Functional Loss Associated with Brain injuries
Taste can be affected by a traumatic brain injury. The most common reason that taste is affected is that smell has been affected. Smell makes up a large part of our sense of taste. Our taste buds alone can only detect sweet, salty, bitter, sour, and umami. All of the nuances of taste actually come from smell. This means that if you disrupt the sense of smell, the sense of taste is affected. Damage to the craniofacial bones can damage the cribriform plate and the ophthalmic nerve, which transmits the elements of smell to the cortex. If the brain is otherwise affected by trauma, the smell part of the cerebral cortex can be damaged directly, leading to a distorted sense of taste.
Disorders of either taste or smell can result in a loss of taste. These include:
- Anosmia-a total loss of the sense of smell
- Hyposmia-a partial loss of the sense of smell
- Hyperosmia-an enhanced sense of smell
- Parosmia-having false smells or perceiving smells that aren’t there
- Dysosmia-having a distortion of the perception of smells
- Ageusia-having a total loss of sense of taste
- Dysgeusia-having a distortion or decrease in the sense of taste
- Parageusia-perceiving a bad taste in the mouth
- Dysgeusia-persistent abnormal taste in the mouth
Changes to the senses of taste and smell can affect eating and appetite in many ways. An inability to smell food can decrease the appetite and can lower one's interest in food.
Loss of smell can reduce saliva production so that dry foods might be difficult to eat. The food choices might be limited to certain foods that provide enough flavor. This could lead to an imbalance of nutrients. A loss of enjoyment of food can lead to a form of anorexia. If taste is affected, some foods, such as meats, may taste terrible, and the nutrients in these kinds of foods will be lost.
A brain injury that results in a loss of taste is the primary gustatory center that is probably damaged. There are two substructures: the anterior insula on the insular lobe and the frontal operculum of the inferior frontal gyrus of the frontal lobe. The taste and smell fibers in the brain are closely connected.
Imagine the scenario of a victim who suffers a blow to the head and, even after ten years, has no sense of smell. That can happen if the brain was injured or a part of the nasal system that goes up into the brain to detect smells.
Doctors often overlook the sense of smell while evaluating a patient with traumatic brain injury. They don’t check the sense of smell and don’t even ask the patient about their senses of smell and taste. Smell and taste are closely linked. The absolute sense of taste involves things like detecting sweet, salty, and bitter. It takes the sense of smell to give taste its specific nuances.
Often, people don’t report a loss of sense of smell immediately after a brain injury; instead, they report a loss or change in taste. A complete loss of smell is called anosmia. This is quite noticeable to the patient following a traumatic brain injury; it can seriously affect the individual’s life. Sometimes the patient will lose their sense of smell only to regain it back a short time later. If the patient has not regained the sense of smell after six months post head injury, this is a loss that is likely to be permanent.
The sense of smell is very complicated, and it is difficult to determine the part of the brain involved in it. You can get a loss of smell if there is some kind of craniofacial trauma, especially if the fracture involves damage to the nasal passages. Also, you can have a fracture through the cribriform plate at the top of the nose. This is where scent comes in from the outside and goes up through the ophthalmic nerve. There can be a shearing-type injury to the olfactory nerve. There can be an injury to the primary or secondary olfactory centers located in the frontotemporal region of the brain.
One can lose a sense of smell if one has Alzheimer’s disease or if one smokes. For these reasons, it is not a good idea to assume that a case of anosmia is due to a head injury. A qualified doctor should be able to determine what caused the anosmia. If, in the scenario above, it is determined that the patient is truly anosmic, the brain trauma was most likely the cause of the problem, and it won’t likely turn around. The problem might be from the olfactory nerve, which is the main nerve that gathers scent and recognizes its origins. It’s not clear whether the person would feel certain emotions following the exposure to the scent or not. Most likely, they would not respond to a sense of smell they can’t consciously notice. This is unlike “blindsight,” in which the blind person appreciates the appearance of something even though they are technically blind.
