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PubMed1992

[Cervical root avulsion presenting proximal segmental muscular atrophy of unilateral upper extremity].

A 56-year-old woman noticed non-progressive weakness in the proximal part of the right upper extremity from her childhood. At the age of 37 years, she was diagnosed as "spinal muscular atrophy" by an orthopedic surgeon. At the age of 56, neurological examinations revealed muscular atrophy and weakness confined to the right deltoid, biceps brachii and brachioradialis together with minor sensory disturbance in the lateral side of the right shoulder and forearm without pyramidal sign in the lower extremities. The neurological features of this case differed from those of juvenile type of distal and segmental muscular atrophy of upper extremities in distribution of muscular atrophy, and simulated those of cervical spondylotic amyotrophy. Myelography demonstrated root avulsion of the right C5 and C6 roots. CT myelography revealed traumatic meningocele. Therefore a clinical diagnosis of cervical root avulsion resulting from unrecognized birth injury was made. The reason of motor dominant pictures of this case may be vulnerability of the anterior nerve roots to traction injury.

Arm↗

PubMed1992

[A case of malignant glioma associated with verbal recent memory disturbance due to left hippocampal atrophy; case report].

Verbal recent memory disturbance was observed in a patient with a malignant glioma associated with left hippocampal atrophy. A 25 year-old male was admitted because of seizures. CT scan and MRI showed enhanced mass lesions in the left temporal lobe associated with ipsilateral hippocampal atrophy. Neurological examination disclosed right homonymous hemianopsia, word amnesia, alexia, agraphia and acalculia. Neuropsychological examination disclosed verbal recent memory disturbance, which consisted of impaired recall of the precisely memorized words after some interruption. Although hippocampal lesions are known to be often associated with cerebrovascular disease, hippocampal atrophy due to brain tumor is quite unusual. This case suggested that the left hippocampus is closely related to verbal recent memory. Hippocampal atrophy in this case conceivably derived from the decreased arterial flow due to perifocal edema or obstructive hydrocephalus.

Adult↗

PubMedDate not supplied

Subdural hygroma versus atrophy on MR brain scans: "the cortical vein sign".

PURPOSE: To determine if the position of the superficial cerebral cortical veins can be used to distinguish subdural hygroma from atrophy on MR brain scans. METHODS: Retrospective review of MR scans obtained in cases of extracerebral fluid collections, separating these into two groups, ie, subdural hygroma or atrophy. FINDINGS: All cases of atrophy in this study showed cortical veins and their branches traversing widened cerebrospinal fluid spaces over the cerebral convexities. None of the subdural hygroma patients showed this finding. Cortical veins in hygroma patients were seen only at the margin of the displaced cortex, and did not traverse the fluid collections over the cerebral convexities. CONCLUSIONS: The authors call the visualization of cortical veins and their branches within fluid collections at the cerebral convexities "the cortical vein sign." They believe this sign to be prima facie evidence of atrophy; its presence rules out the diagnosis of subdural hygroma in the region of interest.

Atrophy↗

PubMedDate not supplied

[Cerebral atrophy in multiple sclerosis patients treated periodically with boluses of methylprednisolone].

INTRODUCTION: In the last years advances in the treatment of the remittant and secondary progressive forms of the multiple sclerosis (MS) have taken place. In the primary progressive forms (PP) the side effects of potentially useful drugs prevent their use; in some studies an improvement of the evolution with the intravenous administration of periodic pulses of methylprednisolone (MP) has been observed. OBJECTIVE: To evaluate if periodic pulses of intravenous MP injected every 4-6 weeks increase the degree of cerebral atrophy of the patients with PP MS. PATIENTS AND METHODS: We studied 11 patients with PP MS treated during 33 months with periodic pulses of intravenous MP. The degree of cerebral atrophy was evaluated in axial cuts of 10 mm of studies of magnetic resonance with the indices of Evans, bicaudate, bifrontal, frontal spears and bithalamic. The statistical evaluation of the results was made applying the test of Wilcoxon-Mann-Whitney. RESULTS: There are not statistically significant differences in the degree of cerebral atrophy with any of the used indices. CONCLUSIONS: Periodic pulses of intravenous MP do not accelerate the cerebral atrophy in patients with progressive forms of multiple sclerosis.

Adult↗

PubMed2003

[An autopsy case of multiple system atrophy with a heteroallelic ceruloplasmin gene mutation].

