impact. After a closed head injury, neurons may be damaged in other parts of the brain due to compression or stretching as a result of the injury, causing diffuse axonal damage . “Secondary injuries” also occur after a TBI. These secondary effects can sometimes cause damage to more brain tissue Assessment and diagnosis of traumatic brain injury When a head injury results in loss of consciousness, altered consciousness (i.e., drowsiness), neurologic impairment (i.e., weakness, slurred speech), or cognitive deficits (i.e., memory loss), then brain injury is likely. Neuropsychological assessment is of limited utility in the acute stages following a mild injury as most difficulties resolve in one to three months. For more significant injuries, detailed neuropsychological testing should occur no earlier than six weeks post- injury, to allow for the patient to recover from the acute effects of the injury (Silverberg et al., 2020). The neuropsychological evaluation begins with a detailed history, particularly of the head injury and what happened before, during, and after the event or accident. Information is gathered from the patient, witnesses, and medical records. Special attention is paid to altered or loss of consciousness, depth of coma, if applicable, and the extent of memory loss that a patient has for the event. Posttraumatic amnesia is memory Changes in emotion and personality following head injury Often more devastating than the cognitive impairments are the changes in emotion and psychiatric symptoms that follow a TBI (Hendrickson et al., 2018; Yrondi et al., 2017). Brain injury can cause personality changes and emotional dysregulation, especially if the injury was sustained to the frontal or temporal lobes. Persons may be more disinhibited or may be apathetic and lack interest and motivation. The changes in emotions and personality may be due to brain damage, psychological Diagnosis, course, and etiology of multiple sclerosis Multiple sclerosis (MS) is a demyelinating disease, that is, the myelin covering of neurons is broken down. As outlined in Chapter 2, myelin helps to make neural communication fast and accurate; thus, when myelin is disrupted, neural communication is disrupted. The areas of demyelination in the brain create lesions that can be seen on an MRI scan, which is a useful and recommended tool for accurate diagnosis. The cause of MS is not known but it is considered an autoimmune disorder that may be triggered by a virus or environmental factors (Bjelobaba et al., 2017). There is no cure for MS, but there are treatments that appear to slow disease progression. Subtypes of multiple sclerosis There are four subtypes of MS with different presentations and courses (Doshi & Chataway, 2016). The relapsing- remitting type is most common and is characterized by relapses with periods of recovery in between; recovery can be complete or there may be minor, residual symptoms. There is no disease progression between relapses. Another type is secondary-progressive, in which the disease begins as relapsing-remitting but eventually there is progression of the disease. In the primary progressive type, there is disease progression from the outset, without Prevalence of multiple sclerosis The highest rates of MS are in North American and Europe (more than 100 cases per 100,000) while the lowest levels are in Eastern Asia and Sub-Saharan Africa (2 cases per 100,000) (Leray et al., 2016). Since the disorder is more common in northern versus southern latitudes, an environmental contribution to the disorder is implicated. There is also a genetic component to the Neuropsychological evaluation in multiple sclerosis Cognitive impairment is common in MS (Benedict et al., 2020). The nature and severity of cognitive deficits vary by subtype (Planche et al., 2016). Variable cognitive symptoms across
than the primary injury. For example, edema , or swelling of brain tissue, can occur and damage neurons. Other possible secondary effects are ischemia, or disruption of blood flow to brain tissue, and epilepsy , which is a disorder characterized by multiple seizures. loss for events that occur after a head injury; the length of the amnesia can be an indicator of the severity of the brain injury, with longer memory loss indicating greater severity (Silverberg et al., 2020). Neuropsychological testing should thoroughly cover all cognitive domains because deficits following a TBI can vary. The most common deficits following a moderate to severe head injury are in attention and processing speed (i.e., persons are easily distracted and slower at processing information). Deficits in learning, retrieval of information from memory, auditory or visual processing, and executive functions also are common. The vast majority of persons who suffer a mild TBI will recover in days to weeks, but a substantial minority will suffer residual deficits in attention, processing speed, and executive functions that are exacerbated by premorbid and concurrent psychological factors (Iverson et al., 2017). reactions to the brain injury and subsequent impairments, or, most likely, a combination of both factors (Dromer et al., 2021). Education about these changes is particularly useful for patients and families, who may not know that emotions and personality can be altered by a brain injury. Behavioral and pharmacologic treatments of emotional disorders should be pursued and neuropsychologists can provide some guidance as to potentially useful interventions.
NEUROCOGNITIVE DISORDER DUE TO MULTIPLE SCLEROSIS
MS is a heterogeneous disorder because different areas of the brain can suffer demyelination, producing different constellations of symptoms. Common symptoms at onset are muscle weakness, paresthesias (sensations of tingling or numbness on the skin), walking or balance difficulties, fatigue, and visual disturbances (Izquierdo, 2017). Diagnostic criteria for MS are dependent on evidence of lesions (in the brain and/or spinal cord) that progress over time (Thompson et al., 2018). Cerebrospinal fluid markers are increasingly recognized to have utility in diagnosis. periods of recovery. For example, to be diagnosed with primary progressive MS, a person must exhibit one year of disease progression plus two of the following criteria: (1) evidence of a brain lesion in one area characteristic for MS, (2) evidence of lesions in the spinal cord, and/or (3) positive cerebrospinal fluid findings. Finally, in the progressive-relapsing type, there is disease progression from the outset with periods of acute relapse; this is the most severe and least common subtype of MS. disorder. Monozygotic twins, who share 100% of their genes, have concordance rates of up to 30%, whereas siblings have 2%-5% lifetime risk (Howard et al., 2016). MS is about twice as common in women as in men. Disease onset occurs between the ages of 20 and 40 for the majority of cases.
individuals is typical, from mild and transient impairments, which are most common, to severe and permanent impairment (Benedict et al., 2020). Even mild cognitive impairments may
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Book Code: SWUS1524
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