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Query: UMLS:C0030552 (paresis)
 5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cerebral malaria (CM) is the most severe manifestation of human malaria yet is still poorly understood. Mouse models have been developed to address the subject. However, their relevance to mimic human pathogenesis is largely debated. Here we study an alternative cerebral malaria model with an experimental Plasmodium berghei Keyberg 173 (K173) infection in Sprague Dawley rats. As in Human, not all infected subjects showed cerebral malaria, with 45% of the rats exhibiting Experimental Cerebral Malaria (ECM) symptoms while the majority (55%) of the remaining rats developed severe anemia and hyperparasitemia (NoECM). These results allow, within the same population, a comparison of the noxious effects of the infection between ECM and severe malaria without ECM. Among the ECM rats, 77.8% died between day 5 and day 12 post-infection, while the remaining rats were spontaneously cured of neurological signs within 24-48 hours. The clinical ECM signs observed were paresis quickly evolving to limb paralysis, global paralysis associated with respiratory distress, and coma. The red blood cell (RBC) count remained normal but a drastic decrease of platelet count and an increase of white blood cell numbers were noted. ECM rats also showed a decrease of glucose and total CO2 levels and an increase of creatinine levels compared to control rats or rats with no ECM. Assessment of the blood-brain barrier revealed loss of integrity, and interestingly histopathological analysis highlighted cyto-adherence and sequestration of infected RBCs in brain vessels from ECM rats only. Overall, this ECM rat model showed numerous clinical and histopathological features similar to Human CM and appears to be a promising model to achieve further understanding the CM pathophysiology in Humans and to evaluate the activity of specific antimalarial drugs in avoiding/limiting cerebral damages from malaria.
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PMID:Young Sprague Dawley rats infected by Plasmodium berghei: A relevant experimental model to study cerebral malaria. 2874 9

The Fahr syndrome (FS) is a rare degenerative neurological disorder (its prevalence is <0.5%). FS is distinguished by the presence of abnormal bilateral intracranial calcifications with a predilection for the basal ganglia, also presented by movement disorders such as parkinsonism, paresis, and speech disorders. Chronic subdural hematoma (CSH), which is typically the result of mild head trauma, is a regularly encountered condition in elderly. A 63-year-old man has referred to our clinic from another hospital with a history of mild head trauma approximately a month ago. At the time of admission, the patient's Glasgow Coma Scale point was 15 points. In the history, there was only mild ataxia and right-sided hemiparesis. The laboratory examination revealed no electrolytes level abnormalities and normal endocrinal test examinations. Computed tomography revealed bilateral calcifications of basal ganglia, dentate nuclei which were misinterpreted as intracerebral contusion; with CSH of left temporal and parietal region. The hematoma was evacuated by burr-hole drainage. The patient was discharged 5 days after the surgery. The pathophysiology of FS is still unrevealed. There are some suggestions such as secondary to local disturbance of blood-brain barrier or a calcium neuronal metabolism disorder. However, on the other hand, local blood-brain barrier disturbance would also take part in CSH pathology. We hypostasized that patients with the history of FS, who had mild head traumas, might prone to subdural collections. On the other hand, FS and CSH coexistence is very unusual. Neurosurgeons might keep in mind FS when bilateral calcifications are seen in a patient.
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PMID:Chronic Subdural Hematoma Associated with Fahr Syndrome: A Clinical Association or Just a Simple Coincidence? 2949 31

Wernicke encephalopathy (WE) is a neurological emergency that develops in the setting of thiamine deficiency, and is characterised by symptoms of confusion, ophthalmoplegia and gait ataxia. Less recognised signs and symptoms include vestibular dysfunction, hearing impairment, peripheral neuropathy, and in severe cases, coma. This case study describes a non-alcoholic patient, who presents with significant auditory and vestibular changes in addition to the classic symptoms of WE. This case report describes a non-alcoholic patient who developed deafness, severe horizontal canal paresis and symptoms of palinacousis in the setting of WE as a complication of a recent gastric sleeve operation.
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PMID:Wernicke encephalopathy hearing loss and palinacousis. 3118 20

