Dot-like Lesions Research Articles

HTRA1-related cerebral small-vessel disease causes cerebral microbleeds on the brainstem surface

Background and objectivesCerebral autosomal recessive arteriopathy with subcortical infarcts and leukoencephalopathy (CARASIL) has recently been known as HTRA1-related cerebral small-vessel disease (CSVD), it is caused by variants in HTRA1. Recently, it has been reported to develop in heterozygotes with some variants of the gene. Multiple prospective studies have reported that the frequency of heterozygous HTRA1 variants developing CSVD is 2 - 6.5 % in CARASIL. Heterozygous variant cases lack unique clinical features, have an older age of onset, and are difficult to detect. Characteristic findings are required to identify such cases. MethodMagnetic resonance imaging (MRI) images of cases that experienced cerebral infarction and carried heterozygous variants in HTRA1 were reviewed. ResultsFour cases of heterozygous HTRA1-related CSVD in two families (Family 1: c.754G > A, p.A252T; three males. Family 2: c.497G > T, p.R166L, one female). In all cases, white matter lesions with lacunar infarcts were observed in the periventricular and basal ganglia, external capsule, and brainstem. Moreover, T2 star weighted image (T2*WI) low presented dot-like lesions were present along the surface of the brainstem, which have only been reported in one homozygous case. Susceptibility-weighted imaging (SWI) was performed in two cases, and the dot-like lesions on T2*WI resembled a pearly tiara along the surface of the brainstem. ConclusionBrainstem surface on T2*WI low showed dot-like lesions, which are not generally observed in patients with stroke and can be characteristic of HTRA1-CSVD associated with heterozygous variant. The pathology requires further investigation for diagnosis.

NI-8 LATE-DELAYED MRI FINDINGS AFTER RADIOTHERAPY: DOT-LIKE ENHANCED LESION

Abstract Introduction Late-delayed radiation reactions after radiotherapy include brain atrophy, leukoencephalopathy, radiation necrosis, and cerebrovascular disease. We will discuss the contrast-enhanced SPGR to detect dot-like enhanced lesions that are considered to be late late-delayed radiation reactions. Material and Methods One hundred eleven patients (62 males and 49 females; median age at irradiation: 49 years) who had received radiotherapy since 1994 and were alive since 2010, had dot-like lesions by contrast-enhanced SPGR, and had a PFS OS of at least 24 months were included in the study. Of these, 64 had high-grade glioma, 4 had low-grade glioma, 15 had PCNSL, 7 had metastatic brain tumors, 9 had germ cell tumors, 5 had medulloblastoma, and 7 had other tumors, with a mean follow-up of 89. Results Contrast-enhanced SPGR showed dot-like or rod-like findings in 23/111 patients (20.7%). Contrast-enhanced FIESTA and Flair-Cube were also detectable in some cases. However, it was difficult to detect by contrast SE-T1WI, SE-T2WI, or contrast SE-Flair. The lesions appeared a median of 49 months after irradiation (IQR 34, 103. Range 25-298). There were no lesions that increased in size, and multiple lesions appeared during the course of the study in 8/23 (34.8%) of the patients. All lesions occurred within the irradiated field and were seen in patients receiving a total dose of 50 Gy or more, but not in patients receiving whole-brain irradiation alone or whole-brain irradiation plus boost at 50 Gy or less. Discussion and Conclusion It is difficult to elucidate the pathogenesis without pathological evidence, but it is one of the late-delayed radiation reactions that occur more than 2 years later, and it is presumed to be vasculopathy or granulation reaction in the Virchow-Robin space. It tends to increase over time and is not considered to be a condition that causes sudden clinical manifestations.

