A monoclonal antikeratin antibody, designated AEl, was used to stain frozen sections of normal and abnormal human skin by the immunofluorescence and peroxidase-antiperoxidase techniques. In normal human epidermis and ichthyosis vulgaris, a nonproliferative epidermal disease, this antibody selectively stained epidermal basal cells. Very different staining patterns were observed in various other epidermal diseases. A suprabasal staining pattern was observed in psoriasis (16 cases), verruca (9), seborrheic keratosis (5), actinic keratosis (2), as well as the epidermis adjacent to certain epidermal neoplasms (4). Basal cell carcinoma (7) showed weak, homogeneous staining. In contrast, a disorganized pattern consisting of cells with various staining intensities was observed in Bowen's disease (2) and squamous cell carcinoma (4). Although the biochemical basis for these altered staining patterns remains to be elucidated, these results provide further evidence that epidermal keratin expression can be affected by various disease states. Moreover, our data suggest that a common alteration in keratin expression, as defined by the suprabasal AEl staining pattern, exists in psoriasis and a number of other benign hyperproliferative epidermal diseases.
The purpose of this study was to evaluate cerebrovascular reactivity (CVR) of major arterial vascular territories, particularly in the contralateral hemodynamically unaffected hemisphere, in patients with unilateral internal carotid artery (ICA) steno-occlusive disease compared to control subjects with risk factors for cerebrovascular disease. Methods: In this retrospective observational study, twenty-seven patients with right-sided unilateral ICA steno-occlusive disease (age range, 25 to 91 years; 17 males) and twenty-one patients with left-sided unilateral ICA steno-occlusive disease (age range, 24 to 83 years; 14 males) and 41 control subjects were studied. CVR was quantitated as the change in blood oxygen level dependent (BOLD) MRI signal (as a surrogate of cerebral blood flow), in response to a consistently applied step change in the arterial partial pressure of carbon dioxide (PaCO2). The CVR of each major arterial vascular territory was assessed in the ipsilateral hemodynamically affected hemisphere and compared to the corresponding territory in the contralateral hemisphere. Results: In patients, a significant reduction in CVR was observed in the ipsilateral anterior circulation compared to that of the corresponding territory on the contralateral side (0.027 ± 0.083 vs. 0.109 ± 0.066% BOLD change/mm Hg, p < 0.0001) and to controls (0.195 ± 0.054% BOLD change/mm Hg, p < 0.0001). The CVR of the contralateral anterior circulation was reduced on average by 50% compared to controls (p < 0.0001). Conclusions: The implication of these findings is that unilateral carotid stenosis affects the vascular reserve of both sides of the brain compared to control subjects. This indicates that the collateral blood flow support from the contralateral to the ipsilateral hemisphere comes at a cost of reduced reserve capacity in the contralateral hemisphere. The findings suggest that there may be a reduction in functional hyperemia associated with neuronal activation, not only affecting the hemisphere ipsilateral to an occlusion, but also the hemisphere contralateral to an occlusion. It remains to be determined if ‘stealing' from the ‘rich' to support the ‘poor' has clinical consequences over the long term.
Acute subdural hematoma (aSDH) is associated with a 60-80% mortality rate and is considered a neurosurgical emergency. Although it is most often treated with emergent surgical decompression, patients may be managed conservatively when they are neurologically intact or the hematoma is small. Typical progression of aSDH resolution occurs over weeks, and is characterized by corresponding changes on radiographic imaging where bright aSDH becomes first isointense at about two weeks and then hypointense on noncontrast computed tomogram (CT) head imaging. If there is continued bleeding acutely, however, the SDH may increase in size leading to transtentorial herniation and subsequent clinical deterioration of the patient.Interestingly, there are a number of case reports in the literature describing the event of spontaneous aSDH resolution. Several hypotheses have been put forward to explain this phenomenon including redistribution of subdural blood and dilution by cerebral spinal fluid (CSF) 1 . Cerebral atrophy, as well as cerebral swelling were both identified to facilitate aSDH resolution 2,3 . Here we describe a patient with an unexpected resolution of an acute SDH in the setting of a bleeding diathesis, and propose that in this patient, coagulopathy contributed to the spontaneous resolution of the hematoma. CASE PRESENTATIONOur patient is a 73-year-old gentleman who had acute onset of left-sided weakness. His strength was 4-/5 in the left upper and lower extremities. He was alert and oriented, with stable vital signs. His past medical history was significant for myelodysplastic syndrome with chronic pancytopenia, and atrial fibrillation on warfarin therapy.On admission, significant findings on bloodwork included platelet count of 17 x 10 9 /L and an international normalized ratio (INR) of 1.6. Non-contrast CT head scan performed at the initial evaluation demonstrated a moderate-sized acute subdural hemorrhage over the right convexity ( Figure 1A). He received vitamin K and platelets, and was admitted for observation. Five hours later, his level of consciousness decreased, and he required intubation. A follow-up non-contrast CT head demonstrated dramatic enlargement of the acute SDH with uncal herniation ( Figure 1B). He received a platelet transfusion and the prothrombin complex concentrate on formulary, Octaplex, in anticipation of emergent surgical evacuation. However, the patient's family instead opted for comfort measures.Over
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