Isolated naratriptan-associated ischemic colitis.

We report a 41-year-old woman who developed histology- and colonoscopy-proven ischemic colitis with the use of naratriptan not exceeding the maximum 2 doses a day and 3 days per week and without a known medical or cardiovascular history. By exclusion of other causes of colonic ischemia, naratriptan was considered the sole causal agent. Discontinuation of naratriptan resulted in a complete clinical recovery. To date, our patient is the youngest known patient to develop ischemic colitis on isolated naratriptan in the setting of no known medical risk factors or predisposing medical condition. Even though triptans are commonly used for the abortive treatment of migraine headaches, such a reported side effect is rare; however, careful assessment and individual patient-based treatment is advised.

Neuroimaging in Secondary Headache Disorders.

A secondary headache may develop de novo or in patients with a history of primary headaches, and a thorough history and neurological exam often helps to suspect a secondary etiology. The causes of secondary headaches include tumors, vascular etiologies, structural brain disorders, infection, inflammation, and alterations of cerebrospinal fluid pressure dynamics. Computed tomography (CT) is very sensitive for detecting acute hemorrhage but magnetic resonance imaging (MRI) is preferred over a head CT in subacute and non-emergent cases. Obtaining the correct diagnosis may include incorporation of intravenous contrast agents, special imaging sequences, and functional imaging techniques.

Hiccups as a migraine aura.

OBJECTIVE: To report a case series of hiccup as a migraine aura. BACKGROUND: Hiccup is a syndrome of inappropriate muscle contraction. To our knowledge, hiccup as a migraine aura has not been reported. CASE SERIES: We describe series of patients who presented with hiccups as their migraine aura symptom. CONCLUSION: Hiccups can present as a primary aura symptom in patients with migraine.

Unilateral pupillary mydriasis from nebulized ipratropium bromide: A false sign of brain herniation in the intensive care unit.

Although there are many causes of anisocoria in the intensive care setting, the development of unilateral mydriasis in patients with intracranial hemorrhage or tumor is a neurological emergency, as it may herald the onset of uncal herniation. We describe two patients with a hemiparesis from neurosurgical disorder who subsequently developed a fixed and dilated pupil. The pupillary abnormality was caused by nebulized ipratropium bromide in both cases, and resolved when the medication was discontinued. Nebulized ipratropium may leak from the mask into ipsilateral eye and cause mydriasis in patients with facial weakness. This benign cause of anisocoria in the intensive care setting is distinguished from uncal herniation by the laterality of neurologic findings, and lack of mental status change, ptosis, and extraocular movement impairment.

Progressive weakness with respiratory failure in a patient with sarcoidosis.

A 29-year-old African American woman with an 8-year history of biopsy-proven renal sarcoidosis and end-stage renal disease requiring hemodialysis was admitted to the hospital with progressive weakness and shortness of breath for 2 months. Eight months prior to admission, she was prescribed 15 mg of prednisone twice a day and 200 mg of hydroxychloroquine sulfate twice a day for hypercalcemia and elevated angiotensin-converting enzyme level. As her laboratory abnormalities improved, the prednisone dose was gradually decreased, and hydroxychloroquine was continued. Six months earlier, she noticed numbness in her feet and progressive loss of muscle bulk in her feet and hands. She also noticed difficulty reaching overhead, getting out of a chair, and climbing stairs. She denied any pain or muscle cramps. Results of electrophysiological tests at that time, which included nerve conduction studies and needle electromyography, revealed moderately severe axonal sensorimotor polyneuropathy. Her weakness worsened and so she was admitted to the hospital and subsequently transferred to our facility for further management.

Where (in the brain) do semantic errors come from?

BACKGROUND: Semantic errors result from the disruption of access either to semantics or to lexical representations. One way to determine the origins of these errors is to evaluate comprehension of words that elicit semantic errors in naming. We hypothesized that in acute stroke there are different brain regions where dysfunction results in semantic errors in both naming and comprehension versus those with semantic errors in oral naming alone. METHODS: A consecutive series of 196 patients with acute left hemispheric stroke who met inclusion criteria were evaluated with oral naming and spoken word/picture verification tasks and magnetic resonance imaging within 48 h of stroke onset. We evaluated the relationship between tissue dysfunction in 10 pre-specified Brodmann's areas (BA) and the production of coordinate semantic errors resulting from (1) semantic deficits or (2) lexical access deficits. RESULTS: Semantic errors arising from semantic deficits were most associated with tissue dysfunction/infarct of left BA 22. Semantic errors resulting from lexical access deficits were associated with hypoperfusion/infarct of left BA 37. CONCLUSION: Our study shows that semantic errors arising from damage to distinct cognitive processes reflect dysfunction of different brain regions.

Characteristics and reversibility of dementia in Normal Pressure Hydrocephalus.

Studies of the cognitive outcome after shunt insertion for treatment of Normal Pressure Hydrocephalus have reported widely mixed results. We prospectively studied performance of 60 patients with Normal Pressure Hydrocephalus on a comprehensive battery of neuropsychological tests before and after shunt surgery to determine which cognitive functions improve with shunt insertion. We also administered a subset of cognitive tests before and after temporary controlled drainage of cerebrospinal fluid to determine if change on this brief subset of tests after drainage could predict which patients would show cognitive improvement three to six months after shunt insertion. There was a significant improvement in learning, retention, and delayed recall of verbal memory three to six months after surgery (using paired t-tests). The majority (74%) of patients showed significant improvement (by at least one standard deviation) on at least one of the memory tests. Absence of improvement on verbal memory after temporary drainage of cerebrospinal fluid had a high negative predictive value for improvement on memory tests at 3-6 months after surgery (96%; p=0.0005). Also, the magnitude of improvement from Baseline to Post-Drainage on few specific tests of learning and recall significantly predicted the magnitude of improvement after shunt surgery on the same tests (r2=0.32-0.58; p=0.04-0.001). Results indicate that testing before and after temporary drainage may be useful in predicting which patients are less likely to improve in memory with shunting.

One-step synthesis of oxazoline and dihydrooxazine libraries.

The reactions of 1,2- and 1,3-hydroxyalkyl azides and aldehydes in the presence of Lewis acid result in the one-step construction of oxazolines and dihydrooxazines, respectively. The reaction was adapted to parallel synthesis using a polymer-bound phosphine to scavenge excess hydroxyalkyl azide. Thus, a 60-member library of various disubstituted oxazolines and di- and trisubstituted dihydrooxazines was generated.

Restoring cerebral blood flow reveals neural regions critical for naming.

We identified areas of the brain that are critical for naming pictures of objects, using a new methodology for testing which components of a network of brain regions are essential for that task. We identified areas of hypoperfusion and structural damage with magnetic resonance perfusion- and diffusion-weighted imaging immediately after stroke in 87 individuals with impaired picture naming. These individuals were reimaged after 3-5 d, after a subset of patients underwent intervention to restore normal blood flow, to determine areas of the brain that had reperfused. We identified brain regions in which reperfusion was associated with improvement in picture naming. Restored blood flow to left posterior middle temporal/fusiform gyrus, Broca's area, and/or Wernicke's area accounted for most acute improvement after stroke. Results show that identifying areas of reperfusion that are associated with acute improvement of a function can reveal the brain regions essential for that function.