Symptomatology in Practice After a CVA

(1)

Neurorehabilitation Centre at CNA, Breda, Noord-Brabant, The Netherlands

Summary

A CVA is a very serious and sudden occurrence. This is thus a specific symptom of this CNS disorder, in contrast to dementia, Parkinson’s, and MS, which are characterized by their progressive course. Over the last few decades, the care for CVA patients has improved enormously, and much expertise has been gained in terms of insights into the impairments that result from a CVA. The experience thus gained can be transposed to the other CNS disorders described in this book. There are, namely, many commonalities, and this provides the opportunity to place neurorehabilitation in a broader perspective. This chapter lists the symptoms that may be an indicator for the occurrence of a CVA, which is followed by the description of the symptomatology after a cerebrovascular accident (CVA). Given that patients are permitted direct access to physiotherapy in the Netherlands, the physiotherapist must be able to recognize symptoms at an early stage. This chapter also examines the causes and risk factors of a CVA. When these are recognized, it is possible to take specific actions that reduce the chance of a CVA.

1.1 Introduction

A CVA is a very serious and sudden occurrence. Suddenly, from 1 s to the next, you may be paralyzed on one side, be aphasic, or feel that the world around you is going so fast that you can no longer make any sense of it. This is thus a specific symptom of this CNS disorder, in contrast to dementia, Parkinson’s, and MS, which are characterized by their progressive course.

The care for CVA patients has improved enormously in recent decades, and much expertise has been gained relating to insights into the impairments that result from a CVA. The experience thus gained can be transposed to the other CNS disorders described in this book. There are, namely, many commonalities and this provides the opportunity to place neurorehabilitation in a broader perspective.

This chapter lists the symptoms that may be an indicator for the occurrence of a CVA, which is followed by the description of the symptomatology after a cerebrovascular accident (CVA). Given that patients are permitted to directly access physiotherapy in the Netherlands, the physiotherapist must be able to recognize symptoms at an early stage. This chapter also examines the causes and risk factors of a CVA. When these are recognized, it is possible to take specific actions that reduce the chance of a CVA.

1.2 Early Identification, Causes, and Risk Factors

Studies have shown that people who experience a CVA have often had TIAs (transient ischemic attacks) previously. If you recognize the acute symptoms and any phenomena that occur with a TIA, you can decide whether to refer the patient for more extensive tests. Early identification of symptoms according to the FAST system is of great relevance:

F	Face	Is one side of the face drooping?
A	Arm	Can the patient keep both arms stretched out?
S	Speech	Is the patient’s speech still clear and coherent?
T	Time	Starting time of the symptoms?

◘ Table 1.1 Lists the symptoms to which one must be alert.

Table 1.1

Acute symptoms and possible symptoms of a TIA that may occur

Acute symptoms	Possible symptoms that may occur
Dizziness and/or balance impairments	Unilateral paralysis
Severe headache	Heightened reflexes on the paretic side
Frequently blue, swollen face	Unilateral sensory impairments
Loss of consciousness	Unilateral visual impairments
Slow and snoring breathing	Swallowing impairments
Possibly wide, light-insensitive pupils	Possible aphasia (word-finding problems)

When acute symptoms and phenomena that occur are identified early, thrombolysis can be performed within 4.5 h of the CVA in the hospital. This is done where there is a cerebral infarction caused by a blood clot. This can clearly reduce the severity of the permanent sequelae. If it is not possible to take action within this time frame, rapid admission to the stroke unit is then indicated, so that intensive rehabilitation is then possible.

A cerebrovascular accident can have various causes:

1.

Cerebral infarction (80%)
2.

Cerebral hemorrhage (including subarachnoidal hemorrhages) (20%)

Knowing the causes that can lead to CVA offers opportunities to influence these factors in a positive manner. In the preventive sense, it is therefore important to know the causes (C), as well as the risk factors (RF). Risk factors can, namely, lead to a cause (see ◘ Table 1.2).

Table 1.2

Cerebral infarction, cerebral hemorrhage, and subarachnoidal hemorrhage: causes and risk factors

Cerebral infarction	Cerebral hemorrhage	Subarachnoidal hemorrhage
Arteriosclerosis (C)	Arteriosclerosis (C)	Arteriovenous malformation (C)
Space – occupying lesion (C)	Space – occupying lesion (C)	Aneurysm (C)
High cholesterol (RF)	Aneurysm (C)	High blood pressure (RF)
Cardiac arrhythmias (RF)	Use of anticoagulants (RF)	In combination with use of oral contraceptives (RF)
Operation (RF)	Congenital bleeding disorders (RF)
Diabetes mellitus (RF)	Diabetes mellitus (RF)
High blood pressure (RF)	High blood pressure (RF)

1.3 Symptomatology After a CVA

The sequelae as a result of a cerebral infarction or cerebral hemorrhage are directly related to the scope and the locality of the lesion. The sequelae are, for each individual, very diverse in nature. The following primary impairments can occur as a result of a lesion in the brain:

1.

