Spreadsheet: 139498d1328276114-excel-2007-copy-data-from-cells-in-one-workbook-to-another-based-on-the-cell-headings-jama-eletters-data
Sheet: 299 9 1046

305 9 923 | Response ID | Status | Title, Author | Responder | [NAME] | Response
 | jama_el;166 | P | Alcoholic neuropathy and dementia - it may not be what it seems to be! [NAME], February 27, 2008 | [NAME],  MD, PhD  University of Alberta, Edmonton, Canada | [EMAIL] | What are the principal causes and diagnostic considerations in evaluating nervous system abnormalities in a 74-year-old man who is an active drinker?  Alcoholic neuropathy affects axons in a length dependent fashion (dying back), with symptoms more prominent in distal limbs. Numbness and paresthesias, and weakness affect feet earlier than hands. Involvement of small nerve fibers causes intractable burning pain and impairment of proprioception manifests as "sensory" ataxia. Focal ("compression") neuropathies are more common and difficult to tease out from the polyneuropathy.   Chronic alcohol intake may cause acute [NAME]'s encephalopathy, which is followed by chronic memory and personality changes - Korsakoff psychosis. More commonly, generalized brain atrophy leads to a slowly progressive dementia. Age, poor diet, self- neglect, and repeated head trauma from falls may contribute to memory deficits. Other CNS manifestations include midline cerebellar degeneration ("cerebellar" ataxia) and degeneration of the corpus callosum with personality changes and dementia. Finally, poor diet with vitamin B12 deficiency may manifest as combined subacute degeneration of spinal cord causing gait ataxia, dementia and depression.   How does one decide if the symptoms or signs are related to alcohol?  Healed skin bruises/fractures from repeated falls, tremors, and polyneuropathy may be clues to excessive alcohol intake. A cognitive deficit from alcoholic liver damage is suggested if aspartate aminotransferase level is more than twice that of alanine aminotransferase. Increased gamma-glutamyltransferase is the most sensitive but nonspecific indicator of alcoholic liver disease. Chronic anemia and low albumin levels are other nonspecific abnormalities.   On neuropsychological testing patients may have a particular pattern of memory loss and frontal lobe deficits. Brain imaging typically shows midline cerebellar or global brain atrophy, more advanced for age.(1)   As far as cognition is concerned, does alcohol have a "safe dose" threshold?  Low to moderate ethanol consumption decreases and excessive drinking increases risk of ischemic stroke - the J-shaped effect,(2) which may also be true for cognition. Bordeaux et al showed an inverse relationship between incidence of dementia in elderly population and wine intake(3) and data from Rotterdam study suggested that risk of "vascular" dementia reduces with moderate consumption of alcohol.(4) The Copenhagen City Heart Study showed that moderate amount of wine but not beer or other spirits may have a protective effect on all types of dementia suggesting that flavinoids in the wine may have an antioxidant effect.(5) Small sample size and confounding effects of cerebrovascular disease and dietary habits of the participants prelude any definite conclusions from the available data.   What do you recommend for Mr. E?  Mr. E needs a multidisciplinary approach since it's not clear whether all findings can be explained by excessive alcohol. [NAME] needs to be better characterized and entrapment neuropathies ruled out. Repeat nerve conduction studies and genetic testing may be needed for Charcot-Marie-Tooth disease, if warranted. Elevated CPK levels may be from axonal neuropathy.   [NAME] ataxia can be central and MRI of the brain and spinal cord may be considered to assess cerebellum and posterior columns. Widespread brain atrophy would suggest cognitive decline to be alcohol related. To rule out B12 deficiency methyl-malonic acid and homocysteine levels should be measured.   Neuropsychological testing is critical to assess and characterize his cognitive deficits and to rule out depression.   Support from community resources in stopping drinking is mandatory. Improved diet, supplementation of vitamins and treatment of high blood pressure will be important.   References 1. [NAME], [NAME], Mittleman [NAME], et al. Alcohol consumption and subclinical findings on magnetic resonance imaging of the brain in older adults. The Cardiovascular Health Study. Stroke 2001;32:1939-46. 2. [NAME]© L, [NAME], [NAME], et al: Alcohol consumption and the risk of ischemic stroke. The Framingham Study. Stroke 2002;323:907-12. 3. [NAME], [NAME], [NAME], et al: Wine consumption and dementia in the elderly: a prospective community study in the Bordeaux area. Rev Neurol (Paris) 1997;153:185-192. 4. [NAME], [NAME], Witteman [NAME], et al. Alcohol consumption and the risk of dementia: the Rotterdam Study. Lancet 2002;359:281-286. 5. [NAME] T, Thudium D, [NAME] and type of alcohol and risk of dementia. The Copenhagen City Heart Study. Neurology 2002;59:1313-1319.
