Neurologic Diseases and Conditions
After studying Chapter 13, you should be able to:
1. Name the main components of the nervous system.
2. List some of the problems to which the nervous system is susceptible.
3. Describe how data are collected during a neurologic assessment.
4. Name the common symptoms and signs of a cerebrovascular accident (CVA).
5. Name the three vascular disorders that may cause a CVA.
6. Define a transient ischemic attack (TIA).
7. Distinguish between (a) epidural and subdural hematomas and (b) cerebral concussion and cerebral contusion.
8. Describe three mechanisms of spinal injuries.
9. Name the goals of treatment of spinal cord injuries.
10. Explain the neurologic consequences of the deterioration or rupture of an intervertebral disk.
11. Describe the symptoms of a migraine.
12. Explain why cephalalgia sometimes is considered a symptom of underlying disease.
13. Describe first aid for seizures.
14. Explain how the symptoms of Parkinson’s disease are controlled.
15. Describe the progression of amyotrophic lateral sclerosis (ALS).
16. Discuss restless legs syndrome.
17. Discuss transient global amnesia.
18. Distinguish between trigeminal neuralgia and Bell’s palsy.
19. List the diagnostic tests used for meningitis and explain how the causative organism is identified.
20. Name the common causes of encephalitis.
21. Explain the pathologic course of Guillain-Barré syndrome.
Orderly Function of the Nervous System
The nervous system is a complex, sophisticated, and elaborate network of many interlaced nerve cells (neurons) that make up the brain (Figure 13-1, A), the spinal cord (Fig 13-1, B), and the nerves. Electrical impulses are carried throughout the body by the neurons (Figure 13-1, C, and Figure 13-2). This entire system regulates and coordinates the body’s activities and produces responses to stimuli, which help the body adjust to changes in its environment, both internal and external.
The nervous system is composed of two divisions: the central nervous system (CNS) and the peripheral nervous system (PNS). The CNS includes the brain and spinal cord. Its function is to process and store sensory and motor information and to govern the state of consciousness. For example, the structures of the brain that control the intellectual functions of thinking, willing, remembering, and deciding, and those that control personality, are located in the frontal lobe of the cerebrum. Coordination, equilibrium, and posture are coordinated in the cerebellum area of the brain. The hypothalamus regulates the secretion of hormones from the pituitary gland and regulates many visceral activities. Five pairs of the 12 cranial nerves originate in the medulla oblongata, an extension of the spinal cord; the medulla also contains vital centers that help regulate heart rate, blood pressure, and respiration. All the sensory and motor nerve fibers pass through the medulla oblongata, connecting the brain and the spinal cord. The spinal cord, a continuation of the medulla oblongata, extends to the first lumbar vertebra. It is divided into 31 segments, each giving rise to a pair of spinal nerves that act like a telephone switchboard, or reflex center, carrying impulses to and from the brain (Figure 13-1, D).
Enrichment
Neurologic Assessment
Neurologic assessment relies on a step-by-step collection of data to evaluate the neurologic status and cognitive function of a person. The examination is appropriate after head trauma occurs or cranial surgery is performed or when a neurologic disorder, such as a brain tumor, is suspected. Observations and findings are graded on a scale and documented. The assessment is done within the constraints of circumstances (e.g., the location [the scene of an accident or a physician’s office] and the patient’s state of consciousness).
Neurologic assessment begins with a thorough medical history, noting past and current problems, and a record of medications being taken. The patient’s comprehension and judgment are noted during the examination.
The patient’s mental status may be graded with the Glasgow coma scale, which is a standardized system for assessing the response to stimuli. E13-1
Next, more sophisticated mental functions are tested, including speech, language, and writing skills. Is the patient having difficulty in putting words together, or is speech slurred? Do the patient’s ideas and thoughts make sense? Behavior, emotional state, long-term and recent memory, and attention span are observed.
