Acquired Brain Injury by Dong Y. Han PsyD

Author:Dong Y. Han, PsyD
Language: eng
Format: epub
Publisher: Springer Publishing Company, Inc.
Published: 2016-12-07T05:00:00+00:00

PATHOPHYSIOLOGY

The pathophysiology of each aforementioned substance class (alcohol, inhalants, sedatives, and stimulants) will be discussed in turn by class in the sections that follow.

Alcohol

Alcohol is a central nervous system (CNS) depressant. The CNS depressant effects of alcohol may cause impaired coordination, gait ataxia, slurred speech, and impaired saccadic movements of the eyes. In addition to the physical presentation associated with the acute effects of alcohol, intoxicated individuals demonstrate reduced capacity for response inhibition, which has been identified in studies of event-related potentials (ERP; Oscar-Berman & Marinković, 2007). However, of greater significance to acquired brain injury are the effects of long-term alcohol abuse/misuse characterized by dependence and withdrawal. The most extreme presentation of alcohol-related cognitive deficits is reflected in Wernicke–Korsakoff’s syndrome in which profound anterograde memory loss is evident. Wernicke–Korsakoff’s syndrome is attributable to a deficiency of thiamine caused by a dietary pattern in which the vast majority of calories consumed are alcohol related rather than more nutrient-rich foods. This thiamine deficiency results in “bilateral necrosis of the mammillary bodies and of a variety of medial diencephalic and other periventricular nuclei” (Blumenfeld, 2002). This deficiency and related Wernicke–Korsakoff’s syndrome characterized by gait ataxia, acute confusion, lasting and profound impairment in memory consolidation, and confabulation represent the most significant cognitive presentation of acquired brain injury secondary to alcohol misuse. However, less significant cognitive presentations are associated with cerebral atrophy, white and gray matter loss, and reduced volume in the prefrontal cortex (Allen, Frantom, Forrest, & Strauss, 2006). In addition to the direct impact of prolonged exposure of the brain to alcohol, the indirect impact of alcohol on the brain caused by impaired liver functioning is also a significant potential source of acquired brain injury associated with alcohol exposure. Allen et al. (2006) identify significant impairment of memory, eye tracking, and hand–eye coordination in individuals with cirrhosis related to alcohol use when compared with individuals with non–alcohol-induced cirrhosis.

In addition to the potential long-term impact on the individual consuming alcohol, significant dysfunction of the CNS, craniofacial anomalies, disrupted free and postnatal growth, and markedly increased risk of intellectual disability and behavioral problems are associated with prenatal alcohol exposure, and may be described as fetal alcohol syndrome (FAS) or alcohol-related neurodevelopmental disorder (ARND) (Guerri, Bazinet, & Riley, 2009). These significant impairments and developmental disruption may be attributable to impaired functioning of glial cells, resulting in hypoplasia of the corpus callosum and anterior commissure, and microglial apoptosis (Wilhelm & Guizzetti, 2016).

Inhalants

Inhalants are broad and varied with regard to chemical type. The National Institute on Drug Abuse (NIDA, 2012) defines inhalants as “the wide variety of substances—including solvents, aerosols, gases, and nitrites—that are rarely, if ever, taken via any other route of administration” (www.drugabuse.gov/publications/drugfacts/inhalants). The pathophysiology of the particular inhalants is varied and related specifically to the particular inhalant. However, the most commonly inhaled substances for recreational use is toluene, which has a direct effect on the CNS as it readily passes through the blood–brain barrier, where it inhibits glutamate-activated ion channels (Cruz, Rivera-García, & Woodward, 2014).

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