Inflammatory and infectious disorders of the brain

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Inflammatory and infectious disorders of the brain


The diversity of neurological sequelae that may occur after an inflammatory disorder in the brain (brain abscess, encephalitis, or meningitis) provides a range of challenges to the rehabilitation team. The therapist must identify the problems underlying the individual’s movement dysfunctions without the template of the cluster of “typical” problems available with some other neurological diagnoses. Each client presents a combination of problems that is unique to that client and that requires the creative design of an intervention program. The following discussion of the therapeutic management of individuals recovering from an inflammatory disorder in the brain focuses on the process of designing an intervention plan to address the specific dysfunctions of the individual client. Because the management of the clinical problems is built on an understanding of the underlying pathological condition and because therapists may not be as familiar with these disease processes, an overview of the inflammatory disorders of the brain is presented.

Overview of inflammatory disorders in the brain

Categorization of inflammatory disorders

Inflammatory disorders of the brain can be categorized based on the anatomical location of the inflammatory process and the cause of the infection, as follows:

In most individuals, the defense mechanisms of the central nervous system (CNS) provide protection from infecting organisms. Compromises of the protective barriers can result in CNS infections as complications of common infections. The response of the CNS to the infection depends on several factors, including the type of organism, its route of entry, the CNS location of the infection, and the immunological competence of the individual. CNS infections occur with greater frequency and severity in individuals who are very young or elderly, immunodeficient, or antibody deficient.

The inflammatory process may be a localized, circumscribed collection of pus; may involve primarily the leptomeninges; may involve the brain substance; or may involve both the meninges and the brain substance. The infecting agents may be bacteria, viruses, prions, fungi, protozoa, or parasites. The most common agents producing meningitis are bacterial; the most common agents producing encephalitis are viral. However, bacterial encephalitis and viral meningitis also are disease entities. The following overview of the inflammatory processes within the brain is organized based on the anatomical location of the infection. More comprehensive discussions based on specific infecting organisms can be found in the references at the end of the chapter.1 The site of the infection will determine the signs and symptoms of the CNS infections, whereas the infecting organism determines the prognosis, including the time course and severity of the problems.2

Brain abscess

Brain abscesses occur when microorganisms reach brain tissue from a penetrating wound to the brain, by extension of local infection such as sinusitis or otitis, or by hematogenous spread from a distant site of infection. The route of infection influences the CNS region involved. The extension of a local infection tends to produce a solitary brain abscess in an adjacent lobe. Multiple abscesses may originate from the spread of microorganisms through the blood. The introduction of microorganisms by a penetrating trauma may result in an abscess soon after the trauma or several years later. As with the disorders presented in the subsequent discussions, circumstances that result in a compromised immune system (chronic corticosteroid or other immunosuppressive drug administration, administration of cytotoxic chemotherapeutic agents, or human immunodeficiency virus [HIV] infection) may predispose the individual to develop opportunistic infections.

The site and size of the abscess influence the initial symptoms. Evidence of increased intracranial pressure, a focal neurological deficit, and fever are described as the classic presenting triad.3 However, the classic triad occurs in less than 50% of patients.4 Most individuals experience an alteration of consciousness. In 47% of the cases, the frontal, parietal, or temporal lobe is involved.4,5 Medical management of the abscess typically consists of antibiotic therapy (depending on the infecting agent and size and site of the abscess) and, often, surgical aspiration or excision. Bharucha and colleagues3 describe neurological sequelae in 25% to 50% of the survivors, with 30% to 50% having persistent seizures, 15% to 30% having hemiparesis, and 10% to 20% having disorders of speech or language.


