Hypoxic Ischemic Encephalopathy In Adults Radiology – dagorcraft what is anoxic encephalopathy

1 from the department of neuroradiology, national neuroscience institute, singapore (A.N.H., C.C.T.L.); department of diagnostic radiology, singapore general hospital.

International brain injury association – ibiahypoxic- ischemic brain injury is a diagnostic term that encompasses a complex constellation of pathophysiological and molecular injuries to the brain induced by hypoxia, ischemia, cytotoxicity, or combinations of these conditions (busl and greer 2. The typical causes of hypoxic- ischemic brain injury – cardiac arrest, respiratory arrest, near- drowning, near- hanging, and other forms of incomplete suffocation, carbon monoxide and other poisonous gas exposures, and perinatal asphyxia – expose the entire brain to potentially injurious reductions of oxygen (i.What is anoxic encephalopathy

although the concept of hypoxic- ischemic brain injury is generally well accepted in clinical medicine, there remains a lack of consistency with respect to the terms used to denote this type of injury, particularly in the neurorehabilitation literature (arciniegas 2. Anoxic brain injury,’ ‘anoxic brain damage,’ and ‘anoxic encephalopathy’ are the most commonly used clinical and research descriptors of this condition, and generally are used as synonyms for hypoxic- ischemic brain injury. However, these terms overstate the severity of one pathophysiologic contributor to injury – decreased delivery of oxygen to the brain, most accurately described as hypoxia rather than as anoxia – and ignore entirely the often concurrent and more injurious decrease in perfusion of the brain (i.What is anoxic encephalopathy with respect to the use of ‘anoxia’ in these diagnostic terms, true anoxia (frank absence of oxygen in the blood) is a rare and debatably survivable event: although complete cessation of respiratory function eliminates introduction of new oxygen into the circulatory system, oxygen remains available, albeit in rapidly diminishing quantities, in the blood for extraction and use by brain tissue for at least several minutes thereafter. With respect to the omission of ‘ischemic’ from these diagnostic terms, purely hypoxic injuries (i.

Greer 2. 00. 6; busl and greer 2. The term ‘anoxic encephalopathy’ is problematic for these reasons as well as the fact that it describes a consequence of injury, i.What is anoxic encephalopathy

Radiology cases and radiology case reports. Anonymous said. What i do not understood is in fact how you are not really much more neatly-liked than you may. Learn about encephalopathy, a term that means brain disease, damage, or malfunction. Learn about encephalopathy symptoms, treatment, and types. OBJECTIVE. Wernicke’s encephalopathy is an acute neurological syndrome resulting from thiamine (vitamin B1) deficiency. Early recognition is important because timely. B. Adults and children after fontanelle closure either transcranial spectral doppler sonography, power M-mode doppler sonography, or transcranial color-coded duplex. · perinatal hypoxic-ischemic encephalopathy (HIE) is an important cause of brain injury in the newborn and can result in long-term devastating consequences.What is anoxic encephalopathy

For these reasons, hypoxic- ischemic brain injury (HI- BI) more accurately and completely describes the pathophysiology of this subcategory of acquired brain injuries. HI- BI therefore is recommended for use over ‘anoxic brain injury’ or other variants of it as the term with which to deescribe such injuries in clinical and research contexts.

Hypoxic-ischemic brain injury most often results from insults such as cardiac arrest, vascular catastrophe, poisoning (such as carbon monoxide intoxication or drug.

Pathophysiology of hypoxic- ischemic brain injury. Diminutions in circulating oxygen levels may result from a failure of gas exchange in the lungs, decreases in blood- oxygen saturation from pulmonary dysfunction or interference by other gases (e.What is anoxic encephalopathy decreased perfusion of the brain occurs when blood flow to it is partially or completely restricted (e. These conditions deprive the brain not only of oxygen but also glucose and all other nutrients as well as the nutrient/waste exchange process required to support brain metabolism, resulting in the development of a hypoxic- ischemic state.

This state is characterized by cellular energy failure, membrane depolarization, brain edema, excess neurotransmitter release (particularly the excitatory amino acid neurotransmitters) and uptake inhibition, increases in intracellular calcium, production of oxygen- free radicals, lipid peroxidation, and disturbances in autoregulation of cerebral blood flow at the micro- and macroscopic levels (calvert and zhang 2.What is anoxic encephalopathy busl and greer 2. Hypoxic and hypoxic- ischemic states at least transiently disrupt brain function and, if sufficiently severe and/or prolonged, may lead to neuronal death and irreversible brain injury. It is important to acknowledge that the pathophysiologic processes occurring in HI- BI also are characteristic of the non- hemorrhagic forms of stroke. However, the term ‘stroke’ is generally used to denote injury resulting from focal or multifocal ischemia (i.