We reported a 69-year-old woman with multiple system atrophy (MSA), who had a heteroallelic missense mutation (G1874A, Gly-->Glu) in the exon 11 of the ceruloplasmin (Cp) gene. At the age of 64, she began to complain of progressive gait disturbance, which was resistant to anti-Parkinsonian drug treatment. Neurological examination revealed parkinsonism such as rigidity, akinesia, mild tremor and postural instability, accompanying saccadic eye movement, dysarthria, dysphagia, orthostatic hypotension and bladder disturbance. She showed neither cerebellar signs nor dementia. Serum Cp and copper concentrations were 13-18 mg/dl and 38-56 micrograms/dl, respectively, which were decreased to about a half of normal values. Brain MRIs revealed high intensity areas in the bilateral putamens in the T2-weighted image, and mild pontine base atrophy. She died of respiratory failure due to laryngeal paresis after five years from the onset. Neuropathological examination revealed brown-colored putamens, where there was severe neuronal cell loss with gliosis. Though atrophy of the pontine base was mild, transverse myelinated fibers were pale in Klüver-Barrera stain. There were Purkinje cell loss of moderate degree and appearance of torpedos in the cerebellum. Both silver staining and immunohistochemical staining to alpha-synuclein showed glial cytoplasmic inclusions, which were found predominantly in the putamens. These clinical features and neuropathological findings were compatible with multiple system atrophy (MSA). Iron staining of the brain revealed iron deposition in the putamens and the substantia nigra, but not in the pontine base nor in the cerebellum. Furthermore, we failed to reveal it in both the liver and the pancreas as well as the thalamus and the caudate nucleus, which were common sites of iron deposition in the previous cases of Cp gene mutation. We have already reported three other MSA cases with a- or hypo-ceruloplasminemia with similar clinical and pathological features to this case. One of them, in which gene analysis was also available, did not have any mutations in its Cp gene. Therefore, the gene mutation of this case may not be a direct cause to MSA, but the fact that the most cases of MSA with hypoceruloplasminemia showed striatonigral degeneration (SND) type implies some relationship between hypoceruloplasminemia and SND.

Aged↗

PubMed2004

Voxel based morphometry reveals a distinct pattern of frontal atrophy in progressive supranuclear palsy.

BACKGROUND: Frontal lobe atrophy is a well known neuropathological feature of progressive supranuclear palsy (PSP), accompanied by characteristic neuropsychological deficits. OBJECTIVE: To determine subregional frontal lobe atrophy patterns in patients with PSP using voxel based morphometry (VBM). METHODS: VBM is an observer unbiased volumetry which allows the investigation of the entire brain. An optimised protocol for normalisation, segmentation, and correction for volume changes in preprocessing was used. Grey matter, white matter, and cerebrospinal fluid (CSF) partitions in 12 patients with probable PSP were compared with 12 healthy controls matched for age and sex. RESULTS: In PSP patients, the following cortical areas were decreased in volume (p(corr)<0.05): the prefrontal cortex, predominantly the medial frontal gyri and a cluster in the left lateral middle frontal gyrus; the insular region including the frontal opercula; both supplementary motor areas; and the left medio-temporal area (V5). White matter comparisons revealed a volume reduction in both frontotemporal regions and the mesencephalon. Analysis of the CSF compartment showed no significant regional changes between the groups. CONCLUSIONS: Frontal atrophy in PSP predominantly involves mesio-frontal targets of striatal projections. This atrophy pattern probably accounts for cardinal PSP associated behavioural deficits.

Atrophy↗

PubMed2003

Smoking enhances age related brain atrophy--a quantitative study with computed tomography.

This is a prospective study done on Bangladeshi people during the period from January 1999 to December 2002. Cases were collected from the department of Medicine in Sir Salimullah Medical College, Dhaka; Sher-e-Bangla Medical College, Barisal and Bangabandhu Sheikh Mujib Medical University, Dhaka. We examined the chronic effect of smoking on brain atrophy quantitatively with Computed Tomography (CT). Study was performed on 219 smokers and same numbers of non-smokers from 40 to 70 years old with neither neurological nor focal abnormality in brain CT. Brain atrophy index (BAI) which was a quantitative marker of brain atrophy reported previously, was calculated from each brain CT. Smokers showed a significant increase in BAI compared to non-smokers in groups 50-54 years (p<0.01), 55-59 years (p<0.01), 60-64 years (p<0.05) and 65-70 years (p<0.05). It was suggested that age-related brain atrophy was increased by chronic smoking through advanced atherosclerosis.