Meningitis (synonymous with leptomeningitis) denotes an infection spread through the cerebrospinal fluid (CSF) with the inflammatory process involving the pia and arachnoid maters, the subarachnoid space, and the adjacent superficial tissues of the brain and spinal cord. Pachymeningitis denotes an inflammatory process involving the dura mater. Meningitis can be caused by a wide variety of organisms, some of which cross the blood-brain barrier and the blood-CSF barrier. The CSF also can become contaminated by a wound that penetrates the meninges as a result of trauma or a medical procedure, such as implantation of a ventriculoperitoneal (VP) shunt. Once the organism compromises the blood-brain and blood-CSF barriers, the CSF provides an ideal medium for growth. All the body’s typical major defense systems are essentially absent in the normal CSF. The blood-brain barrier may impede the clearance of infecting organisms by leukocytes and interfere with the entry of pharmacological agents from the blood. The infecting organism is disseminated throughout the subarachnoid space as the contaminated CSF bathes the brain. Entry into the ventricles occurs either from the choroid plexuses or by reflux through the exit foramen of the fourth ventricle. The spread of the organism through the CSF circulation accounts for the differences in the variety and extent of the neurological sequelae that can result from meningitis.

Bacterial meningitis

Clinical problems.

The diagnostic categorization of meningitis depends on the infecting agent (e.g., Haemophilus influenzae meningitis, Streptococcus pneumoniae meningitis, and viral meningitis) and on the acute or chronic nature of the meningitis (acute, subacute, or chronic meningitis). The term acute bacterial meningitis denotes infections caused by aerobic bacteria (both gram-positive and gram-negative).5,6 The most common infecting organism producing acute bacterial meningitis varies according to the age of the population. During the neonatal period and in the older adult, infections by gram-negative enterobacilli, especially Escherichia coli, and group B streptococci occur most frequently. Typical causative agents in children include H. influenzae, Neisseria meningitidis, and S. pneumoniae.7 S. pneumoniae, N. meningitidis, and H. influenzae are the most common causes of community-acquired meningitis.5,7,8 Individuals with a condition such as sickle cell anemia, alcoholism, or diabetes mellitus and individuals who are immunosuppressed are at increased risk.1,9 Meningococci have been implicated in meningitis that strikes young children most often but can also infect adolescents and young adults. Freshman who live in dormitories are almost four times more likely to get meningitis than other college students.

An example of an organism that uses a typical systemic route of bacterial infection is the H. influenzae organism—a member of the normal flora of the nose and throat. During an upper respiratory tract infection, the organism may gain entry to the blood. The route of transmission of the organism from the blood to the CSF is not well established.

The circulation of CSF spreads the infecting organism through the ventricular system and the subarachnoid spaces (Figure 26-1). The pia and arachnoid maters become acutely inflamed, and as part of the inflammatory response, a purulent exudate forms in the subarachnoid space. The exudate may undergo organization, resulting in an obstruction of the foramen of Monro, the aqueduct of Sylvius, or the exit foramen of the fourth ventricle. The supracortical subarachnoid spaces proximal to the arachnoid villi may be obliterated, resulting in a noncommunicating or obstructive hydrocephalus caused by the accumulation of CSF. As the CSF accumulates, the intracranial pressure rises. The increased intracranial pressure produces venous obstruction, precipitating a further increase in the intracranial pressure. The rise in the CSF pressure compromises the cerebral blood flow, which activates reflex mechanisms to counteract the decreased cerebral blood flow by raising the systemic blood pressure. An increased systemic blood pressure accompanies increased CSF pressure.

The mechanism producing the headaches that accompany increased intracranial pressure may be the stretching of the meninges and pain fibers associated with blood vessels. Vomiting may occur as a result of stimulation of the medullary emetic centers. Papilledema may occur as intracranial pressure increases.

Other routes of bacterial infection may involve a local spread as the result of an infection of the middle ear or mastoid air cells. Meningitis may occur as a complication of a skull fracture, which exposes CNS tissue to the external environment or to the nasal cavity. Fractures of the cribriform plate of the ethmoid bone producing CSF rhinorrhea provide another route for infection. Meningitis may be a further complication to the clinical problems of a traumatic head injury.

Clinical features of acute bacterial meningitis include fever, severe headache, altered consciousness, convulsions (particularly in children), and nuchal rigidity. Nuchal rigidity is indicative of an irritative lesion of the subarachnoid space. Signs of meningeal irritation are painful cervical flexion, the Kernig sign, the Brudzinski sign, and the jolt sign.10 Cervical flexion is painful because it stretches the inflamed meninges, nerve roots, and spinal cord. The pain triggers a reflex spasm of the neck extensors to splint the area against further cervical flexion; however, cervical rotation and extension movements remain relatively free.

