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It is well known that many physical conditions cause a loss in cognition.

Breast Cancer

Cognitive function is a multidimensional concept that includes attention, concentration, learning, memory, problem-solving ability, visuospatial abilities, mental flexibility, psychomotor efficiency, and manual dexterity. Cognitive impairment has long been associated with adjuvant therapy for breast cancer may be diffuse, affecting all of these processes and may persist for years. The most frequently reported deficits are difficulties with attention and concentration, learning new information, and recalling recently learned information (affecting patients in the range of 26 – 44% of patients). No specific domain of cognitive function has been identified as being more impaired than others as a result of chemotherapy, being a global pattern of dysfunction. Schagen, SB, et al. Cognitive dysfunction and chemotherapy: Neuropsychological findings in perspective. Clin Breast Can. December, 2002; 3(Suppl 3): S100 – S108. The mechanism for cognitive impairment function has not been identified and may be multifactorial and have not included any measures of such variables as fever, depression, anxiety, additional medication, etc. The incidence and severity has not been well documented. Bender, CM, et al. Cognitive function and reproductive hormones in adjuvant therapy for Breast Cancer: A critical review. J Pain Sympt Manage. May, 2001; 21(5): 407 – 24.

A large percentage of patients (31 – 75%) receiving adjuvant postoperative chemotherapy suffered cognitive impairment including attention, mental flexibility, speed of information processing, visual memory, and motor function. The cognitive impairment was not affected by or associated with anxiety, depression, or fatigue. Schagen, SB, et al. Cognitive deficits after postoperative adjuvant chemotherapy for breast carcinoma. Cancer. 1999; 85: 640 – 50; Brezden, DB, et al. Cognitive function in breast cancer patients receiving adjuvant chemotherapy. J Clin Oncol. July, 2000; 18(14): 2695 – 2701; Ahles, TA, et al. Breast cancer chemotherapy-related cognitive dysfunction. Clin Breast Can. December, 2002; 3(Suppl 3): S84 – S90; Schagen, SB, et al. Cognitive dysfunction and chemotherapy: Neuropsychological findings in perspective. Clin Breast Can. December, 2002; 3(Suppl 3): S100 – S108. This cognitive function can continue in patients being treatment with tamoxifen. Paganini-Hill, A and Clark, LJ. Preliminary assessment of cognitive function in breast cancer patients treated with tamoxifen. Breast Can Res Treat. 2000; 64: 165 – 76. The cognitive deficit can have a late onset. Schagen, SB, et al. Cognitive deficits after postoperative adjuvant chemotherapy for breast carcinoma. Cancer. 1999; 85: 640 – 50. Only 50% of affected patients show cognitive improvement one year post therapy. Wefel, JS, et al. The cognitive sequelae of standard-dose adjuvant chemotherapy in women with breast carcinoma: Results of a prospective, randomized, longitudinal trial. Cancer. 2004; 100: 2292 – 9. This impairment may last up to two years following treatment and will show improvement in most cases four years following treatment. Ahles, A, et al. Neuropsychologic impact of standard-dose systemic chemotherapy in long-term survivors of breast cancer and lymphoma. J Clin Oncol. January 15, 2002; 20(2): 485 – 93; Schagen, SB, et al. Late effects of adjuvant chemotherapy on cognitive function: A follow-up study in breast cancer patients. Ann Oncol. 2002; 13: 1387 – 97. This deficit has been found to last up to 10 years following chemotherapy treatment, occurring in 39% of patients. Ahles, TA, et al. Breast cancer chemotherapy-related cognitive dysfunction. Clin Breast Can. December, 2002; 3(Suppl 3): S84 – S90. Once the onset of the deficit has occurred, it does not worsen over time. Schagen, SB, et al. Cognitive dysfunction and chemotherapy: Neuropsychological findings in perspective. Clin Breast Can. December, 2002; 3(Suppl 3): S100 – S108.

There has been no pattern of mental fatigue and reduced motivation found during testing following adjuvant therapy. DeJong, N, et al. Course of mental fatigue and motivation in breast cancer patients receiving adjuvant chemotherapy. Ann Oncol. 2005; 16: 372 – 82.