The cranial nerves are assessed by testing the patient’s sense of smell, visual acuity, eye movements, muscles of mastication, taste perception, facial muscles, hearing, and tongue movements and swallowing. E13-2
Motor function is evaluated by testing muscle tone and strength. Asymmetry in size, shape, or strength of corresponding muscles may be significant. Changes in extension and flexion of muscles and spasticity or flaccidity of muscles are noted.
Coordination and balance are assessed by watching for unsteadiness or a shuffling gait or the dragging of a foot. The patient is asked to perform rapid alternating movements and tasks to demonstrate fine motor coordination. A reflex hammer is used to test deep tendon reflexes in the arms and legs; any depression or hyperactivity is recorded.
Sensory examination determines diminished or abnormal sensation. A cotton ball is brushed against the skin at different points. A slight pin stick tests for superficial pain. Temperature and vibration tests also are done.
Findings lead the clinician to begin focusing on any problem area. The need for further testing also is indicated as abnormal assessment findings emerge.
The vast network of nerves throughout the rest of the body is part of the PNS (Figure 13-3, A). Peripheral nerves connect with the spinal cord at many levels, and the information (impulses) they carry travels to and from the brain and spinal cord. Sensory (afferent) nerves transmit impulses from parts of the body (e.g., skin, eye, ear, and nose) to the spinal cord and brain. Motor (efferent) nerves transmit impulses away from the CNS and produce responses in muscles and glands. The PNS contains 12 pairs of cranial nerves (Figure 13-3, B), and 31 pairs of spinal nerves (Figure 13-3, C). Refer to Figure 6-12, Dermatomes, to compare innervations of spinal nerves E13-3 and the sympathetic and parasympathetic nerves. The sympathetic and parasympathetic nerves make up the autonomic nervous system (ANS), which regulates the involuntary muscle movements and glandular actions of the body. The PNS also controls all conscious activities, which greatly affect unconscious processes, such as the heart rate and bowel functions. E13-4
Four major blood vessels on each side of the head supply the brain with essential oxygen and nutrients. The carotid arteries (two internal and two external) originate from the two common carotid arteries and are located in the anterior portion of the neck; the two vertebral arteries, located within the vertebral column (Figure 13-4), join with the two anterior and posterior cerebral arteries and the two anterior and posterior communicating arteries to form the brain’s vascular system in a roughly circular configuration of arteries known as the circle of Willis. Branches from the circle of Willis supply blood to all portions of the brain (Figure 13-5). Areas of the brain that depend on a single branch for survival are especially vulnerable to any disruption in the blood flow (e.g., thrombus or embolus). (See “Vascular Disorders” section.)
Like the rest of the body, the nervous system is susceptible to a variety of problems. Defects in the circulatory system of the brain can lead to vascular disorders and damaged brain cells. The brain also can be damaged by injuries, infections, metabolic derangement, inherited defects, congenital defects, degeneration, and tumors. Because of the complex nature of the CNS and the PNS, damage to either of the systems can cause extremely diverse symptoms.
Common problems within the nervous system that necessitate attention from health care providers include the following:
• Motor disturbances, other disturbances of movement, or paralysis
• Altered levels of consciousness
• Sensory disturbances or numbness
Vascular Disorders
Cerebrovascular Accident (Stroke)
Symptoms and Signs
CVAs are the number one cause of adult disability. Because of the inadequate blood supply, the physical and mental functions controlled by the affected area of the brain fail to operate properly (Figure 13-6, A).
