scholarly journals Chronic Neurological Disease Due to Methylmercury Poisoning

Author(s):  
Alan C. Jackson

AbstractOrganic mercury, especially methylmercury, poisoning causes chronic neurological disease predominantly affecting the brain. There have been documented exposures from eating fish from contaminated waters in Japan and in northwestern Ontario and in Iraq from eating bread made from seed wheat treated with methylmercuric fungicide. The neurological disease is called Minamata disease in Japan. Visual field constriction due to involvement of the calcarine cortex, sensory disturbance due to involvement of the somatosensory cortex, and cerebellar ataxia due to involvement of granule cell neurons of the cerebellum are common and characteristic features due to methylmercury poisoning. Other neurological features include dysarthria, postural and action tremor, cognitive impairment, and hearing loss and dysequilibrium. In contrast, peripheral nerve disease is more characteristic of inorganic mercury intoxication. Similarly, psychosis is more typical of exposure to inorganic mercury, which has been documented in the felt hat industry (“mad hatter”). Laboratory tests (e.g., on blood and hair and toenail samples) are of limited value in the assessment of chronic neurological disease due to mercury poisoning because they may not reflect remote neuronal injury due to mercury. Methylmercury also causes injury to fetal brains during development. There is no effective treatment.

2020 ◽  
Vol 3 (1) ◽  
pp. 51-53
Author(s):  
Rano Azizova ◽  
◽  
Umida Shamsiyeva ◽  
Mirzohid Turabbayev ◽  
Begzod Jorayev ◽  
...  

Traumatic brain disease (TBHD) is a pathological process triggered by the damaging effect of mechanical energy on the brain and is characterized — with a variety of clinical forms — by the unity of etiology, pathogenetic and sanogenetic mechanisms of development and outcomes.


1986 ◽  
Vol 71 (6) ◽  
pp. 749-753 ◽  
Author(s):  
J. E. Maddison ◽  
D. Yau ◽  
P. Stewart ◽  
G. C. Farrell

1. Cerebrospinal fluid (CSF) γ-aminobutyric acid (GABA) levels were measured in a dog model of spontaneous chronic portosystemic encephalopathy. 2. Dogs with congenital portacaval shunts (intra- or extra-hepatic) develop neurological features of abnormal psychomotor behaviour and depressed consciousness that are consistent with the symptoms of chronic portosystemic encephalopathy in humans. In the five dogs studied, plasma ammonia was elevated, as was CSF tryptophan, both usual biochemical abnormalities in portosystemic encephalopathy. 3. CSF levels of GABA in five dogs with portosystemic encephalopathy (100 ± 13 pmol/ml) were not significantly different from those in five control dogs (96 ± 14 pmol/ml). CSF levels of GABA were not altered after ammonia infusion. 4. If enhanced GABA-ergic neurotransmission, due to influx of gut-derived GABA into the brain, is responsible for the pathophysiology of chronic portosystemic encephalopathy in this model, it is not reflected by increased levels of GABA in CSF.


Author(s):  
Oliver Cousins ◽  
Angela Hodges ◽  
Julia Schubert ◽  
Mattia Veronese ◽  
Federico Turkheimer ◽  
...  

Open Biology ◽  
2018 ◽  
Vol 8 (7) ◽  
pp. 180074 ◽  
Author(s):  
Gabriela O. Bodea ◽  
Eleanor G. Z. McKelvey ◽  
Geoffrey J. Faulkner

Over the past decade, major discoveries in retrotransposon biology have depicted the neural genome as a dynamic structure during life. In particular, the retrotransposon LINE-1 (L1) has been shown to be transcribed and mobilized in the brain. Retrotransposition in the developing brain, as well as during adult neurogenesis, provides a milieu in which neural diversity can arise. Dysregulation of retrotransposon activity may also contribute to neurological disease. Here, we review recent reports of retrotransposon activity in the brain, and discuss the temporal nature of retrotransposition and its regulation in neural cells in response to stimuli. We also put forward hypotheses regarding the significance of retrotransposons for brain development and neurological function, and consider the potential implications of this phenomenon for neuropsychiatric and neurodegenerative conditions.


