I still continue to get many questions from the readers of my blog regarding multiple sclerosis (MS). A significant majority of them write to me because they are concerned they may have MS either because of white matter lesions found on a MRI scan of the brain or because they are plagued by various non-specific signs and symptoms. Though I have written about this before, I thought this shall be a good time to go over how the diagnosis of MS is made. What are the symptoms that raise the suspicion for MS, what are the clinical signs on examination that suggest MS and finally what are the tests that may help to confirm the diagnosis.
Before I dwell deeper into this topic, please remember: THE DIAGNOSIS OF MS IS A CLINICAL ONE. Meaning that it can be made on the basis of a history and clinical examination itself. No tests are needed in such a situation to confirm the diagnosis. Of course as it is often in medicine–it is always not that easy.
So let us begin—
Clinical history: Are there any points in the clinical history of the patient that suggest the diagnosis of MS? Patients with MS may give a history of neurological symptoms and signs (remember signs are elicted on clinical examination-meaning when the doctor examines you) that wax and wane (relapsing and remitting MS). A patient may present with acute loss of vision in one eye along with pain in the eye (I am talking about optic neuritis). As the doctor dwells deeper into the history, the patient volunteers that a couple of years ago he had a similar problem in the other eye which had resolved on its own and he had not been investigated further. Hmmm–now we have history of 2 attacks separated in time. As a neurologist this makes me think of MS as a possible diagnosis. The problem with MS though is that it may present with non-specific signs or symptoms or rather it may present with signs and symptoms that localize to different parts of the central nervous system (CNS). By CNS I mean the brain and the spinal cord. So for example patients may present with numbness on weakness on one side of the body (this localizes to the contralateral motor or sensory cortex), problems with the bladder (incontinence–this usually localizes to the spinal cord), problems with balance and coordination (their gait is off and they may have a prominent tremor in their limbs–this localizes to the cerebellum or the brain stem), double vision (this localizes to the cranial nerves which control the movement of the eyes). Virtually any part of the central nervous system can be involved–hence the presentation is at times non-specific. BUT WHAT HELPS US AS DOCTORS IS WHEN WE GET HISTORY WHICH SUGGESTS A DISEASE DISSEMINATED IN SPACE AND IN TIME. Meaning a disease process which is involving different parts of the central nervous system and which has shown evidence of multiple attacks separated by time. REMEMBER MS IS NOT A MONOPHASIC ILLNESS (it relapses and remits!!!)
Clinical examination: So what are the clinical examination findings which make me as a neurologist think of MS in a patient. There are certain neurological signs which have been said to be pathogonomic of MS (meaning the presence of these signs virtually seals the diagnosis of MS). These include certain eye signs. Bilateral internuclear opthalmoplegia (INO) (who said neurology was easy!!!) is one such sign. This is an eye-sign in which the patient’s eyes do not move as directed by the examiner. One eye fails to adduct (that is move inwards) while the other eye abducts (moves outwards) but the abducting eye shows a nystagmus (shaky side to side movement). Other eye signs such as an afferent pupillary defect (this is elicted by shining a penlight into the eye) also raise suspicion for MS. What we as neurologists look for though is this–we look for signs that suggest the disease is disseminated in the CNS. REMEMBER WHAT I TOLD YOU ABOUT MS. IT IS A DISEASE WHICH IS DISSEMINATED IN TIME AND SPACE.
Tests: so when a diagnosis of MS cannot be made on the basis of history and examination alone, we as doctors have to fall back on tests to rule in or rule out the diagnosis. No test seals the diagnosis of MS by itself. They just help to add to our certainity. I shall discuss the various tests namely –imaging studies such as MRI scan of the brain and spinal cord., evoked potential studies such as visual evoked potential (VEP), somatosensory evoked potential (SSEP), brain stem auditory evoked potential (BAEP), spinal fluid (CSF) examination in the next post.