Even minimal and subtle cognitive deficits may be profoundly and unacceptably disturbing in a patient’s quality of life following adjuvant treatment for breast cancer. Olin, JJ. Cognitive function after systemic therapy for breast cancer. Oncology. May, 2001; 613 – 624

Cerebellar Ataxia

The relationship between the cerebellum and the frontal cortex is also poorly understood. Another study has demonstrated that patients with idiopathic cerebellar degeneration exhibit slowing of cognitive information processing. These findings suggest that the cognitive slowing may be due to a disruption of neural circuits between the cerebellum and the frontal cortex. Kawabata, TH, et al. Prolonged P3 latency and decreased brain perfusion in cerebellar degeneration. Acta Neurol Scand. 1999; 100: 310 – 316. These patients have been found to suffer from significant deficits in verbal and nonverbal intelligence, verbal associative learning, and visuospatial skills. Subclinical involvement of auditory and somatosensory pathways at the level of the brainstem were also detected. These deficits were not readily explained by associated motor impairment. Akshoomoff, NA, et al. Contribution of the cerebellum to neuropsychological functioning: Evidence from a case of cerebellar degenerative disorder. Neuropsychologia. 1991; 30(4): 315 – 328.

Chronic Pain

Neurocognitive difficulties are often reported by chronic pain patients. Greater pain severity has been associated with poorer neurocognitive performance in several studies. Memory functions have been found to be affected in distressed chronic pain patients. Unfortunately, there is little evidence concerning the relation between the variables of pain severity, psychological distress, and neurocognitive performance. Iezzi, T, et al. Predictors of neurocognitive performance in chronic pain patients. Int J Behav Med. 2004; 11(1): 56 – 61.

A physician should attend to the psychological impairments resulting from chronic pain syndrome and specify functional limitations when limitations of attention, concentration, or the inability to tolerate environmental stress and distraction might make the individual ineffectual or a risk to others. Ashburn, MA and Rice, LJ, eds. The Management of Pain. (Churchill Livingstone 1998): 67.
Functional pain limitations include measures of a patient’s concentration and cognitive processes, activities of living, emotional status, and functional abilities, as perceived by the patient and physicians. Functional performance evaluation in patients with chronic pain. Evaluation and Treatment of Chronic Pain. Aronoff, GM, ed., 3d., (Williams & Wikins 1998): 603 – 615; Rucker, KS. Standardization of chronic pain assessment: A multiperspective approach. Clin J Pain. 1996; 12: 94 – 110.


Overall, the natural course of neurocognitive disorders associated with HIV infection remains poorly understood. neuropsychological testing is effective in evaluating suspected HIV neurocognitive disorders by quantifying the severity of cognitive impairment and defining the patterns of involvement. Gendelman, H., et al, eds. The Neurology of AIDS. (International Thomson Publishing 1998).

The neurocognitive effects of HIV have been studied extensively. The two levels of neurocognitive impairment are mild (deficits in two or more cognitive areas that interfere at least mildly with daily functioning) and dementia (severe neurocognitive which interferes markedly with daily functioning to the point that diagnosed persons are typically unable to work and may not be able to care for themselves). There is criterion overlap between these two types of neurocognitive impairment with no bright line test for differentiation. In general, cognitive impairment is characterized by mental slowness, forgetfulness, and poor concentration accompanied by behavioral changes including apathy, lethargy and diminished spontaneity. Gendelman, H., et al, eds. The Neurology of AIDS. (International Thomson Publishing 1998) These two levels of cognitive impairment are experienced by 30% of symptomatic HIV patients. Unfortunate consequences of cognitive deficits include the inability to operate a motor vehicle and adhere to a medication regimen. McArthur, JC, et al. Human immunodeficiency virus-associated dementia: An evolving disease. J NeuroVirology. 2003; 9: 205 – 221; Benaslem, MK, and Berger, JR. HIV and the Central Nervous System. Comp Ther. 2002; 28(1): 23 – 33. Most HIV-infected patients do not meet the criteria for diagnosis of dementia. The mild form of neurocognitive impairment can cause deficits which interfere with the ability of patients to complete normal activities of daily living as well as negatively impact on treatment adherence. Oaul, RH, et al. Neurocognitive manifestations of human immunodeficiency virus. CNS Spectrums. December, 2002; 7(12): 860 – 6.