Sensorimotor impairments
2.

Communicative impairments
3.

Cognitive and behavioral changes
4.

Imbalance in the workload and capacity model as a result of socio-emotional problems

◘ Figure 1.1 shows the neural organization of our brain and provides an insight into the relation between the localization of the lesion on the one hand and the symptomatology that occurs as a consequence of that lesion on the other hand.

Fig. 1.1

Cerebral lobes, cerebellum, and brain stem

◘ Table 1.3 provides a simplistic view of the neural organization of our brain. It gives an insight into the relation between the localization of the lesion on the one hand and the symptomatology that occurs as a result of that lesion on the other hand.

Table 1.3

Locality of lesion and possible symptomatology

Locality of lesion	Possible symptomatology
Frontal lobe	Ability to think, executive functions, behavior, visual center, part of the speech (Broca’s aphasia)
Occipital lobe	Processing of visual stimuli, face perception
Parietal lobe	Spatial organization, motor skills, and sensation
Brain stem	Vital functions, such as blood pressure, respiration, temperature, etc.
Cerebellum	Movement sequences (sequence), tonicity regulation, and coordination of movement
Temporal lobe	Memory, concentration, taste, and a part of the speech (Wernicke)
Limbic system	See ► Sect. 8.4

We can see that a lesion in the cerebellum would therefore not cause any loss of function; it would mainly cause a loss of coordination. This has to do with the neural organization in the brain, and it is good to be aware of this so that the observed symptomatology can be related to the lesion in the brain.

The primary impairments named previously, which can occur as a result of a CVA, are discussed below. Although these impairments seldom occur in isolation and they do influence each other, it is necessary to describe each of them independently. This provides clarity and offers ways of unraveling, to some extent, the complexity of the symptoms.

1.4 Sensorimotor Impairments

The term «sensorimotor» is a combination of sensory and motor. Sensorimotor impairments lead to diminished motor function. This term indicates the close link between the sensory system and motor skills, also known as sensorimotor integration.

The most frequent sensorimotor phenomena as a result of a CVA are spastic hemiparesis and loss of sensation. These are expressed on the heterolateral side of where the lesion occurred. In other words, an infarction in the linker hemisphere causes a hemiparesis on the right side of the body. Depending on the localization, the face, arm, leg, and trunk can be involved (◘ Fig. 1.2).

Fig. 1.2

Right-sided spastic paresis resulting from left-hemisphere infarction

It is known that proximally the extremities are bilaterally innervated from the corticospinal tracts (Ghez 1991) and that we find unilateral innervation more distally in the extremities. Because of this, distally there is reduced spare neural capacity in respect of plasticity, and the CVA patient has less chance of making a full recovery.

The unilateral innervation also explains why substantial loss of motor function of the wrist and finger extenders and of the foot flexors occurs so frequently in CVA patients.

In most CVA patients, no substantial loss of function is observed in the muscles of the trunk. This is because these fundamental muscle groups are bilaterally innervated. This is essential, considering that these muscle groups must function as a good «suspension system» for the organs and also fulfill a supporting function for respiration. There is, however, frequently a reduced adaptive capacity of the trunk musculature (see below under «Reduced Adaptive Capacity of the Trunk»).

1.4.1 Primary Motor Impairments

When a CVA has occurred, primary and secondary motor symptoms can be distinguished. The primary motor symptoms can be subdivided on the basis of tonicity into positive and negative symptoms.

Positive Symptoms

Spasticity

Central muscle-tone dysregulation (CMD) is characteristic of a CNS disorder. Spasticity is a manifestation of muscle-tone dysregulation that we frequently see as a result of a CVA. There is spasticity when increased resistance is felt with passive motion in combination with heightened myotatic reflex activity (Lance 1980).

Spasticity is negatively influenced by fatigue, pain, speed, and stress. The spasticity will be more prominently present under the influence of these stressors, and functioning will be negatively affected.

Spasticity can be measured using the scales developed by Ashworth and de Tardieu. The Ashworth Scale is a test whereby the tone is manually tested in a passive manner.

The test does not take account of the relation between the heightened tonicity on the one hand and the starting position of the patient and the related, associated muscles reactions on the other side. This causes limitations with regard to the reliability of the test. A five-point scale is used for the test:

1.

Tonicity not heightened.
2.

Slightly heightened tone: a catch followed by a minimum resistance during the rest of the range of motion (ROM).
3.

Moderately heightened tone: a clear resistance during the ROM.
4.

Substantially heightened tone: considerable resistance and passive movement are difficult.
5.

Rigidity: passive repositioning is virtually impossible (◘ Fig. 1.3).