The Kernig sign refers to a test performed with the client supine in which the thigh is flexed on the abdomen and the knee extended (Figure 26-2, A). Complaints of lumbar or posterior thigh pain indicate a positive test result.10 This movement pulls on the sciatic nerve, which pulls on the covering of the spinal cord, causing pain in the presence of meningeal irritation. The same results are achieved with passive hip flexion with the knee remaining in extension. This is the same procedure described by Hoppenfeld11 as the straight leg raising test for determining pathology of the sciatic nerve or tightness of the hamstrings. Passive hip flexion with knee extension can be painful because of meningeal irritation, spinal root impingement, sciatic nerve irritation, or hamstring tightness. The Brudzinski sign refers to the flexion of the hips and knees elicited when cervical flexion is performed10 (see Figure 26-2, B). These signs will not be present in the deeply comatose client who has decreased muscle tone and absence of muscle reflexes. The signs may also be absent in the infant or elderly patient. Finally, the jolt test, which has the patient turn his or her head from side to side quickly (two to three rotations per second), has a positive result if the maneuver worsens the patient’s headache.10

The diagnosis of bacterial meningitis can be established based on blood cultures and a sample of CSF obtained by a lumbar puncture. CSF pressure is consistently elevated. The CSF sample in bacterial meningitis typically reveals an increased protein count and a decreased glucose level.

The type and severity of the sequelae of acute bacterial meningitis relate directly to the area affected, the extent of CNS infection, the age and general health of the individual, the level of consciousness at the initiation of pharmacological therapy, and the pathological agent involved. Some of the common CNS complications include subdural effusions, altered levels of consciousness, seizures, involvement of the cranial nerves, and increased intracranial pressure.

Potential neurological sequelae.

Even with optimal antimicrobial therapy, bacterial meningitis continues to have a finite mortality rate, which varies with the infecting organism, age of the individual, and time lapse to initiation of treatment, and has the potential for marked neurological morbidity. Neurological sequelae occur in 20% to 50% of the cases.1,9 Bacterial meningitis is considered a medical emergency; delays in initiation of antibacterial therapy increase the risk of complications and permanent neurological dysfunction.1,9

Reports of the long-term outcome of individuals with bacterial meningitis indicate that up to 20% have long-term neurological sequelae.1,5 The sequelae may be the result of the acute infectious pathological condition or subacute or chronic pathological changes. The acute infectious pathological condition could result in sequelae such as inflammatory or vascular involvement of the cranial nerves or thrombosis of the meningeal veins. Cranial nerve palsies, especially sensorineural hearing loss, are common complications. The risk of an acute ischemic stroke is greatest during the first 5 days.9 Weeks to months after treatment, subacute or chronic pathological changes may develop, such as communicating hydrocephalus, which manifests as difficulties with gait, mental status changes, and incontinence.10,12 Approximately 5% of the survivors will have weakness and spasticity.6 Focal cerebral signs that may occur either early or late in the course of bacterial meningitis include hemiparesis, ataxia, seizures, cranial nerve palsies, and gaze preference.1,13 Cognitive slowness has been found in 27% of clients after pneumococcal meningitis, even with good recovery as documented by a Glasgow Outcome Scale score of 5.14

Damage to the cerebral cortex can result in numerous expressions of dysfunction. Motor system dysfunction may be the observable expression of the damage within the CNS, but the location of the damage may include sensory and processing areas, as well as those areas typically categorized as belonging to the motor system. Perceptual deficits or regression in cognitive skills may present residual problems. Cranial nerve involvement is most frequently expressed as dysfunction of the eighth cranial nerve complex and produces auditory and vestibular deficits.

Aseptic meningitis.