Nitin Sethi, MD
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Tags: clinical history, examination, MRI, MS, Multiple sclerosis, spinal tap, SSEP, tests, VEP
Post Traumatic Epilepsy
Nitin K Sethi, MD
Assistant Professor of Neurology
New York-Presbyterian Hospital
Weill Cornell Medical Center
New York, NY 10065
In this post I shall discuss the entity called post traumatic epilepsy/ post traumatic seizure disorder. Epilepsy is a condition characterized by two or more seizures in a person’s lifetime. Broadly speaking epilepsy can be of two kinds:
1. Primary Epilepsy
2. Secondary Epilepsy
Patients who have primary epilepsy have seizures usually due to an underlying genetic predisposition. They do not have a secondary cause for their seizures and neuroimaging is usually normal. On the other hands patients who have secondary epilepsy usually have seizures secondary to something (example secondary to brain tumor, secondary to an abscess in the brain, after a stroke and so forth). Under this category of secondary epilepsies is included post traumatic epilepsy (as the name suggests patients have seizures secondary to brain trauma).
Let me explain with the aid of an example. Let us assume our patient (we shall call him Philip) is a 27-year-old healthy male with no significant medical or surgical history. Bikes are his passion especially Harleys. Have you seen the ones they show on American Chopper. But we are digressing from our story line. Philip loves to ride them fast. A bright sunny Sunday morning finds him zipping down FDR drive at 80 mph. With a bike under me, I felt like a real man. And then disaster strikes. Philip’s bike gets clipped by a speeding SUV. Philip is flung from the bike and hits the ground hard. Did I mention he was not wearing a helmet at this time. He is rushed to the nearest hospital. A lacerated spleen, couple of broken ribs and a fractured collar bone. Not too bad you might say. He shall live to ride another day. But all is not so rosy. Philip does not regain consciousness and does not respond to verbal commands. A quick CT scan yields the answer. Philip has suffered extensive bleeding in the brain (neuro trauma). He is admitted to the neurological ICU. Recovery is painfully slow and after a months stay in the hospital, Philip is discharged to a sub-acute rehab facility. Alls well that ends well? Not quite done yet, I am afraid. Six months after his motorbike accident, Philip is again rushed back to the hospital after a witnessed tonic clonic convulsion. He is evaluated by a neurologist (like me) and a diagnosis of post traumatic epilepsy is made.
So what exactly is post traumatic epilepsy? As the name suggests epilepsy develops after head injury. Seizures can occur anytime after head injury. If they occur immediately after head injury it is referred to as immediate post traumatic epilepsy (also called impact seizures, as seizures occur at the time of impact to head). If seizures occur within the first month after head injury it is referred to as early post traumatic epilepsy. Patients may have their first seizure as long as 18 months after head trauma. This is referred to as late post traumatic epilepsy.
Patients develop post traumatic epilepsy as a result of scarring of brain tissue. They usually have convulsions. The treatment of post traumatic epilepsy is essentially the same as that of any other type of epilepsy. Once the seizure type is characterized, the right anti-epileptic drug is usually effective in controlling the seizures.
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Tags: epilepsy, neuro trauma, seizure, trauma
Braindisease Weblog
I wanted to thank all my readers for their comments and suggestions. I shall try to improve this blog further. Bear with me though, it is a solo endeavor. Most of the posts are written on the run and so if my grammer or spelling is off, please excuse me.
Personal Regards,
Nitin Sethi, MD
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Disclaimer
Please do read my disclaimer. The purpose of my blog is purely educational and to disseminate information about neurological and neurosurgical diseases and condition. It is not meant to diagnose yourself over the Internet.
The information provided in this blog should not be used during any medical emergency or for the diagnosis or treatment of any medical condition. A licensed medical professional should be consulted for diagnosis and treatment of any and all medical conditions. Call 911 if you have a medical emergency.
Links to other sites are provided for information only — they do not constitute my endorsements of those sites.
Any duplication or distribution of the information contained herein is strictly prohibited.
Nitin Sethi, MD
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Tags: blog, diseases, neurology, neurosurgery, website
Incidentally discovered aneurysms in the brain-what to do about them?
