Structurally distinct neurons are responsible for receiving and sending specific messages to the brain about the body's internal and external environment. There are five major types of sensory receptors [3,4]:

The principal extracellular cation is sodium; the main intercellular cation is potassium. With stimulation of the cell, the charge is reversed, as sodium moves into the cell and potassium moves out. This reversal results in a flow of electric current. With sufficient stimulation, the reversal of polarity travels along the entire axon. This process, known as an action potential, requires only a few milliseconds. Quickly, electrical forces and ion concentration forces re-establish the resting membrane potential. If a stimulus is not sufficient to produce an action potential and another stimulus occurs before the membrane has completely stabilized, depolarization will be facilitated [5,6,7].

The hypoglossal nerves exit from the medulla oblongata and pass through the hypoglossal canals located beneath the tongue. These nerves are responsible for tongue movement [8].

The cerebellum modulates and coordinates skeletal muscle activity and maintains body posture and muscle tone. It controls movement with both excitatory and inhibitor signals, which modulates fine movements in ways the cerebral cortex is incapable of carrying out. Each hemisphere influences the movement of the ipsilateral side of the body and modifies activity initiated elsewhere in the body. There is no conscious input [10].

The occipital lobes contain the primary visual and visual association areas. The primary visual areas receive information and perceive color, while the visual association areas give visual input meaning and have a role in visual reflexes for fixing the eyes on a stationary or moving object. Injury to the medial surface on the dominant side can result in loss of the ability to recognize objects and know their function, although recognition of faces still is possible. A consequence of damage to the nondominant side may be the inability to recognize faces and differentiate various animals, such as horses and elephants [1,2].

In the spinal cord, the inner layer of dura is continuous with the spinal dura mater. The spinal dura extends to the second sacral vertebrae, where it joins with the external filum terminal and attaches to the back of the first segment of the coccyx. The middle layer of the meninges, the arachnoid, is a thin, fibrous membrane that adheres closely to the inner surface of the dura, allowing only a narrow space between the two. The inner layer of the meninges, the pia mater, adheres so closely to the brain that it follows the contour of the fissures and sulci. The space between the pia mater and arachnoid is bridged with weblike strands of arachnoid called trabeculae. A rich network of pia blood vessels extends into the brain. The area between the arachnoid and pia mater is called the subarachnoid space. Located here are arteries, veins, arachnoid trabeculae, and CSF. Within the spinal cord, fibrous bridges join the pia mater with the arachnoid and dura mater. These bridges, known as denticulate ligaments, help to stabilize the cord within the spinal canal [14].

The viability and functioning of the CNS are dependent on a rich and continuous blood supply. The brain utilizes approximately 20% of the body's oxygen supply and requires about 400 kcal of glucose per day. The average cerebral blood flow is about 750 mL per minute [14].

Three major factors that have a direct and potent effect on cerebral blood flow are elevations in concentrations of carbon dioxide, hydrogen ions, and oxygen. The increase in hydrogen ion concentration causes vasodilation of the cerebral vessels. Vasomotor reflex response that affects the body's general vascular perfusion also affects the perfusion of blood in the CNS. Vasomotor centers in the pons and medulla maintain vascular tone through impulses transmitted via the spinal cord to all blood vessels in the body. The reticular areas of the brain stem and hypothalamus have both excitatory and inhibitory effects on vasomotor activity. The hypothalamus also influences vasoconstriction activity through excitatory or inhibitory action on the vasomotor centers. It also helps to regulate total body water (and therefore blood pressure) by increasing or decreasing the release of antidiuretic hormone [14].

Inflammatory processes affecting nervous tissue alter the metabolism and thus the tissue's nutritional immune processes. Causes of CNS inflammation include trauma, lumbar punctures, and infectious processes, such as meningitis.

The loss of vibratory perception in the lower extremities usually begins at about 50 years of age. Touch becomes significantly diminished due to skin changes and a decrease in the number of sensory receptors. This fact may be particularly significant to nurses during neurologic assessment. Corneal sensitivity, an accurate measurement of sensory perception, shows a decrease with age. Visual, auditory, gustatory, and olfactory senses are also diminished [16,17].

Bowel and bladder function is controlled by various components of the autonomic nervous system. For patients with known or suspected CNS deficits, it is important to thoroughly review symptoms such as constipation, urinary retention, and fecal and urinary incontinence. Symptoms of ataxia (i.e., lack of muscle coordination) should raise concern about degeneration of the posterior tracts of the spinal cord or cerebellar dysfunction. Spasticity of muscles occurs with CVA and multiple sclerosis. In contrast, flaccidity (i.e., decreased or absent muscle tone) can result from isolation of muscles from neuronal impulses. Fasciculations—fine, rapid, twitching movements originating in small groups of muscle fibers—are often present in patients with ALS [18,19].