Adult↗

PubMedDate not supplied

Regular hemodialysis reverses gastric mucosal atrophy of patients with chronic renal failure.

BACKGROUND/AIMS: Gastric mucosa of patients with chronic renal failure on regular hemodialysis is known to retain fundic glands relatively intact, but no evidence for regeneration of fundic glands by hemodialysis has been provided to date. This study was performed to investigate endoscopically and histopathologically if hemodialysis to treat renal failure would regenerate the background gastric mucosa and to elucidate factors associated with the mucosal regeneration. METHODOLOGY: First, the relationship between duration of hemodialysis and the degree of atrophy of the background gastric mucosa was investigated in patients with chronic renal failure treated and not treated by hemodialysis. Treated patients were further divided into long-term group treated for 4 years or longer and short-term group treated for shorter than 4 years. The degree of atrophy of gastric mucosa was evaluated by hematoxylin-eosin staining, PAS-alucian blue staining and immunohistochemical staining to detect Ki-67 expression using biopsy specimens obtained from gastric mucosa. The labeling index is the proportion of positively labeled cells with respect to the total number of cells. The proliferative index was calculated by multiplying the labeling index and the proliferative zone (length of the area between the uppermost and lowest labeled cells). Serum gastrin, glucagon and cholecystokinin were assayed as well as urine epidermal growth factor to elucidate factors associated with regeneration of gastric mucosa. Helicobacter pylori infection was examined by ELISA. RESULTS: In the long-term group, the degree of atrophy of gastric mucosa was endoscopically evaluated to be C1 type. In both of the two hemodialysis groups, endoscopically identified fundic gland region was histologically confirmed to be fundic glands by both hematoxylin-eosin staining and PAS-alucian blue staining. Epithelial cell proliferative index was significantly higher in long-term and short-term hemodialysis group than non-hemodialysis group (P=0.0001). No significant difference in serum gastrin, glucagon and cholecystokinin as well as urine epidermal growth factor was detectable among the three groups. Most patients of both hemodialysis groups were H. pylori-negative. CONCLUSIONS: A possibility of regeneration of the background gastric mucosa in proportion to the duration of hemodialysis was suggested on the basis of histopathological evidence. The observed regeneration of gastric mucosa was ascribable to elimination of factors associated with atrophy of gastric mucosa including H. pylori by hemodialysis.

Aged↗

PubMed2004

[Secondary glaucoma due to progressive iris atrophy--a century after the first description. Case report].

The iridocorneal endothelial syndrome (ICE) consists of some disorders, like: progressive essential iris atrophy, Chandler disease and the iris nevus syndrome that are characterized by corneal endothelium proliferation and migration, iris atrophy, corneal oedema and/or pigmentary iris nevi. Secondary, refractory glaucoma affects about 50% of patients with progressive essential iris atrophy. Medication of glaucoma is only initially effective. Some conventional filtering surgeries, to control glaucoma are often unsuccessful. Presented case of our patient with primary essential iris atrophy, with secondary glaucoma shows surgical problems. Multiple filtration surgery with or without antiproliferative agents turn out not to be sufficient. In conclusion, intraocular pressure was effectively lowered with iridocleisis technique.

Adult↗

PubMed2002

Cognitive impairment in dementia: correlations with atrophy and cerebrovascular disease quantified by magnetic resonance imaging.

This project assessed the contributions of atrophy and cerebrovascular disease (CVD) to cognitive impairment in dementia. Ten individuals with clinically diagnosed pure VaD were age-, sex-, and education-matched to individuals with AD. All participants underwent neuropsychological testing and MRI which were processed to generate quantitative indices of atrophy and CVD. A linear regression, including thalamic lesion and vCSF volumes, predicted cognitive status (R2 = .74; p < .0005). Three VaD subgroups were identified: thalamic lesion (n = 4), hippocampal infarcts (n = 3), and other (n = 3). In participants without thalamic lesion, vCSF predicted general cognition (R2 = .48), hippocampal atrophy predicted memory impairment (R2 = .33), and white matter lesions predicted executive dysfunction (R2 = .48). Both atrophy and CVD burden correlated highly with cognitive impairment and should be simultaneously assessed in studies of brain-behaviour relations in dementia.