Nitin K Sethi, MD
Assistant Professor of Neurology
New York-Presbyterian Hospital
Weill Cornell Medical Center
New York, NY 10065
Recently I saw a patient in my office. She had undergone a MRI scan for headache. The MRI scan revealed a 4 mm aneurysm in the left middle cerebral artery with a 2 mm neck. I reassured her that the aneurysm was not the cause of her headache and that she more than likely had migraine headaches when she asked me the million dollar question which I had been expecting all along.
Dr. Sethi, but what to do about the aneurysm? Can it rupture? Do I need surgery to take care of it she asked me? I answered her questions according to the best scientific evidence I had at my disposal. That patient visit though got me thinking about how many patients face the same dilemma. That is the purpose of this post. When aneurysms are discovered incidentally in the brain, what needs to be done?
In keeping with my style of writing, I shall keep this simple. Simply put when an aneurysm is discovered in the brain, there are 2 avenues open to us.
Avenue 1. DO NOTHING (otherwise called the WAIT AND WATCH policy). The aneurysm may never rupture in the patient’s lifetime so why touch it. The wait and watch policy works best for aneurysms which are small in size (less that 5 mm in size, some books say aneurysms less that 7 mm in size may be safety observed). Small sized aneurysms in hard to reach areas of the brain can be justifiably observed. What do I mean by hard to reach areas of the brain? Let me explain with the aid of an example. Let us assume Kim our fictitious patient has a 3 mm aneurysm in the cavernous portion of the left internal carotid artery. This is the portion of the internal carotid artery that traverses the cavernous sinus. Now this area is difficult to reach “safely” by the neurosurgeon. The risks of surgery are tangible and may outweigh the potential benefits (remember as the aneurysm is small in size the risk of rupture is low). Better to wait and watch rather than go about chasing this aneurysm.
I said WAIT AND WATCH not WAIT AND FORGET. Meaning the patient should be advised to remain in follow up. The aneurysm should be followed by serial MRI scans done at intervals varying from 6 months to 1 year. Initially the follow up is more frequent, once we have documented that the aneurysm is not increasing in size, the scans can be repeated less frequently. If the aneurysm starts increasing in size then a more “active” course can be pursued. If the patient is hypertensive, good blood pressure control should be the goal as risk of aneurysm growth and rupture increases if blood pressure remains elevated.
Avenue 2. PURSUE AN ACTIVE STRATERGY. Simply put it means “taking care” of the aneurysm surgically either via open craniotomy or via an endovascular approach. Let me explain this. Let us assume Kim has a 10 mm sized aneurysm is the right middle cerebral artery territory. We can approach this aneurysm in 2 ways. First is via an open craniotomy, meaning that open up the skull (we call this a craniotomy), visualize the aneurysm and then secure it with a clip or a band. Once the aneurysm is clipped it cannot rupture as it is excluded from the circulation. PROBLEM SOLVED!!!
Second approach is via an endovascular route. No craniotomy is required. The endovascular surgeon or the interventional neuroradiologist threads a catheter via the femoral artery in the groin and reaches the aneurysm in the brain. Once there he coils it (coils of platinum coated with a thrombogenic material are deployed inside the aneurysm). Over time the aneurysm clots and seals itself from the circulation. PROBLEM SOLVED!!!
Broadly speaking endovascular coiling is superior to open craniotomy (at least in some respects). As no craniotomy is required hospital stay is shorter and post-operative recovery quicker. The endovascular surgeon can reach areas where the neurosurgeon may fear to tread. Certain aneurysm though are not amenable to coiling (example those with a broad neck as the coils fall out). Also once an aneurysm is coiled it takes time before it gets completely thrombosed, surgery on the other hand takes care of the problem then and there.
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Tags: aneurysm, clipping, coiling, craniotomy, endovascular surgery, incidental aneurysm, intracranial hemorrhage
I recently did an interview on the doctor patient relationship. Here I reproduce just a small part of it.