Aseptic meningitis refers to a nonpurulent inflammatory process confined to the meninges and choroid plexus, usually caused by contamination of the CSF with a viral agent, although other agents can trigger the reactions. The symptoms are similar to those of acute bacterial meningitis but typically are less severe. The individual may be irritable and lethargic and complain of a headache, but cerebral function remains normal unless unusual complications occur.5,15 Aseptic meningitis of a viral origin usually causes a benign and relatively short course of illness.16,17

A variety of neurotropic viruses can produce aseptic (viral) meningitis. The enteroviruses (echoviruses and the Coxsackie viruses), herpesviruses, and HIV are the most common causes.5,7,18 The primary nonviral causes of aseptic meningitis are Lyme Borrelia and Leptospira.19 The diagnosis of this type of aseptic meningitis may be established by isolation of the infecting agent within the CSF or by other techniques. The glucose level of the CSF in bacterial meningitis is usually depressed; however, the glucose level in viral meningitis is normal.2

Treatment of aseptic meningitis consists of management of symptoms. The condition does not typically produce residual neurological sequelae, and full recovery is anticipated within a few days to a few weeks.


Clinical problems.

Encephalitis refers to a group of diseases characterized by inflammation of the parenchyma of the brain and its surrounding meninges. Although a variety of agents can produce encephalitis, the term usually denotes a viral invasion of the cells of the brain and spinal cord.

Different cell populations within the CNS vary in their susceptibility to infection by a specific virus. (For example, the viruses responsible for poliomyelitis have a selective affinity for the motor neurons of the brain stem and spinal cord. Viruses such as Coxsackie viruses and echoviruses typically infect meningeal cells to cause the benign viral meningitis discussed in the previous section.) In acute encephalitis, neurons that are vulnerable to the specific virus are invaded and undergo lysis. Viral encephalitis causes a syndrome of elevated temperature, headache, nuchal rigidity, vomiting, and general malaise (symptoms of aseptic or viral meningitis), with the addition of evidence of more extensive cerebral damage such as coma, cranial nerve palsy, hemiplegia, involuntary movements, or ataxia. The difficulty in differentiating between acute viral meningitis and acute viral encephalitis is reflected in the use of the term meningoencephalitis in some cases.

The pathological condition includes destruction or damage to neurons and glial cells resulting from invasion of the cells by the virus, the presence of intranuclear inclusion bodies, edema, and inflammation of the brain and spinal cord. Perivascular cuffing by polymorphonuclear leukocytes and lymphocytes may occur, as well as angiitis of small blood vessels. Widespread destruction of the white matter by the inflammatory process and by thrombosis of the perforating vessels can occur. Increased intracranial pressure, which can result from the cerebral edema and vascular damage, presents the potential for a transtentorial herniation. The likelihood of residual impairment of neurological functions depends on the infecting viral agent. Patients with mumps meningoencephalitis have an excellent prognosis, whereas 55% of the individuals with herpes simplex encephalitis treated with acyclovir have some neurological sequelae.6 Because of the slow recovery of injured brain tissue, even in patients who recover completely, return to normal function may take months.20

Plum and Posner21 discuss viral encephalitis in terms of five pathological syndromes. Acute viral encephalitis is a primary or exclusively CNS infection. An example would be herpes simplex encephalitis, in which the virus shows a partiality for the gray matter of the temporal lobe, insula, cingulate gyrus, and inferior frontal lobe. Other examples are the mosquito-borne viruses, such as the St. Louis encephalitis, California virus encephalitis, and most recently the West Nile virus (WNV). From 1999 to 2005 in the United States, the incidence of infection from the WNV has increased from 62 cases to 3000 cases.22 Currently all states have some level of WNV activity, and only four states are without human cases (Figure 26-3). The majority (80%) of people infected by the WNV will be asymptomatic; of the remaining people infected, less than 1% will develop severe illness.23 Risk of neuroinvasive disease from WNV is 40%; neuroinvasive disease involves meningitis, encephalitis, or poliomyelitis, with wide variety in clinical presentation (Figure 26-4).24 Parainfectious encephalomyelitis is associated with viral infections such as measles, mumps, or varicella. Acute toxic encephalopathy denotes encephalitis that occurs during the course of a systemic infection with a common virus. The clinical symptoms are produced by the cerebral edema in acute toxic encephalopathy, which results in increased intracranial pressure and the risk of transtentorial herniation. Reye syndrome is an example. Global neurological signs, such as hemiplegia and aphasia, are usually present, rather than focal signs. The clinical symptoms of the previous three syndromes may be similar. Specific diagnosis may be established only by biopsy or autopsy.