The symptoms and signs of a stroke reflect the portion of the brain affected (Figure 13-6, B). Common stroke symptoms include the following:
• Sudden aphasia, dysphasia, or difficulty understanding language
• Sudden weakness, numbness, or paralysis of the face, including one-sided drooping mouth and eyelid (hemiparesis)
• Sudden confusion or impaired consciousness
• Sudden loss of vision, blurred vision, unequal pupils, or diplopia
• Sudden onset of dizziness, loss of balance, or loss of coordination
A severe stroke can result in coma and death. Early recognition of symptoms and prompt medical intervention can help reduce the chances of disability and death. E13-5
Patient Screening
Any individual experiencing sudden onset of weakness, numbness or paralysis, difficulty speaking or understanding language, confusion or loss of consciousness, loss of vision or double vision, loss of balance or coordination, and dizziness requires immediate assessment and aggressive intervention. These individuals should be immediately entered into the emergency medical system (EMS) by the medical office or a family member. Occasionally, the onset of symptoms may be insidious over a period of a few hours or even a day.
Etiology
A CVA is usually the result of one of three types of vascular disorders: occlusion of an artery caused by an atheroma; sudden obstruction by an embolus, including a cerebral thrombosis (clot), embolism (moving clot), or other moving emboli; and a cerebral bleed. E13-6 These vascular disorders most often are caused by atherosclerosis (see “Atherosclerosis” section in Chapter 10) and hypertension (high blood pressure). Strokes also can result from blood disorders, arrhythmias, systemic diseases (e.g., diabetes mellitus and syphilis), hyperlipidemia, rheumatic heart disease, or head trauma. A high-fat diet, lack of exercise, cigarette smoking, obesity, and a family history of atherosclerotic disease are contributing factors.
A cerebral embolism is also a blockage, but it is caused by a foreign object, or embolus. This embolus can be a piece of arterial wall, a small blood clot from a diseased heart, or a bacterial clot; usually, platelet fibrin from an ulcerated arterial wall of the heart or valve of the heart is the causative factor. Atrial fibrillation may be a cause of the release of the embolus from the inner chambers of the left side of the heart. It is carried in the bloodstream until it becomes wedged in a blood vessel and obstructs the flow of blood to an area of the brain.
With a cerebral hemorrhage, the cerebral artery is not blocked but instead ruptures, flooding the surrounding brain tissue with blood. E13-7 The initial effects of a hemorrhage may be more severe than those of a thrombosis or embolism, and the long-term effects are much more serious (Figure 13-6, C). (Refer to the Enrichment box on Arteriovenous Malformations [AVM].)
Diagnosis
Physical examination of the patient leads the physician to suspect a CVA and to gauge impairments on a functional scale. It can be confirmed by magnetic resonance imaging (MRI), computed tomography (CT), cerebral angiography, or electroencephalography (EEG). Blood tests for bleeding and clotting disorders may be performed. Cardiac monitoring may show atrial fibrillation or other arrhythmias.
Treatment
Immediate appropriate medical intervention (within 3 hours) from onset of stroke symptoms may limit brain damage and thereby improve the prognosis. Anticoagulants (warfarin sodium [Coumadin], thrombolytic agents, and antiplatelet medications [aspirin]) may be given orally or the thrombolytic agent heparin may be administered intravenously. A recently introduced protocol includes having the individual immediately chew an aspirin if possible. Surgery to improve circulation within the cerebral arteries or to remove clots is considered. Other therapeutic measures include surgery to repair broken or bleeding blood vessels and drugs to prevent or reverse brain swelling. Antiarrhythmic drugs are administered for arrhythmias. Long-term treatment for CVA depends on the size and location of the stroke and the presence and severity of impairments. The goal of medical treatment is to restore lost functions and treat underlying disorders. A team approach to rehabilitation includes help from family members and a medical team of speech, physical, and occupational therapists; nurses; and doctors.
Prevention
Prevention of stroke includes positive lifestyle changes to reduce controllable risk factors, such as smoking, excesses in diet and alcohol consumption, untreated high blood pressure, and uncontrolled diabetes. Other risk factors over which the individual has no control include family history of stroke and age. Approximately 80% of CVAs are preventable with patient education and control or modification of risk factors. Control of atrial fibrillation is important.