Alzheimer Disease↗

PubMed1992

[Hereditary dentatorubropallidoluysian atrophy--clinical variants in a family and degeneration of cerebral white matter in a proband].

We describe a family with hereditary dentatorubropallidoluysian atrophy (DRPLA). 4 patients through 3 successive generations showed a wide clinical variety. The female proband with onset in the elderly developed choreiform involuntary movement, dementia, hyperreflexia and, at the progressive stage, mild ataxia. However she had never displayed epilepsy and myoclonus. The 2 sons showed dementia, choreoathetoid movement and ataxia. The grandson developed typical signs and symptoms of progressive myoclonus epilepsy. The brain CT in the proband showed severe cerebellar and brain stem atrophy, moderate cerebral cortical atrophy and diffuse low density lesions in the deep cerebral white matter. Her neuropathological examination revealed the atrophy and gliosis of cerebral and cerebellar white matter concomitant with both dentatorubral and pallidoluysian system degeneration. The present study indicates that hereditary DRPLA can include multiple clinical variants even in the same family and the degeneration of cerebral and cerebellar white matter besides dentatorubral and pallidoluysian system.

Adolescent↗

PubMed2004

[Clinical study of 83 cases with spinal muscular atrophy in children].

OBJECTIVE: Spinal muscular atrophy (SMA) is a common autosomal recessive disorder and represents one of the most common genetic causes of death in childhood. The last 10 years have seen major advances in the field of SMA, but no curative treatment is available so far. This study aimed to analyze the clinical characteristics of SMA, improve the clinical diagnosis of SMA, and explore the importance of gene diagnosis and prenatal diagnosis of SMA by gene deletion analysis. METHODS: Totally 83 cases with SMA including 55 males and 28 females were enrolled in this study. The age was between 1 day and 14 years (average 23.7 months). The clinical characteristics and changes of electromyography were assessed in all cases. The muscular biopsy was performed in 2 of 83 cases. The deletion of survival of motor neuron gene (SMN) was detected by PCR and restriction endonuclease spectrum analysis in 13 of 83 cases. RESULTS: The 83 cases were subdivided into three clinical groups based on age of onset of symptom, age at death and achievement of certain motor milestone, 60 cases with type I, 19 cases with type II and 4 cases with type III. They were all characterized by symmetric muscle weakness (more proximal than distal) associated with atrophy, absence or marked decrease of deep tendon reflexes. Electromyographic studies showed a pattern of denervation with neither sensory involvement nor marked decrease of motor nerve conduction velocities in all cases. Muscle biopsy provided evidence of skeletal muscle denervation with groups of atrophy in 2 cases. The SMN detection revealed deletion of exon 7 and exon 8 in 11 of 13 cases, only lacking exon 7 in 1 of 13 cases and lacking exon 8 in 1 of 13 cases. CONCLUSION: SMA is characterized by degeneration of lower motor neuron associated with muscle paralysis and atrophy. The definite diagnosis of SMA will rely on the typical clinical characteristics, changes of electromyogram and muscle biopsy and gene deletion analysis. Gene diagnosis of SMA can provide a basis for prenatal diagnosis which is of great importance in preventing SMA.

Adolescent↗

PubMed1992

Expression of human ornithine aminotransferase (OAT) in OAT-deficient Chinese hamster ovary cells and fibroblasts of gyrate atrophy patient.

Gyrate atrophy is a hereditary chorioretinal degenerative disease caused by a deficiency of the mitochondrial enzyme, ornithine aminotransferase (OAT). Recent investigations have demonstrated the molecular genetic defects of OAT in gyrate atrophy patients. We constructed a eukaryotic expression vector (pcDHOAT) which contains the SV40 promoter and human OAT cDNA. We used OAT(-) Chinese hamster ovary (CHO) cells, which have negligible OAT activity, and fibroblasts from a gyrate atrophy patient (GA35 cell), which have negligible OAT mRNA and enzyme. Incorporation of pcDHOAT and synthesis of human OAT mRNAs and active enzyme were demonstrated in both cell types. The level of expression of human OAT was low in the GA35 cells in comparison to the CHO cells. Despite the limited success, the ability to express active OAT in these OAT-deficient cells using an expression vector offers possibilities of replacement gene therapy for gyrate atrophy.