Progressive viral infections occur from common viruses invading susceptible individuals, such as those who are immunosuppressed or during the perinatal to early childhood period. Slow, progressive destruction of the CNS occurs, as in subacute sclerosing panencephalitis. The final category of encephalitis syndromes consists of “slow virus” infections by unconventional agents (the prion diseases) that produce progressive dementing diseases such as Creutzfeldt-Jakob disease and kuru.25

Clinical picture of the individual with inflammatory disorders of the brain

An individual within the acute phase of meningitis or encephalitis or with residual neurologic dysfunction from these disorders may demonstrate signs and symptoms similar to those of generalized brain trauma, tumor disorder, or other identified abnormal neurological state. The variability in the clinical picture is reflected in the inclusion of the category “infectious diseases that affect the central nervous system” in the Guide to Physical Therapist Practice.27 Practice patterns for physical therapists that apply to this population include the following:

Although these patterns have been identified within the physical therapy practice patterns, the concepts and selection of evaluation and intervention procedures are just as applicable for occupational therapists and other individuals working on movement dysfunction. In the acute phase the inflammatory process may result in impairments in arousal and attention that range from nonresponsiveness to agitation. The degree of agitation may range from mild to severe, depending on both the client’s unique CNS characteristics and the degree of inflammation. The agitated state may be the result of alterations in the processing of sensory input, with the consequence of inappropriate or augmented responses to sensory input. The client may respond to a normal level of sound as though it were an unbearably loud noise. Low levels of artificial light may be perceived as extremely bright.

Perceptual and cognitive impairments may be present, resulting in a variety of functional limitations and disabilities. Clients may have distortions in their perception of events as well as memory problems. As their memory returns, accuracy of time and events may be distorted, leading to frustration and anxiety for both the client and those family members and friends who are interacting within the environment.

In addition to alterations in mentation, the individual may demonstrate impaired affect, such as a hypersensitivity or exaggerated emotional responses to seemingly normal interactions. For example, when upset about dropping a spoon on the floor, a client may throw the tray across the table. When another individual was told his girlfriend would be a little late for her afternoon visit, the client became extremely upset and stated his intent to kill himself because his girlfriend did not love him anymore.

Because of the variety of pathological problems after acute inflammation, the client may have residual problems manifested as generalized or focal brain damage. The specifics of these impairments cannot be described as a typical clinical picture because they are extremely dependent on the individual client. These variations require the therapist to conduct a thorough examination and evaluation process to develop an appropriate individualized intervention program. Although content from the Guide to Physical Therapist Practice has been incorporated into the discussion of the examination, evaluation, and intervention processes, the model presented provides a structure that can accommodate the specific disciplinary expertise of both occupational and physical therapists.

Examination and evaluation process

Just as the medical intervention with clients who have an inflammatory disorder of the CNS is, to a large extent, symptomatic, so is the intervention by therapists. Designing an individualized intervention program based on the client’s problems requires a comprehensive initial and ongoing evaluation to define the impairments, functional limitations, and disabilities and to note changes in them. Although the discussion of examination procedures is separated from the discussion of intervention strategies, it must be recognized that the separation is artificial and does not reflect the image of practice. The evaluation process should be considered in relationship to both the long-term assessment of the individual’s changes and the short-term within-session and between-session variations. For example, documentation of the level of consciousness of a client on day one of intervention will provide a starting point for calculation of the distance spanned at the time of discharge. Perhaps more critical to the final outcome is determination of the level of consciousness before, during, and after a particular intervention technique to determine its impact on the individual’s level of arousal and ability to interact with the environment. The evaluation process is a constant activity intertwined with intervention. The observations and data from the process are periodically recorded to establish the course of the disease process and the success of the therapeutic management of the client.