You can read the whole interview on Multiple Sclerosis Central.com by clicking on the following link.
http://www.healthcentral.com/multiple-sclerosis/c/73302/70302/patient
I have asked Doctor Nitin Sethi to contribute to this discussion through an interview about this very topic of the doctor-patient relationship. Doctor Sethi will discuss this relationship from a doctor’s point of view and in part two of this series we will examine the same relationship from a patient’s perspective. The patient will be me. I do encourage you to offer your viewpoints through the form of comments to these articles.
I introduce to you: Nitin K Sethi, MD who is the Assistant Professor of Neurology at New York-Presbyterian Hospital of Weill Cornell Medical Center located in New York City.
What do you feel are some of the personal qualities which are important for a doctor to develop rapport and trust with patients?
A lot has been written about doctor patient relationship and what qualities define it. Nowadays in medical school itself there is a thrust not just to produce smart doctors but also to produce more humane doctors. A study had shown that student doctors (medical students) have the highest levels of empathy. As they go through their long training (residency and at times fellowship), this empathy progressively decreases. One may argue that “experienced” doctors become less humane. I do not buy that argument. I feel the empathy gets replaced by knowledge. You know what you are dealing with and you understand disease pathology better. This might make a doctor sound aloof and like a “machine”. He is very good at what he does but he is cold and aloof.
My patients frequently tell me that they left their previous doctor because he would not hear them out or he was not caring enough. They rarely say I left him because he was incompetent. I want to make this point to answer your question. Some of the smartest doctors I know (people I would go to if I had a neurological problem) do not have the greatest bedside manners. They are not most suave. But as a patient I would rather go to a competent doctor than to one who says all the right things in the right way but is not the smartest light.
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Tags: doctor, health, Multiple sclerosis, patient
Hypothermia and Brain Arrest Protocol
Nitin K Sethi, MD
Assistant Professor of Neurology
New York-Presbyterian Hospital
Weill Cornell Medical Center
New York, NY 10065
Recently I attended the American Academy of Neurology (AAN) annual meeting held in Seattle. One of the topics of interest was the use of hypothermia to improve the outcome of patients after cardiac arrest or traumatic brain injury. Since the neurological outcome of patients presenting after a cardiac arrest (whether in hospital or out in the field) is usually dismal, I thought this shall be a good topic for me to discuss here.
The brain needs oxygen to survive and does not do well if deprived of oxygen. Hypoxia (lack of oxygen) occurs after cardiac arrest (the circulation of blood to the brain is interrupted when the heart stops beating as occurs in a cardiac arrest). If the circulatory flow is not rapidly reinstituted (meaning the heart is not restarted) irreversible neuronal death ensures. The usual scenario is as follows. A patient suffers an out of hospital cardiac arrest. A call goes out to 911. The EMS team is on the scene shortly. The patient is noted to be either in cardiac arrest (we call this asytole) or the heart is beating but ineffectively and there is no palpable pulse (we call this ventricular fibrillation). The heart is revived by either injecting drugs or shocking (with the help of a hand held defibrillator) and there is return of palpable pulse. Alls well you might say but the story is far from over!!!
Even though the heart has been revived the brain has taken a hit. During the time when the heart had stopped, there was a lack of blood flow and oxygen to the brain and irreversible neuronal death has occured. So we have a patient whose heart is now beating but the brain is dead. This patient may never make a meaningful neurological recovery. Some of these pateints end up in persistent vegetative state (PVS) or minimally conscious state (MCS).
By the time, I as a neurologist am called to see the patient, there is precious little I can do. The brain is already dead!!! I can just prognosticate and tell the family that their loved one shall never have a meaningful neurological recovery. In other words, I help them in deciding when to pull the plug!!! Nothing makes me feel more helpless. I did not enter neurology to prognosticate, I entered neurology and medicine to save a life and heal.