Animals↗

PubMed1991

[Study on argyrophilic inclusions of multisystem atrophy (Oppenheimer)].

UNLABELLED: Non-hereditary olivo-ponto-cerebellar atrophy (OPCA) and striato-nigral degeneration (SND) have been looked upon as a single disease entity called multisystem atrophy (MSA) by Oppenheimer. This study revealed that both intracytoplasmic argyrophilic inclusions (AI) in pontine neurons and glial (argyrophilic) cytoplasmic inclusions (GCIs) widely distributed in the CNS are characteristics of MSA. MATERIALS: a) 12 cases with MSA, b) 16 cases with autosomal dominant (AD) form of spinocerebellar degeneration (SCD): AD form of OPCA 5 cases, Joseph disease 4 cases, AD-dentatorubropallidoluysian atrophy (Naitoh & Oyanagi's form) 6 cases, AD-spastic ataxia (Brown) 1 case, c) 4 cases with autosomal recessive (AR) form of SCD: AR form of OPCA 1 case, myoclonic epilepsy with ragged-red fibers (MERRF) 1 case, complicated form of spastic paraplegia 2 cases, d) 6 cases with non-hereditary SCD including intoxications: late cortical cerebellar atrophy 1 case, alcoholic cerebellar degeneration 2 cases, phenytoin-induced cerebellar degeneration 1 case, neuroleptic malignant syndrome 1 case, and e) 27 cases with other neuropsychiatric diseases: Alzheimer disease 20 cases, progressive supranuclear palsy 5 cases, schizophrenia 2 cases. METHOD: We examined 10 mu-thick paraffin sections stained with HE, Klüver-Barrera, Bodian, Holzer, Gallyas, and Bielschowski methods. RESULTS: AI in pontine neurons were found only in two cases of MSA. Interestingly no AI could be detected even in cases with AD form of OPCA showing mild degeneration in the pontocerebellar system. On the other hand, GCIs were found in all cases with MSA irrespective of the degree of degeneration in the olivo-ponto-cerebellar or striato-nigral system. However, there was no GCIs in cases with other form of SCD and other neuropsychiatric diseases. Gallyas stain was the best method for detecting GCIs. GCIs were widely distributed in the CNS except for superficial layers of the cerebral cortex, the cerebellar cortex, and the dorsal column of the spinal cord. There were also many GCIs in the putamen, pontine base, and cerebellar white matter, even though these sites were well preserved.

Alzheimer Disease↗

PubMed2006

Hypometabolism exceeds atrophy in presymptomatic early-onset familial Alzheimer's disease.

UNLABELLED: The aim of the present study is to compare brain atrophy with hypometabolism as preclinical markers of Alzheimer's disease (AD) by studying presymptomatic individuals from families with known early-onset autosomal dominant AD (FAD) carrying mutations in the Presenilin 1 gene. METHODS: Seven asymptomatic at-risk FAD individuals (age, 35-49 y; 4 women; education >/= 12 y) and 7 matched healthy control subjects received complete clinical, neuropsychologic, MRI, and (18)F-FDG PET examinations. Regions of interest (ROIs: whole brain [WB], hippocampus [Hip], entorhinal cortex [EC], posterior cingulate cortex [PCC], inferior parietal lobule [IPL], and superior temporal gyrus (STG]) were drawn on the MRI scans of all subjects and used to measure volumes on MRI and glucose metabolism (MRglc) from the MRI-coregistered, atrophy-corrected PET scans. RESULTS: Compared with controls and after correcting for head size, MRI volume reductions in FAD subjects were restricted to the IPL (18%, P < 0.02). After atrophy correction and adjusting for pons MRglc, PET MRglc reductions were found in all FAD subjects compared with controls in the WB (13%), bilaterally in the IPL (17%) and in the STG (12%), and in the left EC (21%), PCC (20%), and Hip (12%) (P values < 0.05). PET MRglc measurements were consistently less variable than MRI measures, yielding significantly larger effect sizes in separating FAD from controls. CONCLUSION: Presymptomatic FAD individuals show widespread MRglc reductions consistent with the typical AD PET pattern in the relative absence of structural brain atrophy. These data further suggest that PET MRglc measures may serve as biomarkers for the preclinical diagnosis of AD.

Adult↗

PubMed1991

Activation of the ubiquitin-ATP-dependent proteolytic system in skeletal muscle during fasting and denervation atrophy.