There have no studies concerning the effect of neurocognitive deficits on a person’s ability to maintain employment. Since a person may remained employed, but may be working at a less demanding and less remunerative occupation makes such studies difficult. Further, there has been little research concerning the effects of neurocognitive deficits on a patient’s quality of life although these deficits have been associated with a higher rate of mortality. Gendelman, H., et al, eds. The Neurology of AIDS. (International Thomson Publishing 1998). In general, it has been found that cognitive impairment in any cognitive domain is associated with a poor quality of life. Affected persons with impaired executive and attentional functions and slowed processing speed are less able to employ effective coping strategies to manage stressors. It has been further revealed that self-reported measures of cognitive functioning correlate significantly with objective measures of cognitive functions. Tozzi, V, et al. Neurocogntive performance and quality of life in patients with HIV infection. AID Res and Human Retroviruses. 2003; 19(8): 643 – 52.

Neuropsychological testing is effective in evaluating suspected HIV neurocognitive disorders by quantifying the severity of cognitive impairment and defining the patterns of involvement. This testing allows for determination of whether a person suffers from mild neurocognitive disorder rather than HIV dementia. Gendelman, H., et al, eds. The Neurology of AIDS. (International Thomson Publishing 1998). Neuropsychologic functioning has been demonstrated to be independent of depression. Milliken, CP, et al. Fatigue in HIV/AIDS is associated with depression and subjective neurocognitive complaints but not neuropsychological functioning. J Clin Exp Neuropsychol. 2003; 25(3): 201 – 15.

Fatigue and depression do not appear to affect neuropsychological functioning in HIV/AIDS patients. Millikin, CP, et al. Fatigue in HIV/AIDS is associated with depression and subjective neurocognitive complaints but no neuropsychological functioning. J Clin Exp Neurpsych. 2003; 25(2): 201 – 215.


Neuropathic symptoms in hypothyroidism are also common, occurring in 40 – 60% of patients. Neuropathic symptoms include paresthesias painful dyesthesias. Patients may have symptoms of mononeuropathy, polyneuropathy, and cranial nerve neuropathy. One-third of patients have gait unsteadiness. This may include gait ataxia and poor coordination. In rare cases, dyarthric speech has occurred. Neurocognitive impairment may be a prominent feature of hypothyroidism, especially in older patients. This will include slowness in comprehension, diminished attention span, poor recent memory, difficulty with word fluency, and impairment abstract thinking. Even with treatment, resolution of cognitive impairment is slow and can be incomplete. Id.; Whybrow, PC and Bauer, M. Behavioral and psychiatric aspects of hypothyroidism. Braverman, LE and Utiger, RD, eds. The Thyroid: A Fundamental and Clinical Text. 9th ed. (Lippincott, Williams & Wilkins 2005): 842 – 9.

This general decline in cognitive and behavioral function is an integral part of hypometabolic state. The neuropsychiatric symptoms suffered by patients with hypothyroidism may lead to an incorrect diagnosis of a depressive state. Many of these patients will exhibit melancholic symptoms such as crying, loss of appetite, insomnia, and diminished interest in and responsiveness to others. Other patients become fearful, suspicious, and delusional. Although depressed mood seems to predominate, specific mental state and thought content varies with the individual patient. Cognitive changes such as alterations in attention, concentration, perception, and speed of thought appear to be the most common clinical manifestations. Objective psychological testing has revealed impairments in cognitive function including deficits in memory and learning, attention, visuoperceptual and construction skills, and psychomotor slowing. There is a high incidence of hypothyroidism in patients diagnosed with bipolar (manic-depressive) illness. Brain scan imaging techniques are being developed in an effort to better delineate this condition. Whybrow, PC and Bauer, M. Behavioral and psychiatric aspects of hypothyroidism. Braverman, LE and Utiger, RD, eds. The Thyroid: A Fundamental and Clinical Text. 9th ed. (Lippincott, Williams & Wilkins 2005): 842 – 9; Bauer, M, et al. Thyroid, brain and mood modulation in affective disorders: Insights from molecular research and functional brain imaging. Pharmacopsychiatry. 2003; 36 Suppl 3: S215 – S221.