Fig. 1.3

Substantially heightened muscle tone: considerable resistance and passive movement is difficult

With the Tardieu Scale, the stretch velocity is measured in relation to the muscular response (also called catch). In this way, the dynamic component of the muscle length is determined. R1 is the catch that is felt with rapid movement, and R2 is the catch felt with slow movement (see ► Example from Practice 1.1). This clinimetrical finding is clinically relevant, because the velocity-dependent effect can be included in the test. With regard to spasticity, it is known that velocity can have a negative influence on the degree of spasticity.

Example from Practice 1.1

Luke is given an injection with Botox in connection with the high tension in his calf muscles. To collect objective data, among other things, the degree of spasticity is determined using the Tardieu Scale. When the foot is slowly repositioned to dorsal flexion, we achieve 5° of dorsal flexion (=R2).

When the velocity-dependent component is added (the foot is rapidly moved into dorsal flexion), the foot does not pass the neutral position, but the catch occurs at 5° of plantar flexion (=R1). The difference between R1 and R2 is the degree of spasticity, thus in this case 10°.

Spasticity occurs frequently in stereotypical patterns. To be able to recognize these, here is a list of how these are often manifested in the extremities after a CVA.

Upper extremity:

1.

Shoulder: retraction, endorotation, and depression
2.

Elbow: flexion and pronation
3.

Pulse: palmar flexion and ulnar deviation
4.

Fingers: flexion
5.

Thumb: adduction and flexion (◘ Fig. 1.4)

Fig. 1.4

Spastic pattern – upper extremity

Lower extremity:

1.

Hip: retraction, endorotation, and elevation
2.

Knee: extension and endorotation
3.

Ankle: plantar flexion and inversion
4.

Toes: clawing or flexion (◘ Fig. 1.5)

Fig. 1.5

Spastic pattern – lower extremity

Insight into these spastic patterns not only makes it easier to recognize pathological motor skills, but it offers also starting points for physiotherapy interventions if you opt for the «feeling» relearning of motor skills (see ► Chap. 10).

Hyperreflexia

Hyperreflexia is a heightened myotatic activity that can be diagnosed by evoking the reflexes. The most commonly used tests are the Achilles tendon reflex, the knee jerk reflex, and the biceps reflex of the arm. In some cases this heightened myotatic activity is so prominently present that you can observe the heightened reflex when, for instance, you tap someone on the thigh. This hyper-myotatic activity leads to uncontrolled tensing of all muscle fibers. Because of this, no adequate response can take place when, for example, an unexpected situation occurs.

Example from Practice 1.2

Mrs. M. has suffered an infarction in her left hemisphere. Dissociated movement is very difficult for her. During the gait analysis, a circumduction of the leg was observed during the swing phase. The foot is placed in midstance on landing.

There is some dissociation, but as soon as something unexpected happens (she is, e.g., overtaken by someone or there is a strange sound that makes her jump), her whole right leg then stiffens. An examination reveals that, among other things, there is hyperreflexia in her right leg. In her ADL this regularly bothers her. She jumps when, for example, the front doorbell rings or the telephone. The consequence is that she does not have her right leg under control and this results in losing her balance. This has caused her to fall once.

Attention is paid to this during treatment. Walking is practiced in a quiet space, and the course she has to walk is made increasingly more difficult. This is expanded into an environment with more stimuli. Finally situations are practiced by means of badminton. Her balance was evaluated with the Berg Balance Scale.

Hypertonia

Hypertonia is a heightened basic muscle tension in the musculature without the presence of heightened resistance with passive movement and a heightened myotatic reflex activity (e.g., an increase of the muscle tone in the musculus trapezius descendens with stress at work). In practice hypertonia and spasticity are regarded as synonyms; however this is not therefore correct.

The possibility of influencing hypertonia by means of physiotherapy intervention is good, in contrast to spasticity.

Rigidity

Rigidity is a form of central muscle-tone dysregulation (CMD), which manifests in the form of a heightened tone in both the agonist and the antagonist. This form of tonic dysregulation is seen with subcortical lesions. The basal ganglia also lie in the subcortical structures. This is the reason that rigidity is also the term used for the Parkinson’s patient. A typical consequence of rigidity is a slowed and reduced flexibility of the motor skills.

Clonus

Clonus is a series of rapid involuntary rhythmic muscle contractions, evoked by a rapid stretching of the musculature (e.g., the calf muscle). What then occurs is a slow tensing and relaxing in the muscles that may or may not extinguish.

Example from Practice 1.3

Mr. F. has a partial spinal cord injury and is hindered by substantial clonus. He indicates that it plays up when he is going up- or downstairs but especially when climbing. When he puts his foot down, his foot begins to shake, giving him the sensation that he is being pushed backward.

On analyzing him going up- and downstairs, we see the clonus is caused by the weight on the ball of his foot. When the weight is shifted to the front, you first get a dorsal flexion in the foot. This creates pressure on the ball of the foot and stretches the calf muscles. These factors provoke the clonus.

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