The man suddenly had difficulty swallowing and was weak... It's the common drug that's causing the trouble!

What happens to a 59-year-old male patient who suddenly has symptoms such as speech, dysphagia and weakness in his right limb?patientsrecently had a history of pancreatic neuroendocrine tumor surgery, which has been treated for the past six weeks for meldonium and cyclopasis due to concurrent abdominal infectionspatients were admitted to hospital for "vague speech, difficulty swallowing and right limb weakness", and the examination found that the patient had moderate sound impairment, eye tremor, upper limb movement disorder and free dissonality gait, and no clinical eye muscle paralysis or brain disease was foundhad an MR test because he suspected he had a strokeFigure 1MRI brain (Figure 1, Figure 2)shows the symmetrical T2 weighted high signal of the two-sided toothcore (A, long arrow), the extended myelin back side (A, the long arrow), the vestibular nerve core (B, long arrow), the olive core (B, short arrow), the extended nerve core (B, arrow) and the top cover (C, arrow)No significant change sseen in the inside of the hypothalamus (D)
figure 4 DWI showed a high signal signal of the two-sided toothed nucleus and the upper olive nucleus
diagnosed with M.Mand clinical data as: mitanencephalitoThe diagnosis is based on neuroimaging and long-term history of the use of mitanolin, and other possible diseases are ruled outAfter the deactivation of methazole, the patient's neurological function defect sparsed gradually 1 methazoleenenen (MIE) metformin is a widely used and well-tolerated anti-anaerobic bacteria drug MIE is a rare disease with central nervous system toxicity, first reported in 1995, its incidence and potential mechanism is unclear some people speculate that the neurodysfunction is caused by the binding of metazole or its metabolites to neuronal RNA, while others believe that the free radicals formed in the neurotransmitters of catecholamines (such as norepinephrine and dopamine) and methanol are the root causes of neuronal damage there are no identified RISK factors for MIE Liver disease is reported to be the most common disease of the past in patients with MIE (15%) MIE is usually a combination of diabetes, hypertension, hyperlipidemia, and pancreatic neuroendocrine tumors Kim et al have shown that the cumulative dose range of mitanetin in patients affected by MIE is 21 to 135g, with a duration of 14 to 90 days The above patients took a total of 53g of mitanetin for more than 6 weeks before being diagnosed with MIE Clinical Performance: Most MIE patients develop cerebellum dysfunction, followed by mental changes and seizures The most common cerebellum signs are conjure disorders and sound-comtosis Mr Performance: Several radiological features of MIE are reported in the literature Two-sided symmetry T2-weighted high-signal lesions can be found in the cerebellum tooth core, middle brain, bridge back, back myelin and bolumna, but usually affect the toothed nucleus If the back of the brain bridge is affected, the lesions often occur in the fissotic nucleus, the vestibular nerve nucleus, and the upper olive nucleus The burden of the body is often in the pressure The location of T2-weighted high-signal lesions in the above patients was consistent with the distribution of the most frequently reported affected areas Prognosis: Most MIE patients have a good prognosis after discontinuing mitanetin Most patients experience either improved symptoms (29%) or made a full recovery (65%) and a small number had permanent cognitive impairment Patients with mental changes or seizures are more likely to make a full recovery than those with cerebellum dysfunction these patients had mild residual motor disorders in their last neurological assessment On the other hand, the continued use of methazole in MIE patients may lead to irreversible adverse consequences, with occasional reports of fatal sexual encephalopathy 2 differential diagnosis The main differential diagnosis to be considered is The Venik Encephalopathy, a disease caused by thiamine deficiency Clinical symptoms and radiology performance similar to MIE can be presented Clinical manifestations are described as classic triple sepsis of mental and consciousness disorders, comorbidities and palsy of the eye Typical imaging of Wernicke's encephalopathy is the two-sided symmetry T2-weighted high signal of gray matter around the nipple body, the inner thalamus, and the guide pipe, which is particularly special in MIE (Figure 5) However, atypical imaging manifestations similar to MIE can be seen in non-alcoholic patients They include t2-weighted signal abnormalities in the toothed nucleus, cerebellum, cerebral nerve nucleus, and the pressure of the argon body Figure 5 MRI shows the symmetry T2 weighted high signal of the inside (A) of the two-sided thalamus brain, gray matter (B) around the guide pipe, and the extended myelin back side (C) 6 dispersive weighted imaging high signals are found in the tail core (D), the hypothalamus nucleus (E), and the gray matter (F, characteristic "?" shape) The corresponding ADC low signal appears in the tail core, conforming to dispersion restriction (G), and the corresponding low ADC signal is not found in the inside of the thalamus brain or around the pipe 7 Intravenous contrast, the gray matter (J and K, long arrow), nipple body (J and L, short arrow), the inner thalamus (L, long arrow) and the top cover (L, arrow) are strengthened therefore, the identification between MIE and non-alcoholic Wernicke encephalopathy can be difficult, especially in patients with a history of gastrointestinal surgery and systemic infection, because they are both present with thiamin deficiency and the risk of treatment with methicillin fortunately, , atypical symptoms of non-alcoholic Vernik encephalopathy are usually associated with more specific typical symptoms Although the above patients considered the differential diagnosis of Venik encephalopathy, there are no symptoms such as obromitagia or mental and mental disorders that are noteworthy In addition, the lack of typical nipple body, inner hypothalamus and gray matter around the water mains is inconsistent with Wernicke's encephalopathy bromomethane poisoning It is a rare toxic encephalopathy whose imaging characteristics are very similar to MIE: a two-sided symmetry T2 weighted high signal is located on the cerebellum toothy nucleus, bridged back side of the brain, the extended myelin back side, the body pressure section and the brain nerve nucleus however, the above-mentioned patients have no history of exposure to fumigation or related industrial exposure multiple sclerosis myeloid diseases, such as multiple sclerosis, can show damage to the brain stem and the cerebellum However, lesions are usually asymmetric and do not selectively affect the brain nerve nucleus this type of disease can be seen around the ventricle, cortical, sub-screen and spinal cord T2 weighted high-signal lesions, active lesions showed restrictive diffusion and increased contrast Depending on the location of active lesions, there may be multiple forms of clinical seizures and different acute manifestations multifocal cerebral infarction its lesions are usually randomly distributed within the brain, there is evidence of limited diffusion, and the radiology results of our case are not consistent 3 summary
metastis is a commonly used antibiotic, and patients with long clinical histories can use high cumulative doses Mitanienenenenenenis is a rare but important subacute complication with characteristic MRI Two-sided symmetry T2-weighted high-signal lesions are mainly found in the cerebellum tooth core, middle brain, bridge brain back side, extended myelin back side and the body pressure early recognition of these imaging performance, timely discontinuation of drugs, can improve the prognosis, prevent irreversible nerve damage The main identification consideration is The Wenick encephalopathy, especially the non-alcoholic Wenick encephalopathy, which has atypical manifestations author: MaGic Source: