Ischaemic CVE develops when cerebral blood supply is occluded. This can be due to obstruction by blood clots that have formed on athersclerotic plaques on the walls of blood vessels (Wilkinson 1999). Occlusion of cerebral arteries can also occur because of blockage of the lumen of the blood vessels by embolitic material travelling from other parts of the circulation (Atchison 1999).
Haemorrhage accounts for 20% of CVE (Gleb 2000). Haemorrhagic CVE occurs when an aneurysm in a blood vessel in the brain bursts or when hypertension causes rupture of blood vessels (Cohen 1999). As with ischaemic CVE, haemorrhagic CVE causes death of cells and loss of function. These types of CVE are associated with a higher fatality rate than other forms of CVE. The aneurysm is often a congenital abnormality. Rupture of blood vessels may also be a result of hypertension, a significant risk factor for CVE (Gleb 2000).
The neurological deficits following CVE are dependent on the area fed by the interrupted blood supply and the duration of the loss (Atchison 2000).
Motor control is located in the frontal lobe of the cerebral cortex (Young 1997). The opposite side of the brain controls movement of each side of the body. Each hemisphere of the brain contains a contralateral representation of the body (Young 1997). Therefore, because the man in this case study is experiencing right-sided motor dysfunction he is likely to have experienced a CVE in motor cortex of the left hemisphere of his brain.
Movement results from a balance between the central nervous system and peripheral nerve input. Three major components of the brain control voluntary movement; the motor areas of the cerebral cortex, the descending motor tracts from the cerebral cortex and brainstem, and the basal ganglia and cerebellum (Porter 1999).
The primary role of the basal ganglia is to integrate visual, vestibular and other sensory inputs into movement (Fitzgerald 1992). The cerebellum regulates maintenance of posture and balance and regulates the sequence of motor movements. The basal ganglia and cerebellum influence motor function via feedback loops that interconnect with the cerebral cortex (Iyer 1999).
The cerebral cortex and the other structures that contribute to the execution of movement send electrical stimulation to effector muscles via the spinocortical tracts, through the spinal cord, to the skeletal muscle (Greenstein 2000). The contralateral manifestation of the motor dysfunction is due to the pathway taken by the fibres on the journey to the skeletal muscle.
After leaving the cerebral cortex the neurones in the spinocortical tract pass through the internal capsule, into the midbrain and down to the medulla where a portion of the fibres cross to the opposite side of the spinal cord (Cohen 1999). A CVE may occur at any point on this journey from the cerebral cortex. Above the medulla the dysfunction will occur on the contralateral side to the damage.
The location of the disruption of arterial blood supply determines the resulting functional dysfunction (Fitzgerald 1992). Motor dysfunction, as experienced by the man in the case-study, is likely to result from occlusion or haemorrhage of the middle cerebral artery. The internal capsule is a frequent location for CVE (Fitzgerald 1992). As the corticospinal tract containing the descending motor control neurones passes through the internal capsule, an individual experiencing motor dysfunction is likely to have a lesion in that area.
The physical consequences of the CVE in the internal capsule for case-study are likely to be initial flaccid hemiplegia, which is followed by development of permanent spastic hemiparesis. The spasticity will characteristically be exhibited as flexion of the upper limb and extension of the lower limb on the contralateral side to the brain damage (Wilkinson 1999).
Increased reflexes will be present which will lead to motor problems for the patient. Unintended movements will occur which can disrupt purposeful movement. Hyperreflexia occurs because the inhibition of lower motor neurones by the damaged upper motor neurones is no longer present, causing them to over respond to stimuli or even to stimulate muscle groups to contract spontaneously (Gertz 1996).
Because movement also requires normal cerebellar and basal ganglion and sensory function, lesions in these parts may alter the quality of movement experienced after a CVE. Dysfunction resulting from damage to these systems includes clumsy, stiff, slow and involuntary movements (Wilkinson 1999). Disruption of the blood supply to these structures by the pathological mechanisms that cause CVE will cause the death of neurones that contribute to motor control (Cohen 1999).
The physical disruption experienced by the patient in the case study can not be generalised from text-book examples. Prediction of function or rate of recovery in patients who have experienced CVE is difficult due to individual variability of anatomy, especially of blood supply to the cerebral cortex, and extent of ischaemic damage (Atchison 2000). The amount of physical disability that an individual experience is determined not only by any physical difficulties, but also the psychological reactions to the CVE. Physical difficulties such as spasticity may be enhanced by emotional upset or by trying to hurry (Atchison 2000).
The patient in the case-study will have to learn to cope with the often painful, uncontrollable, unexpected motor patterns that result from the CVE in the left middle cerebral artery.
References
Atchison and Hansen (2000) Conditions in Occupational Therapy, Lippincott Williams and Wilkins, Philadelphia
Cohen (1999) Neuroscience for Rehabilitation, 2nd Edition, Lippincott Williams and Wilkins, Philadelphia
Department of Health (2001) National Service Framework for Older People – Standard 5, Department of Health, London
Fitzgerald (1992) Neuroanatomy; Basic and Clinical, 2nd Edition, Bailliere Tindall, London
Gertz (1996) Neuroanatomy Made Easy and Understandable, 5th Edition, Aspen Publishing, Maryland
Gleb (2000) Introduction to Clinical Neurology, 2nd Edition, Butterworth – Heinemann, Boston
Greenstein (2000) Colour Atlas of Neuroscience, Thieme, New York
Iyer et al (1999) Motor 1: Lower Centres, in Cohen (1999) Neuroscience for Rehabilitation, 2nd Edition, Lippincott Williams and Wilkins, Philadelphia
Porter (1999) Motor 2: Higher Centres, in Cohen (1999) Neuroscience for Rehabilitation, 2nd Edition, Lippincott Williams and Wilkins, Philadelphia
Warlow (1987) Strokes, MTP Press, Lancaster
Wilkinson (1999) Essential Neurology, Blackwell Science, Oxford
Young P, and Young H (1997) Basic Clinical Neuroanatomy, Williams and Wilkins, London