So that is why hypothermia for cardiac arrest sounds so promising. Recent studies have shown that if the brain is cooled (there are different ways to cool the brain from using high tech cooling blankets and beds to more primitive but equally effective techniques like bags of ice) to 32-34 degree centigrade for 12-24 hours following cardiac arrest, neuronal death does not occur. Till the heart is revived, the brain remains viable!!!
This research has led to the institution of a Brain Arrest Protocol in some big academic centers. Once a patient who has suffered a cardiac arrest is received, hypothermia protocol is immediately instituted. This has resulted in improved survival rates in these critically ill patients. Patients not only survive but they survive with good neurological outcomes.
If the hypothermia is prolonged or if the temperature is lowered too low it can cause complications and increase the risk for sepsis and cardiac arrhythmia. Hence this protocol is at present still in its infancy but I have a feeling this shall become a standard of care very soon.
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Tags: brain arrest, brain damage, cardiac arrest, hypothermia, MCS, minimally conscious state, persistent vegetative state, PVS
Is it a seizure or is it syncope? the story continues….
So our story ended with John in the ER. As many of you rightly guessed the first case scenario represents a typical syncopal episode while in the second case John had a generalized convulsion (seizure).
So what are the points in the history which favor syncope and which favor a seizure?
When a patient presents to a neurologist with an episode of loss of consciousness, it is imperative that we try to elucidate the underlying cause. As you can imagine the treatment of both these conditions is very different.
Syncope (fainting) can come either from the heart (we call this cardiogenic syncope) or from the brain (we call this neurogenic syncope or vasodepressor syncope or more commonly as vasovagal syncope). So for example you can faint (have a syncopal episode) if you have a sudden massive heart attack, or a transient arrhythmia of the heart (the heart beat fluctuates). As you can imagine these are potential lethal causes and hence patient’s who present with syncope are frequently evaluated for these cardiac conditions. Tests like ECG, prolonged 24 ECG (electrocardiogram) and sometimes an echocardiogram are ordered. Vasovagal syncope on the other hand is more benign and our patient John likely had a vasovagal syncopal episode in case scenario No 1. Another classical example of vasovagal syncope is when someone faints when he or she sees blood for the first time (frequently reported in medical students when they go into the OR for the first time).
So what are the points which favor syncope?
1. Feeling light-headed prior to the episode
2. Feeling dizzy as if you are about to faint.
3. Blurring of vision at the onset of the episode ( Doctor I felt light headed, a little woosy, my vision started to go black and then I passed out)
4. Syncope usually occurs in an upright position (patient is usually standing when it occurs). Syncopal patients usually do not shake (that is they do not have convulsive movements. There is an entity called syncopal convulsion where in the episode starts with a syncope but then goes on to become a seizure. I shall not go into the details here as then it shall become confusing).
5. Usually the loss of consciousness is of very short duration. Once they fall to the ground and the blood rushes to their brain (as gravity has been eliminated), they rapidly regain consciousness.
6. They are not confused after the episode. They come around rapidly and know where they are (they are not confused and disoriented after the episode).
7. Syncopal patients usually do not bite their tongue or have loss of bladder control (wet their patients) during an episode.
What are the points which favor a seizure?
1. Patients who have a seizure do not get the type of prodomal symptoms which patients with syncope do. Meaning they do not feel light-headed, dizzy as if they are about to pass out. Seizures frequently occur out of the blue with no warning whatsoever. That said and done, some patients with seizures which come from the temporal lobe may get an aura. Multiple different types of auras have been reported in temporal lobe epilepsy (smell of burning rubber, metallic taste in the mouth, a rising sensation in the tummy among many others).
2. Seizures can occur in any position-standing, sitting, lying in bed and frequently in sleep too.
3. Patients who have a convulsion shake. We call this tonic clonic movements of the arms and legs (first they are noticed to stiffen up, the eyes may roll up or get deviated to one side and later jerking of the arms and legs occur).
4. The tongue may get caught inbetween the teeth as the patient is stiffening up or when they are having a convulsion (shaking). This frequently leads to a tongue bite (usually on the lateral border of the tongue).