Patient Teaching
Review warning signs of a stroke with the patient and family, and instruct them concerning the importance of quickly seeking medical intervention for any signs of impending stroke. E13-8 Assist the family in finding appropriate medical equipment for home use that will facilitate the home care and safety of the patient. Talk with the family about achievable goals. Assist the family by providing referrals to support groups and encouraging them to seek available help in the community. Generate print-on-demand electronic materials when possible as teaching tools.
Enrichment
Arteriovenous Malformations
Formed during fetal development, arteriovenous malformations (AVM) are abnormal structures of the blood vessels (see Figure 13-6, C). Etiology of this congenital condition that is rarely discovered before the age of 20 years is unknown. Although usually found in the brain, AVMs may be located in any vascular structure. Blood normally flows from the artery through capillaries to the veins. In arteriovenous malformations, an abnormal connection is noted in which the capillaries are lacking. As a result, arterial blood moves directly into the veins, giving the blood vessels the appearance of a tangled mass of arteries and veins. These fragile vascular structures have a tendency to bleed and often result in hemorrhage. When located in the brain, symptoms of the bleeding are similar to those of a stroke. The patient complains of generalized or region-specific headache. Vomiting, stiff neck, confusion, lethargy, generalized weakness, visual problems, and irritability may be noted. As the bleeding progresses, speech may become impaired, muscle weakness and paralysis may be noted in the face, ringing in the ears may be reported, and dizziness and syncope may follow. Some patients may lose consciousness.
Enrichment
Cerebral Aneurysms
A cerebral aneurysm, a cerebrovascular condition, is an abnormal localized weakening, thinning, or dilation of the wall of a cerebral artery or vein resulting in a ballooning of the blood vessel. Leakage or spilling of blood results in a hemorrhage in the brain. E13-8 Pressure caused by the bulging vessel is placed on a nerve or brain tissue. Cerebral aneurysms often cause no symptoms and go unnoticed until rupture or leakage occurs with blood being released into the brain, causing a stroke and resulting brain damage. Cerebral aneurysms can occur in any part of the brain; however, many commonly occur near the base of the brain in the circle of Willis (see Figure 13-5). E13-9
Diagnosis of a cerebral aneurysm usually occurs with onset of symptoms of a cerebral bleed. Occasionally diagnosis is made incidental to imaging examination for other causes.
Treatment when diagnosis is made is surgical repair of the vessel. Frequently, the rupture is too acute with rapid onset such that surgical intervention is unsuccessful and brain damage occurs.
Transient Ischemic Attack
Symptoms and Signs
Transient cerebral ischemia can occur in various sites and therefore various diagnostic codes are used. After the physician has diagnosed the site of the ischemia, refer to the current edition of the ICD-9-CM coding manual to confirm the appropriate code for transient cerebral ischemia. TIAs often are referred to as “little strokes” or “ministrokes” because they resemble a stroke caused by an embolism. The individual may report sudden weakness and numbness down one side of the body, dizziness, dysphagia, confusion, difficulty seeing with one eye, and/or loss of balance. The individual may complain of a sudden onset headache. Usually, TIAs do not cause unconsciousness. These little strokes are often manifested as recurring episodes, lasting from just seconds to possibly hours, with symptoms gradually subsiding. The symptoms of a true stroke (or CVA) last longer than 24 hours, but TIAs should not be discounted as a minor condition because often they are important signals of an impending stroke (CVA). The symptoms, like those of a stroke, depend on which part of the brain is affected. Differentiation between a stroke and a TIA is the duration of symptoms and lack of permanent brain damage.
Etiology
The most common cause of TIA is a piece of plaque, formed by atherosclerosis, which breaks away from the wall of an artery or heart valve and travels to the brain (Figure 13-7). This is known as an embolus or moving clot. Platelet fibrin emboli from an arterial ulcer are often the causative factor. Arterial vascular spasms and minute blood clots also may be etiologic factors. Unlike strokes, TIAs do not normally cause permanent damage to the brain tissue.