Cerebral microbleeds are associated with blood pressure levels in individuals with hypertension

ABSTRACTObjective: Cerebral microbleeds (CMBs), which appear as small dot-like hypointense lesions, are strongly associated with cerebrovascular disease. Recently, numerous investigations have suggested that hypertension and age are risk factors for CMBs; however, whether blood pressure grade and age rank are related to the severity of CMBs remains unclear. The purpose of this research was to assess the association between cerebral microbleeds and blood pressure levels.Methods: In total, 460 consecutive hypertension patients (214 males and 246 females; aged 44–96 years, mean age 60.95 ± 6.82 years) from Lishui Central Hospital were enrolled and classified as CMB or non-CMB patients according to magnetic resonance imaging (MRI). Gradient echo T2*-weighted MRI was used to detect CMBs. Differences in blood pressure, CMB severity, and other patient characteristics were compared between the two groups. Multifactorial logistic regression was used to analyze the correlation between blood pressure and microbleeds.Results: In our study, CMB lesions were identified in 123 patients (26.7%), including 39 patients with CMB lesions located deep in the brain. In the hypertensive population, smoking is an independent risk factor for CMBs. Additionally, systolic blood pressure (SBP), diastolic blood pressure (DBP) and age are also independent risk factors for CMBs. Furthermore, a modest correlation was noted between the number of microbleeds and grade of hypertension.Conclusions: This study provides novel evidence that microbleed severity is associated with hypertension grade. This conclusion emphasizes the importance of antihypertensive therapy in hypertension patients to avoid an increase in CMBs.

Cerebral microbleeds: Beyond the macroscope.

While being increasingly recognized in clinical routine, brain microbleeds remain a puzzling finding for physicians. These small dot-like lesions are thought to be old perivascular collections of hemosiderin deposits. They can be found in different neurological settings such as cerebrovascular or neurodegenerative diseases. While their microscopic size would suggest considering these lesions as anecdotal, they are now regarded as biomarkers of severity of an underlying cerebrovascular disease. Their natural history and the interactions with surrounding brain cells remain unknown. However, their presence may impact therapeutic decisions. Deciphering the biological mechanisms leading to, or following microbleeds would enable us to address a key question: do microbleeds arise and impact the surrounding parenchyma like a miniature version of intracerebral hemorrhages or do they represent a different kind of injury? We hereby discuss, based on both clinical and experimental literature, the gap between the definition of microbleeds coming from neuroimaging and the pathophysiological hypotheses raised from histopathological and experimental data. Our analysis supports the need for a convergent effort from clinicians and basic scientists to go beyond the current "macro" view and disclose the cellular and molecular insights of these cerebral hemorrhagic microlesions.

Nodding syndrome in Uganda is a tauopathy

Nodding syndrome is an epidemic neurologic disorder of unknown cause that affects children in the subsistence-farming communities of East Africa. We report the neuropathologic findings in five fatal cases (13–18 years of age at death) of nodding syndrome from the Acholi people in northern Uganda. Neuropathologic examination revealed tau-immunoreactive neuronal neurofibrillary tangles, pre-tangles, neuropil threads, and dot-like lesions involving the cerebral cortex, subcortical nuclei and brainstem. There was preferential involvement of the frontal and temporal lobes in a patchy distribution, mostly involving the crests of gyri and the superficial cortical lamina. The mesencephalopontine tegmental nuclei, substantia nigra, and locus coeruleus revealed globose neurofibrillary tangles and threads. We conclude that nodding syndrome is a tauopathy and may represent a newly recognized neurodegenerative disease.

The Time Course of Percheron Artery Ischemic Coma on Imaging: A Retrospective Cohort Study

