Rationale:Delayed post-hypoxic leukoencephalopathy(DPHL)is usually an overlooked condition,which arises as a result of a multitude of reversible and irreversible conditions.Patient’s Concern:A 50-year-old female with...Rationale:Delayed post-hypoxic leukoencephalopathy(DPHL)is usually an overlooked condition,which arises as a result of a multitude of reversible and irreversible conditions.Patient’s Concern:A 50-year-old female with a history of epilepsy,who developed DPHL 12 days after respiratory failure secondary to barbiturate toxicity.Diagnosis:DPHL on magnetic resonance imaging of the brain.Interventions:Mechanical ventilation was initiated for respiratory failure and hemodialysis for barbiturate toxicity.Outcomes:The patient developed akinetic mutism due to infirmity and had a residual disability,which led to permanent dependency.Lessons:The diagnosis of DPHL is often delayed or missed,given the rarity of this condition and its inconsistent clinical symptomatology.Diagnostic delay can be avoided by early recognition of the classical“delayed onset”symptoms.展开更多
Objective:To describe the clinical fea-tures of delayed post-hypoxic leukoencephalopathy after smoke inhalation from dry burning.Methods:We col-lected the clinical history and examination data of a pa-tient who presen...Objective:To describe the clinical fea-tures of delayed post-hypoxic leukoencephalopathy after smoke inhalation from dry burning.Methods:We col-lected the clinical history and examination data of a pa-tient who presented with delayed post-hypoxic leukoen-cephalopathy due to smoke poisoning.Results:Patients exposed to heavy smoke from dry burning carbonization can develop delayed post-hypoxic leukoencephalopathy.Conclusion:Delayed post-hypoxic leukoencephalopa-thy after smoke poisoning during cooking is rare.Fam-ily should bring patients to a hospital as soon as possi-ble when observing abnormal neurologic symptoms after smoke inhalation to prevent irreversible damage to the brain.展开更多
Chronic post-hypoxic myoclonus,also known as Lance-Adams syndrome(LAS),is a rare complication of successful cardiopulmanry resuscitation often accompanied by action myoclonus and cerebellar ataxia.It is seen in patien...Chronic post-hypoxic myoclonus,also known as Lance-Adams syndrome(LAS),is a rare complication of successful cardiopulmanry resuscitation often accompanied by action myoclonus and cerebellar ataxia.It is seen in patients who have un-dergone a cardiorespiratory arrest,regained consciousness afterwards,and then developed myoclonus days or weeks after the event.Worldwide,122 cases have been reported in the literature so far,including 1 case of Chinese.Here we report 2 Chinese LAS patients with detailed neuroimagings.Cranial single photon emission computed tomography(SPECT)of patient 1,a 52-year-old woman,showed a mild hypoperfusion in her left temporal lobe,whereas patient 2,a 54-year-old woman,manifested a mild bilateral decrease of glucose metabolism in the frontal lobes and a mild to moderate decrease of the N-acetyl aspartate(NAA)peak in the bilateral hippocampi by cranial[18F]-fluorodeoxyglucose positron emission tomographic(PET)scan and cranial magnetic resonance spectroscopy(MRS),respectively.We also review the literature on the neuroimaging,pathogenesis,and treatment of LAS.展开更多
文摘Rationale:Delayed post-hypoxic leukoencephalopathy(DPHL)is usually an overlooked condition,which arises as a result of a multitude of reversible and irreversible conditions.Patient’s Concern:A 50-year-old female with a history of epilepsy,who developed DPHL 12 days after respiratory failure secondary to barbiturate toxicity.Diagnosis:DPHL on magnetic resonance imaging of the brain.Interventions:Mechanical ventilation was initiated for respiratory failure and hemodialysis for barbiturate toxicity.Outcomes:The patient developed akinetic mutism due to infirmity and had a residual disability,which led to permanent dependency.Lessons:The diagnosis of DPHL is often delayed or missed,given the rarity of this condition and its inconsistent clinical symptomatology.Diagnostic delay can be avoided by early recognition of the classical“delayed onset”symptoms.
文摘Objective:To describe the clinical fea-tures of delayed post-hypoxic leukoencephalopathy after smoke inhalation from dry burning.Methods:We col-lected the clinical history and examination data of a pa-tient who presented with delayed post-hypoxic leukoen-cephalopathy due to smoke poisoning.Results:Patients exposed to heavy smoke from dry burning carbonization can develop delayed post-hypoxic leukoencephalopathy.Conclusion:Delayed post-hypoxic leukoencephalopa-thy after smoke poisoning during cooking is rare.Fam-ily should bring patients to a hospital as soon as possi-ble when observing abnormal neurologic symptoms after smoke inhalation to prevent irreversible damage to the brain.
基金the National Natural Science Foundation of China(No.30600193)the Youth Talent Special Fund of the Health Bureau of Zhejiang Province,China(No.2004QN012)the Health Bureau of Zhejiang Province,China(Nos.2000A114 and 2007A100)
文摘Chronic post-hypoxic myoclonus,also known as Lance-Adams syndrome(LAS),is a rare complication of successful cardiopulmanry resuscitation often accompanied by action myoclonus and cerebellar ataxia.It is seen in patients who have un-dergone a cardiorespiratory arrest,regained consciousness afterwards,and then developed myoclonus days or weeks after the event.Worldwide,122 cases have been reported in the literature so far,including 1 case of Chinese.Here we report 2 Chinese LAS patients with detailed neuroimagings.Cranial single photon emission computed tomography(SPECT)of patient 1,a 52-year-old woman,showed a mild hypoperfusion in her left temporal lobe,whereas patient 2,a 54-year-old woman,manifested a mild bilateral decrease of glucose metabolism in the frontal lobes and a mild to moderate decrease of the N-acetyl aspartate(NAA)peak in the bilateral hippocampi by cranial[18F]-fluorodeoxyglucose positron emission tomographic(PET)scan and cranial magnetic resonance spectroscopy(MRS),respectively.We also review the literature on the neuroimaging,pathogenesis,and treatment of LAS.