5. When the patient stiffens up, the muscles of the urinary bladder go into a spasm and the patient may end having loss of bladder control (wet their pants). This may also occur when the seizure finally ends and the muscles relax.
6. Frequently patients after a seizure are confused and disoriented for a while. We call this the post ictal state.
7. Seizures frequently lead to loss of muscle tone. The patient falls and hits the ground hard. This may lead to cranio-facial injuries and even fractures. Patients with syncope on the other hand do not fall hard, rather thay seem to ease themselves to the ground.
As you can see now syncope and seizures may resemble each other superficially but a good history is usually able to clarify the diagnosis.
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Tags: convulsion, epilepsy, post ictal state, seizure, syncope, vasovagal syncope
Is it a seizure or is it syncope: going over the basics again
Nitin K. Sethi, MD
Assistant Professor of Neurology
New York-Presbyterian Hospital
Weill Cornell Medical Center
New York, NY 10065
I have written about this before but thought this would be a good time to go over the basics again. So let us begin with an example. Our main actor (lets call him John) is working in his office. The clock strikes 12 and he decides to step outside to smoke. It has been a tough day at work for John. Went out with a couple of friends last night and had one too many Jack Daniels on the rocks (with a slice of lime!!!). This liberal indulgence in the bubby resulted in John waking up dehydrated and with the worst hangover of his life. That combined with a cold he is still nursing and you can imagine John is a very unhappy camper.
So John steps out to smoke. Lights up and takes a deep puff. Ahhhhhhhhhhhhhh. And then it happens. He feels light headed, dizzy, his vision starts to grey and before he knows it he is on the floor. His friend who sees him fall, rushes to help him. By the time he reaches John, John is already coming around. He attempts to get up on his feet and asks his friend what happened. He is alert and oriented and apart from a bruised ego, he feels well.
Now lets go to case scenario number 2. John is again our main actor. In this case though John is having a good day. He slept well the night before and steps out to have a smoke. He lights up. Ahhhhhhhhhhh. Life sure feels good. And then it happens. He stiffens up. A cry is heard (we call this the epileptic cry) and then he takes a hard fall to the ground. After falling to the ground, he is noted to “shake” by his friend who has since rushed to his side ( I saw him shaking–both arms and legs, it was horrible. He was foaming at the mouth and I thought he was going to die is how his friend describes the event to the EMS later on!!!). After a minute, John stops shaking but he does not come around immediately. He remains confused and disoriented till the arrival of the EMS 15 minutes later. John later tells the doctor in the ER that he has bitten his tongue and lost control of his bladder (wet his pants) during the episode.
So after presenting these two case scenarios, my question to you is in which scenario did John have a syncope (fainting episode) and which was a seizure?
In the next post we shall pick up John’s story from the ER. Hopefully we can make him feel better.
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Tags: fainting, loss of consciousness, passing out, seizure, syncope, tongue bite
Epidural hematoma: when a “minor” head injury may prove to be fatal
Nitin K Sethi, MD
Assistant Professor of Neurology
New York-Presbyterian Hospital
Weill Cornell Medical Center
New York, NY 10065
Many of you must have read about the tragic demise of actress Natasha Richardson from blunt (closed) head trauma she sustained after falling on a ski slope. While exact details about the extent and nature of her injuries are unclear, it drew attention to blunt (closed) head trauma. I shall discuss about the same here.
Broadly speaking head injuries can be of two types: penetrating head injuries and closed head injuries. An example of a penetrating head injury is a gun shot wound to the head or when a person is involved in a motor vehicle accident with significant polytrauma (including fracture of the skull and bleeding into the brain). Penetrating head injuries are usually easily identified by first responders (emergency medical services such as the ambulance crew responding first to the call). Usually there is an obvious scalp laceration and blood is seen oozing from the site of the injury. Later when the patient is transferred to the hospital, the extent of the injury can be better documented. For this usually a CT scan of the brain is done (at times a MRI brain may be carried out). Penetrating head injuries vary depending upon the mechanism of injury (example velocity, trajectory and size of the bullet in the case of gun shot wounds to the head). Patients with penetrating head trauma are critical and require urgent stabilization usually in an intensive care setting.