Background: We investigated the time course of awakening events in acute Percheron artery ischemic coma (PAIC), which was previously unknown. Methods: Patients who had newly identified acute PAIC in 2010-2013 and had not received thrombolytic therapy were enrolled prospectively. The lesion sizes of PAIC were measured using diffusion-weighted imaging (DWI). The time course of PAIC was also assessed using the Glasgow Coma Scale. Findings: Ninety-three patients met the inclusion criteria, of whom 63 and 30 had transient PAIC and persistent PAIC, respectively. The time course of awakening events in persistent PAIC decreased over time, with large lesions in the bilateral paramedian thalamus/rostral midbrain on DWI almost in all patients and the artery of infarction either at Percheron artery or at a variant of the top of basilar artery; whereas awakening events in transient PAIC increased over time, with small or dot-like lesions in the paramedian thalamus/rostral midbrain in 30.2% cases, and the rest in naturally recanalization of infarcts or TIA. Lesion volumes were larger for persistent PAIC than for transient PAIC (median, 2.4 cm3 vs. 0.03 cm3, P <0.0001). In a proportional hazards ratio (HR) analysis, lesion volume was associated with mortality (HR, 1.8; 95% confidence interval[CI],1.096-2.810). Transient PAIC was associated with much better survival than persistent PAIC (HR, 13.5; 95% CI, 10.29-29.31). Interpretation: The time course of awakening events in transient PAIC differed from that in persistent PAIC. Persistent PAIC was associated with large ischemic lesions in the paramedian thalamus /rostral midbrain, and with high mortality. Funding Statement: This work is supported by a grant from National Clinical Key Specialty Construction Project (20160001), the Medical Research Council, affiliated Shuyang Hospital of Xuzhou Medical University, China. Declaration of Interests: Authors have no conflict of interest. Ethics Approval Statement: This study was approved with a waiver of informed consent by the Ethical Committee of the Shuyang People’s Hospital.

En-Face Optical Coherence Tomography of Acute Syphilitic Posterior Placoid Chorioretinopathy

ABSTRACTPurpose: To report a unique case series of acute syphilitic posterior placoid chorioretinopathy (ASPPC) correlating en-face optical coherence tomography (OCT) with standard imaging modalities.Methods: In this retrospective case series, multimodal imaging was performed in three ASPPC patients at the time of disease presentation.Results: Clinical and laboratory findings were consistent with the diagnosis of ASPPC. In all the study patients, multiple hyperreflective dot-like lesions distributed in the macular area and observed with en-face OCT at the level of retinal pigment epithelium (RPE) corresponded to the nodular RPE elevations on cross-sectional OCT and to the hyperautofluorescent spots on fundus autofluorescence. In addition, the cross-sectional OCT scans showed disorganization of the outer retinal bands and punctate choroidal hyperreflectivity.Conclusion: By combining en-face OCT with multimodal imaging analysis, we propose that a primary inflammation at the level of the choroid may be the pathogenic mechanism for the occurrence of outer retinal band abnormalities.

A quantitative study of tau pathology in 11 cases of chronic traumatic encephalopathy.

To quantify tau pathology of chronic traumatic encephalopathy (CTE) and investigate influence of dot-like lesions (DL), brain region, comorbidity and sporting career length. Densities of neurofibrillary tangles (NFT), astrocytic tangles (AT), DL, oligodendroglial inclusions (GI), neuropil threads (NT), vacuoles, neurons and enlarged neurons (EN) were measured in tau-immunoreactive sections of upper cortical laminae of frontal and temporal lobes, hippocampus (HC), amygdala and substantia nigra (SN) in 11 cases of CTE. DL were a consistent finding in CTE. Densities of NFT, NT and DL were greatest in sectors CA1 and CA2 of the HC. Densities of AT were lower than NFT, small numbers of GI were recorded in temporal lobe and low densities of vacuoles and EN were consistently present. β-Amyloid-containing neuritic plaques (NP) also occurred at low density. Densities of NFT, NT, DL and AT were greater in sulci than gyri, while vacuole density was greater in gyri. Principal components analysis (PCA) suggested that sporting career length and densities of NFT in entorhinal cortex, NT in CA2 and SN and vacuolation in the DG were significant sources of variation among cases. DL are frequent in CTE suggesting affinity with argyrophilic grain disease (AGD) and Parkinson's disease dementia (PD-Dem). Densities of AT in all regions and NT/DL in sectors CA2/4 were consistent features of CTE. The 11 cases are neuropathologically heterogeneous which may result from genetic diversity, and variation in anatomical pathways subjected to trauma.

Is There an Association between Cerebral Microbleeds and Leukoaraiosis?