HI- BI denotes global (i. Having said that, not all areas of the brain are equally vulnerable to the injurious effects of hypoxia and hypoxia- ischemia: injury from these processes tends to be most pronounced in the superior brainstem, cerebellum, white matter and subcortical structures supplied by the distal branches of deep and superficial penetrating blood vessels, cerebral white matter at the zones between the major cerebral artery territories (so called ‘border zones’ or ‘watershed areas’), CA1 region of the hippocampus, and neocortical layers 3, 5, and 6 (injury to which produces ‘laminar cortical necrosis,’ referring to the death of cells in these layers, or lamina, in the cortex) (arbelaez, castillo et al.What is anoxic encephalopathy chalela, wolf et al. Busl and greer 2. Neurological and neurobehavioral consequences of hypoxic- ischemic brain injury.

ADA2. Adenosine deaminase 2. AHA 2008. American heart association guidelines 2008. AIS. Arterial ischemic stroke. CBP 2010. Canadian best practice guidelines 2010. Neurology articles covering symptoms, diagnosis, staging, treatment, prognosis, and follow-up. Peer reviewed and up-to-date recommendations written by leading experts.

The consequences of HI- BI commonly include seizures (event- related and recurrent), disturbances of sensorimotor function, and a broad array of cognitive, emotional, and behavioral disturbances (anderson and arciniegas 2. Lu- emerson and khot 2. Seizures and myoclonus.What is anoxic encephalopathy

As many as one- third of individuals sustaining an HI- BI develop seizures in the immediate post- injury period, typically beginning within 2. The development of such seizures most likely reflects the effects of injury- induced excitotoxic processes on cortical neurons. Most post- hypoxic seizures usually are partial complex or myoclonic in character and occur intermittently.

The occurrence of early seizures does not necessarily portend the development of post- hypoxic epilepsy or persistent post- hypoxic myoclonus nor does it invariably predict poor neurological or functional outcome. However, the post- hypoxic status epilepticus (SE) or myoclonic SE is associated, almost invariably, with a fatal outcome from the HI- BI (rossetti, logroscino et al.What is anoxic encephalopathy it is likely that mortality associated with SE is a reflection of the severity of underlying injury rather than the development of SE per se, although the possibility of SE aggravating the underlying neurological injury has not been definitively excluded. The frequency of late seizures after HI- BI is not well established, although common clinical experience suggests that a nontrivial minority of individuals experience this problem.

Treatment of post- hypoxic epilepsy and/or myoclonus follows that of other secondary epilepsies and myoclonus, and generally is similarly effective. Movement disorders. Post- hypoxic parkinsonism, dystonia, chorea, athetosis, and tremor are rare but potentially disabling consequences of HI- BI.What is anoxic encephalopathy among these problems, post- hypoxic parkinsonism and dystonia are most common. Post- hypoxic parkinsonism is generally symmetric and predominantly akinetic- rigid (i.

The development of this condition most likely reflects the vulnerability of the globus pallidus and the substantia nigra – pars reticularis to the adverse effects of hypoxia and/or ischemia. Post- hypoxic dystonia, which tends to reflect injury to the putamen, is often asymmetric initially but over time may progress to a more symmetric and generalized form. Although these conditions may develop in the early post- injury period, they often are delayed sequelae of HI- BI, developing months or years after injury. Unfortunately, these conditions appear less responsive to pharmacologic treatment than primary parkinsonism (i.What is anoxic encephalopathy parkinson’s disease) and idiopathic dystonia, perhaps reflecting hypoxic- ischemic- induced damage and/or destruction of the neurons in these structures that ordinarily are the targets of these pharmacotherapies. Disorders of elementary sensorimotor function. Injury to descending corticospinal tracts, whether in the deep white matter of the cerebral hemispheres, in the crus cerebri at the level of the midbrain, or in the spinal cord, may produce impairments of elementary motor function.

Involvement of the corticospinal tracts at the level of the cerebral hemispheres or upper brainstem may produce variable patterns and severities of motor weakness, up to and including quadriplegia. An uncommon but remarkable post- hypoxic motor syndrome is the ‘man in a barrel’ syndrome, or bibrachial paresis; this condition is characterized by bilateral proximal upper extremity paresis with preservation of lower extremity function, and reflects hypoxic- ischemic injury to the ‘watershed’ zone of white matter between the anterior and middle cerebral artery territories.What is anoxic encephalopathy similarly, paraparesis and quadriparesis are potential consequences of hypoxic- ischemic watershed infarctions in the upper and lower thoracic and lumbar regions of the spinal cord. Rehabilitative interventions for these problems, and complications of them such as spasticity, contractures, gait and mobility impairments, follow those applied for similar motor impairments due to other causes. The effectiveness of these motor- specific rehabilitative interventions in this population is not well established, but common clinical experience and several rehabilitation outcome studies (shah, al- adawi et al. Burke, shah et al. Shah, carayannopoulos et al.