Observation of current functional status

The examination process should be conceptualized as a decision-making tree that requires the therapist to determine actively which components are to be included in a detailed examination and which can be eliminated or deferred. The first step in this process is the observation of the client’s current functional status. If the client is comatose and nonmobile, the focus of the initial session might be an assessment of the stability of physiological functions, level of consciousness, responses to sensory input, and joint mobility. If the client is an outpatient with motor control deficits, the initial session might focus on defining motor abilities and components contributing to movement dysfunctions with a more superficial assessment of physiological functions and level of consciousness. The therapist must be alert to indications of the need for a more detailed evaluation of perceptual and cognitive function (e.g., the client cannot follow two-step commands, indicating the need to assess cognitive skills).

Some of the components discussed in this process may be examination skills that are more typically possessed by other professions (e.g., assessment of emotional or psychological status). The inclusion of these items is not meant to suggest that the therapist must complete the formal testing. The items are included to indicate factors that will affect goal setting for the client and that will have an impact on the intervention strategy. Although the therapist may not be the health care team member who has primary responsibility for evaluation of these areas, he or she should recognize these areas as potential contributors to movement dysfunctions.

Observation of the current functional status of the client provides the therapist with an initial overview of his assets and deficits. This provides the framework into which the pieces of information from the evaluation of specific aspects of function can be fit. The therapist must not allow assumptions made during the initial observation to bias later observations. The therapist might note that the client is able to roll from the supine to the side-lying position to interact with visitors in the room. When the same activity is not repeated on the mat table in the treatment area, the therapist, knowing the client has the motor skill to roll, might conclude that he is uncooperative or apraxic or has perceptual deficits. The therapist may have failed to consider that the difference between the two situations is the type of support surface or the presence or absence of side rails, which may have enabled the client to roll in bed by pulling over to the side-lying position. It is characteristic of human observation skills that we tend to “see” what we expect to see. The therapist must attempt to observe behaviors and note potential explanations for deviations from normal without biasing the results of the subsequent observations.

The following discussion of the specific considerations within the examination process does not necessarily represent the temporal sequence to be used during the data collection process. As different items are discussed, suggestions for potential combinations of items will be made. The sequence of the process is best determined by the interaction of therapist and client. Figure 26-5 outlines the components that should be considered during the evaluation process and provides a synopsis of the following discussion.

The general philosophy in the evaluation of the client with neurological deficits as a result of brain inflammation is a whole-part-whole approach. General observations of the client’s performance provide an overall description of the client’s abilities while indicating deficits in his or her performance. The cause(s) of the deficits (impairments) are explored to provide the pieces of data defining her or his performance. These pieces of data then are arranged within the framework provided by the general observation to define the whole of the client’s assets and deficits. As the whole picture is established (with the realization that it will be constantly adjusted), the process of goal setting is initiated. These goals need to consider the patient’s and family’s desires. The process presented for refining evaluation data into an intervention plan is applicable whether the client’s neurological dysfunction is the result of a bacterial or viral infection, cerebrovascular accident, trauma, or other factors.

Evaluation of physiological responses to therapeutic activities

It is assumed that the therapist enters the initial interaction with a client after reviewing the available background information. This may provide the therapist with information on the baseline status of the client’s vital physiological functions. Any control problems in these areas should be particularly noted. Until the therapist determines that the vital functions, such as rate of respiration, heart rate, and blood pressure, vary appropriately with the demands of the intervention process, these factors should be monitored. The monitoring process should include consideration of the baseline rate, rate during exercise, and time to return to baseline. The pattern of respiration and changes in that pattern also should be noted.

Other tests and measures of the status of ventilation, respiration, and circulation may be indicated in specific individuals. Individuals with limited mobility or motor control of the trunk or those with cranial nerve dysfunctions may demonstrate difficulty with functions such as moving secretions out of the airways. Inactivity during a prolonged recovery period may result in cardiovascular adaptations that compromise endurance and contribute to increases in the perceived exertion during activities.

Autonomic nervous system dysfunctions may be expressed as inappropriate accommodations to positional changes, such as orthostatic hypotension. Clients with depressed levels of consciousness may display temperature regulation dysfunctions. One mechanism for assessing the client’s ability to maintain a homeostatic temperature is to review the nursing notes. The events surrounding any periods of diaphoresis should be examined. If no causative factors have been identified, then interventions that involve thermal agents as discussed elsewhere in this text should be used judiciously.