Bowel and bladder function is controlled by various components of the autonomic nervous system. For patients with known or suspected CNS deficits, it is important to thoroughly review symptoms such as constipation, urinary retention, and fecal and urinary incontinence. Symptoms of ataxia (i.e., lack of muscle coordination) should raise concern about degeneration of the posterior tracts of the spinal cord or cerebellar dysfunction. Spasticity of muscles occurs with CVA and multiple sclerosis. In contrast, flaccidity (i.e., decreased or absent muscle tone) can result from isolation of muscles from neuronal impulses. Fasciculations—fine, rapid, twitching movements originating in small groups of muscle fibers—are often present in patients with ALS [18,19].

The Glasgow Coma Scale is an objective measure of level of consciousness that can also be somewhat predictive of recovery. Eye, motor, and verbal responses are measured. Coma is defined as a score of 7 or less. With a score of 3 or 4, there is an 85% chance of dying or remaining vegetative. A score greater than 11 is associated with an 85% chance of moderate disability or good recovery. Response to pain is also significant in determining the prognosis [20,21].

Observation of the patient's station (i.e., manner of standing) and gait can provide useful insight. A decortication response is indicative of cortical damage, and unusual gait, stance, or settling posture can result from motor or sensory deficits. With decorticate posturing, the patient demonstrates hyperflexion of the upper extremities and hyperextension of the lower extremities. With decerebrate posturing, both the upper and lower extremities are hyperextended. This response indicates brain-stem injury [20,21]. Postures can also be influenced by mental and physical problems.

Electroencephalography (EEG) is essentially a noninvasive test that records a portion of the brain's electrical activity. The EEG is valued for its ability to reveal abnormal brain-wave patterns that help in diagnosing seizure disorders, brain tumors, abscesses, and psychiatric disorders. Diagnosis is made by evaluating patterns and characteristics of brain waves recorded, along with the patient's clinical state. An absence of brain waves generally establishes brain death; however, acute drug intoxication or severe hypothermia can also cause a flat EEG [22,23,24].

Cerebral angiography (also referred to as intra-arterial digital subtraction angiography) is used to diagnose intracranial lesions. With this approach, a radiopaque contrast medium is injected into blood vessels of the head and neck to allow visualization of intracranial and extracranial vessels on x-ray. Cerebral angiography can reveal aneurysms, arteriovenous malformations, and displacement of vessels by masses, edema, or herniation. The test is also used during surgery to check the position and integrity of aneurysm clips [22,23,24].

Lumbar puncture can be done at the bedside or in the diagnostic lab. The procedure is done with the patient positioned to one side (typically the left) with head and knees flexed toward the abdomen. The patient is assisted in maintaining this position, which separates the vertebrae, allowing the needle to enter the subarachnoid space at the level L3-to-L4 or L4-to-L5. Aseptic technique is required [22,23,24]. In some patients, particularly those who are overweight, sitting and leaning forward may provide better access.

Because CSF is in contact with the components of the CNS, it can be valuable in the diagnosis and evaluation of CNS disease progression or healing process. CSF is colorless and consists of water and traces of protein, glucose, sodium, chloride, and potassium. The average volume in adults ranges from 100–150 mL. CSF pressure in the supine patient ranges from 7–20 cm/H₂O. Fluid that is dark in color or even pink-tinged indicates hemorrhage or a cerebral bleed [22,23,24].

For the physically impaired or obtunded patient, careful positioning with pillows and special devices promotes drainage of secretions, maintains a patent airway, and reduces the risk of aspiration. This includes careful positioning during meals, supplemental oral intake, nasogastric feedings, and oral care. A suction machine should be at hand if choking is a risk or secretions are unmanageable. Active or passive range-of-motion exercises and frequent position changes help to promote mobilization of secretions [20].

Impairment of cardiac output can follow injury to the brain stem's vasomotor center, which influences cardiac function via the autonomic nervous system. The brain stem's vasomotor center also controls blood pressure. With sharp elevation in blood pressure initiated to perfuse a severely edematous brain, the vasomotor center initiates a reflex slowing of the heart, reduces contractility, and produces vasodilation. Cardiac output can also be compromised by anoxia stemming from alterations in respiratory function [18,19].

Urinary retention or incontinence can result from diseases affecting the cerebral cortex, spinal cord, and/or peripheral nervous system. Patients with CNS dysfunction often experience both a diminished awareness of bladder fullness and a decreased ability to empty the bladder. Alterations in consciousness from trauma, electrolyte imbalance, anoxia, and disease processes can produce temporary or permanent urinary incontinence [18,19].

