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, which are as follows:

• A.
  

  Brain abscess

  
  
• B.
  

  Meningitis (leptomeningitis)

  
  
  
  
  • 1.
    

    Bacterial meningitis

    
    
  • 2.
    

    Aseptic meningitis (viral)

  
  
  
  
• C.
  

  Encephalitis

  
  
  
  
  • 1.
    

    Acute viral

    
    
  • 2.
    

    Parainfectious encephalomyelitis

    
    
  • 3.
    

    Acute toxic encephalopathy

    
    
  • 4.
    

    Progressive viral encephalitis

    
    
  • 5.
    

    “Slow virus” encephalitis

  
  

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. 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.

Meningitis

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). ^, 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 . S. pneumoniae, N. meningitidis, and H. influenzae are the most common causes of community-acquired meningitis. ^{, ,} Individuals with a condition such as sickle cell anemia, alcoholism, or diabetes mellitus and individuals who are immunosuppressed are at increased risk. ^, 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 when compared with 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 ( Fig. 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 meninges, showing the layers of the dura, arachnoid, and pia mater and their relationship to the subarachnoid space and brain tissue. CNS , Central nervous system.

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. 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 patient supine in which the thigh is flexed on the abdomen and the knee extended ( Fig. 26.2 A). Complaints of lumbar or posterior thigh pain indicate a positive test result. 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 Hoppenfeld 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 performed (see Fig. 26.2 B). These signs will not be present in the deeply comatose patient 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.

(A) Kernig sign. (B) Brudzinski sign.

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.

Medical management.

Medical management of bacterial meningitis consists of the initiation of the antimicrobial regimen appropriate to the infecting organism and procedures to manage the signs and symptoms of meningitis that have been described in the preceding paragraphs. Medical intervention strategies in both these areas change with the development of new pharmacological agents. Thus medical management can change within short periods. The reader is encouraged to always review recent literature for additional information on current aspects of the medical management of the patient with meningitis.

Prevention.

Vaccination has significantly decreased the incidence of meningitis from H. influenzae type B in young children and infants. College freshmen who live in dormitories are four times more likely than other college students to develop meningococcus meningitis, and there is now a vaccine that has shown promise in reducing the outbreak rate.

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. ^, Bacterial meningitis is considered a medical emergency; delays in initiation of antibacterial therapy increase the risk of complications and permanent neurological dysfunction. ^,

Reports of the long-term outcome of individuals with bacterial meningitis indicate that up to 20% have long-term neurological sequelae. ^, 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. 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. ^, Approximately 5% of the survivors will have weakness and spasticity. 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. ^, Cognitive slowness has been found in 27% of patients after pneumococcal meningitis, even with good recovery as documented by a Glasgow Outcome Scale score of 5.

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. ^, Aseptic meningitis of a viral origin usually causes a benign and relatively short course of illness. ^,

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. ^{, ,} The primary nonviral causes of aseptic meningitis are Lyme Borrelia and Leptospira . 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.

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.

Encephalitis

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 20% to 60% of the individuals with herpes simplex encephalitis treated with acyclovir have some neurological sequelae. Because of the slow recovery of injured brain tissue, even in patients who recover completely, return to normal function may take months.

Plum and Posner 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 St. Louis encephalitis, California virus encephalitis, and most recently West Nile virus (WNV). While from 1999 to 2005 in the United States, the incidence of infection from the WNV increased from 62 cases to 3000 cases, the incidence has decreased in recent years to 2097 cases in 2017. Currently all states have some level of WNV activity, and only two states are without human cases ( Fig. 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. Risk of neuroinvasive disease from WNV is 40%; neuroinvasive disease involves meningitis, encephalitis, or poliomyelitis, with wide variety in clinical presentation ( Fig. 26.4 ). 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.

West Nile virus (WNV) activity in the United States 2018.

(From https://www.cdc.gov/westnile/statsmaps/preliminarymapsdata2018/activitybystate2018.html .)

Clinical Presentation of West Nile Virus.

Weak limbs at the peak of paralysis are darkened. Degree of darkness corresponds to the severity of weakness. Duration of weakness and characteristics (age [years] and sex [ F, female; M, male] are listed below each patient).

(From Cao NJ, Ranganathan C, Kupsky WJ, Li J. Recovery and prognosticators of paralysis in West Nile virus infection. J Neurol Sci. 2005;236:73–80.)

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.

Medical management.

The medical management of virally induced encephalitis has been, and with many infecting agents remains, primarily symptomatic. In some cases, intensive, aggressive care is necessary to sustain life. Pharmacological interventions are available to treat some viral infections, such as herpes encephalitis. The probability of neurological sequelae differs according to the infecting agent. Aggressive management of increased intracranial pressure is required because persistently elevated intracranial pressure is associated with poor outcome. ^, Further information concerning the clinical features, medical management, and potential for neurological sequelae of a specific type of encephalitis should be sought in the literature based on the infecting agent.

Clinical picture of the individual with inflammatory disorders of the brain

An individual within the acute phase of meningitis or encephalitis or with residual neurological 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. It is therefore important for return to optimal function and return to quality life that the therapist understands the impairments of body functions and structures, the patient’s activity limitations and participation restrictions, given the unique personal and environmental factors.

