Multiple cerebral infarction linked to underlying cancer: a review of Trousseau syndrome-related cerebral infarction

2021 ◽  
pp. 1-7
Author(s):  
Chao Zhen ◽  
Yabo Wang ◽  
Haifeng Wang ◽  
Dongmei Li ◽  
Xin Wang
Keyword(s):  
Cerebral Infarction ◽  
Degradation Products ◽  
Early Recognition ◽  
Short Term ◽  
Arterial Embolism ◽  
Trousseau Syndrome ◽  
Appropriate Treatment ◽  
Multiple Cerebral Infarction ◽  
Arterial Thromboembolic Events ◽  
The Brain

Trousseau syndrome is a cancer-associated hypercoagulative state leading to venous or arterial thromboembolic events. Cerebral infarction is the most common result of arterial embolism and the pathogenesis is complicated, mainly associated with hypercoagulation and non-bacterial thrombotic endocarditis. On magnetic resonance imaging, multiple lesions are dispersed in more than two territories of the brain, often simultaneously involving the bilateral anterior and posterior circulation. Elevated plasma levels of D-dimer and fibrinogen degradation products may be seen in these patients. There are high rates of short-term recurrence of stroke and sudden death, highlighting the need for early recognition and appropriate treatment of Trousseau syndrome-associated cerebral infarction.

scholarly journals Thymoma associated paraneoplastic encephalitis (TAPE), a potential cause of limbic encephalitis

2019 ◽  
Vol 12 (8) ◽  
pp. e230709 ◽  
Author(s):  
Henry Liu ◽  
Randall S Edson
Keyword(s):  
Short Term Memory ◽  
Early Recognition ◽  
Autoimmune Encephalitis ◽  
Memory Deficits ◽  
Response To Therapy ◽  
Tumour Resection ◽  
Short Term ◽  
Paraneoplastic Encephalitis ◽  
Appropriate Treatment ◽  
Simplex Virus

A 59-year-old man presents with expressive aphasia and short term memory deficits. Shortly thereafter, he started developing staring spells and intermittent right hand spasms, preliminarily thought to be simple partial seizures. Subsequent MRI brain imaging was highly suggestive of herpes simplex virus (HSV) encephalitis; however, HSV PCR from cerebrospinal fluid was negative. On further testing, the patient was found to have an autoimmune encephalitis thought to be related to an incidentally found thymoma. His clinical presentation, in conjunction with imaging and response to therapy, was strongly suggestive of thymoma associated paraneoplastic encephalitis. Early recognition is the only way to ensure prompt initiation of appropriate treatment. Immunotherapy and cancer directed therapy (including tumour resection, if indicated) have been shown to have favourable outcomes, improved speed of neurological recovery and reduced risk of relapses. Without treatment, progressive neurologic deterioration can occur over months to years, eventually resulting in death.

scholarly journals Carbonic Anhydrase II Deficiency in a Saudi Woman

2015 ◽  
Vol 8 ◽  
pp. CCRep.S16897 ◽  
Author(s):  
Omar N. Alhuzaim ◽  
Ohoud M. Almohareb ◽  
Safiya M. Sherbeeni
Keyword(s):  
Carbonic Anhydrase ◽  
Dna Analysis ◽  
Early Recognition ◽  
Autosomal Recessive Disorder ◽  
Deficiency Syndrome ◽  
Sequence Variant ◽  
Appropriate Treatment ◽  
Carbonic Anhydrase Ii Deficiency ◽  
Renal Tubular ◽  
The Brain

Objective Carbonic anhydrase (CA) II deficiency is a rare autosomal recessive disorder caused by mutation in the CA II gene that leads to osteopetrosis, renal tubular acidosis (RTA), and cerebral calcification. Our aim is to present a patient with the classic triad of CA II deficiency syndrome to enhance the awareness about this rare syndrome. Methods We describe the clinical and radiological findings of a Saudi woman patient with CA II deficiency syndrome. Results A Saudi woman in her 20s presented to our hospital for evaluation of increased bone density. She was known to have delayed developmental milestone with growth retardation and poor scholastic performance. She had multiple fragile fractures started at the age of 15 involving the lower extremities. A physical examination revealed dysmorphic features and intellectual disability with intelligence quotient (IQ) of 36. The initial blood workup showed a picture of distal RTA with hypokalemia, and the radiological imaging confirmed the presence of osteopetrosis and multiple kidney stones. The combination of osteopetrosis with RTA raised the possibility of CA II deficiency. Therefore, computed tomography (CT) of the brain was done and showed intracranial calcification involving the basal ganglia. She was started on potassium chloride and sodium bicarbonate. In addition, she underwent right-sided percutaneous nephrolithotripsy. Her DNA analysis came to show a sequence variant c.232+1G>A, which was detected in both of the CA II genes (homozygous). Conclusion Early recognition of the disease is a key, as an early appropriate treatment institution is essential in order to prevent further complications.

