CVAs may be caused by thrombotic or embolic occlusion of cerebral vessels (ischemic stroke) or a rupture in a blood vessel (hemorrhagic stroke). Approximately 88% are ischemic strokes and most of these are caused by thrombosis (American Heart Association, 2004; Bowman, 2005). Almost all elderly people have some degree of blockage of the arterial supply to the brain, mostly due to arteriosclerotic plaques in one or more feeder arteries. The plaque activates platelets that secrete growth factors, encouraging further proliferation of the plaque. Eventually, these plaques grow large enough to occlude the vessel or may rupture, releasing emboli (Messing, 2003). Hemorrhagic strokes most often result from high blood pressure and cause the most fatalities of all strokes (Bowman, 2005). Risk factors for CVAs include hypertension, cardiovascular disease, atrial fibrillation, diabetes mellitus, cigarette smoking, hyperlipidemia, heavy alcohol use, and obesity (Bowman, 2005).

The location and extent of the ischemia determine the type and severity of the resulting deficits. These deficits may include the following (Bowman, 2005):

Depression is common among people living with the consequences of stroke and among their caregivers. In a study of 80 stroke survivors and their spouses, Ostwald (2004) reported that depression and stress in stroke survivors are predicted by functional status and perception of recovery, whereas depression and stress in spousal caregivers are associated with perceived caregiver burden and age.

Rehabilitation after stroke requires an interdisciplinary team, including physicians, nurses, social workers, counselors, physical therapists, occupational therapists, speech therapists, and dieticians. Patients who have had a stroke are at risk of developing another stroke, so it is important to institute measures to prevent a recurrence. Prevention strategies include control of hypertension, control of blood lipids, anticoagulant therapy, and treatment with antiplatelet agents, such as aspirin, clopidogrel, or dipyridamole (Ezekowitz, 2004).

The cause of AD is not known, but it is associated with age and there is some evidence that genetic factors play a role; approximately 10% of cases are familial. Alterations in brain tissue seen in AD include the formation of beta-amyloid neuritic plaques (also called senile plaques) between neurons and neurofibrillary tangles within neurons (Delagarza, 2003; Messing, 2003). Structural changes include a thickening of the leptomeninges, shrunken gyri, widened sulci, enlarged ventricles, hippocampal shrinkage, and generalized atrophy (Black, 2005). Biochemically, there is a 50% to 90% reduction in the activity of choline acetyltransferase, the biosynthetic enzyme of acetylcholine. The severity of the cognitive losses with AD is roughly proportional to the loss of choline acetyltransferase (Mayeux & Chun, 1995). These changes lead to the memory failure, personality changes, and functional disabilities seen in AD, and these structural and chemical changes become more widespread as the disease progresses.

Memory disturbances are usually the first sign of AD. Individuals with early AD may become irritable, suspicious, agitated, apathetic, or dysphoric. As the disease progresses, language disturbances and apraxia occur, swallowing may become difficult, and irritability and depression worsen (Black, 2005). These behaviors can place a great deal of both physical and emotional stress on the caregivers and may eventually lead to institutionalization of the patient.

Up to 25% of people with AD become clinically depressed (Mayeux & Chun, 1995). However, depression may be difficult to diagnose due to the cognitive and functional changes associated with the disease.

Malnutrition and weight loss often occur with AD and are associated with mortality risk and cognitive decline (Guerin, Soto, Brocker et al., 2005). Problems contributing to decreased oral intake include anorexia, agnosia, swallowing problems, functional impairment, and social support issues (Feldman & Woodward, 2005). The final stages of AD are characterized by an inability to ambulate independently, inability to dress without assistance, inability to bathe properly, urinary and fecal incontinence, and inability to communicate meaningfully (NHPCO, 1996).

Medications that inhibit the degradation of acetylcholine are the mainstay of therapy for AD, but they can cause cholinergic side effects, such as nausea, anorexia, vomiting, and diarrhea (Delagarza, 2003). These acetylcholinesterase inhibitors include donepezil (Aricept), galantamine (Reminyl), memantine (Namenda), rivastigmine (Exelon), and tacrine (Cognex) (Delagarza, 2003; Hodgson & Kizior, 2006). Some studies show cognitive improvements with vitamin E and selegine (Eldepryl), but the evidence is not strong (Birks & Flicker, 2003; Tabet, Birks, & Grimley Evans, 2000). These medications should be discontinued when dementia is severe (Delagarza, 2003).

Symptomatic treatments of depression, anxiety, and agitation and of the side effects of medications are important supportive interventions throughout the course of the disease. Nutritional support may be helpful in early and mid-stages of the disease. However, enteral feedings in advanced dementia do not appear to improve outcome and may put the patient at risk for complications (Finucane, Christmas, & Travis, 1999).

The cause of ALS is unknown, but about 5% to 10% of cases appear to have a genetic link; others are believed to be sporadic. Many different causes of sporadic ALS have been proposed, including exposure to heavy metals, viral infection, and autoimmune disorders, but there is no strong evidence for any of these theories (Rowland & Shneider, 2001). The pathology of ALS includes the replacement of large motor neuron cell bodies of the anterior horn of the spinal cord by fibrous astrocytes, resulting in gliosis. Abnormal protein aggregation, disorganization of intermediate filaments, and glutamate-mediated excitotoxicity are proposed to be involved in mediating this process (Messing, 2003; Rowland & Shneider, 2001).