Diagnosis
A physical examination and history are the first steps in diagnosing the problem. Next is determining the source of a possible embolus. A likely source of emboli is the carotid arteries. Cranial MRI scan, CT scan, and an EEG are all helpful in confirming the diagnosis; however, all can appear normal.
Treatment
Treatment depends on the location of the TIA and the underlying cause. Anticoagulants commonly are used during an episode to lessen the frequency or chance of recurrences. Recent protocol is to have the patient chew an aspirin tablet as soon as symptoms appear. In certain cases, surgery may be attempted to increase the blood flow to the affected area.
Prevention
As with CVA, prevention includes positive lifestyle changes to reduce controllable risk factors such as smoking, excesses in diet and alcohol consumption, untreated high blood pressure, and uncontrolled diabetes. Other risk factors over which the individual has no control include family history of stroke and age. Oral contraceptives may cause strokes so females taking oral contraceptives must be made aware of symptoms and signs of a stroke and instructed to seek medical attention when experiencing any symptoms.
Patient Teaching
As with patients who have suffered a stroke, instructions should be given concerning possible symptoms of an impending stroke. The family members should be encouraged to seek medical intervention for the patient at the first sign of a stroke. Give instructions for monitoring blood pressure and emphasize the importance of complying with the prescribed drug therapy. Use customized electronically generated educational materials when available to reinforce the treatment plan.
Head Trauma
Head trauma usually results in brain injury. Ranging from mild to life-threatening or fatal, traumatic brain injury may be the result of several types of insults to the head. Included in the forms of traumatic brain injury are concussions, contusions, closed head injuries, open head injuries, linear fractures, comminuted fractures, compound fractures, and contrecoup injuries. Concussions, contusions, and injuries where the cranial vault is not violated are types of closed head injuries; fractures to the cranial vault are open head injuries and include linear, depressed, comminuted, compound, and basilar skull fractures (see Figure 13-11). E13-10
Epidural and Subdural Hematomas
Description
An epidural hematoma is a collection or mass of blood that forms between the skull and the dura mater, the outermost of the three meningeal layers covering the brain. With a subdural hematoma, the blood collects or pools between the dura mater and the arachnoid membrane, the second meningeal membrane (Figure 13-8). E13-11
ICD-9-CM Code 852 (Subarachnoid, subdural and extradural hemorrhage, following injury)
ICD-10-CM Code S06.6X0A (Traumatic subarachnoid hemorrhage without loss of consciousness, initial encounter)
(S06.6X0(7th digit)-S06.6X9(7th digit) = 10 codes of specificity)
S06.4X0A (Epidural hemorrhage without loss of consciousness, initial encounter)
(S06.4X0(7th digit)-S06.4X9(7th digit) = 10 codes of specificity)
S06.5X0A (Traumatic subdural hemorrhage without loss of consciousness, initial encounter)
(S06.5X0(7th digit)-S06.5X9(7th digit) = 10 codes of specificity)
Intracranial injuries are coded according to site, type of wound, state of consciousness, or length of unconsciousness. Refer to the current editions of the ICD-9-CM and ICD-10-CM coding manuals for verification of the appropriate code once the diagnosis has been confirmed.
Symptoms and Signs
Pressure on the brain resulting from either of these hematomas can result in impaired functioning of the brain or possible death. E13-12
Symptoms of an epidural hematoma typically appear within a few hours of head trauma. They include sudden headache, dilated pupils, nausea and often vomiting, increased drowsiness, and perhaps hemiparesis. If the hematoma is not treated promptly, unconsciousness, coma, and death occur. Deterioration of the patient’s condition can be rapid. This is a neurologic emergency.
