Based on your two given case scenarios for your written assignment.
Identify one tertiary (functional problem) that is common to both your patients and then, by highlighting the similarities and differences between the two cases, explain why the underlying primary and secondary problems present and how they result in this tertiary deficit.

This following literature will compare two patient case studies, suffering the same functional problem, but with different underlying causes due to differing pathologies. Similarities and differences of each patient’s primary and secondary problems will be discussed, and how they result in their shared functional problem of limited bilateral upper limb function.

Primary deficits caused by the initial pathology, result in alterations to the nervous system impacting on normal movement (Shamway-Cook & Woollacott, 2007). This is caused by altered sensory input, and motor output, and an altered cognition in order to process and interpret the information (ref). As a result of these primary problems, patients have further cardio-respiratory and musculoskeletal problems, whereby joint range of movement and alignment are affected (ref). Changes are seen in muscle structure, with a reduction in soft tissue length leading to additional weakness. This is due to disuse or altered movement from these further impairments. Fatigue overrides further movement due to disuse, reducing exercise tolerance and the patient’s ability to regain optimal function (Shamway – Cook & Woollacott, 2007).

The lateral pre-motor cortex can also be affected and is influenced by sensory cues such as visual or touch receptors and responds to reaching, grasping and bringing the hand to the mouth (ref). Patient A’s sensory input has been impaired as a result of neglect. This perceptual-cognitive impairment should usually process and interpret sensory information (carr and shepherd), however due to the lesion in the right hemisphere the patient doesn’t respond initially, unless the left side is within the patients’ vision. The primary sensory cortex, superior parietal lobe and the frontal lobes also give rise to corticospinal projections causing reduced innervation to the descending pathways causing muscle weakness, along with damage to the reticulospinal pathways affecting muscle tone (ref). The supplementary motor cortex can also be involved and is responsible for the planning and organization of complex bilateral upper limb movements. (Edwards, 2002). Decreased innervations cause the cortices projecting motor-activity information to the descending pathways to become inhibited, reducing neural drive into the motor neurone pool in the spinal cord leaving patient A with reduced innervation to the upper limb muscles. Muscle co-ordination can also be affected due to the reduced input in the higher brain regions and lack of feedback, causing movement to be uncoordinated and not finely tuned (Carr & Shepard, 2004).

Primary changes differ in both case study, mainly due to the different pathologies. However, they do lead to similar secondary changes that impact the functional movement of upper limb function. Patient A presents with secondary problems of weakness, resistance and over activity to handling. Spasticity can be seen 4-6 weeks post stroke as a result of exaggerated stretch reflex activity, muscle stiffness and decreases in muscle length (ref). This is potentially evident in the patients’ left upper limb due secondary changes within the muscles as a result of the initial pathology. Muscle atrophy can occur, causing type ΙΙ muscle fibres to become weak due to a lack of sarcomeres and decreased inhibition to the muscles (Shamway – Cook & Woollacott, 2007). Patient A has a flexor pattern in his left upper limb. Persistent posturing of a flexed elbow may also be due to neural factors causing increased stiffness and shortening of muscle fibres within the elbow flexors, while the elbow extensors are in a sustained resting length.

Increased hypertonia in the right upper limb suggests tonal changes caused by the further secondary changes. Muscle inactivity can cause shortening of the soft tissues reducing the patients’ range of movement. If soft tissue loses its elasticity; this further impairs the patients’ movement and increases resistance when a muscle is moved causing a loss of dexterity, increased stiffness and affecting joint alignment. Contractures at these joints may also be forming at this stage, due to further reduced mobility (Dobkin & Carmichael, 2005). Reduced movement has a further impact of other body systems such as the cardiovascular system, decreasing the patients exercise tolerance and increasing fatigue. The patients’ circulation has been compromised through immobility and this is evident through this left hand and feet becoming oedematous (ref).

Patient B has bilateral upper limb function problems due to primary problems of demyelinating lesions, also known as plaques, affecting the white matter of the brain, spinal cord and cerebral hemispheres (ref). Oligodendrocytes form a myelin sheath around axons, which are needed for efficient axonal conduction during an action potential (ref). Destruction of myelin and degeneration of oligodendrocytes inhibit action potential conduction, therefore messages are slowed or blocked to the upper limb muscles, causing weakness and sensory abnormalities reducing upper limb function. (Lundyb- Ekman, 1998) Ataxia also affects upper limb function (ref). This is caused by the decreased transmission of sensory inputs (ref). Visual and sensory inputs send information via the spinothalamic tract to the spinal cord, brain stem and cortex (ref). Mossy fibres travel from the medulla and enter the cerebellum to transmit the sensory information received (ref). Mossy fibres synapse with purkinje cells to allow the plan of action from the motor cortex. The cerebellum compares the sensory information to the plan and detects any changes. In Patient B sensory and visual information are reduced due to demyelination of lesions within the posterior column also degeneration in action potentials, therefore the cerebellum is unable to receive correct sensory information and make any correct changes to motor output. Decreased innervation of action potentials also causes damage to the corticopsinal tract pathway, resulting in weakness and reduction in movement. The end result leaves patient B with an ataxic movement that commonly affects the upper limbs, reducing functional activities to be smooth and co-ordinated. Patient B’s secondary problems are similar to patient A as she also suffers with weakness, with reduced activity mainly in her left upper limb caused my muscle atrophy and soft tissue changes. Increased tonal changes are also seen in the right upper limb, however, the patient is able to actively flex her right arm, but this is poorly controlled. This is possibly due to ataxia and/or spasticity after the patients’ recent relapse, caused by a reduction in sensory input or loss of postural sense. Opposed to secondary changes of reduced tissue length and/or possibly a resting

length seen in patient A, yet both similar due to lack of sensory input, the output result is different. Patient, A has sensory changes mainly through the left side, reduced joint range of movement and decreased activity due to neglect. Patient B has reduced awareness of light touch through both lower limbs and upper limbs, due to a recent relapse. This reduction in sensory awareness gives rise to uncoordinated output movements of ataxia. Sensory relapse can also involve loss of position sense within the hands. Further differences in patient B are the patient presents with cognitive difficulties that reduce information processing when planning and executing a movement, such as using both upper limbs, this reduces the patients overall functional capability. Cardiorespiratory changes are again similar to patient A due to the decreased movement causing an increase in fatigue and respiratory weakness that can cause deterioration in the patient’s performance. Differences are, if bilateral arms are weak there is likely to be weakness within the diaphragm, respiratory muscles and bulbar palsy, especially after a MS relapse if lesions are found within the medulla.

Despite there are some similarities and differences in patient A and patient B’s primary and secondary problems, they nevertheless share a similar tertiary problem of reduced upper limb function.

References:

Wade, D.T (1992) Measurement in neurological rehabilitation. United States: Oxford Press.