Upper motor neuron degeneration causes hyperactive tendon reflexes, Babinski’s reflex, and clonus. Lower motor neuron disease leads to weakness, muscle wasting, muscle cramps, and muscle fasciculations (Rowland, 1995). Interestingly, the following functions do not appear to be affected by ALS: cognition, sensation, bladder and bowel control, autonomic function, and extraocular movements. Involvement of the corticobulbar tracts causes dysphagia and dysarthria (Black, 2005; Rowland, 1995).

The functional decline and uncomfortable symptoms of ALS cause distress to both the patient and the family. A study by Adelman and colleagues (2004) showed that caregivers accurately report information about a patient’s physical function but that both patients and caregivers overestimated the psychosocial impact of the disease on the other. Caregivers rated patients as having less energy, greater suffering, and greater weariness than the patients indicated for themselves, and patients rated caregivers as more burdened than the caregivers reported for themselves.

The only medication approved in the United States for the treatment of ALS is the glutamate antagonist riluzole (Rilutek). In a review of studies on riluzole, Miller and associates (2002) concluded that it probably prolongs survival by about 2 months and may improve bulbar and limb function, but it does not improve muscle strength. A longer survival benefit may be possible if riluzole is started early in the course of the disease (Wicklund, 2005). Many other treatments have undergone trial, including antioxidants, amino acids, neurotrophins, human insulin-like growth factor, creatine, minocycline, selegiline, and amantadine, but either these medications were ineffective or results were inconclusive (Mitchell, Wokke, & Borasio, 2005; Orrell, Lane, & Ross, 2005; Parton, Mitsumoto, & Leigh, 2005; Wicklund, 2005).

Individuals with ALS experience many discomforts that must be addressed to optimize quality of living.

The main manifestations of HD include choreiform and athetoid movements, accompanied by cognitive and behavioral changes, eventually involving dementia. HD, the most common hereditary cause of chorea, is transmitted in an autosomal dominant pattern, with complete penetrance (Ravina & Hurtig, 2002). Additional features of the inheritance of HD include anticipation, a trend toward earlier onset in successive generations, and paternal descent, which refers to the tendency for anticipation to be most pronounced in individuals who inherit the disease from their father (Yamada, Tsuji, & Takahashi, 2002). Clinical manifestations usually begin between the ages of 30 to 40 years (Black, 2005). About 6% of the cases start before the age of 21 years (juvenile-onset HD) with an akinetic-rigid syndrome (the Westphal variant). Approximately 28% of cases start after the age of 50 years (late-onset HD). “Senile chorea” is simply chorea in an older person and is considered a diagnosis of exclusion; however, the majority of cases likely have HD (Quinn, 2003).

HD is caused by an anomaly of chromosome 4 and is fully penetrant, so the children of an affected parent have a 50% risk of developing the disease (Harper, 2002). The gene abnormality appears as an excessively long repeat of trinucleotides CAG, the length of which determines not only the presence of the disease but also the age of onset (Adams & Victor, 2001). The pathological process in HD is characterized by severe neuronal loss and gliosis occurring selectively in the caudate nucleus and putamen (basal ganglia), with vulnerability in other regions, such as the deep layers of the cortex (Paulsen, Zhao, Stout et al., 2001). Further studies in HD patients have shown alterations in the metabolic activity in muscle tissue and the basal ganglia. (Gu, Gash, Mann et al., 1996; Lodi, Shapira, Manners et al., 2000). Changes in the concentration of neuropeptides in the basal ganglia have also been found, including decreased substance P, methionine enkephalin, dynorphin, and cholecystokinin and increased somatostatin and neuropeptide Y. Positron emission tomography (PET) has shown reduced glucose utilization in an anatomically normal caudate nucleus (Yamada et al., 2002).

Early signs and symptoms of HD include subtle abnormal eye movements, uncoordinated fine motor movements of the hands and face, clumsiness, impulsiveness, decreased concentration, and increased fluctuations of impulsiveness, anxiety, and restlessness. Poor self-control may also be reflected in outbursts of temper, fits of despondency, alcoholism, or sexual promiscuity. Disturbances in mood, particularly depression, are common (almost half of the patients in some series) and may constitute the most prominent symptoms early in the disease (Adams & Victor, 2001).

As HD progresses, physical, emotional, and cognitive symptoms become more compromised. Speech, walking, swallowing, and motor control also worsen throughout the disease trajectory. In many individuals, the involuntary, forceful, random movements worsen in an unpredictable manner and the patient is seldom still for more than a few seconds (Adams & Victor, 2001). Anxiety, stress, and lack of appropriate amounts of sleep can aggravate chorea involvement, adding to the patient’s increased fatigability. Thus, with the progression of HD, signs, symptoms, and functional decline become more debilitating. Surprisingly, during periods of sleep, the chorea movements subside and the individual is able to fully rest. Other clinical features in advanced stages of HD include urinary incontinence, motor instability, and loss of proper swallowing, which causes aspiration and cachexia. The hyperkinetic state combined with abnormalities of muscle and adipose tissue metabolism is the postulated explanation for cachexia (Lodi et al., 2000; Sanberg, Fibiger, & Mark, 1981). Inevitably, complications of functional decline and onset of infections (such as pneumonia and aspiration pneumonia due to impairment of swallowing, choking, and coughing) contribute to the cause of death in these individuals.

Juvenile-onset HD often presents between the ages of 15 to 18 years (Davis, Cheema, Oliver et al., 2005). Early signs and symptoms of juvenile-onset HD include poor school performance, difficulty in comprehending new information, slowness and stiffness, awkwardness in walking, clumsiness and frequent falls, slurred speech, choking and drooling, behavioral changes, personality changes, and slowness in responding. Seizures occur in 25% to 30% of children and usually develop after the first obvious motor abnormalities appear (Huntington Society of Canada, 2000