| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Antonio Culebras, MD, International Newsletter Editor
For most of us, war is something experienced through watching news broadcasts and reading the daily newspaper. However, for some of our colleagues—fortunately few—war is their daily reality. Cognizant of the profound and intense experiences that war can provoke, Neurology is privileged to publish a first-hand account of the perceptions of critical care in Iraq as narrated by neurologists Geoffrey Ling and Cornelius Maher, who spent time there.
see page 14
Delayed orthostatic hypotension as a cause of orthostatic intolerance
Gibbons and Freeman report that 39% of patients with orthostatic hypotension (OH) have blood pressure (BP) fall only after 10 minutes of tilt-table testing. A further 15% had BP fall between 3 and 10 minutes. The authors suggest that delayed OH is a mild or early form of sympathetic adrenergic dysfunction.
|
see page 28
The editorial by Cheshire and Phillips notes that the current definition of OH is a reduction in systolic BP of at least 20 mm Hg or diastolic BP of at least 10 mm Hg within 3 minutes of standing or upright tilt table testing. Autonomic laboratories assess adrenergic function by tilting patients for 3 to 5 minutes. In the Gibbons and Freeman study of 108 patients with OH, only 50 met the criterion for OH within the first 3 minutes of testing, while BP drops in the rest were delayed. They predict that delayed OH will come to be appreciated as a distinct physiologic entity. However, proof that delayed OH is abnormal will require correlations with daily symptoms and neurologic findings as well as comparison to normal controls. Moreover, whether delayed OH warrants the same intensity of treatment as early OH is unclear and must await prospective outcome studies.
see page 8
Apathy vs depression in PD
Kirsch-Darrow et al. compared apathy and depression in 80 patients with PD vs 20 patients with dystonia. Depression occurred similarly in PD and dystonia patients. What distinguished the groups was the much higher frequency of apathy in PD. Apathy may be a core feature of PD and is not limited to patients with depression.
|
see page 33
The editorial by Irene Richard notes that apathy is a mental state characterized by diminished goal directed speech, motor activity, and emotion. Patients with apathy demonstrate a general sense of indifference but their mood is neutral. In depression, mood is distinctly negative and causes emotional suffering. The recognition that apathy can be present without depression is important so that we do not inappropriately diagnose and treat a depressive disorder that is not present. With apathy, it is generally the spouse, family, or friends, and not the patient, who complain.
see page 10
Predicting seizure recurrence after AED withdrawal
Cardoso et al. found that seizure recurrence after AED withdrawal in patients who had been seizure free for >2 years was more frequent in those with hippocampal atrophy or hyperintense T2 signal.
see page 134
The editorial by Anne Berg and Jerome Engel explores the relationship between hippocampal atrophy and seizure control. The study by Cardoso et al. is informative for decisions regarding AED withdrawal, but also suggests the need for longer-term studies to determine the natural history of hippocampal atrophy with respect to AED response and seizure recurrence.
see page 12
Memantine and behavior in AD
Memantine is approved for treatment of dementia in moderate to severe AD. Cummings et al. report that memantine decreased agitation and irritability in patients with AD who were also receiving treatment with donepezil. Few adverse events were observed.
|
see page 57
Elevated cortical zinc in AD
Religa et al. report that zinc levels (but not those of other metals) are twofold elevated in postmortem neocortical samples taken from AD cases vs controls. This increase correlated with increased ß-amyloid levels and dementia severity.
see page 69
Free copper, MMSE, and CSF markers in AD
Squitti et al. found that in AD and healthy subjects, lower MMSE scores were associated with higher free copper (not bound to ceruloplasmin) and lower CSF ß-amyloid concentrations. A free copper blood-to-brain and APP-driven brain-to-blood flux is postulated. Impairment in copper flux may have a deleterious effect in AD.
see page 76
Call-Fleming syndrome associated with antidepressant use
Noskin et al. describe two cases suggesting a potential relationship between the use of antidepressants and development of reversible cerebral vasoconstriction and stroke.
see page 159
Stroke center designation improves quality of care
Gropen et al. studied the impact of early recognition and transport of patients with acute stroke to stroke centers designated by the New York State Department of Health based on compliance with Brain Attack Coalition criteria. More patients received timely thrombolytic therapy and stroke unit admission.
see page 88
Neurologic prognosis and withdrawal of life support after cardiac arrest
Geocadin et al. studied the use of clinical examination, SSEPs, and EEG in the decision-making that patients’ families and physicians face after cardiac arrest. In comatose patients with poor prognosis, withdrawal of care was most expeditious when cortical N20 potentials were absent, followed by uncertain, then normal SSEPs.
see page 105
Is all medication overuse headache just a form of migraine?
Paemeleire et al. report patients with cluster headache who have medication overuse altering their headache phenotype. Each of the patients reported a personal or family history of migraine or severe headache. The new findings converge with those from rheumatology and GI studies to suggest that a subgroup of migraineurs are susceptible to the effects of medication overuse.
see page 109
Hypothalamic stimulation in chronic cluster headache
Leone et al. report that continuous hypothalamic stimulation produced lasting pain resolution or reduction in 13 of 16 patients with chronic drug-refractory cluster headache, without persistent side effects.
see page 150
Related Articles
Neurology 2006 67: 10-11.
Neurology 2006 67: 105-108.
Neurology 2006 67: 109-113.
Neurology 2006 67: 12-13.
Neurology 2006 67: 134-136.
Neurology 2006 67: 14-17.
Neurology 2006 67: 150-152.
Neurology 2006 67: 159-160.
Neurology 2006 67: 28-32.
Neurology 2006 67: 33-38.
Neurology 2006 67: 57-63.
Neurology 2006 67: 69-75.
Neurology 2006 67: 76-82.
Neurology 2006 67: 8-9.
Neurology 2006 67: 88-93.
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