The rapid atrophy of skeletal muscles upon fasting or denervation is due largely to an increased rate of protein breakdown. Blocking the lysosomal or the Ca(2+)-dependent pathways did not prevent increased proteolysis in muscles from fasted animals or following denervation. In contrast, upon food deprivation, the nonlysosomal ATP-dependent process increased by 150-350%. After refeeding, this process returned to control levels by 24 h. Similarly, within one day after denervation of the soleus, proteolysis increased by 50-250%. By contrast, the residual energy-independent process did not change in fasting or denervation. Because the ATP-dependent process might involve activation of the ubiquitin-ATP-dependent pathway, we measured the levels of mRNA for ubiquitin [Ub] in the atrophying muscles. After food deprivation, the levels of polyUb transcripts increased 2- to 4-fold in the soleus and extensor digitorum longus (EDL) muscles, and returned to control levels within 1 day of refeeding. After denervation of the soleus, a 2- to 3-fold increase in polyUb mRNA also occurred within 1 day. The muscle content of ubiquitinated protein also changed in parallel with Ub mRNA levels under these conditions. Thus, polyUb genes appear to be selectively induced in atrophying muscle, and levels of Ub mRNA and ubiquitin-protein conjugates change coordinately with the rate of ATP-dependent proteolysis. These data suggest that in atrophying muscle the ATP-Ub-dependent system plays an important physiological role in the degradation of the bulk of cell proteins.

Adenosine Triphosphate↗

PubMed1991

[A new type of complicated form of hereditary spastic paraplegia showing mental deterioration, quadriplegia with muscular atrophy, sensory disturbance, extrapyramidal disorders, and epilepsy].

UNLABELLED: This study proposes a new type of complicated form of hereditary spastic paraplegia (HSP) and some problems on a clinico-pathological classification of HSP. The present study includes three male and two female patients from two families (A and B). In the family A, four siblings (two males and two females) were affected. Spastic paraplegia developed as an initial symptom. In the family B, a man was affected with spastic paraplegia which had started at the age of eleven. His two half-sisters are normal. All parents in two pedigrees are healthy. The parents in the family B are first cousins. CLINICAL FEATURES: Their physical development was normal, but all of them showed mild mental retardation. Gait disturbance due to spastic paraplegia and mental deterioration developed at the age of high teens. At the age of high 20's, they became unable to walk, because of progressive spastic paraplegia and other complicated neurological impairments including pyramidal disorders in the upper limbs, generalized neurogenic muscular atrophy, sensory disturbance and bradykinesia. Some cases showed rigidity and/or spasticity. At the age of high 30's, they became bed-ridden, because of quadriplegia with generalized muscular atrophy. Three cases in the family A suffered from convulsions which started at the high 30's. Mild athetoid movement in the face and neck was observed in three cases in the family A. All patients became apathetic and indifferent at least by the age of 40. Laboratory findings and data: CT scan yielded brain atrophy and dilatation of the lateral ventricles, atrophy of the corpus callosum and hyperostosis of the cranium.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1991

Atrophie blanche. A clinicopathological study of 27 patients.

Twenty seven patients (8 males and 19 females) with atrophie blanche were observed in the past 7-years. The mean age at onset was 32 years (ranging from 23 years to 57 years) and 19 years (ranging from 11 years to 36 years) for male and female patient, respectively. The mean disease duration was 2.5 years (ranging from 2 months to 16 years) prior to their consultation. Sixty-three percent of them had summer exacerbation. Four patients had essential cryoglobulinemia, one of whom also developed bilateral iliofemoral artery stenosis one year later. Twelve patients also manifested concurrent purpura pigmentosa chronica (PPC)-like lesions. The observation of the natural course and clinical morphology, being divided into white atrophy-predominant and ulcer-predominant type, led to the impression that atrophie blanche and livedo vasculitis are synonyms with the same disease spectrum. Furthermore, white atrophy is not ulcer scars but lesions de novo suggesting dermal vasculopathy. An attempt was made to explain the uniqueness of clinical morphology. First line treatment included local wound care, bed rest and low-dose aspirin plus dipyridamole. Thirteen patients responded to these treatment either at the first attack or the recurrent episodes. Heparin (5000 units subcutaneous injection once daily) was effective for control of intractable painful ulceration in active stage in 70% of the remaining patients.

Adolescent↗