Cerebral microbleeds (CMBs) are small dot-like lesions appearing as hyposignals on gradient echo (GRE) T2* magnetic resonance (MR) sequences, whereas the leukoaraiosis (LA) indicates the presence of patchy areas of hypersignal on fluid-attenuated inversion recovery (FLAIR) MR sequences in the periventricular white matter. The purpose of this work was to evaluate the association between LA and CMBs. Eighty-five consecutive (men 55; median age 64 years) patients were retrospectively analyzed using a 1.5 T system; CMBs were studied using a T2*-weighted GRE sequence and classified as absent (grade 1), mild (grade 2; total number of microbleeds, 1-2), moderate (grade 3; total number of microbleeds, 3-10), and severe (grade 4; total number of microbleeds, >10). LA was assessed with FLAIR MR sequences and was graded based on the European Task Force on Age-Related White Matter Changes as follows: 1 (no lesions), 2 (focal lesions > 5 mm), 3 (early confluent lesions), and 4 (diffuse involvement of an entire brain region). We considered 170 cerebral hemispheres. The prevalence of CMBs was 24.7% (42 of 170), whereas the prevalence of LA was 27.1% (46 of 170). A statistically significant correlation was observed between LA and CMBs (correlation rho = .495, P value = .001). Multiple logistic regression analysis showed an association between CMBs and cerebrovascular symptoms (P = .0023). Results of this study suggest an association between CMBs and LA. Moreover, we found that LA is associated with the presence of cerebrovascular symptoms.

Transient global amnesia.

Transient global amnesia (TGA) is a sudden and severe anterograde memory disturbance accompanied by various degrees of retrograde amnesia and sometimes executive dysfunction. TGA affects elderly individuals and men and women equally. During the episode, patients cannot recall novel episodic information and therefore repeatedly ask the same questions. They are not fully oriented to space and time. Diagnostic criteria first established in 1985, and elaborated in 1990, demand that there is no clouding of consciousness, other impairments of cognition, or a history of epilepsy or head trauma. An episode of TGA resolves within 24 h leaving a memory gap for the length of the attack. While in rare cases TGA might happen repeatedly, it mostly occurs as a single attack. TGA is considered a benign disorder as memory deficits resolve completely and do not lead to long-term sequelae. In up to 90% of reported TGA cases, a precipitating event - mainly described as physical or emotional stress - is present. The cause of TGA has been a matter of long-standing debate among researchers. In search of an answer, several possible causes (ischemia, migraine, epileptic seizures, or, more recently, a disturbance of venous hemodynamics) have been hypothesized. However, to date there is no scientific proof of any of these mechanisms. By using diffusion-weighted MRI 24-48 h after a TGA episode, small dot-like lesions have been detected in the hippocampus. This has led to the implication that the selective vulnerability of CA1 neurons to metabolic stress might play a role in the pathophysiology of TGA.

Microbleeds in vascular dementia: Clinical aspects

Microbleeds are small dot-like lesions which can be appreciated on gradient echo, T2*-weighted magnetic resonance images as hypointensities. They are considered as an expression of small vessel disease on MRI, next to lacunes and white matter hyperintensities (WMH). Microbleeds are relatively common in vascular dementia, with reported prevalences between 35% and 85%. In the context of vascular dementia, microbleeds are mainly thought to result from hypertensive vasculopathy, but the frequent co-occurrence of lobar microbleeds suggests that neurodegenerative pathology and/or cerebral amyloid angiopathy is also of importance. The presence of multiple microbleeds in vascular dementia or in patients with vascular cognitive impairment is related to worse performance on cognitive tests, mainly in psychomotor speed and executive functioning. They may have some predictive value in terms of predicting development of (vascular) dementia, mortality and disability. Data on the occurrence of stroke and post-stroke dementia in patients with microbleeds are to date not available. New definitions and diagnostic criteria for vascular dementia and vascular cognitive impairment are needed and should take into account microbleeds.

Microbloedingen bij de ziekte van Alzheimer: de onschuld voorbij?