 | jama_el;159 | P | Is It Really Memory Loss? [NAME], February 23, 2008 | [NAME],  Ph.D.  Johns Hopkins, Physical Medicine & Rehabilitation | [EMAIL] | Mr E presents with several overlapping physical and cognitive concerns, and therefore would best be served by a multidisciplinary team. I would refer to neurology and physical medicine for greater clarification of Mr E's gait abnormalities. If they are not accounted for by his CMT, possible diagnoses are cerebellar dysfunction such as found in alcoholic cerebellar degeneration and Wernicke encephalopathy, or even atypical Parkinson disease.(1)   His medical doctors are the authority on his physical symptoms, but to paraphrase [NAME], all the privilege I claim for my own profession is that of testing longest: Mr E's cognitive symptoms can be best understood through a complete neuropsychological assessment, the goal aptly summarized by Mr E himself: To determine if his cognitive problems are due to "alcohol, something else, or just age." Given Mr E's age, poorly controlled hypertension, and drinking history, cognitive dysfunction could have several possible causes: alcohol-related dementia, vascular dementia, and mild cognitive impairment are all differential diagnoses to be considered. However, the patient's ability to describe his troubles indicates that he is able to form new memories, which would not be the case in the severe anterograde amnesia typical of [NAME] syndrome.(2) His account is more typical of a problem in sustained attention or working memory.   Subjective perceptions of memory complaints are often indicative of depressed mood.(3) Mr E's mood is certainly a source of concern. He evidently had significant problems coping with a change in his vocational status 10 years ago, has difficulties in family relationships, and now appears disheartened by his progressive physical limitations.   As for his alcohol consumption, his past elevated MCV suggests that his enjoyment has been in the hazardous drinking range. Several brief screening instruments are available to identify hazardous and at-risk drinkers in primary care settings.(4) Based on the Comorbidity-Alcohol Risk Evaluation Tool, which uses comorbidity-specific thresholds,(5) Mr E still meets criteria for at-risk drinking.   No clear dose-response relationship between alcohol and cognitive impairments exists, so a better question for a clinician to ask is, "What level of alcohol consumption would be unsafe for this particular patient?" Alcohol use is related to impaired cognition, increased risk of stroke, contraindicated with antihypertensive medications, and is related to noncompliance with medication regimens. For this patient already at risk of falls, the safest dose is none.   Treatment plans should take into account that Mr E is still relatively cognitively intact, with a high degree of self-awareness. He is a good candidate for a brief motivational interviewing intervention. A recent meta-analysis found this technique was effective in reducing alcohol consumption, with effect sizes ranging from 0.18 to 0.60.(6) My recommendations are best summarized by paraphrasing an Englishwoman of more recent vintage: Try to make him go to rehab. Physical medicine and rehabilitation, that is, where a multidisciplinary team can develop a comprehensive plan to address Mr E's upper extremity functioning, gait and balance problems, cognitive concerns, emotional health, and coping behaviors.   References   1. [NAME], [NAME], [NAME], [NAME], [NAME], [NAME]. Ten steps to identify atypical parkinsonism. J Neurol Neurosurg Psychiatry. December 1, 2006 2006;77(12):1367-1369. 2. Johnson-Greene D D, J. Neuropsychology of Alcoholism. In: Horton AM WD, ed. The Neuropsychology Handbook. 3rd ed. New York: Springer Publishing Co.; 2007:733-756. 3. Bolla K, [NAME], Bonaccorsy, C., & Bleecker, ML. Memory complaints in older adults. Fact or fiction? Archives of Neurology. 1991;48(I):61-64. 4. Moore AA BJ, Babor TF, Hays RD, [NAME]. Beyond alcoholism: identifying older, at-risk drinkers in primary care. Journal of studies on alcohol. 2002;63(3):316-324. 5. Moore AA, Giuli L, [NAME] R, et al. Alcohol Use, Comorbidity, and Mortality. Journal of the American Geriatrics Society. 2006;54(5):757. 6. [NAME], [NAME], [NAME]. The efficacy of motivational interviewing as a brief intervention for excessive drinking: a meta-analytic review. Alcohol Alcohol. May 1,2006;41(3):328-335.