The neuropsychiatric effect is so pronounced that it has been recorded in subclinical hypothyroid patients in a study of elderly patients. This lesser version of hypothyroidism is believed to be a predisposing factor for depression, cognitive impairment, and dementia. Davis, JD, et al. Cognitive and neuropsychiatric aspects of subclinical hypothyroidism: Significant in the elderly. Curr Psych Rep. 2003; 5: 384 – 90.

Multiple Sclerosis

Prevalence of cognitive loss is present in as high as 50% of MS patients. The cognitive deficits are typically not appreciated or noted by treating physicians and may occur early in the disease course. Tasks affected include recently memory, sustained attention, speed of cognitive processing, and conceptual reasoning. Changes in neurologic disability are poor predictors of the degree of cognitive dysfunction. Some MRIs revealing cerebral damaged may be positively correlated with the severity of cognitive loss. Some patients experiencing cognitive loss have trouble accepting this problem. In many cases, they will not inform their treatment providers of the problem. Schiffer, RB. Cognitive Loss. In Multiple Sclerosis in Clinical Practice. van den Noort, S, and Holland, NJ, eds. (Demos Medical Publishing 1999): 99 – 105. Also affected are the following processes: learning, recall of new information, speed of information processing, visualspatial abilities, executive functions (reasoning, problem solving, and planning), as well as timed performance. Poor memory is a common complaint among MS patients. Joy, JE, and Johnston, Jr., RB, eds. Multiple Sclerosis: Current status and strategies for the future. (National Academy Press 2001): 115 – 117. See also. LaRocca, NG. In Multiple Sclerosis” Diagnosis, medical management and rehabilitation. Burks, JS, and Johnson, KP, eds. (Demos Medical Publ. 2000: 405 – 423.


Emotional distress does not have a positive association with cognitive function. In addition, disease activity has not been associated with cognitive function although fatigue measures have demonstrated a significant relationship. Denburg, SN, Carbotte, RM, and Denburt, JA. Psychological aspects of systemic lupus erythematosus: Cognitive function, mood, and self-report. J Rheumatol. 1997; 27: 998 – 1003.

As many as 66% of lupus patients report cognitive deficits which are often associated with information processing and working memory, but can also affect immediate memory or recall, fluency, attention, speed of information processing, psychomotor speed. The cognitive dysfunction demonstrated falls into the “subcortical” pattern similar to that suffered by multiple sclerosis patients. Shucard, JL, et al. Working memory and processing speed deficits in systemic lupus erythematosus as measured by the paced auditory serial addition test. J Int’l Neuropsyh Soc. 2004; 10: 35 – 45.

Postpump Syndrome

There is substantial medical authority which states that many persons suffer from cognitive impairment following CABG surgery. Even after a substantial period of recovery, there remain a proportion of patients who suffer cognitive decline which sufficiently disabled them from returning to employment. Dijk, D.V., M.D., et al. Cognitive Outcome after Off-Pump and On-Pump Coronary Artery Bypass Graft Surgery. Journal of the American Medical Association (JAMA). 2002; 287: 1405 – 12; Newman, Mark F., et al. Longitudinal Assessment of Neurocognitve Function after Coronary Artery Bypass Surgery. New England Journal of Medicine. 2001; 344: 395 – 402. This testing revealed that over 30% of CABG patients suffered cognitive decline 12 months after surgery. Unfortunately, the final numbers were reduced since many patients (12%) did not undergo follow-up testing after the original 3 month testing period. Id. at 1409. Cognitive decline was defined as a 23% decline in performance at the 3 month testing mark. Id. at 1311. A similar study found that 20 – 35% of patients undergoing cardiac surgery suffered postoperative neuropsychological dysfunction for up to several months. Rodig, R., et al. Evaluation of Self-Reported Failures in Cognitive Function after Cardiac and Noncardiac Surgery. Anaesthesia. September, 1999; 54(9): 826 – 830. Similar results were seen in several other studies yield a 22.5% affected rate (2 months post surgery in six studies) in the review article published by Van Dijk, et al. Neurocogntivie Dysfunction after Coronary Artery Bypass Surger: A Systematic Review. Journal of Thoracic and Cardiovascular Surgery. 2000; 120: 632 – 9. The twenty-three selected studies reviewed all employed neuropsychologic testing for assessment purposes with a 20% testing deficit as the threshold for determining cognitive impairment. The use of neuropsychological testing for determination for this purpose has been found to be essential. Stump, David A. Selection and Clinical Significance of Neuropsychologic Tests. Annals of Thoracic Surgery. 1995; 59: 1340 – 4.