Subdural hematomas often exhibit symptoms similar to those of an epidural hematoma, except that the onset is delayed because of a slower accumulation of blood. This delayed onset may mimic the symptoms of a TIA, stroke, or dementia. Diplopia is a common occurrence in patients with a subdural hematoma.
Patient Screening
Most trauma victims with closed and open head injuries will be transported to an emergency facility for treatment. When a head injury is not obvious, the onset of symptoms may be insidious. When a family member, or possibly the injured individual himself, calls in complaining of head pain and onset of other neurologic symptoms after head trauma, instruct the family member to have the victim of the trauma transported to an emergency facility for immediate assessment. Emphasize that the victim should not drive. The victim of any acceleration-deceleration type injury, such as motor vehicle accidents or falls, requires prompt assessment and follow-up intervention.
Etiology
Both types of hematomas can result when blood from ruptured vessels seeps into and around the meningeal layers. Head trauma is the usual cause; a blow to the head can cause an epidural hematoma, or the head striking an immovable object (sudden acceleration or deceleration injury) can cause a subdural hematoma. Sudden acceleration or deceleration causes the brain to strike the skull or to tear vessels within the brain or meninges. Subdural hematomas often occur among the elderly or alcoholics as a result of falls. Cerebral hematoma often follows a skull fracture.
Diagnosis
The clinical findings noted upon examination of the patient, along with a history of recent head trauma, suggest to the physician the possibility of either an epidural or a subdural hematoma. Cranial radiographic films, CT scans, and cerebral arteriograms locate the hematoma and rule out other causes of the symptoms. Prompt investigation of the condition is vital. Obtaining the history of the mechanism of injury and time of the initial insult is an additional aid in determining the diagnosis.
Treatment
If the person loses consciousness because of head trauma, rapid medical attention is needed. A craniotomy, cranial trephination (bur hole, a hole made in the skull with a drill to relieve pressure by draining off the blood that has accumulated), may be necessary. This procedure is performed to remove the accumulated blood and to cauterize the bleeding vessels if increasing intracranial pressure indicates a life-threatening situation. When this procedure is performed promptly, a complete recovery is possible. A patient not losing consciousness but displaying symptoms, either immediately or delayed, should be seen by a physician as soon as possible for evaluation.
Prognosis
Unchecked bleeding enlarges the hematoma and increases pressure on the blood vessels supplying the brain tissue, depriving them of oxygen. Additionally, when pressure is allowed to build within the skull, herniation of the brain tissue downward through the foramen magnum compresses the brainstem and vital centers, resulting in death. Prompt assessment and intervention are the keys to a good prognosis.
Patient Teaching
Provide postsurgical instructions for care of the incision. Instruct caregivers to assess for indications of neurologic changes and other signs of increased intracranial pressure. Encourage the use of seat belts, child restraint seats, and helmets for contact sports and cycling. Generate print-on-demand electronic materials when possible as teaching tools.
Cerebral Concussion
Description
A cerebral concussion is a possible bruising of the cerebral tissue that is caused by back and forth movement of the head, as in an acceleration-deceleration insult. Blunt force trauma also may result in a cerebral concussion.
ICD-9-CM Code 850.9 (Cerebral concussion, unspecified)
ICD-10-CM Code S06.0X9A (Concussion with loss of consciousness of unspecified duration, initial encounter)
Cerebral concussions have various codes according to the level of consciousness and duration of any periods of unconsciousness and are designated by the addition of the fourth digit. Refer to the current editions of the ICD-9-CM and ICD-10-CM coding manuals to determine the appropriate code.
Symptoms and Signs
With a cerebral concussion, patients may experience a loss of consciousness. It often is referred to as being “knocked out.” This state may last from a few seconds to several minutes and may be followed by a varying period of amnesia, lasting from 12 to 24 hours. Respirations become shallow, pulse rate is depressed, and muscle tone is flaccid. Symptoms appearing after the person has regained consciousness may include headache, nausea, vomiting, diplopia or blurred vision, and photophobia (sensitivity to light). Persons with this injury may exhibit irritability, decreased levels of concentration, and amnesia.