Muscular dystrophy is a hereditary, degenerative neuromuscular disorder characterized by chronic, progressive wasting and weakness of voluntary muscles. Far more common in men than women, the disease affects both children and young adults. The nine different types of muscular dystrophy (i.e., myotonic, Duchenne, Becker, Emery-Dreifuss, limb-girdle, facioscapulohumeral, congenital, oculopharyngeal, and distal) vary in the age of onset, rate of symptom progression, and clinical manifestations. All types exhibit degenerative changes in the muscle fibers [29,30].

The choreiform movements are the most striking characteristic of Huntington chorea. They begin slowly, usually first in the face and upper extremities. Facial grimacing and jerking limb movements occur. Over time, movements become frequent, erratic, and violent [29]. Choreiform movements can occur both at rest and during voluntary movements. In advanced stages of Hunting disease, choreiform hyperkinesia occurs alongside dystonic postures of the limbs or trunk before they typically decrease in intensity [32].

In the peripheral form of neurofibromatosis, multiple cutaneous and subcutaneous nodules occur. Cutaneous tumors are palpated in the dermis as discrete soft or firm papules varying in size from millimeters to centimeters. If pressed, these soft nodules feel like a seedless grape, which aids in distinguishing lesions of neurofibromatosis from other tumors. Subcutaneous tumors are usually multiple, assuming two forms: discrete or plexiform neuromas. Discrete tumors are firm nodules that attach to the peripheral portion of a nerve. These nodules may cause neurologic or paresthetic pain to pressure and rarely cause weakness, atrophy, or sensory loss in the distribution of the affected nerve. The number of nodules varies from a few to thousands, and the size varies from pea-sized to orange-sized. Plexiform neuromas are an overgrowth of subcutaneous tissue and can reach enormous sizes. The face, scalp, chest, and neck are typically affected with growths that feel like a "bag of worms" when palpated. The hypertrophy is highly disfiguring and often accompanied by underlying bone abnormalities. These tumors, if large enough, can cause increased ICP and brain stem compression [33].

Clinical manifestations of arteriovenous malformations include seizures, hemorrhage, headaches, motor and sensory deficits, organic mental impairments, visual dysfunction, and syncopal episodes. The most common are seizure activity and hemorrhage [35,36].

Hemorrhagic strokes are categorized by the location of the hemorrhage, either intracerebral or subarachnoid, with the former being more than twice as common—because of this, the term hemorrhagic stroke often refers to intracerebral hemorrhage (ICH) [38,39,40]. ICHs are characterized by bleeding directly into the brain parenchyma [40,41]. Intraventricular hemorrhage describes bleeding that extends into the ventricles [41,42]. Nontraumatic ICH is categorized as primary (unrelated to congenital or acquired lesions), secondary (caused by a congenital or acquired condition), or spontaneous (unrelated to trauma or surgery) [41].

The signs and symptoms of ICH include headache, vomiting, seizures, depressed consciousness, meningeal irritation, and blood-tainted CSF. The onset of symptoms may occur within seconds to minutes after the start of an ICH. Individuals with this type of stroke often feel more ill than those with an ischemic stroke.

ICH is the least treatable type of stroke [43]. Functional independence is regained within six months in approximately 20% of survivors [44]. The morbidity and mortality depend on the volume and location of the hematoma. The one-year mortality rate varies according to anatomic location, with the highest mortality rate (65%) associated with ICH in the brain stem; the rate is 57% for lobar hemorrhage, 51% for deep hemorrhage, and 42% for cerebellar hemorrhage [45]. Overall, 46% of patients with ICH survive one year and 29% survive five years [46].

Communicating hydrocephalus, the third most common complication of subarachnoid hemorrhage, can occur with the bleed or weeks later as a result of a malabsorption or blockage of CSF [59]. Hydrocephalus should be suspected if any of these signs appear [59]:

Mental status changes

A decrease in level of consciousness

Dementias

Flat affect

Urinary incontinence

Disturbances in gait

The risk of ischemic stroke is dangerously high in the period following a TIA. Research indicates that one-half of subsequent strokes occur within the first 48 hours, and a meta-analysis showed that approximately 5% of patients who have a TIA will have an ischemic stroke within seven days of that event [71,74].

The ictal phase is the duration of the actual seizure activity. The patient experiences a paroxysmal, uncontrolled, abnormal, and excessive discharge of electrical activity in the brain. There are also corresponding EEG changes [84]. The clinical manifestations will coincide with the type of seizure activity that the patient is experiencing.

Cluster headaches are one of several types of trigeminal autonomic cephalalgias, primary headaches characterized by unilateral pain in the trigeminal nerve region. As defined by the International Headache Society, cluster headaches are attacks of severe unilateral pain in the orbit and/or the surrounding region of the eye that last 15 to 180 minutes [95]. The term "cluster" refers to the headache attacks occurring in daily episodes. The patient is headache-free in between the clusters.