 | jama_el;143 | P | A Biopsychosocial Perspective is Essential [NAME], February 5, 2008 | [NAME],  M.D.  University of Wisconsin School of Medicine & Public Health | [EMAIL] | A thorough evaluation of this gentleman with a progressive neurological disorder requires consideration of all relevant biological, psychological and social factors.   His neurological signs and symptoms include muscle wasting, deformity of both hands, [NAME] on tandem walking, sensory loss, possible fasciculations, memory loss and word-finding difficulties. The most plausible explanation is that Mr E's excessive alcohol use is exacerbating a pre-existing neurological condition such as Charcot-Marie-Tooth syndrome.   Other considerations include: amyotrophic lateral sclerosis, B12 deficiency, neurosyphilis, cerebrovascular disease, Alzheimer disease, Parkinson disease, frontotemporal dementia, multisystem atrophy and late-onset Friedreich ataxia - but none of these would account for the full range of symptoms. Excessive alcohol use by itself is a possibility, though Mr E's presentation is not consistent with [NAME] syndrome. Mr E is prescribed ranitidine, which has been found to inhibit alcohol dehydrogenase and therefore increase the toxic effects of alcohol.(1)   Further evaluation should include an assessment of mood and anxiety disorders, since both are common in older adults and are comorbid with alcohol use disorders.(2) Mr E should be screened for suicidal ideation, since older men comprise the demographic at highest risk of suicide.(3) Neuropsychological testing would help delineate the exact nature and severity of cognitive symptoms.   The NIAAA recommends that older adults consume no more than one standardized drink per day.(4) Mr E has, at the very least, "at-risk drinking," that is, drinking that may bring about adverse consequences. Further elucidation of his history may indicate evidence supporting a diagnosis of either alcohol abuse or dependence.   The relationship between alcohol use and cognition may be described as a J-shaped curve: modest alcohol use confers the lowest risk of cognitive decline, complete abstinence results in slightly higher risk, and excessive use results in high risk.(5) It is likely that Mr E's alcohol use puts him on the ascending limb of this curve. Given that alcohol is a neurotoxin, any alcohol use is likely to contribute to progression of Mr E's underlying neurological condition. Therefore, I would recommend complete abstinence from alcohol. Once he stops drinking alcohol, he should be monitored for alcohol withdrawal syndrome.   If Mr E has difficulty quitting on his own, I would refer him to a substance abuse treatment program. Older adults may have better outcomes than younger adults in substance abuse treatment programs.(6)   Since Mr E's alcohol use escalated after he retired, one could surmise that the loss of his career as an attorney for an international firm was a significant psychological blow, as well a possible financial stressor. He is separated from his family, suggesting that boredom, loneliness and isolation may be contributing to excessive alcohol use. Alcohol, in a maladaptive way, helped fill a void left behind by retirement and estrangement from his family. Mr. [NAME] should seek out new relationships and new activities to fill the void left behind by alcohol. If Mr E turns out to be suffering from a mood or anxiety disorder, this should be addressed as well.   References   1. [NAME], Roine R, Frezza M, et al. Effects of ranitidine on blood alcohol levels after ethanol ingestion. Comparison with other H2-receptor antagonists. [NAME]. 1992;267(1):83-6. 2. Kessler RC, Berglund P, Demler O, et [NAME]. Lifetime prevalence and age-of-onset distributions of DSM-IV disorders in the National Comorbidity Survey Replication. [NAME]. 2005;62(6):593-602. 3. Conwell Y, [NAME] PR, [NAME]. Risk factors for suicide in later life. Biol Psychiatry. 2002;52:193-204. 4. National Institute on Alcohol Abuse and Alcoholism. The Physicians' Guide to Helping Patients With Alcohol Problems. NIH Pub. No. 95-3769. Rockville, MD: National Institute on Alcohol Abuse and Alcoholism, 1995. 5. [NAME], [NAME], [NAME], [NAME], Mittleman [NAME], Siscovick DS. Prospective study of alcohol consumption and risk of dementia in older adults. [NAME]. 2003;289(11):1405-13. 6. [NAME], Pettinati H, [NAME]. Alcoholism treatment adherence: older age predicts better adherence and drinking outcomes. Am J Geriatr Psychiatry. 2002;10(6):740-7.