Patient Screening
Individuals who have suffered a head injury and have loss of consciousness are in need of immediate assessment and intervention. In most cases, treatment at an emergency care facility is the optimal choice. The unconscious individual should be transferred to the EMS for immediate assessment and transport to an emergency facility.
Etiology
A cerebral concussion is an injury resulting from impact with a blunt object, either by receiving a blow to the head or by falling. This results in a disruption of the normal electrical activity in the brain, but the brain itself usually is not permanently injured (Figure 13-9). Mild traumatic brain injury (MTBI) is a term that can be applied to this injury.
Treatment
The usual treatment of a concussion is quiet bed rest with observation of the patient for signs of behavioral changes. Recently developed concepts suggest it is acceptable to allow the patient to sleep, but make sure the patient is fully awake when aroused. Any changes noted, including changes in the level of consciousness, could indicate a progressive brain injury.
Prognosis
Prognosis is unpredictable and depends on the extent of the insult and any additional trauma. Cumulative effects may occur with successive mild traumatic head injuries resulting in more severe symptoms. While most symptoms disappear after a few days or weeks, some individuals may experience postconcussion syndrome for weeks or months. Many people recover with no residual damage.
Prevention
Cerebral concussions are difficult to prevent. The consistent use of seat belts, child restraint seats, and the wearing of helmets may help reduce the severity of the injury. Individuals who have experienced a concussion are encouraged to avoid situations where another blow to the head could occur.
Patient Teaching
Encourage all patients to consistently use seat belts, secure children in child restraint seats, and wear helmets for contact sports or cycle riding. Provide family or caregivers with written information about care of a victim with a closed head injury. Provide the patient and family with visual aids depicting the neurologic system and its functions.
Cerebral Contusion
Description
A cerebral contusion is more serious than a concussion. This injury to the brain involves bruising of tissue along or just beneath the surface of the brain and also may be termed a contrecoup insult.
ICD-9-CM Code 851 (Cerebral lacerations and contusions)
ICD-10-CM Code S06.330A (Contusion and laceration of cerebrum, unspecified, without loss of consciousness, initial encounter)
Cerebral lacerations and contusions are coded according to site, type of wound, state of consciousness, or length of unconsciousness. Once the diagnosis has been confirmed, refer to the current editions of the ICD-9-CM and ICD-10-CM coding manuals for assistance in verifying the appropriate code.
Symptoms and Signs
The symptoms and signs of a contusion vary according to the site and extent of the injury, and persist for longer than 24 hours. They may range from temporary loss of consciousness to coma. When conscious, the person may report a severe headache and hemiparesis. Symptoms may be progressive in nature. The person may appear drowsy and lethargic or hostile and combative.
Permanent damage to the brain may result from a cerebral contusion caused by subdural and epidural hematomas (see “Epidural and Subdural Hematomas” section), causing impaired intellect, dysphasia, paralysis, epilepsy, impaired gait, and continuing stupor.
Patient Screening
Individuals who have suffered a head injury and complain of severe headache develop one-sided paralysis and experience a period of unconsciousness and are in need of immediate assessment and intervention. In most cases, treatment at an emergency care facility is the optimal choice. The unconscious individual should be transferred to the EMS for immediate assessment and transport to an emergency facility.
Etiology
A contusion of the brain is caused by a blow to the head or impacting against a hard surface, as occurs in an automobile accident. The twisting or shearing force against the two hemispheres of the brain that occurs when colliding with the cranial bones may damage structures deep within the brain (see Figure 13-9). A contusion often is associated with a skull fracture. This traumatic brain injury may be observed in child, spouse, partner, or elder abuse.
Diagnosis
A thorough neurologic examination is necessary, along with obtaining the history of the mechanism of the injury. CT scans reveal the location and extent of brain damage (Figure 13-10). Cranial radiographic films rule out a possible skull fracture.