Polychlorinated biphenyl induced hepatocyte alterations

1987 ◽  
Vol 45 ◽  
pp. 716-717
Author(s):  
D.N. Collins ◽  
J.N. Turner ◽  
K.O. Brosch ◽  
R.F. Seegal
Keyword(s):  
Lipid Droplets ◽  
Wistar Rats ◽  
Homovanillic Acid ◽  
Polychlorinated Biphenyl ◽  
Corn Oil ◽  
Environmental Pollutants ◽  
Short Term ◽  
Pcb Congeners ◽  
Urinary Levels ◽  
The Brain

Polychlorinated biphenyls (PCBs) are a ubiquitous class of environmental pollutants with toxic and hepatocellular effects, including accumulation of fat, proliferated smooth endoplasmic recticulum (SER), and concentric membrane arrays (CMAs) (1-3). The CMAs appear to be a membrane storage and degeneration organelle composed of a large number of concentric membrane layers usually surrounding one or more lipid droplets often with internalized membrane fragments (3). The present study documents liver alteration after a short term single dose exposure to PCBs with high chlorine content, and correlates them with reported animal weights and central nervous system (CNS) measures. In the brain PCB congeners were concentrated in particular regions (4) while catecholamine concentrations were decreased (4-6). Urinary levels of homovanillic acid a dopamine metabolite were evaluated (7).Wistar rats were gavaged with corn oil (6 controls), or with a 1:1 mixture of Aroclor 1254 and 1260 in corn oil at 500 or 1000 mg total PCB/kg (6 at each level).

Morphological Changes in the Brain of Acutely Ill and Weight-Recovered Patients with Anorexia Nervosa

2014 ◽  
Vol 42 (1) ◽  
pp. 7-18 ◽  
Author(s):  
Jochen Seitz ◽  
Katharina Bühren ◽  
Georg G. von Polier ◽  
Nicole Heussen ◽  
Beate Herpertz-Dahlmann ◽  
...  
Keyword(s):  
Anorexia Nervosa ◽  
Cognitive Deficits ◽  
Time Course ◽  
Morphological Changes ◽  
Meta Analysis ◽  
Short Term ◽  
Clinical Prognosis ◽  
Qualitative Review ◽  
Brain Changes ◽  
The Brain

Objective: Acute anorexia nervosa (AN) leads to reduced gray (GM) and white matter (WM) volume in the brain, which however improves again upon restoration of weight. Yet little is known about the extent and clinical correlates of these brain changes, nor do we know much about the time-course and completeness of their recovery. Methods: We conducted a meta-analysis and a qualitative review of all magnetic resonance imaging studies involving volume analyses of the brain in both acute and recovered AN. Results: We identified structural neuroimaging studies with a total of 214 acute AN patients and 177 weight-recovered AN patients. In acute AN, GM was reduced by 5.6% and WM by 3.8% compared to healthy controls (HC). Short-term weight recovery 2–5 months after admission resulted in restitution of about half of the GM aberrations and almost full WM recovery. After 2–8 years of remission GM and WM were nearly normalized, and differences to HC (GM: –1.0%, WM: –0.7%) were no longer significant, although small residual changes could not be ruled out. In the qualitative review some studies found GM volume loss to be associated with cognitive deficits and clinical prognosis. Conclusions: GM and WM were strongly reduced in acute AN. The completeness of brain volume rehabilitation remained equivocal.

scholarly journals Endocrine Dysfunction in Children with Zika-Related Microcephaly Who Were Born during the 2015 Epidemic in the State of Pernambuco, Brazil

Viruses ◽  
2020 ◽  
Vol 13 (1) ◽  
pp. 1
Author(s):  
Andréia Veras Gonçalves ◽  
Demócrito de B. Miranda-Filho ◽  
Líbia Cristina Rocha Vilela ◽  
Regina Coeli Ferreira Ramos ◽  
Thalia V. B. de Araújo ◽  
...  
Keyword(s):  
Optic Nerve ◽  
Viral Infections ◽  
Case Series ◽  
Optic Nerve Hypoplasia ◽  
Endocrine Dysfunction ◽  
Careful Monitoring ◽  
Early Puberty ◽  
Growth Impairment ◽  
Appropriate Treatment ◽  
The Brain

Congenital viral infections and the occurrence of septo-optic dysplasia, which is a combination of optic nerve hypoplasia, abnormal formation of structures along the midline of the brain, and pituitary hypofunction, support the biological plausibility of endocrine dysfunction in Zika-related microcephaly. In this case series we ascertained the presence and describe endocrine dysfunction in 30 children with severe Zika-related microcephaly from the MERG Pediatric Cohort, referred for endocrinological evaluation between February and August 2019. Of the 30 children, 97% had severe microcephaly. The average age at the endocrinological consultation was 41 months and 53% were female. The most frequently observed endocrine dysfunctions comprised short stature, hypothyroidism, obesity and variants early puberty. These dysfunctions occurred alone 57% or in combination 43%. We found optic nerve hypoplasia (6/21) and corpus callosum hypoplasia (20/21). Seizure crises were reported in 86% of the children. The most common—and clinically important—endocrine dysfunctions were pubertal dysfunctions, thyroid disease, growth impairment, and obesity. These dysfunctions require careful monitoring and signal the need for endocrinological evaluation in children with Zika-related microcephaly, in order to make early diagnoses and implement appropriate treatment when necessary.