Alzheimer disease was first identified and named in 1906 by Dr. Alois Alzheimer, a German neuropathologist [99]. Symptoms seen in individuals with Alzheimer disease are partially the result of damage to the hippocampus and the cerebral cortex, reflected in memory loss, impaired cognition, and atypical behaviors.

There are two types of Alzheimer disease: familial and sporadic. Familial Alzheimer disease follows an autosomal dominant inheritance pattern, while sporadic Alzheimer disease has no known inheritance factor. Familial Alzheimer disease can be further classified as early-onset, when it occurs in individuals younger than 60 years of age, or late-onset, when it affects individuals older than 60 years of age [101].

The onset of Alzheimer disease is slow and insidious; impaired memory is usually the initial symptom, followed later by deficits in other cognitive domains. Symptoms may be present for several months before the family realizes the severity of the problem. In some situations, a spouse may shelter and cover for the patient so even children and friends are unaware. In other cases, it is the death of the healthy spouse that causes other family members to recognize the changes that have occurred in the living partner. After the diagnosis of Alzheimer disease, most patients will survive for 4 to 6 years; however, this number can vary from 3 to 20 years [102].

Motor symptoms can also appear long before diagnosis. In Parkinson disease, the cardinal motor features of bradykinesia, resting tremor, rigidity, and postural/gait impairment reflect parkinsonism [117]. A mnemonic for the core motor features is TRAP [118]:

Tremor at rest

Rigidity

Akinesia (i.e., bradykinesia and hypokinesia)

Postural instability

The most characteristic finding in myasthenia gravis is an increasing weakness of certain voluntary muscles with activity and some improvement with rest. The muscles of the eyes are often most affected. Unilateral or bilateral ptosis and diplopia are common [122].

Primary symptoms of multiple sclerosis are caused by the inflammation and demyelination that arises within focal areas of the CNS. The clinical presentation is varied but, in general, consists of some disturbance in vision, sensation, and/or motor function. The most common primary symptoms in patients with multiple sclerosis are:

Fatigue

Heat sensitivity

Muscle spasms

Dizziness

Pain

Paresthesias

Ataxia

Cognitive changes

Visual complaints

Bowel or bladder dysfunction

Sexual dysfunction

Gait problems

Nausea/vomiting

Speech problems

Tremor

Weakness

Sensory perceptual deficits can occur because of photophobia, hyperalgesia, and hyperirritability. A quiet, dark, non-stimulating environment and limited visiting hours can help reduce photophobia. The potential impact of hypoxia or bladder distention on irritability should be ruled out before considering it a neurologic problem. For headache management, keep the head of the bed elevated, unless contraindicated, with good body alignment and repositioning every two hours [98,140]. Pneumococcal and influenza immunizations are the best preventive measures [140].

Clinical management of encephalitis is mainly symptomatic and supportive. There is no curative drug therapy, but steroids such as dexamethasone (Decadron) may be used to combat cerebral edema. Herpes encephalitis is treated with the antiviral agents acyclovir and valacyclovir; however, antivirals are ineffective for other viral causes [141,142]. Not all patients recover completely. Those surviving an acute episode can have residual neurologic deficits, including seizures, dysphasia, memory loss, and/or personality changes [122].

Herpes zoster (also known as shingles) is a viral disorder that affects the posterior root ganglia. It is characterized by cutaneous eruptions of vesicles along the distribution of involved spinal or cranial nerve roots. The highest percentage of cases involve spinal ganglia. Outbreaks occur mainly in adults and are more common in women than men and during the spring and fall [24,143,144].

Herpes zoster develops from reactivation of varicella virus, which is responsible for chickenpox. Children without immunization can develop chickenpox if exposed to an adult with shingles [24,143,144].

Tumors within the cranium can be either primary or metastatic. Metastatic tumors are found predominantly within the substance of the brain, which they reach through the systemic circulation.

The neurologic status of the patient with acute head trauma should be assessed immediately after respiratory airway patency is established. Level of consciousness is the single most important aspect of the clinical nursing observation. Consciousness is assessed on a continuum from full reaction to no reaction to various kinds of stimuli. The bilateral corneal reflex should also be assessed on schedule [37].

Patients with spinal cord injury are at greatest risk in the first 7 to 10 days after trauma. During this time, shock, pulmonary dysfunction, infection, and paralytic ileus can be major problems. Patients who sustain quadriplegic injuries require intensive total medical and nursing management. The posttraumatic care of these patients mainly involves management of bladder and bowel dysfunction, skin care, nutrition maintenance, and physical therapy [125].