Bilateral middle cerebral artery occlusion is a very rare and dangerous pathology, accounting for less than 1% of stroke presentations. Unless treated, the natural course of the disease leads to coma or death and thus is extremely important to be detected early and managed appropriately. We present the case of a 69-year-old lady who woke with right-sided weakness and was found to have a left middle cerebral artery stroke on arrival to her local hospital, which progressed to bilateral paresis and dysarthria whilst on transfer to a tertiary hospital for definitive management. The patient underwent emergent mechanical thrombectomy of bilateral middle cerebral artery occlusions and made a complete recovery. This case emphasis the importance of the early recognition of rare bilateral middle cerebral artery occlusions and demonstrates that timely and effective treatment can have favorable outcomes for patients.
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PMID:Bilateral middle cerebral artery occlusions: Case report detailing successful treatment with timely mechanical thrombectomy. 3205 60

We report diffusion tensor tractography (DTT) of the corticospinal tract (CST) in a patient with paresis of all four limbs following subarachnoid hemorrhage (SAH) with intraventricular hemorrhage (IVH) after the rupture of an anterior communicating artery (ACoA) aneurysm rupture. The 73-year-old female was admitted to our emergency room in a semi-comatose mental state. After coil embolization-an acute SAH treatment-she was transferred to our rehabilitation department with motor weakness development, two weeks after SAH. Upon admission, she was alert but she complained of motor weakness (upper limbs: MRC 3/5, and lower limbs: MRC 1/5). Four weeks after onset, DTT showed that the bilateral CSTs failed to reach the cerebral cortex. The left CST demonstrated a wide spread of fibers within the corona radiata as well as significantly lower tract volume (TV) and higher fractional anisotropy (FA) as well as mean diffusivity (MD) compared to the controls. On the other hand, the right CST shifted to the posterior region at the corona radiata, and MD values of the right CST were significantly higher when compared to the controls. Changes in both CSTs were attributed to vasogenic edema and compression caused by untreated hydrocephalus. We demonstrate in this case, two different pathophysiological entitles, contributing to this patient's motor weakness after SAH.
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PMID:Injury of Corticospinal Tract in a Patient with Subarachnoid Hemorrhage as Determined by Diffusion Tensor Tractography: A Case Report. 3220 57

We experienced a case of an accidental infantile acute subdural hematoma caused by household minor head trauma(Nakamura type I intracranial hemorrhage)with postoperative hemispheric hypodensity lesion(Big Black Brain)whose pathophysiology was analyzed using perfusion MRI. A ten-month-old boy was admitted to our hospital in a comatose state. His mother revealed that the boy suffered a fall from a sofa bed. A CT scan indicated massive acute subdural hematoma in the left cerebral hemisphere. Emergency craniotomy and hematoma evacuation were performed. On postoperative day 3, CT revealed hemispheric hypodensity, and the boy suffered from status epilepticus. MRI on the following day showed widespread white matter hyperintensity in diffusion-weighted images, and MRA demonstrated dilation of the middle cerebral artery. Perfusion MRI using the dynamic susceptibility contrast method revealed a marked increase in cerebral blood flow in the left hemisphere. These abnormal MRI and MRA findings disappeared on postoperative day 13. Status epilepticus also improved upon administration of multi-antiepileptic drugs. Fundoscopy findings on postoperative day 3 showed small bilateral petechial or brush retinal hemorrhages. However, whole-body examination did not show any problems, and was consistent with the mother's account. Thus, we judged non-abusive head trauma. Although follow-up MRI showed diffuse atrophy of the left cerebral hemisphere, the boy aged well without obvious paresis or verbal developmental delay as judged by a follow-up more than a year later. Based on these results, we speculated that hyperperfusion caused by dilation of the cerebral artery was related to the postoperative hemispheric hypodensity, namely "Big Black Brain".
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PMID:[Surgical Case of Accidental Infantile Acute Subdural Hematoma Caused by Household Minor Head Trauma:Hyperperfusion during Postoperative Hemispheric Hypodensity, Namely "Big Black Brain"]. 3293 13


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