Sleep Apnea

Witnessed apnea includes disheveled sheets due to tossing and turning/restlessness. Nocturia is reported in 28% of patients with 4 – 7 bathroom trips each night. The most common daytime symptoms are fatigue and sleepiness. Sleepiness may be subtle, such as midafternoon drowsiness during meetings, occasional naps. Morning/nocturnal headaches are reported in half of patients. As part of their symptoms, patient may report clumsiness in tasks requiring dexterity, concentration, attention, memory, or judgement and may be of such severity so as to hurt job performance and the ability to hold employment. Family and social life can suffer as well due to various personality changes (anxiety, irritability, aggressiveness, depression) with resulting alienation leading to depression. Bassiri, AG and Guilleminault, AG. Clinical features and evaluation of obstructive sleep apnea-hypopnea syndrome. Kryger, MH, et al, eds. Principles and Practice of Sleep Medicine, 3rd ed., (Saunders 2000):869 – 878.


Claimant suffered a stroke which has produced the common residual effects of speech aphasia, memory impairment, and fatigue. In the study by Peter Hagoort in Impairments of Lexical-Semantic Processing in Aphasia: Evidence from the Processing of Lexical Ambiguities. Brain and Language. 45: 189 – 232 (1993), it was found that stroke victims with aphasia did not suffer from a deficit in their stored memory, but rather could not consciously elaborate as part of their speech resulting in a deficit termed the “impairment in consciousness.”

Memory impairment was found to be independently affected from speech aphasia and not simply a consequence of the language impairment. Beeson, P.M. et al. Memory Impairment and Executive Control in Individuals with Stroke-Induced Aphasia. Brain and Language. 45: 253 – 275 (1993).

Subdural Hematoma

Neuropsychiatric syndromes following traumatic brain injury are not well delineated from classical psychiatric syndromes such as depression, psychosis, or anxiety. Thus, these disorders may present with both features of altered behavior and a brain-based neurological disorder. Increased age is recognized risk factor for development of neuropsychiatric disorder following a traumatic brain injury. 77% of TBI patients will show increased distractibility. Often, slowed information processing speed will be present. These deficits become more apparent when a greater cognitive load (increased demand) is placed on the injured person. Therefore, use of short tasks during testing may not reveal the deficit. Memory is usually the most severely affected due to the high concentration of lesions preferentially found in the frontal and anterior temporal brain structures following closed-head injury. Most recent formed memories tend to most affected with decreased performance on implicit (procedural) memory tasks as opposed to more explicit (factual) memory tasks. 44% of patients with moderate disability will demonstrate memory impairments with larger percentage for more serious cases. Over 50% of patients will experience some specific language deficits. Patients with brain contusions or hematomas tend to show deficits of visual perception. TBI patients also show deficits in executive functions (volitional behavior, planning for the future, purposeful action, and regulating one’s behavior).
Granacher, RP. Traumatic Brain Injury: Methods for Clinical and Forensic Neuropyschiatric Assessment. (CRC Press, 2003): 9 – 30, 47 -55.

Animal experiments have demonstrated that subdural hematoma can cause both immediate and subsequent (progressive) brain dysfunction including cognitive deficits. Eijkenboom, M, et al. Chronic cognitive effects of bilateral subdural haematomas in the rat. Neuroscience. 2004; 124: 523 – 33; Eijkenboom, M, et al. The effects of subdural haematoma on spatial learning in the rat. Neuroscience. 1999; 94(2): 373 – 8.

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