Evaluation of cognitive status

Because the evaluation process encompasses the stages of recovery from the critical acute phase through discharge from therapy, a range of aspects are included under the evaluation of cognitive status. As indicated previously, the observation of current functional status will direct the therapist toward the appropriate component tests and measures.

Acute bacterial meningitis and various forms of viral encephalitis may result in changes in the client’s level of consciousness. Consciousness is a state of awareness of one’s self and one’s environment.21 Coma can be defined as a state in which one does not open the eyes, obey commands, or utter recognizable words.28 The individual does not respond to external stimuli or to internal needs. The term vegetative state is sometimes used to indicate the status of individuals who open their eyes and display a sleep-wake cycle but who do not obey commands or utter recognizable words. DeMeyer29 presents a succinct description of the neuroanatomy of consciousness and the neurological examination of the unconscious patient. Plum and Posner21 also provide extensive information in this area.

Several scales have been developed to provide objective guidelines to assess alterations in the state of consciousness. The Glasgow Coma Scale28 assesses three independent items: eye opening, motor performance, and verbal performance. The scale yields a figure from 3 (lowest) to 15 (highest) that can be used to indicate changes in the individual’s state of consciousness. The evaluation format is simple, and the scale demonstrates both interrater and intrarater reliability. Refer to Box 24-4 for the specific scale. The Rancho Los Amigos scale assesses level of consciousness and behavior.28 The therapist can use assessment tools such as the Glasgow Coma Scale and the companion Glasgow Outcome Scale to determine if the intervention program has resulted in any recordable changes in the client’s level of consciousness. Ideally, the client with decreased levels of consciousness will be monitored at consistent intervals to determine changes in status. Any carryover or delayed effects of the intervention could then be noted. The record of the client’s level of consciousness might also display a pattern of peak awareness at a particular point in the day. Scheduling an intervention session during the client’s peak awareness time may maximize the benefit of the therapy.

Performed in conjunction with the assessment of the client’s state of consciousness is the determination of the individual’s orientation to person, time, place, and situation. Because the individual’s level of orientation (documented as oriented times 4) is frequently recorded by multiple members of the rehabilitation team, the information in the medical chart may provide insights into fluctuations over the course of a day or a week.

Gross assessment of the individual’s ability to communicate, both the expressive and receptive aspects of the process, is an important component of the examination. If a dysfunction is present in the client’s ability to communicate, the client should be evaluated by an individual with expertise in this area so that strategies for dealing with the communication deficit can be developed. Evaluation of the movement abilities of the client with communication deficits requires creative planning on the part of the therapist but usually can be accomplished if generalized movement tasks are used. With the client who cannot comprehend a verbal command to roll, the therapist should use an alternate form of communication, such as manual cueing or guidance. The therapist could structure the situation to elicit the desired behavior by activities such as placing the client in an uncomfortable position or positioning a desired object so that it can be reached only by rolling.

As the therapist progresses through the examination and intervention process, ongoing data collection should be occurring on factors that influence the motivation of the individual. Individuals with damage to certain areas within the frontal lobe will have difficulty with committing to long-term projects and may not be motivated to work during a therapy session by an explanation detailing the relationship of the current activity to the larger goal of returning home. In these situations, the therapist must create appropriate immediate rewards, such as a 2-minute rest break after completion of a specific movement task.

Deficits in cognition may be evident as problems in the area of explicit (declarative) or implicit (procedural) learning. Explicit learning is used in the acquisition of knowledge that is consciously recalled. This is information that can be verbalized in declarative sentences, such as the sequential listing of the steps in a movement sequence. Implicit or procedural learning is used in the process of acquiring movement sequences that are performed automatically without conscious attention to the performance. Procedural learning occurs through repetitions of the movement task (refer to Chapter 4). Because explicit and implicit learning use different neuroanatomical circuits, implicit learning can occur in individuals with deficits in the components underlying explicit learning (awareness, attention, higher-order cognitive processes) (refer to Chapter 5 for additional information regarding implicit and explicit learning).

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