HI- BI survivors with such problems. Watershed infarctions occurring the posterior portions of the cerebral hemispheres may produce disturbances in sensory function, and particularly impairments of visual processing.What is anoxic encephalopathy cortical blindness and the balint syndrome (comprised by ocular apraxia, optic ataxia, and simultanagnosia) are specific examples of disorders of sensory function that may be associated with HI- BI. Optimal rehabilitative strategies for these problems are not well developed presently. Cognitive impairment the most extensively studied neurobehavioral sequelae of HI- BI are cognitive impairments. Most common among these are the disorders of consciousness (e.

Balint’s syndrome (as noted above), anton’s syndrome (anosagnosia for visual impairment), personality changes, behavioral disturbances, and disorders of mood and affect regulation have been reported as well.

Neuroradiology cases: herpes encephalitis MRI.What is anoxic encephalopathy A 2. 9 yo married female brought unconscious to casualty with history of mild fever and headache since 3days. CT brain on admission was normal. Csf showed pleocytosis and elevated proteins.

Infarct ruled out as there is no intra cranial major vessel stenosis or occlusion on MR angio particularly the MCA. Herpes encephalitis. Syn : herpes simplex encephalitis (HSE) caused by herpes simplex virus type 1 (HSV- l).

Location wise typically involves limbic system in that commonly involves temporal lobes, insula, subfrontal area and cingulate gyri. May involve cerebral convexity and posterior occipital cortex. Often bilateral disease but asymmetric. Basal ganglia usually spared. Atypical patterns seen in infants and children where involvement of cerebral hemispheres noted primarily.What is anoxic encephalopathy rarely, may affect mid brain and pons.

Neuroimaging. CT often normal early. May see ill defined areas of low attenuation, mild mass effect in medial temporal lobes, insula. Hemorrhage is a late feature. Patchy or gyriform enhancement of temporal lobes on post contrast is a late feature. On MRI , areas of T2 hyper intensity with restricted diffusion on dw images. Mild, patchy enhancement on post contrast T1 early in disease. Gyriform enhancement is feature of late disease.

May see focal abnormal lepto meningeal enhancement. MR is most sensitive for diagnosis. FLAIR and DWI are the most sensitive sequences sufficient for diagnosis when patient is non co operative. Imaging is often key to diagnosis.What is anoxic encephalopathy

DDs. Limbic encephalitis. A rare paraneoplastic syndrome associated with a primary tumor, often lung.

Predilection for limbic system, often bilateral.- hemorrhage is not present. – imaging may be indistinguishable. Clinically sub acute course.

Symptom onset usually weeks to months (vs acute course, ‘short term’ history in HSE)ischemia : – typical vascular distribution (MCA, ACA, PCA)- acute onset. – restricted diffusion on dw images is more intense compared to herpes. Status epileptius: – active seizures may disrupt BBB, cause signal abnormalities and enhancement. – temporal lobe epilepsy hyperperfusion may mimic herpes encephalitis. Herpes viruses include HSV- l, HSV- 2, epstein- barr, cytomegalovirus (CMV), varicella- zoster virus (VZV), B virus, HSV- 6, HSV- 7. HSV- l infection is common in adults and children, typically related to viral reactivation where as HSV- 2 more common in neonates.What is anoxic encephalopathy initial HSV- l infection usually occurs in oronasopharynx through contact with infected secretions. HSV- l invades along cranial nerves (via lingual nerve, a division of the trigeminal nerve) to ganglia. HSV- l remains dormant in the trigeminal ganglion. HSV- l reactivation may occur spontaneously or be precipitated by various factors like local trauma, immunosuppression, hormonal fluctuations, emotional stress. HSV- l causes acute hemorrhagic, necrotizing encephalitis (primarily involving limbic system)HSV- l causes 9.

Herpes is most common nonepidemic cause of viral meningoencephalitis. Clinical presentation. Age : occurs at any age. Highest incidence in adolescents and young adults. Approximately 3.What is anoxic encephalopathy

Gender: no gender predominance. Most common signs/symptoms : fever, headache, seizures, +/- viral prodrome, other signs/symptoms : altered mental status, focal or diffuse neurologic deficit in less than 3. Children often present with nonspecific symptoms like behavioral changes, fever, headaches, seizures, even coma and death. Patients are typically immunocompetent. HSV- 1 is uncommon in AIDSCSF studies show a lymphocytic pleocytosis and elevated protein. Polymerase chain reaction (PCR) of CSF, most useful for diagnosis with sensitivity/specificity of 9.

EEG shows temporal lobe activity. Natural history prognosis: early diagnosis and treatment with antiviral agents can decrease mortality, may improve outcome.What is anoxic encephalopathy

Mortality ranges from 5. Despite acyclovir therapy, ~ 5. Treatment: antiviral therapy with intravenous acyclovir.