scholarly journals Expression Analysis of Zinc Transporters in Nervous Tissue Cells Reveals Neuronal and Synaptic Localization of ZIP4

2021 ◽  
Vol 22 (9) ◽  
pp. 4511
Author(s):  
Chiara A. De Benedictis ◽  
Claudia Haffke ◽  
Simone Hagmeyer ◽  
Ann Katrin Sauer ◽  
Andreas M. Grabrucker
Keyword(s):  
Brain Function ◽  
Zinc Homeostasis ◽  
Zinc Transporters ◽  
Excitatory Synapses ◽  
Short Term ◽  
Synaptic Localization ◽  
Zinc Levels ◽  
Rat Astrocyte ◽  
Cellular Zinc ◽  
The Brain

In the last years, research has shown that zinc ions play an essential role in the physiology of brain function. Zinc acts as a potent neuromodulatory agent and signaling ions, regulating healthy brain development and the function of both neurons and glial cells. Therefore, the concentration of zinc within the brain and its cells is tightly controlled. Zinc transporters are key regulators of (extra-) cellular zinc levels, and deregulation of zinc homeostasis and zinc transporters has been associated with neurodegenerative and neuropsychiatric disorders. However, to date, the presence of specific family members and their subcellular localization within brain cells have not been investigated in detail. Here, we analyzed the expression of all zinc transporters (ZnTs) and Irt-like proteins (ZIPs) in the rat brain. We further used primary rat neurons and rat astrocyte cell lines to differentiate between the expression found in neurons or astrocytes or both. We identified ZIP4 expressed in astrocytes but significantly more so in neurons, a finding that has not been reported previously. In neurons, ZIP4 is localized to synapses and found in a complex with major postsynaptic scaffold proteins of excitatory synapses. Synaptic ZIP4 reacts to short-term fluctuations in local zinc levels. We conclude that ZIP4 may have a so-far undescribed functional role at excitatory postsynapses.

Superior Orbital Fissure Syndrome due to Sinusitis: Report of Two Cases

2005 ◽  
Vol 19 (4) ◽  
pp. 417-420 ◽  
Author(s):  
Fabio de Rezende Pinna ◽  
Daniel L. Dutra ◽  
Maura C. Neves ◽  
Fabrizio Ricci Romano ◽  
Richard L. Voegels ◽  
...  
Keyword(s):  
Early Recognition ◽  
Complete Recovery ◽  
Ocular Motility ◽  
Intravenous Antibiotic ◽  
Superior Orbital Fissure ◽  
Adequate Treatment ◽  
Superior Orbital Fissure Syndrome ◽  
Brain Involvement ◽  
The Brain ◽  
Anatomic Region

Background The potential morbidity and mortality of sphenoid sinus infectious processes are related to their proximity to vital structures within the orbit, such as the cavernous sinus and the brain. Involvement of the posterior orbit can result in superior orbital fissure syndrome, a rare entity affecting structures that cross this anatomic region. Early recognition of this syndrome is mandatory. Delays in adequate treatment may compromise the patient's prognosis. Methods We present two cases of incomplete superior orbital fissure syndrome due to infectious processes of the posterior ethmoid and sphenoid sinuses. Conclusions In our experience, endoscopic decompression of the lamina papyracea shows complete recovery of extrinsic ocular motility in these patients and should be combined with intravenous antibiotic therapy.

Changes of PACAP levels in the brain show gender differences following short-term water and food deprivation

2007 ◽  
Vol 152 (2-3) ◽  
pp. 225-230 ◽  
Author(s):  
P. Kiss ◽  
D. Reglődi ◽  
A. Tamás ◽  
A. Lubics ◽  
I. Lengvári ◽  
...  
Keyword(s):  
Gender Differences ◽  
Food Deprivation ◽  
Short Term ◽  
The Brain

Toluene-induced leukodystrophy from glue sniffing

2021 ◽  
pp. practneurol-2021-002942
Author(s):  
Yue Hui Lau ◽  
Ahmad Shahir Mawardi ◽  
Norzaini Rose Zain ◽  
Shanthi Viswanathan
Keyword(s):  
Basal Ganglia ◽  
Cognitive Decline ◽  
Early Recognition ◽  
Cerebellar Atrophy ◽  
Premature Mortality ◽  
History Of ◽  
The Brain

A 33-year-old man with a history of chronic toluene abuse through glue sniffing, developed tremors, cerebellar signs and cognitive decline. MR scan of the brain showed global cerebral and cerebellar atrophy with symmetrical T2-weighted hypointensities in the basal ganglia, thalami and midbrain. After stopping glue sniffing, his tremors, ataxia of gait, speech and cognition partially improved. Early recognition and intervention of toluene-induced leukodystrophy could prevent ongoing morbidity and premature mortality.

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