In addition to brain injury due to blunt or penetrating injuries or DAI, brain injury may be due to a number of other causes. These include metabolic factors such as
hypoxia/anoxia; hypoglycemia, hypothyroidism, and cer-tain vitamin deficiencies; exposure to CNS toxins such as heavy metals or other industrial/environmental toxins;
drugs of abuse, including toxic inhalants and carbon mon-oxide poisoning; and passage of electrical current through the brain in electrocutions or lightning-related injuries.
Another important and increasingly common kind of brain injury occurs as a complication of coronary artery bypass surgery. This kind of diffuse brain injury is believed to result, in part, from gaseous or particulate microemboli released into the cerebral circulation as a result of complications of the bypass procedure itself or F I G U R E 4 – 1 . The Orientation Log.
inappro=inappropriate; incorr=incorrect; MultiChoice=multiple choice; phon=phonetic; Spon=spontaneous.
Source. Adapted from Jackson WT, Novack TA, Dowler RN: “Effective Serial Measurement of Cognitive Orientation in Rehabil-itation: The Orientation Log.” Archives of Physical Medicine and Rehabilitation 79:718–720, 1998.
F I G U R E 4 – 2 . Neurobehavioral Rating Scale––Revised.
F=female; M=male; Mod.=moderate.
Source. Adapted from Vanier M, Mazaux J-M, Lambert J, et al: “Assessment of Neuropsychologic Impairment After Head Injury:
Interrater Reliability and Factorial and Criterion Validity of the Neurobehavioral Rating Scale—Revised.” Archives of Physical Medicine and Rehabilitation 81:796–806, 2000. Used with permission.
surgical manipulations that occur during and immediately after the time the patient is on bypass. The kinds of neu-rological, cognitive, and behavioral sequelae that occur with these kinds of brain injury are similar to those seen with TBI, both with respect to the types and severity of deficits and the dysfunction and disability they may cause.
As is the case with TBIs, the specific neurocognitive and behavioral sequelae that occur are dependent on the regions of the brain that have been damaged.
Anoxia/Hypoxia
Anoxia is defined as inadequate oxygenation of body tis-sues. Anoxic brain injury owing to a lack of oxygen in the ambient air is known as anoxic anoxia. Anoxia owing to acutely decreased blood volume or lowered hemoglobin concentration in the blood is referred to as anemic anoxia, and anoxia owing to insufficient cerebral blood flow because of cerebrovascular accidents, arrhythmias, or car-diac arrests is called ischemic anoxia. Finally, there is toxic anoxia, which is because of toxins or metabolites that may interfere with oxygen utilization.
In general, hypoxia with ischemia is more harmful than hypoxia alone because potentially toxic metabolic products such as lactic acid may contribute to tissue dam-age. The nature of hypoxic ischemic injury is neuropatho-logically different from traumatic injury, in that the former affects the neurons themselves, whereas the latter tends to be an axonal phenomenon. In addition to cardiac and respiratory arrest, anoxic brain injury occurs in cases of near drowning, strangulation, and anesthetic accidents (Wilson 1996).
Although the brain comprises only 2% of the body’s total weight, it accounts for a disproportionate 20% of the total oxygen utilization and 65% of the glucose uptake.
Approximately 15% of the cardiac output is directed to the brain to meet its energy needs (Kuroiwa and Okeda 1994; White et al. 1984). When disruption of the oxygen delivery system occurs, a series of cerebrovascular ho-meostatic mechanisms become activated to maintain ade-quate oxygen supply to the brain (Cohen 1976; Strand-gaard and Paulson 1984). When there is a sustained disruption in oxygen supply (for a period of 4–8 minutes or longer), cerebral infarction and/or disseminated cellu-lar death may occur (Bigler and Alfonso 1988; Caronna 1979; Cohan et al. 1989; Cohen 1976; Strandgaard and Paulson 1984; White et al. 1984).
The mechanism of anoxic brain damage comprises a complex cascade of time-dependent alterations in neuro-nal function, metabolism, and morphology (Haddad and Jiang 1993; Pulsinelli et al. 1982). The most important acute effect of hypoxia on the brain is the release of
exci-tatory neurotransmitters, leading to an influx of sodium, cellular edema, and consequent cellular injury (Hansen 1985; Kjos et al. 1983; Rothman and Olney 1986).
Longer-term effects are due to an increase in neuronal ex-citability, which results in calcium influx, formation of oxygen-free radicals that injure cells, and eventual cell death (Ascher and Nowak 1987; Choi 1990; Gibson et al.
1988; Haddad and Jiang 1993; Hansen 1985; Maiese and Caronna 1989; Schurr and Rigor 1992; Siesjo 1981;
White et al. 1984).
Whether a patient with hypoxia will develop neuro-logical signs depends more on the severity and duration of the process causing hypoxia than its etiology (Berek et al.