It is the closed head injuries though which can be a little deceiving and that is where I shall like to steer this discussion. The mechanism of closed head injuries is usually blunt trauma to the head (example a fall, a blow to the head while boxing and so on). One special type of closed head injury is a concussive injury from an improvised explosive device (IED). These IED related injuries have become the signature injury in the battlefields of Iraq and Afghanistan. But moving away from the battlefield, closed head injuries are frequent. Most of them are mild as the ones sustained while playing contact sports like football or boxing or when you get up in the middle of the night to go get a glass of water only to bump your head against a door. One “sees stars” for a while but is none the worse for wear apart from a bruised head and maybe ego (especially if you are like me and love to box). But can seemingly innocuous looking closed head injuries prove to be fatal? Can a “minor” fall or blow to the head kill you?
Well yes and this brings us to epidural hematomas. Let us assume you suffer a “minor” closed head injury. What you may ask exactly is “minor” closed head injury. Well it usually refers to an injury in which there is no prolonged loss of consciousness (example is a concussion after a blow to the head or a fall). As the scalp is not lacerated there is no obvious external bleeding. The patient may suffer a minor black out (loss of consciousness for a few seconds to minutes) but soon is awake and seems alert and able to answer questions.
Imagine a boxer, who walks into a straight right. BOOM!!! Down he goes. The referee counts him out. It is a KO. The ring side doctor rushes in. The boxer eyes are glazed but he is coming around and slowly is able to get up and walk out of the ring unassisted. Nothing but a bruised ego and a black eye. He shall live to fight another day you may say as a spectator but the next day you read in the papers that the boxer was found dead in his bed. What happened here? Well the answer is simple. Even though the boxer seemed to have a suffered a “minor” closed head injury, a far more sinister injury process started silently in the brain. The blow to the head caused one of the small arteries (usually a branch of the middle meningeal artery) to start leaking blood. This blood starts collecting in the potential space between the brain and the skull (we call this the epidural space and hence a collection of blood in this space is called an epidural hematoma). As the leak is small, the patient seemingly recovers and looks fine. He may answer questions appropriately and hence may decide not to seek further medical attention. This interval where the patient (in our case our boxer) looks fine and seems to have recovered from the head blow is called the LUCID INTERVAL (the patient is lucid, makes sense and looks normal). But things are already starting to go wrong. The small leak from the ruptured blood vessel leads to progressive accumulation of blood in the epidural space. When the epidural hematoma becomes large, it has no place to expand (remember there is a rigid bony skull which prevents the blood from coming out). So the underlying brain starts getting squashed. This leads to a depression in the level of consciousness as the pressure inside the brain increases. If the elevated intracranial pressure is not brought down urgently the patient may die (we call this herniation of brain due to elevated intracranial pressure).
Could our boxer have been saved? Yes by all means. If he had been kept under observation (sometimes we like to observe patients with closed head trauma overnight in the hospital), then the first signs of raised intracranial pressure would have been picked up. Usually this is a change in the level of consciousness (the boxer would have become drowsy or hard to wake up, may have complained of headache). An urgent CT scan would have revealed the epidural collection of blood and neurosurgical evacuation of the blood would have been carried out (the skull is opened and the blood is drained out. The bleeding vessel is identified and cauterized to achieve homeostasis).
So what are the take home points from our boxer’s story?
-some “minor” looking closed head injuries can indeed prove to be fatal.
-patients should be observed after a closed head injury. If the decision is made not to go to the hospital, have a friend or family member check on the patient at multiple points.
-the earliest change in the patient’s level of consciousness warrants a stat transfer to the nearest hospital and further investigations.
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Tags: closed head injury, concussion, epidural hematoma, head trauma, IED
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- Is it a seizure or is it syncope: going over the basics again
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