It is common to find some vision loss after a head injury, but it isn’t diagnosed right away as other things take precedence. An examination can be interfered with by unconsciousness, combativeness, or lack of cooperation. The degree of total injury doesn’t predict the degree of vision loss. There are obvious injury types, such as periorbital hemorrhage, ecchymosis around the eye, or lacerations of the eye. Obvious evidence of eye trauma can be missing so that the loss of vision is initially not noticed.
The visual system can be damaged at several levels. The patient may have eye trauma or may have optic nerve damage. The visual cortex can be affected by the head trauma the patient received. Anywhere along the path of the visual cortex to the eyes can affect vision. In the emergency room, priority will be given to the vital functions, and it is only when these are taken care of. The patient is out of the emergency room that the ophthalmologist can assess the patient.
There should be a cursory exam in the emergency department and a more complete exam once the patient has been admitted. The examination should include inspection of the eyes and of the periorbital area. If the patient is conscious, visual acuity should be assessed, evaluation of the pupils, and a funduscopic exam. The traumatic loss of vision can be related to direct eye trauma associated with severe head trauma. If ocular trauma such as a penetrating injury or a traumatic hyphema, this requires emergent ophthalmological treatment. If there is a blood clot near the optic nerve, the neurosurgeon needs to be involved as this can be treated.
The examination begins with an external inspection. Look for signs that the globe has been lacerated. Look for a foreign body in the eye that may be embedded. You can easily see lid lacerations, a hyphema, an abnormal placement of the eye, and a collapsed globe. The eye should not be touched and should have a shield over it. Visual acuity can be assessed using a bedside card. Make sure you know if they have glasses or contacts because they are often lost in the trauma. While in the emergency room, you can hold up fingers to basically assess vision. Pupils can easily be assessed, regardless of the responsiveness of the patient. If just one eye has lost vision, there will be a difference in pupillary responsiveness.
The pupils, in cerebral trauma, will be sluggish in nature when a light is shined on them. The pupils might also have anisocoria, which is unequal pupils, that occurs from carotid dissection.
Conscious patients can have their extraocular movements assessed. Patients may complain of double vision. Abnormal eye movements can indicate brainstem or cranial nerve injury. You should also do a funduscopic examination in the ER without dilating the pupils. A brain CT without contrast remains the best neuroimaging scan for trauma victims. It can show areas of blood as well as areas of contusion in the brain. If it shows damage in the visual cortex, one can assume that some visual loss is present.
Visual loss following head trauma is common, and the diagnosis can be challenging for the neurologist called to perform an emergency room assessment. The approach to the patient with post-traumatic visual loss is complicated by a wide range of potential ocular and brain injuries with varying pathophysiology.
The lack of sleep can lead to depression, fatigue, irritability, and anxiety. The individual with traumatic brain injury feels as though they have a diminished sense of well-being. If lack of sleep becomes severe, it can cause difficulty with work performance, workplace accidents, or traffic accidents. Studies have shown that people with a traumatic brain injury are three times more likely to have sleep problems when compared to the general public. This means that nearly sixty percent of TBI patients have some kind of long-term difficulty with sleeping. Women have this problem more than men, and the incidence increases with age.
Sleep problems can range from mild to severe. They are usually the result of an injury to one of the sleep centers of the brain. Common sleep problems include:
- Being sleepy all day long
- Having difficulty falling asleep, staying asleep, or getting up too early. You feel less rested and suffer from cognitive difficulties and behavioral problems during the day. Lack of sleep makes it hard to learn new things.
- Delayed sleep phase syndrome. The patterns of sleep are mixed up.
- Narcolepsy: this is falling asleep suddenly during the day.
- Restless legs syndrome involves the uncontrollable urge to move the legs, especially when lying down or at night.
- Bruxism: This is the grinding of teeth or clenching teeth.
- Sleep apnea: having pauses in one’s sleep with secondary loss of oxygenation and loud snoring.