1997). Two factors that determine the vulnerability of cells in a given brain region to hypoxia include distribu-tion of the cerebral blood vessels and adequacy of their baseline perfusion and the specific metabolic and bio-chemical properties of the neural structures involved.
The most vulnerable regions of the brain are the water-shed areas of the cortex. That is because normal cellular metabolism in these areas is dependent on an adequate flow of normally oxygenated blood through the distal ce-rebral arterioles that perfuse them. Cellular and tissue damage occur first in these areas where inadequate oxy-genation of the blood due to hypoxia fails to meet mini-mal metabolic requirements, especially when impaired perfusion is also present (Brierley and Graham 1984; Par-kin et al. 1987). Cells in brain regions with higher meta-bolic demand are also more likely to be affected by oxy-gen deprivation (Moody et al. 1990; Myers 1979). In addition to these general principles, it has been shown that cells in various brain regions respond differentially to the degree and duration of hypoxia. For example, basal ganglia and cerebral cortical cells show signs of necrosis shortly after a cardiac arrest, whereas similar changes in the hippocampus may not be seen until 2–3 days after the event (Kuroiwa and Okeda 1994; Petito et al. 1987; Puls-inelli et al. 1982).
Coma is a frequent outcome of significant and sus-tained hypoxia. The three leading causes of coma in de-scending order of frequency are: trauma, drug overdose, and cardiac arrest (Shewmon et al. 1989). From a prognos-tic point of view, patients with traumaprognos-tic coma have a better chance of recovery than those with nontraumatic coma.
Among patients in the nontraumatic group, recovery gen-erally occurs in the following descending order of fre-quency: metabolic causes, coma secondary to cardiac ar-rest, and coma from cerebrovascular causes (Berek et al.
1997). Clinical outcomes typically depend on the presence or absence of the prognostic factors listed in Table 4–12.
Neuropsychological deficits after anoxic brain damage may include memory and executive dysfunction,
appercep-tive agnosia, and visual deficits. Most patients with anoxic brain damage have preserved attention and concentration abilities. Some patients who have sustained severe anoxic brain injury may remain in a persistent vegetative state with no observable cognitive functioning at all (Parkin et al.
1987; Wilson 1996).
Cognitive Problems After Coronary Artery Bypass Graft Surgery
Approximately 800,000 patients worldwide undergo coro-nary artery bypass graft (CABG) surgery per year (Selnes et al. 1999). CABG is associated with significant cerebral morbidity, manifested by cognitive decline or stroke (Roach et al. 1996; Van Dijk et al. 2002). The incidence of cognitive decline may vary from 3% to 50%, depending on patient characteristics, definition of decline, and the type and timing of neuropsychological assessment (Diegeler et al. 2000; Roach et al. 1996; Van Dijk et al. 2002). Intraop-erative transcranial Doppler monitoring has clearly dem-onstrated that during cardiopulmonary bypass (CPB), microemboli are released into the brain. This release of microemboli is correlated with postoperative neurological deficits (Syliviris et al. 1998). A study comparing the neu-rocognitive effects of CABG with and without CPB sur-gery demonstrated that patients with their first CABG without CPB had less cognitive impairment at 3 months, but by 12 months the differences between the groups had become negligible (Van Dijk et al. 2002).
The emotional and cognitive state before CABG sur-gery is an important factor in the development of anxiety, depression, and cognitive deficits after the procedure (Adrian et al. 1988; Savageau et al. 1982). Even though a
high percentage of patients may exhibit neuropsycholog-ical deficits immediately or during the first few weeks af-ter the surgery, most return to their premorbid level of neuropsychological functioning within several months af-ter the procedure (Frank et al. 1972; Savageau et al. 1982).
Patients about to undergo CABG surgery should be screened for neurocognitive deficits and emotional distur-bances before the procedure (Adrian et al. 1988). Asking patients about their expectations for the outcome of the procedure is also important because these expectations have an important bearing on the postoperative emotional state, cognitive deficits, and recovery from the surgery.
Electrical Injuries
Electrocution can cause brain damage in two ways—
direct cellular damage due to passage of current through brain tissue and cardiac arrest induced by it. Electrical injuries occur as a result of exposure to live wires at work or home or lightning strikes during thunderstorms. The degree of damage is determined by the amount and type of current, duration of exposure, parts of the body affected, and the pathway of current through the body.
Injuries acquired from exposure to electric current at home or work (low voltage injuries <1,000 volts) are dif-ferent from those sustained from lightning or contact with high-voltage wires (high-voltage injuries >1,000 volts). Injuries due to alternating current are more seri-ous in comparison to those from direct current (Browne and Gaasch 1992; Fish 1993). Patients who experience high-voltage electrical injury may initially show some cognitive deficits with confusion and memory loss, which usually clear within a few days. In cases in which these deficits persist, neuropsychological evaluation should be performed because some symptoms may be permanent, especially in cases of direct electrical injury to the brain (Table 4–13).