basicly myogenic or neurogenic. As a complication of diabetes, diabetic autonomic neuropathy can show itself as pupillary disfunction in the eye, so early diagnosis is significant. Pupil findings usually come out in direct proportion to the length and severity of diabetes (14). Rarely they can be seen in the early stages of diabetes; even sometimes before the somatic neuropathy. The findings of cardiovascular system among the systemic autonomic neuropathy findings are vitally important. By determining the abnormalities of pupillary function earlier, growth of autonomic function abnormalities of cardiovascular system may be prevented and measures for diabetic regulation may be taken. Autonomic neuropathy is asymptomatic in early phase and it can be reversible by glisemic control in early stages. From this point, scanning for autonomic disfunction is important to prevent permanent pathologies. Pupil tests can be methods for diagnosis of this situation in the earliest time

 https://lupinepublishers.com/ophthalmology-journal/pdf/TOOAJ.MS.ID.000122.pdf

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[mcatmemoranda]

Seizures

Seizure types in newborns are considerably different from those in older infants.

Unlike older infants, newborns rarely have organized, generalized, tonic-clonic seizures.

Seizures are often subtle and may manifest as jerking or horizontal deviation of the eyes; blinking or fluttering of the eyelids; drooling, sucking, or lip smacking; tonic posturing of a limb; or apnea.

Jitteriness

Jitteriness is distinct from seizure activity.

With jitteriness, the movements are stimulus-sensitive, generalized and symmetric, and can be diminished by gentle, passive flexion of the limbs.

Myoclonic Jerks

Brief myoclonic jerks in and of themselves are not abnormal in infants and are often noted when the infant is falling asleep.

Clonus

Ankle clonus (spasmodic alternation of muscular contractions between antagonistic muscle groups caused by a hyperactive stretch reflex from an upper motor neuron lesion) of up to approximately 10 beats also should be considered normal in the newborn period if no other neurologic signs are present and it is not distinctly asymmetric.

Clonus normally disappears rapidly; more than 3 beats in a child 1-2 months old is abnormal.

[neurologyteachingclub]

Schematic diagram showing the Upper Motor Neuron. For discussion of this image follow ‘Clinical neurology with KD’ podcast episode one -Approach to weakness, in Apple podcast, Spotify or Google podcast. Full notes are available on the neurologyteachingclub.com website. The corticospinal tracts are excitatory and mostly use glutamate as the neurotransmitter. It starts in the motor cortex and ascents in corona radiata to reach the anterior 2/3 of the posterior limb of the internal capsule. In the internal capsule, the fibres to the upper extremity are arranged more anteriorly. They lie close to the corticobulbar fibres, which travel in the genu of the internal capsule. The corticospinal fibres then ascend down in the middle 3/5 of the cerebral peduncle in the midbrain, basis pontis and the medullary pyramids. At the lower end of the medulla, 75%-90% of fibres cross over to the opposite side to form the lateral corticospinal tract in the spinal cord. The fibres then ascend down through the cervical, thoracic, lumbar and sacral spine to reach the corresponding spinal segment it innervates and synapses with alpha motor neurons at that level. A lesion anywhere in this pathway from the motor cortex through corona radiata, internal capsule, midbrain, pons, and medulla and then crossing to the opposite side in lateral corticospinal tract in cervical, thoracic, and lumbar spine can produce weakness with UMN features like spasticity, hyperreflexia and upgoing plantar. #clinicalneurologywithkd #neurologyteachingclub#neurologypodcast #NTC #firstpodcast #neurology #neurosciences #neuro #clinicalneurology #medicine #clinicalmedicine #kdpodcast #mbbs #medicos #doctors #neuroanatomy #casediscussion #medicinecase #casepresentation #medicineresidents #residency #neuroimages #neurophysiology #NEET #mcq #neetpg #uppermotorneuron #corticospinaltract #pyramidaltract https://www.instagram.com/p/CWPTyUYvuNn/?utm_medium=tumblr

[s-camp]

Clonus - (from the Greek for "violent, confused motion") is a series of involuntary, rhythmic, muscular contractions and relaxations. Clonus is a sign of certain neurological conditions, particularly associated with upper motor neuron lesions involving descending motor pathways, and in many cases is, accompanied by spasticity. Just about every definition of clonus talks about the involuntary movement but you can learn to work with it. I know how to trigger most of my bodies responses and how to suppress them. I normally don't go through this shaking while working on the balance board but wanted to show what clonus looks like, and turning it off and on. I regularly excersice and do activities that are the hardest for my body so I can learn to tolerate them or improve the signal. It's been fascinating to me that I can somewhat find the neuro pathways that were damaged by going through certain movements positions. Always learning 😁 #quadriplegic #tetraplegic #sci #spinalcordinjury #paralyzed #improve #everydamnday #recovery #rebuild #gymlife #balance #consistancy #dedication #clonus #physicaltherapy #neuro #neurology #hope #faith #grateful #myjourney #believe