Patient Teaching
As with cerebral concussions, all patients should be encouraged to consistently use seat belts and secure children in child restraint seats when traveling by car and wear helmets when engaging in contact sports or cycle riding. Provide family members or caregivers with written information about the care of a victim with a closed head injury. Instruct family members or caregivers to seek immediate medical attention for the victim should symptoms worsen. Provide the patient and family with visual aids depicting the neurologic system and its functions.
Depressed Skull Fracture
Description
A fractured skull occurs with a break or fracture in one of the bones of the cranium (Figure 13-11). When the skull bones are depressed or torn loose, they are pushed below the normal surface of the skull.
Symptoms and Signs
When a portion of the skull is broken and is pushed in on the brain, causing injury, it is said to be a depressed skull fracture (see Figure 13-11). The symptoms depend on the site of the fracture. For example, a bone fragment pressing on the motor area of the brain may cause hemiplegia (Figure 13-12). Characteristically, symptoms from a depressed fracture are not progressive. They tend to remain static until the depressed bone is elevated and the pressure is relieved. Epilepsy is a common complication of depressed skull fractures (see Figure 13-11 for additional types of skull fractures)
Signs include bleeding from the wound; ears, nose, or around the eyes; changes in pupils (either nonreactive or unequal); bruising behind the ears (Battle’s sign) or around and under the eyes (Raccoon eyes); and clear or bloody drainage from ears or nose. Other signs include headache, stiff neck, nuchal rigidity, nausea, vomiting, visual disturbances, slurred speech, confusion, restlessness, irritability, difficulty with balance, drowsiness, seizures, and/or loss of consciousness.
Etiology
Direct impact on the skull with a blunt object is the most common cause of depressed fractures. Industrial injuries and automobile accidents are two of the many possible causes. Child, domestic, intimate partner, or elder abuse may also be a causative factor. The fractured bone may cut an artery or vein, causing hemorrhage in the brain.
Prognosis
Prognosis is unpredictable; it depends on the extent of the insult, timely intervention, possible complications, additional trauma, and any underlying medical conditions. Successful surgical intervention in which intracranial pressure is relieved and bleeding is arrested usually has a positive outcome.
Patient Teaching
Reinforce the potential dangers of head injuries in children to parents and remind them of the importance of children wearing helmets while cycling and playing contact sports. Advise parents and others to seek professional emergency intervention in the event of a head injury. Provide the patient and family with visual aids depicting the neurologic system and its functions.
Enrichment
Basilar Skull Fracture
A basilar skull fracture is a fracture of the bones of the floor of the cranial vault (see Figure 13-11). This injury usually results from a massive insult to the cranium during a motor vehicle accident or other violent trauma in which the head is struck anteriorly or laterally in the midportion. As with other head injuries, symptoms, signs, and treatment depend on the area involved and the extent of the fracture. Raccoon’s eyes and Battle’s sign are manifestations of basilar skull fracture, and these signs alert the physician to order imaging of the cranial vault for further investigation. Cerebrospinal fluid (CSF) flowing from the ears or nares may be associated with a skull fracture. The level of consciousness is assessed, as are other neurologic signs. Treatment is similar to that of head injuries, including surgical intervention to relieve intracranial pressure. Occasionally, the severity of the fracture causes severing of the pituitary stalk, resulting in panhypopituitarism.
Spinal Cord Injuries
Paraplegia and Quadriplegia
Description
Injuries to the spinal cord affect the innervation of any spinal nerves distal to the point of insult. The extent of the injury and consequential edema often result in the failure of spinal nerve functioning, with resulting loss of motor and sensory function. Paraplegia is loss of nerve function below the waist and paralysis of the lower trunk and legs. Quadriplegia is loss of nerve function at the cervical region resulting in paralysis of the arms, hands, trunk, and legs.
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