2009 ◽  
Vol 169 (5) ◽  
pp. 625-628 ◽  
Author(s):  
Nilgun Erkek ◽  
Saliha Senel ◽  
Avni Sarac ◽  
Ulker Ertan ◽  
Can Demir Karacan

2021 ◽  
Vol 12 (6) ◽  
pp. 118-121
Author(s):  
Ricky Suryamin ◽  
Subagia Santosa Sudjono

Porencephaly is a very unique rare neurological disease identified by the presence of single or multiple cerebrospinal fluid (CSF) cyst inside the brain matter. This is an intra-cranial cyst that rarely occurs in adults. The diagnosis depends on a well-defined CSF fluid space-occupying lesion (SOL) that communicates with the ventricles on a CT scan or MRI of the brain. Cerebral damage during labor or as unknown trauma during infancy can present with porencephaly much later in life. This might be the aftermath of trauma, ischemic, infection or bleeding in the postnatal life. These cysts may be mild enough to show any symptoms or severe enough to cause mental and physical disability. Here we present a case of a 76-year-old female attended in the emergency department with loss of strength in her right arm, four days ago. Porencephaly in adult is a rare neurological disease case. In this case, porencephaly caused by stroke ischemic 4 years ago due to anterior carotid artery embolism.


Author(s):  
G.D. Perkin ◽  
M.R. Johnson

Case History—A 33 yr old woman, known to have epilepsy, now presenting with odd behaviour. An epileptic seizure is a transient occurrence of signs and/or symptoms due to abnormal excessive or synchronous neuronal activity in the brain. Epilepsy is defined as a disorder of the brain characterized by an enduring predisposition to generate epileptic seizures and by the neurobiological, cognitive, psychological, and social consequences of this condition. The definition of epilepsy requires the occurrence of at least one epileptic seizure and evidence for an enduring alteration in the brain that increases the likelihood of future seizures such as an ‘epileptiform’ EEG abnormality, an appropriate lesion on structural brain imaging (CT or MRI), or the presence of recurrent (two or more) seizures. Epilepsy is a common, serious neurological disease, with prevalence 1% and a cumulative lifetime risk of 5%....


2017 ◽  
Vol 08 (01) ◽  
pp. 135-138 ◽  
Author(s):  
Prerna Garg ◽  
Muthusubramanian Rajasekaran ◽  
Salil Pandey ◽  
Gnanashanmugam Gurusamy ◽  
Devanand Balalakshmoji ◽  
...  

ABSTRACTNeuromyelitisoptica (NMO) and multiple sclerosis (MS) were once considered to be differing manifestation of same auto immune disease, NMO predominantly involving the optic nerve and cord. Now with discovery of NMO antibody the concept has changed and a spectrum of disorders with lesions in brain has been identified. Occasionally, brain may be the first or the only site of involvement in these disorders hence it is essential to be aware of this spectrum. The brain lesions in NMO/NMOSD may be located in characteristic regions and present with symptoms mimicking non neurological disease. We herein present a case of an adult female who was admitted with intractable vomiting and hiccups; subsequently on MRI brain found to have very tiny demyelinating foci in Area Postrema.


1985 ◽  
Vol 4 (6) ◽  
pp. 637-642 ◽  
Author(s):  
T. Aoi ◽  
T. Higuchi ◽  
R. Kidokoro ◽  
R. Fukumura ◽  
A. Yagi ◽  
...  

1 Energy dispersive X-ray analysis was performed on the renal tubular cells of two patients with inorganic mercury intoxication. 2 Some lysosomes of these cells consisted of unusual matrices of aggregated electron-dense grains which were positive for mercury, selenium and sulphur. 3 Though maps of the specific X-rays of both mercury and selenium coincided exactly with these lysosomes, the molecular ratio of selenium to mercury ranged between zero and 2.9. 4 It is unlikely that the trace element of selenium and exogenous inorganic mercury are deposited in the lysosomes independent of each other, but rather their coexistence in the characteristic lysosomes strongly suggests a compound formed by binding mercury to the SeH residues of selenoprotein.


Sign in / Sign up

Export Citation Format

Share Document