- Periodic limb movement disorder, which is an involuntary movement of the arms and legs during sleep.
- Sleepwalking or doing complex activities while sleeping.
What causes sleep problems? An injured brain may disrupt the part of the brain that controls the natural wake and sleep cycle. The brain cannot tell the body to wake up or to fall asleep. There are specific chemicals that help us sleep. Having an injury can change how the chemicals talk to one another so that hypersomnia (too much sleep) or insomnia occurs.
The brain can lose the ability to breathe effectively during sleep. This results in periods of apnea during sleep with a loss of adequate oxygenation. This is known as sleep apnea. It can cause daytime somnolence and obesity.
Medications one needs after a brain injury can affect the sleep state or make a person sleepy. Prescription medications that treat depression and asthma can cause insomnia. Stimulants designed to treat sleepiness during the day can cause insomnia at night. Sometimes adjusting the timing of these medications can help with nighttime insomnia.
Most over-the-counter sleep medications contain diphenhydramine, which is not recommended for people with traumatic brain injuries because it can adversely affect memory and learning. It can also cause urinary retention, nighttime falls, constipation, and dry mouth. Taking a nap during the day can disturb sleep during the night. A lack of exercise can disturb sleep. Pain from brain injuries such as chronic headaches can disturb sleep, and so can the pain medications.
Depression is not uncommon after a traumatic brain injury, and this can affect sleep. Some medications for depression can also affect sleep. Alcohol can bring on sleep, but it can also disturb the patterns of sleep. Waking with the symptoms of depression is common after drinking at night.
Caffeine and nicotine from smoking can interfere with sleep. Try not to smoke or have a caffeinated beverage just before sleeping.
Memory loss is one of the more common findings in head trauma. Virtually all patients complain of memory difficulties following a head injury or traumatic brain injury. There are several kinds of memory loss in head trauma. There is retrograde memory. This is a loss of memory of events that took place before the trauma.
Anterograde memory involves the inability to remember new things. There is a memory for music. There is a place in the brain in which all of our memories for music are stored. There are similar memory areas in the brain for taste and smell. We have a memory for the sense of touch or physical things in our bodies. There is a place in the brain where vision and language are stored. There is something called immediate memory. This memory doesn’t last very long, only a few minutes. This is the type of memory that helps you remember a phone number. People with head injuries usually retain immediate memory but have difficulty with short-term memory. Short-term memory is defined in some circles as a memory that is kept for thirty minutes. In a head injury, short-term memory is often impaired.
People can be told a series of activities to do and, in 30 minutes, they will have no memory of having been told to do those things. Your short-term memory relies on the hippocampus in the brain. It is responsible for holding short-term memory and processing it into long-term memory. This part of the brain is severely impacted by brain trauma. Long-term memory can be remembered after a day, after a week, or after 20 years. Most people with a brain injury have relatively intact long-term memories. New information can’t seem to turn into long-term memory, leaving existing long-term memory to be remembered in lavish detail. Today’s time seems to fly by because they have lost all the little things that fill in the day’s time, so time appears to go faster. Those long-term things that are remembered since the incident are remembered faster than before the accident.
Patients with a traumatic brain injury can have one or both of two types of amnesia. They can have retrograde amnesia or anterograde amnesia. As mentioned above, having retrograde amnesia is where the person loses memory of things that happened before the incident. People often lose only a few seconds of retrograde memory, but some lose several hours before the event. Long-term memories tend to return as the patient gets better. They don’t tend to return in any particular order, however. The less the retrograde amnesia, the smaller is the degree of brain injury. The other form of amnesia is anterograde amnesia. All events since the accident have become erased. This type of amnesia is believed to be due to the upset brain chemistry that goes on. As the chemistry normalizes, the anterograde memory returns. Patients can spend several months or more with the inability to create and retain memory.
Editor's Note: This page has been updated for accuracy and relevancy [cha 3.15.21]
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