Microbloedingen zijn kleine ronde laesies (<10mm), zichtbaar als hypo-intense (zwarte) signalen op T2*-gewogen MRI-sequenties (Greenberg et al., 2009). Deze technieken zijn gevoelig voor lokale verstoring van het magnetische veld, bijvoorbeeld door ijzerhoudende materialen. De radiologische afwijkingen corresponderen met specifieke onderliggende pathologische afwijkingen, te weten ophopingen van het bloedafbraakproduct hemosiderine, langs de kleine hersenvaten (Greenberg et al., 2009; Fazekas et al., 1999).

Microsangrados cerebrales múltiples en paciente con hipertensión mal controlada. Un nuevo marcador de vasculopatía hipertensiva

Brain microbleeds are small dot-like lesions appearing as hyposignal on gradient echo T2* MR sequences. They represent microscopic areas of old hemosiderin deposits. They are frequent in the setting of symptomatic cerebrovascular disease and also in older healthy people, which suggests a link with arterial hypertension. Their use as diagnostic or prognostic biomarkers remains uncertain. The appearance of these microbleedings and increasing use of Magnetic resonance imaging (MRI) in the clinical practice causes many clinical dilemmas. We report the case of a woman with difficult to control hypertension, who was admitted with bilateral simultaneous cerebral hemorrhage, multiple microbleedings being observed in the cerebral magnetic resonance. We discuss the identification and meaning of these hemorrhagic lesions.

Brain microbleeds and Alzheimer’s disease: innocent observation or key player?

Brain microbleeds are small dot-like lesions appearing as hyposignals on gradient echo magnetic resonance sequences. In Alzheimer's disease, brain microbleeds are of special interest as they may play a crucial role in the pathophysiology. They may be a missing link between two important theories on the neuropathogenesis of Alzheimer's disease-the amyloid cascade hypothesis and the vascular hypothesis. Moreover, they may affect the clinical course of the disease and may have therapeutic consequences. The aim of this article is to review available data to understand the meaning of brain microbleeds in clinical terms and underlying pathology in the context of Alzheimer's disease. We also review the available evidence and highlight the pitfalls of our current knowledge on brain microbleeds in the setting of clinical trials design.

Optical coherence tomographic findings in bietti's crystalline tapetoretinal dystrophy.

To report the optical coherence tomography (OCT) findings of Bietti crystalline tapetoretinal dystrophy. Observational case report. A subject with Bietti crystalline tapetoretinal dystrophy was evaluated with ophthalmoscopy, fluorescein angiography, and OCT (Stratus). OCT showed thinning and hyporeflectivity of the outer nuclear layer in the macula due to photoreceptor degeneration. The retinal areas showing atrophy of the retinal pigment epithelium displayed greater penetration of the optical beam into the choroid and visualization of residual choroidal vessels. The hyperreflective band normally seen under the neurosensory retina was extremely wide when atrophy of the entire retinal pigment epithelium/choriocapillaris complex was found. Above this band, and within the neurosensory retina, some hyperreflective dot-like lesions were seen that could be related to crystals. In cases of Bietti crystalline tapetoretinal dystrophy, OCT shows changes secondary to fundus atrophy and more specific changes that can be related to the presence of crystals, thereby making OCT particularly useful for demonstrating macular atrophic abnormalities.

Cerebral fat embolism: diffusion-weighted magnetic resonance imaging findings

To demonstrate the diffusion-weighted (DWI) magnetic resonance imaging (MRI) findings, and the follow-up MRI findings, of cerebral fat embolism in the acute stage. The initial DWI and clinical findings of six patients with cerebral fat embolism were retrospectively evaluated. The finding of DWI with a b-value of 1000 s/mm2 (b=1000) was compared with that of DWI with a b-value of 0 s/mm2 (b=0). In three patients who underwent follow-up MRI, the interval change of the lesion on T2-weighted images was investigated. The characteristic DWI finding of cerebral fat embolism in the acute stage was multiple, hyperintense, dot-like lesions disseminated in the brain. These lesions were distributed dominantly in the bilateral border-zone areas. Some lesions had an ancillary location including the cortex, deep white matter, basal ganglia, and cerebellum. The lesions were more intense and numerous in DWI (b=1000) than in DWI (b=0). The findings on the follow-up T2-weighted images were multiple confluent hyperintense lesions in the white matter with progression since the initial MRI. DWI could be a sensitive tool for detecting cerebral fat embolism in the acute phase. It is recommended that DWI be included in the initial evaluation of cerebral fat embolism with MRI.