These 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 patient’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 patient 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. Patients 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 patient 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 response to seemingly normal interactions. For example, when upset about dropping a spoon on the floor, a patient may throw the tray across the table. When another individual was told his girlfriend would be a little late for her afternoon visit, the patient 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 patient 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 patient. 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.

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 patient’s current functional status. If the patient 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 patient 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 patient 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 patient 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 patient 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 fitted. The therapist must not allow assumptions made during the initial observation to bias later observations. The therapist might note that the patient 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 patient 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 patient 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 patient. Fig. 26.5 outlines the components that should be considered during the evaluation process and provides a synopsis of the following discussion.

Flow Chart of the Evaluation Process. ANS , Autonomic nervous system; GCS , Glasgow Coma Scale; RLAL , Rancho Los Amigos Level; PT , physical therapy.

The general philosophy in the evaluation of the patient with neurological deficits as a result of brain inflammation is a whole-part-whole approach. General observations of the patient’s performance provide an overall description of the patient’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 patient’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 patient’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 patient after reviewing the available background information. This may provide the therapist with information on the baseline status of the patient’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. Patients with depressed levels of consciousness may display temperature regulation dysfunctions. One mechanism for assessing the patient’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 patient’s level of consciousness. Consciousness is a state of awareness of one’s self and one’s environment. Coma can be defined as a state in which one does not open the eyes, obey commands, or utter recognizable words. 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. DeMeyer presents a succinct description of the neuroanatomy of consciousness and the neurological examination of the unconscious patient. Plum and Posner 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 Scale 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 Rancho Los Amigos scale assesses level of consciousness and behavior. 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 patient’s level of consciousness. Ideally, the patient 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 patient’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 patient’s peak awareness time may maximize the benefit of the therapy.

Performed in conjunction with the assessment of the patient’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 patient’s ability to communicate, the patient 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 patient 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 patient 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 patient 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 3 ). 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 3 for additional information regarding implicit and explicit learning).

The emotional and psychological aspects of the patient and the higher-order cognitive and retention skills of the patient should be evaluated informally by the therapist, with referral to appropriate professionals if dysfunction in these areas is suspected. A coordinated team approach is necessary for patients with emotional and psychological, cognitive, perceptual, or communication problems or a combination of these problems. A consistent strategy used by all team members eliminates the necessity on the part of the patient of trying to cope with different approaches by different people in an area in which she or he already has a deficit. The impact of cognitive deficits on the process of learning motor skills is further discussed in the next section on movement assessment. The assessment of the impact of perceptual dysfunctions is incorporated within the evaluation of sensory channels.

Examination of functional abilities

As indicated in the introduction to the evaluation of patients with inflammatory and infectious disorders of the brain, the examination process is not compartmentalized. As the therapist is examining the movement abilities of the individual through the format described in the previous section, he or she is also collecting information on the functional abilities of the individual. The components underlying the movement abilities of the patient can be examined within the framework of the basic or instrumental activities of daily living (ADLs), depending on the functional level of the person. The treatment setting and documentation requirements within that setting will determine whether the data on basic ADL and instrumental ADL skills are recorded with use of a formal scale or index or are gathered through an individualized process.

The introduction of specific tasks provides the therapist with the opportunity to observe the preferred posture used to accomplish the different tasks. The therapist should construct situations that require the individual to respond to unexpected occurrences to provide some insight into the person’s ability to adapt to the unexpected. Throughout the process of examining a patient’s movement abilities and functional abilities, the therapist is assessing the individual’s awareness of safety considerations and judgment in attempting tasks.

The presence of motor planning dysfunctions can be noted as the patient attempts a movement sequence or a functional task. The therapist may have to cue the patient physically to initiate the sequence, which then flows smoothly. The therapist may observe that the patient has the correct components to a movement sequence, but that the sequence of the components is incorrect. Or the patient may demonstrate the ability to produce a movement sequence under one set of conditions but not another. Indications of these types of motor planning problems can be observed during the initial interactions with the patient. Similarly, the therapist also should be aware of indications of problems with dexterity, coordination, and agility, as well as with signs of cerebellar dysfunctions.

Another aspect of the evaluation process that can be integrated in the observations of movement abilities is identification of perceptual deficits. Aspects of the patient’s motor performance can provide indications for detailed perceptual testing to classify the deficits. This testing should be conducted by the health care team member qualified in the area of perceptual testing. During the general evaluation procedures, the therapist can screen the patient for signs of perceptual deficits. Patients’ abilities to cross their midlines with their upper extremities can be demonstrated in movement sequences, such as moving from the supine to the side-sitting to the sitting position ( Fig. 26.6 ). The quality of the integration of information from the two sides of the body can be indicated by the symmetry or asymmetry of posture in positions that should be symmetrical. The therapist may suspect that the patient has a deficit in body awareness or body image by the poor quality of movement patterns that are within the motor capability of the individual. Spontaneous comments by the patient as to how he or she feels when moving (“my leg feels so heavy”) also add to the therapist’s assessment of the patient’s body image. Problems with verticality can be seen with the patient who lists to one side when in an upright posture. When the therapist corrects the list to a vertical posture, patients may express that they now feel that they are leaning to one side. Individuals who cannot appropriately relate their positions to the position of objects in their environments may have a figure-ground deficit or a problem with the concept of their position in space. When approaching stairs, these patients may fail to step up or may attempt to step up too soon. These examples should provide an indication of the observations that can indicate the need for detailed perceptual testing.

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