Optical coherence tomography findings in macular cavernous haemangioma

Editor, Cavernous haemangioma of the retina is an unusual vascular hamartoma with presumed autosomal dominant transmission, characterized by clusters of dark red, intraretinal aneurysms, described as ‘grape-like’ lesions (Alexander & Moates 1988). Usually unilateral and clinically silent, the lesion does not normally increase in size (Kushner et al. 1994); however, macular involvement or vitreous haemorrhage can lead to a decline in vision (Pierro et al. 1992). Herein, we present a rare case of macular cavernous haemangioma as well as its morphological peculiar findings as disclosed by optical coherence tomography (OCT). A 62-year-old woman presented with a progressive decrease in vision in the left eye that had been going on for 7 years. Best corrected visual acuity (VA) was 20/20 in the right eye and counting fingers at 1 metre in the left eye. Fundus examination of the left eye revealed an elevated, dark red, macular lesion, with multiple retinal aneurysmatic formations and subretinal as well as intraretinal haemorrhage (Fig. 1). Fundus examination of the right eye was normal. Fluorescein angiography of the left eye showed typical hyperfluorescent dot-like lesions with inferior blockage hypofluorescence known as ‘fluorescence capping’ (Fig. 2) (Messmer et al. 1983). Optical coherence tomography disclosed intraretinal cysts and highly reflective signals from a thickened macula (Fig. 3). At follow-up 2 years later, no changes were seen in this case of macular cavernous haemangioma. Colour fundus photography shows an irregularly elevated vascular mass in the macular region composed of dilated, oval or rounded, thin-walled, saccular blood vessels giving the appearance of a mass of grapes, with associated intraretinal and subretinal haemorrhages. Fluorescein angiography demonstrates multiple hyperfluorescent dots corresponding to aneurysmatic formations and late dye leakage. A typical finding known as ‘fluorescence capping’, characterized by delayed and incomplete perfusion, with progressive filling of the dye in the upper part (arrows) and blocked hypofluorescence in the lower part (arrowheads), is seen in larger aneurysmatic formations. A linear, 5.92-mm OCT scan, centred on the fovea, discloses retinal elevation caused by the tumoral tissue. Optically clear cystic spaces and high reflective signals are seen arising particularly from the inner part of the thickened neurosensory retina. Underneath the lesion, few reflective signals from the retinal pigment epithelium and choroid are observed. No tomographic signals suggesting fluid accumulation are seen in the vicinity of the lesion. Skin and cerebral anomalies have been reported to eventually occur in patients with cavernous haemangioma of the retina. Therefore, an appropriate medical evaluation should be strongly considered in such patients. Family members should also be examined as a dominant inheritance has been suggested (Schwartz et al. 1984; Dellemijn & Vanneste 1993). In our case, no systemic finding was found after clinical and neurological comprehensive evaluation and no other family member was found for evaluation. In respect to lesion location, the optic disc is the most common locality for the tumour and generally no decrease in vision is noted; however, as in the case presented here, decreased VA may occur due to direct macular involvement (Naftchi & la Cour 2002) or, particularly, as secondary to vitreous haemorrhage (Messmer et al. 1983). Optical coherence tomography was useful to reveal low reflectivity vesicular formations and focal regions of highly reflective signals, most likely corresponding to the red blood filled ‘cysts’ that, at least in part, lie in the plane of the inner retinal layers; additionally, no evidence of perilesional exudation was seen. These findings are consistent with a previous histopathological description of the entity, in which the tumour was composed of telangiectatic retinal vessels displaying anatomical features normally encountered in retinal vessels and mostly occupying the inner half of the retina (Messmer et al. 1984).

Ozone-induced cell death in tobacco cultivar Bel W3 plants. The role of programmed cell death in lesion formation.

Treatment of the ozone-sensitive tobacco (Nicotiana tabacum L. cv Bel W3) with an ozone pulse (150 nL L(-1) for 5 h) induced visible injury, which manifested 48 to 72 h from onset of ozone fumigation. The "classical" ozone symptoms in tobacco cv Bel W3 plants occur as sharply defined, dot-like lesions on the adaxial side of the leaf and result from the death of groups of palisade cells. We investigated whether this reaction had the features of a hypersensitive response like that which results from the incompatible plant-pathogen interaction. We detected an oxidative burst, the result of H2O2 accumulation at 12 h from the starting of fumigation. Ozone treatment induced deposition of autofluorescent compounds and callose 24 h from the start of treatment. Total phenolic content was also strongly stimulated at the 10th and 72nd h from starting fumigation, concomitant with an enhancement in phenylalanine ammonia-lyase a and phenylalanine ammonia-lyase b expression, as evaluated by reverse transcriptase-polymerase chain reaction. There was also a marked, but transient, increase in the mRNA level of pathogenesis-related-1a, a typical hypersensitive response marker. Overall, these results are evidence that ozone triggers a hypersensitive response in tobacco cv Bel W3 plants. We adopted four criteria for detecting programmed cell death in ozonated tobacco cv Bel W3 leaves: (a) early release of cytochrome c from mitochondria; (b) activation of protease; (c) DNA fragmentation by terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling of DNA 3'-OH groups; and (d) ultrastructural changes characteristic of programmed cell death, including chromatin condensation and blebbing of plasma membrane. We, therefore, provide evidence that ozone-induced oxidative stress triggers a cell death program in tobacco cv Bel W3.

Cutaneous Current Marks Due to a Stun Gun Injury

Histological changes of the skin following electrical injury with a stun gun have rarely been described. We report the case of a 61-year-old man who died after having been tortured with a stun gun during a robbery. At autopsy two reddish, dot-like lesions where found on the chest and histological examination revealed electric current-related changes. Only a few reports concerning micromorphological cutaneous changes following stun gun injury have been reported; therefore further investigations concerning the frequency and type of histological findings due to stun gun injuries will be necessary in order to provide sufficient characteristic data for a conclusive interpretation.

Chronische Granulomatöse Chorioretinitis bei Tuberkulose

Though the incidence of tuberculosis decreased substantially during the second half of the century, a steady increase of new cases has been observed within the last decade. Among other reasons, the growing number of immunodeficient patients (e.g. HIV, therapy with immunosuppressive agents) and migration from underdeveloped to industrial countries contribute to this finding. A 57-year-old male patient presented with a history of chronic bilateral chorioretinitis of unknown origin. During the last months a marked decrease in visual acuity of the left eye was noted. Prior diagnostic attempts had not led to a specific diagnosis. Notable was the history of long-term systemic corticosteroid therapy for chronic obstructive lung disease. Funduscopy of the right eye revealed a choroidal granuloma with adjacent serous retinal detachment. Both eyes showed multiple dot-like lesions in the retinal pigment epithelium of the posterior pole. Finally the diagnosis could be made by isolating Mycobacterium tuberculosis from sputum samples and gastric aspirate. Within a few weeks after starting tuberculostatic therapy the ocular symptoms regressed and the visual acuity improved significantly. Securing the diagnosis of tuberculous uveitis is often difficult. The differential diagnosis includes other granulomatous ocular inflammations. The detection of Mycobacterium tuberculosis and the clinical course make the diagnosis most likely. Tuberculosis should always be included in the differential diagnosis as a possible etiology for uveitis, particularly in those cases taking a chronic course. Despite the recent emergence of drug-resistant strains in most cases tuberculosis is a well curable disease.